3rd Yr Surgery - by S. Das - Sixth Edition (1) - 196-1237

!'■!■■' ' . • ' , ■ ■.
A CONCISE
TEXTBOOK
OF
SURGERY
A CONCISE
Somen Das
M.B.B.S. (Cal.), ER.C.S. (Eng. & Edin.)
Senior Consnltant Surgeon
AUTHOR OF
A MANUAL ON CLINICAL SURGERY,
A CONCISE TEXTBOOK OF SURGERY,
A TEXTBOOK ON SURGICAL SHORT CASES,
A PRACTICAL GUIDE TO OPERATIVE SURGERY
&
UNDERGRADUATE FRACTURES & ORTHOPAEDICS.
SIXTH EDITION
KOLKATA
2010
All Rights Reserved
This book or any part thereof must not be reproduced in any form
without the written permission of the author, DR. S. DAS.
Copyright © DR. S. DAS.
First Edition ......................................... June, 1994
Second Edition ............................ September, 1999

Reprinted - August, 2000
Third Edition ........................................ June, 2001

Reprinted - September, 2002
Reprinted - August, 2003
Reprinted - April, 2004
Reprinted - May, 2005
Fourth Edition ................................February, 2006

Reprinted - July, 2006
Reprinted - January, 2007
Reprinted - July, 2007
Fifth Edition .......................................March, 2008

Reprinted - October, 2008
Reprinted - March, 2009
Sixth Edition .......................................... July, 2010
US $ 27.00 Rs. 778.00

ISBN-978-81-905681-2-8
Published by
Dr. S. Das.
13, Old Mayors' Court,
Kolkata - 700005.
INDIA
Email - drsdaslOO@rediffmail.com
Website : http://www.surgerybooksbydrsdas.com
in this profession and I have consulted many books and various established global journals.
I must acknowledge with thanks the masters of Surgery including my late father from whom I have
learnt this subject and technique of writing a textbook, all my patients who have offered themselves to be
photographed and repeated examinations, all my students whose questions made me think and showed me
the way to write this book and lastly my colleagues who have encouraged me in this work. I owe a deep
debt of gratitude to vast number of students and young teachers from all comers of Indian subcontinent
who had requested me and even pressed me to write a comprehensive textbook which they felt absence
of. In fact it is only for them I could venture and complete this task. If this book helps the great mass of
medical students to learn the basis of Surgery, I shall consider that it has done its job.
This book is fully dedicated to the memory of my late father Dr. K. Das, FRCS (Eng. & Edin.).
He, I believe, does not require any introduction. He was a doyen among surgeons with towering stature,
professional excellence and academic brilliance. His legendary personality will always be remembered by
the future generation. He also cherished the desire to write a Textbook of Surgery. But his health did not
permit. How better can one pay tribute to this great teacher of Surgery than to dedicate this Textbook
to his memory by fulfilling his ambition. This book is dedicated to commemorate his 25th death anniversary
(12th January, 1993). I tried my best to bring out this book in 1993, but the Type Setters, Processors and
Printers did not lend their support, so I was late in publishing this book.
June, 1994. S. DAS.

13, Old Mayors’ Court,
Calcutta - 700 005.
Preface To The Sixth Edition
It is a pleasure to acknowledge my sense of gratitude to the teaching faculty and the students
of the Indian Subcontinent, who have widely accepted, appreciated and recommended this book.
This book is now an accepted Textbook in major teaching institutions of this country. It has
transcended other Foreign Textbooks in terms of sales and popularity. This has definitely encouraged
me to bring out this edition.
Surgery is advancing very fast. This edition mirrors the important changes which have taken
place recently. This book provides an update for the students both the undergraduate and the
postgraduate. The trend is now towards minimal access surgery, it has gone upto needlescopic
laparoscopy and the scope and application of these are discussed in almost all the chapters. I have
always averted altercations and only accepted facts have been enumerated. I have not shown any
interest to embellish this edition with coloured photographs as these are more ornamental and do
not always help the students to understand their implications.
The success of this book reflects the wide appeal of its presentation of the fundamentals of
surgical practice in a direct and concise way. Editing a warmly accepted book is more of a challenge
which I am well aware of and it may be assured that an honest attempt has been made. All the
chapters have been updated and recent advances are included. What I have not changed is the basic
idea — that one should have a clear conception of this subject based on Anatomy, Physiology and
Pathology to know the symptoms and signs of surgical diseases and their respective treatment in the
present scenerio. To let the readers know about the primary intention of this book, I have not
reprieved preface to the first edition.
Now standard radiology has largely been replaced by Ultrasound Scanning, Computerised
Axial Tomography and Radioisotope Scanning. Nuclear Magnetic Resonance is now increasingly
used to get improved quality of imaging. So more space has been provided for these investigations
in this edition. Without surgical anatomy and physiology no chapter of a Surgical Text can be
complete and I have provided adequate emphasis on these sections.
I again thankfully acknowledge the inspiration received from my colleagues and the students
to bring out this edition. I am grateful to the patients who voluntarily submitted themselves to the
trouble of being photographed. I am obliged to the great mass of students who made me feel the
dearth of a proper book on this subject and their difficulties to understand this subject. My sincere
thanks to the DTP composer, processor and printer on whom depend the quality of production of
this treatise.
My obeisance to the stalwarts of this field without whose contributions surgery would not have
progressed to this level.
13, Old Mayors’Court, S. DAS.

Kolkata - 700 005.
July, 2010.
A CONCISE
TEXTBOOK OF SURGERY
DEDICATED
TO THE MEMORY OF MY FATHER
Late Dr. K. Das, F.R.C.S. (Eng. & Edin.)
Whose blessings have only made thtis venture possible
&
TO THE MEMORY OF MY MOTHER
Late Mrs. Gitanjali Das
Who had always inspired me during my father’s absence to achieve this goal.
Preface To The First Edition
While I was a medical student, I felt dearth of a
single comprehensive textbook in Surgery which could
provide all the informations an undergraduate should know
to become a full-fledged doctor. My friends also shared
the same idea. Most textbooks of Surgery originate from
the West and present whimsical and often desultory
approach to the subject. These authors deal with certain
topics of their interests in great depth while leave other
topics which are not of their interest though of similar
importance, if not more, to the students. So being
constantly insisted and hard pressed by my beloved
colleagues and students, I ultimately ventured to write a
Textbook on Surgery, which should be complete,
comprehensive and exam-oriented. My intention has been
to write in a clear, concise and easily understandable way,
in my own style keeping always a vigilant watch to the
students’ interest. I was never keen in providing numerous
illustrations in this treatise, as I had already submitted a
total of more than 1,500 illustrations in my other three well-established books —- ‘A Manual On Clinical
Surgery’, ‘A Practical Guide To Operative Surgery’ and ‘A Textbook On Surgical Short Cases’. I did not
want to repeat my illustrations from these books. In this text I have included more than 400 illustrations,
which I think will help the students in understanding the subject.
This book is primarily intended for the undergraduate, though I believe it should prove useful to
those aspiring for diploma and postgraduate degrees in Surgery. In each chapter I have included a section
of Embryology and Surgical Anatomy to help the students to understand Surgery. Reasoned explanation
based on Physiology and Pathology has been included in each chapter to explain the symptoms, signs and
treatment.
Surgery has been full of exciting developments in last few decades. I have tried to include these
developments without increasing the bulk of the book. I have tried to cover all aspects of Surgery with
same depth. The various sophisticated investigations which are now available in developing countries like
ours have made the diagnosis simpler and faster, though these investigations are more expensive and often
inaccessible to the remote health centres. These investigations like Ultrasound, Computed Tomography
(CT), Magnetic Resonance Imaging (MRI), Radionuclides are all discussed with reasonable depth and
illustrations but without unnecessary details to increase the bulk of the book. Thus all relevant and up-
to-date materials have been included in a pertinent and precise manner emphasizing the common surgical
problems which a student must know to become graduate and ultimately a successful clinician. Covering
the whole field of Surgery has been my intention with particular emphasis on those which are required for
examinations both undergraduate and postgraduate. In treatment my approach has been rational and I have
mentioned only those which are accepted and left those which are still in the experimental stage. I could
not resist myself in including a few very update topics like Laparoscopic Cholecystectomy, Extracorporeal
Shock Wave Lithotripsy (ESWL) etc. though these seem to be less important from undergraduate examinatio
point of view, yet it may quench the thirst of a few inquisitive students. Although surgery is becoming
increasingly specialised and fragmented, yet all surgeons must be exposed in the beginning to the widest
possible spectrum of surgical practice, and here lies the importance of this type of text which cannot be
ignored in years to come.
In preparing a textbook like this, I have freely utilised the knowledge and experience of the stalwarts
Contents
CHAPTER_______________________________________________________________________PAGE
1. WOUND HEALING ..... 1
2. SHOCK ..... 11
3. FLUID, ELECTROLYTE AND ACID-BASE BALANCE ..... 24
4. HAEMORRHAGE, HAEMOSTASIS AND BLOOD TRANSFUSION ..... 42
5. NUTRITION (INCLUDING PARENTERAL NUTRITION) .... 56
6. BURNS ..... 61
7. BOIL, ABSCESS, CARBUNCLE, CELLULITIS AND ERYSIPELAS ..... 77
8. SPECIAL INFECTIONS ..... 86
9. CYSTS ..... 94
10. COMMON TUMOURS AND MISCELLANEOUS LESIONS OF THE SKIN ..... 102
11. ULCERS, SINUS AND FISTULA ..... 156
12. TETANUS ..... 169
13. GAS GANGRENE ..... 174
14. SKIN GRAFTING ..... 178
15. DISEASES OF ARTERIES ..... 187
16. DISEASES OF VEINS ..... 256
17. DISEASES OF THE LYMPHATIC SYSTEM ..... 286
18. THE PERIPHERAL NERVES ..... 312
19. AMPUTATION ..... 337
20. THE HAND ..... 349
21. THE FOOT ..... 371
22. THE SPINE AND PELVIS ..... 387
23. THE HEAD ..... 420
24. SWELLINGS OF THE JAW ..... 448
25. MOUTH, TONGUE AND LIPS ..... 461
26. CLEFT LIP AND CLEFT PALATE ..... 479
27. SALIVARY GLANDS ..... 485
28. THE NECK ..... 501
29. THE THYROID AND PARATHYROIDS ..... 526
30. THE ADRENAL GLANDS ..... 561
31. THE BREAST ..... 573
32. INJURIES OF THE CHEST ..... 621
33. DISEASES OF THE CHEST (INCLUDING THE MEDIASTINUM AND
THE DIAPHRAGM) .... 632
34. THE HEART AND PERICARDIUM .... 657
35. THE OESOPHAGUS ..... 676
36. THE STOMACH AND DUODENUM ..... 708
37. THE LIVER AND PORTAL HYPERTENSION .... 758
CHAPTER PAGE
38. THE BILIARY SYSTEM 786

39. THE SPLEEN 821
40. THE PANCREAS 836
41. THE SMAL^ INTESTINE 869
42. INTESTINAL OBSTRUCTION 880
43. THE PERITONEUM, OMENTUM AND MESENTERY 893
44. THE VERMIFORM APPENDIX 904
45. THE COLON 917
46. THE RECTUM AND ANAL CANAL 949
47. UMBILICUS AND ABDOMINAL WALL 988
48. HERNIAS 995
49. THE KIDNEY AND URETER 1031
50. THE URINARY BLADDER 1105
51. THE PROSTATE AND URETHRA 1137
52. TESTIS, EPIDIDYMIS AND SCROTUM 1173
53. THE PENIS 1204
INDEX 1217
CHAPTER
DISEASES OF
ARTERIES
ARTERIAL OCCLUSION
Arterial stenosis or occlusion is a common arterial disease which is mainly caused by
atherosclerosis, emboli or trauma. In various places the symptoms produced by arterial occlusion
are different e.g. in lower limb it causes intermittent claudication, rest pain and gangrene. In
the heart it causes angina pectoris and myocardial infarction. In the brain it causes transient
ischaemic attacks and hemiplegia. In the kidney it causes hypertension. In the intestine it causes
abdominal pain and infarction.
Arterial occlusion is of two types — chronic arterial occlusion and acute arterial occlusion.
CHRONIC ARTERIAL OCCLUSION

AETIOLOGY AND PATHOLOGY.—
1. ATHEROMA.— By far the main cause of chronic arterial occlusion is atheroma. This
disease characteristically affects the large systemic arteries like the aorta and its main branches.
Although coronary and cerebral vessels are also commonly involved. Two types of atheroma
are seen —
Type I. Yellow plaques in the tunica intima.— In the subendothelial layer foam cells accumulate
and later breakdown to release fatty material into the intima, thus yellow plaques or fatty streaks
are formed. This type of pathology is not much concerned in narrowing of the arterial lumen,
but it more often causes weakening of the wall to cause dilatation or aneurysm formation.
Type II. Accumulation of fatty material in the intima with additional fibrosis.— This is more
common type and is seen in the middle and old age individuals. It is often called atherosclerosis
and causes varying degrees of arterial occlusion. The lesion is composed of a central mass of
fatty, yellow porridge-like material which consists predominantly of cholesterol and its esters
and is surrounded by dense fibrous tissue which gives it a white pearly appearance. In advanced
cases ulceration may be superadded resulting in thrombosis. The fatty material also subsequently
undergoes dystrophic calcification, which may be seen on straight X-ray.
Aetiology of this atheroma is not very clearly known, but there are theories which are almost
acceptable.
(a) In human beings atheroma is common in a few conditions accompanied by
hypercholesterolaemia e.g. hereditary hypercholesterolaemia, myxoedematous subjects, diabetics
etc.
(b) Nowadays it is held that cholesterol in the blood is not solely responsible, but it is
mainly the p-lipoprotein (which include cholesterol), which is concerned in the formation of
atheroma.
The P-lipoproteins are absorbed into the intimal layer especially in areas of endothelial
damage due to stress. Once the P-lipoprotein is in the intima, it splits up into cholesterol and its
188 A CONCISE TEXTBOOK OF SURGERY
esters which are retained, whereas the other lipid components e.g. phospholipids are rapidly
removed. Normally the cholesterol is kept in solution by phospholipids. As phospholipids have
been removed, accumulation of cholesterol in the intima causes' the fibrous tissue reaction which
leads to atheroma formation.
It should be remembered that unsaturated fat of vegetable origin lowers the blood cholesterol
level. Similarly oestrogens lower the blood cholesterol level and may explain the lower incidence
of atheroma in females.
2. TRAUMATIC.— Injury to the arterial walls by fractures, adjacent missiles or continuous
rubbing may cause thrombosis formation and also narrowing of the arterial wall to cause arterial
occlusion.
Other rare causes are —
3. INFECTIVE.— Arterial damage may occur by acute inflammatory lesion in the vicinity.
These are mainly seen in small arteries. Similarly in chronic infective diseases, it may produce
endarteritis obliterans to cause thrombosis and narrowing of the vessels. This was previously seen
in cases of syphilis. But nowadays this is uncommon and sometimes seen in the arteries in the
wall of the tuberculous cavity in the lung.
4. THROMBOANGIITIS OBLITERANCE (BUERGER’S DISEASE).— See page 219.
5. RAYNAUD’S DISEASE.— See page 210.
6. POLYARTERITIS NODOSA.
7. GIANT-CELL ARTERITIS.
CLINICAL MANIFESTATIONS of chronic: arterial occlusion.—
SYMPTOMS.— PAIN is the key symptom of arterial occlusion irrespective of its site. A
careful history has to be taken regarding its mode of onset, its location, distribution and its
character. When arterial occlusion develops over longer periods of time, ischaemia is not manifested
until the demand is increased with exercise.
INTERMITTENT CLAUDICATION.— 'Claudio' means 'I limp'. Intermittent claudication is
the most common complaint of the limb due to chronic arterial occlusion. In this condition pain
is experienced during exertion and gradually disappears within minutes upon cessation of activity.
Such pain is a cramp-like pain felt in the muscles. The group of muscles which will be affected
by this pain depends on the site of arterial occlusion. This pain is due to accumulation of excessive
P substances in the muscle which are not absorbed properly due to inadequate blood supply. As
mentioned just now the pain is felt in a group of muscles and which group will be involved
depends on the site of arterial occlusion. As for example in case of aortoiliac obstruction,,
claudication is felt in both buttocks, thighs and calves. In case of iliac obstruction claudication is
felt in the thigh and calf of the same side. In case of femoropopliteal obstruction unilateral
claudication is felt in the calf. In case of Buerger's disease where the arterial occlusion is mostly
in the lower tibial or plantar arteries, claudication is felt in the foot.
On careful enquiry the patient often complains that after walking a distance, which is called
the 'claudication distance’, the pain starts. If the patient continues to walk the metabolites increase
the muscle blood flow and may sweep away the P substances produced by exercise and pain
disappears (grade I). More often the pain continues and the patient can still walk with effort
(grade II). But mostly the pain compels the patient to take rest (grade III, Boyd's classification).
The claudication distance will vary from day to day and will be altered by walking up-hill, the
speed of walking or against the wind. As the disease progresses this claudication distance will
be gradually diminished.
DISEASES OF ARTERIES 189
Intermittent claudication however less commonly occurs in the upper limb due to brachial
artery or axillary or subclavian artery occlusion. Such intermittent claudication, if at all seen, is
only complained of after such activities as writing or manual labour.
REST PAIN.— As the arterial occlusion progresses, intermittent pain of the muscle will be
supplanted by a continuous rest pain at the sites most distal of the arterial supply e.g. toes, foot,
fingers, hand etc. Characteristically this pain is worse at night and is worsened by elevation of
the extremity, whereas it is somewhat relieved by hanging the foot out of the bed or by sleeping
in a chair. This rest pain is mainly due to ischaemic changes in the somatic nerves, so it is the cry
of the dying nerves.
Application of warmth will increase the symptoms of arterial occlusion.
Other points should be noted while taking history e.g. smoking habit of the patient, cardiac
disorders if any, any history of previous trauma, familial history, occupational history, if the
patient is diabetic or not and the drug history.
PHYSICAL EXAMINATIONS.—
A. INSPECTION.—
1. Change in colour is the most noticeable feature of an ischaemic limb. Congestion and
purple-blue cyanosed appearance particularly in dependency is noticed in chronic arterial
insufficiency. The colours are quite different from chronic congested extremity with venous
insufficiency. When the limb is elevated it becomes pallor.
2. Signs of ischaemia.— Characteristic changes due to arterial insufficiency often occur
at the most distal distribution of the concerned artery. These are thinning of the skin, diminished
growth of hair, loss of subcutaneous fat, shininess, trophic changes in the nails which become
brittle and show transverse ridges and minor ulceration on the pressure areas e.g. tips of toes,
ball of the foot, heel and malleoli. It must be remembered that ulceration from venous insufficiency
is virtually unknown below the level of the malleolus. To the contrary most ulcers from arterial
insufficiency begin over the toes or at the most distal parts of the arterial trees. Ischaemic ulcers
are never seen on the leg or about the ankle without involvement of the toes.
3. Buerger’s test.— The legs of normal individual even if they be raised by 90° remain
pink. But in case of an ischaemic limb elevation to a certain degree will cause marked pallor. The
angle between the limb at which such pallor appears and the horizontal plane is known as
'Buerger's angle' or the 'vascular angle'. If the vascular angle is less than 30°, it indicates severe
arterial occlusion.
4. Capillary filling time.— After elevating the legs, the patient is asked to sit up and
hang his leg down by the side of the table. A normal leg will remain pink. But an ischaemic leg
will change its colour from pallor to pink. This change of colour takes place slowly and is called
the 'capillary filling time'. An ischaemic limb further changes its colour and becomes purple-red.
This is due to the filling of dilated skin capillaries with blood.
5. Venous refilling.— The extremities are elevated until collapse of vein has occurred.
The extremities are then quickly lowered and the time required for the veins to refil particularly
on the dorsum of the foot or hand is noted. Normally venous refilling will occur within 10 to 15
seconds. Longer time for filling means arterial insufficiency. Time more than 1 minute denotes
severe degree of arterial occlusion.
Of course this test cannot be performed in presence of venous varicosities with incompetent
valves.
6. Pre-gangrenous state.— The combination of rest pain, colour changes, hyperaesthesia

with or without ischaemic ulceration is frequently referred to as 'pre-gangrenous' state.
7. Established gangrene.— When the arterial occlusion is severe and is existing for
quite a long time, gangrenous changes will be seen. This is the final stage and it is the dry
gangrene, which is characteristic of chronic arterial occlusion. It starts peripherally in the toes and
extends proximally to involve gradually the entire foot and leg.
Line of demarcation is often seen between the gangrenous part and the normal living limb.
This line of demarcation is a line of inflammatory zone. Only in case of ainhum, this line of
demarcation is very deeply marked mainly at the base of the little or the 4th toe.
B. PALPATION.—
1. Skin temperature of the ischaemic limb is always colder than the normal limb.
2. Capillary refilling.— The tip of the nail or pulp of a toe is pressed for a few seconds
and the pressure is then released. The time taken for the blanched area to turn pink is a crude
indication of capillary blood flow.
3. Venous refilling.— The two index fingers are placed side by side on a vein. The
fingers are now pressed firmly and the finger nearer to the heart is moved proximally keeping
the steady pressure on the vein so as to empty a short length of vein between the two fingers.
The distal finger is now released. This will allow venous refilling to be observed. This is poor in
case of ischaemic limb. This is known as Harvey’s sign.
4. Palpation of peripheral pulses — is the most important feature of the examination.
In the lower extremity, the femoral, popliteal, posterior tibial and dorsalis pedis pulses are felt
(See Fig.15.1 in the next page). In the upper extremity the brachial, radial and ulnar pulses are
felt. The integrity of the palmar arterial arch is tested by performing the Allen test. The patient
is asked to make a tight fist. The radial and ulnar arteries at the wrist are occluded. The patient
now slowly opens his hand. With the hand in a relaxed position, the integrity of the radial artery
in the hand is determined by releasing radial compression and noting the return of colour. The
manoeuvre is repeated releasing the ulnar artery while the radial artery remains compressed.
The disappearing pulse.— When peripheral pulses are apparently normal, exercising the
patient to a point of claudication may unmask the effect of arterial obstruction and the previously
palpable pulse may disappear. After rest of couple of minutes the pulse reappears. This is known
as 'disappearing pulse'. The reason is that exercise causes vasodilatation below the slight arterial
occlusion. This needs more arterial flow to the distal part, so that the arterial flow which was
already reduced cannot keep pace with the increasing demand, so that the arterial pressure falls
and the pulse disappears. ••
C. AUSCULTATION.—
1. Arterial bruits.— A systolic bruit over an artery revealed by auscultation indicates
slight occlusion of the artery. Such systolic bruit is conducted distally.
A continuous machinery murmur indicates presence of an arteriovenous fistula.
2. An oscillometer may be of some value in case of extremities with oedema where
peripheral pulses are difficult to palpate. This instrument consists of a blood pressure cuff attached
to a manometer. This cuff is inflated to just above diastolic pressure. This evaluates pulsatile
oscillations of the artery during systolic pressure. It has an advantage that it can quantify the
degree of occlusion used at bedside or even in the office.
SPECIAL INVESTIGATIONS.—
A. GENEFIAL INVESTIGATIONS.—
1. Blood examination should be performed
to exclude anaemia, diabetes, polycythemia, p-
lipoprotein and cholesterol estimations should be
performed.
2. Plain X-ray of the abdomen should be
performed to exclude presence of abdominal aortic

aneurysm by finding arterial calcification at its
wall.
3. E.C.G. should always be performed to
exclude any heart problem.
B. LOCAL INVESTIGATIONS.— These
investigations are designed to detect blood flow,
to know the site of arterial occlusion and its
degree.
1. Doppler ultrasound.— This is based
on the shift in ultrasound frequency that arises if
an ultrasound beam is transmitted to and reflected
from moving blood cells. This is known as doppler
effect. The changes of frequency in the reflected
beam as compared with the transmitted beam are
due to the 'doppler shift'. The frequency shift is
proportional to the velocity of the blood flow. It
may be analysed audibly by listening to the
intensity and pitch of the sound and may be
recorded graphically either as a simple wave form
or as a more complete sound spectrum analysis.
The last technique makes it possible to obtain
quantitative information about the degree of
stenosis.
The second application of doppler ultrasound
is to determine systolic arterial pressure. The
doppler probe is then used as a sensitive
stethoscope over an artery distal to a pressure
cuff. The cuff is inflated to a supra-systolic level
which will cause cessation of blood flow and
hence disappearance of the doppler signal. The
cuff is gradually relaxed and the systolic pressure Fig. 15.1.— Technique of palpation of the dorsalis
is measured. This technique is often used in the pedis, posterior tibial and popliteal arteries from
lower extremity.
above downwards.
The third application of doppler ultrasound is for vascular imaging. The doppler probe is
moved over the area to image the artery. A storage oscilloscope indicates places where blood
flow is detected and thus an image of the artery is obtained. It also gives information of the
diameter of the artery, its blood flow rates and velocities.
A hand-held doppler ultrasound probe is most useful in the assessment of patients with
occlusive arterial disease. This is a very essential tool. It can be used even at sites where arterial
pulse cannot be palpated. The ankle-brachial pressure-index (ABPI) is the ratio of the systolic
pressure at the ankle with that at the arm. The resting ABPI is normally about 1. Values below
0.9 indicate some degree of arterial obstruction and a value less than 0.3 suggests imminent
gangrene. It must be appreciated that re-testing after exercise is useful to detect intermittent
claudication, as ABPI may be normal at rest. This probe is useful to get an idea about the site of
stenosis. •
2. Duplex Imaging.— In this technique a Duplex scanner uses B-mode ultrasound to
provide images of vessels. There is a second type of ultrasound, namely Doppler ultrasound, in
which the imaged vessels are isolated and the Doppler shift is obtained which is analysed by a
computer in the Duplex scanner itself. In this technique shifts can give detailed knowledge of
blood flow or turbulence inside the vessel. Some scanners have colour coding, in which various
colours indicate change in direction and velocity of blood flow. It can be considered as accurate
as angiography in a few circumstances. In terms of safety this technique is preferred to angiography
if the two tests are considered to be equally useful.
3. Plethysmography.— This is a method of assessing changes in volume due to arterial
supply to that particular part. It has applications in peripheral arterial, cerebrovascular and
venous diseases. As the pressure pulse passes through a limb segment a wave form is recorded
by plethysmography, which determines arterial pressure as well as arterial and venous blood
flow.
This method is one of the earliest methods of measuring blood flow in human limbs. Venous
outflow from a limb is briefly arrested while allowing arterial inflow to measure the volume
change in the limb which is proportional to the arterial inflow. Three systems have been used e.g.
water-filled volume recorder, air-filled volume recorder and the mercury in a silastic strain
gauze. This technique is still a good non-invasive method of measurement of blood flow. But it
has rarely been found suitable for screening method for surgery, as the surgeon is more interested
to know the site of the arterial block rather than to measure the blood flow as such. Recently
segmental plethysmography has been introduced by placing.venous occlusion cuffs around the
thigh, calf and ankle. The cuffs are inflated to 65 mm Hg and the pulsation is the quantitative
measure of the arterial diseases.
4. B-scan ultrasound.— This can be used for visualization of blood vessels as a real-time
echo. The value in the diagnosis of occlusive disease is limited when the vessel wall is extensively
calcified. This B-scan may be used as a guide for precise placement of the doppler sample so that
doppler ultrasound can be combined with this technique to get valuable information.
5. Treadmill.— Sometimes patients cannot assess the claudicating distance, which can be
proper Iv assessed by this technique. It may be used in the detection of a fall in ABPI after exercise
indii.&mg occult arterial stenosis.
b. Phonangiography.— Vibrations of low frequency in the arterial wall due to disturbances
in blood flow can be detected as a noise using a stethoscope. By analysing this sound and its
location information of atherosclerosis and stenosis may be obtained.
7. Determination of ankle pressure.— This is one of the non-invasive techniques used
in verifying the diagnosis of ischaemic disease, in localizing the anatomic site of obstruction and
in choosing the type of operation. This is generally done with a doppler device. In patients without
arterial disease, the ankle/arm pressure ratio is 1 or higher. In claudication, it is generally between
0.5 to 1 and with more advanced degree of ischaemia it is generally less than 0.5. Segmental
pressures are obtained by application of cuffs at different levels of the leg. The pressure gradients
between the levels provide information about the location of the disease.
8. Isotope technique.— Xenon
133 dissolved in isotonic saline is injected
intramuscularly and the clearance of
which has been used to study the* blood
flow in the calf muscles. Recently '.
Technetium has become the isotope of .•
choice though the technique remains -
essentially the same. More recently «£,. *5^-*
intravenous injection of isotope has been - " .$■ r
used to get a direct arterial visualization.

For this a gamma camera is used to
picturise the blood flow in a limb.
9. Electromagnetic flow
meter.— When a column of blood moves
an electric potential is produced which is
proportional to the velocity of blood and
the magnetic field strength. The electric
potential is produced at right angles to
the flow. It bears a linear relationship to
the velocity of the blood flow. Two
electrodes are placed diametrically
opposite to each other in contact with the
arterial wall. This is the 'cuff' type of
electromagnetic flow meter. The
electrodes on the surface of the artery pick
up an electromotive force induced in the
blood by its motion through the magnetic
field and feed it back to suitable electronic
amplification. Such a method can detect Fig.15.2.— Bolus of 99Tcm has been injected i.v., followed
the change in the rate of the blood flow by arterial imaging which is done by a gamma camera. This
of 1%. But the greatest disadvantage of figure is an aorto-iliac irr age showing occlusion of the left
this technique is that the artery has to be external iliac, but patency of the common and superficial
exposed. femoral arteries, suitable for cross-over grafting.
10. Investigation for vasospasm.— In early part of Raynaud's disease or Buerger's disease
vasospasm is the main cause of arterial obstruction. It is at this stage that sympathectomy plays
its greatest role. Later on organic changes develop and sympathectomy does not do much good
to these patients. So, importance of finding out the degree of vasospasm cannot be overemphasized
to assess the value of sympathectomy. The method is nerve block with local anaesthetic e.g. the
posterior tibial nerve behind the medial malleolus, the ulnar nerve behind the medial epicondyle
or spinal anaesthesia in case of whole lower limb. Any rise of skin temperature is recorded and
is compared with the rise of mouth temperature.
13
Rise of skin temp. - Rise of mouth temp.

Brown's vasomotor index = ------------- —----- ----------------------------------------
Rise of mouth temperature
Operation is only advisable when the index is 3.5 or more.
11. Oscillometry.— This is of particular value in detecting arterial pulsation at different
levels of the limb. In embolism, a sudden decrease in the movement of its needle is obtained at
the level of arterial occlusion. In thromboangiitis obliterans, if no pulsation is obtained in the leg,
amputation should be performed in the thigh. But if oscillation can be seen in the leg a lower
amputation should be advised.
12. Arteriography.— This is the most reliable method of determining the state of the main
arterial tree. This procedure gives information about the size of the lumen of the artery, the
course of the artery, constriction and dilatation of the arteries and the condition of the collateral
circulation ('Run off'). Hypaque 45 (Sodium Diatrizoate) is the contrast medium often used.
Either of the following two methods is generally used :
(a) RETROGRADE PERCUTANEOUS CATHETERIZATION.— Under local anaesthesia
with proper aseptic precaution a special needle and a cannula are introduced into the femoral or
brachial artery (Seldinger technique). The common femoral artery is used for aortoiliac, renal,
mesenteric and femoropopliteal arteriography, whereas the brachial artery is used for subclavian,
vertebral, carotid and thoracic angiography. The needle is now withdrawn and a flexible guide
wire is threaded through the cannula. The cannula is withdrawn and a polythene catheter is
passed over the guide wire into the artery for a distance.
To avert the dangers of arteriography namely (i) iodine sensitivity and (ii) dissection of the
arterial wall if the tip of the needle is partly within the wall of the artery, a trial injection of 5 to
10 ml of 45% hypaque is made. This will ascertain the position of the tip of the needle.
Either a free flush arteriography or a selective angiography is performed. In free flush
arteriography the tip of the catheter lies in the main aorta and a 'bolus' of 30 ml of the same
contrast medium is injected rapidly. Series of X-ray exposures are taken to see particularly the
whole length of the arterial tree, the origins and the adjacent part of its branches. In selective
angiogram the tip of the catheter is introduced into the corresponding artery to delineate the
artery and its branches precisely.
(b) DIRECT ARTERIAL PUNCTURE.— This method is used in carotid angiogram.
Abdominal aorta (translumbar route) may also be chosen for this method for aortoiliac and
femoropopliteal arteriography when the femoral arteries are occluded or the retrograde method
has failed to produce necessary information.
13. Digital subtraction angiography (DSA).— This technique is preferred nowadays in
specialized centres. In this technique the angiographic information is digitalised in a computer
system, for which the contrast image is subtracted from the non-required surrounding images.
The result is a greater clarity. DSA may be carried out by arterial or venous injection. The arterial
technique is more or less same as conventional angiography, only fine catheter and less contrast
medium are used. The venous technique offers less clarity than its arterial counterpart, the only
advantage is that it avoids arterial puncture. Higher volume of contrast medium is injected in a
large vein which offers even better clarity than the simple arteriography.
The more sophisticated technique is the introduction of magnetic resonance angiography
without the need of direct arterial puncture. When this technology will advance, obviously the
catheter based contrast studies will be reduced.
MANAGEMENT. — Management of cases of chronic

arterial occlusion can be best described under the
following heads —
A. Conservative methods;
B. Indirect surgery to cause vasodilatation;
C. Direct arterial surgery.
A. ('onscri'alirc methods.- About 65% patients
who first present at a vascular clinic with intermittent
claudication can be treated initially by conservative
methods. Followings are the modalities under this group.
1. Stoppage of smoking.—This often goes a long way
to stop the progression of the disease. It particularly works
wonder in case of Buerger's disease.
2. Diet.— Diet should be so planned as to reduce
weight in case of obese individuals. The diets containing
cholesterol or P-Iipoproteins should be avoided.
3. Lipid abnormalities.— As mentioned earlier raised
P-lipoprotein is probably the commonest abnormality
found in those suffering from atherosclerosis.
Cholestyramine is particularly useful which lowers
cholesterol level.
4. Proper explanation.— In cases of intermittent
claudication if the patients are properly explained that
walking is not doing any harm, the walking distance often
improves. Improvement has even seen probably due to Fig. 15.3.— Aortogram showing occlusion
establishment of adequate collateral circulation in many of left external iliac and superficial femoral
patients within a few months. arteries
5. Exercise, if performed within limits, often reduces pain of intermittent claudication and
may help in spontaneous cure.
6. Diabetes and hypertension, if present, should be treated accordingly. Both these diseases
play a considerable role in the development of atherosclerosis.
7. Care of the feet.— This is particularly required in pre-gangrenous state, patients with rest
pain and in diabetic patients.
(i) The part should not be exposed to excessive cold or heat.
(ii) Stockinette may be used to prevent the feet from exposure to cold or to trauma.
(iii) By reducing exercise, demand of blood supply is diminished, so pain is relieved to a
great extent. This may be performed by reducing walking, stopping cycling and by wearing
shoes with high heel to diminish action of calf muscles.
(iv) Pressure to the affected foot particularly over the heel and malleoli should be avoided.
(v) Even minor trauma by amateur chiropody may start gangrene in pregangrenous toes.
So nail cutting should be done cautiously and at the same time any minor trauma should be avoided.
8. Buerger's position.— In this position the head end of the bed is raised and at the same
time the foot end of the bed is gradually lowered about 6 inches daily. This increases blood
supply to the lower extremity and may improve the condition.
9. Buerger's exercise.— In this exercise the affected lower limb is elevated for 2 minutes and
then lowered below the bed side for another 2 minutes. This process is repeated several times in
one sitting. In a day at least 3 sittings should be performed. This also improves circulation to the
affected lower limb.
10. Analgesics.— Various analgesics may be used, of which aspirin in dispersible form is
probably the best due to its antiadhesive effect on the platelets.
11. Drugs.— Drugs to combat diabetes and hypertension must be used properly. A few
antihypertensive agents, particularly beta-blockers may reduce claudication distance. An anti
platelet agent may be used for patients with occlusive arterial disease. Aspirin in the dose of 75
mg to 300 mg daily is quite a good and easily available drug in this group. If there is raised blood
lipids, drug treatment should be used to reduce these to normal level. It must be appreciated that
vasodilators are generally ineffective. Praxilene (Naftidrofuryl oxalate) may increase the
claudicating distance by allowing a greater oxygen debt to be incurred, but the actual ultimate
benefit is quite negligible. Trental (oxpentifylline) reduces blood viscosity and thus may be of
some benefit, but not quite satisfactory.
Intra-arterial administration of vasodilator drugs at the selective site by injection has been
successful as a temporary method. The drugs used are papaverine, lignocaine and duvadilan
injections.
Paravertebral injection of local anaesthetics near the sympathetic chain has also improved
circulation of the limbs. It is also known as chemical sympathectomy. In case of lower limb, injection
is made by the side of the L2, 3 and 4 vertebrae. For upper limb, injection is made by the side
of T2, 3 and 4. If 1% lignocaine is used, the effect is only temporary. For a more lasting result
about 5 ml phenol solution in water is injected. The procedure is better carried out under X-ray
control and a small injection of contrast medium (Hypaque solution) may precede the proper
injection of phenol. The main danger is to penetrate the aorta or the vena cava which can be
detected by drawing back the piston of the syringe which will show indrawing of blood into
the syringe.
B. Indirect surf/cry to cause vasodilatation.—-
1. SYMPATHECTOMY.— This operation, though not very effective in claudication, yet it
has some beneficial role in cases of rest pain and minor ulceration of the toes and fingers. It is
still very doubtful how much muscular blood supply is improved by sympathectomy, but it is
almost certain that it increases blood supply to the skin and subcutaneous tissue. Its main
indications are —
(i) Rest pain and minor ulceration, which are not amenable to direct arterial surgery. The
role of sympathectomy is probably the best in these conditions.
(ii) Buerger's disease.— In this condition sympathectomy plays a considerable role. The
result seems to be very significant if the Brown's vasomotor index is more than 3.5.
(iii) Raynaud's disease and other vasospastic conditions.— In these cases sympathectomy has
not been able to bring about considerable success.
(iv) Senile gangrene or diabetic gangrene in the elderly.— In these cases sympathectomy is
only advised where direct surgery is not feasible.
Usually one of two varieties of sympathectomy is usually performed.
(a) Lumbar sympathectomy.— This operation is performed in cases of arterial occlusions
of the lower limbs.
(b) Cervico-dorsal sympathectomy.— This is performed for arterial occlusion of the upper
limbs.
DISEASE^ OF ARTERIES 197
2. ADRENALECTOMY.— This operation is only used in cases of Buerger's disease with

some satisfactory results. Bilateral adrenalectomy should be performed.
3. MINOR SURGERIES to reduce muscular activity.— In ischaemic limb if the muscular
activity is reduced, claudication pain will be reduced to considerable extent. This can be achieved
by—
(i) Division of nerves to the gastrocnemius and soleus in the popliteal fossa. These muscles
are the muscles of the calf.
(ii) Tenotomy of the tendo-Achilles diminishes effort of the calf muscles by increasing the
length of its tendon.
C. Divert arterial surgery.— Various surgeries can be recommended according to the
type of occlusion and the artery affected. The followings are the different types of surgery which
are used for chronic arterial occlusions.
(1) Repair of injured artery.— This is performed only when the occlusion is due to
trauma.
(i) After exposing the site of occlusion due to trauma, simple manipulation of fractured
bone ends may cure the arterial occlusion. In certain cases of arterial spasm adventitial injection
of papaverine may cure the condition.
(ii) When the artery is tom, direct end-to-end arterial suturing should be performed with
5/0 atraumatic silk.
(iii) In certain cases a segment of the artery becomes contused or lacerated. In these cases
the affected portion is removed and if this segment is small, end-to-end suturing may become
possible without any tension to the suture line. If the affected segment is long, a Dacron graft or
a reversed long saphenous vein graft may be used to make good the loss of the segment.
(2) Thromboendarterectomy.— This operation is performed when the atheromatous lesion
Fig. 15.4 .— Shows the technique of endarterectomy. See the text for details.
is short and localized and has affected a big artery like aorto-iliac occlusion or less commonly in
femoropopliteal occlusion. Though it may require more extensive operation, yet it has the
advantages of preserving the patient's own arteries and avoiding the use of a prosthesis with its
attendant risks. This operation is also called 'disobliteration' or 'reboring'.
In this operation the whole length of the obliterated segment is explored. When the affected
segment is small, a longitudinal incision is made over the diseased segment and is made deep
till the atheromatous plaque is reached. The diseased intima, atheromatous plaque and the
thrombus are removed through a plane of cleavage through the middle of the tunica media. The
arteriotomy is then closed with continuous 5/0 polypropylene (prolene) suture with or without
a vein patch graft. This patch graft is to avoid constriction following longitudinal suturing. This
is called 'Open endarterectomy'.
In case of longer diseased segment, arteriotomies are made only at the upper and lower ends
of the diseased segment. An endarterectomy loop is inserted through the lower arteriotomy and
is pushed upwards dissecting and separating the atheromatous plaque as far as the upper
arteriotomy. The atheromatous plaque is removed from the upper arteriotomy. The arterial
openings are closed after ensuring good flow. General anticoagulant therapy is instituted. This
is called 'Closed endarterectomy'.
(3) Arterial by-pass grafting.— In this technique the diseased segment is bypassed with
a synthetic graft (knitted Dacron or Teflon) or with reversed autogenous long saphenous vein graft.
Prostheses come in two types — woven and knitted. Woven grafts leak less when first exposed to
blood during surgery. Modern knitted prostheses leak even less as they are sealed with gelatin or
collagen by the manufacturer. In fact there is probably little to choose between the types of Dacron
graft to be used. All achieve fairly satisfactory results. In aorto-iliac occlusion mostly synthetic grafts
are applied, whereas in femoro-popliteal occlusion, autogenous vein graft is mainly used. A
Polytetrafluoroethylene (PTFE) graft may be used instead of autogenous vein graft. This often gives
prolonged patency. In case of aorto-iliac occlusion suture material used is monofilament
polypropylene — 2/0 or 3/0. In femoropopliteal occlusion at the groin, 4/0 or 5/0 polypropylene
is used; whereas in case of further down limb occlusion 7/0 suture material is used.
(4) Balloon transluminal angioplasty.— In this technique a balloon angioplasty catheter
is passed through the arterial stenosis. The balloon is inflated with dilute contrast medium to a
pressure of 5 to 10 atmospheres for a period of 15 to 30 seconds even upto 1 minute, after which
it is deflacted. This is repeated for a few times before withdrawal of the catheter. This balloon
is introduced into the arterial tree using the Seldinger technique. Expansion of the balloon produces
fissures in atheromatous plaques and also ruptures muscle fibres of the tunica media thus widening
the lumen and ensuring blood supply to the distal limb. This technique is mainly used in case
of arterial occlusions of the iliac artery, superficial femoral or renal artery. Gradually the endothelial
lining develops along the fissures in the atheromatous plaque within a few months.
Transluminal angioplasty and stenting.— This is particularly effective to inflate a narrowed
short occlusion. The balloon catheter is inserted over a guide wire. The balloon is positioned
within the stenosis or occlusion which is confirmed by angiography. The problem is that often
the vessel fails to stay adequately dilated after such treatment and in these cases metal stent may
be used. In this technique the balloon catheter is introduced through the expanding stent and
then the balloon is inflated. The stent becomes rigid after being expanded and keeps the vessel
widely patent. The catheter balloon is now deflated and the catheter is removed. There is also a
type of self-expanding stent, which is held compressed by a sheath of plastic before application.
WSEAStES Off- ARJERSE5 199
The stent is positioned at the site of stenosis and the plastic sheath is withdrawn. The stent self-
expands and holds the vessel lumen wide open.
This procedure is not as good as reconstructive surgery, and is only used when latter type
of surgery is not possible. However the advantage of this procedure is that it can be repeated if
stenosis recurs.
(5) Other operative salvage procedures.— These operations should not be performed
only for intermittent claudications as gangrene or loss of limb may result if these operations fail.
(a) Femoro-femoral cross over graft.— In this technique without extensive exploration and
minimizing the operation time, an iliac artery occlusion may be relieved if the other iliac artery
is patent with a strong femoral pulse. 8 mm Dacron graft is placed in a tunnel in the subcutaneous
tissue in the lower abdomen just above the pubis from one groin to the other to connect the
common femoral arteries on each side. So that blood from the patent femoral artery is carried
through the graft to the other femoral artery of the ischaemic side.
(b) Hitch-hike femoro-popliteal-tibial graft.— This technique is adopted in cases of difficult
femoro-popliteal occlusion. A Dacron graft connects the common femoral artery to a
thromboendarterectomised upper popliteal artery. A vein graft is again connected from this
rebored upper popliteal artery to the arteries below the knee.
(c) Axillo-femoral graft.—This technique is used for pre-gangrenous limb in a poor risk
patient with bilateral iliac obstructions. 8 mm Dacron graft is placed in a tunnel in the subcutaneous
tissue extending from the axilla to the groin. In its upper part it is anastomosed with the axillary
artery in an end-to-side fashion. In its lower end it is anastomosed to the femoral artery of the
involved limb in the same fashion. By this blood flows sufficiently from the axillary artery to
revascularise the lower limb.
VARIOUS SITES OF CHRONIC ARTERIAL OCCLUSIONS

AORTO ILIAC OCCLUSION
Actiolog\ and Pathology. Patients are mostly in the 5th and 6th decades. Some degree
of atherosclerosis is almost always seen. The process may be atherosclerosis with intimal thickening
and fibrosis. The thrombus often propagates upto the level of the renal arteries, occluding one
renal artery and extending upto near the origin of the superior mesenteric artery.
Concomitant coronary or cerebral atherosclerosis occurs in 30 to 50% of patients with
symptomatic aorto-iliac disease.
Clinical lea! n res.—
SYMPTOMS.— The classical symptoms are intermittent claudication involving both buttocks,
the thighs and calves with impotence of varying severity in males. Impotence is a characteristic
feature in males with occlusion in the region of bifurcation of aorta and the internal iliac arteries
(Leriche's syndrome). Claudication may be symmetric or asymmetric, depending upon the pattern
of involvement of the iliac arteries. Rest pain and ulceration almost always indicate additional
distal disease particularly in diabetics.
PHYSICAL EXAMINATION.— The principal finding is diminution or absence of femoral pulses,
combined with absence of popliteal pulses. Pulsation of the abdominal aorta may be palpable,
but may be absent if the abdominal aorta is occluded upto the renal arteries. Systolic bruit is often
audible over the aorta or iliac arteries confirming the presence of atherosclerosis. Nutrition of the
extremities is usually normal.
Occasionally an acute episode of

severe ischaemia of toes or feet with
cyanosis and rest pain may be
complained of. The syndrome
probably arises from embolization of
fragments of atherosclerotic plaques
or thrombi dislodged from the surface
of such plaque.
Treat ment.— This depends very
much on the symptom and the
profession of the individual rather
than anything else. For example, mild
claudication in a 45 year old patient
whose occupation necessitates
frequent walking is a strong
indication for operation. Whereas a
retired patient of 70 with angina
pectoris and claudication does not
require operation.
CONSERVATIVE TREATMENT
consists of (i) daily exercise to the point
of claudication. This may not only
increase the walking tolerance, but
also may enhance collateral
circulation. If walking is not feasible,
Fig. 15.5.— Aortogram showing complete obstruction of the a similar exercise may be advised
right common iliac artery. indoors
(ii) Abstinence from tobacco in any form is mandatory. It is almost proved that claudication
improves when smoking is stopped and that the risk of gangrene becomes less than that of the
patients who smoke. It should be remembered that claudication progresses to gangrene 2.3 % per
year.
(iii) Alcohol may be advised for its peripheral vasodilator effect.
(iv) Drug therapy with vasodilators have very limited result.
(v) Care of the feet as mentioned earlier should be carried out rigidly in these cases.
(vi) Attempt must be made to lower blood lipid concentration by diet and drugs, but of course
with uncertain benefit.
(vii) Acetyl Salicylic acid in small doses strikingly alters platelet aggregation and may thereby
prevent intravascular thrombosis.
SURGERY.—
(1) Thromboendarterectomy.— The typical pattern of atherosclerotic involvement is extension
of disease proximally to within 2 to 3 cm from the renal arteries and distally into the common
iliac arteries stopping in about 50% of patients just beyond the bifurcation of the common iliac
arteries. Thromboendarterectomy is mainly preferred when the occluded segment is short i.e.
involving the terminal 5 cm of the aorta and the proximal part of the common iliac arteries. When
the disease is more extensive than this, by-pass graft procedure should be the operation of choice.
The abdomen may be opened through either a long right paramedian or midline or a
supraumbilical transverse incision. Transverse incision is often preferred, as it is less painful and
wound healing is much better as this incision runs parallel to the Langer's lines. The peritoneum
of the posterior abdominal wall is incised over the front of the aorta. The aorto-iliac bifurcation
is clearly dissected out, great care being taken not to damage the wall of the iliac veins which are
often firmly adherent to the adjacent arteries. The extent of the disease is now confirmed by
palpation. The arterial clamps are placed well above and below the diseased segment.
When the diseased segment is short, a long arteriotomy is made over the diseased segment
of the aorta and common iliac arteries. A plane of cleavage is found between the atheromatous
core and the outer half of the tunica media. The core is removed and the distal intima is inspected
to ensure that it is firmly attached to the media. If there is any doubt, it is safer to suture it in
place to avoid dissection.
When the diseased segment is long, this portion of the aorta is dissected clear. The aorta
proximally and the external and internal iliac artery distally are encircled with plastic tapes. 50
mg of heparin is then given by intravenous injection before occlusive clamps are applied. Usually
the external iliac clamps are applied before those of the abdominal aorta to protect from distal
embolization. Incisions are made over the distal common iliac arteries and cleavage planes between
the plaques and the media are developed. A longitudinal incision is made into the aorta above
the level of the inferior mesenteric artery and an appropriate cleavage plane between the arterial
intima and media is indentified. With an arterial stripper, the core of atherosclerotic material is
freed proximally. By blunt dissection the aortic and the iliac core can be mobilized and removed
in one piece. The calibre of the external iliac arteries should be measured by the catheters. A
diameter smaller than 16 F catheter indicates the necessity of extending endarterectomy to the
common femoral arteries.
The aortotomy incision is closed with a continuous 5/0 monofilament non-absorbable suture.
The iliac arteriotomies are closed similarly with a patch graft of either autologous saphenous vein
or prosthetic patch of knitted Dacron. The occluding clamps are sequentially removed to permit
flushing. Once blood flow is restored, heparin is neutralized with protamine, giving 1 mg for
each mg of heparin.
(2) By-pass grafting.— This is a very popular operation in aorto-iliac disease. The superiority
of the previous operative procedure over this has not been demonstrated conclusively as con
comitant aneurysmal disease of the aorta is a definite contraindication to endarterectomy.
Long term patency rate after either procedure ranges from 60% to 90%. But by-pass operation
is more popular in aorto-iliac disease.
Usually a Woven Dacron prosthesis is preferred because of firmer adherence of the neointima
which forms subsequently in the wall of the graft.
The proximal anastomosis is constructed in an end-to-side fashion with a continuous suture
of 4/0 monofilament suture. Soft tissue tunnels are formed by blunt dissection anterior and
parallel to the iliac vessels, through which the limbs of the prosthesis are brought parallel to the
iliac arteries. If the distal anastomosis is performed to the common femoral artery, the graft is
brought to the groin deep to the inguinal ligament. The common femoral artery is incised near
the origin of the profunda femoris artery. A continuous suture of 5/0 monofilament suture is
used for end-to-side suturing with the common femoral artery. This is done on both sides.
The major technical hazard in by-pass grafting is the formation of thrombi in the proximal
or distal arterial tree with subsequent embolization into the extremity. This is avoided by flushing
the graft before the distal anastomosis is completed.
Antibiotics in
large amounts are
always started
Extent of disease Operation before the
operation and
aorta
may be repeated
+ aortoiliac if the operation is
common iliac endarterectomy
continued for
longer period.
(3) Balloon angi
oplasty.— This
technique is
probably suitable
to short seg
aortofemoral mental stenosis.
Dacron bypass The technique has
been described
above.
In approxi
mately 10% of
patients serious
local complica
external iliac tions occur which
endarterectomy
external iliac (extra peritoneal) include rupture of
the vessel with
retroperitoneal
haemorrhage or
total occlusion of
the previously
unilateral stenotic vessel.
iliac femorofemoral The long term
(poor-risk Dacron bypass
patients) (subcutaneous) results are not
known as the
procedure has
been introduced
recently.
(4) Lumbar sym
pathectomy.— This
aortoiliac axillofemoral
is indicated in
(poor-risk Dacron bypass patients with
patients) r\ (subcutaneous)
trophic changes
in the feet not
amenable to
arterial recon
struction ope
rations.
fis .15.6,— Diagrammatic mgaesenAMian erf Jfoe gperatoms to be performed in various Unfortunately,
cases off scato-SBac ©odtetoass.. the benefit of
sympathectomy are unpredictable. In many series signs of improvement were seen in only 20 to
30% of patients. There is no doubt lumbar sympathectomy increases circulation of the skin and
subcutaneous tissue, which provides some protection from trophic changes and ulceration. It
does not increase blood flow to the leg muscles.
FEMORO POPLITEAL OCCLUSION

I’utholo&v.— The most common site for atherosclerotic occlusion in the lower extremity is
the distal superficial femoral artery within the adductor canal almost near the adductor foramen.
From here occlusion extends proximally in the superficial femoral artery till the opening of a
large collateral branch or may extend upto its origin from the common femoral. Occlusion of the
profunda femoris artery is very rare, as it is not an artery of conduction, but an artery of supply.
Usually arteries of conduction are involved by atherosclerosis.
If occlusion affects the popliteal artery or its branches, more serious circulatory insufficiency
appears and ulceration and gangrene of the feet may start. This is more common in diabetics.
Clinical features.— .
SYMPTOMS. — Intermittent claudication of the calf muscles with moderate exercise is the
main symptom.
PHYSICAL EXAMINATION reveals a normal femoral pulse but absent popliteal and dorsalis
pedis pulses. Sometimes dorsalis pedis pulse may be felt at rest, but disappears with exercise,
which is known as the 'disappearing pulse'. The nutrition of the foot is usually normal. But if
occlusive disease is present distally, it may be associated with rest pain and trophic changes in
the foot.
The risk of gangrene developing within 5 years in an extremity with claudication as the only
symptom is about 5%.
Treat incut.— Indications for operation is almost in the similar trend as in aorto-iliac disease,
i.e. it is dependent on the symptom of the patient, his age and his occupation.
CONSERVATIVE TREATMENT.— If this is chosen, it is almost similar to that described in
aorto-iliac occlusion. Only one point requires mention that a good exercise programme of walking
daily has resulted in marked improvement in claudication in at least 50% of patients within 6 to
12 months.
SURGERY.—
1. Endarterectomy.— In this disease open endarterectomy is preferred, in which the whole
length of the occluded portion of the artery is exposed by a longitudinal incision, atherosclerotic
core is removed and the arteriotomy is closed by suturing with a vein patch to prevent constriction.
Endarterectomy has not proved satisfactory in femoro-popliteal occlusive disease. That is why it
is only advocated when a suitable vein is not available for by-pass surgery.
2. By-pass grafting.— By-pass operation with autologus saphenous vein is the standard
technique. In determining the choice of operative procedure, venous by-pass is always favoured
if the saphenous vein is at least 4 mm in external diameter.
The long saphenous vein is carefully removed from the inguinal ligament to the knee joint.
This vein is now reversed to permit blood flow in the direction of venous valves without being
obstructed by them. Now it is attached with end-to-side anastomosis to the femoral and the
popliteal arteries proximally and distally respectively above and below the occlusive disease. If
the long saphenous vein is not of adequate diameter, a suitable cephalic vein is an acceptable
substitute.
3. Profundaplasty.— Recognition of the importance of the profunda femoris has laid to the
development of
the operation of
Extent of disease Operation profundaplasty
aimed speci
fically at in
creasing the
superficial femoropopliteal blood flow down
femoral vein bypass this vessel. This
vessel arises from
the posterior
aspect of the
common femoral
artery and its
orifice is rarely
visualized by
superficial anteroposterior
superficial femoral
femoral endarterectomy X-ray projection.
But this will be
demonstrated on
0 , lateral projection.
mr\ Another peculiar

feature is that in
majority of cases,
if atheroma at all
superficial
+ involves this
deep femoral profundaplasty artery, the athe
± (vein patch)
popliteal romatous ste
nosis is only seen
at its origin. Only
in a few cases
such stenosis
may extend upto
Fig. 15.7.— Operations for femoropopliteal disease : Examples of disease pattern and ^he ^'rs^ perfo-
operations to be performed for each case. These operations should only be done when rating artery.
the aorto-iliac segment is relatively free from disease. This ope
ration of
profundaplasty is aimed at removal of atheromatous stenosis from the origin of the profunda and
then to widen the endarterectomised segment by insertion of a vein patch.
The vessel is dissected out and it is palpated to know the extent of the affected segment by
atheroma. After applying bulldog clamps to all the major branches, the diseased segment is
opened by a longitudinal incision (arteriotomy). This arteriotomy must extend upwards into the
common femoral trunk and downwards into the normal part of the artery. By endarterectomy,
the atheromatous core is removed. The distal intima is carefully examined and stitched to the
underlying media if it be needed. A saphenous vein patch is prepared and sutured into the
arteriotomy to widen the profunda artery. The bulldog clamps are now removed. Many surgeons
carry' out arteriography on the table to ensure no technical error has been made during anastomosis
and there is no obstruction of

the blood flow.
Profundaplasty operation
may be carried out in
conjunction with other
procedures e.g. by-pass graft
operation. Even with no
demonstrable stenosis,
widening of the calibre of
apparently normal profunda
artery gives better results
comparable to only by-pass
operation.
4. Lumbar sympathec
tomy.— When claudication is
the only symptom, this
operation should not be
performed. This operation is
only indicated when trophic
changes are present and direct
arterial reconstruction is not
possible. As mentioned earlier
this operation provides
vasodilating effect on the skin
and subcutaneous vessels
proving some protection from
ulceration and gangrene to the
ischaemic foot.
Lumbar sympathectomy is
used in two situations — Fig. 15.8.— Profundaplasty operation. After opening the origin of the
(i) i4s a limb salvageprofunda femoris artery thromboendarterectomy is performed and the
procedure, as mentioned above. opening is closed with a vein patch.
(ii) y4s an adjunct to
reconstructive arterial procedure.— There is good evidence that the long term patency of
femoropopliteal by-pass graft is improved by simultaneous lumbar sympathectomy. However
this is not widely accepted.
5. Amputation.— In certain cases when there is definite ischaemic change in the distal limb
with ulceration and gangrene, there is probably no way out but to amputate the distal portion
of the limb.
Level of amputation.— This is the main problem as the surgeon has to balance two opposing
factors — on one hand the more distal the amputation, the easier it is for the patient to use a
prosthesis. On the other hand, the more proximal the level of amputation, there is more likely of
primary healing. Presence or absence of pulses, arteriographic picture, the results of doppler studies
are the points to be considered. The general rule is that, when in doubt, the more proximal level
should be chosen to prevent repeated amputation.
The various types of amputation are described in the chapter of 'Amputation' (Chapter 19).
CAROTID OCCLUSIVE DISEASE—

It is mainly atherosclerosis at the origin of the internal carotid artery or a more extensive
occlusion of that artery. Occasionally there may be cerebral embolization from the heart or
fibromuscular hyperplasia of the carotid arteries or obliterative arteritis of the great vessels
(Takayasu's arteritis) or due to blunt or penetrating trauma.
In more than 75% of cases the
plaques are found at the carotid
bifurcation involving distal part of the
common carotid and the proximal
parts of external and internal carotid
arteries.
Carotid stenosis causes transient,
recurrent and progressive strokes
causing hemiplegia on the
contralateral side. The classical stroke
from unilateral carotid disease is
ipsilateral blindness and contralateral
hemiplegia. There may be transient
ischaemic attacks (TIA), which mean
transient monoplegia, transient
hemiplegia or transient ipsilateral
blindness. These episodes clear within
minutes to hours after an abrupt
onset. Between such episodes the
patient is completely well.
Between the transient ischaemic
attack on the one hand and the
massive stroke on the other, a wide
variety of motor and sensory
syndromes are seen.
Fig.15.9.— Internal carotid arteriogram showing stenosis due to 11 cainicni. The ideal patient
atherosclerosis. for operation is one with transient
ischaemic attack without permanent
neurologic abnormality. If the internal carotid has become totally occluded producing a major
neurologic deficit, operation performed within 6 hours after onset of symptoms may produce
dramatic recovery, though the operative mortality is considerably high. But if operation is carried
out beyond 6 hours, the result is miserable.
The operation is carotid endarterectomy followed by suturing with vein patch.
SUBCLAVIAN-VERTEBRAL DISEASE. -
Stenosis involving only the vertebral artery is infrequent. The disease is frequently limited
to the site of origin of the vertebral artery. The atherosclerotic plaque usually has a smooth
intimal surface here.
Symptoms are mainly due to decreased flow to the basi-vertebral system. Concomitant disease
in the basilar artery is quite frequent.
Subclavian steal syndrome is a condition in which there is atherosclerotic stenosis of the
subclavian artery proximal to the site of origin of the vertebral artery. Reduction in pressure in
the subclavian beyond the stenosis results in retrograde flow from the brain stem down the
vertebral artery to the arm (so blood is stolen from brain). The clinical picture is that of syncopal
attacks due to ischaemia of the brain stem, visual disturbances and decreased pulse and blood
pressure in the symptomatic arm. There may be a localized bruit in the supraclavicular space.
Treatment.— Subclavian exposure of the subclavian-vertebral junction is obtained through
a transverse supraclavicular incision. If the atherosclerotic plaque has a smooth surface,
endarterectomy may not be necessary and the lumen of the artery is simply widened known as
patch angioplasty with autologous saphenous vein.
Operations for subclavian steal syndrome are rarely necessary. A by-pass graft from the
ipsilateral common carotid artery to the distal subclavian artery may be necessary in symptomatic
cases. If the common carotid artery is markedly stenotic, axilloaxillary by-pass grafting may be
used.
AORTIC-ARCH OCCLUSIVE DISEASE (TAKAYASU’S ARTERITIS).—
Sometimes a non-specific arteritis affects major branches of the aortic arch and also the
thoracic and abdominal aorta. This is particularly seen in the Orient among young women. This
is known as Takayasu's arteritis, named after an ophthalmologist who described it. But occlusive
disease of the major branches of the aortic arch may also occur due to atherosclerosis in Western
Countries and also due to syphilitic arteritis. Takayasu's arteritis involves all layers of the aortic
wall with proliferation of connective tissue and degeneration of the elastic fibres. Granulomatous
lesions may also be present. Aneurysmal formations — fusiform or saccular varieties are also
noticed. It has been suggested that the disorder may be an autoimmune disease.
l linkul Icaimvs.- In case of atherosclerotic disease symptoms are mild permitting many
pathways for collateral circulation. Ischaemic symptoms of the upper extremities and brain may
occur.
In case of Takayasu's arteritis there is fever, malaise, arthritis and general arthralgia. Some
patients complain of pericardial pain and tachycardia and a few may also vomit. Later on ischaemic
manifestations are seen in the upper extremities and brain.
1 real mi n In case of atherosclerosis, multiple by-pass grafts may be required from the
ascending aorta proximally to the carotid or subclavian artery distally. Endarterectomy usually
is not possible.
In case of Takayasu's arteritis, operative treatment often proves disappointing, as both
endarterectomy and by-pass grafts are liable to reocclude. Since this disorder is an autoimmune
disease, steroids may be administered with some beneficial results. Operation is only recommended
for patients with disabling symptoms.
MESENTERIC ARTERIES OCCLUSION.—
Syndromes of visceral artery occlusion may be acute or chronic.
Acute occlusion of the mesenteric artery causes gross changes which are mainly intense muscle
contraction and bluish white rippling of the seromuscular surface. Later on the bowel relaxes and
the surface becomes pale with bluish tinge. The peritoneal covering loses shiny appearance.
Much later, gross signs of haemorrhage into the mesentery are seen and haemorrhagic infarction
becomes well manifested. The bowel wall becomes swollen and infiltrated with blood and the
mucosa becomes necrotic. Permeability to bacteria and fluid occurs and this causes purulent
peritonitis. With this there is a massive intraluminal loss of plasma and fluid. Leucocytosis goes
above 15000. Metabolic acidosis supervenes.
Superior mesenteric artery embolization.— This is a common example of acute occlusion.

It causes (i) tremendous abdominal pain, (ii) followed by vomiting and diarrhoea with (iii)
evidence of cardiac lesion which may be the cause of embolization.
The diagnosis is confirmed by angiography.
Treatment.— Obviously immediate operation is the treatment of choice. After examining
the whole length of the bowel, one can assess the artery which has been embolized. Through a
transverse arteriotomy, Fogarty catheter is passed and embolectomy is performed alongwith
removal of propagated clot. Following restoration of blood flow, pulsation returns to the mesenteric
artery after an appropriate period of time. Now judgement is made as to whether or not the
intestine should be resected. If this is not required the abdomen can be closed.
M esenterie artery thrombosis.— This is a common example of chronic occlusion. In case
of thrombotic occlusion of the mesenteric artery, illness develops insidiously with a progressive
and steady colicky abdominal pain. This is the pain of intestinal spasm due to ischaemia. Half
of these patients will give a history of prior intestinal ischaemia manifested by weight loss, post
prandial pain and altered bowel habits. Some may give manifestations of other atherosclerotic
occlusions.
Whenever bowel infarction is suspected, aortography should be performed. The intra-aortic
catheter is placed at the level of the first lumbar vertebra and anterior, posterior and lateral films
are taken after injecting the radio-opaque dye. In case of this disease a sharp cut of the superior
mesentery artery is seen within 1 cm of its origin.
Treatment.— Previously thromboendarterectomy was used, but as the operation is very
much time consuming and very traumatic to the already ill patient with intestinal infarction, by
pass graft operation (with aorto-mesenteric graft) is now more popular. The infra-renal lumbar
aorta is exposed. Similarly the mesenteric artery is dissected free of its investment in the mesentery.
A saphenous vein graft is mainly used for end-to-side anastomosis from the anterior surface of
the aorta to the superior mesenteric artery.
Following revascularisation, the need for intestinal resection should be considered. A second-
look operation may be performed.
POPLITEAL ARTERY ENTRAPMENT SYNDROME.
In this condition a developmental anomaly is seen in the popliteal artery. In this case the
popliteal artery, instead of entering the popliteal fossa through the arch of the adductor magnus
muscle, enters the popliteal fossa through the muscle mass of the medial head of the gastrocnemius
muscle. Due to this developmental anomaly, the popliteal artery is exposed to repeated trauma
and severe compression by that muscle. As a result typical atherosclerotic changes appear with
occlusion and thrombosis. Sometimes a post-stenotic dilatation and aneurysm may be formed.
C'linieal features.— The main symptom is progressive intermittent claudication of the leg
and sometimes of the foot. Gradually ischaemic gangrene may develop in the toes and foot.
On examination, the usual finding is diminished or absent popliteal, posterior tibial and
dorsalis pedis pulses. Sometimes all pulses may remain normal, but disappear on dorsiflexion
of the foot. Occasionally when there is aneurysm formation, a pulsatile swelling is seen in the
popliteal fossa.
Treat inent.—
(a) When there is no organic lesion developed in the popliteal artery, various types of
myotomy procedures can be adopted to release it from pressure.
(b) When organic lesion has developed, only correction of anatomic abnormality will not
do and some sort of direct arterial surgery in the form of by-pass graft with autogenous long
saphenous vein or thromboendarterectomy angioplasty should be performed to restore blood flow.
ANTERIOR COMPARTMENT SYNDROME.—
Any condition, which increases fluid in the anterior compartment of the leg, causes increase
of pressure in this closed space surrounded by tough deep fascia. If such swelling continues, first
it obstructs veins. If the intracompartmental pressure exceeds aterial pressure, the arteries will be
occluded with ischaemia of the distal limb. The unyielding walls of the compartment are the
tibia, the interosseous membrane and the anterior crural fascia (deep fascia).
Such increase of intracompartmental pressure may be caused by severe exertion, trauma,
venous or lymphatic obstruction in the proximal limb or a complication of femoropopliteal by
pass or even cardiopulmonary by-pass operation.
Clinical features.— Pain is the first and most important symptom. In the beginning it starts
as a dull ache and soon becomes severe. The pain is located in the anterior compartment of the
leg. Movement increases pain.
As the syndrome progresses, one can see erythema of the skin over the anterior compartment.
On palpation tenderness can be elicited on the anterior compartment. Dorsalis pedis pulse
may be diminished or absent, which is a relatively late sign and is seen after the loss of motor
power of the muscles of the anterior compartment. The first muscles which become paralysed are
the anterior tibial and the extensor hallucis longus, followed by extensor digitorum longus and
other muscles.
Examination will reveal in late cases loss of sensation in the area supplied by the peroneal
nerve.
Treatment.— As soon as the diagnosis is made, decompression of the compartment should
be performed by fasciotomy. The skin is incised 2 cm lateral to the shin bone and is made deep
through the subcutaneous tissue and deep fascia. The muscle bellies will be seen bulging through
the fasciotomy. The incision is extended till the compartment pressure is completely relieved. It
is better to keep the wound open and left for secondary suture. Some surgeons however close the
skin only over the bulging muscles to prevent entry of infection.
RAYNAUD’S SYNDROME
Definition.— -
Raynaud's syndrome is a condition characterized by episodic attacks of vasospasm that
cause closure of the small arteries and arterioles of the distal parts of the extremities in response
to cold exposure or emotional stimuli. Classically the attacks consist of three sequential phases
— (i) intense pallor followed by (ii) cyanosis and (iii) rubor upon warming requiring 15 to 45
minutes for full recovery. However a large number of patients develop only pallor and cyanosis
during attacks.
Fingers and hands are most frequently involved, although in many patients the toes, feet,
ears, nose and lips may be similarly affected.
Aetiology.—
1. The syndrome described by Raynaud now termed as Raynaud's phenomenon is a primary
disorder whose aetiology is still unknown. It is also termed Raynaud's disease. It is much more
common in women with a ratio of about 5 :1. 90% of patients are below 40 years of age. In men
it is usually much less severe in intensity.
14
2. It may be a secondary manifestation of some other probably more serious disease. A

comprehensive list is given below but it is more often associated with Buerger's disease
(thromboangiitis obliterans), scleroderma, cervical rib or other thoracic outlet syndrome and
atherosclerosis.
DISOFtDERS IN WHICH RAYNAUD’S SYNDROME MAY BE SECONDARY ARE :
I. Immunologic and connective tissue disorders —
1. Scleroderma.
2. Systemic lupus erythematosus (SLE).
3. Rheumatoid arthritis.
4. Dermatomyositis.
5. Sjogren's syndrome.
II. Obstructive arterial diseases —
1. Arteriosclerosis.
2. Buerger's disease.
3. Thoracic outlet syndrome.
III. Environmental conditions —
1. Vibration injury.
2. Direct arterial trauma.
3. Cold injury.
IV. Drugs —
1. Ergot.
2. Betablocking drugs.
3. Cytotoxic drugs.
4. Birth control pills.
V. Miscellaneous —
1. Cold agglutinins.
2. Cryoglobulinaemia.
3. Neoplasia.
4. Neurologic disorders.
5. Endocrine disorders.
RAYNAUD’S DISEASE
Maurice Raynaud described this condition in 1862. Publication of Allan and Brown's
observations have put light in the understanding of Raynaud's syndrome. Presently there appears
little justification in attempting rigid separation of Raynaud's disease from Raynaud's phenomenon
(where Raynaud's disease is secondary to some other condition). With the passage of time incidence
of primary Raynaud's disease decreases as some associated disease process is found in more and
more patients.
' Pathophysiology.—
The arterioles penetrate the dermis at right angles with an irregular reticulate pattern and
end in a capillary network. In Raynaud's disease, vasospasm occurs with such severity that
dermal circulation momentarily ceases with the production of severe pallor. If the vasospasm is
less severe, with slowing but not cessation of dermal circulation, cyanosis appears. After some
minutes of pallor, the capillaries and probably the venules dilate due to hypoxia and
accumulation of metabolic products of regional anaerobic metabolism. This is followed by a
slight relaxation of the arteriolar spasm with entry of small amount of blood into the dilated
capillaries. This is rapidly deoxidised and this gives rise to cyanosis. This results from sluggish
flow of blood with an increase in the percentage of reduced haemoglobin in the capillaries.
When the vasospasm subsides, a reactive hyperaemia with vasodilatation develops due to
accumulation of tissue metabolite during the anoxic period and this produces redness or rubor.
Why is there the increased tendency of the dermal arterioles to vasoconstriction ? This is not
definitely known. But there are many theories.
Two types of adrenergic receptors have been identified in the blood vessels. Alpha 2-adrenergic
receptors are present in form on human platelets. A recent study evaluated that there is marked
elevation of Alpha 2-receptor activity in spastic Raynaud's disease. This increased Alpha 2-
adrenergic activity may prove to be the 'local vascular fault' hypothesised by Sir Thomas Lewis
50 years ago.
In majority of patients the episode of vasoconstriction is precipitated by exposure to cold. But
in about 25% of patients intense emotion may be the initiating factor. Only rarely is alone the
significant stimulus without an abnormal sensitivity to cold.
Clinical leaf tires.—
Environment has a role to play in this disease and cool damp climates may increase the
incidence of Raynaud's syndrome or may merely make the underlying abnormality clinically
apparent.
Occupation has also a big role to play in Raynaud's syndrome. Use of vibrating tools or exposure
to chronic cold increase incidence of this condition. Incidence of this condition among chain-saw
operators and miners using vibrating equipment ranges from 40% to 90%. Those who work with
earth impactors or rivetting machines which are also vibrating tools show similar incidence of
this disease. These vibrators seem to disturb the neurovascular controls in the hands. Similarly
this syndrome is reported in about 50% among food workers working in cold environment.
Females comprise 70% to 90% of cases of Raynaud's syndrome. Raynaud's disease is
commoner in younger women. Older males may develop this syndrome usually from
arteriosclerosis.
Three stages are distinctly observed with exposure to cold or emotional disturbances. These
are — (1) Stage of local syncope, (2) Stage of local asphyxia and (3) Stage of recovery.
Stage of local syncope.—With exposure to cold the digital arterioles go into spasm and the
decreased blood flow is evident by pallor or blanching (stage of blanching). This change starts at
the tip of the finger and gradually spreads towards the base.
Stage of local asphyxia.— With gradual warming there is slight relaxation of arterioles. Small
amount of blood passes to the capillaries which become dilated due to accumulation of anaerobic
metabolities from the previous stage. Slowly flowing blood becomes easily deoxygenated and
the part becomes dusky or cyanosed (stage of dusky anoxia). The fingers remain cold and numb.
Stage of recovery.— As the attack passes off and with more warming, the spasm absolutely
disappears and the arterioles relax. The oxygenated blood returns into the dilated capillaries
(under influence of anaerobic metabolites which accumulated in the first stage of pallor) and the
fingers become red (stage of red engorgement) and swollen. There may be burning sensation or pain
produced by the increased tissue tension within the digits.
This condition is commonly bilateral.
Inspection.—
No abnormality is usually detected. In late cases one may find finger tip ulceration. This is
usually associated with obstruction and not only spasm of the arterioles.
Palpation.—
(i) Fingers and hand feel cold.
(ii) Pulses at the wrist are usually normal (cf. Buerger's disease).
(iii) One must exclude other conditions which may be associated with this disease e.g.
thoracic outlet syndrome, cervical rib, scleroderma, atherosclerosis etc.
Patients with scleroderma may have visible changes in their skin and face and may complain
of dysphagia.
In long standing cases the fingers gradually waste, especially the pulps, which become thin
and pointed. Small scars may appear following necrosis of small areas of skin. Small and painful
ischaemic ulcers may be seen on the finger tips. Repeated infections (paronychia) are common
around the nails. These are painful and slow to heal.
‘ The patients may gradually get rest pain and gangrene of the finger tips.
Special Investigations.—
1. Digital plethysmography with digital blood pressure determination.
2. Arteriography.
3. Haemogram, E. S. R., Rheumatoid factor, antinuclear antibody determination.
4. Protein electrophoresis.
TREATMENT.
Conservative treatment should be tried first.
CONSERVATIVE TREATMENT.—
1. Moving to warm climate.
2. Tobacco should be avoided.
3. The part should be protected from exposure to cold.
4. Occupational exposure should be reduced.
5. A variety of vasodilator drugs have been used in this condition. One of the most
widely used drugs is Reserpine. An oral dose of 0.25 to 0.50 mg daily should be prescribed for
2 weeks. Methyldopa may be administered orally. This treatment should be continued for several
weeks. Intra-arterial injection of Reserpine 2 or 3 times yearly may be necessary. Guanethidine
has been claimed to be the most effective drug for the symptomatic treatment of this condition
in the last decade. Phenoxybenzamine and more recently prazocin and pentoxifylline are the
adrenergic blocking drugs which have been claimed to provide good result.
The calcium channel-blocking drugs have been used with success by certain investigators.
Nifedipine is the most potent peripheral vasodilator in this group and has been moderately
effective in the treatment of Raynaud's syndrome. This has produced clinical improvement in
50% to 60% of patients. The combination of Nifedipine with low dose of guanethidine or prazocin
has frequently appeared to improve results while diminishing the incidence of side effects.
Patients with spasmodic Raynaud's syndrome respond better than obstructive Raynaud's
syndrome. Prostaglandin E administered intravenously to these patients have shown benefits as
has been reported from a few hospitals of London.
OPERATIVE TREATMENT.—
There is definitely a place for vascular surgery in cases of arteriosclerosis, emboli, thoracic
outlet syndrome, aneurysm or trauma which may be associated conditions of Raynaud's syndrome.
Although CERVICO-DORSAL SYMPATHECTOMY is recommended for primary Raynaud's
disease, and though there is good immediate result, yet this is often followed by gradual recurrence
of symptoms. Probably
sympathectomy produces
long term good results in
mild Raynaud's syndrome of
the spastic variety and this is
the same group of patients
who respond best to drug
therapy.
Cervico-dorsal sympa
thectomy is of little or no
benefit in patients with
Raynaud's syndrome who
have associated connective
tissue disease.
The question of the day
is whether cervico-thoracic
sympathectomy should be
recommended in all cases of
Raynaud's syndrome or not.
Cervico-Thoracic
Sympathectomy.— In this
technique first, second and
third thoracic ganglia are Fig. 15.10 — Anatomical position of cervical sympathetic ganglia.
removed preserving the
cervical portion of the stellate ganglion proximal to the level where the rami communicantes
from the first thoracic nerve join the ganglion, to avoid Homer's syndrome. So in this operation
the sympathetic trunk from the lower half of the stellate ganglion to the just below the 3rd
thoracic ganglion should be resected. As mentioned earlier initial results are usually good but
recurrence of symptoms in subsequent years is quite common.
For this reason sympathectomy is usually employed only when the symptoms are severe and
other therapy becomes ineffective.
Technique of operation.— See Figs. 8.7 & 8.8 at page 95 of Author's 'A Practical Guide to
Operative Surgery'.
Cervico-thoracic sympathectomy can be performed by one of the three following approaches:-
A. ANTERIOR APPROACH.— The patient lies supine on the table. His neck is extended
by putting a sand bag between the shoulder blades. The head is rotated to the opposite side and
the hand of the corresponding side is pulled downwards. Operation on both sides can be done
in one sitting. An incision is made about 1/2 inch above the clavicle starting from the lateral
border of the sternal head of the stemomastoid muscle to the medial border of the trapezius.
After incising the skin, superficial fascia, platysma and investing layer of the deep cervical fascia,
the clavicular head of the stemomastoid is divided and the inferior belly of omohyoid is retracted
upwards to expose the scalenus anterior and the phrenic nerve. The phrenic nerve is safeguarded
and the scalenus anterior is divided at its insertion to the first rib. The subclavian artery is
exposed. It is retracted upwards with a sling. Its branches are carefully safeguarded. The supra
pleural membrane is detached from the inner border of the first rib. The pleura is pushed
downwards and laterally to

expose the sympathetic trunk and
the corresponding posterior ends
of the ribs. The sympathetic trunk
is divided just below the 3rd
thoracic ganglion. The proximal
divided end is drawn upwards
and all the rami communicantes
joining the 3rd and 2nd thoracic
ganglia are divided. Finally the
sympathetic trunk is divided just
below the level of the attachment
of rami communicantes to the
. Skin incision for cervical sympathectomy.
stellate ganglion. This operation
can also be performed above the
subclavian artery, which is
probably a better approach for the
short necked patients. But in that
case the thyrocervical trunk
should be divided between
ligatures for better exposure.
B. AXILLARY APP
ROACH.— The patient lies
supine with the arm abducted.
An incision, about 5 inches in
length, is made on the medial
wall of the axilla along the line of
the 2nd intercostal space. To reach
phrenic the intercostal space, the fibres of
drawn serratus anterior have to be
medially
divided, but generally the long
pleura thoracic nerve lies a little
posterior to the incision and
subclavian hence less liable to be damaged.
The pleural cavity is opened and
Sibson's fascia is broken through with the finger taking
rib-retractor is used. The lung is
care not to tear the underlying pleura.
drawn downwards and forwards
to expose the sympathetic chain
covered with parietal pleura. The
pleura is incised and the
sympathetic trunk is removed
according to necessity. Bleeding
The sympathetic \ o J**. ! s'/ vessels are secured. The lung is
chain is divided \\ \ . // inflated and the wound is closed
between the with an under-water seal
third and drainage.
fourth ganglia. -—
C. POSTERIOR APP
11.— Steps of cervico-thoracic sympathectomy through
ROACH.— This is probably the
anterior approach.
least popular approach for this operation. A vertical incision is made about 5 cm lateral to the
midline keeping the third rib in the centre. All muscles are divided to reach the ribs. 5 cm of
the posterior end of the 3rd rib along with the corresponding transverse process is excised
subperiosteally. The sympathetic trunk will be exposed and excised according to necessity. For
proper exposure, the 2nd and 3rd intercostal nerves may be required to be divided. The
convalescent period is much prolonged and the operation is a lengthy procedure. For this, scope
of its application is very much limited.
Complications.—
1. Main complication is perforation of pleura leading to pneumothorax.
2. On the left side, lymph fistula due to damage to the thoracic duct may occur.
3. Homer's syndrome, which is manifested by ptosis, myosis, enophthalmos and anhidrosis
of that half of the face, may occur if adequate precaution is not taken.
ACROCYANOSIS
It is a condition in which there is persistent but painless cold and cyanosis of the hands and
feet. Though this condition is often confused with Raynaud's syndrome, yet the italic words in
the first sentence are the distinguishing features from Raynaud's syndrome. The basic pathology
is the slow rate of blood flow through the skin due to chronic arteriolar constriction. This results
in a high percentage of reduced haemoglobin in the blood, in the capillaries and this is the cause
of cyanotic colour. In some patients endocrine dysfunction has been found.
This condition also affects young women. Coldness and blueness of the fingers and hands
are persistently present for many years. The extremities are never completely normal. With heat
the colour may change from deep purple to red. Episodes of blanching (which is a common
feature of Raynaud's phenomenon) is absolutely absent in this condition. The peripheral pulses
are usually normal (same as Raynaud's phenomenon). There are no trophic changes indicative
of chronic tissue ischaemia such as atrophy or sclerosis of the skin or ulceration.
Treatment.—
Avoidence of cold temperature and reassurance are often helpful. One may try vasodilator drugs.
If the condition does not respond to above conservative measures, sympathectomy may be
carried out with reasonably good results.
THORACIC OUTLET SYNDROME

The thoracic outlet syndrome is the collective name which includes (i) cervical rib syndrome,
(ii) scalenus anticus syndrome, (iii) costoclavicular syndrome, (iv) hyperabduction syndrome, (v)
pectoralis minor syndrome and (vi) first thoracic rib syndrome. The syndrome is caused by
compression of the brachial plexus or subclavian artery and/or vein in the region near the
thoracic outlet. The symptoms may arise from neural, vascular or combined compression.
Anatomy.—
The subclavian artery leaves the thoracic cage by passing over the first rib between the
scalenus anticus muscle anteriorly and the scalenus medius muscle posteriorly alongwith the
brachial plexus. It then passes under the clavicle and subclavius muscle to enter the axilla beneath
the pectoralis minor muscle. The subclavian vein passes anterior to scalenus anticus muscle and
is in intimate relation with the head of the clavicle and the most medial portion of the first rib.
A potential area of compression exists firstly in the interscalene triangle between the scalenus
anticus anteriorly, the scalenus medius posteriorly and the first rib interiorly. Distal to this area
is again a narrow space — intercostoclavicular space — between the clavicle and the first rib. In the
axilla where the pectoralis minor tendon is attached to the coracoid process, the axillary artery
may be obstructed where it

travels round the coracoid
process. During hyperabduction
the axillary vessels and the
brachial plexus are bent at an
angle of approximately 90° in this
area and are liable to be
compressed.
Aetiology.—
(i) Cervical rib, which occurs
in approximately 1% of the
population, produces symptoms
in only 10% of cases. Symptoms
due to cervical rib are rare in
children, but are most frequently
seen in thin women in the 3rd
and 4th decades. Unusually well
developed musculature may
predispose to compression. Thin
women with long narrow necks
Fig.15.12.— Schematic diagram of the anatomy of thoracic outlet. may predispose to some variation
in the anatomy of the head and
neck. Gradual descent of the shoulder girdle perhaps from atrophy of the regional musculature
may cause onset of symptoms in the 2nd or 3rd decade.
(ii) A wide scalenus anticus muscle may narrow the space in the interscalene triangle and
may cause symptoms.
(iii) The width of the first rib is also of consideration as wider first rib may give rise to
symptoms.
(iv) Fractures of the clavicle or first rib, which produce subsequently bony callus, may lead
to small subclavian aneurysm, peripheral emboli and ischaemia of the hand.
Pathology.—
Compression of the brachial plexus usually affects its lower trunk (C8 & Tl). The ulnar nerve
is mostly involved.
Vascular symptoms may be intermittent from compression or temporary occlusion of the
subclavian artery. Claudication with exercise, pallor, sensation of coldness, numbness or
paraesthesia are the various vascular symptoms. If this condition continues, there may be
atheromatous changes in the artery or a post-stenotic aneurysm may develop. From these emboli
may be dislodged into the peripheral circulation and produce ischaemia of the fingers or hand.
Thrombosis of the .subclavian artery is a late and dreadful sequence.
Another group of vascular symptoms is due to intermittent vasoconstriction similar to that
seen in Raynaud's phenomenon. Unilateral appearance of Raynaud's syndrome should always gives
rise to suspicion of some pathology of thoracic outlet. The intricate cause is the presence of separate
sympathetic nerve for upper extremity. Usually sympathetic innervation of the upper extremity
is incorporated in the main trunks of the brachial plexus. But in only 10% of cases it comes from
a separate cord which is more prone to direct compression and irritation.
Sometimes venous hypertension of the upper extremity may result from intermittent
compression of the subclavian vein. Acute thrombosis of the subclavian vein may be a result of
thoracic outlet syndrome but the exact pathologic mechanisms are not clear.
Clinical features.—
The symptoms of thoracic outlet syndrome vary depending on whether nerves or blood vessels
or both are compressed. Majority of the patients are middle-aged females, although younger group
may be involved. Usually manifestations of compression of either nerves or the vessels dominate.
NEUROLOGIC SYMPTOMS are pain, paraesthesia and numbness usually in the fingers and
hands in the ulnar nerve distribution. Pain is of insidious onset and of general distribution. It
commonly involves the neck, shoulder, arm and hand. It may even radiate to the anterior chest
or posteriorly to the parascapular region. Paraesthesia and numbness are more specific in
distribution and mostly involve the cutaneous area supplied by C8 and T1 (ulnar nerve
distribution). Later on neurologic deficits in the form of sensory loss, motor weakness and atrophy
may develop.
SYMPTOMS OF ARTERIAL COMPRESSION are seen less frequently in about l/4th of the
cases. These include pain, numbness, paraesthesia, coldness and weakness of the arm or hand.
These symptoms are accentuated by exercise and exposure to cold. Distal embolization may
cause Raynaud's syndrome, which in late cases may produce digital ulceration and even gangrene.
The venous symptoms include oedema, venous distension, pain and cyanosis.
Physical examination.—
The signs of arterial compression may be evident by direct physical examination. There may
be differences in qualities of the pulses between the two arms when the subclavian, brachial and
radial arteries are compared.
Occasionally a subclavian and axillary aneurysm may be palpable in the infraclavicular area.
In mild forms of ischaemia one may find pallor on elevation of the arm. In more chronic
cases one may see atrophy of the skin, brittle nails or even focal ulceration.
In 5% of patients Raynaud's phenomenon can be induced by application of the cold to the
extremity.
Three diagnostic manoeuvres or tests can be applied for thoracic outlet syndrome. These are:
1. Adson's manoeuvre or test.— In this test the patient sits on a stool. The clinician feels his
radial pulse. The patient is now asked to inspire deeply, extend his head backwards and turn his
chin towards the affected side. Deep inspiration, extension of the neck and turning of the head
make the scalenus anticus muscle taut and may decrease or obliterate the radial pulse of the
affected side. The test is said to be positive if there is diminution or obliteration of the radial pulse
of the affected side.
2. Costoclavicular compressive manoeuvre or test.— Patient's radial pulse is felt. The patient
throws his shoulders backward and downward as an exaggerated military position. This will cause
reduction or disappearance of the radial pulse. This is produced by the compression of the subclavian
artery between the clavicle and the first rib. Simultaneously a subclavian bruit may be heard.
3. Hyperabduction manoeuvre.— Patient's radial pulse is again monitored. The affected arm
of the patient is now passively hyperabducted. This will cause reduction or disappearance of the
radial pulse due to compression by the pectoralis minor tendon. An axillary bruit can be heard
near the position of the pectoralis minor tendon.
In 10% of patients there may be signs of venous obstruction such as oedema and venous
distension.
On auscultation one may get supraclavicular bruit.

In only 20% of patients there may be objective signs of nerve compression. The clinician
must examine the sensory system and the motor system thoroughly. Both fine sensation and
crude sensation, sensation of temperature and vibration should be tested. These will be diminished
along the medial aspect of the forearm and hand in case of nerve compression. Strength of the
muscles, particularly the intrinsic muscles of the hand innervated by the ulnar nerve, should be
tested. Muscle weakness or even atrophy is a late feature of nerve compression.
Different ial Diagnosis.—
A few conditions have to be differentiated from the thoracic outlet syndrome. These are :
1. Cervical spondylosis.
2. Cervical disc protrusion.
3. Cervical cord compression.
4. Pancoast's tumour.
5. Brachial neuritis.
6. Raynaud's syndrome or phenomenon.
7. Carpal-Tunnel syndrome.
1. X-ray of the neck and chest.— This will demonstrate bony abnormalities e.g. cervical ribs,
bifid first rib, fusion of the first and second rib and clavicular deformities. This will also show
narrowing of the intervertebral foramina by exostosis or tumour.
2. Myelograms may be necessary to demonstrate protrusion of cervical disc or other causes
of cervical cord compression.
3. Arteriography.— This will diagnose arterial compression and exact location of it. One
may do the arteriogram while he is performing the Adson, costoclavicular and hyperabduction
manoeuvres. Arteriogram may occasionally demonstrate post-stenotic dilatation. When an
arteriogram is normal one should suspect neural compression.
4. Plethysmography may be used to know the arterial compression. By this technique one
can record changes in digit volume with each heart beat and can demonstrate obstruction of the
arterial flow.
5. Electromyographic studies may be performed to establish diagnosis of neural compression.
It is possible to detect sites of compression of peripheral nerves by recording the altered responses
of the distal muscles to proximal electrical stimuli. Nerve conduction times should be recorded
particularly through the ulnar nerve. Such conduction time will be significantly prolonged across
the thoracic outlet to the elbow and wrist. However, variability and unreliability of the nerve
conduction study have limited its usefulness in the diagnosis of thoracic outlet syndrome.
TREATMENT.—
In all cases, except those with complete vascular occlusion or poststenotic aneurysm,
conservative treatment should be given a trial.
CONSERVATIVE MANAGEMENT.— This consists of :
1. Weight reduction.
2. Exercise programme to strengthen the muscles of the shoulder girdle, particularly the
elevators. This will minimise the tendency of the shoulder to droop.
The above-mentioned conservative treatment relieves symptoms in 50% to 70% of patients.
Operation is only advised to those cases who do not respond favourably to this conservative
management.
OPERATIVE MANAGEMENT.— This is indicated to those, who do not respond to four or

more months of trial of conservative management.
Operative treatment includes (i) excision of the cervical rib, (ii) division of the scalenus
anticus muscle, (iii) resection of the clavicle and (iv) division of the pectoralis minor tendon.
(i) Excision of the cervical rib.— One of three incisions may be used for excision of the
cervical rib. These are (a) anterior supraclavicular incision, (b) posterior incision identical to that
used for an upper thoracoplasty and (c) transaxillary incision. See the treatment of cervical rib
later in this chapter for details of these operations.
If sympathectomy is indicated, the parietal pleura is stripped from the chest wall attachments
posteriorly and the sympathetic chain will be exposed for excision.
(ii) For scalenotomy operation anterior supraclavicular incision should be employed. For
further details of this operation, see page 226.
(iii) If the pectoralis minor tendon is compressing the neurovascular structures, division of
this tendon should be undertaken through the same transaxillary incision, at the same time the
first rib is resected.
Mild poststenotic dilatation of the subclavian artery usually does not progress once the
compression is relieved and frequently remains of no clinical consequence. However big aneurysm
of the artery should be excised and replaced with grafts, preferably vein graft.
Thrombosis of the subclavian artery should be treated by thromboendarterectomy or by-pass
grafting of the involved segment.
For venous compression, one has to divide the constricting bands which are merely extension
of the manubrial insertion of the stemomastoid muscle.
Occasionally the head of the clavicle may participate prominently in the compression, so that
it requires resection of the medial half of the clavicle. It is always recommended to do an operative
venogram to confirm that decompression operation has been successful. In extremely rare cases
one may find webs at the junction of the subclavian vein and internal jugular vein. This requires
venotomy and excision of the web with subsequent closure of the venotomy of the subclavian
vein.
BUERGER’S DISEASE (THROMBOANGIITIS OBLITERANS)

Buerger's disease was first described by Winiwarter in 1879, but it is Leo Buerger who
published in details this disease in 1908 and again in 1924. In reality, the classic syndrome
described by Buerger, is uncommon.
Definition.—
It is the inflammatory reaction in the arterial wall with involvement of the neighbouring vein
and nerve, terminating in thrombosis of the artery. Many cases diagnosed as Buerger's disease
are probably presenile atherosclerosis occurring in the 3rd, 4th and 5th decades of the life.
Incidence.—
The disease is found more frequently in men between 20 and 40 years of age. It is uncommon
in women, who constitute only 5% to 10% of all patients with Buerger's disease. This is more
common in the Jewish race.
Aetiology.—
A specific cause of this disease has never been demonstrated.
(i) There is a striking association with cigarette smoking and this disease. Usually 20 or more
cigarettes per day is required for this disease to occur. But it is obvious that there are so many
more smokers than patients with Buerger's disease.
(ii) There may be some hormonal influence which suggests the sex distribution. This disease
occurs rarely even in female smokers.
(iii) Patients with Buerger's disease usually come from lower socio-economic groups and they
often have poor hygiene. Fibrinogen levels are often elevated in these patients and a
hypercoagulable state has been postulated. Hyperaggregability of platelets has been reported.
(iv) Familial predisposition has been reported. A genetic factor is suggested as blacks are
rarely affected.
(v) Autonomic overactivity has also been suggested with severe peripheral vasospasm.
(vi) Recently an autoimmune aetiology has been postulated, based on the finding of both
antibodies and lymphocyte-mediated sensitivity to collagen in this disease.
(vii) There has been some association of this disease with Rickettsial disease.
It appears almost certain that some immunologic process, potentiated by cigarette smoking,
plays a major role in Buerger's disease.
Pat hology.—
An obvious inflammatory process features the Buerger's disease. The diseased artery is
usually surrounded by a dense fibrotic reaction which incorporates the adjacent vein and less
often the neighbouring nerve. This seems to be the characteristic of thromboangiitis obliterans.
The lesions in Buerger's disease are segmental and usually begin in arteries of small and
medium size. Both upper and lower extremities are affected in contrast to arteriosclerosis which
usually spares the upper extremities. In the lower extremities the disease generally occurs beyond
the popliteal arteries, starting in tibial arteries extending to the vessels of the foot. In the upper
extremities it is manifested by arterial involvement usually distal to the forearm in about 30% of
patients. Thromboangiitis has also been described in the G.I. tract, veins, lungs, heart etc.
Early in the course of Buerger's disease, the superficial veins are involved producing the
characteristic migratory, recurrent superficial phlebitis (but the larger and deep veins are seldom
affected).
The acute lesion consists of acute arteritis and periarteritis, acute phlebitis and periphlebitis.
The walls of the vessels are invaded by polymorphonuclear leucocytes. Thrombosis occurs within
the vessels with occlusion of the lumen. Giant cells are often present in the thrombus. Small
micro abscesses within the thrombus may characteristically present. These abscesses have central
foci of polymorphonuclear leucocytes. Only a segment of the vessel is involved, which may be
long or short.
In chronic lesion, the artery and the vein are bound together by fibrous adhesions. The nerve
may also be involved in the same adhesions. Involvement of the nerve is responsible for agonising
pain. The thrombus shows fibroblastic activity and endothelial proliferation. The thrombosis is
now organized into fibrous tissue. The internal and external elastic lamina of the artery are
frequently much thickened.
Thromboangiitis obliterans occurs almost exclusively in males between 20 and 40 years of
age. The typical patient is one who is a heavy smoker and had started smoking at an early age.
One should always suspect the diagnosis of Buerger's disease when a young male smoker presents
with peripheral ischaemia, particularly if the upper extremity is involved and if there is a history of
migratory superficial phlebitis.
SYMPTOMS.—
Due to the peripheral involvement, the
pedal arteries are affected earlier and the
patients complain of pain while walking at the
arch of the foot (foot claudications), somewhat
less often at the calf of the leg, but never at
the thigh or buttock (which is common in
atherosclerosis). In the upper extremity it is
the vessels distal to the wrist that are involved
so claudication is rare in upper extremity.
Pain is typical of intermittent claudication i.e.
pain is increased when the muscle is exercised
and disappears when the exercise stops.
Progression of ischaemia is similar to that
in all chronic progressive arterial occlusions.
Intermittent claudication progresses to rest
pain. Gradually postural colour changes
appear, followed by trophic changes and
eventually ulceration and gangrene of one or
more digits and finally of the entire foot or
hand requiring amputation.
Pain in Buerger's disease also results from
phlebitis and ischaemic neuritis. Gradually
rest pain is so intense that the patient cannot
sleep. Some amelioration may be achieved
by placing the affected limb in dependent
position. The limbs become rubor or red on
dependence and pallor on elevation.
One must remember of occasional involvement of the mesenteric or cerebrovascular
circulation. Symptoms may be complained of from this involvement.
INSPECTION.—
There may not be any specific finding till gangrene develops. The peculiar feature is that the
ischaemic area is usually sharply demarkated with relatively good circulation in adjacent tissues.
Before gangrene one may find signs of chronic tissue ischaemia. These include loss of hair from
the digits, atrophy of the skin and brittle nails. Gradually there may be ulceration or gangrene
of the toes commencing in the distal portion of the digit near the nail and gradually extend
proximally to involve whole of the foot or hand.
PALPATION.—
The most frequent finding is absence of posterior tibial and dorsalis pedis pulses in the feet.
Absence of the posterior tibial pulse is highly suggestive of the diagnosis especially when bilateral.
In the upper extremity the radial pulse may be absent and when bilateral it is also suggestive of
this disease.
Special Invesligations.—
ARTEFUOGF?APHY is obviously the most important investigating procedure. In arteriography,
it is the peripheral arteries which are first involved e.g. digital arteries or dorsalis pedis artery.
While the contours of large arteries are normal and smooth, there are abrupt areas of occlusion
in the arteries of the calibre of tibials, frequently surrounded by extensive collateral circulation
which has been typically termed the 'tree root' or 'spider legs' in appearance. A 'cork screw'
deformity has also been observed in peripheral arteries representing partial recanalisation of the
arteries previously occluded by thrombi.
So the characteristic arteriographic appearance of this disease is the smooth and normal appearance
of larger arteries in combination with the extensive occlusion of the smaller arteries alongwith extensive
collateral circulation.
Treatment..—
CONSERVATIVE TREATMENT has a great role to play in this disease.
(i) Every effort should be made to make the patient stop smoking. Indefinite remissions may
follow stoppage of cigarette smoking.
(ii) Various drugs have been tried with questionable value. This included vasodilator drugs,
anticoagulants, dextran, phenylbutazone and steroids. More recently prostaglandin therapy
(PGA-1) has been advocated to prevent platelet aggregation.
SURGICAL TREATMENT.—
(i) Role of sympathectomy is doubtful. Perhaps 50% of patients are significantly benefited
from this procedure. It has got a specific role in relieving pain.
(ii) Arterial reconstruction is also difficult as the distal arteries are usually involved. It may
be considered in rare cases where there is segmental proximal occlusion. Occasionally patients
with Buerger's disease develop atherosclerosis in major arteries. Such a combination may be
suspected if the popliteal pulse is absent. In these patients arterial reconstruction may be performed
on the atherosclerotic proximal arteries, which in fact causes marked circulatory improvement.
(iii) Microvascular transplantation of free omental grafts to areas not amenable to arterial
reconstruction has been successfully tried.
(iv) Amputation is the only way out when gangrene occurs. The approach is conservative
and lowest possible level should be chosen. When gangrene is confined to a toe, amputation may
be postponed, unless rest pain or infection is rather uncontrollable. Amputation should be limited
to the area of gangrene. When below-knee amputation can remove the gangrenous area, it will
not be justified to go for above-knee amputation.
Prognosis.— The risk of amputation is about 20% within 10 years after onset of symptoms.
Although this varies with the use of tobacco. In a few patients who stop smoking completely,
progression of the disease is greatly restricted.
CERVICAL RIB AND SCALENUS ANTICUS SYNDROME

Surgical Anatomy.—
The costal element may develop from the anterior part of the transverse process of the 7th
cervical vertebra. This may sometimes develop into a rib which is known as the cervical rib. In
extreme rare conditions one may find a 6th cervical rib.
Brachial plexus is formed by lower four cervical nerves (C5, 6, 7, 8) and the first thoracic
nerve. When there is a very small contribution from the first thoracic nerve (Tl), this condition
is known as prefixed brachial plexus. Cervical rib may accompany such condition. Sometimes the
brachial plexus receives a big contribution from Tl and also a small part of T2. This condition is
called postfixed brachial plexus. Such condition even with normal first thoracic rib, may cause
symptoms similar to a cervical rib.
Types of cervical ril>.—
It must be remembered that by mass radiography it has been found out that the cervical rib
(coming out from the 7th cervical vertebra) is present in 0.45% of all individuals. In more than
1/2 cases the cervical rib is unilateral. It is commoner on the right side.
Four types of cervical rib are usually found. These are :
1. Complete cervical rib.— Such rib articulates anteriorly (a) either with the manubrium
stemi or (b) with the first rib.
Incomplete varieties — .
2. The cervical rib ends as a large bony mass.
3. The cervical rib ends tappering connected with a fibrous cord to the scalene tubercle of
the first rib.
4. There is no bony cervical rib, but its place is taken by a fibrous band which is incorporated
in the scalenus medius muscle. Obviously it cannot be demonstrated radiologically.
Pathology.—
The subclavian artery and the brachial plexus pass through a narrow triangle, termed the
scalene triangle, which is bounded anteriorly by the scalenus anterior muscle, posteriorly by the
scalenus medius muscle and inferiorly by the first rib.
When the cervical rib is present, the floor of the triangle is raised. Both the subclavian artery
and the lower trunk of the brachial plexus are raised. The lumen of the subclavian artery becomes
constricted. A small poststenotic fusiform dilatation occurs just distal to the constriction. Within
the dilatation clotting occurs on the intima and then thrombus is formed. Portions of this thrombus
may become detached and give rise to emboli. Sometimes, of course rarely, there may be proximal
extension of the thrombus, so that the opening of the vertebral artery may be involved leading
to cerebrovascular embolic episodes.
Due to presence of the cervical rib or due to postfixed brachial plexus, the lower trunk of the
brachial plexus is lifted up leading to compression of this trunk. Neurological deficiencies may
develop from such stretching or compression. Such deficiencies will be limited to the lower trunk
i.e. C8 and Tl distributions. Irritation of the periarterial sympathetic fibres or damage to the
sympathetic fibres content in the lower trunk will lead to vasomotor disturbances.
Sometimes there may not be only cervical rib or postfixed brachial plexus, but abnormally
well developed scalenus anterior muscle may elevate the first rib and compress on the subclavian
artery and the lower trunk of the brachial plexus to give rise to similar symptoms as those of
cervical rib. This is known as scalenus anticus syndrome.
Majority of the patients who present with symptoms of cervical rib and scalenus anticus
syndrome are women over 30 years of age. Slim women with long narrow neck are more
susceptible.
Various clinical types encountered with cervical rib are —
I. CERVICAL RIB WITH NO SYMPTOMS.— As discussed earlier, while 0.45% of the
general population possess cervical rib, only a few come to the clinician with complaints. In fact
well formed cervical ribs (complete) on X-ray examination are usually without symptoms. It is
often the fibrous band or incomplete cervical rib which produces symptoms.
II. CERVICAL RIB WITH LOCAL SYMPTOMS.— Patients may present with symptoms
locally due to presence of cervical rib. They complain of pain and tenderness in the supraclavicular
fossa. On palpation a bony hard, totally fixed lump may be detected in the supraclavicular fossa.
This is obviously the cervical rib.
III. CERVICAL RIB WITH VASCULAR SYMPTOMS.—
(i) Pain.— It is a common symptom with cervical rib. It is mostly located in the forearm,
but sometimes it radiates to the upper arm. The pain is characteristic of intermittent claudication
i.e. pain appears with the use of the arm particularly when the arm is in raised position at the
time of exercise. The pain is relieved by rest. This pain is of ischaemic muscle.
(ii) The hand of the affected side is colder and paler than its fellow of the opposite side.
Sometimes the hand and the fingers may become cyanosed when it is dependent for long.
(iii) Numbness of the fingers is a very common complaint. In a long continued case there
may be ulceration or even gangrene of the fingers.
(iv) Radial pulse is sometimes as full as that of the other side. But if Adson's test is
performed or the arm is hyperabducted, the radial pulse may become feeble or even absent on
the affected side.
Sometimes a systolic bruit can be heard over the distal part of the subclavian artery.
IV. CERVICAL RIB WITH NEUROLOGICAL SYMPTOMS.— Neurological symptoms from
cervical rib is not that common. Usually the lower trunk of the brachial plexus i.e. C8 and Tl
segments are affected.
(i) Sensory disturbances may be detected along the medial aspect of the forearm, the
hand, the little finger and the medial aspect of the ring finger. Fine sensation may be lost. One
must test crude sensation, temperature sensation, vibration sensation in these parts.
(ii) Motor disturbances are also distributed along C8 and Tl. The muscles of the
hypothenar eminence and other small muscles of the hand supplied by the ulnar nerve are
usually affected. Weakness and in late cases wasting may be noticed.
Again it is emphasized that neurological symptoms are less common in cervical rib than
vascular symptoms. When a case is presented mainly with neurological symptoms alongwith
presence of cervical rib, one must exclude (i) pressure on the cervical roots in the region of the
intervertebral foramina, (ii) protrusion of intervertebral cervical disc, (iii) Carpal-Tunnel syndrome
or (iv) angulation of the ulnar nerve behind the elbow, before one comes to the conclusion that
the neurological symptoms are due to the cervical rib only.
Treatment.—
1. No symptom — no treatment.
2. CONSERVATIVE TREATMENT.— This is indicated in all cases as the first mode of
treatment. This is primarily aimed at strengthening the muscles of the shoulder girdle. Majority
of the symptoms are due to sagging down or drooping of the shoulder.
Conservative treatment includes —
(i) Use of a sling. -
(ii) Physiotherapy and exercises to strengthen the muscles of the shoulder girdle and to
elevate the shoulder.
(iii) Certain analgesics.
(iv) The patient is instructed not to carry heavy weight like a bucket full of water, a heavy
shopping basket etc.
About 80% of cases are relieved of symptoms by this simple conservative management.
3. OPERATIVE TREATMENT.— Operation is advised —
(a) When conservative treatment fails.

(b) When there is vascular symptom.
(c) When there is neurological symptom.
OPERATIONS.—
A. When cervical rib is present — extraperiosteal excision of the cervical rib together with
any bony prominence of the first rib is performed. The whole of the cervical rib must be excised
alongwith its fibrous band if present. Sometimes first rib is also excised when it is noticed that
it is compressing the subclavian artery or the post fixed brachial plexus. The periosteum of the
rib should also be excised, so that there is no chance of regeneration of the rib.
One should also perform scalenotomy i.e. scalenus anticus muscle is divided close to its
insertion.
Excision of the cervical rib.— One of the three approaches may be adopted for excision
of the cervical rib. Anterior approach is by far the most popular.
(a) ANTERIOR APPROACH.— Position.— The patient lies supine on the table. The neck is
extended by placing a sand bag between the patient's shoulders. The arm of the affected side is
drawn strongly downwards.
Technique.— The incision is made one inch above the clavicle starting in front from the
clavicular attachment of the stemomastoid muscle to the anterior border of the trapezius behind.
After incising the skin, superficial tissue and platysma, the investing layer of the deep cervical
fascia will be exposed. It is incised and the lateral border of the stemomastoid is retracted
medially to expose the scalenus anterior muscle lying behind the stemomastoid. When the scalenus
anterior muscle is exposed, a careful search should be made for the phrenic nerve, which lies in
front of the scalenus muscle but behind the prevertebral fascia. The subclavian vein is protected.
The phrenic nerve is protected and the insertion of the scalenus anterior to the first rib or into
the cervical rib, is divided. The knife edge is kept against the bone, so that the subclavian artery
is not injured. The brachial plexus is retracted gently downwards and forwards and the scalenus
medius muscle is defined. The fibres of this muscle, inserted into the cervical rib, are also divided.
The cervical rib is cleared off all attachments and the pleura must be safe-guarded. The rib is next
disarticulated from the transverse process of the seventh cervical vertebra or is divided as far
posteriorly as possible. The periosteum is never lifted off the cervical rib and it is excised along
with the periosteum.
(b) POSTERIOR APPROACH.— The incision is identical to that used for an upper
thoracoplasty. The subclavian vessels and the brachial plexus are easily exposed and are displaced
anteriorly. Cervical rib may be excised through this approach and this provides ample exposure
for reconstruction of the vessels if required.
(c) TRANSAXILLARY APPROACH.— The incision is made in the lower most portion of the
axilla from the pectoralis major anteriorly to the latissimus dorsi posteriorly. The incision is
deepened to the muscle of the chest wall. The serratus anterior and the intercostal muscles are
now exposed. The intercostobrachial nerve is saved. Dissection is continued upward and just
above the first rib one can see scalene muscles which are inserted to the first rib. The scalene
muscles are transected. The cervical rib is identified. Any attachment to the cervical rib is divided
and the cervical rib is removed in its entirety including the periosteum. If required the first rib
is also removed from the costochondral junction anteriorly to the posterior angle of the rib
posteriorly. The parietal pleura usually lies deep to the dissection. In case the pleura is punctured,
the puncture is closed around a catheter whilst the anaesthetist expands the lungs.
15
Scalenotomy.—
Position.— Same as that described for excision of the cervical rib.
Technique.— Incision is same as that applied for excision of the cervical rib. After the scalenus
anterior muscle is exposed, the phrenic nerve is protected and the insertion of the scalenus
anterior is divided from the first rib. After division of the scalenus anterior muscle the subclavian
artery and the brachial plexus will slide forward and will be relieved of compression. The
subclavian artery and the lower trunk of the brachial plexus should be examined carefully whether
they are really relieved of any stretching or compression. Sometimes the nerve trunk appears to
be stretched over the medial tendinous fibres of the scalenus medius. In this case these fibres
should also be divided.
B. When there is no cervical rib — only scalenotomy is performed. A thorough search should
be made for presence of a fibrous band in the substance of the scalenus medius muscle or
neighbourhood. If this be present, it must be excised.
ACUTE ARTERIAL OCCLUSION

Sudden occlusion of an artery is commonly due to A. Emboli or B. Trauma.
Aetiology and Pathology.—
A. Emboli.— The Greek word 'embolus' means 'something thrown in'. Two types of
embolization are seen — (i) cardioarterial embolization and (ii) arterioarterial embolization.
(i) CARDIOARTERIAL EMBOLIZATION.— In about 90% of patients emboli in the lower
extremity originate in the heart. The main three causes are — atrial fibrillation, mitral stenosis
and myocardial infarction.
Atrial fibrillation is often seen in mitral stenosis cases. It may also occur from atherosclerosis
without mitral stenosis particularly in older patients.
With mitral stenosis emboli originate from thrombi which are formed in the left atrium because
of restriction of blood flow through the stenotic mitral valve. These patients may also have atrial
fibrillation which may be the cause of emboli formation.
In myocardial infarction emboli originate from mural thrombi which are formed over the
endocardial surfaces of the infarcts. Such embolization usually occurs in the first 2 to 3 weeks
following infarction.
Other rare causes of cardioarterial embolization are bacterial endocarditis and atrial myxoma.
Sites.— Majority of emboli which arise from the heart usually lodge in the arteries of the
lower extremities. These constitute more than 70% of cases. About 10% to 15% emboli lodge in
the superior extremity. About 10% of emboli lodge in the cerebral circulation intracranially.
Another 5% emboli lodge in the visceral arteries — the superior mesenteric, renal etc.
Emboli of the lower extremity usually lodge at bifurcation of major arteries where the diameter
abruptly narrows. The common sites according to frequency of occurrence are : at the bifurcation
of common femoral artery (about 35%), at the bifurcation of popliteal artery (15%), at the bifurcation
of the common iliac artery (14%), at the bifurcation of the aorta (10%). In the superior extremity
the commonest site is at the bifurcation of the brachial artery (about 10%), followed by axillary
artery near shoulder joint (4.5%).
Effects.— The result of arterial embolization is the immediate onset of severe ischaemia of the
tissues supplied by the involved arteries. If untreated, gangrene occurs in about 50% of cases
depending upon the artery involved. The peripheral nerves are very sensitive to oxygen deprivation.
Ischaemia in these peripheral nerves lead to

pain, paraesthesia and paralysis. Striated
muscles are less susceptible to oxygen
deprivation and necrosis only appears after 4
to 6 hours. This time of course varies
depending on the size of the artery occluded,
collateral circulation and outside temperature.
.
axillary 4.s7
Necrosis may be delayed upto 12 hours if
collateral circulation is good. -brach.ial 9.1?
aorta 9.i£ —
Due to embolization there is sluggish flow co nvmotv
iliac 13.6 i
or stagnation of blood in arteries distal to the external / uln.ar 1.2%
embolus, which will cause secondary iliac 3.0J?—'/ radial 1.2 7-
thrombosis to develop. These secondary common. \/\
femoral 34.0 £
thrombi further occlude major collateral superficial, _
r femoral 4.5?
channels and intensify ischaemia and
gangrene formation. Ultimately circulatory
popliteal 14.2 7-
stasis becomes more extensive to cause venous
thrombosis. posterior*
tibial 2.a 7- —
(ii) ARTERIOARTERIAL EMBOLI
ZATION.— This embolization originates from anterior
tibial 2,&7°—
atherosclerotic plaque which has become
ulcerated. Such ulcerated surface becomes
covered by platelets and fibrin which are Fig. 15.14— Shows frequency of different sites of
intermittently dislodged. These emboli may embolus lodgement,
lodge anywhere, either near the atherosclerotic
artery of some distance away from it. Emboli at the ends of anterior tibial and posterior tibial
arteries may originate from the atherosclerotic plaques in the abdominal or thoracic aorta.
Sometimes progressive ischaemia occurs which terminate to gangrene or repeated embolic episodes
are seen with almost complete recovery between the episodes.
B. Trauma.— Arterial trauma may cause acute arterial occlusion. Most arterial injuries
result from penetrating wounds which partly or completely disrupt the walls of the arteries.
Penetrating injuries may be associated with fractures in the adjacent bones which cause arterial
blockage.
Most arterial injuries are either lacerations or transections of the arterial wall. Less common
injuries are arterial contusion with thrombosis. Rarer causes may be simple spasm of the arterial
wall in association with fractures and/or extensive soft tissue injuries from blunt trauma. Very
occasionally arteriovenous fistula may develop. Sometimes swelling of the surrounding soft tissues
may cause blockage of the artery within the fixed fascial compartments, which are known as a
compartmental syndrome (see above).
Clinical features.— There is nothing specific in the local clinical symptoms and signs of
arterial embolism that distinguishes it any way from other causes of acute limb ischaemia, as
mentioned above.
The best way to distinguish between arterial embolism and other causes of acute limb
ischaemia is to take proper history and to examine the rest of the patient. Valvular heart disease
and recent myocardial ischaemia account for majority of causes. Presence of atrial fibrillation
should always give rise to the suspicion of cardio-genic embolism.
The 5 'P's are the best way to describe the clinical presentation of acute arterial occlusion.
The 5 'P's are — Pain, Paralysis, Paraesthesia, Pallor and absent Pulses.
The onset is almost always abrupt, very rarely it may be gradual. In 80% of cases there is
severe pain referred to the most peripheral portions of the limb. Alongwith the pain, the colour
of the affected extremity becomes extremely pallor or mottling due to alternate areas of pallor
and cyanosis, Neurologic symptoms carry a prognostic value. If motor and sensory functions are
intact, the extremity will survive. In majority of cases there may be some sensory disturbances
which vary from paraesthesia to anaesthesia. Paralysis, either partial or complete may occur in
this condition. Sometimes paralysis with anaesthesia may elude the clinician to divert his attention
towards neurologic disease.
PHYSICAL EXAMINATION.—
Inspection.— The affected extremity looks pale with collapsed peripheral vein.
Palpation.— Local temperature is cold below the site of lodgement of embolus. This temperature
level should coincide with the colour changes.
Palpation of arterial pulse is the most important examination to know the site of obstruction.
The pulse of the main artery if traced down, suddenly the pulsation will be lost at the point of
obstruction. There may be a tender small swelling. It should not be too difficult to determine the
level of occlusion. The guides are palpation of pulses, colour change and temperature change. It
must also be noted that at the site of lodgement of embolus the artery feels firm and often tender.
For practical purposes this means that if the common femoral pulse is absent, the embolus is
either lodged there in which case the artery becomes firm and tender or higher up most probably
in the common iliac in which case the femoral artery is soft and non tender. Similarly the
popliteal pulse becomes absent and the artery is tender when the embolism is within it. Sometimes
the popliteal pulse is full and bounding, even stronger than the normal side. This happens when
a small embolus impacts at the bifurcation of the artery below the level of the knee. The pulse
can usually be traced down to the point where it meets the obstruction; here there is often a
tender small swelling and the pulse is lost.
However the level of ischaemia does not correspond to the level of site of occlusion. An iliac
embolus produces ischaemia at the level of the hip joint, while a common femoral embolus
produces ischaemia distal to the knee. These of course vary with the effectiveness of the collateral
circulation. Palpation of muscle is important. In the early stage a doughy sensation is felt on
palpation. The importance of this feeling is that when the muscles are soft the extremity can be
salvaged with effective embolectomy, regardless of how long the embolus has been present. With
continuing ischaemia, the muscle progresses to necrosis and finally to rigor mortis, at this time
the muscles feel stiff. Palpation of stiff muscle means the necrosis has occurred. At this time
effective embolectony is not possible.
The most important aspect of physical examination is the cardiac examination, which should
not be missed.
As soon as the patient is examined and the diagnosis is made, a critical decision is to
whether an angiography should be performed or not. If performance of angiography delays
operation beyond 4 to 6 hours of 'golden period', it should be omitted. Intraoperative angiography
is alternative, which is particularly useful where the site of embolus is uncertain. .
E.C.G. and Chest X-ray should be performed to evaluate the presence of cardiac diseases.
TREATMENT.—
A. FOR EMBOLUS.—
Arterial embolectomv is the treatment of choice and it should be performed as early as
possible, at least before 4 to 6 hours to prevent muscle necrosis, however it does not guarantee
that claudication will not subsequently develop in the extremity.
As soon as the diagnosis is confirmed and the decision for operation is taken, Heparin, 5000
to 10000 units is given intravenously by continuous I. V. drip.
Some surgeons recommend administration of large doses of Heparin to promote lysis of
emboli and thereby improve the chances of operative success. 30000 units of Heparin is
administered intravenously as a bolus followed by doses of 2000 to 3000 units per hour by
continuous I.V. drip. If clinical improvement occurs, operation may be deferred.
OPERATIVE TECHNIQUE.— For operations on the extremities, local anaesthesia is preferred
in seriously ill patients. Only when the patient is clinically well and the anaesthetist or cardiologist
gives his approval, a general anaesthetic should be considered.
With the lower limb fully prepared and toweled as for a varicose vein operation, a longitudinal
incision is made over the common femoral artery. There is no place for cosmetically pleasing
skin-crease incision in this operation. The femoral vascular sheath is opened and more local
anaesthetic may be needed. The common femoral artery is gently freed from its bed using a
curved forceps e.g. Moynihan's cholecystectomy forceps and a tape is passed under it to lift the
artery. First 1 inch or so of the superficial femoral and the origin of the profunda femoris are
cleared sufficiently to permit the application of bulldog arterial clips. At this stage, 5000 units of
Fig.15.15.— Arteriography showing embolization of the popliteal artery in the first figure. Second figure shows
good arterial flow following embolectomy operation.
heparin may be given intravenously or preferably into the pulsating proximal part of the femoral
artery, particularly if heparin is not given earlier. With the arterial sling tape, a short incision is
made over the common femoral artery, where the embolus is lodged. The embolus characteristically
pops out as soon as the lumen is entered. It is removed. It may be followed by a brisk spurt of
arterial blood, then the proximal clamp is applied with a curved Crafford coarctation clamp. The
distal thrombus is then removed with the Fogarty balloon catheter. Usually No. 5 or 6 is used. With
the balloon deflated, the lubricated catheter is passed through arteriotomy as far as possible
down the main artery. The balloon is gently inflated till resistance is felt in the syringe. The
catheter is now gently withdrawn adding slightly more saline to the balloon as the artery size
increases proximally. A long coiled black thrombus with paler pieces of embolus will then emerge
from the arteriotomy. Several passes may be needed to remove all possible thrombus and to
achieve back-bleed of arterial blood. The same manoeuvre is then repeated down the profunda
femoris artery. Each artery is clipped with a soft bulldog clamp.
If there is larger proximal thrombus, with the removal of the embolus, no spurt of arterial
blood will be seen. In this case the Fogarty catheter is inserted upwards through the arteriotomy
with the distal femoral clipped. It is passed upwards for at least 25 cm. The balloon is inflated
and the catheter is gently pulled down. Portions of the embolus and thrombus alongwith a gush
of arterial blood under full pressure will emerge through the arteriotomy. More than one pass
may be necessary.
Arteriotomy is closed with 5/0 arterial suture preferably prolene. The distal clamps are
removed first and any leaks detected is secured with further interrupted sutures. It is preferable
whenever possible not to reverse the action of Heparin at this point to aid removal of stasis
thrombus from the smaller branches.
In some complicated cases, not all of the thrombus may be removed via the common femoral
arteriotomy. In this case a medial approach to the popliteal artery below the knee and sometimes
the posterior tibial artery at the ankle may be required to be opened for full clearance of extensive
or adherent thrombus from these areas.
In late cases with doubtful limb viability and established muscle contracture, revascularization
of the limb may bring about profound metabolic acidosis from ischaemic areas. Infusion of
sodium bicarbonate solution systemically 100 mol or more should be required. Otherwise a
cardiac arrest may occur.
As with all ischaemic cases, there is risk of anaerobic infection it is advisable to give a
preventive large dose of penicillin.
In the postoperative care, the most important aspect is to see that the peripheral circulation is
adequate. Palpation of arterial pulses is the best clinical sign. Pulses which are difficult to feel can
be checked with the doppler instrument. The mode of heparin administration is important. Some
surgeons do not give heparin for 6 hours postoperatively and then to administer it by intermittent
intravenous injection in doses of 5000 units every 6 hours. Oral therapy with Coumarin derivatives
is started after 4 days and continued as long as the patients are at risk. Later on attention should
be given to the heart problems to cure these.
Intra-arterial thrombolysis.— When the ischaemia is not so severe that arterial
embolectomy is mandatory, it may be possible to treat either the embolus or thrombosis by
intra-arterial thrombolysis. Firstly an arteriography is performed and the occlusion is noted. A
narrow catheter (5F gauge) is passed into the occluded vessel and left embedded within the
clot. A thrombolytic agent is now infused for several hours. Heparin 250 units per hour is also
added to the infusing material. The common thrombolytic agents used are streptokinase,
urokinase and tissue plasminogen activator (TPA). Today TPA is mostly used because of its
relative rapidity of action. It has also least allergic side effects. Angiograms are carried out at
regular intervals to know the extent of lysis. The method is abandoned when there is no further
dissolution of clot. The main contraindications of this technique are recent stroke, bleeding
diathesis and pregnancy.
B. FOR ARTERIAL TRAUMA
The treatment is operation and depends on the type of injury to the artery. If a portion of
the arterial wall is damaged, it can be repaired with a vein patch. If the artery is through and
through divided, end-to-end suturing is the best method. If a portion of artery is contused or
lacerated, this segment should be removed and an attempt is made for end-to-end anastomosis.
If the loss of artery is more than 2 cm, direct anastomosis cannot be performed. In this case
autogenous vein graft in the form of reversed long saphenous vein is mostly used.
Ligation of an injured artery should be performed only in case of injury to the minor arteries
such as the radial or ulnar artery, neither of which is essential for limb survival provided one of
these remains uninjured.
Fat Embolism.—
It occurs after major bone fractures e.g. fracture femur, fracture tibia and fibula or in multiple
fractures. It usually occurs in 24 to 72 hours.
Pathogenesis.— It occurs from aggregation of chylomicrons derived from bone marrow.
Clinical features.— Manifestations can be described under following heads —
Cerebral.— Restlessness, disorientation, constricted pupil, drowsiness, pyrexia and ultimately
coma.
Cutaneous.— Petechial haemorrhages in the skin.
Pulmonary.— Tachypnoea, cyanosis, right heart failure, fat droplets in sputum, froth in the
mouth and nostril and finally respiratory failure.
Kidney.— Blockage in renal arteriole causing renal failure. Fat droplets in urine.
Retina.— Emboli in the retinal artery causing haemorrhages in retina detected in fundoscopic
examination.
Management.—
• Ventilator support.
• Heparinization.
• Hyperbaric oxygen.
• Low-molecular weight dextran.
Air Embolism.—
Causes.—
• Commonest cause is through I.V. drip.
• From traumatic opening of major veins suctioning air inside.
• During fallopian tube insufflation.
• During surgeries of neck and axilla.
• During antifungal pneumothorax.
About 50 ml air should be sucked in to cause air embolism. First air enter the right atrium where
it gets churned to form a foam which enters the right ventricle and blocks the pulmonary artery.
Clinical diagnosis can be made by hearing Mill-wheel murmur over the pericardium by
stethoscope.
Management.—
• Patient is placed in Trendelenburg position. A needle is introduced into the right ventricle
to aspirate air. If this is not sufficient open thoracotomy is performed to aspirate air completely
which is responsible to cause the block.
Therapeutic embolization.—
Indications.—
• To arrest haemorrhage in G.I. bleeding, urinary bleeding etc. Embolization of
gastroduodenal artery or left gastric artery in duodenal ulcer bleeding or gastric ulcer bleeding
respectively. It is also used in bleeding from oesophageal varices.
• In haemangiomas.
• In case of malignancies e.g. hepatoma, renal cell carcinoma etc.
• AV fistulas.
Materials used for therapeutic embolization.—
• Gel foam.
• Quick setting plastics.
• Plastic microphones.
• Wool.
• Ethyl alcohol.
• Stainless steel coils.
• Blood clots.
Decompression Disease or Caisson’s J )isea.se.—
This condition develops from rapid decompression when an individual travels by air or goes
to high altitude or when deep sea divers come to the surface. In this case bubble of nitrogen
blocks the small vessels.
• When lung vessels are affected, chest pain or tightness or choking is complained of.
• In case of spinal cord vessels ischaemia causes neurological deficit.
• When vessels of muscles and joints are affected — it causes tremendous pain.
Treatment.—
• Instead of sudden decompression, gradual decompression is followed.
• Oxygen therapy.
GANGRENE
Definition.— Gangrene is death of a portion of the body with putrefaction. It must be
remembered that gangrene is not just necrosis or infarction, but in every case of gangrene there
should be infection with saprophytic putrifying bacteria which add rottenness to death of the part.
Types of gangrene.— There are two types of gangrene — 1. Dry gangrene and 2. Moist
gangrene.
1. DRY GANGRENE.— The characteristic features are —
(i) The part is gradually deprived of its arterial blood supply.
(ii) There is characteristic colour change — first greenish and finally black due to
haemolysis of the red blood corpusles. The term 'mummification' is applied to such dry and
shrivelled foot, which is exactly like that of a mummy.
(iii) There is mainly arterial occlusion, but the venous outflow remains unimpeded.
(iv) Occlusion of the artery is by a chronic process e.g. atheroma with superadded
thrombosis or due to an acute process e.g. embolus or ligation of one of the main arteries,
(v) There is a definite bright red line of separation appears between the living and dead
tissue. This line indicates a process of inflammation due to the contact of the dead with the still
living tissue. There is dilatation of vessels and an exudation of leucocytes. As the blood supply
of the skin and subcutaneous tissue is less abundant than that of the muscles and bone, destruction
of former will proceed further up the limb than that of the latter, so that the resulting stump will
be conical in form.
(vi) The conditions which produce dry gangrene are senile gangrene, diabetic gangrene,
Buerger's disease, Raynaud's disease, sudden vascular occlusion e.g. embolism, ligation or injury
to the vessel, frostbite and due to escharotics (strong acid or alkalis).
2. MOIST GANGRENE is characterized by moist and oedematous limb, with colour
changes which vary among dark red, green, purple and black owing to sulphurated hydrogen
produced by the putrefactive bacteria acting upon the liberated haemoglobin due to haemolysis
and with horrible odour, which is partly due to nitrogenous products such as indol and skatol
and partly due to nonnitrogenous products e.g. sulphurated hydrogen, butyric acid and lactic acid.
The characteristics of moist gangrene are —
(i) When the vein is obstructed, so that no blood can leave the part. No fresh blood can
enter, so liquifaction and bacterial infection occur to cause moist gangrene.
(ii) The part is cold, pulseless, swollen and oedematous. The colour also changes in this
condition. The skin becomes raised into blebs which contain foul smelling fluid.
(iii) It is characterized by horrible odour.
(iv) There is little attempt at formation of a line of demarcation.
(v) Constitutional symptoms are always grave, which are almost absent in dry gangrene.
(vi) The principal conditions, which may give rise to moist gangrene, are gangrene from
acute inflammation, long-standing venous thrombosis, bed sores and gas gangrene.
Separation of gangrene.— There is always a natural attempt by the living tissue to get rid
of the dead tissue. Due to this a zone of demarcation is usually formed between the living tissue
and the dead or gangrenous part. This is due to the development of a layer of granulation tissue.
These granulations extend into the dead tissue. Ulceration follows and as the zone of demarcation
gradually becomes deeper, a final line of separation forms which separates the gangrenous part
from the living tissue.
In dry gangrene, the final line of demarcation appears in a few days and separation begins to
take place perfectly. The soft tissues are separated quickly, but the bone takes much longer time
to separate. As mentioned earlier the blood supply of the skin and subcutaneous tissue is less
abundant than that of the muscle and bone, so the line of separation appears in a conical manner.
In moist gangrene, there is little attempt at formation of actual line of separation due to more
infection and the disease spreads very rapidly up the limb. So dry gangrene is better than moist
gangrene and every effort should be made to convert moist gangrene to the dry gangrene.
Dry Gangrene Moist Gangrene
• Dry, shriveled, mummified. • Oedematous, putrified and dis
coloured (due to H2S).
• Occurs due to slow and gradual • Occurs due to sudden loss of blood
loss of blood supply. supply.
• Clear line of demarcation is present. • Line of demarcation is vague.

• Cannot extend proximally above • Extends proximally rapidly.
the line of demarcation.
• Causes are mainly atherosclerosis, • Causes are mainly emboli and
thromboangiitis obliterans. trauma leading to acute occlusion.
• Treatment is a limited amputation. • Treatment is high amputation.
CAUSES OF GANGRENE
A. Arterial occlusion.—
1. Atherosclerosis (Senile gangrene); 2. Embolism (Embolic gangrene); 3. Raynaud's
disease; 4. Buerger's disease; 5. Cervical rib; 6. Syphilitic gangrene (due to endarteritis obliterans).
B. Venous obstruction.— Deep vein thrombosis.
C. Nervous diseases.—
1. Syringomyelia; 2. Tabes dorsalis; 3. Peripheral neuritis; 4. Hemiplegia; 5. Paraplegia;
6. Leprosy.
D. Traumatic gangrene.—
1. Direct injury to the main artery; 2. Indirect injury (crushing of the tissues or fractures
when bone fragments press on the main artery).
E. Infective gangrene.—
1. Carbuncle; 2. Cancrum oris; 3. Postoperative progressive gangrene following drainage
of empyema and appendicectomy; 4. Gangrene of the scrotum (Fournier's gangrene ); 5. Gas
gangrene.
F. Diabetic gangrene.— This should be considered as a separate group as one or more
of three factors viz. arterial occlusion, infection and peripheral neuritis play simultaneously to
cause gangrene.
G. Physical gangrene.—
1. Heat — bums and scalds; 2. Cold — frostbite; 3. Eschartics (corrosive) — acids and
alkalis; 4. Electricity; 5. X-ray (irradiation).
Special Investigations.— These are almost similar to those of chronic arterial occlusion
which have been discussed earlier.
TREATMENT.
General treatment.— This includes nutritious diet, control of diabetes, relief of pain and
care of the heart.
Local treatment.—
Care of the affected part.—
(i) The part should be kept dry. An attempt should always be made to keep dry gangrene
as dry as possible and try to convert moist gangrene into dry gangrene. Exposure of the part and
use of fan may help in keeping the part dry.
(ii) The part may be kept elevated, which will reduce pain.
(iii) The part should not be heated.
(iv) The part should be protected particularly the local pressure areas e.g. the heel, the
malleoli, the ball of the toes etc. Otherwise patches of gangrene may develop in these areas. A
bed-cradle, padded or Sorbo rings, foam may be used as preventive measures.
(v) The gangrenous part should be carefully observed and toileted e.g. lifting of the crust,
removal of hard or desiccated skin, release of pus etc. Paring of nails should be done carefully,
as carelessness may increase infection in the gangrenous part to make it a moist gangrene from
the dry one.
1. Sympathectomy.— See chapter 18.
2. Amputation.— It has two aspects —
(i) Limb-saving aspect.— Amputation may be required when gangrene has developed.
But a conservative approach should be adopted. With arterial disease, sympathectomy or direct
arterial surgery may more limit the extent of amputation. Thus a major amputation may be
avoided.
(ii) Life-saving aspect.— In case of a badly crushed limb or a rapidly spreading moist
gangrene and in gas gangrene, amputation is required to save life of the patient.
For further description of amputation, see chapter on 'Amputation'.
3. Direct arterial surgery.— When gangrene has developed from chronic occlusion of artery
due to atherosclerosis, it has a place. Revascularization of the limb may heal the gangrene or at
least considerably limit the level of amputation. In embolism or thrombosis also it has a definite
place in the form of embolectomy or thrombectomy. However in Buerger's disease or Raynaud's
disease it has no place.
DIABETIC GANGRENE
The diabetics possess distinct problems, which make their limbs more liable to gangrene
formation. Mainly three factors play major roles —
1. Sugar laden tissues of the diabetics lower their resistance to infection. So these patients
are more susceptible to infection. After a trivial injury to the toe, sole of the foot or the heel,
within hours or days a virulent necrotising infection may appear which spreads along the musculo-
fascial planes. The infecting organism may often be gas producing of the Clostridial group.
Although any type of infection may occur including fungal infections.
This susceptibility to infection manifests itself in the development of carbuncles in the neck
and in different types of necrotising infections of the abdominal wall after elective abdominal
operations.
2. The second most important factor is liability of formation of atheroma in the arteries of
the diabetic patients. It is very much known that 60% of deaths of diabetics take place from
cerebral haemorrhage as a result of atherosclerotic changes in the cerebral arteries. In the lower
limb however arterial occlusive disease mainly involves the popliteal artery and its branches
down to the pedal arches. Arteries proximal to the popliteal are usually non-affected or if affected
show non-diabetic type of atherosclerosis.
3. The 3rd peculiarity of the diabetes is diabetic neuropathy. This impaires sensation and
thus involves the lower limbs to more injuries and infections. As a result of this the pressure
areas of the foot e.g. the heel, ball of the foot become complicated by trophic ulcers. Due to
neuropathy muscular involvement may also be seen in the form of loss of reflexes and deformities.
The feet may be splayed and deformed. Thick callosities may develop in the sole and if attended
by amateur chiropody, it favours entry of infection.
. • Pain and ulceration of foot.
• There may be loss of sensation.

• Peripheral pulse may be absent.
• Change of colour and temperature where gangrene is impending.
• There may be abscess formation.
Both dry and moist types of gangrene are seen in diabetics.
Dry gangrene occurs more frequently in old diabetic patients. Dry gangrene is only possible
when infection factor is minimum and occlusive factor is maximum. The gangrene slowly
progresses with a line of demarcation.
Moist gangrene is more often seen in young diabetics. Infection plays a major role to form this
type of gangrene, which is very much spreading and often lethal.
Sometimes trophic ulcers are seen at the pressure sites usually at the metatarsal heads
particularly over the first or third metatarsal head. Often
these ulcers are completely anaesthetic and hence
painless. Secondary infection is very common.
Meggitt’s classification of diabetic foot.—
Grade 0 — Foot pain only.
Grade 1 — Superficial ulcer of foot.
Grade 2 — Deep ulcer of foot.
Grade 3 — Ulcer with bone involvement.
Grade 4 — Forefoot gangrene.
Grade 5 — Whole foot gangrene.
• Blood sugar and urine ketone bodies estimate.
• Blood creatinine estimation.
• Pus should be sent for culture and sensitivity.
• Doppler study to know arterial patency.
• Angiogram to know any arterial blockage.
• X-ray if osteomyelitis is suspected.
Treatment.—
• Diabetes should be controlled by drugs and
insulin.
• Vasodilators, dipyridamole, pentoxiphylline, low
dose aspirin etc.
• Care of foot — avoid injury, keep it clean and dry
particularly toe webs.
• Micro Cellular Rubber (MCR) foot wear may be
used.
• When there is infection, antibiotics should be
prescribed.
Problems of diabetic foot.—
Fiq.15.16.— Diabetic arteriosclerotic „ ,, .,
3 * a. m * * Callosities followed by ulceration.
J
gangrene involving the right great toe. Note .
the trophic ischaemic chants in the toes * Abscess and cellulitis of foot,
and foot. * Diabetic wet gangrene.
• Osteomyelitis affecting different bones e.g. calcaneum, cuneiforms, metatarsals.

• Arthritis of joints.
SURGERY.—
Infection.— In many cases infection with Clostridia may necessitate immediate guillotine
amputation through the mid-leg or mid-thigh to prevent death from septic shock. In early cases
of course wide spread incision and drainage with debridement of the wound should be performed.
Careful localized debridement combined with intensive antibiotic therapy has often been successful
in saving the limb. The most important aspect of such debridement is removal of all necrotic
tissues. Inadequate debridement leaving deep necrotic tissues is the main cause of failure of this
technique.
Occasionally radical debridement combined with arterial reconstruction of the tibio-peroneal
artery may save the limb from almost inevitable amputation.
If gangrene has set in amputation may be required. Level of amputation will depend on level
of skin changes and Doppler study.
Trophic ulcers.— These trophic ulcers are sharply demarcated, punched out areas on the
sole of the foot found in diabetics. Treatment consists of local cleansing, protection from trauma
and avoidence of weight bearing. Care of the foot is extremely important and all possible methods
should be adopted to prevent entry of infection.
If superimposed infection occurs, the treatment is local debridement with proper antibiotic
administration.
Gangrene.— Localized dry gangrene of a toe is best treated by postponing operation and
allowing autoamputation to take place over a period of weeks. Sometimes collateral circulation
may develop during this period to permit healing of gangrene.
If spreading gangrene takes place, amputation should be called for. So far as the level of
amputation is concerned, conservative approach should be taken depending on conditions of
peripheral pulses and arteriographic picture.
Role of sympathectomy is very limited in case of diabetic gangrene.
BEDSORES
It is also called decubitus ulcer. This is so called, as this ulcer appears on the points of pressure
when a patient is long bed ridden. Though in majority of old patients who are bed ridden for
a considerable period, bedsores may invariably occur, yet there are a few predisposing factors
which cause bedsores earlier than expected time.
These factors are — (i) sensory loss of the part, (ii) malnutrition, (iii) moisture, (iv) anaemia
and (v) improper nursing.
Before formation of bedsore the area becomes red and if the change of colour persists, the
centre of the area gives way to initiate formation of bedsore.
Treatment.—
PREVENTION.— All possible methods should be adopted to prevent formation of
bedsores. These bedsores usually form over the bony prominences. The methods to prevent
bedsores are —
(i) Frequent change of posture 2 to 4 hourly is important.
(ii) The part should always be kept dry with powder. If there be soakage of the area with
sweat, urine or faeces, the part should be immediately dried followed by sprinkling of powder.
(iii) A ripple bed or water bed has now been introduced to prevent bedsore.
(iv) P.V.C. blocks, foam or sheep skin may be used to protect the pressure points.
(v) Adhesive film e.g. Opsite may be used to prevent soakage of the part.
(vi) Aerosol silicone spray may also be used to keep the part dry.
(vii) The haemoglobin of the patient should be maintained at a normal level. Transfusion
of blood or packed cell may be required.
SURGICAL TREATMENT.— Only when the patient is young and otherwise healthy, operative
treatment may cure the condition. Excision of the ulcer followed by flap pedicle skin grafting is
required.
FROSTBITE
This condition occurs due to exposure to cold. This is mainly seen in the climbers and
explorers. It is sometimes seen in elderly debilitated individuals when exposed to very cold
climate. .
Experimentally it has been demonstrated that freezing begins in the mammalian tissues
when the temperature in the deeper parts reaches 10°C and at -5°C the cells gradually become
frozen. Frostbite only occurs due to prolonged exposure to very cold weather as happened in case
of explorers in high altitudes. A different form of frostbite is produced due to acute exposures
to below 0°C, which is called 'high altitude frostbite', in this case ice crystals deposit on the
tissues.
Pathology.— The severity of frostbite has been grouped into 4 clinical types :—
(i) In first degree frostbite there is oedema and redness of the affected part, (ii) In 2nd degree
there is formation of blisters, (iii) In 3rd degree there is necrosis of the skin, (iv) In 4th degree
there is gangrene of the extremity which requires amputation.
The basic pathology is vasospasm and damage to the vessels walls in the form of vascular
occlusion. This causes sludging of blood and wide spread thrombosis. This is followed by capillary
permeability. With rewarming there is formation of oedema.
Treatment.— Rapid warming of the tissue is the most important aspect of treatment. The
frozen tissue should be placed in warm water with a temperature of 40 to 44°C. Complete
rewarming usually takes 20 minutes. Care must be taken not to use higher temperature which
may cause gangrene instead of being beneficial.
Following rewarming the injured part is elevated to minimise formation of oedema. The
patient should be kept in a sterile environment. Blisters may be opened and necrotic skins are
removed. Antibiotic therapy and tetanus antiserum are given routinely to minimise risk of infection.
Use of intra-arterial vasodilator has markedly improved vasospasm in this condition.
Angiography may be performed to know the extent of vascular stenosis and degree of
functional vasospasm. Fast-acting vasodilator e.g. papaverine has been used with success.
Sympathectomy has been proved beneficial if it is performed within first few days. It should
not be performed too early as it may accelerate oedema formation. If sympathectomy is performed
following pick intensity of oedema, it helps in absorption of oedema and to minimise tissue
necrosis.
If thrombosis is the major problem, heparin or dextran may be used to lessen the degree of
small vessel thrombosis.
Demarcation of gangrene areas should be carefully observed for several weeks before
amputation is performed.
AINHUM
Nothing much is known about this disease. It is more often seen in male Negroes who were
always barefooted since childhood. Ainhum is also reported in countries of Central America and
the East.
The characteristic feature is appearance of a fissure at the level of the interphalangeal joint
of a toe. This fissure takes the form of a fibrous band and encircles the digit, which becomes
gradually necrotic. The most frequently affected toe is the 5th toe, which is followed in order of
frequency by the 4th, 3rd, 2nd and great toe. Sometimes the condition may be bilateral and
occasionally more than one toe may be involved.
Arterial pulsations are usually normal.
Treatment.— In the early stage when the toe has not been necrosed, longitudinal incisions,
one on the medial side and another on the lateral side may be performed through the constricting
band to release it. Z-plasty may be performed instead to relieve constriction.
When the digit becomes necrotic, amputation is the only treatment performed through the
constricting band.
ENDOVASCULAR SURGERY.—
This means surgery within the vessel. Mainly this is applied in case of peripheral vessels e.g.
femoro-popliteal, coronary, cerebral, renal etc.
Varieties.—
• Endovascular atherectomy.
• Endovascular grafts e.g. PTFE, Decron etc.
• Balloon angioplasty.—This method is particularly applied in case of short segment stenosis
in vessels like coronary vessels, renal vessels, ilio-femoral vessels.
• Angioscopy.— Inside of a vessel is visualized with small, flexible fibreoptic scope.
Irrigation is required to avoid opacification by blood.
• Intravascular stenting.— Self expanding stent may be used to expand small stenosed area
of the vessel.
• Intravascular ultrasound to know more about pathology in the lumen as well as the wall
of the vessel.
There are certain complications.—
• Rupture of the vessel.
• Sepsis of the vessel.
• Fluid overload.
• More thrombosis may develop following its use.
• Air embolism.
ANEURYSM
Definition.—
Dilatation of a localized segment of the arterial system is known as aneurysm.
Broadly, an aneurysm can be classified into three types — (a) True aneurysm, (b) False
aneurysm and (c) Arteriovenous aneurysm.
(a) A true aneurysm is one, which contains all the three layers of the arterial wall in the
aneurysm.
(b) A false aneurysm is one, which has a single layer of fibrous tissue as the wall of the
sac and does not contain the three layers of the arterial wall as the covering of the aneurysmal
sac. Majority of the false aneurysms follow trauma. A mycotic aneurysm (which is produced by
growth of microorganisms in the vessel wall) is usually of false variety.
Causes.—
Except traumatic aneurysm all other aneurysms are caused by weakening of the wall of the
artery. This weakness may be either congenital or acquired.
1. Congenital.—
(i) Congenital aneurysm often occurs in the cerebral blood vessels particularly in the
circle of Willis due to congenital deficiency of the elastic lamina at the sites of branching. This
is known as Berry aneurysm. These aneurysms remain symptomless till they rupture and cause
subarachnoid or intracerebral haemorrhage.
(ii) A cirsoid aneurysm is the mass of dilated pulsating serpiginous vessels — both
arterial and venous — which is found in a congenital arteriovenous malformation (See Fig. 3.42
of 'A Manual On Clinical Surgery').
(iii) Congenital arteriovenous fistula may lead to aneurysm.
(iv) A few syndromes, which are rare inherited connective tissue defects such as Marfan's
syndrome and Ehler-Danlos syndrome, may cause congenital aneurysm.
(v) Aneurysm of aorta may occasionally occur proximal to coarctation of aorta.
2. Acquired.—
Acquired varieties can be broadly classified into three groups — A. Traumatic, B. Degenerative
and C. Infective.
A- TRAUMATIC.— Majority of the traumatic aneurysms are false aneurysms and are
fusiform in shape.
(i) Direct trauma such as penetrating wound to the artery may cause such aneurysm.
(ii) Irradiation may cause aneurysm.
(iii) Arteriovenous aneurysm may develop from trauma.
(iv) Indirect trauma may cause aneurysm e.g. at the subclavian artery distal to the point
where it crosses the cervical rib.
B. DEGENEFiATIVE.— This group is by far the most common group.
(i) Atherosclerosis, with associated degenerative changes in the elastic and muscle fibres of
the tunica media, is by far the commonest cause of aneurysm. These aneurysms are most frequently
located in the abdominal aorta and the popliteal artery. This suggests that there may be particular
mechanical strains consequent upon local anatomical factors 'such as lumbar lordosis and the
repeated flexion and extension at the knee. However atherosclerotic aneurysm may occur elsewhere
e.g. in the thoracic aorta and its main branches and in the femoral artery. Most atherosclerotic
aneurysms are diagnosed in patients over 60 years of age, more common in men than in women.
(ii) A peculiar type of congenital abdominal aortic aneurysm is seen in relatively young
South African Negroes. This is attributed to congenital intimomedial mucoid degeneration.
C. INFECTIVE.—
(i) Syphilis.— The vasa vasorum becomes obstructed by intimal proliferation and this
leads to impaired nutrition of the tunica media. Syphilitic aneurysms usually follow syphilitic
arteritis. Now this is a rare entity. This is only seen in the thoracic aorta. This may be fusiform
or saccular in shape.
(ii) Acute infections may lead to aneurysmal dilatation. In about 10% of patients with
abdominal aortic aneurysm, the wall of the sac is thickened and shows extensive active chronic
inflammatory changes with plasma-cell infiltration.
(iii) Non-specific mycotic aneurysm may occur anywhere in the body. The nomenclature
is a misnomer as the cause is not due to fungus but due to bacterial infection. It is mainly caused
by staphylococcus aureus or streptococcus.
(iv) As an occasional complication of subacute bacterial endocarditis, the arterial wall
becomes weak and forms aneurysm. Infected embolus rests on the peripheral arteries and thus
produces weakening of the wall.
(v) Sometimes aneurysm is seen in an artery traversing tubercular cavity in the lung.
(vi) Aneurysm is also seen in an artery situated at the base of a peptic ulcer and is also
infective.
(vii) Arteritis — particularly polyarteritis may cause aneurysm.
According to the shape a true aneurysm may be fusiform, saccular or dissecting aneurysm.
FUSIFORM ANEURYSM occurs when there is uniform expansion of the entire circumference
of the arterial wall. This is the commonest variety and it is a spindle shaped enlargement.
SACCULAR ANEURYSM is an expansion of a part of the circumference of the arterial wall.
This is usually traumatic. When a penetrating wound in the artery does not close spontaneously,
a pulsating haematoma develops which is enclosed by fibrous tissue. Later on this saccular cavity
becomes partly lined by endothelium derived from the intima. This is how a saccular aneurysm
forms.
DISSECTING ANEURYSM occurs when the intima ruptures usually beneath an
atheromatous plaque and the blood is forced through the intima to enter between the inner and
outer coats of the tunica media. The intima and the adjacent part of the media are nourished by
diffusion of the arterial blood. The adventitia and the outer part of the media are nourished by
the vasa vasorum from intercostal and other arteries which form a plexus in the adventitia.
Split occurs between the inner part of the media and the outer part of the media. If the vasa
vasorum fails in its function because of obliteration, this leads to mucoid degeneration in the
ground substance of the media which may result in the appearance of clefts in the vessel wall.
This is one of the most common acute problems involving the thoracic aorta and is usually
associated with arterial hypertension and cystic medial necrosis of the aortic wall. The initiating
lesion is a tear in the intima through which the blood leaks into the wall of the aorta and
dissects it and hence its nomenclature.
SYMPTOMS.—
Aneurysm may be asymptomatic and it is then detected accidentally.
(i) The commonest presenting symptom is a dull aching pain. With abdominal aneurysm
there is dull pain in the centre of the abdomen.
(ii) Acute pain may be complained of if the vessel suddenly stretches.
(iii) A severe pain, bursting in nature, is complained of when an aneurysm ruptures and
a large haematoma forms.
(iv) Referred pain may be due to pressure on a nerve e.g. patients with abdominal aortic
aneurysm may present with sciatica.
(v) Some patients notice a pulsatile mass, which is a common mode of presentation for
femoral and popliteal aneurysms.
(vi) Sometimes patients may present with severe ischaemia of the lower limb. Such occurrence
16
may be seen in aortic and femoral aneurysms, though the incidence is less. But in popliteal
aneurysm such incidence is more.
(vii) Patient may present less severe ischaemia caused by emboli originating in the aneurysm.
The best example of such complication is the multiple small emboli which block the digital
arteries from a subclavian aneurysm leading to Raynaud's syndrome. In the lower limb such
emboli may cause intermittent claudication or rest pain.
(viii) Enlargement of the artery may block the vein by direct pressure or may cause it to
thrombose. The patients present with swollen blue and painful limbs. This is due to venous
thrombosis or obstruction which is more often seen in aneurysms of the aorta, femoral and popliteal
arteries which are closely related to the respective veins.
So aneurysms can cause symptoms due to expansion (acute pain), rupture (severe pain bursting
in nature), thrombosis (leading to ischaemia) or release of emboli (Raynaud's syndrome or
intermittent claudication or rest pain or even gangrene of the foot or toes).
Examination.—
(i) A pulsatile swelling exhibiting expansile pulsation in the course of an artery should be
suspected as aneurysm.
(ii) Pulsation diminishes if a pressure is applied proximal to the swelling. It refills again
in 2 or 3 beats if the proximal pressure is released.
(iii) The swelling is compressible.
(iv) A Thrill may be palpable over the swelling.
(v) On auscultation a systolic bruit may be heard over the swelling.
PRESSURE EFFECTS.—
Aneurysms exert pressure on the adjacent structures. These pressure effects are discussed in
details below.
Effects of aneurysm.—
The main menace of aneurysm is rupture which causes enormous bleeding and ultimately
death of the patient if the condition is not suspected earlier and operation is undertaken. Aneurysm
as such produces A. Effects of pressure on the neighbouring structures, B. Thrombosis and C. Emboli
formation.
A. PRESSURE ON THE NEIGHBOURING STRUCTURES.—
(i) Pressure on veins.— This leads to oedema of the distal limb. This is more commonly
seen in aneurysm of the abdominal aorta, femoral and popliteal aneurysm.
(ii) Pressure on the nerves.— This leads to altered sensation e.g. pain, numbness, tingling
and paraesthesia. Paralysis is rare.
(iii) Pressure on the bones.— This leads to erosion of the bones. Such erosion is seen in
vertebrae by aortic aneurysm. The intervertebral discs are resilient structures and do not undergo
erosion.
(iv) Pressure on adjacent organs.— Pressure of an aortic aneurysm on the oesophagus may
cause dysphagia. In case of abdominal aortic aneurysm the stomach may be pushed forward and
if the aneurysm leaks or bursts into the stomach it causes severe haematemesis.
(v) Pressure on the skin.— This stretches the overlying skin and the skin becomes red and
oedematous showing features of inflammation, as if an abscess lies underneath. Aneurysms have
been incised with the wrong diagnosis of abscess with sinister consequences. So one must be very
careful to exclude aneurysm if the abscess lies in the line of a known artery. In this case one can aspirate
first before making an incision.
B. THROMBOSIS.—
Due to formation of laminated thrombus within an aneurysm, the arterial flow to the distal
segment is diminished. Such thrombosis is very common in aneurysm and this is the reason why
arteriography is not diagnostic of aneurysm as such thrombosis does not show dilated sac in
arteriography. This leads to ischaemia of the distal limb. This is a common occurrence in popliteal
aneurysm. This has some protective influence in preventing rupture.
C. EMBOLI FORMATION.—
Emboli often originate in the aneurysm. The best example is formation of multiple small
emboli from subclavian aneurysm which block the digital arteries. Similarly emboli from the
aortic aneurysm, femoral or popliteal aneurysm may cause intermittent claudication, rest pain or
gangrene of the toes.
ISCHAEMIA IN A CASE OF ANEURYSM may be due to :
(i) Thrombosis in the aneurysm.
(ii) Occlusion of the origin of the emerging artery with
thrombosis.
(iii) Pressure of aneurysm on the nearby branches of the
artery.
(iv) Embolism from the aneurysm.
Complications of aneurysm.—
1. Pressure on the adjacent structures.— See above under
'Effects of aneurysm'.
2. Thrombosis and emboli formation.— These lead to
circulatory insufficiency of the inferior extremity. These have been
discussed above.
3. Infection.— This may occur from organisms in the blood
stream. Signs of inflammation become evident with suppuration,
abscess formation followed by rupture.
4. Rupture.— This seems to be the gravest complication of
aneurysm. This occurs due to avascular necrosis of the vessel wall
(pressure necrosis), more commonly along the sides of the
aneurysmal sac. Rupture leads to haemorrhage. This depends on
the site of the artery involved — either retroperitoneal or
subarachnoid, or in the pleural cavity (haemothorax), in the
peritoneal cavity (haemoperitoneum), in the trachea (haemoptysis),
in the oesophagus, stomach or duodenum (haematemesis). Fig.15.17. Arteriographic
n . . , j -,.is ushered with severe pain •
Rupture
u .* • . , ... study of a man who presented
bursting m nature and with .. . .. . f ,
r,, r ° with claudication. It shows
severe shock. ., ,_______ , ... ,
thrombosed popliteal aneurysm.
5. Spontaneous cure.— Occasionally, particularly in saccular
aneurysm gradual formation of clot in the sac with ultimate fibrosis may lead to consolidation.
This is seen in saccular aneurysm in the peripheral arteries.
Differential diagnosis.—
1. Swelling over an artery.— This also leads to pulsation which is typically called 'transmitted
This pulsation is different from expansile pulsation of aneurysm. When two fingers are
pulsation'.
placed on a pulsating swelling, in case of expansile pulsation the two fingers diverge from each
other, whereas in transmitted pulsation the two fingers diverge from each other, whereas in
transmitted pulsation the two fingers are lifted up without divergence with each arterial beat
(See Figs. 3.23, 3.24 & 3.25 in 'A Manual On Clinical Surgery'). Such cases can be easily
distinguished from aneurysm by the above-mentioned test and by postural change, in which the
swelling will be shifted away from the artery so that it will lose pulsation. A pseudopancreatic
cyst often pulsates being a swelling on the abdominal aorta. When the patient is examined in the
genupectoral position the cyst falls away from the artery and consequently pulsation is vanished.
2. Swelling beneath an artery.— A swelling under an artery will lead to pulsation as the
artery is brought towards the surface. Such pulsation is seen when subclavian artery is pushed
up by the cervical rib. Very careful examination is required to distinguish this condition from a
typical aneurysm.
3. Pulsating tumours.— A few tumours are so vascular that they pulsate e.g. telangiectatic
osteosarcoma, very vascular osteoclastoma, metastasis from hypernephroma, aneurysmal bone
cyst etc. Careful investigation should be performed to differentiate such condition from typical
aneurysm.
4. An abscess.— As has been mentioned earlier in the section of 'Effects of Aneurysm' in
'Pressure on the skin', before making an incision onto a swelling, particularly in the chest wall,
in the groin, in the axilla or in the popliteal fossa, one must ask oneself 'Is it not an aneurysm?'.
See whether it is a pulsatile swelling or not.
1. BLOOD — is examined for cholesterol level and other lipids to exclude atherosclerosis.
W. R. and Kahn test should be performed to exclude syphilis.
2. RADIOGRAPHY.—
(i) Straight X-ray may show (a) calcification of the arterial wall, (b) soft tissue shadow
or (c) bony erosion.
(ii) Arteriography is mainly performed to know about the collaterals above and below
the lesion and also to know the condition of the artery above and below the aneurysm.
Arteriography often fails to show aneurysmal dilatation due to the presence of laminated blood
clot within the sac. To decide the type of surgery needed this investigation is important.
3. OTHER INVESTIGATIONS should be performed to exclude other conditions in the
differential diagnosis and to know the general condition of the patient before undertaking major
surgery for aneurysm. Investigations to know the renal function are highly important for abdominal
aortic aneurysm.
Treatment.—
1. ARTERIAL LIGATION.— This operation is becoming obsolete nowadays, since collateral
circulation maintains blood flow through the aneurysm and if the collateral circulation is
inadequate the risk of gangrene is considered high. This procedure is however suitable for splenic
artery, intracranial aneurysm etc. where adequate surgical facilities for sophisticated surgery is
not available. The different methods of ligation are :
(i) Anel's method.— The ligature is applied just proximal to the sac.
(ii) Brasdor's method.— The ligature is applied just distal to the sac.
(iii) Hunter's method.— The ligature is applied immediately above a branch of the artery.
(iv) Wardrop's method.— The ligature is applied immediately below a branch of the artery.
(v) Antylus’ method.— Two ligatures are applied one proximal and another distal to the
aneurysmal sac.
2. WIRING OF THE ANEURYSMAL SAC.— This is indicated in elderly and poor risk
patients and in cases of difficulty placed aneurysms for operation excision as this may carry high
mortality rate.
A long fine thread of stainless steel wire (200 or 1000 feet in length of No. 3) is introduced
into the aneurysmal sac with a hypodermic needle. The wire gets coiled within the sac and this
leads to clotting, thrombosis followed by fibrosis. This may lead to consolidation.
3. WRAPPING OF THE ANEURYSMAL SAC.— A strip of fascia lata, polythene or
cellophane sheet may be wrapped round the aneurysmal sac to strengthen its wall and prevent
rupture. This may be of value in intracranial aneurysms where surgery is difficult and rupture
or such aneurysm may cause death of the patient. So wrapping and strengthening of the wall of
the aneurysm may save the patient.
4. ANEURYSMORRHAPHY (Matas' reconstructive aneurysmorrhaphy).— This is
particularly suitable in case of saccular aneurysm of arteries like femoral or popliteal. The
aueurysmal sac is totally excised and the defect in the arterial wall is closed by suturing of the
adjacent healthy arterial wall.
5. EXCLUSION AND BY-PASS GRAFTING.— This operation is performed where excision
of the aneurysmal sac is not very safe due to presence of adhesions to the neighbouring vital
structures. These vital structures may be damaged during dissection of the aneurysm. Such cases
are abdominal aortic aneurysm where inferior vena cava lies adherent and femoral artery aneurysm
where femoral vein lies adherent.
In this operation the artery is ligated above and below the aneurysm. The by-pass graft
mostly autogenous vein graft is sutured above and below the ligatures with a small opening in
the artery. Two small openings are made in the arterial wall above and below the ligatures and
the 'by-pass graft' mostly autogenous vein graft is sutured around the small openings so that the
blood flows through the by-pass graft to the distal artery. The excluded aneurysmal sac becomes
thrombosed and shrinks into fibrous mass.
6. EXCISION AND GRAFTING.— This is the most popular operation and should be performed
wherever possible. Dacron graft or autogenous vein may be used for grafting.
7. EXCISION AND END-TO-END SUTURING.— This is only possible in case of peripheral
aneurysm, where after excision of the aneurysm two cut ends can be approximated by mobilization
for end-to-end anastomosis.
ARTERIOVENOUS ANEURYSM
Communication between an artery and adjacent vein leads to arteriovenous aneurysm or
arteriovenous fistula.
Causes.—
(i) Congenital.— It is a direct 'shunt' between an artery and a vein. The lesion is commonest
in the leg, but it may occur in the arm or in the scalp. In the latter position it forms a mass of
dilated vessels known as 'cirsoid aneurysm'.
(ii) Acquired — mainly traumatic either by a penetrating wound or a sharp blow.
Communications develop between the artery and the vein lying close to each other at the time
of injury or during the process of healing communication may develop between the artery and
vein, (a) When the artery and the vein communicate directly through a short wide channel it is
called aneurysmal varix. (b) When the anastomosis becomes indirect through an intermediate sac
lying in the soft tissues it is called varicose aneurysm.
(iii) Iatrogenic.— When arteriovenous fistulas are created surgically, this is called iatrogenic
arteriovenous fistula. In current practice the most common is that used in the forearm or legs to
permit renal dialysis in the management of renal insufficiency. Arteriovenous fistulas have also
been surgically constructed to increase blood flow and patency through vascular anastomoses
such as used in venous reconstructions and limb salvage procedures. For renal dialysis it is
mostly used in the wrist or in the ankle and such temporary arteriovenous fistula is known as
cimino fistula.
A few iatrogenic fistulas may result inadvertently during operations e.g. operations on the
kidney, intervertebral discs, small bowel resection and pelvic surgery.
A few iatrogenic fistulas are made as part of operations e.g. distal splenorenal shunt, coronary
artery by-pass grafting etc.
Manifestations of Arteriovenous Anastomosis.—
A. SYSTEMIC EFFECTS.—
The pathophysiologic changes that follow a direct communication between the arterial and
venous system are demonstrated by presence of a thrill over the site of the lesion. The magnitude
of systemic symptoms is related to the size of the fistula and its position in relation to the heart.
These changes are maximum in case of a large artery. With large shunts directly into the venous
circulation, a sequence of changes occurs that is directly related to the volume of blood passing
through the fistula. Systemic effects are :
(i) Cardiac output increases.
(ii) The heart rate increases.
(iii) Diastolic arterial pressure diminishes with an increase in systolic pressure i.e. increase
of the pulse pressure.
(iv) There are elevated right and left atrial pressures.
(v) The blood and plasma volumes increase in an effort to compensate for the increased
volume of blood in the venous circulation.
(vi) Due to high cardiac output, the heart increases in size and ultimately cardiac
hypertrophy results.
(vii) Large fistulas may ultimately lead to congestive cardiac failure with pulmonary
oedema.
(viii) There is also decrease of peripheral resistance.
(ix) It has been found out that digitalis preparations are usually ineffective. So operation
is justified in these cases.
(x) The Central Venous Pressure (CVP) is often increased.
(xi) Arteriovenous fistulas may be associated with the development of bacterial
endocarditis. This also requires surgical closure of the fistula for permanent cure.
B. LOCAL EFFECTS.—
(i) Aneurysmal dilatation is usually present at the site of the fistula.
(ii) Extensive collateral circulation develops connecting the arteries above and below the
fistula. This collateral circulation can become massive and results in an increase in temperature
both of the skin and of the muscle.
(iii) When such fistula occurs in an extremity, the limb may be increased in length. Increase
in bone growth is probably due to increase in local temperature.
(iv) Presence of a thrill over the site of the lesion is quite characteristic, particularly if the
lesion is located near the surface.
(v) On auscultation, a bruit can be heard almost throughout the cardiac cycle.
(vi) The veins are enlarged and may be to certain extent arterialised.
LOCAL SIGNS.—
1. As mentioned earlier a pulsatile swelling or an aneurysmal dilatation is particularly
visible if the lesion is superficial.
2. One can find the dilated collateral circulation with increase temperature of the skin.
3. Port-wine discolouration of the skin may also be seen due to increased collateral
circulation.
4. Distended superficial veins may also be visible. The veins are often varicosed.
5. Increased length of the limb is often noticed in congenital fistula. This may be noticed
in acquired type if the fistula has developed before completion of bony growth, but this will be
less evident.
6. On palpation a thrill may be detected. Pressure on the artery proximal to the fistula
causes the swelling to diminish in size. The thrill and the bruit cease to exist.
7. Below the fistula the limb is ill-developed, it feels cooler.
8. Below the fistula muscle wasting may be noticed.
9. Below the fistula one may find ischaemic changes o£ the extremity with presence of
even indolent leg ulcer. This is due to inadequate arterial blood supply below the fistula due to
diversion of blood into the veins.
10. Auscultation reveals continuous bruit.
SYSTEMIC SIGNS.—
The signs are similar to what have been described above under the heading of 'systemic
effects'. Here one sign worths mentioning i.e. Branham's sign. If a finger is pressed on the
artery proximal to the fistula, there will be slowing of pulse rate and rise in the diastolic
pressure.
1. Arteriography confirms the diagnosis, as the venous filling occurs with speed. This also
indicates the position of the fistula and its size.
2. Ultrasound.— The lesion and the enlarged veins can be aptly demonstrated by
ultrasonography.
Treatment.—
CONGENITAL LESIONS are not progressive, so excision is only advised for severe deformity
and recurrent haemorrhage.
The ACQUIRED LESIONS are usually progressive and operations are always required.
1. Reconstructive operation is the operation of choice. The vessels are separated. The
intervening sac is excised. The defects in the vessels walls are repaired. In difficult cases it may
be necessary to reconstruct the artery at the expense of the vein. Such reconstruction is performed
with the involved vein (which has been sacrificed) or with Dacron graft. The vein is simply
ligated above and below and the intervening part may be utilized for grafting of the artery.
2. Quadruple ligation.— When reconstruction operation is not possible, ligation of the
involved artery and vein both above and below the lesion may be performed (with four ligatures
— 2 for artery and 2 for the vein).
3. Selective intra-arterial embolization is also a useful technique for treating these lesions.
4. In majority of patients it is possible to close the fistula without any distal ischaemia and
subsequent amputations are not required.
ABDOMINAL AORTIC ANEURYSMS

Abdominal aortic aneurysms are important as they are both common and potentially lethal.
This is the most common of all aneurysms. Its incidence is about 2% in the Western population.
95% are due to atherosclerosis. It is fortunate that about 95 % of these aneurysms occur below
the origins of the renal arteries. If imtreated about 1/2 the patients die within 3 years of the
diagnosis and 2/3rds will be dead in 5 years. The most frequent cause of death is rupture of
the aneurysm.
It has been noticed that there is a steady rise in the incidence of this aneurysm, probably due
to increased longevity of mankind. Most patients are in the 6th or 7th decade. Males are more
often affected than females in the ratio of approximately 10 : 1.
Aetiology and Pathology.— As mentioned above about 95% of this aneurysm are
atherosclerotic in origin. In only minor cases other causes like Marfan's syndrome, syphilis or
trauma may be detected.
This aneurysm characteristically originates just below the renal arteries and extend distally
beyond the aortic bifurcation into the common iliacs. This seldom involves the external iliac
arteries. Small aneurysms limited to the abdominal aorta are also not uncommon. If the diameter
of the aneurysm becomes 10 to 15 cm, it may be discovered accidentally by palpation. There is
usually no impairment of peripheral circulation unless distal embolization from the laminated
thrombus lining the lumen occurs.
Clinical features.— It is difficult to know what proportion of abdominal aneurysms may
cause symptoms, but in many patients the
condition is found by chance during
routine abdominal examination. So most
of the patients remain unaware of their
abdominal aneurysms until a mass is
accidentally discovered.
Low back pain may be caused by
abdominal aneurysms. Such pain is due
to tension on retroperitoneal tissues from
the aneurysm. The symptoms are very
vague. Sometimes pain may be referred
to the groin or thigh due to nerve
compression. Virtually any intra
abdominal condition may be simulated
by an abdominal aortic aneurysm e.g.
peptic ulcer, cholecystitis, pancreatitis,
appendicitis or diverticulitis.
A few patients only complain of a
pulsatile mass in the abdomen.
With beginning leakage of the
aneurysm, it may mimic acute abdominal
conditions e.g. perforated peptic ulcer,
_._„„_,, „, haemorrhagic pancreatitis or generalized
Fig. 15.18.— Calcification in wall of an aortic aneurysm . ...
accidentally revealed in an intravenous pyelogram. ” ‘
PHYSICAL EXAMINATION.— For abdominal aneurysm, the abdomen is palpated with

relaxed abdominal muscles while the patient is taking deep respirations. Careful palpation may
usually delineate the lateral walls of the aorta providing an estimate of its width. A pulsating
mass greater than 1 inch diameter usually establishes the diagnosis of aneurysm.
During physical examination, peripheral pulses should be carefully palpated for associated
occlusive vascular disease. Presence of a bruit over the bifurcation of the carotid artery is
particularly significant because an asymptomatic stenosis of the carotid artery may be revealed.
Leakage may occur either into the peritoneal cavity or into the duodenum or even into the
inferior vena cava. Initially bleeding is into the retroperitoneal space, where it may be contained
for- a while before it proves fatal.
1. Blood.— Haemoglobin estimation, full blood count, ESR, grouping and cross-matching,
blood lipids, electrolytes and urea should be performed.
2. Urine analysis to exclude diabetes is essential.
3. E.C.G., liver function test and chest X-ray should be performed.
4. Straight X-ray of the abdomen is the most useful confirmatory investigation, which often
shows a thin curved line of calcification in the wall of the sac. Less frequently only a soft tissue
mass may be seen. The lateral view is particularly helpful which more clearly shows the calcific
rim or thin line of calcification in the wall of the aneurysm, which may be obscured in the
anteroposterior view by the shadows of the vertebral bodies. An estimate of the size of the
aneurysm can be obtained.
5. Aortography is not without risk and may not be very informative since many aneurysms
contain mural thrombus with a central lumen which approximates to that of a normal aorta and
may mask the true size of the aneurysm. Previously it was used to establish relationship of the
renal arteries with the aneurysm, but renal artery involvement is seen in only 1% of cases and
there is no justification to do this investigation.
However this investigation may be justified only when to be confirmed about the extent of
a suspected extensive lesion and to exclude presence of small aneurysms.
6. Ultrasound scanning has the advantage of being a non-invasive technique.
7. Computerised Tomography (CT) or Magnetic Resonance Imaging (MRI) is best to assess the
extent of the aneurysm. To know the involvement of the renal arteries by aneurysm these
investigations are more helpful than other investigations. It also assists in differentiating from
other abdominal masses.
8. Intravenous pyelography is useful not only as a test of renal function, but also because it
may reveal obstruction of one or both ureters. It should be remembered that ureteric obstruction
is more likely to be due to retroperitoneal inflammatory reaction than to external pressure due
to the aneurysmal sac.
Treatment.—
INDICATIONS FOR OPERATION.—
(i) Aneurysms smaller than 5 cm in diameter can be safely observed till they expand or
become symptomatic.
(ii) Asymptomatic aneurysm measuring more than 5 cm diameter is an indication for
operation unless there are other risks which have already shortened the life expectancy.
(iii) When the aneurysm becomes painful, an emergency operation should be contemplated,
as pain denotes impending rupture. Abdominal tenderness also denotes impending rupture.
PREOPEFtATIVE EVALUATIONS include special investigations mentioned above, an

electrocardiogram, renal function tests (particularly clearance studies) and coagulation studies
including platelet counts. If carotid bruits are heard, cerebral angiogram may be performed. If
angina pectoris is present, coronary angiogram is indicated.
TECHNIQUE OF OPERATION.— Before anaesthesia, heparin is injected 10,000 units
intravenously. After induction of anaesthesia, a self-retaining urethral catheter is passed to monitor
urine flow during surgery and in the first few postoperative days.
A long midline incision is made to enter into the peritoneal cavity. The small intestine is
delivered out and enclosed in a sterile plastic bag or moist towels. The small intestine is packed
away on the right side of the abdomen, the descending and pelvic colon on the left side and the
transverse colon upwards. Goligher's self-retaining retractor is used to retract the abdominal
walls. Other possible causes for the patient's symptoms should be ruled out e.g. peptic ulcer,
carcinoma of the G.I. tract etc.
Now the abdominal aneurysm is assessed properly particularly noting the level of its neck
and the state of its bifurcation. The posterior parietal peritoneum is incised from the ligament of
Treitz to the pelvis below, taking care not to damage the inferior mesenteric vein. The neck of
the aneurysm is identified and a vascular clamp is applied there. This step is performed quickly
in case of leaking aneurysm. The inferior mesenteric artery is dissected out. If trial clamping leads
to cyanosis of the left colon, a cuff of the aorta should be preserved around its origin for later
reimplantation into the graft. Usually the artery is ligated and divided close to the abdominal
aorta. The common iliac arteries are next clamped.
For this, these arteries are mobilized and made
free from the inferior vena cava and iliac veins.
ANTERIOR AORTIC
ABDOMINAL
The aneurysm is now incised longitudinally
ANEURYSM
WALL \ and mass of thrombus within it is removed.
Bleeding from the orifices of the lumbar and
median sacral arteries is controlled by suturing
their orifices within the sac.
Now the inferior end of the aneurysmal sac
is inspected. If a ring of normal aortic tissue can
be identified proximal to its bifurcation, a tube
graft can be used. If the bifurcation is involved
VERTEBRAL
in the aneurysm or if there is aneurysmal
COLUMN
involvement of the iliacs, a bifurcation graft will
be necessary.
A woven or knitted Dacron graft may be
Fig.15.19.— Transverse scan at the level of 4 cm
used. Knitted graft should be preclotted and its
above the umbilicus shows a moderately large
use is associated with blood loss through the
abdominal aortic aneurysm with a large defect in
left lateral wall consistent with rupture. Echo-free interstices. That is why woven Dacron graft is
area in the left paravertebral region represents the more preferred.
haematoma. The graft is now placed inside the aneurysmal
sac. The upper anastomosis is commenced in the
midline posteriorly and picks up a fold of aortic wall at the neck of the sac. The suture line now
proceeds laterally to its side and meets in the midline anteriorly. 3/0 Mersilene suture is often
used for this purpose. The graft is then occluded whilst the proximal aortic clamp is released to
test the adequacy of the suture line. Any leaks should be closed by additional sutures.
If a tube graft is used, it is of such a length that it will be under moderate tension when the
distal suture is completed. The distal anastomosis is carried out in exactly the same manner as
the proximal suture.
When a bifurcation graft is used, the common iliac arteries are transected taking care not to
damage their accompanying veins. Two points should be kept in mind at the time of distal
anastomosis — (i) the intima of the common iliac artery should be carefully anchored by the
suture so as to prevent formation of dissecting aneurysm and (ii) before completion of the distal
anastomosis it is essential to release in turn the proximal and distal clamps to dislodge any
thrombus which may be formed during operation. If required, passage of a Fogarty catheter
distally may be required.
The aneurysmal sac is now approximated around the graft and the posterior parietal
peritoneum is closed.
Left colon should be inspected and as mentioned earlier reimplantation of the inferior
mesenteric artery to the graft may be required.
POSTOPERATIVE COMPLICATIONS.— Early postoperative complications are mainly
cardiac and respiratory complications e.g. ischaemia and infarction (cardiac) and atelectasis,
lower lobe consolidation and 'shock lung' (respiratory). Haemorrhage is now not a very serious
complication and occurs provided that anticoagulation is continued beyond the immediate
postoperative period. Haemostasis must be achieved satisfactorily. Left colon ischaemia due to
lack of collateral blood supply may occur in 10% of cases. Fortunately this often resolves
spontaneously. Other early complications are haemorrhage, thrombosis of the graft, peripheral
emboli, ileus, intestinal obstruction, ischaemia of the left colon and renal insufficiency.
Late complications include graft thrombosis, false aneurysm, aortoduodenal fistula (it should
be suspected whenever haematemesis or melaena occurs in months or years after operation. A
successful outcome may be achieved by prompt operation in which aorta is separated from
duodenum, the holes are closed and some omentum is interposed between two structures).
Neurological complications include sexual dysfunction and spinal cord ischaemia. Renal failure
and infection of the graft are rarely seen.
Endoluminal stent-graft procedure.— It has been a minimally invasive recent treatment
offered by major vascular surgical centres for certain aortic aneurysms. The common femoral
arteries are exposed surgically. Under radiological control a stent-graft delivery system is guided
up into the aorta and is placed within the aortic sac. This stent-graft is placed within the aortic
body and one iliac artery. For the other iliac artery a separate single iliac-stent graft is introduced
from the opposite common femoral artery. One must be careful to see that the upper most level
of the graft and distally at both iliac levels the stent-graft should be bloodtight.
Though this method is a success in the initial stage, but lately there is a possibility of stent-
graft fragmentation and leakage at the interface of vessel and stent-graft.
RUPTURED ABDOMINAL ANEURYSM.—
C linical features.— It constitutes a grave surgical emergency. Two types of rupture may
occur —
In case of anterior rupture there is free bleeding into the peritoneal cavity. This condition is
extremely fatal and only few patients can be brought to the hospital alive. Those who are brought
alive, carries a high risk of surgery due to prolonged period of hypotension and shock.
Posterior rupture produces retroperitoneal haematoma. The onset is characterized by acute
vascular collapse, usually with a flank or abdominal pain. Sudden collapse with a pulsatile mass
in the abdomen is almost diagnostic. But frequent erroneous diagnosis as renal colic or massive
myocardial infarct or pulmonary infarct may be made. So careful abdominal palpation is very
essential in these cases.
If no operation is performed the mortality rate is 100%. If operation is performed as an
emergency procedure 50% survival should be expected.
Operative Treatment.— Operation is performed as quickly as possible, infusing 500 to
1000 ml of fluid every few minutes until serious hypotension has been corrected. It is important
to know that elevation of blood pressure should be avoided until the abdomen has been opened and
proximal control of the aorta is obtained. This must be achieved very quickly by cross-clamping
the aorta below the renal arteries. If necessary the aorta may be compressed through the lesser
omentum till infrarenal control can be obtained. Blood replacement is next considered. The
ruptured aneurysm is widely incised, intra-abdominal clots are evacuated and the renal arteries
isolated. Recently there has been renewed interest in autotransfusion using blood sucked out
from the peritoneal cavity. Stored blood should be warmed before transfusion. Low molecular
weight dextran should not be used as when excreted by the kidneys it may block the renal
tubules. Blood loss should be carefully measured and replaced. Intravenous mannitol (200 ml of
20% solution) or frusemide (Lasix) may be of value particularly in the early post-operative phase,
as renal failure is more common after this type of operation.
POPLITEAL ANEURYSMS
Among peripheral aneurysms this aneurysm accounts for 70% of cases. 2/3rds of popliteal
aneurysms are bilateral. If abdominal aorta is carefully examined, l/3rd of these cases may be
seen to accompany aortic aneurysm.
Almost all popliteal aneurysms are atherosclerotic. It usually involves upper 2/3rds of the
artery.
It usually occurs in men in 6th and 7th decades of life, half of whom are hypertensive.
Clinical features.— It is frequently symptomless and may be self-limiting due to spontaneous
thrombosis.
Two types are usually found— (a) the saccular form, may rapidly expand and rupture, (b) The
fusiform type, which is often bilateral, rarely rupture and may be complicated by distal embolism.
This aneurysm itself presents as swelling behind the knee. Symptoms and signs of progressive
enlargement include local pain, tenderness and swelling of the leg due to compression of the
popliteal vein. Sometimes this aneurysm presents with one of its complications e.g. ischaemic
ulceration of toes due to emboli, sudden onset of severe ischaemia following thrombosis or pain
and haematoma formation due to rupture. It should always be suspected and looked for in cases
with embolism of the toes where there is no other obvious source.
Treat ment.— Operation is almost always justified because of its complications of thrombosis,
embolization, gangrene and rupture. Only small asymptomatic aneurysms in the elderly patients
and thrombosed aneurysms can be left alone.
OPERATIVE TECHNIQUE.— This operation may be performed in prone position with an
incision across the popliteal crease to expose the popliteal artery with the aneurysm. Otherwise
this operation can be performed in supine position with the knee slightly flexed and the incision
is made on the medial aspect of the lower thigh extended across the knee joint into the upper calf.
The upper part of the incision may be deepened to expose the upper part of the popliteal artery.
Exposure can be improved by division of semimembranosus and semitendinosus tendons.
Once the artery is exposed and isolated it is clamped to prevent distal embolization during
operation. Various methods of reconstruction are possible. Perhaps the best is the use of saphenous
vein as a by-pass graft in association with proximal and distal ligation and total obliteration of
the sac. Another method is to lay a graft in the open sac and an end-to-end anastomosis is made
above and below the aneurysm. The aneurysmal sac is not excised because both veins and nerves
are intimately attached to its wall.
DISSECTING ANEURYSM
Aetiology.—
The term 'dissecting aneurysm' is a misnomer and it should be called 'aortic dissection'. The
basic pathology is splitting of the intima, allowing the blood to track into the aortic wall creating
a channel between the intima and the adventitia. This is one of the most common acute problems
involving the thoracic aorta. This tracking of blood into the aortic wall causes distension of the
aorta for which it is called an aneurysm. But this aneurysm develops months or years later, and
such aneurysm is not present during acute dissection.
The cause of weakening of the intima, which causes this condition is not definitely known.
Hypertension is present in about 75% of patients and hypertrophy of the left ventricle characteristic
of hypertension is present in about 90% of cases. The exact nature of degeneration of the aortic
wall is confusing. Cystic medial necrosis has been incriminated. Marfan's syndrome has also been
incriminated particularly when it occurs in younger age group. But in this syndrome there is greater
frequency of dissection in patients with coarctation or congenitally bicuspid aortic valve.
It should be emphasized that this disease is not due to atherosclerosis, which is a disease of
the intima which mostly affects the terminal part of the abdominal aorta. The aortic dissection
is a disease of the media and almost always occurs in the thoracic aorta. Its frequent occurrence in
older age group has led to confusion with atherosclerosis. A distinct abnormality of connective
tissue, known as lathyrism has been incriminated which weakens the cross-linking of collagen.
But confirmation of this condition as probable pathogenesis is still missing.
Pathology.—
Usually the tear of the intima and media is a transverse one in the aorta involving about
1/2 of its circumference. This tear is located in majority of cases (70%) in the ascending aorta, in
the aortic arch in 10% of cases and in the upper descending thoracic aorta in 20% of cases. Three
types have been recognized. In type I, the tear occurs in the ascending aorta, blood entering the
false channel extends along the arch and into the descending aorta and the dissection may extend
distally to reach the abdomen in about half the patients. Proximally the dissection may involve
origins of the coronary artery and the aortic valve attachment. In type II, which is more often seen
in Marfan's syndrome, the dissection is localized to the ascending aorta proximal to the origin
of the great vessels. In type III, the dissection commences in the descending thoracic aorta distal
to the origin of the left subclavian artery and extends distally through the chest into the abdomen.
Type II is uncommon, whereas the risks of complications are more in type I than type III.
As dissection progresses, branch vessels are sheared off, either becoming obliterated or
establishing a communication with the false lumen occluded by the dissection. Proximally the
coronary arteries may be involved. One or more aortic valve casps may be detached causing
aortic insufficiency. Distally, any artery may be involved. Involvement of carotid artery produces
brain ischaemia. Involvement of subclavian artery produces differences in blood pressure between
two arms. Involvement of intercostal arteries may cause spinal cord damage with paraplegia.
Rupture through the serosa causes major internal haemorrhage and sudden death. Rupture
into the pericardial cavity is the most common, probably because the adventitia is thin over the
intrapericardial ascending aorta. Rupture into the left pleural cavity may occur. This causes high
mortality of dissecting aneurysm. About 30% of patients die within 24 hours and about 70%
within 2 weeks and 90%, if untreated, within 1 year. This is the reason why emergency operations
are progressively adopted in the last few years for dissecting aneurysm involving the ascending
aorta.
In very fortunate cases, endothelial lining of the false lumen gives way and blood of the false
track again enters the aortic lumen. This is known as 'healed dissecting aneurysm'. Such patients
have double-barrelled aorta.
Clinical features.— The disease is 3 to 4 times more common in males. It occurs
predominently in older patients beyond the 5th decade, though it may occur in younger age group.
The most characteristic symptom of this disease is excruciating pain, reaching its pick of
intensity immediately. This pain is in the anterior chest, though back pain may occur in about
l/3rd of patients. The pain has a tendency to migrate as dissection extends distally. Pain may
radiate to the neck, arm and to the epigastrium. Only occasionally there may be absence of pain.
Collapse or syncope occurs in about 10 to 20% of cases due to ischaemia of the brain. Signs
of occlusion of other major vessels may be present. Hypertension is present in no less than 80%
of cases.
1. Chest X-ray often shows 'widening of the mediastinum' which is pathognomonic of this
condition. Left pleural effusion may be seen due to extravasation of blood. Sometimes chest
X-ray may be normal.
2. E.C.G.— This condition is often confused with myocardial infarction. Electrocardiogram
is of particular value in differentiating these two conditions.
3. Aortography — is a conclusive evidence of dissecting aneurysm. It is unfortunate that it
may not be possible to do this investigation on acutely ill patients. Aortography shows the double
lumen of the aorta. Sometimes an emergency aortogram should be performed as soon as possible
after admission to hospital.
Treatment.—
1. DRUG THEFtAPY.— Immediate drug therapy has been highly rewarding primarily to
control hypertension and to decrease forceful contractility of the left ventricle. Intravenous arfonad
(trimetaphan) was first used. Later on sodium nitroprusside was used, though it may increase
myocardial contractility and that is why a beta-blocking drug e.g. propranolol was used in
conjunction. Nowadays the regimen which is mostly used is a combination of drugs including
arfonad, reserpin and guanethidine. Some suggested replacing guanethidine with alpha-methyl
dopa.
2. OPERATIVE TREATMENT.—
Indications For Operations.—
(i) When hypertension is not controlled by drug therapy, immediate surgery is indicated.
(ii) When the dissection is continued, which is revealed by continued pain or enlargement
of mediastinal emphysema, immediate operation is justified.
(iii) When immediate rupture seems likely, operation should be performed.

(iv) If there is aortic valvular incompetence, operation should be contemplated.
(v) Signs of proximal aortic dissection and signs of pericardial effusion are indications
for operation.
(vi) Involvement of important peripheral arteries is an indication for operation.
(vii) Nearly all patients with ascending aortic dissection should be managed surgically,
as these cases are threatened with complications like pericardial tamponad (rupture into the
pericardium), rupture into the mediastinum or acute aortic insufficiency.
OPERATION.— Complete transection of the involved aorta followed by end-to-end
reanastomosis with the outer wall of the proximal aorta and both inner and outer walls of the
distal aorta with particular care to suture the inner intimal layer with the outer layer of the
proximal aorta. The result is that the blood within the dissecting aneurysm enters the original
lumen of the aorta distally and as the distal intimal layer is thoroughly sutured with the outer
layer of the proximal aorta, chance of further dissection should be negligible. But unfortunately
as the disease lies in the tunica media, recurrence does happen.
Nowadays the whole of the dissected aorta is excised and the aortic continuity is restored
with a woven Dacron prosthesis. Both these operations are performed with median sternotomy
and cardiopulmonary by-pass.
DISEASES OF VEINS
VARICOSE VEINS
Definition.—
When a vein becomes dilated, elongated and tortuous, the vein is said to be 'varicose'.
Sites.—
The common sites of varicosity are :
1. Superficial venous system of the lower limbs — affecting either the Long Saphenous
or the Short Saphenous vein or the both.
2. Oesophageal varix (affecting veins of the gastro-oesophageal junction).
3. Varicosity of the haemorrhoidal veins (piles).
4. Varicosity of the spermatic veins (varicocele).
In this chapter we shall only discuss varicosity of the superficial venous system of the
lower limbs.
VARICOSE VEINS OF THE LOWER LIMBS

SURGICAL ANATOMY
Venous drainage of the lower limbs can be conveniently described under 3 heads — I.
Deep Veins, II. Superficial Veins and III. Perforating or communicating Veins, which connect
the superficial with the deep veins.
I. Deep Veins.—
The deep veins of the lower limb accompany the arteries and their branches. These veins
possess numerous valves. The main veins are — the posterior tibial vein and its tributaries, the
peroneal vein, the anterior tibial vein, the popliteal vein and the femoral vein.
The characteristic features of the deep veins are :
1. There are numerous valves in these veins. These valves direct the flow of the blood
upwards and prevent regurgitation of flow downwards.
2. Within the soleus muscle, which is the most powerful muscle of the calf there are
venous plexuses or sinuses. These are devoid of valves. These veins empty in segments into the
posterior tibial and the peroneal veins. These posterior tibial veins and the peroneal veins also
receive perforating or communicating veins from the superficial veins and both these perforating
veins and the soleus venous plexuses or sinuses may enter the same sites of these veins.
II. Superficial Veins.—
These veins lie in the subcutaneous fat between the skin and the deep fascia. These superficial
veins of the lower limb are the long and short saphenous veins and their tributaries.
DISEASES OF VEINS 257
LONG (GREAT) SAPHENOUS VEIN.—

It is the longest vein in the body. It begins in the medial marginal vein of the foot and ends
in the femoral vein about 3 cm below the inguinal ligament. It ascends in front of the tibial
malleolus, runs upwards crossing the lower part of the medial surface of the tibia obliquely to
gain its medial border. Then it ascends a finger's breadth behind the medial border of the tibia
upto the knee. Here it runs upwards on the posterior parts of the medial condyles of the tibia
and the femur and along the medial side of the thigh to the saphenous opening. Saphenous
opening lies about 3.5 cm below and lateral to the pubic tubercle. It passes through the cribriform
fascia of the saphenous opening and ends in the femoral vein.
There are about 10 to 20 valves in this long saphenous vein which are more numerous in
the leg than in the thigh. Of these, two valves are almost constant — one lies just before the
vein pierces the cribriform fascia and another at its junction with the femoral vein (this valve is
concerned with saphenofemoral sufficiency).
Tributaries.—
1. At the ankle:
It receives veins from the sole of the foot through the medial marginal veins.
2. In the leg :
(i) It communicates freely with the small saphenous vein.
(ii) Just below the knee it receives three large tributaries — (a) one from the front of
the leg, (b) one from the region of the tibial malleolus (which communicates with the perforating
veins) and (c) one from the calf which communicates with the small or short saphenous vein.
3. In the thigh:
(i) A large accessory saphenous vein — which communicates below with the small
saphenous vein. This receives numerous tributaries from the medial and posterior parts of the
thigh.
(ii) A fairly constant large vein, sometimes called the anterior femoral cutaneous vein
— commences from a network of veins on the lower part of the front of the thigh and crosses
the apex of the femoral triangle to enter the long saphenous vein in the upper part of the thigh.
4. Near the saphenous opening:
Just before the long saphenous vein pierces the saphenous opening it is joined by four veins—
(i) The superficial epigastric,
(ii) The superficial circumflex iliac,
(iii) Superficial external pudendal and
(iv) The deep external pudendal vein, which joins the great saphenous vein at the
saphenous opening.
Surgical importance.—
(a) As there is communication between the long and the short saphenous veins varicosity
may spread from one system to the other.
(b) At the time of operation for varicose vein, when a ligature is advised to the
saphenofemoral junction, the veins draining into the long saphenous vein near the saphenous
opening must be ligated and cut otherwise these small veins will become varicosed due to
incompetent saphenofemoral junction.
(c) In case of varicosity of the long saphenous vein, the small veins from the sole of the
foot and the ankle which drain into this venous system through the medial marginal veins
become dilated and this gives rise to swelling of ankle, which is known as 'ankle flare'.
17
SHORT (SMALL) SAPHENOUS VEIN.—

This vein begins behind the lateral malleolus as a continuation of the lateral marginal vein
of the foot. It first ascends along the lateral border of the tendo Achilles and then along the
midline of the back of the leg. It perforates the deep fascia and passes between the two heads
of the Gastrocnemius in the lower part of the popliteal fossa and ends in the popliteal vein 3 to
7.5 cm above the level of the knee joint.
In the leg it is in close relation with the sural nerve.
This vein possesses 7 to 13 valves, one of which is always found near its termination in the
popliteal vein.
Tributaries.—
It sends several tributaries upwards and medially to join the long saphenous vein. The
most important communicating branch arises from the small saphenous vein before it pierces
the deep fascia and passes upwards and medially to join the accessory saphenous vein. This
communication may occasionally form the main continuation of the short saphenous vein.
III. Perforating or communicating veins.—
These veins communicate between the superficial and deep veins. These always pierce the
deep fascia. There are valves within these veins which under normal conditions allow blood to
Fig. 16.1 .— Direction of blood flow in the

deep, perforating and superficial veins. The
deep vein is shown within the muscle belly
and the perforating veins pass through the
deep fascia to link the superficial and deep
systems, a. Muscle contraction forces blood
proximally in the deep system while the valves
in the perforating vein prevent it from being
pumped from the deep to the superficial
system, b. During muscle relaxation the deep
system is refilled from the superficial system
and the distal limb. c. Muscle contraction in
the diseased limb forces blood into the super
ficial system due to incompetence of perfo
rating venous valves, which results in super
ficial venous dilatation and tortuosity.
flow from the superficial to the deep veins. Only when these valves become incompetent blood
may flow in the opposite direction and thus leads to varicosity of the superficial veins.
When the calf muscles contract the blood is pumped upwards in the deep veins and blood
flow into the superficial veins is prevented by the valves in the perforating veins. During
relaxation of the calf muscles blood is aspirated from the superficial into the deep veins. If the
valves in the perforating vein become incompetent these veins become 'high pressure leaks'
during muscular contraction and this transmission of high pressure in the deep veins to the
superficial veins results in dilatation of the superficial veins producing varicose veins. Perforating
veins are of two types :
(a) INDIRECT PERFORATORS.— There are numerous small vessels which start from
the superficial venous system, pierce the deep fascia and communicate with a vessel in an
underlying muscle. The latter vessel in turn is connected with the deep vein. These indirect
perforators are mostly seen in the upper part of the leg.
(b) DIRECT PERFORATORS.— These veins directly connect the saphenous veins or their
tributaries to the deep veins. A few of these direct veins are constant in number and site. These
are :—
(i) In the thigh.—- Between the long saphenous and the femoral vein in the adductor canal.
(ii) In the leg.— The perforators in the leg are divided into three groups :—
(a) Medial perforating veins.— There are three constant medial leg perforators
situated in line with the posterior border of the tibia 2 inches (5 cm), 4 inches (10 cm) and 6
inches (15 cm) above the medial malleolus. The upper two enter the posterior tibial vein where
an unvalved soleal venous sinus also enters it. The importance of this is that the soleal venous
sinuses are devoid of valves. Moreover the clot arising in the soleal veins may extend into the
posterior tibial vein and then into the perforating veins thus destroying the valves of the
perforators. The lowest perforator has a short course connecting long saphenous with the
posterior tibial vein.
(b) Central perforating veins.— One or two veins connect the short saphenous system
to the veins in the gastrocnemius and soleus muscles. Whereas one enters the muscle on the
medial side close to its junction with the tendo Achilles, the other is situated further up in the
calf. These perforators are insignificant for all practical purposes.
(c) Lateral perforating veins.— There are inconstant perforators at the posterior border
of the fibula. These pass at the levels of 2 inches (5 cm), 5 inches (12 cm) and 7 inches (17 cm)
above the lateral malleolus. These are connected with the peroneal veins.
SURGICAL PATHOLOGY
Under normal conditions the blood from the superficial venous system is passed to the
deep veins through the competent perforators and from the deep veins the blood is pumped up
to the heart by the muscle pump, competent valves and negative intrathoracic pressure. But if
this mechanism breaks down, either due to destruction of the valves of the deep veins (following
deep vein thrombosis), or of the perforators or of the superficial venous system, the blood
becomes stagnated in the superficial veins which become the pray of 'high pressure leaks' and
thus becomes distended and tortuous to become varicose veins. If an individual stands motionless
for a long period of time, venous pressure at the ankle may rise to 80 to 100 mm. Hg and
gradually swelling appears. Even with modest activity of the calf muscles and with competent
venous valves, this pressure is reduced to 20 or 30 mm. Hg.
Aetiology.—
1. Morphological factor.—Varicose veins of the lower limbs are the penalty the man has to
pay for its erect posture. The veins have to drain against gravity. The superficial veins have
loose fatty tissue to support them and thus suffer from varicosity. There are three types of
varicosity — primary varicose veins, secondary varicose veins and congenital varicose veins.
2. Primary varicose veins.— These are more common. This condition is mainly due to defect
in the valves. The defects may be congenital or acquired (either due to thrombosis or due to
inflammation in the veins.)
(i) Defect in the saphenofemoral valve leads to varicosity of the long saphenous vein.
(ii) Defect in the saphenopopliteal valve leads to varicosity of the short saphenous vein.
(iii) Defects in the valves of the perforators lead to varicosity of either long saphenous or
short saphenous system.
3. Secondary varicose veins occur due to venous obstruction e.g.
(i) Mechanical factors e.g. pregnancy or tumours in the pelvis (e.g. uterine fibroids,
ovarian cyst, cancers of the cervix, uterus, ovary or rectum).
(ii) Deep vein thrombosis leading to damage of the valves.
(iii) Hormonal causes — progesterone may cause varicosity in multiparous females.
(iv) Acquired arteriovenous fistula (due to trauma or deliberate shunting for dialysis).
(v) Extensive cavernous (venous) haemangioma.
(vi) Retroperitoneal lymphadenopathy or retroperitoneal fibrosis.
(vii) Iliac vein thrombosis.
4. Congenital varicose veins.— Occasionally varicose veins may develop below 20 years of
age. These cases are mostly due to either congenital arteriovenous fistula or cavernous (venous)
haemangioma.
Predisposing factors.—
(a) Prolonged standing.— During prolonged standing long column of blood alongwith
gravity puts pressure on the weakened valves of the veins. This causes failure of the valves
quickly giving rise to varicosity of the long or short saphenous vein. During prolonged standing
the calf muscles also do not work quite often so the calf pump mechanism also cannot push the
venous blood upwards.
(b) Obesity.— Excessive fatty tissue in the subcutaneous tissue offer poor support to the
veins. This leads to the formation of varicosity.
(c) Pregnancy.— Pregnancy is said to predispose the formation of varicose veins. Varicose
veins are often noticed in multiparous women. Pregnancy acts in various ways — (i) Progesterone
causes dilatation and relaxation of the veins of the lower limb. This may make the valves
incompetent. This hormonal effect is maximum in the first trimester of pregnancy, (ii) Pregnant
uterus causes pressure on the inferior vena cava, thus causing obstruction to the venous flow.
This effect is mostly seen in the last trimester of pregnancy. After each pregnancy both hormonal
and mechanical effects are removed and there is improvement of varicosity. During the
subsequent pregnancy these factors again cause the varicosities to develop in a bigger way.
That is why varicose veins are commonly seen in multiparous women.
(d) Old age.— This causes atrophy and weakness of the vein wall. At the same time with
aging the valves in the veins become gradually incompetent.
(e) Athletes.— Sometimes varicose veins are noticed among athletes. Forcible contraction
of the calf muscles may force blood through the perforating veins in reverse direction. This will
cause destruction of the valves of the perforating veins and ultimately lead to formation of
varicose veins. Similarly Ricksawpullers often suffer from varicose veins.
SYMPTOMS.—
(a) The commonest symptom is tired and aching sensation in the affected lower limb,
particularly in the calf, at the end of the day. The severity of symptoms depends mostly on the
extent of the high back pressure.
(b) Sharp pains may be complained of in grossly dilated veins.
(c) Some patients may suffer from cramp in the calf shortly after retiring to bed. Such
cramp is usually due to sudden change in the calibre of communicating veins which stimulates
the muscles through which they pass.
(d) Pain may be bursting or severe in nature and may be particularly localized to the site
of the incompetent perforating veins. Such bursting pain while walking indicates deep vein
deficiency.
(e) Patients may present with no other
symptom except dilated and tortuous veins of the
leg. These dilated veins may or may not be
associated with the following complications.
(f) There may be other complaints or
complications of the dilated and tortuous veins.
Such as —
(i) Ankle swelling towards evening.
(ii) The skin over the varicosities may itch.
It may be pigmented.
(iii) Eczema of the affected skin.
(iv) Venous ulceration.
(g) In the personal history one may find
that the patient is involved in a job of prolonged
standing e.g. bus or tram conductors.
LOCAL EXAMINATIONS.—
INSPECTION.—
1. When the patient stands up, the veins
become prominent. The varicosities may be either
wide spread or restricted to a single varix. When
such single varix is situated at the saphenous
opening, it is called a 'saphena varix’. It must be
distinguished from a femoral hernia. One can feel
characteristic thrill when the patient coughs. Such
varix disappears when the patient lies down.
When this varix is tapped with a finger, a fluid
thrill may be obtained in the long saphenous vein
lower down in the limb.
2. One must assess in inspection whether
varicosity has affected the long saphenous vein or the short saphenous vein or the both.
3. The skin of the lower part of the leg should be particularly inspected to exclude oedema,
pigmentation, eczema or ulceration.
PALPATION.—
1. The dilated veins are particularly palpated. The saphena varix is palpated and presence
of cough impulse is elicited.
A FEW TESTS are performed to know the details of the varicose vein including the sites
of incompetent perforators.
2. Brodie-Trendelenburg test.— This test is performed to determine incompetency of the
sapheno-femoral valve and other communicating system. This
test can be performed in two ways. In both the methods,
the patient is first placed in the recumbent position and
his legs are raised to empty the veins. The sapheno-femoral
junction is now compressed with the thumb of the clinician
and the patient is asked to stand up quickly, (i) In first
method, the pressure is released. If the varices fill very
quickly by a column of blood from above, it indicates
incompetency of the sapheno-femoral valve. This is called
a positive Trendelenburg test, (ii) To test the
communicating system, the pressure is not released but
maintained for about 1 minute. Gradual filling of the veins
during the period indicates incompetency of the
communicating veins, mostly situated on the medial side of
the lower half of the leg allowing the blood to flow from
the deep to the superficial veins. This is also considered
as a positive Trendelenburg test and the positive tests are
indications for operation.
3. Tourniquet test.— It can be called a variant of
Trendelenburg test. In this test the tourniquet is tied
around the thigh or the leg at different levels after the
superficial veins have been made empty by raising the leg
in recumbent position. The patient is now asked to stand Fig.16.3 — It shows a portion of
up. If the veins above the tourniquet fill up and those Trendelenburg test. Firstly the varicosed-
below it remain collapsed, it indicates presence of leg is to be raised to empty the veins.
incompetent communicating vein above the tourniquet. Now the sapheno-femoral junction is
Similarly if the veins below the tourniquet fill rapidly compressed as in this figure with the
whereas veins above the tourniquet remain empty, the thumb of the clinician and the patient is
incompetent communicating veins must be below the asked to stand up. If the pressure is
tourniquet. Thus by moving the tourniquet down the leg continued for about 1 minute gradual
in steps one can determine the position of the incompetent filling of the veins during this period
communicating vein. indicates Incompetence of the
communicating veins. When the pressure
4. Pratt’s test.— This test is performed to know is released if the varices feel very quickly,
the positions of the leg perforators. Firstly an Esmarch it indicates incompetency of the sapheno
elastic bandage is applied from toes to the groin. A femoral valve. The students are referred
tourniquet is then applied at the groin at the upper end of to Figs. 7.2 to 7.4 of author’s ‘A Manual
the elastic bandage. This causes emptying of the varicose On Clinical Surgery’.
veins. The tourniquet is kept in position and the elastic bandage is taken off. The same elastic
bandage is now applied from the groin downwards. At the position of the perforator, a 'blow
out' or a visible varix can be seen. This is marked with a skin pencil.
5. Perthes’ test (Modified).— This test is primarily intended to know whether the deep
veins are normal or not. A tourniquet is tied round the upper part of the thigh tight enough to
prevent any reflux down the vein. The patient is asked to walk quickly with the tourniquet in
place. If the communicating and the deep veins are normal the varicose veins will shrink whereas
if they are blocked the varicose veins will be more distended.
6. Schwartz’s test.— In a long-standing case if a
tap is made on the long saphenous varicose vein in the
lower part of the leg an impulse can be felt at the
saphenous opening with the other hand.
7. Morrissey’s test or Cough impulse test.— In
this test limb is elevated to empty the veins. The patient
is asked to cough forcibly. An expansile impulse if felt
in the long saphenous varicose vein, it may be presumed
that the sapheno-femoral valve is incompetent. Similarly
if the patient coughs and the sapheno-femoral junction
is incompetent a bruit may be heard on auscultation.
8. Fegan’s method to indicate the sites of
perforators.— In the standing position the places of
excessive bulges within the varicosities are marked with
a skin pencil. The patient now lies down. The affected
limb is elevated and the heel is kept supported. The
examiner palpates along the line of the marked
varicosities carefully, so that he can find gap or small pit
in the deep fascia which transmits the incompetent
perforator. This is marked with 'X'. This is the site of the
perforator. It should tally with the skin pencil mark of
the venous bulge marked before.
F,g. 16.4.- Shows how to perform examlnations._
(i) Examination of
exclude pregnancy or presence of any pelvic tumour as the cause of varicosity. Such varicosity
is called secondary varicosity.
Any dilated collateral veins in the abdomen should be carefully noticed. These veins develop
due to inferior vena caval obstruction particularly thrombosis. Such veins are more often seen in
the flanks communicating with the veins of the chest wall, tributaries of the superior vena cava.
(ii) Vaginal and rectal examinations are must to exclude pelvic tumours.
(iii) Peripheral arterial pulses should also be examined to exclude presence of arterial
insufficiency. Ulcers in the lower limb with presence of varicose veins may not necessarily be
the venous ulcers. Such ulcers may occur due to ischaemia from arterial insufficiency and are
known as 'arterial ulcers'. In these cases varicose vein is the second pathology and not the
cause of the ulcer.
Various special investigations may be performed e.g. ascending phlebography, thermography,
radioisotope scanning, radioactive fibrinogen studies and ultrasonics to know the condition of
the deep vein, position of the thrombus and position of the incompetent perforators. Of the
above-mentioned methods ascending phlebography is the most practical and valuable in the
average hospitals.
Venography.— An ascending venography is performed by cannulating a vein in the foot
and by injecting a contrast medium. A narrow tourniquet is applied just above the malleoli to
direct blood flow into the deep veins. It is a useful investigating procedure for suspected deep
vein thrombosis when ultrasonography is not available.
Descending venography is performed by inserting a cannula in the femoral vein and the
contrast material is injected with the patient standing. The contrast material is heavier than
blood, so flows down the limb through incompetent valves.
Doppler ultrasound is a valuable non-invasive tool, which can be used to demonstrate
saphenofemoral or saphenopopliteal reflux, perforator incompetence and patency of deep veins.
An important recent advance in the investigation of venous disease is colour coded Duplex scanning.
It is possible with this non-invasive technique to map the superficial and deep venous systems.
Blood flow velocity can be measured. The direction of venous flow can be observed and also
the sites of valvular incompetence can be identified.
Photoplethysmography.— The probe is attached to the skin to assess venous filling of the
surface venules. The filling of these vessels indicates the pressure of the superficial veins of the
leg. The patient sits quietly until the trace stabilizes. Then he performs a series of 10 dorsiflexion
of the ankle. The venous pressure falls in the superficial veins of the leg and the skin venules
empty so the photoplethysmography trace falls. The patient then sits and the veins refill. This
refilling occurs faster in case of venous incompetence. The test can be repeated after application
of a tourniquet above the knee to occlude the long saphenous vein and then below the knee to
occlude both long and short saphenous veins. This helps to establish which set of superficial
veins is incompetent.
Duplex Ultrasound Imaging.— In this technique high-resolution B-mode imaging and Doppler
ultrasound are used to obtain images of veins as also to measure blood flow in these vessels.
Direct visualization of veins, anatomical as also functional informations are possible to get.
Modem Duplex ultrasound machines show blood flow as a colour mark that is superimposed
on the grey scale image of the vessel. This technique is most reliable in the investigation of
arteries and veins both their anatomy and physiology. The examination is performed with the
patient standing as the veins are filled in this position. The blood flow in the veins is assessed
exactly in the same way as done in case of hand-held Doppler probe. The calf is compressed to
know the upward flow of the blood towards the heart and is shown as blue in the colour flow
map. The calf is then released. Competent veins show no flow, but incompetent veins allow
reverse flow which is represented as red in the colour flow map.
COMPLICATIONS OF VARICOSE VEINS.—
1. THROMBOPHLEBITIS.— This means inflammation of the superficial veins. In this
case the veins become red and feel like tender cords in the subcutaneous tissue.
Treatment is antibiotic. A foam rubber is placed on the inflamed vein, on which an elastic
bandage is wrapped. Such strapping is continued for a fortnight in which the patient may be
allowed to move about. At night the patient should sleep with legs elevated. After fortnight the
bandage is removed. This usually cures the patient. One may try application of thrombophobe
ointment with disputed result. In case tenderness persists after fortnight, the treatment is repeated.
2. PIGMENTATION.— This is particularly seen in the lower part of the leg. Brownish to
black pigmentation is noticed. This is due to haemosiderin deposits from breakdown of R.B.C.
which have come out of the thin walled veins.
3. ECZEMA (CHRONIC DERMATITIS).— Due to extravasation and breaking down of
R.B.C.s in the lower part of the leg, the skin may itch. The patient scratches which may lead to
eczema formation. Alternatively such eczema may occur following minor trauma or as an allergic
manifestation resulting from various ointment applications.
Treatment is application of ointment containing zinc oxide and coal tar twice daily. One
may try hydrocortisone or betamethazone ointment.
4. ANKLE FLARE.— This has been discussed earlier in this chapter. See page 257 & 284.
5. VENOUS ULCER.— This results more often from deep vein thrombosis than from
varicose vein only. Such ulcers are mostly found on or near the medial malleolus. Following
deep vein thrombosis when recanalization of the deep vein occurs, the valves are either destroyed
or become incompetent due to damage. The valves of the perforators are also damaged. So
venous stasis occurs mostly in the lower and medial part of the leg where there are maximum
number of perforators. Such venous stasis favours local anoxia and oedema. This leads to lipolysis
of the subcutaneous fat. These ulcers must be differentiated from arterial ulcers due to ischaemia
following atherosclerosis. The details of this ulcer have been discussed later in this chapter.
6. HAEMORRHAGE.— Haemorrhage from ruptured varicose vein is not uncommon. Such
haemorrhage may occur externally or internally in the subcutaneous tissue. This may follow
minor trauma. Haemorrhage is usually profuse.
Treatment is simple elevation of the leg and application of a firm pad and bandage.
Tourniquet is not used.
7. PERIOSTITIS.— This occurs in case of long standing cases, particularly if a venous
ulcer is formed over the medial surface of the tibia.
8. CALCIFICATION is occasionally seen in the walls of the veins which are varicosed for
many years.
9. EQUINUS DEFORMITY of the foot may result from long standing varicosity. This is
due to bad practice of the patient of walking on the toes for relief of pain due to varicosity.
After some years the Achilles tendon may be shortened and leads to such deformity.
Treatment is physiotherapy and remedial exercises.
TREATMENT of varicose veins.—
Three modes of treatment are available — A. Palliative treatment, B. Operative treatment
and C. Fegan's injection and compression treatment.
A. PALLIATIVE TREATMENT.— The treatment has a limited scope and its indications are:
1. Those who are pregnant.
2. Those who do not want operation.
3. Those who are waiting for operation.
4. Very early cases of varicosity.
This treatment consists of :
(i) Avoidance of prolonged standing.
(ii) A crepe bandage or elastic stockings are applied from the toes to the thigh. This
should be applied before getting out of the bed in the morning and should be kept till after
getting into the bed at night. So it should be worn all throughout the day and is only taken off
during sleep.
(iii) Whenever the patient sits or sleeps, the limb should be preferably above the heart
level. At least it should be always raised.
(iv) Exercise like 'bicycle riding' in the air while lying on the back, walking etc. should
be performed to strengthen the calf muscles.
B. OPERATIVE TREATMENT.— Indications of operative treatment are :
1. Positive Trendelenburg test.
2. Particularly sapheno-femoral incompetence.
Contraindications are :
1. Pregnancy.
2. Women taking contraceptive pills.
3. Thrombophlebitis.
These cases should be treated first and operation for varicose veins is postponed till the
above complications are got rid of.
There are two types of operation :— 1. Ligation; 2. Ligation with stripping.
1. Ligation.—
(a) Sapheno-femoral incompetence.— The operation is performed under general anaesthesia.
An oblique incision is made just below the groin crease starting from the femoral artery pulsation
to 5 cm medially. All the tributaries of the long saphenous vein are ligated and divided. The
long saphenous vein is now ligated flush with the femoral vein. Particular care is taken to see
that there is no intervening tributary of the long saphenous vein between the ligature and the
sapheno-femoral junction. In the process, the superficial epigastric, the superficial circumflex
iliac, the superficial and deep external pudendal tributaries are ligated and divided. The long
saphenous vein is now ligated distal to the flush ligature and it is divided between the ligatures.
(b) In case of saphenopopliteal incompetence — a ligature is applied at the short saphenous
vein 'flush' with the popliteal vein and another ligature distal to it. The short saphenous vein is
divided between the ligatures.
2. Ligation with stripping.— Stripping operation is mainly performed in long saphenous
vein. Since incompetent perforating veins are hardly found in association with the short
saphenous vein and since stripping the short saphenous vein can not only cause long standing
oedema but may also permanently damage the sural nerve, short saphenous stripping is not
practised.
Technique.— The operation of ligation is similar to that described above.
A transverse or longitudinal incision is made over the long saphenous vein just in front of
the medial malleolus. Care is taken not to injure the saphenous nerve. The long saphenous vein
is cleared from the surrounding structures and lifted with an aneurysm needle. The distal part
is ligated tightly and the ends of ligature are held with a pair of artery forceps, which is used to
lift the vein. Proximal tie is kept loose. The vein is incised between the two ligatures and olive
point of the Myer's vein stripper is pushed up through the vein and through the proximal tie to
emerge through the distal cut end of the long saphenous vein at the groin incision. This stripper
is about 73 cm long. The upper end is now pulled till the acom-head is arrested at the medial
malleolus incision. The proximal ligature here is tightened around the stripper and now the
long saphenous vein is severed between the two ligatures. The ends of the distal ligature are
cut short. The skin is sutured above the acom-head. An elastic bandage is wound from the toes
and gradually followed up, while the stripper is steadily pulled through the groin incision
severing all the tributaries and perforating veins up to the groin incision. The stripper with the
vein is kept aside. The skin margins of the groin incision are now sutured and dressed.
Very often the surgeon may not be lucky to push the stripper right up through the groin
incision. The stripper may be stuck somewhere in between. In these cases incision should be
made over the olive point where it is stuck, the vein is freed and the vein distal to this incision
is stripped. Again the olive point is introduced through the vein here and pushed up. Thus the
operation is performed in stages.
POSTOPERATIVE MANAGEMENT.— At the end of the operation compression bandage
is applied to the limb to prevent excessive bruising. This bandage may be replaced after 1 or 2
days with a thigh-length high-compression stocking. The advantage of this stocking is that it
can be easily removed before taking bath and can then be reapplied.
Complications after surgery.— Bruising and discomfort are the main complications. Slight
pain is often complained of which requires mild analgesic.
Sensory nerve injury in the form of saphenous nerve or its branches which accompany the
long saphenous vein may be damaged; similarly the sural nerve which accompanies the short
saphenous vein may also be damaged. But such damage never occurs in more than 1% of cases
and the area of anaesthesia is so small that it is often not located. However all patients should
be warned before surgery that small areas of numbness and tingling may occur after operation.
After varicose vein surgery motor nerve injury is extremely uncommon unless the popliteal
fossa is explored and the nerves in this region are not taken care of.
Venous thrombosis may follow varicose vein surgery, but usually resolves without any
specific treatment. Deep vein thrombosis may also occur following such surgery. Patients who
have previously suffered from deep vein thrombosis are particularly at risk and they should
receive full prophylactic measures including low-dose subcutaneous heparin in addition to
compression stockings. Patients receiving oestrogen therapy are also at higher risk of venous
thrombosis and heparin prophylaxis should be considered.
Multiple Cosmetic Phlebectomy.— Having dealt with the sources of retrograde flow it
may be required to remove a few superficial veins which may have been dilated over the years
by the unrestrained effects of increased intraluminal pressure.
Technique.— A Beaver miniature blade is used to make a tiny incision immediately over the
vein (which has been marked pre-operatively). With a fine mosquito forceps the vein is gently
taken out to the surface when it is more generously grasped with larger forceps. Fine dissection
may be required to free the varicose vein. The varicose vein is now resected by ligating both
the ends. The skin incision is closed with either subcuticular stitches or with steristrips to make
the closure 'cosmetic'.
C. FEGAN'S INJECTION AND COMPRESSION TREATMENT.— The indications are :
(1) When varicose veins are mostly confined to below knee and are caused by incompetent
perforators.
(2) Recurrent varicosity after operation.
(3) A probable alternative to surgery when the patient refuses it.
Contraindications are :
(1) Deep vein thrombosis — this must be excluded before injection treatment.
(2) Sapheno-femoral incompetence.
In this technique sclerosant like ethanolamine oleate 5% (Ethanolamine B.P.C.) or sodium
tetradecyl sulphate 3% (Thrombovar) is used to damage the intima of the vein and to produce
sclerosis later on. No doubt that intimal damage will take place only when sufficient concentration
of sclerosant is injected, yet one should be cautious not to inject more than sufficient concentration
of the sclerosant lest it may reach the deep veins and should initiate thrombosis there. The
maximum dose at one time and in one point is 1 ml. The injection should be given into an
empty vein so that its walls adhere without any intervening blood clot or thrombosis to yield a
lasting result.
Technique.— The patient is made to stand. The positions of incompetent perforators are
marked with ink. The needles of small syringes containing 1 ml sclerosant solution are inserted
into the ink-marked points. The pistons of the syringes are slightly withdrawn to see if the
venous blood is entering the syringes freely indicating that the ends of the needles are inside
the incompetent perforators. The patient is now asked to lie down on a bed. He is directed to
lift the leg concerned. Thus the veins are made empty. Now the solution is injected. Rubber
pads are pressed on the sites of injection while the needles are withdrawn. A crepe bandage is
applied from the toes to the groin keeping equal pressure throughout over the rubber pads.
Postoperatively, the patient is encouraged to walk as usual. Importance of walking
immediately after sclerotherapy and subsequent extra walking each day cannot be over
emphasized. Such walking is important to discourage clotting from spreading into the deep
veins. If the patient remains comfortable with
compressive bandage it should not be
disturbed for at least 3 weeks. The patient
must attend the outpatient clinic every week. ■■■■■H f
After 3 weeks a new bandage is applied with
less compression for another 3 weeks, after
which the bandages are taken off. Later on
the patient will always be asked to attend . '■ I-
outpatient at regular intervals, so that further , . - v' : -
injection may be carried out to any returning
varicosities. So sclerotherapy is a long term
policy of maintenance rather than the one
time cure intended with surgery. Wati §£ %
VENOUS ULCER
Venous ulceration has two main
aetiologies. Firstly, ulceration may be
associated with demonstrable varicose veins
and secondly, such ulceration may follow
thrombosis and phlebitis in the deep and
perforating veins. This second group presents
as an ulcerated oedematous leg with
demonstrable superficial varices in only
about l/3rd of cases. In all cases of this
second group there will be history of long
standing oedema of the leg.
Pathogenesis.— After the deep vein
thrombosis, if the deep venous system is
allowed to eventually recanalise itself, the
delicate valves will remain impregnated laterally in organised thrombosis. The result is patent
but valveless deep venous system, which transmits the gravitational pressure of the blood column
unimpeded from the level of the heart to the ankles. This is the main predisposing feature in
the pathophysiology of the postphlebitic state. However, valvular incompetence alone is not
enough to produce serious stasis sequels. It must occur through incompetent perforator veins
through which the high deep venous pressure is transmitted to the superficial veins. The location
of these perforating veins determines the predilection of ulcer formation — extending from the
malleoli upto the lower half of the leg. These perforators may have been involved in the initial
thrombosis or may become incompetent by dilatation resulting from the back pressure of the
valveless deep venous system.
Within 10 years of untreated thrombophlebitis, 50% will have venous ulcers.
Fibrinogen escapes through large pores in the venules of these patients with venous
hypertension secondary to venous insufficiency. This fibrinogen accumulation acts as a barrier
to diffusion of oxygen and other nutrients and thus develops thick, hard subcutaneous tissue.
Stasis dermatitis develops with brawny oedema, pigmentation and cutaneous atrophy. Fat necrosis,
tissue death and ulceration follow. It is not until some minor trauma which leads to a skin
break that an actual venous ulcer develops.
Ascending functional phlebography or venography is highly important to formulate treatment
in difficult cases. It will show the size of the lumen of the deep veins, the presence of valves
and existence of high pressure leaks in the calf.
Doppler apparatus may be adopted to indicate the direction of flow in veins.
TREATMENT.—
A detailed history of development and progression of the leg ulceration must be taken.
The patient should be examined in a good light both standing and lying with both lower
limbs completely exposed. One must exclude ischaemic ulcer following arterial abnormality.
Clinical tests for long and short saphenous incompetence must be carried out. In addition the
position of the incompetent perforators should be pointed out. The dimensions and exact site of
ulceration should be recorded. The quantity and nature of discharge is noted and cultured.
A. Conservative Treatment.—
(i) Elevation of the affected limb is important. Vertical leg drainage is a simple and
valuable method of reducing and eliminating leg oedema. The patient is advised to sleep with
the legs at 90° to the horizontal plane by putting a vertical board at the end of the bed or
pushing the bed against the wall. The frequency of daily leg elevation depends on the rapidity
of oedema formation.
(ii) Passive movements to maintain the mobility of the foot and ankle.
(iii) Active movements of the calf muscles.
(iv) A firm elastic 'blue line' bandage is applied spirally from the base of the toes upto
the knee joint. While walking this bandage will alternatively stretch and relax and thus help in
venous pumping. A piece of felt or rubber with bevelled edges are cut to a size more than the
ulcer and is interposed in the bandage over the ulcer to reduce the local oedema. This bandage
must be worn whenever the patient is out of bed. The most important factor in achieving healing
of such ulcer is the use of high levels of compression. Pressure of 30 to 45 mmHg is ideal for
early healing. This can be achieved by the use of compression stockings (class 3 stocking exerts
about 30 mmHg compression at the ankle) or by bandaging. This compression should only be
applied to the ulcer region, so patients should wear below the knee stockings. Those patients
who cannot manage the stocking, can be treated by multilayer bandaging. But this bandaging
must be applied by a person trained in this procedure. The best known of these techniques is
the '4-layer bandage' used at Charing Cross
Hospital, London. In this method pressure
of 45 mmHg can be achieved at the ankle.
It has been shown that 70% of venous
ulcers are healed within 12 weeks. This
bandage must be changed once or twice a
week.
(v) Effective antibiotic from the
culture report should be prescribed
immediately. An analgesic may also be
prescribed if required.
(vi) Most exudative ulcers with
yellow or sloughy base and poor
granulation tissue require daily cleansing
and dressing until the ulcer becomes dry
with healthy granulation at the base.
Hibitane, Eusol or hydrogen peroxide may
be used for this purpose.
(vii) Absorbent or adherent
dressings with spirit applications to
promote drying and scaling may achieve
this aim. Proprietory zinc and calamine Fig. 16.6.— Phlebogram showing translucent areas within
absorbent bandages have proved very the deep veins which are nothing but thrombi.
effective. 'Calaband' and/or 'viscopaste'
have their advocates. Bandages are worn over the dressing and can be left in place upto 1
month at a time, although they are initially changed every week.
(viii) Once the ulcer is clean Orahesive powder may be applied on the surface of the
ulcer. Bandage should be continued from toes to the knee.
(ix) 80% to 90% ulcers will heal with this simple outpatient regimen. But the remaining
patients with extending or longstanding ulceration will prove resistant to this form of treatment
and will require admission to hospital.
B. Surgical Treatment.—
(a) Alongwith the previous conservative regimen, incompetent perforators and varicose
veins may be treated by surgery or sclerotherapy following which the ulcer will heal completely.
(b) Larger ulcers will need a split skin graft after the veins have been treated.
(c) Ascending phlebogram must be performed at this stage if not performed earlier to
detect incompetent calf perforating veins and evidence of damaged deep veins. Normal
phlebogram should arouse suspicion as another cause of ulceration as it is rarely produced by
simple saphenous incompetence.
(d) Subfascial ligation of Cockett and Dodd.— Once the ulcer has healed the
incompetent perforating veins should be identified and divided. An incision is made in the
lower half of the leg 2.5 cm behind the posterior border of the tibia. The incision is deepened
till the deep fascia is reached. The

margins are undermined. The deep
fascia is incised along the line of
incision. The margins of the deep
fascia are lifted up. The perforating
veins are ligatured under direct
vision and divided (Fig. 16.7).
(e) Linton developed a radical
surgical approach. In this technique
the superficial varicosities were
BORDER ligated and stripped with subfascial
LINE OF OF TIBIA ligation of the perforating veins.
(f) A by-pass operation may be
performed for thrombosed deep
veins. Such occlusion is relieved
ACHILLES TENDON before or at the same time that the
incompetent perforators are ligated.
MEDIAL MALLEOLUS The saphenous vein has been used
to by-pass segmental venous
occlusion of the iliofemoral or
femoropopliteal vein. For iliofemoral
occlusion, the contralateral
saphenous vein is passed
suprapubically and anastomosed to
the affected side distal to the
occlusion. This is known as Palma
LATERAL operation.
'gjjg'XriNG gastrocnemius For femoropopliteal occlusion, the
obstructed segment can be by
passed by anastomosis of the
saphenous vein to the popliteal-
tibial trunk below the occlusion at
the level of the knee joint.
UPPER- Better assessment of a case can
be made by (i) isotope clearance
technique perhaps combined with
J- POSTERIOR (ii) foot volumetric studies and (iii)
/BORDER OF
f FIBULA PALPABLE Doppler assessment of reflux. At
MIDDLE THRU MUSCLE present, these techniques are being
combined with ascending and
■ACHILLES
TENDON
LOWER
Fig.16.7.— Cockett and Dodd
DEEP FASCIA operation. The upper figure shows
incision. The lower figure shows that the
SKIN FLAP WITH medial perforating veins are ligated and
SHORT SAPHENOUS VEIN divided, whereas the lateral perforating
veins are exposed.
descending phlebography. Based on these results by-pass surgery, valvular repair, valvular
insertion by-passes and artificial valvular transplantation can be selected and assessed.
(g) Valvular repair.— Venous valves in the deep veins may be repaired if their
incompetence is a consequence of primary valve failure. This may lead to successful long term
maintenance of leg ulcer healing. However these operations are technically difficult and there is
risk of thrombosis which may destroy the reconstructed valve. This valve repair was described
by Kistner. He described two types of repair — internal by incising open the vein and suturing
the valve to make incompetent valve competent. The other type is external suturing i.e. the
valves are sutured from outside the vein without opening it.
Valve transplant by autograft.— A portion of the vein which contains defective valves following
deep vein thrombosis may be replaced by transplanting a segment of axillary vein or brachial
vein of the same person which contains competent valves.
(h) The main stay of the local ulcer treatment is to cleanse the ulcer in simple water and
then to debride the ulcer to remove all sloughs. The skin of the leg becomes scaly, which should
be treated by emulsifying ointment. No local antibiotic should be used, similarly no topical
application has been shown to expedite the healing of a venous ulcer as often such applications
make the skin allergic. Only topical steroids may be applied when there are eczematous reactions
around the ulcers. Some surgeons prefer excision and skin grafting, but effectivity of this
procedure is questioned. Now microvascular free-skin flap transfer offers the prospect of bringing
healthy tissue into the areas of severely damaged ulcerative area of skin.
VENOUS THROMBOSIS
Venous thrombosis is a very common surgical problem, which has great influence on the
morbidity and mortality of surgical patients. _
Aetiology'.— Three factors play major roles in aetiology of venous thrombosis. These are:—
(1) Stasis, (2) injury to the vessel wall and (3) hypercoagulability of the blood.
Stasis is probably the most important clinical factor to cause venous thrombosis. A reduction
of blood flow in the major veins by half has been shown immediately following induction of
general anaesthesia and in debilitating diseases. This decrease in flow persists for the duration
of anaesthesia. Clinical coagulability is raised from the overactivity of the normal blood clotting
mechanism. The increased clotting tendency encountered postoperatively may be the result of
several factors including altered blood elements associated with blood dyscrasias or polycythemia
or may be secondary to dehydration. This hypercoagulability of the blood most frequently occurs
in infection, after haemorrhage and in visceral carcinoma which may cause thrombophlebitis
migrans (Trousseau's sign). Injury to the vein wall is mainly due to trauma or infection.
A few predisposing factors are :— (i) major injuries, (ii) following operation, (iii) visceral cancer,
(iv) tobacco smoking, (v) diabetes, (vi) congestive heart failure, (vii) shock, (viii) polycythemia
vera, (ix) long period of sitting or bed rest, (x) pregnancy, (xi) infection, (xii) varicose vein, (xiii)
obesity, (xiv) using of contraceptive pills.
Nowadays great stress is being led on the hypercoagulability factor. Damage to the
endothelium leads to platelet adherence which is the start of the thrombotic process with fibrin
deposition.
RESULTS of thrombosis are as follows :—
(i) Proximally, thrombosis extends into larger veins, where portions of clot may detach as
emboli to cause pulmonary embolism and infarction, which is fatal.
(ii) Locally the clot ultimately organise into fibrous tissue. While a few veins remain
obstructed following thrombosis, others may recanalise. In both these cases the venous valves
are destroyed leading to chronic venous valvular insufficiency. Occasionally calcification may
be seen in the thrombus in pelvic veins, which are known as phlebolith.
(iii) Distally thrombus causes venous obstruction, which increases distal venous pressure.
This leads to oedema. Venous collateral circulation may open up by the appearance of tortuous
superficial veins. If venous pressure increases to such an extent that it exceeds local arterial
pressure, blood flow ceases and venous gangrene occurs.
Types of venous thrombosis.—
Mainly two types of venous thrombosis are seen —
1. Thrombophlebitis.— This is mainly seen in the superficial veins, particularly in varicose
veins or in veins which have been cannulated for infusion. In these cases venous thrombosis is
associated with acute inflammatory response giving rise to pain, local swelling, redness and
tenderness. Although acute inflammatory changes occur in the vein wall, bacteria are rarely present.
2. Phlebothrombosis (deep vein thrombosis).— Here the thrombus produces little
local signs or symptoms and may be loosely attached to the vein wall, so that emboli may be
dislodged from this thrombus to cause fatal pulmonary embolism.
SUPERFICIAL VEIN THROMBOSIS (THROMBOPHLEBITIS).—
As mentioned earlier such thrombophlebitis occurs more often in varicose veins or after
intravenous infusion. This is also seen in association with polycythemia, polyarteritis, Buerger's
disease and visceral cancer. In both Buerger's disease and visceral cancer, thrombophlebitis may
affect one vein after the other and is typically known as thrombophlebitis migrans. This is known
as Trousseau's sign ( this sign is also used to indicate muscular spasm on pressure over nerve,
seen in tetany).
Clinical features.— The patients usually complain of painful cord-like inflamed area, the
inflamed vein.
Careful palpation will reveal a firm cord along the course of a nonsuperficial vein. There
may be associated redness, tenderness and local induration. Veins of the lower extremity should
be best examined in the standing position.
Treatment.— Operation is almost never required as embolization never occurs. However
thrombophlebitis may be present with deep vein thrombosis, when there will be significant
distal swelling and a phlebogram will diagnose deep vein thrombosis.
(a) Hot baths or compress may be helpful in relieving discomfort. It may also prevent
propagation of thrombus by preventing venous stasis.
(b) Elastic support or crepe bandage should be applied to the part. When it affects the
leg, walking is advised with elastic support. The patient may lie down in bed with legs elevated
above the level of the heart. However sitting or standing should be discouraged though walking
is encouraged.
(c) Anticoagulants or enzymatic clot dissolvers have little effect on the outcome.
(d) Aspirin is quite effective in this condition, though there is hardly any place of expensive
and potentially dangerous 'antiinflammatory' drugs.
(e) The role of antibiotic is debateable. While many surgeons prefer to give a short course
of penicillin or cotrimoxazole, others rule out any benefit which may be achieved due to
administration of antibiotic unless a definite septic cause is obvious. But antibiotic has got a
definite role to play in case of thrombophlebitis due to intravenous infusion.
18
Operative treatment.— Only when there is evidence of ascent of thrombi into the more
proximal vein, ligation of the vein is justified. Ligation of the long saphenous vein at the
saphenofemoral junction using local anaesthesia or short saphenous vein in the popliteal fossa
may be indicated if there is fear of propagation of thrombi proximally. Such ligation is also
required when the vein is becoming recurrent phlebitic.
DEEP VEIN THROMBOSIS (PHLEBOTHROMBOSIS) (DVT).—
The aetiology has already been considered under the heading of 'Venous Thrombosis'. The
main predisposing factors are (1) stasis, (2) increased blood coagulability and (3) injury to the
vessel wall.
Deep vein thrombosis occurs more often after operations, any debilitating illness, immobility
for a considerable period, child birth and some sort of local trauma. A peculiar condition is
'spontaneous thrombosis', which may occur without any definite reason and in this case presence
of visceral neoplasm should be excluded. Another important feature is that postoperative
thrombosis is rare before the age of 40 and is more often seen following operations on the hip
joint, on the prostate, cancer and in obese patients.
The thrombus may commence in a venous tributary of a main vein. The calf is the most
frequent site of thrombosis. From here thrombus extends in a serpentine fashion into the main
deep veins, where a portion may break off to cause pulmonary embolus. Other veins are also
involved less frequently.
Clinical features.— Patients with suspected deep venous thrombosis should be evaluated
and treated promptly in order to lessen the propagation of the thrombus, to limit the damage
to the venous valves and to reduce the potential for pulmonary embolism. Venous thrombosis
often is asymptomatic and clinical indications are present in only 40% or less of patients with
venous thrombosis.
The main symptom, which if at all present, is an aching pain. This pain is aggravated by
muscular activity at the site of the thrombus. Sometimes there is only a feeling of heaviness,
accentuated by standing. If there be a massive thrombosis there may be an extremely severe
aching at the site of thrombosis.
Swelling is another symptom, which is noticeable at the dependent part. This swelling is
usually minimal and only occasionally it may be marked.
PHYSICAL FINDINGS.— The three most important signs which may be present in a case
of deep vein thrombosis are swelling, tenderness and Homans' sign.
Swelling should be searched for with the aid of a measuring tape. In majority of cases there
is so slight swelling that it may be missed by the naked eyes. The other extremity should always
be placed side by side to compare and to exclude swelling on the affected side.
Tenderness over the thrombosed vein can be detected by careful palpation of the calf, popliteal
space and thigh (particularly the adductor canal).
Homans' sign.— Homans was the first physician to emphasize the importance of venous
thrombosis in the legs as source of pulmonary emboli. He described a test which is known as
Homans' sign. In his test passive forceful dorsiflexion of the foot with the knee extended will
elicit pain in the calf. Passive elongation of the gastrocnemius and soleus muscles causes irritative
pain in the calf when the calf veins are thrombosed.
Gentle pressure directly on the calf muscle in the relaxed position will also elicit pain. Care
must be taken to be gentle in manipulation lest it should dislodge emboli to cause pulmonary
embolism.
Moses' sign.— Squeezing of the calf muscles from side to side is painful in case of deep
vein thrombosis.
Various sites of involvement.—
1. Calf vein thrombosis.— The most frequent site of thrombosis is probably the veins of
the calf, particularly in the venous sinuses of the soleus muscle. If untreated, the thrombi may
propagate to involve the femoral vein or even the iliac vein. As mentioned above Homans' sign
and calf tenderness are usually present. Swelling is present in only 50% of cases and it is almost
always minimal.
2. Femoral vein thrombosis.— Quite often thrombosis of calf veins is associated with
thrombosis of the femoral veins. Sometimes there is only thrombosis in the femoral vein. This is
detected by tenderness of the thigh, particularly in the adductor canal. Swelling is usually present
at the ankle or calf level. Homans' sign may or may not be present.
3. Iliofemoral venous thrombosis.— Iliofemoral venous thrombosis may also be associated
with calf vein thrombosis. But it may occur singly. The left leg is more often involved in the
ratio of 3 : 1. The reasons may be (i) apparently longer course of the left vein, (ii) its constriction
by the right iliac artery and (iii) occasional presence of congenital web at its junction with the
inferior vena cava.
In this type there is marked swelling affecting almost the entire leg. This is due to
considerable rise in the venous pressure. Alongwith marked oedema there is also bluish
discolouration. When this bluish discolouration is associated with the pain, the process is called
phlegmasia cerulea dolens. This syndrome may progress to venous gangrene due to massive
thrombosis of all venous drainage of the limb. This should be differentiated from white leg or
phlegmasia alba dolens due to lymphatic obstruction and swelling of the lower limb.
4. Pelvic vein thrombosis.— Thrombosis of the pelvic veins is rare and often involves
branches of the internal iliac veins. This is more often seen in women with pelvic inflammatory
disease. Sometimes it may be seen in men due to involvement of the prostatic plexus. The
diagnosis is difficult unless it involves the common iliac and external iliac veins when
manifestations in the leg will be detected. Sometimes pelvic or rectal examination may help in
the diagnosis.
Special investigations.—
Since clinical symptoms and signs are not very reliable to diagnose deep vein thrombosis,
much reliance is given on special investigations.
1. PHLEBOGRAPHY.— The patient lies on a mobile table in horizontal position. 45%
sodium diatrizoate is injected slowly into a vein on the dorsum of the great toe. A pneumatic
cuff just above the ankle directs the contrast medium into the deep veins. Another cuff at the
mid-thigh position confines the contrast medium initially to the lower leg. The amount and rate
of injection of the contrast medium is controlled by the filling of the veins as viewed on the
television screen. The patient is asked to dorsiflex and plantarflex his foot thus propelling the
contrast medium into the tibial veins. When the veins are filled films are taken of the leg in two
planes. At the end of the procedure the contrast medium is washed off from the leg veins by
injecting 100 ml of normal saline containing heparin.
Ascending functional cinephlebography can be obtained by continuous observation of the flow
of the contrast medium on the television screen as it progresses through the tibial veins. Function
of the valves can be particularly noticed. Similarly the popliteal and femoral veins can also be
assessed. The valvular function is considered to be normal when both the valve cusps are seen
Fig. 16.8.— Ascending phlebography showing normal filling

of the deep veins of the leg and thigh.
to open and close with onward flow of blood and
no retrograde flow occurs even with the Valsalva
manoeuvre.
Radionuclide phlebography.—- The venous
system can be visualized by injection of an isotope.
The definition is not as good as with contrast
phlebography, but thrombi within the thigh and
pelvic veins are readily identified. That is why this
technique has become of special value in iliac
venous system, where X-ray studies are often Fig.16.9.— Phlebogram of the deep veins of the
difficult. leg (tibial veins) showing translucent areas which
2. RADIOACTIVE FIBRINOGEN TEST— indicate thrombi within the veins.
At first l31I-labelled fibrinogen was used.
Subsequently 125I-labelled fibrinogen was employed due to its softer radioaction and its
detectibility with much lighter and mobile apparatus. The thyroid gland is firstly blocked by
sodium iodide (100 mg) given orally 24 hours before the intravenous injection of 100 microcuries
of 125I-labelled fibrinogen. The scintillation counter is first placed over the precordial region and
the radioactivity over the heart is measured. The machine is adjusted so that this reading
represents 100%. The legs are elevated on an adjustable stand to decrease venous pooling and
to give access to the calf for the scintillation counter. Counting is performed along the lower
extremity at two inches interval. Preoperative counting can be compared with the postoperative
counting on the 1st, 3rd and 6th days after operation. An increase in the percentage value of 20
or more represents formation of thrombus in the deep veins of the legs.
The test is positive only during the

active formation or a propagation of a
thrombus. It is more valuable during the
postoperative period to detect the patients
at risk. At the time of formation of
thrombosis, its accuracy is about 90%. This
accuracy falls with established deep vein
thrombosis to about 80%.
3. DOPPLER ULTRASONOGRA
PHY.— This convenient and readily
available technique depends upon the
recognition of distorded flow patterns or
absence of flow in the larger veins. This
technique quite accurately detects the
presence of thrombi in those veins
proximal to the knee. The sensing probe is
placed over the femoral vein in the groin.
Normally it transmits a venous hum and
pressure on the calf will change it into a
'roar' due to increased blood flow. If there
is thrombosis in the calf veins, femoral or
popliteal veins, the 'roar' is not heard.
Fig. 16.10.— Radionudtde venogram. *. Dynamic phase, However this test is relatively insensitive
which shows filling defect in the right calf. Remainder of to calf vein thrombosis.
the right side and whole of the left skte are rearma!. b. 4. PLETHYSMOGRAPHY.— Strain
Static phase, which shows persistence of ladfcmudide in gauge plethysmography quantifies venous
the right catf distal to the fifag defect. obstruction by measuring the rate at which
the calf veins empty when the pressure in a proximally placed pneumatic cuff is released. The
rate of maximum venous outflow is inversely proportional to venous resistance. By inflating a
proximal venous cuff below an occlusive tourniquet, the extent of venous reflux can also be
evaluated.
Other plethysmographic techniques have also been developed e.g. impedence plethysmography.
Significant venous obstruction decreases the venous volume changes occurring with respiration
and intermittent compression with a pneumatic thigh cuff. Liquid blood conducts electric currents
and this instrument is capable of measuring small changes in the electrical resistance of the leg
and thus assesses changes in venous volume. This instrument is however much more reliable
in making correct diagnosis of femoropopliteal and major calf-vein thrombosis than doppler
ultrasonography.
5. VENOUS PRESSURE MEASUREMENT.— A needle is inserted into a superficial vein
of the foot or ankle and this is connected to a saline solution manometer. The pressure is compared
with those in the other leg and arm. This test will however be positive in the presence of
significant venous obstruction only early in the course of the disease before sufficient collaterals
have developed.
6. DUPLEX ULTRASOUND IMAGING.— Due to direct visualization, both functional and
anatomical informations can be obtained.
PREVENTION.— Every care should be taken to prevent formation of deep vein thrombosis.
The main points to be considered in preventing deep vein thrombosis is (a) to minimise venous
stasis, (b) to avoid venous intimal injury and (c) to reduce hypercoagulability.
BEFORE OPERATION.— (i) Prevention must begin before operation. Time spent in hospital
awaiting operation should be reduced to the minimum.
(ii) Leg elevation above the level of the heart is quite effective. A recent venographic
study has demonstrated that the contrast medium remains in the soleal veins in an average of
10 minutes in supine patients with legs in horizontal position. Elevation of legs 20° above
horizontal level causes immediate emptying of dye from the soleal veins.
DURING OPERATION.— (i) Elevation of leg during operation, if possible, is quite effective
in reducing DVT.
(ii) Hypertonic or irritating intravenous solutions should not be used into the veins of
the lower extremity. If they are to be used, it is best given by an indwelling catheter.
(iii) Use of anticoagulants e.g. heparin in small doses has competently reduced the
incidence of DVT. 5000 units of heparin is introduced subcutaneously 2 hours prior to operation
and every 8 hours thereafter for 7 days has considerably reduced the incidence of deep vein
thrombosis as diagnosed by I25I-labelled fibrinogen test.
(iv) Intermittent pneumatic compression, electrical calf stimulation and active plantar
flexion of the feet effectively prevent venous stasis in the soleal veins. During anaesthesia,
passive plantar flexion by pedalling on a motor driven board increases the mean venous
flow. External pneumatic compression is free from side effects and is relatively simple and
cheap. It is very effective in preventing venous stasis. Electrical stimulation of the calf muscles
is another physical method of prophylaxis. It appears to be a less effective measure of
prophylaxis when compared to intermittent pneumatic compression. Simple leg elevation and
plantar flexion of the feet are both inexpensive and effective in preventing venous stasis and
require minimal nursing effort.
AFTER OPERATION.— (i) Low molecular weight dextran has been used to prevent venous
thrombosis. But occasional occurrence of pulmonary oedema and increased incidence of bleeding
and haematomas has been noted after such indiscriminate use of dextran. However dextran
prophylaxis may be advantageous in a selected group of patients who are simultaneously in
need of volume replacement and prophylaxis for thrombosis. Bleeding generally is not a problem
if dosage of 1.5 g/kg body weight is not exceeded. However the risk of fluid overload especially
in the elderly patients should be considered.
(ii) Aspirin in small dose has both been able to reduce postoperative pain and prevent
DVT.
(iii) Elastic stockings have been claimed to reduce DVT by compressing the superficial
venous system which increases the velocity of venous blood flow through the deep veins thus
reducing the venous stasis. The optimal pressure gradient for elastic stockings should be 18 to 8
mm Hg from the ankle to the thigh, which increases venous flow velocity detected with Doppler
ultrasound. However the effect of an elastic stocking in prevention of deep vein thrombosis is
controversial. The available data do not provide sufficient evidence to justify its widespread
use. On the other hand these stockings if not fitted properly to ensure graded compression
from the ankle to the thigh, actually may act as a tourniquet and may increase venous stasis.
(iv) Leg elevation is obviously very important in the early postoperative days.
TREATMENT OF ESTABLISHED CASES.—

CONSERVATIVE TREATMENT.
(i) Bed rest.— Bed rest is indicated for about 7 days after the diagnosis is established.
This is to allow thrombi to become adherent to the vein wall. It also prevents formation of
pulmonary embolus.
(ii) Elevation of legs above the level of the heart decreases the pressure in the veins. It
relieves oedema and pain. It also increases rate of blood flow in the nonaffected veins thereby
preventing venous stasis and formation of new thrombi.
(iii) When walking is started, an elastic stocking should be used. With this the rate of
flow in the vein is increased. Standing and sitting idle should be prohibited. This prohibition
should be for no less than 6 months period.
(iv) Heparin.— This drug prevents thrombus formation by inhibiting the formation of
thromboplastin and also acts as antithrombin to inactivate thrombin. Its effectivity can be
determined by measuring clotting time and partial thromboplastin time (PTT). If clotting time
or PTT is at least twice normal, propagation of thrombi can be prevented. This can be achieved
by administering aqueous heparin in the dose of 5000 to 10000 units intravenously either
continuously or every 4 hours. This therapy is advised for variable lengths of time. It is reasonable
to use for at least 7 days. Gradually the dose is reduced over a period of 3 to 5 days. If the drug
is discontinued abruptly, new thrombosis may be formed. This is known as 'heparin rebound'.
After discontinuing heparin, oral anticoagulant therapy with coumarin derivatives should be
started.
(v) Coumarin derivatives.— These derivatives interfere with 4 factors in the clotting
mechanism, but their main effect is reduction of plasma concentration of prothrombin. So the
effect of these drugs can be determined by measuring prothrombin time, which should be less
than 10% of normal to inhibit propagation of thrombi. Warfarin is used for approximately 4
weeks after venous thrombosis or pulmonary embolism, as recurrence is likely within this period.
In case of patients with iliofemoral venous thrombosis this drug should be continued for 6
months. In case of pregnancy, this drug can pass placental barrier, whereas heparin cannot. So
these drugs should not be used during the first trimester or during the whole period of pregnancy
as bleeding complications in new bom infants may be noticed.
(vi) Fibrinolytic drugs e.g. streptokinase indirectly converts plasminogen to plasmin, which
can lyse clots in deep veins. Streptokinase is derived from streptococcal cell cultures. It is
administered intravenously over 12 hours period. Significant lysis of clot within 5 days has
been demonstrated. However allergic, pyrogenic and bleeding side effects should be considered.
Urokinase directly converts plasminogen to plasmin and it also successfully lyses clots. This
drug has been derived from foetal kidney cell cultures and its cost is considerable.
(vii) Aspirin, dipyridamole and sulphinpyrazone are the pharmacologic agents that inhibit
platelet function and have been used considerably in prevention of venous thrombosis. 1200
mg of Aspirin given daily as a preventive measure in patients following elective hip replacement
have been found to be as effective as warfarin in preventing clinically diagnosed venous
thrombosis and pulmonary embolism.
By-pass procedure.— Simple by-pass with vein or prosthetic material may be used in larger
vessels e.g vena cava and iliac veins. In this technique veins of large calibre are difficult to get,
so some sort of prosthetic material is more often used. Palma operation may be carried out
which involves mobilizing the long saphenous vein of the opposite leg, the distal end is tunnelled
across suprapubically and inserted into the affected femoral vein below the obstruction. Blood
drains from the affected leg via the long saphenous vein into the femoral vein of the opposite
side. In case of obstruction of the superficial femoral vein, the long saphenous vein is connected
to the popliteal vein of the same leg. This is known as May-Husni procedure. In majority of
patients with chronic superficial femoral vein obstruction, the blood flows along the long
saphenous vein to reach the common femoral vein, so no operation is required.
Valvular repair.— When the venous valves in the deep veins are damaged, valve repair is
possible to make them competent. This valve repair was described by Kistner. He described
two types of repair — internal by incising open the vein and suturing the valve to make
incompetent valve competent. The other type is external suturing i.e. the valves are sutured
from outside the vein without opening it.
Valve transplant by autograft.— A portion of the vein which contains defective valves following
deep vein thrombosis may be replaced by transplanting a segment of axillary vein or brachial
vein of the same person which contains competent valves. These operations are particularly
carried out who have previously suffered from deep vein thrombosis.
1. Venous thrombectomy with Fogarty catheter has been successfully applied in cases of
major veins e.g. subclavian, ilial or femoral.
2. Sometimes massive venous thrombosis in the lower limb leads to severe impairment
of blood supply to the limb leading to ischaemia and even gangrene. This is a surgical emergency
and requires quick relief of venous obstruction. This can be achieved surgically by opening the
femoral vein through an incision in the groin and removing all clots from the deep veins of the
pelvis and leg. This operation however is losing popularity and the more modem treatment is
thrombolysis — by passing a catheter into the affected vein and by infusing a fibrinolytic agent
e.g. streptokinase or tissue plasminogen activator (TPA).
3. Prevention of pulmonary embolism by surgical means has been considered. This is
particularly if the patient is already having anticoagulant treatment. Thrombectomy cannot be
said to have contributed significantly to the prevention of pulmonary embolism nor perhaps
either to the reduction of post-thrombotic stasis. However it has a real place as potential cure
for developing venous gangrene. The various methods in this group are —
(i) Ligation of femoral vein below profunda entry; (ii) Ligation of iliac vein; (iii)
Interruption of the venous pathway to the lungs by narrowing the inferior vena cava by sutures,
coarsely serratpd clips or by inserting an umbrella filter.
Objections to these operations include (a) the risk of late stasis effect and (b) thrombus has
been demonstrated beyond these devices at postmortem in patients who have succumbed to
pulmonary embolism.
However very few surgeons now perform the above-mentioned operations. The more
modem treatment is to achieve thrombolysis by passing a catheter into the affected vein and
infusing a fibrinolytic drug such as streptokinase or tissue plasminogen activator (TPA). This is
reducing the need for operation.
4. The most effective preventive measure against secondary embolism is heparin in full
therapeutic dosage upto 60,000 units in 24 hours given by regulated drip. This regimen continued
for 7 to 10 days will largely exclude the problem and operation is only restricted to resistant or
chronic cases of small repeated embolism resulting in pulmonary hypertension. Of course as
with heparin there is the risk of haemorrhage.
PULMONARY EMBOLISM
Pathophysiology.— Thrombi break loose from the deep vein thrombosis, pass through the
right atrium and ventricle and lodge in the pulmonary arteries. This is known as pulmonary
embolism. Small emboli lodging in a lobar or segmental artery may cause death, but the
mechanism is not clearly known. It may be, that intense reflex bronchoconstriction and
vasoconstriction may lead to such death. Single small embolism may also result in infarction,
followed by infection, abscess and empyema.
Multiple small emboli may produce arterial obstruction to such an extent as to cause
pulmonary hypertension and right ventricular failure.
Large thrombus which lodges in major pulmonary artery may cause immediate death due
to vasovagal shock, right ventricular failure and inadequate transfer of oxygen and carbondioxide
in the pulmonary circulation.
Majority of pulmonary emboli originate in the lower extremity (85%). 5% come from pelvic
vein, vena cava or upper extremities. 10% of emboli originate from the right atrium.
Obviously there will be more risk of loosening of thrombus at the upper limit of a long
femoroiliac occlusion, where both the force of venous flow and turbulence will be greater.
Recent studies have demonstrated that both compliance and resistance change in both lungs
irrespective of whether the emboli are small or large. This may be reversed by increasing oxygen
in the inspired air or by administration of isoproterenol, suggesting that the changes are due to
contraction of the smooth muscles in the peripheral airways. As the changes are also seen in
the contralateral lung as well as in the embolised lung, it has been postulated that a humoral
mechanism is present. Moreover that unilateral and bilateral wheezing may be present clinically
following acute pulmonary embolism further supports this concept. It may be that serotonin
may possibly be responsible for this bronchoconstriction.
Clinical features.— Patients usually complain of dyspnoea, chest pain, haemoptysis and
hypotension. Dyspnoea is first to appear, followed by pain which becomes more severe in the
presence of a massive embolus lodged in the main pulmonary artery. The pain is usually
substernal and sharp, stabbing in nature, which occurs during breathing. In case of peripheral
embolus there may be pleuritic pain. Occasionally pain may be epigastric. Haemoptysis is due
to presence of infarction of segments of lung.
PHYSICAL EXAMINATIONS.— Most consistent finding is tachycardia and tachypnoea.
Shock and cyanosis are ominous signs and only seen in massive embolus. Pleural friction rubs
are heard in case of peripheral infarcts. Rales may be heard due to secondary pulmonary oedema.
Small pleural effusions are not uncommon. Dilatation of the cervical veins are due to right
ventricular failure. There may be accentuation of second pulmonary sound.
1. CHEST X-RAY.— The most characteristic finding is diminished pulmonary vascular
markings. But unfortunately this is seen in only 50% of cases and only when the films are taken
within 24 to 48 hours, after which vascular markings may return to normal.
Since pulmonary emboli do not always cause infarction, wedge shaped infiltrate may not
be seen. In many patients the chest X-ray may remain normal throughout the course of
pulmonary embolism.
2. ELECTROCARDIOGRAM.— Though it may show certain changes, yet these are not
specific. The most common abnormality is ST segment depression followed by T wave inversion.
3. CHEMICAL
TESTS.— (i)
Elevation of serum
lactic dehydrogenase
(LDH activity), (ii)
increased serum
bilirubin concen
tration and (iii)
normal serum gluta
mic oxaloacetic tran
saminase (SGOT)
level are the
characteristic triad
seen in pulmonary
embolism. But how
much reliability can
be reposed on this Fig.16.11.— A. Chest film is essentially normal. B. But perfusion lung scan of
triad remains a the same case demonstrates absent perfusion to the entire left lower lobe.
question, as in one
series it was positive in omy i»7o or pulmonary emoou cases.
4. PULMONARY ARTERIOGRAPHY.— This is the most objective and reliable means of
establishing a firm diagnosis of pulmonary embolism. The procedure is to rapidly inject a radio
opaque material into the right atrium or main pulmonary artery through a catheter pushed
through a peripheral vein. The filling defects created in the large pulmonary arteries can be
demonstrated. It also shows changes in the small vessel pattern peripherally. The only
disadvantage of this technique is that it may produce hypotension and it should be carefully
used in patients who are seriously ill.
5. PULMONARY RADIO ISOTOPE SCANNING.— Intravenous injection of radioactive
substances such as macroaggregated particles of human serum albomin tagged with 131I (10 -100
micra) or "mTc followed by scintillation scannings of the chest is a quite reliable method to
diagnose areas of decreased vascularity in the lung field due to pulmonary emboli.
Serial scanning is also of considerable value in following up of patients with pulmonary
embolism demonstrating resolution of the emboli.
TREATMENT.— ,
PROPHYLAXIS.— This has been adequately discussed in the section of 'Deep Vein
Thrombosis'.
TREATMENT OF ESTABLISHED CASES.—
CONSERVATIVE TREATMENT—
1. Anticoagulants.— Anticoagulant therapy is the primary method in the majority of
patients once a diagnosis of pulmonary embolism is established. Heparin is administered in
large doses — 40,000 units or more daily till the clotting time is brought down to at least twice
the normal. In acute stages a continuous intravenous drip of heparin is a reliable method for
maintaining stable and sustained elevation of clotting time. Heparin also acts against reflex
bronchoconstriction in pulmonary embolism. It should be followed by oral anticoagulants for 3
to 6 months or even longer.
2. Fibrinolytic agents — Although much work has been done on the use of fibrinolytic
agents to lyse pulmonary emboli, there is little clear evidence about its usefulness. Streptokinase
is infused through the pulmonary angiogram cannula in an initial dose of upto 6,00,000 units,
followed by 1,00,000 units hourly for upto 3 days. It is important to maintain the treatment for
a sufficient length of time. The pulmonary arteriogram can be repeated to check the progress of
the condition. Streptokinase or more recently urokinase has been used but its effectivity is still
controversial.
3. Essential supportive treatment in the form of correction of metabolic acidosis by infusion
of sodium bicarbonate and improvement of heart function by the use of inotropic drugs should
be considered.
SURGICAL TREATMENT.
(i) Ligation or division.— An analysis has shown that femoral vein ligation is less effective
in the prevention of emboli than the use of anticoagulants.
Ligation or division of the inferior vena cava just distal to the right renal vein has been
performed to prevent passage of thrombi. The operation requires general or spinal anaesthesia.
The incidence of pulmonary embolism following this procedure is generally lower than the
reported incidence following femoral vein ligation. However this technique cannot be used in
desparately ill patients.
The ligation of a vein however results in propagation of the thrombus to the site of the
ligature from its origin. It is also complicated by oedema, pain, recurrent phlebitis and ulceration
of lower limbs,
(ii) Venous interruption.— Interruption of the veins of the lower extremity is indicated if
pulmonary embolus occurs in a patient receiving adequate anticoagulant therapy or in patients
in whom anticoagulant therapy is contraindicated. Phlebography is routinely used to localize
the thrombi. Interruption should always be performed proximal to the site of embolus. It should
be done at the vena cava level in the presence of pelvic vein and iliac vein thrombosis. Interrupted
arterial sutures are placed through the vena cava or a plastic clip (Moretz) is placed across it. A
plastic umbrella grid may also be placed into the inferior vena cava by means of a venous
catheter under radiological control.
Plication of the femoral vein may also be performed to prevent emboli from the calf from
passing upwards. The femoral vein is ligated or plicated just below the point where the profunda
vein joins it. Adequate venous return is possible through the profunda circulation.
(iii) Pulmonary embolectomy.— This operation was first performed by Trendelenburg in 1908.
Later on Kirschner in 1924 correctly performed this operation. It is now probably performed on
those few patients who, having survived a massive pulmonary embolism, are yet unable to
maintain circulation without cardiac massage. It should also be used in the event of failure of
thrombolytic treatment. Nowadays this operation is performed as an emergency procedure with
the use of cardiopulmonary by-pass. This technique clearly represents the most satisfactory
method of management available at this time for those patients who require embolectomy for
massive pulmonary embolism.
In case of chronic pulmonary embolism, selected patients can be well managed successfully
by embolectomy. In many such cases there is marked reduction in pulmonary function associated
with occlusion of more than half the pulmonary arterial bed producing pulmonary hypertension.
The mortality still remains high, even in experienced units.
CHRONIC VENOUS INSUFFICIENCY

Aetiology.— There are mainly three causes of chronic venous insufficiency. These are — 1.
VARICOSE VEINS, which are discussed in detail in the beginning of this chapter; 2. Incompetent
perforators and 3. Deep vein abnormalities.
2. INCOMPETENT PERFORATORS.— There are many perforators between the
superficial and deep veins of the inferior extremity, which are also discussed in the section of
'Varicose veins'. When the valves of these perforators become incompentent, they become dilated
and produce localized dilatations at their junctions with the superficial vein which can be detected
both by inspection and palpation. Defects in the deep fascia through which these dilated
perforators pass may also be palpated. When these perforators become incompetent, high
ambulatory venous pressure developing within the deep veins of the calf during exercise is
directly transmitted through these perforators to the superficial venous system. Ultimately there
is a sustained rise in capillary pressure in the surrounding skin with the development of oedema,
induration, fat necrosis and ulceration.
3. DEEP VEIN ABNORMALITIES.— (i) Deep vein thrombosis is the main deep vein
abnormality which often causes chronic venous insufficiency. Following thrombosis, major deep
veins may become patent by recanalization, however the delicate valves will remain imprisoned
laterally in organised thrombosis. The result is the patent and valveless deep venous system
which transmits the gravitational pressure of the blood column unimpeded from the level of
the heart to the ankles. This is the main predisposing feature in the pathophysiology of the
chronic venous insufficiency, (ii) Occasionally the congenital or familial causes of varicosities
may also cause deep vein abnormalities.
However valvular incompetence alone is not enough to produce serious stasis. It must occur
with incompetent perforators through which the high deep venous pressure in the ambulatory
state is transmitted to the superficial tissues. These perforators may have been involved in the
initial thrombosis or may become incompetent by dilatation resulting from the back pressure of
the valveless deep venous system.
Fibrinogen escapes through large pores in the venules of the skin of chronic venous
insufficient lower limb. The accumulated fibrins cannot be removed due to inadequate blood
flow. This fibrin accumulation acts as a barrier to diffusion of oxygen and other nutrients. As a
result of this the subcutaneous tissue becomes thick, hard and tender, known as liposclerosis.
Fibrin was found in all the biopsies taken from patients with liposclerosis. These changes
alongwith stasis dermatitis which produces brawny oedema, cutaneous atrophy and pigmentation
ultimately lead to tissue death and ulceration.
C linical features.— An aching discomfort in the lower limb is frequently complained of.
Oedema is also seen. There may be associated varicose veins, but this condition is mainly due
to deep vein abnormalities and incompetent perforators. There may be night cramps in the
muscles of the calf and feet. ,
PHYSICAL FINDINGS.— Oedema, brawny induration, brownish pigmentation and
dermatitis are seen followed by the development of venous ulcers. All these are usually seen on
the medial aspect of the leg just above the ankle posterior and superior to the medial malleolus.
Various types of dermatitis may be seen. The venous ulcers are characteristically shallow
with surrounding rims of bluish discolouration and erythema. These may be as deep as the
deep fascia but cannot be deeper than that.
The ulcers may appear spontaneously or follow trivial trauma.

Special investigations are more or less like those described in 'Deep Venous Thrombosis'.
Treatment.—
(i) Elevation of leg.— The frequency of daily leg elevation should be charted according to
the oedema of the leg of the individual.
(ii) Active exercise.— Active exercise, particularly walking with elastic stockings. Elastic
stockings should be used whenever out of bed.
(iii) Those who have already developed venous ulcer, the treatment of venous ulcers as
described in the section of 'Venous ulcer' should be followed.
SURGICAL MANAGEMENT.—
1. Ligation and stripping of long or short saphenous vein.— This can only be performed when
its incompetency has been demonstrated by Trendelenburg test. Indications for this operation
are — (i) severe varicosities, (ii) moderate to severe symptoms of varicosities and (iii) presence
of venous ulcers even with aggressive conservative management. The operative procedure has
been discussed under 'Varicose veins'.
2. Fegan's injection of veins, followed by 6 weeks of continuous elastic compression, is also
discussed in 'Varicose veins'.
3. Ligation of incompetent perforators.— This technique is a valuable adjunct to conservative
therapy. It is particularly effective if performed before the patient has developed an ulcer. The
perforators are ligated subfascially. This techniques was first started by Dodd and Cockett.
Longitudinal incision is made 1 cm behind and parallel to the posterior subcutaneous tibial
border. The incision is made deep till the deep fascia is reached. The deep fascia is also divided
along the line of incision. The margins of deep fascia are now elevated and the perforators are
ligated flush to the deep fascia and then divided. All the tributaries joining these veins are also
ligated and divided. The skin is sutured and a pressure bandage is applied.
4. By-pass operation.— Saphenous vein has been used to by-pass segmental venous
occlusion of the iliofemoral or femoropopliteal veins. For iliofemoral occlusion the contralateral
saphenous vein is passed suprapubically and anastomosed to the affected side. A temporary
arteriovenous fistula distal to the anastomosis may ensure patency. For femoropopliteal occlusion,
the obstructed segment can be by-passed by anastomosis of saphenous vein to the popliteal-
tibial trunk at the level of the knee.
DISEASES OF THE
n LYMPHATIC SYSTEM
The lymphatic system comprises of (a) the lymphatics which commence blindly in the tissue
spaces in most tissues of the body and ultimately empty their contents (lymph) in certain veins,
(b) lymph nodes and (c) epithelolymphoid tissues which are collections of lymphoid tissues in
the walls of the alimentary canal and in the spleen and thymus and this group is ignored in
this chapter.
DISEASES OF THE LYMPHATICS

Acute lymphangitis.—
Lymphangitis is inflammation of peripheral lymphatics. These appear as red streaks
progressing towards the regional lymph nodes. Gradually brawny oedema appears distally due
to coagulation of lymph within the lymphatics.
Acute lymphangitis is more frequently caused by Haemolytic Streptococci, though it can also
occur due to Staphylococcal infections. When infection occurs in the distal limb with organisms
mentioned above, such infection spreads through the lymphatics to the regional lymph nodes.
During this process lymphangitis occurs. This is often associated with enlarged and tender
regional lymph nodes which indicate their involvement. Gradually abscess may occur in the
regional lymph nodes.
Occasionally irritative lymphangitis is noticed following lymphangiography.
TREATMENT.— This condition is usually treated by conservative means. Rest to the part
with elevation and local heat is highly important. Since beta-haemolytic streptococci are the
common infecting organisms, penicillin is the antibiotic of choice, unless culture and sensitivity
tests approve other antibiotic. In case of penicillin resistant Staphylococci, cloxacillin is highly
effective. Incision is almost always contraindicated unless there is definite signs of purulent
accumulation e.g. infected blister or paronychia.
Chronic lymphangitis.—
This condition almost always follows repeated attacks of acute lymphangitis. The clinical
importance of this condition lies in the fact that acquired lymphoedema may be precipitated
due to this condition.
NEOPLASMS OF LYMPHATICS.—
Benign neoplasms.— Peculiarly benign lymphatic tumours are of developmental in origin
and so are seen in children often from birth. These tumours are often seen in the area of the
jugular buds in the neck, though these are also seen in the axilla, shoulder and groin. Localized
cluster of dilated lymph sacs in the skin and subcutaneous tissue which cannot connect into the
normal lymph system grows into lymphangioma or benign neoplasm of lymphatics.
Types.— 3 types are usually seen — (a) simple and capillary lymphangioma; (b) cavernous
lymphangioma and (c) cystic hygroma.
DISEASES OF THE LYMPHATIC SYSTEM 287
(a) SIMPLE AND CAPILLARY LYMPHANGIOMA.— This type presents as circumscribed

lesion which appears as vesicles or small blisters or slightly elevated skin patches. These lesions
are also called lymphangioma circumscriptum. These are typically seen on the innerside of the
thigh, on the shoulder or in the axilla. Lymphangiography reveals that the lesion is separate
from the main lymphatic system.
Treatment is excision, when lymphangiography confirms that the lesion is separate from the
main lymphatic. Otherwise there may be risk of chronic lymphatic fistula.
(b) CAVERNOUS (DIFFUSE) LYMPHANGIOMA.— These present as bigger lymphatic
swellings. These are often found in the face, mouth, lips (causing enormous enlargement of the
lips or macrocheilia) and in the tongue (a common cause of macroglossia). This cyst is often
interspersed among muscle fibres.
(c) CYSTIC HYGROMA.— This is the most common form of lymphangioma. This exhibits
large cyst like cavities containing clear watery fluid. Majority (75%) of the cystic hygromata are
present in the neck. 20% are seen in the axilla. Remaining 5% are found scattered in different
parts of the body — in the mediastinum, groin, pelvis and even retroperitoneum. Peculiarly a
few cervical cystic hygromata may have mediastinal extension extending as far as the diaphragm.
Macroscopically cystic hygroma consists of multiple locules filled with lymph. In the depth
the locules are quite big and towards the surface the locules become smaller and smaller in size.
Clinical features.— As mentioned earlier cystic hygroma is mostly seen in children and are
often reported to be present since birth.
Disfigurement is the main symptom. The swelling is mainly painless, though occasionally
it may be painful when it becomes infected.
These are soft swellings. Fluctuation and fluid thrill are always present. These swellings
are brilliantly translucent. Occasionally haemorrhage within the cyst renders the swelling opaque.
Regional lymph nodes usually do not enlarge until and unless the lesion gets infected.
Treatment.— Surgical excision is the only available treatment. In the neck the lesion is
removed under general endotracheal anaesthesia using transverse incision. The cysts often
encroach deep into the neck involving the vital structures. So careful dissection is required. The
cyst wall often lies close to the carotid artery, jugular vein, vagus nerve and brachial plexus. It
must be remembered that the excision must be complete to avoid any chance of recurrence. This
lesion is a developmental anomaly and is not a malignant tumour, so this condition is rarely
associated with recurrence. But as for all cysts, if cyst wall is left behind fluid may reaccumulate
to cause reappearance of the swelling. That is why macroscopically identifiable cystic wall should
be dissected away to prevent recurrence.
Kinmoth described sclerosing treatment for this lesion in adults with apparent satisfactory
result.
Radiotherapy has no place.
Malignant neoplasms.—
LYMPHANGIOSARCOMA.— This is a rare malignant tumour of the lymphatics. It is
occasionally seen in long standing cases of primary or secondary lymphoedema of the extremities.
It is more often seen in the upper limb than the lower limb. This condition has also been reported
in cases of postmastectomy lymphoedema.
This lesion first appears as a bruise or a purplish discolouration. Later on a skin nodule is
seen, on which ulcers with crusting are noticed which gradually progress to necrosis. Gradually
the whole of skin and subcutaneous tissue are involved.
Microscopically the tumour is composed of neoplastic endothelial cells, with poorly defined
lymph spaces.
This tumour not only locally spreads rapidly, but also metastasises widely.
Treatment is ineffective and these tumours are uniformly fatal.
LYMPHOEDEMA
Pathology.— On an aetiological basis, lymphoedema may be divided into 2 groups :
(a) Primary lymphoedema in which there is a developmental error of the regional lymphatic
system.
(b) Secondary lymphoedema in which there is acquired pathology of the defective local
lymphatic system.
PRIMARY LYMPHOEDEMA.— Family history of primary lymphoedema is sometimes
received. Two main forms of familial (hereditary) lymphoedema are recognized — Nonne-Milroy
(Type I) and Letessier-Meige (Type II), though one type may overlap on the other. Milroy's
disease is probably inherited in an autosomal dominant manner with related abnormalities in
the gene coding on chromosome 5. The disease is characterized by brawny lymphoedema of
both legs, sometimes of the genitalia, arms and even face. Such lymphoedema develops from
birth to before puberty. It is often associated with wide range of lymphatic abnormalities on
lymphangiography. Meige's disease is almost similar to Milroy's disease, except that the
lymphoedema develops between puberty and middle age. This can be divided into three clinical
subgroups according to the age of onset of the swelling.
(i) In lymphoedema congenita, the oedema is present in birth. This was first described by
Milroy in 1892. This variety is comparatively rare and occurs in about 10% of all cases of primary
lymphoedema.
(ii) Lymphoedema praecox starts in adolescents and this constitutes 75% of patients with
primary lymphoedema. In this group is familial type D.
(iii) Lymphoedema tarda constitutes 15% of patients with primary lymphoedema and in
these cases the swelling is delayed until after the age of 35 years.
In primary lymphoedema there is some developmental fault in the lymphatic system and a
family history is found in about l/5th cases. In about 1/2 the patients the malformation is
predominantly unilateral.
Lymphangiography has demonstrated 3 basic types of malformation of this disease —
(a) Aplasia of the subcutaneous lymph trunks in the limbs is found in 13% of patients.
Formed lymphatic vessels are absent, but there are haphazardly arranged lymph spaces with
no attempt to form lymphatic channels. This is a severe malformation and is often associated
with the congenital variety.
(b) In 75% of cases the subcutaneous lymphatic trunks in the leg are hypoplastic. They
may be too small in size and number. The commonest defect in this group is presence of a
solitary lymph vessel, which ascends the limb without normal bifurcation and branching. This
may be termed solitary hypoplasia, which may extend upto the knee or even upto the groin. In
a small number of patients hypoplasia may affect the lymph nodes in the groin while the lymph
trunks remain normal.
(c) The third malformation is the varicose or dilated lymph trunks seen in 12% of patients
with primary lymphoedema. In this condition the subcutaneous tissues are filled with dilated
and tortuous lymphatics which are incompetent and allow retrograde reflux of lymph. This is
often associated with diffuse arteriovenous fistulae. The varicose state may extend proximally
to involve the pelvic and even para-aortic lymph trunks. This allows retrograde flow of intestinal
chyle into the groin and thigh. Chyle-filled vesicles may appear in the skin of the leg and
troublesome leak of milky lymph may develop.
The prognosis of primary lymphoedema depends on the type and extent of the malformation.
While lymphatic function is severely prejudiced in aplasia and the varicose types, hypoplastic
variety is less troublesome.
SECONDARY LYMPHOEDEMA.— This condition may follow involvement of the lymph
channels or lymph nodes by neoplastic or inflammatory process, by surgical excision or by
radiotherapy. In some areas parasitic infestation with filariasis is destructive within the lymph
nodes and may produce secondary lymphoedema. In the majority of cases of secondary
lymphoedema the disease process is a local affair in contrast to the primary lymphoedema
where the malformation is widespread over an entire limb.
Primary lymphoedema is mostly seen in adolescent girls. The swelling begins insidiously
with no apparent cause. The patient first notices a little puffiness around the ankle which
disappears after a night's rest only to return at a late stage of the next day. Gradually the
oedema progresses slowly. Severe swelling is unusual until several years have elapsed. The
most important feature is that the swelling is painless (in contrast to venous disease). The main
complaint of the patient is cosmetic appearance.
Secondary lymphoedema develops much more rapidly. Usually there is clear indication of
the local pathology (as mentioned earlier in the classification). This swelling is usually
accompanied by discomfort in the swollen tissues. Recurrent cellulitis is not uncommon. The
infection is usually streptococcal. High pyrexia and rigors are usually accompanied with.
Clinically, it may not be so easy to differentiate venous from lymphatic oedema. But skin
changes, pigmentation, atrophy and tendency to ulceration favour the diagnosis of post-phlebitic
swelling of venous origin. In a lymphoedema the skin remains usually healthy except slight
thickening, hyperkeratosis and recurrent cellulitis. Pain is an important symptom of swelling of
venous aetiology, which is rarely seen in lymphoedema.
Special in vest igat ions.—
It is often possible to diagnose and manage lymphoedema purely on the basis of history
and examination without any special investigations. But certain investigations may be required
to confirm the diagnosis to suggest management and to provide prognostic information.
A few ROUTINE TESTS are always performed. These are full blood count, urea and
electrolytes, creatinine and liver function tests, chest radiography and blood smear for
microfilariae.
LYMPHANGIOGRAPHY.— In this technique the lymphatics of the lower limb are delineated
with radio-opaque dye. Surgically, a lymphatic trunk of the dorsum of the foot is exposed.
Iodised oil contrast medium (neohydriol ultrafluid lipiodol) should be injected directly into the
exposed lymphatic trunk on the dorsum of the foot. By this contrast medium the lymph nodes
as well as lymph trunks can be well visualized radiographically. The contrast medium is warmed
and injected into the exposed lymph trunk. For a lower limb, approximately 6 ml of solution is
injected over a period of 1 hour. Too rapid injection may produce respiratory distress and
pulmonary oil embolus.
ISOTOPE LYMPHOSCINTIGFtAPHY.— This is now replacing lymphangiography.
19
Radioactive technetium-labelled protein or colloid particles are injected into an interdigital web
space, which are taken up by lymphatics. Serial radiographs are taken with a gamma camera.
This technique offers a qualitative measure of lymphatic function as also certain anatomical
details.
Fig.17.1,— First figure shows normal inguinal and iliac lymphangiograms. Second figure shows normal pelvic
lymphadenograms taken after 24 hours. Lipiodo! is cleared from the vessels, whereas nodes show normal
morphology and granularity.
COMPUTERISED TOMOGRAPHY.— Though a single axial CT slice through the midcalf

has been used as a diagnostic test for lymphoedema, yet CT is mainly used to exclude pelvic or
abdominal mass lesions.
MAGNETIC RESONANCE IMAGING (MRI) — provides clear images of the lymphatic
channels and lymph nodes, so it is an effective diagnostic procedure also to distinguish between
venous and lymphatic causes of a swollen limb.
Treatment.—
PRIMARY LYMPHOEDEMA.— In the beginning conservative management should always be
instituted.
Conservative Treatment.— This is the main stay of treatment. Only 15% of patients require
surgery.
(i) Elevation of the limb at night by raising the footend of the bed on blocks of at least 1
foot high.
(ii) An efficient elastic stocking should be worn constantly by day. Control of lymphoedema
requires higher pressure (30 to 40 mmHg for arm and 40 to 60 mmHg for leg). The patient
should put on the stocking as first thing in the morning before rising and should be worn
throughout the day.
(iii) Pneumatic compression devices are available to control moderate lymphoedema.
(iv) Exercise has got some effect in reducing lymphoedema. Slow and rhythmic isotonic
movements will increase venous and lymphatic return and it also augments muscle pumps.
Exercise also helps to maintain joints mobility. When at rest the limb should be positioned
above the level of the heart.
(v) Drugs.— Benzpyrones of which the flavonoids have received some acceptance. Clinical
trials have shown to improve microcirculatory perfusion, stimulate interstitial macrophage
proteolysis and reduce erythorocyte and platelet aggregations and ultimately exert an
antiinflammatory effect. But acceptance is not overall and there are many criticizers. Diuretics
are of no value in pure lymphoedema and their prolonged use may be associated with side
effects by disturbing the electrolyte balance.
(vi) If eczema is present this is treated by triamcinolone 0.05 to 0.1%. Fungal lesion should
also be treated accordingly.
By instituting this treatment not only the progression of the oedema will be halted, but also
a considerable return towards normalcy may be achieved.
To the contrary, a long standing lymphoedema with secondarily fibrosed subcutaneous
tissue, there will be hardly any improvement with this conservative treatment. If there is recurrent
cellulitis, a prophylactic oral antibiotic may be prescribed for an indefinite period. These cases
are very much suitable for surgery.
Surgical Management.— Main indications are :
(i) Limitation of function of the limb
due to its weight and bulk is the main
indication.
(ii) Recurrent cellulitis is also an
indication.
(iii) In case of women appearance of
swollen leg cosmetically is an indication for
surgical treatment.
Two types of operations have been
Thompson Operation devised — 1. Excisional operations and 2.
Physiologic operations.
1. Excisional Operations.—
(a) Homan’s operation.— Firstly the
skin flaps are elevated, then the subcuta
neous tissue is excised from beneath the
flaps. The skin flaps are now closed
primarily as the width of the limb has been
decreased. The only complication is the
Charles Operation possibility of skin flap necrosis. This
operation should be performed on two
Fig. 17.2- Two excisional operations for lymphoedema.
sides one after the other keeping at least
six months gap between the two operations. This operation is more satisfactory in the calf,
though it can be used even on the upper limb, but must not be performed in presence of
venous obstruction.
(b) Thompson operation.— In this operation long viable skin flap is raised based on
midposterior aspect of the limb. This operation can be performed
on either the medial or lateral aspect of the limb. If both sides of
the limb are to be operated on, an interval of 3 to 6 months should
be given between the two operations. After raising the skin flap,
all the subcutaneous tissue and the deep fascia beneath this skin
flap should be excised. The anterior edge of the skin flap is now
burried deep into the muscle in close relation with the deep
vascular bundle and its related lymphatics. In this way the bulk
of the limb is reduced and the tissue tension is restored by the
overlapping procedure. The dermal lymphatic plexus is brought
in proximally to the deep lymphatic trunks, which are usually
normal in primary lymphoedema. Fig.17.3.— Omentum being
(c) Charles’ operation.— In this operation the whole of the used cis a lymph bearing pedicle
to graft to the inguinal region to
oedematous subcutaneous tissue and the deep fascia are excised.
anastomose with deep lymphatics
The exposed muscle layer is covered with split thickness skin of the inferior extremity.
graft. The main disadvantage is a tendency to hyperkeratosis in
the grafted area which occurs in about l/3rd of patients. The unstable skin frequently develops
minor infections with local ulceration and a weeping eczema state which is troublesome.
(d) Kinmonth's modification of Homan's procedure.— In this operation limb reduction is
usually first done on the medial side and then on the lateral side.
2. Physiologic Operations.—
(i) These operations aim to provide or enhance lymph drainage. Attempts have been
made to create an artificial lymph
channels through the
subcutaneous tissue using
nonabsorbable thread e.g.
prolene. These operations are
controversial.
(ii)
physiologic operation attempt to
link subcutaneous tissue with the
deep lymphatics or to attach
lymphatic-bearing pedicles such as
omentum (See Fig. 17.3) or small
bowel to the root of the affected
limb. Kinmonth and associates
Fig.17.4.— A.— Lymphovenous shunt with lymph node. B.— used an opened defunctionalised
Lymphatic threaded into vein. C.— Micro-surgery by anastomosing small bowel pedicle to construct
dilated lymphatics to the vein. a lymphatic anastomosis with
inguinal nodes. Unfortunately this operation is not suitable for most primary lymphoedema
patients.
(iii) Lymphovenous shunts have been used particularly in secondary lymphoedema cases.
(iv) Microsurgery.— In many sites the dilated lymphatics are anastomosed to veins by
micro-surgery. This has been more used in cases of oedema of the arm.
SECONDARY LYMPHOEDEMA.— In contrast to primary lymphoedema, secondary
lymphoedema hardly shows an improvement with conservative treatment. Surgery is the only
treatment, if it be required.
Surgical treatment.— As the pathology of the secondary lymphoedema is blockage or
destruction of the lymph nodes or lymph trunks, surgical procedures are designed to provide a
lymphatic bridge across the obstructed area or by deliberate creation of a lymphovenous shunt
just proximal to the site of obstruction.
Bridging procedures.— This can be performed by lymphangioplasty which was first introduced
by Handley in 1908 by using various artificial channels. Some surgeons implanted double nylon
strands. Some used polyethylene tubes perforated with lateral holes. These tubes were inserted
from the ankle level to the midabdominal wall. These were removed after 1 year, when it might
be expected that permanent channels had been formed by their presence. However these methods
could not be successful to bring improvement in the oedematous state.
Pedicle flaps of skin and subcutaneous tissue may be used as a lymphatic bridge across the
obstructive region. A thick pedicle from the arm may be transplanted into the thigh and
abdominal wall to by-pass the inguinal obstruction. Such method may be tried to by-pass the
axillary obstruction of post-mastectomy oedema of the arm. But the results have not been much
impressive and it has failed to gain a definite place in the surgical management of secondary
lymphoedema.
Lymphovenous shunts.— In this operation a healthy lymph node proximal to the obstruction
region is isolated, taking great care to preserve its vascular pedicle and afferent lymphatics.
This lymph node is transected through its middle. The cut surface of the distal half is then
implanted into a neighbouring vein e.g. the femoral vein in the groin. A linear venotomy is
used with circumferential suture of the capsule of the lymph node to the edges of the venotomy.
In this way the afferent lymph trunks joining the node will discharge their content directly to
the venous system. This operation provides a sound basis in reducing lymphoedema. However
long term report will be required for proper evaluation of this operation.
Excisional operations.— The excisional operations which mentioned under the surgical
treatment of primary lymphoedema may be applicable to a limb with secondary lymphoedema
if the original disease is inactive.
DISEASES OF LYMPH NODES

Before entering into the various causes of lymph node enlargement, a brief note is given
regarding lymphangiography which has an immense value in localizing lymph node enlargement
in various parts of the body, finding out the pathology of such enlargement and finally the sites
of lymph metastasis in various carcinoma (particularly malignancy of the testis) and malignant
melanoma.
Lymphangiography.— This test is of great value in finding out the causes of lymphoedema,
lymph node enlargement and sites of lymph node metastasis in various carcinoma.
Injection of patent blue dye into the web between the toes will show lymphatics on the
dorsum of the foot. One of these lymphatics is cannulated and ultrafluid lipiodol (Radio-opaque
dye) is injected to visualize on X-ray the main lymphatic channels of the leg and subsequently
the lymph nodes. Irregular filling defect in the lymph node means secondary metastasis. Soap
bubble or foamy appearance is seen in Hodgkin's disease. Coarse nodular storage pattern is
seen in lymphosarcoma and marginal sunburst appearance is the feature found in reticulum
cell sarcoma.
In malignant melanoma, sometimes radio-active phosphorus is added to the radio-opaque
dye for lymphangiography. This will destroy the malignant cells in the lymph nodes. This process
is called 'endolymphatic therapy'.
At present CT scan and high resolution ultrasound have almost replaced lymphangiography
as these modalities are now generally available.
VARIOUS CAUSES OF ENLARGEMENT OF LYMPH NODES —
A. INFLAMMATORY.
(a) ACUTE LYMPHADENITIS.
(b) CHRONIC LYMPHADENITIS.
(c) GRANULOMATOUS LYMPHADENITIS — the aetiologic agents may be bacterial,
viral or fungal. From BACTERIAL origin are tuberculosis, syphilis, tularaemia, brucellosis etc;
From VIRAL origin are lymphogranuloma venereum, cat-scratch disease, infectious
mononucleosis; From PARASITOLOGICAL origin is filariasis due to infestation of Wuchereria
Bancrofti and toxoplasmosis; From FUNGAL origin are blastomycosis, histoplasmosis and
coccidioidomycosis (not actinomycosis, as lymph node enlargement is unusual in this disease).
In this group may be added condition like sarcoidosis, whose aetiology is still controversial.
B. NEOPLASTIC.—
(a) BENIGN — almost non-existent.
(b) MALIGNANT —
1. Primary.—
OLD CLASSIFICATION.—
(i) Giant follicle lymphoma;
(ii) Lymphosarcoma;
(iii) Reticulum cell sarcoma;
(iv) Hodgkin's disease.
NEW CLASSIFICATION.— The classification, which is currently used, is based on the
classification of Rappaport et al and of Lukes et al. It is as follows :
Primary malignant lymphomas can be broadly classified into two groups — (i) Diffuse
lymphomas (56%) and (ii) Nodular lymphomas (44%). The latter type is more prevalent in females
but is distinctly rare in children and blacks. But these two groups are actually types of
proliferation that any of the malignant lymphomas can exhibit at some points of their evolution.
The natural history of the disease is primarily related to the cell type in which a nodular pattern
indicates a slower evolution and a better prognosis than a diffuse one. It is also interesting to
note that most nodular lymphomas change later to a diffuse pattern but maintaining the same
cell composition.
The classification based on cell types are :
(i) Malignant lymphoma, undifferentiated type;
(ii) Malignant lymphoma, histiocytic type;
(iii) Malignant lymphoma, lymphocytic type (poorly differentiated);
(iv) Malignant lymphoma, lymphocytic type (well-differentiated);

(v) Malignant lymphoma, mixed type (histiocytic-lymphocytic);
(vi) Malignant lymphoma, Hodgkin's type — (a) lymphocytic predominance; (b) nodular
sclerosis; (c) mixed cellularity; (d) lymphocytic depletion.
2. Secondary.—
Metastatic lymph node enlargement is often seen from Carcinoma, Malignant Melanoma or
rarely from Sarcoma of the draining region.
C. LYMPHATIC LEUKAEMIA.
D. AUTOIMMUNE DISORDERS.—
(i) Juvenile rheumatoid arthritis (Still's disease).
(ii) Other Collagen diseases such as Systemic lupus erythomatosus, Polyarteritis nodosa
and scleroderma.
Causes of generaliy.ed lymph nodes enlargement.—
1. Tuberculosis;
2. Syphilis — secondary stage;
3. Infectious mononucleosis;
4. Sarcoidosis;
5. Brucellosis;
6. Toxoplasmosis;
7. Hodgkin's disease;
8. Lymphosarcoma;
9. Lymphatic leukaemia.
1. Blood.— Routine examination of blood is essential for (a) leucocytosis particularly
polymorphs (acute lymphadenitis); (b) lymphocytosis (tuberculosis, lymphatic leukaemia etc.);
(c) raised E. S. R. (tuberculosis, secondary carcinoma, lymphosarcoma etc.); (d) W. R. and Kahn
test (syphilis); (e) Microfilaria in the peripheral blood vessels when the patient is sleeping
(Filariasis).
2. Aspiration — of the abscess is essential for diagnosis be it a cold abscess or
lymphogranuloma inguinale. In cold abscess one will look for acid-fast bacilli. In
lymphogranuloma inguinale, pus from unruptured bubo is diluted ten times with normal saline
and sterilized at 60° centigrade, 0.1 ml of the solution is injected intradermally. Appearance of
a reddish papule within 48 hours at the site of injection indicates the test to be positive. This
test is known as Frei's intradermal test, which is specific for lymphogranuloma inguinale.
3. Mantoux test and guineapig inoculation test — are specific for tuberculosis.
4. Gordon’s biological test — is specific for Hodgkin's disease. An emulsion of the
affected lymph nodes is injected into a rabbit intracerebrally. This will initiate encephalitis within
a few days.
5. Biopsy.— This is probably the most important special investigation in this concern. Many
cases may not be diagnosed clinically and with the help of the above special investigations.
Biopsy should be called for in these cases. Under local or general anaesthesia according to the
circumstances, the isolated or matted lymph nodes are excised and examined both macroscopically
and microscopically.
6. Radiological examination.— In case of enlarged cervical lymph nodes, X-ray of the
chest is essential, not only to find out enlargement of the mediastinal lymph nodes, but also to
detect pulmonary tuberculosis or bronchogenic carcinoma as the cause of enlargement of cervical

lymph nodes. Calcified tuberculous lymph nodes may easily be seen in X-ray film. But tomography
will be essential to know particularly about the mediastinal lymph nodes.
7. Mediastinal-scanning — with Gallium 67 is sometimes performed to know whether
the mediastinal lymph nodes are involved or not.
8. Laparotomy.— This seems to be the last court of appeal in Hodgkin's disease. This is
required not only to know the clinical staging of the disease by wedge biopsy of the liver and
by biopsy of the aortic, mesenteric and iliac nodes and a small chip biopsy from iliac bone but
also by splenectomy as the spleen is involved in about 90% of cases of the abdominally involved
Hodgkin's disease and to obviate splenic irradiation due to its complications.
VARIOUS TYPES OF LYMPH NODE INVOLVEMENT ARE
Acute lymphadenitis.—
Due to acute inflammation of the drainage area, the regional lymph nodes become acutely
inflamed and the condition is known as acute lymphadenitis. The affected lymph nodes become
enlarged, painful and tender. The overlying skin becomes warm, red and brawny oedematous.
There is a varying degree of pyrexia. Due to periadenitis, which may be present in all the
severe forms, the lymph nodes may be matted together.
Chronic lymphadenitis.—
The drainage area most carefully be examined, hi the cervical group oral sepsis, recurrent
bouts of tonsillitis and lesions of the scalp are usually the common causes. In the groin, besides
infected cuts and ulcers, walking on bare and cracked feet may lead to this condition amongst
labourers. Painful enlarged lymph nodes are common findings.
BIOPSY will show hyperplasia of the reticuloendothelial cells which may be so great as to
replace the lymphoid tissue. The sinuses, both medullary and peripheral are dilated and filled
with endothelial cells. The whole process is a reticuloendothelial hyperplasia.
Tuberculous lymphadenitis.—
In majority of cases human tubercle bacilli enter the body through the tonsil of the
corresponding side. From there they move to the cervical lymph nodes, so the upper deep
cervical nodes are most often affected. There is no generalized infection, so the cervical nodes
involvement is not secondary to tuberculosis anywhere in the body. In about 80% of cases the
tuberculous process is virtually limited to the clinically affected group of lymph nodes.
Age.— This is commonly found in children and young adults. It may occur at any age. The
incidence in the young has diminished since the introduction of BCG vaccination.
The cervical nodes are most frequently involved followed by mediastinal, mesenteric, axillary
and inguinal nodes according to the order of frequency.
In tuberculosis, the lymph nodes on section show translucent, greyish patches in the early
stage. As the disease advances these become opaque and yellowish, which is the result of necrosis
and caseation. Microscopically the tubercles will be seen which consist of the epitheloid cells and
giant cells having peripherally arranged nuclei in the early stage. After one week, lymphocytes
with darkly stained nuclei and scanty cytoplasm make their appearance. By the end of the
second week caseation appears in the centre of the tubercle follicle. So in the centre of the
tubercle follicle lies eosin stained caseation surrounded by giant cells and epitheloid cells around
which remains a zone of chronic inflammatory cells e.g. lymphocyte and plasma cells, around
which are the fibroblasts.
TREATMENT.—
(i) Antitubercular drugs should be prescribed straightway once the diagnosis is
confirmed. Injection Streptomycin — 0.5 to 1 g I. M. daily, INH in the dose of 300 mg/day and
PAS in the dose of 5 to 15 g/day should be prescribed. The latter two drugs should be continued
for at least 1V4 years. Sometimes the organisms may acquire resistance against these drugs.
Recently Ethambutol in the dose of 25 mg/kg body weight and Rifampicin in the dose of 15
mg/kg body weight are prescribed daily for at least 9 months.
(ii) Sanitorial regime, good food, vitamin supplementation and high protein diet are the
supportive therapies which every patient with tuberculous lymph nodes should receive.
(iii) If the lymph nodes do not respond to the drug therapy or show initial response but
remain static after that, operative removal is justified. Incision is made along the Langer's line
over the affected nodes. With fine dissections the surrounding adhesions are released and the
lymph nodes are removed enmasse.
(iv) If cold abscess has been formed, it is advisable to start the antituberculous therapy
and to aspirate the abscess before it ruptures with sinus formation. Aspiration is performed with
a thick needle through the healthy skin preferably from above. Aspiration is never done through
the most prominent and the most dependent part of the abscess lest a sinus should be formed
along the path of the aspiration.
Syphilitic lymphadenitis.—
In the primary stage the lymph nodes in the groin become enlarged along with presence of
genital chancres. The nodes are painless, discrete, firm and shotty. These nodes do not show
any tendency towards suppuration. In extra-genital chancres occurring in the lips, breasts etc.
the nodes may become inflamed, painful and matted. In the secondary stage generalized
involvement of nodes may occur affecting particularly the epitrochlear and occipital groups.
The characteristics are similar to those found in the primary stage. There may be ulcers in the
mouth and various skin rash (pink macular rash appears 4 to 8 weeks after the sore followed
by the papular eruption and more severe form is the ecthymatous type in which the papule
breaks down quickly and the underlying tissues become eroded or ulcerated). In the tertiary
stage the lymph nodes are seldom involved. Other syphilitic stigmas, positive W. R. and Kahn
tests along with presence of Treponema pallidum in dark ground illumination from the primary
lesion confirm the diagnosis.
(i) W. R. and Kahn test — usually positive.
(ii) Treponema pallidum may be demonstrated in specimens obtained from the genitals
or from the mucocutaneous lesion.
(iii) Some specific tests e.g. treponemal antigen test — treponemal haemagglutination
assay or treponema pallidum immobilization test are of more diagnostic value.
Fllurlai lymphadenitis.—
The inguinal nodes are commonly affected and this condition is more often found in males.
The lymph nodes become enlarged and tender. A history of periodic fever with pain ( especially
during the full or new moon ) is very characteristic. Swelling of the spermatic cord with dilatation
of lymphatic vessels (lymphangiectasis ) is often found in filariasis. There may be thickening of
the skin of the scrotum. Microfilaria can be demonstrated in the blood drawn at night.
Eosinophilia is the rule. Biopsy of lymph nodes may reveal adult filaria.
Lymphogranuloma venereum (Syn. lymphogranuloma Inguinale).— .
It is a type of venereal disease caused by a filtrable virus of the psittacosis-lymphogranuloma
inguinale group. A history of exposure is definite, though accidental infection may occur e.g. in
surgeons operating on infected patients. The primary lesion is insignificant and is not revealed
if leading questions are not put to the patients. The PRIMARY LESION is a type of painless
herpetic vesicles on the genitals. The SECONDARY LESION occurs about 2 to 6 weeks after
exposure. Medial group of inguinal lymph nodes of one or both groins are usually involved.
The lymph nodes become matted due to periadenitis and gradually become liquified. The
overlying skin shows brawny oedema and becomes purple in colour. The liquified mass may
break down and discharge thick yellowish-white pus free from organisms. The sinuses result
which refuse to heal for months or years. In females pararectal lymph nodes are involved through
the posterior vaginal wall and an intense pararectal inflammation with dense fibrosis involve
the rectal wall. This may cause stricture of the rectum. Ischiorectal abscess and rectovaginal
fistula may develop.
(i) Frei's test is quite confirmatory. Pus from unruptured bubo of a patient suffering
from this disease is diluted 10 times with normal saline and sterilized at 60° C. 0.1 ml of this
solution is injected intradermally. Appearance of a reddish papule within 48 hours of at least 6
mm in diameter at the site of injection indicates the test to be positive. This is known as Frei's
intradermal test.
(ii) The Complement fixation test is even more sensitive than the previous one. It shows
positive result in earlier stage of the disease. _
(iii) Biopsy is definitely very confirmative. The earliest change in a lymph node is an
accumulation of large mononuclear cells which form small solid granuloma. Ischaemic necrosis
follows with invasion of polymorphonuclear leucocytes. Gradually stellate abscesses form. A
marginal zone of epitheloid cells and fibroblasts appears.
('at-Scratch disease,—
This disease has always an association with cats, but inspite of the name, there is not
necessarily evidence of a scratch or bite. There is usually an initial skin lesion, which is often
ignored. Enlargement of the regional lymph nodes becomes the main feature of this disease.
Axillary or cervical lymph nodes are more often affected. There may be tiny abscess formation
with suppuration. The primary skin lesion is a red papule in the skin at the site of inoculation
usually appearing between 7 and 12 days following contacts. It may become pustular or crusted.
This condition is caused by a virus of psittacosis-lymphogranuloma group.
(i) The diagnosis can be confirmed by skin testing.
(ii) Biopsy of the lymph nodes will reveal early lesion of histiocytic proliferation and
follicular hyperplasia. Microscopic and macroscopic abscesses are late features.
Infectious mononucleosis (Glandular fever).—
Glandular fever is an acute febrile disease in which the common features are fever,
enlargement of lymph nodes, splenomegaly, sore throat, appearance in the blood of lymphocytes
of unusual type ('Glandular fever cells'). The causative organism is probably virus ofrickettsia group,
though controversy still exists regarding the responsible agent. The generalized lymph node
enlargement is due to intense hyperplasia without loss of architecture. The spleen shows almost
the similar picture. In almost every case there is enlargement of cervical lymph nodes and those
in the posterior triangle are affected as much as those in other groups. The enlarged nodes are
often painful and usually tender. Axillary and inguinal groups are affected less frequently than
the cervical group. Abdominal pain and tenderness are common and may be explained by
mesenteric node enlargement.
(i) Lymphocytosis in the blood is a very characteristic feature of this disease.

(ii) Paul-Bunnell test is diagnostic. It is the increase of agglutinins for sheep's red blood
cells during the acute phase of the disease.
Tularaemia.—
It is a highly infectious disease caused by pasteurella tularensis. The clinical picture resembles
plague and is characterized by an ulcer at the site of infection, enlargement and inflammation
of the regional lymph nodes and severe constitutional symptoms. The disease starts 3 to 5 days
after infection with prodromal symptoms e.g. severe headache, feelings of cold and rise of
temperature. The enlarged local lymph nodes show features indistinguishable from those of
tuberculosis.
Brucellosis (Syn. Undulant fever).—
This is a disease which results from infection with species of bacteria of the genus brucella.
These are small, Gram-negative, non-motile coccobacilli. The onset is gradual with early
symptoms of mild fever, malaise, headache, generalized muscular pain and mild gastrointestinal
disturbances. After some weeks or months a pyrexial attack occurs which lasts a few days to
some weeks. It is usually followed by further pyrexial episodes. With each attack there is
enlargement and tenderness of the spleen and to a lesser extent the liver. In some, lymph node
enlargement is a striking feature. There is usually an accompanying hypochromic anaemia and
leukopaenia.
The lymph node biopsy shows features of either tuberculosis or Hodgkin's disease. Presence
of large cells resembling Reed-Sternberg cells may suggest the latter condition.
Sarcoidosis.—
In this disease there are granulomatous lesions which may be found in any organ or tissue.
The most commonly affected are, in order of frequency, the lungs, the lymph nodes, the skin,
the eyes, the liver, the spleen, the salivary glands, the heart, the skeleton and the nervous system.
The characteristic lesion of sarcoidosis is an epitheloid cell granuloma or tubercle. But there is
never caseation. Probably this is the only criterion which differentiates this condition
microscopically from tuberculous lymphadenitis.
Lymph nodes seldom reach very large size, average diameter being 2 to 3 cm. Enlarged
nodes show no tenderness or periadenitis.
The Kveim test.— This is an intradermal injection of 0.15 to 0.2 ml of 10% saline suspension
of sarcoid lymph node. The positive result is shown in 4-6 weeks by the appearance at the site
of injection of a nodule with the histological pattern of sarcoid. This test is positive in 60 to 85%
of patients with sarcoidosis.
Toxoplasmosis.—
It is a disease caused by an intracellular parasite known as toxoplasma gondii. The parasite
multiplies by longitudinal fission within the endothelial and tissue cells of its hosts. When the
virulent strains are formed these cells rupture releasing the parasites which then invade fresh
cells.
Toxoplasmosis may be transmitted to the foetus in utero by an infected mother when it is
called congenital toxoplasmosis.
The clinical features of acquired toxoplasmosis can be easily described under four headings —
(i) Cerebrospinal form is characterized by meningoencephalitis, fever, severe headache,
vomiting, delirium, convulsions, deafness etc.
(ii) Lymphatic form is characterized by enlargement of one or more groups of lymph
nodes with fever of several weeks duration and marked constitutional disturbances.
(iii) Exanthematous form presents as acute febrile illness with widespread maculopapular
rash, myocarditis and interstitial pneumonitis.
(iv) Latent form in which there are no symptoms or signs of the disease and diagnosis
can only be made by laboratory tests.
Fungal diseases.—
Fungal diseases cause chronic granulomatous process that may or may not be associated
with caseation necrosis. There may be hyperplasia of sinus histiocytes without granulation
formation.
NEOPLASMS
No where in pathology has a chaos of names so clouded as in the subject of lymphoid
tumours. The general term 'the reticuloses' is often used to indicate a proliferation of
undifferentiated cells of the lymphoreticular system. I have used both old and new classifications
to make the students understand both the views clearly.
Neoplasms of lymphoid tissue means malignant lymphoma, as benign neoplasm is almost unknown
in lymphoid tissue.
Glant-cell lymphoma.-—
This condition is also known as follicular lymphoblastoma. It is the most benign member
of this group. It is the least common and constitutes only 5% of malignant lymphoid tumours.
Age.— It usually occurs after the age of 30 years. It is virtually unknown in children.
Clinical features.— It usually presents with enlargement of one group of nodes commonly in
the neck or groin. The nodes are not adherent to one another and are freely mobile. Later on
the condition becomes generalized.
Biopsy shows excess of lymphoid follicles which replace the normal architecture. These
follicles are uniform in size and distribution. This condition is often confused with chronic
lymphadenitis. The sinusoides are obliterated in contradistinction to the dilated sinusoides
characteristics of chronic lymphadenitis.
Lymphosarcoma.—
It is the second commonest among the non-Hodgkin's lymphoma.
(i) Age.— Though it may develop in middle life or later, it is quite common among
children.
(ii) The disease commences locally involving a single node. Gradually the adjoining nodes
are involved. Gradually enlarged lymph nodes can be seen in the neck, mediastinum and
abdomen. In abdomen both retroperitoneal and mesenteric nodes are involved.
(iii) Lymphosarcoma may involve lymphoid tissue other than the lymph nodes as for
example tonsil, pharynx and bowel. The involvement of the small intestine may be so diffuse
that the bowel is converted into a stiff tube. Spleen is involved in about less than half the cases.
(iv) Presence of constitutional symptoms like loss of weight, anaemia, anorexia and
weakness are quite evident. Unexplained fever is present in about 1/4th of cases.
(v) On inspection swelling becomes evident particularly in the neck. The overlying skin
is tense and shiny with engorged veins.
(vi) Palpation reveals an irregular surface, definite but irregular margin and varying
consistency — in places soft, firm in some places and hard in a few.
(vii) Chest X-ray may show enlarged mediastinal nodes.
(viii) Lymphangiography will show involved retroperitoneal lymph nodes with typical coarse
nodular pattern of lymphosarcoma.
(ix) Biopsy reveals — the cut surface is greyish white, homogeneous and bulging. Adhesion
to surrounding nodes is characteristic feature of this condition.
Microscopically, the normal structures of lymph nodes disappear and are replaced by diffuse
arrangements of monotonously uniform large lymphoblasts with hyperchromatic nuclei and
scanty cytoplasm. The follicles have disappeared. Diffuse infiltration of the capsule and
surrounding tissue is one of the most characteristic features. Another important feature is that
there is no increase in reticulum as shown by silver stains. The reticulum fibres which are seen
in this condition represent the original content of the node and these are dispersed by the
infiltration of the neoplastic cells, so that in a given field they appear to be decreased in number.
Reticulum ceil sarcoma.—
It is the commonest among non-Hodgkin's lymphomas.
(i) Age and site are similar to those of lymphosarcoma.
(ii) Occasionally bone and even urinary bladder may be involved.
(iii) Prognosis is also same as lymphosarcoma and that the usual survival is less than 2
years.
(iv) Clinical features are more or less same as lymphosarcoma.
(v) Lymphangiography will show typical marginal sun burst appearance.
(vi) Biopsy.— Macroscopic feature is more or less same as lymphosarcoma.
The microscopic picture shows abundance of reticulum cells with faintly acidophilic cytoplasm.
The nucleus is double the size of a lymphocyte and is commonly infolded giving it a reniform
appearance. There are pseudopod like processes of both cytoplasm and nucleus. The characteristic
feature is the well distribution of silver staining reticulum which has got intimate relations to
the tumour cells either encircling groups of cells or sending fibrils between and around individual
cells.
Treatment of both lymphosarcoma and reticulum cell sarcoma.— If there is no evidence of spread
beyond the area of head and neck, radiotherapy is the treatment of choice. High dose of
radiotherapy nearing 6,000 rads and cobalt may be applied. Both these tumours are radiosensitive.
In case of generalized involvement chemotherapy with multiple drugs should be applied.
NEW CLASSIFICATIONS
Undifferentiated lymphoma.—
This is a malignant proliferation of primitive cells having scanty cytoplasm and a round or
oval nucleus with delicate cromatins and a small, distinct nucleolus. Burkitt's lymphoma is
regarded as a specific variant of this type of lymphoma. It has a peculiar geographic distribution
mostly seen in tropical Africa and New Guinea. Typically Burkitt's lymphoma affects children
and young adults. It has a great tendency of extra nodal involvement such as the jaws, ovaries,
abdominal organs, retroperitoneum and the central nervous system. Untreated cases follow a
rapid fatal course.
Microscopically, the most striking feature is the 'starry sky' pattern resulting from a scattering
of non-neoplastic histiocytes containing phagocytosed nuclear debris among a monomorphic
infiltrate of highly primitive cells.
(i) Age.— Majority of the patients are between the ages of 4 and 8 years. Incidence
gradually decreases as the age advances and only 6% of cases are seen over the age of 21 years.
(ii) Sex.— Males are involved more than the females at the ratio of 2 : 1.
(iii) Mode of clinical presentation.— (a) Facial tumours are by far the most common
presentation, (b) The second most frequent mode of presentation is abdominal tumours. These
fall into three main categories — retroperitoneal mass, liver enlargements and ovarian tumours,
(c) Lesion in the central nervous system is the third mode of presentation with vertebral collapse
and paraplegia, (d) Intracranial lesions with cranial nerve palsies, unilateral or bilateral deafness,
increasing drowsiness and headache are the features, (e) Tumours in other sites like salivary
glands, thyroid glands, skeletal tumours (bones most frequently involved are the femur, humerus,
tibia and the ilium; the chief distinguishing feature between this tumour and osteosarcoma is
the relative absence of pain in this tumour) and breasts, (f) Involvement of peripheral lymph
nodes is characteristically rare.
Treatment.— Burkitt's lymphoma is extremely sensitive to radiotherapy, but local
radiotherapy has been followed by development of tumour in other sites. Radiotherapy to clinically
detectable tumours should be supplemented by chemotherapy to deal with disseminated tumours.
Histiocytic lymphoma.—
Lymph nodes involved by histiocytic lymphoma (reticulum cell sarcoma) may be matted
together and contain large necrotic areas. The nodal architecture is totally or partially obliterated
by proliferation of malignant histiocytes. Variations in cellular and nuclear shape are marked.
The nuclei are large and vesicular with prominent nucleoli and thick nuclear membranes. Mitoses
are common. Fibrosis with hyalinization of the stroma is sometimes prominent separating the
tumour cells in clusters of cords.
Lymphocytic lymphoma.—
The individual nodes are not adherent. They appear highly cellular and occasionally
contain areas of necrosis. In poorly differentiated variant the cells are larger than matured
lymphocytes but smaller than histiocytes. The nuclei are round, oval and irregular with focal
chromatin clumping and a distinct nucleolus. Nuclear indentations are often present. In well-
differentiated lymphocytic lymphoma the cells are similar to normal mature lymphocytes. It is
very difficult to differentiate this type of lymphoma from chronic lymphocytic leukaemia. The
clinical history, the peripheral blood count and the bone marrow findings are required to
make such distinction.
Mixed (histiocytic-lymphocytic) lymphoma.—
This designation should be restricted to tumours in which both histiocytes and lymphocytes
are present in significant amounts. A nodular pattern of growth is common in the early stage,
but majority however develop into a diffuse lymphoma of histiocytic type. Whether the concept
of a mixed lymphoma is valid one needs to be substantiated. The alternative possibility that the
lymphocytes are nonneoplastic and that they represent a reaction to the tumour.
Cllnicopathologic correlation.— The prognosis of a particular lymphoma depends on
the extension of the disease, cell type, nodular or diffuse pattern of growth and fibrosis. Stage I
lesions have good prognosis but unfortunately they comprise only l/3rd of all cases. The routine
use of lymphangiography has demonstrated that most patients with non-Hodgkin's malignant
lymphoma have widespread disease at the time of diagnosis. Spread by involvement of
contiguous lymph node groups is common in non-Hodgkin's lymphoma. It is more common in
the diffuse than in the nodular type.
In regard to cell type the average survival is longer for well differentiated lymphocytic
type, shorter for the histiocytic variety and intermediate for the poorly differentiated lymphocytic
type. In all groups, the survival rates are better in patients with tumours with a nodular pattern
of growth and those associated with a significant degree of stromal fibrosis. In contradistinction
to Hodgkin's disease non-Hodgkin lymphomas involve mesenteric lymph nodes quite commonly.
Non-Hodgkin lymphomas have a much greater tendency to begin or at least to present clinically
as extranodal tumours than Hodgkin's disease. The bone marrow and the spleen are the most
common sites of extranodal spread.
HODGKIN’S DISEASE
(i) Age.— The onset of this disease is about a decade earlier than lymphosarcoma and
reticulosarcoma. The incidence increases in the late 20s, but it is not uncommon in children.
(ii) Sex.— The disease is slightly more common in men than women.
SYMPTOMS.—
I. The symptoms are more local than constitutional except in acute cases. The most
common presentation is painless and progressive, enlargement of the lymph node first detected in the
cervical group on one side and then on the other. This is followed by axillary and inguinal
lymph nodes enlargements. Retroperitoneal lymph nodes are often involved but require
lymphangiography and computed tomography (CT scan) for diagnosis. Mediastinal involvement
occurs in only 6% of patients at the time of diagnosis.
II. Constitutional symptoms (B symptoms) such as fever, night sweat, weight loss and
pruritus usually indicate widespread involvement and poor prognosis. They may appear
simultaneously with lymph node enlargement or may precede that.
(i) A typical fever pattern is a high temperature with rigors occurring in a periodic
fashion alternating with a few days of afebrile period — PeTEbstein fever.
(ii) Malaise, weight loss and pallor are also common constitutional symptoms.
(iii) Itching of the skin or pruritus is unexplained but a quite common complaint of this
disease.
(iv) Pains in the bones and abdominal pain may be complained of. There may be root-
pain and even paraplegia due to collapse of the vertebra secondary to bony metastasis. Root-
pain may be due to deposits in the vertebra or pressure by retroperitoneal nodes on the nerve
roots while they come out from the intervertebral foramina. A peculiar feature of this disease is the
complaint of enhanced pain at the sites of disease induced by drinking alcohol.
(v) Pressure effects by enlarged mediastinal lymph nodes may cause venous engorgement,
cyanosis of the head and neck and difficulty in respiration due to pressure on the bronchus.
(vi) Large masses in the abdomen can obstruct the inferior vena cava and cause oedema
of both the legs.
(i) Site.— Any group of the cervical nodes may be affected including those in the
posterior triangle.
(ii) Temperature and tenderness.— The enlarged lymph nodes are neither warm nor tender.
(iii) Size, shape and surface.— Hodgkin's lymph nodes are ovoid, smooth and discrete. The
nodes show little tendency towards matting or softening.
(iv) Consistency.— The lymph nodes feel elastic and rubbery in consistency.
(v) Mobility.— These nodes can be moved from side-to-side, though their mobility is
rather restricted due to tethering to neighbouring structures.
GENERAL EXAMINATIONS.—
(i) Other groups of lymph nodes may be enlarged.
(ii) Splenic enlargement is a significant finding of this disease and is found in not less
than 75% of cases.
(iii) Hepatomegaly is found in about 50% of cases.
(iv) Progressive anaemia is more or less constant and may be due to splenomegaly or
bony metastasis.
(v) Sometimes jaundice is seen due to
excessive haemolysis of the red cells or
involvement of liver.
(i) In blood, a picture of normochromic
normocytic anaemia is quite evident. About
l/3rd of cases show leucocytosis due to
increase in neutrophil and eosinophil.
(ii) Importance of lymphangiography has
already been discussed.
(iii) Computed tomography (CT scan) is
helpful to detect involvement of retroperitoneal
lymph nodes and mediastinal lymph nodes.
(iv) Chest X-ray also shows mediastinal
lymph node enlargement.
(v) The liver and spleen scan indicate
involvement of these organs or not.
(vi) Bono scan is of value in determining
bone involvement.
(vii) Lymph node scanning has been
performed with Gallium 67 to detect the
clinically doubtful lymph node involvement,
particularly the mediastinal group.
CLINICAL STAGING OF THE
HODGKIN’S DISEASE : Stage I.—
Involvement of a single lymph node region or
involvement of a single extralymphatic organ
or site (I E).
Stage II.— Involvement of two or more
lymph node regions on the same side of the
diaphragm alone or with involvement of limited
contiguous extralymphatic organ or tissue (II E).
Stage III.— Involvement of lymph node
regions on both sides of the diaphragm, which
may include the spleen (III S) and/or limited
contiguous extralymphatic organ or site (III E, Fig. 17.5.— Histology of various types of Hodgkin's
III ES). disease. A.- Mixed cellularity. B.-Lymphocytic
Stage IV.— Multiple or disseminated foci predominant and C - Nodular sclerosis.
of involvement or one or more extralymphatic organs or tissues with or without lymphatic

involvement.
All stages are further subdivided on the basis of absence (A) or presence (B) of the following
systemic symptoms e.g. fever, weight loss more than 10%, bone pain etc.
PATHOLOGICALLY, Hodgkin's disease can be divided into four categories, which is
important so far as the prognosis of the disease is concerned. The more numerous are the
lymphocytes, the more favourable is the prognosis.
Type 1.— Lymphocyte-predominant Hodgkin's disease.
Type 2.— Mixed-cellularity — a diffuse infiltrate of lymphocytes, histiocytes, eosinophils
and plasma cells that obliterate the normal architecture.
Type 3.— Nodular sclerosis is often seen in clinical stage I and is associated with better
prognosis.
Type 4.— Lymphocytes depletion pattern — the most ominous form.
BIOPSY.— Macroscopically the lymph nodes are enlarged but remain discrete till the late
stage of the disease when they become fused. They are firm and elastic and on section shows
uniform grey translucent and moist appearance. Occasionally yellow patches of necrosis may
break the homogeneity.
Microscopically there is an early loss of the follicular pattern due to hyperplasia of the reticular
endothelial elements. Its most important feature is cellular pleomorphism. There are lymphocytes,
eosinophils, plasma cells and histiocytes — all are present in greater or lesser amount depending
on the microscopic type. The initial diagnosis depends on the presence of the Reed-Sternberg
cells, which the pathologists make careful search of. This cell is of relatively large size, its
cytoplasm is abundant either basophilic or amphophilic and two or more vesicular nuclei are
present, each having a thick nuclear membrane and a single prominent acidophilic nucleolus
surrounded by a clear halo. The two nuclei are such that one of which is the mirror-image of
the other, the so called 'mirror-image giant cell'. Cells with one nucleus should not be designated
as Reed-Stemberg cells. These may be designated as atypical mononuclear histiocytes. The Reed-
Stemberg cells are neoplastic reticulum cells. Presence of atypical mononuclear histiocytes with
typical pleomorphism also suggests Hodgkin's disease. When the nucleus is single, it may be
convoluted or ring shaped. Besides these giant cells there are also polymorphonuclears,
eosinophils and plasma cells to add to pleomorphism. Eosinophils are particularly characterized,
being sometimes present in large numbers. In doubtful cases they may help to settle the diagnosis,
but they are not invariably present. This group of cells may be regarded as reactionary and
secondary and they do not form an integral part of the neoplastic process. There is a characteristic
increase of reticulum shown by silver-staining.
According to the cell types the Hodgkin's disease can be classified into four varieties —
In type I i.e. lymphocyte predominant type, Reed-Stemberg cells are scanty, scattered among a
large number of matured lymphocytes and sometimes accompanied by proliferation of benign
appearing histiocytes.
In type II or mixed cellularity there is a significant number of eosinophils, neutrophils, plasma
cells and atypical histiocytes that accompany the Reed-Stemberg cells and lymphocytes.
In type III or nodular sclerosis is characterized by broad collagen bands separating the
lymphoid tissue in well defined nodules. The fibrosis often centres around blood vessels. The
cytologic patterns within the nodules is one of lymphocyte predominance, lymphocyte depletion
or mixed cell type. Clumps of foamy macrophages are sometimes present. In additional to the
typical Reed-Stemberg cells there may be seen a type of giant-cell which is quite large with
20
abundant clear cytoplasm and several nuclei having complicated infoldings and inconspicuous
nucleolus. Some pathologists consider presence of these giant cells is more typical of this type
of Hodgkin's disease than the fibrosis itself. It must be remembered that practically all types
of Hodgkin's disease may exhibit some degree of fibrosis particularly after therapy.
In type IV or lymphocyte depletion there is infiltration predominantly formed by malignant
appearing histiocytes, some of which fulfil the criteria of Reed-Stemberg cells. Lymphocytes are
seen few and far between.
Treatment—
(i) RADIOTHERAPY is the treatment of choice if the disease is confined to a single or
two contiguous node-bearing areas (Stage I) or to lymph nodes one side of the diaphragm
(Stage II). Radiotherapy has also produced a substantial number of prolonged remissions in
patients with generalized disease confined to nodal tissue (Stage III), but radical radiotherapy
is not widely used for this type of patients. Chemotherapy is generally employed in patients
who have Stage III disease or who have disease involving extranodal structures (Stage IV).
It is also used in a few patients with
stage II disease who have severe
systemic symptoms, such as fever, as an
adjunct to radical radiotherapy, but not
as definitive treatment. Megavoltage
radiotherapy allows wide areas to be ^
treated. Supradiaphragmatic disease is
treated by radiotherapy to cervical, jgpr-
axillary and mediastinal nodes. Usually "%• ^~
shields. Radiotherapy is given in the ^

range of 4,000 rads in divided doses mLJ
over several weeks. Infradiaphragmatic I^
disease is treated by fields covering i . * . ‘
para-aortic and iliac nodes in the form
of inverted Y fields.
lot during the last decade in the 1

treatment of Hodgkin's disease /
particularly in Stage III, Stage IV and
those with involvement of extra nodal I’ %
structures and those with systemic \
symptoms (B symptoms). In 1964, a f
combination of agents was devised at the V {VHV
(MOPP) include Mechlorethamine,

Vincristine sulphate, Procarbazine and
Prednisone. Preliminary results reported Fig. 17.6.— The principal lymph nodes to be biopsied during
in 1970 were extremely encouraging. The the operation of staging in Hodgkin's disease marked
remission rate was superior to that as black dots.
previously reported for single drug and even more important a substantial proportion of patients
remained continuously free of disease for 4 years even though no maintenance therapy was
given. MOPP is administered for six two weeks cycles of chemotherapy, with two weeks interval
between each period of drug administration.
Treatment Schedule.—
Each course of therapy consisted of 14 days of treatment. Vincristine Sulphate (1.4 mg/Sq.
M) and Mechlorethamine hydrochloride (6 mg/Sq. M) were given on days 1 and 8 by rapid
I.V. injection. Procarbazine hydrochloride (100 mg/Sq. M) and prednisone (40 mg/Sq. M) were
given orally daily in divided doses for 14 days and then discontinued. After each 14-day
treatment, all therapy was discontinued and was resumed two weeks later (to avoid leukaemia
or thrombocytopaenia).
A complete programme of therapy consisted of 6 to 2 — courses with a rest period after each
course.
LAPAROTOMY FOR HODGKIN’S DISEASE.— Staging Laparotomy is frequently done
for clinical staging of Hodgkin's disease. Its use is based on the following facts :
(i) Hodgkin's disease generally begins in a single area and spreads in non-random manner
via lymphatic channels to contiguous lymph nodes and organs that have prominent lymphatic
tissue components, (ii) Selection of therapy depends on the clinical staging and for this staging
laparotomy is of immense value, (iii) Clinical staging is not frequently accurate only by clinical
examinations and there lies -the importance of staging laparotomy, (iv) Approximately 25% of
clinically staged patients will have their stage of disease increased and approximately 15% will
have their stage decreased following laparotomy.
Staging laparotomy is not applicable to all patients with Hodgkin's disease and should be performed
only in patients in whom the result may change the plan of therapy. Patients with advanced Hodgkin's
disease, clinical stage III B and stage IV do not benefit from staging laparotomy because treatment
will be combination chemotherapy. If there be splenomegaly even in advanced Hodgkin's disease,
splenectomy is of value to control cytopenias, reduce tumour burden and avoid the risk of
radiation to the left kidney and lower lobe of left lung.
Staging laparotomy consists of (i) splenectomy, (ii) liver biopsy, (iii) selective excision of
abdominal and retroperitoneal lymph nodes. Lymph nodes are removed from the coeliac axis
region, from the porta hepatis, from the small intestinal mesentery and mesocolon and pre- and
para-aortic lymph nodes, (iv) a bone marrow biopsy is obtained from the iliac crest. (V)
Oophoropexy (ovarian translocation) may be performed in pre menopausal women in whom
radiation therapy using the inverted Y port is likely. Both ovaries are removed from the potential
field of radiation. Lead shielding is an important adjunct to the protective effects offered by
oophoropexy.
Usually a midline incision is made to expose the abdomen for staging laparotomy. One
may use a long left paramedian incision. Staging laparotomy has minimal morbidity and
mortality rate less than 0.5%.
Prognosis.— 5 years survival rates for Hodgkin's disease are 85% for stage I and II, 70% for
stage III A, 50% for stage III B and 40% for stage IV.
SECONDARY CARCINOMA
Secondary carcinoma is a very common cause of lymph node enlargement in the elderly.
Secondary involvement of lymph node may also occur commonly from malignant melanoma.
HISTORY.—
(i) Age.— Patients are usually over 50 years of age. The exception is papillary carcinoma
of the thyroid in which secondary metastatic lymph nodes may be seen in children and young
adults.
(ii) Sex.— More common in men than in women.
SYMPTOMS.
(i) Painless swelling is the usual presentation. In late stages patient may complain of pain
due to involvement of nerves and surrounding structures.
(ii) General symptoms e.g. anorexia, weight loss, weakness etc.
(iii) Patients may have other complaints such as ulcer in the tongue, hoarseness of the
voice. If the primary is in the chest he may have cough or haemoptysis. If the primary is in the
abdomen he may complain of dyspepsia or abdominal pain.
(i) Site.— The precise location of the gland may give a clue to the site of primary tumour.
Upper deep cervical nodes are involved when the primary lies in the head, face and interior of
the mouth. The middle and lower deep cervical nodes are involved when the primary is in the
larynx or thyroid. Supraclavicular lymph node enlargement indicates thoracic or abdominal
disease. When these glands (Virchow's glands) are enlarged, it is called Troisier's sign.
(ii) Temperature and tenderness.— Skin temperature is usually normal unless the tumour is
very vascular. These nodes are usually not tender.
(iii) Size and shape.— The lymph nodes are irregular, discrete and of varying sizes. Soon
they coalesce and form one large mass, so at that time the nodes are not descrete.
(iv) Consistency.— These nodes are usually hard to feel.
(v) Mobility.— As the nodes are tethered to the surrounding structures, their mobility
becomes restricted. In early stage the nodes can be moved sideways but not vertically. Later on
the nodes become absolutely fixed to the surrounding structures. Gradually the skin may be
involved and is 'pulled' towards the mass.
GENERAL EXAMINATIONS.—
(i) Other lymph nodes should be examined particularly in the pathway in search of the
primary tumour.
(ii) Discovery of the primary growth confirms the diagnosis. Whenever a patient comes with
enlarged lymph nodes it should be routine practise to examine its drainage area. The lymphatic
drainage of the body may be discussed in the following way :—
The cervical lymph nodes receive the lymphatics from the head, face, mouth, pharynx and
neck; the left supraclavicular lymph node (Virchow's) receives lymphatics from left upper limb,
left side of the chest including the breast and also the viscera of the abdomen including both
the testes.
The axillary group of lymph nodes drains the upper limb of that side and the trunk which
extends from the clavicle to the level of the umbilicus (including the breast).
The inguinal lymph node drains the whole of the lower limb, the skin of the lower part of
the abdomen below the level of the umbilicus, the penis, scrotum, perineum, vulva, anus, buttock,
lower part of the back including the terminal parts of the anal canal, urethra and vagina (the
portions which are developed from the ectoderm). That means the drainage area of the inguinal
lymph nodes extends from the level of the umbilicus down to the toes.
Treatment.—
(i) When the primary growth is not detected, the secondarily involved lymph nodes should
be excised.
(ii) When the primary growth is operable, the primary growth is adequately excised alongwith
excision of the involved nodes. In this case block dissection of the neck is indicated, provided
there is no clinical or investigation report that there are more distant metastases. Adherence to
the skin, to the mandible or to the larynx should not be regarded as inoperable for each of
these structures can be sacrificed provided the patient's general condition permits. Now-a-days
the surgeons are more inclined to combine radical neck dissection with simultaneous resection
of the primary lesion. This composite resection is called commando operation.
(iii) When the metastatic nodes are fixed to deeper structures and/ or there are distant metastases,
palliative deep X-ray treatment is indicated or the lymph nodes may be treated by local
radiotherapy such as insertion of radioactive gold seeds. This will reduce the size of the tumour
and relieve pain. High doses of deep X-ray therapy will cause necrosis of the mandible or the
laryngeal cartilages in cases of the cervical nodes.
BLOCK DISSECTION OF THE NECK

The incision is planned to give adequate access to all gland groups. The gland groups
which are removed en bloc are the submental, submandibular, the upper and lower deep cervical
Fig.17.7.— Shows various incisions for block dissection of the neck.

groups, the posterior

cervical group and the
supraclavicular group.
Various incisions have
been advocated by various
surgeons e.g. (i) Crile's T
incision whose horizontal
part starts on the midline
at the tip of the mandible
and curves across to the tip
of the mastoid process and
the vertical limb starts
from the midpoint of the
horizontal limb and runs
obliquely downwards to
the midline of the clavicle; Fig. 17.8.— Shows the initial steps of block dissection operation.
(ii) Martin's double -Y
incision; (iii) Ward's Y incision in which the vertical limb extends from in front of the tragus
down to the middle of the clavicle and the curved oblique limb starts from the middle of the
vertical incision and is obliquely carried
upwards to the tip of the mandible in the
midline and (iv) two horizontal incisions are
made one at upper part of the neck, starting
from the tip of the mandible at the midline
and curves across one side of the neck to the
tip of the mastoid process and the lower
horizontal incision is made inch above the
clavicle. These two incisions are joined by
curved vertical incision joining the midpoints
of both these horizontal incisions.
The skin flaps are reflected including the
underlying platysma muscle and the
dissection of the neck structures begins in the
posterior triangle. The fibro-areolar tissue of
the posterior triangle are dissected away from
the trapezius muscle and is carried
medialward till the phrenic nerve is reached.
The lower end of the stemomastoid muscle
is divided. The muscle is retracted upwards.
The omohyoid is severed and turned aside
so that the entire carotid sheath is now
exposed. The internal jugular vein is
separated from the accompanying vagus
nerve and common carotid artery. Next the
Fig.17.9.- ■ Shows the anatomy of the neck at theinternal
end jugular vein is divided between
of block dissection operation. ligatures just above the clavicle. The
dissection proceeds upwards gradually dissecting the lymph nodes chain alongwith the internal
jugular vein and surrounding fat and fascia. Just above the level of the carotid bulb the
hypoglossal nerve is identified. In the upper portion of the neck the stemomastoid muscle is
again transected at the level of the mastoid together with the tip of the parotid gland. The
submandibular salivary gland is dissected free from its fossa. The lingual nerve and artery will
be seen at the depth. A tiny fibre of the facial nerve which innervates the lower lip will be seen
above the submandibular gland. These nerves are preserved. The spinal accessory nerve is only
sacrificed if it is involved in the growth. It is then divided in two places — in the lower neck
where it enters the trapezius muscle and in the upper neck where it enters the stemomastoid
muscle. The operation is completed with transection of the jugular vein at the extreme upper
part of the neck. The skin is closed with suction drainage.
The structures removed in the block dissection are —
(a) The groups of lymph nodes mentioned above, (b) the stemomastoid muscle, (c) the
internal jugular vein, (d) the submental and submandibular salivary glands, (e) spinal accessory
nerve if it is involved, (f) branches of the external carotid artery or a segment of the parent
trunk itself if involved by growth. Spinal accessory nerve is preserved if not involved in growth.
Particular attention is given to preserve the following structures — (a) the vagus nerve, (b) the
hypoglossal nerve, (c) the lingual nerve and (d) the lowest branch (cervical branch) of the facial
nerve.
Modified radical neck dissection.— This operation is still not very specific. Some surgeons
feel that all the functional structures in the neck including the stemomastoid muscle, the spinal
accessory nerve and the jugular vein should be preserved, removing mainly the lymphoareolar
tissue of the anterior and posterior triangles and the submaxillary gland. Some surgeons feel
that the stemomastoid muscle should be removed to give proper exposure to the carotid sheath
and the jugular vein must be removed as the deep cervical nodes are closely related with this
vein.
Suprahyoid block dissection — may be indicated in cases of carcinoma of the tip of the
tongue, floor of the mouth and lower lip. The advantage is that both sides of the neck may be
operated on simultaneously. Mainly the submental, submandibular and upper deep cervical
nodes are removed alongwith the submental and submandibular salivary glands. The rationality
of this operation is very much questioned as the deep cervical nodes are the main lymph nodes
of the neck of which the lower group is left behind.
THE PERIPHERAL
NERVES
Structure of a peripheral nerve.—
The structure of a peripheral nerve can be compared to an electric cable. It consists of many
fibres, which are nothing but axons of the cells situated either in the central nervous system or
in the ganglion of the autonomic nervous system. Each of these fibres or axons is enclosed in a
myelin sheath, which in its turn is surrounded by a cellular sheath, known as neurilemma or sheath
of Schwann. A small bundle of these fibres is called a funiculus. Individual nerve fibres are
ensheathed and supported within the funiculus by delicate connective tissue called the endoneurium,
which is continuous with septa which pass inwards from the perineurium. Each funiculus is
surrounded by a connective tissue sheath called the perineurium. If the nerve is small, it may
consist of only a single funiculus; but if large, it consists of several funiculi held together and
invested by connective tissue, which is known as epineurium. Majority of the cerebrospinal nerves
are myelinated. The blood vessels form a plexus around the nerve before supplying.
INJURY TO THE PERIPHERAL NERVES

Pathology.—
According to the extent of the damage, injury to the peripheral nerves can be divided into
3 categories
1. Neurapraxia.— This condition is almost equivalent to concussion, in which there is
no organic damage to either the nerve fibre or its sheath, but there is a temporary physiological
paralysis of conduction through the intact nerve fibres. Neurapraxia is produced by minor
stretching or torsion or vibratory effect of a high-velocity missile passing near a nerve. There
may be sensory loss or weakness of muscle groups. During this time there is no reaction of
degeneration in the muscles. Recovery is complete, which may take a period of hours to even a
few weeks.
2. i\xonotmesis.— In this condition there is rupture of nerve fibres or axons within intact
sheaths. Wallerian degeneration occurs in the distal portion of the broken axons leaving the
nerve sheaths empty. Recovery takes place slowly by downgrowth of the axons into the empty
distal nerve sheaths. There may be some loss of nerve fibres owing to the blockage of the
downgrowing axons by intraneural fibrosis. Such intraneural fibrosis occurs at the sites of axonal
rupture and minute intraneural haemorrhages. As the sheaths remain intact, the relative position
of axons are preserved and hence the quality of the regeneration is often good. The time required
for recovery varies according to the level of the lesion — which occurs first in the muscles
nearest to the lesion and last in the peripheral skin, where the anaesthetic area decreases steadily.
In the first 10 days there is hardly any downgrowth of axons and so improvement is not seen.
After this initial delay of 10 days to fortnight, the downgrowing axons proceed distally at the
rate of about 1 mm per day (initially the rate may be 2 mm per day, which diminishes in
THE PERIPHERAL NERVES 313
course of time to 1 mm per day after about a couple of months) till they reach their endings.
On arrival at their endings there is a further delay of 3 weeks or so before the end organs
become fully recovered.
Axonotmesis usually results from a stress, occuiring in association with fractures or
dislocations or from an excessive zealed manipulation to reduce such injuries. It may also occur
from compression by tourniquets, splints or incorrect posture on the operating table. Progressive
compression from crutches, callus or scar tissue in the injured area or by repeated minor
stretching of a nerve, which is often seen in ulnar nerve by cubitus valgus or the same nerve
following fracture of the medial epicondyle may lead to this type of injury.
CLINICAL FEATURES.—
Following an injury, a picture of neurapraxia will be noticed. There is loss of sensation,
tone and power of the muscles with diminished reflex activity of the limb. Later on area of
anaesthesia and paralysis of muscles will be restricted to those which are supplied by the
damaged nerves only. This is due to resolution of neurapraxia to the surrounding nerve fibres
which are intact.
Usually after a fortnight anaesthesia of the skin area and loss of power of the muscles will
be restricted to the actual supply of the damaged nerves. Usually the total area affected is less
than the known anatomical distribution of the nerve due to the fact that a few fibres within the
nerve usually escape.
Secondary effects due to nerve damage will be seen. There may be impaired circulation due
to disuse which makes the affected portion cold and blue. There may be some trophic changes
e.g. the nail becomes brittle and the skin becomes thin. Within 3 weeks the reaction of
degeneration appears in the muscles concerned. The affected muscles no longer respond to
faradic stimulation, but they will respond to the galvanic stimulation. The polarity also changes
so that A. C. C. becomes greater than K. C. C. In late cases the muscle fibres degenerate and
progressive fibrosis replaces degenerated muscle fibres. If this occurs recovery is then impossible.
Sometimes periarticular adhesions may develop around the immobile joints to cause stiffness of
the joints.
TREATMENT.—
Treatment of axonotmesis is maintaining nutrition of the limb and to combat secondary
pathological changes due to nerve injury. This consists of maintaining of muscles and joints in
good working condition till the arrival of downgrowing axons. All affected joints are put through
full passive movements daily to prevent contracture to develop. Exercise of the paralysed muscles
is maintained by physiotherapy. Encouragement to the patient is of utmost necessity to restore
function during the period of recovery. Progress is always checked by taking records of the
electrical reactions of the muscles and skin sensitivity. Electrical reactions change back to normal
in the proximal groups first.
Failure to recover or regression after initial recovery, is an indication for exploration of the injured
nerve. This is required to deal with the perineural scar or to remove intraneural fibroma.
The rates of nerve regeneration are assessed by the following clinical data —
(a) Tinel's sign.— A light patellar hammer is used to percuss from below upwards along
the course of the injured nerve. A tingling sensation is experienced at the level of regeneration.
By the sign one can assess the downward growth of the axons or nerve fibres.
(b) The powers of the involved muscles are tested one by one, so that return of function
of the muscle at different levels are observed and thus the level of regeneration can be detected.
(c) Similarly the sensation of the affected skin is regularly assessed and the rate at which
the pain and touch sensitivity returns from the periphery of the anaesthetic skin is assessed to
know the level of regeneration.
Operative treatment of closed nerve injuries.— Sometimes nerve injury can occur as secondary
to fractures, but bony fragments do not injure the nerve directly and the function of the nerve
is impaired by ischaemia from injury to the blood vessels supplying the nerve. The majority of
these nerve lesions remain in continuity and are non-degenerative in type. In these cases the
treatment is directed to reduce the fracture or dislocation and a conservative treatment is given
for the nerve problem, which consists of prevention of stretching of the muscles supplied by
the nerve by proper splints and prevention of pressure sores.
In about 50% of these cases, nerve injury recovers within a few weeks. Of the other half of
the cases, about 80-90% will gradually recover, that is the proximal nerve fibres will grow down
the degenerated distal fragment. In these cases the quality of regeneration is quite satisfactory
as there is no chance of maldistribution of nerve fibres. In only 10% of cases, there may not be
any evidence of recovery at the expected time. These are the cases which will require exploration.
So when recovery does not reach the first motor branch in the expected time, which is calculated
by the recovery rate of approximately 25 mm (1 inch) in a month, exploration is indicated.
Sometimes closed injuries are associated with considerable pain and paraesthesia. This is an
indication for early exploration.
3. Xvurotmesis.— In this condition there is partial or complete division of the nerve
fibres as well as their sheaths. Partial lesion will produce a lateral neuroma on the nerve. Complete
division will produce a terminal neuroma at the distal end of the proximal segment.
In the proximal segment of the divided nerve there will be retrograde degeneration upto
the first node of Ranvier. After an interval of 10 days to fortnight the distal ends of the axons in
the proximal segment will start to grow downwards. But by this time the gap between the
divided nerve ends has been replaced by organic clots and fibrous tissue, which prevent further
downgrowth of the axons. So suturing of the nerve is the only treatment available if restoration
of function is to be achieved.
In the distal segment of the divided nerve, Wallerian degeneration of the axons occurs,
which is described in detail below. It is only noteworthy here that the schwann cells proliferate
to form a small bulb-like projection from which these cells grow proximally towards the
downgrowing axons by chemotaxis.
In neurotmesis, the quality of regeneration is less perfect even after accurate nerve suturing.
This is due to maldistribution of axons into the distal fragment. That means regeneration of axon
sprouts into the wrong sheath. A motor nerve fibre may grow down a sheath previously occupied
by a sensory fibre. So it cannot function, as it will make no connection with the sensory end-
organ. Similarly, a sensory fibre may grow down the sheath of a motor fibre and cannot make
connection with the motor end-plate. Moreover, a few axons will be wasted in the scar tissue at
the suture line. So the recovery of function will be worst in mixed motor and sensory nerves as
axons of motor fibres may be well united with sensory fibres of the distal fragment. The recovery
will be better if the nerve is pure motor or sensory nerve. Thus recovery from the radial nerve
injury at the elbow will be better than the ulnar nerve or median nerve injury at the wrist.
Neurotmesis is seen in war and severe industrial injuries with extensive soft tissue damage.
It is also sometimes associated with fractures. Cut injuries involving nerve may also cause this
type of injury.
TREATMENT.—
As mentioned above the only treatment available for neurotmesis is suturing of the divided
nerve ends. Such nerve repair can be of two types — primary nerve repair and secondary
nerve repair.
In clean tidy incised wounds when presented within 6 hours of injury immediate suturing
of the divided nerve is the ideal treatment, which is known as primary nerve repair.
In untidy contaminated wounds and in case of incised wounds when presented after 6
hours of occurrence, nerve suturing should be postponed until 3 or 4 weeks after injury. This is
known as secondary nerve repair. If a nerve is seen divided during the course of excision of a
contaminated wound, the ends of the divided nerves are approximated by a stitch of fine silk,
which prevents retraction during the waiting period. The idea of secondary nerve repair is that
— (a) infection of the recent wound does not jeopardise the healing of the nerve suture, but
that of late wound does; (b) the nerve sheath remains delicate and friable in an untidy wound
which is not an ideal tissue for suturing as it is easily tom by slightest tension. After about 3
weeks epineural fibrosis makes the sheath thicker and tougher to facilitate suturing.
DIFFERENT CLASSIFICATIONS OF PERIPHERAL NERVE INJURY

TABLE I
MRC (Medical Research Council of London) classification of motor nerve
dysfunction :—
Grade Clinical Features
MO Complete paralysis.
Ml Flicker of contraction.
M2 Contraction with gravity eliminated.
M3 Contraction against gravity alone.
M4 Contraction against gravity and some resistance.
M4+ Strong contraction but not normal.
M5 Contraction against powerful resistance (normal power of the muscle).
TABLE II
MRC CLASSIFICATION OF SENSORY NERVE DYSFUNCTON
Grade Clinical Features
50 No sensation.
51 Deep pain sensation.
52 Protective sensation i.e. skin touch pain and thermal sensation.
53 S2 with better localization alongwith old sensitivity. Hyper-sensitivity may
be present.
S3+ Object and texture recognition. Two point discrimination is not possible.
54 Normal sensation.
Degeneration and regeneration of nerves after division.—
DEGENERATION.—
When a peripheral nerve is divided, the distal part of the divided nerve shows degeneration,
which is typically known as Wallerian degeneration. In this degeneration — (i) the axis cylinder
becomes fibrillated; (ii) the medullary sheath breaks up into droplets of myelin and (iii) the
cells of the sheath of Schwann are converted into phagocytes which remove the remnants of
the medullary sheath and axis cylinder or axon. The cells of the sheath of Schwann proliferate
forming a slight bulb at the commencement of the distal end from which sprouts of Schwann
cells grow proximally towards the downgrowing axons of the proximal segments by chemotaxis.
The proximal portion of the divided nerve also shows similar Wallerian degeneration, but only
upto the first node of Ranvier. After a short interval which varies from 10 days to fortnight the
axons begin to regenerate and begin to subdivide to produce an excess of end bulbs alongwith
proliferating Schwann cells to produce a swelling at the end, which is known as proximal neuroma
or terminal neuroma.
After incomplete division affecting only one side of the peripheral nerve, a lateral neuroma
or a swelling at the place of incomplete division develops due to proliferating Schwann cells
and axons. Similarly if only the central fibres of a nerve trunk are injured, a central neuroma
may develop.
REGENERATION.—
This is only possible when (i) the nerve remains intact (no complete section), (ii) when,
after complete section, the cut ends are sutured perfectly and (iii) when, only a small gap presents
between the cut ends.
SEDDON’S CLASSIFICATION OF NERVE INJURY
Neuropraxia Axonotmesis Neurotmesis
Motor Loss Complete Complete Complete
Sensory Loss Partial Complete Complete
Autonomic Function Present Absent Absent
Nerve conduction Present Absent Absent
distal to injury
Fibrillation on EMG Absent Present Present
Recovery Rapid 2 mm/day 1 mm/day
(Complete) (Good) (Always imperfect)
♦SUNDERLAND’S CLASSIFICATION
Epineurium Perineurium Endoneurium Axon
1st Degree + + ++
2nd Degree + +
3rd Degree + +
4th Degree +
5th Degree
+ = intact; - - severed
* corresponds to the Seddon's classification in the way that the 1st degree is =
neuropraxia; 2nd degree = axonotmesis; 4th and 5th degree = neurotmesis.
In these successful cases, the axons regenerate crossing the gap in close application to the
Schwann cells from the proximal to the distal cut end. The Schwann cells from the neurilemma
that covers the myelin sheath proliferate actively. This proliferation occurs in the both proximal
and distal ends which move towards each other. If the gap is a small one ultimately they meet
each other and forms empty tubes for regeneration of the axons to occur. The activity of the
Schwann cells increases rapidly after the 4th day after injury and reaches its pick at about the
end of the 3rd week.
Even after accurate suture the quality of regeneration is less perfect than in cases of
axonotmesis owing to wastage of a few axons in the scar tissue at the suture line and
maldistribution of a few axons. The density of the suture line is increased by local sepsis and
inflammation. Maldistribution of fibres is greatest in the case of mixed motor and sensory nerves,
as the motor fibres may enter into the empty tubule of sensory nerves and motor nerve cannot
have any action on the sensory end organ and thus wasted. Such maldistribution is also seen in
motor nerves which supply a large number of small muscles. The result is best in case of a pure
motor nerve which supplies a few groups of large muscles concerned in coarse movements e.g.
the radial nerve. The result is worse in case of mixed sensory and motor nerves supplying a
large number of small muscles concerned in fine movements e.g. the ulnar or the median nerve
at the wrist.
From the above discussion it is clear that while nerve suturing care must be taken to avoid
axial rotation of either cut end to ensure full anatomical continuity.
Following suture there is a period of week before sufficient axons arrive in the peripheral
stump to cause any reflex response to pinching. After crossing the site of severence the axons
grow down the peripheral nerve at the rate of 2 mm per day.
Regeneration is not possible (unsuccessful cases) when (i) there is a big gap between the two
cut ends and (ii) when there is considerable fibrosis between the two cut ends (probably due to
infection).
Secondary pathological changes accompanying nerve injury.—
These pathological changes mainly affect the skin, muscles, neighbouring joints and bones.
1. Skin.— The skin becomes thin and atrophic ulcers may develop. It also shows atrophic
changes e.g. thin and brittle nails etc.
2. Muscles.— (i) The affected muscles become paralysed and flaccid.
(ii) The paralysed muscles become over-stretched due to unopposed action of the
antagonist groups.
(iii) Within 3 weeks reaction of degeneration appears in the affected muscles — the
muscle fibres do not respond to faradic stimulation (with rapid make and break), but they
respond to galvanic stimulation (with slow make and break) due to increase in duration of
chronaxie.
(iv) A change of polarity is seen in the affected muscles in which A. C. C. becomes
greater than K. C. C.
(v) In late cases the muscle fibres degenerate and are progressively replaced by fibrosis,
after which recovery becomes impossible.
3. Joints.— Periarticular adhesions are gradually formed around immobile joints, which
later on become fixed in the position of contracture of this periarticular adhesions.
4. Bones.— These gradually become decalcified due to disuse.
Prevention.— Prevention of these secondary pathological changes are discussed in detail in
the section of treatment for 'axonotmesis'.
Gradation of muscle power.— The muscle power which becomes obviously lowered due
to nerve injury has been graded by numbers according to the Medical Research Council of
London. This gradation is as follows:—
0 = Complete paralysis.
1 = Flicker of contraction.
2 = Contraction with gravity eliminated.
3 = Contraction against gravity alone.

4 = Contraction against gravity and some resistance.
5 = Contraction against powerful resistance (normal power of the muscle).
Signs of regeneration.— After nerve injury or nerve repair one has to assess the
regeneration of the nerve. This can be done by —
• The muscle most proximal to the nerve injury should be tested for muscle power. This
muscle is first rennervated. The most distal muscle is last rennervated.
• Tinel's sign.— Sensation is tested by mild tapping along the course of the nerve distal
to proximal. The first hypersensitive area is the regenerated area. This is called Tinel's sign. As
regeneration progresses the hypersensitive area moves distalwise.
• By EMG (Electromyographic study).— This can diagnose regeneration even before
clinical examination.
CAUSES OF PERIPHERAL NERVE LESION.— These can be divided into two primary
groups — A. Causes of single nerve involvement and B. Causes of multiple nerves involvement.
A. Causes of single nerve involvement.—
1. TRAUMATIC.— It may be due to (a) closed injury which usually causes either
neuropraxia or axonotmesis lesion of the nerve or (b) open injury which usually causes
neurotmesis.
2. INFLAMMATORY.— Herpes Zoster, leprosy, diphtheria.
3. NEOPLASTIC.— Neurofibroma, neurofibrosarcoma.
4. MISCELLANEOUS.— Tunnel syndrome, lead poisoning, arsenical poisoning,
diabetes etc.
B. Causes of multiple nerves involvement.—
1. INFLAMMATORY.— Herpes Zoster, leprosy, diphtheria.
2. METABOLIC DISORDERS.— (a) Vitamin B Complex deficiency (Particularly Bl).
(b) Diabetes mellitus. (c) Alcoholism, (d) Porphyria.
3. IDIOPATHIC.
4. MISCELLANEOUS.— Lead poisoning, arsenical poisoning.
NERVE SUTURE
When nerve injury is associated with complex open wound, priority is given to prevent
infection to occur in the wound, as infection will mar the chance of proper nerve repair. So in
these wounds nerve repair is done as a Secondary procedure after the wound has healed free
from infection.
Primary nerve repair.— .
Indication.— Primary nerve repair is only considered in case of very recent, clean-cut wound,
as for example, occurred after a cut by a piece of glass. It can also be performed in case of
children where the result of this primary suture is good. Under no circumstances primary nerve
repair should be ventured by an inexperienced surgeon.
Technique.— As the nerve ends have retracted and the epineurium is rather filmy, primary
suturing is a difficult affair. Irritant material, such as catgut, dexon, or silk should not be used
for primary nerve repair as replacement fibrosis will mar the possibility of any good result. Non
irritant suture material such as nylon or prolene should be used. Moreover if the nerve ends have
retracted proximally and distally, the original wound may have to be extended appropriately to
trace out the nerve ends. The nerve has to be mobilized and proper orientation (regarding
rotation) can be assessed by the vascular pattern on its surface. A small portion of the nerve is
resected both proximally and distally so that clean-cut ends are available for suturing.
Secondary nerve repair.—
Indication.— Delayed nerve repair is an easier operation and is always carried out except the
indications narrated under primary nerve repair. In secondary nerve repair there is no fear of
infection as the wound has already primarily healed. Moreover the epineurium has proliferated
and becomes thickened for proper insertion of sutures. Though portions of the nerve ends have
to be resected to get healthy nerve ends for suturing, yet this resection may be in smaller amount
should also be carried out in primary nerve repair. Secondary nerve suture should be performed
as soon as the wound has healed, as the chance of successful nerve suture will be diminished if
the delay increases beyond two months.
Technique.— This operation is normally carried out after the original injury has properly
healed. The nerve ends are generally burried in scar tissues. The dissection starts from the normal
tissues lying proximal and distal to the scar tissues and gradually the nerve ends are freed.
TECHNIQUE OF NERVE REPAIR IN GENERAL
An adequate incision is made to isolate the nerve ends. The nerve ends should be freed from
the scar tissue, which is called neurolysis. The approach should be made through an intermuscular
space. If scar tissue predominates and is hard to touch, it is probable that regeneration is completely
blocked. Resection and anastomosis will offer the only prospect of cure. Sometimes Faradic
stimulation of the nerve with bipolar electrodes may give valuable information in this matter.
Trimming of the nerve ends.— After mobilizing the nerve, the nerve ends are trimmed
to excise the scar tissue, the ragged or bruised ends of the cut nerve. Sometimes there may be an
end-bulb, which may be neuroma or glioma. These should also be excised. The ends should be
excised till the healthy bundles will be seen sprouting through the ends. One can even feel the
ends. Presence of any hardness there indicates fibrosis. Presence of healthy axoplasm, which will
be softer in touch, indicates that the resection has been completed and the healthy ends are now
ready for suturing.
Nerve suturing.— Non-absorbable, non-irritant suture material on an atraumatic needle is
used. The epineurium is picked up proximally and distally and the two lateral sutures are
inserted. The ends of these sutures are held with the artery forceps. An anterior and a posterior
sutures are also employed. Generally four sutures suffice and one should not be tempted to
employ more sutures unnecessarily. The lateral sutures are now cut short.
Construction of a new bed.— The sutured nerve should not be allowed to lie on scar
tissue. A new path is constructed by opening a muscle sheath and embedding the nerve within
the muscle fibres. It is better to provide a tantalum foil to warp around the sutured nerve. This
will prevent epineural fibrosis and out-sprouting which may well produce a painful scar.
Immobilization of the limb.— The limb is immobilized in a splint to prevent any strain
on the sutured nerve. This should be kept for no less than three weeks. After this, the splint is
gradually removed.
Methods of approximation of shortened nerve ends.— As has already been discussed

that the two ends of the nerve should be freed and slices are removed from the ends of the
nerve until the projecting fibres are seen and the blood is freely oozing from the cut surfaces.
These slices should be done with the Bard-Parker knife or scalpel and not with the scissors as
this may cause crushing of the nerve-ends. During this process, some shortening of the nerve is
expected. So procedures must be adopted, so that anastomosis is performed without tension.
These devices are :—
(i) Mobilization.— The two ends are dissected from the surrounding structures for a
distance. Care should be taken to preserve the important branches.
(ii) Position of the limb concerned.— The position of the limb will be such that there will
be no tension in the suture line. The limb is held in this position by splints.
(iii) Transposition of the nerve.— By transpositioning the nerve, to shorten its course, may
help to minimise the tension on the suture line. This is done by bringing the ulnar nerve in front
of the medial epicondyle of the humerus or by bringing the radial nerve in front of the humerus.
(iv) Stripping and sacrificing of the branches.— If there are branches near about, it is obvious
that these will anchor the nerve and will prevent proper mobilization. In this case unnecessary
branches can be sacrificed and the important branches may be stripped and further mobilized.
Sometimes it may be necessary to separate the nerve fibres which form the branch from the main
trunk. This will definitely mobilize the main trunk which was previously anchored by branches.
(v) Anchoring the untrimmed nerve ends.— When it is obvious that the two ends of the
divided nerve cannot be brought together, the two untrimmed ends are approximated closely
by tension stitches. This can be done by positioning the limb properly (as for example, flexion
of the limb) to help their approximation. Subsequently the limb is gradually straightened so
that the nerve is stretched. When the limb is more or less fully extended, the second operation
is ventured and proper suturing of the nerve is peformed.
(vi) Bone resection.— When nerve injury is associated with an ununited fracture of the
bone, which needs some operative intervention, one may adopt this procedure. This is occasionally
carried out to repair the radial nerve when it is associated with ununited fracture of the humerus.
(vii) Nerve grafting.— Sometimes the two ends of the cut nerve can only be approximated,
if the limb is acutely flexed. In this case the result will not be good even if the two untrimmed
ends are anchored or the limb is gradually extended. These cases are suitable for nerve grafting.
The donor nerve is generally an autogenous graft from the saphenous nerve of the thigh, sural
nerve of the leg or the medial cutaneous nerve of the forearm. This type of nerve grafting does
not help to restore the motor function but can restore sensory function to some extent. The
epineurium of the graft is to be sutured with the epineurium of the host nerve. When the nerve
is of bigger calibre, cable grafts may be-used, in which nerve of same diameter is sutured in the
form of cable with the host nerve. Nerve grafting does not become successful if the intervening
gap between the nerve ends becomes a mass of dense scar tissue. Microscopic surgery in nerve
grafting is being popularised in States but its superiority is yet to be proved.
RESULTS OF THE NERVE REPAIR

The results of nerve repair, of course, depend on various factors, which will be discussed
in this section :
(A) Preoperative.—
(i) Time.— The earlier the operation is performed, the better will be the result after the
THE PERIPHERAL. NERVES 321
chance of infection has been abolished. After two months, the chance of good result is remote.
(ii) Infection.— This will definitely mar the possibility of good result. Moreover
formation of scar tissue following infection will also lessen the possibility of good nerve repair.
(iii) Preoperative management.— Before the nerve has been sutured, the muscles, which
are supplied by the nerve, should not be kept in stretch. This will definitely decrease the
possibility of good result after nerve suturing.
(B) Operative.—
(i) The nerve affected.— It has already been discussed that the result in mixed motor
and sensory nerve is rather disappointing, whereas the result in pure motor or sensory nerve is
much encouraging.
(ii) Haemostasis.— Surgeon must be careful that haemostasis has been fully achieved
during operation.
(iii) Torsion.— This should not be allowed at the time of suturing of the nerve as this
will cause maldistribution of the nerve fibres in the distal segment.
(iv) Suture material.— It is of great importance that the suture material must be non
irritant, such as nylon or prolene. Irritant suture material will increase fibrosis and hence disturb
good nerve regeneration.
(v) Tension.— Under no circumstances, tension should be allowed to the suture line.
(C) Postoperative.—
(i) Postoperative care.— This is highly important to keep the limb in such a position as
to give relaxation to the paralysed muscles as well as to the sutured nerve. The limb should be
immobilized in this position for at least a month, after that the limb is gradually straightened to
bring to its normal position.
(ii) Infection.— Care must be taken that the wound is not infected.
Treatment of incomplete division. Partial division of a nerve is better left alone. An
attempt at suturing of the partially divided nerve will simply initiate scar tissue formation and
will deteriorate the function of the intact portion of the nerve. There is so much overlapping in
the nervous system that even 4/5th division produces very little disability. Nerve suturing is
only indicated when partial division has resulted in a siginificant deficit.
When nerve suturing is almost impossible. — In certain circumstances, the loss of nerve
tissue is so much that there remains little chance of nerve repairing. In these cases following
methods can be adopted :
(i) Nerve implantation.— In this case, if there is any intact nerve by the side, it can be
divided and the proximal end of the previously intact nerve is anastomosed to the distal end of
the nerve concerned, e.g. the hypoglossal nerve is anastomosed with the distal end of the facial
nerve. Obviously full function cannot be expected, but again uncontrolled contractures may be
found.
(ii) Nerve grafting.— This has already been discussed.
(iii) Tendon transplantation.— When the improvement of nerve function cannot be expected,
relatively unnecessary nearby tendons are transplanted to the paralysed tendons for their
functioning. This is often done in case of radial nerve palsy.
(iv) Arthrodesis.— This is particularly done in case of lower limb where stability is more
important than mobility.
(v) Amputation.— If pressure sores and ulcers have become troublesome, one can try
sympathetic ganglionectomy. But amputation will be the last court of appeal.
21
CRANIAL NERVES
1. Olfactory nerve.— This nerve is injured by fracture of the cribriform plate or by a
blow on the back of the head (contre-coup fracture). When this nerve is injured there is partial
(hyposmia) or total loss (anosmia) of smell of the corresponding side.
2. Optic nerve. — This nerve may be damaged by fracture involving the optic foramen
or by a neighbouring tumour or aneurysm. When this nerve is injured, there may be partial or
complete blindness of the affected eye.
3. Oculomotor nerve.— This nerve is sometimes injured in fracture of the skull affecting
the sphenoidal fissure. This nerve may also be involved by neighbouring tumour or aneurysm.
When this nerve is injured the main feature is dilated pupil on the affected side. With this
there may be ptosis of the upper eye lid due to paralysis of levator palpebrae superioris. There
may be proptosis or unusual protrusion of the eye ball due to paralysis of majority ocular muscles.
Diplopia and external strabismus are due to unopposed action of the external rectus and superior
oblique muscles of the eye ball which are not supplied by this nerve. There will also be loss of
accommodation due to paralysis of the sphincter papillae and the ciliaris.
4. Trochlear nerve.— It is rarely injured alone. It may be injured at the superior orbital
fissure due to fracture. This nerve supplies the superior oblique muscle of the eyeball and its
damage will lead to diplopia and deficient movement of the eye to turn it downwards and
laterally.
5. Trigeminal nerve.— It is the largest cranial nerve and is the main sensory nerve to
the face, greater part of the scalp, the teeth, the mouth and the nasal cavity. Its main motor
supply is to the muscles of mastication. It divides into 3 main branches — the ophthalmic, the
maxillary and the mandibular.
Trigeminal neuralgia.— Pain referred to various branches of the trigeminal nerve is known
as trigeminal neuralgia. In the beginning pain is first confined to one of its main divisions.
Trigeminal neuralgia occurs mostly in the middle aged women. Pain is often precipitated by
exposure to cold, eating, talking, touching certain parts of the face and even during walking.
The pain is often severe.
The cause of trigeminal neuralgia is not well known. When it occurs in younger individuals,
multiple sclerosis is a prominent cause.
Treatment.— Tegretol (carbamazepine) is the most effective drug in this condition. Surgery
is only considered when medical treatment fails. Various operative procedures have been
suggested —
(i) The trunks of the maxillary and mandibular nerves and the trigeminal ganglion itself
is injected with alcohol with varying degrees of success.
(ii) Electrocoagulation of the trigeminal ganglion has also produced some success.
(iii) Excision of the ganglion is a crude method, used for this condition.
(iv) Division of the sensory root of the nerve behind the ganglion is now the operation
of choice when pain is confined to the maxillary and mandibular nerve areas. Endeavour is
made to preserve the ophthalmic fibres which lie in the upper and medial part of the root. This
is to avoid the complications of anaesthesia affecting the surface of the eye. The motor root of
the nerve is left intact.
Open surgery is performed either through the middle fossa or the posterior fossa. Through
the middle fossa the trigeminal ganglion is approached either extra- or intradurally. Through
the posterior fossa the root of the 5th nerve is approached near the cerebello-pontine angle.
6. Abducent nerve.— It is occasionally injured by fracture of the skull which involves

superior orbital fissure. It is rarely involved alone and may be involved with other cranial nerves.
This nerve supplies the lateral rectus muscle of the eye ball and this muscle becomes paralysed
if this nerve is injured leading to internal strabismus.
7. Faciid nerve, 8. \estibulococWear nerve, 9. Glossopharyngeal nerve and 10. \agns
nerve are less involved by trauma.
11. Accessory nerve.—
Causes of injury.—
(i) While removal of cervical lymph nodes.
(ii) Occasionally by fractures of the base of the skull involving the jugular foramen.
It supplies the stemomastoid muscle alongwith the 2nd and 3rd cervical nerves. It also
supplies the trapezius muscle alongwith the 3rd and 4th cervical nerves. Damage of this nerve
will cause complete to partial paralysis of the stemomastoid muscle and the trapezius muscle.
When the nerve is involved in the upper part of the anterior triangle of the neck there may be
paralysis of both stemomastoid and trapezius muscles. If the nerve is injured in the posterior
triangle of the neck, which is more common, only the trapezius muscle will be affected.
Clinical features.— There will be drooping of the shoulder due to trapezius paralysis alongwith
wasting of the trapezius. Trapezius paralysis also unables the patient to continue abduction of
the arm after 90°. Strength of stemomastoid muscle can be tested by asking the patient to turn
his face to the opposite side against resistance.
Treatment.— If the operative assault to the spinal accessory nerve is recognized during
operation attempt should always be made to suture it primarily. It is only in case of this nerve
that secondary suture may not be successful due to retraction of the cut ends.
12. Hypoglossal Nerve.—
(i) It is mostly injured during excision of submandibular salivary glands particularly
due to tumours.
(ii) It is hardly injured in fracture base of the skull as it is protected by a bony butterss
which diverts the fissure of the fracture towards the foramen magnum.
Though this, nerve supplies the Styloglossus, Hyoglossus, Geniohyoid and Genioglossus,
yet its main supply is to the intrinsic muscles of the tongue.
Clinical features.— When hypoglossal nerve is injured there will be hemiparesis of the tongue
of that side, due to which there will be hemiatrophy of the tongue of the corresponding side
and if the tongue is protruded out the tip will be pushed towards the affected side due to
unopposed contraction of the muscles of the sound side. The affected side of the tongue becomes
wrinkled.
BRACHIAL PLEXUS
The lesion in brachial plexus may be either complete or partial.
Complete lesion is rare and occurs only after severe injury. It damages all the roots of the
plexus and is often fatal. In this case, there will be anaesthesia of the whole upper limb except
the upper part of the arm which is supplied by C3, 4 & 5 and by the intercostobrachial nerve.
There will be also complete paralysis of the arm and scapular muscles, occasionally the long
thoracic nerve supplying the serratus anterior or the nerve supplying the rhomboids may escape.
Incomplete lesion may be due to stabs or cuts and may affect any of the roots. But the common
injury is due to traction or pressure, which affects either the upper or lower portion of the
plexus.
UPPER BRACHIAL PLEXUS LESION (ERB-DUCHENNE).— This injury is due to
excessive depression of the shoulder or displacement of the head or the both. It may affect new
bom babies during difficult confinements or adult by a fall of weight on the shoulder. The 51h
and sometimes the 6th cervical roots are involved. The muscles affected are biceps, brachialis,
brachioradialis, supinator and deltoid. So the limb becomes internally rotated, extended at the
elbow and pronated in the well known position of 'policeman taking a tip'. If only the 5th
cervical root is affected, there will not be any sensory change. But if the 6th nerve is also affected,
there will be an area of anaesthesia over the outerside of the arm and upper part of the outerside
of the forearm.
As the innervation of the hand is intact, functional improvement may be obtained
conservatively by maintaining full range of passive movement of the limb to prevent contracture
and the anaesthetic skin is protected to avoid pressure sores etc. In degenerative lesions at the
root level, one cannot expect regeneration. Function of the limb can be best restored by arthrodesis
of the shoulder and elbow joints. One may venture transplantation of muscles from the pectoral
groups to the humerus.
LOWER BRACHIAL PLEXUS LESION (KLUMPKE). This type of lesion can occur
when a falling person clutching at an object and hyper-abducting his arm or failing to obtain a
foot-hold on a passing bus. The first dorsal root (T() is usually affected. The result is paralysis
of the intrinsic muscles of the hand (with claw-hand and features of combined median and
ulnar nerves palsy) with anaesthesia of the inner one and half fingers. There will also be Homer's
syndrome. Very occasionally spasticity of the lower limb may be noticed associated with this
condition, which is a result of damage to the pyramidal tract from haemorrhage following
avulsion of the nerve roots.
Horner's syndrome.— This syndrome occurs due to injury to the sympathetic supply of the
face which accompanies the Tl nerve. This syndrome includes — (i) narrowing of the palpebral
fissure — drooping of the upper eyelid (ptosis); (ii) Enophthalmos due to paralysis of Muller's
muscle, in which the eyeball is recessed backwards; (iii) Myosis, i.e. contraction of the pupil
due to the damage to the sympathetic supply of the muscles of the iris and to the unopposed
action of the oculomotor nerve and (iv) anhidrosis i.e. failure of sweating on the affected side of
the face.
Treatment is conservative. Recovery of function may occur when the lesion is due to
stretching-(neurapraxia). But if the nerves have been ruptured, maldistribution of down-growing
fibres will definitely lead to considerable reduction in functional efficiency.
AXILLARY NERVE
This is also called circumflex humeral nerve, which passes through the quadrilateral space
and winds round the surgical neck of the humerus about a finger's breadth below the centre of
the deltoid muscle.
It is injured —
(i) Due to fracture of the neck of the humerus; (ii) Dislocation of the head of the humerus;
(iii) By a direct blow or (iv) Intramuscular injections.
This nerve supplies the deltoid muscle and a portion of the skin on the lateral aspect of the
arm which overlies the deltoid muscle. It also supplies the teres minor muscle.
When this nerve is injured, the deltoid muscle will be paralysed which will be evident by
failure of abduction of the shoulder. There will be also a patch of anaesthesia over the outer
side of the arm.
LONG THORACIC NERVE (NERVE OF BELL)

This nerve arises from the 5th, 6th and 7th cervical nerve roots. This nerve supplies the
serratus anterior muscle. j
This nerve may be injured — (i) by blows or (ii) by weight or a heavy object falling on the
shoulder or (iii) more often during operation on the breast or the chest wall.
Due to injury of this nerve the serratus anterior muscle becomes paralysed. Paralysis of this
muscle can be well demonstrated by 'winging of the scapula'. When the patient is asked to push
against the wall with outstretched hand, the vertebral border and the inferior angle of the scapula
become prominent from the chest wall — this is known as 'winging of the scapula'. The patient
also feels difficulty in raising the arm above right angle from a position in front of the body
due to inability of rotation of scapula on the chest wall owing to paralysis of the serratus anterior
muscle.
RADIAL NERVE
This is also known as musculospiral nerve.
Sites of injury.— This nerve may be injured in the axilla or in the radial groove. Its main
branch, the posterior interosseous nerve, which is concerned with supplying the extensor muscles
of the wrist and fingers, may be injured at the elbow.
A. IN THE AXILLA —
(i) Crutch palsy — that is pressure with ill-adjusted crutch without proper handgrips.
Paresis of this nerve has occurred only after using 4 hours with this type of crutch without
handgrips.
(ii) Fractures and dislocations of upper end of the humerus, or by attempts at their
reduction.
(iii) Rarely by pressure of a new growth.
B. IN THE RADIAL GROOVE —
(i) Pressure of the arm on the edge of the operating table or on the edge over handle
of a chair or footpath after a heavy slip following excessive drink may bring about injury to the
radial nerve at this site. The latter type is known as 'Saturday night' paralysis.
(ii) Prolonged application of a tourniquet or ill-applied plaster of the middle of the
arm is also liable to damage the radial nerve.
(iii) Fracture of the shaft of the humerus is responsible for radial nerve injury in about
10% of cases.
(iv) During operation on the humerus due to nonunited fracture this nerve may be
injured at this site.
(v) Intramuscular injection of drugs may rarely injure radial nerve.
C. AT THE ELBOW (POSTERIOR INTEROSSEOUS NERVE INJURY).—
(i) Fracture of the neck of the radius or dislocation of the radius.
(ii) During operation of excision of the head of the radius.
A. WHEN INJURED IN THE AXILLA —
1. Motor paralysis —
(i) Triceps muscle — which causes inability to extend the forearm against resistance.
(ii) Extensors of the wrist become paralysed which causes wrist drop which is
diagnostic of radial nerve injury.
(iii) Extensors of the metacarpophalangeal joints due to paralysis of the extensor
digitorum. However the patient can extend the interphalangeal joints with the unaffected
interossei muscles (supplied by the ulnar nerve) and lumbricals (supplied by the median and
ulnar nerves). So when the radial nerve is injured the patient will not be able to extend the
metacarpophalangeal joint, but will be able to extend the interphalangeal joints. So extension of
fingers on the whole is not affected.
(iv) Extensors of the all joints of the thumb (extensor pollicis longus and brevis) are
paralysed. So extension of thumb is not possible in radial nerve injury.
(v) The supinator and brachioradialis are paralysed, yet supination of the forearm is
ably performed by the biceps muscle particularly when the elbow is flexed. But supination is
completely lost when the forearm is extended. However paralysis of the brachioradialis can be
tested by asking the patient to flex the elbow joint keeping the forearm in midprone position
against resistance. This becomes difficult and the muscle will not stand out in case of
brachioradialis paralysis.
2. Sensory loss.— In radial nerve injury in the axilla anaesthesia will be present on the
dorsum of the arm, forearm and back of the hand. There will be also anaesthesia of the dorsum
of the thumb and lateral three fingers upto the proximal interphalangeal joint owing to overlap
by the ulnar nerve and median nerve.
3. Trophic changes.— These changes are usually not much.
B. INJURY IN THE RADIAL GROOVE.—
1. Motor paralysis.— This is similar to the radial nerve injury in the axilla, except that
the triceps and anconeus muscles remain unaffected. This is due to the fact that the branches
supplying all the 3 heads of the triceps and the anconeus arise from the radial nerve before it
reaches the radial groove.
2. Sensory loss.-— In radial nerve injury at the radial groove anaesthesia is limited to a
patch on the back of the hand and radial side of the thumb and the adjoining part of the thenar
eminence, the medial side of the thumb and the adjoining sides of the index middle and lateral
side of the ring finger. There is also anaesthesia on the back of the fingers upto the proximal
interphalangeal joints except in the thumb where it reaches upto the nail, as both posterior
cutaneous nerve of the arm and posterior cutaneous nerve of the forearm arise from the radial
nerve before it reaches the radial groove.
3. Trophic changes are trivial.
C. AT THE ELBOW.— Here the posterior interosseous nerve is mainly injured.
1. Motor paralysis.— The posterior interosseous nerve supplies all the muscles of the
back of the forearm which are concerned with extension of the wrist joint and extension of the
metacarpophalangeal joints of the fingers and extension of all joints of the thumb. It also supplies
the supinator muscle. So 'wrist drop' is the main manifestation of motor loss in case of injury to
this nerve.
2. Sensory loss.— The posterior interosseous being a pure motor nerve, there will be no
sensory loss at its injury.
MEDIAN NERVE
Sites of injury. This nerve is injured either at the elbow or at wrist.
A. AT THE ELBOW.— This nerve may be injured at the elbow —
(i) Due to supracondylar fracture of the humerus or condylar fracture or fracture of
lower end of the humerus.
(ii) Due to dislocation of the elbow which may be anterior or posterior, though posterior
dislocation is much more common.
(iii) This nerve may be injured by application of a tourniquet anywhere in the arm.
B. IN THE WRIST.— The various causes of this nerve injury are :
(i) Cut injury to the wrist from a variety of causes.
(ii) Fracture of lower end of the radius.
(iii) Dislocation of the lunate bone.
(iv) Carpal-Tunnel syndrome.
(v) Compound palmar ganglion.
A. WHEN INJURED AT THE ELBOW —
1. Motor paralysis.— The median nerve with its anterior interosseous branch supplies
all the flexors of the wrist and fingers except the flexor carpi ulnaris and the inner part of flexor
digitorum profundus, as also the pronators of the forearm. So these muscles will be paralysed
when the median nerve is injured at the elbow. As the flexor carpi ulnaris remains active, the
hand will be deviated towards the ulnar side particularly when the wrist is flexed. Flexion of
the index finger will be fully affected though the flexion of other fingers may be carried out
with the help of the medial part of the flexor digitorum profundus which is supplied by the
ulnar nerve. Due to this when the patient is asked to clasp the hands the index finger will fail
to flex giving rise to an appearance of a 'pointing index'. The test is known as 'Ochsner's clasping
test’. Flexion of the terminal phalanx of the thumb becomes impossible due to paralysis of the
flexor pollicis longus and the patient will fail to flex the terminal phalanx of the thumb against
resistance while the proximal phalanx is being steadied by the clinician.
Paralysis of the muscles of the thenar eminence is a characteristic feature of median nerve
injury. On inspection the thenar eminence will be flattened and the metacarpal bone of the
thumb apparently comes on the same plane as the other metacarpal bones giving rise to an
appearance which is typically known as 'Simian' or 'Ape-like' hand. The abductor pollicis brevis,
opponens pollicis and flexor pollicis brevis, which constitute the thenar eminence are paralysed.
Even the first dorsal interosseous and the two lateral lumbricals are also supplied by this nerve.
While supply to the interosseous and lumbrical muscles are not very significant, yet paralysis
of abductor pollicis brevis will be evident by the pen test, in which the patient is asked to touch
a pen, which is kept at a slight higher level than the palm of the hand, with the tip of the
thumb. Paralysis of opponens pollicis will be evident by the failure of the patient to touch the
tips of the other fingers with the tip of the thumb.
As the pronators of the forearm become paralysed, pronation of the forearm becomes feeble
which will be particularly evident if the patient is asked to pronate his semiflexed forearm.
Pronation of forearm becomes almost nil after midprone position, upto which brachioradialis
can pronate the forearm.
2. Sensory loss.— This will be particularly evident by loss of sensation over the lateral
half of the palmar surface of the hand and the palmar surface of the thumb and palmar surface
of the radial two and half fingers. This anaesthesia will be extended over the tip of these fingers
upto the middle of the middle phalanges on the posterior surface of these fingers and upto the
nail bed of the thumb. These areas of sensory loss of course will be gradually reduced due to
overlapping from adjacent nerves.
3. Trophic changes.— These changes are seen in the hand and affected fingers
particularly the index finger. Causalgia may be seen if there is partial injury to the nerve.
B. WHEN INJURED AT THE WRIST.— The median nerve is more commonly injured
at the wrist. But in this case the forearm muscles will not be affected.
1. Motor paralysis.— Only the muscles of the thenar eminence will be paralysed and
wasted. These have been described above and the tests which will be positive are — (i) pen
test, (ii) opponens pollicis test and (iii) 'Ape-like' hand.
2. Sensory loss.— This is similar to that described under injury at the elbow.
3. Trophic changes — are similar to those of injury at the elbow.
ULNAR NERVE
Sin s ni injur This nerve may be injured at the elbow or at the wrist.
A. INJURY AT THE ELBOW.— The causes are :
(i) Supracondylar fracture.
(ii) Dislocation of the elbow.
(iii) Fracture of the medial epicondyle of the humerus.
(iv) Cubitus valgus deformity — in which case this nerve becomes stretched and gets
friction at the groove on the medial epicondyle. This condition may develop many years after
malunited supracondylar fracture.
(v) This nerve may be fixed in the groove behind the medial epicondyle due to
adhesions complicating osteoarthritis which may lead to rupture of axons and progressive
interstitial neuritis, collectively known as ‘entrapment neuropathy'.
B. IN THE WRIST.— Cut injury at the wrist is not uncommon. It must be remembered
that ulnar nerve passes superficial to the flexor retinaculum and hence is more often involved
in cut injuries of the wrist.
( linical (catures.—
A. WHEN INJURED AT THE ELBOW —
1. Motor paralysis.— In the forearm this nerve only supplies flexor carpi ulnaris and the
medial half of the flexor digitorum profundus. There will be slight deviation to the radial side
of the hand when the wrist is flexed. Moreover the tendon of flexor carpi ulnaris just above its
insertion into the pisiform bone will become impalpable when it is paralysed. There will be
weakness of flexion of the little and ring fingers particularly at the distal interphalangeal joints.
Paralysis of the muscles of the hypothenar eminence also occur due to injury to the ulnar
nerve. This nerve supplies the abductor digiti minimi, flexor digiti minimi, opponens digiti
minimi, both the heads of the adductor pollicis and sometimes a small twig to the flexor pollicis
brevis. It also supplies all the interossei probably with the exception of first dorsal interosseous
and to the third and fourth lumbrical muscles. The dorsal interossei are concerned with abduction
of the fingers, while palmar interossei adduct the fingers. Interossei alongwith the lumbricals
flex the metacarpophalangeal joints and extend both proximal and distal interphalangeal joint.
In case of ulnar paralysis a typical claw hand or Main en griffe will be noticed particularly in
late cases. In this condition there is hyperextension of the metacarpophalangeal joints and flexion
of the proximal and distal interphalangeal joints. This deformity is due to paralysis of the
interossei and lumbricals which is characteristically evident in both ulnar and median nerve
palsy and in Klumpke's paralysis (lower brachial plexus lesion in which mostly Tl is affected).
In ulnar nerve paralysis though the first and second lumbricals are exempted yet this deformity
can be obviously noticed in ring and little fingers.
As the dorsal interossei are concerned with abduction of the fingers, if the patient is asked
to abduct the fingers against resistance, he will be unable to do so in case of ulnar nerve palsy.
The palmar interossei are concerned with adduction of the fingers. A card is placed between
the two fingers and asked to grip the card with the two fingers by adducting the fingers and
the clinician tries to pull the card. The latter can assess the strength of the palmar interossei by
the force of pull required for the purpose. This is known as the 'card test'.
Adductor pollicis is concerned with adduction of the thumb. If a patient with ulnar nerve
injury is asked to hold a book between his hand and the thumb with the thumb straight he will
fail to do so and he will try to hold the book by flexing the distal interphalangeal joint of the
thumb with the help of flexor pollicis longus. This is known as 'Froment's sign'.
As interossei alongwith lumbricals through extensor expansions are also concerned with
extension of the proximal and distal interphalangeal joints, the strength of the interossei can be
tested by asking the patient to straighten the finger against resistance while the clinician steadies
the proximal phalanx of that finger.
2. Sensory loss.— Sensory loss will be appreciated on the medial border of the hand
alongwith adjoining l/3rd of the palmar and half of the posterior surfaces and the whole of the
little finger and medial aspect of the ring finger.
3. Trophic changes.— These changes are often well evident in ulnar nerve injury.
B. INJURY AT THE WRIST.—
1. Motor paralysis.— Only the small muscles of the hand are paralysed. The various
tests relating to such paralysis have been discussed above.
2. Sensory loss.— As the dorsal cutaneous branch and the palmar cutaneous branch of
the ulnar nerve arise 5 cm above the wrist joint and middle of the forearm respectively, only
the palmar surface of the fingers will be affected.
SCIATIC NERVE
Causes <>l injury.—-
(i) Subtrochanteric fracture of femur, (ii) Posterior dislocation of hip. (iii) Fracture of the
pelvis, (iv) Penetrating wounds.
Sciatic nerve is hardly involved totally. Incomplete injury is much more common in this
nerve. The lateral popliteal portion is affected nine times more commonly than the medial
popliteal portion as the latter passes down on the inner and deep aspects of the sciatic nerve.
THE COMMON PERONEAL (LATERAL POPLITEAL) NERVE

C auses of injury.—
Besides the causes mentioned above for injury to the sciatic nerve, which mainly involve
the common peroneal portion, this nerve itself may be injured by the following causes —
(i) Fracture of the neck of the fibula, (ii) During subcutaneous tenotomy of the biceps tendon,
(iii) At the time of operation of excision of the upper end of the fibula, (iv) By cut injury, (v) By
pressure of plaster or splint, (vi) Rarely the origin of peroneus longus from the fibula may
entrap this nerve and press on it — 'entrapment neuropathy', (vii) Rarely during operations for
multiple ligation of the varicose vein particularly at the origin of the short saphenous vein.
Motor paralysis.— This nerve mainly supplies the extensor and peroneal groups of muscles
of the leg. So when this nerve is injured, these muscles will be paralysed resulting in the
deformities of 'foot drop' and talipes equinovarus.
Sensory loss.— There will be loss of sensation — (a) lateral side of the whole of the leg, which
is supplied by the lateral cutaneous nerve of the calf of the leg, cutaneous branch of the common
peroneal nerve, though it arises at the level of the head of the fibula and may escape injury when
common peroneal nerve is involved at the level of the neck of the fibula. The lower part of the
lateral part of the leg is supplied by the superficial peroneal (musculocutaneous) nerve.
(b) The dorsum of the foot, which is supplied by the superficial peroneal nerve, and the
cleft between the great toe and the second toe which is supplied by the anterior tibial or deep
peroneal nerve will lose sensation. The medial border of the foot is supplied by the saphenous
nerve, whereas the lateral border of the foot is supplied by the sural nerve so these portions are
exempted.
(c) The dorsum of all toes will lose sensation except lateral side of the little toe which is
supplied by the sural nerve.
Assessment of nerve injury is mainly done by clinical examination, but some neuro-
physiological studies and imaging may be performed to get additional information.
N europhysiologieal inve stigation s. —
Skilled neurophysiologist is required to interprete the results and it takes about 2 to 3 weeks
after a nerve injury when proper neurophysiological assessment can be performed. Two tests
can be done :—
• Nerve conduction studies.— These actually record sensory or motor nerve action
potentials and the conduction velocity through the nerve is calculated for given anatomical
segment flowing of conduction. Slowing of conduction can be identified in case of compression
neuropathy.
• Electromyography (EMG).— In this test muscle axon potentials are recorded in
response to voluntary activity. Abnormalities which are typical of denervation or reinervation
can be assessed. Using these tests it is possible to distinguish between a nerve injury in which
axons have not degenerated distal to the lesion (neuropraxia) and one in which Wallerian
degeneration has occurred (axonotmesis or neurotmesis). However axonotmesis or neurotmesis
cannot be distinguished.
Electromyography helps to read the electrical activity of a muscle during rest and activity.
There is no electrical activity in an intact muscle at rest. During weak contraction it records
single action potential and in powerful contraction an interference pattern is observed due to
more action potentials. Denervated muscle shows denervation potentials which appear within 1
to 2 weeks after injury. If this does not appear by 15 to 20 days it indicates good prognostic
sign.
EMG detects presence or absence of any nerve injury. It also indicates whether any nerve
injury is complete or incomplete and whether regeneration is taking place or not. Even the level
of nerve injury can be determined by showing the changes of denervation of the muscles supplied
by the nerve distal to the nerve injury.
Strength duration curve.— Minimum current used to elicit muscle contraction is called
'rheobase' and it is expressed in milliamperes. 'Chronaxie' is the duration of current required to
excite a muscle with double the rheobase strength, this is expressed in milliseconds. The duration
and strength of the current used to excite a muscle is plotted in a graph as the strength duration
curve. A normal muscle responds to stimuli varying in duration from 300 milliseconds to 1
millisecond without any increase in strength of the current. If the duration of current is decreased,
the strength of current is to be increased to produce contraction. So a strength duration curve
can be plotted known as nerve curve.
A totally denerved muscle needs either more strength of current or for a longer duration.
This is called a curve of denervation.
In case of partially denervated muscle shows a curve in between the above two. Assessment
of recovery can also be assessed by strength-duration curve. If recovery is occurring the curve
will show a shift to the left. On the other hand if degeneration is progressive the shift will be to
the right.
• Magnetic Resonance Imaging (MRI) is now being used more frequently to display
peripheral nerve pathology. This imaging technique is showing promise for the future. Presently
this investigation is mainly used to know the damaged of the cervical nerve roots after brachial
plexus injury.
AUTONOMIC NERVOUS SYSTEM

Causalgia.— .
It is a painful condition which arises from incomplete injury to the nerve. Usually the pain
starts following incomplete injury or division of the nerve, though occasionally such pain may
not appear before 2 or 3 months.
Pathophysiology.— Incomplete division of the nerve gives rise to an impulse which passes
towards sensory nerve endings where such stimuli lead to production of histamine-like substance.
Accumulation of this substance causes vasodilatation and the part becomes red, sweats profusely
and becomes increasingly painful. Gradually the trophic changes may appear.
Treatment.— The condition is so distressing that surgical interruption often becomes
necessary. According to the site, cervico-thoracic or lumbar sympathectomy may be required,
which are discussed below.
Ilyperhidrosis or excessive sweating.—
Some patients may complain of excessive sweating of the hands, axillae or even feet.
Treatment.— If the axillae are affected, local excision of the axillary skin which contains apocrine
sweat glands may be required. These are mapped out by applying sweat-sensitive starch and iodine
dusting on the axilla. In obstinate cases cervico-thoracic sympathectomy may be required.
When the hands are too much sweating, cervico-thoracic sympathectomy should be the
treatment of choice.
When the feet are sweating excessively with sodden and offensive feet, lumbar
sympathectomy is justified.
SYMPATHECTOMY.—
INDICATIONS.— The operation of sympathectomy is carried out for the following basic
conditions :—
(1) CIRCULATORY INSUFFICIENCY OF THE LIMBS.— By far this is the most important
indication of sympathectomy. The arteries which have got smooth muscles in their walls, will
be released of their spasms due to sympathectomy. These arteries are generally medium sized,
small arteries, arterioles and arteriovenous communications. By this, there will be more blood
running through the collaterals giving rise to better 'run-off'. The limb will be warm, pain will
be less and the ulcers may show signs of regression.
The pathological conditions under this category, which are benefited by sympathectomy,
are as follows :
(a) Atherosclerosis.— Where direct reconstructive surgery is not possible, sympathectomy
finds its greatest field. The patient with 'rest pain' and an impending gangrene of the toes,
when shows no segmental blockage in arteriography but shows widespread distal blocks, is
probably a good case for sympathectomy. This will improve the condition by dilating the
collateral circulation. The foot will be warmer, 'rest pain' will be relieved to certain extent, but
unfortunately in many cases this symptomatic relief does not last for a long time. Some vascular
surgeons suspect whether sympathectomy really increases the deep collateral circulation or simply
increases vascularisation of the superficial tissue and skin. But one thing is certain, that if
amputation is at all required, previous sympathectomy will definitely limit its extent.
(b) Raynaud's syndrome.— In this condition, the role of sympathectomy is rather dubious.
The symptomatic relief is rather temporary and almost always fails to yield permanent relief.
(c) Thrombo-angiitis obliterans (Buerger's disease).— In this condition, the distal arteries
are involved while the proximal arteries remain absolutely normal with good volume of pulse.
By sympathectomy, one can only delay the progress of the disease, but cannot have a long term
good effect. This operation also limits the extent of amputation.
(2) HYPERHIDROSIS.— The result of sympathectomy is much better in this condition.
When sweating is sufficiently profuse to make one psychotic, this operation should always be
called for. The sweating will be abolished and the long term result is satisfactory.
(3) CAUSALGIA.— Sometimes the patients complain of persistent pain in the limb following
amputation or partial injury to the nerve. Sympathectomy, if carried out, may give the patient
some relief. But the anatomical or pathological reason of this relief is yet to be found out.
Anatomical Consideration of Sympathectomy.— The pre-ganglionic fibres concerned
with supplying the upper limb are derived from the upper thoracic segments of the spinal cord
— T2 to T7. These fibres reach the sympathetic trunk through white rami communicantes. In the
sympathetic trunk these fibres pass up to synapse about cells, situated mainly in the cervico-
thoracic ganglia, from where post-ganglionic fibres pass to the brachial plexus, mainly the lower
trunk. Most of the vaso-constrictor fibres supplying the arteries of the upper limb, emerge from
the spinal cord in the ventral roots of 2nd and 3rd thoracic nerves. So these arteries can be
denervated surgically by cutting the sympathetic trunk below the 3rd thoracic ganglion, severing
the rami communicantes connected with the 2nd and 3rd thoracic ganglia and dividing the
sympathetic trunk proximally just above the lower half of the cervico-thoracic ganglion (Tl
part) distal to the attachment of the white ramus. The white ramus to the cervicothoracic ganglion
is not cut, as it contains the pre-ganglionic fibres, which pass up the sympathetic trunk to the
superior cervical ganglion, whence post-ganglionic fibres pass to supply the vasoconstrictor and
sudomotor nerves to the face and neck. Destruction of this nerve will result in drooping of the
upper eye-lid (ptosis), enophthalmos, constriction of the pupil and absence of sweating of that
side of the face (Homer's syndrome).
Sympathetic fibres to the lower limb emerge from the spinal cord between T9 and Lr They
pass to the sympathetic trunk and then pass downwards, synapsing with the cells in lower
lumbar and sacral ganglia from where post-ganglionic fibres arise and innervate the vessels of
the lower limb. So removal of the lumbar sympathetic trunk just below the first ganglion
proximally and below the 3rd ganglion distally will denervate the blood vessels of the lower
limb. This denervation is essentially pre-ganglionic and particularly of those vessels below the knee level,
as the cells lie in the lower lumbar and sacral sympathetic ganglia. This may be the main reason
why sympathetic denervation of the vessels of the lower limb is more effective than that of the
upper limb, which is a mixed pre- and post-ganglionic denervation.
CERVICO-THORACIC SYMPATHECTOMY.—
For complete sympathetic denervation of the upper limb, it is advisable to remove the lower
half of the stellate ganglion (first thoracic ganglion) distal to the level where the rami
communicantes from the first thoracic nerve join the ganglion to just below the 3rd thoracic
ganglion with division of all rami communicantes joining the 2nd and the 3rd thoracic ganglia.
For hyperhidrosis of the head and neck removal of the whole of stellate ganglion (thus accepting
the Homer's syndrome) will suffice. For axillary hyperhidrosis, the upper four or five thoracic
ganglia should be removed (so axillary approach is more convenient).
Cervico-thoracic sympathectomy can be performed by one of the three following
approaches:—
A. ANTERIOR APPROACH.— The patient lies supine on the table. His neck is extended
by putting a sand bag between the shoulder blades. The head is rotated to the opposite side
and the hand of the corresponding side is pulled downwards. Operation on both sides can be
done in one sitting. An incision is made about 1/2 inch above the clavicle starting from the
lateral border of the sternal head of the stemomastoid muscle to the medial border of the
trapezius. After incising the skin, superficial fascia, platysma and investing layer of the deep
cervical fascia, the clavicular head of the stemomastoid is divided and the inferior belly of
omohyoid is retracted upwards to expose the scalenus anterior and the phrenic nerve. The phrenic
nerve is safeguarded and the scalenus anterior is divided at its insertion to the first rib. The
subclavian artery is exposed. It is retracted upwards with a sling. Its branches are carefully
safe-guarded. The supra-pleural membrane is detached from the inner border of the first rib.
The pleura is pushed downwards and laterally to expose the sympathetic trunk and the
corresponding posterior ends of the ribs. The sympathetic trunk is divided just below the 3rd
thoracic ganglion. The proximal divided end is drawn upwards and all the rami communicantes
joining the 3rd and 2nd thoracic ganglia are divided. Finally the sympathetic trunk is divided
just below the level of the attachment of rami communicantes to the stellate ganglion. This
operation can also be performed above the subclavian artery, which is probably a better approach
for the short necked patients. But in that case the thyrocervical trunk should be divided between
ligatures for better exposure.
B. AXILLARY APPROACH.— The patient lies supine with the arm abducted. An incision,
about 5 inches in length, is made on the medial wall of the axilla along the line of the 2nd
intercostal space. To reach the intercostal space, the fibres of serratus anterior have to be divided,
but generally the long thoracic nerve lies a little posterior to the incision and hence less liable to
be damaged. The pleural cavity is opened and rib-retractor is used. The lung is drawn
downwards and forwards to expose the sympathetic chain covered with parietal pleura. The
pleura is incised and the sympathetic trunk is removed according to necessity. Bleeding vessels
are secured. The lung is inflated and the wound is closed with an under-water seal drainage.
C. POSTERIOR APPROACH.— This is probably the least popular approach for this
operation. A vertical incision is made about 5 cm. lateral to the midline keeping the third rib in
the centre. All muscles are divided to reach the ribs. 5 cm of the posterior end of the 3rd rib
along with the corresponding transverse process is excised subperiosteally. The sympathetic
trunk will be exposed and excised according to necessity. For proper exposure, the 2nd and 3rd
intercostal nerves may be required to be divided. The convalescent period is much longer and
the operation is a lengthy procedure. For this, scope of its application is very much limited.
LUMBAR SYMPATHECTOMY.—
In lumbar ganglionectomy, the sympathetic trunk is removed from the first lumbar ganglion
to the 3rd lumbar ganglion. It is said that while the first ganglion is concerned with sympathetic
innervation of the upper part of the thigh and the groin, the 2nd and 3rd ganglia are concerned
in innervating the limb distal to the middle of the thigh.
Two types of approach can be made for this operation — the extra-peritoneal approach
and intraperitoneal approach, of which the extra-peritoneal approach has enjoyed greater
popularity due to the fact that the peritoneal cavity is not opened.
EXTRA-PERITONEAL APPROACH.— Operation on both sides can be performed in one
sitting. The patient is placed in the 'kidney position'. Either a transverse incision or an oblique
incision may be applied.
The transverse muscle-cutting incision starts from a point just below the tip of the last rib
to the lateral border of the rectus sheath at the level of the umbilicus. The oblique incision is
commenced from the anterior axillary line and runs downwards and medially to the outer
border of the rectus sheath. The muscles are split in the direction of the fibres in the oblique
incision and divided along the line of the incision in the transverse incision, till the peritoneum
is exposed. The wound is now retracted and the peritoneum is gradually stripped medially and
forwards from that portion of the abdominal wall till the inner border of the psoas major is
exposed. The genital vessels and the ureter are adherent to the peritoneum and will be displaced
with it. The sympathetic chain lies along the medial border of the psoas major muscle being
overlapped by the inferior vena cava on the right side and close to the abdominal aorta on the
left side. The most difficult part is to expose the first lumbar ganglion, which lies high up
covered by the crus of the diaphragm just above the renal vessels. The sympathetic trunk from
the first to the third ganglion is excised. In case of bilateral operation, the first lumbar ganglion
on one side should be preserved, since removal of both ganglia will cause sterility due to failure
of the ejaculatory mechanism.
INTRA-PERITONEAL APPROACH.— This approach is only employed when the abdomen
is opened for some other reason.
Peri-arterial sympathectomy.—
This operation has almost lost its ground except in carotid sinus syndrome. In this syndrome,
the blood pressure of the individual suddenly drops down with pressure on the neck. In this
condition, the carotid sinus is denervated by excising the tunica adventitia containing the
periarterial sympathetic plexus for a distance of 1 inch above and below the bifurcation of the
common carotid artery. With a fine needle, normal saline is injected between the muscular coat
and the tunica adventitia. This will lift the tunica adventitia from other coats of the artery and
will facilitate its excision.
TUMOURS OF THE PERIPHERAL NERVES

Peripheral nerve tumours are generally called neuromas.
Neuromas are of mainly two varieties — true and false.
False neuromas are those which arise from the connective tissue covering the nerve fibre or
from the nerve sheath. Neurilemmoma and neurofibroma are included in this group.
True neuromas are extremely rare and are only seen in connection with the sympathetic
system. The sympathetic system originates from the neural crest and develops along 2 lines:—
(a) Primitive neuroblasts and adult sympathetic cells which may give rise to tumours such as
neuroblastoma and ganglioneuroma respectively, (b) Chromaffin tissue situated mostly in the
adrenal medulla and may produce tumours known as pheochromocytoma.
Neurilemmoma and Neurofibroma have been discussed in detail in Chapter 10 of 'Common
Tumours and Miscellaneous Lesions of the Skin'.
Malignant Schwannoma (Neurilemmoma).—
This tumour is composed of Schwann cells derived from the multipotential neural crest
and capable of forming connective tissue fibres simulating those produced by fibroblasts.
This tumour does not arise from solitary neurilemmoma, but usually arises from the
generalized neurofibromatosis or von Recklinghausen's disease. In fact about half the cases arise
from this disease.
Malignant schwannoma is more often seen in females at younger age — probably hormone
plays some role. The usual site is in the limbs, the commonest location being the thigh. Majority
of this tumour develop along recognized peripheral nerves.
Pathology.— The Schwann cells tend to show their characteristic repigmentation. The earliest
evidence of malignancy is the presence of large hyperchromatic nuclei. In the less malignant
group one may find arrangement of the Schwann cells in palisading and whorling fashion. In
more malignant and anaplastic forms there may be no suggestion of palisading but the elongated
cells are arranged in interlacing bundles. It is often not possible to separate a malignant
schwannoma from various fibrosarcomas and leiomyosarcomas on purely histological grounds.
The fact that the malignant tumour has developed from nerve tissue becomes the only logical
evidence in favour of malignant schwannoma.
The nerve from which the tumour arises seems to be destroyed, though its functions may
be retained to a remarkable degree. It is a more malignant tumour than fibrosarcoma. It is
notorious for local recurrence. This is due to the fact that it shows tendency to spread along
lymph spaces within the nerves. Involvement of lymph nodes is rare.
Treatment.— Due to the tendency for local recurrence, wide resection is always justified. In
grade I cases radical local excision may suffice. In more malignant cases amputation may be
needed. In anaplastic cases amputation with chemotherapy is justified.
TUMOURS OF THE SYMPATHETIC SYSTEM

Three tumours are known in this group. These are neuroblastoma, ganglioneuroma and
pheochromocytoma.
Neuroblastoma.— It is a disease of infancy and childhood, though rare cases have been
reported in adults.
It is a tumour of undifferentiated neuroblasts. It is mostly seen in the adrenal medulla and

is discussed in detail in the chapter of 'The Adrenal Glands' (Chapter 38). Occasionally this
tumour may be seen in the ganglia of the paravertebral chains in both the thorax and the
abdomen.
Ganglioneuroma.— It is also a tumour which develops in childhood, though it manifests
clinically in adults.
It is a benign tumour, though it should be considered as potentially malignant. It consists
of adult ganglion cells, nonmedullated nerve fibres and fibrous tissue.
It arises from the sympathetic ganglia along the paravertebral chain either in the thorax or
in the abdomen.
Pheochromocytoma.— It is a tumour of adrenal medulla and is discussed in that chapter
(Chapter 38).
CHAPTER
AMPUTATION
INDICATIONS.—
(1) CONGENITAL.— Supernumerary digits (polydactylism).
(2) TRAUMATIC.— As the time is passing by, less and less amputations are being performed
due to trauma. Today an increasing tendency towards conservatism has been developed. Of
course, an advance in antibiotics and chemotherapy has also lessen the incidence of amputation.
Even then, in severe wounds and injuries, when the limb cannot be saved in any way, amputations
should be done not only to save the limb, but also to save the patient. If the main vessels are not
destroyed, the limb can usually be saved. In odd cases, the bones and the soft tissues are absolutely
crushed and cannot be saved in any way. Another indication in this group will be gas gangrene
following wound and injury.
(3) INFLAMMATORY.— Amputations from this condition have considerably been reduced
in recent years due to the advent of efficient antibiotics and chemotherapeutics. So amputation
is seldom advised for acute osteomyelitis, diabetic cellulitis or even septic arthritis nowadays. But
occasionally, if destructive bone and joint infection in a finger has made it a liability, amputation
may be advised to prevent spread of infection to the palm and to get maximum function from
the other fingers. Sometimes chronic infection of the foot, such as Madura foot, may require
amputation.
(4) VASCULAR INSUFFICIENCY.— Great majority of patients, requiring amputation, are
victims of vascular insufficiency. The main artery to the limb may be injured which may compel
the surgeon to perform amputation if arterial repair becomes not possible. Vascular insufficiency
from atherosclerosis or other forms of arterial diseases may give rise to intermittent claudication
and later on rest pain. This rest pain is quite intolerable and besides this, gangrene to the distal
part of the limb will also require amputation as the only method of relief to the patient. Amputation
should always be performed through healthy tissues of the limb where vascularisation is normal,
well above the affected part of the artery.
(5) MALIGNANT TUMOURS.— In malignant tumours such as osteosarcoma, fibrosarcoma,
chondrosarcoma etc., amputation is required in most of the time. In osteosarcoma, the trend of
treatment has considerably been changed during recent years. In Standord Cade's regime of
treatment, amputation is lately called for and irradiation is the first line of treatment. This will
reduce the number of unnecessary amputations, where metastasis had already occurred and the
patient would die from metastasis in any way. Incidence of amputation is much higher in cases
of fibrosarcoma and chondrosarcoma.
(6) DIABETES.— Quite a number of patients, who come for amputation, are diabetic.
Diabetic atherosclerosis plays the major part to cause gangrene of the limb. Sugar-laden oedematous
tissue often becomes infected and makes the condition worse which may call for ablation of the
limb. .
22
IDEAL LEVEL FOR AMPUTATION.—

To choose the level at which amputation should be performed, the following factors are
considered :
(1) EXTENT OF THE INJURY OR DISEASE should certainly be considered first. When
atherosclerotic gangrene is the cause for amputation, it should be performed through the well
vascularised part of the limb. No set rule can be observed, as was previously done that even in
case of gangrene of the toes, a mid-thigh amputation was recommended. At present the trend is
to find out the normal vascularised part of the limb proximal to the gangrenous part and
amputation should be carried out through this normally vascularised part. In non-diabetic patients,
healing can be assured if the level of amputation is immediately below the most distal palpable
arterial pulsation. Sometimes, a lower level of amputation is often selected although with an
increased risk of delayed wound healing and of a need for re-amputation. While amputation is
being performed, there should be adequate bleeding from the skin and subcutaneous tissue,
otherwise healing cannot be assured. So conservatism is the plan, which is adopted for amputation.
But for malignant diseases, conservatism is not adopted. To the contrary, amputation should
be done through a level above the joint proximal to the tumour, so that chance of local recurrence
will be minimum.
In case of senile gangrene, conservative approach should be adopted. So, while the gangrene
has involved the fore-part of the foot, Syme's amputation should be performed if it is found that
this part of the limb is well vascularised, otherwise amputation through the leg should be chosen.
Arteriographic X-ray will also give a clue as to which should be the level of amputation. If the
obstruction is found at the bifurcation of the popliteal artery, obviously mid-thigh amputation
will be the best. If the anterior and posterior tibial arteries are well patent, one can go for
amputation through the leg.
In diabetic gangrene, conservative amputation is again followed. But in Buerger's disease, a
mid-thigh amputation is often carried out.
(2) FUNCTION OF THE STUMP— The level at which amputation should be carried out,
does not entirely depend upon the disease. Due consideration must be given to the function of
the stump. The level of amputation should be such that it should be ideal for artificial limb fitting
and only then the proper function of the stump can be obtained. For this, a consultation with the
artificial limb maker should always be made to design the best possible stump. A certain length
of thigh or leg or forearm should be kept for proper fitting of the stump. These levels are called
'optimum levels for amputation'.
In forearm, optimum length is 20 cm (8 inches), measured from the tip of the olecranon. But
under no circumstances, the stump should be less than 8 cm for proper fitting of the artificial
limb. Between these levels as much bone as possible, should be saved.
In arm, the optimum length is again 20 cm (8 inches), as measured from inferior angle of
acromion.
In thigh, the optimum length is 25 to 30 cm (10-12 inches) as measured from the tip of the
greater trochanter. The shortest length should be 10 cm (4 inches).
In leg, the optimum length is 14 cm (5Vi inches). The minimum length should be 7.5 cm (3
inches).
The ideal slump. - The surgeon should know what is meant by the term 'ideal stump',
(i) The stump should be of optimum length; (ii) The end of the stump should be smoothly
rounded; (iii) The stump should be firm; (iv) The opposing groups of muscles should be sutured
AMPUTATION 339
together over the end of the bone. The muscles are sutured in such a way that they will be
converted into fibrous tissue and will serve as an effective cushion, which protects the skin; (v)
The vascularity of the flaps should be normal; (vi) There should be no projecting spur of bone;
(vii) The stump should neither be redundant nor be under tension; (viii) The position of the scar
should be such, as to avoid pressure; (ix) The resulting scar should be fully mobile and should
neither be adherent nor be infolded. In case of upper limb, the scar may be terminal, but in case
of lower limb, a posterior scar is desirable to avoid pressure of weight on the artificial limb. In
case of forearm, the scar should be transverse, as antero-posterior scar may be pulled up between
the two bones.
Types of amputation.— Mainly there are two types of amputations either Guillotine
type or a Flap type.
GUILLOTINE TYPE.— In this type of amputation, all the structures of the limb are divided
at the same level and the wound including the bone is left open. Though it is the most primitive
type of amputation, yet it is used even nowadays in case of gas-gangrene where immediate
amputation in the Guillotine type is performed as soon as possible to save the patient's life.
Otherwise this type of amputation has become obsolete as there is a good chance of secondary
infection, which not only involves the soft tissues but also the bone. Whenever it is used nowadays,
it is always followed by re-amputation at a higher level, in a flap method to cover the bone end
with soft tissues.
FLAP METHOD.— This type of amputation is mostly carried out nowadays. There are
different types of flap method — circular, elliptical, racquet, semicircular or rectangular etc.
In circular method the skin and muscles are divided circularly at a lower level than the bone,
so that they provide a covering for the bony stump. This method has got special advantage in
case of doubtful vascularity as the flaps are not long enough to become devitalised.
In elliptical or oval method the upper end of the ellipse is placed on the level of the bone section
while the lower end should lie at a distance below this, equal to M times the diameter of the
limb. The only advantage of this method is that the scar is not terminal.
Racquet method is often used in case of disarticulation at the metacarpal or metatarsophalangeal
joints and is also applied for disarticulation of the shoulder or the hip joint. The incision for this
type of amputation looks like a racquet, with a straight incision resembling the handle of the
racquet and a circular or elliptical incision, resembling the blade of the racquet, continuous with
the straight incision.
Semicircular or rectangular method is by far the most widely practised amputation. Either two
flaps of equal length or a single flap is used. When a single flap is used, the length should be 1V£
times the diameter of the limb at the level of the bone section. If two flaps are used, they should
cover the same distance. Good blood supply of the flaps must be assured. This is particularly of
concern in case of single long flap. When we are using the term 'flap' it means that it includes
the skin, the subcutaneous tissue along with the deep fascia. The muscles are divided transversely
at a level below the bone section just to allow them to be sutured together over the bone end.
Technique.— It can be best described under the following headings :
APPLICATION OF A TOURNIQUET.— Most of the major amputations should be performed
under bloodless condition by using a tourniquet. At first the limb is held elevated for a few
minutes to drain out the blood. A rubber bandage may be wound to get rid of the venous blood
and then the tourniquet is applied. In arterial degeneration, rubber bandage should not be used
and in certain cases, even tourniquets should be avoided lest it should lead to more arterial
damage. In septic cases and in malignant cases, rubber bandage should be avoided. But tourniquet
may be used even in these conditions. After making the incision, it is the usual practice to get
hold of the named vessels and ligate them properly as the first step of operation.
SHAPING THE SKIN FLAPS.— The skin flaps are first drawn on the skin by a skin pencil,
keeping a provision for certain amount of elastic shortening of the skin. With a scalpel incision
is made along the skin mark through the skin, subcutaneous tissue and deep fascia.
MUSCLES.— Muscles are divided a little below the proposed level of bone section, so that
the opposing groups can be sutured over the bone end for proper round shape of the stump.
Moreover, it will act as a barrier between the scar and the bone, so that the scar will not get a
chance to be adhered to the bone. Whenever opposing groups of muscles will not be available
as in case of amputations through the leg, one group of muscles should be taken over the end
of the bone and sutured to the periosteum of the other side of the bone.
NERVES.— All large nerve trunks should be slightly pulled down and divided as short as
possible, so that the ends will be retracted upwards and will not be involved in the scar. If they
are involved in the scar tissue, continuous pain or pain during movement of the limb will be
intolerable to the patient.
BONE AND THE PERIOSTEUM.— The bone should be cut through the proposed level of
section. The periosteum is generally cut through the same level but it may be stripped only
sufficiently to expose the bare bone and to prevent development of ring sequestrum. In only
below-knee amputation, the periosteum is first cut at the level of the skin incision, and reflected
off the tibia in continuity with deep fascia. Before a saw is used to divide the bone, the muscles
should be well retracted either with a shield or with a towel. When the bone is subcutaneous, it
should be bevelled, so that the sharp edge of the divided bone will not project through the skin.
CLOSURE OF THE WOUND.— Before the wound is closed, the tourniquet is released and
a careful watch is kept on the wound to stop all bleeding vessels. Opposing groups of muscles
are sutured across the bone ends with interrupted stitches. Now the skin and fasciae are sutured
over the muscles without tension. It is a good practice to provide a drain, which should preferably
be a suction drainage (Redivac). The wound is covered with gauze and cotton wool and bandaged
tightly from below upwards. It shouldn't be too tight to endanger the vascularisation of the flaps.
POSTOPERATIVE CARE.— The drain is taken off after 24 to 48 hours. The amputation
stump should be kept in rest. This can be best done by enclosing the stump in a plaster of Paris
cast which should extend above the joint proximal to the stump. This will also prevent flexion
contracture of the proximal joint. This plaster cast should be kept for no less than 3 weeks. The
stitches are removed from 7 to 10 days when the wound is healthy by taking off the plaster cast.
After the sutures have been removed, the plaster cast is reapplied.
Complications of amputation stump.—
EARLY.
1. Reactionary and secondary haemorrhage.
2. Infection of the soft tissues and bone. Abscess may be found which requires drainage and
antibiotic treatment.
3. Amputation may be followed by deep vein thrombosis and pulmonary embolism in the
early postoperative days. So subcutaneous heparin 5,000 units twice daily is strongly advised for
several weeks after operation.
4. Gas gangrene may occur particularly in mid-thigh amputation. Such gangrene usually
occurs from contamination by patient's faeces. In this case a higher amputation may be necessary.
AMPUTATION 341
LATE.—
5. Adherent and painful scar.
6. Stump neuroma, which is proliferation of nerve fibrils at the point of nerve division. In
all amputations there will be some amount of neuroma formation, but painful neuroma is the
result of a faulty technique.
7. Phantom limb.— This is a peculiar phenomenon in which the patient feels that he still
possesses the amputated limb. It occurs in more than 50% of cases.
8. Painful phantom is a distressing condition, in which the patient complains of pain in the
amputated part of the limb, which he actually does not possess.
9. Necrosis of the skin flap may occur if the vascular supply of the flaps are not sufficient
enough.
10. Unresolved infection may lead to osteitis, sequestrum formation and sinus. There may
be a bone spur.
11. Causalgia is nothing but a persistent pain at the end of the amputation stump. This is
mostly seen in case of amputation of digits.
12. Flexion contracture of the proximal joint has already been discussed in the 'postoperative
care'.
13. Jactitation.— It is an intermittent spasm of the amputation stump which becomes very
distressing to the patient.
14. Ulceration of the stump may occur due to pressure effects of the prosthesis. Some patients
may be troubled by cold and discoloured stump particularly during winter due to ischaemia.
INDIVIDUAL AMPUTATIONS
Amputation of the Fingers.—
GENERAL PRINCIPLES.— (1) An attempt should always be made to conserve as much as
possible, as even a small stump may be of tremendous value to the patient. So each case should
be judged according to its merit. (2) Removal of the bone should be reduced to minimum just to
be covered with healthy skin. (3) There should not be any tension while suturing the flaps. (4)
Whenever possible, the scar should be placed dorsally. That means the palmar flap should be
longer to retain the tactile sensation, which is the most important function of a finger. (5) In case
of middle and distal phalanges, it is a golden rule to amputate through the phalanges rather than
to disarticulate the interphalangeal joints. By this, one can preserve the attachment of the flexor
and extensor tendons of the phalanges. (6) Unlike amputations of other parts of the body, in
finger, the flexor and extensor tendons should not be sutured across the bony stump. This will
simply limit the movement of the fingers. (7) In case of working people, the metacarpal heads
should be preserved, even if amputation of the little or index finger is being performed. But for
better cosmetic purpose, the marginal metacarpal bones should be obliquely divided, so that it
will be very difficult to realise that a finger is missing.
AMPUTATION THROUGH THE TERMINAL PHALANX.— As has already been mentioned
every effort should be made to preserve the base of the phalanx which receives the insertion of
the long flexors and extensor tendons. A long palmar flap is kept so that the suture line lies dorsally.
A transverse incision is made on the dorsal surface th inch (7 mm) distal to the prominence
of the knuckle. Two lateral incisions are extended distally from the two ends of this dorsal
incision, so that they meet at the tip of the finger. These lateral incisions should be placed just
behind the digital vessels. The flaps are raised along with the subcutaneous tissue and the knife
is played keeping close to the bone. The phalanx is divided with bone shears just distal to the
attachment of the tendons. The palmar flap is now sutured to the dorsal flap.
AMPUTATION THROUGH THE MIDDLE PHALANX.— A racket-shaped incision should
be made with the handle of the racket placed dorsally. If possible it is always desirable to restore
the insertions of the tendons.
AMPUTATION THROUGH THE PROXIMAL PHALANX.— A long palmar flap is usually
employed to keep the amputation stitches dorsally. The digital vessels will be required to be
ligatured. Special care should be taken in case of the index and the little fingers, where short
stump i.e. less than lVi inches phalanges is of no use. So if amputation has to be done below this
level, it should be done through the base of the proximal phalanx.
But reverse is true in case of middle two fingers. When at least a short stump is essential to
prevent deviation of the other fingers towards the amputated finger. As has already been
mentioned, base of the proximal phalanx should be preserved to restore the attachment of the
interosseous muscles and palmar ligaments which will give a good gripping power to the hand.
This will also allow free action of the lumbricals and interossei of the adjacent fingers.
AMPUTATION THROUGH THE METACARPOPHALANGEAL JOINTS.— This is not
recommended as usual practice, but in cases of fulminating infection, where removal of the
finger is indicated, disarticulation through the metacarpo-phalangeal joint may be carried out.
AMPUTATIONS THROUGH THE THUMB.— As the thumb is the most important of all the
fingers, utmost conservatism is the rule while amputating this finger. Even a stump composed
of only metacarpal bone is very essential to the patient. When the skin has been avulsed and the
bone and tendons are exposed, one should rather go for skin grafting to cover the exposed bone
and tendons rather than to amputate the thumb.
Dtsartleulation at the wrist joint.— Though the movement of pronation and supination
is preserved even after this operation, yet this operation has fallen into disrepute as there is not
much skin to cover the expanded lower ends of the bones of the forearm. Moreover, in the
process of pronation and supination, the scar will be tense. So nowadays it is rather preferable
to carry out amputation through the lower 3rd of the forearm rather than to go for disarticulation
of the wrist joint.
Amputation through the forearm.— The site of election, according to the artificial
limb maker, is 7 to 8 inches from the tip of the olecranon. The shortest stump is about 3 inches.
Between these levels as much of the limb as possible should be saved. Flap method is most
commonly used for upper 2/3 rd of the forearm whereas for the lower 3rd of the forearm the
circular method is commonly practised. The muscles, the vessels and the nerves are dealt with
in the usual manner (see above). Both bones are cleared for a short distance with a periosteum
elevator. The interosseous membrane and muscle fibres arising from it are also divided. It is the
usual practice to divide the radial bone first. The muscles are sutured over the bone ends.
Amputation through the arm.— The site of election is again 8 inches from the inferior
angle of the acromion and the shortest stump allowable is 4 inches. So amputation should be
done through the limb as near the site of election as possible. The flap method is mostly favoured
and the flaps are made lateral and medial, instead of antero-posterior.
Amputation through the shoulder.— This is sometimes necessary in case of malignant
disease of the humerus. But whenever possible a small portion of the humerus along with the
AMPUTATION 343
head and tuberosities should be preserved to maintain the normal rounded contour of the shoulder.
The approach is made by the racquet method. The arm is held slightly abducted and externally
rotated. The incision starts just lateral to the coracoid process and extends downwards in the line
of the humerus to the level of the axillary folds where it splits to encircle the arm. The vertical
part of the incision is deepened and the clavicular fibres of the deltoid and the pectoralis major
muscles are divided. The lateral part of the deltoid is retracted and thus the tuberosity of the
humerus will be exposed. The short head of the biceps and the coraco-brachialis are divided. The
subscapularis muscle and the capsule of the shoulder joint are incised. The head of the humerus
is then dislocated forwards. The axillary vessels are divided between ligatures and the nerve
trunks adjacent to the axillary artery are also divided. The remaining muscles are divided. Flaps
are now sutured with drainage.
Inter-scapulothoracic (fore-quarter) amputation.—This operation is also required
for malignant growth of the upper end of the humerus or scapula. Removal of the whole of the
upper limb together with the scapula and lateral
2/3rd of the clavicle is the aim of the operation.
The incision is shown in Fig. 19.1. Its horizontal
part exposes the clavicle which is divided with the
Gigli's saw at the junction of its inner 3rd and lateral
2/3rd. The lateral part of the bone is now retracted
forward to make a gap through which the subclavian
vessels are divided between ligatures. The trunks of
the brachial plexus are divided at a slightly higher
level. Anteriorly, the pectoralis major and minor
muscles are divided between the chest walls.
Posteriorly, the scapula is raised from the thoracic
cage by incising the muscles attached to the vertebral
border of the scapula. The trapezius, the levator
scapulae, the rhomboid, the serratus anterior and
latissimus dorsi are all divided. The haemorrhage is
arrested. The flaps are united, leaving a drain at the
lower end of the wound. Fig.19.1.— Shows the incision for inter*
Amputations of the toes.— scapulothoracic amputation on the right side
and the incision for amputation through the
GENERAL PRINCIPLES.— (1) As in case of shoulder on the left side.
fingers, amputation should be done through the
phalanx leaving its base to preserve the attachment of the insertions of the tendons. (2) The scar
should lie on the dorsum, so the plantar flap should be longer. (3) In case of great and little toes,
the marginal flaps should be kept, so that the scar will be not on the sides. (4) It is the golden
rule to save the head of the first metatarsal bone, which plays an active part in bearing no less
than l/3rd of the weight.
Amputation through the distal phalanx of the great toe.— This is carried out as in the case of the
finger by keeping a long plantar flap. The knife should bg played very close to the bone so as
to avoid injury to the digital vessels. After amputation of the phalanx, the flap should be sutured
on the dorsum.
Removal of the great toe.— The base of the proximal phalanx should always be preserved if
possible. A long plantar flap should be used to cover the large size of the head of the metatarsal
bone. The sesamoid bones should always

be preserved. A dorsal racquet incision
should be made at about inch distal to
the metatarso-phalangeal joint, the handle
of the racquet lies on the dorsal median
line whereas the racquet is carried round
the great toe.
Amputation through lateral four toes.—
The principle is more or less like that of
the great toe. Amputation through the line
of the proximal phalanx is to be preferred
to disarticulation.
Lis franc’s amputation is nothing
but disarticulation through the
tarsometatarsal joints. A long plantar flap
is required for dorsal scar.
Chopart’s amputation is disarti
culation through mid-tarsal joints, i.e.
talonavicular and calcaneocuboid joints.
In this operation also, a long plantar flap
is kept for dorsal suturing. Both these
amputations have become obsolete
nowadays.
Syrne's amputation.— This
incision starts from below the tip of the
lateral malleolus and is carried across the
sole to a point x/i inch below the medial
malleolus. Under no circumstances this
incision should be carried behind the
medial malleolus as this may injure the
medial calcanean vessels on which the
vascularity of the heel flap will depend.
The completed heel The two ends of the heel incision are
flap, showing the
vital calcaneaI
connected by an incision, which crosses
branches of the
posterior tibia! and
in front of the ankle.
peroneal arteries. Firstly the anterior incision is
deepened, so that the extensor group of
tendons, anterior tibial vessels and nerve
Fig.19.2.— Shows the steps of operation of Syme's
amputation. are severed. The flexor group of tendons,
posterior tibial vessels and nerve are
divided on the medial aspect below the malleolus. The peroneal tendons are cut on the lateral
aspect. The anterior capsule is incised and the foot is forcibly plantar flexed. The foot is now
removed with the calcaneum by dividing the tendo-Achilles. At this stage of dissection, the blade
of the knife should be kept very close to the bone. The lower ends of tibia and fibula are divided
transversely 3/4th inch proximal to the ankle joint. The tendons are cut short. The vessels and
AMPUTATION 345
nerves are dealt with in the usual manner.

The skin flaps are sutured with a drainage.
Pirogoffs modification, is the operation
in which the tuberosity of the calcaneum is left
in the heel flap and is made to unite with the
divided end of the tibia.
Below-knee amputation (Bur
gess).— The site of election of amputation
through the leg is 5Vi inches from the knee
joint and the minimum length is 3 inches of
the tibia. Burgess posterior flap technique is
much preferred in case of patients with
vascular disease for the simple reason that The gastrocnemius-soleus mass is tapered and the
posterior flap completed.
the posterior flap is much more vascular than
the anterior flap. The incision is made as
shown in the figure 19.3. The posterior flap is
made VA times the diameter of the limb and
the width being Vi the circumference of the
leg at the point of bone section.
The anterior incision is made 5Vi inches
below the knee joint level, which is deepened
upto the bone. The periosteum covering the
subcutaneous surface of the tibia is raised and
The skin is
the muscles of the anterior compartment are trimmed and
sutured.
severed. Anterior tibial vessels and the nerve
are divided. The incisions on the two sides of
the leg are gradually deepened. On the lateral
side, attention is given to secure the peroneal Fig. 19.3.
Shows the steps of Burgess below-knee
vessels. The peroneal muscles are divided. The amputation.
fibula is divided about 2 cm above the line of
tibial section. On the medial side, the long saphenous vein is come across in the subcutaneous
tissue, which is divided between ligatures. The posterior incision is deepened through the posterior
group of muscles. In the subcutaneous tissue the short saphenous vein will be come across which
is divided between ligatures. The posterior tibial vessels and nerve are found between the soleus
and the tibialis posterior muscle, where they are divided. The tibialis posterior, soleus and
gastrocnemius muscles remain with posterior flap. The posterior surface of the tibia is freed from
all attachments with a knife, whose blade is kept very close to the bone. Now the tibia is divided
at the proposed level of section. The posterior muscles mass is sutured to the periosteum on the
anterior surface of the tibia and the skin of the posterior flap is sutured to the anterior flap. A
suction drainage is always installed.
The stump is lightly bandaged and the patient may start walking with crutches shortly after
the operation. He/she can wear an ischial-bearing pylon until the wound is healed and stable.
There is another method which is more popular at present and it is known as skew-flap below
knee amputation. Here equally long flaps are developed and they are joined anteriorly 2.5 cm
below the tibial crest and posteriorly at the exact opposite point on the circumference of the leg.
The bone and muscles are divided in the same fashion as mentioned above. The gastrocnemius
flap is sutured over the cut bone end to the anterior tibi.il periosteum with absorbable suture.
Finally drainage and skin sutures are applied as mentioned above. This technique is more in
accordance with the anatomical knowledge of the skin blood supply.
Supra-condylar and Gritti-Stokes’ amputations.— In supra-condylar amputation,
the end of the stump is broad, which previously was condemned by the limb-makers. But gradually,
it is becoming popular and problems of limb-fitting have largely been overcome.
In Gritti-Stokes' amputation, the anterior flap
extends down to the tibial tubercle and the
posterior flap is Vi as long as the anterior one.
The ligamentum patellae is divided near its
insertion. Posteriorly, the tendons of the
hamstrings are divided and the popliteal vessels
and sciatic nerve are dealt with properly. The
femur is divided across at the level of the adductor
tubercle and the articular surface of the patella is
removed. The ligamentum patellae is now sutured
to the tendons of the hamstrings in such a fashion
that the articular surface of the patella will be
apposed to the cut-end of the femur. At the sides,
the remnant of the capsule of the knee joint can
be sutured to the periosteum of the femur. This
results in an end-bearing stump. But the patella
often becomes unstable in the Gritti-Stokes'
Fig.19.4.— Shows the skin incision and operation operation and the long stump excludes the use of
of Gritti-Stokes’ amputation. Note, that white areas a sophisticated knee prosthesis.
are to be amputated and the shaded areas are to For these difficulties, Carden's modification can
be preserved. See the patella. sometimes be used. In this operation, the patella
is removed. But this operation again runs the risk
of avascular necrosis of the thin anterior flap.
Through-knee amputation.— This operation is gradually becoming popular due to its
wide end-bearing stump. The patient is placed in supine position with the knee hanging over the
dropped-end section of the table. The anterior flap extends to the tibial tubercle and the short
posterior flap extends to a level a little below the knee joint. Some surgeons prefer two equal
flaps. The patellar tendon is severed from the tibial tubercle. The quadriceps expansion is divided
and the knee joint is opened. The cruciate ligaments and the two lateral ligaments are divided.
Now the posterior incision is deepened and the main vessels and nerve are tackled in the usual
manner. The hamstring tendons are severed at the level of the knee joint. As much synovial
tissue as possible is removed. The patellar tendon is sutured to the cruciate ligaments which are
in their turn sewn to the hamstring tendons. So the patella remains in its natural position in front
of the knee joint, where it prevent rotation of the socket of the stump.
Healing is usually rapid but so long it continues, an ischial-bearing pylon can be worn for
the purpose of walking training. As soon as the scar is stable, a close fitting socket should be applied
for normal weight bearing.
Above-knee amputation.— The exact level is not so important unless a sophisticated
AMPUTATION 347
knee-joint mechanism is to be
provided, in which case the
lower end of the femur should
terminate well above the knee
joint. The site of election of this
amputation is about 10 inches
(25-30 cm) distal to the tip of
the greater trochanter. The
incision is made as shown in
Fig. 19.6, the vertical part of
which should overlie the
subsartorial canal, so that the
femoral vessels can be
individually ligated at the first
stage of the dissection.
The incision is deepened
through the subcutaneous
tissue and fascia lata. The lower
end of the quadriceps muscles
anterior, posteriorly the
hamstring muscles and
medially the adductors, the
gracilis and sartorius tendons
will be divided. The periosteum
is slightly elevated from the
level of bone section and the
femur is divided through the
proposed level of section. The The patellar tendon is cut,
cut-end of the bone is carefully the knee joint is opened and
bevelled and a few drill-holes the cruciate ligaments are
are made. The adductor exposed for division.
muscles are sutured to the ilio
tibial tract across the end of the Fig.19.5- Shows the incision and operative details of through-knee
femur, which is secured amputation.
through the drill-holes
(myodesis). The hamstrings are sutured to the quadriceps muscle (myoplasty) and the sutures are
again stabilized through the drill holes. The fascia lata is repaired and the skin is closed leaving
a suction drainage.
Nowadays many surgeons prefer curved equal anterior and posterior skin flaps of sufficient
length (PA times the anteroposterior diameter of the thigh).
Healing takes about a fortnight to complete. During this time, the patient can wear ischial-
bearing socket and a pylon for walking training. Sometimes it is advisable to make the patient
lie on his face lA hour twice each day to prevent flexion contracture of the hip. After proper
healing has occurred, an application of a suction socket is very much suitable for proper
mobilization of the limb.
Disarticulation of the hip joint.—

This is indicated in case of osteosarcoma of the
femur. The operation can be done either
through a posterior flap, the anterior part of the
incision lying 1 inch below and parallel to the
inguinal ligament or through an anterior racquet
incision, the handle of the racket is placed over
the femoral vessels and the medial flap is kept
longer so that the scar falls away from the anus.
At first the femoral vessels are ligated and
divided. The femoral nerve is divided in the
usual way. All the muscles are divided by
elevating, abducting, adducting and rotating
the limb. The sciatic nerve, which lies deep to
the gluteus maximus is cut short. If possible, the
head and neck of the femur should be
preserved for better shape of the stump.
Inter-innomi no-abdominal
amputation.— This operation is mostly
undertaken for malignant growths of the
upper end of the femur or pelvic bones.
An elliptical incision is made, the lateral
part of which overlies the iliac crest and its
medial part crosses the medial side of the limb
a little below the perineum. The abdominal The hamstrings are
sutured to the
muscles attached to the iliac crest, are divided quadriceps.
close to the bone and the peritoneum is shifted

medially. The common iliac vessels are
ligatured. The conjoined tendon and the rectus
muscle are severed close to the pubis. The
pubic bone is cleared on its anterior and
posterior surfaces. The symphisis pubis is
divided with a chisel. The posterior surface
of the ilium is now cleared off the muscles. A
Gigli saw is passed through the greater sciatic
notch and the ilium is divided upwards and
The completed
outwards to the posterior part of the iliac crest. stump.
The innominate bone together with the

lower limb is drawn down. The lumbo-sacral Fig. 19.6 .— Shows the skin incision and steps of
trunk, 1st, 2nd, 3rd and 4th sacral nerves and operation of above-knee amputation.
obturator nerves are divided a little higher up.
All the vessels, coming in the way should be divided between ligatures. Separation is completed by
the division of psoas, pyriformis and levator ani muscles. The crus of the penis is separated from the
ischio-pubic ramus. The cut muscles are sutured together to give a support to the peritoneum and
the skin is closed leaving a suction drainage.
THE HAND
INFECTIONS OF THE HAND
Aetiology.— Infections of the hand are more often seen among manual workers and
housewives. Small abrasions, pricks or careless nail paring are the main sources of infection.
Sometimes the cause remains unknown, probably through such a small injury which is forgotten
by the patient.
In most of the cases (more than 80%) the infecting organism is the Staph, aureus, followed
by Strep, pyogenes and gram negative bacilli.
CLASSIFICATION
Infections of the hand can be divided into 2 major headings — localized infections and
spreading infections.
LOCALIZED INFECTIONS
Localized infections are further subdivided into 5 categories according to the type of the
tissue involved. From superficial to deep these are — 1. Subcuticular infection; 2. Subcutaneous
infection; 3. Suppurative tenosynovitis; 4. Pyogenic arthritis of the finger and 5. Infection of the
cellular spaces of the hand.
1. SUBCUTICULAR INFECTIONS
Subcuticular abscess.— It is also called 'intracutaneous abscess' or 'septic blister'. This is
often seen on the palmar surface of the digits and the webs. Pus collects within the layers of the
skin to lift the epidermis from the dermis. Sometimes such abscess may communicate with
subcutaneous abscess through a small hole and this is called a collar-stud abscess.
Treatment is to excise the overlying epidermis to drain the abscess. After excising the
epithelium one should look for any communication with deeper abscess. In that case the small
hole is enlarged to drain the subcutaneous abscess and to lay open the deep abscess.
Acute paronychia.— The inflammation commences beneath the eponychium. Suppuration
usually follows which may burrow beneath the base of the nail. So paronychia means infection
of the nail fold with or without extension deep to the nail. The infection is subcuticular since it
is situated entirely within the dermis in which the nail is developed. The infection arises from
careless nail paring or from manicurist's unsterile instruments.
This is the most common infection of the hand. The diagnosis is obvious on inspection
which shows redness and swelling of the nail fold. It is an excruciating painful condition. In
about less than half the cases the pus can be seen beneath the nail.
Treatment.— When the

condition is in the infective stage,
it may be cured by chemotherapy
and by increasing vascularity of
the part by alternating tying and
releasing a thread starting from
the base of the finger upto the
distal interphalangeal joint. As in
majority of cases the causative
organism is Staph, aureus,
flucloxacillin is quite effective.
Operative treatment is required
Fig.20.1.— The dotted lines of Fig.20.2.— Indicates division of
two sides of the nail-fold indicatethe proximal part of the nail for when an abscess has developed.
the lines of proposed incision tobetter drainage of pus beneath The pus should be let out by
lift the nail-fold from the nail to the nail. lifting the nail fold from the nail
extrude the pus beneath it. till the proximal end of the nail
is reached when a small amount
of pus will come out. This simple operation is quite painful and should be done under digital
block. If pus has spread beneath the nail, the proximal part of the nail has to be separated from
its bed and should be cut across with fine pointed but strong scissors. This will inevitably drain
the whole of the abscess cavity. A simple dressing with penicillin tulle is enough.
Chronic paronychia,— This condition affects women more often than men and those who
do much washing. The onset is insidious (the condition has already existed for months). It
seldom follows acute paronychia. On inspection the eponychium is glazed and faintly pink (cf.
acute paronychia, where it is angry red). The nail may become cross-ridged and pigmented (cf.
acute paronychia in which the nail remains absolutely normal but there may be subungual
extension of pus). This condition may be multiple (cf. acute paronychia which is almost always
a single lesion). This infection may be bacterial or fungal. It is better to do microscopical
examination of scrappings or do special cultures for fungi.
Treatment.— Preventive.— Wearing of rubber gloves at the time of washing has considerably
reduced the incidence of this condition.
Curative.— This indolent infection is best treated by diluted Bradosol solution in spirit in the
ratio of 1 : 500. This should be dropped into the nail fold twice daily. Mystatin ointment is a good
antifungal treatment. Soframycin ointment is good for antibacterial treatment. This treatment
should be continued till the pockets are filled with granulation tissue. At this stage treatment is
discontinued and the hand and fingers should be kept as dry as possible for epithelialisation to
occur.
If the condition does not respond to the above measure and if the infection is a bacterial
one, operative treatment same as described under acute paronychia should be considered. In
this case the whole nail may have to be removed.
Apical subungual infection.— This condition arises from a prick beneath the tip of the
nail causing infection of the space between the subungual epithelium and the periosteum.
Gradually a small abscess develops at the tip of the finger just under the nail. It is exquisitely
painful and gives rise to comparatively little swelling. There is redness around the abscess which
extends along one or both the lateral nail folds and to add to fallacy this may be prolonged
even into the eponychium. In this case the diagnosis of paronychia should be excluded. There
THE HAND 351
is extreme tenderness which is greatest just beneath the free edge of the nail, where the pus
gradually comes to the surface. In advanced untreated cases there is likelihood of development
of osteomyelitis of the end of the distal phalanx.
Occasionally such apical abscess may be seen in the distal flexion crease.
Treatment.— The pus is drained by excising a small V-shaped portion of the nail from the
centre of its free edge. Excision of nail should also include excision of full thickness of the skin
overlying the abscess. The amount of pus evacuated is surprisingly small, yet the relief is great.
The abscess often extends down to the bone.
2. SUBCUTANEOUS INFECTIONS
Pulp space infection (Felon).— It is the second most frequent infection of the hand
and comprises about l/4th of all cases of infections of the hand and fingers. This infection
originates usually from a prick. The index finger and thumb are most often affected.
Surgical anatomy.— The terminal pulp space of the finger is a closed space as proximally
the deep fascia is attached to the thin skin of the distal flexion crease and fuses with the
periosteum of the distal phalanx just distal to the insertion of the deep flexor tendon at the
level of the epiphyseal line. The space is filled with compact fat which is subdivided into 15 to
20 compartments by fibrous septa stretching between the periosteum of the phalanx and the
skin. This arrangement has an important bearing on localization and spread of pulp infections.
The strong proximal boundary of the fascial compartment acts as an effective barrier to infection
spreading proximally to the finger. This leads to increase in
tension within the closed compartments which may affect the
blood supply of the distal 4/5th of the distal phalanx leading
to necrosis of that part of the bone.
Clinical features.—This condition starts with a dull pain,
which becomes worse when the hand hangs down. Gradually
the pain increases in intensity and becomes more severe at
night interfering with sleep. Tenderness is exquisite. The pain
becomes throbbing in nature with the formation of pus inside
the space. With the development of abscess a swelling
becomes obvious. If untreated, the abscess tends to point
towards the centre of the pulp and may ultimately burst.
Neglected cases suffer loss of pulp tissue leading to
desensitised withered finger tip. The regional lymph nodes
are enlarged and tender.
Complications.— (i) Osteomyelitis of the terminal phalanx. Fig.20.3.— The pulp space 'RS.' is
(ii) Pyogenic arthritis of the distal interphalangeal joint, (iii) limited proximally by a septum ‘S’.
Spread of infection to the flexor tendon sheath, probably due Note the distribution of the digital
to the fact that the incision has been wrongly extended artery A’.
proximally to the sheath.
Treatment.— In early stages when there is no pus formation large doses of antibiotic in the
form of flucloxacillin may cure the condition. Once pus has developed operation should be
performed without delay.
Operative treatment.— This condition should be recognized as early as possible and the pus
should be drained before the disease has involved the bone. When following drainage of the
space the wound continues to discharge

with sprouting granulation tissue at the
mouth of the sinus, it is quite certain that
necrosis of the terminal phalanx has
occurred. X-ray will confirm the
diagnosis.
For drainage of the abscess a short
transverse incision is made on the most
swollen, prominent and tender spot. The
incision is deepened till the pus is reached.
For proper drainage a portion of the skin
may require to be excised. After opening
the wound all the pus is drained and the
wound is scraped. If necrosed bone is
detected by X-ray, it should be removed.
Figs.20.4 & 20.5.-™ Transverse incision is being made on
The remaining bone is curetted. If the
the most prominent part of the pulp abscess. The surrounding
skin is excised and the depth of the wound is being curetted.
necrosed bone is left behind, a discharging
sinus will inevitably be the result. In case
of children, regeneration of diaphysis is possible, if the periosteum remains undamaged. In case
of adults no regeneration takes place and the patient is left with a short terminal phalanx covered
with an ugly curved nail.
Infection of the middle volar space.— The fibrofatty tissue which occupies this
space is more loosely packed than that of the terminal pulp space. Though this space is
partitioned above and below by flexion creases, yet abscess may spread into the proximal segment
and the web space. This space is shut off from the dorsal cellular space by fibrous septa extending
from the skin to the periosteum.
Clinical features.— Infection of this space is much less common than the preceding one. The
finger becomes swollen at its middle particularly on the palmar aspect. The middle volar space
becomes extremely tender. The finger is held in semiflexion position and it becomes difficult to
differentiate from suppurative tenosynovitis, the only differentiating feature being relatively less
painful passive movement of the finger and more localized swelling in case of the former.
Infection of the proximal volar space.— The fibrofatty tissue occupying this space
is also loosely packed. Though this space is well partitioned from the middle volar space, yet it
communicates freely with the corresponding web spaces.
Clinical features are more or less same as those of the infection of the middle volar space.
Complications.— The infection in these spaces tend to spread to the (i) web space, (ii)
interphalangeal joint and (iii) tendon sheath.
Treatment.— In the infective stage, the treatment is administration of appropriate antibiotics
in large doses.
Once the pus has been localized in either of the above spaces, the treatment is to drain the
pus. If abscess has spread sidewise, it is better to make a longitudinal incision just in front of the
digital vessels. If the pus is mostly localized at the palmar aspect, a transverse incision should be
made on the site of greatest bulge and tenderness. Great care should be taken not to injure the
tendon sheath or joint at the time of drainage, lest infection should spread into these structures
to cause stiff fingers.
THE HAND 353
Web space infection.—

Surgical anatomy.— The web space is the triangular space between the adjacent fingers bounded
by dorsal and volar skins. On each side these spaces are bounded by the digital slips of palmar
aponeurosis. This space is filled with loose connective tissue and fat. The anterior part of each
web space contains a lumbrical muscle, the digital vessels and nerve. The smaller posterior part
contains the interosseous muscles. Distally the web space is continuous with the loose connective
tissue on the side of the finger. Proximally the web space communicates with the deep fascial
spaces of the palm through the lumbrical canals — the fascial canals containing lumbrical muscles.
Aetiology.— Infection of this space is caused (i) by a skin prick, (ii) from a purulent blister,
(iii) from proximal segment of the finger and (iv) from the deep palmar space through the
lumbrical canal.
Clinical features.— In the beginning the constitutional symptoms are severe. Later on there
is localization of infection within the space, which is indicated by oedema on the back of the
web space.
The bases of the fingers are swollen and the adjacent fingers are widely separated. The
infection usually remains confined to the web space and spreads more towards the dorsal surface,
as the skin here is thinner than the anterior surface. In later stage pus may track across the base
of the finger into the adjacent web space and may also spread proximally along the sides of the
proximal segments of the adjacent fingers.
Maximum tenderness is found in the web and on the anterior surface of the base of one of
the fingers. In untreated cases the pus may get an access through the dorsal skin.
It must be remembered that spread of infection from web space to the deep palmar spaces
through lumbrical canals is almost impossible.
Treatment.— In the diffuse cellulitis stage, antibiotic treatment in high doses (Cloxacillin
and flucloxacillin) and elevation of the hand with a sling is quite effective.
Once the abscess has been localized, the pus has to be drained out. The best approach is a
short transverse incision on the palmar surface about 1 cm proximal to the web margin. The
incision must be short (less than 7 mm) to avoid injury to the digital vessels and nerves. The
incision is deepened and a few strands of palmar fascia are divided. If pus does not come out,
probing may be required. Once a gush of pus comes out, the opening is enlarged. The edges of
the wound are cut to give a diamond-shape opening. If after evacuating pus through the palmar
incision, there is still bulging of the dorsal skin, a counter-incision on the dorsum should be
made to evacuate pus from the dorsal pocket.
3. SUPPURATIVE TENOSYNOVITIS (SYN. THECAL WHITLOW)

Surgical anatomy.— The synovial sheaths of all the fingers extend upto the distal
interphalangeal joints. Proximally, the sheaths of the index, middle and ring fingers end in a
cul-de-sac at the distal palmar crease. The sheath of the thumb is continuous with the radial
bursa, which surrounds the tendon of the flexor pollicis longus and extends proximally to a
point about 1 inch above the crease at the wrist. The synovial sheath, covering the flexor tendon
of the little finger, sometimes has direct communication with the ulnar bursa or common palmar
sheath, which surrounds all the flexor tendons to the four fingers. The ulnar bursa also extends
proximally upto 1 inch proximal to the crease at the wrist. At times, the radial and ulnar bursae
intercommunicate each other, while they lie in the carpal tunnel.
These sheaths are often infected from a puncture wound in one of the digits. There will be
23
swelling of the finger concerned, but this swelling will be much less than what is found in
infection of the middle or the proximal volar space of the finger. The digit will be held in
semiflexed position and will be rigid. This rigidity in flexion may disappear due to spontaneous
rupture of the sheath. Passive extension will lead to acute pain. Tenderness will be present
althroughout the extent of the sheath, but will be maximum over the flexor creases and over
the proximal cul-de-sac of the sheath.
When the synovial sheaths of the flexor tendons become infected with pyogenic organism
and ultimately pus forms within these sheaths, the condition is called suppurative tenosynovitis.
Aetiology.— This condition occurs (i) directly from a puncture wound e.g. a pin-prick, a
needle prick or sharp object penetrating the tendon sheath, or (ii) indirectly, due to spread from
neglected subcutaneous infections (middle or terminal or proximal volar space) or injudicious
incision for drainage of such abscesses.
Pathology.— The infecting organism is usually Staphylococcus aureus or Streptococcus
pyogenes. As soon as the infection enters the sheath, a reactive effusion occurs which spread
for the whole extent of the sheath. Gradually pus forms within the sheath. The sheath gets
swollen. Pressure within the sheath alongwith virulent infection will cause damage to the flexor
tendon inside the sheath. Ultimately stiffness of the finger will ensue.
Clinical features.—This is an infection of the flexor tendon sheath. The infection is mainly a
direct one from a prick of a needle, a thorn or a dorsal fin of a fish. The prick is obviously
through the skin overlying the tendon sheath, mostly through a digital flexion crease as at this
part the skin surface is remarkably nearer to the sheath. Sometimes this condition may develop
from injudicious incision for drainage of the distal pulp space or from spread of infection from
the middle and proximal volar spaces. The whole sheath is rapidly involved. The patient feels
throbbing pain in the affected digit, the finger becomes red and swollen and the patient's
temperature rises. Infection of the thumb or little finger spreads upto the palm to involve the
radial or ulnar bursa respectively. The cardinal features of this condition are : (i) Uniform swelling
of the whole finger except the terminal segment where there is no tendon sheath, (ii) Typically
the finger is held in flexed position which is classically known as 'Hook' sign. This is an early
sign, (iii) Tenderness over the anatomical disposition of the sheath. To determine the area of
tenderness the end of a match stick serves the purpose admirably. Accurate localization of
tenderness is not possible with the examiner's finger tip which covers too wide an area. Usually
the tenderness is most marked at the proximal ends of the sheaths in case of the index, middle
and ring fingers. In case of ulnar bursa, a point of maximum tenderness is obtained over the
part of the bursa lying between the two transverse palmar creases — Kanavel's sign, (iv) The
patient is asked to move the fingers. Slight movement of the metacarpophalangeal joint by
contraction of the lumbrical and interosseous muscles may be possible but movement of the
interphalangeal joints is completely restricted, (v) Any attempt to straighten the finger actively
or passively causes exquisite pain.
Complications.— (i) Necrosis of the tendon and adhesion of the tendon with the sheath result
in permanent stiffness of the finger in flexed position, (ii) Spread of infection from one tendon
sheath to another is not impossible since the ulnar and radial bursae inter-communicate in 80%
of cases and occasionally the tendon sheath of the index or the middle or the ring finger
communicates with the ulnar bursa.
Infection of the ulnar bursa.— This is probably the most serious of all infections in
the hand. The infection may result from a direct spread from tenosynovitis of the 5th finger.
THE HAND 355
The clinical features of this condition are: Flexion of mainly the little finger and other fingers if
the sheaths of their tendons communicate with the ulnar bursa, but if the sheath has already
ruptured this finding may not be present; Fullness of the palm; Maximum tenderness towards
the ulnar side between the two palmar creases (Kanavel's point); Oedematous swelling of the
dorsum of the hand.
Infection of the radial bursa.— In fact true synovitis of the flexor pollicis longus
always brings about this condition. This is evident by the fact that swelling of the thumb is
seen to extend into the thenar eminence. The thumb is held flexed. Swelling may be seen just
proximal to the flexor retinaculum on the lateral side.
TREATMENT.— This should be treated immediately with intensive chemotherapy,
immobilization and elevation of the hand. If after 24 hours of conservative treatment, there is
not much improvement of pain, swelling, tenderness and if the temperature continues to be
high, operation should be performed without delay.
OPERATION.— For the index, middle and ring fingers, a small transverse incision is made on
the proximal cul-de-sac of the tendon sheath
to allow both decompression of the sheath
as well as irrigation with antibiotics. After the
pus has been evacuated, plastic cannula or a
ureteric catheter of suitable calibre is
introduced into the sheath. The sheath is
irrigated with antibiotic solution. Dry
dressing is applied and the hand is
immobilized and elevated in a plaster splint.
If pain, tenderness and fever continue to be
present, it seems that the drainage site has
become blocked. In this case exploration and
irrigation should be repeated without delay.
As soon as the infection has been controlled,
active exercises should be commenced, but
antibiotic therapy should be continued for a
few days more, as there is a chance of relapse
as soon as the movement of the finger is
started.
If the tendon is seen to have sloughed
and non-viable, amputation of the finger
through its base should be considered. If a Fig.20.6.— Incisions for opening infected tendon sheath.
small portion of the tendon has become ‘M’ indicates the median nerve with its main branches.
sloughed one can try to replace this by a graft 1,2,3,4,5,6,7 & 8 indicate different incisions to open the
provided the function of the finger is still tendon sheaths. See the text.
maintained.
For the little finger.— The danger of suppurative tenosynovitis in this finger lies in the fact
that tendon sheath here often communicates with the ulnar bursa and infection spreads to the
ulnar bursa if treatment is not started early. Sometimes there is a constriction in the sheath at
the level of the metacarpophalangeal joint which may prevent spread of infection to the ulnar
bursa in early stage. Whenever the response to conservative treatment is not satisfactory, no
time should be lost in draining the sheath of the little finger by the methods described for other
fingers above.
For radial bursa, three incisions may be necessary for proper drainage. One at the midlateral
line of the proximal segment of the thumb which lies just in front of the digital vessels and
nerve. The second on the perithenar crease and this incision should not extend further than a
finger's breadth distal to the flexor retinaculum, which is located by the scaphoid tubercle, since
a branch of the median nerve to the muscles of the thenar eminence may be injured. Lastly a
transverse incision may be made just proximal to the flexor retinaculum on the radial bursa.
After drainage, irrigation may be done with thin polythene cannula.
In ulnar bursa, incision may be made just in front of the metacarpophalangeal joint of the
little finger. The ulnar bursa is opened. A ureteric catheter may be passed both proximally and
distally for proper irrigation. But a transverse incision 1 cm proximal to the distal crease of the
wrist joint is more often required for proper drainage. Sometimes even after two incisions,
drainage may not be satisfactory. In these cases, the flexor retinaculum has to be divided through
an incision from the proximal incision carried distally for a short distance which skirts the
thenar eminence.
Complications of suppurative tenosynovitis.—
1. Involvement of the forearm.— When the radial or ulnar bursa becomes distended with
pus, it may burst and pus travels proximally in the forearm between the flexor profundus tendons
anteriorly and pronator quadratus and interosseous membrane dorsally. This is the space known
as Parona's space. Pus in this space will not show much swelling, but there will be brawny
induration above the wrist in the flexor surface of the forearm. The pus here is drained by
making incision on the lateral or medial border of the forearm and by pushing a haemostat
through this incision. The jaws of the haemostat are opened and the pus is drained by Hilton's
method. A corrugated drain is then inserted.
2. Suppurative arthritis.— This occurs very rarely as a complication of suppurative
tenosynovitis. This condition may call for amputation except the thumb.
3. Continuation of suppuration — is possible when there is sloughing of tendon or bone
necrosis.
4. Stiff finger — is possible if the condition is not detected in time and treatment instituted.
5. Involvement of median nerve — is possible due to compression of the Carpal-Tunnel by
distension of ulnar or radial bursa. Both the bursae may be distended due to the existent
communication.
4. PYOGENIC ARTHRITIS OF THE FINGER

This type of infection occurs from extension of infection from soft tissues around the joint
like infection of the middle or proximal segment of the finger or suppurative tenosynovitis. Only
very rarely pyogenic arthritis of the finger may occur from perforating wound of the finger.
The infection is first localized in the synovial membrane and in this stage if treatment is
done, disability may be avoided. But unfortunately enough the articular cartilages and capsular
ligaments are very quickly involved resulting in stiffness of the finger, if not properly treated.
Pyogenic arthritis of a finger is suspected, when following a wound, the region of the knuckle
becomes very painful and movement of the joint increases the intensity of pain. Crepitus is a
late sign. When this condition is not associated with an external wound, one must estimate the
blood sugar level to exclude diabetes mellitus.
THE HAND 357
When an external wound is present to show the cause of pyogenic arthritis, immediate
exploration should be carried out under antibiotic cover. The extensor expansion on either side
is transversely incised and a clear view of the joint should be obtained by mobilizing the tendon
towards the opposite side. The pus is drained and a search should be made for any loculated
collection of pus within the joint as is always done to drain any abscess cavity. Loose fragments
of cartilage and necrotic tissues are removed. The joint is irrigated with first normal saline and
then with antibiotic solution. The capsule and the extensor expansion are repaired with fine
sutures of nylon or polypropylene. The skin wound is closed. It should be left open if the
wound is more than 6 hours old and the wound is very much contaminated. The hand is
immobilized in 'optimum position' till the infection has completely subsided.
When pyogenic arthritis is not associated with an external wound, conservative treatment should
always be tried first. An intensive antibiotic therapy should be started immediately and the
fingers and the hand are immobilized in the optimum position. In most of the cases, the infection
subsides with this treatment. But in some cases operative drainage may be required.
5. INFECTION OF THE CELLULAR SPACES OF THE HAND

Cellular spaces of the hand are very important surgically and knowledge of anatomical
extent of these spaces will enable the surgeon to make proper incision for drainage of these
spaces.
Surgical anatomy.— There are superficial and deep palmar spaces in the palm of the
hand, while in the dorsum of the hand, there are subcutaneous space and subaponeurotic space.
SUPERFICIAL PALMAR SPACE lies just deep to the palmar aponeurosis and superficial
to the flexor tendons. Nevertheless, it contains superficial palmar arch and digital branches of
the median and ulnar nerves.
DEEP PALMAR SPACES.— There are two spaces — (i) the middle palmar space and (ii)
thenar space.
(i) The middle palmar space lies deep to the flexor tendons encircled by the ulnar bursa and
superficial to the medial three metacarpal bones with intervening interossei. It is separated from
the thenar space by an oblique septum which is attached deep to the 3rd metacarpal bone and
superficially to the ulnar bursa between the flexor tendons to the index finger and the middle
finger. Distally it is connected with lumbrical canals which extend towards the medial three
webs. Proximally it is continuous deep to the flexor retinaculum with the space of Parona.
(ii) The thenar space lies deep to the thenar muscles and radial bursa and superficial to the
adductor pollicis muscle. Distally it is connected with the lumbrical canal along the lateral side
of the index finger and sometimes into the web space between the index and the middle finger.
It is separated from the middle palmar space by an oblique septum and the flexor tendon to the
index finger lies just superficial to this space.
DORSAL SPACES.— There are two spaces on the dorsum of the hand — a subcutaneous
space and a subaponeurotic space being separated by the aponeurosis which binds the extensor
tendons.
PARONA’S SPACE.— This space lies in the lower part of the forearm anteriorly lying deep
to the flexor tendons and superficial to the pronator quadratus.
Infection of the superficial palmar spaces.^ This results from abrasion of the
skin of the palm. The hollow of the palm is obliterated by the collection of pus within this
space. The skin appears to be whitish and this signifies that the pus is in the superficial palmar
space. Sometimes infection of this space may spread into the subcutaneous tissue through a
small opening in the palmar aponeurosis (collar stud abscess).
Primarily, antibiotic treatment should be started and once the pus is localized, it should be
drained through an incision, placed on the point of maximum tenderness and swelling along
the line of one of the palmar creases. The wound is properly explored and the opening in the
palmar aponeurosis should be extended for proper drainage.
Infection of the middle palmar space.—
Aetiology.— This infection usually originates (i) from blood borne infection of a haematoma
in this space; (ii) from a penetrating wound; (iii) as complication of suppurative tenosynovitis.
Clinical features.—The patients are mostly manual labourers. The main complaint is the
intense throbbing pain in the palm of the hand.
On examination there may not be much swelling of the palm, but obliteration of the normal
hollow of the palm is noticed. This is due to the fact that the pus is situated beneath the thick,
strong and resistant palmar
fascia. Though there may be
TENDON OF FLEXOR ' FLEXOR TENDONS obvious oedematous swelling
POLLICIS LONGUS TO ALL FINGERS of the dorsum of the hand,
IN RADIAL BURSA SUPERFICIAL IN ULNAR BURSA which may be so
considerable that it is often
called 'the frog hand'. This is
because the lymphatics from
the palm pass over the dorsal
aspect of the hand and also
due to the fact that the skin
and subcutaneous tissue on
the dorsum are more loose
and elastic. The fingers are
held in flexed position, as the
palmar fascia becomes
relaxed in this position and
the patient gets less pain.
Fluctuation is difficult to
PALMAR SUBAPONEUROTIC
elicit. Passive extension and
SPACE OR SUB TENDINOUS
flexion are not so painful as
SPACE
in case of suppurative
tenosynovitis.
Fig.20.7.— Diagrammatic representation of the cross section of the hand.
Disposition of the middle palmar, thenar and dorsal spaces are shown with If the condition remains
their important relations. untreated, pus may erode
through the palmar fascia
and then patient gets relief from pain. At this time swelling of the palm becomes obvious.
Treatment.— Intensive antibiotic therapy should be started till the pus is localized. Once
this has occurred, it should be drained. Drainage is provided by making an incision along the
distal palmar crease at its ulnar side. The palmar fascia is carefully divided and a sinus forcep
is introduced and opened to drain the pus liberally. It is often advantageous to divide the
palmar fascia longitudinally to avoid damage to digital vessels and nerves. The pus is mopped
THE HAND 359
out. The skin edges as well as the edges of the palmar

fascia are trimmed for free drainage.
If the pus has tracked down into the lumbrical
canals, it may be drained by incising the web space
as mentioned in the drainage of web space infection.
Infection of the thenar space.— This will
lead to marked swelling in the region of the web
between the thumb and the index finger or between
the index and the middle fingers. Flexion of the
metacarpophalangeal joint of the thumb or the index
finger will be painful.
Drainage is effected by an incision in the line of
this web between the thumb and the index finger. A
sinus forceps is pushed into this wound in front of
the adductor pollicis muscle and the pus will come
out automatically.
T m Fig.20.8.— 1 & 2 are incisions to drain the
Infection of the dorsal space.- These middle pa)mar space while 3 „ to drain the
spaces may be infected by small abrasion, arthritis thenar space,
of the joints etc.
Intensive antibiotic therapy should be started immediately and care must be taken to exclude
possibilities of infection at other spaces, since this will also lead to swelling of the dorsum of the
hand. Infection of these spaces generally subside automatically with antibiotic therapy and
drainage is not required very often.
Infection of the Parona’s space.— Besides proximal extension of the infection from middle
palmar and thenar spaces, this space may be infected in suppurative tenosynovitis. Deep-seated
abscess may develop. Fluctuation is difficult to elicit. But brawny induration that pits on pressure
suggests abscess formation.
Whenever it is suspected that the pus has been localized at this space, drainage is obtained
by a longitudinal incision on the most prominent part of the swelling. Longitudinal incision
will save the blood vessels, tendons and nerves at this region, but transverse incision is of more
cosmetic value, though the risk of injury to nerves and vessels is more in this incision.
SPREADING INFECTIONS
1. Lymphangitis.— Organisms gain entrance through a minute abrasion which is often
forgotten by the patients. Within a few hours the hand becomes swollen and painful with severe
constitutional disturbances like high fever. As the superficial lymphatic vessels from the palmar
aspect courses to the dorsum of the hand, oedema is mostly seen on the back of the hand. The
hand becomes red, warm and tender. Swelling is mostly noticed on the dorsum of the hand. In
fair-skinned individuals red streaks may be noticed along the lymph vessels. The regional lymph
nodes are often enlarged and tender. When infection enters into the lateral half of the hand
involving the thumb and index finger, the axillary nodes are first involved. When infection
affects the medial half of the hand, the epitrochlear group of lymph nodes become enlarged
and tender. When infection enters the middle finger, the first lymph node to become swollen
may be the deltopectoral group and from here infection may enter the general circulation giving
rise to septicaemia.
Treatment.— This is similar to lymphangitis anywhere in the body and is described in page
286.
2. Cellulitis.— This is almost similar to cellulitis anywhere in the body which is described
in page 84. This is primarily treated by antibiotics and operative drainage is only required when
there is localized abscess formation.
General principles of treatment in case of any type of hand infection.—
(i) Intensive antibiotic therapy.
(ii) Rest and elevation of the hand with proper sling.
(iii) As soon as there is evidence of localization of the pus, it should be drained by
properly placed incision under anaesthesia, which may be digital or general. A bloodless field
is preferred as it offers better view to the position of nerves and tendon sheaths and damages
caused to them.
(iv) Evacuation of pus must be complete with debridement of the walls of the abscess
cavity.
(v) Proper postoperative treatment is required in the form of care to the wound and
change of dressings. First change of dressing should be done after 24 hours of operation and
thereafter on alternate days. The dressings should be kept dry.
OTHER LESIONS OF THE HAND

A. CONGENITAL DEFORMITIES
Congenital deformities include : Polydactylism i.e. supernumerary fingers; Ectrodactylism
i.e. absence of digits; Syndactylism i.e. webbing of the fingers; Macrodactylism i.e. overgrowth
of fingers; Congenital contracture of the little finger; Madelung’s deformity i.e. congenital
subluxation of the lower end of the ulna.
Madelung’s deformity.— This is congenital subluxation or dislocation of the inferior
radioulnar joint. This deformity usually consists of (i) relatively short radius, (ii) resultant radial
deviation of the hand, (iii) with prominence of the head of the ulna and (iv) with sometimes
contracture of the little finger.
Club hand.— In this condition the radius becomes absent so that the wrist and hand are
deviated laterally.
Congenital contracture of the little finger — is commonly seen during early childhood.
It is frequently bilateral. In many ways it mimics Dupuytren's contracture, but absence of
thickening of the palmar fascia is the pathognomonic feature of this condition. Moreover the
.ring finger is rarely involved. The pathology is the contracture of the soft tissue.
B. ACQUIRED DEFORMITIES
Dupuytren’s contracture.— It is a localized thickening and shortening of usually
the palmar fascia and rarely the plantar fascia. The fascia is thickened to form nodules and it
contracts so that eventually the affected fingers are drawn into flexion.
THE HAND 361
AETIOLOGY.—
(i) The cause of Dupuytren's contracture is not known definitely.
(ii) It is known to be familial. This curious disorder is of autosomal dominant inheritance.
(iii) It is believed to be due to repeated trauma to the palm, which has been seriously
questioned. That it is often bilateral and may involve even the feet speaks against traumatic origin.
(iv) It occurs in association with epilepsy, alcoholic cirrhosis, pulmonary tuberculosis and
also diabetes.
(v) This condition is occasionally associated with Peyronie's disease of the penis.
PATHOLOGY.— Usually the disease starts near the base of the little finger and later on it
involves the base of the ring finger. Less often the middle and index fingers may be involved.
A fibrous plaque develops at this region of the palmar fascia. Histologically such plaque contains
tom collagen fibres and altered blood pigments. As the palmar fascia gradually thickens and
shrinks, its distal prolongations pull the fingers into flexion. The distal prolongations of the
palmar fascia are attached to the sides of the proximal and middle phalanx. From the palmar
fascia there are some superficial attachments to the skin of the palm, which also shrink to pucker
the palmar skin. In long standing cases, nodules can be palpated in the palmar fascia and gradually
permanent changes take place in the metacarpophalangeal and proximal interphalangeal joints,
so that the fingers cannot be made straight.
History.—
Age and Sex.— Dupuytren's contracture usually begins in middle age, progresses so slowly
that many patients do not present until old age. Men are affected 10 times more than women.
Symptoms.—
(i) In the early
stage the patient may
complain of pain on
grasping. Later on the
condition becomes
painless and the
deformity increases.
(ii) The patient
notices that he cannot
fully extend the
metacarpo-phalangeal
joints of the ring and
little fingers.
(iii) G r a d u a l l y
when the contraction of
the palmar fascia
becomes severe the
fingers are pulled
down into the palm of
the hand and become
useless.
(iv) The patient Fig.20.9.— Shows a typical case of Dupuytren’s contracture of the left hand,
tifHilo rinht ic nni+o nnrmal
may notice thickening in the tissues in the palm near the base of the ring or the little finger —
may be years before contracture develops. The nodule gradually enlarges and spreads strands
of contracting fascia which become prominent.
(v) Dupuytren's contracture is commonly bilateral and may also occur in the foot.
(vi) Family history.— This condition is familial and often runs in families.
Local examinations.— Palpation of the palm of the hand reveals firm, irregular shaped nodule
with indistinct edges, proximal to the base of the ring or little finger. The contracted strands
can be felt running from the nodule to the base of the ring and little fingers. These also spread
to the centre of the flexor retinaculum proximally. These bands get tighter and more prominent
if the fingers are extended.
The skin of the palm is puckered and creased. It is tethered to the underlying nodule.
The metacarpo-phalangeal joint and the proximal interphalangeal joints are flexed, as the
palmar fascia extends distally to be attached to both sides of the proximal and middle phalanges. The
distal interphalangeal joint is never flexed, on the contrary may be hyperextended.
Flexion deformity of the fingers is not lessened by flexion of the wrist joint (cf. Volkmann's ischaemic
contracture).
There may be thickening of the subcutaneous tissue on the dorsum of the proximal
interphalangeal joints of the affected fingers. These are known as Garrod's pads.
TREATMENT.—
(i) In early cases this condition may be treated by night splintage and gentle stretching.
(ii) Established condition of Dupuytren's contracture requires operation. The following
operations may be performed according to the severity of the case :—
Fasciotomy.— In this procedure the taut fascia is divided with a tenotome, which is inserted
horizontally. The skin is carefully separated from the fascia and the contracted bands are divided.
This procedure is repeated in other places of the fascia using separate points of entry till all the
contracted bands are divided. This operation can only be performed in early cases. A few
surgeons claim good results.
Fasciectomy.— In this operation an incision is made on the distal palmar crease. The palmar
fascia is carefully dissected free. The contracted portion of the fascia is excised. If necessary a Z-
shaped incision is made over the proximal phalanx to excise the prolongation of the palmar
fascia in the proximal and middle phalanges.
After any operation a removable splint is used to maintain the corrected position. This
splint is continuously used except during daily wax baths and exercises. After 6 weeks this
splint is only used at night for further 6 months.
Amputation — may only be advised when the little finger is severely affected and the joint
capsules are so secondarily contracted that it cannot be straightened even after fasciectomy.
STENOSING TENOVAGINITIS
De Quervaln’s Disease.—
De Quervain first described this condition in 1895. In this condition the fibrous sheath
containing extensor pollicis brevis and abductor pollicis longus tendons becomes fibrosed and
thickened, so that the intrathecal lumen becomes narrowed. It occurs at a point about IV2 inches
or 3.25 cm above the tip of the radial styloid process. It is on the lateral aspect of the lower end
of the radius where the tendons lie in shallow bony groove.
THE HAND 363
AETIOLOGY AND PATHOLOGY.—

(i) It usually occurs in individuals who use their thumbs to a great deal. The cause is
friction between the tendon sheath against the bone which leads to thickening and stenosing of
the tendon sheath.
(ii) A blow to the tendon sheath or tendons against the bone has also been incriminated
to cause this pathology. This leads to oedema of the tendon sheath and ultimately fibrosis.
(iii) Degenerative changes of the fibrous sheath and tendons have also been incriminated
to cause this condition.
CLINICAL FEATURES.— The patients are usually middle aged individuals between 40
and 50 years of age. This condition is more often seen in women.
Main symptom is pain on the radial side of the wrist particularly following actions like
wringing cloths. There is also weakness of the grip and weakness of the thumb. Pain becomes
aggravated by abduction and extension of the thumb. In course of weeks pain becomes so severe
that the wrist is almost disabled.
On examination, a visible swelling may be seen just above the radial styloid process. The
swelling is better felt than seen. There is also tenderness on the swelling. The swelling is a
cartilaginous-like thickening. Crepitus on movement can be elicited. If the thumb is passively
adducted across the palm, pain is complained of. Similarly pain becomes severe when the patient
extends the thumb against resistance.
TREATMENT.—
Conservative treatment in early stage by immobilizing the tendon with a plaster case including
the forearm, hand and thumb upto the distal crease — often gives relief in 70% of cases. Injection
of hydrocortisone and xylocaine or novocaine to the thickened sheath is also effective.
Operative treatment is imperative for cure in established case of this condition. The skin and
the deep fascia are divided longitudinally. The branches of the radial nerve are carefully
preserved. The fibrous sheath is then slit open. A portion of the tendon sheath may be removed
if required. The sheath is kept open. The deep fascia and skin are sutured.
Trigger Finger.—
This is a condition of stenosing tenovaginitis of flexor tendons. In this condition there is
obstacle to voluntary flexion or extension of the finger. When the finger is extended, it is difficult
to do so, but when the obstructed portion is crossed, the finger suddenly straightens with a
snap, hence it is called 'Trigger finger'.
AETIOLOGY AND PATHOLOGY.— A small thickening is found on the flexor tendon where
it passes beneath the pulley in front of the metacarpophalangeal joint. A portion of the sheath
in the region of the pulley may be thickened or constricted pressing upon the tendon causing
an enlargement of the tendon on each side of the constriction. Rheumatoid tenosynovitis is one
of the causes of this condition.
CLINICAL FEATURES.— This condition is seen more often in adults, though children are
also affected.
In adults the middle finger or the ring finger is most commonly affected. The first complaint
is that the affected finger refuses to be clenched when the other fingers are clenched easily.
Similarly when the fingers are made straight, the affected finger remains bent. As if the tendon
is getting arrested at a particular point. If the finger is passively moved passed this position, the
finger jerks with an audible snap. In case of straightening such snap is almost like the trigger of
a gun hence it is called Trigger finger'.
On careful examination a tendon nodule can be felt on the affected finger in front of the
metacarpophalangeal joint.
In children the thumb is often affected. Even both thumbs may be affected. The condition
is a stenosing tenovaginitis of the flexor pollicis longus. A palpable nodule or thickening may
be felt in front of the metacarpophalangeal joint.
TREATMENT.—
Conservative treatment.— Injection of hydrocortisone into the tendon sheath may relieve the
condition, but complete cure is only possible by operation.
Operative treatment.— Through a short transverse skin incision on the palmar surface opposite
the metacarpophalangeal joint, the affected fibrous sheath is exposed. The fibrous sheath is incised
longitudinally, so that the flexor tendon moves freely. Care must be taken to avoid injury to the
digital nerve. This operation can be performed at about the age of 1 year.
Mallet Finger.—
This results from injury to the extensor tendon of the terminal phalanx. It usually occurs if
the finger tip is forcibly bent during active extension of the other joints of the finger and the
extensor muscle is in full command, e.g. while making a bed or catching a ball.
PATHOLOGY.— Mallet finger occurs
when the terminal slip of the extensor tendon
to the distal phalanx is avulsed or it has pulled
off a fragment of bone (its insertion) from the
dorsal aspect of the base of the distal phalanx.
CLINICAL FEATURES.— The peculiar
deformity is obvious. The terminal joint of the
finger is kept flexed. The patient fails to extend
the terminal phalanx. Passive extension is
possible, but when it is released the terminal
phalanx falls back into flexed position under
the influence of the long flexor tendon.
TREATMENT.— If radiologically, there
Fig.20.10.— Mallet finger. The terminal slip of the is no fracture, the injury should be treated
extensor tendon to the distal phalanx is avulsed. by a splint in which the terminal phalanx is
held in full extension (hyperextended) for 6
weeks. The splint used is either Oatley splint or mallet finger splint, which leaves the proximal
joints free to move. Most tendons unite by this time and the patient regains active extension.
Occasionally slight deformity may persist, though active extension is possible. This should be
accepted, as gradually it may improve and if operation (suturing of the tendon) is performed at
this stage it may stiffen the distal interphalangeal joint.
If X-ray reveals that there is a fracture, the treatment is operation and the fractured fragment
should be sutured back into place.
Mallet Thumb .— This resembles mallet finger. The extensor pollicis longus may be cut
anywhere or it may rupture at the wrist in rheumatoid arthritis or it may rupture following
fracture of the lower end of the radius.
TREATMENT is always operation. Only when it is a clean cut, primary suturing may be
possible. In majority of cases the tendon ruptures and ends are frayed. It is better to suture the
cut distal end to another tendon e.g. extensor indicis propius, extensor pollicis brevis or extensor
THE HAND 365
carpi radialis longus.

Carpal-Tunnel Syndrome.—
This is a condition in which the median nerve is compressed at the wrist as it passes through
the carpal tunnel — the space between the carpal bones posteriorly and the flexor retinaculum
anteriorly. In the normal carpal tunnel there is exactly room for the flexor tendons and the
median nerve, so any swelling here is likely to result in compression of the nerve.
CAUSES.— The compression can be caused by skeletal abnormalities, swelling of other tissues
within the tunnel or thickness of the retinaculum. The syndrome is however common in (i)
menopausal women, (ii) in rheumatoid arthritis and (iii) in pregnancy. This condition may occur
in (iv) osteoarthritis and even with (v) myxoedema. (vi) Malunited Colles' fracture may occasionally
cause this condition. In rheumatoid arthritis there may be chronic inflammatory thickening of the
tendon sheaths with increase in the bulk, (vii) In some cases cause remains unknown, these cases
may be due to stenosing tenovaginitis due to affection of the flexor retinaculum.
SYMPTOMS.— Age and Sex.— As mentioned earlier this condition is particularly common
in middle-aged women at the menopause. It is about 8 times more common in women. If it
occurs in younger patient, the cause may be rheumatoid disease, pregnancy or tenosynovitis.
(i) Pins and needles in the fingers particularly the index and the middle fingers and
sometimes thumb, is the common presenting symptom. It must be remembered that the little
finger should never be affected as it is supplied by the ulnar nerve.
(ii) Pain and paraesthesia occur in the distribution of the median nerve. Such pain is usually
worse at night and it wakes the patient up at night with burning pain, tingling and numbness.
The fingers may feel swollen. Hanging the arm over the side of the bed or getting up or walking
about may relieve pain. This pain radiates up along the forearm upto the arm. The fingers may
feel stiff, particularly in the morning, may be due to compression of the flexor tendons.
(iii) Loss of function.— As the compression increases, neurological symptoms appear with
paraesthesia and numbness. Patient notices that she cannot do delicate movements and often
drops small articles. Patient also feels inco-ordination of the fingers. There is actually no loss of
muscle power, but there is loss of fine discriminatory sensation. Ultimately there may be some
loss of motor function of the muscles of the thenar eminence and of the first two lumbricals.
SIGNS.—
(i) Examination of the hand is often negative. Slight tenderness over the carpal-tunnel
may be elicited.
(ii) If the fingers and wrists are held fully flexed for a few moments, an increase in pain
is noticed.
(iii) By the above procedure one can also assess the pattern of sensory changes.
(iv) The patient is often not sure of the precise distribution of paraesthesia. Light touch
sensitivity and two-point discrimination may be reduced in the skin innervated by the median
nerve.
(v) In late cases there may be wasting of the thenar muscles with altered sensation of
the median nerve area.
(vi) Movements.— All movements of the joints of the hand, active and passive, are normal.
Only abduction and opposition of the thumb may be weak.
SPECIAL INVESTIGATIONS.— Electromyography and conduction studies on the median nerve
confirm the diagnosis. The latter demonstrates delay at the carpal-tunnel.
TREATMENT.—
Conservative treatment.— This consists of —
(i) Injecting hydrocortisone into the flexor sheaths at the carpal-tunnel.
(ii) Wearing a cock-up splint etc.
In majority of cases conservative treatment fails and surgery is the treatment of choice.
Operation.— The best treatment is longitudinal division of the flexor retinaculum. This relieves
the patient immediately. Neurological deficit may take time to recover or may not recover fully.
In case of rheumatoid tenosynovitis additional synovectomy may be required.
Volkman’s ischaemic contracture — is due to vascular injury which results in muscular
infarction and subsequent contracture. In the stage of ischaemia the signs like pain, pallor, puffiness
(oedema), pulselessness and paralysis (five 'p's) will be seen. Pain on passive extension of the
fingers is probably the first sign to appear. The radial pulse is constantly absent and the skin
temperature of the affected hand will definitely be lower than its healthy counterpart. In the stage
of contracture the fingers become flexed but they can be, at least partially, extended when the
wrist is flexed (cf. Dupuytren's contracture in which the affected finger can never be extended).
Burns contracture can be diagnosed easily by history itself.
Attrition rupture of the extensor pollicis longus is also a condition most commonly
seen in middle-aged women. This is usually due to rheumatoid arthritis or occasionally may
complicate a Colles' fracture. While working with the thumb suddenly the patient experiences
a snap and the thumb falls adducted helplessly and the patient fails to extend the terminal
interphalangeal joint of the thumb. Treatment is mentioned above in 'Mallet Thumb'.
C. SWELLINGS OF THE HAND

1. Implantation dermoid.— Implantation dermoid is caused by prick by different
pointed objects such as needle, bone of a fish etc. The epithelium of the skin is driven in and
causes such condition. A soft cystic swelling is found mostly in the finger and occasionally in
the hand which is neither attached to the skin nor to the deeper structures. Fluctuation can be
elicited.
2. Ganglion.— Ganglion is a localized, tense cystic swelling in connection with the
joint capsule or tendon sheath. It contains clear gelatinous fluid.
AETIOLOGY.— The aetiology is yet to be known.
Myxoid degeneration of fibrous tissue of capsule, ligaments and retinaculae has been
suggested. This is sometimes initiated or excited by injury.
According to some, ganglion arises from small bursa within the substance of the joint capsule
or the fibrous tendon sheath. This bursa becomes distended possibly following trauma giving
rise to a ganglion.
Synovial herniation as the probable cause of ganglion has been rejected.
PATHOLOGY.— Ganglion is a cystic swelling containing clear gelatinous fluid or viscous
fluid. It is surrounded by fibrous capsule and it possesses small pseudopodia.
SITES.—
1. The commonest site is on the dorsum of the wrist. Other probable sites are : 2. Front of
the wrist, when it may compress a nerve causing numbness or weakness. 3. The dorsum of the
foot. 4. The palmar aspect of the hand. 5. The flexor aspect of the fingers, where small ganglions
may develop.
THE HAND 367
The tendons on the dorsum of the wrist from lateral to

medial are —
(i) Abductor pollicis longus. \ Surrounded
r' ' ° f by a common
(ii) Extensor pollicis brevis. J sheath.
(iii) Extensor carpi radialis longus. 1 Surrounded
(iv) Extensor carpi radialis brevis. J sheath”111111011
(v) Extensor pollicis longus.
(vi) Extensor indicis.
(vii) Extensor digitorum.
(viii) Extensor digiti minimi.
(ix) Extensor carpi ulnaris.
CLINICAL FEATURES.— The patient often is a young
adult.
The most common presenting symptom is painless
lump. Occasionally there may be considerable pain, which
is often seen in case of ganglion on the flexor aspect of the
finger.
On examination, the lump is well defined, cystic swelling,
but it is often felt firm or even hard (as the cyst is very
tense). Mobility is not much, though it can be moved with _ _
great difficulty sideways. It is immobile along the axis of the
tendon. When it arises from the fibrous sheath of a tendon, Fig.20.11. Implantation dermoid
the swelling becomes fixed as the tendon is made taut. cyst ând.
TREATMENT.—
Conservative treatment.— (i) A strike on the cyst will cause rupture of the cyst with apparent
belief of cure (previously it was done with the holy ________________________________________
Bible in the West). But with this treatment recurrence
is common.
(ii) Aspiration of the cyst and injection of
sclerosing solution (3% sodium murrhuate or 5%
phenol in almond oil) or hydrocortisone is another
well known treatment of this condition. This
injection may be repeated followed by crepe
bandaging. This has also not succeeded to claim cure
in majority of the cases.
Operative treatment.— Complete excision of the
ganglion is the best treatment. This is usually done
by using a tourniquet. The ganglion is removed
completely. Care must be taken to remove all the Fig.20.12.— Ganglion on volar aspect of
pseudopodia and the fibrous layer from which they the wrist. (Courtesy Dr. Yogesh Salphale)
arise.
The excised specimen should be sent for biopsy as very occasionally there may be some
neoplastic change, particularly synovioma.
3. Glomus tumour.— See Chapter 10 'Common Tumours and Miscellaneous Lesions of
the Skin'.
4. Compound palmar ganglion.— Chronic inflammation sometimes distends the

common sheath of the flexor tendons in front of the wrist both above and below the flexor
retinaculum. This is known as compound palmar ganglion.
Pathology.— The common causes are tuberculosis and rheumatoid arthritis. The ulnar bursa
which covers the flexor tendons of the fingers are usually affected. It is so named, as there are two
swellings — one above the flexor retinaculum and
the other below the flexor retinaculum almost in
the hollow of the palm. The synovial membrane,
which is involved, becomes thick and villous. The
amount of fluid is increased and it may contain
fibrin particles in the shape of 'melon seeds'. The
lining membrane contains granulation tissue. The
tendons eventually become fray and may rupture.
(i) Almost all the patients are below 40
years of age.
(ii) Pain is unusual.
(iii) There may be paraesthesia due to
median nerve compression.
(iv) The swelling is an hour-glass swelling
on inspection.
(v) On palpation it is neither warm nor
tender. Fluid from one part can be pushed to the
other part (known as cross-fluctuation). (See Fig.
21.1 in the author's 'A Text Book On Surgical
Short Cases'). The swelling is cystic with
fluctuation test positive. Transillumination test is
negative. There may be wasting of the muscles of
the hand and fingers. Occasionally cold abscess
may result.
Treatment.— If the condition is tuberculous,
Fig.20.13. A compound palmar ganglion. antitubercular treatment is started. The wrist is
rested in a splint. The ganglion is aspirated and streptomycin is instilled.
If no improvement is noticed after 3 or 4 months of conservative treatment, the entire flexor
sheath is dissected out with excision of all the diseased synovial membrane.
If the case is rheumatoid disease, the treatment is complete excision of the affected synovial
sheath and ulnar bursa keeping the flexor tendons intact.
INJURIES OF THE HAND AND FINGERS

Evaluation of the injury.— Whenever a case of hand injury comes to the emergency
department, a careful assessment of the injury is highly important. While doing this careful
assessment is made regarding —
(i) Arteries.— If there is any arterial injury which artery is injured and how much is the
severity of haemorrhage. The state of blood supply to the finger distal to the arterial injury
should be noted.
THE HAND 369
(ii) Nerves.— This is highly important to know if there is any nerve injury and if so
which nerve is injured and what is the type of injury i.e. neurapraxia, axonotmesis or neurotmesis.
(iii) Tendons and their sheaths.— Sometimes only tendon sheath may be lacerated without
injury to the contained tendon. This may not be clinically detected unless the wound is explored.
Tendon injury however is clinically detectable by active movement.
(iv) Bones.— Presence and extent of bony injury should be detected clinically and
radiologically.
(v) Joints.— Injury to any joint of the hand and fingers should be ascertained clinically
and radiologically.
Principles of treatment.— Injuries of the hand and fingers should be considered with
due respect since this portion of the limb is most vital and if activity of hand is lost, the patient
may loose his earning. So all injuries of hand and fingers should be admitted to the hospital
except very trivial injuries, which can be treated in outpatient department or emergency.
Operation should be performed under anaesthesia and only injuries of the distal 2/3rd of
the finger can be treated under local anaesthesia of digital block. Injuries proximal to these are
treated under general anaesthesia.
These cases should always be operated on in the operation theatre under strict asepsis.
Tourniquet.— Tourniquet is essential in hand surgery. It offers a bloodless field which gives
better view to the nerve and tendon injuries. Moreover it prevents a bloody field in which it is
difficult to operate. The maximum safe time for a tourniquet is V/i hours and recording of time
is essential at the time of application of tourniquet.
Cleaning of the wound.— Injuries of the hands and fingers are almost always contaminated
to certain degree and they should be cleaned properly before operation is started. First of all a
sterile piece of gauze is used to cover the wound surface and the surrounding skin is thoroughly
cleaned with soap and water. Ether soap may be used to clean the greasy material and a brush
or a piece of gauze may be used to clean the dirt. Cetavlon is next used as an antiseptic solution
in the surrounding skin. After the surrounding skin has been well cleaned, the piece of gauze
covering the wound is removed and the wound itself is cleaned with soap-water solution,
cetavlon and hydrogen-peroxide.
The hand is well draped and kept on a hand-rest with a proper mould to keep the fingers
stretched to facilitate subsequent operation.
Excision of the wound or debridement.— The exact aim behind this operation has already been
discussed in the 'treatment of open fractures'. Any ragged skin, subcutaneous tissue and fascial
margins are excised. Any contamination, dirt or non-viable tissues should be removed. After
this, the wound will look healthier and may bleed from a few points, which should be secured
and ligated with fine catgut.
If the excision has to be extended for a wider exposure and better excision of the wound, it
should be extended along the 'principle of incision', described below.
Principles of incisions.— In a finger, the incision should be made transversely either on the
palmar or on the dorsal surface. An attempt should always be made to put the incision on the
crease line.
In the palm, again transverse incisions are ideal and they should be placed on the flexion
creases. If a longitudinal incision is at all required, it should be made oblique along the perithenar
crease or it may be placed on relatively immobile hypothenar eminence.
Closure of the wound.— When the wound is less than 6 hours old and is relatively clean,
24
primary suture is permissible if the wound margins yield themselves to apposition without any
tension whatsoever. If the wound is more than 6 hours old or it is quite contaminated or the
skin margins cannot be apposed without tension, it is better to leave the wound open. The
wound should then be covered with penicillin tulle or sofratulle and kept pressed with roller
gauze, cotton and bandage in 'optimum position'. If after a few days, the wound seems to be
healtheir and the skin margins can be apposed properly without tension, a 'delayed primary
suture' is advised.
Some complicated injuries of the hand and Jlngers.—
(!) Bursi linger.— This is the result of a compression injury, which will burst the skin
open leaving the tendons, bones and joints exposed. As there is too much oedematous swelling
of the subcutaneous tissue and soft tissues of the finger, it is usually impossible to close the
wound without tension. What should be done is to apply loose stitches one or two at the margins
of the wound and to apply pressure bandage to keep the wound edges approximated. This will
only cover the tendons and bones and so minimises infection therein.
(2) Wounds with rained skin flaps.— In these cases, one has to assess about the viability
of the flap. If the flap is viable, it should be secured in position with fine stitches with a very
tiny drain just beneath the flap to prevent haematoma formation. A pressure bandage is applied.
Care must be taken not to produce any tension during suturing of the flap as this will inevitably
lead to necrosis of the flap.
When the viability of the skin flap is in doubt, the subcutaneous tissue of the flap should
be removed and the flap is kept in position with fine sutures. The flap now acts as a whole
thickness free skin graft. But this technique is not at all risk-free since necrosis of the flap will
lead to infection of the wound which will cause disaster. So it is better to excise the doubtful
flap and to deal with the skin loss as will be described in the next section.
(3) Wounds with skin loss.— The principle, which should be followed in these types of
wound, is that the loss of skin should immediately be made good by skin grafting as this will
prevent infection of the tendons and joints, which might have been exposed.
Full-thickness skin graft is ideal for replacing skin on the palmar aspect of the finger and
the palm. Partial-thickness skin graft cannot be a very satisfactory permanent skin replacement
on palmar aspects of the fingers and the hand as it does not possess wearing qualities, but it
may be used as temporary measure for closure of the wound which will be replaced later on by
full-thickness skin graft.
Two methods of full-thickness skin graft have been tried — the free graft and the pedicle
graft. While the 'free graft' has the advantage that it can be performed in a single operation,
but its main disadvantage is that the chance of 'take' is certainly less. On the other hand, pedicle
graft requires operation in stages, but it enjoys the advantage of better 'take'.
DIFFERENT TYPES OF GRAFT, which can be used to make good skin loss in hand and
fingers, are described below :
FREE GRAFT.— Full-thickness free graft is often taken from the skin behind the ear as
this part of the skin has got good sensory appreciation and is hairless. The graft is secured with
fine silk sutures with the margin of the wound. A pressure bandage is applied. The wound
behind the ear is now closed by slightly undermining the skin margins. As has already been
discussed, the question of taking is a problem of this graft. Yet the graft from the skin behind
the ear, because of its rich sub-dermal vascular plexus 'takes' much better than the other free
skin grafts.
THE HAND 371
ROTATION FLAP— Sometimes small wounds on the palmar or dorsal surface of the finger
or hand, exposing the tendons, can be made good by rotational flap taken from the lateral
surface of the finger or from the skin over the hypothenar eminence of the palm.
PEDICLE GRAFT.— So far as 'take' is concerned, these grafts are by far better than the
free graft. Pedicle graft can be taken from various places such as :—
Cross finger flap, which means that the wound of one finger is made good by transfer of a
pedicle flap from the side of another finger. The flap should be planned properly, so that the
flap can be placed on the wound of the affected finger without tension and two fingers concerned
will be kept immobilized for the period until a successful 'take' is assured. The denuded area of
the finger from which the flap has been taken is covered with a split-skin graft. Thenar flap is a
satisfactory method of pedicle graft, particularly for skin loss at the finger tip. A small flap is
taken from the skin of the thenar eminence with the base attached proximally and this flap is
fixed to the tip of the finger, which will require skin graft. For this the finger should be kept
immobilized in a splint, until the 'take' is assured. The denuded area of the thenar eminence is
closed by undermining the skin margins and suturing.
Pedicle graft from the thigh or abdomen is required, when the skin loss of the hand or finger is
too much. In the thigh, actually a bridge graft is applied on the denuded area of the palm. The
hand is immobilized in that position until the 'take' is assured. In abdomen, the pedicle is taken
from the abdominal wall and the hand is immobilized with the abdomen till the 'take' is complete.
(4) Wounds with division of the tendons.— Many injuries of the hand and fingers are
associated with division of tendons. It is always advisable to ascertain in the first opportunity
the tendons, which have been divided, by clinical examination. Sometimes clinical examination
may not give a definite indication about the tendon injury due to the severity of the injury and
inability of the patient to move the fingers inspite of no tendon injury.
The principle of repair of the tendons differs according to whether they are flexor tendons
or extensor tendons. Simply because of the fact that flexor tendons are enclosed within fibro-
osseous compartments in two places (a) at the carpal tunnel and (b) in front of the phalanges,
these flexor tendons require more expert supervision. Whereas extensor tendons, being
surrounded by only paratenon, pose no difficult problems of repair.
FLEXOR TENDONS.— For successful repair strict asepsis must be maintained, (a) If only
the wound is very recent, clean cut and uncontaminated, (b) when the facilities in the operation
theatre are adequate and (c) when the surgeon's competence is beyond doubt, primary repair
may be ventured. Otherwise debridement of the wound aiming at healing by first intention
should be the motto and tendon repair is carried out at a later date i.e. 'secondary repair'. At
this time the two ends of the tendon may be brought together loosely with a black silk suture,
so that at the time of secondary repair much time will not be wasted in finding out the proximal
end of the cut tendon.
The principles are laid as follows :—
(i) When the profundus tendon is cut within Vi inch (1 cm) of its insertion i.e. beyond
the limit of the flexor tendon sheath, repair by direct suture is indicated.
(ii) If the profundus tendon is divided just beyond the level where it emerges between
the two slips of the superficialis tendon, it is left alone. Attempt at repair may interfere with the
function of the intact superficialis tendon. The loss of flexion at the terminal interphalangeal
joint is not very serious disability and can be partially made good by arthrodesis of the distal
joint in semi-flexion position.
(iii) When both the superficialis and profundus tendons are divided within the tendon
sheath, the superficialis tendon is sacrificed to get the full function of the more important
profundus tendon which is then repaired. The whole of the distal segment and the proximal
segment of the superficialis tendon to a level well above the wound are excised. The profundus
tendon is always repaired as a secondary procedure at a later date. Free tendon graft extending
from the middle of the palm to its insertion into the terminal phalanx should be contemplated
and direct suture should be avoided as it may lead to subsequent restriction of movement within
the fibrous sheath. The fibrous sheath must not be sutured, rather it may be split open by a
lateral incision so that it may not constrict the tendon during healing.
(iv) Controversy still exists in case of flexor pollicis longus tendon. As the room within
the fibro-osseous canal is more than that of the flexor tendons of the fingers, some surgeons
prefer to repair by direct suture. According to others free tendon graft, as done in the case of
other fingers, is probably better and will yield better function of the thumb.
(v) If the flexor digitorum superficialis tendons are only cut repair is not required, since
this may hinder a good movement of the more important profundus tendon.
(vi) At the wrist and forearm the severed flexor tendons are usually repaired by direct
suture — either primary or secondary. When both superficialis and profundus tendons are cut
the former is excised proximally and distally well beyond the wound margins and the profundus
tendons are repaired as usual. When the repair is done within or near the carpal tunnel, the
flexor retinaculum is left unsutured.
EXTENSOR TENDONS.— Divided extensor tendons are generally repaired by direct suture
— primary or secondary. Fine silk is better than wire as suture material. When the extensor
tendon is divided posterior to the finger joints, capsule of the joint may be cut as the tendon
here expands and forms a part of the capsule. In this case primary repair is advised after
thorough cleaning.
Postoperative treatment.— After tendon repair, the fingers and the wrist are kept in
such a position as the tendon, which has been repaired, remains relaxed. For this, in case of
flexor tendon, a plaster of Paris cast is placed on the extensor surface of the forearm, wrist and
fingers so that the fingers and the wrist are in flexed position. A cotton wool and a gauze ball
should be placed in the palm so that the fingers can be flexed slightly. In case of extensor
tendon, a plaster cast or a splint may be used to keep the wrist and the fingers extended. Slight
active use of the fingers should be started, this will prevent adhesion formation and will keep
the joints mobile. Immobilization should be continued for at least 6 weeks.
(5) Wounds with division of nerves.— Very often the wounds of the hands and fingers
are associated with nerve injuries. In these cases also injuries of nerves may not be assessed
properly even by careful clinical examination. Proper wound exploration is therefore required
to know definitely which nerve has been severed.
As a rule, in case of clean cut wound with least contamination and when the wound is less
than 6 hours old, one may proceed to suture the nerve. When the wound is not very clean-cut,
contaminated and is more than 6 hours old, it is always preferable to leave the nerve suture at
the primary stage and should be done as secondary suture 3 weeks later after proper wound
healing. If the wound is slightly contaminated, it is better to have the nerve suturing as primary
procedure. The digital nerves can be exempted from this rule as being entirely sensory nerves.
Whenever possible primary suture should be attempted.
THE FOOT
RARE CONGENITAL DEFORMITIES. -

There may be supernumerary toes, absence of toes, bifid foot, overlapping 5th toe elc. These are
often associated with congenital deformities of the fingers.
SWELLINGS.— Corns and callosities occur at the sites of intermittent pressure. A corn
consists of a conical wedge of highly compressed keratotic epithelial cells. This occurs over a very
limited area and impinges on the nerve endings. This gives rise to pain. A callosity on the other
hand is distributed over a comparatively large area. This is nothing but a greatly thickened and
cornified skin which ceases at the periphery where it is being continued with the normal skin.
A soft com occurs where the skin is macerated between the toes. This is commonly seen
in the cleft between the 4th and 5th toes where the soft skin is subjected to pressure between
the bases of the proximal phalanges.
Plantar wart is commonly seen on the weight-bearing portion of the sole. These warts are
dark and exquisitely tender. These differentiate this condition from com or callosity. When seen
through magnifying glass, one may find red or black spots which are haemorrhages from
attenuated fronds of the submerged papillomas.
A ganglion is more or less similar to that found in the hand and wrist.
A bursa superficial to the tendo Achillis may be enlarged due to inflammation.
Swelling of the ankle joint may be due to effusion in the joint.
Other causes of swellings of the foot are the tumours affecting the foot. Of the tumours the
commonest is malignant melanoma followed by squamous cell carcinoma. Malignant melanoma
occurs mainly on the medial aspect of the sole where the skin is relatively soft. The swelling is
asymptomatic in the beginning. Pigmentation and ulceration are the usual features. Regional
lymph nodes are always enlarged and occasionally the liver may be involved by metastasis.
Squamous cell carcinoma on the other hand affects the weight-bearing areas of the forefoot
where the skin is relatively hard. Due to pressure of the weight the tendons and bones are soon
infiltrated and the tumours become fixed to the deeper structures.
ULCERS.— Ulcers of the foot are more often seen in tropical countries and are caused by
various infective agents. Of these tuberculosis is by far the commonest. Besides these infective
ulcers, one may come across perforating ulcers in denervated sole. These are mainly situated
on the weight-bearing zones, such as ball of the great or little toe or heel. These ulcers are
usually surrounded by indurated skin and the ulcers tend to perforate right up to the bone
justifying its nomenclature. Ulcers may develop from ingrowing toe-nail and subungual
exostosis due to repeated friction of the skin against the nail or the bony exostosis. The surface
becomes granulating.
Madura Foot (Mycetoma Pedis).—
It was first identified in Madura, Tamilnadu in India by Gill. It is a chronic granulomatous
condition with multiple discharging sinuses in the foot.
Organisms responsible are — mainly Nocardia Madurae followed by Nocardia brasiliensis,

Nocardia asteroides and Actinomyces israelii. These are filamentous organisms similar to
actinomycosis.
Pat hologv.— •
Organisms enter the foot who walk bare footed through abrasions or cuts of the foot. These
organisms enter the deeper plane and starts granulomatous inflammation. Gradually painless,
pale, firm nodules are formed which gradually become vesicles which in turn ultimately burst
to form discharging sinuses.
Granules are discharged from the sinuses, which may be red, yellow and black. In red and
yellow types deeper tissues including bones are involved causing necrosing osteomyelitis. Tendons
and nerve tissues are resistant to invasion. In black type the infection mainly remains
subcutaneous, though deeper tissues e.g. muscles, tendons and nerves may be involved.
It must be remembered that the regional lymph nodes are not involved until and unless
secondary infection takes place.
• Patients are mainly from South India or Africa.
• They present with painless swollen foot. When hand is involved it is called Madura
hand.
• Gradually multiple discharging sinuses develop.
• Regional lymph nodes usually do not enlarge unless there is secondary infection.
Differential Diagnosis.—
• Tuberculous foot.
• Chronic osteomyelitis.
• Actinomycosis.
Investigations.—
• Discharge granules should be examined under microscopic which reveal filamentous
organisms.
• Culture is performed in Saboumond's dextrose Agar medium.
• Actinomycosis granules show sun-ray appearance with gram-positive centre and gram-
negative clubs.
Management.—
• Rest and elevation of foot with antibiotics.
• A long course of Dapsone in the dose of 100 mg bd improves this condition in majority
of cases. It should be accompanied by broad spectrum antibiotics to deal with secondary infection,
if any. Amphotericin is also a specific antifungal drug.
• Long term penicillin has been tried.
• Specific drug is antifungal drug — amphotericin, dapsone.
• Non-specific drug like iodide may be tried.
• In severe cases amputation may be required.
The other rare cause of ulcer in the foot is Kaposi’s sarcoma. This is commonly seen in
the Jews, Italian and Eastern Europeans. Males in the middle of their lives are more susceptible
to this condition. Multiple, painless, plum-coloured nodules particularly affecting the lower
extremities are the characteristic features of this condition. The last but not the least is the
malignant melanoma in the list of causes of ulcer of the foot.
THE FOOT 375
PAIN IN THE FOOT

Pain in the foot can be classified according to the region affected :—
A. Pain in the heel; B. Pain in the mid-foot or C. Pain in the fore-foot.
A. P<iin in the licel.— This can be subdivided into —
(a) Pain within the heel e.g. fracture or disease of the calcaneum (osteomyelitis or tumour
or Paget's disease) and arthritis of the subtaloid joint;
(b) Pain behind the heel e.g. tendo-Achillis bursitis, retrocalcaneum bursitis, apophysitis
of the calcaneum (Sever's disease) and rupture and paratendinitis of the tendo-Achillis;
(c) Pain beneath the heel e.g. infracalcaneum bursitis and plantar fasciitis (Policeman's heel).
Calcanean spur.— This is usually revealed in X-ray and is a bony projection forwards
from undersurface of the calcaneal tuberosity. It is nothing but ossification of the plantar fascia
at its calcaneal end. This has very little significance so far as the pain in the heel is concerned.
That means if a patient complains of pain in the heel and on X-ray one can find the presence of
calcanean spur, the clinician cannot infer that the calcanean spur is the cause of pain. Very often
inflammation of the soft tissue or a bursa beneath the spur gives rise to pain.
B. Pain in the mid-fool.—
A strain on the inferior calcaneonavicular ligament (spring ligament) occurs when the foot flattens
rapidly due to weakness of the short muscles of the sole or after prolonged confinement in the
bed.
Kohler's disease (osteochondritis of the navicular bone) is another cause of the pain in the
mid-foot. The usual victim is the child under 5 years of age. Painful limp with tenderness over
the navicular bone is the diagnostic consideration, the navicular bone becomes dense with altered
shape.
An 'overbone' connecting the dorsal surfaces of the medial cuneiform and the base of the 1st
metatarsal bone gives rise to pain in the mid
foot. A tender and bony lump just proximal
to the base of the 1st metatarsal bone is the
diagnostic feature of this condition.
C. Pain in the fore-fool or
metatarsalgia.—
(a) DISORDERS OF THE FOOT
may give rise to pain in the fore-foot e.g.
splay foot associated with hallux valgus,
curly toes, a claw-foot with claw toes etc.
* (b) DISORDERS OF INDIVIDUAL
TOES e.g. hallux valgus, hallux rigidus,
ingrowing toe nail, hammer toe etc.
Curly toes.— The metatarsophalangeal
joints are hyperextended and the toe joints
are flexed. Several toes are generally
affected. The condition is often bilateral and
may be associated with pes cavus
deformity. A positive family history is often
j•Liu■ ji
on 3 „ , Fig.21.1.— While the right foot is normal, the left foot is
elicited. Painful callosities may develop ., , , , ,
, affected with claw foot and daw toes,
the dorsum of the toes.
(c) SPECIAL VARIETIES OF METATARSALGIA : This includes (i) Freiberg's disease.—

This is nothing but crushing type of osteochondritis affecting the head of the 2nd or 3rd metatarsal
bone. It is generally seen in young adults and girls predominate. A bony lump or irregularity is
palpable which is tender and the affected joint becomes irritable. X-ray shows dense and the
flattened epiphysis; increase in joint space and a thick neck (similar to what is seen in Perthes'
disease).
(ii) Morton's metatarsalgia.— This is a fibroneuroma affecting usually the 3rd digital nerve
just before its division into two branches. Middle-aged women are more often affected. Sharp
intermittent pain shoots into the affected toes. Sensation may be diminished in the adjacent toes.
Localized tenderness can be elicited over the neuroma. Relief is obtained by taking the shoe off
and squeezing or massaging the fore-foot.
(iii) March or stress fracture.— This usually affects the 2nd or 3rd metatarsal bone. It occurs
in young adults after unaccustomed long walk. Swelling and tenderness may be felt on the
dorsum of the affected metatarsal bone. X-ray appearance is at first normal but later on one
may find a fusiform callus around a fine transverse fracture in about 2 to 3 weeks time.
INGROWING TOE NAIL

This means one side of the nail of the toe curls inwards too much deep into the side of the
nail-bed and grows to form a lateral spike. This usually occurs on one side of the nail. It usually
predisposes to painful infection of the over-hanging nail fold. Local suppuration may cause
granulating fleshy mass to appear at the side of the nail. This condition mostly occurs in the
great toe.
CAUSES.—
(i) Excessive sweaty foot; (ii) Using of excessive tight shoes; (iii) Cutting the nail too short
and convexly; (iv) Idiopathic — where no definite cause can be found out and this condition
may be seen in families.
Clinical features.— The side of the nail curls in and digs towards the bone. The skin lateral
to the nail over hangs it which is called overhanging nail fold which becomes infected and
painful. Sometimes granulation tissue can be seen at the edge of the digging nail.
Treatment.—
(i) The foot should be kept clean and dry.
(ii) Tight shoes should be avoided.
(iii) When infection is present, a portion of gauze, soaked in alcohol should be tucked in
at the place of ingrowing toe nail.
(iv) Soframycin ointment should be applied at the ingrowing toe nail.
Conservative treatments cannot cure long standing cases, nor it can cure the idiopathic cases
where the toe nail curls in deep into the nail bed.
OPERATIVE TREATMENT.— This includes radical removal of the affected side of the nail
alongwith the comer of the germinal envelop to prevent recurrence.
A V-shaped wedge including about a third of the breadth of the nail alongwith the nail fold
is excised from the lateral aspect of the toe. An attempt should be made to close the gap with silk
sutures. This operation is not always successful as often spicules of nail grow at the edges irregularly
and give rise to pain. In these cases radical excision of the nail bed should be advised.
THE FOOT 377
Radical excision of the nail bed.— An incision is made to

raise a rectangular flap of nail fold and the nail is extracted.
The proximal one-third of the nail, which corresponds to the
extent of the lunula is completely removed. This part of the
nail bed is responsible for the growth of the nail. The excision
of this part should be radical so much so that the bone will be
exposed. Particular attention should be taken at the angles,
which sometimes may be missed and will be responsible for
regrowth of the nail which may dig in and will cause
recurrence of symptoms. The distal portion of the nail bed is
undermined and the tip of the distal phalanx is sometimes
excised to bring the distal part of the nail bed close to the nail
fold for suturing.
Onychogryphosis.— In this condition there is Fig.21.2.— Shows the method of
overgrowth of the toe nail which becomes crooked and excision of the V-shaped wedge of the
thickened. Usually the big toe is involved. It mostly occurs in nail including its matrix for ingrowing
elderly people. The nail may be so curled as to resemble Ram's toe nail.
horn.
Fig.21.3.— It is a diagrammatic representation of the steps of the operation of radical excision of the nail bed.
Fungus infection or trauma seems to be the cause of this condition.

Treatment.— The nail is cut from the base by a gigli saw. The remaining nail is dealt with
filling regularly so that it does not recur.
If the condition recurs the radical excision of the nail bed as mentioned above should be
considered.
Paronychia.— This is much less common than in fingers. Although it may be seen in great
toes.
Aetiology is mostly (i) an ingrowing nail or (ii) abrasion of the eponychium with contaminated
scissors.
Clinical features are similar to those of paronychia of the finger.
Treatment is also similar to that of paronychia in the finger. Only when there is ingrowing toe
nail, radical excision of the nail bed becomes essential after controlling infection.
INFECTIONS OF FOOT
This can be divided into minor infections and major infections.
Minor infections.- These include ingrowing toe nail, fungal infections, infected blisters
and infected bursitis.
Except ingrowing toe nail, others usually occur in bare footed individuals. Minor bacterial
infections lead to lymphangitis toe and regional lymph nodes enlargement and tenderness. Blood
examination, wound swab, culture and sensitivity should be performed to identify the organisms.
Blood culture may help in certain cases. Imaging and MRI offer an idea about the extent of
tissues involved in infection.
TREATMENT.— Basic principles include rest, elevation and antibiotics. When slough has
formed surgical debridement is necessary with desloughing agents and regular dressing to recover
formation of granulation tissue.
Ingrowing toe nail treatment is different. At first local antibiotic ointment with bandaging
and keeping the part dry may help. If this does not cure the condition wedge resection of the
nail and nail bed should be performed. But when it is recurrent the nail should be removed
with whole of the nail bed (Zadek's operation). Fungal infection of ingrowing toe nail may
cause thickening and distortion of the nail which is called onychogryphosis.
Major infections.- Diabetes is the main cause of major infections. When the infection is
superficial it may lead to ulcer formation. If the infection is deep it may involve the deeper
tissues including muscles, bones (osteomyelitis) and joints (arthritis). With neuropathy sensation
is lost and infection spreads to glucose laden tissue which lead to ulcer formation at the pressure
areas e.g. sole of the foot and under the heads of metatarsals. Arterial blockage further aggravate
the situation.
TREATMENT.— If ulceration is present, deslough the ulcer and excise hyperkeratotic tissues
followed by regular dressing. To make the patient mobile a skin tight POP cast is applied which
is changed weekly.
Deep infection without abscess formation and ulcer, is treated by rest, elevation of foot and
antibiotics. Any abscess formation needs drainage and debridement. Once the ulcer has healed
appropriately insoles and soft soles in the shoes should be used.
If gangrene develops, amputation is the only answer and the level of amputation should be
through properly vascularised tissues for proper wound healing.
Other major infections of foot are tuberculosis, guinea worm infection, osteomyelitis,
arthritis etc.
INFECTION OF THE SPACES OF THE FOOT.— By this we mean pyogenic infection
of the foot and in many respects, it is similar to that of the hand. In the sole, there are the
superficial plantar space and deep plantar space lying superficial and deep to the plantar aponeurosis
respectively.
Infection of the superficial fascial space is mainly seen in (i) the sole of the foot (in
those who walk bare-footed), (ii) the web space, (iii) Interdigital subcutaneous space and (iv)
the heel space.
Infection of the deep fascial space.— There are three deep fascial spaces in the sole —
medial, central and lateral. The medial and lateral spaces are less important and are rarely
infected. The central plantar space is divided into four compartments between five layers of the
muscles. The diagnosis is made by the history of a penetrating injury, pain, tenderness and
THE FOOT 379
swelling. The swelling becomes more prominent on the dorsum even if the pus is situated
under the sole.
Treatment.— Once the abscess has been localized, it should be drained by an incision made
parallel to and just above the medial border of the foot.
Infection of web space.— There are four web spaces in the foot, but infection is more
common in the web space between the great toe and the second toe which is the largest web space.
Clinical features are similar to those of the hand.
Treatment is also similar to those of the hand — that pus should be drained as soon as it
becomes evident in the web space. Transverse incision is often may not be possible and in this
case longitudinal incision may be preferred particularly saving the digital vessels and nerves.
TUBERCULOUS ARTHRITIS OF FOOT

Mostly the subtalar joints are affected. This may spread to the midtarsal joints. So far as the
tarsal bones are concerned, calcaneum is mostly affected.
The disease starts as synovitis or as an osteomyelitis. Walking becomes painful. The ankle
is swollen and the calf is markedly waisted. The movements are restricted. The skin feels warm.
In late cases sinus formation is noticed.
X-ray — is quite diagnostic. It shows rarefaction of the affected bones. The affected joints
become narrow and the joint space becomes irregular. When a cold abscess is formed in a bone
particularly calcaneum, an osteolytic round lesion can be seen (see Figs. 21.7 & 21.8 of Author's
'A Manual On Clinical Surgery').
Treat men I.— The general treatment is same as tuberculous infection of bone and joint
anywhere in the body. To give rest to the foot, a removable splint is used and the foot is kept
in neutral position. When the disease is arrested, the patient may be allowed with a non-weight-
bearing caliper. As the condition improves, gradual weight bearing is started and ultimately the
caliper is discarded.
If tuberculous arthritis has destroyed the joint, stiffness is inevitable and arthrodesis is the
best treatment.
PAINFUL HEEL
This is a common complaint, which is often received from an individual of any age. 'Painful
heel' may be caused by various conditions, which can be best classified according to the age
group in which they commonly occur :—
1. IN CHILDREN.—
Sever’s disease.— This is a type of osteochondritis which affects the epiphysis of the
calcaneal tuberosity, into which the tendo-Achilles is inserted. This usually occurs in boys around
10 years of age. It is a type of 'traction osteochondritis'. Patient complains of pain and tenderness
at the insertion of the tendo-Achilles. X-ray shows increased density and fragmentation of the
apophysis.
Treatment is to avoid wearing flat-heeled shoes. Instead he should wear high-heel shoes.
Avoidance of strenuous activities and too much walking should also be advised.
2. IN ADOLESCENTS.—
Calcaneal Knob.— This is an uncommon condition affecting girls of teen age. The
posterolateral portion of the calcaneus becomes prominent and it rubs against the shoe
causing pain.
A soft pad may be used at the heel of the shoe. If this does not cure the condition, the
knob should be chiselled off.
3. IN YOUNG ADULTS.—
(a) Bursitis.— The bursa just superficial to the calcaneal tuberosity or just above the
insertion of the tendo-Achilles may become inflamed due to ill-fitting shoes. Such bursitis is
more common in young women. Localized pain and tenderness are the main complaints with
some redness of the skin over the inflamed bursa.
Using of soft shoes often cure the condition. Rest and avoidance of shoes for a time may
also cure such condition. If the above measures fail, it may be required to excise the bursa.
(b) Acute plantar fasciitis.— This condition is an acute infection of the plantar fascia
just in front of the calcaneus. This condition may follow gonorrhoea. Patient complains of pain
and tenderness in the posterior part of the sole just in front of the calcaneus.
Rest and protection of the painful area with antibiotics often cure this condition.
(c) Following fracture of the calcaneus patient may complain of 'painful heel' for
quite a long time.
4. IN MIDDLE AGED.—
(a) Chronic plantar fasciitis.— This is often called 'policeman's heel'. The exact
pathology is not known. There is pain and tenderness below the calcaneus. This condition is
more often seen in men between 40 and 60 years of age.
A soft pad may be used just below the tender area. If this does not help, injection of
hydrocortisone should be made at the most tender spot. If the above measure also fails, division
of the plantar fascia is indicated.
(b) Bong spur from the undersurface of the calcaneal tuberosity is often seen in X-ray
with the patient complaining of 'painful heel'. Significance of finding a bony spur is questioned.
It may not be the cause of 'painful heel' and may be a simple association.
Injection hydrocortisone often helps to cure this condition. If it does not cure, the bony
spur is chiselled off with division of the plantar fascia.
(c) 'Paget 's disease affecting calcaneus may cause 'painful heel'.
5. AT ANY AGE.—
(a) Chronic osteomyelitis, in the form of Brodie's abscess, may affect the calcaneus
to cause painful heel. This may occur at any age. On X-ray one will find a translucent area
surrounded by sclerosed bone.
(b) Tuberculous osteomyelitis may be rarely seen in calcaneus to cause 'painful heel'.
PLANTAR FASCIITIS
This is a common cause of pain in the heel. It occurs from the inflammation of plantar
aponeurosis at its attachment on the tuberosity of the calcaneum. The pain is first complained
of in the early morning and gradually improves with activity. On examination there is marked
tenderness just in front of the calcaneal tuberosity on its medial aspect. It is often known as
‘policeman’s heel’.
X-ray may show a sharp bony spur projecting from the tuberosity of the calcaneum. Its
significance is questioned and it may not be the cause of 'painful heel' and may be a simple
association.
THE FOOT 381
Treatment.— Analgesics and heel-pad usually help. If this does not cure, injection
hydrocortisone may be tried. The last court of appeal is to chisel off the bony spur with division
of the plantar fascia.
HALLUX VALGUS
This is valgus deformity of the hallux, that means the great toe is deviated laterally at the
metatarsophalangeal joint.
Aetiology.—
1. Congenital.— In congenital hallux valgus, the first metatarsal bone is adducted and this
is known as 'varus first metatarsal'. This is often a familial condition.
2. Acquired.—
(i) Shoes.— Constant wearing of pointed shoes with high-heel which is commonly
practised by the girls of the Western World, is often the cause of such deformity. Of course such
deformity is only seen in middle-aged women who have continually used this type of shoe
from teen ages.
(ii) In middle aged women with increasing weight, the forefoot often splays, so that
the first metatarsal bone becomes more varus leading to this deformity.
Pathology.— The main feature of this condition is prominence of the head of the first
metatarsal bone and lateral inclination of the great toe.
Undue prominence of the head of the first metatarsal bone will lead to the following
secondary pathologies :—
(a) A protective bursa develops over the medial aspect of the head of the first metatarsal
bone, this is known as 'bunion'. This bursa becomes often inflamed due to rubbing or friction
against the shoe.
(b) An exostosis may develop from the medial side of the head of the first metatarsal
bone due to pressure on the periosteum.
(c) Osteoarthritis may later develop in the first metatarsophalangeal joint due to
malalignment.
The proximal phalanx of the great toe is inclined laterally towards the second toe which is
crowded and may become deformed. Due to the lateral inclination of the great toe the long
tendon of the hallux is also shifted laterally giving rise to 'bow-string' effect which causes an
increase of the deformity gradually.
Clinical features.— Hallux valgus is often bilateral. It is mostly seen in middle-aged women.
If it occurs in adolescents, it is mostly congenital and a strong familial tendency is noticed.
This condition may be painless. But if the patient presents with pain, it is usually due to (i)
an inflamed bunion, (ii) associated with splay forefoot or (iii) a hammer toe.
Treatment.— A . IN ADOLESCENTS.— At this age operation is usually justified —
(i) Simmond’s operation.— In this operation varus osteotomy of the first metatarsal bone
is performed near the base of the first metatarsal bone and a wedge of bone is inserted into the
medial aspect of the osteotomy. This wedge of bone is usually got from the chiselling of the
prominent metatarsal head. At the same time the adductor hallucis tendon is reinserted into the
metatarsal neck.
(ii) In older patients osteotomy of the first metatarsal bone is performed obliquely through
its distal third and the distal portion is displaced laterally alongwith the toe which is displaced
medially and a Kirschner wire is inserted from the tip of the toe to the base of the first metatarsal
bone. The whole foot is kept immobilized in plaster.
B. IN ADULTS.— •
Conservative treatment.— There is a place of conservative treatment at this age of patients.
The shoe should be wide with the front part soft. Padding may be used to protect the bunion
and hammer toe. Foot exercises and physiotherapy are advised to cure splay foot and
metatarsalgia.
Operative treatment.— This is often justified when the symptoms are not relieved by
conservative measures.
1. Keller’s operation.— This is a quite successful
operation in majority of cases particularly in presence of
symptoms of arthritis. A curved incision is made on the medial
aspect of the joint. Soft tissues are denuded off the proximal half
of the phalanx taking particular care not to damage the tendons.
The medial part of the head of the first metatarsal is also cleared.
The proximal third of the proximal phalanx is excised. The
prominent medial portion of the head of the first metatarsal with
exostoses is also trimmed off. A flap of soft tissue may be
interposed between the metatarsal head and the phalanx. The
incision is sutured. Postoperative immobilization is done by
compressive bandaging for 3 weeks followed by gradual, active
exercise.
2. Mayo’s operation.— In this operation the head of the Fig.21.4 .— Keller’s operation.
Interrupted lines indicate the
first metatarsal bone is excised and the prominent medial portion
portions of the bones to be
of the base of the proximal phalanx is trimmed. So Mayo's excised. See the text.
operation is just the reverse of Keller's operation.
3. Arthrodesis of the metatarso-phalangeal joint may be performed to abolish pain. The
articular cartilages with a portion of the base of the proximal phalanx and the head of the
metatarsal are removed alongwith any osteophytes present. A position of a few degrees of
dorsiflexion and slight abduction of the toe is obtained and fixed with a screw passing obliquely
from the innerside of the metatarsal to the outerside of the phalanx or by staples or by two
transfixion wires and a compression clamp. Complete immobilization is required by plaster of
Paris until fusion occurs in 6 weeks or more.
4. McBride operation.— In this operation the conjoined tendons of adductor hallucis
and the lateral head of the flexor hallucis brevis are transferred from the proximal phalanx to
the lateral side of the head of the first metatarsal bone. The lateral sesamoid bone and the
osteophytes are removed to get normal alignment of the hallux. .
5. When there is gross varus deformity of the first metatarsal bone and the patient is
below 50 years, Keller's operation may be combined with an osteotomy near the base of the
first metatarsal bone. Plaster immobilization is required for 6 weeks.
6. Bunionectomy.— Excision of the bunion with excision of underlying prominent portion
of the head of the metatarsal bone is a simple method which often reduces the symptoms. The
medial ligament of the joint may be reconstructed for better result.
7. Radical operation.— In this operation main defects are corrected e.g. (a) deformity of
the first metatarsal is corrected; (b) Such correction is maintained and (c) restoration of muscle
THE FOOT 383
balance. The proximal l/3rd of the proximal phalanx is removed alongwith exostosis. Adduction
of metatarsal bone is corrected by osteotomy at its base and inserting a wedge from the exostosis
removed from metatarsal head. Tendon of adductor hallucis is transformed to the metatarsal
head to restore muscle balance and to maintain correction.
HALLUX RIGIDUS
It is a condition of stiffness of the metatarso-phalangeal joint of the great toe, particularly

characterized by absence of dorsiflexion. In the initial stage plantar flexion is possible, but in
late cases all movements of the joint are abolished.
CAUSES.—
I. Congenital.— There are two types —
(a) The first metatarsal bone is short and is elevated to cause the metatarso-phalangeal
joint hyperextended to allow the ball of the foot to reach the ground. This extreme position
may cause degeneration of the joint and ultimately hallux rigidus.
(b) In this condition hallux rigidus is associated with flat foot. The first metatarsal bone
remains more horizontal than normal and the head of the bone is rotated upwards, so that the
dorsal portion of the articular surface does not become articular. This exposed area undergoes
disuse changes e.g. osteophytic outgrowth and fibrillation. This alongwith reflex spasm of the
muscles causes rigidity of the metatarso-phalangeal joint with particular restriction of its
dorsiflexion.
II. Acquired.— This may be of two varieties also —
(a) When the great toe is longer than the second toe, it is liable to be pressurized
against the toe-cap of the shoe. Splitting osteochondritis of the first metatarsal head occurs
followed by hallux rigidus.
(b) The most common cause of acquired hallux rigidus is the inflammatory changes of
the metatarso-phalangeal joint particularly rheumatoid arthritis. The limitation of joint movement
is the result of muscular spasm in the initial stage to prevent movement of the painful joint.
Later on articular changes occur alongwith changes in the capsule and ligaments to cause
permanent stiffness.
In all the varieties the joint becomes the site of characteristic osteoarthritic changes later on.
Clinical 1’calures. Adult males are more often affected by this condition. This is also
seen in adolescents of either sex.
Pain is the most important symptom, which is experienced on walking particularly during
dorsiflexion of the joint. The joint is sometimes swollen with periarthritis.
Attempts to move the joint are painful in the early stage. Later on stiffness is permanent,
when attempts at passive movements become painless. Abnormal degree of dorsiflexion is
sometimes seen in the interphalangeal joint.
X-ray shows narrowed joint space. There is sclerosis in the adjacent bones with osteophyte
formation. Later on signs of osteoarthritis become evident.
Treatment.—
CONSERVATIVE TREATMENT.— All cases of hallux rigidus should be given a trial of
conservative treatment. Relief may be obtained by restricting the movement of the joint either (i)
by thickening the sole of the shoe, or (ii) by fitting a metatarsal bar to the sole of the shoe, or
(iii) by insertion of a thin plate of steel between the two layers of the sole. Particularly in
adolescents better result can be expected. The deformity can be over-corrected under anaesthesia
and this position of dorsiflexion is maintained by a walking plaster case. The plaster case is
kept for 6 weeks. This method is also very helpful for young individuals.
OPERATIVE TREATMENT.— In ADOLESCENTS and YOUNG individuals conservative
treatment is quite successful in bringing relief to the patients.
(i) If this fails, osteotomy of the first metatarsal bone should be considered.
In ADULTS, if pain is not relieved by conservative method —
(ii) Arthroplasty of the joint in the form of Keller's operation or Mayo's operation should
be considered. This of course causes weakness of the joint.
(iii) Arthrodesis is particularly considered in case of manual workers. But this should not
be considered in acute phase and in women who often wear high-heel shoes.
(iv) In case of mild hallux rigidus with exostosis on the dorsum of the first metatarsal
head, the exostosis should be chiselled off.
METATARSALGIA
Pain in the metatarsal region is called 'metatarsalgia'.

CAUSES.— The causes of metatarsalgia can be best described under 3 heads —
1. Static.
2. Inflammatory.
3. Traumatic.
1. Static variety.— (i) The various deformities of the foot may be included in this group.
Splay foot with hallux valgus and curly toes are often seen in middle-aged women. This is a
frequent cause of metatarsalgia.
(ii) Claw foot with claw toes also causes metatarsalgia as the weight is borne in a limited
area.
(iii) Metatarsus primus varus and metatarsus hypermobilis also cause metatarsalgia.
(iv) Deformities of the toes e.g. hammer toe, claw toes and curly toes also produce
meta tarsalgia.
(v) Hallux disorders e.g. hallux valgus, hallux rigidus or ingrown toe-nail also cause
meta tarsalgia.
2. Inflammatory.— Rheumatism of the metatarso-phalangeal joint, gout etc. may cause
metatarsalgia.
3. Traumatic.— Injury to the forefoot causes metatarsalgia for quite a long time. In this
group one special variety is worth mentioning i.e. stress fracture.
Stress fracture.— It is also known as march fracture. It usually occurs in young adults
after unaccustomed long walk. It usually affects the second metatarsal or the third metatarsal
bone. An almost invisible crack fracture occurs at the neck of the metatarsal bone. The affected
region becomes painful and tender. On palpation a thick tender area can be recognized, which
is nothing but an excessive callus formation around a fine transverse fracture. X-ray may not
show any abnormality in the early stage, but later on fusiform excessive callus may be seen
around fine transverse fracture at the neck of the metatarsal bone.
Two special varieties of meta tarsalgia are very important and are discussed separately. These
are :—
1. FREIBERG'S DISEASE (Kohler's disease of the metatarsal head).— It is a type of
THE FOOT 385
crushing osteochondritis of the head of the metatarsal bone. Most frequently the second
metatarsal bone is affected, rarely the third and even more rarely the others may be affected.
Pathological changes are similar to any crushing osteochondritis i.e. the bone becomes dense
with rarefied areas in between, associated with indentation or collapse of the articular surface.
Young adult women are more often affected. Pain in the forefoot is the most common
symptom which becomes exaggerated during movements. There may be considerable oedema.
On palpation the metatarsal head becomes thick and tender.
X-ray changes are — (i) broadening of the metatarsal head, which becomes irregular, wide
and flat; (ii) thickening of the neck; (iii) increase of the joint space; (iv) thickening of the shaft of
the metatarsal bone; and (v) detached portions of the articular surface may remain free in the
joint.
Treatment is to give rest by application of walking plaster cast. If pain persists, operative
treatment in the form of excision of the head may be considered, but it obviously will weaken
the transverse arch of the foot.
2. MORTON’S METATARSALGIA.— A painful neuroma of the digital nerve which causes
shooting pain towards the contiguous sides of the two toes is the characteristic feature of this
special type of metatarsalgia. It may affect any or all of the digital nerves, but is most common
in relation to the third or fourth metatarsal space.
Women between 40 and 50 years are mostly affected. Sharp intermittent pain is the most
important only symptom which shoots into the adjacent toes. The pain is mostly experienced
with the shoes on, possibly because the metatarsal bones squeeze the neuroma at this time. On
examination localized tenderness can be felt at the neuroma. Sensation may be diminished at
the distribution area of the affected digital nerve.
Treatment.— Conservative methods like insertion of transverse metatarsal bar in the sole of
the foot may provide relief. But in intractable cases, the neuroma should be excised either through
dorsal incision (more commonly used) or through plantar incision.
HAMMER TOE
The DEFORMITIES which occur in a hammer toe are :—

(a) Hyperextension of the metatarso-phalangeal joint;
(b) Hyperflexion of the proximal interphalangeal joint and
(c) Hyperextension of the distal interphalangeal joint; (d)
Callosities or adventitious bursa may develop over the
dorsum of the proximal interphalangeal joint due to
pressure against shoes.
The second toe is commonly affected.
CAUSES.— (i) The toe may have been too long, (ii)
The shoes used may be too short, (iii) Presence of hallux
valgus.
TREATMENT.— CONSERVATIVE TREATMENT.—
Padded corrective strappings should be recommended for
children or in early cases. But late cases cannot be treated
by conservative method and operative treatment should be Fig.21.5.— A typical case of
recommended. Hammer toe.
25
OPERATIVE TREATMENT.— This treatment should be deferred till 15 years of age for
proper union of the epiphysis. An oval incision is made on the dorsal surface of the proximal
interphalangeal joint to excise the callosities and adventitious bursa if present there. The joint
surface are excised, the deformity is corrected, the toe is straightened. The joint is now
arthrodesed with a piece of Kirschner wire pushed from the tip of the toe through the joint.
The end of the wire should be protected at the tip of the toe and is kept in position for 6 weeks
which is followed by a collodion splint for 3 weeks.
RUPTURED TENDO-ACHILLES
It is the commonest tendon to rupture. The pathology is almost same as ruptured biceps
tendon. Avascular degeneration is the main pathology which causes rupture.
The patients are usually over 40 years of age. The usual history is that while running or
jumping, suddenly the patient feels as if he has been struck just above the heel. Since then he is
unable to stand on his toes. Such rupture occurs when the calf muscles contract, but is resisted
by the body weight and at this time a degenerated tendon ruptures.
On examination a gap may be seen and felt about 3 to 5 cm above the insertion of the tendo-
Achilles. This gap is more felt with dorsiflexion of the ankle. Plantar flexion of the foot is weak.
It must be noticed that though the patient finds difficult to stand on tip-toe on the affected side,
but it is never completely absent.
Simmond's test.— With the patient in prone position, if the calf is squeezed, in normal person
the foot will be plantar flexed. But if the tendo-Achilles is ruptured the foot does not undergo
plantar flexion.
Sometimes a diagnosis of incomplete tear of tendo-Achilles is made, when no gap is detected
in the tendon. It must be remembered that when the tear is even one day old, it may be difficult
to feel the gap. Moreover the patient may be able to stand on his toes by using his long flexors
of the toes. A correct diagnosis of incomplete tear can only be made during operation.
Treatment.—
Particularly in early cases, the tendon may be sutured with the foot in passively plantar
flexed position. After operation a plaster is applied with the foot in equinus position for 8 weeks.
A shoe with raised heel is worn for a further 6 weeks.
In late cases, suturing may be extremely difficult and may not give expected result. It is
very difficult to bring down the contracted upper end to normal position. One may try tendon
lengthening operation and then suturing.
387
CHAPTER- 22
THE SPINE AND PELVIS

SPINA BIFIDA
Congenital defect in the posterior bony wall of the spinal canal involving the laminae, is known as spina
bifida. This is most commonly seen in the lumbo-sacral region. Sometimes the contents of the canal may
protrude through the defect.
Development of the spinal cord.—
(i) During the 2nd week of intrauterine life a dorsal groove appears on the surface of the embryo, which
is known as the neural groove.
(ii) The margins of the neural groove unite so that it becomes converted into a tube from which the nervou
system is developed. This tube is known as neural tube and the lumen within it is called the neural canal. This
neural canal persists as the central canal. The neural tube becomes separated from the surface by an ingrowth
of the mesoderm.
Development of the vertebral column.—
(i) In front of the neural tube there is a solid rod of cells, known as the notochord. Around the notochord
the vertebral bodies develop. In each segment bars of cartilage appear on either side of the notocord, which
develop into vertebral bodies.
(ii) From each of the bodies there extend two projections which grow round the neural tube to form the
vertebral arch. During the 4th month they fuse with each other posteriorly to form the vertebral arches.
(iii) Such fusion first occurs in the thoracic region. From there fusion extends upwards and downwards.
(iv) Failure of fusion of these arches gives rise to spina bifida.
Incidence.— The incidence of spina bifida (excluding spina bifida occulta) is 0.1%.
Types of spina bifida.—
1. Spina bifida occulta.
2. Meningocele.
3. Meningomyelocele.
4. Syringomyelocele.
5. Myelocele.
Myelocele is the commonest type of spina bifida, if the spina bifida occulta is excluded. But unfortunately
many cases with myelocele are still bom. Even if they bom alive, death occurs within a few days from infection
of the cord and meninges.
1. SPINA BIFIDA OCCULT A.— In this condition though there is failure of the neural arches to unite,
and a small gap exists in one of the vertebral arches, usually in the lumbar or sacral regions, yet there is no
protrusion of the cord or membranes. Frequently one vertebra is affected. The gap is filled with fibrous tissue.
As a rule, there is no projection on the surface to indicate this defect, though a local patch of hair, a naevo-
lipoma or a depression in the skin suggests the underlying bony deficiency.
A fibrous band, the membrana reuniens connects the skin to the spinal theca. At one stage the spinal cord
reaches the distal end of the vertebral column. Gradually the cord lags behind in growth, so that at brith the di
end of the cord lies at the third lumbar vertebra. Later on due to more development of the vertebral column, th
distal end of the cord lies at the lower end of the first lumbar vertebra in adults. With the growth of the body
the membrana reuniens pull on the theca and nerve roots. This causes some neurological deficiencies e.g. foot
drop, nocturnal enuresis or backache. Such symptoms appear late in childhood or in adult life.
Many cases of spina bifida occulta are symptomless. Either they remain undiagnosed or diagnosed by
accident when an X-ray is taken for some other reasons.
Clinical features.— (i) Present since birth.
(ii) There is some abnormality in the local skin — either a skin dimple or a local patch of hair or a naevo-
38S A CONCISE TEXTBOOK OF SURGERY
lipoma or simple lipoma.

(iii) Neurological examinations must be performed, as in adolescent or in adult life manifestations of su
deficiency may be revealed in the form of backache, nocturnal enuresis, local anaesthesia, local paresis or e
foot drop.
(iv) X-ray is often confirmatory as it will show the bony defect.
Treatment.—
If there is any symptom, opera
tion should be performed.
(a) Presence of tuft of hair or
lipoma may lead to cosmetic
complaint and this is treated by
excision of these lesion.
(b) If there are neurological
symptoms due to membrana
reuniens, the membrana reuniens
•Horizontal and Vertical Sections of a Spinal Meningocele.is excised in its whole length from
the skin through the vertebral gap
to the spinal meninges.
(c) Orthopaedic, urological or
neurological symptoms may not
be due to traction by the membrana
reuniens alone, but are more likely
to be due to compression of the
cord by extradural or intradural li
pomas. Such lesions should be ex
cised. Sometimes a condition,
called diastematomyelia in which
■ a Meninoo-myelocele. the cord is split in the midline by a
bony spur, may be seen. This
abnormality is usually associated
with presence of tuft of hair on the
overlying skin. Myelography
should always be performed be
fore the operation.
2. MENINGOCELE — In
this condition protrusion of me
ninges occurs through the defect in
the neural arch. Such protrusion
contains only cerebrospinal fluid.
Diagram of a Syrinoo-myelocele. So it gives rise to a cystic swelling.
Usually the duramater stops at
the margin of the defect and the pia
Fig. 30.1.— Vertical and horizontal sections of Meningocele,
Meningo-myelocele and Syringo-myelocele are shown.
and arachnoid protrude. The over
lying skin remains intact.
It is common in the lumbosacral region. Menigocele also occurs in the skull, where it is more common i
the occipital region or at the root of the nose.
Clinical features.— (i) It is present since birth.
(ii) It is a cystic swelling, that means fluctuation test is positive.
THE SPINE AND PELVIS 389
(iii) It is a highly translucent swelling.

(iv) It is compressible.
(v) Expansile impulse is present when the child cries or coughs.
(vi) The overlying skin is normal and free.
(vii) On careful palpation the edge of the bony defect is palpable.
(viii) Neurological manifestations are usually absent (cf. meningo-myelocele, where neurological manifes
tations are usually present).
(ix) When this condition is associated with hydrocephalus this combination is known as Amold-Chiari
syndrome.
(x) X-ray is confirmatory and will show the bony defect.
Complications are — (i) Infection and (ii) Rupture.
Treatment.—Operation should be performed as early as possible, but child’s condition and strength should
be sufficient to withstand operation. This operation is often performed within a few days of birth. If the operat
is delayed, the overlying skin may become atrophic and may ulcerate.
The principles of operation are — (i) The skin and the sac are opened with incisions perpendicular to each
other. This will minimize the chance of postoperative C.S.F. leakage.
(ii) The redundant part of the sac is excised.
(iii) The margins of the excised sac are sutured together in the midline.
(iv) To strengthen the bony gap, the adjacent erector spinae muscles and the overlying fasciae are
approximated over the gap with the help of lateral release incisions (to minimize tension on the suture line).
(v) The skin is closed.
3. MENINGOMYELOCELE.— In this condition the normally developed spinal cord or cauda equin
is protruded alongwith the meninges and these structures may be adherent to the posterior aspect of the sac.
Clinical features.— (i) Though myelocele is the most common type of spina bifida (many cases are still
bom), yet meningomyelocele is the commonest variety of spina bifida in the living children.
(ii) The bony defect may usually extend over 3 or more segments.
(iii) At the summit of the swelling skin may be absent or atrophic, so here the meninges are exposed. That
is why complications like infection and rupture are not uncommon.
(iv) In transillumination test the nerves may be seen within the sac (cf. meningocele), though it is a
translucent swelling.
(v) Neurological manifestations are almost always present.—There may be sensory disturbances alongwith
trophic changes in the lower extremities. There may be motor disturbances and in advance cases one may find
extensive paralysis of the legs. Bilateral talipes is quite common in this condition, as also urinary incontinence.
(vi) X-ray will show the bony defect. There may be other abnormalities of the vertebrae, like scoliosis or
kyphosis or even haemivertebra.
Complications.—
(i) Infection, i
(ii) Rupture. ) Very common.
(iii) Urinary obstruction, hydronephrosis and urinary tract infection.
Treatment.— Operation must be performed as early as possible. Child's condition should also be
considered, as it should withstand operation.
Delay in operation may cause (i) infection within the sac and postoperative problems.
(ii) The sac may rupture and will make operation extremely difficult with infection spreading through
the subarachnoid space.
(iii) There will be more adhesion of nerves with the wall of the sac, which will be difficult to separate.
(iv) Gradually extensive paralysis of the legs and incontinence may occur, so that surgical intervention ma
become contraindicated.
STEPS OF OPERATION.—
(i) The sac is opened and the redundant membrane is excised. Meticulous care must be taken to sepa
all the nerve fibres which are adherent to the posterior wall of the sac and then they are replaced into the
canal.
(ii) The membranes are sutured in the midline deep to the bony defect.
(iii) Adjacent erector spinae muscles and the overlying fasciae are brought in the midline and sutured
lateral release incisions are made to minimize tension on the suture line of the muscles. The skin is closed
without tension. If difficulty is encountered to bring the skin in the midline, a rotation flap may be used.
(iv) Further care of these children may be necessary. Repeated orthopaedic and urological surgery ma
necessary to rectify orthopaedic defects and urinary incontinence. C.S.F. shunts may be necessary for
hydrocephalus.
4. SYRINGOMYELOCELE.— In this condition the central canal of the spinal cord is dilated and
spinal cord lies within the sac together with the peripheral nerves arising from the cord.
This is the rarest variety of spina bifida.
Gross neurological deficits and paralytic manifestations are present.
5. MYELOCELE.—This is the gravest form of spina bifida, in which besides the bony defect there i
defect of development of the spinal cord. The development is arrested before the time of closure of the ne
furrow. So that the posterior part of the spinal cord is not developed. The elliptical raw surface of the neu
furrow can be seen, deep to which lies the anterior part of the spinal cord. At the top end of the defect the
canal of the spinal cord opens on the surface and discharges the cerebrospinal fluid constantly.
Majority of the cases are still bom. Even if a few bom alive, they die within a few days from infection o
the cord and meninges.
TORTICOLLIS
Two conditions should be considered — I. Congenital torticollis or infantile torticollis and II. Acquired
torticollis or secondary torticollis.
I. CONGENITAL TORTICOLLIS.—
This condition usually occurs due to infarction of the central portion of one stemomastoid muscle at th
of birth. At birth, the central part of the muscle may be found to be swollen, which is known as ‘stemoma
tumour’. The infarcted muscle is gradually replaced by fibrous tissue which fails to elongate as the child g
to cause progressive deformity. The deformity is that the mastoid process of the affected side comes closu
the clavicular origin of the stemomastoid and the face of the individual is directed away from the side of
lesion (as if the affected stemomastoid muscle is contracting). This condition is analogous to the developm
of Volkman’s ischaemic contracture of the limbs.
CAUSE.—
(i) Idiopathic, where definite cause is unknown.
(ii) The stemomastoid muscle might have been injured at birth. A history of difficult labour or breech
delivery is often obtained. Association of hip dysplasia is a supporting evidence.
Pathology.— A ‘Stemomastoid tumour’ appears about 2 to 3 weeks after birth as a spindle-shaped swe
in the stemomastoid muscle. The tumour gradually becomes absorbed and finally disappears before 6th m
Microscopically, the stemomastoid tumour consists of young cellular fibrous tissue with remnants of the
original muscle fibres here and there which are undergoing degeneration. After one year, the stemomasto
muscle is reduced to fibrous tissue. There is also some thickening and contraction of the deep cervical fasc
scalenus anterior and medius muscles. Gradually the vessels on the affected side of the neck become shor
and smaller in calibre.
SECONDARY CHANGES.— Due to the shortening of stemomastoid muscle and deformity of the face, a few
secondary changes gradually appear when the child grows older. These secondary changes are :
(i) Well marked asymmetry of the face, which becomes shorter from above downwards and wider fr
side to side on the affected side.

(ii) Frontal eminence on the affected side becomes flattened, whereas there is well marked protrusion of
the occipital region on that side.
(iii) The vault of the skull is projected backwards on the affected side, whereas it projects forwards on the
opposite side. This deformity of the skull is almost similar to that found in the thorax in thoracic scoliosis, th
is why this deformity is called ‘scoliosis capitis’.
(iv) Occasionally the mastoid process becomes abnormally larger and an exostosis develops in it, a simila
exostosis may appear on the clavicle at the side of attachment of the clavicular head of the stemomastoid mu
(v) A compensatory cervical scoliosis may develop.
(i) In 20% of cases the ‘stemomastoid tumour’ is noticed in first few weeks of life. It is a well defined
swelling involving the middle of one stemomastoid muscle. At this stage there is neither deformity nor
limitation of movement.
(ii) Within a few months the ‘stemomastoid tumour’ disappears.
(iii) Deformity does not become apparent until the child is 3 or 4 years old. This occurs as the unaffected
stemomastoid grows normally but the affected stemomastoid fails to grow at that pace and at the same time
fibrous tissue in it contracts.
(iv) The mastoid process comes closure to the sternal notch on the affected side, so that the ear becomes
lower and further forward on the affected side. The face turns towards the other side.
(v) The stemomastoid muscle feels cord-like on the affected side.
(vi) X-ray does not reveal any abnormality.
Treatment.—
PROPHYLAXIS.— When a ‘stemomastoid tumour’ is noticed at birth, effort should be made to prevent
torticollis from developing. Every day the infant’s head should be manipulated gently into a position which
elongates the affected stemomastoid muscle to the full extent. This is continued so that the muscle when bein
replaced by fibrous tissue will not be shortened. The baby is laid to sleep on alternate sides.
CONSERVATIVE TREATMENT.— When the deformity is detected early, stretching and splintage
method may cure the condition. Daily stretching of the affected stemomastoid is done followed by application
of a splint or a linen skull-cap attached by tapes tight under the axilla. This treatment is continued until the c
naturally comes to hold its head correctly. The cap is worn at night for further 6 months to prevent recurrenc
OPERATIONS.— If the deformity is not seen until the age of 3 to 4 years and if the conservative method
fails, operative treatment should be called for. One of the three operations should be considered.
1. Subcutaneous tenotomy of the lower end.— The lower end of stemomastoid muscle is divided with a
tenotomy knife. Though this operation has a good cosmetic value, yet it is not without risk as there are quite
a few vessels around, which may be injured leading to excessive haemorrhage. So these vessels are to be avo
carefully.
2. Open division of the lower end.— This operation is much more preferred to the previous one to avoid
the risk of haemorrhage.
A transverse incision is made about 2 inches in length with its centre over the lower part of the stemomas
muscle one inch above the clavicle. After incising the skin, platysma and deep fascia, both the heads of the
stemomastoid muscle are divided. The anaesthetist then twists the child’s head to obtain correction of the
deformity. The surgeon at that time looks for any other shortened structures which might intervene the
correction of the deformity. These shortened structures should be divided till complete over-correction is
achieved. Sometimes the scalenus anterior muscle and the carotid sheath are found shortened. In these cases
these structures should be carefully divided. Care must be taken to protect the phrenic nerve and contents of
carotid sheath. When it is sure that the deformity is over-corrected, the skin and the platysma are sutured wi
a suction drainage. This operation is completely safe.
The head should be maintained in the over-corrected position for 6 weeks either by a plaster cast or
preferably with a torticollis harness. When the normal position has been attained, active exercises should be
started.
3. Open division of the upper end.— This procedure is not often performed, though its advantage is t
the scar is hidden by the hair. This operation may be combined with any of the above two operations. Singu
this operation is less effective than the previous one. In this operation care should be taken to avoid damage
the spinal accessory nerve.
H. SECONDARY TORTICOLLIS.—
Torticollis or wryneck may develop secondary to a few conditions. These conditions can be broadly
classified into a few groups — 1. Traumatic, 2. Inflammatory, 3. Spasmodic and 4. Miscellaneous.
1. Traumatic.— Injury to the cervical spine and prolapsed cervical disc and cervical spondylosis are the
main causes in this group.
2. Inflammatory.— Suppurative inflammation of the cervical lymph nodes, tuberculous infection of the
cervical lymph nodes and vertebral tuberculosis (caries spine) of the cervical region are the main causes in th
group.
3. Spasmodic.— Within this group are included neurological and psychological disorders which cause
marked spasm of the stemomastoid muscle. Sometime violent jerking may occur at attempted correction.
4. Miscellaneous.— Scarring of the skin following bums, ocular disorders are the main causes in this
group.
The distinguishing features between primary and secondary torticollis are that the latter condition does n
start in infancy and that there is no facial asymmetry in the latter condition.
Treatment — of secondary torticollis is mainly that of the primary cause.
PROLAPSE OF INTERVERTEBRAL DISC
Anatomy.— Intervertebral discs are interposed between the vertebral bodies. These discs act as shock
absorber for the spinal column. It also provides mobility between the bodies of the vertebrae. Each intervert
disc consists of a central semifluid spongy material known as 'nucleuspulposus' which is surrounded by a tou
fibrous ring, known as annulusfibrosus. Annulus fibrosus has got attachment with the adjacent vertebral bod
Microscopically, it consists of dense fibrous tissue which is arranged in concentrical laminae convex from
above downwards and a wider zone of fibrocartilage. Within each lamina the majority of the fibres lie in par
and run obliquely between the two vertebrae.
The nucleus pulposus contains the remnant of the notochord. Microscopically it reveals fine fibrillar
structure with clear stroma resembling connective tissue, mucin and fibroblastic cartilage and notochordal c
The borders of the nucleus are not distinct as they gradually merge into annulus fibrosus.
The intervertebral disc is enclosed between the fibrocartilaginous plates above and below which are attac
to the vertebral bodies. During flexion of the spine the disc is deformed and the nucleus and annulus fibrosu
bulge backwards slightly into the neural canal. The nucleus pulposus is normally under tension and provide
constant pressure on the annulus fibrosus which is held in place by ligaments.
Causes of prolapse.—
1. Traumatic.— 80% of cases of prolapse of intervertebral disc are traumatic in origin. There may be a
history of sudden severe strain which may tear the posterior longitudinal ligament so that the tense nucleus
pulposus bulges backwards through the annulus fibrosus. The patient’s occupation may be such that continu
flexion strain may cause prolapse e.g. porter, fireman etc. The disc mostly herniates backwards just lateral to
the posterior longitudinal ligament.
2. Increased tension.— The nucleus pulposus may absorb fluid and swell, so that this bulges the annulus
or even bursts through it. Such absorption of fluid may occur in some physical illness and emotional stress.
3. Degeneration.— In about 15% of cases prolapse of intervertebral disc is degenerative in origin. The
disc loses elasticity and its fluid content decreases. The weakened disc cannot resist body weight and is liabl
to herniate. There is no history of injury. Disc degeneration is characterised by (a) reduction in the amount o
hyaluronic acid and keratosulphates, (b) increase in fibrillation and precipitation of collagen and (c) increase
in the lower molecular weight glycoproteins. These changes result in decrease of the gel property of the disc
and disturbance of its normal function. Simple unequal stress or minor trauma with thepresence of these ch
will cause increase in the intradiscal pressure which will lead to protrusion or prolapse of the disc.
Sites.— Protrusion of the disc is most common in the most mobile positions of the spine, as these portion
are subjected to greater stress and strain. According to frequency the sites are :—
1. Lumbosacral region — above and below the L5 vertebra i.e. L4/5 and L5/S1. 80% of disc prolapse
occurs at this region.
2. Lower cervical region — above and below the C6 vertebra i.e. C5/6 and C6/7. 19% of disc prolapse
occurs in this region.
3. Dorsal region — which constitutes 1% of all disc prolapses.
Pathology.— The commonest type of protrusion is a circumscribed bulging of the disc with attenuated
annulus fibrosus. Sometimes the nucleus may herniate through the annulus fibrosus. The herniated materia
press on the duramater causing backache or on the nerve roots causing sciatica and/or backache. At first ther
is oedema which increases the symptoms. Gradually oedema subsides and the prolapsed material shrinks. I
remain prolapsed and become adherent to the nerve root sheaths or may slip back into its own place. The pr
on the nerve roots is extradurally.
There is narrowing of the intervertebral joint space, which is noticed in X-ray in 50% of cases.
Prolapse of the disc increases mobility between the vertebrae which ultimately develops intervertebral
arthritis. Thus it disturbs the mechanism of the intervertebral joints. There may be osteophyte formation and
compensatory thickening of the ligamenta flava to check abnormal mobility.
There may be protrusion of nucleus pulposus into the body of a vertebra, which is recognised as a Schmo
node in X-ray. Such node is also seen in Scheuermann’s disease.
Particularly in the lumbar region a lateral protrusion will press on the roots of the cauda equina. The ner
root which comes out from the corresponding intervertebral foramen is compressed against the lateral marg
of the prolapse, whereas the nerve root coming out from the next intervertebral foramen is pressed by the in
margin of the prolapse.
A. CERVICAL DISC PROTRUSION -
CLINICAL FEATURES.— Cervical disc protrusion is relatively uncommon.
In case of midline protrusion which is rarer than lateral protrusion the anterior part of the cord is slightly
compressed with compression of the anterior spinal artery and anterior spinal veins. Compression of the ant
spinal artery will disturb the pyramidal and spinothalamic tracts and will damage to certain extent the anter
horns. Compression of the anterior spinal veins will cause stasis and congestion of the anterior horns below
level of the lesion. Symptoms like those of disseminated sclerosis or primary lateral sclerosis may appear. Th
may be spastic paralysis and secondary atrophic changes due to involvement of the anterior horns.
Lateral protrusions which are more common will first cause pain and stiffness of the neck. The pain often
radiates to the scapular region and sometimes to the occiput. Cervical prolapsed disc does not involve multi
nerve roots, but it affects a single nerve root which emerges above the corresponding vertebra i.e. C6 nerve r
is involved in case of C5/6 protrusion.
When the C6 root is involved pain will be complained of at the shoulder tip, outer border of the upper ar
and dorsum of the forearm. There will be sensory loss along the lateral border of the upper arm and lateral b
of the forearm. There will be weakness of the biceps, diminished biceps and supinator jerks.
When the C7 nerve root is involved, in case of C6/7 protrusion, pain will be complained of at the shoulde
tip, back of the upper arm and back of the forearm. Sensory loss can be detected on the posterior aspect of th
forearm and of all the fingers except thumb and little finger. There will be weakness of the triceps and extens
muscles of the wrist and fingers and there will be diminished triceps jerk.
It must be noted that true cervical disc protrusions are uncommon. This diagnosis is only accepted if ther
is definite evidence of filling defect in myelography.
Treatment.—
1. Rest.— A cervical collar often gives comfort and it prevents unguarded movement. For minor cases
this may give permanent relief.
2. Traction.—Traction of the cervical spine will increase the disc space so as to cause the disc to slip back
into its normal position. This is achieved by skull traction. Weight upto 40 lb. may be used for 20 minutes da
or continuous traction may be used with 10 lb. for two days or more. The patient is sedated during the tractio
3. Operation.— If the symptoms are severe enough and show neurological symptoms which are not
improved by the above methods, operation is performed to remove the disc by anterior approach. Previously
posterior approach was used and the disc protrusion was exposed by hemilaminectomy or full laminectomy
In case of midline protrusion there is risk of damage to the anterior spinal artery which may cause permanen
paralysis. But nowadays anterior approach is preferred, followed by vertebral fusion by inserting bone graft.
By this the normal intervertebral space is restored.
B. LUMBAR DISC PROLAPSE.—
Clinical features.— In the lumbar region the roots of the cauda equina run obliquely, so a lateral protrusion
may press on more than one roots. Protrusion of the intervertebral disc may be central, paramedian or latera
of which the commonest is the lateral to the posterior longitudinal ligament. This lateral protrusion almost
always presses on the nerve root. Usually the nerve root that comes out from the corresponding intervertebr
foramen is usually compressed. The root may be compressed backwards and medially or the protrusion may
displace the root laterally and presents itself in the angle between the spinal cord and the nerve root. The
paramedian type of protrusion usually affects two nerve roots — one nerve root against the lateral margin of
the protrusion and the nerve root below is caught against its inner margin.
SYMPTOMS.—
Pain.— The typical syndrome of lumbar disc protrusion is low backache followed by referred sciatic pain.
In almost all the cases there is an initial period of low back pain, which is later followed by pain which radiat
down the thigh and leg following the nerve roots which are compressed. In l/3rd of cases sciatica (referred
sciatic pain) precedes backache and in l/4th of cases both backache and sciatica are complained of simultane
ously.
The onset of pain may be acute following trauma e.g. lifting weights in a stooping position etc. The pain m
appear hours or days or even weeks after trauma. In this case the onset should be considered subacute. In a f
cases the patients are subjected to habitual back strain and the patients complain of intermittent, increasing
backache. In this case the onset may be considered chronic.
The pain is usually described as a dull ache, a stabbing pain or a shooting pain. The site of pain is indicate
usually in the lower lumbar region and usually in the midline. The pain may be referred to one or both sacro
iliac joints, to the buttock or distally to the lower limb. The pain is accentuated by coughing in the distributio
of the affected nerve.
Other symptoms.— Paraesthesia, pins and needles are sometimes complained of in the distribution of the
affected nerve. Patient may complain of tenderness in the muscles and weakness of the muscles supplied by
affected nerve roots.
It must be remembered that small protrusions cause very severe pain, as there is maximum friction of the
nerve root without much loss of conduction. Larger protrusion causes less pain, as it fixes the nerve root firm
and there is less friction, but since the conduction is diminished, so neurological signs are more marked.
PHYSICAL SIGNS.— The back and the lower limbs of the patient are examined carefully.
Examination Of The Spine
.—
Inspection.—Lumbar scoliosis is often noticed in lumbar disc protrusion. When the nerve root is medially
displaced by the protrusion, the patient tends to stand with a tilt of the trunk away from the affected side to
more friction of the nerve root. On the contrary when the nerve root is displaced laterally by the protruding d
the patient tends to stand with tilt towards the affected side. This is a protective mechanism to avoid stretch
ing of the nerve root over the protrusion.
Palpation.—Palpation of the spine should be carried out carefully. Local tenderness over the interspinou
ligament or just lateral to the spinous process over the affected intervertebral space can be detected in majo
of cases. Often the
pain is referred to
the buttock or the
lower limb when the
affected area is
pressed with a
thumb. A diagnosis
of disc protrusion
can be made with
confidence when
this sign is detected.
Movements.—
Some limitation of
J®, forward flexion of
the spine is obvious
with this condition.
Fig. 30.2.— A. Shows that the disc protrusion is displacing the nerve root laterally, so that the Similarly backward
patient stands with a tilt towards the affected side to avoid friction. B. Shows that the disc extension is also
protrusion is displacing the nerve root medially, so that the patient stands with a tilt towards sound
side to avoid frictions. limited to certain
extent. Lateral flex
ion of the spine is more limited on one side or the other depending on the displacement of the nerve root b
protruded disc. When it is laterally displaced lateral flexion of the spine on the affected side will not be lim
whereas on the opposite side will be extremely restricted. Similarly with medial displacement of the nerve
lateral flexion of the spine on the affected side will be very much restricted. In one word restriction of the la
flexion of the spine will be seen on the opposite side of scoliosis.
Examination Of The Lower Limbs.—
It should be remembered that central prolapse produces backache and bilateral leg signs. Paramedian pro
lapse causes pain which is made worse when the patient bends laterally on the other side. Lateral prolapse (w
the prolapse is lateral to the nerve root) causes pain which increases when he bends laterally towards the a
side.
Lateral prolapse below the 5th lumbar vertebra presses only on the first sacral root (SI). Lateral prolapse
of the disc above the 5th lumbar vertebra may press on the 1st sacral (S1) or 5th lumbar (L5) or both nerve r
(i) Muscle wasting.— This can be noted by inspection or by measuring the circumferences of the thigh
and calf. In case of involvementof 4 th or 3rd lumbar root there will be wasting of the quadriceps muscle, w
in case of involvement of the first sacral root, there will be wasting of the calf muscles.
(ii) Motor power.— In case of involvement of the 4th or 3rd lumbar root there will be weakness of the
quadriceps muscle. Whereas in case of involvement of the 5th lumbar root, there will be weakness of the
extensor hallucis longus muscle and anterior tibialis muscle. So dorsiflexion of the ankle joint will be weak
similarly there will be weakness of extension of the toe. In case of involvement of 1st sacral root, there will
weakness of plantar flexors and flexor hallucis longus, so there will be weakness in plantar flexion of the an
and flexion of the great toe.
(iii) Tendon reflexes.— In case of involvement of the 4th lumbar and 3rd lumbar roots there will be
diminished knee jerk. In case of involvementof the 1st sacral root there will be very much diminished or ab
ankle jerk.
(iv) Sensory impairment.— In case of involvement of the 3rd lumbar root, sensory loss can be detected in
the lower thigh. In case of involvement of the 4th lumbar root, sensory impairment can be detected along th
anteromedial surface of the leg from the patella downwards with some sensory impairment of the side of th
thigh. In case of involvement of the 5th lumbar root, sensory impairment is detected in the back of the thigh
most of the lateral aspect of the leg and dorsum of the foot. In case of involvement of 1st sacral root (which
suggests protrusion of L5/S1
disc) sensory impairment is
noticed on the sole and outer
margin of the foot with loss of
ankle jerk.
In short, in case of L51S1
disc protrusion, usually the 1st
sacral nerve root is involved
and there will be sensory im
pairment of the sole and outer
margin of the foot and in the
dorsum of the web between the
great and the second toe with
absence of the ankle jerk.
In case of L4/5 disc
protrusion, usually the 5th
lumbar root is involved, in
which there will be sensory
impairment of the dorsum of
the foot, lateral aspect of the
leg and back of the thigh, there
will be weak dorsiflexion of
the ankle and great toe but no
alteration of the ankle jerk.
In case of upper iumbar
disc(L3/4 or L2/3) prolapse,
there will be sensory impair
ment of the front of the lower
thigh and side of the thigh and
anteromedial aspect of the leg.
A IB There will be weakness of
quadriceps muscle and tibialis
Fig. 30.3.— Shows segmental sensory distribution of the nerves of the lower anterior. There will be weak
limb. A. Shows the anterior aspect of the lower limb. B. Shows the posterior
aspect of the lower limb.
dorsiflexion of the ankle and
extension of the knee and there
will be diminished knee jerk.
(v) Straight leg-raising test.— The patient lies supine on the examining table. First exclude that there is
no compensatory lordosis by insinuating a hand beneath the lumbar spine. The patient is now asked to raise
lower limb keeping knee straight. He should continue to raise the leg till he experiences pain as evidenced by
watching his face. The angle at which the pain is felt is recorded. To be sure the test is repeated and as the an
is approached additional care is exercised to note when the pain starts. If the pain is evoked under 40° it sugg
impingement of the protruding intervertebral disc on a nerve root. If the pain is evoked at an angle above 40
it indicates tension on nerve root that is abnormally sensitive from a cause not necessarily an intervertebral d
protrusion.
At the angle when the patient experiences first twinge of pain, the ankle is passively dorsiflexed. This causes
aggravation of the pain due to additional traction to the sciatic nerve (Bragard’s sign). It suggests irritation
one or more nerve roots either by disc protrusion or from some other space occupying lesion. This second p
of the test is important to differentiate sciatica from diseases of the sacro-iliac joint. In the latter condition
straight leg-raising test will be positive but there will be no aggravation of pain during passive dorsiflexion
the ankle.
1. X-ray.—Anteroposterior and lateral views of the whole lumbar spine and sacrum should be tak
routinely. This is to exclude any bone pathology and to detect disc prolapse. Pathological narrowing of the
S
intervertebral space is noticed in X-ray in l/3rd of cases of disc
prolapse. Various other bone deformities may be detected by X-
ray which are the causes of backache.
2. Myelography.— Visualisation of disc prolapse by

radio-opaque medium e.g. lipiodol, myodil or pantopaque. 3 to
5 ml of solution is injected slowly into the subarachnoid space.
This is followed by X-ray screening on a tilting table. Filling
defect of the radio-opaque medium is diagnostic of lumbar disc
prolapse. The radio-opaque medium should be aspirated after
the examination is over. Myelography is of tremendous impor
tance in excluding a tumour of cauda equina to be differentiated
from disc prolapse. It must be remembered that negative myelo
graphy does not rule out presence of disc prolapse.
3. Epidurography.— Injection of water soluble contrast
medium into the epidural space is often preferred due to the risk
of possible long term sequel of oily contrast medium. The most
commonly used medium is Urografin (sodium diatrizoate)
premedication. But it is preferred to negative surgical exploration.

5. Magnetic Resonance Imaging (MRI).—This investigation has recently brought about revolution in
investigation of disc prolapse. Where facilities of this investigation are available, this has certainly surpassed
the previous investigations so far as its diagnostic efficacy is concerned (See Fig.30.6).
Treatment.—
5 CONSERVATIVE
TREATMENT.—
Except rare eases of
... jgtt. paraplegia due to massive
: -4S . protrusion, which is a sur
':‘ - \ .; j gical emergency, all cases
f MM " I HH Hi of prolapsed intervertebral
• Fj,* disc should be given a trial
r- m, 1)1 conservative treatment
initially. In a proportion of
i cases this treatment may
H| „ ^ring about comPlcle and
£^>?r'V permanent relief.
•A’"' * ■*' nal point in conservative

‘ * ’ NHHHmHHHHRMIHH treatment is rest to the
Fig. 30.5.— Discography showing a normal L4/L5 disc, but a protruding L5/S1 disc. lumbar spine. The patient
should go to bed with
boards placed under the mattress. Strict recumbency for 3 weeks is essential.
If the attack is less severe, the patient may get out of the bed earlier and a corset is worn. He must avoid
stooping or lifting weight.
Immobilisation in plaster of Paris jacket may be recommended after a few days rest in bed when pain has
subsided considerably. This should be worn for 2 to
3 months. This plaster jacket should extend from the
nipples to the pubis.
2. Traction.— In severe cases skin traction
may be applied to one leg or to the pelvis. The traction
may have opened up the disc spaces to cause reduc
tion of the prolapse. If this is not believed, traction
certainly enforces rest. This is an effective means to
enforce rest. Traction may be applied minimum for 1
hour daily for 3 weeks.
3. Other methods.—Injection of 0.5% solu
tion of procaine epidurally has been claimed to
reduce prolapse. About 50 ml should be injected.
Injection of 2 mg of chymopapaine into the disc
space has also been claimed to reduce prolapse. The
enzyme is said to dissolve the nucleus pulposus.
The majority of cases can be cured by the conser
vative method. Operation is only indicated if the
symptoms persist or neurological signs develop.
Fig. 30.6.— MRI shows protrusion of the L5/S1 disc. OPERATIVE TREATMENT.
It also denotes an element of disc degeneration. Removal of the disc is the main operation. It was
previously performed by hemilaminectomy. A midline incision is made. The muscles are stripped off from th
outer surfaces of the laminae with a wide chisel. The adjacent margins of the two laminae and the ligamentum
flavum are removed. The nerve root and the duramater are gently retracted to expose the intervertebral disc.
prolapsed, bulging of the disc can be noticed. The disc material is extracted out piecemeal with pituitary force
Almost the entire disc should be removed.
The disc above must be inspected even when the prolapse has already been detected and removed.
Nowadays a full laminectomy is not performed, as it causes weakness of the spine. An interlaminar
approach with excision of the ligamentum flavum and little, if any, of parts of the adjacent lamillae. This is cal
'fenestration operation'.
Many orthopaedic surgeons recommend immediate spinal fusion in every case operated for prolapse
intervertebral disc. This is because they are concerned with the mechanical aspects of the spinal column after
removal of the intervertebral disc. But an intelligent compromise is to chalk out a few indications for spinal
fusion. The indications for spinal fusion are :—
(i) Presence of osteoarthritis ; (ii) Instability is anticipated (when pain is not relieved by rest, particularly
at night, as the patient wakes up when he turns over in the bed); (iii) In case of heavy manual workers; (iv) Wh
associated with congenital malformations or spondylolisthesis.
Bosworth’s method of posterior spinal grafting is mostly used. A bone graft from the superficial cortex of
the posterior part of the ileum is removed and is notched at either end to receive the spinous process above an
below. The area to be fused is stripped off its cortical bone and the two spinous processes are cut flush with th
laminae. The graft is inserted with the patient in flexion and the spinous processes separated. The lumbar spin
is then extended and the graft is automatically fixed between the spinous processes. The fusion is further
reinforced by separate iliac strips.
CERVICAL SPONDYLOSIS
It is the commonest disorder of the cervical spine. It is a degenerative condition of the lower cervical region
and is characterised by :—
(i) Degeneration of the intervertebral disc with extrusion of the disc material;
(ii) Surrounding fibrosis which may spread to the nerve roots ;
(iii) The edges of the vertebral bodies hypertrophy,which is known as ‘lipping’;
(iv) There is also degeneration of the neurocentral joints of Luschka with the formation of osteophytes
which project into the intervertebral foramen producing neurological symptoms.
It is in fact osteoarthritis of the intervertebral joints.
Clinical features.— Patients are usually over 40 year of age.
SYMPTOMS.—
(i) The most important complaint is pain in the neck which appears gradually and becomes worse in
the morning at the time of getting up.
(ii) The pain may radiate widely — to the occiput, to the frontal region, to the shoulders and down one
or both arms.
(iii) Weakness, paraesthesia and clumsy finger movements are sometimes complained of in the upper
limb.
PHYSICAL SIGNS.—
(i) Inspection — does not reveal any abnormality.
(ii) Palpation.— Some tenderness in the affected cervical region may be elicited.
(iii) Movements of the neck are usually restricted to certain extent. Pain is usually complained of at the
extreme of movements.
(iv) Neurological examination of both the upper limbs is highly important and it may reveal involve
mentof nerve roots. Examination for sensory loss, motor weakness and of tendon reflexes should be performed
X-ray.— This is diagnostic and it shows diminution of disc spaces. ‘Lipping’ is also evident. Osteophytes
can also be seen.

Angiography—may reveal restriction of movement of vertebral and basilar arteries with the movement o
the neck. This occurs due to fibrosis from spondylosis which engulfs the arteries and restricts their movem
as also cause constriction in those arteries. Patient may feel dizzy or even black out with movements of the
Treatment.—
(i) Heat and massage to the neck and shoulder girdles are often relieving.
(ii) Cervical collar is highly effective as it minimises neck movement and relieves symptoms.
This is required when conservative treatment fails to relieve symptoms and there are neurological signs
which are not relieved by the above means.Spinal fusion is the main operative treatment, but it should be a
with removal of osteophytes which press on the nerve roots and removal of bony ridges if they are detecte
pressing on the anterior surface of the cord.
LUMBAR SPONDYLOSIS
The pathology is almost similar to that of cervical spondylosis. This affects mainly the lower lumbar ver
tebrae.
Clinical features.— Backache is the main symptom. Sciatica may also supervene when the nerve roots are
compressed by osteophytes.
Treatment is rest and lumbar corset to limit movement of the lumbar spines.
Spinal fusion is rarely indicated.
SPONDYLOLISTHESIS
Though this is an orthopaedic problem, but it was
first noticed by an obstetrician named Killan in 1853.
Though he considered it to be chiefly affecting women,
yet later on orthopaedic surgeons have discovered
that this condition affects males more often than
females.
This is a deformity of the lumbosacral region
produced by gradual slipping forward of the lumbar
spine on the sacrum. The main pathology is a separa
tion of the body of the vertebra from its posterior
articulation, lamina and spinous process due to de
fect in the pedicles. The pedicles are concerned with
holding the vertebral body in front with the laminae
and spinous process behind. Due to the defect in the
pedicle (pars interarticularis), the laminae with the
spinous process are left in their normal position,
whereas the vertebral body moves forward alongwith
the spinal column.
The shift is almost always seen between L5 and
the sacrum or between L4 and L5.
Fig. 30. 7.— Spondylolisthesis showing a gap in the Pathology.— The spondylolisthesis can be clas
pars interarticularis indicated with an arrow. sified into 4 varieties :—
The figure shows forward displacement of L5 on SI.
1.
variety, in which there is a defect or gap in the pars interarticularis (spondylolysis). It runs in families and i
familial condition. The condition is usually revealed later in life, probably due to continuous stresses.
A NEW BOOK
UNDER AUTHORSHIP OF DR. S. DAS
UNDERGRADUATE
FRACTURES &
ORTHOPAEDICS
UNDERGRADUATE
FRACTURES
&
ORTHOPAEDICS
S.Das
edition MBS S. (Cat). F.R<XS. A
It is a concise, complete and exam-oriented book, which

is fully coloured. This book not only provides a clear concept
on the subject, but also is extremely useful in answering
MCQs for MD/MS entrance examinations. It is also helpful
for the postgraduate students to learn 'the basics of fractures
2. Congenital.— The superior sacral facets are defective,which is responsible for the forward slip of the
5th lumbar vertebra alongwith the spinal column above. The incidence is about 10% to 20%.
3. Degenerative.—Degenerative changes of the discs and the facet joints may cause forward slip, which
is more common at L4/5 level. The incidence is about 25%.
4. Traumatic.—Trauma may lead to fracture of the pars interarticularis or the pedicle leading to traumati
spondylolisthesis. The incidence is approximately 5%.
It is the pars interarticularis which is the part of the pedicle between the superior and inferior articular face
When the pars interarticularis is in two pieces, the gap is occupied by fibrous tissue, then the vertebra is divid
into two parts—a posterior part which consists of the spinous process, laminae and inferior articular facets an
an anterior part which consists of the vertebral body and the superior articular facets. In spondylolisthesis wh
there is a gap in the pars interarticularis the posterior part of the affected vertebra remains in line with the low
part of the vertebral column, whereas the anterior part moves forward alongwith the upper part of the verteb
column.
Even if there is no gap in the pars interarticularis it may be elongated or the facets may be defective to caus
spondylolisthesis. Because of the deformity, the spinal canal is not narrowed, but the nerve roots may be
compressed by the narrowed intervertebral foramina.
SYMPTOMS.— Backache is the main symptom. In children the condition may be painless, when unduly
protruding abdomen may draw the notice of the observant mother. Even in adolescents and young adults
backache is the main symptom. It is usually of gradual onset and of long duration. Pain is usually intermittent
which gets worse after exercises. It is dull ache in character. Sciatic pain along one or both lower limbs is
sometimes complained of. The pain is usually relieved by rest.
This condition is considered to be the most common cause of low back pain and sciatica in children and
adolescents.
PHYSICAL SIGNS.—
(i) The trunk is shortened.
(ii) Deep transverse furrows are seen on both sides of the trunk between the ribs and the iliac crest.
(iii) There is diminution of space between the ribs and the crest of the ilium and between the xiphoid proce
and the pubis.
(iv) The sacrum
is unduly prominent.
There may be promi
nence of the 5th lumbar
spine above which a
depression can be seen.
(v) A consider
able amount of lordosis
may be noticed.
(vi) Occasion
ally there may be lum
bar scoliosis.
X-ray.—The ant-
teroposterior v i e w
shows that the upper
border of the 5th lum
IB bar vertebra is lower
Fig. 30.8.—The figure demonstrates Ullman’s sign. A.— Normal. and almost at the same
B.— Spondylolisthesis. See the text. level with its transverse
processes.
The lateral views demonstrate the forward shift. Normally, when the anterior border of the first sacral b
is drawn upwards vertically, it will be seen to be well in front the anterior border of the 5th lumbar body, b
in spondylolisthesis this will cut through the body of the 5th lumbar vertebra This is known as Ullmann's s
The defect of spondylolisthesis is best shown in oblique view as this enables to visualise the pars
interarticularis. An outline of ‘Scot’s Terrier’ can be easily seen in this view with the neck formed by the pa
interarticularis. When there is a break in the pars interarticularis the terrier is decapitated.
Treatment.—
When the symptoms are slight, conservative treatment can be started. The objectives of this treatment a
— (i) reduction of stress and (ii) restoration of tone of the spinal muscles. These can be achieved usually by
rest and lumbar corset. This should be added by exercises — particularly extension of the spine to strength
the spinal muscles.
When symptoms are more serious and cannot be relieved by simple measures as mentioned above, ope
treatment should be considered. There are various types of operations —
1. Direct repair.— Through posterior approach the gap in the pars interarticularis is thoroughly rawed
and then fixed with bone chip grafts and a screw. Both sides are fixed. The method can be applied only wh
there is a minor gap without much slipping. The advantage of this operation is that movement of the spine
not sacrificed. The nerve roots should be relieved from adhesions in the intervertebral foramina.
2. Posterior spinal fusion.—The advantage of fusing the bodies of the vertebrae is that it prevents furthe
displacement. When there is slipping on the 5th lumbar vertebra on the sacrum, the spinous processes of th
L5 and SI are fused with bone grafts.
3. Anterior fusion.— This is more popular method of spinal fusion in this condition. The approach may
be intraperitoneal or extraperitoneal. After lifting the iliac vessels and the sympathetic plexus, an excellent
exposure of L4 and SI should be obtained. By means of an osteotome a rectangular gap is produced betwee
the sacrum and displaced vertebra extending backward for about 2 cm. The gap is produced by removing
portion of the body of the L5 vertebra, SI vertebra and the intervening intervertebral disc. Autogenous bon
grafts are taken from the crest of the ilium. These grafts are fitted accurately in the gap produced by the
osteotome, alongwith correction of the slip or deformity.
The patient should be kept recumbent in a plaster shell for at least 3 months. A successful solid fusion u
gives complete relief.
Traumatic spondylolisthesis.— This usually occurs after hyperextension injury which may have fracture
a lamina or may have strained the pre-existing congenital defect of pars interarticularis. In case of only trau
spondylolisthesis a plaster jacket is worn for 3 months. This will heal the fracture. If spondylolysis is prese
spinal fusion is indicated.
LOW BACK PAIN

Low back pain is a very common symptom in early adult life and middle age. It is the commonest symp
complex related to the musculo-skeletal system. Almost all adults can remember of having sufferred from
backache at least once in their life time.
The causes of low back pain can be classified in the following way :
(A) In the back.—
(i) CONGENITAL —
(a) Spina bifida; (b) Spondylolisthesis; (c) Hemivertebra (when one of the two centres of ossif
for the vertebral body fails to develop); (d) Split vertebra (when there is a definite gap between the two cen
of ossification); (e) Abnormality in the articular processes (articular facets of the 5th lumbar vertebra may t
the form like that of articular processes of the thoracic vertebra); (f) Besides lack of fusion between the two
halves of the neural arch which produces the condition of spina bifida, the lamina may fail to fuse with the bo
of vertebra; (g) Sacralisation of the transverse process of the 5th lumbar vertebra.
(ii) TRAUMATIC —
(a) Lumbosacral strain;
(b) Injuries to the intervertebral joints, ligaments and muscles. These injuries are produced by external
violence which may overstretch the spinal column. The pain is sudden and although increased by certain
movements, it is a constant excruciating pain during the acute stage which is only partly relieved by rest. It is
sometimes difficult of find out the exact side of the lesion. In case of muscle strain the common site being the
origin of the sacrospinalis from the back of sacrum or the origin of the gluteus maximus from the posterior
superior iliac spine. The underlying pathology is simply the rupture of some fibres with consequent exudation
and swelling. Novocaine injection abolishes the local pain. In ligamentous injury the pain is deep-seated and
can be elicited both by pressure with the finger or by movement of the spine.
(c) Spondylolisthesis.— Many orthopaedic surgeons are of the opinion that trauma plays a significant
role so far as the aetiology of this condition is concerned. Minor repeated trauma may lead to this condition
which may be incriminated as a congenital lesion.
(d) Compression fracture;
(e) Vertebral process fracture (transverse and spinous processes);
(f) Ruptured disc.
(iii) FUNCTIONAL DEFECTS —
(a) Anteroposterior imbalance (pregnancy, pot belly, fixed flexion deformity of the hip joints etc.);
(b, Lateral imbalance (scoliosis, leg length discrepancy etc.).
(iv) INFLAMMATORY —
(a) Pyogenic osteomyelitis;
(b) Tuberculosis;
(c) Arthritis;
(d) Brucellosis;
(e) Ankylosing spondylitis;
(f) Myositis;
(g) Fibrositis.
(v) DEGENERATIVE —
(a) Osteoarthritis (spondylosis);
(b) Senile osteoporosis;
(c) Degenerative disc disease.
(iv) NEOPLASTIC —
(a) Primary tumours e.g. multiple myeloma, eosinophilic granuloma (Calve’s disease), haemangioma,
osteoid osteoma;
(b) Metastatic tumours from breast, bronchus, kidney, suprarenal, prostate, thyroid and gastro
intestinal tract.
(B) Other than the back.—
(i) ABDOMINAL DISORDERS, e.g. pancreatitis (very important), cholecystitis, biliary calculus, peptic
ulcer, hiatus hernia etc.;
(ii) PELVIC DISORDERS, e.g. inflammatory condition of the ovaries and tubes, intrapelvic tumour etc.;
(iii) GENITO URINARY CAUSES, e.g. renal infection, renal or ureteric calculus, prostatitis, prostatic
carcinoma, seminal vesiculitis etc.;-
(iv) VASCULAR DISORDERS, e.g. ischaemic pain from occlusion of the aorta or iliac arteries and
aneurysmal dilatation of the aorta may cause backache.
Two conditions worth special mention. These are — Lumbosacral strain and Fibrositis (Lumbago).
LUMBOSACRAL STRAIN (SPRUNG BACK)

It is the commonest variety of acute backache. This is usually caused by strain, stretching or tearing of various ligaments
of the vertebral column (interspinous ligaments, ligamentum flavum, anterior and posterior longitudinal ligaments and the
capsule of the posterior facet articulation). This condition develops from mechanical stress and strain which the lumbosacral
region renders itself. The commonest site is the lumbosacral region as the name suggests. It is the site of great shearing strain
and it is the junction between the mobile and fixed parts of the spinal column. Lumbosacral strain can occur in both acute
and chronic forms.
The acute form.— It may be due to sudden blow forcing the joint into positions beyond the normal range of movement,
or by an effort to prevent aheavy material falling or by a sudden body movement. In these cases the spinal muscles are caught
unaware, so the ligaments sustain the full force of injury.
One can elicit the history of recent trauma. Pain and tenderness are localised to the lumbosacral region. All the
movements of the spine are restricted. The patients usually are able to bend forward only by flexing the hip joints keeping
the lumbosacral region rigid. Very rarely pain may radiate to the lower limb, but it seldom goes beyond the knee joints.
Treatment.—
(i) Rest in bed for 7 to 20 days on a firm bed with pillows beneath the knees.
(ii) Local heating in the form of hot water bag or infra red lamp or short wave diathermy usually relieves symptoms.
(iii) Non-steroidal anti-inflammatory analgesic drugs should be prescribed.
(iv) When the acute symptoms have subsided gradual spinal exercises should be instituted.
Almost all such cases can be successfully treated by this non-operative means. Recurrence is prevented by regular
exercises.
Chronic form.— The onset of this condition is usually insidious, but it may follow an acute strain which has been
unrecognised or untreated. It occurs mostly in individuals with poor musculature and an increase in the normal lumbar
lordosis (usually a woman with pendulus abdomen). Gradually the attacks become more and more frequent and the pain
becomes constant as the age advances. In certain cases there may be narrowing of the intervertebral disc space with
narrowing of the intervertebral foramina causing nerve root pressure.
The symptoms of chronic cases vary. Some patients only complain of ‘weakback’ whilst others complain of pain and
restricted movements of the spine. Sciatic pain may be present when there is nerve root pressure by narrowing of the
intervertebral foramina.
Treatment.—
(i) Main treatment is to increase the muscle tone by various spinal exercises. These should be designed to flatten the
lumbar lordosis and to improve posture.
(ii) Lumbosacral belt or corset is only useful in cases with pendulus abdomen.
FIBROSITIS (LUMBAGO)
Fibrositis causing backache often reveals one or more tender nodules lying superficially in the erector spinae or its
attachments or in the region of the muscular attachments to the crest of the ilium.
In the lumbar region it is called 'lumbago'.
Aetiology is not very clearly known. It may be rheumatic fibrositis or local muscular spasm due to nerve root irritation.
It may be caused by some internal derangement in the low lumbar intervertebral joints.
Clinical features.— Pain comes on suddenly while the patient bends his back and it is very severe. The lumbar region
is almost immobilised by muscular spasm. Extension of the spine is almost impossible. If the tendon nodules are found,
pressure on these nodules aggravates pain and novocaine injection relieves the pain. Recurrence is common and the
condition may be chronic. Neurological signs are usually absent, but if present they indicate disc prolapse.
Treatment.—
(i) Rest on firm bed relieves the symptoms.
(ii) Manipulation of the lower lumbar region usually brings about recovery in majority of cases.
SCIATICA
It is a symptom and not a disease. The symptom is pain, which starts in the back and radiates down one
both lower limbs. Straight-leg raising test, if positive, is diagnostic of this condition. Bragard’s sign (see
‘Straight Leg Raising Test’) is more confirmatory. Lasegue’s sign is present in all cases. If the knee is kept in
full extension and the foot is dorsiflexed, the hip cannot be flexed to any extent without giving rise to great
due to direct stretching of the nerve.

According to various nerve root/roots affected, various dermatomes of the lower limb may show diminis
sensation. Similarly there may be muscle weakness according to the nerve root affected. Knee jerk or ankle je
may be diminished or absent according to the root affected.
CAUSES OF SCIATICA —
A. PRIMARY SCIATICA (Rare).— This may occur due to neuritis (often a polyneuritis) which may be
(i) toxic, e.g. from alcoholism, lead or arsenic poisoning or from diabetic or syphilitic neuritis.
(ii) Such neuritis may be infective, e.g. rheumatism, syphilis, focal sepsis etc.
B. SECONDARY SCIATICA.— This is usually due to compression of nerve roots. The causes are —
(a) In the vertebral canal —
(i) Prolapsed disc.
(ii) Caries spine.
(iii) Tumour of the cauda equina or meninges.
(iv) Tumours of the vertebral column.
(b) In the vertebral foramen —
(i) Tumour of the nerve root.
(ii) Lymphadenomatous deposit.
(iii) Spondylolisthesis.
(iv) Lumbago.
,. " —
(v) Ankylosing spondylitis.
E
(c) In the pelvis
'S£y- (i) Compression by an abscess,
v' (ii) Compression by a tumour.

Prolapsed disc is by
TUMOURS OFfar the most
THE common cause of
VERTEBRAL
sciatica. COLUMN
The majority of the tumours of the vertebral column
are malignant. The probable tumours are :
Benign tumours.— These include chondromas,
osteoma, Fibroma, haemangioma and giant-cell tumour.
These tumours only become evident when they cause
spinal compression by pressing on the anterior surface of
the cord.
Malignant tumours.— These can be primary or
secondary. PRIMARY TUMOURS are usually seen in
children and young adults and these are multiple my
eloma, Hodgkin’s disease, chondrosarcoma and fibro
sarcoma. These tumours also present with spinal cord
compression. Occasionally they may present as palpable
swelling, particularly when the tumour affects the neural
arches.
Treatment is first deep X-ray therapy. If it does not
work operative removal is indicated.
SECONDARY TUMOURS.— Malignant tumours
from various parts of the body often metastasise in the
vertebral bodies. Such secondary deposits are in fact the
commonest tumours in the vertebral column. The malignant lesions which often metastasise to the vertebral
column are : Breast carcinoma, prostatic carcinoma, hypernephroma, bronchogenic carcinoma, thyroid
carcinoma in order of frequency. Majority of these secondary deposits are carried by blood vessels from the
primary sites to the vertebral column. There is a rich venous plexus in the extradural space and around the
vertebral bodies which often carry directly the malignant cells from their
primary sites. The common examples of such metastasis are from carci
noma prostate and carcinoma breast. Majority of such lesions are osteol
ytic, except a few from carcinoma of the prostate which may be of
osteosclerotic type. Collapse of vertebra is not uncommon in osteolytic
lesion when it has destroyed considerable portion of the vertebral body.
One malignant tumour directly invades the vertebral column and that
is malignant neuroblastoma of the sympathetic chain. This tumour invade
the vertebral column through intervertebral foramen.
Clinical features.— Majority of the primary carcinomas of the
vertebral column occur in children and young adults, whereas secondary
deposits in the vertebral column are common in aged people above 40
years of age.
SYMPTOMS.— The most common presenting symptom is the local
pain and radicular pain in the distribution of one or more spinal roots.
Such pain is slow on onset and is aggravated by movement of the spine.
So the patients often remain static in a chair or in bed for hours. Any
increase in the intradural pressure e.g. coughing, sneezing or defaecation
will cause increase of pain.
Occasionally deposits may develop painlessly till there is sudden
collapse of the affected vertebra or vertebrae producing severe acute
backache and sudden paralysis.
Any patient above 40 years of age when complains of backache, should
be investigated properly to exclude secondary deposit in the spine.
PHYSICAL SIGNS.— Careful examination should be made to ex
clude neurological manifestations in the lower limb. Two types of lesion
Fig. 30.10.— Shows the relative may be noticed in this condition — (i) lower motor neurone lesion and (ii)
position of spinal segments to
vertebrae. upper motor neurone lesion.
(i) In lower motor neurone lesion
and paralysis cf individual muscles and decrease in muscle tone. Reduction in tendon and cutaneous reflex
will also be obvious. There may be wasting of muscle in late cases.
(ii) In upper motor neurone lesion, in which ihe pyramidal tract of the spinal cord is pressed upon, the
will be spastic paralysis with increase of tendon reflexes and positive Babinski sign.
Examination of the spine is also important though it should be done with utmost gentleness. Localised
tenderness and abnormality of the alignment of spinous processes are important diagnostic features of
secondary metastasis in the spinal column.
Relationship of the spinal segments to vertebrae is important. As the spinal cord ends at the lower level
the first lumbar vertebra, the spinal segment does not correspond to the vertebrae (see Fig. 30. 10 ).
In the cervical region the spinal cord segment is one above in number than the corresponding vertebral
i.e. 6th cervical cord segment is opposite to the 5th cervical spine.
In the upper thoracic region the spines are two lower in number than the corresponding cord segment i.
the 3rd thoracic spine corresponds to the 5th thoracic cord segment.
In the lower thoracic region the spines are three lower in number than the corresponding cord segment
is 8th spine corresponds to the 11th thoracic cord segment. 12th thoracic spine corresponds to 4th lumbar
segment. In the 1st lumbar vertebral canal all the distal segments of the cord lie as the spinal cord ends at the
lower border of the 1st lumbar vertebra.
Treatment.— Treatment of the secondary deposits in the spinal column varies with the type of the primary
tumour. When it is secondary to the breast carcinoma or prostate carcinoma, treatment is mainly hormone
therapy. Stilboestrol works in secondaries of prostate carcinoma, whereas adrenalectomy and oophorectomy
are good for secondaries of breast carcinoma. These are discussed in details in the corresponding chapters.
In secondaries from other carcinomas deep X-ray therapy is quite helpful. Support to the spine with plaste
jacket and analgesics are also required as adjuvant measures. Intrathecal phenol (5% in myodil) injections are
quite helpful in relieving agonising pain.
Operation of laminectomy with decompression of the cord and excision of as much of the tumour as possi
may be performed in cases of unrelieved pain with deteriorating neurological state. But this is an extreme ste
and when the patient’s general condition is already poor, one must not add to the burden of suffering withou
definite chance of improvement.
TUMOURS OF THE SPINAL CANAL
Tumours inside the spinal canal are divided into two groups — I. Intradural tumours, which are situated
inside the duramater and II. Extradural tumours, which are situated outside the duramater but inside the spin
canal.
I. Intradural tumours.—
These tumours are further subdivided into 1. Extramedullary tumours, which constitute about 80% of thes
tumours and which are situated outside the spinal cord and 2. Intramedullary tumours, which coustitute only
20% of these tumours and are situated within the spinal cord.
1. EXTRAMEDULLARY TUMOURS.— Two varieties are usually found in this region — neurofi
bromas and meningiomas.
Neurofibromas are common in males and usually arise from posterior nerve roots, so situated in the
posterolateral aspect of the spinal cord. These tumours gradually become extradural and may even find their
ways through the intervertebral foramina to reach outside the vertebral column.
Meningiomas are more common in women. These are usually of the size of grapes. These are usually
attached to the duramater and indent the spinal cord.
2. INTRAMEDULLARY TUMOURS.— The peculiar feature is that majority of these tumours are
situated in the cervical region. Usually 3 varieties are detected — (i) gliomas, (ii) ependymomas and (iii)
vascular malformations.
(i) Gliomas are usually diffuse and are irremovable.
(ii) Ependymomas arise from the ependyma lining of the central canal. These tumours are either soli
or cystic. These can be excised.
(iii) Vascular malformations are rare and usually no treatment is available for them.
II. Extradural tumours.—
These tumours are situated outside the duramater but inside the spinal canal. This is the area which is rich
in venous plexus.
The most common tumour in this region is the secondary bony metastasis. The other tumours are lipoma,
angiolipoma, liposarcoma, Schwannoma and meningioma and other primary bone tumours e.g. chordoma,
osteoclastoma, aneurysmal bone cyst and sarcoma.
SCOLIOSIS
The normal spine in human being is straight when seen from behind. Deviation of the spine to one side is known as
‘scoliosis'.
Scoliosis can be broadly classified into — A. Non-structural group and B. Structural group. The main difference is that
in the non-structural group the vertebrae are not rotated and the scoliosis is transient and not fixed.
A. NON-STRUCTURAL SCOLIOSIS.—
This is also called mobile or transient scoliosis. This can be divided into three groups — I. Postural scoliosis, II.
Compensatory scoliosis and III. Sciatic scoliosis.
I. Postural scoliosis.— This is common in adolescent girls. The primary curve is often convex to the left and is
usually mild.
The scoliosis disappears when the child bends forwards. This is diagnostic of this condition. In structural scoliosis the
curve becomes accentuated on bending. Spontaneous recovery is almost invariable and thepatients may be instructed spinal
exercises to bring about good tone of the spinal muscles and a good postural habit, v
II. Compensatory scoliosis.— Such scoliosis occurs as compensation of a short leg. The diagnostic feature is that the
scoliosis disappears when the patient sits down. This cancels inequality of the length of the lower limbs. Short stemomastoid,
ocular disorders and abnormalities of the chest may also cause compensatory scoliosis of the cervical and thoracic region.
m. Sciatic scoliosis.—Prolapsed intervertebral disc presses on the nerve root to cause sciatica. Depending on whether
the prolapse is pushing the nerve root laterally or medially there may be scoliosis towards the affected side or towards the
normal side respectively. '
B. STRUCTURAL SCOLIOSIS —
This is also known as fixed scoliosis. In this condition there is always rotationof the vertebra in the fashion that the bodies
rotate towards the convexity of the curve and the spinous processes rotate towards the concavity.
There are usually three curves — the middle one is known as the primary curve and is the main scoliosis. The above
and below the main curve are the compensatory curves which later on also become fixed.
In case of structural scoliosis the deformity gradually worsens till the spinal growth of the individual ceases. This can
be assessed by the complete appearance of the iliac apophyses on X-ray, which is known as ‘Risser's sign . The deformity
increases with the spinal growth. This is due to the fact that greater pressure is probably exerted through the epiphyses on
the concave site, this minimises growth on this side and so increases the deformity.
Varieties.—
1. Congenital.— Congenital defects in the vertebrae e.g. hemivertebra, fused vertebrae, absent discs, absent ribs etc.
may cause scoliosis. From outside there may be a pad of fat, dimple, excess hair or angiomas associated with such congenital
deformities. Congenital scoliosis is usually mild, but occasionally it may be severe. Neurological manifestations are not seen
in congenital scoliosis except when it is associated with spina bifida.
2. Paralytic.— Poliomyelitis, muscular dystrophies and cerebral palsy may cause scoliosis. Unbalanced paralysis,
particularly of the lateral abdominal muscles and intercostal muscles cause scoliosis. Such scoliosis usually appears some
years after the original disease and gradually increases progressively.
3. Neurofibromatosis.— About l/3rd of multiple neurofibromatosis cases develop scoliosis. Such scoliosis usually
occurs in the thoracic region and may become severe. Characteristic pigmentation of the skin known as Cafe-au-lait spots
are usually always present to diagnose such condition.
4. Idiopathic.— By far this is the commonest variety. As the name suggests, the cause is not known. Genetic factors
seem to play a considerable role. The diagnosis is reached by excluding other varieties of scoliosis. Some sort of mental
defects usually accompany this condition. Such scoliosis is more often seen in adolescents which may affect any area of
the spine. Sometimes idiopathic scoliosis is seen in infants, when the primary curve is always thoracic.
Some rare varieties of fixed scoliosis are as follows. These constitute only 5% of all structural scoliosis.
(a) Dystrophies.— In some bone dystrophies and malformation syndromes there may be associated scoliosis. This
is particularly seen in Marfan’s syndrome and osteogenesis imperfecta.
(b) Syringomyelia.— High thoracic scoliosis is common in syringomyelia. Neurological deficits in the form of loss
of sensation, weakness of muscles, trophic changes are seen in the upper limbs with claw hand.
(c) Friedreich’s ataxia.—It is arare familial condition which is associated with scoliosis and pes cavus. The condition
is seen between the ages of 5 and 15 years. This condition is characterised by ataxia, tremor, slurred speech and clumsiness.
As mentioned above idiopathic scoliosis is common in young adolescent girls.
Symptoms.—The main presenting symptom is the deformity. High scoliosis is usually seen in adolescents. Lumbar and
lower curves are seen later in life.
Backache is sometime the presenting feature particularly with congenital variety.
Physical signs.— Some abnormalities like lipoma, angioma, dimples, naevi, excess hair and angiomas are sometimes
seen in congenital scoliosis. Skin pigmentation in the form of Cafe-au-lait is often seen in neurofibromatosis varieties.
Neurological signs should always be looked for. The heart and lungs should always be examined thoroughly to find out
abnormalities there. A portion of cases of thoracic scoliosis is associated with congenital heart diseases. Similarly diseases
of cardiorespiratory system are seen particularly in thoracic scoliosis more as a result of scoliosis.
On careful inspection one can easily detect the deviation of spinous processes from the midline. One can also assess the
protrusion of the rib angles due to rotation of the vertebrae. One side of the chest looks flattened whereas the other side looks
projected. In case of high scoliosis, the level of the shoulders may not be in one line, one shoulder will be highly placed than
its felow. In case of lumbar scoliosis one hip will be more prominent than the other.
On careful palpation one can assess the rotation of the vertebrae involved in scoliosis. When the patient bends forward
the scoliotic curve becomes more obvious. This is diagnostic of structural scoliosis and is due to rotation of the vertebrae.
X-rays may reveal congenital abnormalities, if present. The angle of curve is usually measured by X-ray.
Treatment.—
CONSERVATIVE TREATMENT.— It is intended to correct the deformity to certain extent and to prevent further
increase of deformity in the growing child.
1. Exercises.—These help to make good posture of the body to hide the deformity. These also help to keep the back
supple which will be of help subsequently after treatment.
2. Supports.— The intentions for some sort of support to the spinal column are :— (i) to correct the deformity to
certain extent and to minimise the increase of deformity till spinal maturity is achieved when operation can be recommended;
(ii) to correct the deformity in case of minimum to medium deformity.
The Milwaukee brace is now established as an essential part of this treatment. Milwaukee brace and vigorous exercise
are started early inpatients with curves of mild or moderate severity. The correction will be achieved if treatment is continued
till the patient attains spinal maturity. Proper use of Milwaukee brace has resulted in fewer patients with idiopathic scoliosis
requiring surgery. The most favourable response to this treatment has been observed in patients with curvatures under 40
degrees and under 13 years of age. In Milwaukee brace there are adjustable steel supports transferring stress direct from the
chin and occiput to the iliac crest. By extending the steels the curve can be straightened gradually.
Another support therapy is the plaster jacket. A window in the plaster is so placed that breathing tends to straighten the
curve.
Indications.— (i) Failure of Milwaukee brace conservative method.
(ii) Too late cases for conservative treatment e.g. when the patients are over 15 years of age and the curves are over
50 degrees.
(iii) When the thoracic curves are over 60 degrees — these cases usually show a tendency to increase the deformity
and operation is the only treatment available.
Pre-operative correction.— Several methods of correction have been used e.g. plaster cast with windows and wedgings
which are first done, followed by spinal fusion and post-operatively plaster splintage is continued for many months.
Though the above technique is very straight forward, yet it is not very effective. So complex instrumentation is now
becoming increasingly popular.
Halo-pelvic traction pre-operatively may be used. A metal halo (hoop) is screwed to the outer table of the skull and a
second hoop is anchorded with transfixing screws to the pelvis. The two hoops are gradually moved apart with correcting
steel rods.
A halo-femoral traction may be used with the patient on a Stryker bed, where traction is applied through the halo-fixed
in the skull and counter traction through femoral skeletal pins.
Harrington instrumentation can be used for corrections.
Operation.— The spine is first exposed widely through a long skin incision. All soft tissues including ligaments and
facet joints capsules are removed to expose bony surfaces. The spinous processes are chiselled off at their bases. The laminae
and the transverse processes are decorticated. The iliac cancellous strips are laid down over the decorticated bony surfaces.
These are laid down in layers. Such spinal fusion should extend from neutral vertebra proximal to the neutral vertebra distal
including all vertebrae within the major curve. Sometimes a series of wedges are excised each including the disc and
vertebral end-plates. Staples and screws are fixed to the vertebra] bodies. Thus deformities are corrected alongwith spinal
fusion.
A well moulded plaster cast is used for post-operative immobilisation. Harrington instrumentation may also be used,
which affords temporary internal fixation and an accessory correction device. The total period of plaster cast immobilisation
is usually from 9 to 12 months depending upon the length of the fusion. Recumbency should be for 3 to 4 months, after which
the patients can be ambulatory.
KYPHOSIS
Alterations in the normal anteroposterior curvatures of the spinal column is known as kyphosis. In fact it indicates excess
dorsal convexity of the spinal column. Like scoliosis a few varieties of kyphosis are non-structural and can be cured easily,
whereas others are of structural variety. i
NON-STRUCTURAL KYPHOSIS —
1. Postural Kyphosis.—It is quite common in adolescent girls and in women after child birth. Postural kyphosis may
be associated with other postural defect e.g. flat feet. This type of kyphosis can be easily treated by exercise and postural
training.
2. Compensatory.— A few kyphoses may appear as compensatory measure for other deformities such as congenital
dislocation of hip, fixed deformity of the hip or excessive lumbar lordosis.
3. Mobile kyphosis.— Such kyphosis is seen in differentmuscle weaknesses and as compensatory to lumbar lordosis.
This kyphosis may later on cause backache. This can also be treated easily by exercises and postural training. Certain muscle
dystrophies and poliomyelitis may also cause thoracic kyphosis.
STRUCTURAL KYPHOSIS —
There are various causes which may lead to structural kyphosis. Two varieties of kyphosis can be considered — 1.
Angular kyphosis or kyphos or hump back and 2. Round back or smooth kyphosis with a long gentle curve.
1. Angular kyphosis.— This is a sharp kyphosis or kyphos which is caused by affection of less number of vertebrae,
usually maximum of 3 or 4 varieties. The causes are :— (i) Traumatic — crush fracture or pathological fracture from
secondary metastasis, (ii) Inflammatory — tuberculosis or caries spine, (iii) Calve’s disease.
Calve's disease is a rare condition of eosinophylic granuloma affecting one vertebral body. The affected body becomes
flattened but the disc spaces remain normal. This condition is usually seen in children and the presenting feature is backache
and angular kyphosis. Treatment is a few months rest on firm bed or plaster shell.
2. Round back or smooth kyphosis.— A various conditions may lead to such deformity. According to age the causes
can be further classified into —
(i) Adolescents — Scheuermann’s disease.
(ii) Young adults — Ankylosing spondylitis.
(iii) Elderly individuals — Senile kyphosis and Paget’s disease.
Scheuermann's disease.—
AETIOLOGY.— Scheuermann himself considered this condition to be due to osteochondritis. Lambrinudi suggesled
that the epiphyseal plates are damaged due to excessive flexion of the vertebral column when there is limited flexion in the
hips due to tight hamstrings. The actual cause is still debateable.
The PATHOLOGY is that the epiphyseal plates are irregularly ossified, more dense and fragmented.
CLINICAL FEATURES.— This condition is seen in teen agers.
Symptoms.— The majority of the patients present due to increasing dorsal convexity of the back. A few patients may
complain of backache.
Physical examinations.— A smooth thoracic kyphosis is almost always seen. A compensatory lumbar lordosis is often
accompanied with. Spinal movements are usually normal or limitations are not detected very much. Straight-leg raising is
often limited to 60° due to tight hamstrings.
X-ray shows that bodies of a few thoracic vertebrae are wedged — mostly involved are thoracic 6th to 10th vertebrae.
The epiphyseal plates are dense and fragmented. The vertebral bodies may contain small translucent areas near the disc
spaces which are known as Schmorl’s nodes. The disc spaces are usually normal or slightly narrowed in the front.
TREATMENT.— A little deformity with no pain requires no treatment. When the deformity is slight and there is little
pain, various exercises should be recommended to strengthen the extensor muscles of the spine. Pain usually disappears
within a few months in these cases.
When the pain is severe and the deformity is considerable, the patient should lie flat on a firm bed or on a posterior plaster
shell. This is continued till the spinal growth is complete. When pain disappears, the patient may be allowed up wearing a
brace or plaster jacket by day and sleeping on plaster shell at night.
ANKYLOSING SPONDYLITIS —
AETIOLOGY.— The cause of this condition is not known very clearly, but an autoimmune reaction seems
to play a main role. Genes also carry this disease as it is often found in relatives of patients. Infection of prost
Reiter’s disease, psoriasis and ulcerative colitis are somehow or other associated with this disease.
PATHOLOGY.— The primary lesions are in the joints of the vertebral column. The early changes are
similar to those of rheumatoid arthritis. Some of the earliest and most characteristic changes occur in the
sacroiliac joints, where the disease seems to start. The early lesion is a type of synovitis with increased
vascularity and infiltration of lymphocytes and plasma cells. The intervertebral discs are first replaced by
vascular connective tissue and then undergo ossification which particularly affects the periphery of the annu
fibrosus and the intervertebral ligaments. There is destruction and narrowing of the joint spaces, which appe
in X-ray as haziness of the opposed surfaces of the bones. Later on ossification of the peripheral region of th
discs including spinal ligaments occur so that the whole spinal column is converted into a rod of bone.
CLINICAL FEATURES.— This is a disease of young adults. Individuals between the ages of 15 and 35
are usually affected. Men are more commonly affected than women.
Symptoms.— The commonest symptoms are pain and stiffness of the spine. The onset is insiduous. In the
beginning the symptoms are intermittent and only felt on getting up in the morning. A few patients may
complain of pains in various joints particularly in the lower limbs. Pain along the distribution of the sciatic n
or sciatica is sometime complained of, but the peculiarity is that it alternates from one side to the other. Vag
symptoms like malaise, fatigue, loss of weight and chest pains are also complained of. Ankylosis of the
costovertebral joints results in fixation of the thorax with interference in respiratory movements, so respirat
disease is apt to appear in late cases.
Physical signs.—The pathological process may stop at any stage. In about half of the patients it stops befo
any significant deformity can be seen. In a small number of cases it may pursue a long course for many year
till the entire spine becomes stiff like ‘bamboo spine’.
The back forms a continuous curve with dorsal convexity from the head to the sacrum. Even in milder ca
the normal lumbar lordosis is absent. Some tenderness may be elicited at the sacro-iliac joints in the beginni
but in late cases tenderness over the manubrio-stemal joints and symphysis pubis may be detected.
Movement of the spine is very much affected due to stiff lumbar spine. But even then flexion is possible b
mobile hips. Extension and lateral flexion of the spine are also limited.
X-ray.— Earliest changes are seen in the sacro-iliac joints. The joint line becomes blurred with irregular
surrounding sclerosis. The joint space is also gradually diminished and ultimately obliterated. Similar chang
are also seen in manubrio-stemal joint and symphysis pubis in late cases.
In the spine the vertebral bodies look ‘square’ by losing their normal anterior concavity. Calcification of
intervertebral ligaments and the peripheral parts of the disc spaces can be noticed. When such calcification i
completed, the vertebral column looks like a ‘bamboo spine’.
TREATMENT.—
1. Physiotherapy and exercise.— Though ankylosing spondylitis has got some link with inflammatory
disorders, rest has hardly achieved any place in its treatment. Physiotherapy and spinal exercises with deep
breathing are helpful in keeping the spine mobile. Swimming is also helpful. The patient should sleep on a h
bed or on a plaster cast to prevent occurrence of kyphosis.
2. Drugs.— Salicylates are helpful in mild cases but phenylbutazone is effective in moderate and severe
cases. Indomethacin in the dose of 25 mg thrice daily is also beneficial in moderate cases. Steroids are not he
ful, except when the disease is associated with severe iritis.
3. Radiotherapy.— It may be used as palliative measures, but its effectivity is less in an established case.
4. Operations.— This has practically no place in this condition. When the hips are also stiff, one may
perform total hip replacement to get mobility of the body as a whole.
Senile kyphosis.—
Degeneration of the intervertebral disc is probably the cause of senile kyphosis. Senile osteoporosis has a
got some contribution. In osteoporosis the vertebral bodies become soft and biconcave, whereas in true seni
kyphosis the disc spaces become narrowed, though the vertebrae are also slightly wedged. Ultimately os
teoarthritis of the intervertebral joints take place.
FRACTURES AND DISLOCATIONS OF THE SPINE

The importance of fractures and dislocations of the spine lies in the question of spinal cord damage. On t
basis the spine fractures are classified into two categories — stable fractures and unstable fractures.
I. Stable fractures.— This means the spinal cord is rarely damaged in these fractures and movemen
the spine is safe.
II. Unstable fractures.— In these fractures the spinal cord may be damaged, in case it has escaped it may
be injured by subsequent movement.

The students must note that stability does not depend on the fracture itself, but on the integrity of the
ligaments, particularly the posterior ligament complex. This complex
consists of the supraspinatous ligament, interspinatous ligament, the cap
sules of the facet joints
and possibly also the "
ligamcntum flavum.
Mechanism of in- t i HH -
jury.— In this section
we shall consider the
types of forces which
produce various types
of spinal injuries.
Mainly there are 4 types
of forces which may
cause spinal injuries.
These are: 1. Compres
sion forces, 2. Hinging
forces, 3. Shearing
Fig. 30.11.— Burst fracture of L3.
forces and 4. Direct
This fracture is stable, but painful
enough to merit support. injuries. Fig. 30.12.— Anterior wedge fracture.
Fig. 30.13.— Burst fracture. Fig. 30.14.—- Upper figure shows anterior wedge
fracture due to slight forward hinging force. The lower
1. COMPRESSION FORCES.— Such forces can figure shows vertebral fracture plus ligamentous injury
(extremely rare) due to vigorous forward hinging force
only be applied to straight portion of the spine. In fact (flexion injury).
there is no straight portion of the spine, except sometimes
the cervical and the lumbar spines may become straight instead of lordosis. In that way these forces cannot
jure the thoracic spine. When a person falls from a height the lumbar spine may be compressed; similarly if
weight falls on the head the cervical spine may be compressed. In compression force the nucleus pulposus s
the vertebral end-plates and fractures the vertebra vertically, with greater force the disc material may be for
into the vertebral body. Such fracture is known as ‘burst fracture'. This is a very stable fracture.
2. HINGING FORCES.— There are two types of hinging forces — forward hinging forces and backw
hinging forces.
Forward Hinging forces are common in lumbar spine injuries. This may occur when the patient falls from
the bent position or a weight falls on his bent back. The anterior portion of the vertebral body crushes, but the
posterior ligament complex remains intact. This is known as 'crush fracture’. This is a stable fracture. Forward
hinging injuries are rare in the neck as the chin touches the sternum before hyperflexion can occur.
This type of force can cause ‘wedge fractures’ in the thoracic region. This is probably commonest in the tho
racic spine. It should be borne in mind that this type of fracture can also be pathological due to malignant de
posits or osteoporosis.
Backward Hinging forces more commonly involve the cervical region rather than lumbar region. There
is hardly any chance of thoracic region to be affected by this type of force. In the cervical region this type of
injury may be caused by diving into shallow water. This will fracture the arch of the atlas or of the axis.
Occasionally the anterior ligament may be tom instead of any fracture. This is also a stable injury as the post
ligaments complex remains intact.
Backward hinging force causing lumbar injuries is less common. This may cause fracture of the lamina. I
may happen that the young toddler who falls repeatedly on his buttocks may sustain this type of injury whi
may well be the starting point of spondylolisthesis, which is recognised later in life.
3. SHEARING FORCES.— In this type of force there is rotation of the spinal column associated with
flexion. This injury is also common in the lumbar region. When a weight falls asymmetrically on the back or
a person falls from a height with the body twisted, such
type of injury may occur. A slice of bone is sheared off
from the top of one of the vertebral body and the posterior
facet may be fractured. The posterior ligament complex
tears, causing the injury an unstable one. Another type of
shearing force may be come across in which there is a
combination of flexion force with forward shearing —
the so-called ‘seat-belt fracture’, which is caused by
motor car accident. The pelvis is anchored to the seat by
the seat-belt and during accident the body is thrown
forwards. The posterior ligaments are torn, there may be
no bony fracture, but the upper facet may leap-frog over
the lower. This is also an unstable injury.
In the neck similar type of injury can occur due to fall
from a motor cycle or horse. A whip-lash injury of the
neck may also tear the posterior ligament and permit
Fig. 30.15.-—Combination of flexion and rotation
can cause dislocation in the cervical spine.
forward dislocation. It should be noted that as the facets
are relatively horizontally placed in the cervical region,
forward dislocation is more common in this region without fracture of the facets.
This type of force can also cause ‘true fracture dislocation’ in the thoracic region. The importance of this
type of fracture in the thoracic region is that almost invariably paraplegia results as the spinal canal is quite
narrow in the thoracic region.
4. DIRECT INJURIES.— Such injury causes avulsion fractures. In the cervical region the 7th spinous
process may be avulsed by direct injury, which is known as ‘Clay-Shoveller's fracture’. In the lumbar spine
the transverse processes may be fractured by direct injury and are often missed considering it to be muscle
injuries.
Before concentrating on the clinical examination of a patient with spinal injuries to detect the region of th
spine affected and the type of fracture, due attention should be given to the general examination of the patient.
The patient should be considered as a whole and careful examinations should be performed to exclude injur
to the chest, abdomen, head and the limbs. Head injuries,
chest injuries and abdominal injuries are more serious
and are threat to life. The limb fractures and dislocations
should be excluded and if have occurred should be
treated alongwith the spinal injuries.
Usually the patient is first seen lying supine on a
stretcher or trolly. To examine the back, the patient is
carefully turned to one side in one piece by two or three
persons.
Inspection.— The skin of the back is inspected for
abrasions or bruising which indicate the probable level
of injury.
Palpation.— The whole of the spinal column is
palpated systematically. The spinous processes and the
muscles by the side are carefully palpated. When there is
Fig. 30.16.— Continuation of flexion and rotation
readily causes an unstable fracture dislocation.
a gap in the spinous processes, this indicates injury to the
posterior ligament complex and the injury is probably an
unstable one.
Examination of lower limbs.— Buttocks and lower limbs should be carefully examined to assess the neuro
logical damage.
X-ray — is extremely important. The patient must be handled very carefully in the X-ray department.
Anteroposterior and lateral views must be taken. An oblique view is also very helpful which is centred throu
the spinous processes. First of all the bodies of the vertebrae should be carefully examined. Next the facets an
neural arches are examined. Lastly dislocations should be excluded.
MANAGEMENT —
1. BURST FRACTURES.— These are stable fractures.
In the thoracolumbar region.— The posterior portion of the fractured vertebral body is very close to the
duramater and nerve roots. That is why these fractures should always be treated in a plaster jacket, even tho
these are stable fractures. The plaster jacket is applied in the neutral position of the spine and not with
hyperextension of the spine. The plaster jacket should be kept for 6 weeks, which is replaced by a polythene
jacket for another 6 weeks. This polythene jacket however may be taken off during sleeping and washing.
In the neck.—A plaster collar should be applied for burst fractures, which should be worn for 6 weeks. Aft
that it is replaced by a polythene collar, till consolidation of the fracture is seen on X-ray.
Some burst fractures in the neck may be serious and may cause cord damage. Whenever there is evidence
of cord damage, skull traction should be applied. Skeletal skull traction should be used for this purpose. Suc
traction should be continued for 6 weeks, which is followed by a plaster or polythene collar till consolidation
of fracture is seen on X-ray.
It must be remembered that any neck injury associated with spinal cord damage is best treated with skele
skull traction. So long it is with this traction an unstable neck injury is safe.
2. CRUSH FRACTURES OR ANTERIOR WEDGE FRACTURES.— These fractures are caused by
forward hinging and are always stable.
In the thoracolumbar region.— Though previously these fractures were treated by a plaster jacket for 3
months with hyperextension of the spine, this is notrequired and even the vertebral body may recollapse wit
such plaster. These fractures are best treated by activity. When the back is painful and the muscles are in spa
radiant heat should be applied to the affected region. The patients should be turned on their faces several tim
a day and are taught how to use spinal exercises. As soon as the patient is comfortable, he can be ambulant a
be back to work. However spinal exercises should be continued.
In the thorax.— In this region also these fractures are treated by activity. Many of these fractures in this
region arc however pathological and should be treated accordingly.
In the neck.— These fractures are uncommon in the neck. A card-board or felt collar should be worn for
comfort. These collars are removed at night.
3. LAMINAR FRACTURES.— These are caused by backward hinging force.
In the thoracolumbar region.— These fractures are also best treated in a plaster jacket for 6 weeks, followed
by a polythene jacket till union is confirmed in X-ray.
In the neck.— A polythene collar is used. This is fitted in the neck in neutral position. It should be worn fo
3 months by which union can be expected.
4. Unstable fractures.—A. Management Of Fractures —
In the THORACOLUMBAR REGION.—
Fractures WITH Paraplegia.— Two types are available —
(a) Conservative method.— This method is not much practised nowadays, since it has the risk of causing
more damage to the spinal cord. The patient is turned every two hours on to his side in one piece by three nu
The skin is carefully cleaned, powdered and the bed-sheets are smoothed. By this the bedsores are avoided. A
two weeks, the patient can be moved easily and gradually union is expected.
(b) Operative method.— The spinal fusion is performed with plates which are attached on each side of the
spinous processes. Usually two spinous processes above and below the affected vertebra are fixed. This meth
is a safe procedure, which gives adequate facility for proper nursing. The patient also becomes comfortable.
Treatment of paraplegia should also accompany the treatment of fractures. Management of paraplegia is
described below.
Unstable fractures WITHOUT PARAPLEGIA.— The spine must be made stable as slight movement may
damage the spinal cord. This can be achieved by spinal fusion with plating.
However such fractures can also be treated by immobilisation of the spine in plaster bed. The patient is ta
to operation theatre and is placed prone on the operating table. He is now X-rayed. If reduction has been
achieved, plaster is applied to the posterior half of the trunk upto mid-thigh. Now the patient is taken to bed
is laid on the plaster back slab. For cleaning, which should be done at least once a week, the patient is turned
in prone position, the plaster shell is taken off and the back is cleaned and powdered. The patient is again lai
on the posterior plaster shell. After 6 weeks the fracture becomes almost stable, so a plaster jacket is applied
with the spine in neutral position. The patient should wear this plaster jacket for further 6 to 12 weeks, till un
is evident in X-ray. The patient however is allowed up and mobile so long he is in plaster jacket.
Sometimes by the prone position reduction is not achieved. This indicates locked facets. The table should
be hinged at the level of the fracture to reduce it. If the facets are still locked, the patient is anaesthetised and
gentle manipulation combined with traction may achieve reduction. If this also fails, open reduction should b
done operatively under direct vision. Following open reduction internal fixation should be performed. When
there is considerable bony damage, plates and bolts may be used for internal fixation. But if it is mainly
ligamentous injury, bone grafts should be used alongwith plates and bolts for internal fixation, as ligament r
takes longer time and may cause breakage of the plates before complete healing leading to further displacem
and injury to the spinal cord.
IN THE NECK.— Dislocations with or without fractures are more common in the neck which are unstable
injuries. These are best treated by skeletal skull traction for 3 weeks. This will cause reduction at the same tim
will give stability to the affected site. Now spinal fusion is performed with bone grafting. The spinous proces
and laminae above and below the fracture are decorticated. Bone grafts are laid along them and the processe
are fixed with wires. Anterior fusion may also be performed by fusing vertebral bodies anteriorly with bone
block inserted into them. The skull traction is continued throughout the operation and postoperatjvely till the
wound heals. The traction is then removed and a collar is applied. The collar should be worn till union of the
graft is confirmed by X-rays.
B. Management Of Paraplegia.— Three varieties of cord lesion occur —
(i) Cord concussion.— In this condition there is flaccid motor paralysis, sensory loss and visceral loss
below the level of cord lesion. It is in fact a functional damage rather than organic lesion. So recovery is usual
complete, which begins within 8 hours.
(ii) Cord transection.— In this condition there are two phases — firstly a phase of cord shock, which is
a temporary condition and is usually followed by irrepairable damage of the spinal cord. In the stage of cord
shock there is flaccid motor paralysis, sensory loss and visceral paralysis below the level of the cord lesion.
When the stage of shock disappears, the distal part of the spinal cord below the level of transection acts lik
an independent structure. So all visceral reflexes return, but they act independently without the influence of
upper motor neurone. There is spastic paralysis with increased muscle tone, tendon reflexes become
exaggerated and clonus appears.
(iii) Root transection.— Flaccid motor paralysis, sensory loss and visceral paralysis occur in the distribu
tion of damaged root.
Management.—
1. Treatment of skin.— Skin care is highly important in paraplegic patients. Anaesthetic skin may develop
pressure sores or bed sores within a few hours. Immediate plating of the spine is of considerable help to nurs
of the skin. Every 2 hours the patient is gently rolled to one side and his back is carefully washed, dried and
powdered. Creases in the bed sheets should be smoothened. After 4 weeks the skin usually becomes tolerant
and cure becomes easy. If at all bed sores develop, they usually do not heal without excision and skin grafting
2. Bladder and bowel care.— In specialised paraplegic centres intermittent catheterisation under aseptic
precautions can be performed. But in general hospital it is better to provide continuous drainage through a fi
Gibbon catheter. The catheter drains into a disposable polythene bag which is changed every day. Daily blad
wash with proper antibiotics should be advised. A self retaining Foley catheter should replace Gibbon cathete
Later on two types of incontinence may be seen:— (i) An automatic bladder which contracts reflexly when th
bladder is full to certain extent and (ii) overflow incontinence where bladder continues to distend till it is
manually emptied by suprapubic pressure or it is drained when it is extremely full.
A few patients are left with a high residual urine after emptying the bladder. Special investigations like
cystography and cystometry should be performed. Such patients may require transurethral resection of the
bladder neck or sphincterotomy. But these operations should be considered only when 3 full months of bladd
training has been completed.
The bowel should be drained with the help of timely enemas and aperients. Abdominal exercises can also
help for training of bowel habit.
3. Muscles and joints care.— Proper splints should be used to prevent flexion contractures in case of
paralysed muscles. The concerned joints should be moved passively through their full ranges at least twice da
Muscle tone may gradually come back. If not, one may consider operations like transfer of tendons.
FRACTURES OF THE PELVIS

Four types of fractures of the pelvis are seen —
I. Avulsion fractures.— These are relatively unimportant traction injuries associated with violent muscle
action. A portion of the bone which gives attachment to the concerned muscle becomes fractured and detache
from the parent bone.
II. Isolated pelvic ring fractures.— In this condition the pelvic ring is broken in only one place. So
displacement is slight and complications are also rare.
III. Pelvic ring disruption.— In this condition the pelvic ring is broken in two places. So displacement is
severe and complications are more.
IV. Sacro-coccygeal injuries.
I. AVULSION FRACTURES.—
Mechanism.— This usually occurs in athletes and in adolescents. Violent muscle contraction separates the
apophyses which give attachment to these muscles. The muscles concerned are the satorius, rectus femoris and
the hamstrings.
Usually three sites are affected:—(a) Anterior superior iliac spine avulsion due to contraction of the satorius
muscle which is attached to that, (b) Anterior inferior iliac spine is avulsed due to violent contraction of rectus
femoris attached to it. (c) A portion of ischeal tuberosity may be avulsed by strong hamstring contraction.
Clinical features.— After the injury the patient usually complains of pain in the fractured site.
On examination, the exact site of avulsion becomes tender. If the concerned muscle is made taut against
resistance, it is extremely painful.
X-ray shows avulsion of the apophysis concerned.
TREATMENT.— Simple rest for a few days is all that is required. The muscle concerned should be
completely relaxed. Normal activities can be resumed when pain disappears and the patient feels comfortable.
II. ISOLATED PELVIC RING FRACTURES.—
Here the pelvic ring is broken in only one place. Displacement is slight and intrapelvic viscera are hardly
damaged.
Mechanism.— A direct blow to the side of the pelvis or to the front of the pelvis may cause such injury. Thre
types of fractures are usually seen in this group — (i) fracture of the ilium, (ii) fracture of the acetabulum with
central dislocation of the hip and (iii) fracture of the pubic rami one or both on one side only.
Clinical features.— After the injury the patient cannot walk, or if he can walk it is with extreme pain.
On examination, one can see bruising of the affected side. T endemess of the affected region can be elicited.
X-ray will categorically show the type of fracture.
TREATMENT.— Fractures of the ilium and pubic rami need only rest. When pain goes off and the patient
is comfortable, he can move about. In case of central dislocation of hip, skeletal traction should be applied. Onl
when there is acetabular fracture with large portion of the roof or posterior wall detached, open reduction and
screw fixation become necessary.
III. PELVIC RING DISRUPTION.—
In this condition the pelvic ring is broken in two places. There is obviously considerable displacement and
there is also chance of injury to the intrapelvic structures.
Mechanism.—Usually 3 types of pelvic ring disruptions are seen, each is caused by a different type of force.
The 3 different types of forces are :—
(i) Compression force.— Lateral force from both sides may fracture the side wall of pelvis on both sides,
This injury may be an associated with medial displacement of the hip.
Anteroposterior compression force may fracture both pubic rami on both sides. The central segment will
be pushed backwards damaging the urethra.
(ii) Hinge force.— This force is applied from front to one side of the pelvis. Such force is seen in run-over
accidents. One-half of the pelvis is usually affected and the symphysis pubis is forced apart in front whereas
in the back there is usually fracture at the sacro-iliac region. So that the whole pelvis is actually ‘opened up’.
The other half of the pelvis usually remains intact.
(iii) Vertical force.— It is almost like the previous force but it comes from down upwards. Such force
usually occurs when an individual falls from a height on one leg. The affected side of the pelvis fractures on
two places, the pubis in front and the ilium behind. The portion of the pelvis lying in between the two fractures
is pushed upwards.
Symptoms.— After the injury patient is unable to move. He may not be able to pass urine. There is
considerable pain which becomes worse on movement and even on coughing. Internal haemorrhage is usually
considerable so much so to produce shock.
Physical Examinations.— There may be considerable bruising and swelling of the affected region.
27 '
Palpation will reveal tenderness but this is so diffuse that it is of no diagnostic value. When pubic rami ar
fractured and there is considerable suprapubic tenderness one must be very careful to assess urogenital d
The urinary bladder and urethra should be investigated properly to exclude any damage in those regions
hinge fractures the gap may be felt in the symphysis which is abnormally large. In vertical force fractures
is a possibility of damage to the nerve roots and particularly the sciatic nerve. This should be excluded.
X-ray.— This is diagnostic and indicates the type of fracture. From the type of fracture one can assess t
type of injuring force. In compression injury both pubic rami are fractured on both side. In hinge force fra
there is an abnormal gap at the symphysis pubis and there is a fracture near or subluxation at the sacro-il
In vertical force fractures the pubic rami and posterior portion of the ilium are fractured on same side wit
upward shift of the segment of pelvis between the fractures.
TREATMENT.—
1. TREATMENT OF SHOCK.— This must be done immediately with infusion of intravenous saline
and/or dextrose. Blood transfusion should also be given. Resuscitation of the patient is extremely import
2. TREATMENT OF PELVIC VISCERAL INJURIES.— Mainly the urinary bladder and urethra are
ruptured when pubic rami are fractured. This may also occur when the symphysis pubis is forced apart a
hinged type of injury. The patient is asked to pass urine. If he can pass urine and the urine is clear then no
should be done except to keep watch on the patient particularly his subsequent urines. If the patient fails
urine, a soft rubber catheter should be passed through urethra.
Intrapelvic rupture of urethra.— This is the commonest injury in case of pubic rami fractures. In this case
soft rubber catheter cannot be passed through urethra into the bladder. The bladder should be opened
suprapubically and a sound is passed from above. By ‘rail-roading’ methods a self retaining catheter is
introduced into the bladder. The ruptured urethra is now approximated and sutured. The suprapubic bla
drainage is continued alongwith a corrugated rubber drain to the retropubic space in front of the bladder
is known as Cave of Retzius.
Urinary bladder rupture.-— Such rupture may be exlraperitoneal or intraperitoneal. The management o
such rupture has been discussed in detail in Chapter - 58. It must be remembered here that suturing of th
is required alongwith bladder drainage and a drain to the retropubic space (Cave of Retzius).
3. TREATMENT OF FRACTURE.—
(a) Compression type of fractures.— In this type of fracture reduction is not required. All that is re
quired is rest. The patient should lie in bed for 3 weeks. During that period movement of the lower extrem
particularly the hip joints should be performed. After 3 weeks when the patient is almost comfortable he
get up and walk normally. Gradual spinal exercises should also be started. Weight-bearing is not harmfu
there is no damage to the line of weight transmission.
It must be remembered that this type of fracture is particularly liable to cause damage to the urethra a
urinary bladder. Such injury should be excluded or managed properly.
(b) Hinge type of fractures.— These fractures should be reduced. The patient should be general
anaesthetised and is rolled to the unaffected side. A compression force is applied to the affected pelvis so
it gradually ‘closes’. After reduction that means after proper alignment of the pelvis, a firm binder or a lu
sacral corset should be used. If reduction fails, internal fixation with wire should be considered. The wire
passed through drill holes or through obturator foramina to bring the two pubic bones together. The pati
remains in bed for 3 weeks. During this period he must move his lower limbs. After that the patient is allo
up with crutches. Weight-bearing is not allowed till union occurs. This usually takes another 6 weeks. Th
is worn for 3 months.
(c) Verticalforce injuries.— Under general anaesthesia the fracture is reduced by pulling the leg of th
affected side. This will bring down the fractured segment in line with the other side of the pelvis. Skeletal
is applied and is continued for 6 weeks till the fracture unites. Traction is then removed and the patient is
up with crutches. Weight-bearing is not allowed for 3 months from the date of injury.
COMPLICATIONS.—
(i) Intrapelvic haemorrhage which is often considerable to cause oligaemic shock.

(ii) Paralytic ileus.
(iii) Urogenital damage, particularly the urinary bladder and urethra. This is the most important complic
tion and adequate attention should be given to this complication.
(iv) Persistent sacro-iliac pain.
(v) Sciatic nerve injury particularly in vertical force fractures. Such nerve injury usually recovers, but
occasionally exploration may be required.
IV. SACROCOCCYGEAL INJURIES.—
Three types of injuries may occur in this group — fracture to the sacrum, fracture to the coccyx and sprai
in the sacro-coccygeal joint.
Mechanism.— A blow from behind usually causes fracture of the sacrum. A fall on the buttock usually
causes fracture of the coccyx or sprain of the sacro-coccygeal joint.
Clinicalfeatures.— The patient usually complains of pain in the buttock after injury. Tenderness is usually
localised on the fractured site, but sometimes it may be generalised affecting the whole of middle of the butt
Careful examination may elicit the type of fracture. Occasionally the roots of the sacral nerves may be dama
giving rise to neurological deficits in the areas of supply of the affected nerve roots.
X-ray.— This is highly significant and diagnostic. The fracture of the sacrum may or may not be associate
with displacement. When the fracture is displaced the lower fragment is usually pushed forwards. In case of
fractured coccyx the lower fragment is usually angulated forwards. If the X-ray does not reveal any fracture,
a sprain of the sacro-coccygeal joint should be the diagnosis.
TREATMENT.—If the fracture is displaced, reduction of the fracture should be attempted per rectum. Af
reduction the patient should take rest. During rest lower limbs should be moved. When the pain is relieved,
normal activity should be resumed. Sometimes the patient only complains of pain near the coccygeal region
the time of sitting. In these cases the patients should be advised to use Sorbo cushion when sitting. If the pai
is not relieved with this measure injection of local anaesthetic to the tender spot or even excision of the coccy
should be considered.
420
CHAPTER - 23
THE HEAD
THE SCALP
Surgical Anatomy.— There are 5 layers of the scalp after its 5 letters, viz. — S-skin; C-connective tissue;
A-aponeurosis; L-loose areolar tissue and P-pericranium. The skin is quite dense and contains many sebace
glands. The connective tissue layer, which binds the skin to the galea aponeurotica, is also very dense and
contains vessels and nerves. For this layer, the superficial 3 layers namely — skin, connective tissue and ga
aponeurotica behave as one layer. From this layer, the scalp wounds bleed profusely and the bleeding does
stop by itself which is usual in case of bleedings any where in the body. This is because of the fact that the v
walls are firmly anchored to the fibrous septa, which traverse through this layer and prevent the vessels fro
retraction. The galea aponeurotica is a dense aponeurosis, continuous in front with the frontalis muscle (whic
is not attached to the bone but is attached to the eye-brow and root of the nose), behind with the occipitalis
(which is attached to the occipital bone) and laterally with the temporal fascia (which is attached to the
zygomatic arch). The loose areolar tissue is said to be ‘the dangerous layer of the scalp’, as the emissary veins
connecting the dural sinuses with the veins of the scalp, traverse this layer. So infection of this area is likely
spread into the cranium. The pericranium is like the periosteum, which is loosely attached to the skull excep
at the suture lines, where it is firmly attached. So any collection of fluid underneath the pericranium takes t
shape of the bone concerned (cephal haematoma). The blood supply of the scalp is very rich so that the vita
of an even detached part of the scalp is maintained through a narrow pedicle.
Scalp Wounds.—These wounds should not be considered too trifle, on the other hand they should be tre
with considerable seriousness. Even the smallest scalp wound may lead to fulminating cellulitis of the scalp
Moreover, if it be associated with depressed fracture of the skull it becomes more dangerous, since infection
may travel through the tom duramater to form cerebral abscess.
First-aid treatment.— The first step is to know the extent and severity of the wound, which should be don
with utmost care and after wearing gloves. An X-ray is essential to know if it is associated with a depressed
fracture or not. This preliminary examination alongwith necessary neurological examinations will certainly
the seriousness of the condition and will also give a clue whether the case should be transferred to a neurol
department or not.
Shaving.— The half of the scalp should be shaved for a distance of about 5 to 7 cm around the wound. Fi
the hair is thoroughly washed with soap and water and then a razor is used to shave the surrounding area.
shaving, the surrounding scalp is washed again with soap and water and cleaned with a sterile swab.
Debridement.— In case of small wounds of the scalp, debridement can be performed under local
anaesthesia. 2% lignocaine solution is injected into the surrounding healthy tissue circumferentially around
wound to anaesthetise the wound, which is to be debridcd. Under no circumstances should the injection be
into doubtfully contaminated tissue, since infection may spread through this procedure.
Debridement of the large wounds of the scalp should better be performed under general anaesthesia.
Debridement is done as in case of wounds in other parts of the body. All the contaminated and devitalis
tissues should be removed. If the margins of the wound are contaminated and bruised, these should be exc
Arrest of haemorrhage.— As the vessels of the scalp are firmly anchored to the fibrous septa of the
connective tissue layer and are thus prevented from normal retraction, bleeding from the scalp is usually pr
and very difficult to control. Sometimes patients may come to the emergency department with scalp injury
which bleeds profusely. In that case a rubber tourniquet may be used around the circumference of the head
stop bleeding as the vessels of the scalp enter it through its periphery. A tight capeline bandage serves the
purpose of arresting haemorrhage.
In case of planned operations, the incision should be made vertical as the vessels of the scalp run vertica
THE HEAD 421
But in certain operations, transverse incisions are to be used. In these cases, the incision should be made in
segments and as soon as the incision is made the assistant presses the scalp near the cut edges against the s
with finger tips. This pressure will minimise the blood loss. Before releasing the pressure, artery forceps are
applied to the cut edges of galea aponeurotica and this layer is everted by holding the artery forceps. This w
occlude the bleeding vessels. In neurosurgical practise, Raney clips are often used.
Scalp suturing.— In case of small wounds of the scalp, interrupted one layer suturing will be enough. Th
one layer suturing should be through the skin, connective tissue and galea aponeurotica.
In case of larger wounds of the scalp or wounds after debridement, suturing should be performed in tw
layers. Firstly the galea aponeurotica is sutured with fine silk or chromic catgut and then the skin edges are
sutured by another layer of interrupted non-absorbable sutures.
In case of loss of scalp, rotation flap technique may be adopted to make good that loss. In certain cases,
simple undermining of the wound margins may be enough to bring together the wound margins.
Infections of the scalp.— As mentioned above infections of the scalp most commonly occur following
scalp wounds. Due to extreme vascularity of the scalp, wounds usually heal without much spread of infect
or infection remains localised. Rarely infection may spread in the loose areolar tissue deep to the galea
aponeurotica. This is dangerous as the emissary veins connecting the dural sinuses with the veins of the sca
traverse this layer. So infection may spread to dural sinuses through these emissary veins. That is why this
is called ‘the dangerous layer of the scalp’.
When a patient presents with scalp infection following trauma, wound toileting should be performed
immediately and a swab is sent from the scalp wound for culture and sensitivity tests. A broad spectrum
antibiotic is started in the beginning and as soon as the culture report is received, appropriate antibiotic is g
instead. If pus accumulates in the loose areolar tissue, adequate incision should be made to drain the pus.
Sometimes multiple incisions may be required. It must be remembered that if the scalp wound is very much
lacerated, tetanus and gas gangrene are potential dangers.
Subperiosteal infection is rare. Sometimes such infection may lead to subperiosteal pus formation and scal
oedema, both of which usually form swelling of the scalp which is peculiarly known as ‘Pott's puffy tumou
Subperiosteal infection should be considered as serious as it is often associated with intracranial abscess eit
extradural or subdural. So these cases should be investigated properly to exclude intracranial abscess forma
Subperiosteal infection often occurs as complication of osteomyelitis of the skull or it may occur as a sequel
of chronic frontal sinusitis.
SWELLINGS OF THE HEAD
1. Sebaceous cysts.— Sebaceous cysts of the scalp are not uncommon. These are usually multiple. The
surrounding becomes bald due to interference of blood supply from pressure of the cyst. Main complicatio
of sebaceous cysts of this area are infection and ulceration.
2. Dermoid cysts.— Such cysts are commonly seen over the external angular process. Dermoid cysts are
basically congenital, but may not become obvious until the patient becomes adult. The interesting feature o
dermoid cyst of the head is that it may have communication with an intracranial dermoid through a narrow
in the skull. Dermoid cyst of the head usually causes saucerization of the skull bone with sclerotic margin w
is easily felt with the tip of the finger. So X-ray of the skull is mandatory in case of dermoid cyst of the head
either to detect bony defect of the skull or to detect a gap in the skull through which there may be commun
with intracranial dermoid. When such communication becomes wide, impulse on coughing may be elicited.
3. Meningocele.— A soft fluctuant swelling in the midline of the head usually just above the nose is
nothing but meningocele. Such swellings are translucent and provide impulse on coughing.
4. Osteomyelitis with subperiosteal infection.— As mentioned earlier ‘Pott's puffy tumour’ is a
peculiar swelling of the head. It is painful and oedematous.
TUMOURS.—
TUMOURS OF THE SOFT TISSUES.—
1. Squamous cell and basal cell carcinomas are not uncommon in the head. Such tumours usually
present as small ulcers which are ignored in the early stages. Presence of such tumours is indicated by repeate
bleeding on combing of hair. These tumours in the scalp are slow growing and spread for months or even yea
Gradually these tumours tend to invade deeply and involve all the layers of the scalp. Gradually they may ero
the skull.
Treatment.— Biopsy is essential to confirm the diagnosis. Once the diagnosis is confirmed the tumour is
excised alongwith a considerable healthy scalp margin. Resulting scalp defect is made good with rotation flap
2. Papilloma.—This tumour may be single or multiple in the scalp and cause discomfort on combing the
hair. Repeated irritation of this tumour during combing may encourage malignant changes.
3. Lipoma.
4. Melanoma.
5. Cirsoid aneurysm.—This is a haemangioma of artery. Usually the superficial temporal artery and its
branches are affected. The area becomes bald. The underlying bone also becomes thinned out by pressure of
the aneurysm. X-ray of the skull is obligatory to exclude any presence of perforation of the skull which indica
that a part of the tumour is intracranial. Erosion of the skull can also be detected in X-ray.
The main complication of this tumour is the risk of serious haemorrhage following ulceration.
Treatment.— It is easier to treat this tumour in early stages. The feeding artery or arteries are ligated and
the tumour is excised. Big cirsoid aneurysm is difficult to treat as radical excision is almost impossible. The m
feeding vessels are ligated and this may reduce the size of the tumour at the same time minimise the risk of
serious haemorrhage from ulceration. But if intracranial connection is there the tumour continues to be large
and treatment becomes unsuccessful.
TUMOURS OF BONE (SKULL).—
These are characterised by hardness and absolute immovability due to fixation with the skull.
I. Benign tumours include ivory osteoma, which is quite rare and arises in the region of air sinuses and
osteoclastoma occasionally develops in the diploe and is extremely rare.
II. Malignant tumours include (i) osteosarcoma which is not quite common, but when occurs, it is quite
vascular and may be pulsatile. It sometimes may occur secondary to Paget’s disease.
(ii) Secondary carcinoma is in fact the commonest malignant tumour in this region. The primary is usua
seen in the breast, kidney, thyroid, prostate or suprarenal. The peculiarity of secondary tumour from breast is
that it is usually multiple. The peculiarity of secondary from adenocarcinoma of the kidney or hypernephrom
is that the tumour becomes very vascular and may pulsate.
Secondary tumours are often evident on skull X-ray as clear areas with irregular margin.
HEAD INJURY
The term ‘head injury’ includes injury to the scalp, skull and/or brain. It goes without saying that injury to
the brain is by far the most important. Injury to the scalp has already been described.
FRACTURE OF THE SKULL
Fractures of the skull can be broadly classified into two heads — I. Fracture of the vault of the skull and
II.'Fracture of the base of the skull.
I. FRACTURE OF THE VAULT OF THE SKULL
Whenever a patient comes with head injury, the patient must be shaved completely and thorough
examination of the injury must be made to know if it is associated with the fracture of the skull or not. Two ty
of fractures of the skull can be seen — A. Closed fractures and B. Open fractures.
A. Closed fractures.— In these cases the fractured site is not exposed outside, that means the scalp
remains intact, though it may be bruished or grazed.
B. Open fractures.— When the fracture of the skull is exposed outside through the laceration of the scalp,
THE HEAD 423
it is called open fracture. The danger of such fracture is that it can be easily infected and it may give an access
to the infection to reach deeper to cause meningitis or even brain abscess.
MECHANISM.— Fractures of the vault of the skull are mainly caused by one of the three types of injury
— (i) compression of the sphere, (ii) by local indentation and (iii) by tangential injury.
(i) Compression of the sphere.— When the head is compressed against a hard flat surface, it renders the
spherical skull more ovoid and a linear fracture starts from the point of maximum convexity through the thin
areas of the bone. The fracture line often deflects from the bony buttresses towards the base of the skull. So it
must be remembered that many fractures of the base of the skull are produced by extensions of the fissures
starting in the vault.
(ii) Local indentation.— This may produce closed pond depressed fractures caused by a large round
object in which the scalp may be bruished but remains intact and the skull becomes indented but not indriven
so that the underlying dura remains intact. There may be bruising of the underlying brain surface but it is not
penetrated. Local indentation of the skull may also be produced by small objects which cause compound (open)
depressedfractures. The scalp is lacerated, the fractured skull is depressed and indriven lacerating both the dura
and the subjacent brain. There is immediate risk of infection and a later risk of epilepsy resulting from the
contracting fibrous scar of the healing brain.
(iii) Tangential injury.— This type of injury causing fracture of the vault of the skull is rare. A tangentially
directed violence which may secure a grip on the skull may lift it up producing a horse-shoe shaped fracture
surrounding the calverium.
TYPES OF FRACTURES.— Fracture of the vault of the skull may be either of the following types —
1. Linear fracture (crack or fissure).— Such fracture is usually caused by compression of the sphere.
This fracture is quite common and is result of skull distortion. This fracture may be continuous to the base of
the skull causing fracture of the anterior cranial fossa or middle cranial fossa or posterior cranial fossa. A linea
fracture of the squamous temporal bone is of special significance, which may give rise to extradural
haemorrhage by injury to the middle meningeal artery or one of its branches.
2. Simple and comminuted linear fracture.— This is the most common type of fracture involving the
vault of the skull. The significance of this fracture is that it indicates that there may be a deceleration or
acceleration primary brain injury. Similarly it may also indicate in certain areas possibility of extradural or
subdural haemorrhage. The fracture itself has little significance and its own treatment should not get much
significance as it is a simple fracture without laceration of the full thickness of the scalp.
3. Depressed fractures.— As mentioned earlier there are two types of depressed fracture — closed or
open. Obviously the open depressed fracture possesses immediate risk of infection to be carried down to the
underlying meninges and also to the brain itself. It should be remembered that a depressed fracture becomes
significant when the degree of depression is greater than the depth of the inner table of the skull. Depressed
fracture may cause several complications which are narrated below —
(i) Dural tear.— Depression of the skull bone fragments may tear the underlying dura mater. This
simply is an indication for surgery.
(ii) Pressure on the cerebral cortex.— If the depression of the bony fragments is more it may even cause
pressure on the cerebral cortex. Itgoes without saying that such depressed fracture requires immediate operati
for elevation.
(iii) Underlying haemorrhage.— Though this is not a very common complication of depressed fracture,
yet it is possible that depressed fracture causes underlying haemorrhage, which may increase the intracranial
pressure leading to cerebral compression. CT scan may evaluate such haemorrhage.
(iv) Epilepsy.— Post-traumatic epilepsy early or late occurs following a depressed fracture. Though
elevation of thedepressed fracture is always indicated when such risk is anticipated, yet it is debatable how mu
this elevation operation contributes in preventing such epilepsy.
(v) Pressure on dural venous sinuses.— Rarely a depressed fracture may compress or obstruct the
superior sagittal sinus or lateral sinus, which may lead to raised intracranial pressure and cerebral compressio
424
A CONCISE TEXTBOOK OF SURGERY
Moreover there is risk of severe haemorrhage from these sinuses if such depressed fractures are attempted
elevate. So these fractures are better left alone and should not be elevated.
Treatment.— If the fracture is a linear one without any displacement, no special treatment is required. Bu
care must be taken to detect any deceleration or acceleration primary injury to the brain and to exclude pre
of any extradural haemorrhage in this case.
When the fracture is comminuted, a thorough examination is made about the fragments. The contaminate
fragments which are absolutely detached, should be removed. Otherwise the fragments should not be dist
if they are not digging in to cause brain damage.
When the fracture is compound, prophylactic antibiotics (particularly broad spectrum which has got
effectivity against gram-positive and gram-negative organisms) should be started immediately on admissi
and is continued for 10 days.
Treatment of depressed fractures.— Whenever a case of depressed fracture is identified, first it should
be assessed whether the fracture is simple (closed) or open (compound). The whole head should be shaved
careful assessment is made to exclude any neurological deficit. If there is laceration of the scalp, debrideme
should be made to an absolute minimum remembering that scalp will be used to cover after treatment of
depressed fracture.
If the depressed fracture has a depression greater than the depth of the inner table of the skull, it should
elevated. A burr-hole is made through the normal skull by the side of the fractured portion. Through this b
hole an elevator (Adson's elevator) is introduced and the underlying dura is gently separated from the ove
bone fragments. The depressed fragments are now cautiously lifted up and the dura is inspected to exclud
dural tear. If any of the fragments is contaminated and fully detached, it should be removed.
An assessment should be made from the site of the fracture whether any dural sinus may be injured or
as injury to the dural sinus will cause serious haemorrhage.
TREATMENT OF DURAL TEAR.— It is always essential to have a look at the dura mater beneath a
depressed fracture of the skull. It may be tom or it may be seen bulged and plum-coloured to suggest the p
of subdural haemorrhage. In this case an incision should be made on dura and to have a look inside to stop
subdural haemorrhage.
When there is dural tear, the whole extent of the tear must be exposed by removal of the overlying skull
required. The ragged edges of the dura mater should be excised, but care should be taken not to excise too
and not to increase the tear as this may lead to spread of infection into the subarachnoid space. This will al
give rise to difficulty in closing the tear. The dura mater should always be closed preferably by interrupted
sutures with nonabsorbable material such as fine silk.
If there is dural loss, the defect is made good with a transplant from fascia lata or pericranium, provided
dura mater is not much contaminated.
When the dural tear is associated with too much contamination, it is best left alone as done in case of wounds
in other parts of the body. A late primary suture is performed at a later date.
Sometimes haemorrhage from dural vessels becomes troublesome and difficult to control. These dural
vessels are too tiny to be picked up with artery forceps. So they are best tackled by diathermy coagulation.
vessels of course can be under-run with suture. Sometimes simple oozing is the main problem, when the m
graft from temporalis muscle should be used to stop the oozing.
When the tear of the dura mater has involved a dural sinus, venous bleeding may make the surgeon worried.
In case of small tear, a graft of pericranium may be sutured over the tear to stop bleeding. In case of large t
a muscle graft may be required to stop bleeding. This muscle graft is usually taken from the temporalis mu
and is hammered to form a flat sheet, which is placed over the dural tear and sutured. A piece of oxycel m
be similarly used to stop bleeding.
When associated with injury to the brain.— Sometimes in depressed fracture, fragments of the skull may
dig in to cause brain damage. In this case a wide exposure is required to see the extent of brain damage. Th
treatment is to remove all devitalised cerebral tissues, extravasated blood, any foreign body and detached
THE HEAD 425
fragment of bone. After that, the damaged brain tissue is cleared off by a combination of irrigation and suct
Warm saline is injected into the damaged brain tissue and the nozzle of the suction apparatus is kept very c
to the damaged area so that all devitalised brain matter and blood clot may be removed by suction. Haemo
is controlled very meticulously giving no chance to further haematoma to form.
Skull reconstruction.—If bone fragments are removed from the skull, the skull deficit should be made goo
The removed bone fragments may be cleaned and replaced in a mosaic fashion and the pericranium and sc
are closed carefully in layers over these bone fragments. If this is not possible skull defect may be made goo
with insertion of moulded tantalum plates or acrylic inlays. These are performed 3 to 6 months after the hea
injury.
II. FRACTURE OF THE BASE OF THE SKULL
As mentioned earlier linear fracture of the vault of skull may extend into the skull base.
(a) Fracture of the anterior cranial fossa.— In this fracture there will be haemorrhage from the nose
(epistaxis) and/or escape of cerebrospinal fluid (CSF rhinorrhoea) and even brain matter through the nose.
will be evidence of haemorrhage in the orbital cavity by the presence of ecchymosis starting in the lower ey
and gradually involving the upper eyelid. There may be subconjunctival haemorrhage, the posterior limit o
which cannot be seen and excessive haemorrhage may push the eye forward. The olfactory nerve (first cran
nerve) is frequently tom and unless its fellow of the other side is also damaged, partial anosmia may pass
unrecognised. The optic nerve usually escapes injury. The 3rd, 4ih, 1st division of the 5th and 6th cranial ne
may be injured at the sphenoidal fissure. 3rd nerve palsy produces a dilated pupil in a conscious patient.
(b) Fracture of the middle cranial fossa.— Haemorrhage and escape of cranial contents (CSF and brain
matter) may be expected from the ear (CSF otorrhoea) and the mouth. This usually occurs if the basal fractu
is associated with disruption of the dura mater and rupture of the tympanic membrane. Occasionally there
be epistaxis when the nasal sinuses are affected. Of the cranial nerves, the 7th nerve (facial), the 8th nerve an
occasionally the 6th nerve may be injured. Facial nerve injury will cause paralysis of the facial muscles. Inju
to the 8th nerve will cause deafness and injury to the 6th nerve will result in internal strabismus.
(c) Fracture of the posterior cranial fossa.— Extravasation of blood may be seen in the suboccipital
region producing a swelling at the back of the upper part of the neck and ecchymosis near the tip of the ma
process (Battle's sign). Such ecchymosis appears within 3 or 4 days of trauma. The 9th, 10th and 11th crania
nerves are occasionally injured at the jugular foramen, but the 12th nerve usually escapes as it is protected b
strong bony buttresses.
The students should remember certain IMPORTANCES OF SKULL FRACTURES :—
1. In certain places (linear fracture in squamous part of the temporal bone) vault fractures characterist
cally may injure the middle meningeal artery to cause extradural haemorrhage.
2. Compound fractures may result in infection of the meninges and the brain.
3. Depressed fracture of the vault may cause dural tear and even injury to the cerebral cortex.
4. Compound fractures may result in infection of the meninges and even of the brain.
5. Fracture of the base of the skull may cause injury to the various cranial nerves except the 2nd and th
12th. Such injury to the nerve may be caused by complete tear of the nerve (causing immediate and parman
paralysis) or compression of the nerê by blood clots (the paralysis is temporary and appears after a few da
of injury) or due to involvement of the nerve in scar or callus formation during the healing process of the fr
(such paralysis occurs after a few weeks and is usually permanent if not relieved).
6. In basal fractures there may be escape of blood — epistaxis in anterior cranial fossa fracture, bleedin
from the ear or epistaxis (if the nasal sinuses are involved) in middle cranial fossa fracture, swelling at the n
of the neck and patch of ecchymosis over the mastoid process (Battle's sign) in posterior cranial fossa fractu
7. Escape of cranial contents may also occur in basal fractures. It is usually CSF and may by associated
with brain content. In anterior cranial fossa CSF rhinorrhoea may be seen and in middle cranial fossa fractu
CSF otorrhoea may be seen.
It cannot be too impressed that management of such cases should be done with prophylactic antibiotics
(broad spectrum covering both gram-negative and gram-positive organisms), as meningitis, is a very commo
complication from such disorder.
8. In basal fracture of anterior cranial fossa, air may enter the cranial cavity producing intracranial
aerocele.
9. Medicolegal.— It must be confessed at the end that even if skull fracture is of little significance
surgically, its importance for medicolegal reasons should not be ignored.
INJURY TO THE BRAIN

Mechanism and pathology.—
Injury to the brain can be divided into two parts. In thefirst part injury is inflicted on the brain at the mom
of impact of injury. This is due to diffuse neuronal lesion and may be called ‘primary brain injury’. In the second
pari due to brain swelling or oedema or intracranial haemorrhage resulting from trauma to the head and the
patient gradually loses consciousness a few hours after injury or trauma. This is called ‘secondary brain lesion'.
Primary brain injury.— Brain has certain amount of mobility inside the skull box, though such movement
has been greatly restricted by the presence of falx and tentorium. The dura mater is more or less firmly attach
to the skull and merges with the falx and tentorium. Between the brain and the dura mater there is a space w
consists of two compartments — subdural space and subarachnoid space separated by the arachnoid. In the
subarachnoid space there is CSF fluid. With age the brain shrinks, so its mobility increases. So there is more
chance of injury to the brain in old individuals.
The brain injury is usually caused by displacement and distortion of cerebral tissues occurring at the mom
of impact. Shearing forces cause widespread damage to neurons, nerve fibres, supporting tissues (glia) and
blood vessels.
TWO TYPES of brain injury are seen — 1. The first type is due to movement of the brain within the skull
box causing shearing forces due to deceleration or acceleration. Such injury is often caused by traffic accidents
when the moving head strikes an immovable object e.g. the footpath or road. In case of acceleration injury th
stationary skull is struck by a moving object e.g. assault, in which the brain rapidly accelerates against the
stationary midbrain. Three types of brain injury are seen in this category —
(a) When the head is struck from in front, both the cerebral hemispheres are displaced posteriorly agains
the static midbrain, hypothalamus and brain stem.
(b) When the head is struck from behind or in front at one side or the other, one cerebral hemisphere mo
against the other, so that the junctional tissues of the commissures and corpus callosum are damaged.
(c) In some cases the grey matter of the cortex moves over the white matter leading to tear of nerve cells
and axon fibres of that region. This damage may be diffuse and may occur far away from the site of the blow
to the head.
Clinical effect of such distortion of brain is loss of consciousness. Such loss of consciousness may be
persisting if there is significant neuronal damage. Neuronal damage also causes focal neurological deficit.
Distortion or neuronal damage of the midbrain usually causes deterioration in the level of consciousness. It m
be remembered that the brain stem reticular formation is responsible for normal consciousness probably thro
activation of cortical mechanism. It cannot be impressed too hard that damage to the brain may well occur
without appreciable injury or fracture of the skull bone.
2. Secondary type of brain injury is due to localised injury to the brain against rough internal confi
of the skull, falx and tentorium. Where the skull is smooth there is less or no damage to the brain. Where the
internal portion of the skull is rough the brain lying against such portion may be injured if it impacts on it. So
the temporal lobe of brain may be damaged against the sharp sphenoid ridge. The inferior surface of the fron
lobe may be damaged by the rough anterior cranial fossa floor. The occipital pole which lies against the meet
place of the falx and tentorium may be damaged. Corpus callosum may be damaged against the sharp edge o
THE HEAD 427
the falx. Cerebral peduncles may be damaged by the sharp edge of the tentorium.
To indicate the type of brain damage three terms are being used from old days. These terms are — cerebral
concussion, cerebral contusion and cerebral laceration.
Cerebral concussion.— This is a brief temporary physiological paralysis of function without organic
structural damage. In concussion there is a transient loss of impairment of consciousness, dizziness or mild
confusion, which is usually followed by complete recovery. It may be short lasting from 1 minute to '/2 an hou
or it may be long lasting where it may be prolonged for hours or even a day. With the loss of consciousness the
patient falls down. He becomes pale andcovered with cold clammy sweat. The temperature drops below norm
The pulse becomes imperceptible. Gradually the temperature rises and the pulse becomes full and bounding.
The cause of concussion is not very clearly known. Many theories have been suggested. Cerebral anaemia
has been incriminated as cause of concussion. Severe compression of the brain causes emptying of the vessels
which leads to anaemiaT Gradually refilling of the vessels takes place and the condition recovers. Some believe
that it is due to molecular disturbance of the hypothalamus and brain stem. Some believe that it is due to abrup
stretching of the delicate anterior and posterior perforating arteries causing transient ischaemia of the midbrain
Some believe it is due to a wave of pressure transmitted through the CSF on to the floor of the 4th ventricle.
Cerebral contusion.— In cerebral contusion there is shearing damage to the nerve cells and axons either
superficially in the cortex or deeply in the cortex between grey matter and white matter. There may be bruising
and haemorrhages due to tearing of small blood vessels within the brain substance. Brain oedema is the most
important pathological process in cerebral contusion. There is also congestion and dilatation of blood vessels
within the brain. Both brain oedema and congestion contribute to swelling of the brain. So in cerebral contusion
there is damage to nerve cells and axons with bruise and swelling of cortical gyri.
Cerebral laceration.— In this condition the brain surface is tom or lacerated with effusion of blood into
the cerebrospinal fluid. Such laceration is usually due to impact of the brain cortex against die rough internal
bony ridges or the edges of the falx or tentorium. The internal changes of the brain i.e. shearing damage to the
nerve cells and axons and brain oedema which are seen in cerebral contusion are also seen in cerebral laceratio
Often the laceration is most severe on the side opposite to that on which the blow is struck. This condition is
known as ‘contrecoup injury’. Partly as the result of tissue destruction and partly as the result of gliosis, a series
of atrophic changes may follow the injury. The damaged part of the brain shrinks and fluid accumulates in the
subarachnoid space. This may be associated with great mental impairment. A scar may develop at the area of
injury which undergoes contraction over a period of months and years exerting pull not only locally but also
on the whole framework of the brain. This causes epilepsy in the future (traumatic epilepsy of the Jacksonian
type).
Cerebral irritation.— It is a vague term which is often vaguely used. Such cerebral irritation may occur
at any time within 48 hours of injury. In this condition the patient curls up on his side with knees drawn up an
arms flexed (an attitude of flexion) and also resents all interference and avoids light. He takes no interest in the
surroundings. Recovery is apparently complete, but in majority of cases headache, irritability, depression, lack
of concentration, defective memory and change of personality may be expected. Cerebral irritation is said to
be due to localised oedema which occurs around the area of contusion or laceration in the brain.
SEQUELAE OF CONTUSION OR LACERATION.— Unless the patient succumbs to severe contusion
or laceration of the brain, one or more of the following features may be seen later on —
(i) As mentioned earlier in contusion or laceration the grey matter may move against the white causin
rupture and degeneration of some axon fibres in that region. This may lead to some change in personality and
defective memory. Post-traumatic amnesia (PTA) also occurs in this condition. The duration of PTA is the best
guide to assess the severity of head injury. This is the time between the head injury and return to continuous
memory. PTA commonly persists for a while after return of consciousness. If it is less than an hour, the injury
can be regarded as slight, if it is between 1 to 24 hours head injury is moderate, if it persists between 1 to 7 days
it is severe. There is another type of amnesia, which is known as retrograde traumatic amnesia (RTA). This
means loss of memory for events before the occurrence of the accidents.
(ii) Cerebral irritation, as mentioned above, may also take place after cerebral contusion or laceration.
(iii) Due to damage of brain tissue, after recovery the patient may complain of headache, photophobia,
nausea and vomiting, depression, lack of concentration or delerium. This is often called post-contusional
syndrome.
(iv) The damaged portion of the brain at the time of healing and neurological proliferation a firm tissu
formed. Such scar tissue undergoes contraction over a period of months and years exerting a constant pul
the brain not only locally, but also on the whole frame work of the brain. This may cause traumatic epilep
the Jacksonian type after a few years of head injury.
(v) Contusion or laceration may cause permanent damage to an important focal centre of cerebral cort
e.g. anosmia in case of injury to the inferior aspect of the frontal lobe; hemianopia and blindness in case of
occipital lobe lesion, ataxia and nystagmus are features of cerebellar lesion and these focus the attention to
posterior fossa.
(vi) If contusion or laceration gives rise to haemorrhage or oedema, features of cerebral compression may
set in.
Secondary pathologies.—
(a) Brain swelling.— The brain often reacts to any insult be it traumatic or inflammatory or neoplastic by
swelling due to oedema. Initially oedema is localised to the demaged part of the brain, but it gradually exte
rapidly throughout one or both the cerebral hemispheres. So there is considerable rise in intracranial press
which may lead to cerebral compression.
(b) Haemorrhage.— After brain injury there may be extradural or subdural or subarachnoid or subcortic
haemorrhages. Such haemorrhage may be the result of arterial or venous bleeding. These haemorrhages h
been described later on.
(c) Brain necrosis.— In case of cerebral contusion or laceration alongwith oedema and venous engorge
ment ischaemia to a localised part of the brain is not unusual. This may lead to necrosis of that localised p
of brain. Such necrotic changes may occur in one of the temporal lobes or frontal lobes.
(d) Coning.— This means herniation of contents of brain. When contents of supratentorial compartmen
herniate through the tentorial hiatus due to compression in the supratentorial compartment it is called con
Similarly when the contents of the infratentorial compartment herniate through the foramen magnum due
increased pressure within that region it is also called coning. When there is compression of the supratento
compartment, usually the medial part of the temporal lobe (the uncus) herniates through the tentorial hiat
causes pressure on the ipsilateral third cranial nerve (oculomotor nerve). The result is early constriction an
dilatation of the pupil of the same side (Hutchinson’s pupil). The midbrain is distorted and gradually disp
away to be impacted against the free edge of the tentorium on the other side. This may interfere with the
descending motor pathways coming from the opposite hemisphere. This causes hemiparesis on the oppos
side of the injury. This ultimately leads to deterioration in the level of consciousness due to pressure on th
reticular formation of the brain stem(See Fig. 31.3).
Cerebral compression.— Following head injury, the brain may be compressed due to one of the followin
reasons —
(i) Intracranial haemorrhage or haematomas.
(ii) Oedema around the contused or lacerated brain tissue which spreads to whole of cerebral hemisph
(iii) Retention of CSF in the lateral ventricles.
(iv) Failure of absorption of CSF by the basal systems and arachnoid granulations which are blocked b
the effused blood.
Cerebral compression is characterised by the following CLINICAL FEATURES —
(a) The patient after being conscious or irritable for a while, passes into profound unconsciousness.
Progressive deterioration in the level of unconsciousness is the main feature.
(b) The pulse becomes slow and bounding (of high volume).
THE HEAD 429
(c) Respiration becomes slow and deep, frequently stertorous. The patient's cheeks flap with respiration.
(d) His face becomes flushed.
(e) The temperature becomes unequal being higher on the paralysed side.
(f) Hemiparesis may be seen on the opposite side of head injury as the contralateral crus of the midbrain
is pressed against the edge of the tentorial hiatus.
(g) The pupil on the side of the lesion, after initial contraction, dilates with poor reaction to light
(Hutchinson's pupil). In the last stage both the pupils become dilated and fixed without reaction to light.
INTRACRANIAL HAEMORRHAGES
Haemorrhage from any intracranial vessel may occur in head injury. This may occur above or below the
tentorium cerebelli and becomes responsible for causing brain compression. It requires sometime to develop
cerebral compression. In this period the patient remains conscious and this period is typically known as the
‘lucid interval'. This period varies according to the type of the vessel (whether artery or vein) and the calibre
of the vessel injured.
SUPRATENTORIAL HAEMORRHAGE is by far much commoner and includes intracerebral haemor
rhage, subdural haemorrhage and extradural haemorrhage.
Intracerebral haemorrhage.—
This is least common and least significant of all supratentorial haemorrhages. This is produced by arleiial
bleeding from an area of surface laceration. Very rarely a major intracerebral vessel e.g. a central artery ruptur
Intracerebral haemorrhage hardly causes cerebral compression of considerable magnitude. When a central
artery ruptures, the bleeding may become fatal, as it may rupture into the ventricle causing intraveniricular
haemorrhage, the main symptom of which is hyperthermia. Epileptic fits may be seen with localised paralysis.
Alarming haemorrhage may also occur from pre-existing vascular lesion e.g. an aneurysm or arteriovenous
malformation. So arteriography is advisable if time permits before surgery in these cases. The symptoms and
signs develop from 1 to 10 days after head injury. Of course this period depends on the type of vessel ruptured
or any pathology associated with it.
Intracercbral haemorrhage may be small enough and blood clots or haematomas in the brain may produce
signs and symptoms which mimic those of cerebral tumours. CT scan and arteriography may be helpful in pro
diagnosis. Removal of such masses may be effective particularly when these are situated in the anterior part o
the frontal or temporal lobe.
SUBDURAL HAEMORRHAGE.—
This condition is about 6 times commoner than extradural haemorrhage. It is caused by —
(i) Laceration of the cortex associated with venous or arterial haemorrhage, the haematoma of which
collects under the dura mater. This type of haemorrhage is less significant and less dangerous.
(ii) Significant subdural haemorrhage is causcd by rupture of superior cerebral veins. These veins run
upwards along the surface of the cerebral hemispheres and then pierce the arachnoid mater and enter into the
subdural space before it reaches the superior sagittal sinus. So these veins are fixed on one side to the arachno
mater and surface of the brain and on the other side to the dura mater lining the sagittal sinus. Between these
two fixed points, these veins lie free and remain mobile in the subdural space. Impact to the front or back of th
head may lead to rupture of these veins causing subdural haemorrhage. The cerebral hemisphere moves
alongwith the lower parts of the superior cerebral veins, whereas the upper parts of these veins are fixed to th
superior sagittal sinus into which they drain. This causes alarming haemorrhage in the subdural space. Subdu
haemorrhage is much commoner in the elderly as the brain atrophies in these individuals giving rise to more
space for the brain to move within the skull. In these individuals subdural haemorrhage may occur following
a trivial injury or shaking of head.
In about 50% of cases this condition is bilateral, that means veins of both sides are tom.
Clinical Features.—
(a) As subdural haemorrhage is often
accompanied with severe primary brain
damage, so there is no definite lucid inter-
vai. The primary brain damage, which usu-
causes early unconsciousness, is rap
idly followed by unconsciousness due to

cerebral compression from acute subdural
haemorrhage. So there is no typical lucid
interval in these cases.
(b) Level of unconsciousness deterio
rates very quickly than in extradural haem
orrhage.
(c) Symptoms and signs of cerebral
compression become more evident in this
Fig.31.1. Shows how subdural haematoma is produced by condition. In bilateral cases such symptoms
tearing of superior cerebral veins at the level of the arachnoid. ,. ,,,
See ^ t t and signs are seen on both sides.
(d) When subdural haemorrhage is less
dramatic and delayed by seveial days, it is called subacute subdural haematoma. In this type the symptoms
iess dramatic and consist of headache which
,..-v .V;/’;"’ is unduly severe and prolonged, mental
' apathy, slowness to respond to questions.
. | Tflc Pal‘cnt may 8° 'nt0 c°ma when the
, >;•& M ,Snjb;\ midbrain pressure-cone develops.
W*j (c) When subdural haematoma ap-
W 1 iXm IP* 1 V pears further late and it becomes difficult to
remember head injury as the cause of such
■ ~ abnormal bchaviourof the patient, it iscalled
&. .*§> ■» ..Iconic subdural haematoma.
Treatment.— In case of acute subdural
h icmorrhage immediate operation is the only
way to save the patient. Extensive craniot
omy should be performed todetect the haem
orrhage and the haemorrhagic vessel. The
haemorrhagic vessels are carefully secured
and ligated. Burr-holes are of no value, as it
is extremely impossible to localise the site
of haemorrhage precisely inspite of all in
vestigations. CT scan and arteriography, if
time permits, should be performed before
operation to give some idea as to the site of
haemorrhage. The haemorrhaging vessel is
ligated and haematoma cleared off.
The patient may succumb to the exten
sive brain damage which may associate acute
Fig.31.2.— CT scan showing subdural haemorrhage. subdural haemorrhage inspite of proper treat
Also note deviation of midline structures.
ment.
THE HEAD 431
EXTRADURAL HAEMORRHAGE
It is the haemorrhage in the space outside the dura mater, but inside the skull. The importance of extrad
ral haemorrhage lies in the fact that it is
amenable to surgery and if the case is not
diagnosed in right time the patient may
die. Probably in no other lesion in head
injury surgery has got such a definite
role to play to save the patient.
VESSELS AFFECTED.—
1. The classical syndrome of ex
tradural haemorrhage results mostly from
injury to the main trunk of the middle
meningeal artery or more commonly one
of its branches — anterior or posterior.
The anterior branch is more commonly
injured than the posterior in the ratio of
5 : 1 . Such bleeding usually takes place
in the middle cranial fossa. The mecha
nism of such injury and its outcome are
discussed in detail below.
2. Middle meningeal vein at times
may be torn to cause extradural haemor
rhage. As this bleeding is less forcible, it
rarely causes danger to the patient.
3. Sometimes bleeding may
occur in the posterior cranial fossa and
the source is a torn posterior meningeal
Fig.31.3.— Schematic diagram showing how .supratentorial
haematoma (extradural or subdural haemorrhage) causes stretching of artery over the occipital lobe.
the 3rd cranial nerve, tentorial hernia and distortion of midbrain leading 4. Extradural haemorrhage may
to loss of consciousness. also occur by fractures of the anterior
fossa when branches of the internal maxillary or anterior meningeal vessels may be torn. In this case a simil
deterioration in level of consciousness will be noticed when the haematoma enlarges to a big size.
5. Very occasionally the bleeding may occur from one of the venous sinuses — either superior sag
sinus (in the anterior or middle cranial fossa) or from the transverse sinus (in the posterior cranial fossa).
MECHANISM OF MIDDLE MENINGEAL ARTERY BLEEDING.— Extradural haemorrhage from
injury to the trunk of the middle meningeal artery or one of its branches occurs due to relatively trivial in ju
which comes from lateral direction. A blow on the thin bone of the temporal plate may be caused with a go
ball or cricket ball or football. This causes a fracture in the squamous part of the temporal bone which drive
the dura inwards. The middle meningeal artery leaves the bony canal in the pterion, crosses the extradural
and gains attachment to the outer surface of the dura mater. Usually the part which crosses the extradural s
(free part) becomes tom. Of course sometimes the anterior branch or posterior branch of the middle mening
artery is injured due to direct trauma of the fractured bone fragments against these arteries.
The blood which escapes from the tom vessel passes in three directions :
(i) Some of it passes outwards through the fracture to form a boggy swelling due to haematoma u
temporal muscle. This finding not only is an indication for admission of a conscious patient to the hospital,
also indicates occurrence of extradural haemorrhage.
(ii) Some of escaping blood gravitates down into the base of the middle cranial fossa.
(iii) Some part of the escaping blood gradually moves upwards separating the dura mater from inside th
skull just outside the underlying motor cortex of the cerebral hemisphere. This haematoma is the most impor
in causing lethal problems of extradural haemorrhage. The amount of this haematoma depends on the ease w
which the dura mater is stripped off from the inner surface of the skull. In children and young adults extradu
haematoma very easily takes a big size and a big extradural haematoma is often possible without fracture in
children due to excessive elasticity of the skull. With advancing age the dura mater becomes more adherent to
the scar and haematoma takes sometime to form which is considered as ‘lucid interval'. When the haematoma
has reached a considerable size, it causes sufficient rise in intracranial pressure to cause cerebral compression
Uncus herniates through the tentorial hiatus with such rise of intracranial pressure and the midbrain gets
distorted at the tentorial hiatus This causes unconsciousness clue to pressure on the reticular system of the
midbrain. The time taken to form such a big
haematoma as to cause sufficient rise in
intracranial pressure to cause unconscious
ness following injury is the period known as
‘lucid interval'. The uncus first irritates and
then stretches the oculomotor nerve (3rd
cranial nerve) to cause constriction of pupil
for a short period. This is followed by dila
tation of pupil due to paralysis of the said
nerve. This occurs on the side of head injury.
With more haematoma formation and with
the greater rise of intracranial pressure, im
paction of mid-brain cone occurs and this
cause decerebrate rigidity with fixed dilata
tion of both pupils which fail to react to light.
This is an ominous sign and the case is
probably too late for operation.
HISTORY.— Patient or his associates
often give history that a laterally directed
blow of relatively trivial nature has caused
the head injury. There may or may not be a
short period of concussion. When there is an
initial cerebral concussion, the patient be
comes unconscious immediately after head
injury. After a short while he usually recov
Fig.31.4.— CT scan showing extradural haematoma with
deviation of midline structures towards the sound side. ers completely and continues what he was
doing. This injury is often seen in football
ers , who after initial unconsciousness, recovers completely and plays for the rest of the game. Later on the pa
gradually complains of headache and drowsiness which is followed by unconsciousness due to cerebral
compression. This is the period known as the ‘lucid interval’ and this is time taken by the haemorrhage to be
big enough to cause cerebral compression.
In certain cases, the lucid interval may not be seen and the patient remains unconscious throughout, thoug
his level of unconsciousness may deteriorate later on. This occurs — (i) when primary cerebral injury is more
severe to cause a prolonged concussion, so that by that time sufficient blood accumulates to set in cerebral
compression; or (ii) when bleeding is too rapid and produces sufficient big haematoma before the patient
recovers from usual concussion.
History must be taken whether the patient was alcoholic or uraemic or opium poisoned or in diabetic com
This only complicates the physical finding.
THE HEAD 433
(i) The site of injury has to be examined properly. Often a haematoma may be detected at the temporal
region which immediately should arouse suspicion of extradural haemorrhage.
(ii) Depth of consciousness has already been discussed.
(iii) Eyes.— As mentioned earlier when the medial part of the temporal lobe herniates through the tentoria
hiatus, it first stretches the oculomotor nerve and then paralyses it. So pupil on the side of head injury will fir
be constricted due to irritation of oculomotor nerve which will be followed by dilatation due to paralysis of t
nerve. When the uncus has been sufficiently herniated to cause the mid-brain to be pushed to the opposite sid
and be pressed against the tentorial edge, this causes the opposite oculomotor nerve to be pressed above the
tentorial margin. The nerve is first irritated and then paralysed. So in the 2nd stage when the pupil of the inju
side becomes dilated due to paralysis of the oculomotor nerve of the same side, the pupil of the other side
constricts as the nerve of the other side becomes irritated. Finally the pupils of both sides become dilated, fixe
and not reacting to light. This characteristic papillary change is known as ‘Hutchinson's pupil'.
(iv) Paralysis.— When blood is collected over the motor cortex from below upwards, it causes pressure
on the cortex to cause paralysis following a short phase of twitching. This paralysis occurs on the opposite sid
of the body and in a descending order — first the face, then the upper limbs and lastly the lower limbs as the
are represented in an inverse manner on the motor cortex.
When blood sufficiently accumulates to cause cerebral compression and herniation of the medial part of th
temporal lobe, the brain stem is pushed to the opposite side. The opposite crus is pressed against the opposit
tentorial margin and so paralysis of the same side of the body (hemiparesis) occurs as the side of injury. This
is because the opposite crus contains motor fibres of the affected side of the body as the decussation of the m
fibres takes place at the medulla oblongata.
If cerebral compression is not relieved impaction of mid-brain cone at the tentorial orifice occurs. This
results in decerebrate rigidity with bilateral fixed dilated pupils.
(v) Pulse and blood pressure.— During cerebral concussion the pulse becomes rapid and thready and the
blood pressure falls down. With the appearance of cerebral compression the pulse becomes slow and boundi
with the blood pressure rises. This is an attempt to maintain the essential cerebral circulation against cerebral
compression.
(vi) Respiration.— In concussion respiration becomes slow and shallow. With the advent of cerebral
compression the respiration becomes slow and deep and ultimately Cheyne Stokes' respiration starts which
indicates grave prognosis.
(vii) Temperature.— With the appearance of cerebral compression, the temperature may rise upto 100° F.
The temperature is slightly higher on the paralysed side (Victor Horsley's sign).
Posterior branch bleeding.— In case of haemorrhage from the posterior branch of the middle meningeal
artery, paralysis of the other side of the body in descending order is not usually come across, as the clot, in th
case, is situated not over the motor cortex but at a distance posterior to the motor cortex. The signs of cerebra
compression i.e. deterioration of level of consciousness, initial constriction followed by dilatation of pupil on
the side of injury and hemiparesis on the same side of the body as the injury due to impaction of the contralat
crus will be noticed.
Extradural haemorrhage of venous origin.— As mentioned earlier extradural haemorrhage may be
caused by injury of a major sinus or by tearing of a meningeal vein. Haemorrhage from venous origin takes s
more time to produce cerebral compression. In case of injury to the superior sagittal sinus, the clot may comp
on the upper end of one or both motor cortices. This may cause unilateral or bilateral leg weakness.
Treatment.— ■
The aim of treatment in extradural haemorrhage is to detect and evacuate a haematoma before it causes
deterioration and secondary brain damage. In this case when the diagnosis is almost certain, the patient shou
be transferred to a neurosurgical department and surgical action should be taken without delay and without
special investigations. In some cases CT scanning may be performed, particularly in a patient who is already
28
in coma.
The next thing is to decide the side to be explored. This is determined by :
(i) The side of temporal haematoma formation;
(ii) The side which shows fracture of skull on X-ray;
(iii) The side on which the pupil first dilates and
(iv) The side from which calcified pineal gland has been shifted on X-ray.
Preoperative preparation.— General anaesthesia with endotracheal intubation and controlled ventilation
are usually used. If these facilities are not available, the operation can be performed under local anaesthesia w
endotracheal tube in position to prevent airway obstruction. After deciding the side to be explored, the patie
face is turned to the opposite side. The head should be thoroughly shaved, or at least half of the head (the sid
to be operated on) must be shaved. Sterile towels are placed in such a fashion so that it allows access to the
temporal, parietal and frontal regions. Blood must be drawn for grouping and cross-matching and at least ab
of blood should be made available at hand at the time of operation.
Operation.— The main aim of operation is to detect the exact site of extradural haemorrhage and to stop
the bleeding after evacuating all blood clots.
Burr-hole exploration versus craniotomy.—
Exploratory burr-holes were usually made to detect extradural haemorrhage. These ‘blind’ burr-holes hav
several draw backs and at least one of them is that it often fails to reveal the clots. The reason for this is that
extradural haematoma often occurs in an atypical position. A more important factor is that the majority of
intracranial haematomas found in head inj ury patients are intradural and these cannot be reliably localised.
holes therefore often cause unnecessary delays.
EXPLORATORY BURR-HOLE.— This should be made at a region where the middle meningeal artery
divides into its anterior and posterior branches after it has come out from the bony canal of pterion. The surf
marking of this is at a point 2 inches behind the external angular process and 2 inches above the zygomatic
process. The burr-hole made to explore this site is called the temporal burr-hole. For this a vertical incision of
3 cm length is made just above the zygomatic arch midway between the external angular process and the ext
auditory meatus. The incision is made through the skin, connective tissue, galea aponeurotica, the temporali
fascia and the temporalis muscle. The temporalis muscle and the fascia are retracted to expose the underlyin
temporal bone. A small burr-hole is made at this region. If the burr-hole has been made just at the site of
extradural haemorrhage, the haematoma will be seen through the burr-hole as black currant jelly. Obviously
this bleeding is from the middle meningeal artery. The burr-hole may be enlarged with a bone nibbler, which
is known as craniectomy. When extradural clot is seen, the clot has to be removed. Very often after the clot is
removed, the fresh blood will gradually well up the wound and will obscure the view. To have a clear view,
continuous irrigation with warm saline alongwith suction is started. The main intention is to locate the bleed
artery. When this is seen, it is best to coagulate it with diathermy electrode. If this is not possible the bleeding
vessel should be under-run with suture. Neurosurgeons often prefer silver clips for this purpose. When the
middle meningeal artery is tom at the bony canal in the pterion, the canal is plugged with bone wax or simpl
with a match stick. If the dural sinus is torn, muscle graft from the temporalis muscle is probably the best to
control haemorrhage. The muscle graft is placed outside the dura mater and is stitched to the pericranium. T
dura mater is then hitched to the surrounding bone by passing sutures through the superficial layer of the du
This step is essential to prevent reaccumulation of haematoma. Next the muscles, temporal fascia, galea and
the skin are closed in layers without drainage and the head is dressed using gauze and a crepe bandage.
When the standard temporal burr-hole fails to locate the extradural bleeding, a parietal burr-hole should be
made. Often the haemorrhage comes from the posterior branch of the middle meningeal artery. In this case a
vertical incision is made above and behind the external auditory meatus and the skull is opened 4 cm behind
and above the external auditory meatus. If this burr-hole also fails to locate the extradural bleeding, a frontal
burr-hole should be made.
If the temporal fracture or evidence of external trauma is on the site opposite to the first dilating pupil, th
THE HEAD 435
compressing lesion is likely to be contre-coup. In this case the burr-hole should be made on the opposite side
of the external trauma. But this is extremely rare.
Craniotomy with osteoplastic flap.— From the description above, it is clear that valuable time may be
wasted in making unsuccessful burr-holes. So many neurosurgeons prefer to do temporal craniotomy to get
wider access for quick decompression of the brain. But this requires experience and familiarity with
neurosurgical instruments. A U-shaped incision on the scalp, the base of which is looking downwards is mad
The flap is raised. 5 or more burr-holes are made on the sk:<ll on the imaginary line to lift the osteoplastic fla
~ Two holes at the base of the flap are placed a bit
nearer to each other than the scalp incision, so that
the bone flap may break easily through the nar
row base. A curved deceptor is used to separate
the dura mater from the skull by insinuating it
through the burr-holes. By means of a special
guide, a Gigli saw is passed between the adjacent
holes and the intervening part is divided in a
manner that will make an outward bevel on the
bony flap. This will prevent the flap from sinking
below its normal level when placed in its position
after operation.
Postoperative care.— The skin sutures are
removed on the 5th day. Antibiotics should be
used. Prophylactic anticonvulsant drugs should
be given for 6 weeks.
Fig.31.5.— Shows how osteoplastic flap is made with the MANAGEMENT OF HEAD INJURY
help of Gigli saw through the burr-holes. Management of head injury can be conven
iently described under several heads :
1. Attending the patient in the casualty department.
2. Indications for admission.
3. General nursing care.
4. Deterioration of level of consciousness.
5. Indications for surgery.
6. Special investigations.
7. Non-surgical treatment.
8. Early complications.
9. Late complications of head injury.
1. Attending the patient in the casualty department.— Whenever a patient comes to the emergency
department with head injury, the main concern of the attending physician is to (a) exclude other surgically
remediable injuries e.g. intrathoracic and inlraabdominal injuries which are more dangerous and may quickly
be fatal.
(b) To see that there is no airway obstruction.
The esssential steps to be considered in emergency department are —
(i) Protection of the airway.—This is particularly essential when the patient is unconscious and vomiting.
False teeth should be removed. His face should be turned to one side, mouth suction and insertion of a pharyn
airway are essential. Some patients may require a cuffed endotracheal tube for proper airway protection.
(ii) Proper history taking.— The nature of injury should be enquired into. History of unconsciousness and
whether there was ‘lucid interval’ or not should be found out. Enquiry should be made about PTA and RTA.
Whether the patient was alcoholic or not before the trauma. Whether the patient is a diabetic or not or whethe
the patient is an opium addict or not.

(iii) Careful clinical examina-
':’; don.— Level of consciousness is the most
7\* important single criterion which cannot be
* .ii.'.' jgjlfrA over emphasised. Both pupils should be
examined about its size and reaction to light.
jfj j ture of long bones. The nose, mouth and car

BjV are examined clearly to exclude blood or
|i I I fl examination. The spine including ccrvical

H• ^ ' |l region should be examined carefully to
*s Mpftf! J| exclude any injury there. The chest, abdo-
llof J mCn Un<^ ^C^‘S sôu^, exam‘ncd ,h°r-
BV Km| J ^ 2. Indications for admission.— Two
^^ ' types of patients require admission in the
V' X'T'^r ‘^ P the patients who require thorough obscrva-

• "' * >• lion for at least 24 hours, despite the patient
* jfiMbeing perfectly well at the lime of admis-
Hl sion. Type B arc the patients who have
suffered serious injury and require treat-
mcnt possibly surgery. The indications for
admission are —
Fig.31.6.— CT scan showing intra-cerebral haematoma. (j) Any degree of depression of
level of consciousness after injury.
(ii) Persistent headache or vomiting (vomiting may indicate simple cerebral concussion).
(iii) Skull fracture.
(iv) Focal neurological signs.
(v) Absence of proper history (relatives or friends or those present during accident are not available).
(vi) Patient with alcohol intoxication.
3. General nursing care.— This has already been described to certain extent in number 1.
(i) Posture.— An unconscious patient should lie in prone position or in supine position with face turned
to one side. If the blood pressure decreases, the head end of the bed should be lowered.
(ii) Airway must always be kept clear. Secretions should be sucked out repeatedly. A pharyngeal airwa
may be introduced or if possible an endotracheal tube may be inserted. Controlled ventilation may be used
spontaneous respiration is inadequate.
(iii) Bladder may be catheterised continuously, particularly in unconscious patient.
(iv) Attention to skin, eyes, mouth and bowels should be maintained particularly in unconscious patient
(v) Nutrition, in unconscious patient, should be maintained. Nasogastric tube feeding is good enough fo
this purpose. If this fails parenteral nutrition should be considered.
4. Deterioration of level of consciousness.— A close watch should be kept on the patient to find out if
cerebral compression is setting in. The level of consciousness is of immense importance in a case of head inju
Deterioration of this level of consciousness often indicates cerebral compression from rising intracranial
THE HEAD 437
pressure. But certain other conditions which may cause deterioration of level of consciousness should be bor
in mind. These are (i) blood loss from other injuries, (ii) airway obstruction and inadequate ventilation, (iii)
hypoinfusion, (iv) meningitis etc. It cannot be over-impressed that deterioration of level of consciousness
should be assumed to be due to intracranial haematoma and cerebral compression unless proved otherwise.
In monitoring the patient the points to differentiate cerebral concussion from cerebral compression shoul
be remembered. These are :
Cerebral concussion Cerebral compression
(0 Unconsciousness from the time of injury. (i) Two periods of unconsciousness with a lucid
interval in between.
(ii) Pulse is quick and thready. (ii) Pulse is slow and bounding.
(iii) Blood pressure is normal or slightly lowered.(iii) Blood pressure is raised.
(iv) Pupils are slightly dilated, equal and reacting(iv) Pupils show typical changes known as Hutch
to light. inson's pupils.
(v) Respiration becomes slow and shallow. (v) The respiration becomes slow and deep; later
on Chevne Stokes respiration may start with
grave prognosis.
5. Indications for surgery.— With the appearance of signs of cerebral compression i.e. deterioration in
level of consciousness, slowing of pulse rate and rising of blood pressure, the patients are probably needing
surgery. These patients should be referred to neurosurgical department. If acute extradural haemorrhage is
suspected, surgery should be advised without any special investigation.
6. Special investigations.—
Skull X-ray.— The importance of skull X-ray in head injury is described below :
(i) If it indicates fracture of skull, it gives more weight to a head injury case and is a definite indication
for admission.
(ii) If it indicates a depressed fracture, it may need surgery.
(iii) Finding of a linear fracture at the squamous part of the temporal bone always gives a suspicion to
occurrence of extradural haemorrhage.
(iv) It may show a calcified pineal gland and its shift to one side or the other may indicate space occupyin
lesion on the opposite side which may well be a haematoma as a cause of cerebral compression.
(v) It may show presence of intracranial air or foreign bodies.
(vi) It may give evidence of associated injuries to the base of the skull or face.
Importance of skull X-ray on arrival of a case of head injury cannot be over-emphasised. A few skull
radiographs are usually required from different views. Besides the usual A. P. (antero-posterior) and lateral
view, the right and/or left lateral, the half-axial (35°) and the anteroposterior at an angle of 20° are taken. A
tangential view including a Towne’s projection may be helpful in case of depressed fracture to know the amo
of depression. It should be borne in mind that it is harmful to move the head in different positions for the pu
of taking plates.
X-ray of the cervical spine.— Only lateral view may be taken to exclude any fracture or fracture-
dislocation there.
Chest radiography.— Once the patient is in X-ray department it is not a bad idea to take the chest X-ray
alongwith the skull X-ray if any injury is suspected there.
For further special investigations the patient should be transferred to the neurosurgical clinic. It is wise to
give osmotic diuretics (described later in this section) to achieve temporary improvement during transfer.
Echo encephalography.— It is a simple and non-invasive method to detect shift of the cerebral midline.
Obviously the presence of haematoma may be indicated by shift of the cerebral midline to the opposite side.
While it is more informative in case of extradural haemorrhage, it is not so in case of subdural haemorrhage
in case of the latter, haemorrhage is bilateral in 50% of cases. The problem of detecting the midline clearly i
always there and even with the experienced observers. Introduction of automated machines have reduced
problem. Neurosurgeons are gradually becoming sceptical about the value of this technique and its popula
is going down rapidly with the introduction of CT scan.
Carotid angiography.— In the absence of availability of CT scan, this investigation is still a valuable
method. It plays an important role to demonstrate extracerebral haematomas (extradural or subdural). The
technique consists of injection of a dye (10 ml of 35% diodone) into the common carotid artery followed by
skiagraphy immediately. It should be said in the passing that this investigation can only be performed whe
patient’s condition is not so acute and he does not require immediate operation, as this is a time consuming
investigation. Carotid angiography will indicate the presence of subdural haematoma by displacement of t
cortical vessels away from the inner table of the skull. In case of extradural haemorrhage the middle cerebr
artery will be displaced inward and the anterior cerebral artery will also be displaced to the opposite side a
the midline. If there be subtemporal haematoma or subcortical bleeding in the temporal lobe, the middle ce
artery will be displaced upward.
Ultrasonography.— It does demonstrate the presence of haemorrhage and its site by positioning the
midline structures with their characteristic echoes. But the informations from this investigation are no way
to those obtained from CT scan.
Intracranial pressure monitoring.— It is a sophisticated method of investigation. Intracranial pressure
is raised due to many of the complications of head injury. Measurement of intracranial pressure has a clear
in the management of patients with head injuries particularly with intracranial haematomas. But the expert
needed to measure intracranial pressure accurately may not be available in many institutions. Its particular
is in postoperative care after the haemorrhages have been operated on. Its value in indicating the type of
haemorrhage and its site before operation is still very doubtful. It should be remembered that an extremely
intracranial pressure may shut off cerebral blood flow.
Computed axial tomography (CT scan).—This investigation has definitely been the most popular among
the neurosurgeons. It conveys much more informations about the intracranial contents than any previous
technique. This non-invasive investigation is easy and safe to perform. It also eliminates exposure to
conventional X-ray investigations.
The patient lies on a movable couch, so that the part to be investigated can be moved within the scannin
gantry. The head is scanned from above downwards in a series of transverse planes. The information is fed
a computer and it produces a record in which high density objects e.g. bone or tumour or clot appear white
less density objects e.g. brain substance appears grey and even less dense objects like oedema are coloured
mottled and the ventricular fluids as black. CT scanning may show a fracturc of the skull and may be partic
useful in demonstrating basal or orbital fractures, yet its major contribution is in the demonstration of
haematomas. It also demonstrates lesions such as contusions and presence of tumours, infarctions, ventricu
displacement and hydrocephalus. Its major importance lies in detecting clots in atypical positions, which ar
always missed in other investigations.
In one word all the patients, except those who need immediate surgery for decompression, should be se
for CT scanning. This investigation has become also Valuable in chalking out a rational and coordinated str
for head injury management. It has largely replaced other methods of investigation.
7. Non-surgical treatment.— The last decade has seen the application of various forms of ‘aggressiv
medical management. These approaches are based upon measurement of intracranial pressure (ICP) and
application of measures aimed at either treating or preventing rise of ICP. The various drugs which are use
this respect are the osmotic diuretics, steroids, hyperventilation and barbiturates.
OSMOTIC AGENTS.— The basis for the use of osmotic diuretics is to raise the osmolarity of the plasma
so that fluid from the brain will be drawn to the extracellular compartment and later into the blood, thus br
oedema and swelling are reduced. So the solution used are hyperosmolar, nondiffusible (these should not c
THE HEAD 439
the blood brain barrier) and are not excreted too rapidly by the kidneys. Today the most commonly used os
agent is 20% mannitol. This is given intravenously to an adult in a volume of 250 ml over the course of 20 to
30 minutes (0.25 to 1 g/kg body weight). The effect of mannitol lasts for only 3 to 4 hours. So this may be
repeated at 6 or 8 hours intervals. The students are hereby cautioned about the potential dangers of the use
such intravenous mannitol. Care must be taken to see that (i) satisfactory renal function is maintained, (ii) fl
and electrolyte replacement should be accurate and (iii) if the blood becomes hyperosmolar, the rate of
administration should be minimised.
Students are further cautioned against indiscriminate use of this agent in all cases of head injury. This sh
not be used in the acute stage when possioility of intracranial haemorrhage has not been excluded. But in ce
cases to get more time before surgery, such agent may be used with care.
Frusemide is another agent in this group, which is often used. Intramuscular inj. of 40 to 80 mg produces
a rapid diuresis which increases osmolarity of the blood and hence absorbs extrafluid from the brain.
STEROIDS.— The rationale for widespread use of steroids in head injury has largely been their benefits
in oedema due to brain tumour. But it has been questioned whether or not steroids has any effect on ICP or
outcome of head injury patients. Some authors of course claim reduction in mortality. In high doses they ha
been used in head inj ury cases (Dexamethasone or Betamethasone in the dose of 60 mg/day) .But even at p
there is no clear evidence that steroids do improve the outcome of head injury cases.
HYPERVENTILATION.— The claim that hyperventilation to a Pa C02 of 20 to 25 mmHg lie mainly on
induction of cerebral vasoconstriction by this method and so reducing ICP. With hyperventilation the reduc
of ICP lasts longer than after administration of mannitol. Although hyperventilation has been used frequent
in Western Countries in head injury cases, there is no convincing evidence of its value.
BARBITURATES.— Barbiturates reduce ICP by reducing cerebral blood flow and by protecting the brain
from damage by reducing its metabolic requirements. These are used in high doses which suppress EEG. It
carries a risk of cardiovascular depression which may be fatal. The value of this treatment is also unproven.
On the whole the effectivity of various medicines just described above in head injury cases is still debatab
It is more advisable not to give too much stress on these agents. Whenever possible intracranial haematoma
should be evacuated as expeditiously as possible and the rest is treated with a high standard of intensive car
The ultimate outcome of the patients depends mainly on the severity of brain damage.
8. Early complications of head injury.—
(i) LEAKAGE OF CSF.— CSF rhinorrhoea or CSF otorrhoea means a communication has been
established between the intracranial cavity and the nose or the ear. It indicates fracture of the base of the sku
and tear of the dura mater. Sometimes brain matter may come out with CSF. These are usually treated with
prophylactic antibiotics (mainly broad spectrum effective against gram-positive and gram-negative organ
isms). The indications for anterior fossa exploration are (a) CSF rhinorrhoea persisting for more than 10 days
(b) an aerocele, (c) attack of meningitis and (d) presence of fracture involving the frontal or ethmoid sinus. T
fractures are reduced in these cases.
(ii) AEROCELE.— Entry of air into the cranial cavity only occurs when there is CSF rhinorrhoea. Such
aerocele is seen in the subarachnoid space or in the substance of the frontal lobe or in the ventricular system
Aerocele occurs when the patient blows his nose in a case of CSF rhinorrhoea. Treatment is almost similar to
that of CSF rhinorrhoea.
(iii) MENINGITIS.— This often occurs in major head injuries particularly with basal skull fracture.
Meningitis usually takes place not before 48 hours of injury. Neck stiffness, which is a common sign of
meningitis, is also seen in case of subarachnoid bleeding. Lumbar puncture to diagnose meningitis should n
be done casually and is only performed when its indication is clear and there are no signs of cerebral
compression. In cerebral compression there is a risk of pressure-cone being formed by the impaction of med
into the foramen magnum while draining the cerebrospinal fluid. This is fatal.
(iv) FAT EMBOLISM.— It is difficult to differentiate from systemic fat embolism due to multiple
injuries with limb fractures from neurological deterioration due to head injury. Neurological features due to
embolism usually do not appear before 48 hours of injury. The finding of fresh petechiae over the upper par
of trunk and in the axilla is of fat embolism. The pupils which vary in size from moment to moment but rem
equal with presence of retinal haemorrhages are signs of fat embolism. In case of absence of positive signs of
fat embolism, either X-ray of the skull should be taken to exclude intracranial haematoma or to obtain a CT s
for proper diagnosis.
(v) BRAIN-STEM INJURY.— This term indicates injury to the pons and medulla. This is often due
to increased intracranial pressure of the supratentorial compartment. The typical features are extensor spasm
of all 4 limbs, arching of the trunk (opisthotonus), a rapid pulse, rapid and shallow respiration, small pupils
pyrexia.
(vi) POSTERIOR FOSSA COMPRESSION.— In this region extradural haemorrhage may occur due
to tear of the lateral sinus. Compression occurs on the cerebellum and medulla. The most important physica
sign is shallow an irregular respiration followed by deterioration of level of consciousness. CT scan is helpfu
in diagnosing this condition.
(vii) PITUITARY FAILURE.—This may result if basal fractures pass across the pituitary fossa causing
acute damage to the pituitary gland. Profound fall in blood pressure, tachycardia and hypothermia are seen
deterioration in level of consciousness. High dosage of steroids should be given in the dose of hydrocortison
— 200 mg 6 hourly on 1st day followed by reduced and maintenance dosage later on.
9. Late complications of head injury.—
(i) Chronic subdural haematoma.
(ii) Post traumatic epilepsy.
(iii) Headache.
(.iv) Hydroccphalus.
INTRACRANIAL INFECTIONS
Intracranial infections include osteomyelitis of the skull, extradural abscess, subdural abscess (empyema)
and intraccrcbral or brain abscess.
OSTEOMYELITIS OF THE SKULL —
Osteomyelitis of skull is quite rare.
PATHOGENESIS.— Osteomyelitis of the skull occurs from 3 major sources of infection — (i) infection from a wound of the scalp,
(ii) infection from middle ear, paranasal sinus or mastoid air cells, (iii) haematogenous spread from anywhere of the body.
ORGANISMS.— Though any organism may be the causative agent, yet by far the most common is Staphylococcus aureus followed
by B. proteus and B. pyocyaneus (both these organisms usually come from middle ear infection).
PATHOLOGY.— Infection spreads through the diploic spaces. The infection also spreads under ti.s outer periosteal layer or
pericranium. This pericranium is attached firmly at the sutures of the skull so osteomyelitis of the skull is usually limited to the bone
concerned. Osteomyelitis of the skull causes pitting oedema of the scalp over the affected area and this collectively known as ‘Pott’s puffy
tumour’. Gradually the blood supply to the skull gets damaged and therefore necrosis and sequestration of the bone may take place. Very
commonly infection spreads to the extradural space.
CLINICAL FEATURES.— Fever, malaise and leucocytosis are the general signs and symptoms. Locally a swelling may be detected
in the skull with quite tenderness. Sometimes the infection may remain indolent for sometime and only manifests itself by drainage through
an area of scalp. More often the infection is quite virulent and may spread into the intracranial structures.
TREATMENT.— Appropriate antibiotics should be started immediately once suspicion of osteomyelitis of the skull is made. If a
portion of bone is dead, it has to be excised. Care must be taken to be certain that no infection remains in the extradural space after excision
of the bone.
EXTRADURAL ABSCESS.—
PATHOGENESIS And PATHOLOGY.— Such abscess is usually caused by (i) spread of infection from osteomyelitis of the skull;
(ii) spread of infection from the middle ear, (iii) from frontal sinus and (iv) from mastoid air cells. In case of middle ear infection, it
commonly reaches extradural spread through the tegmen lympani. When an epidural abscess is formed, the dura mater acts as a protective
barrier against inward spread of infection. But unfortunately infection often breaks through the dural barrier and has resulted in meningitis
or brain abscess. Infection may spread into the subdural space by direct extension along emissary veins and dural sinuses.
CLINICAL FEATURES.— These are almost similar to those of acute osteomyelitis of the skull. There may be acute headache.
Tenderness can be elicited over the area of extradural abscess by percussion on the local area of the skull. Seizures and focal neurologic
deficits may be seen and are mostly due to thrombophlebitis of superficial cortical veins.
THE HEAD 441
TREATMENT.— Appropriate antibiotic should be started immediately. Once the abscess has been formed, it should be drained
through burr-hole. Any necrosed skull bone nearby should be excised. Drainage of the infected sinus or mastoid air cells are to be performed
for complete cure of the condition.
SUBDURAL ABSCESS —
PATHOGENESIS And PATHOLOGY.— Subdural abscess is also caused by infections of the middle ear, paranasal sinuses and
mastoid air cells. Infection of paranasal sinuses is a very common source of subdural abscess. Infection spreads into the superior sagittal
sinus and to the cerebral veins, where it causes septic thrombophlebitis and thus infects the subdural space. The abscess gets a wide space
to extend over the cerebral hemispheres and it often spreads bilaterally. In other cases infection extends along emissary veins and via dural
sinuses into the sudural space through cerebral veins.
ORGANISMS.— Here also the common causative organisms are S. aureus, B. Proteus and B. pyocyaneus. Since there is no natural
barrier to spread of the infection, subdural infection is quite dangerous and the surface of entire hemisphere may be involved within a very
short period. Progression to the opposite hemisphere occurs beneath the falx.
CLINICAL FEATURES.— Symptom pattern of a patient with subdural infection may vary. A history of chronic synusitis or chronic
ear infection may be received. Suddenly a rise in temperature with chills and convulsion may occur indicating appearance of subdural
infection. Severe headache with mild weakness and numbness of the opposite side of the body will be complained of. This is soon followed
by convulsion and unconsciousness. Initial examination may reveal signs of meningitis. Lumbar puncture shows increased cell counts, but
sugar content of CSF remains within normal limits. Microscopic examination of CSF may fail to reveal any bacteria.
Gradually there will be total loss of function of the involved hemisphere. The condition may be aggravated by increase of intracranial
tension and herniation of the temporal lobe. This will be indicated by dilated pupil on the involved side, hemiparesis of the same side of
the lesion and beginning of decerebration.
TREATMENT.— Treatment of subdural empyema or abscess is early burr-hole and drainage. Once increased intracranial pressure
has been developed with deterioration of level of consciousness and shift of the midline structures, external decompression by removing
osteoplastic flap and opening of the dura mater are mandatory. This is indeed a big operation on a patient with very bad general condition.
The operation must be performed under proper antibiotic cover.
BRAIN ABSCESS.—
PATHOGENESIS And PATHOLOGY.— The brain is quite resistant to infection by various organisms. Brain abscess cannot be
formed unless that portion of the brain is already damaged by anoxia, haemorrhage or trauma. The infection once formed within the brain
is gradually walled off by granulation or glial tissue. This formation of wall is so efficient that it completely isolates the infection not only
from the rest of the brain tissue but also from the systemic blood supply. Hence it is difficult to cure such brain abscess by systemic
antibiotics.
Cerebral abscesses may occur from either of the 3 sources — (i) direct extension from middle ear, paranasal sinuses or mastoid air cells
(this is the commonest route of infection), (ii) blood bome infection from anywhere in the body, but most common is intrathoracic sepsis,
(iii) by direct traumatic penetration — infection through this route lias been greatly minimised by adequate surgical care of the wound and
proper antibiotic protection. The middle ear infection is the most common source of infection for brain abscess. The temporal lobe of
cerebral hemisphere is the common site for abscess formation from such infection. Haematogenous abscesses may occur following
bacteraemia, but such infection is more common from intrathoracic sepsis e.g. lung abscess, infected bronchiectasis, empyema, cyanotic
heart disease and subacute bacterial endocarditis. It must be remembered that in cyanotic heart disease the commonest cause of cerebral
dysfunction is a cerebral abscess with symptoms of seizures or neurologic loss. These cases should always be sent for CT scan to rule out
abscess. Infected clot from lung passes to the left heart, thence via the carotid into the middle cerebral circulation. Such infection is usually
implanted deep in the white matter near the ventricle in parietal or temporal lobe.
CAUSATIVE ORGANISMS.—In brain abscess the organisms commonly seen are Streptococci (particularly the anaerobic strains),
Pneumococci and Staphylococci in that order of frequency.
CLINICAL FEATURES.— 3 stages have been recognised in clinical features —
Acute stage.— This is characterised by acute pyogenic encephalitis without pus formation and the symptoms and signs are almost
similar to the subdural abscess.
Subacute stage.— This starts at about 3 weeks following infection. In this stage there is formation of a glial wall which is thickest
towards the cortex and thinnest towards the ventricle. Gradually a unilocular or multilocular cavity is formed within the wall containing
active organisms.
Chronic stage.— As the glial wall becomes thicker in 6 weeks a chronic abscess is formed. At this stage there may be no signs of
systemic reaction to infection e.g. no fever or leucocytosis. But there will be progressive focal neurological deficit and an increasing mass
as a space occupying lesion which simulates a tumour.
Clinical diagnosis of brain abscess depends on 3 findings — (i) Evidence of infection, (ii) Focal neurological symptoms and signs and
(iii) Features of raised intracranial pressure.
(i) Evidence of infection.— A recent middle ear infection or frontal sinusitis is usually obtained. Similarly history of intrathoracic
infection may be received. In the acute stage there will be fever, high white cell count (above 10,000 in majority of cases) and tachycardia.
ESR is also raised in majority of cases.
(ii) Focal neurological symptoms and signs.— These will depend on the site of lesion. In case of cortical lesion anywhere and
particularly in frontal lobe lesion, epilepsy is an early symptom. In temporal lobe abscess, contralateral hemiparesis and dysphagia may
be noticed. In cerebellar abscess nystagmus, ataxia and incoordination on the side of lesion may be detected.
(iii) Features of raised intracranial pressure.— The symptoms of raised intracranial pressure are headache, vomiting and
deterioration of level of consciousness. The signs of this condition are depressed conscious level, slowing of pulse rate, rising pressure and
papilloedema.
TREATMENT.—In acute stage, antibiotics, anti-inflammatory agents e.g. steroids and careful control of fluids are the treatment of
choice. Repeated CT scans are necessary to monitor the progress of the treatment and to detect formation of capsule. This usually takes
10 to 20 days.
Once abscess has been demonstrated, it has to be drained (i) either by intermittent tapping through a perforator opening, (ii) by constant
drainage or by (iii) excision of the abscess.
A burr-hole is made in the appropriate site, the dura mater is opened and a blunt brain cannula is inserted into the abscess cavity. The
pus is aspirated and an antibiotic is inserted. Previously a radio-opaque contrast medium (1 ml of steripaque) is introduced into the abscess
cavity through the brain cannula. The pus should be immediately sent for culture and sensitivity test. High doses of penicillin are started
intravenously as the organisms are mostly Streptococci. Metronidazole or Chloramphenicol are the antibiotics of choice in B. proteus or
B. pyocyaneus infections.
Further progress and shrinkage of the abscess are assessed by radiography with contrast medium or by CT scan.
If the abscess fails to shrink to the expectation of the surgeon, excision of the abscess should be performed.
Steroids and osmotic agents may be given to reduce oedema around the brain abscess. Prophylactic anticonvalsants should be given
for 6 months.
The main dangers of abscess of the brain are (a) acute oedematous response of the brain, (b) rapid rise in intracranial pressure and (c)
rupture of untreated cerebral abscess into the ventricular system which is rapidly fatal. Due to failure to diagnose early and presence of
concurrent thoracic and cardiac diseases, the mortality rate of brain abscess is high even upto 40 to 50 per cent.
INTRACRANIAL TUMOURS
Classification.— This can be best classified under two headings ■— A. Extracerebral and B. Intracerebral.
A. EXTRACEREBRAL TUMOURS may be 1. Meningioma, 2. Acoustic neuroma, 3. Pituitary adenoma,
4. Craniopharyngioma, 5. Teratoma, 6. Cholesteatoma, 7. Pinealoma, 8. Chordoma and 9. Retinoblastoma.
B. INTRACEREBRAL TUMOURS may be 1. Glioma, 2. Metastatic carcinoma, 3. Haemangioma, 4.
Colloid cyst, 5. Sarcoma and 6. Tuberculoma.
Important tumours are described below :—
1. Gliomas (43%).— These are subdivided according to the stage of development of the glial cells into
— (a) Astrocytoma, (b) Oligodendroglioma, (c) Spongioblastoma polare, (d) Mcdulloblastoma, (e) Glioblas
toma multiforme and (f) Ependymoma.
(a) ASTROCYTOMA.— It is benign growth composed of star-shaped adult neuroglial tissue. It may
occur at any age. In children it affects the cerebellum whereas in adults it affects the frontal lobe most comm
These tumours occur as one of the 3 forms —
(i) Diffuse or infiltrating variety, which is probably the most common. The margins are not recognised
properly. It may affcct any part of the brain, but the brain stem is more often affected. Its total removal is alm
impossible.
(ii) The solid form.— It is usually circumscribed and can be removed totally.
(iii) The cystic form.— In fact the tumour is not cystic but it is nodular. From the surface of the nodule
a fluid is secreted which forms a cystic cleft between the tumour and compressed normal brain. Its removal
also easy in the sense that the tumour is enucleated through the cystic cleft.
The actual behaviour of astrocytoma depends on its cellular type. Astrocytomas are now classified into 4
grades according to the proportion of adult and primitive cells which they contain. Grade I means more adu
cells and this is relatively benign whereas grade IV means more primitive cells and it is more malignant.
(b) OLIGODENDROGLIOMA.— It is also an adult cell tumour, the cells having short stunted processes
It affects the deep parts of the cerebrum in adults. It is less malignant than other gliomas.
(c) SPONGIOBLASTOMA POLARE.— It arises from primitive unipolar or bipolar cells. It usually
affects the optic chiasma, third ventricle and hypothalamus in young subjects. It is often difficult to remove
tumour, but fortunately enough this tumour is more radiosensitive. It may produce seedling metastasis in th
cerebrospinal fluid.
(d) MEDULLOBLASTOMA.— It is a highly malignant growth and affects the vermis of the cerebellum
in children. It grows rapidly and gives rise to seedling metastases throughout the cerebral hemisphere and s
meninges. It is radiosensitive.
(e) GLIOBLASTOMA MULTEFORME.— Itarises as a result of malignantdegeneration in a pre-existing
THE HEAD 443
astrocytoma and therefore occurs in the cerebrum of adult males. It contains all varieties of glial cells includi
giant cells.
(f) EPENDY
mour found mostly in fourth ventricle. Age of predilection
is 2nd and 3rd decades. These tumours arc also growing and
^ I of low malignancy. When occurs in cerebral hemisphere, it
Hr* / ;irW m t may become somewhat more malignant like malignant
• Hk v ^ sentially benign growths originating in the arachnoid villi

^ and may gain attachment to the dura mater. Meningiomas
mjl which is called meningioma plaque. The tumour cells o

I •• invade the skull through dilated emissary veins. Gradu
■ ^ one can sec bone destruction and reactive hyperostosi
situations, they are called parasagittal, when occurring

Fig.31.7.— Cystic astrocytoma showing along the superior longitudinal sinus; frontobasal, when
ventricular shift. occurring on the cribriform plate, sphenoid wing and tuber-
culum sellae, and posterior, when occurring at the cerebellopontine angle and jugular foramen.
3. Pituitary adenoma (12 %).— There are three types of adenoma: chromophobe, acidophil and basophil.
(;a)Chromophobe adenoma affects usually women between the ages of 20 and 50 years. Headache and
bitemporal hemianopia are the characteristic features, (b) Acidophil adenoma gives rise to gigantism in childre
and acromegaly in adults, owing to excessive production of growth hormone by the acidophil cells and inhi
bition of basophil sex secretion, (c) Baso
phil adenoma gives rise to Cushing’s syn-
^._ drome. Females are mostly affected. There
îs accumulation of fat in the trunk, neck
and face.
4. Acoustic neurofibroma (Sch-
,V -/ : wannonia) (8% ).- Schwannoma mainly
affects the sheath of the auditory nerve
.M.■' ' '" s§| (8th cranial nerve) and that is wh> it is
often called acoustic neurofibroma. It is
"\v. ly the most frequent variety of subtentorial
i tumouroccurring in adult life. Sometimes
... " -v it may be multiple in association with vo
_ Recklinghausen’s disease. It sometimes
■<- V ., , v " ; A ’ ^Jjp * may occur in association with spinal
meningiomas.
5. Metastatic tumours.— A few
primary tumours arc notorious to
produce metastasis in the brain. The
commonest primary site is the lung.
#'
Other primaries e.g. breast cancer,
Fig.31.8.— Skiagram showing hypertrophied bone overlying
adenocarcinoma of kidney, neuroblas-
a parasagittal meningioma. toma, malignant melanoma, intestinal
carcinoma, carcinoma of prostate etc. are known to metastasise in the brain. It is more common
than other primary intracerebral tumours.

6. Craniopharyngiomas.—These growths produce large masses, in which there are cystic cavities li
with ciliated epithelium and containing cholesterol crystals. More than 50% of these growths are calcified.
Though these tumours are usually suprasellar, yet these may be infrasellar and even they may not be cystic
Sometimes these tumours may cause hydrocephalus and raise intracranial pressure to a considerable extent
obstructing the flow of CSF.
CLINICAL FEATURES.— Clinical features of brain tumours can be best described under 4 stages —
STAGE I.—There is always an initial silent period which varies in length according to the rate of the grow
and position of the tumour. Those tumours which are not near any area of the brain to produce symptoms o
due to pressure will have a longer silent period. During this period the tumour gradually takes up the
subarachnoid space. It then flattenes the ventricle till the brain has no more room within the skull. Obstruct
of CSF flow from the vcntricles contribute a lot to increase of intracranial pressure. Similarly oedema aroun
the brain tumour also contributes to the increase of intracranial pressure. It will then produce the symptom
raised intracranial pressure of stage III.
STAGE II.— This includes epilepsy and focal syndromes.
Epilepsy, if starts first time in adults, a brain tumour should be suspected as the cause of such epilepsy. C
scan and more recently Magnetic resonance imaging (MRI) are best investigating tools available in the hand
of surgeons to diagnose a brain tumour at this stage. Epilepsy in a patient between the ages of 30 and 50 yea
is mainly due to the development of a brain tumour.
Focal syndromes depend on the site of the tumour. If the tumour is situated in a particular lobe near an
important area its local effect produces a few symptoms, which the students should remember.
In frontal lobe tumours, there occur (i) changes in personality, (ii) weakness of the opposite side of the face
and (iii) inability to count correctly due to involvement of Broca's area on the left side in right-handed perso
In parietal lobe tumours, the signs arc (i) aslereognosis, i.e. failure to recognise the size, shape and form of
different objects, (ii) exaggerated deep reflexes, (iii) weakness on the opposite side.
In temporal lobe tumours, the signs are (i) aphasia, (ii) hemianopia and (iii) uncinate fit with hallucination
of smell in lesions of the uncinate gyrus.
In cerebellar tumours, the signs arc (i) ataxic gait with Romberg's sign, (ii) asthenia with absence of tendon
reflexes, (iii) strabismus, (iv) nystagmus, (v) stiffness of the neck etc.
STAGE III.— This is due to raised intracranial pressure. These symptoms occur earliest in midline and
posterior fossa tumours, early in temporal and parietal lobe tumours and late in frontal lobe tumours. In a
meningioma the onset may be delayed for several years. Ilence the absence of these symptoms does not exclude
presence of an intracranial tumour. The symptoms of raised intracranial pressure are — (a) headache, (b)
effortless vomiting, (c) deterioration of level of consciousness and (d) dimness of vision.
The signs of raised intracranial pressure are:— (a) Lowering of level of consciousness, (b) slowing of pulse
rate, (c) rise in blood pressure and (d) papilloedema.
STAGE IV.— This is the stage of cone formation. When intracranial pressure increases to the extent that
the medial border of temporal lobe of one hemisphere is forced through tentorial opening, this causes press
on the mid-brain which contains reticular formation which is concerned with consciousness. Similarly press
on the contralateral crus will cause hemiparcsis on the side of the lesion. The herniation will also put pressu
on the oculomotor nerve of that side to cause first irritation and then paralysis of that nerve. Ultimately bila
cone formation will cause decerebrate rigidity and death of the patient. The signs of the stage of coning are:—
(a) paroxysmal headache, (b) drowsiness, (c) deterioration of level of consciousness, (d) unilateral pupillary
dilatation, (e) unconsciousness, (f) neck stiffness, (g) unilateral hemiparesis, (h) decerebrate rigidity.
SPECIAL INVESTIGATIONS.— Besides examination of the urine and blood (including W. R., urea,
N.P.N. and E.S.R.) the following special investigations are essential.
1. Lumbar puncture.— One should not do lumbar puncture in ease with papilloedema. This is mainly indicated
to exclude non-tumourous conditions.
THE HEAD 445
(a) Pressure should be measured by a manometer. Normally, it is about 120 mm of water. Any pressure above 160
mm would mean a raised intracranial pressure. If the pressure is high only a very small quantity of fluid should be drained
since there is always the danger of herniation of the temporal lobe through the tentorium cerebelli and of the medulla through
the foramen magnum. Although brain tumours are usually associated with increased pressure, yet a normal or even low
pressure as measured by lumbar puncture is not unusual.
(b) The cellular content is not markedly increased in the majority of cases, but in 10% of cases it is raised. In glioma
it is more seen. Generally less than 50 cells are found, but one may find upto 100 cells due to necrosis of malignant glioma
close to the ventricle.
(c) Protein content.— Considerable increase in protein content is sometimes found in neurofibromas of the
auditory nerve and in meningiomas; in the latter condition it may rise up to 500 mg or even more. Normally, the protein
content of the cerebrospinal fluid is 20-30 mg per cent. Protein content is generally increased in cases of tumours. Site of
tumour is important in this respect and intraventricular or paraventricular tumours produce more protein level in CSF.
Increase in number of cells and protein content (approximately 80 mg/100 ml) are seen in acute stage of cerebral abscess.
Gradually the number of cells is reduced but the protein content increases to even 120 mg/100 ml.
(d) Wassermann reaction of the cerebrospinal fluid should also be tested.
2. Skiagraphy.— Straight X-ray films of the skull reveal many facts :
(a) When the intracranial tension is increased, note the following points : (i) separation of all the sutures of the
vault in children; (ii) hammer markings or ‘beaten silver’ appearance of the skull; (iii) simple dilatation of pituitary fossa
with thinning or erosion of the posterior clinoid processes (this is the most important finding).
(b) In meningioma (i) the skull shows three types of involvement: erosive, hypertrophic and sclerotic — the first
type is frequently encountered in the vault and the last one at the base of the skull, whilst hyperostosis is found in either place;
(ii) enlarged vascular groove caused by engorged meningeal veils; (iii) calcification in the tumour.
(c) Astrocytoma also shows calcification. About 40% oligodendroglioma calcify.
(d) In suprasellar cyst, patchy calcification is characteristic. Widened but shallow sella turcica with erosion of the
clinoid processes is often evident.
(e) Pituitary adenoma causes enlargement of the pituitary fossa; the enlargement is great and rarely regular — a
fact that differentiates extrapituitary causes of enlargement of the pituitary fossa (internal hydrocephalus, suprasellar cyst).
(f) Displacement of the calcified pineal body — ‘pineal shift' — is indicative of a large tumour in the opposite
hemisphere.
(g) Over half of the cases of craniopharyngioma and some tuberculomas show calcification.
X-ray of the chest should be taken for primary focus in the lungs since 30 percent of bronchial carcinoma comes with
cerebral symptoms before any chest symptoms.
3. Ventriculography is done by passing abrain cannula into each lateral ventricle through ahole bored in the skull
7 cm above the external occipital protuberance and 3 cm from the middle line. The direction of the cannula will be so guided
as to aim at the pupil of the same side. The ventricle will be found at a depth of about 5 cm from the surface. 5 ml of fluid
is slowly withdrawn and a little less than 5 ml (to allow expansion at body temperature) or air is introduced. Skiagrams arc
taken immediately after. By means of ventriculography any alteration of the size, shape and position of the ventricular
system can be clearly visualized. Myodil ventriculography can be done, by pushing 1.5 ml of myodil through anterior horn
of the lateral ventricle.
4. Encephalography is the skiagraphy taken after replacing the cerebrospinal fluid by air or oxygen through a
lumbar or cisternal puncture. First a lumbar puncture is performed and the operation table is tilted to about 45°, so that the
head is uppermost, then for every 11 ml of fluid withdrawn 10 ml of oxygen is injected until about 45 ml has been introduced.
This is immediately followed by skiagraphy. X-ray pictures will show gas in the basal cistemae, over the cortex and in the
ventricles. This investigation is dangerous in cerebral tumours and should be reserved for low pressure cases with symptoms
of epilepsy.
5. Carotid angiography is the skiagraphy taken immediately after the injection of 8-12 ml of 45% Hypaquq into
the carotid artery. Three lateral films are exposed at intervals of two seconds. This is followed by further injection to obtain
anteroposterior vessels. This method is helpful to demonstrate the presence or absence of an aneurysm or of an angiomatous
tumour such as a meningioma.
6. Vertebral angiography.— 30 ml of 50% Hypaque is used for this. Either retrograde method through the
brachial or femoral artery or horizontal approach just above the atlas is made.
7. Electro-encephalography is a modem method of localizing brain tumour. A cerebral tumour is electrically
dead compared with the normal cortex. Tumours produce delta or theta waves on the surface. Occasionally it gives a clue
as to which side carotid angiography is to be carried out.
8. Cerebral Puncture.— If secondary carcinoma or malignant glioma or cyst is suspected cerebral puncture is
very valuable investigation. A burr-hole is made on the site of the cyst or a tumour and aspirating needle or ventricular
cannula is introduced into the cyst or the tumour for aspiration. A cyst produced by astrocytoma contains golden yellow
coloured fluid. A malignant cyst contains muddy non-clotting fluid. Meningiomas provide resistance to the aspirating
cannula. After aspiration, air or thorotrast injected into the cavity in order to produce a picture of the cyst.
9. Biopsy.— A sample of the tumour may be obtained by the brain cannula during ventriculography or by means
of a special punch such as that designed by Jackson.
10. Echoencephalography.— Displacement of the midline structures above the tentorium can be detected by
reflecting the sound waves from both sides of the skull off those structures. A shift of more than 0.5 cm will be revealed
by this technique.
11. Scintillation-encephalography.— Radioactive iodinated human serum albumin is used for this. On the 3rd
day after giving this isotope the scanning is done.
12. Brain Scan.— Intracranial tumour and other space-occupying lesions can now be diagnosed with no morbidity
by brain scanning with a certainty of 80%-90%. A locally increased concentration of injected radioisotope substance may
be found. It can be visualised by an external scanner or camera, which produces a map of the radioactive distribution in the
head. Its usefulness is immense and to narrate in short the main points are : (i) detection and localisation of primary brain
tumours; (ii) detection of cerebral metastases; (iii) differentiation between diffuse and focal inflammatory diseases, i.e.
between diffuse meningo-encephalitis and localised brain abscess; (iv) in the assessment of head injury, i.e. differentiation
among simple concussion, contusion, extradural and subdural haemorrhages; (v) assessing the effect of carotid stenosis on
cerebral blood flow and how it improves after endarterectomy.
In case of brain tumours, arteriography, ventriculography, pneumoencephalography can be used but they are complex
and not without morbidity. Electroencephalography is not precise in localising a brain tumour. Ultrasonic encephalography
is more recent and quite safe, but indicates only lateral shift of the midline structure of the anterior half of the cranium. To
the contrary radioisotope scanning is simple and free from risk. Even when angiography or ventriculography has revealed
the site of lesion, scanning may give additional information which will be of great diagnostic value. The most commonly
used isotopes are 131I, "“Tc, etc. The optimum time for scanning in 13,I is about 24 to 48 hours whereas in "”Tc the optimum
time for scanning is about 1 to 3 hours. Brain tumours are demonstrated as areas of increased activity on the scan or camera
pictures. Intracranial non-malignant cyst lesions do not show significant uptake. The overall accuracy of detection of brain
tumours by scanning varies from 65% to 93%.
13. CT Scanning .— When available, this has become the major method of diagnosis of brain tumours. It indicates
presence of the tumour with or without ventricular displacement or distension. It is also possible to know the type of the
tumour. Meningiomas, schwannomas and pituitary adenomas enhance scanning vividly, whereas gliomas show variable
patterns of enhancement. Sometimes exact nature of the tumour cannot be assessed by this investigation.
14. Magnetic Resonance Imaging (MRI).— The human body is a chemical composition made up of several
elements such as Hydrogen, Carbon, Nitrogen, Sodium, Phosphorus, Potassium etc., in various chemical combinations. It
has been observed that the atoms of some of these elements, having odd number of protons in their nuclei, have magnetic
properties. The magnetic properties of the protons of these elements have been utilised to produce Magnetic Resonance
signals and images. The most abundant of these in the human body, is the proton of Hydrogen atom in the form of water
and various other Organic compounds such as fats, cholesterol etc. These Hydrogen protons (Minute magnets) in the human
body are in a random orientation pointing in different directions. The patient is placed in the centre of a huge, powerful
cylindrical magnetic system. Under its influence the patient’s tiny hydrogen proton magnets tend to align themselves in the
directionof the external magnetic field. These tiny magnets of the human body are then subjected to an interplay to additional
magnetic influences, in the form of Radiofrequency waves, magnetic gradient coils etc., to elicit Magnetic Resonance
signals.
The various types of signals elicited are labelled Tl, T2 relaxation signals. The Magnetic Resonance Signals have
specific tissue characteristics. These are analysed by a computer and reconstructed mathematically by a method called
Fourier Transformation into sectional images of the human body. The most utilised proton for imaging the human body is
the protons of Hydrogen element; Hydrogen being most abundant in human tissues.
The various types of images exhibit specific tissue characteristics, by which the tissues can be identified. For
examples —
Tl T2
Fat Bright Dark
Muscle Grey Grey
CSF/Clear Fluids Black White
Brain white matter Bright Dark
THE HEAD 447
Brain grey matter Dark Bright

Bone, Air and Flowing Blood Dark Dark
MRI IN BRAIN IMAGING.— The\maximum application of MRI is in the study of the brain. The unique contrast
resolution obtainable in MR imaging provides excellent white and grey matter differentiation. S ince bone does not interfere
with the imaging and artefacts, which are hindrance in CT scanning are not present, excellent anatomical details of the brain
and other structures in the middle and posterior cranial fossa are brought out.
With the introduction of MR imaging, statistics reveal, MR imaging of the brain detects at least 30 per cent of
pathological lesions not demonstrated in CT examination. It is more sensitive than CT in detecting cerebral infarcts within
a few hours of onset. It is particularly valuable in detecting cerebral brain stem infarcts. MRI is indispensable for detecting
lesions in middle and posterior cranial fossa, small acoustic neuromas and pituitary microadenomas. MRI is invaluable for
not only detecting, but also staging intracranial neoplasms for surgical or radiotherapeutic management. It helps in early
detection of cerebral metastases and for evaluating patients with epileptic foci.
TREATMENT.— The primary goal of management of intracranial tumour is total surgical excision or
extirpation of the tumour. Unfortunately, in case of brain tumour surgical removal is not always possible or e
desirable, since the resulting neurologic deficit may cripple the patient’s life. In these cases palliation by parti
removal of the tumour or relief of raised intracranial pressure should be achieved. Further treatment of the
tumour X-ray therapy and/or chemotherapy may control the tumour or give significant relief to allow the
patient’s existance relatively comfortable.
Management of intracranial tumour can be divided into 2 groups — 1. Release of raised intracranial pressu
and 2. Local treatment of the brain tumour.
1. Release of raised intracranial pressure.— This can be achieved by various means —
(i) Tapping of cystic tumours.
(ii) Tapping the ventricle and its drainage through a posterior parietal burr-hole when the lateral
ventricles are dilated in case of posterior fossa and 3rd ventricle tumours.
(iii) Partial removal of the tumour, particularly the supratentorial ones.
(iv) Administration of 20% of mannitol solution to produce temporary improvement.
(v) Dexamethasone in doses upto 24 mg/day may bring about relief and even inprove focal syndrome
in patients with malignant tumours.
2. Local treatment of the brain tumour.—
Craniotomy is usually performed by raising an osteoplastic flap. The individual tumours are tackled as
below —
Malignant gliomas.— The pathology of the tumour is established by frozen section or smear. In case of high grade malignancy only
the tumour is removed by rongeur and suction. In low grade malignant tumours, the removal should be more aggressive with a portion of
normal tissue. Haemostasis is obtained by packing, diathermy, hydrogen paroxide or by application of tantalum clips to larger vessels.
Meningiomas.— In these cases clipping or diathermy of feeding vessels are first performed to reduce the bulk of the tumour. Now the
meningiomas are removed alongwith the adjacent dura mater. In case of the basal tumours total removal may not be possible.
Benign astrocytoma and haemangioma.— These benign tumours should be totally removed. As these tumours are mainly seen in
cerebellum, posterior fossa craniectomy is needed.
Acoustic neuroma.—The approach is again posterior fossa craniectomy. The tumour is totally removed with preservation of the facial
nerve. Operating microscope is of great help in dissecting the tumour out from the brain stem. Trans-sphenoidal approach has now been
used with success.
Metastasis.— Usually these tumours cannot be operated on. Particularly when the primary is bronchial carcinoma or melanoma the
results are disappointing. When the metastasis is well circumscribed then only it can be removed totally with blunt dissection, rongeur and
suction.
Craniopharyngiomas.— These tumours in or above the sella may be evacuated by frontal craniotomy or by trans-sphenoidal surgery.
If the tumour blocks the 3rd ventricle, the CSF may be short circuited to the cistema magna by leading a catheter from the ventricle through
a burr-hole opening in the skull, thence under the skin and occipital muscle to drain into the cistema magna which is exposed above the
foramen magnum. This is known as ventriculo-cisternostomy operation ofTorkildsen.
Radiotherapy.— Malignant astrocytoma grade in and IV and medulloblastoma respond more favourably
to radiotherapy.
Chemotherapy.— The results of chemotherapy are still not very conclusive.
448
CHAPTER - 24
SWELLINGS OF THE JAW

CLASSIFICATION OF JAW SWELLINGS
A. Arising from the mucoperiosteum i.e. Epulis. There are five varieties of Epulis —
(i) Fibrous.
(ii) Granulomatous.
(iii) Myeloid.
(iv) Sarcomatous.
(v) Carcinomatous.
B. Arising from tooth germ i.e. odontomes. The different varieties are —
1. Epithelial odontomes i.e. arising from epithelium elements —
(i) Dental cyst.
(ii) Dentigerous cyst.
(iii) Adamantinoma.
THE FOLLOWINGS ARE RARE VARIETIES —
2. Connective tissue odontomes i.e. arising from connective tissue elements —
(i) Fibrous odontome.
(ii) Cementomes.
(iii) Sarcomatous odontomes.
3. Composite odontomes i.e. arising from both epithelial and connective tissue elements —
(i) Radicular odontome.
(ii) Compound follicular odontome. l ,
. ■, r Extremely rare.
(ui) Complex composite odontome. 1
C. Osseous tumours—any bone tumour can affect the jaw. But there are few bone tumours which occur
more often in the jaws. These are discussed later in this chapter.
D. Inflammatory group —
(i) Alveolar abscess.
(ii) Osteomyelitis.
(iii) Actinomycosis.
EPULIS
The word ‘Epulis’ is an old term which means ‘upon the gum ’. So ‘epulis’ is a swelling situated on the gum.
It arises from the alveolar margin of the jaw. It can originate from the bone, the periosteum or the mucous
membrane. The different varieties are described below.
Fibrous Epulis.—
It is the most common of all the varieties of epulis. It arises from the periosteum at the neck of an incisor
or premolar tooth. As it grows, it separates the teeth and ultimately loosens them.
PATHOLOGY.—
It is fibroma and is composed of fusiform cells with many new blood vessels.
(i) It is a firm nodule at the junction of the gum and tooth.
(ii) It becomes polypoid in shape.
(iii) It is a slow growing tumour.
(iv) It is often seen in relation to the incisor or premolar tooth.
(v) It is not tender.
(vi) The adjacent teeth may be slighdy separated and be loosen.
SWELLINGS OF THE JAW 449
(vii) Draining lymph nodes are not enlarged.

COMPLICATIONS.—
(i) It may undergo malignant change — fibrosarcoma. Then it looks soft bluish red. It grows rapidly and
often bleeds.
(ii) It may recur after excision if its root is not thoroughly excised.
TREATMENT.—
Excision is the treatment of choice. Adjacent tooth or teeth and resection of a wedge of bone with its root
must be performed to prevent recurrence.
Granulomatous Epulis.—
It is often called false epulis as it is a mass of granulation tissue around a carious tooth or at the site of
irritation by a denture.
A similar condition may be found temporarily during pregnancy which is known as gingivitis gravidarum
(i) The mass looks bright red.
(ii) It is soft or firm in feel.
(iii) It easily bleeds on touch, as it is a mass of granulation tissue.
(iv) It is often associated with a carious teeth, so it is found in those who do not maintain oral hygiene.
Offensive smell of mouth is often associated with. This may be due to infection of the epulis.
(v) Sometimes ill-fitting denture may cause such swelling.
(vi) The draining lymph nodes may be enlarged and tender.
TREATMENT.—
(i) Extraction of the carious tooth associated with the swelling.
(ii) If ill-fitting denture is the cause, it should be replaced.
(iii) Maintenance of oral hygiene.
(iv) The granulation tissue is scraped away and is examined histologically.
(v) The mass of granulation tissue may be diathermised.
Myeloid Epulis (Syn. Giant-Cell epulis).—
It is an osteoclastoma and arises from the underlying bone.
PATHOLOGY.—
Microscopically the stroma consists of fifcrocellular tissue. Multinucleated giant cells, as found in typical
osteoclastoma, are found scattered.
(i) Although the underlying mass is firm due to ex
pansion of the marginal bone under cover of the mucoperi-
osteum, yet the gum covering it becomes hyperaemic, oede
matous and soft to touch.
(ii) It is plum-coloured due to high vascularity.
(iii) It is always sessile.
(iv) It is more rapidly growing tumour than the other
varieties of epulis.
(v) The adjoining teeth are separated and loosened.
(vi) X-ray may be performed to show typical soap-
bubble appearance of osteoclastoma.
COMPLICATIONS.—
(i) Ulceration.
(ii) Serious haemorrhage.
TREATMENT.—
Fig.32.1.— Benign giant cell epulis of the gum.
(i) In case of small swelling, the treatment is curet
29
450
tage and filling the cavity with cancellous bone chips.

(ii) In case of large tumours, radical excision of the bone should be performed requiring graft in cas
mandible. The graft is often taken from a rib.
Carcinomatous Epulis.—
It is an epithelioma of the gum. It usually arises from the mucous membrane of the alveolar margin. Bu
may arise around a tooth or in a socket. It is an infiltrating lesion, which becomes infected and painful. In l
stage the lesion fungates giving rise to ulcerated form.
(i) It may present as a lump or an ulcer.
(ii) It is a painful lesion.
(iii) Soon it invades bone.
(iv) The growth ultimately fungates.
(v) Regional lymph nodes are always involved.
(vi) Biopsy should be performed to confirm the diagnosis.
TREATMENT.—
(i) Adequate resection of the growth alongwith surrounding healthy tissue should be performed. T
entails excision of the maxilla in case of upper jaw or excision of the mandible in case of lower jaw. The def
is made good by grafting.
(ii) Radiotherapy may be tried in selected cases.
I
ODONTOMES
Odontomes are cysts or tumours arising from the epithelial or mesothelial elements from the tooth germ
In the development of the tooth, downward extension of epithelium takes place which later forms the enam
organ. A cluster of this epithelium persists as ‘epithelial debris’ from which the epithelial odontomes are
formed. Epithelial odontomes are much commoner and three varieties are commonly seen e.g. dental cyst,
dentigerous cyst (follicular odontomes) and adamantinoma.
DENTAL CYST (syn. Radicular cyst, periodontal cyst).—
This is the most common of all the odontomes. It is associated with chronically infected pulpless tooth.
PATHOGENESIS.—
The continued irritation of infection appears to stimulate the remaining nests of cells (epithelial debris)
proliferate. The centre of the mass becomes necrosed, then liquified and finally converted into a cyst.
PATHOLOGY.—
The dental cyst is lined by squamous epithelium. The contents may be fluid or semisolid containing cell
debris, cholesterol crystals and foreign body giant-cells.The fluid is sterile unless secondary infection occur
If the infection remains active, the epithelium is destroyed and the cyst is surrounded by a fibrous wall.
the infection diminishes, the epithelial wall persists and the cyst continues to grow at the expense of the
surrounding structures and causes expansion of the alveolus.
(i) These cysts can appear at any age, but commonly seen in and around middle age.
(ii) It is more frequent in the upper jaw. In this place if it attains a large size, it may encroach the antrum
and may rarely open into it.
(iii) It is always associated with a normally erupted tooth, but chronically infected or carious tooth.
(iv) It is usually painless, unless infected when it becomes painful.
(v) When the bone is thinned out, there may be ‘egg-shell crackling’.
(vi) If the bone is completely destroyed, fluctuation may be present.
(vii) X-ray is helpful in diagnosis. A circular radiotranslucent area will be seen in relation to the root of t
affected tooth. The margin of the cyst is sclerosed.
TREATMENT.—
(i) Pre-and postoperative dental hygiene must be maintained.
(ii) The affected carious tooth should be removed.
(iii) The cyst is approached intraorally. The whole epithelial lining is removed. The cyst wall is curetted
and the soft tissue is pushed in. The cyst is obliterated and the wound is sutured.
DENTIGEROUS CYST (syn. Follicular odontome or cyst).—
This cyst is usually associated with non-erupted
permanent tooth. The swelling consists of a cyst
containing a tooth, most commonly an upper or a
lower third molar tooth lying obliquely in the cyst
with viscid fluid.
PATHOLOGY.—
The follicle consists of an inner epithelial lining
and an outer connective tissue covering. The lining
epithelium is squamous cell epithelium. The content
is more or less similar to that of the dental cyst i.e.
fluid or semisolid content with cholesterol crystals
and giant-cells. The cyst continues to grow and may
attain a very large size. If occasionally infection
occurs, the epithelium is destroyed and the cyst
remains small. Within the cyst the tooth lies either
free in the cavity obliquely or embedded in the wall
of the follicle.
(i)
Fig.32.2.—Skiagram showing a large dentigerous cyst in- the second and third decades.
volving the posterior portion of the left side of mandible. (jj) The common locations are ‘in order of
Note the unerupted first molar tooth beneath the swellinq. .. , .. ,..,, ...
frequency the msndiDulsr third molcir, m3xili3.ry
third molar and mandibular second premolar.
(iii) This cyst grows larger and expands the outer table of the jaw causing egg-shell crackling.
(iv) It is a painless swelling unless infected.
(v) The lower jaw is more often affected.
(vi) Counting of tooth may help, as the non-erupted tooth causing dentigerous cyst will be missing.
(vii) Radio graphically it appears as a well defined radiolucency around the crown of the unerupted tooth.
The larger cysts are rarely multilocular. Ridges of bone on the side walls cause pseudotrabecular or soap-bubble
appearance in X-ray.
TREATMENT.—
(i) Total excision of the cyst wall is imperative. Intraoral approach is made. A transverse incision is made
on the outer table. The mucoperiosteum flaps are raised. The cyst is entered. The cyst wall is completely excise
and curetted. The hollow is obliterated by pushing in soft tissues and with bone chips. The mucoperiosteal flap
are sutured.
(ii) If the cyst is a big one, total excision is not possible. The cyst is marsupialised. The cyst is first deroofed
by excising the outer table of the cyst. The interior of the cyst is curetted thoroughly and is marsupialised.
ADAMANTINOMA (syn. Ameloblastoma; Multilocular cystic disease; Eve's disease).—
Adamantinoma is a true neoplasm of the odontogenic epithelium. It is an epithelial tumour arising from
ameloblasts (enamel-forming cells). It is more common in the coloured. Pathologically it behaves and looks like
a basal cell carcinoma.
PATHOLOGY.—
Macroscopically it is filled with transparent fluid or jelly. Microscopically it varies in appearance
considerably. There is an outer layer of columnar cells—the ameloblasts and acentral core of ‘star cells’ wit
large vacuoles in the cytoplasm. Sometimes this tumour is composed of epithelial strands or islands of var
sizes. On the periphery of these island are these tall columnar ameloblasts-like cells. The central cells may
degenerate leaving cystic spaces.
Adamantinoma can occur elsewhere than the jaw. These sites are :
(a) In the stalk of the pituitary where it is known as suprasellar tumour. Both the pituitary stalk and
enamel organ arise from the oral epithelium and this may be the reason of appearance of similar tumour in
pituitary stalk.
(b) Adamantinoma may occur in the tibia. This is an extremely rare tumour and may be explained o
the basis of abnormal embryonic epithelial invaginations.
Spread.— This tumour is a locally invasive tumour and is not known for distant spread. It does not
metastasize to lymph nodes.
(i) It is a rare tumour of the jaw.
(ii) It commences usually in childhood or early adult life. In some series majority of the patients wer
in 4th or 5th decades.
(iii) It shows a slight predilection for males.
(iv) It is usually found in the molar area of the mandible.
(v) It is a slow growing tumour and it exists for even years before the patients present before the
clinician.
(vi) It is a painless tumour.
(vii) It causes expansion mostly of the outer table, so the swelling is more evident from outside than f
inside the mouth.
(viii) Cystic degeneration leads to areas of softening and egg-shell crackling on palpation.
(ix) It should be remembered that unlike the previous odontomes it is not associated with any cariou
tooth or any missing tooth.
(x) X-ray shows large loculi and also a fine honey-comb appearance. Small multiple translucent area
separated by fine bony trabeculae will give rise to such honey-comb appearance.
Differential Diagnosis.—Two conditions very much mimic adamantinoma. These are (i) osteoclastoma or
giant-cell tumour affecting the mandible and (ii) Giant-cell reparative granuloma. See page............
TREATMENT.—
(i) It is a locally invasive tumour almost like basal-cell carcinoma, so simple enucleation and curetta
will invariably lead to recurrence.
(ii) Radiotherapy is ineffective.
(iii) Therefore resection of the tumour alongwith a margin of healthy bone is essential for permanent
cure. Normal relationship is maintained by dental fixation. If no recurrence takes place after several month
a bone graft should be used to make good the mandibular defect.
(iv) If the tumour is very large affecting the major part of the mandible, hemimandibulectomy may b
necessary. The mandibular defect is substituted by a prosthesis or a silastic rod carved to the design and m
over a K-wire. After a few months the holding prosthesis is replaced by a block bone graft or a narrow can
bone graft put in a tray of tantalum mesh bone implant.
OSSEOUS TUMOURS
BENIGN TUMOURS —
(a) Fibro-osseous group.
(b) Paget’s disease (this may not be considered as a typical tumour).
(c) Osteoclastoma.
(d) Giant-cell reparative granuloma.
MALIGNANT TUMOURS OF THE MAXILLA.—
(a) Osteosarcoma.
(b) Columnar cell carcinoma of the maxillary antrum.
(c) Squamous cell carcinoma derived from epithelium overlying the hard palate, tooth socket or the gum.
(d) Invasion of the maxilla by sarcoma of the ethmoid.
(e) Burkitt’s tumour.
MALIGNANT TUMOURS OF THE MANDIBLE —
(a) Primary malignant neoplasm is extremely rare.
(b) Secondary malignant neoplasm may occur from (i) carcinoma of the tongue, (ii) floor of the mouth,
(iii) carcinoma of the lip, (iv) metastatic involvement of the facial lymph nodes which lie injuxtaposition of the
mandible near the groove for the facial artery.
THE FIBRO-OSSEOUS GROUP

The jaws are mainly membrane bones so fibro-osseous dysplasia is often seen here. In this tumour there is
varying amount of fibrous tissue and bone. If the fibrous tissue element is more with myxomatous degenerati
the tumour will be soft in major parts.
If only one tumour is found it is called monostotic fibrous dysplasia. If the condition is diffuse it is called
polyostotic fibrous dysplasia.
If the tumour is composed of solely bone, the condition is called ivory osteoma if it is localised. If this bony
tumour is diffuse, it is called Leontiasis ossea.
X-ray appearance of fibrous dysplasia are strips and bubbles within the jaw. Ivory osteoma is a benign den
localised tumour.
(i) Fibrous dysplasia is more often seen in the 1 st or 2nd decade and its growth stops when the individ
is fully grown.
(ii) Such tumour has been associated with dental sepsis or some sort of oral sepsis.
TREATMENT.—
When the individual is fully grown, excision of the tumour is made under antibiotic cover.
PAGET’S DISEASE OF THE JAW

This condition may arise as a part of generalised Paget’s disease or it may be confined only in the jaws.
(i) Pain is almost always present.
(ii) Old people are usually involved.
(iii) Radiological appearance is very characteristic.
COMPLICATIONS.—
Osteosarcoma is a known complication of Paget’s disease.
OSTEOCLASTOMA
This is an extremely rare tumour in the jaw, more seen in the lower jaw. It may occur under the gum as
myeloid epulis. It has often been confused with giant-cell reparative granuloma. Osteoclastoma, giant-celled
reparative granuloma and adamantinoma mimic one another and their differential diagnosis is important and
discussed after the description of the giant-celled reparative granuloma.
GIANT-CELLED REPARATIVE GRANULOMA
This lesion occurs due to haemorrhage within the bone marrow.
PATHOLOGY.—
Macroscopically it consists of opaque, semisolid, dark-red material.
Microscopically there are multinuclear giant cells which are few in number and distributed unevenly. It
often difficult to distinguish this lesion from the so-called ‘brown tumour of hyperparathyroidism’.
(i) It occurs more often between the ages of 10 and 25 years.
(ii) Females are frequently involved than males.
(iii) The swelling is painless.
(iv) It often involves the mandible rather than the maxilla.
(v) X-ray shows round or oval area of radiotranslucency. It expands and thins out the cortex but do
not perforate it.
DIFFERENTIAL DIAGNOSIS.—
(i) Osteoclastoma.
(ii) Adamantinoma.
(iii) Brown tumour of hyperparathyroidism.— Serum calcium level must always be determined to
exclude this condition. X-ray of other parts of the skeleton is also necessary.
TREATMENT.—
(i) Thorough curettage through external incision is the treatment of choice. The bone cavity should no
be opened into the mouth.
(ii) This condition usually does not recur. In case it recurs one should again exclude hyperparathyroidism.
DIFFERENTIAL DIAGNOSIS OF ADAMANTINOMA, OSTEOCLASTOMA

AND GIANT-CELL REPARATIVE GRANULOMA
Adamantinoma Osteoclastoma Giant-cell Reparative

Granuloma
25 to 40 years. 10 to 25 years.
Males are more often af Females are more often

fected. affected.
Relatively rapid growingA slow growing lesion.
tumour.
Mandible is more often Mandible is more often

affected. affected.
Both the inner and outer Both tables are expanded.
tables are expanded.
Painless. Painless.
Usually does not fungate.Usually does not fungate.
Soap-bubble appearance Rounded or oval translu

with larger cysts and fine cent area which expands
or ill-defined trabeculae the cortex but does not per
(pseudo-trabeculae). forate it. There is hardly
There may be perforation any trabeculae.
of cortex.
9. Histology.— Peripheral columnar cells Multinucleated giant cellsMultinucleated G-cells are

with central core of ‘star are many in number in fewer in number and dis
cells’ with large vacuoles fibrocellular stroma. tributed unevenly.
in the cytoplasm.
10. Radio Not radiosensitive. Radiosensitive. Being not a typical tumour
sensitivity.— this is not questioned.
11. Recurrence.— Recurrence is common. Recurrence is common. Does not recur.
12. Malignancy.— It is a locally malignant It is treacherous and may Malignancy is never seen.
tumour. turn into malignancy par
ticularly if it recurs.
OSTEOSARCOMA OF THE JAW

Maxilla is more often affected, particularly the maxillary antrum, whose prognosis is the worst. The best
prognosis is seen in lesions of the mandibular symphysis. Cases of parosteal osteosarcoma has also been
reported. It affects mostly the anterior aspect of the jaw, but the condition soon shows itself on the inferior or
palatal surface.
PATHOLOGY.—
Osteosarcoma seen in maxilla is mostly of round-celled variety. Only rarely it may be highly differentiated
fibro-myxo chondrosarcoma.
(i) Though any age and both the sexes may be involved, yet women around 40 years are the common
victims.
(ii) Pain and swelling are the main complaints.
(iii) Nasal obstruction and epiphora (abnormal outflow of tears down the cheek due to obstruction of th
lacrimal ducts) occur late in the disease.
TREATMENT.—
Radiotherapy followed by surgery, if required, is the treatment of choice. High voltage radiotherapy is
applied. 6 weeks after conclusion of the radiotherapy the growth is exposed and biopsies are taken from vario
parts. If any such biopsy shows malignant lesion, excision of the maxilla is advised.
CARCINOMA OF THE MAXILLARY ANTRUM

PATHOLOGY.—
Two varieties of carcinoma are seen in the maxilla — (a) columnar cell carcinoma of the maxillary antrum
and (b) squamous cell carcinoma arising from the epithelium overlying the hard palate or the gum.
Lymph node metastasis occurs early as in other carcinomata. Mostly the deep cervical groups are involved.
(i) Patients are usually above 40 years of age.
(ii) Both sexes are almost equally involved.
(iii) Foul, purulent and blood-stained discharge from the nose is the common symptom.
(iv) If the growth originates on the floor of the antrum, toothache is the main complain and the dental
surgeon is often consulted.
(v) If the growth involves anterolateral wall of the maxillary antrum, swelling will be seen on the face.
(vi) If the medial wall of the antrum is affected, nasal obstruction and epiphora are the usual complaints.
(vii) If the roof of the antrum is invaded there will be proptosis and diplopia.
(viii) If the floor of the antrum is involved, the hard palate will show bulging.
(ix) Cervical lymph nodes should always be examined as lymph node metastasis is quite early in
lesion. About l/3rd of the cases will show such metastasis.
(x) Biopsy may be required to confirm the diagnosis.

TREATMENT.—
Radiotherapy is the main mode of treatment.
A course of high voltage radiotherapy or gumma rays are given. 6 weeks after conclusion of the radiatio
therapy, when it is assumed that tissue reaction due to radiotherapy has subsided, palatal antrostomy is
performed. Irradiated growths are biopsied from different sites of the antrum. A portion of the wall is also
biopsied. The middle and the inferior turbinate bones with portions of the tissues are also removed with a
diathermy needle. These biopsy specimens are examined histopathologically to detect presence of any resid
growth.
If no growth is detected, nothing more is required.
If biopsy shows residual growth is present, a hollow plastic applicator made by dental surgeon, filled wi
wax and radium tubes, is inserted for further irradiation. Radium needles may be applied directly if the gro
are found in the post-ethmoidal region.
If cervical nodes are involved, block dissection of the neck should be performed.
SURGERY.—
If radiotherapy cannot control the disease upto the expectation, excision of the maxilla should be perform
Nowadays sophisticated prosthesis has been constructed, so there is little deformity after this operation.
Cytotoxic drugs may be tried if recurrences occur after radiotherapy and excision.
Role of Cryosurgery and Laser ablasion should be reviewed.
BURKITT’S TUMOUR
In many parts of Africa this is the commonest neoplasm in children of first decade. It is a type of multifo
lymphoma whose aetiology is not very clear. Viral origin has been strongly suggested. Age distribution has
very characteristic in the sense that majority of the patients are in the range of 3-7 years of age. Involvement
becomes progressively diminished as age increases.
Maxillary tumours generally present in relation to the molar and prcmolar teeth. As the tumour develops
alveolus expands on both sides and the affected teeth loose their attachments to the bone. Subsequently the
tumour develops around the teeth with an external swelling which appears under the cheek distorting the f
Mandibular tumours develop in the same way with marked distortion of the face though without significan
ulceration and often with surprisingly little evidence of pain. Multiple jaw lesions with involvement of seve
jaw quadrants are one of the characteristic features. When two jaw quadrants are involved it is nearly alway
the maxilla and the mandible of the same side.
Radiological features of this tumour in the jaws are disappearance of the lamina dura round the affected
teeth. Subsequently multiple small areas of bone dissolution appear and eventually coalesce forming larger
areas of bone destruction. So the bone involvement is essentially osteolytic.
Abdominal tumours are the second most frequent mode of presentation. Retroperitoneal mass, liver
enlargement or ovarian tumours may be seen. The adrenal and pancreatic involvements are also common.
Enlargement of mesenteric lymph nodes can give rise to an epigastric mass. Splenic involvement is not very
significant.
Lesion involving the spinal nerves is the 3rd commonest mode of presentation. Radiographs frequently sho
paravertebral mass in the lower dorsal or upper lumbar region. Intracranial lesions in the form of cranial ne
palsies may be seen in this condition. This tumour may affect the salivary gland, the thyroid, the breast, the
and lymph nodes.
Treatment.—
Burkitt’s lymphoma is exceedingly sensitive to radiotherapy. But this tumour is multifocal, so remission
from local radiotherapy have been followed by development of tumours in other sites. That is the reason wh
chemotherapy is without doubt the treatment of choice. Not only has the tumour been shown to be exceedingly
sensitive to a wide range of chemotherapeutic agents, but also cures have been observed in higher proportio
of patients thus treated than in any form of cancer other than choriocarcinoma.
CHEMOTHERAPY is best administered systemically, either orally or intravenously according to the dru
used. This ensures that treatment reaches all tumours and shrinks in demonstrable tumours can be assumed
reflect similar changes in those that remain undetected. Intra-arterial administration has proved effective fo
dealing with local tumours but in view of the disseminated nature of the disease, results have been short-liv
The drugs which are extensively used with good results have been the Methotrexate, Cyclophosphamide an
Vincristine sulphate. Methotrexate has been used orally in the dose of approximately 1 mg/kg/day for 4 to
days. Cyclophosphamide is given orally or intravenously in a dose of 30 to 40 mg/kg as a single injection o
in divided doses over 2 to 3 days by mouth. This dose may be repeated twice if complete remission has bee
obtained. Vincristine sulphate is used intravenously in a dose of 0.05 to 0.15 mg/kg boby weight.
Role of SURGERY is limited to taking biopsies and removal of ovaries when they are replaced by massiv
tumours. In jaw lesions biopsy is best performed with a Volkmann’s spoon after removing a loose tooth.
Role of RADIOTHERAPY is restricted to the localised disease.
LONG TERM RESULT.— Long term result of Burkitt's lymphoma following chemotherapy is quite
encouraging. Long term remissions can be expected in majority of patients having total or almost total clinic
remissions of jaw lesions unless tumours in other sites develop subsequently. It has been shown that if patie
survive for more than 500 days after first admission to hospital they can be considered as potential cures. O
few patients who have remained symptom free for over a year have subsequently died from their tumours.
MALIGNANT NEOPLASMS OF THE MANDIBLE

As has already been mentioned, there is hardly any primary malignant neoplasm of the mandible. Mand
is sometimes directly involved from advanced cancer of the tongue, floor of the mouth, carcinoma of the lip
from metastatic facial lymph nodes.
Treatment.— Surgery is the main treatment as radiotherapy causes necrosis of the mandible. The growth
is resected alongwith a healthy portion of mandible on both sides. Hemimandibulectomy may also be perfo
according to the extent of involvement of the mandible. The gap is made good by prosthesis or bone graft.
ALVEOLAR ABSCESS
Alveolar abscess, when occurs from the milk tooth, can affect either jaw; but when it occurs from perman
tooth, usually the lower jaw is involved, particularly the molar tooth.
PATHOLOGY.—
Alveolar abscess usually arises from acute pulpitis. Infected pulp exerts pressure through the root canal i
the bony tissue around the apex of the tooth. Localised abscess forms. This abscess gradually points toward
the outer surface with exception of the upper lateral incisor tooth, in which case the abscess gives rise to swe
on the palate and in case of abscess in the impacted 3rd molar tooth which may burst through the medial wa
of the alveolus.
COMPLICATIONS.—
(i) If not treated properly, alveolar abscess will cause osteomyelitis of the jaw.
(ii) Alveolar abscess may burst and cause Ludwig's angina.
(i) Alveolar abscess is most often seen during childhood and early adult life.
(ii) Pain is the first symptom which is dull and constant.
(iii) Swelling of the cheek almost always follows pain.
(iv) There is redness and oedema of the gum near the affected tooth.
(v) The regional lymph nodes become inflamed and tender.
(vi) X-ray may show rarefaction around the apex of the affected tooth, but this takes time for resorption
of bone to occur.
TREATMENT.—
(i) As soon as the diagnosis has been made antibiotics should be started. Penicillin, erythromycin and
cloxacillin are quite effective in this disease.
(ii) Hot intraoral irrigations are also effective in giving relief to the patients. Cold application may be
used externally. Hot applications are usually avoided externally as they promote the abscess to point externa
which is cosmetically not accepted by many patients.
(iii) Once the abscess has been formed, drainage must be performed. It is usually done intraorally by
incising the periosteum. When alveolar abscess develops from milk tooth, it maybe extracted. When alveolar
abscess develops from permanent tooth, proper dentistry is vital, otherwise it may lead to osteomyelitis.
OSTEOMYELITIS OF THE JAW

PATHOLOGY.—
Three varieties of osteomyelitis are noted in the jaw. These are (i) Acute osteomyelitis (rare), (ii) Subacute
osteomyelitis and (iii) Chronic osteomyelitis.
Acute osteomyelitis.—
This often occurs in infants as a complication of specific fever e.g. measles, scarlet fever etc. It may also
be caused by spread of infection from the antrum or the dental sac of the first molar tooth. In case of measles
either the maxilla or the mandible may be involved, whereas in the latter case maxilla is more often involved
Puffiness of the eye-lids and swelling of the maxilla become obvious. The patient runs temperature. There
may be a discharging sinus if the abscess has naturally drained. Pressure on the maxilla will cause discharge
of pus through the sinus.
TREATMENT.—
Appropriate antibiotics should be given. A polythene catheter is introduced by trocar and cannula via the
nose and the cavity is irrigated with normal saline twice daily.
Subacute osteomyelitis.—
This is the commonest among the different varieties of osteomyelitis affecting the jaw.
Pathogenesis.—
(i) Spread of apical dental abscess.
(ii) Spread of alveolar abscess.
(iii) Fracture of the jaw.
The causative organism is usually the staphylococcus aureus.
The mandible is mostly affected. The reason is that it possesses a single tenuous blood supply along its long
axis, which is easily obstructed by infection or trauma. Obstruction of blood supply will cause bone necrosis
and subsequently osteomyelitis of the jaw. The maxilla is protected by a series of vertical arteries with
anastomosis, so obstruction of a single artery cannot cause necrosis of the bone.
Pain, swelling and tenderness are three main features of the osteomyelitis of the lower jaw. Increased
pressure in the dental canal compresses the inferior dental nerve and this will cause numbness of the chin in
distribution of mental nerve. This is diagnostic. Gradually the swelling points externally or internally and if t
swelling bursts, a sinus is formed externally or internally. This will relieve pain.
X-ray will show bone necrosis in about 3 weeks time or more.
TREATMENT.—
(i) Antibiotic should be started immediately.
(ii) Operation is needed to relieve tension and to get rid of disease and dead bone (sequestrum).
Chronic osteomyelitis.—
Mandible is more often affected than maxilla. Causes are :
(i) Fracture of the mandible.

(ii) Alveolar abscess — X-ray will show local osteitis with sequestrum almost similar to Brodie's
abscess. But sequestrum formation is not that common as these bones are membranous bones.
(iii) Radiation and chemical necrosis.— Radiation often causes necrosis of the mandible. Phosphorus
poisoning may also cause chronic osteomyelitis which is rare nowadays. Arsenic or Mercury may cause chr
osteomyelitis of the mandible.
(iv) Tuberculosis, syphilis and actinomycosis may rarely cause chronic osteomyelitis.
X-ray.— This may reveal only periosteal reaction or local osteitis. The most important finding is formatio
of a cavity due to osteolytic lesion with surrounding sclerosis (almost like Brodie’s abscess) with or without
sequestrum formation. Sequestrum formation is not so common as in long bones, as these bones are
membranous bones. Bone necrosis becomes evident in X-ray not before 3 weeks.
TREATMENT.—
Sequestrectomy is the treatment of choice. A suitable incision is made at the dependent part of the affecte
area of the mandible. The involucrum is chiselled and the cavity is made open. If there is any sequestrum, it
removed. The cavity is packed lightly with petroleum jelly gauze. Appropriate antibiotics should be given.
ACTINOMYCOSIS
This disease is caused by Actinomyces Israelii, an anaerobic gram-positive branching filamentous
organism. This organism often lives as a harmless parasite in tonsillar crypts and dental cavities of an otherw
normal mouth (normal commensals of the mouth). If the organism invades tissue, it causes a subacute pyogen
inflammation with considerable induration and sinus formation.
PREDISPOSING FACTORS.—
(i) Trauma, (ii) presence of carious tooth, (iii) secondary bacterial invasion and (iv) hypersensitivity
important predisposing factors in the development of lesions in the mouth.
PATHOLOGY.—
In tissues the actinomyces grow in the form of yellow colonies which are easily seen in the pus by the na
eye. These constitute the well known ‘ sulphur granules’ or less known ‘Fish-roebodies’. If one of these granu
is crushed under a cover glass and examined unstained, two elements can be distinguished — branching
mycelial filaments and club forms. The filaments constitute the greater part of the body, whereas the clubs a
pear-shaped bodies which form fringes round the periphery of the colony. These clubs probably represent
means of defence against the protective forces of the tissues and are produced as deposition of lipid materia
derived from the host tissues. The filaments are gram-positive, whereas the clubs are gram-negative. The
characteristic radial arrangement is responsible for the familial term ‘ray-fungus’.
THE MICROSCOPIC APPEARANCE is that of a suppurating granuloma which consists of pus-filled cor
in which there may be numbers of mycelial colonies. More peripherally there is cellular infiltrate which cons
of mononuclear histiocytes, lymphocytes and occasional giant-cells. Dense scar gradually replaces all other
elements and imparts characteristic woody, indurated nature of the lesion. It must be remembered that myc
may not be found in sections of the tissue and should not be accepted as the only point of diagnostic value.
Myecelium is more often seen in soft areas and in pus rather than in a piece of hard tissue.
SPREAD.—
(i) Spread by lymph stream is practically unknown, so the draining lymph nodes will never be enlarged
(ii) Spread by blood stream is uncommon but a lesion may rupture into a vessel and give rise to metasta
in distant organs. The liver, the brain and the heart are the organs which may be involved. Only in rare cases
the kidney, the spleen and the ovaries may be involved.
FOUR MAIN CLINICAL FORMS OF ACTINOMYCOSIS ARE SEEN. These are (a) Facio-cervical, (b)
Ileo-caecal, (c) Thoracic and (d) Hepatic. Facio-cervical is the commonest with about 60% occurrence,
followed by ileo-caecal 25%.
FACIO-CERVICAL ACTINOMYCOSIS
Tissues of the face and neck including the tongue and mandible are mainly affected. The swelling is
characteristically seen over the angle of the mandible.
(i) The swelling is mostly seen over the angle of the mandible often adjacent to a carious tooth.
(ii) The onset is insidious.
(iii) The condition is painless.
(iv) The gum becomes indurated and simulates bony swelling.
(v) The overlying skin of the adjacent face and neck is bluish in colour.
(vi) An abundant fibrous tissue reaction leads to brawny induration of the neck.
(vii) Softening occurs in patches, abscesses develop and eventually burst to cause multiple sinuses.
Chronicity, dense induration and sinuses surrounded by bluish skin are the most characteristic features of
cervico-facial actinomycosis.
(viii) The pus which is discharged through the sinuses is usually thin and may contain tiny sulphur
granules. These granules are most readily found in the pus of a newly opened lesion. When the lesion is old
discharging for sometime, it may not be possible to demonstrate sulphur granules. In such cases it is best to
a considerable amount of secretion to collect before examining it. The grains may be recognized at the botto
of such collection.
(ix) X-ray appearance is characteristically negative and this distinguishes this condition from os
litis of the jaw. Some amount of multiple sclerosis may be seen in long standing cases.
TREATMENT.—
Treatment of this condition is mainly medical. Actinomyces are sensitive to penicillin, tetracycline and
lincomycin. An intensive course of penicillin e.g. 10 mega units i.m ./day is administered for a prolonged p
The dose is gradually reduced to 4 mega units daily and this is continued for even 3 months.
Penicillin therapy may be supplemented by tincture iodine orally. The iodides may help to resolve fibrosis.
Role of surgery is restricted to chronic and resistant cases which are not responding to antibiotics properly
Drainage of the abscesses should be performed by widening open the sinuses. Roller gauze soaked in tinctu
iodine (2%) should be loosely packed after opening the abscess cavity. This will help the antibiotics to work
better.
In some resistant cases radiotherapy may be tried, but its efficacy is not much.
461
CHAPTER - 25
MOUTH, TONGUE AND LIPS
MOUTH
STOMATITIS
Stomatitis is a general term used to describe any kind of inflammation of the lining of the mouth. Such
inflammation may affect the surface of the tongue also.
Causes.— Such inflammation of the mouth may be caused — (i) by Injury, (ii) Mechanically, (iii)
Chemically, (iv) Thermally, (v) by Radiotherapy, (vi) Idiopathic and (vii) by Malnutrition.
TRAUMATIC STOMATITIS
Traumatic stomatitis is commonly caused by (i) vigorous use of hard tooth brush, (ii) Ill-fitting dentures, (iii) Jagged
teeth, (iv) Simple cut or bum of the mouth.
Simple cut or bum of the mouth usually heals by itself. Traumatic stomatitis is soon covered by a thin grey glistening
coagulum. As the mouth is painful, movements are obviously restricted. Salivation is increased. The tongue is quoted with
fur.
Treatment.— Frequent washing of the mouth with saline or thymol. A few drops of Detol may be instilled in a glass
of warm water and rinsing the mouth with such water is quite effective in controlling the stomatitis.
APHTHOUS STOMATITIS
This condition is usually associated with generalised debilitating diseases.
Though there may be recurrent solitary aphthous ulcer, yet multiple ulcers are more common. In the beginning on the inside of the
mouth one can see small vesicles with hyperaemic base. Such vesicles are painful and tender. These vesicles break and form small white
circular, deep ulcers. These ulcers are also very painful.
Treatment.— A swab should be taken from the ulcer and it is sent for culture and sensitivity test. If pathogenic organisms are
discovered proper antibiotic should be started. Otherwise maintenance of oral hygiene is the most important step in the treatment. Mouth
should be kept clean and it should be rinsed thrice with diluted Detol-water or Listerin-water solution.
MONILIAL STOMATITIS (THRUSH)

Such type of stomatitis is seen — (i) in infants within first few weeks of life, (ii) in people suffering from debilitating
disease, (iii) as a complication of prolonged antibiotic therapy, which changes the balance of the bacterial flora in the
alimentary canal and (iv) in diabetic patients.
This condition mostly occurs due to a fungus known as Candida albicans.
(i) This disease starts as spots on the buccal mucous membrane. These spots are small red patches which appear on
the buccal mucosa and the tongue. These turn white as white exudate composed of desquamated epithelial cells are entangled
in the mycelium.
(ii) Mouth is painful and there is excessive salivation.
(iii) Sometimes swallowing is also painful if the infection has spread into the pharynx.
Treatment.— The mouth should be kept clean by the use of glycerin or thymol applied on a swab stick. Nystatin is
the specific antibiotic against this fungus and this should be used immediately. Particular care should be taken to keep the
utensils clean which the patient use.
RECURRENT APHTHOUS ULCERATION
This is mainly seen in adults. The ulcers are usually seen on the inner sides of the lips and cheek' and on the undersurface
of the tongue. These ulcers recur in different parts of the mouth. There is a familial predisposition, but this lesion is not
contagious. Women are more often affected.
These ulcers are very painful and there is excessive salivation. These ulcers heal by themselves within a fortnight.
462
Treatment.— A culture should be taken from the lesion and appropriate antibiotic should be used if pathogens are
detected. Oral hygiene is very important.
VINCENT'S ANGINA (SYN. ULCERATIVE STOMATITIS; ACUTE ULCERATIVE GINGIVITIS)

Causative organisms.— Borrelia Vincenti is an anaerobic spirochaete. This is responsible to cause this lesion. This
spirochaete can be seen in wet smear by dark ground illumination. Another organism called B. fusiformis, a gram negative
rod with pointed end, is also seen in these lesions. Both these organisms may be found in normal mouths, but are particularly
found in large numbers in association with this disease. Whether these are the cause of this disease or secondary invaders
is yet to be answered.
(i) Early adult individuals are more often involved. It is rarely seen after the age of 35 years.
(ii) Acute condition starts with prodromal symptoms e.g. malaise, pyrexia and increased salivation.
(iii) After about a couple of days of such prodromal symptoms patient complains of dull toothache and gum bleeding.
ON EXAMINATION.—
(i) Bad smell is almost invariably associated with this disease. Excessive salivation is also common.
(ii) Gums are swollen and red, particularly between the incisors and around the 3rd molars.
(iii) The affected areas of the gum are red and inflamed. Small ulcers can be seen on the gum which are covered with
yellowish slough or membrane.
(iv) The condition is extremely painful.
(v) If the membrane is peeled away the gum bleeds and the small ulcers are revealed.
(vi) If the condition remains untreated, such lesions spread to the cheeks, palate, fauces and even to the pharynx.
Tongue is rarely affected. When the fauces are involved the condition must be differentiated from diphtheria and secondary
syphilis.
(vii) The regional lymph nodes become enlarged and tender.
Treatment.— (i) Penicillin is the drug of choice and should be given parenterally.
(ii) The membrane should be swabed away with pledgets of cotton wool soaked with hydrogen peroxide. Mouth
should be kept clean by repeated mouth washes.
(iii) When acute attack has subsided proper dental treatment is required for carious tooth or disease of the periodontol
tissues.
ANGULAR STOMATITIS (SYN. CHEILOSIS: PERLECHE)

As the name suggests cracks or superficial ulceration at the comer of the mouth is known as angular stomatitis. This
condition must be differentiated from congenital and tertiary syphilis.
Causes.—
(i) In children who rub and lick the comers of the mouths often suffer from this disease.
(ii) Over closure is the commonest cause of angular stomatitis in older patients.
(iii) When the oral mucosa is atrophied or there is tendency to seborrhoeic dermatitis, this condition may appear.
(iv) Dribbling of saliva through the comers of the mouth often cause this condition.
Such cracks may be infected by Candida albicans and streptococci.
(i) Inflamed red brown fissures at the comers of the mouth are the common presentation. It often appears in children
of school going age.
(ii) Gradually fissures turn into scars.
Differential Diagnosis.— Most important is syphilis either congenital or of secondary stage or of tertiary stage.
Treatment.—
Improvement of general hygiene. One can apply Mercurochrome or Gentian violet at the cracks. Vitamin supplemen
tation particularly vitamin B complex, vitamin C and oral iron preparation are important.
CANCRUM ORIS (SYN. GANGRENOUS STOMATITIS)

This condition is now extremely rare. It used to be associated with measles, malnutrition and serious diseases such as
the blood dyscrasias (particularly leukaemia). Nowadays, if this disease is at all seen, it is often a complication of leukaemia.
(i) The lesion begins as an area of oedema and induration on the lip. The area becomes ischaemic and necrotic. The
area of necrosis spreads steadily and large areas of lips, cheeks and jaws may be destroyed.
MOUTH , TONGUE AND UPS 463
(ii) It is an extremely painful condition.

(iii) The patient is very ill and anorexic. There is often high temperature.
Treatment.— Proper antibiotics should be started immediately. Systemic Penicillin and Metronidazole are quite
effective. The general treatment of the disease which remains in the background should be treated simultaneously. High
protein diet and vitamin supplementation are essential. Healing takes place with gross scarring which may prevent proper
movement of the jaw. Excision of the scarred tissue with skin grafting is then required.
STOMATITIS WITH MALNUTRITION

Various types of stomatitis often remain associated with malnutrition. The mucosa of the tongue may undergo atrophy.
Similarly thinning of the oral mucosa makes the mouth more susceptible to trauma, hot drinks and spices.
Vitamin B.—In this group nicotinic acid deficiency will lead to Pellagra (means rough skin). This will cause excessive
salivation. The epithelium of the tongue becomes desquamated. The inside of the mouth becomes fiery red and painful.
Riboflavin deficiency will also lead to atrophy of lingual papillae.
Vitamin C.— Deficiency of this vitamin will cause scurvy. Features of stomatitis due to this disease are loosening of
the teeth and bleeding gums.
Iron.— Iron deficiency anaemia in women about manopause is particularly known as Paterson-Kelly syndrome. This
syndrome is the combination of smooth tongue, desquamation of buccal and pharyngeal mucosa and subsequently
dysphagia.
SYPHILIS
All three stages of syphilis cause some abnormality in the mouth.
Primary stage — chancre on the lip or tongue.
Secondary stage — ‘Snail-track’ ulcers, mucous patches and Hutchinson’s Wart.
Tertiary stage — gumma, chronic superficial glossitis and gummatous parenchymal infiltration.
Chancre on the lip.— This is almost same as the primary chancre on the genitalia. It is highly contagious.
The initial lesion is an elevated but flat pink, painless macule. This gradually grows into hemispherical papu
The mucosa covering it breaks down leaving a superficial ulcer. This ulcer is painful unlike its genital
counterpart. Regional lymph nodes become enlarged, discrete and tender.
The ulcer ultimately heals and the lump also dissolves leaving only a fine superficial scar.
Snail-track ulcers.— These are commonly seen on the pillers of the fauces. These are linear ulcers which
are covered with white boggy epithelium which makes them look like snail tracks. Such ulcers develop from
coalescence of mucous patches.
Mucous patches.— These patches are greyish-white red patches seen on the inside of the lips, cheeks and
on the pillers of the fauces. Oedema and desquamation of epithelium cause such ulcers white. When the grey
white patch of dead epithelium separates the underlying mucosa bleeds. Mucous patches are highly contagio
Hutchinson’s Wart.— It is a type of condyloma which affects midline of the tongue. Condyloma is
hypertrophied epithelium, broad based and flat. It is highly contagious.
Gumma.— This is mostly seen on the tongue, but rarely affects the lips and the cheeks. Gummata are also
seen in the hard palate and nasal septum which may lead to perforation of the palate and nasal septum causi
collapse of the bridge of the nose.
Gumma in the tongue is painless, hard and discrete mass. It usually develops in the anterior 2/3rds of the
tongue. It is often confused with nodular carcinoma of the tongue.
Gummatous parenchymal infiltration usually involves the tongue and makes it stiff, big, thick and irregular.
Chronic superficial glossitis.— This condition may be caused by other factors, which will be discussed
later in this chapter. Tertiary syphilis is one of the causes which produces this condition. It is a precancerous
condition.
CYSTS IN THE MOUTH
The following types of cysts may be found in the mouth —
1. Mucous retention cyst;

2. Ranula;
3. Sublingual dermoid.
MUCOUS RETENTION CYST
Such retention cyst may occur anywhere on the mucous surface of the mouth. The inner surface of the li
and the whole of the inside of the mouth contain many small mucous secreting glands.
Cause.— Obstruction of the duct of one of these glands will give rise to mucous retention cyst.
HISTORY.—Age.— This cyst can occur at any age.
SYMPTOMS.—■ (i) The main complaint is a small lump on the inner side of the lip or cheek.
(ii) It is a painless swelling and grows slowly.
(iii) The swelling may interfere with eating and may get bitten in the process.
EXAMINATIONS.— (i) This type of cyst is more common on the lower lip and on the inside of the chee
at the level of bite of the teeth.
(ii) The colour of the cyst is usually pale pink of that of overlying epithelium. The content looks grey
glairy appearance of the mucus. If the overlying epithelium has been damaged by the teeth it will be white
scarred.
(iii) Size and shape.— This cyst is usually spherical and of 0.5 to 2 cm in diameter.
(iv) Surface is smooth.
(v) Consistency is either soft or hard depending on the tension of fluid within the cyst.
(vi) Fluctuation test and transillumination test usually cannot be performed as the cyst is not big enou
(vii) Mobility.— The cyst can be moved and the overlying mucous membrane is not fixed to the cyst.
(viii) The local lymph nodes are not enlarged.
Treatment.—
Complete excision of the cyst under local anaesthesia is the treatment of choice. If the cyst is a big one,
general anaesthesia may be required.
Cryosurgery may be tried if possible.
RANULA
Ranula is a transparent cyst on the floor of the mouth on one side or the other. The term ranula is a Latin
word which means a ‘small frog’. As the swelling looks like the belly of a frog, Hippocrates gave this name
The cyst is considered to be a mucous retention cyst arising from the glands of Blandin and Nuhn situat
on the floor of the mouth. It is also considered by a few as dilatation of the duct of the sublingual salivary g
but this theory is not entirely satisfactory. This cyst is usually unilateral.
Pathology.— The cyst contains clear ropy fluid or jelly-like fluid. It is lined by columnar or cuboidal
epithelium, which in turn is covered by delicate capsule of fibrous tissue.
HISTORY.—
(i) Age.— Ranula is mostly seen in children and young adults.
(ii) Sex.— Both sexes are equally involved.
SYMPTOMS.—
The only complaint of the patient is a swelling in the floor of the mouth, which has grown gradually over
a few weeks. When the swelling suddenly grows in size it may be painful.
EXAMINATIONS.—
(i) Site.— The typical position of the swelling is on the floor of the mouth, below the tongue and on
the side of the frenum. The Wharton’s duct will be seen running over the surface of the swelling.
(ii) Colour.— It is slightly bluish or greyish in colour, which is very diagnostic.
(iii) Temperature and tenderness.— The swelling is neither warm nor tender.
MOUTH , TONGUE AND UPS
465
(iv) Size and shape.— Ranula is a spherical swelling whose top half is visible. The size varies from -1
to 5 cm in diameter.
(v) Surface and Edge.— The surface is smooth but the edge is difficult to feel as it is deep between the
arches of the mandible.
(vi) Consistency.— The swelling is soft or hard according to tension of fluid inside the swelling, but it
is a typical cystic swelling.
(vii) Both the fluctuation and the transillumination tests are positive. The ranula is typically known as
brilliant translucent swelling.
(viii) Mobility.— The overlying mucous membrane can be moved over the swelling. The cyst itself can
be moved over the underlying structures, but such mobility is restricted due to lack of space around.
(ix) The local lymph nodes should not be enlarged.
Types of Ranula.—
1. Simple ranula.— When the ranula is situated only in the floor of the mouth without any cervical
prolongation it is called a simple ranula.
2. Deep or plunging ranula.— When the intrabuccal ranula has a cervical prolongation it is called deep
or plunging ranula. The cyst is often considered to be derived from the cervical sinus. Such prolongation com
down along the posterior border of the mylohyoid muscle and appears in the submandibular region.
Deep or plunging ranula can be diagnosed by inspecting the submandibular region in all cases of ranula.
a swelling can be inspected in the submandibular region, bidigital palpation should be performed. One finger
is placed inside the mouth on the ranula and the other finger is placed on the swelling in the submandibular
region. If pressure on the first finger causes sense of fluctuation on the 2nd finger or vice versa, then it is a
plunging ranula.
Complications.— 1. Infection; 2. Bursting; 3. Repeated trauma; 4. A big ranula may cause difficulty in
speech or eating.
Treatment.—
(i) Complete excision.— This is definitely the ideal treatment. Cyst often bursts before dissection is
completed. That is why a small amount of the content is aspirated out and thus complete excision becomes ea
as the tension within the cyst is decreased.
(ii) Partial excision with marsupialisation.— The major part of the cyst wall together with its overlying
mucous membrane is excised. The cut edge of the cyst wall is sutured with the cut edge of the mucous memb
Thus the remaining portion of the cyst is always exposed to the floor of the mouth and will never get opportu
to form a retention cyst again.
(iii) Deep or plunging ranula should be excised completely. The incision is made on the neck transversally
over the swelling along the skin crease. Some surgeons prefer to remove the whole cyst through oral approac
If successful this treatment is cosmetically better, but often a portion of the cyst wall may not be removed and
will cause recurrence. That is why cervical approach is often advised.
SUBLINGUAL DERMOID CYST

Students are referred to chapter 36 ‘The Neck’ for detail discussion of this cyst.
Only one point is to be stressed here that the sublingual dermoid cyst is a mtdline swelling in the floor of
the mouth, whereas ranula is unilateral swelling in the floor of the mouth. Sublingual dermoid is a congenital
swelling as it is formed at the point of fusion of the two mandibular arches and this cyst develops from the
secretion of the sequestrated surface ectoderm at the fusion site. This cyst is whitish in colour and opaque (tra
illumination is negative as the cyst contains sebaceous material), whereas ranula is a transparent bluish cyst
which is brilliantly translucent.
30
466
TUMOURS OF THE CHEEK

Papilloma.—
1. A true papilloma is not very common.
2. It is soft and fleshy in consistency.
3. It does not turn into malignancy.
Treatment.— Papilloma should be totally excised alongwith an adequate normal margin of tissue.
Fibroepithelial polyp.—
1. It occurs from repeated trauma by the teeth.
2. So it is almost always seen on the inner side of the cheek at the level of the bite.
3. It is a core of fibrous tissue covered by mucous membrane of the cheek.
4. It is firm in consistency in comparison to the papilloma which is soft.
Treatment.— It is totally excised with a small margin of healthy tissue.
Lipoma.—
1. This may occur anywhere inside the mouth where there is fat.
2. Usually it is seen in the cheek.
3. The features are same as lipoma anywhere in the body.
Treatment is excision.
Haemangioma.—
1. It rarely occurs in mucous membrane of the cheek or the floor of the mouth. It may occur in the lip.
2. Recurrent bleeding is the characteristic feature.
3. It is often congenital.
Treatment.— (i) Injection of boiling water inside the haemangioma.
(ii) Injection of a sclerosant solution inside the haemangioma.
(iii) Excision of the haemangioma is the best treatment if possible.
(iv) Cryosurgery may be tried.
Neurofibroma.—
It may appear as solitary tumour along the course of a nerve, particularly the lingual nerve. This is a soft
fusiform, fibrous mass. Neurofibroma may also appear as pedunculated swelling. It may also present as a d
thickening of the gum gradually involving the cheek or the floor of the mouth.
Salivary tumours.—
There are buccal and retromolar salivary glands besides the ectopic glands in the cheek. Pleomorphic
adenoma is the commonest, but other tumours like adenoid cystic carcinoma (cylindroma) (not uncommon
muco-epidermoid carcinomas are also seen.
Treatment is complete excision of the tumour if it is pleomorphic adenoma and total excision with a marg
of healthy tissue if it be cylindroma.
Mixed salivary tumours.—
Ectopic salivary glands are situated in the mouth and may give rise to such tumours.
Treatment is complete excision.
CARCINOMA OF THE CHEEK
This condition is more common in Indian subcontinent than in Western countries. The reason is that peo
of this subcontinent often indulge in chewing the betel-nut and keep the quid of it in the cheek. Such carcino
is often called verrucous carcinoma (tobacco chewer’s carcinoma).
Such cancers are initially soft, non-indurated papillary growths which later ulcerate. The lesion graduall
invades and destroys the underlying soft tissues and bone. There may be leukoplakia to start with and this
ultimately turns into malignancy.
In Western countries, it is more common among those who smoke heavily and drink alcohols. A few
carcinomas may arise in Candida infected speckled leukoplakia.
MOUTH , TONGUE AND LIPS 467
PATHOLOGY.—These carcinomas are usually squamous cell carcinoma. There are numerous branching
projections of well differentiated epithelium each of which is covered by a layer of parakeratotic cells. At the
base of the lesion rete pegs are long and club-shaped and extend into chronically inflamed connective tissue.
Dyskeratosis and cellular pleomoiphism are minimal. Differentiation is constantly maintained.
SPREAD to regional lymph nodes may occur but distant metastasis is rare. Local recurrence rate is high.
CLINICAL FEATURES.— Carcinoma of the cheek is presented as an ulcer, a fissure or a papilliferous
growth. Most of the verrucous carcinomas are papilliferous growths. There may or may not be foul-smelling
discharge. Carcinoma of the cheek is usually a slow growing tumour.
Cervical lymph nodes should always be palpated as secondaries are common in the regional lymph nodes
TREATMENT.— (i) Adequate excision often gives satisfactory result.
Where the facilities of radiotherapy are available, surgery is indicated in —
(a) Recurrent tumours; (b) Residual tumours; (c) Radiotherapy failure cases.
Where facilities of radiotherapy are not available surgery is the main treatment.
The resulting defect may be made good by rotation flap or reflecting a flap of skin from the temporal regio
Pedicle grafts may be applied. When the skin from the temporal region is taken, the buccal aspect of the cheek
is now lined with the skin.
(ii) Radiation therapy plays an important role in the treatment of carcinoma of the cheek. If the service of
experienced radiotherapist is available, this treatment may be tried first. Interstitial radiation may be given by
192Iridium wire. External irradiation is given by megavoltage machines.
(iii) If cervical nodes are involved block dissection is necessary.
THE TONGUE
LEUKOPLAKIA
The essential process in leukoplakia is a slowly progressive hyperkeratosis. There is proliferation and
heaping up of the cornified epithelium with the formation of milk-white patches. This condition may occur
anywhere in the mouth, but most commonly seen on the tongue. In this case the tongue looks as if it has been
smeared with white paint. The condition in the tongue is called CHRONIC SUPERFICIAL GLOSSITIS.
Leukoplakia are now more often involving the lips and occasionally the cheek, gum and palate.
Leukoplakia may be seen in other places such as the larynx, glans penis, vulva and the perianal region. He
we shall discuss the leukoplakia on the tongue or chronic superficial glossitis.
AETIOLOGY.— The 6 well known aetiological factors of chronic superficial glossitis are —
(i) Smoking; (ii) Syphilis; (iii) Sharp tooth; (iv) Sepsis; (v) Spirits; (vi) Spices.
These are classically known as 6 ‘S’s.
PATHOLOGY.— The condition is confined to the anterior 2/3rds of the tongue. It usually starts at the edg
and gradually spreads on to the dorsum. The surface may become fissured and cracked due to contraction of
the underlying scarred tissue caused by chronic inflammation.
Macroscopically, the affected area of the tongue shows milk-white patches with cracks and fissures. In
course of time atrophy tends to succeed hypertrophy, the thickened papillae disappear and the white membra
is worn off. The surface becomes smooth and red.
Microscopically, the epidermis is greatly thickened and shows excessive comification. The prickle cell layer
hypertrophies and swollen cells with nuclei reach the surface (parakeratosis). The underlying tissue is infiltra
with chronic inflammatory cells of the small round type to be replaced later by fibrous tissue.
The practical importance of leukoplakia is the danger of its developing into carcinoma. It is considered to
be a premalignant condition. As many as 32% has developed into carcinoma in one study.
HISTORY.— (i) Age.— Usually middle-aged or elderly people are affected. Majority of the patients are
above 50 years of age.

(ii) Sex.— Men are affected more than women.
SYMPTOMS.—The main complaint is that the tongue has become white at places and has developed cr
and fissures. Occasionally there may be a lump.
EXAMINATIONS.— On examination, leukoplakia may be seen in one of the 4 clinical stages :—
Stage I.— Appearance of thin grey transparent film on the affected part of the tongue. This thin milky fi
may be wide spread.
Stage II.—This thin film turns opaque and white. This is leukoplakia. In the beginning it looks soft, but lat
on cracks and fissures appear.
Stage III.— Hyperplasia causes small nodules and warty outgrowths. Desquamation also appears simul
neously which leaves areas of smooth red and shiny tongue.
Stage IV.— This is the stage of appearance of clinically detectable carcinoma. This lesion possesses all th
characteristic features of primary carcinoma. The carcinomatous change usually occurs within the fissures.
should be suspected if there is local thickening, bleeding or pain.
Treatment.—
(i) Being a premalignant condition it should be biopsied as soon as such condition is detected.
(ii) Small patches of leukoplakia should be removed.
(iii) When a large area of leukoplakia is detected and confirmed by biopsy, one should wait and watch.
patients must be examined every month to note the progress of the disease. Appearance of ‘warty excresce
or small lump should arouse suspicion and these portions should be excised and examined histologically.
(iv) Role of radiotherapy is very intricate. It does improve the condition initially, but it increases the cha
of malignancy. Moreover, to add more problem such malignant lesions become resistant to further radioth
ULCERS OF THE TONGUE

The various types of ulcers are as follows :—
(i) Aphthous ulcer;
(ii) Traumatic or dental ulcer;
(iii)Chronic non-specific ulcer;
(iv) Post-pertussis ulcer;
(v) Syphilitic ulcer;
(vi) Tuberculous ulcer;
(vii) Carcinomatous ulcer;
(viii) Herpetic ulcer;
(ix) Ulcers due to glossitis.
Aphthous (dyspeptic) ulcer — is a small painful ulcer seen on the tip, undersurface and sides of the tongu
in its anterior part. The ulcer is small, superficial with white floor, yellowish border and surrounded by a
hyperaemic zone. This condition is quite painful and usually starts in early adult life. These ulcers tend to r
and show a familial predisposition. Women suffer from this condition more often than men.
Dental ulcer — is caused by mechanical irritation either by a jagged tooth or denture. These ulcers occur
at the periphery or on the undersurface of the tongue at the sides. This ulcer is elongated. It often presents
slough at its base and surrounded by a zone of erythema and induration. This ulcer is quite painful.
Syphilitic ulcer.— Mainly ‘snail-track’ ulcers are seen in various parts of the mouth in second stage of
syphilis. These ulcers are particularly rare in the tongue. The syphilitic conditions which are more often see
in the tongue are the gumma and chronic superficial glossitis.
Tuberculous ulcer.— Young adults are usually involved. Such ulcers are shallow, often multiple and
greyish yellow with slightly red undermining margin. These ulcers are seen at the margin, tip or dorsum. T
ulcer when occurs in the anterior 2/3rd of the tongue becomes very painful. Tuberculosis of the lungs or la
is frequently associated with. There may be enlarged cervical lymph nodes which in late cases may be matt
and even with cold abscess formation.

Post-pertussis ulcer occurs only in children with whooping cough. It is usually seen at the upper part of
frenum linguae and in the undersurface of the tip.
Chronic non-specific ulcer usually occurs in the anterior 2/3rd of the tongue. No aetiological factor can be
found out. It is moderately indurated and not very painful.
Carcinomatous ulcer.— It usually occurs in elderly individuals above the age of 50 years. Common site
is at the margins particularly in anterior 2/3rds of the tongue. It may occur at the dorsum when superimposed
on chronic superficial glossitis. It is usually single, but may be multiple if superimposed on chronic superficia
glossitis.
SYMPTOMS.—
It is usually painless to start with. Ulcer and excessive
salivation are the two important symptoms. Later on the condi
tion becomes painful and pain may be referred to the ear. There
may be lump in the neck.
SIGNS.—
The ulcer is irregular in shape, has a raised and everted edge
with indurated base. Induration is most important. The floor of
such ulcer is often covered with necrotic debris. Cervical lymph
nodes are usually enlarged. These are discrete, hard and mobile
in the early stage but become fixed to the underlying structures
in late stages.
Herpetic ulcer.— Such ulcer is common in children and
Fig.33.1.—A typical carcinomatous ulcer of the young adults. This occurs due to herpetic affection of the
tongue. Note the raised, everted and indurated lingual nerve. Acute neuralgic pain is often associated with on
margin of the ulcer. the affected side. Gradually vesicles appear which later on burst
to form multiple superficial ulcers which are extremely painful.
Ulcers due to glossitis.— Such ulcer occurs in chronic superficial glossitis. In this case the aetiology is
mainly smoking and hence this ulcer is called ‘smoker’s ulcer’. The ulcers are usually superficial and multiple
with hyperaemia. Patient usually complains of pain during taking food.
NEOPLASMS
BENIGN NEOPLASMS
Benign neoplasms are rare in the tongue. These are —
(i) Papilloma;
(ii) Haemangioma;
(iii) Lipoma;
(iv) Lymphangioma;
(v) Neurofibroma;
(Vi) Lingual thyroid;
(vii) Salivary gland tumour;
(viii) Osteoma.
Papilloma.— It is the most common benign tumour of the tongue. It can be sessile or pedunculated. The
main complaint is the presence of wart for quite a long time. It is painless. It is not associated with lymph nod
enlargement.
Differential Diagnosis.— The most important is Hutchinson’s wart (see above ‘syphilis in the mouth’).
Treatment.— It should be excised alongwith a wedge of normal tissue at the base. The excised tumour shou
be sent for histopathological report.
Haemangioma.— Almost always haemangioma of the tongue is of cavernous variety i.e. venous type. The
main complaint is the purplish swelling of the tongue, which often bleeds due to trauma.
Treatment is excision of the tumour.
Lipoma.— In tongue lipoma is usually small and the patient seeks advise due to presence of an abnorm
swelling.
Treatment is excision.
Osteoma—is a clinical curiosity. Sometimes a hard swelling may be seen in the posterior third of the ton
just beneath the foramen caecum. Such osteoma seems to have arisen from remnant of a branchial arch.
Treatment is excision of the growth.
Lingual thyroid.— This is discussed later in this chapter.
Lymphangioma and neurofibroma are discussed later under the heading of ‘Macroglossia’.
CARCINOMA OF THE TONGUE

Carcinoma of the tongue is a common lesion. It accounts for more than half of all intraoral carcinomas.
(i) Pipe smoking;
(ii) Syphilis;
(iii) Chronic superficial glossitis;
(iv) Alcohol;
(v) Chronic irritation from sharp tooth, oral sepsis and spices may play roles in initiating carcinoma;
(vi) Betel-nut.
Pathology.—
Carcinoma of the tongue occurs mostly on the anterior 2/3rds at or near the edges and 50% of carcinom
are seen in this region. 20% is seen in the posterior third of the tongue. In the dorsum and in the tip 10% ea
In this latter region it usually arises in a gummatous ulcer. 10% can occur on the undersurface of the tongu
MACROSCOPICALLY, four types can be seen —
(i) An ulcer,
(ii) A warty growth,
(iii) An indurated plaque or mass,
(iv) A fissure.
The ulcerative variety is by far the commonest. Sometimes no lesion can be seen but an induration can b
felt. The warty form is usually superimposed on leukoplakia.
(i) Ulcerative variety.— This type is almost always seen near the edge of the tongue. The ulcer looks
irregular and the edges are raised and everted. The floor is covered by a yellowish-grey slough. The most
characteristic feature is that the base is indurated. Even if the ulcer is shallow, the base will be felt to extend
more deeply, as the growth is invasive.
(ii) Warty growth.— When carcinomatous, it usually possesses a broad and indurated base. This form
develops when an excess of proliferating filiform growth occurs. Rarely it takes a cauliflower type look. Th
type is often superimposed on a previous leukoplakia.
(iii) An indurated plaque or mass.— In this case submucous plaque which is typically indurated can be fel
(iv) A fissure.— This type is usually presented as a chronic fissure which refuses to heal. This type often
follows chronic superficial glossitis or syphilis. Some degree of induration is almost always present.
MICROSCOPIC FEATURES depend mostly on the part of the tongue affected.
I. In the anterior 2/3rd epidermoid carcinomas with cell-nest formation is mostly seen. The reas
the anterior 2/3rds of the tongue is covered by thick stratified, comified epithelium with numerous papilla
submucous tissue is sparse and there are no racemose glands. The degree of differentiation will depend oh
grade of the tumour. Differentiation is less in case of cancer tongue than in case of cancer of the lip, that is w
prognosis of tongue cancer is worse than that of lip cancer.
II. In the posterior 3rd of the tongue it may be (i) basal cell type, or (ii) transitional type or (iii)
lymphoepithelioma. In the posterior 3rd of the tongue there is little or no comification, there are abundant
racemose glands and numerous collection of lymphocytes near the basal layer of the cells. S o the above varie
of carcinoma are seen in this region.
Very rarely one can come across adenocarcinoma or malignant melanoma in the tongue.
Spread of carcinoma.—
1. LOCAL SPREAD.— As carcinoma in other parts of the body local spread occurs by infiltration and
invasion. Carcinoma of the anterior 2l3rds of the tongue usually starts on the lateral margin of the tongue and
invades the floor of the mouth early but it remains limited to the side affected and does not extend to the othe
side across the midline.
Carcinoma of the posterior 3rd of the tongue tends to spread to the corresponding tonsil, epiglottis and soft
palate.
2. LYMPHATIC SPREAD.— Like other carcinomas in the body lymphatic spread is quite early.
Regional lymph nodes are affected by embolic spread and not by permeation, so that the intervening tissue is
not involved.
(i) From the tip the lymphatics pass through the floor of the mouth to the submental groups of lymph
nodes of both sides. One set of lymphatics from the tip of the tongue also pass to the juguloomohyoid gland.
(ii) From the anterior 2/3rds the lymphatics drain into the submandibular lymph nodes lying in relatio
to the submandibular salivary glands. Some of the glands may be embedded in the substance of salivary glan
(iii) On the posterior third of the tongue lymphatics drain into the jugulodigastric group of the upper d
cervical nodes on both sides of the neck. A few pass to juguloomohyoid group.
(iv) The central lymphatics from either side of the median raphe of the tongue pass vertically downwar
in the midline of the tongue between the two genioglossi which often decussate and then pass some to the lef
and some to the right to the jugulodigastric group of lymph nodes.
The jugulodigastric group of the upper deep cervical nodes ultimately receives the efferent lymphatics fro
the submandibular and submental groups, so that in later stages the jugulodigastric group will be involved
regardless of the original site of the tumour.
It should be remembered that secondary infection of the growth also causes enlargement of the draining
nodes. So enlargement of the draining lymph nodes do not always mean lymphatic metastasis.
More patients with posterior 3rd cancer present with lymph node metastasis. The reason is that the growth
remains occult and when the patient presents it is in relatively late stage.
3. BLOOD SPREAD.— It is very rare and extremely late in occurrence. It is only seen when the growth
is in the extreme posterior part of the tongue.
HISTORY.—
(i) Age.— The patients are usually over 50 years of age. The pick incidence is seen in the 6th decade.
(ii) Sex.— Though previously males were affected more when syphilis was not uncommon, yet now the
incidence is almost equal in both the sexes with probably slight preponderance towards males. Increase in
female incidence may be attributed to increase in smoking habit among females. Decrease in male incidence
is attributed to low incidence of syphilis, decreased use of the clay pipes, improved standard of oral hygiene a
decrease in consumption of country liquor.
SYMPTOMS.—
(i) The commonest complaint is a painless lump or an ulcer on the surface of the tongue. Many patients
ignore the condition at this stage, until and unless some more symptoms develop within a span of a few mon
(ii) Excessive salivation gradually appears alongwith the growth. An old patient sitting in the outpatient
department repeatedly spitting into his handkerchief is a good indication of carcinomaof the tongue. In late st
the saliva becomes blood-stained.
(iii) Foetor oris is another symptom which is often accompanied with carcinoma of the tongue. Offensive
smell in the mouth occurs due to bacterial stomatitis as the patient is unable to swallow saliva.
(iv) Ankyloglossia or immobility of the tongue occurs due to extensive carcinomatous infiltration of the
lingual musculature. It becomes even worse when the floor of the mouth is involved and ultimately this cau
difficulty in speech.
(v) Pain.— Carcinoma is always painless to start with, but in late cases the patient may complain of pain
due to involvement of the nerves. Pain may be experienced in the tongue or may be referred to the ear. Whe
the lingual nerve is involved pain may be complained of and such pain may be referred to the ear through
auriculotemporal nerve another branch of the 3rd division of the 5th cranial nerve (mandibular nerve).
(vi) Hoarseness of the voice and dysphagia.— Both these symptoms are only complained of when the
growth is in the posterior 3rd of the tongue and has involved pharynx and larynx.
(vii) Lump in the neck — due to enlarged cervical lymph nodes.
It must be remembered that growth situated on the posterior 3rd of the tongue often escapes notice of an
intelligent patient and even the clinician if he does not examine the case carefully. Such patients often presen
with hoarseness of the voice, dysphagia, difficulty in speech or even lump in the neck.
EXAMINATIONS.—
(a) Site.— As has already been mentioned carcinoma is most common in the anterior 2/3rds of the tongu
at or near the edges.
(b) Growth itself.—
(i) A carcinomatous ulcer of the tongue looks irregular in shape with typical raised and everted edge,
yellowish-grey slough on the floor and thin serous discharge. Induration at the base is the most characteristi
finding. It often bleeds to touch.
(ii) Papilliferous or Warty carcinoma looks like a papilloma which is usually pallor than the
surrounding epithelium. The base is broad and firm and indurated. It may be of any size.
(iii) Carcinomatous lump is often oval in shape with long axis parallel to the long axis of the tongue.
Its size varies from 2 to 5 cm in diameter. Its surface is irregular, the edge is indistinct and the consistency is
hard (most important feature).
(iv) Carcinoma in the form of fissure is rare. It looks as a deep linear ulcer with no detectable edge. It
is often secondary to chronic superficial glossitis or syphilis.
It is important to examine thefloor of the mouth, gums, the jaw, tonsils andfauces. Palpation of the posterior
part of the tongue and laryngoscopy examination are highly important if one does not want to miss growth i
the posterior 3rd of the tongue.
(c) Examination of lymph nodes, particularly the submandibular, submental and jugulodigastric groups,
are important. It is again stressed that enlargement of the draining lymph nodes does not necessarily mean
lymphatic metastasis, but this may be caused by secondary infection of the growth.
TREATMENT —
Treatment can be divided into two groups — A. Treatment of the primary growth and B. Treatment of th
secondary lymph nodes.
A. Treatment of the primary growth.—
Ancillary treatment.— (i) A swab from the ulcer is taken for bacteriological report, culture and sensitivity
tests. Suitable antibiotic should be started immediately.
(ii) Mouth should be cleansed by antiseptic mouth washes.
(iii) If there is presence of carious tooth or gingivitis this should be treated simultaneously.
(iv) Investigation must be made to exclude syphilis.
Two modes of treatment may be used for primary growth — SUGERY and RADIOTHERAPY.
SURGERY.— (a) If the growth is less than 1 cm in diameter — the growth is removed alongwith a wide
margin of mucosa of not less than 1 cm. This excised growth should be sent for histopathological examinatio
Monthly follow-up should be continued.
(b) In case of larger growth preliminary treatment should be radiotherapy. Only in those cases where
radiotherapy fails to respond, surgery is indicated. In these cases if the growth is localised to anterior 2/3rds
the tongue, partial glossectomy or subtotal glossectomy should be carried out.

(c) When the growth reaches within 2 cm of the jaw, radiotherapy may not be successful as this cause
necrosis of the mandible. In these cases hemimandibulectomy may be required alongwith excision of the
growth.
RADIOTHERAPY.— (a) When the growth is more
than 1 cm in diameter in the anterior 2/3rds, the preliminary
treatment is radiotherapy in the form of interstitial radio
therapy. Radium needles, Radon seeds or radioactive tan
talum wires or192 Iridium wire are placed in the growth in
one plane with a distance of 1 cm. When the growth is
deeper and extends more than 1 cm into the tongue, it is
difficult to treat these growths with interstitial radiother
apy and teletherapy should be used.
(b) Teletherapy — in which cobalt 60 unit is used.
This therapy is particularly useful in the posterior l/3rd of
the tongue, where interstitial radiotherapy is also difficult
to employ. When the lesion is large than 2 cm in diameter
it is usually irradiated by external beam irradiation. The
submandibular nodes are also included in the field even if
no nodes are palpable.
(c) If there is large tumour with palpable nodes,
both primary and the neck are irradiated to 4500 rads. Then
6-8 weeks later an excision is carried out in continuity
(Commando operation).
CHEMOTHERAPY.— Role of chemotherapy in tongue cancer is still in doubt. Regional intra-arterial ad
ministration of a cytotoxic drug e.g. amethoprin (50 mg/day for 5 days) may reduce the size of the growth, b
long term result is not encouraging.
B. Treatment of the secondary lymph nodes.—
(a) When the lymph nodes are not enlarged, regular follow-up should be carried out.
(b) If the lymph nodes are palpable and they are secondarily involved by metastasis, the treatment is
block-dissection. Sometimes block-dissection may be performed alongwith haemiglossectomy and this is
called Commando operation.
(c) When the enlarged lymph nodes are fixed and cannot be excised, deep X-ray therapy may be
employed. Role of radiotherapy is extremely poor so far as treatment of secondaries is concerned.
PALLIATIVE TREATMENT.—
1. In case of large fixed primary growth deep X-ray therapy will be tried.
2. When the primary recurs even after radiotherapy and surgery, cryosurgery may be tried.
3. In case of extreme pain due to advanced growth, blocking of the trigeminal nerve with 5 % phenol m
be considered.
Patients with tongue cancer die from following conditions:—
(i) Cancerous cachexia and starvation.
(ii) Inhalation bronchopneumonia.
(iii) Asphyxia due to oedema glottis or cervical lymph nodes pressing on air passages.
(iv) Haemorrhage from involved cervical lymph nodes ulcerating and eroding an artery.
Prognosis.— The 5 years survival rate of cancer tongue is not more than 25%.
A FEW RARE ANOMALIES OF THE TONGUE

Macroglossia.— Painless diffuse enlargement of the tongue is called macroglossia. Acute inflammation of the tongue
may cause such enlargement but as it is not a painless condition it should not be included under the heading of macroglos-
sia. CAUSES of macroglossia are:—
1. Lymphangioma;
2. Haemangioma;
3. Neurofibroma;
4. Muscular macroglossia;
5. Primary mesodermal amyloidosis;
6. Infiltrating carcinoma.
LYMPHANGIOMA.— In'this condition there is
dilatation of the lymph spaces. The enlargement of the
tongue may be diffuse or localised. Recurring attacks
of inflammation are not uncommon. With each attack
the tongue becomes larger and more indurated. The
surface may become ulcerated. The lower lip may be
everted and the teeth deformed. The condition is usu
ally present at birth. This condition may be associated
with cystic hygroma. The swollen tongue protrudes
Fig.33.3.— Mucosal neuroma of the tongue, which is not a permanently from the mouth .
common finding. At times it is seen in association with medul Treatment is by excision. Radiotherapy may help.
lary carcinoma of the thyroid. HAEMANGIOMA.—Widespread haemangioma
may cause macroglossia. There may be arteriovenous
fistula between the lingual artery and vein. In this case the large tongue pulsates.
Treatment.—- Partial excision should be performed. In case of arteriovenous fistula ligation of both lingual arteries
should precede partial excision.
NEUROFIBROMA.— It is a rare cause of macroglossia. It usually occurs in association with Von-Recklinghausen's
disease. Itoften affects one side of the tongue. Veiy rarely onemay find mucosal neuroma of the tongue (it is often associated
with medullary carcinoma of the tongue) (Fig. 33.3).
Treatment is haemiglossectomy.
MUSCULAR MACROGLOSSIA.— This condition is only seen in cretins. The tongue protrudes out of the mouth and
may become dry and cracked.
Treatment is partial excision, particularly the portion which protrudes out of the mouth.
CONGENITAL FISSURED TONGUE

Very rarely one can come across a congenital fissured tongue or congenital furrowing. In such cases fissures are mainly
transverse, though there may be a deep furrow in the middle of the tongue. Fissures may appear in the tongue due to
hereditary or acquired syphilis, chronic superficial glossitis and even in carcinoma. In syphilis and in chronic superficial
glossitis the fissures are usually longitudinal.
FURRING OF THE TONGUE

In acutely ill person with malaise and anorexia or with peritonitis, the normal movement of the tongue is very much
hampered. In these cases there may be (a) accumulation of food debris between the filiform papillae of the tongue, (b) there
may be overgrowth of normal bacterial flora of the mouth and (c) the desquamated cells are not normally removed by
movement of the tongue. So these products accumulate on the tongue to form ‘furring’ of the tongue.
In normal individuals fuiring of the tongue is only noticed in case of excessive smokers. But in such cases the fur is thick
and it is brown or black in colour.
MEDIAN RHOMBOID GLOSSITIS
It is a rare developmental anomaly. A reddish patch is found in the midline just in front of the circumvallate papillae
due to inadequate covering of the tubercular impar.
The importance of this condition is that it is often confused with (a) syphilitic wart or (b) carcinoma of the dorsum of
the tongue.
If these two pathologies can be excluded, no definite treatment is necessary for this condition.
HAIRY TONGUE
The condition is characterised by hypertrophy of the papillae. A fungus, Aspergillus Niger is often responsible for this
condition. Hypertrophy of papillae becomes covered with such fungi and mass of bacteria and give dark colour to the tongue.
Thus the dorsum of the tongue appears to have a patch of hairs and this condition is often called ‘black hairy tongue’.
Treatment.— Daily brushing of the area with a tooth brush dipped in a solution of 40% urea in water. It usually cures
this condition.
LINGUAL THYROID
Sometimes a round red swelling may be seen at the back of the tongue at the foramen caecum .This condition
is called lingual thyroid and contains thyroid tissue at the foramen caecum from where the thyroid diverticulum
starts in embryo. It must be remembered that this may be the only
thyroid tissue present in the individual.
COMPLICATIONS are (i) Haemorrhage, (ii) Respiratory
obstruction, (iii) Dysphagia and (iv) Impairment of speech.
TREATMENT.— L-thyroxin replacement therapy is given
to reduce the size of the swelling. If normal-thyroid is present,
excision may be advised.
LIPS
PIGMENTED LIPS
Brown pigmented spots on the lips, inside of the cheeks and
on the palate are found in Peutz-Jeghers' syndrome (familial
intestinal polyposis). In Addison’s disease black spots may be
seen on the lips.
Fig.33.4.— Lingual thyroid located in the
region of foramen caecum. MACROCHEILIA
Unlike macroglossia there are only two conditions which may give rise to macrocheilia — (a) lym
phangioma (which is much more common) and (b) chronic inflammation.
NEOPLASMS
BENIGN NEOPLASMS
Benign tumours may arise from any of the tissues forming the lips — the skin, fat, fibrous tissue, muscles,
blood vessels, lymphatics, nerves and specialised glands. The benign tumours which are seen in the lips are —
(0 Naevi;
(ii) Papilloma;
(iii) Fibroma;
(iv) Lipoma;
(v) Haemangioma;
(vi) Lymphangioma;
(vii) Pyogenic granuloma;
(viii) Keratoacanthoma;
(ix) Leukoplakia;
(x) Ectopic salivary tumour.
Ectopic salivary tumour.— Though this is extremely rare, yet it is seen in young adult males. Usually the
upper lip is involved. This is mostly seen on one or other side at the site of the right or left fusion line.
MALIGNANT NEOPLASMS
By far the commonest malignant lesion is the squamous cell carcinoma of the lip. Besides this one may co
across basal cell carcinomas and melanomas arising from the skin of the lips.
CARCINOMA OF THE LIP
Certain important points.—
(i) Lip carcinoma accounts for approximately 15% of all malignant diseases of the face and head and
roughly 1% of all cancers.

(ii) The lower lip is affected in more than 90% of cases, upper lip in only 5% of cases and 2% occurs at
one of the angles of the mouth.
(iii) 90% of the cases are seen in males.
(iv) This carcinoma is rarely seen in individuals below the age of 40 years. Incidence increases with
advancing age with highest incidence in the 6th decade.
(v) Carcinoma of the lip is rarely seen in blacks.
(vi) Persons with light-coloured skin, blue eyes and light colour hair when exposed to sunlight appears t
be highly susceptible.
(vii) There is a definite correlation between lip cancer and exposure to sunlight.
(viii) Persons who work in the outdoors or at higher elevations where the effects of actinic irradiation are
stronger, are more susceptible to the development of this cancer.
(ix) Other predisposing factors are — (a) syphilis, (b) excessive use of the tobacco (particularly smoking
of pipes and keeping ‘Khainy ’ between the lower lip and gum), (c) heavy alcohol consumption and (d) prev
gumma irradiation.
Pathology.— MACROSCOPIC ALLY, the disease begins as a flat nodule or an indurated crack at the skin
vermilion junction. Almost all lip cancers originate in this area. Then it may take either of the two forms — (1)
indurated nodule, warty mass or exophytic lesion or (2) endophytic lesion or ulcerated lesion. The ulcer pres
hard and raised edges characteristic of malignancy. As the ulcer spreads it gradually destroys the lip and the
tissues covering the chin. It may finally involve the mandible. If the carcinoma involves the commissure, the
prognosis is worse.
MICROSCOPICALLY, epidermoid carcinoma accounts for 99% of all lip cancers. These are usually well
differentiated, mostly grades I and II. Basal cell carcinoma occasionally appears on the lips. Melanoma is als
occasionally seen primarily in the lip.
SPREAD.— The disease is locally malignant. Lip cancer spreads to regional lymph nodes late. The route
is to the facial and submental lymph nodes and the nodes along the anterior portion of the submandibular g
The efferents from all these nodes reach the upper deep cervical group. The lymphatics from the upper lip d
into the preauricular and submandibular lymph nodes directly. Lymph node involvement may be noted within
3 months of the disease but frequently it is delayed for 9 to 12 months.
It should be remembered that the lymph nodes may be involved, but may not show any enlargement OR
may be enlargement of lymph nodes but it is inflammatory and not malignant.
Invasion of the mandible may also occur but late. It occurs via direct soft tissue extension usually entering
the mental foramen to reach the marrow cavity. Some pathologists presume that the lower jaw may be invol
along the perineural lymphatics.
Distant metastasis to the lungs and liver may occur late. This is also extremely rare.
DEATH occurs usually due to uncontrolled tumour in the neck.
HISTORY.—
Age, sex, occupation, ethnic group and geography have already been considered above.
Past history.— Patient may give a previous history of blistering due to actinic cheilitis; thickening due to
solar keratosis or white patches due to leukoplakia.
Occupation and habits.— The patient is often an outdoor worker. He may be a chain pipe smoker
(particularly clay pipes).
SYMPTOMS.—
(i) Usual presentation is a nodule or an ulcer which fails to heal.
(ii) The lesion may bleed or there may be offensive discharge.
(iii) The lesion is painless.
(iv) Patient may draw attention of the clinician to the swellings under his chin (lymph node involvement
EXAMINATIONS.—
The cancer starts as a small lump or nodule which ultimately ulcerates and develops a typical everted ed
of carcinomatous ulcer.
(i) Base is hard and indurated.
(ii) Floor is covered by a thick greyish-yellow slough. It is a mixture of necrosed tissue and inflammatory
exudate. It is thin, as the ulcer is repeatedly rubbed by the tongue.
(iii) Edge.— The edge of the ulcer is proliferated
and everted. This is red and bleeds easily.
(iv) Discharge — is thin, watery and slightly blood
stained. It is often infected though rarely purulent.
(v) Mobility.— The lump is invariably fixed to the
subcutaneous structures of the lip, but can be moved
with the lip. It is usually separated from the jaw and is
freely mobile over the jaw. Only in late cases it may be
fixed to the gum and jaw.
(vi) Lymph nodes.— All the draining lymph nodes
should be carefully examined. These are preauricular,
facial, submental, submandibular and upper deep cer
vical groups. If the lymph nodes are enlarged, it should
Fig.33.5.— A typical squamous cell carcinoma of lower
lip. For characteristic features see the text. be noted whether they are tender or not and whether
their consistency is firm or hard. Their mobility must be
GENERAL EXAMINATION should be performed to exclude distant metastasis.

DIFFERENTIAL DIAGNOSIS.— A few conditions mimic carcinoma of the lip and these are —
(i) Syphilitic chancre;
(ii) Keratoacanthoma;
(iii) Pyogenic granuloma;
(iv) Keratoses;
(v) Leukoplakia.
Treatment.—
SURGERY.—
1. SMALL PRIMARY lip cancers of the well differentiated type are adequately treated by local
resection. The V-excision is a popular method.
2. FOR LARGER LESIONS excision of more than half of the lip may be required.
3. Excision of the lesion should accompany a wide margin of surrounding healthy tissue. In these cases
thorough knowledge of local and distant flap techniques may be required for lip reconstruction.
RADIOTHERAPY still has many advocates as a primary modality in the treatment of lip cancer. A typica
course of radiation therapy lasts several weeks with daily treatments 5 times a week which is followed by
breakdown of the tumour and slow healing. In favourable lesions the cure rate for radiation therapy is 80% t
90% almost similar to surgery. However the radiation therapy produces considerable morbidity and usually
does not treat the regional nodes. Prior radiotherapy may increase the problem of wound healing if recurren
develops and surgery is then required.
TREATMENT OF SECONDARY LYMPH NODES.— When regional lymph nodes are involved, these
should be excised and examined histopathologically. Metastasis, if reaches cervical nodes, may reqire cervica
block dissection.
MELANOMAS OF THE LIP require wide surgical resection in continuity with node dissection of the
neck. Both radiotherapy and chemotherapy are ineffective in melanoma.
KERATOACANTHOMA
11113 is a cutaneous tumour which arises from the hair follicles on the lips. It is a benign tumour and runs a self-limited course. This
tumour is limited to white races and mostly seen in individuals between 50 and 70 years of age.
Actinic rays, chemical carcinogens, genetic factors, viral factors and trauma may play role in its aetiology.
CLINICALLY, the tumour appears as dome-shaped lesion with a pink hue. Gradually the dome breaks to reveal central keratin plug.
This plug ultimately detaches leaving an ulcerated lesion. If untreated it may produce a cicatricial deformity of the lip. It is a rapidly growing
lesion which reaches maximum size within 6 weeks and resolves spontaneous within four to six months from onset.
TREATMENT is surgical excision and primary closure. The specimen must be sent for histopathological report.
This condition often resembles carcinoma and histopathological report must be asked for to be definite about the diagnosis.
KERATOSES
These are scaly slightly raised lesions at the vermilion-cutaneous junction. It usually occurs in elderly patients with fair skin who are
chronically exposed to sunlight. This makes this condition so similar to lip carcinoma.
TREATMENT.— Full thickness of the skin should be excised and the tissue should be sent for histopathological report.
PYOGENIC GRANULOMA
This is a localised superficial polypoid mass, devoid of epithelium. It grossly resembles polyp of granulation tissue. This lesion may
occur at any age. Patients complain of pain of variable nature. It tends to bleed by trauma.
TREATMENT is surgical excision and histopathological examination of the excised lesion.
479
CHAPTER - 26
CLEFT LIP AND CLEFT PALATE
EMBRYOLOGY.—
The face is formed by five processes which surround the opening — the stomodeum — at the anterior end
of the embryo. These five processes are :
(1) Frontonasal process at the upper and central part — it is a single process.
(2) Maxillary processes at the upper and lateral part of the face — one on each side.
(3) Mandibular processes at the lower lateral aspect of the face — one on each side.
FRONTONASAL PROCESS.— Due to appearance of the olfactory pits at 5th week one on each side of
the midline at the inferior aspect of the frontonasal process, the process is divided into a central part called
median or medial nasal process (M. N. P.) and two lateral parts called the lateral nasal processes (L. N. P.). T
olfactory pit is destined to form the nostril. The medial nasal process develops a bulge on each side known a
the globular process.
Medial nasal process and globular process form: (i) The septum of the nose; (ii) The philtrum of the upper
lip and (iii) the premaxilla.
Lateral nasal process forms the side of the nose. It does not take any part in the formation of the upper lip.
MAXILLARY PROCESS.— Forms: (i) The cheek; (ii) the whole of the upper lip except the philtrum; (iii)
most of the upper jaw; (iv) the palate.
MANDIBULAR PROCESS.— Forms the lower jaw.
The upper lip is thus formed centrally from the superficial part of the medial nasal process, which is called
the philtrum. Lateral to this is formed by the maxillary process from each side which fuses with the medial n
process. So defect in fusion of the medial nasal process with the maxillary process will lead to the developme
of hare-lip or cleft lip.
The palate develops from three components — (i) premaxilla, which is developed from the medial nasal
process and (ii) two palatine processes of maxilla coming one from each side and fuse in the midline and also
with the premaxilla to form the palate. Defect in this fusion will lead to the development of the cleft palate.
CLEFT LIP
Developmental error in the formation of the upper lip will lead to the formation of cleft lip.
Classification.— A. Cleft lip may be :
1. Central (very rare).— It is due to failure of fusion of the two bulbous extremities of the median nasal
process (globular processes).
2. Lateral (the common variety).— It is the cleft between the philtrum (the central part of the upper lip
formed by the M. N. P.) and the lateral part of the upper lip (formed by the maxillary process). The cause is
imperfect fusion of the median nasal process with the maxillary process. Remember that the lateral nasal
process is not at all concerned. As the lateral variety is much more common, the condition should be called cleft
lip and not the hare-lip, as a typical hare-lip is a midline variety.
Lateral variety may be:
(i) Unilateral, which is commoner or
(ii) Bilateral, which is rare.
B. A cleft lip may be :
(i) Incomplete, in which the cleft has not extended upto the nostril and the upper part of the lip has fus
normally.
(ii) Complete.— In this case cleft lip extends to the floor of the nose. This is often associated with
flattening and widening of the nostril of the affected side.
C. Cleft lip may be :
(i) Simple ox
(ii) Compound, when the cleft lip is associated with a cleft in the alveolus.
D. A cleft lip may be :
(i) Uncomplicated or
(ii) Complicated i.e. associated with either cleft alveolus and/or cleft palate. A complete cleft lip may
be complicated whereas there is no chance of an incomplete cleft lip to be complicated.
Upper cleft lip may be occasionally associated
'” ,':v with presence of two small blind tubes in the lower lip.
!' , - 1 These are lined with squamous epithelium. These
; ■" ■.• often show hereditary tendency. These are called
■fcf '. inferior labial sinuses or mandibular recesses. The
;” The lower lip.— The lower cleft lip is extremely

uncommon If it occurs it is usually central, due to
failure of fusion of the two mandibular processes.
r.,f ' J jii substantial part of the areola as well as nipple into its
J, , agfir jgp mouth, sucking becomes dificult to a certain extent
■ : jflpPQP but not greatly. For bottle feeding, the hole of the teat
^ shoul(* ^ enlarged with a red hot needle. ^ ^
Fig.34.1.— Bilateral incomplete cleft lip. Treatment.

OPTIMUM TIME FOR REPAIR.— It is generally
advisable to perform the operation at the age of 3 months, when the baby is 5 to 6 Kg. in weight. This is alw
performed before the time for primary dentition, to avoid defective dentition. If the patient comes late, oper
should be performed, but the final result may not be satisfactory. If there is any protruded tooth, which ma
pressure on the suture line, it should be extracted.
This time is preferred as :
(i) The lip is larger and thick at this age, so that technically repair will be easier.
(ii) The baby is sufficient to accept general anaesthesia and operative assault.
(iii) Feeding with dropper in the post-operative period is not difficult.
(iv) It facilitates sucking.
(v) It helps in developing of the alveolus. In case of cleft alveolus early operation helps in closure of the
alveolar gap.
(vi) Defective speech is avoided.
(vii) When cleft lip is associated with cleft palate, early reconstruction of the lip will reduce the gap in th
palate.
Technique of operation.— There are numerous techniques by which this defect can be closed by plastic
surgery. The operation, advocated by Mirault, which was modified by Blair, is widely practised for unilater
cleft lip and will be described here. Another technique, which was advocated by Millard, is a popular altern
method.
MIR AULT-BL AIR OPERATION.— This operation is performed in 3 stages — In the first stage, adequat
CLEFT LIP AND CLEFT PALATE 481
mobilisation of the lip lateral to the cleft, the ala of the affected nostril and a considerable part of the cheek is
performed. This is done to avoid tension on the suture line after plastic repair. The lip is everted and an incisi
is made in the groove between the lip and the maxilla. The flap is dissected off the maxilla for a considerable
distance. Bleeding is checked by firm pressure with gauze.
In the second stage, the margins are made raw by cutting the whole thickness of the lip. The margins are
cut in a fashion as shown in Fig. 34.2 or Fig. 34.3. To facilitate this cutting in particular fashion and for proper
Fig.34.2.— Shows how to repair unilateral cleft

lip by Mirault-Blair technique. Lower figure shows
a typical case of unilateral cleft lip.
plastic repair, an ink mark is first made on the lip.

In the third or the last stage, the skin flaps are sutured in such a manner that the continuity of the red margi
of the lip is properly maintained. A rubber tube of proper size is introduced through the nostril first and then
the repair is started. The mucous membrane and the muscle are sutured separately with chromic catgut. The s
is sutured with fine silk or nylon.
The gap of the floor of the nostril must be repaired. Correction of the deformity of the nostril should also
be done.
If there is associated alveolar cleft it need not be repaired, as orbicularis oris if effectively reconstructed,
obliterates the alveolar gap spontaneously.
Postoperative care.—
After the operation is completed, the suture line is smeared with collodium and a Logan's bow is fixed to
relieve the tension on the suture line. The sutures are removed on the 5th postoperative day. The patient’s han
should be fixed in splints, so that he will not be able to touch the operation site.
Operation for bilateral cleft lip.— Sometimes both the maxillary processes fail to fuse with the medial
nasal process, which forms the philtrum. This philtrum with the premaxilla then projects forwards for a li
distance. In this case, the premaxilla has to be pushed back to fix with a notch in the anterior aspect of the
IB c
Fig.34.3.— Shows the steps of Millard rotation advancement repair,
a comparatively easier technique.
septum. The repair of the cleft is performed in the same way as the unilateral cleft.
CLEFT PALATE
Palate is developed from three components — (i) the premaxilla, developing from the medial nasal pro
(M. N. P.) and it bears the incisor teeth and (ii) the two palatine processes one from each maxillary process
line of fusion is in the form of Y.
Cleft palate is due to failure of fusion of these three processes. Cleft palate may be :
(i) Complete.— There is a gap between the two halves of the palate in its entire length. So that nose an
mouth become interconnected. In front, this gap may pass on one side of the premaxilla or on both sides. I
latter case the premaxilla is not attached to the palate, but hangs down from the septum of the nose some
in front of (anterior to) where it ought to be.
(ii) Incomplete.— The two halves of the palate fuse together from before backwards. The last parts to fu
are the two halves of the uvula. Incomplete fusion therefore may be :
(a) Bifid uvula.
(b) The whole length of the soft palate.
(c) The whole length of the soft palate and the posterior part of the hard palate.
In incomplete cleft palate, the anterior part of the palate is always normally formed.
Problems with cleft palate.—
1. Difficulties in sucking.— The negative pressure which is required for sucking connot be produced. S
spoon feeding is to be resorted to.
2. Difficulty in eating.— Regurgitation of food into the nose makes eating difficult. But adults are seen
with cleft palate who have grown up without surgery and are well nourished.
3. Difficulty in speech.— A person with cleft palate is unable to pronounce the palatal consonents. Thes
are B ,D, K, P, T. There is nasal intonation. This is due to the fact that air comes out through the nose while
4. Difficulty in hearing.— If palatal repair is not done, acute or chronic otitis media may develop.
In flammatory oedema of the pharyngeal mucosa and defective muscular activity will impede the ventilat
drainage of the middle ear through the Eustachian tube. This may lead to accumulation of inflammatory e
and deafness.
CLEFT LIP AND CLEFT PALATE 483
5. Dental problems.— Various problems of dentition may be due to irregular development of the
alveolus. The alveolar cleft interferes with the dental lamina and the upper lateral incisor may be small, absen
or even duplicate. All the incisors are badly displaced in bilateral cleft! Relative mandibular prognathism may
also result.
6. Defect in smelling.— This is due to contamination of the nasal mucous membrane with the oral
organisms through the cleft palate.
7. Repeated respiratory tract infection.
8. There may be chance of aspiration bronchopneumonia.
Treatment.—
Optimum time for operation.— Repair should be carried out at the age of 1 to 1V2 years i.e. before the child
acquires the bad habit of nasal speech.
Some surgeons prefer early repair of the cleft palate, as they think that the children start making efforts to
produce understandable sounds earlier. But early repair may lead to maldevelopment of the maxillae in later
life. So closure of the hard palate defect should not be performed till the facial development is well advanced
i.e. till the time of secondary dentition. A plate is constructed which will cover the cleft to facilitate feeding and
which will mould, the parts of the palate into the optimum position for surgical repair. Fresh plates will be
constructed at intervals to continue the moulding until the alveolar processes are aligned.
Operations for repair.—
1. LANGENBECK'S OPERATION.— In this operation the margins of the cleft are pared, the nasal
septum is defined and separated off the upper surface of the cleft palate. The mucoperiosteal flaps are lifted up
from the hard palate with a suitable raspatory. Two release incisions are made one on each side just medial to
the alveolar margins. The mucoperiosteal flaps are mobilised till the release incisions are reached. The cleft
then repaired in the midline by bringing in the mucoperiosteal flaps and the nasal mucosa medially. Repair
done in three layers — nasal mucosa, the soft palate muscles with interrupted catgut sutures and the muco
eriosteal flaps with interrupted silk suture.
2. WARDILL’S OPERATION (FOUR-FLAP OPERATION).— The main problem of Langenbeck’s
operation is tension in the suture line. Slight tension at the suture line will lead to failure of union due to lo
of vascularity and necrosis of the mucoperiosteal flaps. Moreover the length of the palate remains short afte
repair in Langenbeck’s operation, so nasal speech continues to be present.
These are the reasons why Wardill’s four-flap operation has become more popular than the previous on
The modifications of this operation are :
(i) The two flaps of the cleft palate are divided obliquely upto the releasing incision just medial to
alveolar margin. So now four-flaps are available. The anterior two flaps are brought to the midline and sutu
Now the posterior two flaps are not only brought to the midline but also pulled posteriorly to lengthen the
(See Fig 4.7 of Author’s ‘A Textbook on Surgical Short Cases’). This operation definitely increases the length
of the palate so that the space between the oropharynx and nasopharynx is diminished. The flaps wheneve
sutured should be done in three layers — the nasal mucosa is sutured with fine catgut. The muscles of the s
palate are sutured with No. O catgut, whereas the mucoperiosteal flap on the buccal side is sutured with fin
silk. All sutures should be interrupted.
(ii) Tension at the suture line is further reduced by breaking the hamulus process on each side, thus rel
the tensor palati muscle.
(iii) Pharyngoplasty.— This operation is aimed at reduction of the diameter of the nasopharynx. It also
makes prominent the ridge of Passavant. A transverse incision is made on the posterior pharyngeal wall at
level of Passavant’s ridge through the mucous membrane and the constrictor pharyngis superior at the leve
the anterior arch of the atlas. The flaps are undermined considerably in all directions. The incision is closed
vertically taking big bites from the salpingopharyngeal folds. Thus not only the diameter of the nasopharyn
is reduced, but also the muscular folds become prominent particularly at the time of deglutition.
In Dennis-Browne's pharyngoplasty operation, a purse string suture is applied to the mucous membrane
on the posterior pharyngeal wall at the level of the Passavant’s ridge.
The airway is kept clear for the first 24 hours. Oral cleanliness is maintained. Fluid diets are started exce
milk as it clots on the suture line. Later on intensive speech training is very important.
485
CHAPTER - 27
There are three pairs of major salivary glands—the Parotid, the Submandibular and the Sublingual glands
Besides these there are also the anterior lingual glands and numerous small glands in relation to the mucous
membrane of the lips, cheek and roof of the mouth and in the mucous membrane of the tongue. There are als
numerous small labial, buccal and palatal glands.
PAROTID GLAND
This is the largest salivary gland and lies below the external acoustic meatus,between the mandible and the stemomas-
toid. It projects forwards on to the surface of the masscter where a small part of it may be detached and lies between the
zygomatic arch above and the parotid duct below. The detached portion is called accessory parotid gland.
This gland forms an irregular, lobulated yellowish mass.
COVERINGS.— Parotid gland is covered by a true capsule which is nothing but condensation of fibrous stroma of the
gland. On its outer side the true capsule is covered by a layer from the deep cervical fascia which is called a false capsule.
At the inferior border of the parotid gland the investing layer of deep cervical fascia splits to enclose the parotid gland. The
superficial layer which covers the parotid gland extends upwards under the name of the parotid fascia and is fixed to the
zygomatic arch. The deep part of the fascia which passes deep to the parotid gland is attached to the styloid process and the
mandible and acquires the name of the stylomandibular ligament. It is also attached to the tympanic plate and blends with
the fibrous sheaths of the muscles related to the gland. The stylomandibular ligament is thickened and it intervens between
the parotid and the submandibular glands. It must be remembered that the parotid fascia is quite thick and tough so much
so that the parotid abscess does not show fluctuation until very late.
SURFACES OF THE GLAND.— The parotid gland is pyramidal in shape and presents superficial, anteromedial,
posteromedial and a small superior surfaces. The lower part of the gland tapers to a blunt ending.
The superficial surface is covered by the skin and the superficial fascia which contains the facial branches of the great
auricular nerve and the superficial parotid lymph nodes. The posterior border of the platysma also lies in this superficial
fascia.
The anteromedial surface is grooved by the posterior border of the ramus of the mandible. It covers theposteroinferior
part of the masseter muscle, the adjoining part of the mandibular ramus and the lateral aspect of the temporomandibular joint.
It also passes forwards on the deep aspect of the ramus to reach the medial pterygoid muscle. The branches of the facial nerve
emerge from under cover of the anterior margin of this surface.
The posteromedial surface is moulded on the mastoid process, stemomastoid muscle, the posterior belly of the digastric,
the styloid process and the styloid group of muscles. The external carotid artery grooves this surface before it enters the
substance of the gland. The styloid process and the styloid muscles intervene between the gland on the superficial side and
the internal carotid artery and the internal jugular vein on the deep side. The anteromedial and the posteromedial surfaces
meet along a medial margin which may project deeply as to be in contact with the side wall of the pharynx.
The superiorsurface isconcave and is related to the cartilaginous part of the external acoustic meatus and to the posterior
surface of the temporomandibular joint. The auriculotemporal nerve winds round the neck of the mandible and enters the
gland through this surface.
The lower extremity of the gland overlaps the posterior belly of the digastric and the carotid triangle to a variable extent.
STRUCTURES WITHIN THE GLAND.— (i) The External Carotid Artery pierces the posteromedial surface of
the Parotid gland and divides into its terminal branches — the maxillary artery and the superficial temporal artery — within
its substance. The maxillary artery leaves the anteromedial surface and runs deep to the neck of the mandible, while the
superficial temporal artery gives off transverse facial branch and then ascends to appear at upper limit of the gland. The
posterior auricular artery may arise from the external carotid artery within the gland and then leaves through the
posteromedial surface.
(ii) On a more superficial plane than the external carotid artery lies The Retromandibular Vein which is formed
in the upper part of the gland by the union of the maxillary and the superficial temporal vein. The retromandibular vein
emerges from the gland behind its lower extremity and joins the posterior auricular vein to form the external jugular vein.
Before it leaves the gland it gives off a communicating branch which leaves the gland in front of its lower extremity and
joins the facial vein.
(iii) On a still more superficial plane the Facial Nerve traverses the gland. It enters the upper part of the posteromedial
surface and passes forwards and downwards behind the posterior border of the ramus of the mandible where it divides into
two main divisions — (a) the temporofacial nerve, which runs sharply upwards and (b) the cervicofacial nerve, which
continues the course of the parent nerve downwards and forwards. The temporofacial nerve further subdivides into the
temp >ral and zygomatic branches, whereas the cervicofacial nerve further divides into the buccal, the mandibular and
the i ;rvical nerves. These five branches leave the anteromedial surface of the gland.
iv) The Auriculotemporal Nerve, which encircles the middle meningeal artery, runs backwards under cover of
the neck of the mandible and passes laterally behind the temporomandibular joint to enter the upper part of the parotid gland.
It ultimately leaves the gland through the superior surface and ascends posterior to the superficial temporal vessels.
So, mainly the contents are the external carotid artery and its terminal branches, the retromandibular vein and its main
tributaries and the facial nerve and its main branches. These three structures are placed in such a manner within the gland
that the artery lies in the deepest plane, the vein lies in the middle and the facial nerve lies in the most superficial plane. Within
the parotid gland the facial nerve and the retromandibular vein divide the parotid gland into two parts — the superficial
part and the deep part by the faciovenous plane, which is known as Patey's faciovenous plane.
Parotid Duct.— It carries secretion of the parotid
gland to the mouth. It is about 5 cm in length. It comes
out through the anterior border of the gland, crosses the
Masseter muscle and at the anterior border of this muscle
it turns inwards nearly at a right angle, passes through the
corpus adeposum of the cheek (suctorial pad of fat in the
infant) and pierces the Buccinator. It then runs for a short
distance obliquely forwards between the Buccinator and
the mucous membrane of the mouth and opens into a
small papilla in the mucous membrane of the cheek
opposite the crown of the second upper molar tooth. The
duct can be felt as it dips inwards at the anterior bordei
of the masseter by pressing the index finger backwards
on this border of the muscle (with the teeth clenched to
make the muscle taut) and moving the finger up and
down across the line of the duct.
Vessels and Nerves.— The external carotid artery
supplies this gland through its small branches while the
artery is within the gland.
Fig.35.1 .-A diagram showing disposition of parotid gland, The lymPh vessels 611(1 into the 2 or 3
'^P11 nodes on
parotid duct and branches of the facial nerve. surface of the parotid glands known as parotid lymph
nodes. From these nodes efferents pass to the superficial
and deep cervical lymph nodes.
The nerve supply of the parotid gland is derived from both parasympathetic and sympathetic systems. The secretomotor
or parasympathetic supply is through the auriculotemporal nerve, but these nerves are derived from the inferior salivary
nuclcus via the otic ganglion through the tympanic branch of the glossopharyngeal nerve. The sympathetic supply comes
from the plexus around the external carotid artery.
SUBMANDIBULAR SALIVARY GLAND
It consists of a large superficial part and a smaller deep part which are continuous with each other round the posterior
border of the mylohyoid muscle.
THE SUPERFICIAL PART.— This part is situated in the digastric triangle. It has three surfaces — an inferior, a lateral
and medial surfaces. This gland is also covered on both aspects by splitting of the investing layer of the deep cervical fascia.
This fascia splits, the superficial part covers the submandibular gland and is attached to the inferior border of the mandible.
The deep part covers the medial surface of the gland and is attached to the mylohyoid line on the medial surface of the
mandible.
The inferior surface, which is in fact the superficial surface of the gland is covered by the skin, platysma and the deep
fascia. It is crossed by the facial vein and the cervical branch of the facial nerve. It is also in close relation with the
submandibular lymph nodes and a few may actually be embedded within the gland.
The lateral surface is in relation with the submandibular fossa of the inner surface of the body of the mandible and with
the insertion of the Medial pterygoid muscle. The facial artery is embedded in a groove in the posterior and superior part
of the gland. The artery first passes up between the lateral surface of the gland and the medial surface of the mandible and
then curves downwards to reach the lower border of the mandible.
SALIVARY GLANDS 487
The medial surface is related in front to the mylohyoid muscle separated by the mylohyoid nerve and vessels. Posteriorly this surface
is in relation with the styloglossus muscle, the stylohyoid ligament and the glossopharyngeal nerve which separate it from the wall of the
pharynx. In the intermediate part the medial surface is in relation to the hyoglossus muscle, the lingual nerve, the submandibular ganglion,
the hypoglossal nerve and the deep lingual vein (in that order from above downwards).
THE DEEP PART.— This part of the submandibular gland lies in the interval between the Mylohyoid muscle below and laterally
and the Hyoglossus and Styloglossus muscles medially. It is related above to the lingual nerve and the submandibular ganglion and below
to the hypoglossal nerve and deep lingual vein.
The gland can be felt bidigitally between the index fmger placed on the floor of the mouth and the thumb placed outside medial and
just in front of the angle of the mandible.
The SUBMANDIBULAR DUCT is also about 5 cm in length. It begins by numerous branches in the superficial part of the gland
and emerges from the middle of the surface of that part of the gland a little behind the posterior border of the mylohyoid. It then runs
through the deep part of the gland and comes out of the gland to run between the mylohyoid and the hyoglossus. It then passes between
the sublingual gland and the genioglossus and opens by a narrow orifice on the floor of the mouth on the summit of the sublingual papilla
at the side of the frenulum of the tongue. On the Hyoglossus it lies between the lingual nerve and hypoglossal nerve but at the anterior
border of the muscle it is crossed laterally by the lingual nerve.
Vessels and Nerves.— The arteries come from the facial and lingual arteries.
The nerves are derived from the submandibular ganglion through which it receives filaments from the chorda tympani of the facial
nerve (parasympathetic supply) and through the lingual branch of the mandibular nerve (sympathetic supply).
THE SUBLINGUAL SALIVARY GLAND

This is the smallest of three main salivary glands. It is situated beneath the mucous membrane of the floor of the mouth in contact
with the sublingual fossa of the inner surface of the mandible close to the symphysis. It is almond shaped, narrow and flattened. It is related
above to the mucous membrane of the mouth which is raised in the form of sublingual fold. It is related below with the mylohyoid. In
front it is related to the fellow of the opposite side and behind it is related to the deep part of the submandibular gland. Laterally it is related
to the inner surface of the mandible and medially with the genioglossus muscle from which it is separated by the lingual nerve and the
submandibular duct.
PAROTID GLAND
Acute suppurative parotitis.— Acute inflammation of the salivary gland most frequently occurs in the
parotid, but occasionally the other salivary glands may be involved.
Causative organism is mainly the staphylococcus aureus, but streptococcus viridans or pneumococci may
be involved.
Organisms reach the gland from the mouth through the Stensen’s duct. Blood-borne infection is rare.
Two aetiological factors play major role in causing infection of the salivary gland. These are (i) when the
salivary flow is reduced—owing to dehydration (following major surgical operations) or starvation or following
radiotherapy and (ii) partial obstruction of the duct with retention of secretions — owing to presence of calculus.
CLINICAL FEATURES.— Patient mainly complains of pain and swelling of the side of the face.
On examination, there is brawny oedematous swelling over the parotid region with all signs of inflammation.
The temperature is usually high over 38°C. There may be widespread cellulitis of the overlying skin which looks
dusky red. If the parotid gland is pressed, pus may be seen coming out through the internal opening of the parotid
duct. This pus should be sent for culture and sensitivity test. Fluctuation may not be possible to elicit in the early
stage when there is pus in the parotid gland due to presence of a dense fascia which is derived from the deep
cervical fascia and covers the superficial surface of the gland being closely adherent to the gland and attached
to the zygomatic arch. Once pus has penetrated this dense fascia fluctuation can be elicited. But it is a late stage
and should not be allowed to reach.
TREATMENT.— (i) To improve general state of the patient.
(ii) Meticulous oral hygiene should be practised. Teeth should be cleaned with tooth paste and tooth brush.
Sodium bicarbonate mouth wash should be used for edentulous patients. Dentures should only be used during
meals.
(iii) Soft diet should be prescribed as chewing is painful.
(iv) A suitable antibiotic should be started immediately.
(v) Gentle parotid massage at regular intervals is quite helpful in extruding the pus.
(vi) When the pus stops draining through the duct and local and general conditions deteriorate, drainage
488
of the gland should be considered. Brawny induration over the parotid region is another indication for drainage
of the gland. When such is seen over the lower pole, drainage is more essential, as an abscess of the lower pole
may drain spontaneously into the external auditory meatus.
Incision is made vertically in front of the tragus and
curves under the lobe of the ear to reach the tip of the mastoid
process and then comes forward towards the lower pole of the
gland. Skin and subcutaneous tissue are cut along the line of
the incision and are retracted transversely. The transverse
incision is made on the dense parotid fascia and a pair of
mosquito artery forceps is pushed in and opened. Pus will be
seen coming out from beneath the fascia. Transverse incision
is made to protect the facial nerve which is also placed
transversely. The abscess is drained by Hilton’s method to
protect the facial nerve. A corrugated rubber-sheet drain is
inserted. When the swelling is reduced and drainage of pus
ceases, the wound in front of the ear is sutured under local
anaesthesia.
Acute parotitis.—This condition may be due to a virus
or more rarely by tuberculosis or actinomycosis, or cat-
scratch disease.
Mumps is a viral disease which often causes acute
Fiq. 35.2 — Left sided sialogram showing dilatation of the parotitis. It is a non-suppurative condition. It may be unilat-
main duct only with narrowing of the terminal portion. , .,,. , ,....,.
eral to start with but becomes bilateral within a few days. It
is associated with constitutional disturbances and other manifestations of mumps.
Recurrent subacute and chronic parotitis (sialoadenitis).— This condition often occurs (i) as a sequel
to an episode of acute inflammation or (ii) as the result of intermittent obstruction by a calculus or (iii) by an
autoimmune disease or (iv) when it occurs on both sides Sjogren’s syndrome should be suspected.
Recurrent attacks of pain and swelling and discharge of small amount of pus in the saliva are the typical
complaints. Due to retained secretions, ductules dilate and the acini become atrophic. The gland is progressively
replaced by chronically inflamed scar tissue. Even in Sjogren’s syndrome patients may complain of unilateral
pain and swelling. This is often due to calculus as a complication of reduced salivary flow of Sjogren’s syndrome.
A sialogram should always be performed. A sialogram or sialography is the method of taking radiograph
of a salivary gland following injection of suitable radio-opaque fluid e.g. Lipiodol or Hypaque (sodium
diatrizoate) into the duct system of the salivary gland. A fine polythene catheter is introduced into the orifice
of the duct. The outer end of the catheter is now fixed with a syringe containing the radioopaque fluid. Depending
on the size of the gland 0.5 to 2 ml of solution is pushed through the catheter. Radiographs are taken. Any
radiolucent obstruction, narrowing or dilatation of the duct is well shown through this radiography. The position
and size of the salivary neoplasm can also be detected. Fistula or abscess cavity may also be detected. If any extra
glandular mass displaces the salivary gland or the duct, this can be detected by such sialography. In the condition
of recurrent subacute parotitis one may find multiple, small proximal dilatations, which are called ‘punctate
sialectasis’, which is characteristic of this condition, Sjogren’s syndrome or following irradiation of the parotid
gland. In this condition there may be grossly distortion of the duct system with localised dilatation of the duct
with inspissated debris.
TREATMENT.— (i) Infection should be controlled by antibiotics.
(ii) If stone is present it should be removed.
(iii) If the duct is constricted and causing obstruction to the flow of saliva, it should be dilated through the
mouth.
(iv) Duct irrigation or even radiotherapy may be required when there is no stone or definite constriction of
the duct.
SALIVARY GLANDS 489
(v) Total conservative parotidectomy is advocated if the above measures fail. Superficial parotidectomy is
contraindicated as the remaining sialectatic deep lobe may produce a troublesome postoperative salivary fistula.
NEOPLASMS OF THE SALIVARY GLANDS

Approximately 75% of the neoplasms of the salivary gland occur in the parotid glands. In the parotid glands
80% tumours are benign and of these 80% are pleomorphic adenomas. The remaining 20% is composed of
definite carcinomas alongwith the mucoepidermoid and acinic cell tumours which are generally considered to
be cancers with variable aggressiveness.
About 15% of salivary tumours occur in the submandibular salivary glands. Of these 60% are benign. Of
the benign tumours 90% are pleomorphic adenomas.
10% of salivary tumours occur in the sublingual salivary glands and minor salivary glands situated in the
palate, lip and cheek. Majority of these tumours (60%) are malignant. 40% are benign and of which almost all
are pleomoiphic adenomas. The most common cancers in the salivary glands in the descending order of
frequency are mucoepidermoid carcinoma, adenoid cystic carcinoma, adenocarcinoma, epidermoid carcinoma,
undifferentiated carcinoma and carcinomas arising in the pleomorphic adenomas.
CLASSIFICATION:
A. Epithelial tumours.—
BENIGN.—
1. Pleomorphic adenoma (mixed tumour).
2. Oxyphil adenoma.
3. Papillary cystadenoma lymphomatosum (Warthin’s tumour).
4. Basal cell adenoma.
MALIGNANT.—
1. Mucoepidermoid carcinoma.
2. Adenoid cystic carcinoma.
3. Acinic cell adenocarcinoma.
4. Papillary adenocarcinoma.
5. Squamous cell carcinoma.
6. Undifferentiated carcinoma.
7. Carcinoma arising in pleomorphic adenoma.
B. Connective tissue tumours.—
BENIGN.—
1. Haemangioma.
2. Lipoma.
3. Neurilemmoma.
4. Fibroma.
MALIGNANT —
1. Malignant lymphoma.
2. Benign tumours as mentioned above may turn malignant.
C. Metastatic tumours.
Tumours mostly affect one of the 3 major salivary glands. Tumours of the minor salivary glands are
encountered most frequently in the palate. The upper lip is second in frequency. These tumours are occasionally
seen in the nasopharynx, larynx, bronchi and nasal sinuses.
PLEOMORPHIC ADENOMA (MIXED TUMOUR)
This is the commonest tumour of the major salivary glands and its marked feature is histologic diversity.
It is called ‘mixed’ as there is cartilage besides epithelial cells.
Sites.—
Though this tumour usually occurs in the major salivary glands, yet it may occur in the salivary glands of
the palate, upper lip and buccal mucosa. Tumours of the minor salivary glands, including mixed tumours, are
encountered most frequently in the palate. The upper lip is second in frequency. This tumour most commonly
occurs in the parotid and about 90% is seen in this gland. 7% is seen in the submandibular gland. In the parotid
gland the commonest location is the tail of the gland.
Pathology.—
Pleomorphic adenoma is basically a benign tumour. Recurrence rate, which are reported to be as high as
45%, was mostly due to fault in the surgical technique in the form of simple enucleation which was often used
earlier. It must be remembered that the tumour capsule, which may be well formed over much of the area, is often
incomplete. Careful examination reveals presence of tiny excrescences which project from the lobulated surface
of the main tumour. It is from these that the recurrences develop sometimes years after treatment of the mixed
tumour.
MACROSCOPICALLY, the tumour forms a rubbery, resilient mass with a bosselated surface. Consistency
depends on the presence of pseudocartilage and the degree of cellularity. Extensions from the tumour invade the
normal salivary gland tissue. On section, this tumour shows a somewhat glistening, mucoid appearance with
zones of apparent cartilage.
MICROSCOPICALLY, two main groups of cells can be distinguished, (i) One group comprises well
differentiated epithelial cells which may be arranged in acini, cords or sheets. A trabecular pattern and well-
formed tubular structures may also be detected. In about l/4th of the cases islands of squamous epithelium can
be seen; this represents squamous metaplasia, (ii) The other group consists of spindle or stellate cells usually
separated by abundant intercellular mucoid materials. At places this material closely resembles cartilage. The
spindle shaped cells are myoepithelial in nature. Both epithelial and myoepithelial cells secrete the mucoid
material which resembles cartilage. Occasionally sufficient mucoid material may accumulate to produce a cystic
part of the swelling. It characteristically possesses a pleomorphic stroma with pseudocartilaginous, lymphoid,
myxomatous and fibrous elements besides the epithelial cells. The rarity of mitotic figures and absence of necrosis
are of help in the differential diagnosis with true malignant neoplasm.
Regarding origin of this tumour two theories are in vogue, (a) The first is that the mixed tumours are
embryonic tumours arising from the embryonic rests from invagination of the oral ectoderm, (b) The second view
is that this tumour is adenoma of-the salivary gland and the cartilage is not true cartilage but pseudocartilage.
The tumour epithelial cells produce mucin. This mucin looks like homogeneous cartilage and the cells it contains
may lie free in small spaces around which there may be a fibrillar condensation, so that a pseudocapsular
appearance closely resembling a cartilage is produced.
HISTORY.—
(i) Age.— It is more frequent around 40 years of age, but it is also seen in children.
(ii) Sex.— Slightly higher incidence in women has been noticed.
SYMPTOMS.—
The patient complains of a painless swelling of the side of the face which has been present for months or
years. It is a slow growing tumour and gradually increases in size.
EXAMINATIONS.— "
(i) Site.— The typical site of the tumour is below the lobule of the ear. The tumour gradually takes the
position of the inferior part of the parotid gland just posterior and superior to the angle of the mandible.
(ii) Temperature and tenderness.— The temperature and colour of the overlying skin are normal.
Tenderness is conspicuous by its absence.
(iii) Shape.—The tumour tends to be round or oval when it is small. As it grows bigger, it becomes lobulated.
(iv) Surface.—Its surface is smooth. Sometimes it is bosselated and is occasionally crossed by deep furrows.
(v) Edge.— The margin is quite distinct.
(vi) Consistency.— It is firm and rubbery to feel. Variable consistency is a marked feature of this condition.
SALIVARY GLANDS 491
(vii) Fixity.— It is neither adherent to the skin nor to the masseter muscle.
(viii) Involvement of the facial nerve.— Even when the tumour is a huge one, the facial nerve is not invol
and remains free. Involvement of facial nerve, indicated by paralysis of the involved facial muscles, indi
infiltration of the nerve and it is a sure indication of carcinomatous change in a pleomorphic adenoma.
(ix) Cervical lymph nodes — are not enlarged.
(x) Examination of the inside of the mouth.— This is only required when such tumour arises from the
deep part of the parotid gland. This is an extremely rare incident. In this case the tumour pushes the to
the pillar of the fauces towards the midline.
MALIGNANT TRANSFORMATION.— Though rare yet malignant transformation of this tumour may occur in approximately 3 to
5% of cases after perhaps it exists for more than 10 or 20 years. Malignant transformation is apprehended when the tumour (a) becomes
painful; (b) starts growing rapidly; (c) feels stony hard; (d) gets fixed to the masseter deeply or to the skin superficially; (e) involves the
facial nerve — an important feature; (f) the cervical lymph nodes are enlarged and (g) causes restriction of movements of the jaw.
Investigations of salivary neoplasms.— At present CT and MRI scannings are the most helpful imaging techniques for
parotid and mandibular tumours. These imaging techniques particularly MRI indicate accurately the borders of the tumour and indicate
whether it is a circumscribed benign tumour or diffuse invasive malignant tumour. Moreover the anatomic relationship of the tumour
with surrounding structures will also be identified.
Fine needle aspiration (FNA) biopsy is much better than open biopsy. It is said that provided the needle gauge does not exceed 18G
there is no risk of seeding of viable tumour cells. About accuracy, there is a question mark, though the advocates of this technique claim
a very high accurate rate.
Open incisional biopsy is not recommended for neoplasms of the major salivary glands. An incision into a poorly encapsulated
tumour will spill the tumour cells into the surrounding tissue planes, which will lead to multiple local tumour recurrences even many
years after surgery unless they are subjected to radical postoperative radiotherapy, which should be avoided in the management of
benign disease. However it has a place in two cases — (i) for tumours of the minor salivary glands particularly in the palate, where there
is less chance to open up other tissue planes; and (ii) when there is skin infiltration or ulceration.
Treatment.— This tumour is radioresistant, so excision is the treatment of choice.
(i) There is no place of incisional biopsy, though fine-needle biopsy has been advocated by a f
Biopsy of the parotid carries a risk of damage to the facial nerve. For tumours of the minor salivary glan
palatal region, preoperative biopsy is a must. Where service of expert cytologist is available, fine-needle
aspiration biopsy can be performed. This type of aspiration biopsy guided by computed tomography is a
valuable means to detect the nature of deep lobe tumours.
(ii) Enucleation is followed by recurrence in as many as 50% of cases, as there are tumour extension
outside the capsule of the tumour within the normal salivary tissue.
(iii) Attempt at excision of these tumours with a cuff of surrounding normal tissue is also accompan
injury to one or more branches of the facial nerve. So this treatment did not receive wide acceptance.
(iv) Superficial parotidectomyis the treatment of choice. This operation is also known as Patey's operati
In this operation, after isolation of the facial nerve and its branches, the superficial portion of the parot
is dissected from the underlying tissues and removed with the tumour inside it. This operation brings d
recurrence rate to minimum, as also assures against injury to any branch of the facial nerve.
(v) The excised mass is now sent for frozen section. If a low grade malignant lesion such as an acin
adenocarcinoma, an adenoid cystic carcinoma or a low grade mucoepidermoid carcinoma is detected, th
remainder of the gland should be removed probably with the sacrifice of the facial nerve.
If a high grade malignant lesion is detected e.g. anaplastic adenocarcinoma or squamous cell carcin
radical neck dissection should be accompanied by removal of the remainder of the gland.
(vi) If the tumour is a simple pleomorphic adenoma, no further treatment is required except regular
(vii) Majority of the tumours of the salivary glands are radioresistant. However the more malignant les
demonstrate considerable sensitivity to radiotherapy and this treatment may be considered as adjuvant
excisional surgery when required.
(viii) In case of submandibular gland neoplasms, the whole gland is excised with particular care to preserve
the lingual and hypoglossal nerves.
(ix) In case of palatal growth an incision is made over the tumour. The periosteum is raised from the
the greater palatine vessels are mobilised, clamped, diathermised beyond the tumour. The whole tumou
The palatal bone may need to be sacrificed when it is invaded by the tumour clinically or radiographica
PAPILLARY CYSTADENOMA LYMPHOMATOSUM

(SYN. WARTHIN’S TUMOUR; ADENOLYMPHOMA)
HISTOGENESIS.— This tumour is derived from salivary tissue inclusions in lymph nodes, which th
often found in the parotid gland. This tumour was previously considered to be teratoid or branchiogen
Pathology.— The most important feature of this tumour is that it only involves the parotid gland and
almost always occurs in the lower portion of the parotid gland overlying the angle of the mandible. This
represents about 5% to 15% of the parotid tumours. It is a benign, encapsulated tumour. It is extreme
growing. It has a greater tendency to occur bilaterally
Gross appearance is soft and frequently cystic. The cyst usually contains glairy brown mucus. The
microscopic picture is quite different from any other tumour in the salivary glands. Irregular papillary pr
of tall columnar epithelium with eosinophilic and finely granular cytoplasm projects in the cystic spac
cores of the papillary processes contain abundant lymphoid tissue with germ centres.
HISTORY.— (i) Age.— This tumour appears in the middle and old age. Inspite of its suggested origin
tumour is rare in childhood. The usual period of appearance is the fifth and sixth decades.
(ii) Sex.— It is the only salivary gland tumour which is much commoner in men.
(iii) Ethnic group.—This tumour is more common in the white. This has never been recorded in Negr
SYMPTOMS.— The usual complaint is a painless slow-growing tumour over the angle of the jaw. Th
swelling may be bilateral.
EXAMINATIONS.— (i) Site.— This tumour has a peculiar predilection to develop in the lower part of
parotid gland. This is slightly lower than the common site of pleomorphic adenoma.
(ii) Number.— More than one tumour may be found at times either on one side or both sides.
(iii) Temperature and tenderness.— The overlying skin looks normal and not warm. The tumour is nev
tender.
(iv) Size and shape.— This tumour does not attain a large size and the usual size is 1 to 3 cm in dia
It is spherical in shape.
(v) Surface — is smooth and well defined.
(vi) Edge — is distinct.
(vii) Consistency.— This tumour is soft, cystic and sometimes fluctuant. Though there are cysts, yet
usually not translucent.
(viii) Mobility.— This tumour can be moved a little in all directions. This tumour is not fixed to the s
deeper structures.
(ix) Facial nerve — is never involved.
(x) Cervical lymph nodes — are not enlarged.
DIAGNOSIS.— A peculiar feature of this tumour is that it shows ‘hot’ spot in 99raTc-pertechnetate s
Other tumours of the parotid show ‘cold’ spot. So this is a great diagnostic index without biopsy.
Treatment — is superficial parotidectomy.
OXYPHIL ADENOMA (SYN. ONCOCYTOMA)
This is a typical benign tumour which grows slowly and does not become large. Microscopic feature
more or less similar to Warthin’s tumour except that there is no lymphoid element in this tumour. It i
entirely of large cells with eccentric nuclei and granular acidophilic cytoplasm. The cytoplasm is granu
is full with mitochondria. Mitotic figures are absent.
These tumours appear as nodules in the salivary glands. This tumour is predominantly seen in the
gland, though it occurs in the submandibular gland also.
Treatment.— Simple excision is all that is necessary. These tumours do not become malignant and o
rarely recur if incompletely removed.
MUCOEPIDERMOID CARCINOMA
This accounts for 6% to 10% of all neoplasms in the major salivary glands. This occurs more freque
SALIVARY GLANDS 493
the parotid gland. This tumour has variable level of aggressiveness and divided into low grade and high grade
types. The majority are slow growing cancers which can be successfully treated by adequate radical excision.
On cross section this tumour may be solid, cystic or semicystic. The fluid within the cyst is clear or mucous or
thick turbid secretion. Microscopically four cell types can be identified — (i) mucin producing, (ii) squamous,
(iii) intermediate and (iv) clear cells. The intermediate is considered to be the precursor of the mucin producing
and squamous cells. Clear or hydropic cells may be present in large number.
The low grade type presents as a well circumscribed mass having cystic areas with mucinous material.
Microscopically mucin producing cells predominate.
The high grade variety is grossly infiltrative and has less tendency to cyst formation. In this variety squamous
cells predominate over the mucin producing cells.
Clinically, the tumour varies from soft cystic to hard in consistency. Soft cystic tumours are low grade
malignant, whereas hard tumours are of high grade variety. They usually do not cause facial paralysis. The more
malignant variety invades surrounding structures and is relatively fixed. These occasionally metastasise to deep
cervical lymph nodes or even lungs.
ADENOID CYSTIC CARCINOMA (SYN. CYLINDROMA)
It is a poorly encapsulated infiltrating tumour. This tumour is believed to arise from the ducts and is unique
in being as common in submandibular gland as in the parotid gland. It also occurs significantly in accessory
salivary glands. This is known as cylindroma. This tumour also occurs in the trachea, bronchi, paranasal sinuses,
pharynx and lacrimal glands.
The microscopic pattern of adenoid cystic carcinoma has certain well defined characteristics. Nests of
columnar cells are seen arranged concentrically around a gland like space filled with mucin or mucohyaline
material. The tumour cells are small, dark staining and with relatively little cytoplasm.
This tumour is treacherous as it appears rather benign. But microscopic variations may occur in which
pseudoglandular spaces do not occur and only small nests of highly infiltrative tumour cells are seen. These
tumours show tendency to recur and often involve the perineural spaces.
Clinical features.— This tumour is comparatively slow-growing. Local pain is sometimes a prominent and
early symptom. Due to its affinity to invade perineural lymphatics, there may be areas of anaesthesia of the skin
and high frequency of facial nerve paralysis. Local lymph node involvement may occur. It may also be fixed to
the underlying bone due to fixation with the periosteum. It may invade the medullary bone for many centimetres
before showing significant bone resorption. Consistency tends to be hard.
Treatment.— When this tumour is diagnosed, a radical surgical approach should be used no matter how
benign it appears under the microscope. In case of inoperable recurrences radiotherapy may be applied. Unlike
other tumours of the salivary gland, it is more radiosensitive.
ACINIC CELL ADENOCARCINOMA

This tumour again occurs almost exclusively in the parotid glands. Two-thirds of the tumours occur in
women and are most common in 4th and 5th decades. It is a rare tumour with low grade clinical malignancy.
Clinically it presents as round or ovoid encapsulated tumour which is usually solitary. Local recurrences
are quite common.
Pathology.— Grossly the tumour is an encapsulated round mass which is greyish-white on cut surface. This
tumour is known for its highly cellular nature and relative absence of supporting stroma. The tumour cells are
round or polygonal resembling serous cells of the salivary glands. Nuclei are small, darkly stained and uniform
in appearance. The cytoplasm is basophilic and granular with coarse secretory granules. Lymphoid tissue may
be prominent. This tumour tends to involve the regional lymph nodes.
Treatment is again radical excision.
PAPILLARY ADENOCARCINOMA
This is an extremely rare tumour. It grows large. Haemorrhage and necrosis are common. This tumour can
also be differentiated into high grade and low grade. Variety is based on presence or absence of stromal invasion.
The low grade variety is prognostically similar to low grade mucoepidermoid carcinoma and the high grade
variety has a poor prognosis comparable to that of adenoid cystic carcinoma.
Microscopically it shows well defined papillary structures and mucin in the stroma.
SQUAMOUS CELL CARCINOMA

This tumour probably arises from squamous metaplasia of the lining epithelium of the ducts. This tumour
is also rare, but it is seen in the submandibular gland where prognosis is even worse than that in the parotid.
Pathologically this tumour is more or less similar to epidermoid carcinoma anywhere in the body with local
invasion and spread to lymph nodes.
This is the only tumour in the salivary gland which responds to radiotherapy. So irradiation therapy is often
helpful.
METASTATIC CARCINOMA
The two tumours that most commonly metastasise to the parotid gland are (i) epidermoid carcinoma of the
skin and (ii) malignant melanoma.
In the submandibular gland the most common tumour is a metastatic carcinoma in the submandibular lymph
nodes.
DUMB-BELL PAROTID TUMOUR
Very rarely parotid neoplasm may arise from the deep part of the gland and gradually enlarges medially
passing between the styloid process and the mandible. It ultimately presents as a swelling on the lateral wall of
the pharynx or posterior pillar of the fauces or as a swelling of the soft palate. There is virtually no visible or
palpable swelling in the preauricular region. If the growth is a slow growing one, it is usually a pleomorphic
adenoma and no biopsy is required. If the growth is relatively rapid, it should be biopsied through a small incision
on the posterior pillar of the fauces. Computed tomography often demonstrates the tumour with its size and
anatomical position.
Treatment is surgical excision of the tumour alongwith a margin of normal tissue and a covering- of
connective tissue. The incision is almost like that of parotidectomy with a submandibular extension. It may
require the mandible to be divided anterior to the mental foramen so that the angle may be retracted upwards.
It may also require division of the styloid process between the origin of the stylopharyngeous and the styloglossus
and stylohyoid muscles to facilitate dissection of the tumour under direct vision.
CARCINOMA OF THE PAROTID GLAND

Regardless of the pathological variety, carcinoma of the parotid gland is being considered in this section.
HISTORY.— (i) Age.— The patients are usually over 50 years of age.
(ii) Sex.— Males and females are equally affected.
SYMPTOMS.— The most common complaint is rapidly growing swelling on the side of the face. The
swelling may be painful. Pain is more felt during movement of the jaw. Pain may radiate to the ear, to the face
or to the neck.
There may be a history of a painless lump for quite a few years and recently the swelling has suddenly
increased in size.
EXAMINATIONS.— (i) Site.— It is in the parotid region.
(ii) Temperature and tenderness.— The overlying skin may be somewhat warm. When the skin is
infiltrated it may look reddish-blue. Tenderness is usually not present.
(iii) Size and shape.— Carcinoma is usually of big size as it grows bigger within a short time. It may be of
any shape.
(iv) Surface.— It is irregular.
(v) Consistency.— The mass is usually hard, but may be firm.
(vi) Fixity.— The swelling is often fixed to deeper structures. When the masseter is made taut by clenching
SALIVARY GLANDS 495
the teeth, the swelling becomes fixed and cannot be moved along the line of the fibres of the masseter. But slight
sideways movement may be present. The skin may be free but a few carcinomas show a tendency to infiltrate
the skin. In that case the skin cannot be lifted up off the tumour.
(vii) Regional lymph nodes are often enlarged and hard.
(viii) Facial nerve is often involved by carcinoma of the parotid. This will lead to paralysis of the facial
muscles.
(ix) General examination.—In case of few carcinomas, blood-borne metastasis may be present particularly
to the lungs.
Treatment of malignant tumours.— SURGERY is the main treatment, though a few carcinomas like
squamous cell carcinoma and cylindroma recurrences may be treated by radiotherapy. When the tumour presents
with clinical signs of malignancy, a fine-needle biopsy is almost always performed if the lump is easily accessible.
In case of relatively inaccessible growth an open biopsy is performed for frozen section during the operation,
followed by a radical excision.
(i) Total parotidectomy with sacrifice of the facial nerve should be the treatment of choice, particularly in
cases of low grade malignant lesions such as acinar cell adenocarcinoma, adenoid cystic carcinoma and low
grade mucoepidermoid carcinoma.
(ii) In case of high grade malignant lesions e.g. high grade mucoepidermoid carcinoma, undifferentiated
carcinoma and squamous cell carcinoma radical neck dissection should be accompanied by complete parotidectomy.
(iii) In a few cases of low grade malignant lesion one may try to save the facial nerve alongwith total
parotidectomy, though technically it is difficult.
(iv) Local recurrences should be treated by radiotherapy.
(v) When complete removal is not possible, superficial parotidectomy with radium implantation should be
the treatment of choice.
(vi) When the tumour is completely fixed and irremovable only palliative deep X-ray therapy is advised.
(vii) The facial nerve, which is sacrificed during the operation, may be grafted using the great auricular
nerve. A few immediate reconstructive techniques have been used when facial nerve grafting is not possible.
These techniques include immediate transfer of the masseter muscle to the paralysed comer of the mouth, use
of dermal ligaments and modified tarsorrhaphy to support the paralysed eye lids. When a portion of the mandible
has been excised, primary bone grafting may be used to replace the mandible.
RADIATION THERAPY.— If the surgeon feels that there is residual cancer after radical resection, or if the
pathologists report ‘cancer is extending to the margin of the resection’, in such cases postoperative cobalt
therapy should be initiated as soon as satisfactory wound healing has been obtained.
Other advanced parotid cancers that are clearly non-resectable may be controlled for many months by
appropriate X-ray therapy.
CHEMOTHERAPY.— In occasional circumstances, methotrexate or 5-fluorouracil therapy may cause
limited regression of malignant neoplasms of the parotid or submandibular gland. But its efficacy is not
established for long term palliation. Infusion with cyclophosphamide (Cycloxan or Endoxan) by retrograde
catheter into the superficial temporal artery has produced marked regression in certain cases of advanced parotid
carcinoma.
SUBMANDIBULAR GLAND TUMOURS.— Due to deep location of the gland, lymph node dissection
should be performed more often than in parotid malignancy. Radical excision of the submandibular gland with
adjacent mandible, a portion of the mylohyoid muscle, a portion of the tongue and lymph node dissection of the
neck are performed to give adequate removal of the growth alongwith a considerable margin of healthy tissue.
Occasionally such removal may require sacrifice of the lingual and hypoglossal nerves.
MINOR SALIVARY GLAND TUMOURS.— A biopsy is always taken preoperatively. Almost 75% of
salivary gland tumours in the palate prove to be malignant. Patients with such tumours require full-thickness
resection of portions of the hard and the soft palate. Hard palate defects may be managed by the use of dental
prosthesis, whereas defects of the soft palate are managed by immediate reconstruction using a flap of mucosa
and muscle from the posterior pharynx. Subsequently, pedicle flap reconstruction of the palate may be performed.
SJOGREN’S SYNDROME.— This syndrome consists of clinical triad — (i) dry eyes (keratoconjunc
tivitis sicca), (ii) dry mouth (xerostomia) and (iii) rheumatoid arthritis. Other connective tissue disease e.g.
systemic lupus erythomatosus, scleroderma, or polyarteritis nodosa may be present. When other connective
tissue disease is present the condition is called secondary Sjogren’s syndrome. When only the clinical triad (as
mentioned above) is present, it is called primary Sjogren’s syndrome.
PATHOLOGY.— The salivary and lacrimal glands are infiltrated with lymphocytes with extensive
replacement and destruction of the acinar parenchyma. There is mucous gland metaplasia of the duct epithelium
which may lead to formation of gelatinous saliva in some patients. The ductal epithelium becomes hyperplastic
forming casts within the lumen. This may cause blocking of smaller ducts. There may be localised strictures and
dilatations of the duct. There may be ascending infection to complicate the condition. In general hypergamma
globulinaemia, eosinophilia, leukopenia and cryoglobulinaemia are often noticed as laboratory findings. This
condition is regarded as an autoimmune disease and very much resembles Hashimoto’s disease of the thyroid.
One can find autoantibodies such as rheumatoid factor, antinuclear factor and salivary duct antibody in the
serum. One can perform uptake study by "Tc-pertechnetate scan.
CLINICAL FEATURES.— Progressively severe dry mouth is the main complaint. Gradually caries of teeth
occur with fall of teeth. Dentures are difficult to wear due to stickiness of the mouth. The tongue becomes cracked.
Attacks of mondial stomatitis is also complained of. Swelling of the salivary glands in the form of localised
nodules should arouse suspicion and must be differentiated from malignancy. Rheumatoid arthritie mainly
affects the small joints and is generalised.
MIKULICZ’S DISEASE.— It is characterised by the triad which includes — (i) symmetrical enlarge
ment of all salivary glands, (ii) enlargement of the lacrymal glands which causes narrowing of the palpebral
fissures and (iii) dryness of the mouth.
PATHOLOGY.— It is also considered to be an autoimmune disease of the glands with microscopic feature
almost similar to Sjogren’s syndrome.
CLINICAL FEATURES.— This condition occurs more often in women. Majority of patients are over 40
years of age. The condition develops slowly and painlessly.
COMPLICATIONS.— (1) Rare complication of Mikulicz disease is the development of malignant
lymphoma within the involved salivary glands.
(ii) There may be occurrence of malignant variant of Mikulicz disease, which is an extremely rare
occurrence and is characterised by repeated local recurrences and eventually lymph node metastasis.
Management.— (i) The condition may resolve by itself after several months or years.
(ii) Steroids and immunosuppressive agents may be used, but should be aware of the side effects. Such
treatment may increase the risk of ascending infection.
(iii) Meticulous oral hygiene with tooth brush and fluoride tooth paste with special 1% chlorhexidine
gluconate preparation to control caries and tooth loss in Sjogren’s syndrome is very important.
(iv) Dry eyes may be treated with obliteration of the lacrymal punctum by diathermy, to be followed by
instillation of artificial tears.
(v) Radiotherapy may reduce enlargement of the salivary glands of Mikulicz disease, but increases dryness
of mouth and tendency towards infection.
(vi) Surgery.—When the above conservative measures fail, surgery in the form of superficial parotidectomy
and excision of the submandibular salivary glands will definitely reduce the deformity. The lacrymal glands
should be left alone.
PAROTID FISTULA
A parotid fistula may arise from the parotid gland or the parotid duct. Such fistula may be internal when
it opens inside the mouth or external when it opens to the exterior.
CAUSES.— Parotid'fistula may occur from :
(i) Penetrating injury particularly by glass splinters.
(ii) Rupture of parotid abscess.
SALIVARY GLANDS 497
(iii) Inadvertent incision for drainage of parotid abscess.

(iv) Complication of superficial parotidectomy.
Clinical features.— The main complaint is an opening in the cheek with discharge. On careful questioning
it will be evident that discharge comes out only during meals. There may be excoriation of the neighbourhood
skin.
Special Investigations.— A sialogram should be performed with watery solution of lipiodol. This will give
an indication whether the fistula is in relation to the main duct, ductule or to the gland.
Treatment.— (i) When the fistula is connected with the main duct—reconstruction of the duct by Newman
or Seabrock’s operation should be performed. In this
technique one polythene catheter is passed through
the parotid duct opening in the mouth in a retrograde
fashion into the parotid duct upto the fistula. Anoth
er probe is introduced through the external fistula. A
horizontal incision is made on the cheek. The ducts
are dissected and the divided ends are identified and
made free. The catheter wire is passed into the distal
and proximal ends of the duct. If repair without
tension is possible the ends of the divided duct are slit
longitudinally and then joined by oblique suture line
to avoid stricture. Suture is performed by using 6/0
silk or dexon or prolene which are placed in the
submucous coat of ducts interruptedly. The adjacent
connective tissues are approximated with great care
so that there is no chance of recurrence. The skin
incision is now closed. The end of the catheter which
comes out through the parotid duct opening into the
mouth is anchored to the oral mucosa to prevent its
slipping out. This catheter is kept in situ for 2 weeks,
after which it is removed.
If a portion of the duct has been destroyed and
direct suturing is impossible, continuity can be
restored using a rectangular pedicle flap of mucosa
Fig. 35.3.—Shows the technique of suturing the parotid duct in case from the inner aspect of the cheek. This flap is now
of recent injury. In this method suturing is performed over a piece
rolled into a tube and anastomosed to the proximal
of Silkworm-Gut instead of tantalum wire.
cut end of the duct.
(ii) If reconstruction fails, the auriculotemporal nerve which carries secretomotor fibres to the parotid gland
is resected.
(iii) If the above method fails, complete parotidectomy is advised preserving the facial nerve.
AURICULOTEMPORAL SYNDROME
(SYN. FREY’S SYNDROME)
Partial injury to the auriculotemporal nerve gives rise to such syndrome. This type of injury —
(i) May be congenital, possibly due to birth trauma.
(ii) May be accidental.
(iii) May be caused by inadvertent incision for drainage of parotid abscess.
(iv) May occasionally follow superficial parotidectomy.
In this condition (a) there is flushing and sweating of the skin innervated by the auriculotemporal nerve
particularly during meal and (b) presence of cutaneous hyperaesthesia in front and above the ear, the area
supplied by the auriculotemporal nerve.
32
The EXPLANATION of this syndrome is —

(i) The similar postganglionic parasympathetic fibres become united to the sympathetic nerves from
superior cervical ganglion which are concerned to supply vessels and sweat glands of that region. This
flushing and sweating of the skin.
(ii) Following injury to the auriculotemporal nerve, postganglionic parasympathetic fibres from the
ganglion grow down the sheaths of the cutaneous filaments, so hyperaesthesia follows stimulation of th
secretomotor nerves.
TREATMENT.— If the symptoms persist, the treatment is avulsion of the auriculotemporal nerve in
of the auricle where it lies just posterior to the superficial temporal vessels.
SUBMANDIBULAR SALIVARY GLAND

SIALOLITHIASIS
Salivary stones are more common in the submandibular salivary gland than in the parotid gland be
the saliva of the submandibular salivary gland is more viscid and saturated in calcium salts. Such ston
more frequently within the duct of the submandibular gland (Wharton’s duct). Less commonly the calcu
occur within the gland substance.
AETIOLOGY.— Pathogenesis of calculus formation is unknown. It has been suggested —
(i) That chronic inflammation may cause inspissation of the saliva and deposition of calcium salts.
(ii) That retention of secretion may cause calculi formation. Such retention is more common in the
submandibular salivary gland as the duct has a very curved route and the secretion from the superficia
up and reach the submandibular duct through the deep part which is not a dependent drainage.
Composition of the stone.— A salivary gland calculus is composed of cellular debris and mucus in t
centre, but the main content is calcium and magnesium phosphate. Such combination is found in tarta
tooth.
Clinical features.— Painful swelling during meals is the most important symptom. Such pain may be
preceded by salivary colic. When this history is forthcoming, the patient should be given some lemon ju
the swelling can be produced. At this time if one examines the orifice of the affected duct, it shows little
ejection of saliva.
SUBMANDIBULAR CALCULI
HISTORY.—
(i) Age.— Majority of the patients are young to middle age. This condition is rarely seen in children.
(ii) Sex.— Males and females are almost equally involved.
SYMPTOMS.—
(i) The main complaint is pain and swelling beneath the jaw just before and during meals. Both the
symptoms last throughout the meal. After certain period the pain and the swelling gradually subside. S
and swelling may persist. Some patients may give a typical history of colic just before the meals.
(ii) Some residual pain and swelling beneath the jaw may be the constant complaint.
(iii) Some discomfort or swelling may be complained of in the floor of the mouth.
(iv) Patient may be able to relieve his symptoms by pressing on the gland. On the other hand such a
may lead to ejection of foul tasting fluid in the mouth (purulent saliva).
(v) Patient may give previous history of similar symptom on the other side of the face.
EXAMINATIONS.—
Sometimes the submandibular gland will be swollen when the patient presents to the doctor. If such
is not present, the clinician can produce the condition artificially by instilling a few drops of lemon juice
the patient’s mouth. This will cause pain and swelling of the gland. The clinician must look at the openi
the involved duct and no saliva is seen to be coming out through that orifice. Usually there is no temper
SALIVARY GLANDS 499
but slight tenderness is expected. The distended gland feels elastic, rubbery and firm. Bimanual palpation is
important. For this clinician places index finger of one hand on the floor of the mouth and fingers of the other
hand on the outer surface of the lump just below the mandible. The finger inside the mouth can feel the deep
part of the salivary gland. To exclude impaction of the stone in the duct, the whole duct must be palpated
bimanually.
Inspection of the floor of the mouth is very important. The patient is asked to open his mouth and lift his
tongue to the roof of the mouth. This allows proper inspection of the floor of the mouth with the help of a torc
Orifices of the submandibular (Wharton’s) ducts are situated on the either side of frenulum linguae. It is noted
whether the orifice looks inflamed or swollen due to impaction of a stone in the duct. A stone may be impacte
in the ampulla just beneath the orifice and may be seen if inspected carefully. In case of presence of stone in on
duct, saliva will not come out from this orifice. This may be tested by placing two dry swabs one on each orific
and some lemon juice is dropped on the dorsum of the tongue. A minute later the patient is asked to move the
tongue up. The swab on the orifice of the duct where the stone is impacted will remain dry, whereas the other
swab will be wet.
Treatment.—
All cases should be X-rayed before they go to the operation theatre to locate the exact position of the stone
A. STONE IN THE SUBMANDIBULAR DUCT.—
If the stone is palpable near the orifice of the duct it can be removed by an incision made directly over it
through the mucous membrane of the mouth. The stone is steadied between the thumb and index finger, the
overlying tissues will be infiltrated with local anaesthesia. An incision is made directly upon the stone, which
is extracted with a small scoop. A stay suture may be passed under the duct to bring it up into the top of the w
as also not to allow to slip the stone posteriorly into the gland and then incision is made on the wall of the duc
to remove the stone.
B. STONE IN THE SUBMANDIBULAR GLAND.— Excision of the salivary gland is advised.
OTHER INDICATIONS FOR EXCISION OF THE SUBMANDIBULAR SALIVARY GLAND ARE :
(i) When the gland is chronically inflamed.
(ii) When the gland is the site of stone formation.
(iii) Any tumour of the gland.
(iv) Secondary carcinoma of the submandibular lymph nodes.
Operation.— A curved incision is made over the lower third of the gland about 5 cm long in the line of skin
crease (Langer’s line). The skin and platysma are divided in the same line to avoid injury to the cervical branch
of the facial nerve. The posterior end of the incision should lie at least 2 cm distant from the angle of the mandi
The anterior facial vein is found within the fat superficial to the gland. This vein is divided between ligatures.
The lower pole of the gland is freed keeping close to the surface of the gland and is turned upwards and forwa
The posterior belly of the digastric and the stylohyoid muscles are identified. These are retracted backwards w
a retractor. The facial artery with its venae comitantes will be seen emerging from deep to the muscles and
entering to the deep surface of the gland. It is divided between ligatures very carefully with double ligation of
the proximal end as the artery tends to retract beneath the muscles. The gland is now drawn down and is separ
from the lower border of the jaw dissecting close to the gland. If the lower pole of the gland is now retracted
backwards the posterior border of the mylohyoid muscle will be seen. It is separated with scissors from the gro
between the superficial and deep parts of the glands. Small arteries entering the gland from the muscle should
be divided between ligatures or sealed with diathermy. The deep part of the gland is now drawn down with ca
not to injure the lingual nerve. The nerve is separated under direct vision. The hyoglossus muscle is exposed w
submandibular ganglion. The submandibular duct is drawn down through the loop of the nerve. The duct shou
be clamped and divided between ligatures as forward as possible. So that major portion of the duct remains wi
the gland. All throughout the process, the dissection should be kept close to the gland so that the hypoglossal
nerve is not injured. Sometimes veins from the gland may drain into the venae comitantes of the hypoglossal
nerve. These should be divided between ligatures with great care. The submandibular gland is now taken away
and the wound is closed in layers with vacuum drainage.
PAROTID CALCULI
Parotid calculi are not as common as submandibular calculi. Calculus in the duct of the parotid gland gi
rise to the same symptoms as mentioned in sialolithiasis. Plain radiograph may detect large stones. Sialogra
may be required to identify and locate the smaller ones.
Treatmen t.—When a calculus is palpable from the mouth, it may be removed with an incision made dire
upon it through the mucus membrane. In case of calculi anterior to the accessory parotid gland an intraoral
incision is made around the parotid papilla. The flap is raised which includes the parotid duct for a distance
the cheek till the calculus is reached. The calculus is removed, the duct is reinserted and intraoral incision ar
the parotid papilla is sutured.
In case of calculi in the intraglandular portion of the duct, these are approached from outside through
preauricular incision as made for parotidectomy. The duct is identified at the anterior border of the gland an
traced forwards and backwards till the calculus is discovered. The calculus is extracted and the duct is kept
or sutured with fine suture material. Care must be taken to conserve any branch of the facial nerve.
Papillary stenosis.— Ulceration at the opening of the parotid or submandibular duct may occur following
trauma from a denture. This ulceration may subsequently heal by stenosis causing obstruction to the flow of
saliva. Ulceration of the parotid duct opening or papilla may follow irritation from a sharp tooth or bite of th
cheek.
In case of stenosis resulting from fibrosis of the ulcer, treatment is papillotomy with suture of the duct li
with the oral mucus membrane.
501
CHAPTER - 28
THE NECK
SWELLINGS
Swellings in the neck may be due to various causes. These swellings, for ease of description, can be divided
into A. Midline swellings and B. Lateral swellings.
A. Midline Swellings.— From above downwards —
1. Ludwig’s angina.
2. Enlarged submental lymph nodes.
4. Thyroglossal cyst
5. Subhyoid bursitis.
6. Goitre of the thyroid isthmus and pyramidal lobe.
7. Enlarged lymph nodes and lipoma in the suprasternal space of Burns.
8. Retrosternal goitre.
9. Thymic swelling.
10. Bony swellings arising-from the manubrium stemi.
A few swellings may appear anywhere in the midline which are swellings of the skin and superficial fascia
(sebaceous cyst, lipoma, fibroma, neurofibroma etc.) and dermoid cyst.
In the midline, the common swellings are :
1. Submental lymph nodes.
2. Thyroid gland enlargement.
3. Thyroglossal cyst.
5. Lipoma.
B. Lateral Swellings.— For benefit of description lateral swellings can be better described according to
their locations in either of the three triangles of the neck — (a) submandibular triangle, (b) carotid triangle or
(c) posterior triangle.
(a) In the SUBMANDIBULAR or DIGASTRIC TRIANGLE :
1. Enlarged lymph nodes.
2. Enlargement of submandibular salivary gland.
3. Deep or plunging ranula.
4. Extension of growth from the jaw.
5. Sjogren’s syndrome.
(b) In the CAROTID TRIANGLE :
1. Aneurysm of the carotid artery.
2. Carotid body tumour.
3. Branchial cyst
4. Branchiogenic carcinoma.
5. Thyroid swelling.
6. Lymph node swelling.
7. Stemomastoid tumour in a new bom baby.
8. Laryngocele.
(c) In the POSTERIOR TRIANGLE :
1. Enlarged supraclavicular lymph nodes.
2. Cystic hygroma.
3. Pharyngeal pouch.
4. Subclavian aneurysm.
5. Cervical rib.
6. Clavicular tumours.
7. Lipoma (Dercum’s disease).
8. Cold abscess.
In addition to the above list the following lesions can occur anywhere in the neck. These are :
1. Sebaceous cyst.
2. Lipoma.
3. Neurofibroma.
4. Haemangioma.
Common lateral swellings are :
1. Lymph node swelling.
2. Salivary gland enlargement.
3. Thyroid enlargement.
4. Branchial cyst.
5. Lipoma.
For clinical diagnosis the swellings of the neck can be divided into ACUTE SWELLINGS and CHRONIC
SWELLINGS.
Acute swellings are:
(i) Ludwig’s angina.
(ii) Boil.
(iii) Curbuncle.
(iv) Acute lymphadenitis.
Chronic swellings may be further subdivided into (a) cystic swellings, (b) solid swellings and (c) pulsatile
swellings.
(a) CYSTIC SWELLINGS are :
(i) Branchial cyst.
(ii) Thyroglossal cyst.
(iii) Dermoid cyst.
(iv) Cystic hygroma.
(v) Sebaceous cyst.
(vi) Cystic adenoma of the thyroid gland.
(vii) Cold abscess.
(viii) Abscess of the lymph nodes.
(ix) Plunging ranula.
(x) Pharyngeal pouch.
(xi) Laryngocele.
(xii) Retention cyst of salivary gland.
(b) SOLID SWELLINGS are:
(i) Swellings arising from the thyroid.
(ii) Swellings arising from the salivary gland.
(iii) Lymph node swellings.
(iv) Branchiogenic carcinoma.
(v) Stemomastoid tumour.
(vi) Carotid body tumour.
(vii) Cervical rib.
(c) PULSATILE SWELLINGS are :
THE NECK 503
(i) Aneurysm of the carotid artery.

(ii) Aneurysm of the subclavian artery.
(iii) Carotid body tumour.
(iv) Lymph node swellings lying in close proximity to the carotid artery will elicit transmitted pulsatio
(v) A few primary toxic goitres.
The various pathological swellings are now described in detail in the following section.
DEVELOPMENT OF BRANCHIAL ARCHES —
The lower part of the face and the whole of the neck, which subsequently intervene between the mouth and the
pericardium, owe their formation to the development of a series of six visceral arches. These arches, in lower vertebrates,
provide for water-breathing animals an efficient respiratory apparatus which are called ‘gills ’. The branchial clefts in these
animals breakdown and a series of gill slits develop which communicate between the exterior and the inside of the pharynx.
Periodically the oxygen-bearing water is taken into the pharynx through the mouth and expelled through the gill slits. In
its passage it bathes into the endodermal surfaces of the branchial arches filled with capillaries. The blood gives up its
carbondioxide and absorbs fresh oxygen in its place.
In human beings at first the arches form rounded ridge-like projections in the overlying ectoderm and corresponding
projections in the entodermal floor of the pharynx. These ridges are separated from one another by a series of furrows, where
the surface ectoderm and the pharyngeal entoderm come into direct contact with each other. The ectodermal furrows are
termed the branchial clefts and the entodermal furrows the pharyngeal pouches. At this stage the pharynx possesses a wide
roof and a wide floor which meet on each side and there is no true lateral wall.
So each arch consists of an ectodermal covering, a mesenchymal core and an entodermal covering. The mesenchymal
core gives rise to skeletal element, striated muscles, vessels and nerves. The innervation of the muscle masses once
established will persist, no matter how far the muscle may migrate from the site of its development.
Mesodermal derivatives of the branchial arches.—
FIRST ARCH OR MANDIBULAR ARCH :
I. Skeletal elements.—The skeletal element of first arch is termed Meckel’s cartilage. Its dorsal end forms — (i) the
incus; (ii) the malleus with its anterior process. The intermediate portion disappears but its sheath persists as (iii) anterior
ligament of the malleus and (iv) sphenomandibular ligament. The succeeding portion is enveloped by the (v) developing
mandible. The part extending from-the mental foramen to the symphysis menti is by cartilaginous ossification and the rest
is membraneous bone.
II. Muscular elements develop into (i) tensor tympani, (ii) tensor veli palatini and muscles of mastication which
include (iii) the masseter, (iv) temporalis muscle, (v) medial and lateral pterygoids, (vi) mylohyoid and (vii) anterior belly
of the digastric.
HI. Nerve.— Mandibular division of the trigeminal nerve (5th cranial nerve).
IV. Artery.— The first aortic arch disappears entirely. According to some the maxillary artery may be the remnant of
the first aortic arch.
SECOND ARCH OR HYOID ARCH :
I. Skeletal elements.— The dorsal end forms the (i) stapes. Thereafter it forms as it passes ventrally (ii) styloid
process, (iii) stylohyoid ligament, (iv) the lesser cornu and (v) the upper part of the body of the hyoid bone.
EL Muscular elements form (i) the stapedius, (ii) the stylohyoid, (iii) the posterior belly of the digastric, (iv) all
muscles of facial expression including occipito-frontalis and buccinator, (v) the platysma, (vi) the auricular muscles.
III. Nerve.— The facial nerve (7th cranial nerve) is the nerve of this arch.
IV. Artery.— The dorsal end of the second arch remains as the stem of the stapedial artery whilst the remainder of the
artery disappears.
THIRD ARCH :
I. Skeletal elements.— The dorsal portion does not chondrify. The ventral portion chondrifies and persists as the
(i) greater comu of the hyoid bone and (ii) lower part of whole of the body of the hyoid.
II. Muscular elements.— The stylopharyngeus can be attributed definitely to have been derived from the third arch.
HI. Nerve.— The glossopharyngeal nerve (9th cranial nerve).
IV. Artery.— The whole of the artery of the third arch persists. The external carotid artery appears as a sprout from
the middle of the third arch and grows headwards. The ventral portion of the arch upto the sprout forms the common carotid
artery and the dorsal portion from the sprout forms the internal carotid artery.
FOURTH ARCH :
I. Skeletal elements.— (i) Thyroid cartilage, (ii) some controversy remains regarding the epiglottis. Though a few
consider this to have developed from this arch, but majority agree that this is developed in the substance of the hypobranchial
eminence and does not represent a branchial arch cartilage.
II. Muscular elements.— Muscles of the pharynx which are supplied by the (i) superior laryngeal nerve and also
(ii)cricothyroid.
HI. Nerve.— The superior laryngeal nerve.
IV. Artery.— On the right side it forms the first part of the right subclavian artery. On the left side it forms the main
part of the arch of the aorta.
FIFTH ARCH :
I. Skeletal elements.— (i) Some consider that cricoid develops from this arch. It probably also contributes to the
development of (ii) thyroid cartilage.
II. Muscular elements.— It is confusing regarding development of other muscles of the larynx. A few may develop
from this arch.
HI. Nerve.—It is controversial which is the nerve of this arch. But in lower animals the nerve to the fifth arch is a branch
of the vagus.
IV. Artery.— The artery of this arch disappears.
SIXTH ARCH :
I. Skeletal elements.—Many believe that (i) cricoid cartilage and (ii) arytenoid cartilage are derived from this arch.
II. Muscular elements.— (i) All intrinsic muscles of the larynx except cricothyroid; (ii) All muscles of the pharynx
except Stylopharyngeus; (iii) All the muscles of the palate except the tensor palati.
III. Nerve.— The recurrent laryngeal nerve canying the fibres of the cranial accessory nerve.
IV. Artery.— The ventral part forms both the branches of the pulmonary artery. The dorsal part disappears on the right
side, while it persists on the left side as ductus arteriosus communicating with the arch of the aorta. Ductus arteriosus after
birth becomcs obliterated and forms ligamentum arteriosum.
BRANCHIAL CYST
DEVELOPMENT.—
The second arch or the hyoid arch grows ventrally as also caudally and it grows at a greater pace than th
third and the fourth arches. The second arch gradually overlaps over the third and fourth arches at the end
the fifth week. The ridge produced by this arch grows downwards and meets caudally a smaller bridge term
the epipericardial ridge just above the pericardium. According to some it meets the fifth arch and the two fuse
A small depression is formed which lies superficial to the third and fourth arches and deep to the second ar
This depression is called nreccvical sinus. Ultimately this sinus disappears. But if this sinus persists, it forms
a cystic swelling at the upper part of the neck, which
is called the BRANCHIAL CYST. So in fact, third
and fourth arches do not take part in forming the
ectodermal covering of the neck. From the ridge
formed by the second branchial arch develops the
stemomastoid and the trapezius muscles. If the sec
ond arch fails to fuse with the 5th arch or epiper
icardial ridge, a fistula develops and it connects the
precervical sinus. It is called BRANCHIAL SINUS
OR FISTULA.
OTHER THEORY of branchial cyst is that it may
develop from the inclusion of parotid epithelium in
the upper deep cervical lymph nodes (Illingworth).
Pathology.—
The cyst is usually lined by stratified squamous
epithelium. If it arises from the internal branchial
furrow the epithelium may be columnar and ciliated.
The striking feature of this cyst is that its wall contains large amount of lymphoid tissue. For this, the cyst is
THE NECK 505
prone to infection and this has laid to Illingworth’s theory of inclusion of ectopic epithelium in upper deep
cervical lymph nodes. The contents are viscid, mucoid, cheesy material and cholesterol crystals in large
numbers.
1. Age.— Though congenital, yet it does not manifest itself before puberty. Majority of the patients
are between 20 to 25 years or even later. This is because the fluid which it contains takes this time to accumula
2. Sex.— Equal distribution of sex is noticed.
SYMPTOMS.—
Painless swelling in the upper and lateral part of the neck is the main symptom. If infected the swelling may
be painful and it becomes difficult to differentiate from acute lymphadenitis, chronic lymphadenitis or
tuberculous lymphadenitis and cold abscess.
PHYSICAL EXAMINATIONS.—
(i) Site.— Branchial cyst occupies upper and lateral part of the neck deep to the upper-third of the
stemomastoid muscle. It protrudes from beneath the anterior border of the stemomastoid. The stemomastoid
muscle develops from the migrated myotome in the ridge of the second branchial arch which covers the pre-
cervical sinus. The branchial cyst develops from the precervical sinus, so it will always be deep to the
stemomastoid muscle.
(ii) Size and shape.— It may be round, but is usually oval in shape with its long axis running forwards
and downwards. It is of variable size and may attain the size of an orange. Majority are between 5 to 10 cm in
diameter.
(iii) Surface is smooth and the edge is distinct, but yields under the palpating fingers. The overlying skin
looks normal, though if infected, may be red and angry looking.
(iv) Consistency is soft When the content is under tension, feel may be firm or even hard. Fluctuation
test will be positive, but is difficult to elicit when the cyst is small and the stemomastoid muscle is thick.
(v) Transillumination test is usually negative, but may be positive if the content is clear fluid (rarely
present).
(vi) Mobility.— The lump is not freely mobile as it is particularly deep to stemomastoid.
(vii) Regional lymph nodes are usually not palpable unless the cyst is infected.
(viii) The cyst cannot be reduced or compressed.
(ix) On aspiration cholesterol crystals can be demonstrated in the aspirated fluid.
Students should remember that cysts containing cholesterol crystals are :—
1. Branchial cyst.
2. Dental cyst.
3. Dentigerous cyst.
4. Cystic Hygroma (not always).
5. Old hydrocele.
6. Thyroglossal cyst (not always).
Complications.—
(a) Recurrent infection due to presence of lymphoid tissue in the wall of the cyst.
(b) The cyst may burst or due to inadvertent incision a fistula may develop, which is often called an
acquired branchial fistula.
Treatment.—
Excision is the treatment of choice. Incision is made parallel to the skin crease (along the Langer’s line). One
must be particular not to leave behind a portion of the cyst wall. To ensure this, dissection must be made
carefully. Some amount of the content may be aspirated before dissection so that the wall of the cyst may be
grasped with suitable forceps without injuring it. Sometimes it extends between the origins of the internal and
external carotid arteries upto the pharyngeal wall. Hypoglossal and glossopharyngeal nerves lie deep to the cy
and they should be protected. The cyst usually lies deep to the posterior belly of the digastric. The spinal
accessory nerve also lies deep to the cyst and should be protected.
BRANCHIAL FISTULA
By the term ‘branchial fistula’ we mean congenital branchial fistula developed from failure of fusion
between the second branchial arch with the 5th.
‘Acquired branchial fistula’ may occasionally be seen due to (i) infection of the branchial cyst and
subsequent rupture or (ii) due to inadvertent incision on the infected branchial cyst with the wrong diagno
of an abscess. It is usually situated in the upper or middle thirds of the neck and often continues to dischar
Congenital branchial fistula is often a branchial sinus without any communication inside. From the
development it is clear that branchial fistula represents a persistent second branchial cleft which covers the
and fourth branchial arch. So usually there should not be any internal opening and in the true sense it is a
‘branchial sinus’. The membrane which intervenes between the second branchial cleft and the second branc
pouch which forms the supratonsillar fossa at times may disappear or perforate by injudicious use of prob
then a branchial sinus becomes a branchial fistula and opens in the anterior aspect of the posterior pillar of
fauces, just behind the tonsil.
Course of the branchial fistula.— From its opening on the skin the fistula passes subcutaneously to the
level of the upper border of the thyroid cartilage where it pierces the deep fascia. The fistula then passes th
the bifurcation of the common carotid artery being superficial to the internal carotid artery and deep to the
external carotid artery. As the fistula arises from the second branchial cleft being covered by the second
branchial arch superficially, so all the structures derived from the second arch will be superficial to this fis
and the structures developed from the third branchial arch will lie deep to this fistula. Internal carotid arte
derived from the third arch while the external carotid artery sprouts out of the third arch and immediately
becomes superficial, so the fistula traverses between these two arteries. The fistula passes deep to the poste
belly of the digastric and the stylohyoid muscle. It crosses superficial to the internal jugular vein and the
hypoglossal nerve, the glossopharyngeal nerve and the stylopharyngeus muscle (derivatives of 3rd arch).
pierces the superior constrictor muscle and opens on the posterior pillar of the fauces behind the tonsil.
Pathology.— The fistula has a muscular coat and an inner epithelial lining. The stratified squamous
epithelium or pseudostratified ciliated columnar epithelium forms the epithelium lining. According to a fe
pathologists columnar ciliated epithelium forms the epithelium lining. But since this fistula is remnant of
branchial cleft there is more possibility that the lining will be stratified squamous variety. Patches of lymph
tissue may be seen deep to this epithelial lining. Due to the presence of lymphoid tissue recurrent inflamm
is common and not infrequently the epithelial lining is replaced by chronically inflamed granulation tissue
It often discharges from the external opening either mucoid or mucopurulent fluid.
Diagnosis.— (i) It may be unilateral and in 30% of cases it may be bilateral.
(ii) It may be seen at any age but most commonly seen in 2nd decade. As the condition is not much
troublesome patients often come to the clinician late.
(iii) The position of the external opening of the fistula is quite characteristic. It is nearly always situated in
the lower third of the neck near the anterior border of the stemomastoid muscle (cf. branchial cyst which is
situated in the upper part of the neck, so the acquired branchial fistula is seen at this region).
(iv) The surrounding skin may be excoriated due to discharge.
(v) Swallowing will cause the external fistula to be tucked in causing the dimple prominent.
Treatment.— If the fistula becomes troublesome with discharge of mucus and repeated inflammation, the
treatment is excision of the fistula track. A sinogram may be made by injecting radio-opaque dye into the
fistulous track to know the upper limit of the fistula.
First method.— A ureteric catheter may be passed up the track. An incision is made high up in the neck
the skin crease (Langer's line) and the dissection is continued to get the upper limit of the track to the fork
the common carotid artery towards the pharyngeal wall. When the upper dissection is completed, the exte
orifice is freed by a small elliptical incision on the skin and whole of the lower part of the track is dissected
THE NECK 507
through the upper incision. Both the incisions are closed.

Second method.— In the beginning an elliptical incision is made around the external opening and the
dissection is continued upward through the superficial fascia and platysma upto the upper border of the th
cartilage where it penetrates through the deep fascia. Gentle traction to the fistula track will facilitate
identification of the fistula and its dissection upwards. A second incision may be required above the upper
of the thyroid cartilage transversely placed along the Langer’s line. The upper part of the track is dissected
through this incision upto the pharyngeal wall. This is ‘stepladder pattern’ dissection of the branchial fistula
Both the incisions are closed with or without drainage. During dissection one must be careful, as many imp
nerves and blood vessels, which have been discussed earlier, are around.
Complete removal is necessary to avoid recurrence.
BRANCHIOGENIC CARCINOMA
This is a rare tumour which arises from the remnants of the branchial clefts. This is a deep-seated carcino
with no other primary tumour ever discovered. As a matter of fact a clinical diagnosis of branchiogenic
carcinoma is rarely justified until and unless one very clearly excludes primary growth in the mouth, tongu
pharynx, larynx and external auditory meatus. Again at times a primary carcinoma of the mouth or pharyn
remain silent for months, the only evidence of its presence being a deep-seated cervical lymph node.
This carcinoma is commoner in males and is situated deep in the neck near the bifurcation of the commo
carotid artery. It infiltrates the surrounding structures and metastasises to the regional lymph nodes. Micros
cally, the tumour consists of squamous or transitional cells arranged in masses, in the centre of which cavitie
may appear due to necrosis. Lymphoid tissue may be seen here and there, as is seen in a branchial cyst.
CYSTIC HYGROMA
It is a cystic swelling which contains multiple locules of clear lymph.
DEVELOPMENT.— In human embryo at about the 6th week the lymph sacs develop six in number from
which the lymph vessels are derived. One pair in the neck called jugular lymph sacs develop near the origin
the internal jugular vein. One at the retroperitoneal tissue and another lymph sac is called cy sterna chyli. A
pair develops near the inguinal region below the bifurcation of the common iliac vein. This pair is called
posterior lymph sac.
The jugular lymph sac is first to appear at the junction of the subclavian vein with the anterior cardinal v
which ultimately forms the jugular vein. Sequestration of a portion of the jugular sac from the lymphatic sys
which fails to join the regular lymphatic system accounts for the appearance of cystic hygroma.
Pathology.— The swelling consists of aggregation of cysts which contain clear lymph. It can be considered
as a multilocular swelling containing clear lymph. Each locule is lined by a single layer of endothelium. Tha
is why this swelling is a brilliantly translucent swelling. Many locules or cysts may intercommunicate with o
another. Cystic hygroma may infiltrate into the muscle planes and these extensions may grow deep.
Sites of cystic hygroma.—
(i) Posterior triangle of the neck is the commonest site. The swelling gradually extends upwards toward
the ear or downwards towards the axilla. The swelling may attain such a huge size that it becomes difficult
know which is the actual site of origin. In a few text books it is described as an anterior triangle swelling.
(ii) In the cheek.
(iii) In axilla.
(iv) In the groin. 1
(v) In the mediastinum. J rare'
These sites should be carefully looked for such swelling.
Age.— It is the earliest swelling one can see in the neck. It manifests in early infancy. Occasionally it is
present at birth. Rarely it may be present before birth and if attains a large size may obstruct labour.
SYMPTOMS.—The only complaint is the lump or swelling. The parents bring the children for disfigure
ment.
(i) Site.— Its usual position is at the lower third of the neck in the posterior triangle.
(ii) Size and shape.—The size varies extremely. It is usually round in shape with smooth indistinct margin
which yields to the palpating finger.
(iii) Surface.—Surface is smooth or lobulated. When multiple cysts or locula remain very near the surface,
it may be lobulated. Usually large cyst remains towards the surface and gives a smooth surface.
(iv) Consistency.— It is extremely soft and cystic and fluctuation test is positive.
(v) Impulse on coughing.— This swelling gives an impulse on coughing. When the child coughs or cries
the swelling visibly increases in size.
(vi) Compressibility.— The swelling is partially compressible, as the fluid in one loculus passes into the
others. But this cannot be reduced.
(vii) Translucency test.— It is a brilliantly translucent swelling and this is important for differential
diagnosis. During this test multiple septi may be noticed.
(viii) Regional lymph nodes are not enlarged.
Complications.—
(i) Sometimes the growth is extremely rapid and may cause respiratory difficulty. In this case immediate
aspiration of as much content as possible is necessary. Tracheostomy may be required if this does not relieve
respiratory difficulty.
(ii) Swelling may become infected as a result of nasopharyngeal infection.
(iii) Spontaneous recovery may take place particularly when the swelling becomes inflamed. Subsequent
fibrosis will help spontaneous regression.
Treatment.—
Excision is the treatment of choice. Such excision may be delayed under strict follow-up till the child attain
a reasonable age for excision.
Preliminary injections of boiling water into the cysts at weekly interval will cause regression of the swellin
to a certain extent. The cyst wall becomes more fibrous. This should be followed by excision of the cyst.
Preliminary injection will facilitate dissection. One must be careful to excise all the extensions through the
muscle planes.
Dangers of incomplete removal.— (i) It may cause recurrence.
(ii) Continuous fluid and electrolyte loss through the open cysts will cause dehydration of the child.
(iii) It may lead to wound infection.
Radiotherapy may be tried in case of recurrence and when surgery is not possible. This swelling is
radioresistant and hardly acts to radiotherapy.
THYROGLOSSAL CYST
It is a cystic swelling developed in the remnant of the thyroglossal tract.

Development.— From the ventral portion of the entoderm between the first and second branchial arch, a
diverticulum extends downwards and forms the median thyroid diverticulum. This diverticulum moves
downwards and comes in front of the thyroid cartilage to form the isthmus and pyramidal lobe of the thyroid
gland. This tract is known as thyroglossal tract. The hyoid bone which is developed from the second and third
branchial arches come in very close relation with this tract. The entoderm from where the tract or the
thyroglossal duct started ultimately forms the foramen caecum of the tongue.
The course of the thyroglossal tract or duct.—The thyroglossal duct passes down from the foramen caecum
of the tongue between the genioglossi muscles. Then it passes along the midline downwards. It descends eith
in front of the hyoid bone or through the hyoid bone or it hooks below and behind the hyoid bone and then
THE NECK 509
descends downwards along the midline to the upper border of the thyroid cartilage. It then moves slightly t
the left and ultimately ends in the pyramidal lobe of the thyroid gland.
Ultimate fate of the thyroglossal duct.— (i) From the origin of the duct in the foramen caecum ectopic
thyroid tissue may develop and form lingual thyroid. This lingual thyroid is a red rounded swelling at the ba
of the tongue at the foramen caecum. It may represent the only thyroid tissue present.
(ii) The entire duct usually disappears except the lower portion which forms the isthmus of the thyroid
gland and the pyramidal lobe.
(iii) The upper portion of the duct from the foramen caecum to the hyoid bone may disappear but the res
of the duct or tract persists as the levator glandulae thyroidae.
(iv) While the tract disappears, a portion of the duct may remain patent which gives rise to a cystic swell
due to accumulation of secretions and this is known as thyroglossal cyst. This is an example of tubulodermoid.
(v) An ectopic thyroid may occupy subhyoid position in the midline and simulate a thyroglossal cyst. It
may be the only thyroid tissue present in the body.
Pathology.— The thyroglossal cyst is lined by pseudostratified ciliated columnar epithelium. There may
be squamous lining and mucous glands. There may be some lymphoid tissue outside the epithelial lining, fo
which this cyst is prone to become infected. It may contain thyroid tissue. The contents are usually mucoid a
become thickened by desquamated epithelial cells or debris. Cholesterol crystals may be present. Carcinoma
tous changes may occur in a thyroglossal cyst.
History.— 1. Age.— Thyroglossal cyst may appear at any age, but majority of the patients are between 15
to 30 years of age.
2. Sex.— This cyst is more commonly seen in women.
Symptoms.— 1. The commonest symptom is a painless swelling in the neck. It is usually a midline swellin
except when it is below the thyroid cartilage where it may shift to one side, more commonly to the left.
2. Duration of symptoms.— The lump may be present for many years before the patient comes to the
doctor. It is usually an increase in size which brings the patient to a clinician.
3. Pain in the cyst is almost always associated with infection of the cyst.
4. Systemic symptoms are never seen in this condition.
Examinations.— 1. POSITION.— A thyroglossal cyst may develop anywhere along the thyroglossal tract
starting from foramen caecum to the isthmus of the thyroid gland, but according to frequency, its position m
be as follows :—
(a) Subhyoid position (below the hyoid bone);
(b) In the region of the thyroid cartilage (may be deviated to the left side);
(c) Suprahyoid position (above the hyoid bone);
(d) At the level of the cricoid cartilage;
(e) In the floor of the mouth;
(0 Beneath the foramen caecum.
2. SIZE AND SHAPE.—Thyroglossal cyst is spherical or oval with the long axis along the thyroglossal
tract. The cyst varies in size from 0.5 cm to 5 cm in diameter. Due to prominence of the swelling being in fron
of the neck, patient often presents early even when it is small.
3. TENDERNESS.— The cyst only becomes tender if it is infected.
4. CONSISTENCY.— Though it is a cystic swelling, yet the consistency is often firm or hard depending
upon the tension of fluid within the cyst.
5. FLUCTUATION TEST is usually positive. When the cyst is a small one, Paget's test should be
performed.
6. TRANSELLUMINATION TEST may occasionally be positive, but due to the thick content with
epithelial debris it is usually negative.
7. MOBILITY.—The cyst can be moved sideways but not vertically (along the length of the thyroglossal
duct) as the cyst is tethered by the remnant of the thyroglossal duct.

The cyst moves with deglutition (because the swelling is attached to the hyoid bone.by fibrous tissue).
The PECULIARITY of the thyroglossal cyst is that it moves up with protrusion of the tongue. This can be
examined by asking the patient to open her mouth. The clinician holds the cyst with his thumb and forefinge
The patient is asked to protrude her tongue. The clinician willfeel that the swelling slips out of his grip and m
up. Absence of this sign does not exclude the diagnosis as majority of the cysts are below the level of the hyoid
bone and usually loses attachment with the tongue and so this test becomes negative.
8. REGIONAL LYMPH NODES are usually not enlarged unless the cyst is infected.
1. Subhyoid bursal cyst.— Though this cyst moves on deglutition, yet it does not move up with protrusio
of the tongue. Moreover this cyst has a particular position with transversally oval in shape, whereas thyrogl
cyst is usually spherical and differs in position.
2. Sublingual dermoid is often difficult to differentiate from suprahyoid thyroglossal cyst. Again mobility
with deglutition and protrusion of the tongue will help in the diagnosis.
Complications.—
1. Recurrent infection;
2. Fistula formation;
3. Carcinoma, though rare, may arise in the thyroglossal cyst. Mostly this is adenocarcinoma of thyroid
origin due to inclusion of the thyroid tissue in the wall of the duct.
Treatment.—
A thyroglossal cyst should be excised as a routine, as due to the presence of lymphatic tissue in the wall
infection is inevitable. An infected cyst often looks like an abscess and incision will lead to the formation of
a sinus. Excision of the cyst should also include any persistent portion of the track, otherwise recurrence is
inevitable. The intimate relationship between the track and the body of the hyoid bone, necessitates excision
of a segment of the bone from the midline to make sure that this portion of the track has been excised.
THYROGLOSSAL FISTULA
Aetiology.— It is never congenital. This acquired sinus or fistula originates from —

(i) Bursting of an infected thyroglossal cyst.
(ii) An incision on the infected thyroglossal cyst with the mistaken diagnosis of an abscess.
(iii) Incomplete removal of the thyroglossal cyst.
Pathology.— It must be remembered that though a thyroglossal sinus or fistula is an acquired condition it
is almost always associated with the congenital abnormality of peristence of the thyroglossal tract. This tract
is lined by columnar epithelium. This sinus is covered with a hood of skin with its concavity downwards du
to more growth of the neck as a whole in comparison to that of the thyroglossal tract. This sinus often discha
mucus and is the site of recurrent attacks of inflammation.
Clinical features.— (i) It is usually seen between the ages of 15 to 40 years.
(ii) The patient often gives history that the fistula closes by itself. After an interval of time it becomes
infected and painful, then it starts discharging with relief of pain. After a few days the fistula closes again.
On careful enquiry one can get the history of presence of a previous swelling (thyroglossal cyst) which was
infected and subsequently burst with the development of this sinus or somebody attempted incision of the cy
to drain it.
(iii) The position of the fistula is usually in the midline but varies — it may be either suprahyoid, subhyoid
or in front of the thyroid cartilage.
(iv) The fistula may be infected with red hot surrounding skin. Otherwise the skin around the fistula is
usually normal.
(v) Characteristic feature of the fistula is that it is covered with a hood of skin or semilunar fold of skin
THE NECK 511
just above the fistula. If the tongue is protruded the fistula will be pulled up with prominence of the dimple.
Treatment.—
Excision of the fistula alongwith the thyroglossal tract as far as possible upto the base of the tongue is the
treatment of choice. If a portion of the thyroglossal tract is left behind there is chance of recurrence. Presence
of any ectopic thyroid tissue along the thyroglossal tract must be excluded since excision of this thyroid tissu
may lead to myxoedema since this may be the only thyroid tissue present in the body.
Sistrunk’s operation is usually performed where a horizontal elliptical incision is made circumcising the
sinus opening and the tract is followed up and dissected upto the hyoid bone. Another transverse collar incis
is made in front of the hyoid bone and a portion of the middle of the hyoid bone is excised and the tract rema
attached to this excised portion of the hyoid bone. The tract is further followed up to the base of the tongue an
excised.
SUBLINGUAL DERMOID CYST
It is a congenital sequestration dermoid cyst and is formed by inclusion of the surface ectoderm at the fusi
line of the first branchial arch or the mandibular arch. Such cysts are always in the midline and may be above
or below the mylohyoid muscle.
Pathology.—It is a thin walled cyst lined by squamous epithelium and the wall contains hair follicles, swe
glands and sebaceous glands. The content is cheesy material which is sebaceous material secreted by the
sebaceous glands in the lining epithelium. Unlike other dermoid cysts, it never contains hair.
Types.—Usually this is a midline cyst, yet a few dermoid cysts are seen to be of lateral variety. These latera
variety cysts usually derive from the second branchial cleft. So the types are :
1. MEDIAN VARIETY —
(a) Supramylohyoid variety;
(b) Inframylohyoid variety.
2. LATERAL VARIETY —
(a) Supramylohyoid variety;
(b) Inframylohyoid variety.
Clinical features.— 1. Age.— Though it is a congenital swelling, yet patients usually present between the
ages of 10 and 25 years.
2. Sex.— Both sexes are equally involved.
SYMPTOMS.—
Patients usually complain of a painless swelling under the tongue in the floor of the mouth or just below the
point of the chin. It is usually painless, but when the swelling suddenly increases in size, patient may complai
of pain. Very rarely the contents become infected and the cyst becomes painful and tense.
Physical examinations.—
1. MEDIAN VARIETY :
(a) Supramylohyoid Variety or Sublingual Variety :—
(i) It is a midline swelling on the floor of the mouth.
(ii) Mucous membrane of the mouth over the swelling is usually normal. The cyst is usually spherical
and by the time the patient comes to the clinic it is usually 2 to 7 cm in diameter.
(iii) The surface is smooth with definite edge.
(iv) It is a cystic swelling and fluctuation test is positive. Bimanual palpation will reveal the extents of
the cyst and gives a better idea regarding fluctuation.
(v) Transillumination test is usually negative (cf. ranula).
Ranula.—It is usually on one or the other side and not a typical midline swelling. It is a brilliantly transluce
swelling.
(b) INFRAMYLOHYOID or CERVICAL VARIETY :—

(i) It is a swelling in the submental region and gives rise to a ‘double chin’ appearance.
(ii) The overlying skin is usually normal.
(iii) Bimanual palpation will give a clear idea regarding the extent of the cyst and fluctuation.
(iv) Fluctuation test is positive.
(v) Transillumination test is negative.
(vi) It does not move up with deglutition.
(vii) It does not move with protrusion of the tongue.
(i) Suprahyoid thyroglossal cyst — which moves up with protrusion of the tongue.
(ii) Submental lymph node swelling.
2. LATERAL VARIETY :
(a) SUPRAMYLOHYOID VARIETY:—
It is an opaque cystic swelling in the floor of the mouth on one side or the other. Transillumination test
negative.
Ranula — transillumination test is positive.
(b) INFRAMYLOHYOID VARIETY I—
It is a cystic swelling in the submandibular region. Bimanual palpation is extremely necessary to know t
extent of the cyst and to exclude plunging ranula.
(i) Plunging ranula — transillumination test is positive.
(ii) Submandibular lymph node swelling — solid swelling.
(iii) Submandibular salivary gland swelling — solid swelling.
Treatment.—
Total excision is the treatment of choice.
Supramylohyoid varieties are approached through the floor of the mouth.
Inframylohyoid varieties are approached through the neck by curved incision along the Langer’s line ov
the cyst. Plastic surgeons would prefer to excise these cysts through the floor of the mouth by retracting the
posterior border of the mylohyoid muscle.
DEEP OR PLUNGING RANULA
When a typical ranula is associated with cervical prolongation, it is called a deep or plunging ranula. Th
type of ranula passes beyond the floor of the mouth along the posterior border of the mylohyoid muscle an
appears in the submandibular region. For description of ranula the students are referred to the chapter of
‘MOUTH’. This ranula may be derived from the cervical sinus and thus an embryological remnant.
Diagnosis.— Whenever a case of ranula is detected on the floor of the mouth, the submandibular region
of the neck should be examined by inspection and palpation.
Bidigital palpation of the swelling.— One finger is placed in the oral cavity and the other on the
submandibular region of the neck. Cross fluctuation can be elicited by pushing one finger and palpating th
impulse by the other finger and vice-versa.
Complications.— (i) This may burst due to repeated trauma and reappear.
(ii) Ranula may be rarely infected.
(iii) A big ranula may cause difficulty in eating and speech.
(i) Sublingual dermoid.— This swelling is more often a midline swelling. This swelling is not translu
whereas a plunging ranula is brilliantly translucent.
THE NECK
513
(ii) Lipoma.
(iii) Submandibular lymph node swelling.
(iv) Submandibular salivary gland swelling.
Treatment.—
Treatment is excision of the ranula. In case of deep or plunging ranula, the incision should be made on the
neck along the Langer’s line. So the approach is through the neck. Excision must be complete and no wall of
the sac is left behind.
STERNOMASTOID TUMOUR (CONGENITAL TORTICOLLIS, FIBROMATOSIS COLI)
Though it is called congenital torticollis, yet it is not a true congenital abnormality.

Aetiology.—(i) Infarction of the central portion of one stemomastoid muscle at the time of birth is the most
accepted aetiology. The infarcted muscle is gradually replaced by fibrous tissue which contracts. This infarct
is often caused by a temporary acute venous obstruction within the muscle substance in utero or during labo
(ii) Many pathologists consider that it is a congenital anomaly and may be associated with other congeni
anomalies such as dislocation of the hip.
(iii) The same theory of infarction remains but some pathologists consider that the stemomastoid branch
of the superior thyroid artery is affected. This is an ‘end artery’ which supplies the middle part of the
stemomastoid muscle. It is often found obliterated in association with stemomastoid tumour.
(iv) Trauma.— Trauma may be inflicted to the stemomastoid muscle during delivery and may tear a few
of its fibres. A haematoma results and which is replaced by fibrosis and tumour formation.
Clinical features.—Age.— This is one of the earliest swellings found in the neck. It may be noted within
several days to several months after birth.
SYMPTOMS.— The mother often notices the lump. So the main complaint is the swelling. She may also
find that the child keeps his head turned to one side—torticollis. Any attempt to turn the head straight will ca
pain. As the child grows the head becomes turned to one side and tilted towards the other side — torticollis.
usually does not appear before the age of 4 years as it becomes obvious with the growth of the length in neck
At this age the fibrous contracture of the affected stemomastoid will cause this deformity.
EXAMINATIONS.—
(i) Position.—The stemomastoid tumour usually lies in the middle of the stemomastoid muscle i.e. in the
middle third of the neck on its lateral side.
(ii) Tenderness.—This tumour may be tender in the first few weeks of the life. The child often cries as soo
as the swelling is palpated.
(iii) Size and Shape.— It is usually 1 to 2 cm in diameter. The swelling is fusiform in shape along the long
axis of the stemomastoid muscle.
(iv) Surface.— The surface is usually smooth.
(v) Edge.— The anterior and posterior edges of the tumour are distinct but the superior and inferior edge
are indistinct and continuous with the normal stemomastoid muscle.
(vi) Consistency.— In the beginning the swelling is firm, but gradually it becomes harder and begins to
shrink within the muscle to become impalpable later on.
(vii) Mobility.— The swelling is mobile sideways but not along the length of the stemomastoid muscle.
(viii) The regional lymph nodes are not enlarged and normal.
The neck.— All the movements of the neck should be examined. The child is too young to move the neck
actively as the clinician advises. Manipulate the head and neck very gently. Some sort of torticollis may be
present. There may be restriction of movements due to spasm of the stemomastoid muscle. Otherwise the ne
movements may be normal.
Gradually the swelling of the stemomastoid tumour subsides within a few months. The stemomastoid
muscle becomes contracted with the development of torticollis. The muscle at this stage will feel like a tight
33
cord.
The eyes.—Examine the eyes, particularly the movements of the eyeball to exclude presence of any squin
The torticollis may be secondary to squint and not a sternomastoid tumour.
X-ray.— All cases should be X-rayed to exclude any bony abnormality e.g. hemivertebra as the primary
pathology. But this is extremely rare.
Treatment.—
(i) If the sternomastoid tumour is noticed at birth, infant’s head is gently manipulated through the full
range of movement everyday. If this is maintained, the muscle will not get scope to be shortened and tortico
may not appear.
(ii) When the condition is noticed only after the torticollis has developed —
(a) A brace or harness may be used to correct the torticollis. Daily physiotherapy should be given to
stretch the affected sternomastoid muscle. But this may not be successful to correct the deformity.
(b) So operation is the only treatment of choice in this condition. The best technique is to divide the
sternomastoid muscle at its distal or proximal attachment by open method. In majority of cases both the head
(sternal and clavicular) at the lower end are divided by open method. Subcutaneous tenotomy is a blind
technique and should be avoided in children lest it should injure the major blood vessels deep to the
sternomastoid muscle. During division one must be careful not to injure the spinal accessory nerve or to inj
any blood vessel. Any soft tissue contracture (e.g. deep fascia etc.) or neighbouring muscle contracture (e.g.
scalenus anterior etc.) should be divided.
Postoperative care.— After operation the neck is kept in over-corrected position for about 6 months with
torticollis harness. After 6 months physiotherapy should be continued for both active and passive moveme
of the neck.
CAROTID BODY TUMOUR (POTATO TUMOUR; CHEMODECTOMA;

NON-CHROMAFFIN PARAGANGLIOMA)
Carotid body is a chemoreceptor organ situated near the bifurcation of the common carotid artery on ea
side. In the carotid body there are receptors which are stimulated by the rise in the PC02 or H+ concentratio
of arterial blood or a decline in its P02. Hyperventilation is produced by increase in arterial PC02. So these a
respiratory chemoreceptors and chemical control of respiration is adjusted by these chemoreceptors. Caroti
body consists of a number of separate lobules around which there is no true capsule. Within each lobule the
are solid nests of large pale-staining epitheloid cells or chief cells which are supported by a connective tissue
frame work in which there is sponge-like arrangement pf capillary sinusoids in addition to myelinated nerv
fibres and ganglion cells. The chief cells have finely granular eosinophilic cytoplasm and small uniform nuc
The chief cells are the chemoreceptor cells. There are also sustentacular cells surrounded by sinusoidal vesse
The sustentacular cells appear to be interposed between the blood and the chemoreceptor cells. The myelin
nerve fibres loose their myelin sheath and become non-myelinated nerve fibres which remain in contact wi
the cell membranes of the chemoreceptor cells but do not penetrate into these cells. The carotid body and th
aortic body are the chief peripheral chemoreceptors present in the human body. The carotid body is supplie
by the glossopharyngeal nerve whereas the aortic body is supplied by the vagus nerve. Through these affer
nerves impulses reach the respiratory centre. When the arterial blood becomes deficient in 02 or it contains
excess of C02 or H+ these cells are stimulated and thus respiration is stimulated (Hyperpnoea). PaC02 value
must be quite high to stimulate these peripheral chemoreceptors (carotidbody and aortic body), but slight C
excess or H+ excess will stimulate central chemoreceptors. Each carotid or aortic body is also called glomus.
The staining reactions of glomus tissue suggest that both acetylcholine and catecholamines are present. The
blood flow to each carotid body is enormous and much more than the blood flow to the brain and kidney. C
body is part of the non-chromaffin paragangliomas. So carotid body forms a part of the chemoreceptor syst
as well as non-chromaffin paraganglioma.
THE NECK 515
Sites.— (i) The carotid body and (ii) the aortic body are the two principal chemoreceptors. Besides these
there are (iii) chemoreceptors in the brain stem (central chemoreceptor) located near the respiratory centre its
on the ventral surface of the brain stem. These central chemoreceptors may also be present in pons, midbrain
and even in cerebral cortex. There are also (iv) pulmonary and (v) myocardial chemoreceptors in the pulmon
and coronary vessels respectively.
Other sites of non-chromaffin paragangliomas.—
(i) The carotid body at the medial aspect of the common carotid artery at the point of bifurcation, (ii) T
aortic body near the arch of the aorta at the points of origin of the left coronary artery and the innominate arter
(iii) The glomus jugulare, which is located in the adventitia of the jugular bulb, (iv) The glomus intravagale,
which is associated with ganglion nodosum of the vagus nerve, (v) The paraganglion tympanicum, which is
distributed along the tympanic branch of the glossopharyngeal nerve.
Besides these, tumours of chemoreceptor tissue have been found (vi) in the femoral canal in relation to the
femoral artery, (vii) in the small bowel mesentery and (viii) in the retroperitoneum.
Pathology.— The tumour is well capsulated. It looks yellow or orange on cut surface. This is a firm,
homogeneous and compact tumour, almost looks like a potato. So it is called the ‘potato tumour’. It is so
intimately adherent to the carotid artery that it is often impossible to excise the tumour without sacrificing pa
of the common, internal or external carotid artery.
Histologically, this tumour is composed of characteristic cell nests and alveolar arrangements of chief cells.
It almost shows the same histologic pattern of a normal carotid body. Occasionally this tumour may demonst
a moderately severe degree of nuclear pleomorphism. This tumour is considered to be a benign tumour and
remains localised for years. But regional metastasis occurs in about 20% of cases. Biologically aggressiveness
which gives rise to local or distant metastasis is seen in less than 5% of cases.
1. Age.— Highest incidcnce is seen between the ages of 40 and 60 years of life.
2. Sex.— This tumour occurs with equal frequency in men and women.
3. Though majority are unilateral, occasionally bilateral tumours may be seen. Tumours arising in other
non-chromaffin paraganglioma may be noticed.
4. A strong familial incidence has been recorded.
5. The main symptom is slow growing painless swelling at the bifurcation of the common carotid artery.
Since the swelling is painless, it attains the size of at least a plum before the patient comes to a clinician. It
increases in size very slowly.
6. Usually there is a long history.
7. If the lesion lies deep to the bifurcation of the carotid artery, compression of the oesophagus or larynx
is the first complaint.
8. Homer’s syndrome may be present. Similarly there may be unilateral paralysis of the vocal cord.
9. Patient may suffer from symptoms of transient cerebral ischaemia, e.g. blackouts, transient paraesthe-
sia or paralysis. But these are rare since compression of the carotid artery by the tumour is very slow. Pressure
on the tumour may give rise to syncopal attack.
(i) Position.— This tumour is situated at the bifurcation of the common carotid artery and therefore is see
in the upper part of the anterior triangle of the neck at the level of the upper border of the thyroid cartilage or
just below the level of the hyoid bone, under cover of the anterior edge of the sternomastoid muscle. The tumo
is beneath the anterior edge of the sternomastoid muscle and deep to the deep cervical fascia.
(ii) Tenderness and temperature.— This tumour is hot tender or hot and the overlying skin looks normal.
(iii) Size.— Carotid body tumour varies in size from 2 cm to 10 cm in diameter.
(iv) Shape.— Carotid body tumour is initially a round shaped swelling, but as it grows bigger, it becomes
irregular in shape, with narrower lower end caught between the bifurcation of the common carotid artery.
(v) Surface.— The surface is usually smooth, but it may be slightly bosselated.
(vi) Edge.— The edge is usually distinct

(vii) Consistency.— The majority of these tumours are solid and hard. This is called potato tumour.
(viii) Pulsation.— This tumour sometimes, not always, pulsates. This may be a transmitted pulsation as the
tumour lies on the carotid artery. Sometimes the external carotid artery runs over the superficial aspect of
tumour and this causes a pulsating tumour (expansile pulsation). Occasionally this tumour may be so vascu
that it pulsates (expansile pulsation).
(ix) Mobility.— This tumour cannot be moved vertically, though it can be moved sideways.
(x) Lymph nodes.— The regional lymph nodes are usually not enlarged.
1. Cervical lymph node enlargement, whatever may be the pathology.
2. Stemomastoid tumour.
3. Branchial cyst
4. Aneurysm of the carotid artery.
5. Thyroid gland enlargement.
6. Aberrant lateral thyroid.
1. Arteriography will definitely diagnose the condition and it will show splayed carotid fork due to
presence of tumour at the bifurcation. It may show the abnormal tumour vessels within the tumour.
2. Open biopsy is definitely confirmatory, but is dangerous as it may injure the carotid artery.
Treatment.—
Surgical excision is the only treatment available in this condition.
(i) In case of old individuals with a long history the tumour may be left as it is without any interference.
(ii) Otherwise in all cases the tumour should be explored by an adequate incision. If the tumour can be
dissected easily from the carotid artery, it should be removed.
(iii) When the tumour is large and inseparable from the carotid artery, the tumour should be resected
alongwith the bifurcation of the carotid artery. In such cases it is essential to maintain the blood supply to
brain by a temporary by-pass system. After excision of the tumour alongwith the bifurcation of the carotid
artery, continuity of the arteries is restored by dacron graft or autogenous vein graft.
(iv) This tumour is radio-resistant.
(v) General surgeons if come across carotid body tumour where adequate facilities are not avilable the
may simply take biopsy and handover the case to the neurosurgeons.
SUBHYOID BURSAL CYST

It is an enlargement of the subhyoid bursa with accumulation of inflammatory fluid within it. So it may
called subhyoid bursitis. The subhyoid bursa is situated below the hyoid bone and in front of the thyrohyoid
membrane.
(i) Pain with swelling just below the hyoid bone in the midline is the characteristic feature of this condition.
(ii) The swelling is oval with long axis placed transversely parallel to the hyoid bone (cf. thyroglossal c
(iii) As mentioned earlier it is also a midline swelling, which moves up with deglutition as it is attached
the hyoid bone. But it does not move with protrusion of the tongue.
(iv) It is a cystic swelling, so fluctuation test is positive. Transillumination test is negative as the fluid, i
contains, is turbid and not clear.
Treatment.— Complete excision of the cyst by making a transverse incision along the Langer’s line over
the cyst is the only treatment.
THE NECK 517
THE SWELLINGS, WHICH MOVE UP WITH DEGLUTITION, ARE:

1. Thyroid swellings.
2. Ectopic thyroid.
3. Thyroglossal cyst
4. Subhyoid bursal cyst or subhyoid bursitis.
5. Enlarged pretracheal lymph nodes which are fixed to the trachea.
6. Laryngocele.
Only thyroglossal cyst moves up also with protrusion of the tongue.
COLD ABSCESS IN THE NECK
A cystic lateral swelling of the neck may be due to cold abscess. ‘Cold abscess’ is an abscess which arises
from tuberculous origin. It is called ‘Cold’ as it is not as hot and red as pyogenic abscess. It is also much less
painful than pyogenic abscess.
Causes of cold abscess other than tuberculosis.—
1. Actinomycosis.— The pus from this fungal infection is also cold in nature and it produces multiple
sinuses.
2. Gumma degeneration may produce cold abscess but this is extremely rare.
3. Leprosy.— Nodular leprosy may produce cold abscess from degeneration.
Aetiology.— Cold abscess in the neck may be derived from aetiological sources.
1. From caseation of the tuberculous lymphadenitis in the cervical region. The cold abscess is often seen
in the anterior triangle.
2. From tuberculosis of cervical spine. In the case the cold abscess is usually present in the posterior
triangle.
PATHOLOGY.—
A. From tuberculous lymphadenitis.— Usually one group of cervical nodes is first infected. Most
frequently the upper jugular group of lymph nodes is affected. The source of infection is obviously the tubercle
bacilli and it is mostly the ‘human’ type and not the ‘bovine’ type that is responsible for tuberculous cervical
lymphadenitis. The tubercle bacilli gain entrance through the tonsil of corresponding side. The first stage is the
stage of lymphadenitis. In this stage the lymph nodes remain descrete and slightly tender. In the second stage
the lymph nodes become matted with perilymphadenitis. In the third stage the caseating material liquifies and
breaks through the capsules of the lymph nodes and a ‘cold abscess’ forms. In the beginning the cold abscess
remains deep to the deep cervical fascia. In a few weeks time the deep cervical fascia becomes eroded at one
point and the pus flows through the small opening into the superficial fascia. Now it is called a collar-stud
abscess. This means that the pus deep to the deep cervical fascia becomes continuous with the pus in the
superficial fascia through a small opening in the deep cervical fascia. The superficial abscess gradually enlarge
and forms the cold abscess which becomes obvious on inspection. In untreated cases the skin will soon become
red over the centre of the cold abscess. Gradually the skin in the centre gives way and a discharging chronic
sinus forms.
B. From caries (tuberculous) spine of the cervical region.— Cold abscess from tuberculosis of the
spine may either rupture anteriorly or posteriorly.
(a) Anterior rupture.— When the cold abscess ruptures anteriorly the pus will at first lie deep to the
prevertebral layer of the deep cervical fascia. Gradually it may follow one of the following tracks —
(i) The pus may flow downwards remaining behind the prevertebral fascia and enter into the superior
mediastinum.
(ii) The pus may flow laterally deep to the prevertebral fascia and behind the carotid sheath to reach the
posterior triangle behind the sternomastoid muscle.
(iii) In the upper cervical region the pus may bulge forward into the posterior wall of the pharynx and
forms the retropharyngeal abscess. It is central in position, but acute retropharyngeal abscess arising from
pharyngeal lymph nodes lies in front of the prevertebral fascia and will be on one side of the median septu
which stretches from the prevertebral fascia to the posterior wall of the pharynx.
(iv) In the lower cervical region the cold abscess may press forward on to the posterior wall of the
oesophagus.
_______ (v) In the axilla.— The pus flows through
M
fidBjSQPP J ^ into the open mouth of the axillary sheath, which
J J 4 nothing but a tubular sheath of the prevertebral fascia
j / carrying brachial plexus and the subclavian artery
towards the axilla. Thus the cold abscess gains the
, J axilla and upper part of the arm through the a
(b) Posterior rupture.— When the cold

abscess ruptures posteriorly it comes into the spinal
'! canal. From here it follows the anterior primary
< division of the cervical spinal nerves and appears in
f S ^ mn the posterior triangle.
From the posterior triangle the cold abscess may
travel along the cords of the brachial plexus and the
axillary artery into the axilla. From the axilla the
^ abscess may move further down along the course of
. the brachial artery.
CLINICAL FEATURES —
Fig.36.2.— Shows a tuberculous ulcer in the 1, Age.— No age is exempted, but cold ab-
lower part of the neck. ^ of[en seen jn youngI childrcn.
2. Sex.— No sex predilection is noticed.
3. Patients often give history of neckache (caries of the cervical region).
4. Patient may give a history of solid swelling previously in the region of the cold abscess.
5. Later on the patient presents with a swelling in the neck which is rather painless.
6. Other features of tuberculosis e.g. evening rise of temperature, anorexia, loss of weight, anaemia,
coughing etc. may be present.
7. There may be a family history of tuberculosis.
ON EXAMINATION.—
1. Site.—When it is secondary to tuberculous lymphadenitis cold abscess is in the anterior triangle. W
it is secondary to caries of the cervical spine cold abscess is seen in the posterior triangle.
2. Tenderness is slightly present.
3. Temperature is usually normal or slightly hot over the swelling. There is no brawny induration or
oedema as seen in pyogenic abscess.
4. The swelling is cystic, soft with an indistinct margin. Fluctuation test is always positive.
5. Transillumination test is usually negative (in contradistinction to cystic hygroma).
6. Matted lymph nodes may be palpable at the margin and in the depth of the cold abscess.
THE NECK 519
E.SJ?. (very diagnostic).

2. Sputum examination may show acid fast bacilli.
3. Aspiration of the abscess material should be examined in the following ways :—
(i) Ziehl-Neelsen stain for acid fast bacilli. Gram stain may be performed to exclude secondary
infection.
(ii) Culture of the material for tuberculosis.
(iii) Guineapig inoculation test.
4. Mantoux test is usually positive.
5. Other lymph node biopsy to know whether that is also affected by tuberculosis or not.
6. X-ray of the neck (anteroposterior and lateral views).— This is particularly required when there is
suspicion of caries spine affecting cervical region. The findings would be —
(i) Diminution of joint space between the affected cervical vertebrae.
(ii) Osteoporosis of the affected cervical vertebrae and destruction.
(iii) Soft tissue shadow of paravertebral cold abscess.
(iv) Calcified lymph nodes may or may not be seen.
7. X-ray of the chest — to exclude pulmonary tuberculosis with presence of affected hilar lymph nodes.
TREATMENT.—
Treatment consists of general treatment and local treatment.
GENERAL TREATMENT.—
1. Antitubercular drugs should be given according to the age of the patients. Injection Streptomycin,
INH and PAS were the usual combination for quite a long time. This treatment should be continued for at leas
1 ’/ years. Injection Streptomycin is given I.M. 1 g. daily for at least 3 months. INH is given 300 mg daily and
PAS 5 to 10 g. daily. These are adult doses. Presently various other antitubercular drugs have come up as
tuberculous bacilli are becoming resistant to the usual treatment described above. Rifampicin and Ethambutol
are often used now-a-days in the doses of 15 mg/kg body weight and 25 mg/kg body weight respectively. Wi
these drugs and other sophisticated drugs antitubercular treatment has been reduced to 9 months instead of
1V2 years previously.
2. Good food particularly high protein diet is extremely necessary. Vitamin supplements should always
be given, particularly vitamin B-complex and vitamin C.
3. Sanitarium regime is also necessary.
LOCAL TREATMENT.—
1. When the cold abscess is a small one, it may resolve with general treatment and no special treatment
is required.
2. When a big abscess is not responding to general treatment, aspiration is advised.
Technique of aspiration.— The needle should be inserted through healthy skin from above (avoiding
dependent part) to avoid chance of sinus formation. If aspiration is performed through the most prominent pa
of the skin which has become red and the most dependent part, there is every possibility that a sinus will deve
along the aspirated track.
3. When there are enlarged lymph nodes not responding to general treatment, excision of the lymph node
should be performed and those should be sent for histopathological report.
4. When the cold abscess is secondary to caries spine of the cervical region, immobilisation of cervical
spine is required with a plaster jacket known as Minerva jacket. It extends above covering the scalp and neck
(exposing the face and ear only) and extends below upto the nipple line in the chest. The plaster immobilisatio
is continued for 3 to 6 months.
5. When the cervical vertebrae are destroyed and become unstable, cervical spine fusion operation is
performed.
COLLAR-STUD ABSCESS
This has already been described above in the section of pathology. It is a bi-locular abscess with one locule
deep to the deep fascia and another locule in the superficial fascia. Both the locules intercommunicate with
other through a small perforation in the deep fascia. This may occur anywhere in the body.
Types.—
1. Pyogenic.— When a pyogenic abscess develops deep to the deep fascia and gradually the pressure
mounts so that the deep fascia perforates, the pus comes out into the superficial fascia. Such collar-stud abs
is more often seen in the hand where deep fascia is the palmar fascia.
2. Tuberculous.— This is more often seen in the neck from caseating tuberculous lymph nodes. The col
abscess beneath the deep fascia erodes and a portion comes out into the superficial fascia.
PHARYNGEAL POUCH (DIVERTICULUM OF THE PHARYNX)
AETIOLOGY.— Such diverticulum arises as a protrusion or herniation of the mucosa of the pharynx
through a weak spot in the posterior pharyngeal wall, known as Killian s dehiscence. This weak area lies
between the upper oblique fibres (known as Thyropharyngeus) and the sphincter-like transverse fibres (know
as Cricopharyngeus) of the inferior constrictor muscle of the pharynx. Both these parts of the inferior constric
muscle of the pharynx have different nerve supplies and functions.
THYROPHARYNGEUS PART.— The fibres of this part of inferior constrictor of pharynx are oblique in
direction as the fibres take origin (mainly) from the oblique line of the lamina of the thyroid cartilage and sp
backwards and medially and are inserted with the muscle of the opposite side into a fibrous raphe in the po
midline of the pharynx. Its main nerve supply comes from the pharyngeal branch of the vagus nerve which a
from the upper part of the inferior ganglion of the vagus nerve and consists principally of the fibres from th
cranial root of the accessory nerve. The main function of this part of the inferior constrictor muscle is to pro
the food following deglutition.
CRICOPHARYNGEUS PART.— The fibres of this part of the inferior constrictor arise from the side of
the cricoid cartilage and pass backwards horizontally to be continuous with the fibres of the opposite side an
are continuous below with the circular fibres of the oesophagus. This muscle surrounds the narrowest part
the pharynx and acts as a sphincter. During swallowing the Cricopharyngeus relaxes so that the bolus of fo
passes unhindered. Failure of such relaxation will result in an increased pressure within the lower part of th
pharynx and will cause herniation of the pharyngeal mucous membrane posteriorly through the weak spot
known as Killian’s dehiscence. Such herniation is known as pharyngeal pouch or diverticulum of the phary
So it is a pressure diverticulum or pulsion diverticulum of the pharynx which is often miscalled as diverticulum
of the oesophagus. The nerve supply of this part of inferior constrictor mainly derives from the recurrent
laryngeal nerve and external laryngeal nerve.
The course of the diverticulum.—To start with it is a midline swelling of the posterior aspect of the pharynx
As the diverticulum enlarges in size the resistance of the vertebral column pushes it to one side or the other
usually to the left side.
CLINICAL FEATURES.— (i) Age.— The sufferers are usually old people.
(ii) Sex.— It is commoner in men at the ratio of 2 : 1.
The course of the diverticulum can be divided into 3 stages for facility of description of clinical features.
STAGE I.— This is the stage of initial bulging and it is symptomless. The pathology can only be detected
as an accident during the course of a barium swallow examination for some other reason. At this stage ther
only a small diverticulum in the posterior aspect of the pharynx which has not touched the vertebral colum
In only extremely rare cases the patient may complain of a sensation of foreign body in the throat.
STAGE II.— In this stage the diverticulum is large, more globular and still lies in the posterior midline, b
touches the vertebral column. The main symptoms at this stage are :
(a) Regurgitation of undigested food material at different times e.g. at the time of turning to one side
or the other at night or even during swallowing at the next time of eating.
(b) Such regurgitation may awaken the patient from sleep with a sense of suffocation and violent
THE NECK 521
coughing.
(c) Occasionally abscess of lung may result from regurgitation of food into the air passage.
At this stage operation and excision of the pouch is indicated.
STAGE III.— In this stage the diverticulum becomes even bigger in size and is pushed to the left side by
the vertebral column. The fundus of the pouch becomes dependent and lies in the posterior triangle of the ne
The mouth of the pouch looks horizontally upwards. The main symptoms are :
(a) Symptoms of the second stage persist.
(b) In about l/3rd of cases a swelling is visible in the posterior triangle of the neck and the swelling
becomes larger as the patient drinks.
(c) Dysphagia is the main symptom of this stage and in fact many patients come to the clinician only
with this symptom. This is due to the fact that the pouch compresses the oesophagus and the dysphagia resu
(d) A gurgling noise may be heard in the neck as the patient swallows.
(e) Due to semi-starvation there is progressive loss of weight and gradually the patient may become
cachectic in the long run.
(f) Aspiration of the contents of the pouch may lead to lung abscess, aspiration pneumonia etc. and
cause more problem to the disease.
So in this stage the main complaints are regurgitation, increasing dysphagia and visible swelling in the ne
The features of the swelling in the neck caused by the 3rd stage of pharyngeal pouch are :
(i) Site.— The swelling usually lies in the posterior triangle of the left side. That means such sw
is always posterior to the sternomastoid muscle and in front of the trapezius muscle. This swelling lies usuall
inferior to the level of the thyroid cartilage as the position of the Killian’s dehiscence is below the Thyrophary
geus muscle which corresponds to the level of the thyroid cartilage. This swelling lies deep to the deep cervic
fascia, so when the sternomastoid m uscle is made taut there is slight decrease in the prominence of the swell
as the deep cervical fascia also becomes taut by that manoeuvre.
(ii) Size and shape.— It is usually globular in shape, but the size varies according to the duration of th
swelling.
(iii) Surface is usually smooth and the edge is indistinct.
(iv) Consistency.— It is soft and cystic. It can be reduced. Fluctuation test is positive, but transillumi
nation test is negative.
(v) Fixity.— This swelling is not mobile and is fixed to the surrounding structures.
Special Investigations.— Two investigations are important in this regard —
1. RADIOGRAPHY.— With a very thin emulsion of barium, barium swallow examination should be
performed. Anteroposterior view may not be very helpful as the barium filled pharyngeal pouch will
superimpose on the beginning of the oesophagus and may look like a septum obstructing the commencemen
of the oesophagus. The best view to diagnose pharyngeal pouch is the semi-lateral view. If the pouch is
compressed one will see in the screen the barium to be spilled into the oesophagus. Moreover one can see the
overflow of barium emulsion into the oesophagus. One may find the fundus of the pouch invading the super
mediastinum.
Chest X-ray is essential to exclude associated lung abscess or aspiration pneumonitis.
2. OESOPHAGOSCOPY.— This investigation is not as necessary as the previous one. It is also
dangerous. The instrument may perforate the fundus of the pouch, which is quite thin and fragile.
TREATMENT.— In STAGE I — operation is not indicated and the diverticulum is almost ignored until
and unless the patient comes with more symptoms of stage II.
In STAGE II and STAGE III — operation is strongly advised and the pharyngeal pouch is excised with
cricopharyngeal myotomy (almost similar to Heller’s operation).
OPERATION.— Endoscopy is first performed with two ideas — (i) to pack the pouch with ribbon gauze
and (ii) to pass a nasogastric tube into the oesophagus to determine the position of the sac.
Either a transverse incision at the level of the cricoid cartilage is made or an oblique incision along the
anterior border of the left sternomastoid muscle is made.

The lateral lobe of the thyroid gland is first mobilised. To do this the superior pole of the thyroid gland is
ligated and divided, the middle thyroid veins are ligated and divided and even the inferior thyroid artery ma
have to be ligated and divided. Once the lateral lobe is mobilised and retracted forward the pharyngeal pouc
will be visible near the beginning of the oesophagus. With great care the whole pouch is gradually freed from
the surrounding structures. Once the neck of the pouch is well defined by the position of the nasogastric tube
and the ribbon gauzepack an incision is made on the neck of the pouch to incise only the outer layer of the po
keeping intact the mucous membrane. Then the mucous membrane is also divided at the neck, This dissectio
is important to permit closure of the neck of the pouch in two layers — outer fibrous layer and inner mucous
membrane layer. During suturing of the layers the mucous membrane is first sutured with atraumatic 2/0 ca
and the fibrous layer is closed over mucous membrane by interrupted sutures of fine silk. During closure of t
neck of the pouch care must be taken not to narrow the beginning of the oesophagus.
Cricopharyngeal myotomy is now performed in all cases like Heller’s operation. The hypertrophied circular
muscle is divided vertically till the submucosa is reached.
The incisional wound is closed
with drainage.
POST-OPERATIVE CARE.—
The patient is fed through nasogas
tric tube for 3 days, after which the
tube is removed. Only liquids are
given for the next 3 days by mouth.
After this semisolid diet is started
gradually.
OPERATIVE COMPLICA
TIONS.— (i) Infection.— If the
pouch is perforated during freeing
of the pouch, there is a chance of
infection of the wound and even
mediastinitis.
(ii) Fistula.— This only
occurs if the two layers are not
A IB meticulously sutured during clo
sure of the neck of the pouch. So
Fig.36.3.—Excision of the pharyngoesophageal diverticulum with concomitant this step of operation is extremely
cervical oesophagomyotomy. In Fig. A. Cricopharyngeal myotomy is being per important. In case a fistula occurs it
formed after isolating the diverticulum. In Fig. B. the diverticulum is excised to
show the final appearance after operation. Arrow shows the cricopharyngeal
usually closes by itself i f the begin
myotomy. ning of the oesophagus is not nar
rowed.
LARYNGOCELE
This is a narrow-necked air-conlaining diverticulum resulting from herniation of the laryngeal mucosa. It may be located
internal or external to the laryngeal skeleton.
An internal laryngocele may displace and enlarge the false vocal cord and may result in hoarseness or airway
obstruction.
External laryngocele passes through the thyrohyoid membrane and presents as a swelling in the neck over the
thyrohyoid membrane.
Laryngoceles are more common in glassblo wers, wind instruments musicians and others who develop high intraluminal
pressures.
THE NECK 523
1. As mentioned earlier it is more common among trumpet players and persons with chronic cough.
2. This is a smooth ovoid swelling which is tympanic.
3. The swelling becomes prominent when the patient is asked to blow or perform Valsalva manoeuvre.
4. The swelling is boggy in feel and may be resonant on percussion.
5. Sometimes laryngocele may fill with mucoid fluid and may become infected, in which case the term laryn-
gopyocele is more appropriate.
6. There may be hoarseness of voice.
7. The swelling moves up with the larynx, on swallowing. This is quite diagnostic.
Treatment.—
Laryngoceles are excised through transverse cervical incision. The sac is dissected from the surrounding tissue upto
the point where it comes out through the thyrohyoid membrane. The neck is ligated and divided and the whole sac is excised.
The membrane is repaired by invaginating the stump of the neck almost like the stump of the vermiform appendix.
CERVICAL RIB
A rib arising from the 7th cervical vertebra is called a cervical rib. Cervical rib rarely causes a visible swell
and if there is a swelling in the subclavian triangle at the position of the cervical rib, one should think of
subclavian artery aneurysm rather than a cervical rib.
The patients with cervical rib usually present with neurological and vascular symptoms in the arm. It mus
be remembered that presence of cervical rib does not always cause symptoms and many such cervical ribs have
been passed unnoticed or detected in the course of routine X-ray examination.
There are mainly four varieties of cervical ribs seen in clinical practice :—
(a) A complete rib which articulates anteriorly with the manubrium sterni or the first rib.
(b) An almost complete rib with the free end of the rib expands into a bony mass. This variety may give
rise to a visible swelling in the subclavian triangle in the neck.
(c) A true incomplete rib ends into a fibrous band which is connected to the scalene tubercle of the first
rib.
(d) An only fibrous band all along which is closely
applied or incorporated in the scalenus medius muscle. This
can give rise to symptoms, but may not be revealed by X-ray.
scale rv us
Pathology.—
GTVtlCUS The brachial plexus and the subclavian artery emerge
between the scalenus anticusand scalenus medius ensheathed
by axillary sheath, a prolongation of the prevertebral fascia
cervical
rib which covers these muscles. So brachial plexus and sub
clavian artery come out through a triangle formed anteriorly
by the scalenus anticus, posteriorly by the scalenus medius
and below or the base by the first rib. When there is cervical
rib the subclavian artery and the first thoracic nerve are lifted
ubclaviarv. up and this is the main pathology which gives rise to both
rterij vascular and neurological symptoms.
Vascular symptoms are caused by the constriction of the
lumen of the subclavian artery as the artery is lifted up by the
cartilacj iaous cervical rib. Such constriction is followed by post-stenotic
boss
dilatation where clotting occurs in the intima of the artery.
Fig.36.4.— Figure shows how the neurovascular Mural thrombus may become detached and give rise to
compression is brought about by cervical rib. Sub
emboli. Rarely proximal extension of the thrombus may
clavian artery and brachial plexus are shown to be
compressed by the cervical rib. affect the vertebral artery and cause cerebrovascular em
bolic episodes.
Neurological symptoms are caused by pressure on the first thoracic nerve from below by the cervical rib.
1. LOCAL SYMPTOMS.— Patients may present with a lump in the lower part of the neck. Sometimes
tenderness can be elicited in the supraclavicular fossa. The lump is bony hard in consistency and fixed. In the
cases if both the wrists are dragged down and the radial pulses are felt on both sides, the pulse on the affected
side will be feeble.
2. VASCULAR SYMPTOMS.—
(i) Pain is the most important symptom. Pain radiates from the neck to the upper arm and forearm. Pa
is aggravated by the use of the arm and more so when the arm is in the raised position during exercise. Pain i
relieved by rest. This pain is the ischaemic muscle pain, similar to intermittent claudication of the leg. Later o
pain becomes almost similar to the ‘rest pain’.
(ii) Numbness is often complained of in a case of cervical rib. When numbness is due to vascular
pathology, some trophic changes may be seen. Arteriography will reveal that the subclavian artery is almost
occluded.
(iii) Temperature and colour changes.— The affected upper limb is often colder than its fellow. It often
looks unduly pale. There may be some change in the radial pulse of the affected side than that of the normal s
If the distal part of the subclavian artery is auscultated, a systolic bruit may be detected. Raynaud’s phenome
may be seen.
3. NEUROLOGICAL SYMPTOMS.— Pain and tingling of the hand and forearm particularly on the med
aspect may be noticed. The hypothenar eminence may be wasting in late cases. Some form of hypoaesthesia
or anaesthesia may be detected in the skin supplied by the Tt segment. Weakness of the muscles of the hand
is detected.
Vasomotor disturbances like coldness of the fingers, cyanosis, excessive sweating may be noticed. Trophic
changes like ulceration and lately ulceration of the tips of fingers are not uncommon.
Signs.—
I. In the Neck.— A lump may be palpable in the supraclavicular region (subclavian triangle). The lump
be hard bony mass, which obviously indicates the anterior portion of the cervical rib. The lump may be
bosselated. Occasionally there may be a pulsatile swelling in the sub
clavian triangle which indicates elevated subclavian artery due to pres
ence of cervical rib just beneath the artery.
There may be slight lowering of the shoulder girdle of the affected side
due to muscular wasting. In fact this drooping of shoulder girdle is more
often responsible for the symptoms which are collectively known as
cervical rib syndrome.
II. In the limb.—
(i) Sensory changes in the form of paraesthesia or rarely anaes
thesia are mainly noticed on the medial aspect of the forearm and hand
(along the distribution of the C8 and Tj).
(ii) The motor changes are mostly noticed in the small muscles
of the hand (supplied by the segment Tj). There may be loss of tone and
muscle power of both thenar and hypothenar muscles. The movements of
the finger become clumsy and incoordinated. The thenar, hypothenar
muscles, interossei and lumbricals are mainly involved. Occasionally one
may find clawhands.
Fig.36.5.— Adson’s test. See the text. (iii) Vasomotor disturbances e.g. cyanosis, excessive sweating
This test can be performed by sitting or and coldness of the fingers may also be noticed.
standing posture. Probably standing (iv) Vascular sign may be detected, if the patient stands in front
position is better.
of the clinician, who feels both his radial pulses by his two hands. The
THE NECK 525
patient’s hands are now dragged down as far as possible and again the radial pulses are felt. The radial pul
on the affected side will be obviously diminished or obliterated.
III. Adson's test.— This test is posi
tive in presence of cervical rib and scalenus
anticus syndrome due to compression of the
subclavian artery. The patient sits on a stool. He
is instructed to take a deep breath in and to turn the
face to the affected side. The examiner examines
his radial pulse, which is often obliterated due to
compression of the subclavian artery.
Treatment.—
(i) In MILD CASES various exercises
may be advised to strengthen the muscles of the
shoulder girdle. This often relieves the symp
toms.
(ii) In ADVANCED CASES the only
treatment is excision of the cervical rib or the
corresponding fibrous band or dividing the
Fig.36.6.— First figure shows how the lower trunk of brachial scalenus anterior muscle which is known as scale-
plexus and subclavian artery are being compressed by the notomy. It must be remembered that it is essential
cervical rib. In the second figure it is shown how scalenotomy to remove the cervical rib alongwith its perios
may help the patient in relieving compression.
teum so that there is no chance of regeneration.
See chapter XV ‘DISEASES OF ARTERIES’ for further details.
CERVICAL LYMPH NODE ENLARGEMENTS

In the neck the most common swelling is the cervical lymph node enlargement. The anatomy of the cerv
lymph nodes and the clinical examination are discussed in detail in my ‘A Text Book On Surgical Short Cas
Chapter IX. The various causes of cervical lymph node enlargements are similar to those of any lymph node
enlargement in the body. These are discussed in details in CHAPTER 7 7 of this treatise. Secondary carcinom
of cervical lymph nodes is extremely common and in fact any neck swelling in an elderly patient should aro
suspicion of this condition. This subject has also been discussed in detail in chapter 17. The students must go
through this section and block dissection of the neck in that chapter.
526
CHAPTER - 29
THE THYROID AND PARATHYROIDS

EMBRYOLOGY —
The thyroid gland is developed as a median thickening of the entoderm. In the floor of the pharynx between the levels
of the first and second pharyngeal pouches gradually a median diverticulum is formed in the latter half of the fourth week
immediately caudal to the tuberculum impar. It grows caudally as a tubular duct which bifurcates and subsequently divides
into a series of double cellular plates from which the isthmus and the lateral lobes of the thyroid gland are developed. As
the thyroid primordium descends, it acquires mesodermal contributions such as the parafollicular C-cells which will
ultimately secrete calcitonin. These parafollicular C-Cells are derived from a bud which is known ultimo-branchial body
which arises from a diverticulum of the fourth pharyngeal pouch of each side and amalgamates with the corresponding
lateral lobe of the thyroid. The connection of the median diverticulum with the pharynx is termed the thyroglossal duct. The
site of its connection with the epithelial floor of the mouth is marked by the foramen caecum on the tongue. Except the distal
part of the duct which usually differentiates to form the pyramidal lobe of the thyroid, the rest of the duct disappears.
Occasionally a portion of the thyroglossal duct may persist and give rise to the formation of cyst in the midline of the neck,
which is called thyroglossal cyst.
ANATOMY
The thyroid gland is a highly vascular organ, situated in front and sides of the lower part of the neck, opposite the 5th,
6th, 7th and 1st thoracic vertebrae. It is ensheathed by the pretracheal layer of the deep cervical fascia and consists of right
and left lobes, connected across the median plane by a narrow portion, termed isthmus.
The lobes are conical in shape and the lateral surface of each lobe lies in relation with the sternothyroid and more
superficially with the sternohyoid and superior belly of the omohyoid, which in their turn are overlapped below by the
anterior border of the stemomastoid. The medial surface lies over the larynx and trachea. At the upper part, the external
laryngeal nerve passes deep to this surface on its way to Cricothyroid. At its lower part, the recurrent laryngeal nerve lies
between trachea and oesophagus. The postero lateral surface is in relation with the carotid sheath. The posterior border is
important in the sense that it is closely related to the inferior thyroid artery below and with an anastomosing branch, which
connects this vessel to the posterior branch of the superior thyroid artery. In addition, the parathyroid glands are related to
this border.
The isthmus lies in front of the second and third rings of the trachea. Anteriorly, it is in relation with pre-tracheal fascia,
sternothyroid, sternohyoid, anterior jugular vein, the fascia and the skin in that order from deep to the superficial aspect.
Sometimes a 3rd conical lobe, called pyramidal lobe, extends from the upper part of the isthmus towards the hyoid bone.
Between the gland and its sheath are net works of anastomosing blood vessels.
Coverings.— The thyroid gland is covered by two capsules — 1. True capsule and 2. False capsule.
1. The true capsule or fascia propria is a fibrous capsule which envelops the gland and sends numerous fibrous septa
into it.
2. False capsule is a fascial sheath derived from the pretracheal layer of the deep cervical fascia. This layer when
it reaches the lateral border of the thyroid splits into two laminae — anterior and posterior to enclose the thyroid gland. The
two laminae meet on the other lateral border of the thyroid and becomes continuous as pretracheal layer. This sheath is
thickened on the postero-medial aspect of each lobe which is known as ligament of Berry. This ligament extends from the
posteromedial border of the thyroid lobe to the cricoid cartilage.________________________________________________
The thyroid moves with deglutition due to its attachments with the larynx and trachea as follows :—
(i) Ligament of Berry on either side.
(ii) Posterior lamina of the pretracheal fascia which is closely adherent to the trachea on the back.
(iii) Sometimes a fibromuscular slip may extend from the pyramidal lobe to the inferior border of the hyoid bone
which is known as levator glandulae thyroidae.___________________________________ __________________ _______
Blood supply.— Arteries, which supply the thyroid gland, are the superior and the inferior thyroid arteries. An
additional branch by the name of arteria thyroidea ima which comes from the brachio-cephalic trunk or the arch of the aorta
also supplies the thyroid. A few unnamed arteries from the trachea also supply the thyroid gland. Afterpartial thyroidectomy,
they maintain the blood supply of the remaining glandular tissue. The veins form a plexus on the surface of the gland and
in front of the trachea. From, this plexus, the superior and middle thyroid veins drain into the internal jugular vein; whereas
the inferior thyroid veins drain into the corresponding brachiocephalic veins.
Lymphatics of the thyroid gland communicate freely with the plexus on the wall of the trachea. Lymphatics from the
THE THYROID AND PARATHYROIDS 527
gland drain to the prelaryngeal nodes above the isthmus and to the pretracheal and paratracheal nodes. Some may drain into
the brachiocephalic lymph nodes in the superior mediastinum. Laterally the gland is drained by vessels which accompany
the superior thyroid vein to the deep cervical lymph nodes. Some lymph vessels from the thyroid gland may drain directly
into the thoracic duct.
Nerve supply of the thyroid gland is derived from sympathetic and parasympathetic nerves. The SYMPATHETIC
supply comes form the superior, middle and inferior cervical ganglia. These nerves form plexus surrounding the blood
vessels of the thyroid gland and follow them to reach the gland. The PARASYMPATHETIC supply is derived from external
laryngeal nerve and the recurrent laryngeal nerve which are branches of the vagus nerve.
The superior laryngeal nerve which is a branch of vagus nerve divides into internal and external laryngeal nerves. While
the internal laryngeal nerve is mainly a sensory nerve to mucous membrane of the larynx as far below the vocal cord, the
external laryngeal nerve is important so far as the thyroid gland is concerned. It descends under cover of the sternohyoid
in company with the superior thyroid artery but on a deeper plane. So while tying the superior thyroid artery during subtotal
thyroidectomy one has to be cautious not to injure this nerve. This nerve goes deeper and lies on the inferior constrictor of
the pharynx and then reaches the Cricothyroid, which it supplies. So during ligation of the superior thyroid artery one should
be as close to the superior pole of the thyroid as possible, since this nerve passes deeper and escapes injury. Cricothyroid
is concerned with regulating the degree of tension of the vocal cords. The recurrent laryngeal nerve which is also a branch
of vagus nerve is important as it lies close to the inferior thyroid artery and is liable to be injured while ligating the inferior
thyroid artery. On the right side this nerve hooks round the first part of the right subclavical artery and ascends obliquely
to the side of the trachea behind the common carotid artery. Then it follows groove between the trachea and the oesophagus.
Near the lower pole of the lobe of the thyroid gland the nerve is always intimately related to the inferior thyroid artery —
it may cross either in front or behind the artery or may pass between its branches. On the left side it hooks round the arch
of the aorta and ascends to the side of the trachea and follows the groove between the trachea and the oesophagus. It supplies
all the muscles of the laiynx except the Cricothyroid. So if this nerve is involved in ligature and is injured there will be failure
of adduction and abduction of the vocal cords. The Posterior crico-arytenoids open the glottis while the Lateral crico-
arytenoids and Transverse arytenoid close the glottis. Besides muscular supply the recurrent laryngeal nerve supplies the
mucous membrane of the larynx below the vocal cords.
HISTOLOGY —
The thyroid is made up of multiple acini or follicles. Each spherical follicle is surrounded by a single layer of cells and
filled with pink-staining proteinaceous material called colloid. When the gland is inactive, the colloid is abundant, the
follicles are large and the cells lining them are flat. When the gland is active, the follicles are small, the cells are cuboidal
or columnar and the edge of the colloid is scalloped, forming many small 'reabsorption lacunae'. The microvilli project
into the colloid from the apices of the thyroid cells. The individual thyroid cells rest on a basement membrane which
separates them from the adjacent capillaries.
Second group of cells, called C cells, is also present alongwith the thyroid cells. These cells are derived from
neuroectoderm and are part of the APUD cells. In fish and amphibians these cells are present in a separate ultimobranchial
body. But in human being these cells are incorporated into the thyroid gland as part of the lateral thyroid lobes.
PHYSIOLOGY
The principal hormone secreted by the thyroid is thyroxin, an iodine-con taining aminoacid. Triiodothyronine (iodine molecule in 3,5,3
positions), trace amounts of reversed triiodothyronine (iodine molecule in 3,3,5 positions) and other compounds are also liberated.
THYROID HORMONE SYNTHESIS.— Ingested iodine is converted into iodide and absorbed in the small intestine. 98% of the
absorbed iodide is taken up by the thyroid. At normal plasma iodide level excretion through urine is about 15 (J.g/day. To replace this small
loss from the body a minimum daily intake of approximately 20 pg is required. The thyroid concentrates iodide by actively transporting
it from the circulation to the coUoid. The transport mechanism is called the ‘iodide trapping mechanism’. In the thyroid gland iodide is
oxidised to iodine by the enzyme called peroxidase. This iodine in matter of seconds is attached to the 3-position of tyrosine molecule to
form monoiodotyrosine. Monoiodotyrosine is next iodinated in the 5-position to form diiodotyrosine. Two diiodotyrosine molecules then
undergo an oxidative condensation, with the liberation of an alanine residue and the formation of thyroxin. This thyroxin remains in peptide
linkage to thyroglobulin. Triiodothyronine is probably formed by condensation of monoiodotyrosine with diiodotyrosine and ‘reversed
triiodothyronine’ is formed by condensation of diiodotyrosine and monoiodotyrosine. When TSH is administered, thyroid function is
stimulated, iodide uptake is increased, thyroxin synthesis is enhanced and more thyroxin is secreted. Blood flow in the thyroid gland
increases, the cells hypertrophy and the weight of the gland rises. TSH acts by increasing cyclic AMP formation.
The free thyroxin secreted by the thyroid is bound in the blood stream to plasma protein. The amount of protein-bound iodine (PBI)
in the plasma normally ranges from 3.5 to 8.0|lg/l 00 ml. The plasma proteins which bind thyroid hormones are (i) thyroxin-binding globulin
(TBG) (otl and Ci2 globulin), (ii) thyroxin-binding prealbumin (TBPA) and (iii) Albumin. Most of the circulating thyroxin is bound to TBG,
only small amounts of thyroxin are bound to TBPA and practically none to albumin. Amount of thyroxin bound in normal plasma is 7 pg/
100 ml to TBG, 1 (ig/lOOml lo TBPA and none to albumin. So total protein-bound thyroxin is 8 pg/100 ml. Triiodothyronine shows less
affinity to be bound to plasma protein. This correlates well with the fact that triiodothyronine has a much shorter half-life than thyroxin
and that its action on the tissues is much more rapid. Free thyroxin exists about 0.004 ug/100 ml. This is in equilibrium with the 9 Jig/100
ml bound to protein in plasma. It is the free thyroxin in the plasma which is physiologically active and it is this fraction which inhibits the
pituitary secretion of TSH. The plasma of hyperthyroid patient contains excess of free thyroxin.
Effects of thyroid hormones.—
1. CALORIGENIC ACTION.— Thyroxin increases Oj consumption of almost all metabolically active tissues. The exceptions are
brain, testes, uterus, lymph nodes, spleen and anterior pituitary. Thyroxin actually depresses the 02 consumption of the anterior pituitary
presumably because it inhibits TSH secretion. Thyroxin increases the basal metabolic rate (BMR). It also increases nitrogen excretion. If
food intake is not increased endogenous protein and fat stores are catabolized and weight is lost. The catabolic response in skeletal muscle
is sometime so severe that muscle weakness is a prominent symptom and creatinine excretion is marked. When metabolic rate is increased
the need for all vitamins is increased and vitamin deficiency syndromes may be aggravated. Peripheral resistance decreases because of
cutaneous vasodilatation. But cardiac output is increased, so that pulse pressure and cardiac rate are increased. In the absence of thyroxin
a moderate anaemia occurs as a result of decreased bone marrow metabolism and poor absorption of vitamin B12 from the intestine.
2. EFFECTS OF NERVOUS SYSTEM.— In adult, hypothyroidism produces slow mentation and increased CSF protein level.
Thyroxin reverses these changes and large doses cause irritability and restlessness. These latter effects are probably secondary to increased
sensitivity to circulating catecholamines with consequent increased activation of the reticular activity system.
In infants, thyroxin has additional actions on the nervous system possibly because the blood-brain barrier is not developed. In
hypothyroid infants myelination is defective and mental development is seriously retarded. The mental changes are irreversible if thyroxine
replacement is not instituted soon after birth.
Thyroid hormones also exert effects on the peripheral nervous system. The reaction time of stretch reflexes is shortened in
hyperthyroidism and prolonged in hypothyroidism. Measurement of the reaction time of the ankle jerk and knee jerk has attracted
considerable attention as a clinical test for evaluating the thyroid function, though this reaction time is also affected by certain other diseases.
3. EFFECTS ON CARBOHYDRATE METABOLISM.—Thyroxin increases the rate of absorption of carbohydrate from the gastro
intestinal tract. In hyperthyroidism therefore the blood glucose rises rapidly after a carbohydrate meal, sometimes exceeding the renal
threshold. The increased catabolism of this condition and elevated level of epinephrine keep liver glycogen depleted. So the blood glucose
falls rapidly as glucose is catabolized.
4. EFFECTS ONCHOLESTEROLMETABOUSM.— Thyroxin stimulates both cholesterol synthesis and the hepatic mechanisms
that remove cholesterol from the circulation. But the latter process exceeds that of the former so that the plasma cholesterol level falls in
hyperthyroidism.
5. RELATION TO CATECHOLAMINES.— Thyroxin potentials the effects of catecholamines and vice versa, but the basis of this
interaction is not known. Although catecholamine secretion is usually normal in hyperthyroidism, the cardiovascular effects, tremors and
sweating produced by thyroxin can be blocked by drugs such as reserpine, guanethidine and propranolol, the beta-adrenargic blocker.
Obviously many of the effects of thyroxin, especially those on the nervous and cardiovascular systems are due in large part to adrenargic
nervous system.
6. EFFECTS ON GROWTH AND DEVELOPMENT.— In hypothyroid children bone growth is slow and epiphyseal closure is
delayed. In absence of thyroxin, pituitary growth hoimone content and secretion are depressed. Thyroxin potentiates the effect of growth
hormone on the tissues.
Control of thyroid secretion.— TSH, which is an anterior pituitary hormone, stimulates the thyroid to produce thyroxin. Thyroxin
in its turn inhibits TSH secretion, which is known as feed-back mechanism. Electrical stimulation of the hypothalamus causes increased
TSH secretion. The substance that stimulates TSH secretion from hypothalamus is thyrotropin-releasing factor (TRF). This releasing factor
is apparently secreted in the portal vessels in the median eminence. The part of the hypothalamus which is concerned with production of
TRF is t' , eg ion in and above the rostral end of the median eminence. TRF production is increased by cold and decreased by heat.
Antithyroid drugs.—There are two major categories of antithyroid drugs. The first, comprising perchlorate and thiocyanate, prevents
uptake of iodine by the thyroid gland. The second group includes organic substances like thiourea derivatives and neomarcazole, which
prevent the binding of iodine to tyrosine radicals. The action of this group of drug is independent of the level of blood iodide.
ASSESSMENT OF THYROID FUNCTION

It is generally agreed that no single procedure consistently yields reliable basis for diagnosis and therefo
a combination of the various tests is generally required. These tests are combined to provide a correct over
assessment of thyroid function. The tests can be divided into two major groups—In-vitro tests and In-vivo
In-vitro tests
1. Serum protein bound iodine (FBI).— Measurement of PBI has dominated In-vitro tests of thyroid function
for over 20 years. It is cheap and has a high degree of reproducibility. But its drawback is the lack of specificity and that
it measures non-hormonal forms by iodine in the blood. Iodine contamination of the environment is.increased steadily such
as with (i) X-ray contrast media, (ii) expectorants containing iodide, (iii) oral contraceptives etc. So with these
contaminations false high results of serum PBI can be expected. Similarly false low results may also be due to lowering of
TBG. This is often seen (i) as hereditary, (ii) when excessive androgens are used and (iii) in renal failure.
2. Serum T4 and T3.—The most useful index of thyroid function is the direct measurement of circulating thyroid
hormones. This is mostly done by radioimmunoassay method. Normal range of serum T4 is 4.5 to 11 (O.g/100 ml and normal
range of serum T3 is 100 to 160 ng/100 ml. 99.9 percent of serum T4 is bound to protein and 99.5 percent of serum T3 is
bound to protein. Only free T4 and free T3 are physiologically active, so estimation of these by radioimmunoassay is more
important. Normal free T4 is 10 - 30 nml/L, whereas normal free T3 is 3.5 - 6 fimol/L. However only in T3 toxicity
measurement of serum T3 is diagnostic.
3. T3 resin uptake.— The radioactive tri-iodothyronine (T3) is added to the system. This will be bound either by
the resin or by the unoccupied thyroxin-binding globulin (TBG) as TBG has a greater affinity for T4 than for T3. So
radioactive T3 added to the system will be bound to the resin if TBG is saturated with endogenous T4 and the T3 ‘uptake’
by the resin will be high. In hyperthyroidism the number of free binding sites of TBG is low because most of them are
already carrying hormone whereas in hypothyroidism the number of free sites is high. Nowadays sephadex or thyopac has
been used to replace the resin as the secondary binder. The fraction of labelled T3 taken up by the resin is compared with
that taken up by a standard serum and the result is expressed as the resin uptake ratio. The normal range is 0.90 to 1.20 i.e.
taking 100% as the mean normal value for free binding sites, a figure of 89% or less suggests hyperthyroidism and a figure
of 121% or more suggests hypothyroidism.
4. Free thyroxin index.— In patients with an increase TBG the serum T4 rises into the hyperthyroid range and
because of the increase in binding sites on the serum proteins the T3 resin uptake moves into the hypothyroid range. A
mathematical combination of serum T4 and T3 resin uptake has been derived that gives normal values in euthyroid
patients with abnormal levels of TBG. Free thyroxin index (F.T.I.) can be calculated as F.T.I. = serum T4 (or PBI) X T3
uptake percent. The normal range of F.T.I. is from 3.7 to 8.6. It is probably the best parameter of thyroid function at the
present moment.
5. Serum thyroid stimulating hormone (TSH).— The serum concentration of TSH is measured by immu
noassay technique. The normal serum TSH level is low, being about 1 jju (m units) per ml or upto 5m U/L. It is raised in
primary hypothyroidism (may be over 40m U/L) and almost undetectable in hyperthyroidism. As the normal level of TSH
is very low, it is of little help in the diagnosis of hyperthyroidism, but it is a most sensitive test of primary hypothyroidism.
The circulating TSH level is always raised in primary hypothyroidism often over 40 nu/ml. Raised TSH level may be
found in patients following radioiodine therapy even though they are euthyroid. This is also seen following subtotal
thyroidectomy.
6. Tests of hypothalamic-pituitary axis or the TRH test.— When thyrotropin-releasing hormone, a iiypo-
thalamic-releasing factor, is given intravenously in a dose of 200 (ig to a normal individual. The level of TSH in the serum
rises from the basal level of about 1 pu/ml (m unit/L) to a mean peak concentration of about 10 fiu/ml at 20 minutes and
returns to normal by 120 minutes. In hypothyroidism there is an exaggerated rise of an already elevated TSH level, but in
hyperthyroidism there is no response of an already depressed TSH level. It is particularly relevant to the diagnosis of T3
thyrotoxicosis if it is not possible to measure the circulating serum T3 level. The TRH test replaces the T3 suppression
test. T4, antithyroid drugs, corticosteroids, oestrogens and levodopa will modify the TSH response to TRH. The main
indications for TRH test are in cases of mild hyperthyroidism when the diagnosis is in doubt, in hypopituitarism and in
ophthalmic Graves’ disease. TRH test does not seem to give any added information to a single TSH determination in the
diagnosis of primary hypothyroidism.
In-vivo tests
1. Uptake tests.— In general, the rate at which the thyroid gland traps iodine reflects the rate of secretion of
thyroid hormone into the circulation. Thus in hyperthyroidism both the proportion the tracer dose taken up and the rate at
which it takes places are increased. A tracer dose (5 microcuries) of ,3II is given which is absorbed from the small intestine
into the blood. The thyroid and the kidneys compete for it. In hyperthyroidism the thyroid uptake is rapid and little is
excreted in the urine. The thyroid content of l31I is determined with a suitable detector. The best time to measure the
isotope uptake is between 10 to 120 minutes after administration. The greatest rate of accumulation is more apparent in the
early phase of uptake than at 24 hours after administration. This early uptake enables the diagnosis to be confirmed at the
patient’s first visit to the clinic. The normal value is approximately 30% in 24 hours. I32I and ""Tc are more often used
nowadays as they have low radiation and short lives (the half life of 132I is 2.3 hours as opposed to 8 days of l3'I). This test
however should not be done in children or during pregnancy, but the low-energy isotopes like l32I or <WmTc may be used.
2. T3 suppression test (Werner).— This test is useful in differentiating thyrotoxicosis from other causes of
raised uptakes, such as (i) single goitre from iodine deficiency, (ii) in studing the autonomy of thyroid nodules, (iii) in
checking the response of antithyroid drug in treatment of thyrotoxicosis, (iv) in assessment of ophthalmic Graves’ disease
where the patient may be euthyroid, but uptake is not suppressed. Less suppression is characteristic of thyrotoxicosis. The
initial uptake is measured as has been described in the earlier section. Then 40 ng of tri-iodothyronine (T3) is given orally
8 hourly (total 120 Mg) for 5 days, after which the uptake is repeated. T3 is preferred to T4 because of its rapid effect and shorter
34
half-life. Patients with non-toxic goitre show an average fall of uptake of about 50 to 80% as opposed to 10 to 20% in case of toxic
goitres.
3. TSH stimulation test.— This was introduced to distinguish between the primary and secondary hypothyroidism. An injection
of TSH will cause a rise in uptake in patients with hypopituitarism but no rise with primary thyroid failure. The uptake is measured
before and 24 hours after an injection of 10 i.u. of bovine TSH.
4. Thyroid scan.— Automatic scanning machines are now widely used to obtain information about the size, shape and position
of the gland and the topographical distribution of the tracer isotope. Both 1311 and ”"Tc are being used. 1311 scan is obtained at 24 hours
and "Tc scan is obtained at about half an hour. The scan will distinguish between functioning and non-functioning thyroid nodules. It
is very much indicated (i) when a solitary nodule is palpated, (ii) in cases of suspected retrosternal goitre, (iii) ectopic thyroid tissue and
(iv) in the diagnosis of toxic nodular goitre — either a solitary toxic nodule or a part of toxic multinodular goitre. A single non
functioning thyroid nodule is an indication for surgery. Only histological examination can establish whether it is a carcinoma or one of
other causes of non-functioning nodules such as adenoma, a cyst, or a focal area of autoimmune thyroiditis. This test mainly differentiates
between which part of the gland is functioning (hot) and which part is non-functioning (cold). A functioning nodule is unlikely to be a
carcinoma. If it is autonomous, all the isotope is concentrated within the nodule and the rest of gland shows little activity. Such nodules
are likely to become toxic and produce hyperthyroidism. More commonly a nodule is functional but not autonomous, in which case both
the nodule and the rest of the gland take up the isotope.
5. Thyroid autoantibodies.— Antibodies against thyroid microsomal antigen (now known as thyroid peroxidase (TPO)) and
thyroglobulin in the serum are useful in determining the various causes of thyroid swellings and dysfunction. Serum level above 25 units
ml-1 for TPO antibody and litres greater than 1 : 100 for anti-thyroglobulin are considered abnormal and may be the cause of the existing
disease. Exceptions are always there, as histologically proved autoimmune thyroiditis have been shown to be seronegative sometimes.
Miscellaneous other tests

1. Serum cholesterol determination.— Although serum cholesterol level is knowr. to vary widely in both normal and diseased
condition, the value is usually elevated in patients with hypothyroidism. This test (the physiology of which has been explained in the
section of ‘Physiology’) is helpful in diagnosing hypothyroidism.
2. Tendon reflexes.— Particularly ankle jerk and knee jerk are being tested. The relaxation is quite slow in hypothyroidism.
3. Measurement of LATS and antibodies in the serum.— Presence of LATS in the serum is quite diagnostic of Graves’
disease and has aetiological significance. Measurement of antithyroglobulin and thyroid antimicrosomal antibodies is helpful in
autoimmune thyroiditis.
Summary.— The above-mentioned tests mainly indicate the function of the thyroid either hypo- or hyperthyroidism. Underlying
pathology can also be detected through these tests to facilitate to choose the type of treatment to be instituted. But various other special
investigations will be required to diagnose definitely the type of thyroid swelling. This will be discussed below alongwith the description
of various diseased conditions of the thyroid.
GOITRE
The term goitre is derived from the French word ‘goitre’, which is originally derived from the Latin word
‘guttur’ —means ‘throat’. We use the term ‘goitre’ to denote enlargement of the thyroid gland irrespective of
its cause. A few texts have described ‘goitre’ as benign enlargement of the thyroid gland usually associated
with normal production of thyroid hormone.
Goitre is classified as follows :
1. Simple goitre — (a) diffuse hyperplastic goitre; (b) nodular goitre; (c) colloid goitre.
2. Toxic goitre — (a) diffuse toxic goitre (Graves’ disease); (b) toxic nodular goitre; (c) toxic nodule.
3. Neoplastic goitre — (a) benign tumours; (b) malignant tumours.
4. Thyroiditis — (a) autoimmune thyroiditis; (b) subacute or granulomatous or de Quervain’s thyroidi
(c) Riedel’s thyroiditis.
5. Other rare conditions.
SIMPLE GOITRE
Aetiology.— This goitre is mainly formed due to stimulation with increased TSH. TSH secretion is increa
low level of circulating thyroid hormones. So any condition which will lead to decrease in production of thy
may lead to formation of simple goitre. The followings are the causes of formation of such goitre.
(a) Familial goitre.— This goitre may be seen in families. The inborn error in metabolism is generally inh
an autosomal recessive gene. There is enzyme deficiency within the thyroid gland. This may impair iodine a
oxidation or coupling of iodotyrosine. This leads to formation of decreased level of thyroid hormones which
TSH secretion and a simple goitre is formed. It must be remembered that although there is no enzyme defici
thyroid gland and there is adequate iodide in food and water, failure of intestinal absorption may produce i
(b) Endemic goitre (Iodine deficiency).— In certain places there is very low iodide content in the water an
inhabitants do not get even minimum requirement of iodine. This leads to formation of reduced levels of thyro
hence the goitre. These areas are the regions of the Alps, the Andes and the Himalayas. In the United States, th
regions are the mountainous areas, the upper north west America and around the great lakes. In Great Britain
is found in Derbyshire, Yorkshire and Southern Ireland. The famous Nile valley (also known as Struma Valley
are these areas. In low land areas around the lakes the soil lacks iodide. Calcium is goitrogenic and places whe
plenty of chalks and lime stones, goitre is endemic. Excess ingestion of iodine may develop goitre with thyroto
is known as ‘Jodbasedow disease.’ It must be remembered that the daily requirement of iodine is about 0.1 to 0
(c) Dyshormonogenesis or enzyme deficiency.— In non-endemic areas many sporadic goitres are due to enzym
of varying severity which lead to low thyroxin discharge, so TSH level goes up, which leads to formation of th
deficiency is often due to a genetic defect and is seen in families. It is often same as familial goitre as described
(d) Coitrogens.— There are certain goitrogens which have low iodine content and those who consume such
may produce this type of goitre. These are vegetables of the brassica family i.e. cabbage, turnips, kale, brussel,
sprout etc. Certain drugs such as P.A.S., thyocyanate, antithyroid drugs are also goitrogenic. Iodides in large q
also goitrogenic as they inhibit the organic binding of iodine to produce ‘iodide goitre’.
(e) Physiological.— In certain cases when there are high metabolic demands diffuse hyperplastic goitre ma
seen. Such conditions are puberty, pregnancy etc. In these conditions there is more demand of thyroid hormon
normal and if the thyroid gland fails to rise to the occasion, excessive TSH secretion will lead to this type of go
(0 Sporadic goitre.—This term is applied to an enlargement of the thyroid gland for which no definite caus
established. The diagnosis is mainly made by exclusion of other conditions. It may be due to impaired efficienc
thyroid gland or due to hypersecretion of TSH.
Pathology.— The thyroid gland is diffusely enlarged and smooth. It may be nodular. There are certain stage
through which this type of goitre gradually passes through. In thefirst stage due to TSH stimulation the lobules
composed of active follicles. This is called the ‘stage of diffuse hyperplasia’. When TSH stimulation ceases by
ingestion of iodine the second stage appears. Tliis is the ‘stage of involution’ forming large follicles filled with
colloid. If this condition continues i.e. in the third stage the gland enlarges to an enormous extent which is know
as colloid goitre. Sometimes due to fluctuating TSH levels a mixed pattern develops with areas of active lobules
and areas of inactive lobules. Inactive lobules gradually coalesce to form multinodular structure. There may be
haemorrhage or necrosis involving such nodules. Most of these nodules are inactive, but scattered between the
nodules are areas of normal thyroid tissue and focal areas of lymphocytic infiltration. There may be gross or
microscopic evidence of degeneration of the nodules with cyst formation, haemorrhage or calcification.
DIFFUSE HYPERPLASTIC GOITRE.—
Clinical features.— Females are more often affected in the ratio of about 9 : 1 . The age incidence varies,
but the condition usually starts in the teenagers, but patients may come to the clinic with multinodular goitre,
nodular goitre or colloid goitre in middle ages. If history of goitre and hypothyroidism starts from early childh
some inherited defect may be present. A family history is important in these cases. A deaf and goitrous patient
since infancy is known as Pendred’s syndrome.
SYMPTOMS.— Most patients with this type of goitre are asymptomatic. The most common symptom is the
swelling of the neck. If the goitre is too big there may be pressure effect on the trachea or on the oesophagus
(dysphagia). There may be distension of jugular veins due to pressure effect. Involvement of the nerves such a
recurrent laryngeal nerve or Horner’s syndrome is very rare and this usually suggests a neoplastic lesion. On
rare occasion there may be sudden pain with increase in size of the gland due to large haemorrhage within a
cyst or a degenerative nodule. This is an emergency condition and requires immediate attention.
SIGNS.— On inspection there is diffuse swelling of the thyroid gland which moves on swallowing. A
thyroid swelling always moves up on swallowing except (a) there is intrathoracic extension, (b) thyroiditis,
extending into adjacent structures, (c) carcinoma with invasion of surrounding tissues etc. On palpation the
thyroid is uniformly enlarged. Its consistency is softer than the gland of a patient with Graves’ disease.
NODULAR GOITRE.—
Patients are usually females and in their late thirties or forties. The symptoms have been more or less
described under diffuse hyperplastic goitre. On examination the nodules may be palpable which are usually
multiple. Occasionally a solitary nodule may be palpable but there are usually multiple small nodules which
remain impalpable. The nodules are usually colloid, cystic, degenerative, haemorrhagic or may form calcificati
COLLOID GOITRE.—
The patients are usually above 25 years of age, but occasionally patients may be seen with colloid goitr
their late teens. The symptoms have been described under diffuse hyperplastic goitre. On palpation there
diffuse swelling of the thyroid gland which is quite soft. One must palpate the common carotid artery and
trachea for pressure effect. Enquiry must be made regarding dysphagia i.e. pressure effect on the oesopha
Hardly there is any neurological involvement of recurrent laryngeal nerve or in the form of Horners’ synd
Diagnosis — is quite easy. The patient is euthyroid, the gland is soft and smooth on palpation. The glan
moves on swallowing. If there is certain amount of pain one should exclude carcinoma, but more often it
to haemorrhage in a simple nodule. One must exclude secondary thyrotoxicosis. Differential diagnosis fro
lymphadenoid goitre is difficult.
Complications.— This is particularly concerned in case of nodular goitre and colloid goitre. The usual
complications which may be seen in these two types of goitre are:
(a) Secondary thyrotoxicosis.— This may complicate about 30% of nodular goitres. This is discussed
later in this chapter.
(b) Tracheal obstruction.— This may be due to substemal prolongation of the goitre or may be seen in
goitres. Haemorrhage into a nodule can produce acute respiratory obstruction which requires immediate
(c) Carcinoma.— Though this is not common, yet one should exclude this possibility in case of all
nodular goitres. Its incidence has been quoted as below 5% and mostly follicular type of carcinoma is seen
these cases. Incidence of cancer has been reported more in endemic areas. Rapidly growing nodules in lon
standing goitres should always be suspected and subjected to aspiration cytology.
Special Investigations.— 1. Assessment of thyroid function is essential to exclude mild hyperthyroidism.
2. Straight X-ray of the neck and chest may show tracheal deviation or compression or sometimes
calcification of the goitre. This also ascertains the diameter of the lumen of the trachea. The study may rev
whether the goitre has extended into the thorax or not.
3. Barium swallow X-ray is indicated only if the patient complains of dysphagia.
4. Occasionally needle biopsy may be required to differentiate from diffuse thyroiditis.
5. In case of nodular goitres a few other tests may be required to exclude carcinomatous involvemen
These tests have been described later in this chapter.
Prevention and treatment of NON-NODULAR goitre.— In endemic areas (areas of Great Britain, Sub-
Himalayan areas of India, parts of U.S.A., Switzerland etc.) all table salts should contain iodide. This will
considerably reduce the incidence of endemic goitre. If the goitre is drug induced, discontinuance of the
offending drug is advised. All other non-nodular goitres should be treated with administration of thyroxi
the dose of 0.3 mg/day for a few months and then gradually the dose is reduced to 0.1 mg/day for a few
This treatment usually reduces the size of goitre particularly the diffuse hyperplastic variety. A little iodin
therapy may help to decrease the size of the goitre. Indications for operation are: (i) Cosmetic reasons when
the goitre does not respond to medicine; (ii) When there is pressure symptom or sign and when there is p
(iii) Rapid increase in size of the gland due to intraglandular haemorrhage; (iv) In case of presence of intra
goitre which is causing respiratory obstruction.
Operation.—In above conditions where operation is required in case of non-nodular goitres, the operat
is partial thyroidectomy. The technique is essentially same as subtotal thyroidectomy performed in case o
primary hyperthyroidism, but in these cases the amount of thyroid tissue left is same as the size of the no
thyroid gland. After thyroidectomy there is often need for supplemental hormone therapy.
In case of intraglandular haemorrhage causing acute respiratory obstruction aspiration is justified follo
by administration of thyroxin. In case of failures to relieve tracheal obstruction one may have to excise a
portion of the thyroid including the cyst. In case of congenital goitre in the new born with tracheal obstru
the best treatment is to resect the thyroid isthmus rather than tracheostomy.
Treatment of MULTINODULAR goitre.— This type of simple goitre is almost irreversible. Following
administration of thyroxin or thyroid extract in the dose of 120 to 180 mg/day, near about 50% of cases of
multinodular goitres show reduction in size. In majority of cases though there is decrease in overall size y
nodularity persists. So majority of these patients require surgery in the form of partial thyroidectomy. Sometimes
multinodular change is only seen in one lobe, probably with minimal involvement of the opposite lobe. In this
case total lobectomy should be performed. There is also a chance of carcinoma to be present within such
goitre. This also increases the indication for operation of this type of goitre. Postoperatively 0.1 mg of L-
thyroxin should be given daily to prevent recurrence by depressing TSH for indefinite period.
Treatment of COLLOID goitre.— For cosmetic reason treatment is always partial thyroidectomy. Ap
proximately normal amount of thyroid tissue is preserved and the rest is excised. The problem which one may
face is that the major functioning thyroid tissue may be removed in the process and what is left behind is not
absolutely functioning. So the patient will be in hypothyroid state following operation and will require
replacement hormone therapy in the form of L-thyroxin tablet for the rest of the life.
RETROSTERNAL GOITRE
Retrosternal goitres mainly derive from the lower pole of the multinodular goitres. In men whose necks are
short and the pretracheal muscles are strong, the negative intrathoracic pressure tends to draw the goitre into
the superior mediastinum. Only occasionally a few retrosternal goitres develop from ectopic thyroid tissue.
According to the degree of descent these goitres can be classified into (i) Substernal goitre — when the
goitre is palpable from the neck by insinuating finger behind the sternum, (ii) Plunging goitre — this goitre is
normally not palpable from the neck but in case of increased intrathoracic pressure such as during coughing or
sneezing the goitre is pushed into the neck, (iii) Intrathoracic goitre — when the goitre is completely inside the
thorax and is never palpable from the neck.
CLINICAL FEATURES.— This goitre may remain symptomless, but its main symptom is obstructive.
Obstruction to the trachea causing dyspnoea, obstruction to the oesophagus causing dysphagia or obstruction
to the major veins in the thorax causing engorgement of the neck veins is usually come across. This type of
goitre may turn toxic or malignant.
SPECIAL INVESTIGATIONS.— 1. X-ray of the chest may show compression on the trachea or calcification
of the goitre.
2. Barium swallow X-ray may be required in case of dysphagia to know the position and amount of
compression on the oesophagus. .
3. Thyroid scan is required to differentiate a retrosternal goitre from a mediastinal tumour.
4. Assessment of thyroid function is required in the form of serum T4, free thyroxin index and thyroid
uptake studies to know whether the goitre has been toxic or not.
TREATMENT.— In case of symptomless goitres treatment may not be required. In case of obstruction
there is no place for thyroxin, antithyroid drugs or radioiodine. Resection of the retrosternal goitre is the
OPERATION.— The cervical part of the goitre is first mobilised through the characteristic neck incision
(described later in this chapter). The superior thyroid vessels, middle thyroid veins and the inferior thyroid
artery are ligated. The retrosternal goitre is gradually mobilised from the neck and pulled up into the neck.
Since the blood supply is mainly derived from the inferior thyroid vessels, there is hardly any chance of
excessive haemorrhage. The recurrent laryngeal nerve should be identified and saved from injury. The goitre
is then excised alongwith the lobe of the thyroid gland from which it has originated. Only in case of excessive
adhesions, one may have to excise the goitre piecemeal.
ISOLATED THYROID SWELLING OR CLINICALLY ‘SOLITARY NODULE’
Thyroid swelling which appears to be isolated, and confined to one or other lateral lobe or to the isthmus is
not uncommon. Most of these swellings are simple nodular goitre formed by inactive colloid or apparently
localised manifestations of simple multinodular goitre. This group also includes the neoplastic group either
benign or malignant, cysts and localised chronic lymphocytic thyroiditis.
Solitary Nodule.— CLINICAL FEATURES.— A clinically solitary nodule is often a cluster of nodules of
non-toxic goitre usually between 1 and 4 cm in total size but occasionally much larger. In 50 to 60 percent of
patients when the gland is exposed it is evident that the process is in fact generalised with subclinical nod
elsewhere in the affected lobe or in the other lobe.
The patient complains mainly of the localised swelling in the neck which moves on deglutition. Only o
patient may complain of acute pain and increase in the size of swelling when there is haemorrhage inside
nodule. On palpation it is a smooth softish swelling, which has a very definite margin unlike carcinoma p
the anaplastic variety. The benign adenomatous swellings are also circumscribed but they feel firm.
Main problem is the DIAGNOSIS of such solitary nodule. History of irradiation to the head and neck
should arouse suspicion of a malignant swelling.
1. Thyroid function tests are not very useful as diagnostic test since most patients with thyroid cancer
and benign thyroid swellings are euthyroid. But this test if shows toxicity indicates a nodular toxic goitre
will be discussed under the heading of ‘toxic goitres’.
2. Radioactive scan is very helpful to differentiate ‘hot’ from ‘cold’ nodules. Hot nodules are unlikely
to be carcinoma and indicate to be toxic nodules. ‘Cold’ nodules are more suspicious. They may be cystic o
solid. Incidence of carcinoma in cold solitary swelling is about 15 to 20%. 80% or more are benign.
3. Ultrasonography is now commonly used in the diagnosis of localised thyroid swelling. This is high
accurate in determining the physical characteristic of the swelling and cysts or areas of cyst formation are
reliably differentiated from solid swellings. But ultrasound is highly inaccurate in predicting the underlyi
pathology. So this test is mainly used to differentiate cystic from solid lesion. Most cystic lesions are benig
except a few papillary carcinoma which may be cystic. That is why it was losing popularity, but now it is a
gaining popularity to be used as an adjunct to aspiration cytology.
4. Fine Needle Aspiration cytology (FNAC) — is now the investigation of choice in discrete thyroid nod
It is a simple technique and can be quickly performed even in outpatient department. Though this techniq
been claimed to have very high accuracy rate to diagnose different types of nodules, thyroiditis, papillary
medullary carcinoma, anaplastic carcinoma and lymphoma, yet it cannot distinguish between a benign fo
adenoma and follicular carcinoma as this distinction is dependent mainly on histology, which can even in
capsular or vascular invasion. There can also be unsatisfactory aspirates particularly in cystic swellings, in
only cyst fluid comes out with only few thyroid follicular cells on which the report depends. Nowadays u
is used to guide the needle to achieve the specimen from the cyst wall to know more about the disease.
5. Needle biopsy, particularly in solid group, is quite helpful for first hand knowledge. Concern about
dissemination of cancer cells along the needle track has been exaggerated but the technique has the disadv
of causing occasional morbidity such as pain, haematoma and transient recurrent laryngeal nerve palsy. T
also difficulty to take sample from small isolated swelling. Three major techniques have been used in perf
needle biopsy. These are: (a) Fine needle aspiration
biopsy; (b) Large needle aspiration biopsy and (c)
Cutting needle biopsy, (a) Fine,needle aspiration
using 21- to 25- gauge needle provides a specimen
for cytologic study, (b) The large needle techniques
provide tissue for histologic study. The advantages
of fine needle aspiration are numerous. It is safe, rap
cheap and well tolerated by patients. Even lesions
smaller than 0.5 cm can be sampled. The most
important factor is an experienced cytologist to
interpret the findings. This method usually allows th
cytologist to differentiate neoplastic from non
neoplastic nodules. Papillary, medullary and
anaplastic cancer are claimed to be easily recognized
The main limitation of this technique is its inability
Fig. 37.1.— Shows ultrasonic examination of a thyroid swelling. (0 differentiate between benign and malignan
The figure is a horizontal section showing a simple cyst with a . . , . . . T . . . . ,
clearly defined cyst wall. follicular neoplasms. In this situation total
thyroidectomy is recommended since 40% of these lesions are found to be malignant or to perform lobectom
and to wait for histology report to come. The subsequent treatment has been discussed under follicular carc
Large needle aspiration biopsy is performed with 16- or 18- gauge needle. A small clump of cellular materia
is obtained for histologic study. The tissue obtained in this manner is not as good for histologic study as tha
obtained by (c) cutting needle biopsy using Silvermann needles. This latter technique is applied only in nodul
more than 2 cm in diameter. This latter technique however has not been as popular as fine needle aspiration
to the complications of haematoma, injury to trachea or recurrent laryngeal nerve palsy.
6. CT and MRI.— Sophisticated scanning devices like CT (Computed Axial Tomography) and MRI
(Magnetic Resonance Imaging) could not prove very successful at present stage so far as investigation of
thyroid nodules are concerned. These investigations, though provide excellent anatomical detail of the thyro
nodules, are still confined to the use in assessing retrosternal or recurrent swellings.
7. Thyroid autoantibodies to a variety of thyroid antigens are detectable in the serum of patients with
autoimmune thyroid disease. Detection of such thyroid autoantibodies is not so important in case of solitary
nodules, but it is more important in case of generalised thyroid swelling. Only occasionally chronic lympho
thyroiditis may produce localised swelling or localised lymphoma may develop within a thyroid affected by
chronic lymphocytic thyroiditis which shows thyroid autoantibodies in the serum.
8. Chest radiography is necessary when there is tracheal deviation or compression or to know if there is
any retrosternal extension, particularly when the swelling has been suspected as malignant by other investig
TREATMENT.— We are only concerned with simple nodular goitre in this section. In finding out the
diagnosis of a localised thyroid swelling the various special investigations which have been narrated just
above should be performed. Once the diagnosis is established that it is neither a toxic, nor neoplastic, nor a
cystic swelling, but a simple nodular goitre, the treatment becomes mainly cosmetic. If there is no pressure
symptom or acute increase in swelling due to haemorrhage, the nodule may be left alone particularly in case
patients above 40 years of age. As the estimated risk of malignancy is about 5% to 30%, moreover not infreq
such goitre turns toxic, the treatment is excision of the solitary nodule alongwith a margin of normal thyroid
tissue all around. The excised nodule should be sent for histopathological report. If carcinoma is detected by
histological examination, total thyroidectomy is advised.
TOXIC GOITRES
Whatever may be the causes, thyrotoxicosis refers to an accumulation of clinical manifestations which are
due to excess secretion of active thyroid hormones.
CAUSES OF THYROTOXICOSIS are :
(a) Graves’ disease; (b) Toxic multinodular goitre; (c) Toxic adenoma. Rare causes are — (d) Early s
of de Quervain’s thyroiditis; (e) Jodbasedow syndrome; (f) Thyrotoxicosis factitia; (g) Struma ovarii;
(h) Iatrogenic hyperthyroidism; (i) Disseminated thyroid autonomy; (j) Neonatal thyrotoxicosis.
Broadly speaking there are two distinct types of toxic goitres — 1. Primary toxic goitre and 2. Secondary toxic goitre
GRAVES’ DISEASE OR DIFFUSE TOXIC GOITRE OR PRIMARY TOXIC GOITRE
It is a diffuse goitre affecting whole of functioning thyroid tissue causing hypertrophy and hyperplasia d
to abnormal thyroid stimulants such as LATS. It is usually seen in younger women and is frequently associa
with eye signs. It is always associated with primary thyrotoxicosis.
Aetiology.— The cause of Graves’ disease is not very clearly known. It is considered to be a systemic
autoimmune disease in which there are three components — (i) Hyperthyroidism, (ii) Exophthalmos and
(iii) Dermopathy called pretibial myxoedema. It is believed that hyperthyroidism results due to abnormal
thyroid stimulant such as thyroid-stimulating antibody (TSH-RAb) that binds to TSH receptor sites.
These are mostly detectable in the serum of the patients suffering from hyperthyroidism in Graves’
disease. It is usually seen in younger women and 50% of patients have family history of autoimmune
endocrine diseases.
There are other contributory factors in the aetiology of this disease. They are : (a) Heredity, (b) Sex, and
(c) Emotional disturbances, (a) Heredity.— Graves’ disease is often seen in several members of the same
family. Other thyroid disorders (particularly Hashimoto’s thyroiditis) are also seen in these families. (b)Sex—
There is hardly any doubt that this condition affects females more often than males in the ratio of about 6:1.
(c) Emotional disturbances.— Different types of stresses have been incriminated as the cause of this condition
but its importance is still questioned.
Pathology.— In Graves’ disease the thyroid is uniformly enlarged and the surface is characteristically smo
though slight nodularity may be detected. Microscopically the thyroid is hyperplastic and the epithelia which
the acini are high columnar instead of flattened cuboidal type which is found in normal thyroid gland. There
minimal amount of colloid in the acini and many of them are even empty and others contain vacuolated coll
The nuclei of the thyroid cells exhibit mitoses. Papillary projections of the hyperplastic epithelium into the a
common. Lastly there is increase in vascularity and lymphoid tissue around the acini.
CLINICAL FEATURES.— In Graves’ disease a classical triad, composed of goitre, thyrotoxicosis and
exophthalmos, is seen. Occasionally one of these features may occur singly or in any combination. Graves’ d
most commonly becomes clinically apparent in young patients, though this can occur at all ages. It is hardly
before 10 years of age and in the elderly. As has already been quoted the female/male ratio is about 6:1.
(i) GOITRE.— Barring a few cases in which thyroid may not be seen to be enlarged (not more than 2%
of cases), thyroid is usually enlarged to varying extent. The enlargement of thyroid is diffuse and symmetric
Even the pyramidal lobe may be enlarged and may become palpable. Obstructive symptoms due to enlargem
of the gland from encroachment on the trachea or oesophagus are rare. On palpation the gland surface is
characteristically smooth, but it is often irregular with fine nodularity. Extreme vascularity is very characteri
Bruit may be heard on the goitre, but it is best heard on the superior pole on either side.
(ii) THYROTOXICOSIS.— There are groups of symptoms in thyrotoxicosis.
Patients with thyrotoxicosis are extremely excitable, restless, emotionally unstable and often complain of
insomnia. Muscle weakness, wasting, fatigue are common in thyrotoxicosis. Muscle weakness is most eviden
proximal limb muscles. In extreme cases myopathy may be seen. Muscle problems are more often seen in ma
than females. Physical examination of patients will demonstrate tremor of the extended and abducted fingers
Tendon reflexes will be hyperactive in this condition. This group of symptoms is more marked in patients w
Graves’ disease than in patients with multinodular toxic goitre, toxic adenoma or rare cases of hyperthyroid
A few features due to increased calorigenesis are quite evident in thyrotoxicosis. The patients often feel
warmer and gradually become intolerable to heat. There is increased sweating and thirst. There is weight loss
inspite of increased appetite. These manifestations of increased calorigenesis are also more marked in patients
with Graves’ disease than in other causes of thyrotoxicosis.
Cardiovascular manifestations are more marked in older patients with toxic multinodular goitre. Thyroto
cosis, when affects previously existent multinodular goitre or nodular goitre, is called SECONDARY
THYROTOXICOSIS. Tachycardia is a characteristic feature of this condition and sleeping pulse rate is mostl
80. Patients may experience palpitation. Cutaneous and peripheral vasodilatation results in low diastolic pre
There is increased cardiac output and hence high systolic pressure. Combination of high systolic pressure an
diastolic pressure will produce increased pulse pressure and water-hammer pulse. Atrial fibrillation, which
paroxysmal in the beginning and gradually becomes continuous, is also a common finding of secondary thy
Congestive cardiac failure with ankle oedema and dyspnoea is occasionally seen in secondary thyrotoxicosis
Changes of the skin and its appendages are often seen in thyrotoxicosis. The skin becomes warm and mo
There is facial flushing and perspiration. The nail becomes soft and increasingly fragile. There may be clubbi
of the fingers and toes. The hair becomes fine and readily falls out with combing. Gynaecomastia may be see
due to hepatic dysfunction and incomplete metabolism of circulating oestrogen. Menstrual periods are often
scanty or absent and return to normal when thyroid function is controlled. Libido may be increased but ferti
is reduced with high rate of miscarriages.
Pretibial myxoedema is thickening of the skin with mucin like deposit in the lower part of the leg. In the
early stage the skin becomes thick and red. Sometimes the whole leg below the knee is involved. This condit
is almost associated with exophthalmos and high level of TSH-RAb.

Thyrotoxicosis has got a peculiar action on gastrointestinal tract. Diarrhoea or increased frequency of
defaecation is most often complained of. Excess of thyroid hormone results in increased bone turn-over, whic
in its turn produces hypercalcaemia, though no increased incidence of renal calculi has been noticed.
(iii) EXOPHTHALMOS.— ‘Exophthalmos’ means protrusion of the eyeball. Relation of exophthalmos w
disease is very peculiar. On one hand it is true that severe thyrotoxicosis may not be necessarily accompanied
on the other hand exophthalmos may be the only manifestation of Graves’ disease. Only in l/3rd of cases, the
manifestations and the signs and symptoms of thyrotoxicosis begin simultaneously. It may be unilateral or bilat
eye signs of Graves’ disease are various. The important ones are — (i) spasm of the upper eye lid with lid retr
proptosis with widening of the palpebral fissure; (iii) supraorbital and infraorbital swelling; (iv) congestion, o
chemosis of the conjunctiva; (v) in severe cases the papilloedema and comeal ulceration may occur; (vi) extern
ophthalmoplegia or weakness of the extrinsic ocular muscles is present in about 40% of cases of Graves’ disea
rotation with lateral rotation of the eyeball is most commonly affected. It must be remembered that true exopht
proptosis of the eye caused by infiltration of the retrobulbar tissue with fluid and round cells. This may be ass
some degree of retraction and spasm of the upper eye lid. Though spasm and retraction of the upper eye lid m
when hyperthyroidism is controlled particularly by administration of beta-adreneigic blockers, yet exophthal
progresses after thyrotoxicosis has been relieved by surgical treatment and radioactive iodine. The extent of e
or proptosis can be measured with an exophthalmometer, which indicates the distance between the horizonta
anterior convexity of the cornea and the bony margin of the orbit. In a person with normal vision reading of m
mm is abnormal. Oedema of the eye lids, chemosis and congested conjunctiva with venous congestion is a sig
exophthalmos which is classically known as 'malignantexophthalmos".
Clinically exophthalmos can be divided into two categories — (a) Apparent and (b) True.
(a) Apparent.— Such exophthalmos is mainly due to spasm and retraction of the upper eyelid. This is
mainly caused by sympathetic nerve irritation which supplies the Muller’s muscle (the unstriped muscle fibre
and the levator palpebrae superioris.
(b) True.— Such exophthalmos can be further subdivided into mild form and severe form —
(i) Mild form is due to persistent contraction of the Muller’s muscle probably due to continued
sympathetic stimulation.
(ii) Severe form is due to infiltration of the retrobulbar connective tissue with fluid, fatty deposits and
round cells. This occurs probably due to lymphatic or venous obstruction. Gradually there is oedema of the
eyelids, chemosis and congested conjunctiva, which becomes progressive and classically known as ‘Malignan
exophthalmos’.
Cause.— Progressive exophthalmos occurs due to liberation of a special pituitary hormone known as
exophthalmos producing substance or hormone (EPS or EPH). That, it is not due to T.S H., is proved by the
fact that exophthalmos cannot be produced experimentally by administration of T.S.H. and partial relief of
malignant exophthalmos can be achieved by pituitary ablation or stalk section.
The degree of exophthalmos can be best measured by an instrument known as ‘exophthalmometer’.
Malignant exophthalmos is more commonly seen in male and is associated with increased lacrimation and
pain in the eye. Eye sight may be lost. Exophthalmos is usually a self limiting disease and may even regress to
varying extent. Hypothyroidism however increases proptosis. Lateral tarsorrhaphy operation helps to protect
the eye. Improvement has been reported with massive doses of prednisolone ar.d with metronidazole. When
the eye is in danger orbital decompression may be required.
OTHER EYE SIGNS are as follows
(i) Von Graffe’s sign.— When the patient is asked to look down, his upper eyelid fails to follow the
rotation of the eye ball and thus lags behind.
(ii) Joffroy’s sign.— When the patient is asked to look upwards with the head fixed, there will be absence
of wrinkling on the forehead.
(iii) Moebius’ sign.— Failure of convergence of eye balls.
(iv) Dalrymple's sign.— Normally the upper sclera is not seen. But when this sign becomes positive the
upper sclera will be seen due to retraction of the upper eyelid.

(v) Stellwag's sign.— Absence of normal blinking i.e. staring look.
Diagnosis and Special Investigations.— The tests to assess thyroid function are enough to give indication
that the clinician is dealing with a case of thyrotoxicosis. These are described above in the section of ‘Asses
Of Thyroid Function’. This alongwith generalised enlargement of the thyroid and exophthalmos leaves litt
doubt that he is dealing with a case of Graves’ disease. About 30% cases of Graves’ disease have circulating
antibodies against gastric parietal cells. A high titre of thyroid autoantibodies is also found in about '/3rd o
patients with Graves’ disease. Wayne’s clinical diagnostic index is very helpful in detecting a case of
thyrotoxicosis. The chart is given below : —
Wayne’s Clinical Diagnostic Index
Signs Present Absent Symptoms Present Absent
Palpable thyroid — +3 -3 Palpitations — +2
Exophthalmos — +2 Excessive sweating — +3
Lid retraction — +2 Appetite increased — +3
Finger tremor — +1 Appetite decreased —— -3
Bruit over thyroid — +2 -2 Weight increased —— -3
Atrial fibrillation — +4 Weight decreased — +3
Pulse rate — Preference for cold — +5
90 per minute — +3 Preference for heat —— -5
80 per minute — — -3
Index over 19 indicates toxic goitre. Index below 11 indicates non-toxic goitre.
T3 thyrotoxicosis is diagnosed by estimating T3 in the serum. It may be diagnosed when the routine test
thyroid function are within the normal range yet the clinical picture is very much suggestive of thyrotoxico
HYPERTHYROIDISM DUE TO OTHER CAUSES.—
JODB ASEDOW SYNDROME.— It is a case of diffuse toxic goitre when large doses of iodide are given
to a hyperplastic endemic goitre. These are often seen in European countries. This type of hyperthyroidism
usually temporary, but rarely it may be persistent.
EARLY STAGE OF DE QUERVAIN’S THYROIDITIS.— In early stages of subacute or acute forms of
autoimmune thyroiditis or of de Quervain’s thyroiditis, mild hyperthyroidism may occur due to liberation
excess thyroid hormones from damaged tissues of thyroid.
THYROTOXICOSIS FACTITIA.— When thyroxine is taken in the dosage more than normal requiremen
(0.15 to 0.25 mg) per day, hyperthyroidism may occur. But if the dose is below the normal requirements it
suppresses normal hormone production by the thyroid.
NEONATAL THYROTOXICOSIS.— This may only occur when TSH-RAb titre is raised in the child.
This only occurs when the baby is born to hyperthyroid mother or to euthyroid mother who had treatment
earlier thyrotoxicosis. In fact TSH-RAb titres are present in both the mother and the child as this can cross t
placental barrier. Such hyperthyroidism in a new born baby gradually subsides in months time and TSH-R
titre falls in the baby’s serum.
SECONDARY CARCINOMA.— This can rarely produce mild hyperthyroidism when excess hormone i
produced from the thyroid.
.TREATMENT.— There are three main approaches to the treatment of this condition. These are :
(I) Antithyroid drugs; (II) Radioactive iodine and (III) Surgery. Besides these three main types of treatment
non specific measures such as rest, sedation and beta-adrenergic blockers are helpful to treat this condition.
Each case should be judged on its merit.
(I) Antithyroid drugs.— These are used to restore the patient to euthyroid state and to maintain th
a long period in the hope that a permanent remission will occur. These drugs interfere with organic bindin
iodine in the thyroid or inhibit coupling of iodothyrosines and hence decrease the formation of thyroid hor
So these drugs actually do not treat the underlying cause of the disease, but only reduce the amount of thy
hormones. Only recently it has been claimed that propylthiouracil (PTU) decreases thyroid-stimulating
immunoglobulines. Mainly two types of drugs are used. One is propylthiouracil, another is carbimazole. As
the potency of the latter drug is about 10 times that of the former, the dose required is 100 to 300 mg of the
former every 6 to 8 hours or 10 to 20 mg of the latter every 6 to 8 hours. Carbimazole should be started in a
high dose of 10 mg 4 times a day for about 14 days, when some improvement in the degree of thyrotoxicos
is noted and then in the euthyroid state a maintenance dose of 5 mg 3 times a day is given for 6 to 12 mont
Thyroxin 0.2 mg may be given in addition to the antithyroid drugs to minimise the size of the goitre quick
and to counteract any chance of iatrogenic thyroid insufficiency. In order to be effective the anti thyroid ta
must be taken every 6 to 8 hours. Many patients do not take the tablets properly and in such cases thyrotox
invariably recurs. These cases are better treated by surgery or radioactive iodine.
Only in limited number of patients (approximately 5%) side effects of antithyroid drugs become evident
These include skin rash, fever, peripheral neuritis, polyarteritis, agranulocytosis and aplastic anaemia. The
two are dangerous complications and in the event of agranulocytosis the drug should be discontinued.
Propylthiouracil may cause prothrombin deficiency responding to Vitamin K therapy. The most serious
complications of antithyroid drugs are agranulocytosis and aplastic anaemia.
(3 adrenergic blockers e.g. propranolol and nadolol are also antithyroid drugs and may be used. It mus
remembered that basically antithyroid drugs are used to restore an euthyroid state and to maintain this for
prolonged period so that permanent remission can occur This is assessed by the fact that production of thy
stimulating antibodies (TSH-RAb) will diminish or disappear.
Advantages.— 1. Patients always choose this treatment rather than surgery or radioactive iodine. 2. Belo
45 years with diffuse small goitre this should be the preliminary treatment in all cases. 3. It is the treatmen
choice during pregnancy and in cases of children. 4. This therapy should be advised in cases with high titr
thyroid antibodies. 5. This treatment is also advised in cases of proptOsis of recent onset.
Disadvantages.— 1. It is impossible to give guarantee to the patients whether they will be cured or not. 2
Treatment is prolonged. 3. The failure rate is very high (more than 50%) even after a course of VA to 2 year
4. Some goitres enlarge and become very vascular following this treatment, even if thyroxin is given at the
same time. 5. Its side effects and complications are to be considered.
(II) Radioactive iodine.—This treatment destroys thyroid cells and reduces the mass of thyroid func
ing tissue. An objection to radioactive iodine therapy in the young patient is based on subsequent genetic
damage, leukaemia and subsequent development of carcinoma. But many reports have failed to show that
incidence of carcinoma appears to be increased. Anyway, most centres have restricted the use of radioactiv
iodines to adults over the age of 40 years and are never advised to pregnant women and nursing mothers.
Incidence of leukaemia is little, if at all, increased by this therapeutic modality. The possibility of genetic
abnormalities in the offsprings following radioiodine treatment is also very minimal.
The average dose for diffuse toxic goitre is 7 to 9 mCi of l3lI. In case of toxic nodular goitre this dose is
increased to 12 to 15 mCi. Approximately 8500 rads dose is given to the thyroid. Response is slow and a
definite improvement is obtained in 8 to 12 weeks time. If there is no improvement after 12 weeks a furthe
dose is required. In about 20% of cases two or more doses become necessary.
Advantages.— 1. It does neither require a prolonged drug therapy nor surgery. 2. It is the cheapest thera
of the three.
Disadvantages.— 1. There is a chance of developing thyroid insufficiency and permanent myxoedema.
2. It requires some time to control the disease. 3. Nodules may develop in thyroid during this therapy. 4. T
therapy is not very satisfactory in cases of nodular toxic goitre. 5. There is a very high incidence of hypothy
as the years pass by. At the end of 10 years there is 70% incidence of hypothyroidism and it may reach 100
if the patients live long enough subsequent to therapy. So a long follow-up is required.
(Ill) Surgery.— This is aimed to reduce the active thyroid mass and is generally planned to leave a remn
which eliminates both hyperthyroidism and goitre. In cases of big diffuse toxic goitre and toxic nodular go
this is the treatment of choice. In case of autonomous toxic nodule, surgery is the easy method of treatmen
one may try with radioiodine in cases of above 40 years of age.
Advantages.— 1. Immediate cure. 2. No prolonged treatment. 3. No long follow-up is required. 4. Subtotal

thyroidectomy also makes possible the simultaneous removal of an incidental papillary carcinoma, which is
noted in 2% of cases. 5. The patients can leave the hospital by 5 days and resume work within 1 month.
Disadvantages.— 1. Recurrence of thyrotoxicosis occurs in about 5% of cases. 2. Every operation carries
morbidity and mortality. 3. Postoperative thyroid insufficiency may occur. 4. Parathyroid insufficiency may
also complicate surgery. 5. Recurrent laryngeal nerve may be injured.
PREOPERATIVE PREPARATIONS.— (i) Any antithyroid drug should be prescribed before operation to
bring the patient to the euthyroid state. Propylthiouracil is usually used in the dose of 100 mg. thrice daily. La
doses may be required if rapid control is desired. It is preferable to do the operation about 2 months after the
has been brought to euthyroid state. If surgery is performed too soon after control of thyrotoxicosis, there is a
of thyroid crisis, (ii) It is customary to treat controlled thyrotoxic patients with iodide or iodine. 10 drops of Lug
solution 3 times daily for 10 days prior to surgery is often used for this purpose. Potassium iodide tablets 60 m
times daily may be used instead of Lugol’s solution. Iodine is given to decrease the size and vascularity of the
gland. Thyroxin may be used instead of iodine. The former will suppress the TSH increase due to use of antith
fi. drug, which will also decrease the
vascularity of the gland, (iii)
Propranolol (Beta-adrenergic
blocker) (40 mg t. d. s.) has added
safety to the operation for Graves’
disease. This drug decreases the
pulse rate, tremor and anxiety,
although thyrotoxicosis remains.
Usually this drug is given 7 days
prior to operation. Propranolol,
when given preoperatively, should
be continued postoperatively also
for 7 days.
Subtotal thyroidectomy.—
After the patient is prepared for
subtotal thyroidectomy, three
investigations are to be carried out
before one should venture for
operation — (a) Laryngoscopy to
see the condition of the cords to
exclude injury to recurrent
Fig. 37.2.— The figure shows a ligature being passed round the superior
laryngeal nerve during operation.
thyroid artery. The ligature round the inferior thyroid artery is not shown.
The dotted line shows the line of division of thyroidectomy. So laryngoscopy should also be
performed just after operation.
Only in 3% of cases there may be symptomless cord paralysis. These cases are to be segregated from cord
paralysis due to recurrent laryngeal nerve injury during operation by laryngoscopy preoperatively. (b) Thyroid
scan to differentiate between multinodular toxic goitre and autonomous toxic nodule to assess the type of
surgery to be performed, (c) Detection of thyroid antibodies.
Technique.—General anaesthesia with endotracheal intubation is advised. The neck of the patient is extend
by placing of pillow between the shoulder blades. An incision is made one inch above the sternal ends of the
clavicles starting from lateral margin of one sternomastoid to the lateral margin of the other sternomastoid. Th
incision is deepened to cut the subcutaneous tissue. The platysma is incised slightly higher than the skin incisi
for better scar. The flaps of the skin, subcutaneous tissue and platysma are raised upwards to the upper borde
the thyroid cartilage and below to the suprasternal notch. The investing layer of the deep cervical fascia is inci
vertically in the midline. The veins which are coming in the way should be divided between ligatures. The
infrahyoid muscles are retracted. The anterior surface of the gland covered with pretracheal fascia is expose
This fascia is incised and a finger is insinuated to know the whole extent of the goitre. If by retraction of the
infrahyoid muscles proper exposure of the thyroid lobes is not attained, these muscles can be divided as hig
as possible to cause minimum damage to the nerve supply which comes from below. Thyroid lobes are then
mobilised. The superior pole of the’gland is first delivered at the wound where the superior thyroid vessels
clamped as close to the gland as possible to prevent injury to the external laryngeal nerve and then divided.
lateral lobe is now retracted forward when the middle thyroid vein at the middle of the gland will be found
is tied and divided. Next the inferior thyroid artery is ligated in continuity far away from the gland to avoid
to the recurrent laryngeal nerve. The recurrent laryngeal nerve often lies between the branches of the inferio
thyroid artery so that identification of the nerve is important. The nerve passes into the larynx immediately
behind the inferior cornu of the thyroid cartilage, which is an important landmark. A traction on the ligatur
the trunk of the inferior thyroid artery will make the nerve taut and can be felt easily. Parathyroid glands ar
protected by careful inspection before resection. Now subtotal resection of each lobe is carried out leaving a
remnant of'/gth of each lobe (4 to 5 Gm on each side). Absolute haemostasis must be secured. If a parathyroid
gland is accidentally excised, it should be autotransplanted into a pocket, formed within the stemomastoid
muscle. The pretracheal muscles are sutured. The platysma muscle is sutured separately and then the woun
is closed with a suction drainage into the deep cervical space.
Postoperative care.— (i) Indirect laryngoscopy should be performed in all cases before leaving hospital,
(ii) Serum calcium should be estimated after 6 weeks to exclude parathyroid insufficiency, (iii) After 6 mont
and then at yearly intervals investigations should be performed to exclude recurrence of thyrotoxicosis or
thyroid insufficiency.
Postoperative Complications.—Postoperative complications after thyroidectomy can be broadly divided
into 2 groups — A. Immediate complications and B. Late complications.
A. IMMEDIATE COMPLICATIONS.—
1. Haemorrhage.
2. Infection.
3. Recurrent laryngeal nerve paralysis.
4. Thyroid crisis or storm.
5. Respiratory obstruction.
6. Parathyroid insufficiency or tetany.
B. LATE COMPLICATIONS.—
1. Thyroid insufficiency.
2. Recurrent thyrotoxicosis.
3. Progressive exophthalmos.
4. Hypertrophic or keloid scar.
1. HAEMORRHAGE, which may be primary or reactionary may complicate the convalescent period. Bleeding in this
condition has a separate importance in that it accumulates behind the infrahyoid muscles and may lead to serious respiratory
difficulty by giving pressure on the trachea. In this condition one should re-explore the wound, evacuate the haematoma
and the bleeding vessels should be secured. A small subcutaneous haematoma may however be aspirated. The best
preventive measure to avoid this complication is to attain absolute haemostasis before closing the wound.
2. INFECTION.— Incidence of wound infection is almost similar to any other operation. This has been extensively
reduced by achieving proper haemostasis at the site of surgery and by the use of suction drainage instead of conventionally
used corrugated rubber drain.
3. RECURRENT LARYNGEAL NERVE PARALYSIS.— It is usually temporary and is caused by pressure on the
nerve by haematoma or oedema. This may occur unilaterally or bilaterally. The temporary paralysis usually recovers in 3
weeks to 3 months time. If recovery does not occur within this period permanent injury to the nerve should be suspected.
Permanent injury to the nerve is extremely rare (0 to 2% of cases) and may be caused from undue stretching or by its inclusion
in a ligature.
Injury to this nerve should be avoided at all costs. This can be done by (i) first identifying this nerve before ligating the
inferior thyroid artery; (ii) The inferior thyroid artery is ligated as far away from the thyroid as possible to keep the nerve
safe; (iii) The posterior lamina of the pretracheal fascia should be kept intact as the nerve lies behind the fascia.
The recurrent laryngeal nerve supplies all the muscles of the larynx, except cricothyroid, which not only renders the
vocal cords tense, but also adduct the vocal cords by rotating arytenoids medially. It also supplies sensory branches to the
laryngeal mucous membrane below the level of the vocal cords. In case of unilateral nerve injury, the vocal cord of the
affected side will be motionless, while the opposite vocal cord will cross the midline to accommodate itself to the affected
one. This may cause hoarseness of voice, cough and tendency of fluids to go down the larynx during deglutition. In majority
of cases these difficulties pass off in a few months as accommodation occurs. In case of bilateral nerve injury, both the vocal
cords will be motionless, the so-called ‘cadaveric position’. So immediate asphyxia may occur as soon as the endotracheal
tube will be withdrawn by the anaesthetists. Immediate tracheostomy is the life-saving measure.
SUPERIOR LARYNGEAL NERVE PARALYSIS.— This is extremely rare. Even if it occurs it hardly affects
functioning of the vocal cords. However if the superior and recurrent nerves are both injured, the vocal cord assumes a
position midway between abduction and adduction and remains without tension as seen in the dead. This is known as
cadaveric position of the cord.
4. THYROID CRISIS OR STORM is a severe thyrotoxic reaction and appears suddenly within 3 or 4 days after
operation. It is an acute exacerbation of hyperthyroidism. It occurs if a thyrotoxic patient has not been brought down to
euthyroid state before operation. It is characterised by tachycardia, fever (which may rise upto 105° F or more), restlessness,
delirium etc. The treatment is mainly preventive and the patient must be brought to euthyroid state before operation. When
the condition has already developed, the treatment is as follows :—
Treatment.— (i) The patient should be sedated immediately with morphin or pethidine, (ii) Hyperpyrexia should be
controlled by Ice-bag, tepid sponging, hypothermic blanket, rectal ice irrigation and the patient should be kept in an
airconditioned room, (iii) Oxygen is administered and intravenous drip of glucose-saline should be started to combat
dehydration, (iv) Potassium may be added to control tachycardia, (v) Cortisone is often highly effective and 100 mg. cortisol
may be administered, (vi) Lugol's iodine (20 to 40 min. upto 100 min. in 24 hours) should be given intravenously. Thereafter
it may be given orally 60 min. every 8 hours for 48 hours. Gradually the dose is reduced, (vii) Propranolol (beta-adrenergic
blocker) should be used in the dose of 20 to 40 mg 6 hourly, (viii) For atrial fibrillation, digitalis may be cautiously
administered since it may overburden the heart which is already weak in these cases.
The mortality rate of this condition is approximately 10%.
5. RESPIRATORY OBSTRUCTION is mostly due to laryngeal oedema. Besides tension haematoma, laryngeal
oedema may be caused by anaesthetic intubation and surgical manipulation. When the goitre is very vascular there is more
chance of such oedema. If releasing the tension haematoma does not immediately relieve airway obstruction, the trachea
should be intubated immediately in the idea that laryngeal oedema is thecause of respiratory obstruction besides haematoma
only. Intubation in presence of laryngeal oedema may be very difficult and may call for assistance of an experienced
anaesthetist as repeated attempts may cause more oedema and may lead to cerebral anoxia. The endotracheal tube can be
left in place for several days and steroids should be given to reduce laryngeal oedema. Only in rare cases tracheostomy may
be necessary.
6. TETANY.— Damage of the parathyroid glands resulting in tetany has been reported in about 1 to 3 per cent of cases
subjected to thyroidectomy for thyrotoxicosis. Majority of cases present within 2 to 5 days after operation but a few may
be delayed for 2 to 3 weeks. Mostly it is transient and recovers spontaneously. The serum calcium level falls and the treatment
is administration of 20 ml of 20% calcium gluconate solution with some parathormone.
7. THYROID INSUFFICIENCY.— In 10 to 30% of patients subjected to thyroidectomy for thyrotoxicosis
permanent hypothyroidism may complicate. The appearance of this condition is very insidious and may be difficult to
diagnose. It usually represents a change in the autoimmune response to the thyroid cells rather than operative removal of
too much of thyroid tissue. This usually appears within 2 years of operation and may be delayed for 5 years or more.
Treatment is administration of L-thyroxin.
8. RECURRENT THYROTOXICOSIS may occur in approximately 5-10% of cases after.operation. This may occur
either due to inadequate removal of the thyroid tissue or to subsequenthyperplasia of the remaining thyroid tissue. That is
why while deciding the amount of thyroid tissue to be removed in case of toxic goitres, err should be made towards leaving
too little tissue. If at all this occurs the condition should be treated by antithyroid drugs in case of patients below 40 years
and radioiodine in cases of patients above 40 years of age.
9. PROGRESSIVE OR MALIGNANT EXOPHTHALMOS.— Occasionally this may occur after operation. While
thyrotoxic features regress, exophthalmos may increase.
10. KELOID SCAR.—To avoid such scar platysma should be incised at a level just above skin incision. A fewpersons
are vulnerable to produce hypertrophic scar. Such unseen scar may occur following wound infection.
Choice of therapy.— It is well appreciated that each case should be considered individually. Various factors are considered, particularly
the age, facilities available, wish of the individual patient, profession of the patient etc. A list is provided below to set a guideline.
DIFFUSE TOXfC GOITRE.— In patients under 45 years surgery should be advised for large goitre and antithyroid drugs or
radioiodine for the small goitre. For patients over 45 years radioiodine is preferred.
TOXIC NODULAR GOITRE.— It does not respond to antithyroid drugs or radioiodine, so surgery should be advised.
TOXIC NODULE.— In this case both surgery or radioiodine may be used, but surgery is preferred as the result is certain and
without morbidity. For patients over 45 years one can consider radioiodine as the other thyroid tissues do not take up iodine, so
treatment is satisfactory and the risk of delayed thyroid insufficiency is much less.
RECURRENT THYROTOXICOSIS AFTER SURGERY.— Here further surgery has almost no place, so radioiodine is the preferred
treatment. Only in case of young women intending to have children radioiodine should be avoided and antithyroid drugs should be used
CHILDREN AND ADOLESCENTS.— These cases should be treated with antithyroid drugs as radioiodine is not used due to a
theoretical risk of inducing carcinoma at later age. Surgery is also avoided as there is increased risk of recurrence as the thyroid cells are
more active in the young. Antithyroid drugs should be continued till late teens, if there is failure in treatment total or near-total thyroidectomy
may be advised at this stage.
PREGNANCY.— In these cases radioiodine is totally contraindicated due to the risk to the foetus. The problem of surgery is
miscarriage or abortion. Antithyroid drugs have also problems as this may cause thyroid insufficiency in the mother and the baby may
bom goitrous and hypothyroid as both TSH and antithyroid drugs cross the placenta. The only solution is surgery in the 2nd trimester
Careful administration of antithyroid drugs may not produce any complications.
SECONDARY TOXIC GOITRE

When toxicity superimposes on previously pathological goitre, it is called secondary toxic goitre. Toxic
multinodular goitre and toxic adenoma are examples of secondary toxic goitre. As the features of toxicity
appear at a variable interval from the appearance of the thyroid swelling, hence called secondary toxic goitre.
Differences between primary and secondary toxic goitres are :—
Primary Secondary
1. Goitre appears alongwith toxic symptoms. 1. Goitre appears first and toxic symptoms appear much
later.
2. The patients are usually young. 2. The patients are usually older, almost always above 35
years of age and may occur even much later in life.
3. Female/male ratio is about 6:1. 3. Female/male ratio is about 8 : 1.
4. The symptoms appear suddenly and are seldom mild. 4. Symptoms appear gradually and are usually mild.
5. Nervous manifestations dominate. 5. Cardiovascular manifestations are more dominant.
6. Exophthalmos and eye-signs are quite common. 6. Exophthalmos and eye-signs are virtually never seen.
7. The goitre is uniform, firm and moderate in size. 7. Goitre is usually nodular and may be quite big.
TOXIC MULTINODULAR GOITRE
Aetiology and Pathology.— This is usually superimposed on a long standing non-toxic multinodular goitre.
Macroscopically the gland contains multiple nodules, many of which contain aggregates of irregular cells and considerable
amount of colloid. These nodules are rather inactive, but it is the internodular thyroid tissue which becomes overactive. In
some cases a few nodules may be overactive and in these cases it is more or less like autonomous thyroid nodules, which
are independent of stimulation by TSH. But the former case of hyperthyroidism is due to LATS overactivity.
Clinical features.— The patients are usually middle aged — 40 to 60 years of age. Females are more often
affected than males. The syndrome is that of secondary thyrotoxicosis. Exophthalmos is rarely present. There are
features of hyperthyroidism with more cardiovascular manifestations. There may be symptoms related to obst
of the trachea and/or oesophagus. On inspection a bigger thyroid can be seen than Graves’ disease. On palpat
multinodularity becomes obvious. The surface is irregular and is relatively firm than a non-toxic goitre.
Diagnosis and Special Investigations.— Radioiodine uptake of these cases is generally less than that in
Graves’ disease. Thyroid scan is essential which will demonstrate ‘hot’ areas.
Treatment.— Surgery is probably the best treatment of this condition. Subtotal thyroidectomy is the type
of operation required. This condition does not respond so rapidly to radioiodine or antithyroid drugs in
comparison to Graves’ disease. Moreover the goitre is often large and uncomfortable.
TOXIC NODULE
Aetiology and Pathology.— This is most often a follicular tumour of unknown origin. It is autonomous and its
overactivity is not due to LATS. It is also independent of TSH stimulation as administration of exogenous thyroid extract
fails to suppress the secretion of triiodothyronine and thyroxin.

Clinical features.—This condition occurs in younger age groups, usually in the thirtees and forties. Fem
again are more often affected. The symptom is a thyroid swelling which is a slow growing mass in the nec
Symptoms of hyperthyroidism will be present. Exophthalmos is absent as in case of toxic multinodular go
On inspection, the thyroid nodule is quite obvious which moves on swallowing. Patient may complain of
sudden increase in the size of swelling due to necrosis and intraglandular haemorrhage. With larger lesion
cervical compression may be present. Palpation reveals a solitary nodule within the thyroid which can be
well palpated by Lahey’s technique. No bruit over the thyroid is audible.
Diagnosis and Special Investigations.— Thyroid scan is the most essential investigation to indicate that th
nodule is ‘hot’. Often investigation of thyroid assessment tests may be performed to ascertain the thyroid
the type of thyrotoxicosis. The students are referred to the section of ‘Solitary Nodule’ for special investiga
Treatment.— The choice is between surgery and radioiodine. As autonomous nodule uptakes radioiod
which destroys active cells, radioiodine works in this case. Over the age of 40 years radioiodine may be tr
Below 40 years of age surgery should be the treatment of choice.
RARE CASES OF THYROTOXICOSIS
1. EARLY STAGE OF SUBACUTE OR DE QUERVAIN’S THYROIDITIS may cause mild hyperthyroidism due to excess
liberation of thyroid hormones from damaged thyroid. Ultimately hypothyroidism is almost the rule. In early stage or stage 1 the thyroid
is swollen and painful with thyrotoxic symptom lasting for about 1 to 2 months. Gradually the patient becomes euthyroid with an
enlarged, firm and toxic nontender goitre. The ESR is almost always elevated.
2. JODB ASEDOW SYNDROME.— Large doses of iodine given to hyperplastic endemic goitre may produce hyperthyroidism.
3. THYROTOXICOSIS FACTITIA.— Sometimes hyperthyroidism may develop by taking L-thyroxin in large doses. The dose
of this drug should not exceed 0.4 mg a day.
4. STRUMA OVARII.— Thyroid tissue in the ovary sometimes makes the patient thyrotoxic.
5. IATROGENIC HYPERTHYROIDISM.— Over-treatment of hypothyroidism may lead to thyrotoxicosis. The treatment of
hypothyroidism is to administer thyroid extract or L-thyroxin. But the dose should be small in the beginning and within several weeks
the dose should be increased to 0.2 mg of L-thyroxin daily. Abrupt increase in the dose of the drug in the beginning for a long period may
lead to this condition.
6. DISSEMINATE THYROID AUTONOMY.— Sometimes large mass of secondary carcinoma may produce sufficient thyroid
hormone to bring the patient to hyperthyroid state.
7. NEONATAL THYROTOXICOSIS.— This occurs due to high LATS titre present in the mother’s serum and crosses the
placental barrier to reach the foetus. So the mother is usually hyperthyroid. This hyperthyroidism of the new bom baby gradually
subsides in one month’s time as the LATS titre naturally falls.
____________ TUMOURS OF THE THYROID____________

BENIGN TUMOURS
These are mainly adenomas particularly follicular adenoma.
ADENOMA
Almost all benign thyroid tumours arise from glandular epithelium and are termed adenomas. These benign
tumours are true neoplasms and usually occur in middle life. Women are about 5 times more commonly a
than men. Adenomas vary size from a few millimetres to even larger than 10 cm. This tumour always pos
a well defined margin.
Follicular Adenoma.— Almost all thyroid adenomas show follicle formation to a varying degree. Follic
adenomas are usually cellular but may contain a variable amount of colloid. The distinction between a tru
and an isolated nodular goitre may be difficult but the presence of well-defined capsule is a definite distin
feature. Many follicular adenomas show evidence of function and take up radioiodine but they rarely hyp
to a degree that results in hyperthyroidism. It must be remembered that ‘toxic adenoma ’ is usually part of a tox
nodular goitre rather than a true neoplasm. It is unknown whether follicular adenomas show transition over t
to carcinoma but current opinion is that the majority of thyroid carcinomas are malignant from inception. The
most important clinically relevant fact about follicular adenomas is that many of these tumours cannot be
distinguished from follicular carcinoma on clinical, isotopic, ultrasonic or cytological ground and the only
method of making the distinction is by careful histological examination for evidence of capsular or angioinva
Microscopically follicular adenomas show consistent pattern of follicles. According to the size of the
follicles and to the degree of follicle formation, this adenoma has been subclassified into embryonal, foetal
(microfollicular) and simple. In the embryonal type there is poor or absent follicle formation and requires
meticulous histological scrutiny for evidence of capsular or angioinvasion which means that it should rathe
called follicular carcinoma.
Hurthle cell (Askanazy or Oxyphil) adenoma is a variant of follicular adenoma. It is composed entirely o
large acidophilic granular cells popularly known as Hurthle cells. These are metaplastic thyroid epithelium
found in many pathological conditions of the thyroid and particularly in chronic lymphocytic thyroiditis.
Hurthle cell adenomas usually do not show follicle formation and contain little or no colloid.
Papillary adenoma.— It is a benign neoplasm showing papillary processes. If such tumours are ever ben
they are rare. So grossly all papillary tumours should be regarded as papillary carcinomas. However
conventional histologic examination may show encapsulation and absence of capsular or angioinvasion eve
on meticulous scrutiny to support the view that on rare occasions a papillary neoplasm may be benign.
Clinical features OF BENIGN TUMOURS.—Patients usually present with slow growing swellings of the
neck. No other complain is usually evident. One must remember that a thyroid swelling to be palpable it mu
be of at least 1 cm in size. There is no evidence of cervical node involvement. Only in cases of bleeding insid
the tumour it may cause pain and rapid increase in swelling.
Diagnosis and Special Investigations OF BENIGN TUMOURS.— Straight X-ray of the neck is useful
as it may demonstrate encroachment of the trachea. Other investigations have been discussed previously in
section of ‘Solitary nodule’.
Treatment OF BENIGN TUMOURS.— As malignancy cannot be ruled out with emphasis, excisional
biopsy is the treatment of choice. Usually a lobectomy and removal of the adenoma with surrounding health
tissue is performed. The specimen may be sent for frozen section analysis while the patient is anaesthetised.
the report is a benign tumour, no further removal of thyroid tissue is necessary. After operation with benign
tumours it is better to treat the patients with replacement doses of L-thyroxin. Since this may reduce the num
of recurrent nodules. The patient must be followed-up carefully for a long period.
If biopsy report reveals malignancy, near-total thyroidectomy is justified.
MALIGNANT NEOPLASMS
The classification of malignant thyroid tumours should be as follows :
, ... _ „ . . / (a) DIFFERENTIATED.
A. Follicular cell origin undjffhRENTIATED.
(a) DIFFERENTIATED:
(i) Papillary carcinoma (60%);
(ii) Follicular carcinoma (15%);
(iii) Mixed papillary and follicular carcinoma.
(b) UNDIFFERENTIATED:
Anaplastic carcinoma (13%).
B. Parafollicular cell origin :
Medullary carcinoma (6%).
C. Non-thyroid cell origin :
(i) Malignant lymphoma (4%);
(ii) Sarcoma;
(iii) Metastatic carcinoma.
The incidence of thyroid carcinoma in clinically evident solitary thyroid nodules that are surgically resect
varies from 15% to 30% in different series. Thyroid carcinoma is rare in children and increases in frequency
with increasing age. These tumours also demonstrate a 3:1 female predominance. There are about 30 to 40 ne
cases of thyroid cancer per million per year, of which annual mortality from thyroid cancer is about 4 to 5 pe
35
million in a year. Difference between incidence and mortality reflects the favourable prognosis of most thyro
carcinomas, though these lesions have the potentiality to aggressiveness and metastasis.
Aetiology.— 1. Iodide deficiency or goitrogenic drugs administered over a long period may produce
papillary carcinoma. 2. External irradiation and administration of 131I have both induced thyroid carcinoma
experimental animals. Carcinogenic effect of ionizing radiation is thought to work by two mcchanisms — (a
Cellular injury with altered cell division and replication of nuclei acids and (b) the injured cells produce less
thyroid hormone leading to TSH stimulation which is itself carcinogenic. 3. Ionizing radiation in childhood
young ages directed at the thymus or cervical lymph nodes has been shown to be definitely carcinogenic for
human thyroid. That is why administration of 131I for treatment of hyperthyroidism should be restricted to t
patients above 40 years of age. Also the fact is that large radiation dose which is administered in these cases
is less liable to produce carcinoma since all or most of the thyroid epithelium is destroyed. The small dose m
be dangerous. 4. Autoimmune thyroiditis has been incriminated to increase incidence of thyroid cancer.
Spread of thyroid cancers.—
1. Direct spread.— All carcinomas of the thyroid spread directly into the surrounding normal thyroid
tissue by infiltration. Anaplastic carcinoma is particularly known to directly spread outside the thyroid and
involve the neighbouring structures. The tumour first infiltrates into the infrahyoid muscles and then gradu
into the trachea, oesophagus, recurrent laryngeal nerve, carotid sheath and even sternomastoid muscles. Du
to this direct spread the tumour becomes fixed and irresectable. Papillary carcinoma, though known for its
multicentricity, yet its direct spread is least. Follicular carcinoma occupies a middle position and anaplastic
carcinoma has greatest affinity for direct spread.
2. Lymphatic spread.— All thyroid carcinomas spread by lymphatics to variable extent. Papillary
carcinoma is particularly notorious for lymphatic spread and it often spreads so early that the cervical lymp
nodes become palpable when the primary growth remains impalpable (which is known as ‘lateral aberrant
thyroid'). Multicentricity of this carcinoma has often been incriminated to lymphatic spread within the rich
intrathyroid lymphatic plexus. The regional lymph nodes which are involved are the deep cervical nodes
(jugulo-digastric and jugulo-omohyoid) and the pretracheal, prelaryngeal and paratracheal groups of lymph
nodes. The lymph node metastasis is usually homolateral.
3. Blood spread.— Thyroid carcinoma is also known for its blood spread. Follicular carcinoma and
anaplastic carcinoma are particularly notorious in this respect. Blood spread mainly occurs due to angioinva
of the tumour emboli. Through blood spread the lungs, ends of long bones, skull and vertebrae are often aff
Sometimes such metastases may be so vascular that they become pulsatile.
One characteristic feature of metastatic lesions of thyroid is that these lesions show remarkable degree of
differentiation, so that they closely resemble normal thyroid tissue rather than primary carcinoma. That is w
metastatic enlargement of deep cervical nodes in case of papillary carcinoma almost looks like normal thyro
and it was previously called 'lateral aberrant thyroid’. Similarly distant metastatic lesions often look like
normal thyroid and were previously called ‘benign metastasising goitre’.
PAPILLARY CARCINOMA
This is the most common form of thyroid cancer and constitutes about 60 to 70 per cent of the thyroid can
It constitutes 80% of thyroid cancers in children.
Pathology.— Papillary carcinomas are unencapsulated tumours that tend to invade lymphatics and to
spread to the normal surrounding thyroid tissue. This carcinoma is composed of columnar thyroid cells
arranged in papillary projections with connective tissue vascular stalks. The nuclei show characteristic vesic
appearance. Sometimes the tumour may contain localised deposits of calcium in connective tissue layers wh
are calledpsammoma bodies. It must be remembered that the mixed carcinomas containing both papillary and
follicular elements behave like the papillary carcinoma. Multicentricity of the primary tumour is the most
important feature of this cancer. It is found in no less than 80% of cases of this cancer if the gland is thoroug
examined. Multicentricity has often been incriminated due to lymphatic spread in the rich intrathyroidal lym
THE THYROID AND PARATHYROIDS
547
plexus. Lymph node metastasis is also quite early. A higher incidence of node involvement is found in children
It must be emphasized here that presence of nodal metastasis correlates with recurrence though it has little effe
on mortality particularly in patients below 40 years of age. Another important feature is that this cancer is
dependant on TSH stimulation. The tremendous potentiality of this tumour to metastasise to regional lymph
nodes while itis of microscopic size has given rise to the development of ‘lateral aberrant thyroid'. In fact these
are palpable regional lymph nodes which have become enlarged while the primary tumour is still small and n
palpable.
Clinical features.— It is the most slow growing among the malignant tumours of the thyroid. Though this
neoplasm can appear at any age, yet the pick incidence is in the third and fourth decades. It occurs 3 times mor
frequently in females than in males. The age has particular bearing on prognosis of the case. It shows a peculiar
tendency to become more malignant with advancing age. 10 years survival in patients with pulmonary
metastasis has been reported to be 83% in those under 40 years of age, whereas not one patient above 40 years
of age survived.
The lesion usually presents as an asymptomatic nodule within the thyroid gland. In good number of cases
there is regional lymph node enlargement. Pressure symptom, fixity of the thyroid lesion and distant metastas
are all late in this condition. The size of the primary lesion has an impact on prognosis. When the tumour is lar
than 1.5 cm the chance of recurrence is more frequent and death from cancer occurs more often. The peculiar
fact is that the presence of regional lymph node metastasis is of less importance in determining prognosis. This
is due to the fact that the younger patients who show better prognosis are most likely to have nodal metastasis
However in patients over 40 years of age, presence of nodal metastasis is associated with worse prognosis.
Diagnosis and Special Investigations.— 1. Straight X-ray of the neck may reveal calcium flecks
suggesting psammoma bodies. 2. Radioiodine scan shows ‘cold nodule’. 3. Ultrasonography determines that
it is a solid lesion. 4. Needle biopsy is helpful to diagnose this condition.
Treatment.— In majority of circumstances it is not possible to be definite about the diagnosis of this
condition. The treatment of this condition is obviously surgical excision. The best approach would be to resect
the entire lobe containing the tumour and the isthmus and to send this for frozen section biopsy and to wait, w
the patient is anaesthetised, for the result to come. Once the papillary carcinoma is the histological finding the
treatment is NEAR-TOTAL THYROIDECTOMY. Due to multicentricity of the tumour, this is the treatment
of choice. Near total thyroidectomy should be associated with removal of the pretracheal, paratracheal and the
lymph nodes in the tracheoesophageal groove upto superior mediastinum.
Following thyroidectomy all individuals with papillary carcinoma should be placed on suppressive dose of
thyroid hormone for life. The dose is approximately 0.3 to 0.4 mg of thyroxin daily to suppress TSH production
to which this tumour is very much dependant. Other ancillary modes of treatment such as radioactive iodine,
external irradiation and chemotherapy will be discussed later in this chapter.
FOLLICULAR CARCINOMA
This group comprises 15% to 20% of all thyroid cancers.
Pathology.— Macroscopically it appears to be an encapsulated lesion. Microscopically this tumour has
follicles and like adenocarcinoma the cells are crowded. There is also existence of lumen in the acini which may
or may not contain colloid. The nuclei of the cells are often vesicular. The most important feature is capsular
invasion and angioinvasion (vascular invasion). This is the most reliable criterion of malignancy. This
carcinoma usually does not metastasise to regional or distant lymph nodes. Multicentricity, which is common
in papillary carcinoma, is also much rare in this condition. Instead, haematogenous spread to distant sites such
as bone, lung and liver occurs quite early. There are in fact two varieties of follicular carcinoma: (a) The one
is encapsulated, well differentiated and of low grade malignancy and is difficult to distinguish from a benign
adenoma. Only capsular invasion and vascular invasion are the distinguishing features. This lesion usually doe
not metastasise. (b) The other variety shows vascular invasion quite early and the primary tumour is the most
aggressive of all well-differentiated carcinomas.
Hurthle cell carcinomas are histologically distinct from follicular tumours. The prognosis of this tumour
is intermediate between the two types of follicular carcinoma. This tumour has a tendency to occur bilater
and metastasise locally, so there is a high incidence of local recurrence.
Clinical features.— This carcinoma tends to occur in older age group, with a pick incidence in the 5th
decade. It is three times more common in females than in males. Patients may present with a long history
goitre. Sudden recent change in the form of increase in size or diffuse swelling into a firm nodule is observ
Very often an asymptomatic, slowly enlarging thyroid nodule is the presenting feature. Regional lymph n
are seldom involved. Pain and invasion to adjacent structures are late manifestations. Distant metastases a
frequent, of which bony, pulmonary and liver metastases are the dominant ones. The bony metastases are
usually osteolytic. This tumour shows good response to radioiodine.
Treatment.— Encapsulated and low grade follicular carcinoma, which shows a low incidence of distant
metastasis later on, is often treated with thyroid lobectomy. The other lobe is carefully examined to exclud
lesion there. Many surgeons, of course, favour near-total thyroidectomy not because of multicentricity, bu
facilitate later treatment with radioiodine if metastases occur. If it is seen that the regional lymph nodes ar
affected, these nodes should be dissected out. But if the lymph nodes are not affected there is no indicatio
radical neck dissection as this tumour does not show an early lymphatic metastasis.
Suppressive thyroid hormone therapy is advocated in all patients for the rest of the life.
Even in aggressive follicular carcinoma, near total thyroidectomy and post-operative radioiodine thera
with thyroid hormone has shown a great improvement in the result.
Increasing age has an adverse influence on survival. Presence of distant metastasis is obviously associa
with bad prognosis. But the size of the primary tumour and presence of regional lymph node metastasis d
have important prognostic value.
Other adjuvant treatments for differentiated carcinomas.—
A. L-THYROXIN.— Following surgical treatment in cases of papillary and follicular carcinomas,
patients should be treated with L-thyroxin to suppress TSH level. Increased TSH level has been shown to
stimulate growth of carcinomas. Regression of metastatic lesions has been observed with thyroxin treatme
B. RADIOIODINE THERAPY.— Post-operative 131I scans are always performed following operation
for well differentiated thyroid carcinoma. These scans are usually performed 1 to 3 months after operation
weeks prior to scan no thyroid hormone should be given to the patient in order to achieve maximal conce
of TSH which stimulates uptake of 131I by the metastatic lesions. To make radioactive iodine treatment most
effective all normal thyroid tissue should be removed surgically. Only in younger patients with papillary
carcinoma less than 1.5 cm in size this radioiodine therapy is contraindicated. Ablation of residual thyroid
can usually be accomplished with one dose of 30- millicuries (mC) of 131I. When there are metastases the d
should be increased to 150 mC of I31I. Female patients should always be screened for pregnancy prior to
radioiodine. If there is no metastasis similar scans are performed at 6 months intervals upto 1 year and the
3 to 5 years. As soon as metastasis is seen that is ablated with radioiodine therapy.
Serum thyroglobulin is helpful in detecting metastasis. After total thyroidectomy thyroglobulin level s
be below 1 ng/ml of serum during T4 therapy. If this value goes above 10 ng/ml it suggests metastasis.
C. EXTERNAL IRRADIATION.— It has very limited value in differentiated carcinomas of thyroid. It
is only applied (i) when thyroid cancer has invaded trachea or oesophagus and (ii) when metastatic lesion
not take up radioiodine effectively.
D. CHEMOTHERAPY.— Its scope is also very limited. When metastatic lesions have spread widely a
no longer take up radioiodine, chemotherapy may be tried. The single most effective drug is Adriamycin
(Doxorubicin).
ANAPLASTIC CARCINOMA
This constitutes about 10% to 15% of malignant tumours of the thyroid.
Pathology.— This carcinoma may develop from a previous nodular goitre. It may even develop from pr
existing well differentiated thyroid carcinoma. Macroscopically the tumour is not encapsulated and usually
extends into the remaining thyroid tissue and even outside the thyroid to involve adjacent structures.
Microscopically the cells are variable from spindle shaped, small cells to multinucleated giant cells. Presence
of mitosis is very characteristic in this carcinoma. In some cases there may be areas of papillary or follicular
carcinoma. These lesions grow rapidly and have marked propensity for local invasion. It often causes tracheal
or oesophageal obstruction. By the time the patients come to surgeons, there is already invasion to trachea or
oesophagus or adjacent structures of the neck precluding surgical resection. Regional lymph nodes are
frequently enlarged. Distant metastases to the lungs and bones are not uncommon.
Clinical features.— This carcinoma usually affects patients over 50 years of age, with an increasing
incidence in successive decades. Patients generally present with an enlarged thyroid which may or may not be
painful. The gland is often fixed and shows poor movement on swallowing. Encroachment of adjacent structu
is quite noticeable. The consistency of the gland is hard or very firm.
Treatment.— Total thyroidectomy with modified neck dissection is the treatment of choice, but in many
patients the thyroid is not resectable. The diagnosis is best made by needle biopsy or by taking a small portion
of thyroid to relieve airway obstruction where facilities of needle biopsy are not available. Tracheostomy may
be necessary to relieve airway obstruction. Radioactive iodine is ineffective as the tumour cannot take up iodin
External irradiation is very important to afford palliation for pain. Chemotherapy is not that effective as external
irradiation yet Adriamycin or combination of Chlorambucil, Adriamycin and Vincristine may be helpful to the
patient. Anyway 80% of patients die before completion of 1 year.
MEDULLARY CARCINOMA
The main characteristic features of medullary carcinoma are (a) its non-follicular histological appearance,
(b) its origin from parafollicular C-cells and (c) its secretion of calcitonin. It shows almost equal sex incidence
in contrast to all other diseases of the thyroid. It shows familial incidence with autosomal dominant inheritanc
when it is associated with phaeochromocytoma and parathyroid hyperplasia to form the second type of multip
endocrine adenomatosis (MEAII) or multiple endocrine neoplasia (MEN Type II). Calcitonin is secreted by
C-cells derived from the neural crest and are part of the APUD series of polypeptide-secreting cells. These
C-cells migrate to the lateral thyroid lobes in the foetus and are mostly found in the posterolateral areas of the
upper and middle thirds of each lobe. It constitutes about 5% to 9% of all thyroid carcinomas.
Pathology.— Macroscopically the size may vary from nonvisible to 10 cm or more. Particularly in familial
cases bilateral growths with multicentricity are noticed. But in sporadic cases single nodules are most often see
Microscopically it does not show the typical follicular pattern of the thyroid gland, but it is composed of a solid
mass of cells and hence it is called ‘medullary’. There is often presence of amyloid in the stroma. Presence of
granules of thyrocalcitonin in the medullary carcinoma cells by electron microscopy indicates that these
neoplasms arise from the parafollicular cells. Some of these neoplasms histologically resemble carcinoids.
Mitotic activity, vascular and lymphatic involvement are common. C-cells hyperplasia is considered to be
precursor of medullary carcinoma. Microscopically it is often diagnosed as anaplastic carcinoma. This tumour
spreads first to lymph nodes of the neck and superior mediastinum. Later on distant metastasis may involve th
lungs, liver, adrenals, bone and other organs. The peculiar feature is that in bone the metastatic lesion is
osteoblastic. In only advanced cases one may find local invasion to the trachea and oesophagus. —
Clinical features.—This tumour may occur from children of 2 years of age to 80 to 90 years. It shows about
equal incidence in both female and male. In familial cases the average age is the early 20s. Only in 28% to 30%
of cases it shows familial nature. Patients present with a single or multiple nodules in the thyroid. Rarely is the
mass of sufficient size to produce tracheal compression, dysphagia or local pressure symptoms. Rapidly
growing and poorly differentiated neoplasms are invasive and more frequently cause local symptoms, which
include cervical discomfort, pain referred to the ear or jaw, dysphagia, dyspnoea and hoarseness. Hoarseness
may be due to secondary invasion of the recurrent laryngeal nerve. Hoarseness or dysphagia is rare only in 10
of cases. Majority of patients suffer from diarrhoea. Increased motility and impaired absorption of water and
electrolytes have been held responsible for diarrhoea. Serotonin, calcitonin or prostaglandin E2 has also b
considered responsible for such diarrhoea. About 1/5th of the cases show cervical lymphadenopathy wh
present Ectopic production of ACTH by this carcinoma has been demonstrated in most cases. Patients ma
present with kidney stone (due to hyperparathyroidism) and/or with symptoms of pheochromocytoma.
Occasionally it may be associated with Cushing’s syndrome.
Medullary carcinoma of thyroid has been a part of multiple endocrine neoplasia type II or multiple en
adenomatosis (MEAII). This is further divided into Ha and lib. The former consists of medullary carcinom
pheochromocytoma and parathyroid hyperplasia, while the latter (the rare variety) is characterised by the
concurrence of medullary carcinoma, pheochromocytoma, multiple mucosal neuromas, ganglioneuromat
and a typical facial appearance. The MEA Ha is also known as Sipple’s syndrome. Both these syndromes
inherited as autosomal dominant traits. The parafollicular cells have the biochemical feature of APUD cel
The medullary portion of the adrenal gland that gives rise to pheochromocytoma also comes from the neu
crest and has the APUD cells characteristic. The presence of parathyroid hyperplasia seems to be due to
overactivity of parathyroid following low calcium level in the serum due to excess calcitonin from medul
carcinoma. But some workers have reported elevated levels of the parathyroid hormones in patient with
carcinoma.
Diagnosis and Special Investigations.— Medullary carcinoma is usually associated with an elevated
serum calcitonin level measured by radioimmunoassay. Following a bolus intravenous injection of penta
(0.5 M-g/kg), pick CT (calcitonin) level is detectable in 1 to 3 minutes. Pentagastrin stimulation test has b
successful in detecting patients with early MEA Ha or MEA lib who have no clinical or radiological evide
of medullary carcinoma and even no increase in calcitonin level. The diagnosis of pheochromocytoma de
on careful analysis of the levels of urinary catecholamines and catecholamine metabolites. This is especial
important since this lesion may be unsuspected clinically. The determination of 24-hour urinary total
catecholamines, metanephrines or vanillyl mandelic acid (VMA) will almost always prove the diagnosis o
pheochromocytoma. The best test for invaluating adrenal gland size prior to surgery is computed tomogr
scanning (CT Scan). The diagnosis of hyperparathyroidism in patients with MEA 2 depends largely on se
measurements of blood calcium levels. Determination of peripheral plasma parathyroid hormone levels m
be misleading. Any history of recurrent renal stones should of course make the search for hyperparathyro
even more vigorous.
Treatment.— Total thyroidectomy is the treatment of choice for medullary carcinoma of thyroid. The
reason is that it frequently exists in various parts of the gland with multicentricity. In case of incomplete
resection, recurrence can be expected. If the lymph nodes are palpable one sided or bilateral neck dissection
should be performed according to the case. To resect lymph nodes in the superior mediastinum, sternal s
incision may be required. Medullary carcinoma does not respond to thyroxin therapy or radioiodine or to
external irradiation. Chemotherapy with Adriamycin has led to some remissions of medullary carcinoma an
should be tried if the metastatic disease is progressive.
It is now known that almost invariably all four parathyroid glands are involved. If the patients are fou
be hypercalcaemic prior to thyroidectomy, one can expect to find enlargement of parathyroid glands at su
The operative procedure of choice is a subtotal parathyroidectomy i.e. excision of 3'/2 glands.
If pheochromocytoma is detected, a bilateral total adrenalectomy may be necessary due to multicentri
and bilateral nature of the lesion. This should be done by bilateral subcostal incisions and exploration of b
adrenal glands and the sympathetic chain. Adrenal medullary hyperplasia in normal sized adrenal gland
common finding in these cases. In case of unilateral pheochromocytomas, it is advisable to remove only th
tumourous gland. Such patients should be followed carefully at yearly intervals. Preoperatively these pat
should receive alpha-adrenergic blockers e.g. phenoxybenzamine (50 to 200 mg/day) and beta-adrenergic
blockers e.g. propranolol (40 mg/day). Postoperatively these patients will require long term glucocorticoi
mineralocorticoid as replacement therapy.
Prognosis.— 5 years survival rate in patients without lymph node metastasis is about 70% to 80%, wher
with lymph node metastasis it is approximately 40%,to 50%.

MALIGNANT LYMPHOMA
This condition does not produce any special feature. On FNAC the condition is suspected. Ultimately dia
settled by receiving sufficient material by large-needle (Trucut) or open biopsy. Previously this condition wa
as small round-cell anaplastic carcinoma. This condition may be large enough to cause tracheal compression
When the diagnosis is established by biopsy, radiatidn is the main treatment and it offers a very good res
Radical surgery is almost unnecessary. If there be any tracheal compression, isthmusectomy may be perform
The prognosis is good if there is no involvement of cervical lymph nodes. Occasionally this tumour may
a part of wide spread malignant lymphoma disease, whpn the prognosis is miserable.
THYROIDITIS
\
Infective thyroiditis is quite rare. Chronic thyroiditis is more common which includes Hashimoto’s disea
de Quervain’s thyroiditis and RiedeFs thyroiditis. \
ACUTE SUPPURATIVE THYROIDITIS
This almost invariably follows an acute upper respiratory tract infection. This disease is characterised by severe pain
in the thyroid and in the adjacent neck, fever, chill and rigor. Patient may complain of dysphagia. In case of abscess
formation pus may extend into the deep spaces of tbe neck and into the superior mediastinum.
Treatment consists of extensive antibiotic and drainage of abscess if it has formed.
HASHIMOTO’S DISEASE OR AUTOIMMUNE THYROIDITIS
It is also called lymphadenoid goitre or chronic lymphocytic thyroiditis. It is the most common form of thyroiditis. It is almost 5 to
10 times more common than de Quervain's thyroiditis.
Aetiology.— It is an autoimmune disease. The thyroid gland seems to become sensitive to its own cell constituents and thyroglobulin.
Four autoantigens have been detected — (i) Thyroid cell microsomes, (ii) Thyroid cell nuclear component, (iii) Thyroglobulin, and (iv)
Nonthyroglobulin colloid. Only antimicrosomal (MCHA) and antithyroglobulin (TGHA) antibodies can be measured in the patient’s
serum. Genetic predisposition is evident. Members of the family with this disease hav« an increased incidence of spontaneous
hypothyroidism, goitre, Hashimoto’s disease and less often thyrotoxicosis. Pernicious anaemia and autoimmune gastritis may be seen in
the same family which confirms its autoimmune nature. Peculiarly papillary carcinoma may coexist with this condition.
Pathology.— In majority of cases thyroid is symmetrically enlarged and semifinn in consistency. In occasional cases the enlargement
may be asymmetric and even nodular! Microscopically there is disruption of epithelial cells and remaining epithelial cells become larger
and show oxyphilic changes (Askanazy cells). Lymphocytic infiltration is very prominent and it may be either focal or diffuse. The
thyroid tissue may degenerate at places and is replaced by fibrous tissue.
Clinical features.— Again the patients are women in most of the cases and the disease occurs in fifties. The onset is insidious and
may be asymptomatic. The main complaint is enlargement of the neck with slight pain and tenderness in the region of the thyroid. The
patient may become mild hyperthyroid initially, but hypothyroidism is inevitable. Patient may complain of shortness of breath, fatigue
and increase in weight — all related to hypothyroid state. Palpation reveals a diffusely enlarged thyroid gland which may be lobulated.
Occasionally it may be nodular. The consistency is firm or rubbery depending upon the degree of fibrous tissue present. Less is the
fibrosis the gland will feel soft and rubbery, whereas in case of more fibrosis the gland will be firm. Increased incidence of rheumatoid
arthritis, haemolytic anaemia, myasthenia gravis and pernicious anaemia may be seen alongwith this disease. Addison’s disease, diabetes
mellitus and ovarian insufficiency may also be seen as part of autoimmune disease.
Special Investigations.— Thyroid functional tests usually indicate hypofunction. Diagnosis is confirmed by demonstration of high
litres of antibodies in the serum. Needle biopsy is also confirmatory. Where facilities for needle biopsy are not available, excisional
biopsy is indicated.
Treatment.— This disease usually causes GENERALISED ENLARGEMENT of the thyroid. If the goitre is quite small and the
patient is euthyroid no treatment is required. When the patient is hypothyroid and there is a goitre, full replacement doses of thyroxin is
required. Surgical treatment is only required (i) when there are pressure symptoms, (ii) in case of an extremely enlarged goitre, (iii) for
cosmetic reason when the patient wants it and (iv) when it is difficult to exclude malignant neoplasm. The surgical procedure is usually
subtotal thyroidectomy with clearing of the trachea.
When the disease is NODULAR, suppressive hormone therapy with thyroxin may be tried, if one is sure of absence of malignant
neoplasm. But majority surgeons like surgical excision in the form of lobectomy and excision of the isthmus as excisional biopsy to
exclude malignancy. It must be remembered that majority carcinomas associated with Hashimoto’s disease are of papillary variety.
After surgery suppressive therapy with thyroid hormone should always be given postoperatively.
SUBACUTE THYROIDITIS OR DE QUERVAIN’S DISEASE

It is also called granulomatous thyroiditis. The aetiology is rather controversial. Some advocate of its viral origin and
others are in the opinion that it is an autoimmune disease. The latter has almost universally been denied. The disease often
follows an upper respiratory tract infection.
Pathology.— There is enlargement of follicles of thyroid with infiltration by lymphocytes, neutrophils and large
mononuclear cells. Foreign body type of Giant cells containing many nuclei are quite common in this lesion.
Clinical features.—Itusually affects individuals from 3 years to 75 years, yet it seems to be common in forties. Females
are more often affected than males. The thyroid becomes acutely congested, swollen and mildly tender. Prodromal
symptoms like fever and malaise are present. The gland is usually adherant to the surrounding tissues but unlike Riedel's
thyroiditis it can be dissected free very easily. This disease can be divided into four stages. In stage I the thyroid becomes
acutely congested, swollen and mildly tender. The patient may be thyrotoxic and this stage lasts for 1 to 2 months. In stage
II the gland remains enlarged but becomes non-tender and the patient becomes euthyroid. In stage HI the patient gradually
turns to hypothyroid state. In stage IV remission or recovery may occur. It takes about 6 months to complete the four stages.
Diagnosis and Special Investigations.—Even though the patient is febrile, WBC count remains normal. ESR is almost
always elevated. Needle biopsy or fine needle aspiration makes the diagnosis with certainty.
Treatment.— This disease is specifically treated with corticosteroids. Prednisolone in the dose of 40 mg daily for 7
days and then the dose is gradually reduced over 1 to 2 months is the effective form of treatment. Salicylates and thyroid
hormone may be added to this therapy to make it quite successful. Surgical treatment is contraindicated as possiblity of
recovery less to normal thyroid function is there.
RIEDEL'S THYROIDITIS
It is a very rare form of thyroiditis, in which chronic inflammatory process involves one or both lobes of the thyroid.
This inflammatory process extends beyond the limit of the thyroid and involves surrounding fasciae, muscles, nerves, blood
vessels, trachea and oesophagus.
Pathology.— Thyroid follicles become small and few in number. They are replaced by dense fibrous tissue.
Clinical features.— This disease also occurs in women more frequently. The average age of the patient is about 50.
Symptoms are mosdy due to compression of the trachea, oesophagus and recurrent laryngeal nerve.
Special Investigations.— Hypothyroidism is almost always evident in thyroid function tests. Thyroid autoantibodies
have been demonstrated in the serum, though in lower titres than in patient with Hashimoto's disease.
Treatment.—Thyroxin is again the treatment of choice, as this relieves hypothyroidism. Surgical treatment is justified
when pressure symptoms are the main features. Extent of removal depends on the amount of involvement of the gland in
this disease. When one lobe is involved, lobectomy with isthmusectomy is indicated. When there is bilateral involvement,
the isthmus and as much of each lobe as possible should be resected.
HYPOTHYROIDISM
This is a medical condition and is more elaborately described in the text books of medicine. Here it is described in
nutshell to acquaint the students of this condition which may be a sequel of overzealous thyroidectomy, after treatment with
radioactive iodine and after various forms of thyroiditis.
Clinical manifestations.— Hypothyroidism is seen in three groups of patients.
(a) In the new bom it is termed cretinism. Mental retardation, poor growth, difficult to nurse the baby and dwarfism
are the features seen in this condition.
(b) Thyroid failure during childhood or adolescence is known as juvenile hypothyroidism. The child appears younger
with low intellect and mental deficiency. There may be abdominal distension, umbilical hernia and prolapse of rectum.
(c) Hypothyroidism in the adult is very rare and majority of the patients are female. In mild cases only tiredness and
weight gain may be present. In severe cases increasing fatigue is evident. Weight gain is a characteristic feature, the skin
becomes thickened and puffy. Non-pitting bogginess of the skin is apparent in hands and feet. Muscle cramps are common
and may be accompanied by paresthesia. Intellectual function and speech may be impaired. Dementia may develop.
Cardiovascular manifestations are related to reduced cardiac output which resemble those of congestive cardiac failure.
There is narrowing of pulse pressure in contradistinction to hyperthyroidism where the pulse pressure is high. Resting pulse
is slow and blood pressure may be elevated. Shortness of breath and pulmonary effusions are evident in late cases.
Abdominal distension due to G. I. tract gases or ascites may be present.
Treatment.—This is obviously the replacement therapy with thyroid hormone either in the form of L-thyroxin or thy
roid extract. The treatment should begin with low dose — 0.5 mg daily and within several weeks this can be increased to
1 mg daily. This gradual increase in the dose is due to avoid cardiac problems related to an increased demand on the
myocardium, the maintenance dose of L-thyroxin is 1.5 mg daily and the maintenance dose of L-triiodothyronine is 0.75
mg daily. The maintenance dose for thyroid extract is 60 to 120 mg daily. The dose is adjusted by following the clinical signs
and symptoms as well as the F. T. I. and T4 levels in the blood.
ECTOPIC THYROID TISSUE

Usually there are three places where aberrant thyroid tissues may be found — (i) Lingual thyroid, (ii) Thyroglossal ec
topic thyroid and (iii) struma ovarii.
Lingual thy
roid.— This
forms a red
rounded swelling
in the middle at the
junction of ante
rior^ and poste
rior 1/3 of the
tongue. It may
cause impairment
of speech and
haemorrhage.
Very occasionally
it may cause res
piratory obstruc
tion or dysphagia.
Fig.37.3.— Diagram of lingual thyroid. It must be remem
bered that it may
be the only thyroid present in the patient.
It is mainly treated with suppressive dose of thyroxin to reduce the size
of the swelling. When it is causing difficulty to the patient inspite of
thyroxin therapy, excision or ablasion with radioiodine is indicated. Fig.37.4.— Lingual goitre.
Thyroglossal ectopic thyroid.— Occasionally it forms a swelling in the upper part of the neck which may be mistaken
as a thyroglossal cyst. It may be the only thyroid tissue present in the patient.
If the swelling is disturbing, excision may be advised alongwith postoperative thyroxin therapy, if there is absence of
normal thyroid.
Struma ovarii.— Ovarian teratoma may include thyroid
m. .... ... tissue. This is unique in ovary only. This teratoma is malignant.
m&sfy' Occasionally hyperthyroidism may be present due to added
secretion from this thyroid tissue.
THYROGLOSSAL TRACT
This tract extends from the foramen caecum of the
tongue to the isthmus of the thyroid. Usually this tract
disappears, but occasionally it may persist and ultimately
a cyst or fistula may develop from this tract which is
known as thyroglossal cyst or thyroglossal fistula.
Thyroglossal cyst.— It appears from cystic degencra-
v'?-’: tion of a part of the thyroglossal tract. It is often compli-
|W* I cated with infection as it is lined by nodules of lymphatic
tissue which communicate by lymphatics with the lymph
' nodes of the neck. This cyst is always in the midline. The
Fig.37.5.— Thyroglossal cyst. commonest position of the thyroglossal cyst is just below
the hyoid bone (subhyoid thyroglossal cyst). But it may be
seen just above the hyoid bone or in front of the thyroid cartilage.
A thyroglossal cyst is always excised. When it is presented with infection and abscess formation, incision
and drainage is the treatment of choice. Once infection is controlled, it should be treated by complete excision
usually with removal of central portion of the hyoid bone.
Thyroglossal fistula.—This fistula forms following infection of a thyroglossal cyst or following its incom
plete removal. The opening of the fistula also varies in position from just above the hyoid bone upto the isth
mus of the thyroid. Thyroglossal fistula is lined by columnar epithelium and serous secretion is discharged.
hood of skin with its concavity downwards is often seen in lbngstanding cases.
The treatment is excision of the whole thyroglossal tract through the central core of lingual muscles. The
operation for excision of thyroglossal tract is known as Sistrunk’s operation. It is always advisable to excise
middle of the body of the hyoid bone as thyroglossal tract is very closely related to this bone.
PARATHYROID
Embryology.—Thetwosuperiorparathyroids arise from the fourth branchial pouch. They descend along with the thyroid and continue
to remain in close association with the upper portion of the posterior aspect of the two lateral lobes of the thyroid. These positions in adult
life are relatively constant. Occasionally they may descend as far as the superior portion of the posterior mediastinum and it must be
remembered that when they descend to the mediastinum they always lie posterior to the inferior parathyroids.
The two inferior parathyroids arise from the third branchial pouch alongwith the thymus and descend during the foetal life with the
thymus. These positions are variable starting from below the mandible to the level of the heart. They usually lie in the lower part of the
posterior aspect of the two lateral lobes of the thyroid either within the thyroid capsule or outside it or even outside the pretracheal fascia.
They may descend from their normal positions to the superior mediastinum and even to anterior mediastinum upto the pericardium. But
it must be remembered that they are almost always supplied by the inferior thyroid arteries.
ANATOMY
Parathyroid glands are small, yellowish brown, ovoid and lentiform bodies. These usually lie between the posterior borders of the lobes
of the thyroid gland and its capsule. Usually they are 4 in number, two on each side and are called from their positions, the superior and
inferior parathyroids. There is an anastomotic artery connecting the superior and inferior thyroid arteries and runs along the posterior
border of the lobe of the thyroid gland.lt usually passes very close to the parathyroids, which forms a good guide to them. These glands
vary in number. There may be multiple glands or only three glands.
The superior parathyroid gland is more constant in position and is usually situated at the middle of the posterior border of the thyroid
gland. However it may lie at a higher level.
The inferior parathyroid gland may lie in various positions e.g. (i) within the fascial sheath of the thyroid gland near the lower pole;
(ii) behind and outside the fascial sheath of the thyroid; (iii) within the substance of the lobe of the thyroid gland near the lower end of its
posterior border.
Hie superior parathyroid glands are usually supplied by the anastomotic artery connecting the superior and inferior thyroid arteries
while the inferior parathyroid glands are supplied by the inferior thyroid artery. Only occasionally the inferior parathyroids when they lie
abnormally in the mediastinum may receive supply from thymic vessels, internal mammary vessels or rarely from the aorta.
Histology.— Each parathyroid has a thin connecting tissue capsule from which septa pass into the gland but do not subdivide it into
distinct lobules. In children the gland consists of columns or cords of the principal cells (or chief cells). There are three varieties of chief
cells according to the depth of staining — (a) dark chief cells, (b) light chief cells and (c) clear chief cells in which the cytoplasm is not
easily stained. At about 10 years of age other cells appear — which are called oxyphil or eosinophil cells. The chief cells are concerned
with secretion of parathormone, whereas the function of oxyphil cells is not known. With the age the number of oxyphil cell increases. The
oxyphil cells are larger than the chief cells and contain more cytoplasm which stains deeply with eosin.
PHYSIOLOGY
Calcium metabolism.— Parathyroid hormone is one of the most important factors affecting calcium metabolism. Adult human body
contains about 1110 gm calcium (1.5% of body weight). Most of the calcium is in the skeleton. The plasma calcium, normally about 10
mg/100 ml is partly bound to protein and partly diffusible. It is the free, ionized calcium which is necessary for coagulation, cardiac and
skeletal muscle contraction and nerve function. Calcium in the bone is of two types — (i) readily exchangeable reservoir and (ii) stable
calcium what is only slowly exchangeable. Plasma calcium is in equilibrium with the readily exchangeable bone calcium. A high protein
diet increases absorption of calcium from the intestine. Excess dietary calcium is excreted in the stools, but most of the calcium liberated
during bone resorption is excreted in the urine. The main action of VITAMIN D is to facilitate intestinal absorption of calcium. Vitamin
D3 is produced in the skin of mammals by the action of sunlight. In Vitamin D deficiency the protein matrix of new bone fails to mineralise
producing rickets in children.
Parathyroid hormone.— This hormone acts on kidney and skeleton directly and on the gastrointestinal tract indirectly.
In the kidney, this hormone decreases calcium clearance and causes increased excretion of phosphate in the urine. The latter action
is due to inhibition of reabsorption of phosphate from the proximal convoluted portion of the renal tubule. This hormone also increases
bicarbonate excretion. Decrease in tubular reabsorption of phosphate causes phosphaturia and low plasma phosphate level. This causes
increase in plasma calcium.
In the skeleton, parathyroid hormone promotes release of calcium from the bone by active transport process. It stimulates osteoclastic
activity and may even convert osteoblasts to osteoclasts. There is evidence that both calcium-mobilising and phosphaturic actions of
parathyroid hormone are modified through formation of cyclic AMP.
In gastrointestinal tract, this hormone has a direct stimulatory effect on intestinal absorption of calcium. This occurs only when
Vitamin D is present.
REGULATION OF PARATHYROID SECRETION is mainly by the circulatory level of ionized calcium. When the calcium
level is high, secretion is diminished and calcium is deposited in the bones. When the calcium level is low, the secretion is
increased and calcium is mobilized from the bones. Elevated plasma phosphate level is said to stimulate parathyroid secretion.
There is no trophic hormone which influences the secretion of parathyroid hormone.
In conditions such as chronic renal disease, in which the plasma calcium is chronically low, feed-back stimulation of the
parathyroid glands causes compensatory parathyroid hypertrophy and secondary hyperparathyroidism.
HYPERPARATHYROIDISM
PRIMARY HYPERPARATHYROIDISM
Aetiology.—The aetiology of primary hyperparathyroidism is not known, (i) A renal leak of calcium,
which may result in hypocalcaemia, stimulates parathyroid glands ultimately to autonomous hyperfunction
stage, (ii) Low dose ionizing irradiation in childhood has increased incidence of hyperparathyroidism.
FAMILIAL HYPERPARATHYROIDISM usually occurs with multiple endocrine neoplasia. There are 2
types of this neoplasia — MEN-1 (Wermer’s syndrome) and MEN-2.
MEN-l.—This includes hyperparathyroidism (chief cell hyperplasia) in 90% of cases. Multiple pancreatico
duodenal neuroendocrine tumours causing Zollinger-Ellison syndrome in approximately 50% of cases
which may be benign or malignant. There is also benign pituitary adenoma which may be functioning or
non-functioning in 40% of cases which may cause acromegaly or cushing’s syndrome or there may be
hyperplasia of the adrenal cortex and carcinoid tumour. Duodenal ulceration is a common feature of this
syndorme. Other associated disorders include thyroid neoplasms (adenoma or differentiated thyroid
carcinoma), adrenal neoplasms and lipomas. Students are referred to page 677 for further description. It is a
autosomal dominant disorder which is associated with mutation of the MEN-1 tumour suppressor gene on
chromosome 11.
MEN-2.—This is also known Sipple’s syndrome. In this case there is medullary carcinoma of the thyroid
with pheocromocytoma and hyperparathyroidism. This syndrome is further divided into type 2a and type
2b. In type 2a hyperparathyroidism is seen in 25% of patients, whereas in type 2b there are additional
neurofibromas affecting lips, eyelids and face producing swellings in these regions, megacolon and
ganglioneuromatosis. Hyperparathyroidism is rarely seen with this syndrome.
Familial isolated hyperparathyroidism — is a rare autosomal dominant disorder, in which the risk of
parathyroid carcinoma is about 20%.
Pathology.— In majority patients with primary hyperparathyroidism the main pathology is adednoma of
the gland (85%), or rarely hyperplasia of the gland (14%) or every rarely carcinoma of the gland (1%).
Parathyroid adenoma mainly involves chief cells and sometimes oxyphil cells. There is ususally a ‘rim’ of
normal parathyroid tissue around the adenoma. Adenoma usually involves a single gland. Multiple adenom
are seen in patients over 60 years of age.
Parathyroid hyperplasia usually involves all 4 parathyroid glands, but the enlargement may be asymmetric.
Again chief cells are mainly affected, though oxyphil cells may be involved.
Parathyroid carcinomas are grey-white in appearance while hyperplasia is usually brown in colour. The
gland becomes adherent to the adjacent tissues.
Thyroid cysts are extremely rare and occur from degenerative change in hyperplastic or adenomatous
gland.
Clinical features.— Primary hyperparathyroidism is more common in females than males. The incidence
increases with increasing age, though it may be seen between the ages of 20 and 60 years. Hyperparathyroid
presents in multiple ways. The symptoms and signs can be grouped into four varieties. The first are the
symptoms due to raised level of calcium in blood and urine. The second group comprises the clinical features
due to abnormal deposition of calcium in soft tissues. The third group comprises the effects of bone resorptio
and is seen in its most florid form in Von Recklinghausen’s disease. The fourth group comprises the various
bizarre forms of presentation.
I. HYPERCALCAEMIA.—When the level of calcium rises the patient feels unwell, loses appetite and th
is followed by nausea and vomiting. Deposition of calcium crystals on the renal tubules results in polyuria,
dehydration, increased thirst and constipation. There is muscle weakness followed by inability to concentrat
Patient also complains of drowsiness. There may be numbness around the lips and chin. Finally cardiac arres
may occur, the heart being in systole. This clinical picture is due to high level of calcium and nothing else.
II. CALCIFICATION IN SOFT TISSUES.—Mainly the kidney is affected. Calcification in the kidney is an
important clinical manifestation of hyperparathyroidism. Stones may be formed in the renal tubules or in the
calyces giving rise to renal or ureteric colic. Calcium deposited in the renal parenchyma is known as
nephrocalcinosis. It is usually associated with considerable renal insufficiency. When hyperparathyroidism
is corrected, further stone formation is prevented, though pre-existing stones may need to be surgically
removed. Calcium is laid down frequently in and around joint capsules and tendons of the lower limb. This
may lead to weakness and spontaneous rupture of tendons. Calcium deposits may also be seen in blood
vessels and symptomless calculi have been found in the pancreas and salivary glands.
III. BONE DISEASE.—Skeletal changes are probably always present in some degree in hyperparathy
roidism. The degree of bony involvement varies so widely as to be undetectable in some patients while others
have gross generalised cystic bone disease known as osteitis fibrosa cystica. If the disease is diagnosed at an
early stage, radiological evidence of skeletal involvement may not be present. Backache, shoulder pain or
generalised aches in the spinal region or limbs may be the early symptom of bone involvement. Bony
tenderness may follow and sometime there are gross deformities such as kyphoscoliosis, obvious bony
swellings and fractures. Radiological subperiosteal resorption of bone is the earliest and most consistent
finding, which occurs especially in the middle phalanges of the index and middle fingers in the adult.
Erosion under the periosteum is common. Other bones commonly involved are the tibia, distal ulna, neck of
femur, pubis and outer third of clavicle. Diffuse demineralisation affecting the skull may present a hazy
outline and ground glass appearance. At a later stage bone cysts are formed. The commonest sites are the
medullary parts of the long bones. The overlying cortex may be thinned and pathological fractures may
occur through these cysts. Large cystic swellings may be seen in the jaw. In its most advanced form the
vertebrae may collapse causing kyphoscoliosis; cystic disease in the ribs leads to chest deformity; lower limb
bones are susceptable to fracture and the pelvis becomes triradiate. It is said that cystic disease of the jaw
indicates that all four parathyroid glands have been involved in adenomatous change.
IV. BIZARRE PRESENTATIONS.—
1. Gastroduodenal Ulcer.—An increased incidence of peptic ulcer disease has been seen in patients
with primary hyperparathyroidism. It has been clearly shown that an acute rise in serum calcium increases
acid and pepsin secretion and that this effect is abolished by vagotomy. But it is also demonstrated that
simply infusion of parathyroid hormone (PTH) into the gastroepiploic artery causes excessive secretion of
gastrin though blood calcium level remains normal, thus demonstrating direct effect of PTH on gastric
secretion. It has also been shown that the basal secretion of gastric acid was raised in hyperparathyroidism
and this level returned to normal only after parathyroidectomy. A parathyroid adenoma may occur in
association with Zollinger-Ellison syndrome as a part of the multiple endocrine neoplasia (MEN) Type I.
Pituitary tumours usually chromophobe adenoma and adrenocortical tumours have also been associated
with this condition.
2. Pancreatitis.—Association of pancreatitis with hyperparathyroidism was reported four decades
ago. Widespread calcinosis of the pancreas has been found in many patients with hyperparathyroidism. The
reason of pancreatitis in hyperparathyroidism is not very clearly known, though pancreatic disorder may lead
to hyperparathyroidism by release of glucagon which produces hypocalcaemia thereby excites parathyroid
to secrete more parathyroid hormone. Gallstone disease was also seen in hyperparathyroidism. This is
presumably due to high concentration of calcium in the bile. This on the other hand may produce pancreatitis
3. Hypertension.—Relationship of hypertension in hyperparathyroidism is also dubious. Though
hypertension has been incriminated as relating to kidney, yet the blood pressure returns to normal after
parathyroidectomy. It has been suggested that hypercalcaemia may be associated with hypertension as a
result of direct effect of calcium ions on vascular tone.
4. This condition may remain associated with medullary carcinoma or papillary carcinoma of the thyroid.
PHYSICAL SIGNS.—It must be remembered that diseased parathyroid glands are rarely palpable. So
much so that if a swelling is detected in the posterior aspect of the thyroid gland in a case of
hyperparathyroidism the swelling is something else than an enlarged parathyroid gland.
Special Investigations and Diagnosis. —

1. SERUM CALCIUM LEVEL.—A high calcium level is almost always expected in a case of hyperparathyroidism. The
normal range usually varies from 8.5 to 10.5 mg/100 ml. While withdrawing the blood for serum calcium estimation, the patient
should be fasting and a tourniquet should not be used. Haemoconcentration resulting to rise in serum calcium when tourniquet
is used has probably been overexaggerated. If the blood is stored for sometime before analysis serum calcium level may come
down. Hypoproteinaemia may show low calcium level and may mislead a case of hyperparathyroidism. In this case an index can
be found out by multiplying observed serum calcium level by 7.4 and dividing the product by the patient’s total protein value.
Calcium level x 7.4
Index = --------------------------------------------
Protein level of the blood
A diet rich in phosphate (e.g. cheese) tends to lower serum calcium level. One must be careful to exclude other causes of
hypercalcaemia e.g. metastatic bone disease, sarcoidosis, Vitamin D intoxication, myelomatosis, milk-alkali syndrome, prolonged
immobilisation, severe Paget’s disease, Hodgkin's disease, leukaemia etc.
Cortisone in the dose of 150 mg/day for 10 days is helpful to differentiate this condition. Blood is taken for calcium
estimation before the cortisone therapy and on the 5th, 8th and 10th day after beginning cortisone therapy. Hypercalcaemia due
to hyperparathyroidism will remain unaffected by cortisone therapy whereas in other cases the calcium level will come down.
2. SERUM ALKALINE PHOSPHATASE.—Approximately 40% of patients with hyperparathyroidism will have increased
level of serum alkaline phosphatase. Some degree of bone affection is expected in these cases.
3. DETERMINATION OF PARATHYROID HORMONE(PTH).—The development of radioimmunoassay technique has
helped in determining parathyroid hormone in the blood, though this facility is available only in a few centres.
4. SCANNING the neck after radioactive tracer dose of 75 Se-Selenometheonine has been widely used in the past but little
nowadays. The reason is that it is not specifically taken by parathyroid tissue even when the thyroid is blocked by iodide.
5. CATHETERISATION AND RADIOIMMUNOASSAY.—A catheter is passed via femoral vein through the inferior and
superior vena cava, brachiocephalic and jugular vein into the neck. Serial blood samples are taken at various sites under
fluoroscopic control. Each sample is subjected to radioimmunoassay for PTH and a high level of PTH is expected adjacent to
the parathyroid tumour. This technique represents a real advance in localisation of parathyroid tumours.
6. PREOPERATIVE LOCALISATION.—Before operation, a few investigations may be made to localise parathyroid
adenoma —
(a) CT Scanning is particularly helpful when the gland is situated in the mediastinum rather than in the neck.
(b) Ultrasonography is the simplest non-invasive method which sometimes help in localising the gland, though its
accuracy depends much on the skill and experience of the investigator. The result of positive localisation is approximately 75%.
(c) Magnetic Resonance Imaging is potentially the most useful for localisation of parathyroid. Initial studies suggest
about 85% detection rate with lesions smaller than'0.5 cm diameter.
(d) Thallium-Technetium isotope subtraction scan is however more helpful in localising parathyroid adenomas. First the
thyroid is outlined with technetium 99m. Thallium-201 is then administered. This isotope is taken up by both thyroid and
parathyroid. Both the images of technetium 99m and thallium-201 are taken by a gamma camera. These two images are now
subtracted by computer and thus the parathyroid adenoma is localised as ‘hot spot’.
(e) Technetium — 99m (”mTc)-Labelled Sestamibi (MIBI) isotope scans identify approximately 80% of abnormal
thyroid glands. This is mostly used nowdays.
Single-photon emission computerised tomography (SPECT) allows more accurate 3-dimensional localisation of abnormal
parathyroid tissue.
7. DYE STUDIES DURING OPERATION.—The dye orthotoluidine blue causes blue staining of various organs e.g. the
thyroid, parathyroid etc. After intravenous injection the thyroid is also stained blue alongwith parathyroid, but thyroid
staining soon disappears leaving the parathyroid well coloured and therefore easily visible. This preoperative dye localisation
study can give an easier access to the tumour.
Treatment. — MEDICAL TREATMENT has come up in primary hyperparathyroidism. The treatment
includes use of oestrogen supplements or biphosphonate therapy to lower the serum calcium level. This is
supported by adequate hydration and avoidance of calcium intake. If the patient is on thiazide diuretic it
should be stopped.
Presently calcium receptor agonists are being experimented in the treatment of this condition, the
therapeutic potential of which is still under consideration.
Surgery.—The treatment of primary hyperparathyroidism is surgery. The only exception is the
asymptomatic patient who may be followed up intermittently without operative intervention. Even in this
group of patients some surgeons have questioned whether or not they will become progressively osteoporo
with chronic disease, or may develop hyperparathyroid crisis (will be discussed later in this chapter) or will
be lost in follow-up. Importance of a meticulous, systematic and time-consuming search cannot be over
emphasized. By far the best chance of discovering parathyroid gland is during the first neck exploration and
subsequent operations will make recognition of parathyroid tissue extremely difficult.
General anaesthesia is used and the neck is opened through a transverse cervical incision similar to that
used for subtotal thyroidectomy. The strap muscles are retracted sideways after dividing them in the midline,
a lobe of the thyroid gland is elevated and rotated medially. One must remember the possibility of potential
damage to the superior and particularly the recurrent laryngeal nerve in this case! The tissues inferior to the
thyroid lobe are cleaned to expose the recurrent laryngeal nerve and the inferior thyroid artery. In the
majority of patients the nerve lies in the tracheoesophageal groove, less commonly lateral to the trachea. The
external laryngeal nerve, branch of the superior laryngeal nerve lies immediately adjacent and medial to the
superior thyroid artery at the superior pole of the thyroid lobe. Now one should look for the parathyroid
glands. The upper parathyroid glands are more easily found and are usually located on the posterior surface
of the thyroid lobe at the middle or just above this level. The lower glands are larger than the upper ones, but
less constant in location. These glands are usually more anteriorly placed than the upper glands and anywher
from the middle of the thyroid lobe upto the anterior mediastinum. But the majority of parathyroid glands in
the mediastinum can be removed through cervical incision. After removal of the suspected parathyroid
glands they should be sent for frozen section biopsy. It is convenient if the biopsy report becomes available
immediately when the patient is anaesthetised preferably through a two-way microphone-loud speaker link
between operation theatre and pathology department.
• When an adenoma develops in a parathyroid gland the colour becomes predominantly reddish-brown.
An adenoma appears soft, smooth and homogeneous on section, whereas hyperplastic gland tends to be
irregular in outline. If a parathyroid adenoma is found and the other parathyroids appear normal, the
adenomatous gland should be removed.
If all four glands are found to be hyperplastic, three and half glands are removed leaving the half of the 4th
gland with a long black silk suture. The idea is that it may be required to remove a part or whole of it later on.
• When inferior parathyroid glands are not available near the thyroid gland, the thymus can be drawn up
into the neck by gentle traction to search for parathyroid glands. The thymic tissue when displayed should
always be cut open to exclude presence of small parathyroid adenoma within its substance. Finally it should
be remembered that the parathyroids may be found behind the oesophagus or pharynx and exploration is not
complete without search in these areas.
POSTOPERATIVE MANAGEMENT.—Two small suction drains are inserted into the cervical wound.
Half hourly observations are kept on patients for evidence of Chvostek’s sign of facial nerve irritability or for
presence of Trousseau’s sign of carpal spasm on inflation of a sphygmomanometer cuff above systolic blood
pressure. The early symptoms of hypocalcaemia e.g. tingling or numbness about the lips and on finger tips
are also sought for. Serum calcium estimation is done in the evening of operation and also on the following
morning. Milder degrees of hypocalcaemia are treated by oral calcium in the form of effervescent tablets.
Should the patients become severely hypocalcaemic, 10 ml of 10% calcium gluconate is given by slow
intravenous injection. Depending on the degree of hypocalcaemia, Vitamin D may be given in an initial dose
of 8 mg of dihydrotachysterol per day. The dose is adjusted according to the daily level of serum calcium.
PARATHYROID CARCINOMA.—It is only responsible for approximately 1% cases of
hyperparathyroidism. There are symptoms of severe hypercalcaemia and very high PTH level. It may present
with a palpable mass.
Histologically diagnosis is difficult and requires expert in this field.
TREATMENT is surgery as described above. The whole mass is excised with ipsilateral lobectomy of
thyroid and excision of ail lymph nodes involved. Death is usually caused by uncontrolled severe
hypercalcaemia. Survival rates are not very discouraging and it is approximately 85% for 5 years and 50%
for 10 years.
Sometimes recurrence is seen with increasing calcium and PTH levels. Re-exploration may be required in
these cases.
Persistent and recurrent hyperparathyrodism.— Students should keep in mind that preoperative
localisation of abnormal parathyroids is not that important in case of first exploration, but it is extremely
important if recurrent exploration is required. First of all biological investigations should be performed to be
definite that it is a case of recurrent hyperparathyroidism. ■
Mainly CT/MRI scan, ultrasound or sestamibi scanning are performed to localise abnormal parathyroid.
Selective arteriography may be required to identify the glands. Selective venous sampling to measure PTH
levels in the veins of the neck or the mediastinum may regionalise abnormal parathyroid tissue.
Fluorodeoxyglucose positron emission tomography (FDG-PET) scanning is sometimes useful.
Re-exploration for parathyroid surgery is associated with certain risk of recurrent laryngeal nerve injury
and subsequent hypocalcaemia. For this rapid PTH assay is used to demonstrate the fall in PTH level after
excision of abnormal parathyroid tissue. If PTH levels fall below 50% of the previous value in 15 minutes
after excision, it is better to terminate the operation to reduce surgical morbidity from further handling.
HYPERPARATHYROID CRISIS
This term has been used to describe the clinical dilemma in which the patients become acutely ill with severe symptoms
of hypercalcaemia requiring urgent treatment. It characteristically starts with rapid development of muscular weakness,
fatigue, nausea, vomiting, drowsiness and confusion. Repeated copious vomiting leading to hypovolaemia and prerenal
uremia so that the patient becomes drowsy and confused. Cardiac arrhythmia may ensue. The serum calcium level ranges from
16 mg to 20 mg/100 ml. The parathyroid gland or glands are usually enlarged and even in l/3rd of cases the gland may be
palpable. The aetiology is still unknown.
Treatment.—For restoration of blood volume with promotion of diuresis intravenous fluid is essential. This itself brings
about dramatic improvement in the clinical state of the patient. Further reduction of serum calcium may be obtained by the
use of phosphate either by tablet or intravenous infusion. Oral phosphate is given in an effervescent tablet providing 100 mg
of elemental phosphorus. Upto 3 gm of phosphate may be given on each day for 2 or 3 days. This tablet is very irritant to G.I.
tract and limits its use. Intravenous infusion of biphosphonate (pamidronate 60 to 90 mg I.V. in 5 hours) should be
administered. Particularly in elderly patients care must be taken to avoid precipitating congestive cardiac failure and electrolyte
imbalance. Side effects of this biphosphonate therapy include fever, myalgia and pain at the infusion site. An isotonic solution
of sodium sulphate given in a dose of 3 litres in 9 hours has been shown to reduce serum calcium level rapidly.
Once the patient’s serum calcium has fallen to less dangerous level arrangements should be made for parathyroidectomy
as soon as practicable. This of course is the main treatment of this condition.
SECONDARY AND TERTIARY HYPERPARATHYROIDISM

SECONDARY HYPERPARATHYROIDISM develops in chronic renal failure and malabsorption syn
drome. In chronic renal failure there is phosphate retention leading to hyperphosphataemia. This leads to
hypocalcaemia which triggers off the parathyroid hyperplasia.
When this reactive response of the parathyroid becomes autonomous, adenomata develop and produce
the biochemical changes of primary hyperparathyroidism. This condition has been described as TERTIARY
HYPERPARATHYROIDISM. The hypocalcaemia associated with chronic renal failure often disappears with
haemodialysis even if the serum phosphate level remains the same. It is uncommon to have bone pain in this
condition.
Therapy should be directed forwards controlling the serum phosphate by dietary restriction and maintaini
adequate calcium intake. Administration of Vitamin D sterols and reducing aluminium in the diet and in the
dialysate bath may help in this condition. If these medical measures fail, parathyroidectomy is indicated.
HYPOPARATHYROIDISM
Causes.—The most common cause of hypoparathyroidism is damage to the parathyroid gland during thyroid surgery.
Bruising or slight damage to the blood supply of the parathyroid may cause transient hypocalcaemia. It takes about 3 days to
reach low calcium level and returns to normal calcium level in three days thereafter. The sooner after surgery the serum
calcium falls, more is the likelihood of parathyroid gland injury.
• Idiopathic hypoparathyroidism is a rare disease and may be due to the presence of antibodies aginst parathyroid tissue.
These patients may also have antibodies against thyroid, adrenal and gastric parietal cells.
• Another form of hypoparathyroidism is seen in childhood and appears to be familial (familial hypoparathyroidism). This
is due to prenatal suppression of foetal parathyroid glands by the hyperparathyroid mother.
• Only occasionally there may be congenital absence of parathyroid gland and thymus, so these children in addition to
hypocalcaemia suffer from absence of the thymus-dependent lymphoid system (DiGeorges Syndrome).
Clinical features.—Hypoparathyroidism causes hypocalcaemia. This is manifested by —
• Numbness and tingling in the fingers, toes and circumoral area.
• Mental symptoms in the form of anxiousness and depression are also common.
• Tetany may develop characterised by carpopedal spasms, convulsion and laryngeal stridor which may prove fatal.
Physical examinations.—Two signs are very important —
• Chvostek’s sign i.e. abnormal contraction of facial muscles elecited by tapping on the facial nerve anterior to the ear.
• Trousseau’s sign is elicited by occluding blood flow to the forearm for 3 minutes with sphygmomanometer cuff applied
to the arm and raising the pressure above systolic level. This will induce carpopedal spasm i.e. metacarpophalangeal joints are
flexed with extension of interphalangeal joints and adduction of the thumb causing Obstetrician's hand. Similar technique
may be applied in the foot which causes extension of the ankle joint and flexion of the toes
Diagnosis.—
• Estimation of serum calcium level indicates usually below 7 mg/100 ml.
• ECG changes include prolonged QT intervals and QRS complex changes.
Treamment— is calcium therapy.
• In case of mild hypocalcaemia, oral calcium e.g. calcium lactate or calcium gluconate, with vitamin D are adequate. Milk
may also be supplemented
• In case of servere hypocalcaemia, 10 ml of 10% calcium gluconate solution is given by slow intravenous injection (to
avoid cardiac erythmia). Magnesium supplements may also be required.
APUDOMAS
‘Apudomas’ are endocrine tumours which arise from apud cells. The ‘apud’ cells are distributed widely in the body and
have common cytochemical characteristics related to the synthesis of polypeptides and amines. The name ‘apud’ was first
proposed by Pearse in 1968 and is derived from the initial letters of three main properties of these cells — viz. (i) high content
of /Imine, (ii) the capacity for amine Precursor t/ptake from the environment and (iii) presence of amino acid Decarboxylase
for conversion of amino acids to amines.
The average diameter of these ‘apud’ cells is 100 to 200 (im and contain dense storage granules of their polypeptide
products. Majority of gastrointestinal apud cells possess long apical processes which reach the glandular lumen ending in tufts
of microvilli.
Pearse suggested that neural crest cells should be considered as ancestors of these apud cells. It is well accepted fact at the
present moment that all apud cells, be it in the carotid body, the thyroid, anterior pituitary, elementary tract and even
parathyroids, arise from the neural crest or neuroectoderm.
Apudomas can be conveniently classified into the following groups : —
A. Orthoendocrine —
1. Tumours secreting normal polypeptides of their cells of origin e.g. insulinoma, gastrinoma (Zollinger-Ellison syndrome),
pancreatic glucagonoma, calcitoninoma (medullary carcinoma of the thyroid).
2. Tumours secreting normal amines of their cells of origin e.g. pheochromocytoma, neuroblastoma and ganglioneuroma
(all arising from adrenal medulla) and carcinoid tumour.
B. Paraendocrine Apudoma Syndrome (PES) —
1. Tumours of endocrine glands secreting hormones characteristic of other glands.
2. Tumours of organs, not usually regarded as endocrine in nature, secreting hormones e.g. oat cell carcinoma of bronchus
producing ectopic ACTH, Schwartz-Bartter syndrome producing ADH and WDHA syndrome which is non-13 islet cell tumours
of the pancreas presenting with Watery Diarrhoea, //ypocalcaemia and hypo-or /Ichlorhydria.
MULTIPLE ENDOCRINE NEOPLASIA (MEN), in which more than 1 endocrine glands become the site of neoplasia.
1. Multiple endocrine neoplasia type / (MEN 1).— In this group the parathyroid glands are most frequently involved
(Chief cell hyperplasia) (90%) producing hyperparathyroidism, which is often mild. There is often pancreatic islet cell
tumour (80%) causing Zollinger-Ellison syndrome. The anterior pituitary is involved next (65%) causing acromegaly or
Cushing’s syndrome. There may be hyperplasia of the adrenal cortex and carcinoid tumour Duodenal ulceration is a common
feature of this syndrome. It may be related to hyperparathyroidism as hypercalcaemia promotes the secretion of gastrin.
Parathyroidectomy often reduces the secretion of acid and sometimes cures duodenal ulceration. In fact operation for
duodenal ulcer should be postponed until all endocrine lesions have been treated. Unless the patient has a pancreatic
gastrinoma, for which total gastrectomy should be performed, he may not need any further operation.
2. In type 2 (MEN 2), which is known as Sipple’s syndrome, there is medullary carcinoma of the thyroid with
pheochromocytoma and hyperparathyroidism. Pheochromocytoma requires the most urgent treatment as treatment of other
lesions may precipitate a fatal hypertensive crisis. That is why in all cases of medullary carcinoma of thyroid or
hyperparathyroidism investigations must be performed to screen out presence of pheochromocytoma. This type 2 syndrome
has been further subdivided into type 2a and type 2b. The type 2a has just been described.
In type 2b there are additional neurofibromas affecting lips, eyelids and face producing swellings in these regions.
Megacolon and ganglioneuromatosis may also be found.
561
CHAPTER - 30
THE ADRENAL GLANDS

Development.—
The adrenal gland is composed of a cortex and a medulla each having different embryologic, histologic and functional
characteristics. The adrenal cortex is mesodermal in origin and arises from the coelomic epithelium between the 4th and
6th weeks of foetal life. It gradually differentiates into a thin peripheral neocortex and a thick inner ‘foetal zone’. By the
4th month of embryonic life the adrenal glands are about 3 to 4 times larger than the kidneys, but they gradually decrease
in size thereafter till they assume normal adult size after first year postpartum. During the process of revolution the inner
foetal zone gradually involutes.
The medulla is derived from the chromaffin ectodermal cells of the neural crest during the 7th week of embryonic life.
These cells split off from the sympathetic ganglion cells and migrate further ventrally so as to lie ventrolateral to the aorta,
where they form, paraganglia. Several such nodules near the cranial ends of the gonads combine into a large mass of cells
lying between the dorsal aorta and the dorsomedial border of the mesonephros. Here they come into approximation with
the adrenal cortex and gradually form the adrenal medulla.
In lower animals the adrenal cortex and medulla remain completely separate. During the course of development
medullary and cortical tissue may be left behind in v arious locations to form accessory adrenal cortex or medulla. Incidence
of extra-adrenal medullary tissue is quite high (approximately 1 out of every 8 cases of medullary hyperfunction) in
comparison to extra-adrenal cortical tissue (approximately less than 1 out of 1000 cases of adrenocortical hyperfunction).
Accessory medullary tissues are mostly found in the paraganglia around the aorta near the adrenal glands, in the
mediastinum, in the pelvis near the bladder and occasionally even in the neck or the sacrococcygeal, vaginal or anal regions.
Accessory adrenocortical rests are most commonly found close to the adrenal within the kidney, in the ovarian pedicle, in
the broad ligament, in the ovary itself and in the testis.
Anatomy.—
Each adrenal gland lies along the anteromedial border of the superior pole of the kidney. The triangular-shaped right
adrenal gland lies close to the inferior vena cava and is usually intimately related with the bare area of the liver anteriorly.
The left adrenal gland is crescentic in shape and lies between the kidney and the aorta. Each adrenal gland is approximately
4 g. in weight. These glands are firmer than the surrounding perirenal fat and are easily palpable. The adrenal cortex is bri ght
yellow and much thicker than the medulla, which is usually reddish brown.
The adrenals are highly vascular and the arterial supply comes from the 3 sources — (i) from the inferior phrenic artery
superiorly (Superior adrenal artery), (ii) the abdominal aortamedially (Middle adrenal artery) and (iii) renal artery inferiorly
(Inferior adrenal artery). Additionally numerous small arterial branches feed each gland. The right adrenal receives primary
blood supply from the superior and inferior adrenal arteries, whereas the left adrenal is supplied by the middle and inferior
arteries. The extreme variability of the arterial supply of the glands has been recognised in recent years due to arteriography
of the glands performed so frequently. Variation from the classic blood supply is often said to be the rule rather than
exception.
The adrenal veins are more constant. There is usually 1 large vein for each adrenal gland. The vein from the right adrenal
gland drains into the inferior vena cava. The vein from the left adrenal gland drains primarily into the left renal vein, though
infrequently it may drain into the inferior vena cava.
The lymphatics form plexuses within the subcapsular portion of the adrenal cortex and these alongwith the lymphatics
from the adrenal medulla drain to the adjacent para aortic and renal lymph nodes.
Nerve supply is not apparent for the adrenal cortex though the adrenal medulla is richly supplied by sympathetic nerves.
Physiology.—
HISTOLOGY.— The adrenal cortex in the adult comprises of 3 distinct zones — (a) a peripheral zona glomerulosa,
(b) an intermediate zona fasciculata and (c) inner zona reticularis adjacent to the medulla. Each of these zones has
characteristic light and electron microscopic features which distinguish one from the others. There are also functional
differences — (a) aldosterone is produced exclusively in the zona glomerulosa, (b) glucocorticoids or cortisols are
produced in the zona fasciculata, (c) androgens are produced in the zona reticularis.
Adrenal medulla constitutes 10% of the total gland weight. Adrenal medullary cells are polyhedral in shape and are
arranged in cords. They contain catecholamines and precipitate chromium salts that stain brown with haematoxylin and
eosin stain. On electron microscopy, coarse vesicles containing epinephrine and norepinephrine can be identified.
36
ADRENAL CORTEX
Physiology of the mineralocorticoids.—
The major mineralocorticoid in man is aldosterone, which is primarily produced by the zona glomerulosa. The action of aldosterone
appears to be primarily on the renal tubule producing proximal resorption of sodium and chloride and distal resorption in exchange for
potassium and hydrogen. In one word the action of aldosterone is sodium retention.
Under normal conditions the secretion of aldosterone is regulated by complex and multifactorial system. The different factors include
A.C.T.H., the renin-angiotensin system and the serum concentrations of sodium and potassium. Roughly 30% of aldosterone secretion is
influenced by A.C.T.H. The remainder depends primarily on the secretion of renin-angiotensin system. Due to fall in blood volume there
is fall in pressure in the afferent renal arteriole. This influences releases of renin by juxtaglomerular cells. The renin combines with
angiotensinogen manufactured in the liver to form angiotensin I, which is converted by a converting enzyme in the pulmonary circulation
to angiotensin II. Angiotensin II stimulates the zona glomerulosa of the adrenal cortex to release aldosterone. The feed-back mechanism
for regulation of aldosterone production depends upon aldosterone-induced renal retention of sodium, which raises the blood volume and
turns off the production of renin. In case of renal artery stenosis, in which there is permanent fall in afferent arteriolar pressure, there is
hypertrophy of the juxtaglomerular cells with permanent rise in secretion of renin producing increased aldosterone secretion seen in
secondary aldosteronism. Either a reduction in renal arterial pressure or a decrease in the serum sodium concentration will stimulate
secretion of renin from the juxtaglomerular cells. Low sodium diets appear to produce renal vascular constriction even with insignificant
changes in serum levels to cause renin release. Aldosterone secretion in normal patients has been shown to increase in response to
catecholamine infusion or electrical stimulation of the renal sympathetic nerves. From this it is established that the sympathetic nervous
system plays a role in aldosterone secretion. Aldosterone is metabolised in the same fashion as cortisol.
Clinical states associated with elevated aldosterone production can be subdivided into — (a) primary aldosteronism and (b) secondary
aldosteronism. — (a) Patients with adrenal cortical glomerulosa cell tumours secrete aldosterone in an autonomous manner and this is
known as primary aldosteronism.
(b) Hypovolaemia from any cause will effect release of renin which ultimately causes excessive aldosterone secretion, which is
known as secondary aldosteronism.
Physiology of the glucocorticoid.—
Glucocorticoids in human beings are mostly cortisol and corticosterone. These are called glucocorticoids as these enzymes exhibit
potent effects on carbohydrate metabolism by promoting gluconeogenesis and deposition of liver glycogen. It is mainly the cortisol which
induces significant glucocorticoid effect. Glucocorticoids influence glucose metabolism directly in the liver by stimulating intrahepatic
synthesis of glucose and glycogen. There is also decrease in glucose utilisation by muscle, skin fibroblasts and fat cells causing catabolic
effect in these tissues with release of fatty acids, glycerol and aminoacids into the circulation, thus providing substrate for iiver
gluconeogenesis. With increase in plasma glucocorticoid levels many tissue are affected. There is redistribution of body fat characterised
by truncal obesity and peripheral thinning. The mechanism for this centripetal fat accumulation is unknown. Glucocorticoids induce
profound catabolic effects in muscles producing muscle weakness and negative nitrogen balance. Diabetes mellitus may become clinically
apparent due to increased gluconeogenesis and peripheral insulin resistance. Glucocorticoids are also potent immunosuppressive agents.
Potent immunosuppressive regimens that contain glucocorticoids result in increased occurrence of malignancy particularly of the lymphoid
tissue. Glucocorticoid retard wound healing by decreasing collagen formation and impeding fibroblasts response. Osteoporosis is another
manifestation of glucocorticoid administration, though the mechanism is not prefectly known. Psychological derangements, especially
depression are frequently associated with prolonged administration of glucocorticoids. Prolonged glucocorticoid administration may
produce lenticular cataracts or comeal ulcers. Though cortisol and corticosterone are primarily recognised as glucocorticoids these steroids
have mineralocorticoid effects also.
CONTROL.— Undernormal conditions in adults 10to30mg per day of cortisol is produced. The hypothalamus secretes CRF, which
promotes release of A.C.T.H. from the anterior pituitary. A.C.T.H. stimulates the adrenal cortex to produce and release cortisol. Rising
blood levels of cortisol inhibit further release of CRF from the hypothalamus and thus a negative feed-back regulatory mechanism is
established. Normally there is diurnal variation in release of CRF, A.C.T.H. and therefore cortisol. An important features of Cushing's
syndrome is failure of this diumal variation, so that A.C.T.H. is secreted constantly round the clock probably due to continued CRF stimulus.
After trauma this feed-back mechanism is disturbed by other central nervous system mechanism, so that CRF and A.C.T.H. are secreted
inspite of rising levels of cortisol.
METABOLISM of cortisol.— In the blood, cortisol exists in 3 states — (i) free, (ii) bound and (iii) conjugated.
(i) In the free state cortisol is metabolically active compound available to the tissues. For transport and protection, it is bound to
a substance known as corticosteroid-binding globulin (CBG or transcortin), which is a-globulin. When the level of free cortisol nses in
the plasma above a fixed level, it is excreted unchanged in the urine as urinary free cortisol. Measurement of this compound provides the
most precise reflection of the amount of cortisol produced by the body.
(ii) Approximately 75% of cortisol is bound to transcortin, 15% is bound to albumin and 10 to 15% remains free. Plasma transcortin
level is increased during pregnancy or by administration of oestrogen. Hypoalbuminaemia may cause decreased plasma cortisol level. The
plasma half-life of cortisol is 90 minutes.
(iii) After clearance from plasma the majoirty of the bound cortisol is metabolised in the liver. Here cortisol undergoes transformation
to inactive metabolites including dihydro- and tetrahydrocortisol, cortone and cortolone. These are conjugated with glucoronic acid and
become water soluble. These are now easily excreted in the urine, where they may be measured as 17-hydroxy or 17-ketogenic steroids.
Physiology of sex hormones.—
Normally, the gonads produce for greater amounts of oestrogen or androgens than does the adrenal cortex. However with congenital
adrenal hyperplasia or adrenal cortical tumours, the adrenals may produce large amounts of biologically active androgens or oestrogen s.
The resultant clinical abnormalities present in female children are adrenal virilism due to excess adrenal secretion which produces clitoral
THE ADRENAL GLANDS 563
hypertrophy, labial fusion etc. Whereas in male children the same adrenal excess will produce increased muscle mass, accelerated growth
of axillary and pubic hair. With elevated oestrogen levels, girls experience precocious breast enlargement and menstrual bleeding, whereas
in boys it develops gynaecomastia.
The androgens are conjugated and excreted in the same fashion as cortisol. Androgens are also influenced by A.C.T.H. secretion, but
they cannot inhibit A.C.T.H. secretion by feed-back mechanism.
CUSHING’S SYNDROME
Cushing’s syndrome is caused by increased plasma glucocorticoid level due to enhanced production of
cortisol by the adrenal cortex. This may be the result of adrenal cortical adenoma or carcinoma or due to
increased secretion of A.C.T.H. Adrenal hyperplasia is the most common, followed by adrenal adenoma,
carcinoma and ectopic A.C.T.H. source, pituitary tumours secreting A.C.T.H. in that order of frequency. This
syndrome may occasionally occur due to iatrogenic administration of corticosteroids.
Pathology.—
Harvey Cushing in 1932 ascribed the syndrome to basophilic adenoma of the anterior pituitary. Adrenal
cortical hyperplasia is the most common cause of Cushing’s syndrome. Such hyperplasia is mainly due to
increased production of A.C.T.H. with loss of normal diurnal variation of A.C.T.H. release and failure of feed
back mechanism. Hyperplasia may also be caused by excessive A.C.T.H. secretion either from the tumour of
the pituitary or from an ectopic tumour. Both the adrenal glands become hyperplastic and the sharp edges o
the gland become thick and rounded. Microscopically, widening of the cortex mainly involves the zona
fasciculata.
Adrenal adenoma is sometimes seen in Cushing’s syndrome associated with atrophy of the remainder co
and cortex of the opposite side. This atrophy is due to inhibition of A.C.T.H. secretion by the excess cortisol
secreted by the autonomous tumour.
Adrenocortical carcinoma is seen in 10% of cases of Cushing’s syndrome. This tumour sometimes occurs
in young children and wide spread metastases may occur which are also hyperfunctioning.
This disease is mostly seen in the 3rd and 4th dccades, though its occurrence has been noticed in children
below 1 year of age and in old individuals above 70 years of age.
Cushing’s syndrome is 4 times more common in women than in men. Adenomas are more common in
women than in men.
SYMPTOMS AND SIGNS.— Obesity is present in almost every case. The peculiarity is that there is
truncal fullness with relatively thin limbs. There is excessive accumulation of fat around the head and neck
giving rise to typical ‘moon fades’ and ‘buffalo hump’. Purple striae are often seen on the abdomen and
occasionally on the extremities. A large percentage of female patients become hirsute with acne and
ecchymosis. Oligomenorrhoea and amenorrhoea may be present. Impotence may occur in men.
Elevated blood pressure usually of a moderate degree is often seen in large percentage of patients. This
increased blood pressure is due to sodium retention and atherosclerosis, which account for death in 40% of
patients with Cushing’s syndrome.
Muscle weakness and bone pain particularly backache are quite common. The weakness is due to muscle
wasting, but may be due to decrease in potassium concentration. The bones become osteoporotic and
pathological fractures may occur in advanced cases. The neurologic symptoms including headache, irritabilit
depression and mental symptoms are also come across.
Many patients with Cushing’s syndrome demonstrate decreased glucose tolerance and become diabetic.
Such diabetes is often controlled by diet, though some patients may require insulin. Some patients may show
hypercaleiuria, though serum calcium concentration is usually normal unless associated with multiple
endocrine neoplasia type I and associated hyperparathyroidism. Serum potassium may be decreased with
metabolic hypokalaemia.
Diagnosis of Cushing's syndrome depends on demonstration of hypercortisolism.
1. The most useful screening test is the determination offree cortisol in urine. Values in excess of 100
|ig/24 hours suggest increased cortisol production. When screening tests are abnormal, further tests should
performed to know the reason of increased cortisol production — whether it is adrenal, ectopic A.C.T.H. or
pituitary-hypothalamic aetiology.
2. Plasma A.C.T.H. measurement.— Normally A.C.T.H. levels range between 10 and 100 Pg. per ml.
Highest plasma levels are seen in early morning hours and lowest concentrations are found in the late evenin
Patients with adrenal neoplasms show low plasma A.C.T.H. levels and this is virtually diagnostic of an
adrenocortical neoplasm. In basophilic pituitary tumours (Cushing’s disease) plasma A.C.T.H. levels may be
as high as 200 to 500 Pg. per ml. Sometimes due to neoplasms that ectopically produce this hormone, plasma
A.C.T.H. level reaches the highest level often exceeding 1000 Pg. per ml.
3. Dexamethasone suppression test.—Dexamethasone is more potent than cortisol in inhibiting A.C.T.H.
release from the pituitary gland. The patient ingests 1 mg of dexamethasone at midnight. At 8 a.m. the next
morning a plasma sample is taken for cortisol measurement. In normal subjects the level should be less than
5 jj.g/100 ml. Plasma values above 5 |ig/100 ml. suggests Cushing’s syndrome.
4. Metyrapone test.— Metvrapone blocks 11-P-hydroxylase and conversion of 11-deoxycortisol to
cortisol in the adrenal cortex. This results in increase in A.C.T.H. secretion which stimulates the adrenal corte
to produce increased amounts of cortisol precursors e.g. 11-deoxycortisol. These compounds are detected in
urine as increased amount of 17-hydroxycorticosteroids. In this test metyrapone is administered orally in the
dose of 10 mg./kg. body weight every 4 hours for 6 dosage. In normal subject there is a twofold or greater
increase in total urinary 17-hydroxycorticosteroids on the day or on the subsequent day of the test.
5. A.C.T.H. stimulation test.— Administration of A.C.T.H. demonstrates elevation in urinary free
cortisol in pituitary-dependent Cushing’s disease. In patients with adrenocortical neoplasia or ectopic A.C.T
secretion this increase in urinary free cortisol is not found.
6. CT scan— accurately finds out almost all adrenal tumours in patients with Cushing’s syndrome. This
method of investigation is now very popular and has almost replaced other techniques for detection of pituit
microadenoma in Cushing’s disease. CT is also reliable in detecting nodules in the lungs, mediastinum and
pancreas, which are potential sites of ectopic ACTH production.
7. X-ray of the sella turcica and angiography of the adrenal.— X-ray should be performed in all cases.
Enlarged sella turcica may be noted in patients with pituitary tumours as in case of Cushing’s syndrome. X-r
of bones in general may frequently demonstrate osteoporosis and even pathological fractures.
Angiography may be performed to localise adrenal tumours or to demonstrate adrenal hyperplasia. Mor
recently 131Iodocholesterol emission photoscanning has been effective in demonstrating adrenal lesion in
Cushing’s syndrome.
Treatment.—
MEDICAL TREATMENT.—- Medical treatment is restricted to (i) inoperable carcinoma of the adrenal
cortex with metastases or (ii) extremely poor surgical risk.
Three drugs have been tried in this syndrome —
(a) Metyrapone may be used in the dose of 2 to 6 g. per day in divided doses by mouth. This drug is
capable of reducing plasma cortisol level. In both adrenal hyperplasia and tumours this drug has been effect
(b) Aminoglutethimide is an anticonvulsant with the trade name Elipten. This drug acts by blocking
steroid synthesis as some point between cholesterol and pregnenolone. Thus it causes decrease in cortisol lev
in plasma. The dose is about 1 to 2 g. per day. This drug is also effective in Cushing’s syndrome due to aden
and carcinoma, though it is not effective in A.C.T.H. producing oat cell carcinoma. This drug however has be
banned due to its effect of hirsutism and goitre producing.
(c) O, P-DDD is a drug which directly damages the adrenocortical cells. It has been used primarily to
treat metastatic adrenocortical carcinoma. It is given in the dosage of 10 to 20 g. per day for prolonged period
This drug has been used in the dosage of 2 to 5 g. per day to treat Cushing’s syndrome due to hyperplasia or
adenoma. The side effects of this drug are numerous including nausea, skin rashes, pigmentation, blurring o
vision, nystagmus etc.

1. Pituitary irradiation.— In case of Cushing’s syndrome due to adrenocortical hyperplasia pituitary
irradiation is the best treatment. The idea is to reduce A.C.T.H. secretion from the pituitary and thus to prev
adrenal hyperplasia. The usual radiation dose is 4000 to 5000 rads to the pituitary fossa using a60 cobalt or hi
energy source. The cure rate varies from 10 to 60% average being 30%.
Recently 90Yttrium implantation in the pituitary fossa has been used for Cushing’s disease.
2. Transsphenoidal hypophysectomy.— The effect of this operation is almost similar to pituitary
irradiation. With transphenoidal surgical technique the neurosurgeon can remove pituitary tumour and achi
remission of Cushing’s syndrome. In a large percentage of patients with Cushing’s disease the pituitary glan
were found to have microadenomas. It should also be noted that the secretion of other anterior pituitary
hormones can be preserved in the majority of patients following transsphenoidal surgery. The benefits from
transsphenoidal hypophysectomy appear to present striking improvements over those achieved by transfron
hypophysectomy or total adrenalectomy. Obviously in subjects with small pituitary adenomas, a transsphe
noidal approach is the procedure of choice.
3. Adrenalectomy.— Patients who fail transsphenoidal hypophysectomy are candidates for this opera
tion. Patients with severe Cushing’s syndrome may be offered this operation.
Although bilateral adrenalectomy is usually curative in patients with Cushing’s disease, but there have b
reported cases of recurrent hypercortisolism presumably due to ectopic adrenal tissue. Incomplete resection
adrenocortical tissue or rupture of cortical adenoma during surgery may cause recurrence.
Transabdominal, back and flank approaches have been made for adrenalectomy in Cushing's syndrome.
entire gland containing the tumour is excised. If there is bilateral adrenal hyperplasia, the left side is operated
on first as exposure is easier in this side. If the gland appears normal or enlarged it should be removed. If the
gland appears atrophied, it is biopsied, left undisturbed and the wound is closed considering that the diagno
was wrong and the patient has adrenocortical tumour on the opposite side. The right side is then exposed.
ALDOSTERONISM
Increase of aldosterone secretion gives rise to a condition known as hyperaldosteronism. Primary aldoster
onism was first described by Conn in 1955. In this condition there is excess aldosterone secretion, where
A.C.T.H. plays a minor but interesting role. Secondary aldosteronism is due to decreased renal arterial pressure
for which there is excess secretion of renin from juxtaglomerular cells of kidney which acts on angiotensinog
to convert it into angiotensin II which is the chief stimulus to aldosterone production.
Pathology.—
About 90% of patients with primary aldosteronism have benign solitary adrenocortical adenoma more
common on the left than on the right side. The size of the tumour has little relation to the degree of
hypersecretion. Adenomas are bilateral in 5% of cases. Bilateral adrenal glomerulosa cells hyperplasia also
causes primary aldosteronism. Rarely primary aldosteronism may be produced by adrenocortical carcinoma
Macroscopically, the tumours are discrete and circumscribed. On cut section these are bright canary yello
The cells do not look like those of zona glomerulosa, but these are often hybrid cells with features of both zon
glomerulosa and zona fasciculata.
The patients are mostly between the ages of 30 and 50 years, though this disease has been found in childre
of 3 years and in the old of 75 years. It is twice as common in women than men.
The signs and symptoms are mild and nonspecific. The patients often complain of frontal headache, musc
weakness, fatigue, polyuria, nocturia and thurst. Moderately severe diastolic hypertension is noted. Occasion
ally patients may have tetany. Hypocalcaemia and hypernatremia are most characteristic features.
1. Plasma potassium and sodium.— In primary aldosteronism there is typically low potassium and high
- A CONCISE TEXTBOOK OF SURGERY
566
plasma sodium level, though normokalaemic primary aldosteronism has been reported. In secondary aldos
onism there is also low plasma potassium level, though plasma sodium concentration is normal or low. The
greater the degree of secondary aldosteronism and renin secretion, the lower the sodium level.
Chlorothiazide may be used as a diagnostic aid to produce profound depression of plasma potassium le
in patients with primary aldosteronism.
2. E.C.G.— The E.C.G. changes are characteristic of hypokalaemia, which becomes normal after
removal of aldosterone-secreting tumour.
3. Urinary potassium and sodium measurements.— In hyperaldosteronism there is excessive loss of
potassium in the urine. The urine becomes alkaline. There is systemic metabolic alkalosis with elevated
bicarbonate level.
4. Urinary specific gravity.— Patients with hyperaldosteronism characteristically produce large volume
of urine with low specific gravity. This is resistant to ADH, so that there is no increase in the specific gravity
level with the administration of Pitressin.
5. Aldosterone excretion in the urine.—In normal individuals with salt intake patients usually excrete less
than 10 |ig per day of aldosterone in the urine. In primary aldosteronism patients excrete aldosterone betw
15 and 50 ng per day.
6. Spironolactone test.— 100 g. of Aldactone 4 times a day is given for 3 days while the patient is on
normal sodium intake. The serum potassium level should rise by a minimum of 1 mEq/Litre if there is
hyperaldosteronism. Patients with other causes of hypokalaemia will not show any increase.
7. Plasma renin level.— If primary aldosteronism is present the value will be normal or low, whereas in
secondary aldosteronism this level will be high.
Treatment.—
Majority of patients with primary hyperaldosteronism have adrenocortical adenomas or bilateral adrena
hyperplasia. Rarely such disease may be caused by adrenocortical carcinoma. The treatment of choice is
resection of the adrenal gland containing the lesion. In small number of patients the increased aldosterone l
can be suppressed by administration of drugs.
MEDICAL MANAGEMENT.— Spironolactone is an antagonist of aldosterone, but does not alter the
production of aldosterone by the adrenal. Spironolactone reduces serum sodium and elevates serum potass
levels. The hypertension is reduced. The headaches and nocturnal polyuria also disappear. This substance o
course does not have similar effect in secondary aldosteronism.
The increased aldosterone levels can be suppressed by the administration of dexamethasone. 2 mg of
dexamethasone may be administered daily for 2 weeks. Patient’s blood pressure becomes normal with a
decrease in serum aldosterone level.
SURGICAL TREATMENT.— As mentioned earlier ideal treatment for adrenal cortical adenoma is surgic
extirpation.
Preoperatively, the patient should be on low sodium and high potassium intake. The serum potassium l
should be raised to 3 mEq per litre prior to surgery. Spironolactone may be used in this respect, though in
majority of cases this is not required.
Operative technique.— Posterior approach is often preferred in primary aldosteronism. The adenomas are
seldom bilateral. The affected gland is removed entirely.
If no adrenal tumour is palpable during surgery, the adrenal which yields higher aldosterone content in
venous blood should be removed. Microscopic adenomas have been found in such gland.
In patients with adrenocortical hyperplasia total or subtotal adrenalectomy should be carried out. Adren
venous blood should always be sampled for localisation for aldosterone producing tumours.
ADRENOGENITAL SYNDROME
This syndrome may appear at 3 different times of life — at birth, in childhood or in adult.
(a) At birth.— Congenital adrenogenital syndrome showing manifestations at birth is by far the most
common variety. In female child congenital adrenal hyperplasia produces pseudohermaphrodite, while in ma
child it produces macrogenitosomia praecox.
The treatment is usually not operative, though in occasional cases plastic operations may be required on th
genitalia of female pseudohermaphrodites.
(b) In childhood.—In this age group adrenogenital syndrome is often due to adenoma or carcinoma of the
adrenal cortex. In the female it produces masculinisation and in the male it produces sexual precocity.
(c) In adult life the adrenogenital syndrome is usually due to tumour. It is seen more commonly in women
in whom it produces virilism with or without signs of Cushing’s syndrome. In the male, where it is less comm
it produces feminisation.
Adrenogenital syndrome refers to any situation in which there is over-production of androgens. That is wh
this syndrome is more marked and distressing in the females than in the males.
In a variety of situation in young women, including the Stein Leventhal syndrome, there is mild
oveiproduction of androgens leading to hirsutism, acne and amenorrhoea. There may be slight increase in 17-
ketosteroid excretion. Treatment is by administration of corticosteroid or oestrogen.
Oestrogen secreting tumours.— Feminising adrenocortical tumours are rare. The tumours are usually
large and are palpable in about 1/2 the cases. The pick incidence of feminising tumours is between the ages of
25 and 45 years. If this tumour occurs in young girls, it results in striking premature sexual development. Sign
of Cushing’s syndrome is frequently present as well.
In males the presenting sign is usually gynaecomastia, feminising hair change and atrophy of testis and
penis. In females the diagnosis is often not made unless it presents as Cushing’s syndrome.
There is marked increase in urinary oestrogen, 17-hydroxycorticosteroids and 17-ketosteroids.
TREATMENT is by surgical excision as soon as the diagnosis is made. If the tumour is malignant, surgical
excision should be followed by radiotherapy. Metastases may occur in the liver, lungs, bones and even to the
brain. Oestrogen secreting tumours in men are often malignant and radical resection with lymphadenectomy
should be the treatment of choice as this tumour is relatively insensitive to irradiation and chemotherapy.
ADRENOCORTICAL INSUFFICIENCY OR ADDISON’S DISEASE

OR CHRONIC HYPOCORTICISM
This disease is of less importance to the surgeons. This condition is due to progressive destruction of the three zones
of the adrenal cortex and medulla with lymphocytic infiltration.
Though the cause is still not very clear, yet autoimmune disease is held responsible for 60% of cases. Other autoimmune
diseases such as thyroiditis (Hashimoto’s disease), pernicious anaemia, hypoparathyroidism and gonadal failure are seen
associated with this condition.
T uberculosis still accounts for 10 to 20% of cases of this disease. Amyloidosis and metastatic carcinoma are other causes
of this condition.
This disease often commences in the 3rd or 4th decade. Males and females are equally affected.
The major signs and symptoms of Addison's disease can be divided into 2 groups — (a) those related to glucocorticoid
deficiency and (b) those related to mineralocorticoid deficit.
The most frequent complaints are weakness, weight loss, fatigue. Hyperpigmentation is the form of irregular dusky
pigmentation of the skin due to deposits of melanin are noted in approximately 90% of cases. It occurs mostly on the extensor
surfaces, on the palmar creases and on the buccal mucosa. Pigmentation in the mouth is a striking feature of this condition.
Patients are usually hypotensive with low sodium level and elevated potassium level. Nausea, vomiting and diarrhoea occur
in approximately half the cases.
The characteristic laboratory findings are marked hyponatraemia, hyperkalaemia and decreased blood volume.
Hypercalcaemia may be present.
High plasma concentration of ACTH with decreased concentration of plasma cortisol is confirmatory of this condition.
Treatment.—
It is mainly medical. Hydrocortisol sodium succinate should be administered in the dose of 100 mg intravenously every
568
8 hours till the patient becomes stable. Intravenous fluids are also required in the form of normal saline and 5% glucose.
Monitoring of serum potassium and sodium should be performed frequently.
When the condition goes to chronic stage, it requires administration of corticosteroids in the form of cortisone acetate
25 mg in the morning and 12.5 mg in the afternoon.
Waterhouse-friderichsen syndrome.—
Severe systemic bacterial infections particularly with meningococci or Ps. aeruginosa may cause massive bilateral
adrenal cortical haemorrhage with endotoxic shock. Most cases occur in infants, though adults are also involved particularly
in bums.
Patients often present with hyperpyrexia, rigors, cyanosis and vomiting. Profound vascular collapse resulting from
endotoxaemia and acute corticosteroid deficiency is very lethal. Petechial haemorrhages in the skin which coalesce to form
purpuric rashes may be seen.
Bilateral tenderness 2 inches (5 cm) below the costal margin with clear urine and absence of any sign in the lungs is
confirmatory of this condition. The petechial spot in the skin may be punctured and the smear should be examined for
diplococcus.
■ Treatment.— Successful treatment of this disorder depends upon early diagnosis and administration of high doses of
corticosteroid and appropriate antibiotics. Hydrocortisone sodium succinate should be administered intravenously, or
intramuscularly if the veins are not available, in the dose of 100 mg every 8 hours. Proper antibiotic should be administered
intravenously. Oxygen should also be administered.
ADRENAL MEDULLA
Physiology.—
The cells of the adrenal medulla secrete a large number of biogenic amines which are known as catecholamines. Mainly 3
catecholamines are found in adrenergically innervated human tissues—dopamine, norepinephrine and epinephrine. These catecholamines
are synthesised in the brain, the nerve endings of sympathetic neurones, chromaffin cells of the adrenal medulla and certain other extra
adrenal neural crest tissues. L-Tyrosine, an aminoacid derived from the diet or by endogenous conversion of phenylalanine, is converted
by tyrosine hydroxylase to L-dihydroxy phenylalanine (DOPA). Dopa is decarboxylated to L-dihydroxy phenylethylamine (Dopamine)
by aromatic L-aminoacid decarboxylase. Dopamine is hydroxylated by dopamine (3-hydroxylase to L-norepinephrine. PNMT (phenyle-
thanolamine N-methyl Transferase) is responsible for transformation of L-norepinephrine to L-epinephrine. PNMT.is available exclusively
in the adrenal medulla and the organ of Zuckerkandl.
Epinephrine accounts for 80% of total catecholamines in the human adrenal medulla, norepinephrine accounts for approximately 20%
and dopamine represents a very small fraction. There are cytoplasmic granules which are storage vesicles for dopamine, epinephrine and
norepinephrine in the cells of adrenal medulla and sympathetic nerve endings. Excitation of these cells stimulates expulsion of the granular
contents into the extracellular fluid and circulation. Dopamine is found in several other locations notably the liver and lungs.
Fate of catecholamines.— Once the catecholamines are released from the adrenal medulla into the circulation, they undergo biologic
inactivation by one of 3 routes —
(i) The most important for epinephrine and norepinephrine is the uptake and retention of these substances into the post-ganglionic
neurones and sympathetic nerves.
(ii) The second uptake mechanism involves inactivation of circulating amines, particularly epinephrine, in peripheral tissues e.g.
cardiac and vascular muscle cells, collagen and elastin. This 2nd uptake mechanism is less important than the first.
(iii) Catecholamines are inactivated by one of 2 enzymes, catechol-O-methyl transferase (COMT) or monoamine oxidase (MAO).
While COMr is responsible for inactivation of circulating catecholamines, MAO is mainly responsible for inactivation of catecholamines
in the cytoplasm of nerve endings and peripheral tissues. The metabolites of enzymatic degradation of catecholamines are nor-
metanephrine, metanephrine and VMA (Vanillyl Mandelic Acid) and Methoxy hydroxy phenyl glycol (MHPG). These are available in the
urine and can be measured for diagnostic purpose in pheochromocytoma. Free catecholamines may also be excreted in the urine.
PHEOCHROMOCYTOMA
This is a functionally active chromaffin tumour, which may be located in the adrenal medulla or other
of sympathetic ganglia or chromaffin tissue. The term is derived from the Greek word Phaios which mean
and chroma means dusky as this tumour stains deep brownish colour when exposed to chromium salts. Th
tumour is derived from primitive cells originating in the neural crest, which can differentiate to form
pheochromocytes. This tumour has a tendency to produce large amount of catecholamines, primarily
norepinephrine.
Pathology.—
Pheochromocytomas often involve the right rather than the left adrenal medulla and in 10% of cases it
be bilateral.
Macroscopically, this tumour tends to be circumscribed and yellowish brown, but occasionally this may
attain a large size. Large growths frequendy exhibit areas of necrosis, haemorrhage or cyst formation. When
treated with solution of chrome salts, this tumour turns dark brown to almost black.
Microscopically, the cells are arranged in cords and trabecullae. The cells are large polyhedral or irregular
pheochromocytes, many of which show pleomorphism. The tissues are traversed by thin walled vessels, the
walls of which are lined by the cells of the tumour.
About 8% of these tumours behave in a malignant fashion.
Pheochromocytomas may develop at all ages, but are usually encountered between the ages of 20 and 50
years.
This tumour presents a clinical picture in a bizarre fashion which is often referred to as adrenal-sympath
syndrome. The most constant feature of this syndrome is paroxysmal or persistent arterial hypertension. The
patient complains of sweating, palpitation and headache. Death may occur from myocardial infarction or
cerebrovascular accident. The patient may present with diabetes mellitus.
Occasionally pheochromocytoma may present in a relatively asymptomatic patient as only diastolic
hypertension detected during routine evaluation. Itis said thatO. 1 to 0.2% ofpatients with diastolic hyperten
harbour pheochromocytomas.
The signs and symptoms of pheochromocytomas are due to increased secretion of epinephrine and
norepinephrine. The secretion may be constant or intermittent accounting for persistent or paroxysmal natu
of the symptoms. Usually patients with paroxysmal hypertension are more symptomatic than those with
sustained hypertension. In small doses norepinephrine stimulates arteriolar tone and causes increased vascu
resistance and diastolic pressure. When the secretion is mainly epinephrine, the effects include sweating,
tachycardia and hyperglycaemia. However hypertensive episode may be stimulated by injection of drugs e.
histamine or glucagon or by injection of contrast materials used for arteriography.
1. Diagnosis of pheochromocytoma is confirmed by documenting increased excretion rates of urinary
epinephrine and norepinephrine or their metabolites (metanephrine, normetanephrine or VMA). 90% of the
cases can be accurately diagnosed by this technique.
2. Measurement of plasma epinephrine and norepinephrine is generally not useful, though particularly
with paroxysmal hypertension these levels may be raised.
3. Provocative test by intravenous administration of histamine, a drug that provokes secretion of
catecholamines into the circulation of patients with pheochromocytoma, thereby evokes a hypertensive
episode. Unfortunately false-negative and false-positive reactions occur with these tests in approximately 20
of cases. These tests are also associated with significant degree of morbidity. Tyramine or glucagon may also
be used for provocative tests.
LOCALISATION OF ADRENAL TUMOURS.—
1. Conventional urography may show downward displacement of the kidney if a large adrenal mass is
present.
2. Ultrasonography.— This technique is rarely able to identify adrenal neoplasm smaller than 2 to 3 cm
in size.
3. Computed tomography.— The greatest advantage of this technique is its ability to detect lesions less
than 2 cm in size. The smallest lesion identified was 1 cm in diameter. This technique offers great promise in
the identification of both primary and metastatic adrenal lesions.
4. Adrenal imaging.— By using 131I-19-iodocholesterol attempts have been made to image various
tumours in the adrenal glands. But this has not been much successful. 131IMIBG has been used recently with
more success (about 80% in pheochromocytoma).
5. Arteriography.— Although associated with some risk, this technique has been used to localise
pheochromocytomas, which are highly vascular. But this technique may induce hypertensive crisis.
6. Adrenal venography.— This has an advantage of sampling the adrenal venous blood for measurem
of corticosteroids or catecholamines to localise functioning tumours and also localising the tumour by injecti
contrast medium into the adrenal vein.
Treatment.—
MEDICAL TREATMENT.— The main treatment of pheochromocytoma is surgery. The place of medical
treatment is restricted to (i) in preoperative preparation, (ii) for patients who refuse surgery and (iii) for patie
who have functioning metastases.
Oral administration of phentolamine (Regitine) may be used to control symptoms in the dose of 25 mg ev
3 hours. Intravenous phentolamine has been proposed for difficult cases to control hypertension. Addition o
reserpine has also been advised to control hypertension. More recently phenoxybenzamin (Dibenzyline), an
adrenergic receptor blocking agent has been used to achieve reduction of chronic blood pressure in patients
pheochromocytoma with good result, a-methyl dopa is also been used with some success.
p-adrenergic receptor blocking agent e.g. propranolol has been used with success particularly in patients
who are being prepared for surgical treatment and to treat malignant pheochromocytomas. The dose used in
these cases is about 60 mg per day by mouth in 3 or 4 divided doses.
OPERATIVE PROCEDURE.— Many surgeons advocate anterior transabdominal approach for all adrena
neoplasms regardless of the type. This approach is probably good considering that pheochromocytomas may
be bilateral and may occur in extra-adrenal sites. But some surgeons yet prefer posterior approach as this tum
is mainly a unilateral tumour. Posterior incisions are better tolerated by the patients. The adrenal gland
containing the tumour should be removed entirely. Technique of adrenalectomy is discussed at the end of th
chapter.
NEUROBLASTOMA
This tumour is almost confined to children and more than 50% occur within first 2 years of life and 80%
before 10 years of life. This tumour is one of the most frequent abdominal neoplasms observed in infants and
children below 5 years of age. Only occasionally this tumour has been reported in adults.
Pathology.—This tumour tends to occur more on the left side. Macroscopically, the tumour is soft in
consistency and may attain a large size. It is bilateral in a few cases.
Microscopic picture is masses of undifferentiated small round cells, which are known as neuroblasts. Fibril
are arranged in longitudinal bundles or in round whorls around the cell masses giving a characteristic
appearance of rosette or pseudorosette.
SPREAD of the tumour is important as patients are often brought in due to metastasis.
(i) Blood spread metastasis is quite common particularly to the bones (30%), liver (20%), skull or brain
(11%) and lungs (9%). There is special predilection for metastasis in the skull and orbit, so that the patient
presents with protrusion of the eye with haemorrhage in the surrounding tissues. When proptosis develops
a young child, the clinician must examine its abdomen to exclude neuroblastoma. Probably metastasis in the
skull from the adrenal occurs through the vertebral system of veins. Metastases however are also seen in the
long bones, ribs and sternum.
(ii) Lymphatic spread, though occurs, is usually late. Regional lymph nodes are involved in 25% of cases.
Cervical lymph nodes are also seen to be involved in 5% of cases.
Clinical features.— Abdominal mass or swelling is the most common symptom. There is often weight los
vomiting and abdominal pain. Pallor is often well noticed. Liver enlargement due to liver metastasis is not
uncommon. Hypertension may be an additional finding in a few cases.
Patients often present with metastasis particularly in the skull. So the parents of the children first point ou
swelling of the head, proptosis with or without ecchymosis of the eyelid. Occasionally blindness is complain
of. Sometimes this tumour is presented with extensive bony metastasis, pallor and severe anaemia without o
findings.
Special Investigations.— 1. Urinary excretion of catecholamines or metabolites of catecholamines may be
elevated. As this tumour is more embryonic in nature, it tends to secrete large amounts of dopamine instead
epinephrine or norepinephrine. The urinary VMA level is often elevated. Metabolite of dopamine e.g. HVA i
more often elevated in case of this tumour.
2. Liver function tests are of not much value even with hepatic metastases.
Treatment.—
Total excision of the adrenal gland alongwith the tumour is the treatment of choice. Sometimes this tumou
bleeds a lot which becomes hazard for operation. Fresh blood replacement is required.
Excision should be followed by postoperative irradiation.
Combined chemotherapeutic drugs should be prescribed for metastatic cases.
Prognosis is often regarded as hopeless, but this view must now be modified. Sometimes this tumour show
a change from the malignant to the benign form. Widespread necrosis may occur in the tumour which destro
many of the tumour cells. Although mortality of the neuroblastoma is high, there is a better prognosis if the
diagnosis is made before 1 year of age. The more mature is the tumour the better is the prognosis. If metastas
are not present at the time of treatment, the prognosis is better.
GANGLIONEUROMA
This is the rarest of the medullary tumours. As pheochromocytoma it occurs in adults. It is a benign tumo
and least harmful among the 3 tumours of the adrenal medulla.
The tumour is composed of adult nerve cells and fibres. It produces no hormonal secretion.
This tumour is often asymptomatic and detected accidentally.
It sometimes presents as a fusiform radio-opaque lesion in the paravertebral gutters in straight X-ray in th
course of routine investigations. There is no other diagnostic laboratory findings.
ADRENALECTOMY
Usually the left side is explored first, due to the fact that the left gland is more often affected by adenomas
or carcinomas. If a tumour is found adrenalectomy is carried out. If the leftgland is seen to be atrophic, it is hi
probable that there is a tumour on the right side, which should be operated on. If the left gland is seen to be
hyperplastic or normal subtotal (90%) adrenalectomy should be performed. If after performing left sided
adrenalectomy, it is found that the patient will not tolerate a bilateral operation, exploration of the right side
should be postponed.
When the bilateral adrenalectomy has to be performed, anterior approach should be adopted. If the lesion
is localised to one side (aldosteronoma) and has been identified with certainty, thepostero-lateral approach is
used.
POSITION.— The patient lies supine on the table with a slightly arch over the raised gallbladder bridge.
This can also be achieved with the break of the table under the 12th thoracic vertebra. The pelvis is secured w
wide strapping.
INCISION.— For anterior approach, a long left paramedian incision is made from the xiphisternum above
to well below the umbilicus. If access is inadequate, the incision is extended laterally through the rectus musc
at the level of the transpyloric plane to the costal margin.
A curved transverse incision, convex upwards with its centre 5 cm above the umbilicus, is sometimes
preferred. This not only gives a better access, but being transverse, the incision heals rapidly.
For postero-lateral approach, an incision is made over the 11th rib from the lateral border of the
sacrospinalis to the abdominal wall. Extraperitoneal approach is made as done for kidney operation.
TECHNIQUE —ANTERIOR APPROACH.—
LEFTSIDE.—
After opening the abdomen, the small intestine is packed downwards. The costal margin is retracted upw
very strongly. A hand is insinuated to push the spleen medially and the posterior layer of the lienorenal ligam
is incised. The spleen is further turned medially together with the tail of the pancreas and the splenic vessels.
The left adrenal is identified above the kidney. The gland is first palpated between the finger and the thum
The large adrenal vein is identified, emerging from the inferomedial angle and draining into the renal vein
vein is carefully divided between ligatures. The gland is gradually mobilised and the fine medial arterial
attachments are cauterised with diathermy. The gland is now freed and removed.
RIGHT SIDE.—
The falciform ligament is divided. The liver is retracted upwards and the hepatic flexure of the colon an
duodenum are packed downwards. The inferior vena cava is seen deep to the duodenum. The posterior pa
peritoneum is incised transversely just above the duodenum to the border of the inferior vena cava. The la
of the posterior parietal peritoneum are reflected upwards and downwards. The fat around the upper part
kidney is cleared off. The adrenal gland will be exposed. On the medial side of the gland, one or more adre
veins will be seen draining to the inferior vena cava. These are divided between ligatures. Great care must
taken not to injure the inferior vena cava. The gland is gradually mobilised and the residual arterial bleedi
is stopped by diathermy cauterisation.
It is always essential to search for ectopic adrenal tissue before completing the operation. The wound is
closed in layers.
POSTEROLATERAL or POSTERIOR APPROACH.— Incision is made over the 11th rib. The 11th rib is
resected. The lumbodorsal fascia is incised and the sacrospinalis muscle is retracted medially. The kidney i
pushed below manually. Care should be taken to identify the pleura and preserve it. The arteries and vein
adrenal gland are identified, tied securely and divided. The adrenal gland is then removed and the wound
sutured. If the pleura has been injured, a small chest tube is put inside the pleural cavity and under-water
drainage is given. The chest tube is removed on the 2nd postoperative day.
When bilateral adrenalectomy will be required, corticosteroids should be administered preoperatively.
Cortisone acetate should be given I.M. in the dose of 50 mg. 48 hours and 24 hours prior to surgery and on
morning of surgery. This dose is continued till 3rd or 4th postoperative day after which the patient can be
cortisone acetate orally. During surgery at the time of removal of adrenals 100 mg. of hydrocortisone sodiu
succinate is given i.v. and additional same dose at 8 and 16 hours postoperatively.
573
CHAPTER - 31
'■
THE BREAST
EMBRYOLOGY
The human breast makes its appearance in the 6th week of foetal life as an ectodermal thickening extending from the
axilla to the groin. This is called the mammary ridge or milk line. In human beings the distal 2/3rds of this line disappears
rapidly. Only the pectoral portion thickens and takes the appearance of a lens-shaped thickening. Gradually from this
thickening on the milk line growth of ectoderm occurs in the form of 15 to 20 solid cords to form the rudimentary mammary
gland. These cords show bulbous dilatations at their ends from which alveoli of the gland develop. The solid cords develop
in the 5 th month of foetal life and these gradually turn into ducts by hollowing during 7th or 8th month of foetal life. At this
period the skin from which the ducts develop show a small depression which corresponds to the nipple and the ducts turn
to be milk ducts. In the later weeks of foetal life the alveoli become canalized. Just before or soon afterbirth themasenchym
underlying this depression proliferates and makes it everted to form the nipple. The areola is slight thickening in the skin
which contains a few glands of Montgomery. The areola, soon after birth, distinguishes itself by slight increase in
pigmentation. The 15 to 20 milk ducts and their alveoli ultimately form 15 to 20 lobules at the age of puberty.
Soon after birth bilateral or unilateral enlargement of the breast occurs in majority of infants. In half of these cases the
swelling is accompanied by secretion of creamy fluid similar to colostrum, which is called ‘Witch's milk'. This is due to
increase of oestrogen level in the infant's circulating blood which is nothing but of maternal origin. This disappears after
2 weeks when the oestrogen level automatically falls.
ANATOMY
The breast is a modified sweat gland lying on the pectoral fascia and musculature of the chest wall and surrounded by
skin and subcutaneous fat. Transversely it extends from the side of the sternum to near the mid-axillary line. Vertically it
extends from the 2nd to 6th rib. The superolateral part of the breast is prolonged upwards and laterally towards the axilla
forming the axillary tail of Spence, which pierces the deep fascia to lie in close relationship with the pectoral group of axillary
lymph nodes. The foramen of the deep fascia through which the axillary tail reaches the axilla is called Langer's foramen.
Neoplasms or deformities affecting this tail are often confused with the lymph nodes enlargement. The deep surface of the
breast is slightly concave and is in direct relation with the deep fascia which separates the breast from the following muscles
— Pectoralis major, Serratus anterior, Obliquus extemus abdominis and the aponeurosis of the last muscle as it forms the
anterior wall of the sheath of the rectus abdominis. 2/3rds of the breast lies on pectoralis major and fascia covering it, lateral
’/ rd lies on serratus anterior and inner and lower most small portion lies on aponeurosis of external oblique muscle. Between
the breast and the deep fascia there is a space containing loose areolar tissue which is known as retromammary or
submammary space and this allows the breast to be movable on the deep fascia covering Pectoralis major. Only when
advanced cancer of the breast has involved the fascia covering pectoralis major the breast becomes fixed to certain extent.
Portions of the fibrous tissue of the breast extend from the surface of the glandular breast anteriorly to intermingle with the
superficial layer of the superficial fascia. Similarprocesses from the deep surface of the gland cross the retromammary space
to fuse with the pectoral fascia. These are called ligaments of Cooper.
The nipple is a cylindrical or conical eminence which projects from just below the centre of the anterior surface of the
breast and usually lies at the level of the 4th intercostal space. It is traversed by 15 to 20 milk ducts (lactiferous ducts) which
open by minute orifices on its wrinkled tip. The bulk of the nipple is made up of unstriped muscle fibres arranged circularly
and longitudinally, though majority are arranged circularly and there contraction causes erection of the nipple and serves
to entry of the milk into the ducts. Longitudinal muscles when contracted cause retraction of the nipple. The base of the nipple
is encircled by a more pigmented skin which is called areola. The subareolar area contains much smooth muscle. The fibres
of the areola are arranged in cortcentric rings as well as radially and are inserted into the base of the dermis. They function
to contract the areola and to compress the base of the nipple. The skin of the areola contains numerous sebaceous glands
called the areolar glands which become enlarged during pregnancy and lactation to form 'Montgomery glands'. Fatty
secretion of these glands provides a protective lubricant for the skin of the areola and nipple during lactation. There is no
fat immediately beneath the skin of the areola and nipple.
Structure.— The breast consists of (a) gland tissue, (b) fibrous tissue and (c) fatty tissue in the intervals between the
lobes. The gland tissue is of pale reddish, firm and a lobulated mass. It consists of 15 to 20 lobes connected together by
areolar tissue. The lobes in their turn are composed of lobules which consist of a cluster of rounded alveoli which open into
the smallest branches of the lactiferous ducts. These branches unite to form larger ducts which ultimately end into the milk
ducts or lactiferous ducts each of which drains a lobe of the gland. According to the number of the lobes lactiferous ducts
also vary in number from 15 to 20. These ducts converge towards the areola beneath which they form dilatations which are
called ampulla or lactiferous sinuses, which serve as reservoirs for milk. At the base of the nipple these ducts again become
contracted and pursue a straight course to the summit of the nipple. Each duct is composed of areolar tissue containing
longitudinal and transverse elastic fibres. These ducts are lined by columnar epithelium resting on a basement membrane.
In fact this basement membrane is a second flat layer of cells and acts as a ‘reserve layer’ which may proliferate to produce
more layers of cells. The potential alveoli remain solid, more or less spherical masses of granular polyhedral cells before
pregnancy. True secreting alveoli only develop during pregnancy, when the ducts branch markedly and their terminal parts
possess lumens which increase in size as milk is secreted into them. The secretory activity of the cells lining the alveoli
increases progressively during the latter half of pregnancy. The secretion in later stages of pregnancy and for a few days
after parturition is known as colostrum. It contains cells called colostrum corpuscles which have numerous fat globules in
their cytoplasm. The nature of these cells is not much known, but it may be the inner most cell lining of the primitive alveoli
which undergo fatty degeneration and are shed into the alveolar lumen. True milk secretion commences a few days after
parturition. The milk distends the alveoli which are then lined by a single layer of granular, short columnar cells on a
basement membrane. The cells become flattened as the secretion increases in quantity.
Subcutaneous tissue encloses the gland and sends numerous septa into it to support its various lobules. The fibrous septa
run from the pectoral fascia around the breast lobules through the overlying fat to the superficial fascia and dermal layer
of the skin. These are suspensory ligaments of Cooper which permit considerable mobility of the breast itself. These
ligaments may become contracted by fibrosis in cancer of the breast, thus causing the overlying skin to become pitted and
retracted.
Arterial supply.— There are three major arterial supply to the breast. 1. Perforating branches of the internal
mammary artery which penetrate through the 1st, 2nd, 3rd and 4th intercostal spaces just lateral to the sternum through the
pectoralis major and enter the medial part of the breast. This supplies more than 50% of the blood to the breast. 2. The lateral
mammary branches of the lateral thoracic artery is the second source of blood supply to the breast. The lateral thoracic artery
is a branch of axillary artery and courses along the lateral border of the pectoralis minor muscle. 3. The third source of blood
supply comes from the pectoral branch of the acromiothoracic artery, also a branch of axillary artery. This supplies the
posterior part of the breast. The other sources of blood supply come from (i) the superior thoracic branch of the first part
of the axillary artery, (ii) lateral perforating branches of the intercostal arteries and (iii) branches from subscapsular artery
which contribute very small amount of blood supply.
Venous drainage.— Venous drainage of the mammary glands can be broadly classified into (i) the deep veins and
(ii) the superficial veins.
1. The deep veins of the mammary glands drain along the routes of the corresponding arterial supply. So the major
venous drainage is through the perforating veins into the internal mammary veins. The next way of drainage is through
multiple tributaries following the path of the lateral thoracic artery into the axillary vein. In contradistinction to the arterial
supply the third major way of venous drainage is along the lateral perforating branches into the intercostal veins. This last
route has got tremendous surgical importance in the sense that the intercostal veins communicate with the vertebral veins.
This is the reason why breast cancer metastasises so easily to the vertebral bodies, sacrum or pelvis even without presence
of metastasis in the lungs. This occurs by straining or coughing when the flow pattern within the valveless anastomosing
veins changes and the blood from the breast flows down along the vertebral plexus.
2. The superficial veins are quite rich and sometimes become dilated during pregnancy and over underlying neoplasms
such as soft fibroadenoma, sarcoma and sometimes in carcinoma. The majority of these superficial veins drain into the
internal mammary vein and axillary vein. Some of these veins also drain into the superficial veins of the neck.
The lymphatics.— Without doubt an adequate knowledge of the lymphatic drainage of the breast is very essential
since this is the route through which carcinoma of the breast metastasises early. Like venous drainage, the lymphatics of
the breast are also classified into the (i) superficial lymphatics draining the skin overlying the breast and (ii) deep lymphatics
draining the mammary gland.
1 .By far most of the lymphatics from the skin overlying the breast alongwith the subareolar plexus drain into the pectoral
group of axillary lymph nodes. Only a small part overlying the medial part of the breast drains into the internal thoracic
(mammary) group of lymph nodes. The lymphatics from the medial aspect of the breast often decussate in the midline and
drain into the internal mammary group of the other side also. The internal mammary lymph nodes are 4 to 5 in number on
each side and are placed at the anterior ends of the first, second and third intercostal spaces lying along the side of the interna
mammary vessels.
2. Lymph vessels of the mammary glands originate in a plexus in the interlobular connective tissue and in the walls
of the lactiferous ducts. These plexuses also communicate with the plexus of minute vessels on the deep fascia underlying
the breast. Efferent vessels from these plexuses pass around the anterior border of the axilla pierce the axillary fascia and
THE BREAST 575
end into the pectoral group of axillary lymph

nodes. Some lymph vessels from the upper part
of the breast may drain into the infraclavicular or
interpectoral nodes in the deltopectoral groove
or direct to the apical group of lymph nodes. A
few lymph nodes lie between thepectoralis major
and minor muscles, which are known as ‘Rotter’s
nodes’. Only a few lymph vessels may pass
directly to the subscapular group of axillary
lymph nodes. 75% of the lymphatics from the
breast drain into axillary lymph nodes. The
lymphatics from all the groups of the axillary
lymph nodes ultimately drain into apical group
of lymph nodes and from there the efferent
vessels unite to form the subclavian trunk which
also drains the supraclavicular lymph nodes and
opens into the right lymphatic duct on the right
side and to the thoracic duct on the left side. The
subclavian trunk however may drain into the
junction of internal jugular vein and subclavian
vein directly on both sides.
Majority of the lymph vessels from the medial
aspect of the breast which comprises even less
than 25% oflymph drainage follow the perforat
ing branches into the internal mammary group of
lymph nodes. Only occasionally a few lymph
vessels from the breast may follow the lateral
cutaneous branches of the posterior intercostal
arteries to the intercostal lymph nodes.
Fig.39.1.— The lymphatic glands which are concerned with drainage of A few lymphatics from the inferior and medial
lymphatics of the breast and are commonly involved by carcinoma of the part of the breast may pierce the rectal sheath to
breast. 1. Internal mammary; 2. Supraclavicular; 3. Infra-clavicular reach the extraperitoneal space. Here they com
(Delto-pectoral); 4. Pectoral; 5. Subscapular; 6. Brachial ; 7. Apical. municate with the extraperitoneal plexus of
lymphatics. This may be a route of peritoneal
dissemination of cancer cells in breast cancer.
CONGENITAL ANOMALIES OF THE BREAST

Amazia.— Absence of breast is more common in men. It may be associated with absence of sternal portio
of the pectoralis major. Absence of breast may be seen on one or both sides. Athelia is absence of nipple whic
is extremely rare.
Polymazia.— Accessory breasts are very rare though it has been recorded in the axilla (commonest), groi
or very rarely in the thigh. When present they may function during lactation. Supernumerary nipples are
occasionally seen along the primitive milk line. In fact accessory breasts and accessory nipples are usually du
to persistence of the portions of the milk line which fail to disappear during development. Polythelia is multi
nipples which may be seen anywhere along the milk line.
Treatment is excision of accessory breast.
Varginal hypertrophy.— This is also a rare anomaly in otherwise healthy girls in puberty. The breasts
attain huge dimension so much so upto the level of the genitalia. The only treatment is plastic surgical repair
which is known as reduction mammoplasty.
Asymmetric breasts.— Usually the breasts develop at the same pace, but occasionally one breast may
either develop rapidly or slowly in comparison to the other. In case of such complaints the patients are instru
to wait until maturation is complete when a plastic

surgical procedures may be required to adjust the'
difference.
Gynaecomastia (gynaecomazia).— When there
is breast-like swelling in males, the condition is called
gynaecomastia. The breast is enlarged to certain ex
tent, while the nipple and areola may or may not
assume the same feminine characteristics.
Slight swelling of the breast in adolescent boys is
not uncommon. This is due to the change in the
hormonal pattern during that age. The condition may
be unilateral or bilateral.
Pathophysiology. — Gynaecomastia implies pres
ence of a female-type mammary gland in the male.
Most examples of gynaecomastia are PHYSIOLOGIC
which occur either in the (i) neonatal period and
mostly in the (ii) adolescence or sometimes in (iii) old
individuals. In adolescence there is an excess of oestradiol
relative to testosterone. In old individuals, the plasma
testosterone level falls.
PATHOLOGICALLY gynaecomastia may be caused
from the following conditions —
Fig. 39 2.— A case of gynaecomastia in a patient with I.
oat cell carcinoma of the lung.
in the secretion of oestradiol from the testicles (ledig
cell and sertoli cell tumours, choriocarcinoma, embryonal carcinoma) or non-testicular tumours (adrenal
cortical neoplasms, lung carcinoma, hepatocellular carcinoma). Endocrine disorders such as hyperthyroidism
and hypothyroidism or hepatic disease (non-alcoholic or alcoholic cirrhosis) may initiate oestrogen excess.
II. Androgen deficiency states such as aging may initiate gynaecomastia physiologically between
the ages of 50 and 70 years. Certain conditions e.g. Klinefelter syndrome (XXY), Kallmann syndrome,
eunuchoital males (congenital anorchia), hereditary defects of androgen biosynthesis, ACTH deficiency
etc. may cause gynaecomastia.
III. Secondary testicular failure may cause gynaecomastia due to trauma, orchitis, cryptorchidism,
irradiation to testis, hydrocele, varicocele, spermatocele and renal failure regardless of cause, may initiate
gynaecomastia.
IV. Drugs with oestrogenic or oestrogen-related activity (digitalis, anabolic steroids etc.) may cause
gynaecomastia. Drugs that inhibit the action or synthesis of testosterone (cimetidine, phenytoin, spironolacton
diazepam) may initiate gynaecomastia. Drugs that enhance oestrogen synthesis, may also induce gynaecomas
(reserpine, theophylline, frusemide).
PATHOLOGY.— In gynaecomastia, particularly the idiopathic variety, the breast shows proliferation
of fibrofatty stroma and ducts without acinar growth.
CLINICAL FEATURES.— Patients usually present with no other complaints but abnormal enlarge
ment of the breast. Unilateral enlargement of the breast is much more common and mostly of idiopathic
variety. Though it is a painless condition, yet a few patients (particularly elderly individuals) complain
of a little pain.
Palpation reveals feel of normal breast which is non-tender and movable over the underlying muscles.
Serious psychological problem may accompany this condition. Various pathologies of the breast may be
associated with this condition.
TREATMENT.— Idiopathic gynaecomazia, which is by far the commonest variety, may resolve by
itself. Sa one should wait and see the progress of the condition. When the condition is due to androgen
THE BREAST 577
deficiency, testosterone administration may cause breast regression. When no cause can be elicited and
in these idiopathic cases when gynaecomastia is progressive, surgical therapy in the form of transareolar
mastectomy is advised particularly in the young adult. Danazol has been successful in certain cases, but
its side effects from the androgenic properties of the drug are disturbing. Tamoxifen citrate also shows
encouraging initial result.
When definite reason cannot be evaluated and there is no sign of regression in a case of gynaecomazia,
excision of the breast mass (simple mastectomy) is indicated. Circumareolar incision should be made
and the breast tissue is removed keeping intact the nipple and the areola. This incision gives the best
cosmetic effect. In case of any doubt of presence of any associated pathology, the excised mass should
be sent for histopathological report. If the breast is of bigger size, a Gaillard Thomas’ incision may be
used.
INJURY
Traumatic fat necrosis.—• Some sort of insult to the breast in the form of injury, indirect violence
from seat-belt injury and administration of subcutaneous infusion into the breast may produce this
condition. Middle aged fatty women are mostly affected. This condition is mostly a chronic one in which
the patient presents with a painless lump which simulates in many respects carcinoma of the breast.
PATHOLOGY.— This is an uncommon lesion. Focal necrosis of fat tissues in the breast followed
by inflammatory reaction and subsequent scarring gives rise to a focus of firmer consistency. This is
capable of confusing with a new growth. The stages are — that in the beginning there is a focus of
haemorrhage, later central liquefactive necrosis of fat surrounded by a zone of inflammation occurs. Later
on well defined nodule of greyish white with firm consistency containing possibly small foci of chalky
white debris is formed. The area is converted into a dense fibrous scar. Histologically, the central focus
of necrotic fat cells is surrounded by lipid-filled macrophages and intense neutrophilic infiltration. This
is followed by progressive fibroblastic proliferation and lymphocytic and histiocytic infiltration to wall
off the focus. Still later foreign body giant cells, calcium salts and blood pigments make their appearance
and the whole focus is replaced by scarred tissue which is walled off by collagenous tissue.
CLINICAL FEATURES.— This condition is without any clinical significance save for its possible
confusion with a tumour. History of injury, no retraction of the nipple, the feel of the lump which is
not very hard and irregular and there is no axillary lymph node enlargement are the features in favour
of this condition. Slight skin retraction may be present and the condition cannot be differentiated from
carcinoma by mammography. Incision on such a lump will show chalky white area similar to that found
in cases of subsiding acute pancreatitis.
TREATMENT.— Whenever in doubt excisional biopsy is the treatment of choice and is usually
required for the diagnosis to be certain.
Haematoma.— This is more often seen after injury. This is mostly an acute condition with bruishing
of the overlying skin. Chronic cases may confuse the clinician as the lump of haematoma may be
reminiscent of a neoplasm. Some sort of discolouration of the overlying skin and history of injury are
helpful in diagnosis.
INFECTION
Inflammatory process in and around the breast can be completely described under the following
headings :—
1. Acute intramammary mastitis; 2. Chronic intramammary mastitis; 3 Subareolar mastitis; 4. Chro
nic subareolar mastitis; 5. Retromammary abscess; 6. Tuberculosis; 7. Syphilis; 8. Actinomycosis;
9. Mondor’s disease.
1. ACUTE INTRAMAMMARY MASTITIS.— The usual sufferers are the nursing mothers in their
first lactations and usually in the first month. It may be seen even upto six months after parturition when
the incisor teeth of the infant are developing.
37
AETIOLOGY.— (i) Development of cracks and bruises in the nipple is the main cause of ascending
infection. Staphylococcus Aureus is the main causative organism, rarely streptococcus has been incrim
inated. Infant’s nasopharynx harbours staphylococci, (ii) Failure of secretion to escape due to blockage
of one or more lactiferous ducts with epithelial debris has been incriminated to precipitate this disease,
(iii) Similarly retracted nipple may also cause this condition, (iv) Stasis in some part of the lactiferous
tree is a major factor in the production of this condition. Streptococci though less commonly involved
in this condition, yet produce diffuse infection with more toxic features.
CLINICAL FEATURES.— The affected breast becomes extremely painful and that is the only symptom
with which the patients present in majority of these cases. Redness, oedema, tenderness and brawny
induration are the features usually associated with this condition. The first stage is the cellulitic stage,
in which the breast as a whole becomes red and extremely painful. Gradually when the abscess develops
redness becomes limited to the area of abscess formation. Moreover brawny induration, oedema and
tenderness are all localised to the area of abscess formation. Fluctuation is very difficult to elicit in the
breast, so the surgeon should not wait for this test to be positive. Oedema, brawny induration and local
tenderness are the three features one should look for to be definite that abscess formation has been complete
TREATMENT.— Support to the breasts and antibiotics are the main points of treatment in the
CELLULITIC STAGE. One must remember that as soon as the ABSCESS FORMATION is complete the
treatment is incision and drainage of the pus from the abscess cavity. Continuous administration of
antibiotic even after formation of abscess may lead to the formation of antibioma with its attendant pain,
chronicity and ill health. Once there is pus, the pus has to be let out by incision and drainage. Incision
must be made on the most prominent and dependent part of the abscess. Then a finger should be pushed
into the abscess cavity and all the loculi should be explored for complete drainage of the pus. One must
be sure that not a single locule has been left intact. This will simply cause chronicity. When the most
prominent point of the abscess cavity is not the most dependent part, incision may be made on the most
prominent part and a counter incision is made on the most dependent part for complete evacuation of
pus. After draining the whole of pus a corrugated rubber sheet drainage should be left in and the skin
incision is left open for further drainage. The breast is now dressed properly with adequate pieces of
gauge and bandage to give it full support.
When the cavity is a big one following drainage of abscess, it may be packed with roller gauge.
Such package becomes necessary to stop oozing haemorrhage from its wall lest a haematoma forms within
cavity which becomes nidus for further infection. Roller gauge should be moderately lightly packed but
not too tightly as it may hinder granulation tissue formation for healing.
Postoperative management includes (i) continuous administration of proper antibiotic following
sensitivity test, (ii) Dressing should be changed every day in the beginning followed by alternate day
change. The drain should be removed after 48 hours.
Suckling may be continued from the opposite breast. The milk from the affected breast is pumped
out, boiled for 5 minutes and then given to the infant.
Weaning or stopping of milk formation is usually not required. It may be required if (a) milk cannot
be properly expressed due to too much pain or (b) the abscess is not healing properly or (c) there is
formation of milk fistula due to injury to Lhe milk duct or (d) the child has been breast-fed for quite
a long time. Weaning is usually achieved by stilboestrol tablets, 10 mg thrice daily.
2. CHRONIC INTRAMAMMARY MASTITIS.— This follows (i) continuous antibiotic treatment
or (ii) inadequate drainage of the abscess cavity or (iii) too tight packing of the abscess cavity. The dull
pain persists and a tender swelling may continue. This condition may simulate neoplasm. Due to
continuous administration of antibiotics given after abscess formation, the wall becomes fibrosed and
pus becomes sterile and the whole mass becomes firm, which is known as 'antibioma'.
Treatment.— Excision of the abscess or incision of the abscess cavity with curettage of its wall.
3. SUBAREOLAR MASTITIS.—-This condition is not a true mastitis. This results from an infected
sebaceous gland of Montgomery of the areola. This may follow a furuncle on or near the areola. The
THE BREAST 579
mammary gland itself is not at all involved. It presents with a small very painful lump on the areola.
Whenever the diagnosis is certain and localised tenderness is present one should incise to drain the pus.
4. CHRONIC SUBAREOLAR MASTITIS.— In this condition abscess develops usually behind
the nipple and points at the edge of the areola avoiding the tough fibromuscular tissue of the areola itself.
These are usually sterile at first presentation but rapidly become colonised with bacteria — aerobic or
anaerobic. These are less painful than lactation abscesses and usually
restricted to a single obstructed duct system. This may be an im
portant aspect of duct ectasia. If this abscess is allowed to burst
spontaneously, the lesion settles temporarily but recurrent abscesses
usually develop. This goes on till a chronic milk fistula develops
at the edge of the areola which continues to discharge. When the
discharge.is stopped, abscess develops, it bursts and the fistula again
opens up. This is called a milk fistula or a mammary fistula.
TREATMENT.— Simple fistulectomy is performed as in case
of fistula-in-ano to lay open the fistula track. The fistula may be
excised to lay open the underlying tissue to be healed by granulation
tissue. In intractable cases major duct excision should be performed.
Only in very recurrent conditions with presence of periductal mastitis
it is better to excise the breast tissue around the involved duct
through a radial incision.
5. RETROMAMMARY ABSCESS.—This condition has nothing
Fig.39.3.—Gaillard Thomas’ incision. The to do with the breast. The infection arises from the tissues deep to
dotted area indicates deep surface of the
the breast, (i) Infected haematoma, (ii) empyema, (iii) tuberculosis
breast which can be readily exposed
through this incision. of the rib or spine and (iv) osteomyelitis of the ribs are the causes
which produce pus deep to the breast.
TREATMENT.— Submammary (Gaillard Thomas’) incision is made in the submammary sulcus and
the breast is lifted up from the underlying pectoral fascia. The incision is then deepened to reach the
abscess cavity. The abscess is drained, a corrugated rubber sheet drainage is introduced and the wound
is dressed properly. This incision has a good cosmetic value.
6. TUBERCULOSIS.— This is usually secondary to pulmonary tuberculosis, chest wall tuberculosis,
cervical lymph node tuberculosis or mediastinal tuberculous lymphadenitis. Blood borne infection seems
to be the cause of this condition.
CLINICAL FEATURES.— Usually women who have borne one or more children are usually affected.
Tuberculous focus is present elsewhere. Chronic abscess in the breast is the first stage followed by fistula
formation. It must be remembered that the condition is much less painful than the pyogenic infection.
The abscess is the cold abscess, so redness and oedema, calor and dolor are conspicuous by absence.
Multiple sinuses with typical bluish hue around them are very characteristic. The diagnosis is made by
blood test, bacteriological examination of the discharge, chest X-ray, lymph node biopsy etc.
Treatment is usually the antituberculous chemotherapy till the disease resolves.
7. SYPHILIS.— All the three stages of the syphilis can be seen in the breast, though they aie
extremely rare nowadays. Primary chancre may be seen on the nipple. Secondary stage of syphilis may
be revealed in the form of mucous patches on the submammary fold. In this stage there may be diffuse
mastitis with swelling and pain in the breast. This is called diffuse syphilitic mastitis. Third stage of
syphilis in the form of gumma is very rare.
8. Actinomycosis.— The features of actinomycosis of the breast are essentially similar to the
faciocervical actinomycosis. Usual chemotherapy is started and if the disease does not respond so
effectively to this chemotherapy, local mastectomy is indicated.
9. Mondor’s disease.— Thrombophlebitis of the superficial veins of the breast or the chest wall
is referred to this disease. The cause is often not known and is a part of spontaneous thrombophlebitis
anywhere in the body.
Clinical feature is presence of painful red indurated subcutaneous thrombophlebitic cord. When the
corresponding arm is raised there may be appearance of groove alongside the indurated vein.
Treatment is rest to the arm and support to the breast by bandaging. Some antibiotic treatment should
be started and thrombophobe ointment may be applied. The condition usually subsides within a few mont
without recurrence or complication.
BENIGN BREAST DISEASE

Until recently, benign disorders of the breast were given less importance than breast cancer. This
has resulted in many patients with benign breast disease receiving less attention from clinicians. Benign
breast disease has also suffered from the major disadvantage of a hopelessly confusing terminology and
inadequate classification. During the past decade there has been increasing interest in this disease. Almost
30% of women suffer from this condition at sometime in their lives. Benign breast diseases can be
classified in the following manner :—
I. Aberrations of normal development and involution (ANDI) —
mostly with cyclical mastalgia.
II. Primary non-cyclical mastalgia —
— musculoskeletal
— cervical root pain.
III. Breast lumps —
— Cysts
— galactocele
— sclerosing adenosis
— fat necrosis
— cyclical nodularity
— chronic abscess
— lipoma.
IV. Benign neoplasms —
— fibroadenoma
— phyllodes tumour
— duct papilloma.
V. Disorders of the nipples and periareolar region —
— nipple discharge and inversion
— mammary fistula
— duct ectasia/periductal mastitis
— retraction
— sepsis.
VI. A few non-breast disorders —
(a) Musculoskeletal —
(i) Tietz’s syndrome — pain at the costochondral junction.
(ii) Pain localised in lateral chest wall.
(b) Referred cervical root pain may present as mastalgia particularly in elderly patients.
Despite complexity of classification, there are relatively few presenting symptoms of benign breast
disease. Symptoms fall into 3 main groups — Breast pain, Lumps and Disorders of the nipples and
periareolar region. The most common symptom is pain which accounts for 50% of cases, followed by
lumps which accounts for 35% of cases. Clinician must be particular to exclude carcinoma while venturing
to diagnose a condition as benign breast disease.
Clinical features.— Breast pain or mastalgia is the most significant symptom.
THE BREAST
581
BREAST PAIN (MASTALGIA).— Pain accounts for upto 50% of patients with benign breast disease.
There are two distinct group of patients with this symptom. One group of patients have symptoms which
bear a definite relationship to the menstrual cycle — this is known as cyclical mastalgia. In the remainder
there is no such correlation — this is known as non-cyclical mastalgia.
Cyclical mastalgia has been described in the section of Aberrations of Normal Development and
Involution.
Non-cyclical mastalgia is less understood than its cyclical counterpart. It is more chronic, unilateral
and located in the medial quadrant of the breast and in the periareolar region. The pain is frequently
described as burning or dragging rather than a ‘heavy feeling’. The mastalgia is sometimes well localised
and are known as ‘trigger spot zones’. It must be remembered that in half of the cases such mastalgia
arises not from the breast but from the surrounding musculoskeletal structures. A careful history and
examination are necessary to come to a diagnosis.
Approximately 40% of the cases of benign breast disease will present as LUMP or LUMPS in the
breast. The main problem is that the patient is afraid of cancer. Clinician must be particular in taking
all cares to exclude carcinoma by various diagnostic aids such as mammography, ultrasonography and
FNAC. The surgeon has two important tasks when confronted with a patient with such lumpy breast.
Firstly, he has to decide whether the lump is truely an abnormality or whether it can be regarded as
being within the spectrum of normality. Secondly if the lump is a true abnormality, whether it is malignant
or not. For this, careful history taking and examination are extremely important.
Management.— Management of benign breast disease depends on the diagnosis. The various
conditions which are included in the classification of benign breast disease deserve separate management
according to the individual case. These have been described in the appropriate sections below.
ABERRATIONS OF NORMAL DEVELOPMENT AND INVOLUTION (ANDI).—

Aberrations of Normal Development and Involution (ANDI) can account for many, if not all, benign
breast disorders. About 2 or 3% of women refer to a clinic with cyclical mastalgia, the symptoms of
which are more severe with distressing discomfort lasting a week or more. In the past all such patients
were described as suffering from ‘fibrocystic disease’, although there is little histological evidence of
either fibrosis or cyst formation. A variety of names have been given to this condition e.g. fibroadenosis,
fibrocystic disease, chronic mastitis, mastopathy etc.
Aetiology.— The fundamental abnormality being relative hyperoestrogenism due to either increased
oestrogen secretion or deficient progesterone production. More recently, abnormal prolacting secretion
has been incriminated. Other aetiological factors include excessive caffeine ingestion or inadequate
essential fatty acid intake. There is a good evidence that essential fatty acid supplement can reduce the
symptoms of cyclical mastalgia. Psychoneurosis has been widely incriminated as an important factor.
Pathology.— Pathology is confusing and there is no set abnormality detected in this condition.
GROSSLY, the affected areas look white or yellow on section and it is of rubbery consistency.
MICROSCOPICALLY, the disease may present one of the following features —
(i) FIBROSIS.— Fat and elastic tissue are replaced by white fibrous tissue. Chronic inflammatory
cells are noticed in the interstitial tissue. Periductal mastitis leads to connective tissue hyperplasia of
the periductal tissue and fibrous stroma. This fibrous tissue compresses the ducts and distorts acinar
patterns. Lymphocyte infiltration is not uncommon in the fibrous stroma.
(ii) CYST FORMATION is most often noticed, though the size of the cyst is variable. The
pathogenesis of such breast cyst is not clear. Early workers suggested that they might simply be distended
ducts or they may result from cystic lobular involution. In the latter cases lobules develop microcysts
which eventually coalesce to be larger cysts. This process is potentiated by obstruction of lobular outflow
and replacement of surrounding stroma by fibrous tissue. More recent investigations have suggested that
the aetiology of these cysts is more complex than previously believed. Two types of cysts are identified.
From simple and uncomplicated cysts aspirated fluid has a high sodium : potassium ratio (above 3) simila
to that found in plasma. The pH of fluid is less than 7.4. It seems that interstitial fluid passively diffuses
through simple membrane to cause such cyst. This cyst tends to be single, non-recurrent and not associated
with increased risk of cancer.
The second type cyst is lined with apocrine epithelium characterised by large columnar cells
resembling those found in apocrine sweat glands. The aspirate fluid shows the ratio of sodium : potassium
to be less than 3. The pH is higher. It is suggested that apocrine epithelium actively secrete potassium
into the cyst fluid. This cyst tends to recur and may be associated with the risk of breast cancer. These
cysts usually arise from a single lobule. The cysts may become large when the solitary draining duct
is blocked by kinking or hyperplasia. Cysts are usually multiple. One cyst may be palpable whereas others
in the surrounding breast tissue are not palpable. This classic diffuse cystic disease is mainly called
Schimmelbush’s disease. When one large cyst becomes tense and blue domed, the cyst is called ‘blue-
domed cyst of Bloodgood’. The cysts usually contain greyish green desquamated cells. Occasionally the
cysts may contain blood due to haemorrhage into the cyst.
(iii) HYPERPLASIA of epithelium lining the ducts and acini may occur. This involves both glandular
tissue and connective tissue. There is considerable hyperplasia of epithelium lining of the acini. The
epithelial hyperplasia may be so extensive that it may result in papillomatous overgrowth within the ducts
and cysts. Hyperplasia may reach such a degree that the ductal lumen may be full of cells.
(iv) PAPILLOMATOSIS is sometimes noticed as papillomatous overgrowth within the ducts.
MACROSCOPICALLY the lesion is of India-rubber consistency ar.d white or yellow in colour. This
is easily distinguished from the hard, gritty and greyish lesion of carcinoma.
A variant of this condition is known as sclerosing adenosis, where glandular proliferation (adenosis)
is so distorted by proliferation of fibrous or myoepithelial cells as to lose the normal lobular arrangement.
This is more common in younger women. It is more solid and fibrous than usual fibroadenosis. It is
sometimes confused with carcinoma on histologic study. The clear difference is absence of mitosis in
this condition, where the nuclei are regular and cystic spaces between cells can be found. See page 702
for more description.
Clinical features.— Breast pain or mastalgia is the most common presentation, which brings the
patient to a breast clinic.
BREAST PAIN (MASTALGIA).— Pain accounts for upto 50% of patients with benign breast disease.
There are two distinct group of patients with these symptoms. One group of patients have symptoms
which bear a definite relationship to the menstrual cycle — this is known as cyclical mastalgia. In the
remainder there is no such correlation — this is known as non-cyclical mastalgia.
Cyclical mastalgia is the common type of breast pain accounting for 40% of all cases referred to
a breast clinic. In this condition discomfort lasts for a varying period of time prior to menstruation and
this is usually seen in premenopausal women with median age of about 35 years. Episodes of discomfort
may last for some months, there may be years of freedom of pain until symptoms begin again. The pain
of cyclical mastalgia is frequently, but not always, bilateral and is usually located in the upper and outer
quadrant. The pain may radiate across the chest wall into the axillae or down the inside of the arm.
The breasts are felt ‘heavy’ and marked nodularity is noticed at the time of discomfort. There are no
mammographic or pathological characteristic of cyclical mastalgia. Indeed this lack of correlation between
clinical, radiological and histological findings is one of the major characteristics of this condition. There
may be almost complete replacement with fat giving a translucent appearance or there may be dense
and nodular appearance in mammography.
Non-cyclical mastalgia are only seen in peri- and postmenopausal women. The pain is frequently
described as burning or dragging rather than a heavy feeling as experienced in cyclical mastalgia. The
mastalgia is sometimes well localised, which is called ‘trigger-spot zone’.
LUMPS IN THE BREAST are the next mode of presentation. Lumps are often found bilaterally,
commonly in the upper and outer quadrants. As mentioned earlier that just before menstruation both
THE BREAST 583
pain and lumpiness increase with some tenderness.

ON EXAMINATION there is hardly any retraction of the nipple. Palpation reveals nodular lesion
with multiple lumps. These lumps are inseparable among themselves and are easily movable within the
breast. These lumps are nothing but larger cysts. The lumps are more obvious when examined between
the fingers and the thumb. The lumps usually disappear when examined by the flat of the hand. The
lumps are not adherent to the pectoral fascia and not to the skin. Axillary lymph node enlargement may
or may not be present. If enlarged they may be slightly tender and firm, no question of being hard. With
transillumination one can identify large cyst but cannot rule out a concomitant carcinoma.
Incidence of cancer is extremely low in this disease. Very occasionally epithelial hyperplasia may
lead to carcinoma particularly when occurs in elderly individuals.
Management.—
Management of cyclical mastalgia.— More than 80% of patients with cyclical mastalgia require
no treatment other than simple assurance that the condition is not a cancer and the patient will be cured
without any medicine. Firm breast support may be required.
About 5% to 10% of patients will continue to have pain despite all assurances. For these patients
specific drug therapy may be considered. A large number of studies evaluating the efficacy of these drugs
have been performed. Many such trials could not become successful as they do not take into account
the natural history of mastalgia. As a result a false impression of benefit may occur merely from natural
remission.
Diuretics and antibiotics have been used without much rationale. Reduction in caffeine or adminis
tration of Vitamin A or B6 have failed to show effect on cyclical mastalgia. Administration of oral
contraceptives may reduce symptoms of cyclical breast pain, but total success can by no means be
guaranteed.
Danazol acts as an antigonadotrophin by its action on the pituitary-ovarian axis. At a dose of 200
to 400 mg daily it depresses production of follicle stimulating hormone and luteinizing hormone and
ovarian function. Danazol is a synthetic steroid which suppresses pituitary gonadotrophin output. It has
no inherent oestrogenic or progestational activity. Side effects are dose related, so the lowest dose
compatible with control of the condition should be used. It significantly reduces breast pain, though it
is associated with side effects in 20% of patients which include masculinization, voice change, amenorrhoea
acne, weight gain and reduction of breast size.
Prolactin lowering agent — bromocriptine is also helpful in this condition as it seems that prolactin
stimulates glandular breast tissue and abnormal prolactin level is detected with cyclical mastalgia. This
significantly reduces symptoms of cyclical mastalgia, though this drug has also side effects e.g. nausea,
vomiting, dizziness and postural hypotension in about 20% of patients.
Antioestrogen drug — tamoxifen has been shown to be of benefit in this condition. 10 mg of tamoxifen
daily provides pain relief. Side effects are also seen in this drug e.g. weight gain and hot flushes.
The suggestion that breast pain may be secondary to a deficit of essential fatty acids has laid to its
treatment with evening primrose oil, a mixture of lanoleic and lanolenic acids. It is given in adequate
dose for over 3 months. Studies have shown that it gives relief to more than 50% of cases. Patients with
cyclical mastalgia should be treated initially with evening primrose oil, followed by Danazol, if the first
fails. Bromocriptin is the 3rd choice. Tamoxifen is used when these drugs fail.
Medroxyprogesterone (Farlutal) in the dose of 10 mg daily in two divided doses has been claimed
to be effective in this condition. The main draw back of this therapy is that it may be associated with
high peripheral oestrogen level. High dose of Vitamin E is also beneficial. Yearly mammograms will
exclude presence of new lesions. Assurance is a major part of treatment of this condition.
Injection of Milk, iodine or even Omnamycin has been claimed to give some relief to the patients
considering it to be a type of non-specific infection.
It is necessary to treat for 3 months and then stop the therapy and wait for relapse. Any relapse
is an indication for restarting treatment, perhaps at a lower dose than originally used. Bromocryptin and
danazol are potentially teratogenic and require the use of a barrier form of contraception as they interfere
with oral contraceptives.
For non-cyclical mastalgia, one must exclude extramammary causes of pain. It may also be necessary
to take a biopsy from the localised tender area, which may have other pathology including cancer. Non
steroidal analgesics or injection with local anaesthetic may be required in intractable cases.
Occasionally, mastalgia may not respond to all medical treatment mentioned above. Consideration
of mastectomy should be given and subcutaneous mastectomy is preferred. But the general impression
is that it should be avoided at all costs. In case of non-cyclical mastalgia surgical excision of ‘trigger-
spot zones’ may be advised, but this approach is not widely accepted.
Management of lumpy breast.— Mammography and ultrasonography should be performed to
exclude other conditions. It may be required to take biopsy from a single or multiple lumps to exclude
other condition.
SURGICAL TREATMENT.— If all the above measures fail excision of the lesion is the treatment
of choice. The excised lesion must be sent for histopathological report to be sure of absence of concomitant
carcinoma.
Indications of Surgery.— (i) Failure of conservative treatment.
(ii) If pain is intolerable.
(iii) Swelling remains inspite of best conservative treatment which is causing anxiety to the patient.
(iv) Clinically the swelling is persistent and it is difficult to exclude presence of concomitant
carcinoma.
(v) In older patients causing anxiety.
Type of operation is usually excision biopsy. Circumareolar incision is a good cosmetic incision. If it
cannot give proper access to the swelling a submammary incision of Gaillard Thomas may be made and
the breast is lifted to reach the swelling. If both the above incisions are considered to fail to provide proper
access, then radial incision or curved incision along the Langer’s line should be made over the swelling.
CYSTS OF THE BREAST

Two types of classification can be chalked out for various types of cysts of the breast :—
TYPE I Classification.—
A. From the ducts —
1. Fibroadenosis (usually multiple).
2. Blue-domed cyst of Bloodgood (solitary).
3. Galactocele.
4. Serocystic disease of Brodie (Cystosarcoma Phyllodes).
5. Papillary cystadenoma.
6. Intracystic papillary carcinoma.
B. From the stroma —
1. Blood cyst (encapsulation of haematoma).
2. Lymphatic cyst.
3. Hydatid cyst.
4. Colloid degeneration of carcinoma.
TYPE II Classification.—
A. From mammary dysplasia —
1. Fibroadenosis (usually multiple).
2. Cyclical nodularity.
3. Blue-domed cyst of Bloodgood (usually solitary).
4. Sclerosing adenosis.
B. From retention cysts —
Galactocele.
THE BREAST 585
C. From tumours —
(a) Benign.—
1. Papillary cystadenoma.
2. Serocystic disease of Brodie (Cystosarcoma phyllodes).
(b) Malignant.—
1. Intracystic papillary carcinoma.
2. Colloid or mucinous carcinoma.
3. Medullary carcinoma.
D. Miscellaneous —
1. Lymphatic cyst.
2. Hydatid cyst.
3. Blood cyst.
Lymphatic cyst and hydatid cysts are very rare. Lymphatic cyst is almost same as that found in the
neck. By far the commonest type of cyst found in breast is due to fibroadenosis. The cysts are usually
multiple, though a solitary cyst may dominate the finding.
Clinical features.— Cysts are classically seen in perimenopausal women between the ages of 45
and 52 or in the last decade of reproductive life. They are usually single at presentation, but it is not
uncommon to see multiple cysts in a breast. In extreme example the whole breast seems to be composed
of a number of cysts.
The breast cysts suddenly appear. The reason is that the cyst exists in a flaccid subclinical state prior
to its presentation as a lump. Cysts may be uncomfortable and are frequently painful. There may be a
vague relationship between discomfort and the menstrual cycle with increasing pain prior to menstruation.
The characteristic features of the cysts are that they are smooth and dent on palpation. They have
a degree of mobility, though not as pronounced as that of fibroadenomas. Normal nodular breast tissue
overlying the cyst may hide its classic smooth nature on palpation.
Mammography and ultrasonography help in the diagnosis, but aspiration of the cyst confirms the
diagnosis. The amount of fluid aspirated is variable, though in average it is about 6 to 8 ml. Occasionally
cyst may contain even 60 or 80 ml of fluid. Cyst fluid varies in colour ranging from pale yellow to almost
black. The aspirate is usually translucent, though it may be thick and turgid.
TREATMENT.— Mammograms should be performed in cases of cysts before aspiration is performed.
When one is very sure of the diagnosis of solitary cyst, aspiration of the cyst is indicated. When aspiration
reveals that the fluid is clear and without presence of blood and if after aspiration no mass can be felt
the diagnosis is a benign cyst and mostly a case of fibroadenosis. The fluid must always be sent for
cytological report. If a mass is felt after aspiration or the aspirated fluid shows presence of blood,
malignancy should be suspected and excision biopsy should be the treatment of choice. When the cyst
disappears after aspiration, the patient should be followed up every two months for recurrence. Reaccumulat
of fluid within the cyst is suspicious of malignancy and should call for excisional biopsy. Majority of
the cases of solitary cyst from fibroadenosis do not recur. In case of multiple cysts the treatment is again
excision of the lesion and biopsy. If a mass does remain after aspiration, further investigation with Fine
Needle Aspiration Cytology (FNAC) or biopsy is indicated.
Recurrence of cyst is a problem. Recurrence is often at a different site from the presenting cyst. About
Vi of the patients develop further cyst within 5 to 10 years. A small number of women develop recurrences
on a regular basis and may attend the breast clinic every 2 or 3 months for cyst to be drained. In these
cases danazol or tamoxifen treatment may be recommended, but efficacy of these drugs is in doubt.
Theoretically patients with breast cyst may be at an increased risk for breast cancer. Mammography
should be performed on women with cysts.
There are two main indications for surgical excision of the cyst. Firstly, if the aspirate is blood
stained, an intracystic carcinoma is suspected. Secondly is the recurrence of cyst. If the same cyst recurs
rapidly more than once, its excision is recommended.
Galactocele.— Accumulation of milk and amorphous epithelial debris due to blockage of a main
duct gives rise to this condition. It presents as a subareolar cyst and mostly seen in patients who have
just ceased lactation. Discharge from the nipple — milky in the beginning and thick greenish discharge
in late cases is quite diagnostic.
TREATMENT.— Excision of the affected duct is the treatment of choice, as infection and abscess
formation in a galactocele is not uncommon.
Sclerosing adenosis.— It is classified as an aberration of normal development and involution of
breast. Microscopically it is characterised by terminal duct lobules and myoepithelial cell proliferation,
increased number of acini and fibrous stromal change. Multifocal and nodular types have been described.
This is a case of mastalgia. Such pain may be due to perineural invasion and there may be ‘trigger spot
zones’. Macroscopically, this condition may have a stellate appearance and may calcify — thus mimicking
carcinoma, both clinically and radiologically. This condition has been confused with carcinoma histo
logically due to increased cellularity particularly in frozen sections.
CLINICALLY, it usually presents as a smooth, relatively mobile mass. Patients within the age group
of 30 to 50 years are usually affected. It is frequently a painful condition and often it presents as mastalgia
rather than a lump.
Sclerosing adenosis is regarded as an abnormality of normal development, characterised by lobular
enlargement and distortion associated with fibrous stromal change.
Fat necrosis.— See page 693.
Cyclical nodularity.— Many patients come to the breast clinics with lumps which are actually
manifestations of cyclical nodularity. It is the mass, rather than pain, which is the predominant feature,
though many patients may admit discomfort or pain in the lump. A careful history will reveal that the
lump has been present for sometime.
Majority of the patients are teenagers, though occasionally older women approaching menopause may
be involved. A large and uncomfortable swelling develops suddenly in the upper and outer quadrant.
Examination reveals a diffuse nodular swelling which may be slightly tender. This may resolve with the
next menstrual cycle. But if it persists, aspiration is indicated followed by mammography. Aspiration
cytology is indicated in older women and biopsy may be needed in suspected cases.
So long as malignancy is excluded this condition requires only assurance.
Mammary duct ectasia.— A variety of names have been given to this condition such as plasma
cell mastitis, mastitis obliterans and granulomatous mastitis.
The primary change in this condition is simple dilatation of the larger periareolar ducts associated
with periductal inflammation. All the ducts may not be dilated, but such change may be bilateral. In
the initial stage one or more of the larger lactiferous ducts are dilated. Usually 3 to 6 ducts are involved
whereas the others remain absolutely normal. The dilated ducts are filled with stagnant brown or green
secretion. Due to this stagnation there is loss of duct epithelial lining. This secretion may be discharged
from the nipple even with slight bleeding. Due to leakage of the secretion through the damaged duct
walls, there may be an irritant reaction in the tissues around the ducts leading to periductal mastitis.
Such periductal mastitis produces a painful mass or even a frank periareolar abscess. Repeated inflam
matory processes cause fibrosis, nipple retraction and even fistula formation. A chronic indurated mass
may form beneath the areola which mimics a carcinoma.
As to the pathogenesis of this condition is concerned, the sole question is ‘what does cause the
initial duct dilatation?’ Suggested possibilities include (i) hormonally induced muscular relaxation of the
duct wall; (ii) Inadequate absorption of secretions or (iii) obstruction of the ducts with squamous debris.
The pathologists who contradict these theories suggest (iv) that the periareolar inflammation is the primary
pathogenic process. This may cause arteriopathy to damage the duct wall. So duct dilatation is secondary
followed by fibrosis and nipple retraction.
CLINICAL FEATURES.— The disease usually appears at or after menopause. A diffuse lump is
THE BREAST 587
the main presentation which may produce nipple retraction. The lump is mostly beneath the areola,
occasionally peripheral lump may be present. Nipple discharge is quite common. Classically it is thick
and creamy but sometimes greenish discharge may be present. This condition may even produce bloody
discharge where no other cause such as papilloma can be detected. Axillary adenopathy is not unusual.
The disease is usually unilateral but may involve the other breast within a few years. Many patients may
complain of mastalgia.
TREATMENT.— In the beginning carcinoma must be excluded as this case is often presented with
a mass or nipple retraction. This is done by mammography and fine needle aspiration cytology. If still
one is not sure, the mass should be excised. When carcinoma has been excluded, antibiotic therapy may
be tried. Flucloxacillin and metronidazole are the appropriate drugs.
If there is a solitary duct fistula, fistulectomy with excision of the involved duct should be considered.
In case of recurrent episodes of plasma cell mastitis and recurrent mammary duct fistula in postmenopausa
women, excision of all major ducts (Hadfield's operation) is indicated. This operation is described in
page 705.
NIPPLE DISCHARGE.— Nipple discharge is quite a common symptom. The patient may fear
cancer and the discharge itself causes annoyance and social embarrassment. In the history the patient
should be questioned whether the discharge is unilateral or bilateral, whether it is associated with a lump
or not, or whether the discharge is blood stained or not.
On inspection, one may detect the duct or ducts from where the discharge is coming out. Excessive
crusting may occasionally be seen on the nipple which is nothing but dried product of secretion. Sometime
a skin disorder such as eczema may be found.
On palpation, the whole breast is examined with particular attention towards the subareolar region.
Gentle pressure on this area may bring out the discharge. Examine the nature of the discharge. Of
paramount importance is whether the discharge contains blood or not. Whether it is fresh blood or dark
in colour.
INVESTIGATIONS.— Mammography and Fine Needle Aspiration Cytology (FNAC) should be carried
out. Mammography is particularly helpful to exclude an underlying impalpable mass. On mammography
the most important feature to be noticed is the intraductal microcalcification of carcinoma in situ. It may
indicate dilated ducts with coarse calcifications of secretory granules. Ductography may demonstrate the
presence of duct papilloma. Cytology from FNAC may reveal malignant cells, but a negative result has
no importance.
Causes of nipple discharge.— There are a number of causes of nipple discharge —
I. Physiological causes.— Discharge of milk is a normal phenomenon during pregnancy and
lactation. Occasionally, blood stained discharge may be observed during pregnancy. This is of no
significance and reassurance is all that is required. In neonates a milky nipple discharge may occur
transiently due to transplacental passage of luteal hormones from the mother’s circulation.
II. Galactorrhoea.— This means secretion of milk not related to pregnancy or lactation. Physi
ological causes include stress and mechanical stimulation of the breast. It may be seen at menarche and
menopause and even may occur years after cessation of breast feeding. In these physiological circum
stances simple reassurance is all that is required.
Galactorrhoea may occur as a secondary phenomenon. It may occur as side effect of drugs that enhance
dopamine activity e.g. chlorpromazine, metoclopromide and methyldopa. Hyperprolactinaemia due to a
prolactin-secreting tumour or from a secondary source of bronchogenic carcinoma may cause galactorrhoea
III. Duct ectasia.— It is a common cause of nipple discharge. It is often bilateral. The character
of the discharge is thick, opalescent and of varying colours. Occasionally the discharge may be blood
stained.
IV. Fibrocystic disease or cystic mastopathy typically produces multiple-duct discharge and is
another commonly associated disease.
V. Duct papilloma.— The discharge is from a single duct. It is either serous or serosanguineous
or frankly blood stained in majority of cases. It may even cause watery discharge. It is often solitary.
Occasionally 2 or 3 papillomas may be found in a single duct. It must be remembered that multiple
papillomas particularly occurring in the periphery of the breast involving more than one duct carry an
increased risk of malignant change. These peripheral lesions are more likely to cause a breast mass than
nipple discharge.
VI. Carcinoma.— Papillary intraductal carcinomas and even invasive carcinomas can present as
nipple discharge. It is usually from a single duct. It may be watery or serous, but often frankly blood
stained.
VII. Cysts.— Nipple discharge is often caused by cysts than is generally appreciated. Some surgeons
believe that these cysts are simple dilated ducts. Gentle pressure on these cysts may produce discharge.
VIII. Idiopathic causes.— A few cases of nipple discharge presented at various breast clinics remain
without causes, despite all attempts at establishing a diagnosis, even with biopsy. After thorough
investigations if no cause can be found out simple reassurance is enough for serous or watery or non
blood-stained discharges. If the discharge is blood-stained, it should be assumed that the cause is there,
but not detected. So careful follow-up is required.
According to the nature .of nipple discharge the following classification may be made :—
Usually seven varieties of nipple discharge may be seen — (i) Milk discharge, (ii) Serous discharge, (ii
discharge, (iv) Greenish discharge, (v) Black discharge, (vi) Pus and (vii) Creamy discharge.
1. Milk discharge.— The surgeon should be acquainted with physiological discharges from the nipple. T
the ductal system of the breast is continuously secreting fluid under normal circumstances, yet it is unc
for women to notice any discharge through the nipple. This is due to reabsorption of secretion. Only in e
rare cases due to excessive physiological activity nipple discharge may be noticed in the second phase of
cycle. Milk discharge is more commonly seen in very late stages of pregnancy. Lactation may continue fo
or years after suckling if the patient continues to express milk because she thinks this should be done. T
physiologfcal galactorrhoea. Drugs including the contraceptive pills may occasionally lead to slight disch
milk perhaps through pituitary prolactin mechanism.
Milk discharge may be seen in case of milk fistula following chronic subareolar mastitis. Milk discharge
occasionally be seen with galactocele.
2. Serous discharge.— Physiologically this may be seen, though very rarely and after continuous use of
contraceptive pills. Serous discharge may be seen in cases of fibroadenosis and mammary duct ectasia, though
greenish-black discharge is more common in fibroadenosis and thick creamy discharge is more often see
mammary duct ectasia. Duct papilloma and non-infiltrating duct carcinoma may produce serous discharge in the
intervals of bloody discharge.
3.Blood discharge.— Though very occasionally blood discharge from the nipple may be seen in bilateral
in pregnancy due to physiological epithelial hyperplasia, yet blood discharge is usually seen in papilloma of the
duct and in cases of duct carcinoma. Benign solitary papilloma is more common in younger women of 15 to 3
years. Multiple papillomas are more often seen in patients nearing menopause. Non-infiltrating or infiltra
of duct carcinoma may cause blood stained discharge which are more commonly seen after the age of 50
4. Greenish discharge.— This is typically seen in cases of fibroadenosis. Similar coloured fluid can also be
obtained from cyst aspiration in similar cases. Serous, brownish or even greenish discharge may also be
mammary duct ectasia.
5. Black discharge.— Old blood looks black and such blackish discharge may occur in duct papilloma or
duct carcinoma which is notorious for blood discharge. Blackish discharge is also occasionally seen in cases
fibroadenosis.
6. Pus.— Rarely discharge of pus may be seen through nipple in cases of acute mastitis.
7. Creamy discharge.— Thick creamy discharge is seen in mammary duct ectasia.
Management of nipple discharge.— 1. Discharge located to one duct, but not blood stained.—
Mammography should be performed in all patients older than 35 years. If carcinoma has been excluded
reassurance is all that is required. But if the discharge continues and is proving intolerable, microdochectomy
should be performed.
2. In case of blood stained discharge from a single duct.— Mammography should be performed
in all patients over 35 years of age. Careful palpation is required to detect any subareolar lump. If bleeding
THE BREAST 589
continues and the duct is located from where bleeding occurs, microdochectomy is performed. When the
duct cannot be located, cone excision of the major ducts (Hadfield’s operation) should be performed.
3. Multifocal and non-blood stained discharge.— Again mammography should be performed in all
patients over 35 years of age. The usual cause of such discharge is duct ectasia. Cefotaxime or flucloxacillin
and metronidazole administration is recommended.
4. Multifocal and blood stained discharge.— Again mammography is performed. Many cases may
be due to duct ectasia which should be diagnosed. In other cases major duct excision (Hadfield) should
be called for.
5. Galactorrhoea if caused by mechanical stimulation and ingestion of the drugs, these should be
stopped. In other cases prolactin level should be detected and if the level is normal, simple reassurance
should be given. If it is due to prolactin-secreting tumour or from bronchogenic carcinoma these should
be treated.
Microdochectomy.— It is a conservative approach, which has the advantage that the patient should
be able to breast feed after the operation. So it is the treatment of choice in case of young women with
single duct discharge. A stiff nylon suture or a fine probe is inserted into the duct from which the discharg
is coming out and is fixed to the skin of the nipple with fine silk stitches. The skin of the incision is
infiltrated with adrenaline in saline. With a pair of fine-pointed scissors a triangular area is cut 1 mm
away from the point of entry of the stiff nylon. With fine-pointed scissors the breast tissue alongwith
the duct is dissected off to reach the depth. An attempt should be made to excise the duct of about 5
cm in length. Usually the papilloma is situated within 4 to 5 cm from the nipple orifice. The specimen
of duct alongwith the triangular skin is removed intact including the stiff nylon. Strict haemostasis should
be achieved and the wound is closed without drainage. A pressure bandage is applied.
Excision of major ducts (Hadfield’s Operation).— A circumareolar incision is made not extending
more than 3/5ths of the circumference of the areola. The incision is made mostly along the lower half
of the areolar margin. The subcutaneous tissue is cut down to the duct system. With blunt dissection
a plane of cleavage is dissected circumferentially around the terminal lactiferous ducts. Once the ducts
are dissected out they are divided close to the nipple and are removed with a conical wedge of tissue
with long axis of 2 to 4 cm and with the base of 1 to 2 cm of the subareolar tissue. The excised material
contains all the major lactiferous ducts. The excised specimen is sent for histological examination. Any
opened ducts are closed by ligature and the cavity in the breast substance is obliterated with deep sutures.
The wound is closed with 3/0 subcuticular dexon suture with a small vaccuum drain. The breast is kept
well supported by strapping.
NIPPLE INVERSION AND RETRACTION.— The terms nipple inversion and retraction, though
been used interchangeably, yet there is a definite distinction. Nipple inversion means congenital failure of
of nipple during development. Nipple retraction means a secondary process in which the nipple is retracte
was normal before.
CONGENITAL NIPPLE INVERSION.— Congenital nipple inversion is a not uncommon problem an
in approximately 25% of all women. This condition tends to be bilateral. This does not always interfer
breast feeding, as the infant creates a ‘teat’ from the surrounding breast tissue. With this condition th
of higher incidence of duct ectasia and periductal mastitis.
TREATMENT.— The patient should be encouraged to breast feed and she should be reassured that n
complication does arise from this condition. A few patients may insist for surgical eversion, but shoul
Mechanical suction device may be used to evert the nipple with some effect. The only surgical way of
the nipple is to divide all the underlying ducts. Furthermore even after such cosmetic surgery the nip
take flattened appearance rather than being protuberant.
NIPPLE RETRACTION.— Nipple retraction of recent origin (not congenital) is usually caused by on
3 conditions — (i) duct ectasia, (ii) carcinoma and (iii) postsurgical retraction.
(i) Duct ectasia.— It must be remembered that in duct ectasia it is usually a slit-like retract
or linear transverse defect. In the early stage it is possible to do digital eversion, though at later stage
more and more difficult. Other features of duct ectasia such as nipple discharge and periareolar absc
present. The condition is often bilateral.
(ii) Carcinoma.— In this condition there is circumferential retraction of the nipple and usually a mass is
detected in the breast. The history is usually shorter and the condition is unilateral. If there is any doubt
mammography is helpful.
(iii) Postsurgical retraction.— Injudicious surgery and an ugly periareolar defect may cause such retraction
in inexperienced hands.
TREATMENT.— In case of nipple retraction due to duct ectasia the treatment is Hadfield’s operation. In c
of carcinoma associated with nipple retraction, the case should be treated according to the type of breast carcin
Cracked nipple.— This condition mostly occurs during lactation. It may indicate the possibility of developin
acute infective mastitis.
To prevent cracked nipple the areola and the nipple should be washed, dried and lubricated with lanolin d
last 2 months of pregnancy and during lactation. If such precautionary measure has not been taken and the nip
is cracked during lactation, no breast feeding should be allowed through the involved nipple and breast pump
be used to empty the breast. The cracked nipple is treated with antibiotic ointment and feeding is only resume
when the condition is cured.
Chancre of the nipple.— It is now an extremely rare condition and almost unseen. It usually occurs either fro
buccal ulcer in the mouth of the partner or from a syphilitic baby. But in case of the latter, the wet nurse
and not the mother, as the mother is immune to reinfection from her own child.
Eczema of the nipple is also a rare occurrence. It must be remembered that it is a bilateral condition in
to Paget's disease, which is a unilateral condition.
For treatment it is better to refer the patient to a skin specialist.
BENIGN NEOPLASMS
1. Fibroadenoma; 2. Phyllodes tumour; 3. Duct papilloma.
1. FIBROADENOMA
The most common benign tumour of the female breast is the fibroadenoma. It is a new growth
composed of both fibrous and glandular tissues.
Aetiology.— This tumour is said to develop as the result of increased sensitivity of a focal area
of breast to oestrogen. It is almost an acceptable fact that there is some relationship between excess
oestrogen level and fibroadenoma. That is why this condition may present simultaneously with fibroadenosis.
Pathology.— These lesions are encapsulated and tend to be spherical but on occasions they may
be multinodular or somewhat irregular.
The gross appearance is characteristic with smooth boundaries and the cut surface is glistening white.
If the epithelial elements are excessive they may appear as light brown areas. Fibroadenoma has mixed
epithelial or glandular and mesenchymal elements. Fibroadenomas typically stop growing when they reach
2 to 3 cm in diameter.
Blacks have greater propensity than whites to develop fibroadenomas and at a younger age. This
lesion invariably has a relationship to oestrogen sensitivity and it occurs predominantly in the 2nd and
3rd decades of life.
Other variants of fibroadenoma are characterised by increased cellularity of the stroma and/or
epithelium. These typically occur in adolescence and bear resemblance to benign phyllodes (leaf-like)
tumours. The predominant carcinoma that presents concurrently with the fibroadenoma is lobular
carcinoma in situ.
On section these lesions are composed of uniform, greyish white, fleshy, homogeneous mass with
fibrous whorls which tend to bulge from the capsule. There may be some minute yellow to pink softer
areas. Fibroadenoma is classified into two varieties according to their origins — either Pericanalicular
or Intracanalicutar.
The breast has two components of connective tissue separated by the elastic lamina which covers
the ductules. When the connective tissue outside this elastic lamina becomes proliferated along with the
THE BREAST 591
glandular element it is called pericanalicular fibroadenoma. When the connective tissue inside the elastic
lamina becomes proliferated alongwith the glandular element, it is called intracanalicular fibroadenoma.
The PERICANALICULAR VARIETY (Hard fibroadenoma) is firmer, smaller with an increase in ducts a
stroma. This tumour can be felt very clearly out of the breast tissue due to its tremendous firmness and
within the breast substance, so it is often called ‘breast mouse’. In this type round or oval gland spaces
single or multiple layers of cells.
The INTRACANALICULAR TYPE (Soft fibroadenoma) is relatively less firm, grows larger and the glan
and the duct system are very much compressed with great distortion due to proliferated surrounding co
pressing on them. Connective tissue is so profuse and rather loose that this type is often referred to as
It must be remembered that both pericanalicular and intracanalicular patterns may coexist within the s
SYMPTOMS.—
(i) The pericanalicular or hard type usually occurs in younger girls between 15 and 30 years of age
or soft fibroadenoma more commonly affects older group from 30 to 50 years of age.
(ii) This tumour is most commonly presented as a painless, slowly growing, solitary lump in the bre
is often seen in the lower part of the breast, fibroadenosis occurs mostly in the upper and outer quadrant of the brea
(iii) Multiple fibroadenomata may be present in about 10% of cases.
(iv) Pain is usually conspicuous by its absence, though it may occasionally be complained of, partic
there is associated fibroadenosis.
(v) Though the hard variety is known for its slow growth and never attains a big size, yet intra
be large in size due to rapid growth. Some discomfort or slight pain may be complained of due to its size
(vi) Discharge through nipple is almost unknown.
LOCAL EXAMINATION.—
INSPECTION does not reveal anything particular and the nipple remains always normal. But in case
intracanalicular fibroadenoma, swelling may be visible.
PALPATION is important.
(a) Fibroadenomas are smooth or slightly lobulated usually measuring 2 to 3 cm in diameter. With
adjacent to the nipple, these are characteristically mobile. Mobility is more in young girls. Mobility lesse
to the restraining effects of surrounding fibrotic tissue. In only 10% of cases there may be multiple fibro
(b) A freely mobile solitary lump within the breast with a round smooth margin is nothing but a fibr
consistency is firm except in case of large intracanalicular variety when consistency may be softer.
(c) The lump is neither fixed to the overlying skin, nor fixed to the fascia covering pectoralis major.
fixed within the breast and is so freely movable, that it is often called a ‘breast mouse’.
(d) The axillary lymph nodes are usually not enlarged.
DIAGNOSIS.— Upto the age of 25 years clinical diagnosis is enough.Mammography has no place in its ro
With increasing age mammography and Fine Needle Aspiration Cytology (FNAC) should be performed to exclude m
Ultrasonography is quite helpful in the differential diagnosis of palpable breast lump. Ultrasonography shoul
with Logic 500 Proserver having a linear multifrequency with a 6-9 MHz probe. A water pack is used for
lesions. The lesions should be viewed in both longitudinal and transverse planes employing low and hig
transducer position. Each breast is examined quadrant by quadrant survey. If the mass is delineated, it
or non- circumscribed. Both benign and malignant lesions are detected by this technique. Confirmation
ultrasonography is made by FNAC or histopathology. It is a well known fact that ultrasonography of the
differentiating cystic from solid masses. Well circumscribed masses are mostly benign and poorly circum
malignant. The accuracy of ultrasound in the detection of solid breast mass is about 65% in Indian stud
correctly diagnosed in about 95% of cases. Detection of carcinoma in breast by ultrasound is more accu
However in Indian studies benign lesions of the breast are more readily diagnosed by the ultrasound tha
Sensitivity of ultrasound in the diagnosis of fibroadenoma of the breast is expected to be more than 80%
TREATMENT.— Excisional biopsy is the treatment of choice. Although a skilled clinician can probably
detect a fibroadenoma with an accuracy of 80% to 85% of cases, yet excision is mandatory. This gives an
opportunity to get the histopathological report. Moreover removal of the tumour will give the patient a
psychological advantage to have been cured from the disease. Periareolar or submammary incision should be
attempted at whenever possible for cosmetic reason. As the tumour is often situated in the lower part of the
breast, submammary incision (Gaillard Thomas’ incision) is often applied. Only when the tumour
cannot be removed through one of these incisions, a radial incision or a curved incision along the line
of Langer is made. The incision is deepened right upto the capsule of the tumour. In case of pericanalicular
variety the capsule is incised and the tumour is removed with a finger which is pushed into the cleavage
between the capsule and the tumour, the adhesions are severed and the tumour is brought out of the
incision. This is called enucleation. In case of intracanalicular variety enucleation may not be possible
and the whole tumour is excised. The dead space is obliterated with catgut suturing. Haemostasis is
attained. The skin is closed. Drainage is only necessary when one is not very sure of haemostasis and
when there is a big dead space.
It is better to send the excised tumour for frozen section biopsy. Only when unfortunately carcinoma
is detected, quadrantectomy or Patey radical mastectomy should be performed according to the size of
the tumour.
The present trend is that in women under the age of 25 years, routine excision is unnecessary because
of greater understanding of the natural history of this condition. If fibroadenomas are left untreated most
will slowly increase in size upto 3 cm in diameter over a period of 5 years. Thereafter they remain static
or may gradually become smaller.
GIANT FIBROADENOMA.— Giant fibroadenoma has a bimodal age of presentation at the
extremes of reproductive life — either in the age group of 14 to 18 years or 45 to 50 years. When occurs
in younger age group it is called ‘juvenile fibroadenoma’. This fibroadenoma is characterised by rapid
growth and acquires a size of at least 4 to 5 cm in diameter, though it may be even more than 10 cm
diameter size.
Histologically one must remember its features to differentiate it from phyllodes tumour. This type
of fibroadenoma contains typical hypocellular stroma and epithelial components showing mild degrees
of hyperplasia and atypia, though mitoses are uncommon. In phyllodes tumour there are more cellularity,
pleomorphism and mitotic activity.
Giant fibroadenoma are more common in black and oriental races. There may be pain associated
with rapid increase of the tumour. On examination the breast is enlarged with displacement of the nipple.
The overlying skin has a characteristic shiny appearance with dilated veins. In neglected cases skin
necrosis may occur. When occurs in teenagers, it may be difficult to differentiate it from varginal
hypertrophy, although the latter is bilateral and not associated with cutaneous or venous changes.
TREATMENT.— Enucleation through an appropriately cosmetic incision (may be a submammary
incision) is the treatment of choice. If there be any discrepancy in the breast size, it attains normality
within a year or two. As there is no evidence to
recur locally or metastasise, mastectomy is
contraindicated.
2. PHYLLODES TUMOUR
This benign tumour has many names —
phyllodes sarcoma, cystosarcoma phyllodes, serocystic
disease of Brodie and benign cystosarcoma. Phyl
lodes tumour shows a wide spectrum of activity
varying from an almost benign condition to a lo
cally aggressive, and sometime metastatic tumour.
Phyllodes tumour, though appears well circum
scribed, is characterised by irregular surface pro
jections. These projections may be cut during sur
gical excision and predispose to recurrence. ‘Phyl
lodes’ is a Greek word which means leaf-like.
This tumour presents as a massive tumour with
an unevenly bosselated surface. Occasionally ulcer-
THE BREAST
593
ation of the overlying skin occurs due to pressure necrosis. Before this, the skin becomes warm, red,
shiny with visible dilated subcutaneous veins. Axillary lymph node metastasis is rare and even when
the tumour turns malignant, lymph node metastasis is late. Similarly when malignant transformation
takes place distant metastasis is also rare.
The cut surface is soft brown in colour and exhibits cysts, necrosis or haemorrhage. As there is
degeneration and cyst formation, the cut surface shows the appearance of leaves arranged side-by-side
(Greek term 'Phyllode' means leaf-like).
Histologically, both epithelial and fibrous stromal elements are present, which show hypercellularity,
much atypia and numerous mitoses. Myxoid stroma is mostly seen, which may have lymphomatous,
chondromatous or osteoid foci.
These may metastasise via blood stream.
Clinical features.— This tumour occurs predominantly in premenopausal women around 40 years
of age. However these may occur in younger women. The tumour grows rapidly to a large size and involve
most of the breast.
PHYSICAL EXAMINATION.—
INSPECTION shows a big swelling with tense glistening skin over it. There are prominent subcu
taneous veins overlying the tumour. Nipple is normal without retraction or discharge.
PALPATION.— (i) The tumour has a fairly smooth margin. Consistency is firm and at places soft.
(ii) The tumour is neither fixed to the skin nor fixed to the deeper structures. Though the skin
overlying the tumour is tense, yet it can be picked up apart from the tumour.
(iii) The axillary lymph nodes are not involved. Similarly there is no distant metastasis.
(iv) There is no retraction of the nipple or discharge from the nipple.
Inspite of its tendency to grow rapidly it is not uncommon to see small tumours which are clinically
indistinguishable from simple fibroadenoma.
Treatment.— This tumour when occurs in young women, represents the benign end of the spectrum.
So simple enucleation is recommended. Older patients require wider excision with 1 cm margin of normal
breast tissue. Large tumours with aggressive history may require even wider excision in the form of
quadrantectomy or even simple mastectomy.
It must be remembered that even with wider excision about 25% of tumours recur within 10 years
time. Such local recurrence should be widely excised in the form of mastectomy with reconstruction.
It is a matter of concern that in less than 5% of cases this tumour may metastasise.
3. DUCT PAPILLOMA
Pathology.— This is a benign tumour, which arises from the lining epithelium of a principal
lactiferous duct. The tumour is usually of small size. It is often said that it is a precancerous condition
and may turn into intraductal papillary carcinoma. But this idea is not correct and almost all intraductal
papillary carcinoma arise de novo and not from the pre-existing duct papilloma. Sometimes the tumour
is so small that it is not palpable but it projects into the lumen and often obstructs the duct so that the
duct becomes dilated and cystic.
The majority of these tumours are single, but bilateral examples are not rare. Only occasionally 2
or more ducts of the same breast may be involved by papillary growth. But the usual presentation is
a single papilloma located in one of the major lactiferous ducts which has a stalk.
It is also important to be familiar with the term papillomatosis — either solitary or multiple.
Papillomatosis is simple epithelial hyperplasia which often remains in association with fibrocystic changes
and occur in young women. Papillomatosis fills the individual ducts like true polyp without any stalk.
(a) Majority of the victims are between the ages of 30 and 50 years.
(b) The commonest and the main symptom is bloody discharge from the nipple. Occasionally dark
blood-stained fluid or even serous fluid may be discharged.
38
(c) Sometimes a small and soft swelling may be palpable beneath the nipple or areola. As the tumour
is soft, it is difficult to palpate and often remains impalpable. If a patient presents with a small mass
beneath the nipple or areola with bloody discharge from the nipple, the diagnosis is almost certain that
the patient is suffering from duct papilloma.
(d) Very often the tumour is not palpable, but as the tumour obstructs the ducts, there is accumulation
of discharge which is palpable as a cystic swelling.
(e) If a swelling is felt beneath the nipple or areola, compression of such swelling will cause discharge
from the opening of the affected duct in the nipple.
(0 Majority of these tumours are benign. Intraductal papillary carcinoma is rare and usually arises
de novo in the duct. Invasion through the duct wall must be identified to confirm malignancy.
(g) Very occasionally the nipple may be unduly prominent or retracted.
(h) The regional axillary lymph nodes are usually not affected if the tumour remains benign.
Ductograms can be very useful in identifying intraductal papilloma.
TREATMENT.— Complete excision of the duct involved alongwith the tumour should be performed.
This operation is called Microdochectomy. This is performed by wedge resection. If the mass can be
palpated the wedge is located over the mass and the whole wedge is excised. If no mass can be felt,
the duct from which blood is expressed should be gently probed. A triangular area is cut 1 mm away
from the probe. The skin flaps are reflected. The fine probe alongwith the duct is excised downwards
till the papilloma is detected. The papilloma is nearly always situated within 4 to 5 cm from the nipple
orifice. The blind wedge resection is carried out with triangular area of skin attached to the fine probe.
After strict haemostasis the wound is closed without drainage. A pressure bandage is applied.
Simple mastectomy is not justified for this lesion.
OTHER BENIGN NEOPLASMS of the breast are (i) neurofibroma, (ii) lipoma and (iii) papillary
cystadenoma. While the neurofibroma and lipoma are the same as are found in the other parts of the
body, papillary cystadenoma is peculiar in the breast. This is a swelling which is composed of cysts
and into these cysts papillomatous processes extend. These extensions are so much that the cysts are
almost filled with these papillomatous processes. So the swelling feels solid and not cystic. It may cause
bloody discharge from the nipple. Treatment is excisional biopsy as this condition is mainly benign.
MALIGNANT NEOPLASMS OF THE BREAST

Malignant neoplasm of the breast is broadly classified into carcinoma and sarcoma.
BREAST CARCINOMA
AETIOLOGY —
1. Age.— Incidence of breast cancer increases with age. It is only occasionally seen in late teens, thereafter
there is a rapid rise in incidence rate upto the age of 50 years. After that the rate slows down though it continu
to rise until old age. Risk of developing breast cancer is only 0.3% between the ages of 20 and 40, but it is mor
than 5% between 50 and 70 years. This accounts that the majority of patients presenting with breast cancer are
over the age of 50 years.
2. Genetic factors.— Family history of breast cancer has often shown an increased incidence in the same
family. The risk is greatest in patients with Ist-degree relatives (mother or sister) affected, particularly if they
under the age of 50 years when the disease developed. With affection of 2nd-degree relatives the risk is less. I
is about 2.2 in case of a history of breast cancer in Ist-degree relatives and only 1 among those with an affected
2nd-degree relatives. There is probably a direct genetic factor involved in it. But it must be confessed that gen
factors contribute only about 5% of all cases, but may account for 25% of cases who present before 30 years of
age. A gene has been identified in high risk families on the long arm of chromosome 17, which is concerned w
the development of breast cancer. The gene is termed BRCA I, which has been discovered by several internati
groups in 1994. It is inherited as a dominant genetic trait. It is a large gene. When BRCA I was identified, a sec
THE BREAST
595
susceptible gene was also discovered in chromosome 13, which is known as BRCA 2, which is considered to be
responsible for approximately 30% of all familial breast cancers. It has been experimented that while BkCA I
predisposes to both breast and ovarian cancer in families, BRCA 2 appears to be restricted to breast cancer, eve
male breast cancer. Together BRCA 1 and BRCA 2 account for approximately 75% of all hereditary breast canc
3. Child bearing and fertility.— Single and nulliparous married women have a relative risk rate of 1.5
compared to parous women. The effect of parity on protective influence depends on the age of the patient at fi
child birth. For those whose first child birth occurred after the age of 30 years, there appears to be virtually no
protective effect. On the contrary some evidences suggest that women whose first child birth was over the age
35 years may have an increased risk of breast cancer. Subsequent pregnancies appear to have no influence on t
risk of developing breast cancer. The protective effect occurs only if the pregnancy continues to full term. If the
is any protective effect of breast feeding is still a matter of debate but majority are in the belief that this has no
protective effect.
4. Age of menarche and menopause.— The girls whose menarche occurs before the age of 12 years have
a relative risk of 2.50 compared to those starting menstruation after 12 years. Reduction in the age of menarche
over the last few decades in the western world as well as in Indian subcontinent probably due to improved nu
and general health may be an important cause of higher incidence in breast cancer. Women in whom menopau
occurs after the age of 55 years have twice the risk of developing the disease compared to women whose meno
started before the age of 45 years. Artificially induced surgical menopause appears to be protective for breast c
5. Geographical.— Breast cancer is commonly seen in Western countries. It is still a rare tumour in Japan.
6. Endocrine.— The role of exogenous hormones, particularly oral contraceptives and hormone replacemen
therapy in the development of breast cancer is still controversial. Small dosage of exogenous oestrogen therapy
for short periods in premenopausal women appear to be safe. When hormone replacements are taken for more
8 years the risk becomes increased in the range of 1.5 to 2.0, particularly in those who are taking oral contracep
from early in life. In postmenopausal women breast cancer is more common in the obese. It may be due to incr
conversion of steroid hormones to oestradiol in the body fat.
7. Diet.— Diets rich in saturated fatty acids may influence the risk of developing breast cancer. Cancer of
the National Academy of Science concluded that fried and high fat foods can increase the risk of developing ca
approximately 2 folds. Similarly high intake of alcohol has been claimed to be associated with an increased risk
of breast cancer. Vitamin C seems to have some protective action. There is a strong relationship between body
weight and breast cancer, although this is critically dependent on age. In women under 50 years of age there is
no relation of body weight with risk of breast cancer. But in women more than 60 years of age, increasing weig
means more risk of cancer.
8. Benign duct disease.— Some pathological entities such as multiple papillomatosis, gross atypia with
hyperplasia are certainly associated with an increased risk of breast cancer (3.0). But it must be carefully remem
that there is no increased cancer risk for two important benign conditions e.g. fibroadenoma and ‘fibrocystic di
PATHOLOGY.— Approximately 50% of breast cancers arise in the upper and outer quadrant, 12%
to 15% in the upper and inner quadrant, 6% to 10% in the lower and outer quadrant, 3% to 5% in the
lower and inner quadrant and 20% in the central or subareolar region. Breast carcinoma is mainly
unilateral condition, but in only 1% to 2% of cases it shows simultaneous bilateral presentation. The
word ‘simultaneous’ must be noted, as there may be much more cases where the other breast is involved
later in life. Over 90% of breast cancers arise in the ductal epithelium and only 10% in the mammary
lobules. Near about 70% of breast cancers are scirrhous type, 6% medullary carcinoma, 3% tubular
carcinoma, 3% colloid carcinoma, 1% Paget’s disease, 2% papillary carcinoma and 6% combined lobular
and ductal carcinoma. Non-infiltrating carcinomas of the mammary ducts constitute 5% of all carcinomas
of the breast.
There are many methods of pathologically classifying breast cancer — most are based on whether
it is derived from the duct system or the lobule. It should be remembered that most tumours arise from
terminal ductules and this fact also explains the common occurrence of mixed tumours with both lobular
and ductal component.
I. DUCTAL CARCINOMA OF THE BREAST.— This is the most common form of breast cancer
accounting for 85% to 90% of all cases.
1. Ductal carcinoma in-situ.— It is characterised by proliferation of malignant breast epithelial cells
confined to the duct system and does not invade the basement membrane or surrounding tissues. It accounts
for 5% of all cases of breast carcinoma. It is mammographically visible by microcalcification. It is detected

in 6% of apparently normal breast in postmortem studies. The most important aspect is its malignant pote
tiality. 30% to 50% show invasive cancer in the same quadrant after an interval of 10 to 15 years. Two main
histological types are detected — (i) the solid or comedo type is most common and more virulent. It is
characterised by the closely packed cells within ductal spaces, so that the breast ducts become swollen. Th
ducts may expand to 1 or 2 mm in diameter. Devoid of blood supply to the centre of the lesion may lead to
central necrosis and then the intraductal spaces remain filled with necrotic cellular debris. Necrosis may
undergo dystrophic calcification, which is fine, linear or branching or focally clustered, when seen on high
quality mammography It may give rise to small palpable lump, (ii) Papillary or cribriform type is characte
by papillary projections of tumour cells into the ductal lumen. Presence of branchings which fill the duct
spaces give rise to cribriform pattern. This type is less likely to form palpable mass. This type does not
calcify to produce mammographic abnormality. These two subtypes may coexist.
2. Invasive ductal carcinoma.— Once intraductal carcinoma has invaded the basement membran
of the duct, it has now the ability to infiltrate into the surrounding breast tissue and is called ‘invasive duc
carcinoma’. A large number of different morphological types of invasive duct cancer is apparent to the
pathologists —
(i) Infiltrating Ductal Carcinoma With Productive Fibrosis (Scirrhous Carcinoma).— It accounts
for 70% of all invasive mammary cancers. This is presented in peri- or postmenopausal women in the 6th
decade as solitary, non-tender, firm and ill-defined mass. The tumour characteristically possesses a poorly
defined border which is better defined by palpation than inspection. Cut surface looks as a central radiatin
stellate tumour with chalky-white or yellow streaks extending into surrounding parenchyma. The histolog
picture reveals variable cellular
and nuclear grade from in-situ
to highly anaplastic variants, sug
gesting significant heterogeneity.
Neoplastic cells are arranged in
small clusters or stocked in single
rows that occupy irregular cleft
spaces between collagen bundles.
Tumour infiltration can shorten
Cooper’s ligaments as they
... j course from the superficial fas
cia of the coreum to the deep
layer of clavipectoral fascia.
Fig.39.5.— Section of a typical scirrhous carcinoma. Note that this tumour possesses With progressive gro
no capsule and has infiltrated the tissues of the breast. The nipple is deeply retracted, ligaments are furthe
to cause skin dimpling directly over the tumour. This with extensive oedema of the skin due to lymphatic
involvement causes the characteristic appearance of ‘peau d’orange". This common cancer is more diag
nosed by exclusion of other types of mammary cancers.
Microscopically, there are cords or islands of malignant cells which infiltrate outside the ducts into a
variable amount of stroma. It may form primitive glandular pattern, but not similar to the tubular carci
noma. The stromal reaction is intense and has led to the term ‘scirrhous carcinoma’ of the breast. This
tumour obviously originates from the duct epithelium.
(ii) Medullary Carcinoma.— This cancer represents 2% to 15% of all breast cancers. The tumour
takes origin from the large ducts. Grossly, the tumour is soft, well circumscribed, bulky, haemorrhagic an
has uniform consistency. Commonly the lesion is deeply placed within the breast and relatively mobile.
This tumour has a smooth contour and may even appear to have a pseudocapsule. Bilaterality is reported
less than l/5th of cases. In less than 10% of cases these neoplasms contain detectable oestrogen or progeste
receptors.
THE BREAST 597
Microscopically this carcinoma is characterised by (a) dense lymphoreticular infiltrate composed pre
dominantly of lymphocytes and a variable number of plasma cells; (b) Large pleomorphic nuclei that are
poorly differentiated and accompanied by active cellular mitosis; (c) Syncytial sheet-like growth pattern
with minimal or absence of tubuloacinar differentiation. This carcinoma is less frequently associated with
lymph node metastases than other types of breast cancer and thus associated with a better prognosis. 5-year
survival rate is better than other invasive ductal and lobular carcinomas. There is often benign or hyper
plastic enlargement of the lymph nodes of the axilla to cause erroneous clinical staging. Axillary lymph
node metastasis is reported in only 45% of cases.
(iii) Tubular Carcinoma.— This type of breast cancer represents only 3% of all breast cancers. It is
well differentiated. Macroscopically this cancer is small — about 1 cm in diameter and scirrhous. Most
commonly this lesion is seen in perimenopausal or early menopausal women. It is hard with radial appear
ance. It is more diagnosed mammographically and has been reported in as many as l/5th of women whose
cancers are detected by screening only.
Histologically tubular differentiation is distinctive. The tumour is characterized by infiltrating tubular
structures, lined by one cell layer and with an open central space. The small tubular pattern and single cell
lining of neoplastic tubules provide important histological characters of the tumour. Absence of myoepi
thelial cells and a well defined basement membrane serve to differentiate this tumour from other invasive
varieties.
Only 10% of patients develop axillary metastasis and is usually confined to small numbers in low
axillary nodes (level I). This carcinoma obviously has a good prognosis and 10-year survival rate is more
than 75%. It is uncommon for well differentiated pure tubular carcinoma to metastasise to distant sites. It is
also associated with very low recurrence rate after treatment. It is not clear whether such tubular carcinoma
may dedifferentiate into more aggressive types of cancers.
(iv) Mucinous (Colloid) Carcinoma.— This carcinoma also develops from the ducts. This uncommon
cancer constitutes only 2% of all breast cancers. It is typically bulky mucinous and is largely confined to the
elderly women. The cut surface looks glistening, glaring and gelatinous. Fibrosis is variable and when
abundant, it imperts a firm consistency to the tumour. Approximately l/3rd of cases have axillary metasta
sis and 5-year survival rate is more than 70%.
Histologically, there are large pools of mucin that surrounds variable group of tumour cells. Signet-ring
cells are not generally seen in mucin-producing breast adenocarcinomas. About 2/3rds of these tumours
contain detectable ER receptors. This mucin is secreted by the carcinoma cells. The 5-year and 10-year
survival rates are reported to be 70% and 55% respectively.
(v) Papillary Carcinoma.— This carcinoma accounts for less than 2% of all breast carcinomas and
are generally seen in old women (around 70 years). Typically this tumour is a small one and rarely attains
a size more than 2 to 3 cm in diameter. It is also subdivided into in-situ and invasive types. This tumour is
easily delineated from surrounding breast tissue by a fibrous covering.
Histologically, there are papillae with well defined fibrovascular stalks and multilayers epithelium
with pleomorphic cells. This tumour has the lowest frequency of axillary nodal involvement and has the
best 5-year survival rate.
(vi) Adenoid Cystic Carcinoma.— This lesion is very rare — less than 0.1% of all types of breast
cancer. These cancers present as small lesions — 1 to 3 cm in diameter. These are characteristically well
circumscribed with well defined margins. The tumour contains dense mucoid material with glandular spaces
Axillary metastases are rare with this type of carcinoma, but distant metastases like pulmonary metastases
are not uncommon.
II. LOBULAR CARCINOMA OF THE BREAST.— This can be conveniently subdivided into in-situ
and invasive forms depending on whether the basement membrane of the lobule has been invaded by the
tumour or not.
Histologically, it is a proliferation of small round epithelial cells within the lumens of multiple breast
acini. So it presents as multiple clusters of epithelial cells forming islands of neoplastic cells maintaining a
lobular architecture. Ducts are also expanded with proliferating cells.

(i) Lobular carcinoma in-situ.— Within this lobule there must be a uniform proliferation of cells.
The most important aspect of this cancer is its potential for becoming invasive. The risk of becoming
invasive following simple biopsy is only 25% over 20 years, which is much lower than that of ductal
carcinoma in-situ. In practice this lesion is only discovered by chance in biopsy specimen undertaken for
some other reason. It never forms a palpable mass and thus missed in physical examination. There is no
typical mammographic finding. Incidence of this type of carcinoma is approximately 3%. It must be re
membered that lobular carcinoma has a high propensity for bilaterality, multicentricity and multifocality.
(ii) Invasive lobular carcinoma.— This accounts for 10% of all breast cancers. The histologic fea
tures include characteristic small cells with rounded nuclei, inconspicuous nucleoli and scanty indistinct
cytoplasm. Clinically this tumour is almost equal to an ordinary infiltrating ductal carcinoma. It produces
no distinguishing mammographic feature. Grossly, this lesion varies from clinically inapparent microscopi
tumour that replaces a portion of the breast to a poorly defined somewhat firm mass. This cancer may
mimic inflammatory or benign lesions. This tumour is particularly known for bilaterality, multicentricity
and multifocality. Examination of the contralateral breast has demonstrated lesions in nearly 40% of cases.
This infiltrating type is very difficult to diagnose from scirrhous type both clinically and microscopically.
Microscopic evidence of preinvasive tumours cells in clusters within the acini in a lobule is the only diag
nostic finding. The prognosis of a classical invasive lobular carcinoma is generally somewhat better than
that of the invasive ductal carcinoma.
Paget’s disease.— Sir James Paget in 1874 described this lesion, which is a chronic eczematous erup
tion of the nipple. Paget’s disease constitutes approximately 1% of the histologic types of breast cancer. It
is almost always associated with an underlying intraductal or invasive carcinoma. This constitutes 1% of al
breast carcinomas. It begins as a weeping eczematous lesion of the nipple which becomes red and thick
ened. The areola and surrounding skin may be involved as well. The surface becomes either scaly and
crusted or moist and oozing. In the beginning no mass may be felt, but eventually a swelling will develop
beneath the nipple in most of the cases. Any eczema
tous lesion of the nipple in a postmenopausal women
should be biopsied to exclude Paget’s disease. This
condition arises from an underlying carcinoma of
the mammary duct, which gradually grows towards
the nipple and invades the skin around the nipple.
Downward growth of this intraductal carcinoma will
only produce the mass below the nipple, which is
rather late. The better prognosis of this condition is
probably due to early diagnosis.
Histologically, presence of Paget’s cell is the most
diagnostic evidence. These cells are distinctly large,
clear and vacuolated with small dark nuclei. These
cells are seen in clusters in the deeper layers of the
epidermis. Epidermis is usually thickened 2 to 3 times
than the normal and this thickening occurs before
ulceration takes place. Round cells and plasma cells
infiltration into the superficial layers of the epider
mis is also a characteristic feature of this condition.
Symptoms include itching, burning, intermittent
haemorrhage and tenderness. Intraductal adenocar
cinomas often involve the epidermis of the nipple
and areola by intraepithelial dissemination. Physi
cal finding may identity a palpable mass Fig.39.6.— Paget s disease of the nipple.
THE BREAST J 99
in the subareolar area. l/4th to l/3rd of patients have axillary node metastasis. In general, this cancer
has a better prognosis than the majority of the lesions due to its early presentation.
Inflammatory carcinoma.— In this condition the tumour cells are very undifferentiated and involve
the subdermal lymphatics quite early. As a result of this there is lymphatic blockage and lymphangitis.
This gives rise to cellulitis of the breast. There is redness, pain and swelling of the involved breast. The
diagnosis becomes difficult from acute mastitis. Axillary lymph node involvement is quite early. It
frequently occurs during lactation, so it is often called ‘lactational carcinoma’. The prognosis is usually
grave.
SPREAD OF CARCINOMA.— Carcinoma of the breast spreads through the following routes :
1. LOCAL SPREAD.— Carcinoma of the breast spreads quite efficiently into the surrounding tissues
by infiltration and invasion. Scirrhous carcinoma is particularly notorious for local spread. Infiltration
is quite efficiently seen in scirrhous carcinoma and that is the reason why it possesses irregular margins.
It is also due to infiltration that the breast carcinoma becomes fixed to the breast substance quite early.
Invasion of the skin causes dimpling of the skin. Invasion of the ligaments of Cooper also causes tethering
of the skin. Invasion into the major periductal tissue causes retraction of the nipple (which is recent in
contradistinction to longstanding retraction of nipple which is congenital) and through the local spread
breast carcinoma gradually invades the pectoral fascia, pectoral muscle and ultimately the chest wall.
Within the breast there are 3 main mechanisms of spread. The most important mechanism is by
direct infiltration into the surrounding parenchyma by remifying projections that give characteristic
stellate appearance of breast cancer.
The 2nd mode of spread is by direct infiltration along the ducts. It is unclear whether such spread
represents actual tumour growth or it reflects a field change of pre-existing in-situ disease. This explains
the phenomenon of multifocal nature of the breast cancer.
The third mode of spread is by local lymphatic and vascular spread within the breast.
2. INTRADUCTAL SPREAD.— Carcinomatous cells in the breast often spread through the ducts
and ductules. The examples are Paget’s disease, lobular carcinoma, tubular carcinoma etc. This explains
the phenomenon of multifocal nature of breast cancer.
3. LYMPHATIC SPREAD.— Breast carcinoma spreads through this route by (i) emboli and (ii)
permeation. Emboli are clusters of carcinoma cells which are swept along the lymphatic vessels to the
regional lymph nodes. By permeation it means that columns of cancer cells grow along the lumen of
the lymphatic channel and gradually proceed to the regional lymph nodes. Lymphatic spread is quite
early in scirrhous carcinoma of the breast. The pectoral group of the axillary lymph nodes is the first
to be involved in majority of cases. Gradually other groups of the axillary lymph nodes are involved.
Carcinoma of the medial part of the breast involves internal mammary group of lymph nodes early. Even
in upper and outer quadrants the breast carcinoma involves internal mammary group in 33% of cases.
Later the supraclavicular lymph nodes, the opposite breast and the mediastinal group of lymph nodes
are involved. Liver is sometimes involved by lymph vessels through the plexus over the sheath of the
rectus abdominis communicating with the subdiaphragmatic lymphatic plexus and through the lymphatics
of the falciform ligament. Supraclavicular lymph node on the left side is often involved due to retrograde
permeation from the thoracic duct.
Cancer cells often involve the cutaneous lymphatics causing oedema of the overlying skin. Due to
involvement of regional lymph nodes and blockage of the lymphatics there is also oedema of the whole
breast. In case of oedema of the breast one can see multiple pin-point depressions (pits) at the sites of
attachment of the hair follicles as these are fixed to the subcutaneous tissue. This almost looks like the
peel of an orange and hence called ‘peau d'orange'. This can be well demonstrated by lifting a portion
of the overlying breast skin with a finger and thumb.
The regional spread of breast cancer is the spread to the axillary, internal mammary and supraclavicular
lymph nodes via lymphatics.
Axillary nodal spread.— Axillary nodes are more commonly involved in breast cancer. Approxi
mately 45% of all patients have nodal disease at presentation. There is a relation between the tumour
size and axillary nodal spread. For tumours less than 2 cm in diameter, the incidence of axillary nodal
spread is less than 20%. For tumours 2 to 5 cm in diameter, nodal involvement is 35% and tumours
greater than 5 cm in size nodal involvement is about 50%. The clinical assessment of axillary nodes
is notoriously unreliable. About 30% of palpable and apparently diseased nodes are found to be
histologically free of metastasis. Conversely upto 30% of clinically normal axillary nodes demonstrate
histological evidence of metastasis. The relationship between axillary nodal spread and prognosis depends
on three factors — (i) the number of nodes affected, (ii) the level of axillary nodal involvement and
(iii) the extent of disease within the nodes themselves.
(i) Number of nodes involved.— Women treated by mastectomy with no axillary lymph node
involvement have 85% survival rate. But with one or two lymph nodes involved at the time of operation
survival rate is 60%. With 5 or 6 nodes affected the survival rate is 45% and with 11 or 12 nodes involved
the survival rate is only 30%.
(ii) Level of disease.— This is a less powerful factor than the number of nodes affected by metastasis
so far as the prognosis is concerned. In patients with disease in level I nodes has a 5-year survival rate
of 65%, those with disease at level II has a 5-year survival rate of 30% and with disease at level III
nodes no patient survives for 5 years.
(iii) Extent of disease in individual nodes.— Deposits less than 2 mm in size can be detected only
by histological methods. When clinically there is no node involvement, such deposits (micrometastases)
may occur in one or two nodes. But their presence in the 3rd node is exceptional in the absence of
macroscopic metastasis. Presence of a single micrometastasis implies a slightly worse prognosis than for
node negative disease, but improved survival compared to patients with a single pathologically obvious
macrometastasis.
By regional lymph nodes we mean axillary (ipsilateral), interpectoral (Rotter’s) nodes and lymph
nodes along the axillary vein and its tributaries which may be divided into the following levels by the
surgeons — (a) level I (low axilla) — lymph nodes lateral to the lateral border of pectoralis minor muscle,
(b) Level II (mid-axilla) — lymph nodes between the medial and lateral borders of the pectoralis minor
muscle and the interpectoral (Rotter’s) lymph nodes, (c) Level III (apical axilla) — lymph nodes medial
to the medial margin of the pectoralis minor muscle including those designated as infraclavicular or apical.
Internal mammary nodal spread.— Metastases in the internal mammary nodes are more commonly
associated with medial and periareolar tumours. Disease affecting the internal mammary lymph nodes
is rare in the absence of axillary nodal spread. Only 8% of patients may have such disease with the axilla
clear. Metastatic disease in the internal mammary nodes alone has the same prognostic implication as
axillary nodal disease. But if both internal mammary and axillary nodes are affected the outlook is poorer.
Internal mammary group of lymph nodes in the intercostal spaces along the sides of the sternum,
when involved by metastasis is coded as a distant metastasis (Ml), alongwith other groups e.g.
supraclavicular (Virchow), cervical and contralateral internal mammary lymph nodes.
Supraclavicular nodes.— Metastatic disease in these nodes implies extensive involvement of the
axillary nodes or internal mammary nodes and is associated with a poor prognosis.
4. SPREAD BY BLOOD.— This spread occurs later than lymphatic spread in case of carcinoma
of the breast. Cancer cells detach as emboli into the venules and are drifted through the venous blood
to the lungs first. If they cross the capillaries of the lungs they reach the left atrium and hence to systemic
circulation. So there is always the chance of lung metastasis first by this route. Even then bony metastasis
is more common as probably lots of emboli pass through the lung capillaries without forming metastasis
there. Skeletal metastasis is the commonest blood borne metastasis from carcinoma of the breast. The
spines are most commonly involved. This involvement may occur through the left heart or through
vertebral veins which communicate through intercostal veins. This latter path explains early involvement
of spine in blood borne metastasis even before the lungs. Lungs are next involved. Liver is also involved
through this route. Brain, adrenal glands and ovaries are also metastasised by this route. The pleural
THE BREAST 601
cavity may be involved from metastasis in the lungs.

5. INTRACOELOMIC SPREAD.— The cancer cells may spread into the peritoneal cavity
from breast cancers. This is mostly through lymphatic spread which involves the subdiaphragmatic
and retroperitoneal lymph plexus from the piexus over the rectus sheath by piercing rectus. Cancer
cells thus reach the peritoneum and considerable peritoneal dissemination may occur. Seedlings
ma\ drop on the ovary and form ovarian metastasis which is so popularly known as Krukenberg’s
tumour. Retrograde lymphatic spread has also been incriminated as the cause of Krukenberg’s
tumour as on section it is found that the medulla of the ovary is first involved in Krukenberg’s
tumour.
CLINICAL FEATURES.— Breast cancer may occur at any age after puberty, though it usually
occurs after 40 years of age.
SYMPTOMS.— (i) Typically, the patient presents with a painless lump in the breast, commonly
in the upper and outer quadrant. A lump in the breast should always be suspected as a carcinoma
unless proved otherwise. Presence of this type of swelling is usually of short duration.
(ii) Pain is conspicuous by its absence. Sometimes a bigger mass may give rise to a discomfort
which is often referred to by the patient as pain. Only inflammatory carcinoma is painful and in
majority of cases it is seen in lactational period. Pain is often complained of in advanced stages.
(iii) Discharge through nipple is not usual. Though blood discharge is quite common in ductal
carcinoma. Discharge of varying nature may be complained of in
case of other carcinomas occasionally.
(iv) Recent retraction of nipple may be noticed by
intelligent patients.
(v) Sometimes patients complain of metastatic symptoms
while they remain unaware of the primary cancer in the breast.
Such symptoms are -— backache, chest pain, haemoptysis,
dyspnoea, jaundice, ascites or enlarged axillary or left
supraclavicular lymph nodes.
On INSPECTION, retraction of nipple or dimpling of the
skin may be obvious, (i) The nipple of the affected side may
be raised from the normal level of its fellow, (ii) Retraction of
nipple can be best ascertained by asking the patient to hold
her arms up. (iii) Peau d’orange may be obvious in a few cases.
Peau d’orange is due to cutaneous lymphatic oedema. Where
Fig.39.7.— An advanced case of the skin is tethered by the sweat ducts, these parts cannot swell
carcinoma of right breast. whereas the other parts of the skin swell up due to lymphatic
oedema. This causes an appearance almost like an orange skin. The same type of condition may
be seen in case of chronic abscess also, (iv) Oedema of the whole arm is sometimes seen as a
complication of breast cancer treatment either after radical axillary dissection or after radiotherapy
or after both of these. It appears at any time from months to years after such treatment. One must
exclude neoplastic infiltration of the axilla which may block lymphatic or venous channels as to
cause this condition. This condition is susceptible to bacterial infection following minor trauma
and requires vigorous antibiotic treatment. Limb elevation, elastic arms stockings and pneumatic
compression devices may be used to manage such late oedema, (v) Red eczematous lesion is
apparent in Paget’s disease, (vi) Nipple discharge is usually insignificant in scirrhous carcinoma, but
bloody discharge is often found in papillary carcinoma.
On PALPATION, the (i) breast lump which is best palpated by the flat of the hand is probably a
case of carcinoma. Fibroadenosis and fibroadenoma are much better palpated with the fingers and
the thumb. The nodularity of the fibroadenosis almost disappears when the less sensible flat of the
hand is used. Fibroadenoma has a very definite margin which is regular and the tumour moves inside
the breast so freely that it is called ‘breast mouse’. On the other hand the carcinoma has got irregu
lar surface, harder in feel and is fixed within the breast substance very early. For this the breast
should be steadied with one hand and an attempt to move the swelling is made with the other hand.
This is not possible in case of carcinoma of the breast. In late cases the tumour becomes fixed to the
overlying skin and/or to the pectoral fascia. In very late cases the growth will fungate through the
skin and by that time probably the growth has been fixed to the chest wall.
(ii) Axillary lymph nodes are always palpable due to their involvement. The nodes become
enlarged and hard which indicate that carcinoma has involved the axillary nodes. In later cases the
nodes become fixed to the underlying structures.
(iii) An attempt should always be made to find out if there is any distant metastasis. The oppo
site breast should always be palpated methodically — all the quadrants, nipple and areola to ex
clude presence of any swelling there. Patient must be asked if she has any complaint like chest pain,
dyspnoea, haemoptysis, pain in the spine, pain in the hip, pain in the neck or any swelling anywhere
in the body. Ribs, spine, sternum, pelvis, upper ends of the femur and humerus should also be exam
ined for presence of any metastasis. Vaginal examination is necessary to detect Krunkenberg’s tu
mour of the ovary or presence of peritoneal metastasis in the pouch of Douglas. The liver should
always be palpated for presence of any swelling there. Percussion and auscultation should be made
on the lungs. Supraclavicular lymph nodes should always be examined. Cases are on record when a
small tumour is associated with supraclavicular lymph node involvement. Remember involvement
of supraclavicular lymph node makes the carcinoma of the breast a stage IV disease.
(iv) In advanced stage, direct invasion of the skin and dermal lymphatics by cancer cells takes
place, which gradually involves larger areas of thorax particularly in case of scirrhous cancer and
the whole area of skin becomes rigid as a coat of armour and is known as Cancer en cuirasse.
Clinical staging.— Clinical staging is an attempt by the surgeon to identify the extent of the
malignant lesion based on clinical examinations and special investigations. Whereas microscopic
typing and grading are important to understand the prognosis of a breast cancer, clinical staging is a
guide to treatment.
There are three methods of clinical staging in use at present : 1. The Manchester system, 2. The
Columbia system and 3. The TNM (tumours, nodes, metastases) system. By far the TNM classifica
tion has achieved widespread acceptance.
1. MANCHESTER SYSTEM —
Stage I : The growth is confined to the breast.
Stage II: The growth is confined to the breast, but palpable and mobile lymph nodes are present
in the axilla.
Stage III : The growth extends beyond the mammary parenchyma as shown by —
(a) Skin invasion or fixation over an area larger than the size of the breast or skin ulceration.
(b) Tumour fixation to the underlying muscle or fascia — Axillary lymph nodes, if enlarged,
are mobile.
Stage IV : The growth extends beyond the breast area; Fixation of the tumour to the chest wall;
Fixation or matting of the axillary lymph nodes, Supraclavicular nodes involvement; Distant me
tastasis.
2. COLUMBIA SYSTEM —
Stage A : No skin oedema, ulceration or fixation of the tumour to the chest wall i.e. the tumour is
confined to the breast substance. Axillary nodes are not clinically involved.
Stage B : No skin oedema, ulceration or fixation of the tumour to the chest wall. Axillary nodes
are clinically involved but less than 2.5 cm in transverse diameter and are not fixed to the overlying
skin or deeper structures of the axilla.
Stage C : Presence of oedema of the skin, skin ulceration, fixity to the chest wall, massive in
THE BREAST .............................. , ________________ 603
volvement of axillary nodes (more than 2.5 cm in trans

verse diameter) and fixation of the axillary nodes to the
overlying skin or deeper structures.
Stage D : All those present in Stage C. Over and above
there may be extensive oedema of the skin, satellite skin
nodules, clinically supraclavicular node involvement,
parasternal metastasis, oedema of the ipsilateral arm and
distant metastasis.
3. TNM SYSTEM.—
This was first presented by the International Union Against
Cancer, which was organised in 1959 by the American College
of Surgeons. It is based on Clinical observation related to
the tumour (T), regional lymph nodes (N) and distant me
tastasis (M). The system is described as follows:
Tumour (T).—
TO : No demonstrable tumour in the breast.
T1S : Preinvasive carcinoma (carcinoma in Situ).
Tl : Tumour of 2 cm or less; skin is not involved or
involved locally in Paget’s disease.
T2 : Tumour size 2 to 5 cm.
T3 : Tumour is greater than 5 cm in size.
T4 : Tumour of any size with any of the following :
Skin infiltration, ulceration, skin oedema, Peau d’ or
ange, pectoral muscle or chest wall attachment.
Regional lymph nodes.—
NO : No clinically palpable axillary lymph nodes.
N1 : Clinically palpable axillary nodes (Nla — metastasis
not suspected, Nib — metastasis suspected).
N2 : Clinically palpable, fixed axillary nodes (metasta
sis suspected).
N3 : Homolateral supra- or infraclavicular nodes consid
ered to contain metastasis; oedema of the arm. Fig. 39.8.— Mammogram showing curvilinear
Distant metastasis.— band (‘Rainbow sign’) which represents the ea
MO : No distant metastasis. est sign of localised skin infiltration. Its prese
M1: Clinical and radiologic evidence of metastasis ex is invariably associated with progressive disea
Appearance of septal thickening is similarly o
cept those to homolateral axillary or infraclavicular lymph grave prognostic significance. Microcalcificatio
nodes; includes skin involvement beyond the breast. may be due to active secretory process by tum
STAGING : cells in an epithelium that is known to be cap
Stage I : Tl, NO or Nla, MO. of concentrating calcium ions.
Stage II : Tl, Nib, MO; T2, NO, MO or TO, Nib, MO; T2, Nla, MO or T2, Nib, MO.
Stage III : T3, N2, MO or T4, N2, MO.
Stage IV : Any T, Any N with Ml.
SPECIAL INVESTIGATIONS.— These are aimed at (i) early diagnosis of the case and (ii) to detect
distant metastasis if present for proper clinical staging. It should be remembered that the tumours do
generally become palpable until they are bigger than 1 cm in diameter. The accuracy of diagnosis of br
cancer on physical examination is only 70% among the most experienced clinicians.
1. Mammography.— This is nothing but an X-ray examination of the breast. Special and careful
niques are necessary with fine-grain X-ray film. It has achieved world wide acceptance in the last decad
Views are taken of each breast from the superior and medial aspects, with the inferior and lateral surfa
the breast respectively against the cassette. Mammography is especially useful in (a) Screening procedure
Clinically undetected cancer has been diagnosed by mammography in 10% of patients. It is particularly usefu
in high-risk populations (relatives of the patients who suffered from breast cancer), (b) It is particularly
useful in older patients with large and fatty breasts where palpation is rather difficult to make the diagnosis
Younger women have dense and active breast stroma which obscures lesions in mammography, (c) Mamm
raphy is very important in examining the opposite breast in women who have already been treated for brea
cancer. This investigation should be a routine in follow-up cases after treatment of breast cancer on one side
(d) In case of a swelling of the breast whose clinical diagnosis has not been certain, mammography has a ver
definite role to play.
Benign lesions are usually well circumscribed and homogeneous and are often surrounded by a zone of
fatty tissue. Calcification if present is usually coarse and is mainly situated at the periphery of the lesion. In
case of carcinomas the margins are poorly defined, the edges are either spiculated or irregular. Fine, stipple
calcification in the soft tissue and periductal region is very suggestive. Thickening and retraction qf the
overlying skin is also seen in a few cases of breast carcinoma. Less certain findings are — increased ductal
and stromal activity. Serial mammograms may be particularly useful, so that progression of this disease can
be detected. It must be remembered that in mammograms radiation risk is considered negligible.
2. Xeroradiography.— It is basically the same technically as mammography, except that the image is
recorded on selenium coated film producing a positive impression to make it easier to the untrained eyes. I
diagnostic capacity is more or less same as mammography.
3. Thermography.— The skin over the malignant tumour of the breast is usually warmer than the
surrounding areas. Special scanners may be used to delineate these “hot spots” on film. Infection may give
false positive result. All cancers are not hot and thus give false negative results. Its main utility may be to
differentiate between malignant and benign tumours. When used in conjunction with physical examination
and mammography it can be expected to increase the number of cancers detected by 3% to 5%.
4. Ultrasound.— This is an important di
agnostic tool in many organ systems, but its ap
plication in breast cancer detection remains in the
development stage. At present, ultrasonic exami
nation of the breast is useful only in differentia
tion between solid and cystic swellings greater than
2.5 cm in diameter. Recent improvement in instru
mentation has helped to detect 0.5 cm solid breast
masses. Fluid-filled lesions lack an internal echo
pattern, whereas solid lesions are filled with in
ternal echoes. If the solid lesions are homogeneous,
the echo pattern is evenly distributed throughout
the mass. Echoes from the boundaries of a benign
lesion are smooth and well-defined. Infiltrating
lesions such as scirrhous carcinomas have jagged
borders. Breast ultrasonograms are of limited use
Fig. 39.9.— Xeroradiograph of a breast showing cluster of
fulness in the detection and diagnosis of breast microcalcification. The causes of microcalcification are —
cancer. If however sophisticated instruments (i)be
Cancer; (ii) Mammary dysplasia; (iii) Fibroadenosis and
come commercially available, gray scale echography (iv) Normal involution.
may become a valuable adjunctive procedure. At
present breast ultrasonograms are of limited usefulness in the detection and diagnosis of breast cancer, but
gray scale echography may become a valuable adjunctive procedure.
5. Aspiration.— This is performed in case of cystic lumps of the breast which were preliminarily thou
to be benign. But if the aspirated fluid is blood-stained, if the mass does not completely disappear on aspira
tion and if the cyst recurs rapidly after two aspirations, excision biopsy should be called for suspecting it to
be malignant. Fluid should be sent for cytology. Though negative result is of little importance, yet the posi
tive result means malignant lesion and calls for wide excision of the lump or mastectomy.
NEW IMAGING FOR BREAST DISEASES
It has been revealed that in the mammography and ultrasonography features of benign and malignant
tumours often overlap, so that biopsy is frequently required to establish the diagnosis. Mammography tend
THE BREAST 605
to underestimate tumour size, multifocality and about 5% to 15% of cancers are not visualised at all with
resultant delay in diagnosis. Ultrasonography however is of limited value in the detection of small tumours
(less than 1 cm), multifocality and intraductal disease. Both imaging techniques have limitations in the as
sessment of irradiated conserved breast and the response to neo-adjuvant chemotherapy.
Several exciting imaging techniques have currently been used. Here 2 new imaging modalities viz. mag
netic resonance imaging (MRI) and nuclear medicines related imaging techniques are discussed.
MAGNETIC RESONANCE IMAGING (MRI) OF THE BREAST.— Contrast enhancement
of MRI of the breast is a new technique. Gadolinium chelate is given as a rapid intravenous bolus
injection. Although dilution occurs in the heart and lungs the contrast agent enters the arterial sys
tem as a bolus. Contrast medium, present in capillaries and extravascular extracellular space pro
vides enhancement. Neo-angiogenesis is a recognised feature of malignant breast tumour. Regions
of hypervascularity, increased capillary permeability and increased interstitial space develop pre
dominantly at the periphery of malignant breast tumours and may create beds for poolling of con
trast material. Although angiogenesis is a definite feature in the growth of malignant tumours, yet it
is not unique to it, as angiogenic benign tumours do exist. The hypervascularity, associated with
benign conditions such as inflammatory lesions most likely account for some of the overlap in en
hancement characteristics. The choice of pulse sequence is the greatest determinant of image qual
ity for breast MR imaging examinations. The goal of the pulse sequence is to provide the highest
contrast between enhancing cancer and normal tissue with the most efficient acquisition times.
The presence of contrast enhancement is very sensitive but not very specific. Two approaches
have been used to improve the specificity of MR imaging in the differentiation of benign and malig
nant tumours, namely, dynamic imaging and high resolution static contrast enhanced imaging. Using
the latter criterion a sensitivity of 95% and a specificity of 86% is shown for the diagnosis of breast
cancer. Correlative studies of MR imaging with serially sectioned pathological analysis of mastec
tomy specimens showed a sensitivity of 95% for MR imaging in the diagnosis of breast cancer,
compared with a sensitivity of only 55% for mammography. Currently there is no single standardised
or a generally accepted technique for all breast MR imaging. However there is uniform agreement
that some form of 3 dimensional Tl-weighted sequence must be used before and after injection of
gadolinium chelate. The dose of gadolinium used in most centres is 0.1 m mol/Kg body weight. Due
to extracellular distribution of gadolinium, rapid imaging within 5 to 10 minutes of injection is
needed as the contrast agent washes out of the tumour into the normal breast parenchyma. The
development of newer, better targetted, contrast agents that stay within the tumour for a longer
period of time will help further advance in the implementation of breast MR imaging.
MRI IN PRIMARY BREAST CANCER.— The potential role of MRI in identifying cancers not
detected with conventional imaging methods has created great interest. The sensitivity of MRI in
the diagnosis of breast cancer reported in most studies varies from 80% to 100% and in all these
studies its sensitivity was greater than mammography and ultrasonography. Moreover mammogra
phy and ultrasonography significantly underestimate tumour size by 14% and 20% respectively,
whereas MRI shows no significant difference compared with that determined by pathological ex
amination. The accuracy of MRI in defining the tumour margins may assist in planning the extent of
surgical resection required to obtain negative resection margins. MRI also plays a role in the local
staging of breast cancer by enabling accurate assessment of tumour size, detection of multicentric
foci, prediction of presence of extensive intraductal component and assessment of nipple-areolar or
pectoralis attachment and axillary nodal involvement. MRI is more competent in detecting multi
centricity of breast cancer than other investing modalities.
MRI may have a role in the diagnosis of axillary nodal metastasis. Nodes measuring more than 5 mm
in diameter and appearing as high signal spots on inversion recovery sequence, are likely to be malignant.
This investigation is getting more and more importance to the breast surgeons. It has been proved
useful as a screening procedure in high risk women. It is probably the best to distinguish scar from
recurrence in women who had previous breast conservative surgery for cancer. It is quite useful for
imaging the breasts with implants. In the management of axilla in both primary breast cancer and
recurrent disease it is said to be an important evaluating tool.
NUCLEAR MEDICINE BREAST IMAGING TECHNIQUE.— These techniques involve the
use of single-gamma or dualgamma (positron emitting) radiotracers and provide functional or meta
bolic information of breast tumours. Single-gamma studies, "Technetium sestamibi and "mTc tetrafosmin
are mostly used in breast scintigraphy due to less favourable washout characteristics. It must be
confessed that mammoscintigraphy has excellent sensitivity in the diagnosis of breast cancers for
tumours larger than 1 cm, but sensitivity is generally poor for smaller, non-palpable or medially
located lesions. Lymphoscintigraphy, with the use of 99mTc colloids is also beginning to be employed
for preoperative and intraoperative localisation of non-palpable breast tumours. However this tech
nique in present days has not succeeded to be used routinely in breast cancer cases.
6. Biopsy.— It is customary when presented with a palpable mass in the breast to remove the
lump for accurate diagnosis. Whatever the degree of suspicion of cancer, most surgeons still prefer
to be quite definite before committing a woman to mastectomy or radiotherapy.
The frozen section histology technique has probably been put to use more often in the manage
ment of mammary lesions than in any other situation. There has been considerable interest recently
in needle biopsy as an alternative to excision biopsy procedure. There were a few false-negative
results, but greater problem was due to false positive results received with cytodiagnosis of aspi
rated material. Drill biopsy has been claimed to avoid this problem. 95% accuracy has been claimed.
No false positive result has been recorded but the cancers less than 1 cm in diameter may be missed
by drill biopsy. Needle can be introduced to the centre of the suspicious area under X-ray control.
With this technique it has been claimed that as small as 3 mm diameter tumours have been success
fully identified and biopsied.
Needle biopsy can easily be achieved for breast lumps greater than 1 cm in size. The skin over
the lump is infiltrated with local anaesthetic, a cutting needle is inserted into the centre of the lump
and an adequate core of material is obtained for routine histopathological examination. There are no
false positives using this technique, but a negative result must be ignored and the lump should be
dealt with by open biopsy. In all cases, a preliminary attempt at needle aspiration should be carried
out to exclude the possibility of a cyst. The advantage of a definite diagnosis of cancer at the first
visit to the clinic is enormous. This enables a search for metastasis to be established immediately. It
enables the surgeon to proceed with a frank discussion with the woman for the need for mastectomy
and it saves the patient from psychological trauma of being subjected to general anaesthesia without
knowing if she will awake with or without her both the breasts.
Fine Needle Aspiration Cytology (FNAC).— It has become an almost routine practice in the
investigation of a breast lump. A 22-gauge needle and an appropriate size syringe is required. If
mammography is necessary, this procedure is postponed, till mammography is done, as a small haematoma
resulting from needle puncture may confuse the mammographic picture. Though its value in breast
cyst is discussed elsewhere, here we shall discuss its investigative potentiality in breast carcinoma.
This method has the advantage that it can be performed as an out-patient procedure. It is relatively
atraumatic. Its disadvantages are that it requires expert and specialised pathological interpretation.
Aspiration cytology cannot differentiate in-situ or invasive cancer, but can distinguish ductal from
lobular carcinoma. False negative results (approximately 15%) are either due to missing the tumour
at the time of aspiration or from failing to aspirate a particularly scirrhous acellular carcinoma.
SEARCH FOR DISTANT METASTASES.—
One should consider breast cancer as a systemic disease. No woman therefore should be sub
jected for mastectomy until a most careful search has been undertaken for distant metastases.
7 Chest X-ray.— This is the simplest method of looking for potential site of visceral metastasis. This should be a routine
investigation for all women with early carcinoma of the breast. Lungs are predominantly involved by blood borne metastasis
THE BREAST 607
which will lodge in a pulmonary capillary and gradually grow into a nodular mass. This is the most common form of pulmonary
matastasis and the lesion will eventually produce a single or more commonly multiple nodular densities seen on chest X-ray.
These densities are not visible in chest X-ray until they become 1 to 2 cm in size. The 2nd mode of lung involvement is through
mediastinal lymph nodes when minute cancer cells spread in a retrograde fashion into the peribronchial lymphatics thus producin
lymphangitic pattern of spread seen on chest radiography. In these cases chest X-ray is characterised by diffuse interstitial infiltra
that is difficult to diagnose until the tumour has spread diffusely throughout the lung. While the blood borne nodular lesions
usually do not produce symptoms until the lung is largely replaced with metastatic tumour, the lymphangitic spread can produce
irritating cough and increasing shortness of breath in early stage of the disease.
Metastatic lesions in the mediastinal lymph nodes will not be visualised by chest X-ray until they reach 2 cm in size,
because the lesions tend to blend with other mediastinal structures. These lesions are usually asymptomatic till the tumour grows
out of the node and invades adjacent structures such as recurrent laryngeal nerve or oesophagus.
8. Bone X-ray.— A skeletal survey is often asked for particularly X-ray of the spine, pelvis, upper ends of the humerus
and femur and skull. Osseous metastasis is the commonest site of metastatic breast cancer in autopsy series. At least 20% of
patients with operable breast cancer will eventually develop clinical evidence of osseous metastasis before death. Osseous
metastases occur through blood (blood-borne) either systemically through the lungs and left heart or via intercostal veins and
disseminate by way of the vertebral veins. The pelvis and the spine are the most frequently involved sites. The lumbar spine
is the commonest site in the spine followed by thoracic spine, sacrum and cervical spine. Other common sites of metastases
in order of decreasing frequency are the femur, ribs, skull, humerus, scapula and clavicle. The commonest type of osseous
metastasis is the osteolytic lesion which destroys bone mineral and produces an irregular lytic lesion on X-ray. At least 50%
of bone minerals must be destroyed before the lesion becomes apparent on the radiograph. 5% to 10% of the bony metastases
from breast cancer are osteoblastic. Thickenings of trabecular pattern which eventually coalesce to form radiographic evidence
of irregular dense masses. The third type of metastatic lesion grows within the bone marrow without any associated damage
to the adjacent bone. The 4th type of bony metastasis is any combination of the previously mentioned three types. It must be
remembered that bony metastasis remains asymptomatic until the metastatic lesion extends to the periosteum. Periosteal distention
or periosteal invasion produces pain and occasionally tenderness at the involved site.
9. Bone scan.— Development of skeletal scintigraphy has undoubtedly improved accuracy for detecting bony metastasis.
Radioactive fluorine was one of the first few bone-seeking isotopes that had successfully demonstrated skeletal metastases earlie
than would be detectable by conventional X-ray. Since then enormous improvement in the sensitivity of the scanning devices
and availability of newer radioactive bone seeking isotopes have made skeletal scintigraphy an attractive method to detect bone
metastasis. So for routine skeletal survey a whole body skeletal scan followed by specific radiology of the areas of abnormal
uptake should be the method of choice. Healing fractures, Paget’s disease and osteoarthritis also show hot spots as bony metastasis.
Obviously presence of bone metastasis detected by scan will put the patient into stage IV category. False positive and false
negative results are disturbing. In suspicious cases shown by the scan, open bone biopsy is the last court of appeal. Inspite
of the fact that radiographic skeletal surveys are normal in almost all patients with operable breast cancer, at least 20% to
30% of these patients will develop clinical and radiographic evidence of metastasis within 10 years following treatment. Since
radionuclide bone scans are known to detect metastatic lesions many months prior, bone scans seem to offer a promising means
in detecting otherwise occult osseous metastasis. Bone scans are obtained by the following techniques. After intravenous injectio
of WmTc phosphonate and diphosphonate, whole body images are obtained with a rectilinear scanner. These rectilinear scans
are supplemented by gamma-camera images of the entire spine plus any area that is equivocally abnormal on rectilinear scan.
It is extremely important to obtain radiographs of any area of increased radioactivity detected by bone scan to eliminate such
lesions as Paget’s disease or degenerative joint disease.
10. Liver scan.— Liver metastases are present in 60% to 70% of patients dying of metastatic breast cancer. Clusters
of metastatic cells lodge in capillaries fed by the hepatic artery. These early metastatic lesions gradually grow into nodular
lesions. In early stages symptoms are rare. Symptoms occur only when there is distension of Glissen’s capsule or obstruction
of the biliary system producing jaundice. Small liver metastases are rarely detected by clinical examination.
Liver scans are obtained following injection of a sulphur colloid labelled ’’Technetium. The colloid particles are taken
up by the reticuloendothelial system and the radioactivity in the colloid particles provides a means of screening the liver. Metastati
lesions in the liver are most accurately diagnosed by detecting focal filling defects. It is rather unfortunate that single defect
smaller than 2 cm in diameter cannot be routinely detected by liver scanning. Quite a large number of patients with metastatic
breast cancers do have hepatic lesions less than 2 cm in size.
11. Computerised Tomography (CT scan) can be used to detect mediastinal or retroperitoneal masses of malignantly
involved lymph nodes.
12. Biochemical studies.— Elevated alkaline phosphatase and gamma glutamyl transaminase are crude estimates of liver
metastasis. Similarly increase in urinary hydroxyproline indicates collagen break down from metastasis. Serum alkaline
phosphatase originates in the liver, bone, intestine, kidney and placenta of pregnant woman. Elevation of serum alkaline
phosphatase is detected in 60% to 90% of cases with liver metastasis, indicating that this is a relatively sensitive indicator of
liver metastasis. But unfortunately a number of other hepatobiliary disorders as well as inflammatory lesions, osteoporotic lesion
and metastatic lesion in the bone may also raise the serum alkaline phosphatase level. Nevertheless the serum alkaline phosphat
has proved to be a very useful screening procedure for either bone or liver metastasis. Significant elevation of the serum alkaline
phosphatase in presence of normal bilirubin and serum glutamic oxaloacetic transaminase is suspicious enough of bone metastas
to indicate the need for additional studies of the bones and livers.
Serum Carcinoembryonic Antigen (CEA) is a valuable indicator in association with liver scan to detect liver metastasis.
If the defects in the liver scan are associated with CEA levels greater than 5 ng/ml, liver metastasis are considered to be presen
So far as the diagnosis of early cases and determination of prognosis are concerned urinary steroids have got some value.
An abnormally low level of aetiocholanolone (a metabolite of the adrenal androgen dehydroepiandrosterone) in relation to the
total amounts of 17-hydroxycorticosteroids in the urine is detected in patients with breast cancer. It also indicates bad prognosis
This is called ‘negative discriminants’. They show poor response to adrenalectomy and hypophysectomy.
TREATMENT.— The choice of treatment of breast cancer varies a lot from surgeon to surgeon.
But basically it is aimed at (i) curing the local disease and (ii) to minimise untoward side effects and
disability.
TREATMENT O F EARLY BREAST CANCERS (STAGE I AND STAGE I I ) . — There are several
options available for this potentially curable breast cancer. The local treatment ranges from lumpectomy
(tylectomy) to super-radical mastectomy.
The traditional surgical treatment for breast cancer involves total removal of the breast. Upto early
1970s breast cancer was treated by total mastectomy, the most commonly performed operation was
Halsted’s radical mastectomy. Later on more conservative operations came into place e.g. tumourectomy,
lumpectomy, tylectomy, segmental mastectomy and quadrantectomy — in which the primary tumour is
removed and the breast is preserved. The terms ‘lumpectomy’, ‘tumourectomy’ and ‘tylectomy’ imply
removal of the tumour with a minimal margin of normal breast tissue around it. ‘Segmental mastectomy’
implies excision of the tumour with a rim of associated normal breast tissue. The term quadrantectomy’
denotes removal of a breast quadrant and involves wider excision of normal breast tissue than segmental
mastectomy.
Majority of women presenting with apparently localised breast cancer have micrometastatic disease
which is not detectable by currently available screening investigations. Survival is determined by the
presence or absence of these micrometastases. The aim of locoregional treatment is to achieve long-term
local disease control. Numerous studies have now shown that although local recurrence may be slightly
more common after breast conservation than mastectomy, disease-free survival and overall survival are
the same. The advantage of conservation surgery is that it offers better cosmetic appearance when
compared with mastectomy which allows increased freedom of dress. In fact local treatment has little
influence on survival. However breast conservation should be combined with some form of systemic
therapy given either as an adjuvant following or as primary systemic therapy prior to surgery.
Studies evaluating simple excision of the tumour without adjuvant radiotherapy have produced
somewhat disappointing results with a local recurrence rate of approximately 25% in 5 years.
Failure of local excision alone laid to the use of adjuvant radiotherapy to the remaining breast tissue.
This combination of conservative surgery with adjuvant radiotherapy has now become a standard
procedure for patients with breast cancer. The results are encouraging with local recurrence rate is under
10%.
INDICATIONS FOR BREAST CONSERVATION TREATMENT.— If the patient prefers to be treated
by total mastectomy, it should be adhered to. Many patients feel more secured after total mastectomy
and others prefer to avoid irradication treatment. The main indications for conservative surgery are as
follows :— (i) Tumour size is of paramount importance. If the tumour is more than 3 or 4 cm in diameter
mastectomy should be recommended. In case of small breasts even smaller tumours may require
mastectomy, (ii) There are doubts whether breast conservation is appropriate for patients with node
positive disease.
Selection of patients for breast conservation.— Patients with palpable breast lesion suspicious of
malignancy should be investigated with Fine Needle Aspiration Cytology (FNAC) and mammography.
Mammography is important as it identifies impalpable multifocal, multicentric or contralateral disease.
All patients with established diagnosis of malignancy should have chest X-ray, full blood count and liver
function tests prior to surgery. Routine bone and liver scans are unnecessary unless symptoms are present
or the results of biochemical screening investigations are abnormal.
Patients suitable for breast conservation surgery are as follows :—
THE BREAST 609
(i) A single clinical and mammographic lesion measuring 4 cm or less without signs of local advance
ment (Tl, T2, < 4 cm), with no extensive nodal involvement (NO, Nl) or metastasis (MO). Tumours bigger
than 4 cm may also be treated by breast conserving surgery in patients with large breast.
(ii) There is no age limit for this surgery and elderly, fit patients are treated in the same way as the
younger.
Using primary systemic chemotherapy it is now possible to shrink large tumours to allow such surgery.
Contraindications to breast conservation surgery are — (i) tumours more than 4 cm in size (T4), (ii) extensive
nodal metastasis (N2) and (iii) with distant metastasis (Ml), (iv) Fixity of tumour with underlying muscles or overly
ing skin, (v) Multicentricity of the tumour which is determined by mammography is a definite contraindication, (vi)
Central lesions (for whom breast conservation surgery would produce an unacceptable cosmetic result). When nipple
has to be sacrificed total mastectomy should be performed, (vii) Poor tumour differentiation is a contraindication,
(viii) Multifocality is also a contraindication to breast conservation.
A few relative contraindications are — (i) when the patients are quite young (under 35 years); (ii) presence of
extensive ductal carcinoma-in-situ and (iii) widespread lymphatic invasion.
1. LUMPECTOMY (TYLECTOMY).— This is sometimes practiced in which the tumour alongwith
a thin rim of the surrounding breast tissue is removed. This seems to be an unsound approach for general
use due to high risk of recurrence. Without radiotherapy the recurrence rate is about 37% after lumpectomy
whereas when radiotherapy is added to lumpectomy the recurrence rate is reduced to 10%. So this treat
ment could not enjoy widespread acceptance.
2. WIDE LOCAL EXCISION.— This is the most descriptive term which was also referred to by
many names e.g. segmentectomy, partial mastectomy etc. In this procedure the malignant tumour is re
moved with a surrounding minimum 2 cm rim of grossly normal breast parenchyma. An even more aggres
sive procedure involves removal of the whole segment of the breast containing the tumour, which is called
quadrantectomy. In modern practice, these limited surgical procedures are always accompanied withpos/-
operative radiation therapy giving at least 4,500 cGy. to the whole breast. Axillary dissection is always
done through a separate incision to take samples of lymph nodes for histopathology report for evidence of
metastasis. There are various options to deal with the axilla which include sampling removal of the nodes
behind and lateral to pectoralis minor (Level II) or perform a full axillary dissection (Level III). A
quadrantectomy, axillary dissection and radiotherapy is known as QUART, which was popularised by Prof.
Umberto Veronesi from Milan. So this conservative breast surgery means wide local excision of the pri
mary tumour, whole breast radiation and a separate axillary dissection. There is considerable evidence that
relapse rate is significantly decreased following radiation therapy in comparison to no radiation therapy. If
an axillary dissection is performed, axillary radiation should not be routine unless there are many positive
nodes. This is to reduce the incidence of ipsilateral arm oedema which is more common following radia
tion. Local recurrence is more common in younger women and in those with high-grade tumours. Patients
whose margins are involved (revealed in biopsy specimen) should have a further local excision or a mastec
tomy before going on to radiotherapy.
Stereotactic wide local excision.— Placement of a hooked wire close to the lesion using either stereotactic or
ultrasound guidance is made. Lateral and craniocaudal mammograms are taken and prior to surgery these films are
discussed with the radiologists. From these mammograms the surgeon calculates the position of the breast lesion and
an incision is made along the Langer’s line directly over the lesion. The incision is deepened and the dissection
proceeds towards the location of the wire. Once the wire has been identified, it is divided with sterile wire cutter. The
proximal part of the wire is removed and the tissue around the distal wire is grasped with tissue forceps. Using
mammograms as a guide, a block of tissue 1 to 2 cm around the mammographic lesion is excised. The completeness of
excision is confirmed by further mammographies. Close co-operation between the surgeon and the pathologist is
required to identify the nature of the lesion and adequacy of the excision.
3. SUBCUTANEOUS MASTECTOMY WITH PROSTHETIC REPLACEMENT.— In this technique
a total mastectomy is performed keeping the skin and fatty envelop of the breast intact. The nipple is
preserved and is attached only to subjacent dermis. It has got tremendous cosmetic value as silastic implants
are used. This operation requires meticulous technique and may be employed only in carcinoma-in-situ
cases. Some breast tissue is invariably left and it cannot be applied to an established invasive carcinoma.
39
4. TOTAL MASTECTOMY.— This is widely practiced in some institutions where it is usually

performed with axillary node biopsy. Overlying skin is removed less so that skin grafting is not required.
Advocates of this treatment believe that internal mammary lymph nodes are also affected, though in less
percentage, as the axillary lymph nodes. So they do not find any justification for a routine radical
mastectomy in all cases. Radiotherapy may be given routinely or may be preserved for those patients
with histologically involved nodes either immediately or when they become clinically apparent. This
method may be the treatment of choice in stage I breast carcinoma. Mcwhirter is the greatest proponent
of this technique in which he used orthovoltage therapy (250 kV) with delivery of 3,500 R to the axillary,
internal mammary and supraclavicular lymph nodes. Later on the used radiotherapy dose was 400 kV
to the axillary and supraclavicular lymph nodes while 250 kV was applied to the internal mammary chain.
5. HALSTED RADICAL MASTECTOMY.— In this classical operation, the following structures
are removed — (1) the whole breast, (2) the portion of the'skin overlying the tumour, which should
always include the nipple, (3) the subcutaneous fat and the deep fascia vertically from the lower border
of the clavicle upto the upper quarter of the sheath of the rectus abdominis and horizontally from the
sternum to the anterior border of the latissimus dorsi, (4) the whole of the pectoralis major (clavicular
part may be spared in growths at the lower part), (5) the pectoralis minor and clavipectoral fascia, (6)
upper part of the aponeurosis of the external oblique and anterior parts of a few digitations of the serratus
anterior, (7) all fatty and loose areolar tissue along with all groups of lymph nodes of the axilla.
The structures to be saved are : (1) the axillary vein and the cephalic vein (in order to prevent oedema
of the upper limb); (2) the long thoracic nerve of Bell, supplying the serratus anterior. The nerve to
the latissimus dorsi may be sacrificed, if required.
POSITION.— The patient lies supine near the edge of the table with the arm of the affected side abducted to right angle
and placed on an arm rest. A sand bag is placed under the scapula.
TECHNIQUE.—
Incision.— The central part of the incision is an ellipse to include the skin overlying the tumour and the nipple. This
incision is prolonged upwards and laterally across the axilla to the insertion of the pectoralis major muscle. The lower end
of the ellipse is carried downwards and towards the umbilicus as far as necessary. No attempt should be made to preserve
any doubtful skin for the purpose of complete subsequent closure of the wound.
Undermining the skin edges.— The skin edges of the incision are undermined leaving sufficient thickness of fat on the
under surface of the skin to ensure its viability. The upper skin flap is undermined upto the clavicle above and to beyond the
midline; the lower flap is undermined laterally to the edges of the latissimus dorsi and below to the upper part of the abdomen.
Clearance of the axilla.— The upper part of the incision is deepened and the skin flaps are reflected to expose the entire
width of the pectoralis major from the clavicle downwards, lying in front of the axilla and the fascial floor of the axilla as
far back as the edge of the latissimus dorsi. An incision is made on the upper border of the fascia covering the pectoralis major.
The upper margin of the fascia is stripped medially as far as the junction between the sternal and the clavicular fibres of the
pectoralis major. A finger is passed between the two sets of fibres and the sternal fibres are divided near their insertion. This
sternal part of the pectoralis major is now retracted medially. If the growth is situated on the upper part of the breast, the
entire insertion of the pectoralis major is divided. The insertion of the pectoralis minor muscle is also divided and is reflected
medially. The thoracoacromial artery, which lies deep to this muscle and the lateral thoracic artery, which runs along the lower
border, should be secured. The clavipectoral fascia, which lies above the pectoralis minor muscle, should also be removed
and care being taken to preserve the cephalic vein. The axilla is now wide open. All fat, lymph nodes and cellular tissues
are dissected out and pushed towards the breast, so that the whole of the lymphatic territory can be removed as a whole with
the breast. The apical glands lie at the medial side of the axillary vein. The dissection is best carried out by means of a finger
covered with gauze. The stripping process is continued till the muscles of the posterior axillary wall (subscapularis, teres major
and latissimus dorsi) and the serratus anterior forming the medial wall are completely exposed. Sometimes the nerve to the
latissimus dorsi may be sacrificed, otherwise this nerve along with the nerve of Bell, supplying the serratus anterior, should
be carefully protected. Warm saline packs are placed on the axilla, while the attention is directed towards the removal of the
breast tissue.
Removal of the breast.— The pectoral muscles are now gradually divided from the chest wall along with upper fibres
of the external oblique. The perforating branches of the internal mammary artery will be encountered. They should be clamped
with forceps before they are divided, otherwise they retract causing difficulty in arresting haemorrhage. Upper part of the rectus
sheath is removed leaving the fibres of the rectus muscle exposed. Finally, the whole mass is removed by dividing the sternal
fibres of the pectoralis major.
Meticulous attention should be paid to arrest haemorrhage. A good search should be made, if there is any glandular tissue
left behind, particularly at the apex of the axilla along the axillary vessels.
Closure of the wound.— Before sewing up the flaps, the arm should be elevated straight above the head. This is to prevent
THE BREAST 611
any functional disability. While suturing the two flaps care must be taken not to do it under tension, as this will lead to
devitalisation of skin flaps and necrosis. If a gap does exist between the flaps, it should be closed with skin graft. Drainage
should always be given, preferably suction drainage, to prevent haematoma formation. Abundant dressings are applied and
bandaged to prevent haematoma formation, which will form a nidus for wound infection. The arm is kept in adduction and
bandaged against the chest wall. After 48 hours, the arm is abducted to 60° to prevent functional disability.
Postoperative care.— The patient should be in the semi-sitting position. The drainage is removed in 48 hours. When
the bandage is released, the arm is kept in abducted position supported by a pillow.
The modern trend is to reserve radiotherapy for tumour recurrences only and it is not given as a routine after radical
mastectomy.
6. MODIFIED RADICAL MASTECTOMY.— This modification was designed to reduce the cosmetic
deformity produced by the classical Halsted radical mastectomy while at the same time the block
dissection of the axilla is performed. Patey, at the Middlesex hospital in London, developed a procedure
that preserves the pectoralis major muscle and sacrifices the underlying pectoralis minor muscle to
remove level I, II and III lymph nodes in the axilla. This is a widely used procedure to treat operable
breast cancer and is the alternative to breast-sparing procedures. In this technique the pectoralis
major muscle remains intact providing a soft tissue covering over the chest wall and almost normal
appearing junction of the shoulder with the anterior chest wall. This avoids a hollow defect inferior
to the clavicle which is caused by removal of the pectoralis major muscle. The result of the operation
and the survival rate is no way inferior to those of radical mastectomy.
Auchincloss left both the pectoralis major and minor muscles intact removing the axillary nodes
and the nodes between the two pectoral muscles. This modification limits the complete removal of
high axillary nodes, but Auchincloss justified that only 2% of patients will be benefited by removal
of this high level lymph nodes. This procedure is also gaining popularity during the last decade in the
United States.
The excision of the breast including excision of the overlying skin and the need for skin grafting
is essentially the same as with Halsted radical mastectomy. This operation now enjoys widespread
acceptance as treatment of early breast cancer, as it gives good local control and allows the full
assessment of the axilla. This prevents further dissemination and lessens the chance of regional recurrence.
This procedure also gives a chance for later breast reconstruction.
7. EXTENDED RADICAL MASTECTOMY.— 21% of the outer quadrant tumours and 43% of
the central and inner quadrant tumours have internal mammary node involvement. Being not satisfied
with the Halsted radical mastectomy where only axillary lymph nodes are dissected out, this technique
includes removal of internal mammary group of lymph nodes as well. In SUPER-RADICAL
MASTECTOMY internal mammary group, mediastinal and supraclavicular lymph nodes are also
removed alongwith axillary node dissection. Both the above techniques are associated with increased
morbidity and mortality. In the first technique ipsilateral half of the sternum and a portion of ribs 2nd
to 5th adjacent to the sternum are removed. The internal mammary lymph nodes lying alongside the
internal mammary artery and accompanying vein alongwith the adjacent pleura are removed. Due to
its high morbidity and mortality rate this treatment has never received popularity.
Management of axillary nodes.— Axillary node sampling has been widely practised. It must be
admitted however that sampling fails to provide as much prognostic information as required in comparison
to full nodal assessment. The supporters of sampling claim that if done properly node-positive patients
can be specifically targeted for adjuvant radiation therapy, whereas full axillary dissection needlessly
overtreats 50% of patients with negative nodes. The available data indicate that adjuvant radiotherapy
provides as good overall control in the axilla as clearance. The whole question of sampling depends
on how well it is done. When inappropriately performed it should be condemned. If done properly it
provides qualitative data and therapeutic advantage same as total clearance.
The role of axillary surgery is still debated, but it is accepted that the presence of metastatic
disease within the axillary lymph node is still the best marker for prognosis. However, treatment of
the axilla does not affect a long term survival, suggesting that the axillary nodes act not as a ‘reservoir’
for disease but as a marker for metastatic potential. It is now known that all hormone receptor-positive
patients, irrespective of age, benefit from tamoxifen. If mastectomy is performed, it is reasonable to

clear the axilla as part of the operation, but if a wide local excision is planned the surgeon should
dissect the axilla through a separate incision. Axillary surgery should not be combined with radiotherapy
to the axilla because of excess morbidity. Removal of the internal mammary lymph node is unnecessary.
Axillary nodal clearance or block dissection of axillary nodes accurately stages the axilla. The
main criticism of clearance is that 50% of patients with negatives nodes do not require this treatment.
In some centres the pectoralis minor muscle is routinely removed or divided, whereas in other centres
it is merely retracted.
Wide local excision should be combined with a procedure to stage the axilla as this provides important
information ahout subsequent adjuvant treatment and prognosis. Two main options are available to stage
the axilla (i) complete axillary node clearance upto Level III or (ii) an axillary node sample. Axillary node
clearance may be associated with greater morbidity, though better than axillary node sampling combined
with axillary radiotherapy. After both complete axillary node clearance and axillary radiotherapy the main
complication is lymphoedema even upto an incidence of 40%.
In the light of currently available information it seems reasonable to perform an axillary node
sample in patients with impalpable breast cancer and to perform a Level III axillary node clearance
in patients with palpable disease.
Axillary node sampling.— This is usually performed through a separate axillary incision in the
skin crease of the axilla and is undertaken immediately prior to wide local excision. The axilla is
entered and the tail of the breast is palpated. If the nodes cannot be identified, the edges of pectoralis
major and lattissimus dorsi muscles are identified. A finger is passed round behind the lower axillary
fats which is situated between these two muscles. At least 4 palpable nodes are excised and are sent
separately for histology. If 4 nodes are not palpable in the lower axilla (Level I) then palpable nodes
from higher axilla (Level II or even Level III) should be excised. It must be appreciated that axillary
node sampling is not merely a Level I dissection, but this should allow dissection of Level II or Level
III. Sometimes Level I axillary nodes remain uninvolved whereas Level II or III nodes are involved
— the so called skip metastasis. Haemostasis in the axilla is secured with diathermy. No drain is
required and the wound is closed in layers with absorbable sutures.
Axillary node clearance.— This operation is also performed through a separate incision before
wide local excision of the breast. S incision is made along the skin creases of the axilla. The skin
incision is deepened and the skin flaps are dissected to the edges of the pectoralis major and lattissimus
dorsi muscles. The pectoralis minor muscle is cleared and divided with retraction of the pectoralis
major muscle. This allows a thorough clearance to be performed. The axillary vein is identified and
the contents of the axilla below the vein are cleared to the apex of the axilla preserving routinely the
long thoracic nerve, the thoracodorsal nerve and vessels and if possible the intercostobrachial nerve.
The undersurface of the pectoralis major muscle is carefully palpated and any palpable interpectoral
nodes are excised. Dissection of the lower axillary contents should continue into the axillary tail of
the breast. A redivac drain is introduced in the axilla and remains in-situ till the volume of fluid in the
drain is less than 30 ml in 24 hours. The wound is closed in layers with absorbable sutures.
SENTINEL NODE BIOPSY
The sentinel node is the first node encountered by tumour cells and the histological status of the
sentinel node predicts the status of the distant lymph nodes. So the sentinel node (SLN) is defined as
the lymph node(s) which is in a direct drainage pathway from the primary tumour. It is at the highest
risk of harbouring metastatic deposits. The other nodes receive lymph from the SLN. Cabanas in
1977 was the first person to introduce the sentinel node biopsy as a staging procedure in penile
carcinoma by directly injecting contrast medium into the dorsum lymphatics of the penis with penile
carcinoma. The first visualised lymph node was designated as the sentinel lymph node. The advantages
of sentinel node biopsy are : (i) it is a minimally invasive technique, whose morbidity and cost are
THE BREAST 613
extremely low. (ii) This can give an idea whether the lymph nodes of axilla are involved or not.
(iii) This approach may obviate the need for axillary lymph node dissection in all breast cancer
patients without compromising staging information.
Lymphoscintigraphy.— This is usually performed a day before operation. A single dose of 10-15
MBq of (99mTc) — labelled Nanocoll in a volume of 0.2 ml is injected subdermally at the tumour site
using a 25G needle. It is confirmed that the lymphatics of the overlying skin drain to the same axillary
sentinel node as the underlying glandular breast tissue. The purpose of this procedure is to find the
location and number of the SLN preoperatively. It also helps to differentiate the SLN from 2nd and
3rd group of nodes.
The surgical approach to the intra-operative detection of a sentinel node may be either by blue
dye lymphatic mapping or by a probe guided surgery. With intraparenchymal injection of the blue
dye alone, the success rate for identification of the SLN varies between 65% and 95%. Whereas the
success rate for operation guided by a gamma detection probe is more than 85% and may be even
100%. Majority follow a policy of preoperative lymphoscintigraphy and the combination of blue dye
lymphatic mapping and probe-guided operation for intraoperative localisation of the sentinel lymph
node. Preoperative lymphoscintigraphy is very helpful in accurate localisation of SLN.
The lymph node which is most medially placed of the pectoral group is often the sentinel node.
In node negative cases the specialised centres mostly perform sentinel node biopsy and send
it for histopathology report. If this node is not involved nothing is further done except a vigilant
follow-up. If this node is involved the question of axillary node sampling or clearance comes in.
This avoids many unnecessary sampling or clearance which is always associated with lot of
morbidity e.g. stiffness of the shoulder, continuous pain along the arm, backache, neckache and rigidity,
headache etc.
SLN biopsy must be performed in a clinical trial setting. We need to await the results of ongoing
randomised trials before adopting this technique for routine management of patients with breast carcinoma.
ADJUVANT THERAPY.—
It should be understood that micrometastases are often established prior to diagnosis and this is
the reason why extensive local treatment in the form of radical mastectomy or extended radical mastectomy
is becoming unpopular. Clinical trials indicate that adjuvant cytotoxic therapy or hormonal therapy,
when used in patients with axillary metastasis but without established distant metastasis, prolong the
disease-free interval and perhaps improve survival rates.
Adjuvant chemotherapy.— If lymph nodes removed at the time of axillary sampling confirm
histologic metastasis, adjuvant chemotherapy should be considered in the postoperative period.
For approximately 20% to 30% of patients, clinically negative axillary nodes will be proved
pathologically positive. A combination of cyclophosphamide, 5-fluorouracil and methotrexate has
been widely used because of its known activity in patient with metastatic disease. The initial
study showed a 30% reduction in mortality in patients receiving 12 cycles of treatment — the effect
is more clearly apparent in premenopausal women with 1 to 3 positive nodes. A 6-cycle course of
treatment is now regarded as standard. A few centres are now recommending this treatment for node
negative women below 50 years. This treatment is mainly recommended to premenopausal women
with positive lymph nodes mainly due to its effect as chemical castration. This combination
polychemotherapy is also effective in women aged over 50 years, may not be to the same degree as in
younger patients. It may be also recommended to node-negative patients, though the survival difference
may be less than 5%.
Chemotherapy may be used preoperatively in cases of large but operable tumours that would
traditionally require mastectomy. The aim of this treatment is to shrink the tumour to enable breast
conserving surgery to be performed.
The toxicity noted with cytotoxic agents for breast cancer is similar to that observed with chemotherapy
of other malignancies. These include nausea, vomiting, alopecia, myelosuppression, thrombocytopenia
etc. These toxic events may be reversible with discontinuance of the cytotoxic agents. A common side
effect of adjuvant chemotherapy in premenopausal patients is cessation of menses, as chemotherapy causes
a pharmacological castration.
Patients with very poor prognosis, such as those with a large number of diseased nodes, may in future
be considered for even more aggressive polychemotherapy such as provided by cyclophosphamide,
adriamycin and 5-fluorouracil.
Very recently Doxorubicin has been introduced in place of adriamycin and the treatment time has
been reduced to 6 months with 4-cycles in therapy. It has been seen that women treated with either high
or moderate dose of intense CAF (Cyclophosphamide, doxorubicin and fluorouracil) has a significantly
longer disease free and overall survival. This high dose of chemotherapy is supplemented with haematopoie
growth factors to accelerate both recovery of peripheral white blood cell count after treatment and to
stimulate the production of circulating haematopoietic cells for harvest and autologous transplantation.
This technical advancement has allowed the oncologist to use Higher dose of adjuvant therapy particularly
in multiple node positive patients with high risk of relapse. Newer combination chemotherapy including
doxorubicin is administered for 4 to 6 months and is just as effective as longer courses of treatment.
Adjuvant hormonal therapy.—
Hormonal receptors.— Within the breast cancer cells are specific proteins that bind and transfer
steroid moieties into the cell nucleus to exert specific hormonal effects. The most widely available receptor
proteins are the oestrogen receptor (ER) and progesterone receptor (PR) proteins. To obtain qualitative
hormonal assay of either hormone receptor, 1 gm of fresh tissue obtained from the tumour is essential.
These receptors are thermal and ischaemia labile. The specimens must be rapidly frozen (-70°C) for
ER and PR assay. After homogenation and centrifugation of the prepared specimen, it is then incubated
with 3H-tritium-labelled oestradiol-17p. Labelled unbound hormone is removed from the incubation
mixture and the bound oestrogen sediment is measured. Binding capacity is expressed in femtomoles.
Values more than 10 fmol/mg protein is considered receptor-positive, whereas values less than 3 to 4
fmol/mg are receptor-negative. 90% or more of well-differentiated ductal and lobular carcinomas are
ER-positive.
In the past oophorectomy, adrenalectomy and/or hypophysectomy were the primary endocrine
ablative procedures commonly used to treat metastatic foci. Oophorectomy was used for premenopausal
patients who presented with skin and/or bony metastasis. Adrenalectomy and hypophysectomy were
effective in individuals who had previously responded to either oophorectomy or exogenous oestrogen
therapy. Receptor activity is the most commonly utilised measure to determine the applicability and
selection of additive hormonal or ablative hormonal procedures. Tamoxifen is a weak oestrogen agonist.
But tamoxifen acts like a competitive antagonist of oestrogen activity in the breast. Its action in tissues
other than the breast are due to oestrogen-like actions. Regardless of its exact mode of action, tamoxifen
can effectively replace oophorectomy. It is as effective as either ablative or additive therapies in treating
hormone-sensitive cancers. Tamoxifen is the most widely used hormonal treatment in breast cancer at
the present day. The effect is greatest in patients aged over 50 years with positive nodes, in whom there
is 20% reduction in annual mortality. There is small, yet significant, effect in node-negative individuals.
The effect of tamoxifen is less apparent in women aged under 50 years. As is the case for adjuvant
chemotherapy, the effect of tamoxifen is found within the first 5-years and continues for at least 10 years.
The role of adjuvant tamoxifen is now well established in women over 50 years of age. The duration
of treatment is usually between 2 and 5 years. The effect of tamoxifen is favourable irrespective of the
oestrogen receptor (ER) status of the tumour, though ER-rich tumours achieve greater reduction in size
with less risk of relapse. Tamoxifen is not without side-effects, particularly in premenopausal patients
with nausea, weight gain, vaginal dryness or discharge. A 24% reduction in mortality in node-positive
patients aged less than 50 years following oophorectomy have been noticed.
Although there is a temptation to combine adjuvant chemotherapy with tamoxifen, there is no evidencr
that their effects are additive. In fact tamoxifen inhibits the action of chemotherapy.
THE BREAST 615
Adjuvant tamoxifen is given for a minimum of 3 years and it is quite free from toxicity, though
venous thrombosis, ophthalmologic complications and slightly increased incidence of endometrial cancer
have been recorded. Under no circumstances therapy should exceed doses more than 20 mg and in excess
of 5 years. Tamoxifen should better be given to women whose tumours are positive for hormone receptors.
It should not be routinely recommended for hormone receptor negative tumours.
Other hormonal agents are also being tried. The notable amongst these is Zoladex — a luteinizing
hormone releasing hormone antagonist. Its effect is same as chemical oophorectomy and has the same
beneficial effects as surgical oophorectomy or irradiation oophorectomy in premenopausal women. In
surgical oophorectomy laparoscopic techniques may be used.
In case of node-negative patients, tamoxifen reduces the clinical incidence of contralateral primary
breast cancer.
Radiotherapy.— Radiotherapy following mastectomy is only used in extensive local disease with
infiltration of the chest wall. After conservative surgery radiotherapy to the remaining breast tissue was
used as a routine procedure, but there is doubt whether all patients should receive such therapy or not.
This adjuvant radiotherapy is not without morbidity. Moreover majority of these patients may not develop
local recurrence. So at present, only patients with higher risk of local relapse and those with extensive
carcinoma or carcinoma at the margins of excision should be offered postoperative radiotherapy.
Breast carcinoma in pregnancy and lactation.— The prognosis of breast carcinoma in pregnancy
and lactation is poor. It has been shown that those women treated for breast cancer during the 2nd half
of pregnancy did significantly less well than those treated in the 1st half of pregnancy or in the 1st six
months postpartum. The following should be the mode of treatment for breast carcinoma in pregnancy
and lactation — (a) In 1st half of pregnancy carcinoma should be treated with radical mastectomy without
radiation or interruption of pregnancy, (b) When breast carcinoma is identified in the 2nd half of
pregnancy, small lesions are not treated until after delivery. If rapid growth occurs or if the lesion has
already reached stage III, pregnancy is terminated, lactation is suppressed and the breast tumour is then
treated, (c) When cancer is discovered during lactation it is treated in the usual manner after suppression
of lactation.
It must be remembered that patients below 35 years of age should be encouraged to be pregnant
after a minimum one year interval following treatment for breast cancer. It is a revealed fact that those
who had subsequent pregnancies following treatment for breast cancer had significantly better 10 year
survival rate than those who did not become pregnant following mastectomy. This may be due to the
interruption in the oestrogen stimulation process, as in pregnancy oestrogen level becomes lower than
in non-pregnant state.
Bilateral breast cancer.— It has been observed that 9% of patients with radical mastectomy develops
a second primary in the opposite breast within 10 years. After treatment of primary breast cancer
approximately 1% of patients develop detectable breast cancer in the opposite breast each year. Yearly
mammogram, frequent physical examinations are essential to detect such bilateral disease. When detected
the treatment is almost same as the primary treatment. For cosmetic reason one can always consider total
mastectomy of the opposite breast with or without insertion of a silastic prosthesis.
MANAGEMENT OF ADVANCED CASES OF BREAST CANCER

Late stages of breast cancer are often accompanied by distressing symptoms. Those of greater
frequency are misery of extensive ulcerating local disease, metastases in bone and dyspnoea from lesions
in lungs. At this stage, effective palliation is essential. Admittedly, there is a wide choice of methods,
but in this section, only available methods of treatment will be described.
Once breast cancer has spread outside the confines of the breast and regional lymph nodes, it cannot
be cured. Stage III and Stage IV breast cancers are usually considered in this group. These cancers,
although not curable, can be offered palliative therapy.
LOCALLY ADVANCED CANCER (STAGE III).— Locally advanced tumours are defined as those
with more than 5 cm in diameter or those with fixed axillary nodes in which there is no evidence of
distant metastasis. In other words locally advanced breast cancer means a very large primary lesion with
or without extensive nodal disease but having no detectable systemic metastasis. Locally advanced breast
cancer corresponds to stage III as defined by AJCC-UICC classification system.
Stage Tumours Nodes
IIIA Nl, N2
fflB N3
any N
Thus locally advanced breast cancer encompasses a heterogenous group of tumours ranging from
a large fungated mass in the breast to a very small mass in the breast with large and fixed axillary lymph
nodes. Locally advanced breast cancer is associated with poor prognosis and high local recurrence rate.
Surgery alone is considered inadequate and multimodality treatment comprising chemotherapy, surgery
and radiotherapy is advocated as the treatment of choice. Management of these cancers is somewhat
disappointing because of poor local tumour control and high incidence of subsequent metastatic disease.
The overall survival rate is less than 20%. There is probably little to choose between mastectomy and
primary irradiation in the management of such cases. A combination of the two may produce improved
local control. There are two principal objectives for the management of locally advanced breast cancer
— (a) To achieve local control and (b) To prevent or delay the distant metastasis. Recently there has
been enthusiasm for using adjuvant chemotherapy in these patients. Combination chemotherapeutic agents
e.g. cyclophosphamide, adriamycin and 5-fluorouracil have effected dramatic regression of the breast
lesion in approximately 60% to 75% of these patients. There is even disappearance of axillary metastasis
in certain cases. After 6-drug cycles, an extended simple mastectomy (inclusive of level I nodes) is
performed to remove residual malignant disease in the chest wall. This is followed by comprehensive
radiation therapy. After this multimodal therapy 5 and 10 year survival rates are reported as 45% and
28%. Median life expectancy of patients with Stage IV breast cancer is only 24 months.
Surgery.— It is mainly reserved for the removal of primary breast tumour. Mastectomy appears to
be the appropriate initial treatment and use of breast-preserving procedure is not recommended. Even
if metastases are present, the persistence of a tumour mass cause additional misery from ulceration or
fungation. In these circumstances, operation is aimed at removal of the breast, containing its tumour.
For the relief of functional disturbance resulting from deposits of the tumour in the abdominal cavity
or spinal canal, surgery may be indicated. Sometimes acute intestinal obstruction may require bypass
operation or impending paraplegia may require a laminectomy, decompression and spinal fusion oper
ation.
The major types of modalities which are in current use for palliation in advanced carcinomas of
the breast are (i) Endocrine therapy, (ii) Chemotherapy and (iii) Radiotherapy.
(i) ENDOCRINE THERAPY.— One of the most important discoveries that has improved the
outlook of patients of breast cancer is the identification of hormone receptors in tumour tissue. Those
tumours which have hormone receptors, response rate to endocrine treatment is more than 50%.
Tamoxifen appears to be the agent of first choice in these patients.
(ii) CHEMOTHERAPY.— Recent trend is to treat these advanced breast cancers with chemotherapy
first. Two types of combination chemotherapy are being used recently — either cyclophosphamide,
Methotrexate and fluorouracil (CMF) or cyclophosphamide, doxorubicin (adriamycin) and fluorouracil
(CAF). These combinations are standard care as the first attack on advanced breast cancer. Cyclophos
phamide, which is a prototype alkylating agent and doxorubicin, which is an anthracycline antibiotic,
considered to be the most active single agent in present days. With this chemotherapy a remission rate
of 50% has been noticed. The basis of chemotherapy is that one must consider the possibility of
THE BREAST 617
micrometastasis which may have developed in these advanced carcinomas.

For some patients who have troublesome local relapse of disease after combined chemotherapy, the
surgeon may be able to salvage the local problem by performing mastectomy. Due to skin involvement
it is necessary to take an extensive area of skin in excision, so that primary closure, even after undermining
the edges, may not be possible. Under these circumstances skin cover can be achieved with either split
skin graft or with a rotational myocutaneous flap.
Management of relapse after adjuvant chemotherapy is as follows :— If the relapse is regional, the
first treatment would usually be tumour excision followed by radiotherapy. For those who develop distant
recurrences, the disease-free interval is an important indicator of the aggressiveness of the disease. If
the disease-free interval is 2 years or more, it is worthwhile giving a trial of endocrine therapy which
is comprised of ovarian radiation or oophorectomy for those still menstruating and tamoxifen (gonadot
rophin releasing hormone analogue) for the postmenopausal. Should the interval be less than 2 years
it is unlikely that there will be response to endocrine therapy, but this may still be tried in those in whom
there is no life threatening disease e.g. lymphangitis carcinomatosa, liver metastases or brain secondaries,
which require chemotherapy.
In patients whose advanced disease responds to chemotherapy the optimal duration of treatment is
unknown, but 6 months is reasonable. Prolonging the course of chemotherapy leads to more toxicity,
but has no impact on survival. There is also no place for maintenance chemotherapy in those who have
had a complete remission of disease.
(iii) RADIOTHERAPY.— Solitary, locally recurrent tumour is best treated with radiotherapy of a
small field. In many cases this simple treatment suffices. Recurrence in multiple intracutaneous areas
of chest wall, which is so popularly referred to as cancer-en-cuirasse, is well treated by superficial beam
treatment particularly by electrons. Osseous metastasis is particularly well treated with a short course
of radiotherapy of 2,000 R over 3 to 5 days. Relief of pain, stabilisation of damaged bone and prevention
of pathological fracture are noticed. When pathological fracture takes place, internal fixation with
endocrine therapy and aggressive local radiotherapy are very effective palliative measures to bring back
function. However in T4 cases or inflammatory carcinomas, initial aggressive chemotherapy is recom
mended and after chemotherapy response is achieved, total mastectomy, radiotherapy, followed by more
chemotherapy is advised. If initial chemotherapy response is not enough after 2 or 3 courses, only
radiotherapy to the breast is advised. In case of brain metastases from breast cancer, radiotherapy is the
only effective means of palliation. High doses of corticosteroids are given in these cases with the beginning
of radiotherapy to reduce brain oedema.
SPECIFIC PROBLEMS IN ADVANCED DISEASES.—
Bone metastases.— Among the patients who develop relapse of breast carcinoma, about 30% will have bone
metastases. Some of these metastases are asymptomatic. However bone metastases can produce pain, pathological fracture,
spinal cord compression and hypercalcaemia. Its of no use carrying out routine bone scans on asymptomatic women being
followed-up after treatment for breast carcinoma. However patients complaining of skeletal symptoms should have these
areas X-rayed together with radioisotopic bone scan.
Treatment of localised painful lesion is by external radiotherapy in order to relieve pain and to prevent further bone
destruction. Lytic bone metastasis in weight bearing bone such as the femur require careful evaluation to determine how
extensive the cortical damage is, since some will benefit from prophylactic pinning followed by radiotherapy in order
to prevent pathological fractures. Reversal of osteolysis has been obtained by radiotherapy. There is evidence that
subsequent progression of bone metastasis can be reduced with biphosphonates. Disodium dichloromethylene diphosphonate
(clodronate) in the dose of 1600 mg/day when administered between 3 and 9 months there is considerable reduction in
the incidence of hypercalcaemia and subsequent skeletal fractures in these patients. Similarly incidence of new metastases
or fractures is also reduced. Moreover there is hardly any side affect. Thus there is a place for clodronate in the palliation
of women with bone metastases.
Brain metastases.— This type of relapse is particularly distressing and usually carries a poor prognosis. Presenting
symptoms include headache, nausea and vomiting fits, paresis and incoordination. Clinical examinations may reveal
evidence of papilloedema with localised central nervous system signs.
Treatment is immediate reduction in cerebral oedema with steroids (dexamethasone 4 mg 4 times daily). The diagnosis
and extent of intracranial disease are confirmed by computed tomographic (CT) scan. Cranial irradiation in short
course is the treatment of choice. Only in rare circumstances surgery may be needed in the form of removal of isolated
cerebral metastasis. Carcinomatous meningitis may occasionally occur causing symptoms of confusion, headache,
nerve root pain or cranial nerve palsy. These cases respond to radiotherapy, but the place of intrathecal chemotherapy
is still controversial. Vertebral bone metastases may cause spinal cord compression giving rise to backache, girdle
pain, limb weakness or even bladder dysfunction. The diagnosis may be confirmed by Magnetic Resonance Imaging
(MRI). After initial steroids, radiotherapy is the main treatment. Occasionally surgical decompression and spinal
stabilisation may be required.
Pleural effusion.— Pleural effusion is a common problem in patients with metastatic breast cancer. In about Vi of
these cases this is the first evidence of recurrence. Patients with pleural effusion usually complain of shortness of
breath, sometimes associated with cough. There may be a dull chest pain and occasionally pleuritic pain. Clinical
examination reveals dullness on percussion and reduced air intake over the lung base on the affected side. An opacity
in chest X-ray may be noticed. Confirmation of diagnosis is made by needle thoracentesis taking enough fluid for
cytological evaluation. Cytological evidence of malignant cells is noticed in approximately 60% of patients. If a
pleural biopsy is performed about 7% to 8% more cases will be confirmed as having metastatic disease. Thoracoscopy
may be of value in confirming the presence of metastasis with parenchymal deposits being identifical in upto 60% of
patients with negative fluid cytology.
Firstly the effusion should be drained to dryness, secondly an effective agent should be instilled (to achieve
pleurodesis) and finally the parietal and visceral pleura must be apposed so that a fibrous reaction can occur. The agent
which is most effective is the talc, which is insufflated after drainage under general anaesthesia and an intercostal drain
is left in place for 5 days. Effusion is controlled in more than 90% of patients. If the patient is too ill to undergo general
anaesthesia, tetracycline (500 mg) can be instilled under local anaesthesia. Only in extreme rare cases, where pleurodesis
may fail due to presence of loculation of effusion, may be benefited from decortication, though it carries a mortality
rate of 5%.
Ascites.— Development of ascites is a relatively uncommon event and the prognosis depends upon whether it is
the result of hepatic metastases or of peritoneal seedlings. Those with hepatic metastasis show poorer prognosis.
In the absence of hepatic metastasis, a first-line diuretic should be tried. If this does not relieve symptoms, para
centesis should be performed. Only in selected cases insertion of peri toneovenous shunt may help in relieving abdomi
nal distension.
PALLIATIVE CARE.— Pain relief is the prime aim in patients with earlier symptoms of advanced breast cancer.
Simple analgesics e.g. paracetamol and aspirin should be given to those with mild pain. Moderate pain will require
nonsteroidal anti-inflammatory drugs e.g. piroxicam, naproxen and diclofenac. If such agents cannot control the pain,
morphine sulphate slow-release tablets should be given together with antiemetics. Diamorphin continuous infusion
may be valuable in the terminal stages of the disease.
Followings are the modes of treatment in various problems of advanced breast cancer —
Problems Treatment
Regional or local recurrence Local radiotherapy.
Skeletal pain Analgesics + Radiotherapy.
Dyspnoea with effusion Intercostal drainage + intrapleural cytotoxic drugs.
Hepatic metastasis Adequate endocrine therapy with corticosteroids.
Hypercalcaemia Corticosteroids, Calcitonin and Phosphates.
Paralysis from cord compression Emergency laminectomy.
BREAST RECONSTRUCTION
Breast reconstruction is now regarded as an integral part of breast cancer management and is requested
with increasing frequency by informed women at the time of mastectomy.
Over the last 35 years a variety of techniques have been described e.g. silicone implants, lattissimus
dorsi (LD) myocutaneous flaps, transverse rectus abdominis myocutaneous (TRAM) flaps and tissue
expanders.
Immediate versus delayed reconstruction.— Approximately 40% of breast reconstruction in the U.S.
is now performed at the time of mastectomy. The advantages of immediate breast reconstruction (IBR)
outweigh the disadvantages in most patients. The advantages are — reduced hospital stay, reduced cost,
reduced disability, reduced time off work, reduced scarring, easier axillary dissection, patient’s
THE BREAST 619
convenience and better reconstruction with improved cosmesis. IBR is unsuitable for ‘high risk’ patients
with obesity, diabetes and smoking habits. Another disadvantage is the time-frame for decision making,
which is short. Complications may be revealed later causing delay in adjuvant treatment. Moreover the
procedure of IBR is lengthy (3 to 6 hours) and require speciality training to achieve good results.
Choosing the technique.— Implants or expanders may be used alone (e.g. subpectoral reconstruction)
or in combination with autologus tissue (e.g. LD flap). Reconstruction using autologus tissue alone, either
as a pedicle flap or a ‘free’ flap (e.g. TRAM flap) provides a third alternative. The world-wide popularity
of expanders implant reconstruction is related to the speed and apparent simplicity of this approach, which
has no donor site morbidity and requires a short hospital stay and little convalescence. Following subpec
toral placement of tissue expander, the breast mould is created by repeated outpatient expansion introduc
ing saline through a remotely-sited or integral injection port. Capsular contraction can be reduced by using
modern texture prosthesis.
Modern breast implants are manufactured with an outer shell of polydimethylsiloxane (silicone) and
contains a ‘filler’ material such as silicone gel which gives the implant its volume. A recent wave of
adverse publicity that silicone is both immunogenic and carcinogenic are unfounded. Some small amounts
of silicone gel ‘bleed’ through the shell of all implants into the surrounding tissues. This sets up a fibrous
reaction which may sometimes lead to ‘adverse capsular contracture’ (ACC) with hardening, distortion and
discomfort which may be bad enough to require treatment by open or endoscopic capsulotomy in some
patients. This implant is widely used in U.K.
1. Reconstruction with subcutaneous or subpectoral implant.— This is the easiest technique to perform. The
subcutaneous technique is often condemned as it frequently causes skin necrosis and extrusion. When inserting the
implant subpectorally care must be taken to ensure that the prosthesis is in an appropriate position. There is a tendency
of such implant to migrate superiorly, so it is necessary to divide the fascial bands between the insertion of pectoralis
muscle and the rectus abdominis. The main problem is the formation of a capsule, which is unsightly and imparts hard
texture to the breast. Capsule formation is less common if ‘texture’ implant is used. The second problem is the lack of
ptosis which occurs in normal breast. The technique of tissue expansion may be used to overcome this problem. The
Becker expander consists of an outer lumen filled with silicon gel and an inner chamber filled with saline with self
sealing side port. This inner chamber with saline is gradually expanded to the desired volume over a number of weeks.
Once expansion is complete the saline chamber is aspirated to allow creation of a reconstructed breast of similar
volume to that of the opposite side alongwith providing some ptosis. The self-sealing side port is then removed under
local anaesthetic. Most implants in current use are made of silicon gel. This material is inert and has a natural feel.
The most commonly adopted technique has been the pedicled lattissimus dorsi myocutaneous flap due to its
proximity and good blood supply. This technique may be combined with an implant. The more recent innovation has
been the rectus abdominis myocutaneous flap. A longitudinal or transverse incision may be used. Majority surgeons
now prefer to use transverse rectus abdominis flap. A few surgeons even use free transverse rectus abdominis flap with
microvascular anastomosis between epigastric and thoracodorsal vessls. Unfortunately it is time-consuming proce
dure which requires specific expertise with microvascular anastomosis.
2. Pedicled or free myocutaneous flap.— One of the two types is usually applied — latissimus dorsi
myocutaneous flap (LD-flap) or transverse rectus abdominis myocutaneous flap (TRAM-flap).
In contrast to prosthesis reconstruction, these autologus techniques are complex and more expensive
procedures which require comprehensive training and experience.
Lattissimus dorsi myocutaneous flap is used mainly in pedicle form and often used due to its proximity
and good blood supply. This technique may be combined with an implant. It is a versatile and reliable
method which results in a ptotic breast. In this technique abdominal weakness is avoided as may occur in
TRAM-flap reconstruction. Complications are mainly related to donor site morbidity including pain, seroma
formation and scarring. Most patients need additional implant/expander. ‘Autogenous’ LD reconstruction
may be considered for small breast cancer in women who have enough dorsal skin and subcutaneous tissue
to create a flap with sufficient volume to replace the breast without the need for a prosthesis.
The TRAM-flap is based on a transversely-sited lower abdominal island of skin and fat, supplied by
perforators arising from the superior and inferior epigastric vessels. Divisions of the inferior epigastric
vessels allow elevation and transposition of the flap, attached to one or both superior epigastric pedicle,
depending on the size of the flap required. Rectus muscle is taken with each pedicle to improve the circu
lation and reduce the likelihood of flap necrosis. Though a longitudinal or transverse incision may be used
for this flap, majority surgeons now prefer to use transverse rectus abdominis flap and hence known as
TRAM-flap. Modern TRAM-flap reconstruction results in a soft natural and ptotic breast and avoids the
need for additional prosthetic volume replacement. Excellent cosmetic results are achieved at the expense
of 5 to 7 days hospital stay, a 4 to 6 weeks convalescent period and an overall complication rate of 16% to
28%. Major complications include abdominal weakness, abdominal herniation and flap loss. Weakness
resulting from bipedicle reconstruction can be avoided by the use of free TRAM-flaps in those patients
unsuitable for single-pedicle procedure. After separating the flap from its native blood supply and transpo
sition into the empty breast pocket, circulation of the flap is re-established by performing a microvascular
anastomosis between the inferior epigastric and the thoracodorsal or internal mammary vessels.
SARCOMA OF THE BREAST

There are various sarcomas which may be found in the breast such as liposarcoma, rhabdomyosarcoma
fibrosarcoma, haemangiosarcoma and lymphosarcoma but these are rare. Cystosarcoma is the most com
mon sarcoma found in the breast. These cystosarcomas may arise from soft (intracanalicular) fibroad
enoma. Histologically spindle cells outnumber any other form of cells.
CLINICAL FEATURES.— Usually 40 to 50 years of females are affected. Cystosarcomas are usually
slow growing tumour and present as a large lobular mass in the breast. On INSPECTION a huge mass can
be seen in the breast. The overlying skin is tense, red with dilated veins. Absence of skin retraction, skin
dimpling and Peau d’orange are obvious. On PALPATION the big mass is much softer in feel than scirrho
carcinoma. Consistency may vary in different places of the tumour. Skin is absolutely free from invasion.
There may be ulceration in the skin through which the tumour may fungate, but this is not due to invasion
into the skin. The tumour is so big that the skin overlying the tumour is stretched and ultimately gives way
A probe may be passed between the ulcerated skin margin and the tumour which is not at all possible had
the tumour infiltrated the skin. The tumour is also free from the underlying structures and it can be movab
along the direction of the fibres of the pectoralis major after this muscle is made taut. Axillary lymph node
involvement is quite late.
Spread of sarcoma.— 1. Like other sarcomas anywhere in the body the spread is mainly through the
blood.
2. Local infiltration is the next type of spread, but it is much less in degree than scirrhous carcinoma.
Local recurrence has been noted after inadequate excision.
3. Lymph spread is rare and very late.
TREATMENT.— Wide local excision in the form of total mastectomy followed by radiotherapy is the
treatment of choice. The tumour should always be sent for histopathological report. In case of small tumou
one may get away with total mastectomy but perform wide excision of the tumour with 5 cm of healthy
tissue around. If local recurrence occurs surgical reexcision in the form of total mastectomy and radio
therapy should be the treatment of choice.
Prognosis.— Prognosis of all sarcomas of the breast are relatively good than other sarcomas in the
body. Only the prognosis of angiosarcoma is worse as it tends to early blood-borne metastasise to the lung
621
CHAPTER - 32
INJURIES OF THE CHEST
Two types of injuries of the chest may be seen — closed and open. In civil practise chest injuries occur
usually from road accidents and stab or gun-shot wounds. In war, of course, chest injuries are more common
and it usually constitutes 10% of all wounds and 25% of those killed in battle. Injuries of the chest may often
be associated with injuries elsewhere, particularly the head, abdomen and the limbs. Chest injuries should
always get priority in the treatment in case of multiple injuries.
FRACTURE OF THE RIBS

Incidence.— Fracture of the ribs usually occurs in closed injuries of the chest. One or more ribs may be
involved. 1st and 2nd ribs are rarely fractured as they are protected by the clavicle. The 11th and 12th ribs are
also rarely fractured as they are floating. Fracture of the ribs is occasionally seen in children as their ribs are m
flexible and elastic.
Types of trauma.— As mentioned earlier fracture of the ribs usually occurs from closed injury of the chest.
The various types of trauma which may cause fracture of the rib are :—
1. Direct trauma.— When chest is struck against a hard object fracture of rib may occur at the site of
trauma. This usually fractures one rib, but two or more ribs may be fractured.
2. Crush injury — This injury is often caused by road accidents and aeroplane accidents. Multiple ribs
may be fractured and the fracture usually occurs at the site of maximum curvatures in a single rib i.e. at the
anterior and/or posterior angles of the rib. So multiple ribs are fractured in two sites. This usually causes ‘ sto
in’ chest or flail chest.
3. Steering-Wheel injury.—This occurs in head-on car accidents in which there is fracture or dislocation
of the upper end of the sternum and bilateral fractures of the ribs at their anterior ends or at the costo-chondra
junctions. Such injury may be prevented by wearing seat belts.
4. Minor trauma.— When the ribs become rigid in elderly individuals, a paroxysm of cough may cause
fracture of rib.
Uncomplicated rib fracture.— Sometimes fracture of the rib is not associated with any complication. The
main complaint of the patient is pain while taking a deep breath in. The pain is also exaggerated during cough
or sneezing.
On INSPECTION, nothing characteristic may be seen except presence of a slight bruising.
On PAT PATTON, local bony irregularity, tenderness and crepitus are the findings of a fractured rib. The
clinician should run his finger along each rib in the region of injury to reveal local bony tenderness. The
‘compression test' is usually positive. The patient stands with both hand on the head and the clinician places
the base of one hand on the sternum and the other hand on the spine and thoracic cage is compressed
anteroposteriorly. The patient experiences pain if any rib is fractured. This is ‘compression test.’
X-ray is usually confirmatory, but it may miss a hair-line crack fracture.
TREATMENT.— The main aim of treatment is to reduce pain, as the fracture heals by itself and does not
require any special treatment for it.
1. Systemic analgesics may be administered orally or by injections every 6 to 8 hours on first 2 or 3 days.
Various analgesics may be tried. Pentazocine has now become very popular in this respect, though it has got
some respiratory depression effect besides analgesia and sedation. Fortwin, Fortagesic and Foracet are the
various available trading drugs containing this product, Acetyl salicylic acid is an old good drug. Micropyrin
and Disprin are the drugs with this pharmacologic preparation. Paracetamol and analgin are also good in this
respect.
2. Local injection.— Analgesics may be injected locally at the fracture site to reduce pain during
respiration. Local anaesthetics particularly the long acting ones e.g. injection Marcaine may be instilled locally
at the fracture site.

Intercostal nerve block.—The intercostal nerves of the affected ribs may be blocked at the posterior axillary
line with long-acting local anaesthetic agents. The nerves just above and below the fractured ribs should als
be blocked in this procedure. It is quite useful in case of persistent pain.
3. Strapping of the chest by immobilising the fractured ribs was a very popular treatment previously du
to its immediate action to relieve pain. But the disadvantages of this strapping treatment are that (a) it dimini
normal respiratory movement, which is more damaging in case of elderly people and (b) it may force the br
rib ends inwards to cause damage to the underlying structures. Such strapping is applied at the phase of fu
expiration. The strapping must include 2 ribs above and below the fractured ribs and the strapping must cr
midline both anteriorly and posteriorly. Elastic corset may be applied as strapping. Local strapping may als
be applied on the affected side only to get away with its disadvantages. It may be advised in case of young
and children.
Complications of fracture of the ribs.— Complications particularly occur when more than 1 ribs are
fractured or more so when ribs are fractured in 2 places. The complications may be described under 2 heads
A. General complications and B. Local complications.
A. General complications.—
Shock (mainly hypovolaemic due to other injuries in the body and neurogenic shock).
B. Local complications.—
1. Surgical emphysema.
2. Traumatic pneumothorax.
3. Traumatic haemothorax.
4. Stove-in chest and flail chest.
5. Pulmonary contusion and laceration.
6. Injury to the heart and pericardium.
7. Traumatic asphyxia.
8. Injury to the diaphragm and diaphrag
matic hernia.
9. Injury to the subdiaphragmatic organs e.g.
liver, spleen, kidneys, colon and stomach.
SURGICAL EMPHYSEMA — This simply
means air in the subcutaneous tissue. It is also called
‘subcutaneous emphysema’.
MECHANISM.— The fractured ends of the
ribs are forced in due to the injuring force and injure
the underlying lung, through which air comes out
into the muscles and subcutaneous tissue of the
chest wall. The fractured ends of the rib move back
to their normal positions and the rent in lung is
sealed off. If the rent in the lung persists, it is called
traumatic pneumothorax. Surgical emphysema
should not be confused with mediastinal emphy
sema, which is a sequel of rupture of the bronchus
or oesophagus and in this condition emphysema is
first noticed in the neck.
CLINICAL FEATURES.—The patient mainly
complains of pain in the chest due to fractured ribs.
Fig.40.1.— A case of surgical emphysema due to On inspection, one may find bruised skin due to
laceration of the right lung from rib fracture. trauma. The affected area around the fractured ribs
INJURIES OF THE CHEST 623
may be seen slightly swollen with air. Such swelling may extend into the neck or to the upper limb of the
corresponding side.
Palpation is important as it will elicit typical crepitus of surgical emphysema.
Percussion may elicit resonant note due to presence of surgical emphysema.
Auscultation reveals the crepitus of the emphysema and there may be absence of breath sounds due to
associated pneumothorax, if present.
X-ray is confirmatory and (i) it will reveal not only fracture of the ribs but also (ii) presence of air in the so
tissues superficial to the fractured ribs (surgical emphysema), (iii) There may be associated pneumothorax
which will also be revealed in X-ray.
OTHER CAUSES OF SURGICAL EMPHYSEMA.—
(i) In case of extraperitoneal injuries of the ascending or descending colon or rectum there may be surg
emphysema in the loin.
(ii) In case of ruptured oesophagus or bronchus there will be mediastinal emphysema, in which air is fir
detected in the subcutaneous tissue of the neck.
(iii) In fractures of the paranasal sinuses, one may get surgical emphysema in the face.
(iv) In extreme occasional cases one may find localised emphysema in the subcutaneous tissue following
thoracic or abdominal incisions.
TREATMENT.—
1. Surgical emphysema itself does not require any treatment as air is usually absorbed from the
subcutaneous tissue.
2. Treatment of fractured rib should draw the attention of the surgeon.
3. One must carefully assess if any of other complications following fracture of ribs has occurred. Such
complications should be treated properly.
4. Traumatic pneumothorax often associates surgical emphysema and a water-seal drain has to be mad
with an intercostal needle inserted through the 2nd intercostal space.
TRAUMATIC PNEUMOTHORAX.— Air in the pleural cavity is called ‘pneumothorax’ and when it is
due to trauma it is called ‘traumatic pneumothorax’. In majority cases of trauma blood is associated with air
the pleural cavity and then it is called haemopneumothorax. Some thoracic surgeons prefer to use this doub
term only when there is sufficient blood in the pleural
cavity which requires removal or loss from the circulating
fxpG.55Cl.CjG volume requires transfusion replacement.
of
There are 3 types of traumatic pneumothorax —
1. Closed pneumothorax.— When air comes out
in the pleural cavity through a small rent in the lung due to
trauma with fractured ends of the ribs and when such rent
is subsequendy closed, it is called ‘closed pneumothorax’.
2. Open pneumothorax.— Air may enter the pleu
ral cavity through a wound in the chest wall and this is
called open pneumothorax. This may be of 2 types—suck
ing or non-sucking variety. When with every inspiration
air is sucked into the pleural cavity, it is called ‘sucking
pneumothorax’.
3. Tension pneumothorax.— When the lacerated
Tij-p(zs o f p iin\otKorax
tvq
lung communicates with abranch of the bronchial tree, this
permits air to enter the pleural cavity from the lung during
Fig.40.2.— Diagrammatic representation of two types inspiration, but does not permit it to escape during expira-
of pneumothorax. A.— Tension pneumothorax and tion as the lcflk in the lung bccomes elosed, SO the rent
B — Open pneumothorax. See the text. becomes ‘valvular*. This condition is called ‘tension pneu-
othorax’. This causes collapse of the lung of the affected side. This displaces the mediastinum to the healthy
de, depresses the diaphragm and compresses the opposite lung due to mediastinal shift to the opposite side.
CLINICAL FEATURES.—Pneumothorax as a whole is easily recognised by varying degrees of dyspnoea,
n, shock and cyanosis. Hyperresonance on percussion note and absence of breath sounds on auscultation are
the two important findings of this condition. In case of tension
pneumothorax there will be shift of trachea and apex beat
towards the opposite side. X-ray is obviously confirmatory.
TREATMENT.—
1. Closed pneumothorax.— Usually closed pneumo
thorax is steadily absorbed and the lungs subsequently re-
expand. The time required for this normal resorption, of course,
depends on the size of the pneumothorax. If the pneumothorax
is embarrassing normal respiration, air should be evacuated from
the pleural cavity by direct aspiration or by pushing an intercos
tal tube through the 2nd intercostal space anteriorly. .
2. Open pneumothorax.— Treatment of this condition
is closure of the wound in the chest wall as soon as possible. This
may be done with a piece of gauze covered with elastoplast or
Fig.40.3.— Shows more clearly how tension by skin stitches. At a later date proper exploration of the wound
pneumothorax takes place. Note the tracheal and debridement is carried out. If at all a thoracotomy incision
shift to the opposite side. isrequireditshouldbedone through the wound ofthechest wall.
3. Tension pneumothorax.— This requires immediate surgical intervention as the condition is fatal. A
wide bore needle is inserted into the pleural cavity through 2nd intercostal space 1 */2 inches lateral to the st
to avoid injury to the internal
mammary artery. This needle
is soon replaced by a self-re
taining tube. To introduce such
tube, a small stab incision is
made at the same spot under
local anaesthesia. The tube is
introduced with the help of a
trocar and a cannula. This tube
is connected to a water-seal
drainage. The tube is kept in
Fig.40.4.— Showing the mechanism of mediastinal flutter and paradoxical respira situ so long as the radiological
evidence of full lung reexpan
tion. In the first figu re, the opening in the chest wall is large, the lung of the affected
side shrinks during inspiration as the air rushes into the pleural cavity through open sion is obtained. If leakage of
wound pushing the mediastinum towards the healthy side pressing upon the
unaffected lung whose aeration is also imparted. In the second figure, during air continues even after 5 days,
expiration, the mediastinum is pushed towards the affected side with air rushingafrom thoracotomy should be per
the good lung to the affected lung. This side-to-side movement of the mediastinum formed to deal with the rent in
is known as ‘mediastinal flutter’ and since the heart and the great vessels are
implicated, it leads to shock with a rapid pulse.
the lung tissue.
During inspiration the affected lung collapses and during expiration it TRAUMATIC HAEM-
expands, i.e. reversal of the normal process. This is referred to as paradoxical OTHORAX.— This means
respiration’. It is more evident from outside in a case of ‘flail chest’ when multipleaccumulation
ribs of blood in the
are fractured at two places.
pleural cavity due to trauma to
the chest. The blood comes from (i) either from the contusion of the lung or (ii) injury to the parietal vessels
(intercostal or internal mammary vessels) or (iii) rupture of intrapleural adhesion or (iv) injury to the heart a
great vessels. Although haemothorax develops at the time of injury in most patients, yet it may be delayed fo
several days. Movement of the diaphragm and thoracic structures cause partial defibrination of blood that is
into the pleural cavity, so the blood remains liquid for a considerable period without being clotted in the ple
cavity. Pleural enzymes begin to produce clot lysis within a few hours after bleeding stops. If not aspirated
early, a deposition of organised fibrin will prevent proper expansion of the lung.
CLINICAL FEATURES.— The symptoms are more or less similar to those of pneumothorax. Physical
signs are those of presence of fluid in the pleural cavity. Dullness on percussion, weak breath sounds, impair
vocal resonance and shifting of apex beat to the opposite side are the features of fluid in the pleural cavity. X
ray is confirmatory and it requires about 400 to 500 ml of blood to be collected for detection in skiagraphy.
TREATMENT.— In one sentence the treatment consists of transfusion to restore blood volume, aspiration
of blood from the pleural cavity and to sedate the patient.
1. Small haemothorax requires simple aspiration. If bleeding recurs, repeated aspirations may be
required everyday. After each aspiration it is a good practice to instil 10 lacs units of penicillin into the pleur
cavity to prevent secondary infection. Aspiration should be continued till X-ray shows full expansion of the
lung.
2. Tube drainage.— Removal of blood from the chest relieves pressure and encourages rapid lung
reexpansion, at the same time this prevents bacterial growth in stagnant fluid. This may be done most effecti
by insertion of an intercostal catheter in the midaxillary line through the 7th or 8th intercostal space. A 2nd tu
may be inserted through the 2nd intercostal space anteriorly if there is an associated pneumothorax. These tu
should be connected to an under-water-seal drainage. The volume of blood draining into the under-water-se
jystem is measured at frequent intervals. This gives not only an indication of the amount of bleeding, but als
the amount of the blood to be transfused intravenously.
3. Thoracotomy.— If haemothorax clots, so that tube drainage becomes impossible or haemothorax
becomes infected, thoracotomy is required.
Indications for thoracotomy are — (a) Bleeding continues as determined by the signs of internal
haemorrhage or if bleeding occurs in the order of 200 ml of blood per hour as coming out through the interco
tube, (b) A large haemothorax exists but intercostal tube drainage is not clearing it properly because of const
blockage by fibrin clot and (c) the haemothorax has become infected.
The operation is performed with endotracheal anaesthesia through the 5th or 6th intercostal space. The
pleural cavity is cleared of fibrin, blood clots and effusions by mop and sucker. Sometimes a dense envelop m
be seen to cover the lung, which does not allow the lung to inflate to the full extent. This envelop is removed
by careful dissection, the process of which is known as decortication. The lung will be seen to re-expand. The
chest is closed in layers leaving a drainage connected with a water-sealed bottle. Drainage is continued till th
radiograph shows the lung to be fully expanded.
STOVE-IN CHEST and FLAIL CHEST.— For practical purposes the two terms ‘stove-in chest’ and
‘flail chest’ are often used synonymously, but there is difference between these two terms.
STOVE-IN CHEST develops from the extensive localised crushing force which produces multiple rib
fractures. This results in depression of the chest wall in that region. Relative immobility leads to accumulatio
of bronchopulmonary secretion. This condition, if associated with depressed fracture of clavicle, becomes a
serious condition.
FI .ATT. CHEST develops when multiple ribs fracture anteriorly at or near the costochondral junctions and
posteriorly near the angles of the ribs. This results in a fragment of the chest wall which becomes unstable ha
no bony connection. This ‘floating segment’ moves in during inspiration due to negative pressure in the pleu
cavity and moves out during expiration due to positive pressure within the pleural cavity. This results in
paradoxical movement of this floating segment of the chest wall. This is also known as paradoxical respiration,
that means the floating segment moves in the opposite direction as the movement of the normal chest wall. T
very badly affects aeration of the lung and progressive accumulation of carbondioxide. So it ultimately leads
to profound hypoxia accentuated by restriction of breathing produced by severe pain associated with this typ
of injury.
40
Three types of flail chest can be seen —

1. In the lateral type, multiple ribs are fractured anteriorly and posteriorly as mentioned above.
2. In anterior type, the anterior ends of a few ribs on both sides are fractured so that the sternum alongw
the anterior fragments of ribs of both sides becomes the floating segment.
Anterior type Lateral type Posterior type
Fig.40.5.— Types of flail chest. See the text.

3. In posterior type, the multiple ribs are fractured at their posterior angles on both sides, so that th
column along with the posterior fragments of the ribs become the floating segment. The effect of paradoxic
respiration in this case is minimal.
EFFECTS of paradoxical respiration—(i) Itcauses imperfectventilation which leads to profound hypoxia.
(ii) With paradoxical respira
tion, there will be also mediastinal
flutter, in which the mediastinum
will move towards the sound side
during inspiration and moves
towards the affected side during
expiration. As the contents of the
mediastinum are the heart and great
vessels, their movements will lead
to severe shock.
(iii) Due to paradoxical respi
ration a portion of inspired air will
flow back to the opposite healthy
lung during inspiration and the
INSPIRATION
EXPIRATION same air will reach the affected
lung through the bronchi during
expiration. This pendulum move
Fig.40.6.— Paradoxical respiration in case of flail chest. The fractured ribs are ment of air from one lung to the
displaced inwards during inspiration and outwards during expiration. other will lead to stagnation of air
and will diminish the amount of air entering both the lungs considerably.
(iv) Paradoxical respiration will also lead to accumulation of bronchopulmonary secretions due to
tremendous pain and relative immobility of the affected lung.
(v) Post traumatic pulmonary insufficiency or wet lung may also occur due to flail chest.
TREATMENT.— Immediate hospitalisation of these patients cannot be over-emphasised. Administratio
of relaxant drugs (this gives quick relief of pain), passage of an endotracheal tube, insertion of intrapleural dra
and mechanical or manual control of ventilation are the key stones of the management.
1. Modem plastic endotracheal tubes can safely be retained upto 5 days. But minimum 2 to 3 weeks are
required for consolidation of fractured ribs, so tracheostomy at a convenient time is always required.
Tracheostomy is extremely needed in this condition and is considered as ‘routine’ in the management of patien
with flail chest. The utilities of tracheostomy are — (a) it reduces dead space (the unnecessary space between
the nose and the trachea is eliminated), (b) It gives better access for tracheobroncheal aspiration or toileting and
(c) it facilitates internal stabilisation of the chest wall through mechanical ventilation. So if facilities for
immediate tracheostomy are available, it should be done. .
2. Mechanical ventilation is highly effective intreatmentof flail chest. It not only controls and minimises
paradoxical respiration, but it acts as an effective ‘internal pneumatic fixation' of the floating segment.
3. Some sortof fixation of the floating segment becomes essential to stop paradoxical respiration. Various
methods have been advocated for this purpose —
(a) For minor injuries, simple pad and strapping may help.
(b) Even in severe cases, external fixation has worked wonder. In these cases towel clips are placed
round the ribs and traction is applied on these towel clips.
(c) Alternatively the fractured ribs may be secured with the use of stainless steel wire.
(d) Operative fixation of fractured ribs may be required in some cases. A long curved incision is made
over the affected side and the latissimus dorsi and serratus anterior muscles are divided. The pleural cavity is
entered by stripping the upper border of one of the ribs. The clotted haemothorax is evacuated. The bleeding
intercostal or internal mammary arteries are ligated. The flail segment is stabilised by inserting lengths of
Kirschner wire or short Rush nails into the medullary cavities of the ribs. Additional fixation may be achieved
by inserting stout sutures through the intercostal muscles. Finally thoracotomy is closed with tube drainage in
the pleural cavity.
Antibiotics should always be given to combat infection.
TRAUMATIC RUPTURE OF THE DIAPHRAGM.— Rupture of the diaphragm may occur from
penetrating injuries or crush injuries to the lower chest or upper abdomen. The abdominal trauma is more ofte
responsible for rupture of the diaphragm than thoracic trauma. The ratio is 5:2. The crushing injury causes
rupture of the diaphragm due to sudden increase of the intra-abdominal and intrathoracic pressure.
The left hemidiaphragm is ruptured more frequently by blunt trauma than the right and the ratio is about
9 : 1 . The right diaphragm is more protected by the liver, whereas the left diaphragm is weakened in the
posterolateral aspect due to the gap for abdominal aorta and the oesophageal hiatus. If the right hemidiaphrag
is ruptured, the liver is usually the only abdominal structure that herniates through the diaphragm. When the
left hemidiaphragm ruptures, which usually extends from the oesophageal hiatus across the cupula towards th
costal margin, the stomach, the spleen, the left transverse colon and/or omentum may herniate through the
rupture.
In case of penetrating diaphragmatic injuries, the hole in the diaphragm is small and herniation occurs rarel
and slowly.
Immediate diagnosis is the key of successful management of this condition. The first chest X-ray may often
show nothing more than a blurring of the diaphragm with or without evidence of a small haemothorax. Effort
should be made to confirm the diagnosis by contrast studies by pushing air through the nasogastric tube or by
the use of pneumoperitoneum or by radioisotope liver and spleen scans. The only characteristic feature is that
on auscultation of the chest one may hear bowel sounds. The confirmative radiographic picture shows hollow
viscera containing air in the pleural cavity.
TREATMENT.— As soon as the diagnosis is confirmed, a thoracotomy incision is made. The herniated
viscera are put back into the abdomen and the diaphragm is sutured by interrupted nonabsorbable suture
material. Thoracotomy is better as (i) adhesions between abdominal viscera and intrathoracic structures can be
seen easily, (ii) reduction of hernia becomes easier and (iii) repair of the rupture of the diaphragm is technically
easier from this approach.

Laparotomy is only indicated when an associated intra-abdominal injury is suspected.
CONTUSION AND LACERATION OF THE LUNG.— Lungs are often injured in moderate to severe
trauma to the chest wall. PULMONARY CONTUSION is the term used to indicate the consequences of blu
trauma to the lung. It often occurs in rapid deceleration of the chest against an automobile steering-wheel
from a height or in blast injuries. Pulmonary contusion is often associated with fracture of the ribs or stern
The contused lung is characterised by capillary disruption that results in intra-alveolar and interstitial
haemorrhage, oedema, fluid obstruction of small airways and leucocyte infiltration. In chest X-ray a fluffy
infiltrate is seen in the contused lung, which increases in density within a day or two. Unless the contusion
involves only a small region of one lung, it may result in serious depression of respiratory function. Italso
loss of pulmonary compliance. Small areas of atelectasis develop.
Contusion generally results in areas of consolidation and usually resolves spontaneously.
PULMONARY LACERATION represents greater extent of pulmonary contusion.
Injury to the lung is clearly evidenced by haemoptysis. In every case of thoracic injury, the patient must
questioned whether he has coughed up blood or not. Even a small quantity of frothy blood, if coughed up
an indication of injury to the lung. Surgical emphysema is another strong evidence of lung injury. It must be
remembered that besides the common surgical emphysema which is seen on the chest wall, injury to the lu
may result in mediastinal emphysema. The various conditions which may develop following contusion an
laceration of the lung are :—
(i) Haemoptysis.
(ii) Surgical emphysema.
(iii) Mediastinal emphysema.
(iv) Traumatic pneumothorax.
(v) Traumatic haemothorax.
(vi) Atelectasis.
(vii) Persistent collapse of the lung in case of grossly lacerated lung.
(viii) Secondary infection of the damaged lung.
TREATMENT.—The extent of lung damage can be assessed by monitoring serial measurements of arte
blood gases. Endotracheal intubation and ventilatory support with assisted ventilation are always required
patients with contusion or laceration of the lung. These patients also require intravenous fluid administrat
as these cases may be involved with multiple injuries. One word of caution should be remembered that lar
volume intravenous fluid administration may worsen the pulmonary oedema which accompanies pulmon
contusion. The rate of I. V. fluid should not exceed 50 to 75 ml per hour. Sometimes 20 to 40 mg dosage of
intravenous frusemide at the intervals of 6 hours may be required to mobilise oedema fluids from the lung
These measures often cure these cases.
Sometimes, in serious conditions, a thoracotomy and repair or resection of the affected segment of the lun
may be required. The indications for this operation are :—
(a) Continued or uncontrolled haemorrhage leading to large haemothorax.
(b) Massive air leak leading to massive pneumothorax.
(c) Presence of mediastinal emphysema.
(d) When assisted ventilation is required for more than 72 hours.
POST-TRAUMATIC PULMONARY INSUFFICIENCY.— There may be an acute respiratory failure
in patients who suffer major thoracic trauma. It is our practice that whenever doubt or controversy clouds
knowledge of a disease process, the issue is usually obscured still further by using confusing nomenclatur
This is particularly the case in case of major damage to the lungs following severe trauma. The clinical fea
of such patient are fairly constant.'
The patient is admitted through the casualty department with injury to the chest and multiple injuries
body including long bone fractures. The patient is pink, but breathing easily and chest radiograph is eithe
normal or shows insignificant fluffy opacification involving perhaps one lobe. Within next few hours a slightly
cyanotic tinge develops. The respiratory rate rises and the pulmonary opacities become more marked. Arterial
blood Pa02 level is below the normal value of 100 mmHg. Obviously an endotracheal tube is passed and the
patient is managed with a mechanical ventilator. Though the condition of the patient improves but further che
X-ray shows that the mottled areas are beginning to coalesce to produce a uniform hazy opacification. Gradua
as time goes by, it seems that the lungs become more and more difficult to inflate and higher and higher
concentrations of oxygen must be delivered to the patient. Ultimately the patient may die despite ventilation
with 100% oxygen forced into the lungs with maximum pressure. At autopsy the lungs are found to have beco
solid almost like liver. A few patients may of course may survive and eventually recover after 2 or 3 weeks of
intensive treatment The various terms e.g. ‘wet lung’, ‘shock lung' ‘congestive atelectasis', ‘adult respiratory
distress syndrome’, ‘crush lung’, ‘blast lung’ and ‘post-traumaticpulmonary insufficiency' have been used for
this condition.
AETIOLOGY.—
(i) This condition usually develops when the lungs become injured with violent crushing injuries of the
rib cage or sudden deceleration forces. A shock wave travels through the substance of the lung. This tears
delicate structures in the alveolar walls. Bleeding occurs into the lung substance due to this tearing and causes
large areas of the lung to become bruised. If there is retention of sputum due to pain or injury to the thoracic
skeleton, the pulmonary function becomes even worse.
(ii) Extrathoracic causes have been widely documented, as similar clinical pattern develops in a patient
who shows no evidence of thoracic injury. Large volumes of crystalloid solutions, if administered instead of
blood, pulmonary oedema may ensue. Even massive transfusions of stored blood may produce micro-emboli
which obstruct small pulmonary vessels.
(iii) It has also been suggested that fractures of the long bones may lead to fat embolism, which causes this
condition. Petechial haemorrhages in the skin and detection of fat in the sputum and urine may help to make
the diagnosis.
MANAGEMENT.— Maintenance of good cardiovascular status and prompt institution of ventilatory
support are required. Monitoring central venous pressure (CVP) is the minimum for guidance of fluid and
diuretic therapy in these patients. Placement of Swan-Ganz catheter to allow measurement of left atrial and
pulmonary artery pressure is ideal. The need for inotropic myocardial support may be assessed by this
technique. Ventilatory support techniques have advanced to allow a wider selection of ventilators and method
of assisted respiration. Concentration of oxygen should be used which maintains the Pa02 at a barely acceptable
level "of about 70 to 80 mmHg. Tracheostomy is almost always required, as mechanical ventilation will be
needed for 2 to 3 weeks.
Antibiotics are used to avoid superadded infection. Diuretic is often prescribed to combat pulmonary
oedema. Digoxin may be administered to increase cardiac competence. The place of steroid therapy is still an
unanswered question. Methyl prednisolone in the dosage of 30 mg/kg body weight given intravenously every
6 hours for 48 hours in combination with ventilatory support may do the tricks in many cases.
TRAUMATIC ASPHYXIA.— This is a rare condition which follows crushing injury of the chest. Blood
from the heart is driven into the veins of the head and neck and upper part of chest causing extravasation of bl
into the conjunctivae and skin of those regions. There is intense venous congestion with dusky appearance of
the head, neck and upper part of the chest. Petechial haemorrhages may follow. There may be retinal
haemorrhage and optic atrophy. The patient may become unconscious. X-ray of the lungs do not usually show
any characteristic feature, but occasionally a picture of miliary spots may be received.
TREATMENT.— These patients should be in propped-up position and oxygen is given. This position will
help in venous drainage. No other special treatment is required except symptomatic treatments.
MEDIASTINAL EMPHYSEMA.— This is a condition in which there is escape of air into the
mediastinum either through wounds of the trachea or bronchi or the oesophagus. The face and neck become
suffused and livid due to pressure on the great veins of the neck at their roots. Surgical emphysema is first
revealed at the neck. This condition threatens life and calls for immediate treatment.
TREATMENT is immediate thoracotomy and repair of the wound or tear through which air is coming
into the mediastinum.
INJURY TO THE HEART AND PERICARDIUM.— Sometimes in thoracic injuries, the heart may be
injured. This may occur by penetrating wound. In this case blood accumulates in the pericardium which
compresses the heart and jeopardises the circulation. This is ‘cardiac tamponade’. Three classical signs are
(i) 'Silent heart’ i.e. diminution of cardiac sound.
(ii) Increased area of cardiac dullness.
(iii) Steady fall of arterial pressure with gradual rise of venous pressure.
TREATMENT is immediate aspiration of the pericardium through the leftcostoxiphoid angle. This is a
saving measure.
Traumatic Chylothorax.— Sometimes after an injury to the thorax with fracture of a rib or ribs, signs of
hydrothorax develop. The radiographic appearance is almost like that of pleural effusion. This is a rare in
and sometimes occur after a large meal when the thoracic duct is distended with chyle. The thoracic duct
injured by the fractured rib. This type of chylothorax is also seen after a stab or gun-shot wound or after
intrathoracic operations or operations at the base of the neck particularly on the left side. It is more often
diagnosed during aspiration of a pleural effusion when chylous fluid is detected.
TREATMENT.—- Repeated aspiration, restricted fluid intake and fat free diet rich in protein are the
preliminary managements of this condition. If with this regime, there is no considerable reduction in the
outpouring of chyle after 7 days, operation is recommended. Undue delay will deteriorate the general con
of the patient.
Operation.— About 6 hours before the operation is started a feed of coloured cream is given to the pati
to delineate the site of injury of the thoracic duct. A low right sided thoracotomy is performed. The thorac
is found along the bodies of the vertebrae between the aorta on the left and the azygos vein on the right si
At the level of the 5th thoracic vertebra, the thoracic duct crosses the midi ine to pass behind the arch of th
The tom duct is identified. Its proximal end is ligated. The thorax is closed with water-sealed drainage.
MANAGEMENT OF OTHER CHEST INJURIES
MANAGEMENT OF OPEN WOUNDS OF THE THORAX.— There are two types of open wounds of
the thorax — sucking and non-sucking.
Sucking wounds are more dangerous and they should be closed immediately either by firm pad or by
temporary suture. If dyspnoea persists, more aspiration of air and blood should be carried out. Endotrach
should be administered and positive pressure respiration is maintained with the patient sedated. When th
patient’s condition permits, he should be moved to the operation theatre.
Operative treatment.— Under endotracheal general anaesthesia, the wound in the thorax is debrided. Th
means the margins of the wound are excised, all damaged and crushed muscles are removed alongwith r
of broken fragments of rib. If the patient’s condition is poor, a rapid examination of the pleural cavity and
lung should be carried out through a limited thoracotomy. This examination is done to exclude any seriou
bleeding or major intrathoracic injury. A small rib retractor is used. The blood is sucked out from the pleu
cavity. If a laceration of the lung is present, it probably has stopped bleeding. The wound is then thorough
inspected for presence of any foreign body, which should be removed. No excision of the lung wound is c
out as gas gangrene is unknown in the lung. A few sutures of fine catgut are inserted to repair the wound
lung. The chest is closed in layers with particular care that approximation of muscle layers has been done
water-seal drainage is instituted.
A few X-rays are taken in the early postoperative days. If the lung is seen collapsed in part or whole,
bronchoscopic examination and bronchoscopic aspiration of the tracheobronchial tree should be carried o
These can be performed through tracheostomy. If there are effusions in the pleural cavity, these should be
aspirated.
THORACOABDOMINAL INJURIES —
Crushing injury, stab and bullet wounds of the lower thorax may involve the abdominal viscera e.g. sple
liver, stomach or intestine. Combined thoracic and abdominal injuries are not uncommon. In nearly all lowe
thoracic injuries, one should always suspect upper abdominal injuries. X-ray should always be taken to excl
such injuries. It is obvious that the abdominal injury is more fatal and should always be excluded before any
treatment of thoracic injury is contemplated.
In thoracoabdominal injuries, it is advantageous to make thoracic approach. This will help to detect the
predicted course of the missile to anticipate the visceral damage. The main indications for operation are signs
of persistent bleeding or evidence of involvement of a hollow viscus. The thoracic approach has the advantages
of (i) easy tackling of the thoracic injuries and (ii) also giving adequate exposure of the upper abdomen throu
the diaphragm to tackle abdominal visceral injuries. The surgeon with little thoracic experience sometimes f
justified in exploring the abdomen only. But there is no doubt that thoracic approach is much convenient to
repair any obvious laceration of the lung and it permits an excellent exposure through the diaphragm to ena
the surgeon to remove a damaged spleen or to suture a wound in the upper 3rd of the stomach.
It is always advisable to make a thoracotomy incision in the 7th, 8th or 9th intercostal space and this inci
should be extended to the upper abdomen. Through this incision it is easy to assess the injury to the spleen,
or stomach or coils of intestine and also to treat these injuries accordingly.
CRUSHING INJURIES OF THE THORAX.— Such type of injuries are more common in wars. In
civilian practice road accidents or aeroplane accidents may produce such injuries to the chest. It may occur d
to a localised blow or an extensive crushing force or by concussion waves from explotions (blast injuries).
Effects of crush injury depend on its severity. The injuries may produce rib fractures, stove-in chest, flail
chest, lung contusion or laceration, myocardial damage or aortic rupture. The greater problem is inability to
cough out bronchial secretions, which leads to shallow respiration with cyanosis. This is associated with
tachycardia and hypotension. Hypoxiaproduces cerebral confusion and restlessness, followed by unconscio
ness in severe cases.
Treatment.—
1. Careful assessment of the damage is highly essential.
2. Position of the mediastinum should be assessed to detect whether there is pneumothorax or haemot
horax or massive collapse of the lung.
3. The chest wall is examined for rib fractures, paradoxical movements, depression (stove-in chest) or
presence of sucking wounds.
4. Stabilisation of the chest wall should be done immediately as mentioned in the section of ‘flail chest
5. Relief of pain should be given with analgesics, morphine and/or intercostal nerve block.
6. Removal of blood or air from the pleural cavity is essential with continuous water-seal drainage.
7. Endotracheal tube should be instituted or a tracheostomy. This is the most important measure. It
permits repeated aspiration of the tracheobronchial tree, eliminates dead space and allows intermittent posi
pressure respiration. This positive pressure respiration should be continued till the blood gas estimations
confirm achievement of normalcy. This usually takes about 10 to 14 days, which cannot be maintained with
endotracheal tube, so tracheostomy becomes necessary in all severe cases of crush injuries.
8. Oxygen is necessary and is usually administered by a mask.
9. Fluid replacement is highly important which should be supplemented with blood transfusion if
considerable blood has been lost due to injury.
632
CHAPTER - 33
DISEASES OF THE CHEST
(INCLUDING THE MEDIASTINUM AND THE DIAPHRAGM)
PLEURAL EFFUSION
The pleural cavity is always bathed by pleural fluid. This fluid is exudated by the visceral pleura and is
absorbed by the parietal pleural. Approximately 1000 ml of this fluid is formed per day. Any disturbance in th
balance of secretion and absorption may result in accumulation of fluid in the pleural cavity, which is known
as pleural effusion.
A minimum of about 300 ml of pleural fluid is generally required before one can radiographically diagnos
a case of pleural effusion. The first indication of which is blunting or abolition of costophrenic sinus or angle.
So when a diagnosis of small pleural effusion is noted on a thoracic roentgenogram, usually considerable flui
is already present and can be obtained by a carefully performed thoracentesis. So radiographers often prescri
a lateral decubitus chest X-ray to be obtained to detect small volume of effusion.
Pleural effusions can be classified into 2 groups — (i) Transudates and (ii) Exudates.
(i) TRANSUDATES have specific gravity less than 1.015 and their protein contents are also less than
3 g/100 ml. Such transudate is clear with a faint yellow tinge and no odour. The common causes of formation
of such transudate are congestive cardiac failure, nephrotic syndrome, ascites and atelectasis.
(ii) EXUDATES, on the other hand, contain protein more than 3 g/100 ml and possess specific gravity mor
than 1.016. Such exudates are caused, by inflammatory diseases and neoplasms of both pleura and lungs and
pulmonary infarction.
A haemorrhagic pleural effusion is not included in transudate or exudate group and it is usually caused by
neoplastic invasion of the pleura, pulmonary infarction, tuberculosis or unrevealed trauma.
Clinical features.— Pleural effusion is usually associated with symptom of dyspnoea. Stony dullness on
percussion, absent breath sounds and absent vocal fremitus on auscultation are the significant signs of pleura
effusion. If the effusion is massive, the mediastinum is shifted to the opposite side causing compression to the
opposite lung. Severe cardiorespiratory embarrassment with cyanosis may also result in massive pleural
effusion. Diagnostic thoracentesis is indicated in most patients with pleural effusion, unless the cause is alread
known. Thoracentesis is best done after careful localisation of the effusion by roentgenogram in frontal, lateral
and oblique planes or by the use of fluoroscopic image intensifier. After thorough infiltration of the skin,
intercostal muscles and the parietal pleural with a local anaesthetic agent, the needle of appropriate calibre an
length is directed j ust above the superior border of the lower rib of the appropriate intercostal space. The nee
is penetrated through the parietal pleura, till fluid is reached. During aspiration low in the costophrenic angle
the needle tip should be directed upwards to avoid puncture of the diaphragm. Removal of all available fluid
usually presents no difficulty unless sometimes after complete evacuation of a massive acute effusion, pain,
discomfort and severe coughing may be initiated. Usually no more than 1500 ml should be aspirated in first
attempt in a case of massive pleural effusion.
Causes of pleural effusion.— There are hundreds of causes of pleural effusion. Here I am giving a short
list of the various causes of pleural effusion of surgical interest according to frequency :—
1. Most common causes.— (i) Congestive cardiac failure; (ii) Infection of the lung and pleura,
particularly bacterial pneumonia; (iii) Neoplasms, of which bronchogenic carcinoma tops the list followed by
pleural metastasis from miscellaneous tumours and lymphoma.
2. Common causes.— (i) Trauma; (ii) Pulmonary infarction and (iii) Lobar atelectasis.
3. Occasional causes.— (i) Tuberculosis; (ii) Viral pulmonary and pericardial infections and (iii) Intra
abdominal infections e.g. subphrenic absccss, pancreatitis etc.
4. Extremely rare causes.— (i) Systemic bacterial infection; (ii) Nephrotic syndrome; (iii) Rheumatoid
DISEASES OF THE CHEST (INCLUDING THE MEDIASTINUM AND THE DIAPHRAGM) 633
arthritis; (iv) Fluid retention and (v) Meig's syndrome.

Of the above causes, subdiaphragmatic or intra-abdominal pathologies as the cause of pleural effusion
deserve special mention. Subphrenic and hepatic abscesses often cause pleural effusion. Cirrhosis of the liver
and pancreatitis are also known to cause pleural effusion in certain percentage of cases. Ovarian fibroma is
sometimes associated with pleural effusion, which is known as Meig's syndrome.. The method of formation of
pleural effusion in these cases are still not clearly known. It may be that passage of fluid from the peritoneal
cavity into the pleural cavity occurs through the lymphatics, whereas others hold the view that the passage o
fluid occurs through recognised or unrecognised openings in the diaphragm.
EMPYEMA THORACIC
The term 'empyema thoracic' is generally applied to pyogenic infections of the pleural cavity associated wit
pleural effusion. A collection of purulent fluid in the pleural space is called ‘empyema’ in wider sense. In fact
all phases of pleural infection from an infected turbid effusion to a mature abscess containing thick pus are
included in this term.
Aetiology.— Empyema usually occurs from primary disease in the neighbourhood, so it is always
secondary.
1. Most commonly, the primary condition is in the underlying lung. Lobar pneumonia and bronchopneu
monia, are the most common causes. But any infective process in the lung may cause empyema e.g. lung
abscess, bronchiectasis and tuberculosis. The infective process usually extend to the pleura either directly or
by the lymphatics, or by blood (haematogenous) spread or by rupture of necrotic pulmonary parenchyma. Lu
infection may itself be secondary to bronchial obstruction either due to bronchogenic carcinoma or bronchiec
tasis. A ruptured emphysematous bleb with spontaneous pneumothorax may also result in an empyema.
2. Empyema may be caused by the source of infection in a mediastinal structure e.g. bronchi; (bron
chopleural fistula) or the oesophagus (perforation, leaking anastomosis); or infected lymph node; or osteomye
litis of the thoracic vertebrae.
3. Empyema may also occur due to causes below the diaphragm e.g. subphrenic abscess or intrahepatic
abscess. In these cases infection probably spread by lymphatics.
4. Infection may also be introduced into the pleural cavity from outside e.g. trauma, operation or needle
aspiration.
So to narrate the sources of infection which may cause empyema are briefly as follows :—
(a) Lung (pneumonia, lung abscess, bronchogenic carcinoma, bronchiectasis, tuberculosis).
(b) From bronchi (bronchopleural fistula).
(c) From the oesophagus (perforation, leaking anastomosis and carcinoma).
(d) From chest wall (wound and osteomyelitis of the ribs).
(e) Postoperatively (thoracotomy).
(0 From other structures of the mediastinum (infected lymph nodes or osteomyelitis of the thoracic
vertebrae).
(g) From below the diaphragm (subphrenic abscess or intrahepatic abscess).
The most common organisms responsible for empyemas are the pneumococci, streptococci and staphylo
coccus aureus. The last named organism is gradually moving to the top position so far as frequency of its
existence and its virulence are concerned. Staphylococcal empyemas are often becoming antibiotic-resistant
and causing real problem to the surgeons.
A few gram-negative organisms are also causing empyema and these are Pseudomonas, Klebsiella
pneumoniae, Esch. coli, Aerobactor aerogenes, proteus, bacteroids and even Salmonella.
Pathology.—In majority of cases empyema is caused by pneumonia of the underlying lung. Previously two
types of empyema were considered — syn-pneumonic and metapneumonic. The syn-pneuinonic empyema
occurs secondary to streptococcal bronchopneumonia and the empyema occurs simultaneous with the bron
chopneumonia. That is why it is called syn-pneumonic. The metapneumonic empyema is seen secondary to
pneumococcal lobar pneumonia and the process of empyema starts after the resolution of pneumonia and
is why it is called metapneumonic.
In case of empyema the actual pleural infection is preceded by the development of a serous effusion. In
next stage the pleura is invaded by organisms. The next stage is the starting of inflammatory changes in th
pleura with exudation of fluid from the pleura. Such exudate is a protein rich effusion. In the next stage fib
is deposited on the surface of the pleura and the nature will try to encircle the septic area with a barrier of f
tissue. At the initial stage the visceral pleura will fuse with the parietal pleura at the periphery of the collec
of fluid. Gradually the fibrin deposits on the pleura are invaded by blood vessels from the adjacent lung an
wall. Granulation tissue is gradually formed which is replaced by fibrous tissue later on.
As the empyema is gradually walled off by adhesions, the fluid also thickenes. Thick pus is an indicatio
that the empyema is localised and cannot spread further. Later on in a case of chronic empyema there is a l
of fibrous tissue superficial to the visceral pleura and deep to the parietal pleura to encircle the empyema. A
of clevage exists between this wall of fibrous tissue and the visceral pleura or the parietal pleura.
The secondary changes in case of chronic empyema are that the lung is encased in a rigid cover of fibrous
tissue and that segment of the lung becomes immobile and functionless. The diaphragm is elevated and fix
The mediastinum is drawn towards the affected side. The ribs are gradually drawn together and finally los
mobility.
The pus within empyema varies with the bacteriology. In pneumococcal and staphylococcal cases it is th
and intensely purulent. In streptococcal infections the pus is at first thin and watery and later on it is more
than purulent, though it contains large number of organisms.
Clinical features.— Three stages of empyema have been recognized — 1. Acute empyema, 2. Subacute
empyema and 3. Chronic empyema.
1. ACUTE EMPYEMA.— In this condition, the patient may be toxic and in shock. There may be pleur
pain. Respiration is shallow and rapid. The signs of presence of pleural fluid will be there. The clinical sign
of fluid in the pleural cavity are — (i) stony dullness on percussion, (ii) diminished breath sounds and voca
resonance on auscultation, (iii) mediastinum is displaced to the opposite side (this is not very prominent in
of empyema), (iv) diminished chest movement on the affected side.
Diagnosis is confirmed by (i) chest X-ray, which shows fluid in the pleural cavity and (ii) aspiration of t
pleural cavity.
A condition of acutefulminating toxic empyema can be considered due to its more toxicity. It usually follow
perforation of oesophagus or rupture of lung abscess. In these cases the patient is severely toxic and unless
empyema is drained quickly under proper antibiotic cover, the condition turns fatal.
2. SUB ACUTE EMPYEMA.— Majority of empyemas, seen in clinical practise, are of this stage. The
onset is insidious and its presence is often overlooked. Suspicion of this condition occurs due to delayed
resolution, prolonged convalescence or persistent fever following a lobar pneumonia. Subacute empyema
occurs due to early administration of antibiotics for the primary condition (i.e. lobar pneumonia or other lu
infection). Clinical signs of presence of fluid in the pleural cavity will be present. Chest X-ray and aspiration
will confirm the diagnosis.
3. CHRONIC EMPYEMA.— Majority of chronic empyemas are due to mismanagement of acute or
subacute empyema. Some are due to failure of diagnosis in the acute or subacute stage. A few cases are due
chronic pathology in the lung (e.g. bronchiectasis, neoplasm etc.), in the pleura (foreign bodies or actinomy
cosis) or in the chest wall (osteomyelitis of the rib).
The main feature of chronic empyema is the absence of toxicity and acute condition. There is no dyspno
or fever or anaemia.
Two types of chronic empyema are seen — (a) closed type and (b) open type.
(a) Closed type.— In this case there is a closed collection of pus completely walled off from its
surroundings. The pus inside is thick. If it be sterile, tuberculosis may be suspected.
(b) Open type.— In this condition empyema cavity is communicated either with a bronchus (which
is known as bronchopleural fistula) or to the exterior through a sinus in the chest wall (which is known as
persistent empyema).
Having confirmed the diagnosis of empyema, it is always essential to know the primary disease. From t
causes mentioned above, it should be the surgeon’s duty to find out the actual cause of empyema. In case o
patients over 40 years of age, it should be suspected to be secondary to a carcinoma and a bronchoscopic
examination should be performed to exclude such possibility. Thoracoscopy is of some help in difficult cas
to know the primary disease.
A complication of chronic empyema needs special mention and this is ‘empyema necessitatis’. In this
condition a neglected or unrecognised empyema thoracis may provide its own drainage by breaking throu
either the visceral or parietal wall. When it breaks its visceral wall, it perforates through the lung and
communicates with a bronchus. This is clinically indicated by sudden expectoration of large quantity of pu
This needs immediate evacuation of the pleura and intensive bronchopulmonary toilet. When chronic emp
thoracis breaks through its parietal wall, it burrows through the chest wall and becomes superficial either i
lateral or anterior aspect probably through the opening for the lateral or anterior cutaneous branches of the
intercostal nerves. This condition is presented as an enlarging local abscess and is diagnosed by presence o
impulse on coughing and reducibility. The treatir ent of this condition is drainage of the abscess and the ch
empyema thoracis.
Management.— The objectives of management of empyema are — (1) control of primary infection and
its secondary manifestations; (2) evacuation of the purulent contents from the empyema sac to prevent
chronicity and (3) reexpansion of the underlying lung in order to restore function. The methods used to ach
these objectives depend upon the stage of the empyema.
Basically the management of empyema arc based on two principles —
1. The use of appropriate antibiotic therapy based upon the bacteriologic diagnosis.
2. Adequate drainage of the pus.
STAGE I (ACUTE EMPYEMA).— If the condition is diagnosed early when the pus is quite thin, repeated
aspirations on alternate days with removal of as much pus as possible is all that is required. Even in this stag
occasionally aspirations fail to control infection and in which case continuous closed drainage should not be
delayed. This is only required if the fluid reaccumulates and infection and toxicity are difficult to control an
if the pus becomes too thick to be aspirated with a needle.
Aspiration.— The pleural punctures should be made on the 8th or 9th intercostal space on the posterior
axillary line. The site of puncture is infiltrated with 1% local anaesthetic solution. A large needle is introduc
and as much fluid as possible should be aspirated. After aspiration, proper antibiotic should be instilled. So
lipiodol is injected into the pleural cavity to know the lower limit of the pleural cavity. The aim should be to
introduce the needle through the most dependent space for proper aspiration.
Drainage by intercostal tube.— Continuous closed drainage is performed through this technique. The site
for insertion of the tube is to the most dependent part of the empyema cavity. Accurate localisation of empy
cavity is facilitated by the use of biplane roentgenogram of the chest or with a fluoroscopic image intensifie
The skin is infiltrated with local anaesthetic down to the parietal pleura. In majority of cases the site for inse
of the tube is the 8th or 9 th intercostal space between the posterior axillary line and scapular line. A stab w
is made for introduction of the trocar and cannula which are pushed into the pleural cavity. The trochar is
withdrawn and a stretched Malecot catheter is quickly introduced. The catheter introducer is removed and
the cannula is removed.
STAGE II (SUB ACUTE EMPYEMA).— In this condition drainage of pus is effected by open drainage
with resection of a short segment of rib. In this condition the pus is too thick and it is often loculated in multiple
pockets. The pus contains too much organised fibrin to be evacuated through aclosed drainage by an interc
tube.
The operation is carried out under local anaesthesia. The site selected for drainage lies immediately abov
the lowest limit of the empyema posteriorly. Usually the 9th or the 10th rib on the paravertebral line is resec
A vertical incision is often preferred as there remains the choice of more than one ribs for resection. The incisi
is made straight through the muscles upto the ribs. The periosteum is incised longitudinally for 5 to 7 cm and
this section of the rib is cleared subperiosteally — first on its superficial surface and then from the inner surfa
About 5 cm of the rib, which is devoid of periosteum is resected with rib shears. Local anaesthetic is injected
again into the inner periosteum with adherent parietal pleura to prevent pleural shock. The empyema cavity
now opened with a small nick and a pair of sinus forcep is introduced for proper drainage. Finally a finger is
introduced to divide the loculi, if present Drainage should at first be closed using an underwater-seal. When
the discharge is reduced to 60 ml daily, open drainage is instituted. Drainage should be continued till the
empyema cavity is completely obliterated. Early removal of the tube is an obvious cause of chronicity. It may
take about 6 to 8 weeks for complete obliteration of the empyema cavity.
STAGE III (CHRONIC EMPYEMA).— In these cases decortication operation is best suited. A postero
lateral thoracotomy is performed through the bed of either the 5th, 6th or 7th rib. The rib is resected from the
transverse process to the costochondral junction. The empyema is opened and mopped dry. The margins of th
membrane are gradually peeled off through the plane of clevage. While peeling it from the lung one should n
injure the lung. After the membrane is completely excised and all bleeding points secured, a drainage tube is
inserted through a dependent intercostal space. The lung is inflated by the anaesthetist and it is seen that noth
is impeding its full expansion. The drainage tube is connected with a water-seal drain and the wound is close
around the drainage tube.
This operation is however a major one, which requires skilled anaesthetist and blood transfusion. It is also
indicated when chronic empyema is secondary to bronchiectasis, lung abscess or carcinoma where the
underlying lung condition can also be dealt with at the same time. This operation however is contraindicated
in the frail and elderly individuals.
Chronic empyema sinus.— This is sometimes seen when the empyema has drained itself to the exterior
through a sinus or following tuberculous empyema, or due to underlying lung disease, or due to retained for
body or due to osteomyelitis of a rib. Management of such a case is to instill radio-opaque iodised oil through
the sinus. This will delineate the empyema cavity. According to the chronicity of the condition the empyema
is treated either by open drainage by rib resection or by decortication operation.
SURGICAL TREATMENT OF PULMONARY TUBERCULOSIS

The introduction of various antitubercular drugs have definitely minimised the scope of operation in case of pulmonary
tuberculosis. These had made both cavitation and endobroncheal tuberculosis quite uncommon. Patients with cavitation or
bronchostenosis respond very slowly to chemotherapy and these are the cases which are more likely to require surgical
intervention.
Operative treatment of pulmonary tuberculosis can be of two types— collapse therapy or resection.
Collapse therapy aims at collapsing the diseased segment of the lung thereby giving rest to the segment which will
promote healing. Resection is complete removal of the diseased segment of the lung. With modem trends in treatment,
collapse therapy, which was widely used previously, is now steadily losing popularity. So most of the patients undergoing
operations are resection operation.
Collapse therapy includes (a) artificial pneumothorax, (b) thoracoscopy and section of adhesions, (c) phrenic crush,
(d) thoracoplasty with apicolysis, (e) extra-pleural pneumothorax and (f) extra-pleural plastic plombage.
ARTIFICIAL PNEUMOTHORAX is the safest and can only be performed when there is no adhesion in the pleural
cavity.
PHRENIC CRUSH is a method inducing deliberate paralysis of the diaphragm, which rises upwards and thus collapses
the involved segment.
EXTRA-PLEURAL PNEUMOTHORAX is to produce pneumothorax in the space between the parietal pleura and the
endothoracic fascia after resecting the posterior few inches of the 3rd or 4th rib. The space is refilled with air periodically.
EXTRA-PLEURAL PLASTIC PLOMBAGE enjoys two advantages over thoracoplasty — (i) there is no subsequent
deformity as no rib is resected, (ii) Plastic plombage prevents paradoxical exertion of the lung. The approach is very much
similar to that of extra-pleural pneumothorax. The periosteum is stripped from the upper 5 ribs. The ribs are not resected.
Polyethene balls are introduced through the ribs until the space between the ribs and the detached muscles and periosteum
is completely filled.
THORACOPLASTY is still the most effective operation among the collapse therapy group. Nowadays its implication
is limited to cases where resection is contraindicated.
Operation.— A J-shaped incision is made 2 inches away and parallel to the thoracic spines and curving forwards
beneath the inferior angle of the scapula. The incision is deepened dividing the trapezius, rhomboids, latissimus dorsi and
serratus anterior. This allows the scapula to be elevated and displaced forwards to expose the upper ribs. The whole of the
first rib is resected sub-periosteally and as much as possible of the 2nd rib and 3rd ribs are resected. This operation is mainly
done for the upper lobe disease. By upper three ribs resection, relaxation may not be adequate. In this case, apicolysis should
be carried out by dividing the intercostal muscles and a plane of clevage is found out between the intercostal muscles and
endothoracic fascia, known as Semb’s space. This space is partially filled with serum which acts as a useful plombage
first stacje second, stacp ttvtrd. steep
Fig.41.1. — Stages of thoracoplasty operation.
preventing expansion of the lobe.

Sometimes upper three ribs resection may not be adequate and a 2nd stage of operation is carried out by removing
posterior 3/4th of the 4th and 5th ribs.
Occasionally a 3rd stage may be required in which posterior halves of the 6th and 7th ribs are removed.
Lung resection.—
INDICATIONS.— 1. Persistently positive sputum cultures following 6 months of continuous optimal chemotherapy
with 2 or more drugs.
2. Localised pulmonary disease by atypical micobacteria with broad resistance to chemotherapy e.g. M. intracellu-
lare.
3. Underlying cavitary disease e.g. bronchiectasis or bronchial stenosis.
4. Presence of a bronchopleural fistula in association with tuberculosis.
5. Massive life threatning haemoptysis or recurrent severe haemoptysis.
6. Presence of a mass lesion suspicious of carcinoma in an area of tuberculous involvement.
Before operation it should be assessed that the patient’s cardiopulmonary reserve is adequate to sustain him through the
contemplated resection.
Preoperatively, bronchoscopy should always be performed to be certain that there is no evidence of endobronchial
tuberculosis or proximal bronchial stenosis.
Operation.— The type of resection depends on the extent of disease. It must be remembered that all diseased tissues
should be resected, though adequate conservation of lung tissue to preserve pulmonary function is desirable. Usually either
alobectomy or pneumonectomy is necessary. It is occasionally necessary to combine upper lobectomy with wedge resection
of the superior segment of the lower lobe to remove all diseased tissues. Wedge or segmental resection is not often applicable
in pulmonary tuberculosis cases. Only occasionally it can be applied when a mass lesion is to be excised to rule out presence
of carcinoma. Lobectomy is the most frequently required procedure, as pneumonectomy is rarely indicated except when
one lung is totally destroyed by the disease. It is sometimes required that stage lobectomies are performed on various sittings.
The operative techniques of lobectomy and pneumonectomy are beyond the scope of this book and the students may
be referred to specialised operative techniques of thoracic surgery.
BRONCHIECTASIS
It is mainly a medical condition, so its aetiology, pathology and clinical features are elaborately described
in any standard textbook of Medicine. Here I shall discuss only the indications and methods of surgical
treatment.
1. Chest X-ray sometimes may be normal in cases of bronchiectasis.
2. Bronchoscopy is helpful in the diagnosis. It also rules out other pathologies like tumour or stenosis in
the bronchi. It can also obtain uncontaminated material from the bronchiectatic cavity for culture.
3. Bronchography.— This is particularly helpful for preoperative evaluation, as every segment of both
lungs may be visualised (Fig. 41.2).
4. Computed tomography (CT scan) is useful in the diagnosis of bronchiectasis and should precede bron
chography.
Surgical treatment.—
INDICATIONS.— 1. Localised bronchiectasis persisting for sometime which is not cured by medicines.
2. In case of generalised disease repeated respiratory infections in multisegmental group is an indication
for surgery. Such disorder tends to develop in early life.
3. Many patients may prefer surgical treatment to repeated postural drainage.
The main aim of surgical treatment is to excise all diseased tissues of the lung, be it a segment or a lobe or
a lung as a whole. So segmental resection, lobectomy or pneumonectomy should be called for according to the
case. Bilateral lobectomy or segmental resection may also
be performed. It must be remembered that modem surgical
approach to bronchiectasis is based upon the principle or
conservation of pulmonary tissue.
The results of resection for bronchiectasis are good.
This is particularly so in case of localised disease than with
multisegmental disease. Patients with diffuse bronchiecta
sis are not good candidates for surgical treatment. In fact
surgical treatment of patients with localised bronchiectasis
yields excellent results with a very low morbidity and
mortality.
LUNG ABSCESS
Necrosis of lung tissue due to localised area of lung infection
is called a lung abscess. Such necrosis is due to thrombosis of the
segmental artery and vein due to virulent infection.
It is usually secondary to primary pneumonia of the lung with
bacterial species that are noted for their necrotising ability. This
so called ‘post-pneumonic abscess’ is frequently located in the
Fig.41 — Bronchography showing dittusc upper lobe.
saccular bronchiectasis of the right lung. Causes of lung abscess.— 1. Aspiration of gastric contents
followed by pneumonia is probably the commonest cause of lur.g
abscess at present. Abscesses which follow aspiration are usually located in the posterior lobes.
2. Lung abscesses may sometime occur due to septic emboli. These abscesses are small and multiple.
3. Pulmonary abscess may develop about a foreign material carried into the lung by a penetrating injury.
4. Lung abscesses may be secondary to chronic upper respiratory tract infection e.g. dental infection, tonsilitis or a
sinusitis.
5. Partial or complete bronchial obstruction is an important cause of lung abscess in which case infection is laid distal
to the growth. The cause of obstruction is often a bronchial neoplasm or rarely bronchial stenosis from previous
inflammatory disease. These cases are seen in patients over 40 years of age.
Causative organisms.— The various organisms which are often found in lung abscesses are — (i) Staphylococcus
aureus, which when infect in infants and young children takes a very acute course and rapidly proceeds to abscess formation.
(ii) Streptococcus.— These are usually less virulent than the staphylococcus ones.
(iii) Pneumococcus.
(iv) Haemophilus influenzae.
(v) Coliform organisms.
(vi) Friedlander — this bacteria is often seen in elderly patients. Such abscesses often slough out and associated
with high mortality.
(vii) Anaerobic organism which comes from dental infection.
Pathology.— As mentioned earlier inhalation or aspiration of infected material is the main cause for lung abscess
formation. Such material obstructs one of the smaller bronchi and causes atelectasis of that particular segment of the lung.
The atelectatic lung is now invaded by pathogenic organisms and suppuration begins. With the infection spreading into the
surrounding tissues involves the segmental artery and veins to cause thrombosis of those vessels. This leads to tissue necrosis
alongwith suppuration which ultimately forms a lung abscess. As pus accumulates, tension rises and eventually the abscess
may rupture into a bronchus. This will cause expectoration of pus. Infection may then subside. But the state of chronic
infection persists. A zone of inflammatory consolidation continues to surround the abscess cavity as it passes to a chronic
stage. Gradually the adjacent lung tissue may be involved and the pus may even spread to the other parts of the lung.
Clinical features.— Usually the patient becomes ill for a few days with dry cough and pleural pain. This is the initial
stage of lung abscess formation. This condition has got no specific clinical feature except expectoration of considerable
quantities of offensive sputum which contains pus and blood. This occurs when the lung abscess forms communication with
bronchi. The diagnosis is usually made on the basis of clinical manifestations of pulmonary infection and expectoration of
foul and putrid sputum.
With successful treatment resolution occurs slowly with diminution of cough and sputum and toxicity. Healing takes
about several weeks to complete and at that time cough and sputum have almost stopped.
1. Usual blood examinations should be performed.
2. Sputum is sent for culture and sensitivity test.
3. Chest X-ray is confirmatory with demonstration of a lesion with an air-fluid level. There are other conditions in
which such air-fluid level can be seen. These are — (a) Cavitated epidermoid carcinoma, (b) Pulmonary mycosis, (c)
Infected bronchogenic cyst, (d) Tuberculous cavity, (e) Hydatid cyst, (f) Histoplasmosis, (g) Expectorated empyema
(connected with bronchus).
4. Bronchoscopy is essential to exclude presence of neoplasm or foreign body.
Treatment.—
MEDICAL.— About 80% to 90% of lung abscesses can be treated successfully with medicines. The main points in
medical treatment are — (i) intense antibiotic therapy and (ii) drainage of the abscess cavity by postural means.
(i) The appropriate antibiotic is selected from the culture and sensitivity test of the sputum. Intense antibiotic
treatment should be given, that means the dose of the antibiotic should be double the normal dose and the course of the
treatment is also prolonged to at least 3 weeks. In case of staphylococcus abscess it should be as long as 6 weeks. It may
be necessary to change the antibiotic during the course according to the periodic culture and sensitivity reports of the sputum.
(ii) Postural drainage should be carried out for 2 hours 3 times daily in the beginning. Formally, repeated
bronchoscopy at intervals for several days to a week was advocated to promote bronchial drainage. Chest X-ray, physical
therapy and appropriate use of bronchodilators should accompany postural drainage. In case of children special procedures
e.g. endotracheal placement of an aspirating catheter should be advised.
SURGIC ALTREATMENT.— Failure of patient to respond to medical management by lack of beginning of resolution
of the abscess is the main indication for surgical intervention. Surgical treatment is also indicated when an associated
carcinoma cannot be excluded. Surgical treatment may be of two types — (a) pneumonotomy, or drainage of abscess and
(b) pulmonary resection.
(a) Pneumonotomy.— It is a technique of direct drainage of lung abscess through the chest wall after subperiosteal
resection of a short segment of rib overlying the abscess. This is particularly suitable for debilitated and elderly individuals
in whom lobectomy seems to be a high risk. Healing of the track through the chest wall requires several months. But
gradually pneumonotomy is less required nowadays due to satisfactory control of lung abscess with antibiotics.
(b) Pulmonary resection.— Usually lobectomy is the operation mostly performed when lung abscess becomes
chronic with a cavity in the lung which is clearly shown by tomography. Care must be taken at the time of induction of
anaesthesia by positioning the patient in a way to prevent spill of the abscess content into the contralateral lung. As an abscess
may extend into the adjacent lobe through the interlobar fissure, one must be careful to assess the need of surgery before
going for a more extensive resection.
LUNG CYST
Rarely, various types of cysts may be found in the lungs. These are basically divided into four groups :—
1. EMPHYSEMATOUS CYST.— These cysts develop due to degenerative changes in the lung with destruction of
normal alveolar frame work and rupture of alveolar walls. Coalescence of alveolar spaces forms an enormous cyst. This cyst
has no epithelial lining and remnants of blood vessels will be seen stretching across the cyst. Such cysts are often associated
with chronic bronchitis. Infection and haemorrhage may occur in this cyst, but spontaneous pneumothorax is the most
common and serious complication of this condition. Treatment is excision of such cyst when it is localised. If such changes
are generalised, excision is then impracticable and obliteration by plication with multiple sutures should be performed.
When spontaneous pneumothorax has already developed pleurodesis should be carried out to prevent further attacks of such
complications.
2. EPITHELIAL CYST.— These cysts are developmental in origin, so these are often associated with other
congenital abnormalities. Such cyst may be solitary and large or multiple and small. The usual symptoms are dyspnoea and
tightness of the chest. Fever, cough and sputum are complained of if these cysts become infected. Haemorrhage also occurs
in these cysts when they are infected. X-ray shows spherical shadows containing air, fluid or both air and fluid.
3. PARASITIC CYST.— Hydatid cyst is by far the most common in this group.
4. PSEUDO-CYST.— These cysts are not true in the sense that these are not cysts to start with, but various
inflammatory conditions of the lung may lead to cavity formation which behave like cyst. These pseudocysts may occur
in association with staphylococcal or pneumonic infection, pulmonary tuberculosis or following lung abscess.
TUMOURS OF THE BRONCHI AND LUNG

BENIGN TUMOURS
It must be borne in mind that in bronchial tree and lungs benign tumours are extremely rare and 98% o
tumours are usually malignant.
Pathology.— Position-wise benign tumours can be divided into two groups — (a) Intrabronchial and (b
peripheral, (a) Intrabronchial tumours arise from the larger bronchi and are seen through the bronchoscope
These are more common. Through bronchoscope only a portion of the tumour may be seen as there may b
large extrabronchial portion known as iceberg tumour, (b) Peripheral tumours are situated in the periphery
the lung and are not visible through the bronchoscope.
Histologically, there are two main types of benign tumours — (a) bronchial adenoma and (b) hamartoma
(a) BRONCHIAL ADENOMA.— This implies a benign neoplasm with gland-like appearance. The t
is actually a misnomer and it includes 3 clearly different groups of neoplasms — carcinoid (70%), cylindro
(adenoid cystic adenoma) and mucoepidermoid adenoma. Most of these tumours characteristically obstru
bronchus, which leads to infection first of the bronchus and then of the parenchyma. Partial obstruction m
lead to a ball-valve effect with resultant emphysema in the involved segment. Partial obstruction may pers
for many years with intermittent infection, cough and sputum production.
On radiographic examination, the mass may be too small to be evident and usually the distal effects of
obstruction steal the show e.g. pneumonia, emphysema and atelectasis. Bronchogram or C.T. scan usually
demonstrate the endobronchial mass. Bronchoscopy and biopsy are the confirmatory tests.
As mentioned earlier, of the three varieties of adenoma, carcinoids from the major groups. Carcinoids
resemble cells from the neural crest which migrate to distant areas of the embryo in the bronchi. These are
composed of small cuboid, uniform cells arranged in pseudoacini in a very vascular stroma. These tumours m
possess endocrine function. This tumour is a type of apudoma. This tumour secretes ACTH, ADH, ADH-like
hormone, angiotensin and HCG (Human Chorionic Gonadotropin).
Cylindromas are of high malignant potential and are sometimes referred to as adenoid cystic carcinoma. T
tumour is more common in large bronchi and is the 2nd most common tumour in the trachea. The majority o
the tumour grows outside the bronchus. The cells are pleomorphic, dark and with frequent mitoses.
Mucoepidermoid tumours.— These are rare and often removal is not complete.
There are rare adenomas like plasmacytoma (a tumour of plasma cells), polyps and oncocytomas (oxyphilic
granular cell adenoma).
(b) HAMARTOMA.— The hamartoma is a composite tumour composed of 2 or more tissue elements.
tumour represents abnormal mixing of various normal components of the organ from which it arises. Thus in
the lung, cartilage, fat, vascular tissue, respiratory epithelium and glandular tissue may be found. The variou
hamartomas are chondromatous, fibromatous, lipomatous, angiomatous, leiomyomatous etc.
Clinical features.— The clinical features can be best described under 3 groups —-
1. Symptoms due to partial or complete bronchial obstruction. This is discussed in the pathology under
the heading of ‘bronchial adenoma’.
2. Recurrent haemoptysis.—Carcinoid adenoma often causes repeated large haemoptysis occurring over
a period of years with complete symptom-free intervals. There may be wheeziness and irritating cough
alongwith this symptom.
3. Various endocrine effects which have been described above (being a type of apudoma).
Diagnosis is mainly made by the history, chest X-ray, bronchography and bronchoscopy. Bronchography
is particularly helpful to know the extent of the tumour and the secondary lung changes due to its presence.
Treatment.— Surgical resection of the tumour is the treatment of choice. This can be done by either of the
2 methods —
1. Bronchotomy.— The tumour is removed with part of the bronchial wall. This is particularly indicated
when there is no extrabronchial extension or there is no secondary lung damage.
2. Lung resection.— This becomes necessary only when there is permanent secondary lung damage due
to presence of the tumour. The lung resection should be extremely conservative i.e. as little lung tissue as
possible should be resected.
PRIMARY CARCINOMA OF THE LUNG
Primary carcinoma of the lung has increased its incidence from an obscure and rarely encountered tumou
at the beginning of this century to one that ranks first among males now. Its incidence has rapidly increased
in the last 30 years. It is now the commonest cancer in males and the 2nd commonest cancer in women very m
competing for thel st place with the cancer of the breast having already advanced ahead of the carcinoma of t
cervix and uterus. It is interesting to note that if a person ceases to smoke, the development of lung cancer is
less likely than if smoking is continued. This increased incidence of this disease is attributed to —
(i) Increase in the habit of cigarette smoking.
(ii) Industrial hazards — inhalation of fumes and dyes and
(iii) Atmospheric polutions including smoke.
This tumour most often occurs in the 5th and 6th decades, though it may occur earlier but only occasional
below 40 years of age.
Aetiology.— 1. The most important aetiologic agent in the development of this disease is cigarette smoking.
The cigarette smoke contains polycyclic hydrocarbons and unbumed tobacco contains N-nitrosonomicotine.
These substances are highly carcinogenic. It has been seen that excessive cigarette smoking for a long period
is required to develop this disease. The great majority of patients have smoked more than 20 cigarettes a day
for more than 20 years when the diagnosis of carcinoma is first made. It should be noted that cigarettes are m
41
dangerous than pipes and cigars in causing cancer of the lung. The histologic changes which are caused by
cigarette smoking are (a) basal cell hyperplasia, (b) stratification, (c) squamous metaplasia and (d) carcinoma
in situ. It should be borne in mind that epidermoid carcinoma mostly originates from cigarette smoking,
whereas adenocarcinoma is mostly seen among non-smokers.
2. Introduction of gasoline engine as the chief motive power is one of the principal characteristics of th
age of industrialisation. Increased use of automobiles nearly parallels the increased incidence of cancer of lu
3. Dust laden with tar, which is often breathed particularly in large cities, is responsible for initiating
carcinoma of the lung. It contains carcinogenic hydrocarbons. Similarly exhaust gases and shoot from cars a
buses are considered to be more dangerous in initiating this disease.
4. In workers exposed to asbestos, who did not smoke, the incidence of lung cancer is similar to that am
smokers. So asbestos is also concerned in initiating this lesion.
5. Chromium, nickel, arsenic and radioactive substances have also been incriminated to cause lung
cancer. Hydrocarbon distillates of coal and petroleum are also concerned in the causation of this tumcur.
6. Sulphurous smoke and fog and tarry particles from the road also contain carcinogenic effect. Worke
in the Chromate industry have a high incidence of lung cancer.
7. Respiratory viruses have also been incriminated to produce this neoplasm in concert with tobacco
smoke.
At the end it must be confessed that in a significant number of patients with primary adenocarcinoma of the
lung aetiology could not be identified and majority of these patients are women.
Pathology.—
ORIGIN.— Majority of primary carcinomas of the lung arise from the surface epithelium of the bronchia
iree, mostly from the basal or mucous cells. A few arise from neurosecretory cells and from those that have o
in the Clara cells of the distal bronchioles.
MACROSCOPIC VARIETIES.— Three main varieties are noticed :—
1. Main bronchus tumours.— These tumours arise in the main bronchus or one of its primary or secon
divisions. These are usually visible through the bronchoscope. These tumours frequently cause bronchial
obstruction and produce early symptoms of bronchial obstruction and irritation. This is the most common
variety.
2. Peripheral tumours.— These arise from
small bronchi. These are usually late in produc
ing symptoms and are often accidentally discov
ered by chest radiography done for some other
reason. These are hardly seen with conventional
bronchoscope, but may be seen with fibre-optic
bronchoscope.
3. Pancoast Tumours.— These are peripheral
lung carcinomas found in the apex of the lung.
This lesion often causes early symptoms due to
invasion into the brachial plexus and sympathetic
chain producing the typical pancoast syndrome,
which includes Homer’s syndrome, lower bra
chial plexus lesion, apical shadow and rib ero
sion. This tumour is relatively of slow growth
variety.
'Scar carcinoma'.— Lung cancer occasion
ally arises at the site of previous pulmonary dis
ease. Such carcinoma has been seen in the sea'
Fig.41.3.— Main bronchus bronchogenic
carcinoma with progressive growth. tissue following tuberculous process, infarcts,
trauma, pneumoconiosis and other inflammatory lesions. Blockage of lymphatics by scar tissue causes
concentration of carcinogen-containing substances, which ultimately produces malignant change. This may be
considered analogous to the skin cancerarising in a bum scar. The majority of such lesions are adenocarcinoma
or bronchiolar cell carcinoma. Most of these lesions are seen in the upper lobe.
is interesting to note that lung carcinomas develop twice as frequently in the upper lobes as in the lower
This neoplasm may be present for several years before symptoms occur and when symptoms occur it has
Fig.41.4.— A.— PA — chest X-ray shows a mass between the aortic knob and the left hilum (located in the posterior
segment of the left upper lobe). B.— CT scan of the same case shows the growth (M) by the side of the descending aorta.
LN — hilar lymph nodes; AA - is ascending aorta and DA is descending aorta.
already attained a minimum diameter of 1 cm,

so that it is large enough to be seen on chest X-
ray.
MICROSCOPIC VARIETIES.—The usual
microscopic varieties which are seen in lung
carcinoma are — (i) squamous cell carcinoma
(epidermoid), (ii) adenocarcinoma, (iii) undif
ferentiated or anaplastic carcinoma (including
small cell, large cell and ‘oat cell’ carcinoma),
(iv) bronchioalveolar (alveolar) cacinoma and
(v) large cell carcinoma.
1. Squamous cell carcinoma.— This is the
most common type and accounts for approxi
mately 50% to 70% of total lesions. This carci
noma is usually seen in smokers and is almost
unknown among non-smokers. Majority of
squamous cell carcinomas occur in the main
bronchi and so are centrally located. It usually
arises after preliminary squamous metaplasia
has replaced the normal respiratory pseudos
Fig.41.5.— PA radiograph showing peripheral carcinoma. tratified epithelium. Though it often occurs in
main bronchi, yet many peripheral tumours and pancoast tumours are of this microscopic variety. When
in main bronchi, this neoplasm often becomes bulky and central necrosis with cavitation is not uncommo
tumour is known for its slow growth, though it involves quickly the hilar lymph nodes, paratracheal and
subcarinal group of lymph nodes.
2. Adenocarcinoma.— Its incidence is about 15% of the total lesion. Its incidence is progressively
increasing. These lesions are more apt to be seen in the periphery of the lung. It is more often seen in fem
and in non-smokers with occupational exposure. Growth is more rapid than squamous cell variety and it ea
metastasises by the vascular route to the liver, brain, bone and adrenals. It sometimes undergoes symmet
expansion in the lung periphery so as to be called a ‘cannon ball’ tumour.
3. Undifferentiated or anaplastic carcinoma.— These highly aggressive type of tumour represents 20
to 30% of the total. 'Oat cell carcinoma' is a highly malignant one among the various types in this group. In
majority of cases it is central in location due to its origin in a proximal bronchus. It not only spreads early
the hilar and mediastinal groups of lymph nodes, this tumour aggressively invades surrounding structur
is also disseminated by early vascular invasion. This variety of carcinoma is often considered not fit for su
resection. The large cell and the small cell varieties are usually peripherally located and lymphatic spread i
not seen in these cases.
4. Bronchioalveolar (alveolar cell) carcinoma.— This tumour arises from the alveoli or from a typical
Clara cells in the bronchioles. It is seen in either of two forms — localised or diffuse. The most characteris
feature of the lesion is its favourable prognosis in comparison to other types of primary carcinomas.
5. Large cell (giant-cell) carcinoma.— It is a variant of adenocarcinoma which deserves separate
classification due to its aggressive clinical behaviour. Its incidence varies from 1 to 10% of total lesions.
Spread.—
1. DIRECT EXTENSION.— The tumour spreads by direct infiltration into the surrounding structure
These are mediastinum, pericardium, pleura and chest wall.
2. INTRABRONCHIAL SPREAD.— This is only seen in case of main bronchus tumour. The tumour
spreads considerably through the submucosa of the bronchial wall for a distance of variable length. It ma
the trachea or the opposite bronchus.
3. LYMPHATIC SPREAD.— This spread is mostly seen in squamous cell variety carcinomas and in
case of main bronchus tumours, (i) First the hilar.group of lymph nodes are affected, (ii) From there grow
spreads via lymphatics to the subcarinal group of lymph nodes (below the bifurcation of the trachea). In
cases the lymphatic spread occurs upwards to involve paratracheal group of lymph nodes (by the side of
trachea), (iii) From the paratracheal group, the supraclavicular nodes (including the scalene nodes) may b
involved. Gradually the inferior deep cervical group is also involved. Left supraclavicular group (Vircho
nodes) is often involved earlier by retrograde permeation. Direct spread may occur within the lung throu
peribronchial and perivascular lymphatics. As a result, multiple nodules may form throughout the lung.
4. BLOOD SPREAD.— Adenocarcinomas, oat cell carcinomas and giant-cell carcinomas are known
metastasise early through blood stream. The liver, brain, bones, adrenal glands and skin are mostly invol
by blood-borne metastasis. In the bones, the ribs, the vertebrae, the pelvis and ends of the long bones are
in that order of frequency.
Clinical features.— As mentioned above many patients remain asymptomatic for quite a few years an
diagnosis is only made by chest X-ray, done for some other reason. This ‘asymptomatic’ group constitutes a
5% of all cases.
Primary lung carcinoma or bronchogenic carcinoma is seen predominantly in men of 45 to 65 years of
with the pick incidence at 55 to 60 years. The diagnosis of this tumour is being made with increasing freq
in women. These patients are usually in their 5th dccade. The disease has been discovered in patients you
than 40 years (incidence is less than 5%). Due importance should be given to the fact that lung cancer in y
individuals is often virulent and that the diagnosis is frequently delayed.
SYMPTOMS from carcinoma of the lung can be best described under 4 heads — 1. Signs and symptoms
due to primary tumour; 2. Signs and symptoms due to secondary invasion; 3. General symptoms and 4.
Endocrine related symptoms. Pancoast tumour deserves special mention as it produces all together different
clinical feature.
1. SIGNS AND SYMPTOMS DUE TO PRIMARY TUMOUR.—
(a) Cough.— This is the commonest clinical manifestation of carcinoma of the lung, which occurs in
more than 75% of cases. Most lesions that produce cough are located in major bronchi and produce irritation
by neoplastic erosion of the mucosa. Sputum production usually accompanies cough and its character is
dependant on the degree of infection accompanying the lesion. It must be noted that intermittent or chronic
cough is quite common among long-term smokers. So it is difficult to establish the onset of symptoms. But
certain change in the character of chronic cough should raise suspicion of this malignant lesion in cases of long
term chain smokers.
(b) Haemoptysis.— This is usually seen in the form of blood streaking of sputum, and massive
haemoptysis is unusual. This type of haemoptysis occurs in about V2 of all patients. It is fortunate that it prompts
the patients to consult a physician.
(c) Chest pain.— This is usually dull and of non-specific type. It is seen in 50% of patients. Such type
of pain is usually seen in cases without chest wall involvement. Gradually when the parietal pleura or chest wa
is involved, a severe and constant pain is complained of locally or referred to other side due to referred pain.
(d) Dyspnoea.— Some degree of shortness of breath may occur in patients with carcinoma of the lung.
This may be due to bronchial obstruction, as wheezing is often a sign associated with this symptom.
2. SIGNS AND SYMPTOMS DUE TO SECONDARY INVASION.—
Invasion of the mediastinum may cause (i) pressure on the superior vena cava causing congestion of veins
of the face and neck, (ii) Pressure on the recurrent laryngeal nerve may cause hoarseness of voice. It may be
due to direct tumour invasion or due to pressure of metastatic lymph nodes, (iii) Pressure on the oesophagus
will cause dysphagia (present in 1 to 5% of cases), (iv) Pressure on the phrenic nerve or invasion into it may
cause its paralysis which will lead to paralysis of the hemidiaphragm, evidenced by continuous elevated posi t
of the affected half of the diaphragm.
Symptoms due to secondary deposits may also be seen —
(i) Cervical lymph node metastasis occurs in 15 to 20% of cases and these nodes may be palpable.
(ii) Hepatomegaly may be present and liver metastasis is seen in 35% of patients died from cancer lung.
(iii) When the bones are involved, localised aches may be complained of.
(iv) If brain is involved, patient may complain of headache and vomiting, epileptic fits or weakness of limb
due to paresis.
(v) Skin nodules are exceptionally rare due to skin metastasis.
3. GENERAL SYMPTOMS.—
(i) Clubbing.— Clubbing is often associated with pulmonary hypertrophic osteoarthropathy. Pulmo
nary hypertrophic osteoarthropathy has been found in 4 to 10% of cases. This lesion produces symmetrical
proliferative subperiosteal osteitis with new bone formation which affects the distal segments of the shafts of
the long bones. Chronic synovitis is also seen with joint pains which may divert the attention of the clinician
to the diagnosis of rheumatoid arthritis. It is interesting to note that clubbing occurs more frequently in patient
with squamous carcinomas and disappears rapidly following excision of the tumour. None of the patients with
clubbing and hypertrophic pulmonary osteoarthropathy had oat cell carcinoma.
(ii) Loss of appetite, weight loss, though common in any other malignant tumours, yet they carry a
prognostic significance in lung carcinoma. These usually suggest that the tumour is probably unresectable or
there is systemic metastases. Deliberate search should be made for systemic metastases by isotope scanning an
computed tomography.
(iii) Neuromyopathies may be present in 15% of cases usually with oat cell carcinoma. The manifes
tations are those of muscular origin consisting of polymyositis and those of neurologic origin with sensory and
motor loss. Remissions follow excision of the primary lesion.
4. ENDOCRINE RELATED SYMPTOMS.—A small percentage of patients with bronchogenic or

carcinoma show manifestations that are considered to be due to elaboration of hormone-like substances b
neoplastic cells. Regression of these symptoms often occurs following resection of the lesion. But these
symptoms and signs do not imply systemic spread of the tumour.
(i) The most common hormonal manifestation is a type of Cushing’s syndrome often associated w
oat cell carcinoma. This should arouse suspicion of bronchogenic carcinoma or carcinoma of lung when o
male patients are involved.
(ii) Antidiuretic hormone is sometimes produced by a poorly differentiated tumour or adenocarci
which is marked by water toxication, hyponatraemia and various cerebral symptoms (e.g. mental confusi
even coma).
(iii) Carcinoid syndrome has been reported in a few patients with oat cell carcinoma and 5-hy
droxy trypL'.min or 5-hydroxytryptophan may be secreted.
(iv) Parathormone may also be secreted by bronchogenic tumours, usually squamous cell carcinoma
and produce symptoms of hypercalcaemia including mental cor fusion.
(v) Ectopic gonadotrophin secretion has been identified with large-cell anaplastic carcinoma. This
may cause gynaecomastia in male patients.
(vi) Certain patients may show hypoglycaemia with bronchogenic or lung carcinomas.
PANCOAST TUMOUR.— A special and well recognised site for bronchogenic carcinoma is the apex o
lung, known as 'superior sulcus tumour’ of Pancoast. Due to its peculiar position it produces peculiar symp
and signs. The tumour invades the superior mediastinum early and involves the brachial plexus and cerv
sympathetic nerves and upper ribs to produce a collection of symptoms known as pancoast syndrome. It
includes (a) Homer’s syndrome, (b) lower brachial plexus palsy, (c) erosion of upper two ribs on X-ray an
pain in the shoulder, arm and axilla, the inner aspect of the upper arm and the scapular region. This is a s
growing tumour.
SIGNS.— Signs are particularly conspicuous by their absence in bronchogenic or lung carcinoma. If su
tumour produces bronchial obstruction, only then a whezee may be heard in the involved area. There may
presence of pleural effusion secondary to the lung carcinoma which will give rise to dullness on percussio
and diminished breath sounds on auscultation.
A few signs may be obtained due to
metastasis of the primary tumour. En
8th cervical nerve larged cervical or axillary lymph nodes
stellate ganglion may be palpable in the supraclavicular or
dome of pleura axillary region respectively. Liver enlarge
ment can be assessed clinically on careful
oesophagus 1st thoracic nerve
palpation.
lower trunk of
laryngeal nerve
brachial plexus Staging of lung carcinoma.— Lung
scalenus anterior carcinoma can be divided into 4 stages
phrenic nerve
■V------ subclavian vein according to the American Joint Com
1st rib mittee for Cancer Staging —
Occult carcinoma.— There is no evi
dence of primary tumour or evidence of
metastasis to the regional lymph nodes or
distant metastasis. But bronchopulmon
ary secretion contains malignant cells.
Invasive carcinoma.—
Stage I.—The primary tumour is with-
Fig.41.6.— Normal anatomy of apex of the left lung. This figure shows out any metastasis to the hilar lymph node
the structures which may be involved by the pancoast tumour to 0r to any distant sites,
produce pancoast syndrome.
Stage II.—The tumour classified as T2 with metastasis to the lymph nodes in the ipsilateral hilar region on
Stage III.—The tumour has metastasis to the lymph nodes on the contralateral hilar region or anywhere in
the mediastinum or with distant metastasis.
1. BLOOD.— (i) Eosinophilia has been found to be associated with a variety of lung carcinomas. This
eosinophilia may be due to manifestation against tumour necrosis or a particular type of haemopoietic horm
may be produced by the tumour cells which stimulates bone marrows to produce more eosinophils.
(ii) Carcinoembryogenic antigen (CEA) levels may be significantly elevated in patients with sma
carcinoma with liver metastasis. Serial estimation of CEA levels may be useful in monitoring response to
chemotherapy.
2. CHEST X-RAY.— Carcinoma of lung may present a variety of roentgenographic manifestations.
The most common presentation is a mass in the hilar region. There may be isolated mass in the peripheral
lung field either with a smooth border (known as ‘coin lesion’) or with irregular margin. Many of these may
be without symptoms and are first noted on a routine chest film. Quite a few patients with lung cancer may n
show any changes on the chest X-ray.
Evidence of secondary invasion or metastases may also be revealed on skiagraphy. These are (i) pleural
effusion, (ii) osteolytic lesions in the ribs or vertebrae and (iii) evidence of paralysis of the phrenic nerve with
an elevated non-mobile diaphragm on the affected side.
3. CYTOLOGICAL EXAMINATION OF THE SPUTUM.— This may diagnose many occult carcino
mas in X-rays. It is successful in more than 60% of cases.
4. PERCUTANEOUS ASPIRATION NEEDLE BIOPSY.— Peripheral lung carcinomas may be diag
nosed more readily by this technique. This is done under local anaesthesia. This is particularly helpful in tho
cases which cannot be diagnosed by bronchoscopy. In one series the needle aspirate demonstrated malignan
cells with 96% accuracy.
5 BRONCHOSCOPY.— This is the fundamental diagnostic technique for patients suspected of lung car
cinoma. With the advent of flexible fibreoptic bronchoscope the success rate has gone upto 70%. With the hel
of bronchoscopy one can do bronchial brushing and cytologic studies of bronchial washings that may be
obtained through broncoscope. The endoscopist must try to assess the proximal extent of the neoplasm as th
resectability of the tumour depends on its closeness with the tracheal carina.
6. MEDIASTINOSCOPY.— This has become a routine practise once the diagnosis is made to see the
mediastinal structures through a small incision in the suprasternal fossa. The mediastinoscope is introduced
through the incision along the anterior course of the trachea. It is also possible to take biopsy from the
paratracheal and hilar lymph nodes. If nodes of the other side are involved resection of the tumour
is contraindicated. Many surgeons now favour a short anterior or lateral thoracotomy in preference to medi
astinoscopy. It is simple and offers better acess to the hilar region. Mediastinoscopy may be associated with
serious and fatal complications including haemorrhage from an arterial or venous source.
7. CT SCAN.— This technique is being utilised not only for diagnosis of lung cancer but also for its
staging. Computed tomography correctly predicts the presence or absence of mediastinal metastasis with
accuracy of more than 90%. If CT of mediastinum demonstrates no lymphadenopathy, mediastinoscopy is
unnecessary. But false positive result may be achieved due to lymphadenopathy from other causes than
metastasis.
8. LIVER, BRAIN and BONE SCANNING.— Following injection of technetium-labelled sulphur
colloid, scanning of liver, brain and bone may be performed to exclude distant metastasis.
9. ROUTINE RADIOGRAPHIC BONE SURVEY for all patients should be considered before opera
tion. Occult skeletal metastasis is seen in 21% of cases. Bone scanning is more successful than conventional
X-ray.
10. BARIUM SWALLOW EXAMINATION of the oesophagus will indicate if it is involved by the lun
cancer or not. Mediastinal glands may press on the oesophagus which will also be revealed by this technique
11. SCALENE NODE BIOPSY or supraclavicular node biopsy may also detect involvement of these
nodes which contraindicate radical resection.
TREATMENT.— Surgical removal of the primary tumour is the treatment of choice. Whenever possible
radical resection of the tumour should be performed.
There are a few instances when the patient cannot be operated on and these cases are considered to be
inoperable. It must be remembered that when a diagnosis of carcinoma of lung is made, half of the patients a
found to be inoperable from the outset Of the 50% upon whom exploratory thoracotomy is performed, half of
these will be found to have such extensive disease that a radical resection cannot be performed. Thus radical
resection is possible in only 25% of patients in the best centres of the world and this figure is much less in our
country.
CONTRAINDICATIONS for operability of the tumour are —
(i) Involvement of the main bronchus within 1.5 cm of the carina.
(ii) Evidence of involvement of the recurrent laryngeal nerve, oesophagus or superior vena cava.
(iii) Involvement of the phrenic nerve.
(iv) Evidence of distant metastasis.
(v) Compression of the trachea.
(vi) Paralysis of the vocal cords.
(vii) Patients are unfit for operation due to their old age and general condition.
(viii) Patients with chronic bronchitis and poor respiratory reserve.
(ix) Patients with serious ischaemic heart disease.
(x) Signs of cardiac involvement
When the patients are fit for operation exploratory thoracotomy should always be peformed. Most surgeo
prefer posterior thoracotomy through the 5th or 6th intercostal space. However an anterior thoracotomy
through the 3rd intercostal space is sometimes preferred by a few surgeons since ventilation is much better
achieved during the operation with this approach.
The extent of lung resection obviously depends on the site of the tumour. For lesions confined to one lobe
lobectomy will suffice. When the tumour has involved the main bronchus, pneumonectomy is the operation of
choice. For carcinomas occurring in the periphery of the lung, particularly in patients with reduced pulmona
reserve, a local wedge resection can be an entirely satisfactory procedure. In certain patients in whom an
extensive pulmonary resection is hazardous, sleeve resection may be performed in which one lobar bronchus
together with a part of the right or left main bronchus is excised and the distal bronchus is then reanastomos
to the proximal bronchus.
Radical excision.— As in cancer anywhere in the body radical resection means excision of the primary
tumour with the regional lymph nodes.
Radical pneumonectomy.—Anaesthesia is given to one lung. At the initial stage the pulmonary veins from
the affected lobe should be tied to reduce the risk of tumour embolism. The remaining vessels are then isolat
and secured by double ligatures before they are divided. The bronchus is divided as close to its origin as pos
without leaving behind any redundant stump which may be devitalised. The paratracheal, subcarinal and p
aortic lymph nodes should be removed with surrounding areolar tissue alongwith lung resection. The bronc
is closed with sutures of wire or nylon using interrupted figure of ‘8’ stitches. Nowadays automatic stapling
device has been introduced to staple for closure of bronchus.
Radical lobectomy.— The relevant artery, vein and bronchus are isolated by blunt dissection. Sometimes
the lobes may be adhered to each other and such adhesions are to be divided by sharp dissection. Thus the lo
is gradually freed from its attachments. The visceral pleura is incised and the lobe with the lobar bronchus is
isolated. The bronchus is divided between clamps close to its origin from the main bronchus. The correspond
vessels are divided between ligatures. The bronchus is closed with interrupted sutures of silk, nylon or steel
A stapler may also be used instead of sutures. The bronchial stump is then over-sewed with mediastinal pleu
Apical and basal pleural tubes are inserted for removal of air and blood respectively and to ensure full expan
of the remaining lung. Any involved lymph nodes in the mediastinum should be removed alongwith
surrounding areolar tissue with lobectomy.
After thoracotomy, it may be seen that the growth is not suitable for radical resection, (i) Spread of the
tumour involving the parietal pleura, (ii) pericardium, (iii) heart or (iv) other mediastinal structures are signs
which indicate non-suitability of the case for resection of the tumour, (v) Involvement of the chest wall in mos
cases indicate non-operability, but in certain cases it is possible to resect the tumour en bloc with the chest wal
If on thoracotomy the growth is not suitable for complete resection, a palliative resection should be
undertaken. By this, it means removal of the portion of the lung with primary tumour. This is quite helpful to
the patients as it will not give chance for subsequent bronchial obstruction to develop. Similarly frank abscess
distal to the lesion is also not possible. Sometimes severe haemoptysis may be relieved by palliative resection
Radiotherapy.— Patients selected for primary radiotherapy treatment include —
(i) those in whom operation is contraindicated or those who refuse surgery;
(ii) those with inoperable lesions;
(iii) those in whom carcinomata recur after previous surgical excision.
The generally recommended dose in the treatment of carcinoma of the lung is 5000 to 6000 rads given
5 times weekly for 5 to 6 weeks.
Preoperative irradiation has only been successful in carcinoma of the superior pulmonary sulcus (Pancoast
tumour) which becomes more operable after this radiation therapy. Otherwise the scope of preoperative
irradiation is not satisfactory due to increased incidence of bronchopleural fistulas following resection and no
improvement in the survival rate.
Postoperative irradiation has a limited scope when the risk of recurrence following surgical therapy is
anticipated. This has also a place when a portion of the growth has not been removed during operation. For s
patients a dose of approximately 5000 rads is given over a period of 5 weeks to the left out primary tumour an
involved lymph nodes.
Palliative radiation therapy can be very useful in improving the quality of life by improving chest pain,
haemoptysis and paroxysmal coughing. Superior vena caval syndrome is also relieved to a great extent. Relie
of pain from bone metastasis is often achieved by palliative radiation therapy. Brain metastases can also be
palliated by whole brain radiation with doses upto 4000 rads given over 4 weeks period. Neurologic deficits
can also be relieved by radiation therapy.
In modem days complications of radiation therapy are usually minor. These include radiation pneumonitis
and oesophagitis. Pneumonitis is generally associated with mild cough, fever and minimal haemoptysis. Late
pulmonary changes include interstitial fibrosis.
Chemotherapy.— Chemotherapy has a particular role to play in small cell carcinoma of the lung (oat cell).
Aggressive chemotherapy is the treatment of choice in this condition. The current treatment protocols of smal
cell carcinoma include cyclophosphamide, doxorubicin and vincristin. Cyclophosphamide is probably the
single most active drug. Adriamycin is also a good potent addition. Recently VP-16 has become an important
chemotherapeutic agent and is often used in combination with doxorubicin and vincristin. When these drugs
are administered in conjunction with a course of radiation (3000 rads), this combination has achieved
considerable remission. The response rate is as high as 75% with limited disease and complete remission has
been obtained in 14% of patients with extensive disease.
For non-small cell bronchogenic carcinomas the effect of chemotherapy has been variable. It is more
effective in adenocarcinoma and large-cell carcinoma than for squamous cell carcinoma. In adenocarcinomas
by using combination of radiation therapy and chemotherapy considerable remission has been achieved. In
these cases 4 drugs therapy should be introduced with cyclophosphamide, adriamycin, methotrexate and cis-
platinum.
For patients with extensive squamous cell carcinoma of the lung several different combination of drug have
been employed with some success.
Immunologic aspects of pulmonary carcinoma.— It is known that depressed cellular immunity is always
associated with a poor prognosis in patients with all type of malignant tumours. In this type of carcinoma a
attempt has been made to increase the immunocompetence of the individual with lung carcinoma. Immuno
erapy of pulmonary neoplasm has been evaluated by the direct intratumour injection of bacille Calmette-
Guerin (BCG). Such injections were made either by the transbronchoscopic route or by percutaneous inject
with aid of the fluoroscope into the pulmonary tumours. Although considerable resolution of the neoplasm
been achieved, yet this technique is in the developmental stage. Complications include fever, empyema and
bronchopulmonary fistulas.
Laser therapy.— YAG laser and carbondioxide laser have been introduced in the treatment of malignant
disease of the main stem bronchi. Y AG (yttrium-aluminium-garnet) laser is safer and produces effective re
especially in patients who have inoperable lesion and who is suffering from massive haemoptysis or when
lesion is obstructing the bronchus causing infection distally. By this technique haemorrhage can be controll
similarly obstruction can be relieved.
SECONDARY CARCINOMA OF THE LUNG

The types of primary tumours which metastasise to the lungs are
1. Carcinomas, of which carcinoma of the breast, kidney, thyroid, colon, prostate, testis and uterus are
important in that order of frequency.
2. Sarcomas, of which osteosarcoma tops the list.
3. Choriocarcinoma, which often metastasises to the lungs.
4. Malignant melanoma.
ROUTES OF SPREAD.—
1. By blood stream.— By far this is the commonest route through which metastasis occurs in the lungs. When
the primary growth is located in the area
of systemic circulation, the cancer cells
in the blood stream meet the first set of
capillaries in the lungs. Here they rest
and gradually proliferate to cause secon-
■ ; dary metastasis.
When the primary growth is located
j] ^ ’ ■■ in the portal circulation, the cancer cells
.Hb in the blood stream meet the first set of
capillaries in the liver, so liver metasta
sis is quite common in G.I. carcinomas.
^relllPw*' 2. By the lymphatics.— Lymphatic
'• : spread into the lungs may occur from
■ cancer of the breast.
;; Types.— Secondary deposits of the
j . '■ ■■■■;> lungs may be of two types:—
: -; 1. A solitary central deposit known
as 'cannon-ball' metastasis. Such me
tastasis is more often seen in carci-
; noma of the kidney, carcinoma of the
breast, osteosarcoma and malignant le
. .. .
sion of the testis.
2.
tered all over the lung. These may be
Fig.41.7. Chest X-ray showing a large round opacity in the right unilateral or bilateral,
lung in a patient who was operated on for anal carcinoma 2 years ago.
This is a typical case of ‘secondary carcinoma of the lung’. Treatment.
SURGERY.— In case of solitary pulmonary metastasis resection is indicated in those patients in whom a
year or more had passed between control of the primary tumour and appearance of the metastasis. In all ev
it is important to assess the extent of the pulmonary lesion before operation. Standard X-ray tomography is
supplanted by computed tomography for this purpose. In evaluation of patients to be considered for resect
of pulmonary matastasis, the exclusion of metastasis to other sites should be as thorough as possible.
Radioisotopic studies, bone marrow biopsy, lymphangiography, various scannings and total body CT scan
should be performed to exclude such possibility.
The extent of pulmonary resection for metastatic lesion is determined by the location of the lesion and the
patient’s pulmonary function. The majority of the patients require wedge pulmonary resection or segmente
tomy, the operative mortality of which is quite low (1%). Pneumonectomy is rarely indicated.
CHEMOTHERAPY.— With increased effectiveness of chemotherapy, this has been used with better
results after excision of lung metastasis particularly in osteosarcoma, carcinoma of the breast and testis.
Nowadays intense RADIOTHERAPY is almost always used following resection with the hope of controllin
secondary tumour growth in the lung and prolonging survival.
In case of bilateral lesions, staged thoracotomies with an interval of several weeks or months have been u
But one must always be sure that no other metastasis exists in other parts of the body.
THE MEDIASTINUM
Anatomy.— The mediastinum is an extrapleural space between the two pleural cavities, bordered on each side by
parietal pleura. It is customery to divide the mediastinum into several areas. The mediastinum is classically divided into 4
compartments —
1. Superior mediastinum — which lies above the plane extending from the lower margin of the manubrium stemi
in front to the lower margin of the 4th thoracic vertebra behind. It contains the upper trachea and oesophagus, the aortic arch
and its branches and the thymus gland.
The inferior mediastinum is further subdivided into 3 compartments —
2. Anterior mediastinum — lies in front of the anterior border of the heart. It contains the thymus gland, adipose and
areolar tissues containing lymphatics.
3. Middle mediastinum — is a triangular area with its
base on the diaphragm and is bounded in front by the anterior
mediastinum and in the back by the posterior mediastinum.
It contains the pericardium and the heart, aorta, tracheal bi
furcation and'fnain bronchi and the bronchial lymph nodes.
4. The posterior mediastinum — is bounded anteriorly
by the middle mediastinum and posteriorly by the anterior
borders of the bodies of the dorsal vertebrae and anterior
surfaces of the ribs and inferiorly by the diaphragm. It
contains the oesophagus, the descending aorta, the sympa
thetic and intercostal nerves and posterior mediastinal group
of lymph nodes.
MEDIASTINAL EMPHYSEMA.—
Introduction of air into the mediastinum produces me
diastinal emphysema or pneumomediastinum. The air usu
ally comes through the rent in the tracheo-bronchial tree or
in the oesophagus. Penetrating wounds injuring these struc
tures or blunt trauma with fracture of ribs or vertebrae may
rarely cause such injury.
On very rare occasions, one may find ‘spontaneous
mediastinal emphysema', in which air leaks out into the
Fig.41.8.—Anatomic subdivision of the mediastinum as mediastinum not following trauma but usually following
seen in a lateral chest X-ray. . , ,,, ..,,
interstitial emphysema of the lung or due to alveolar rupture
following positive pressure ventilation, air by dissecting along the vascular structures of the lung enters the hilum and then
into the tissue planes of the mediastinum.
SYMPTOMS.—These include substemal pain and crepitus in the suprasternal notch and in the neck. Gradually patient
complains of dyspnoea.
Physical signs.— Crepitus in the substemal notch is the pathognomonic sign of mediastinal emphysema. In late cases
mediastinal air may spread to the soft tissues of the neck, chest, abdomen and extremities. The patient may be cyanosed.
There may be prominence of the neck veins when mediastinal air exerts considerable pressure on the superior vena cava.
Circulatory failure may develop.
Chest X-ray is diagnostic and shows presence of air within the mediastinum.
Treatment.— Traumatic mediastinal emphysema calls for immediate surgical attention. Thoracotomy is performed
with closure of the opening in the tracheobronchial tree or oesophagus. The ‘spontaneous’ form is likely to subside itself
without producing significant sequelae. The patient must be observed carefully and as soon as there is manifestation of
increased tension, surgical decompression may be necessary.
MEDIASTINAL TUMOURS AND CYSTS

The various tumours and cysts, which are noticed in the mediastinum can be classified according to their
positions.
1. In the superior mediastinum.—
(a) Thymoma is the most common followed by
(b) Tumours of the thyroid and
(c) Tumours of the parathyroid.
2. In the anterior mediastinum.—
(a) Retrosternal goitre.
(b) Thymoma.
(c) Teratodermoid tumours.
(d) Germ-cell tumours.
(e) Lymphomas.
(f) Parathyroid adenoma.
(g) Lymph node lesions.
(h) Mesenchymal tumours.
(i) Vascular and lymphatic tumours.
3. In the middle mediastinum.— Mainly the cysts e.g.
(a) Bronchogenic cysts.
(b) Pericardial cysts.
4. In the posterior mediastinum.—
(a) Neurogenic tumours, which are by far the most common.
(b) Enteric cysts.
For convenience of description, various mediastinal tumours will be described first followed by mediastina
cysts.
MEDIASTINAL TUMOURS
THYMOMA.—
Thymomas are the most common neoplasms arising in the anterior mediastinum. This is also one of the most common types of
mediastinal tumours. These tumours are also seen in the superior mediastinum. Tliese tumours are rare in childhood and usually appear
in adult life, the pick incidence is between the ages of 40 and 60 years. This tumour occurs in almost equal frequency in males and females.
(i) About l/3rd of thymomas are asymptomatic.
(ii) Compression effects e.g. superior vena caval obstruction, dyspnoea, cough and chest pain are presented by a few patients.
(iii) The most important presentation is myasthenia gravis. It is seen from 10 to 50% of cases of thymomas. Patients with thymoma
and myasthenia gravis are thought to have much poorer prognosis than without myasthenia gravis. But the recent trend is that the survival
is more related to the stage of tumour than to the presence of myasthenia gravis.
(iv) There are reports of thymoma occurring with a variety of clinical conditions e.g. red-blood cell aplasia, Cushing's syndrome,
hypoglobulinaemia, severe collagen vascular disorders and megaoesophagus.
HISTOLOGIC CLASSIFICATION.— Thymomas have been classified simply on the basis of predominance of epithelial or
lymphocytic cells. Thus thymomas may be (i) epithelial type, (ii) lymphocytic type, (iii) mixed type or (iv) teratomatous type. The epithelial
type is the commonest.
BENIGN OR MALIGNANT.— Benign tumours constitute 50 to 65% of cases. These are well capsulaled and do not invade adjacent
mediastinal structures. The malignant varieties are associated with severe and intractable disease and infiltrate locally to the pericardium,
pleura, heart, great vessels or chest wall.
Routine radiography is the main investigation which almost always reveals a thymoma.
Treatment.— Presence of thymoma is themain indication for exploration regardless whether ornot it is associated with any symptom
or not. Median sternotomy is the choice of approach. Benign encapsulated tumours should be completely resected alongwith the entire
thymus and the adjacent adipose tissue of the anterior and superior mediastinum.
In case of malignant thymoma, complete resection is preferred alongwith removal of the involved neighbouring structures.
Radiotherapy in doses of 4000 to 6500 rads is usually given postoperatively to patients with malignant tumours.
After exposure, if complete excision is not possible, interstitial implantation of the residual tumour with U5Iodine is a good procedure
to provide high levels of continuing postoperative irradiation.
TERATODERMOID TUMOURS.—
Mediastinal teratomas arise from cells originating from the branchial cleft and pouch in association with the thymus gland. The
mediastinum is the 2nd most frequent location of teratomas after the gonads in adults and sacrococcygeal area in children. These tumours
are frequently seen in the anterior mediastinum, but rarely these may be located intrapericardially or in the posteriormediastinum. As other
teratomas, mediastinal teratomas are also composed of multiple types of tissues (ectodermal, mesodermal and entodermal) foreign to this
area. Careful histologic examination reveals that ectodermal elements predominate, though mesodermal and entodermal tissues are also
present. These solid teratomas contain well differentiated elements of teeth, bone, cartilage, mucus, fibrous, lipoid and muscle tissue with
nerves, salivary glands, pancreas, thymus and lung.
The term 'dermoid cyst' is used to describe those lesions that are primarily cystic and contain amounts of epidermis, dermal glands,
hair and sebaceous material.
Teratodermoid tumours are most frequently seen in adolescents or in young adults. Both sexes are equally involved. Approximately
80% of these tumours are benign.
Clinical features.— These tumours may also present asymptomatically. Compression to the adjacent structures are the main
presenting features.
(i) Frequent use of chest roentgenography has been able to detect asymptomatic smaller tumours.
(ii) The most important diagnostic test specific for suggesting malignancy is the high serum level of Alphafetoprotein and
carcinoembryonic antigen. These elevated glycoproteins are due to their secretion by the malignant components of the tumour.
Treatment.— Operative resection is the treatment of choice. Even when the tumour is benign it may be attached to the thymus or
pericardium, portions of which should be removed with the tumour.
It is difficult to remove malignant teratomas totally in all cases as they often invade the superior vena cava, pericardium or heart. In
case of incomplete removal, combination chemotherapy including cis-platinum should be given. The prognosis of malignant teratomas is
poor as these tumours often recur locally or metastasise early. Some better results have been claimed by a few surgeons using
chemotherapy.
GERM-CELL TUMOURS —
These tumours arise from primordial mediastinal germ-cells that failed to migrate from the urogenital ridge. Germ-cell tumours
constitute 1 % of all mediastinal tumours. There are 5 types of germ-cell tumours seen in this region — seminoma, embryonal carcinoma,
teratocarcinoma, choriocarcinoma and endodermal sinus or yolksac tumour. About half are seminomas.
Clinical features.— Majority of the patients are symptomatic at the time of diagnosis. Features of compression e.g. retrosternal chest
pain, superior vena caval obstruction and hoarseness of voice are the main symptoms.
Chest X-ray is confirmatory and it shows a large anterior mediastinal mass, which is not very easy to differentiate from other tumours
and cysts of the anteriormediastinum. When malignant these tumours commonly metastasise to the pleura, chest wall, lymph nodes, liver,
bone and retroperitoneal tissue. Choriocarcinoma and embryonal carcinoma are highly malignant neoplasms.
The non-seminomatous tumours produce biologic markers like Alphafetoprotein (AFP) and Human Chorionic Gonadotrophin (HCG)
which are almost diagnostic.
Treatment.— It should be remembered that seminomas are radiosensitive. The general approach is total resection of the tumour by
operation. Pure seminomas should be given radiotherapy which may cure the condition.
In case of non-seminomatous tumours excision followed by chemotherapy is the treatment of choice.
LYMPHOMAS —
Mediastinal lymph node involvement is quite common in cases of disseminated lymphoma. These lymphomas are usually situated in
the anteriormediastinum, although they may involve lymph nodes elsewhere particularly around the bronchi. These lesions are basically
malignant. Such malignant lymphomas may be divided into 2 groups — Hodgkin lymphoma and non-Hodgkin lymphoma. In 50% of
patients with Hodgkin disease mediastinal lymph nodes are involved.
Clinical features.— Mediastinal lymphomas can occur at any age, though these are commonly seen in the 3rd or 4th decades of life.
The main symptoms are cough, fever, chest pain and weight loss.
The main diagnostic investigations are the chest X-ray, CT scan and cervical lymph node biopsy.
Treatment is mainly based on the type of lymphoma.

ENDOCRINE TUMOURS.—
Two types of endocrine tumours are seen in the mediastinum — thyroid tumours and parathyroid tumours. While retrosternal goitres
are sometimes seen, parathyroid adenomas are never seen as swelling of the mediastinum.
Thyroid tumours.— These tumours are either asymptomatic or may produce symptoms of compression. Occasionally retrosternal
goitre may be toxic.
Parathyroid adenoma.— These are usually seen in the anterior or superior mediastinum. Occasionally these may be seen in the
posterior mediastinum in the groove between the trachea and the oesophagus. Most mediastinal parathyroid tumours are hormonally active.
MESENCHYMAL TUMOURS.—
7% of all mediastinal tumours and cysts are the mesenchymal tumours. Lipomas are the most frequently found tumours. Majority of
these are seen in the anterior mediastinum. Due to its soft consistency, it may reach enormous size before causing symptoms. When
symptoms occur, these are mainly due to compression of the neighbouring structures. Operative excision is the treatment of choice.
Othermesenchymal tumours include liposarcoma, fibroma, fibrosarcoma, mesothelioma, myxoma, lieomyosarcoma and rhabdomyo
sarcoma. These tumours are relatively uncommon.
VASCULAR AND LYMPHATIC TUMOURS —
The different types of these tumours which are occassionally found in mediastinum are haemangioma, lymphangioma, haemangio-
endothelioma and lymphangiomyoma. The most common variety is the benign lymphangioma, also konwn as cystic hygroma. These
tumours are usually seen in the anteriormediastinum and in all age groups. These tumours often grow to large size before they are diagnosed
and produce symptoms by compressing adjacent structures. One very rare tumour characteristically located in the posterior mediastinum
is the intrathoracic extramedullary haematopoiesis.
These tumours are usually thin-walled unilocular cysts or multilocular tumours. On chest X-ray these present as round or lobulated
mass of homogeneous density.
NEUROGENIC TUMOURS —
This is the most common neoplasm arising in the mediastinum. It accounts for approximately 21 % of all primary mediastinal tumours
and cysts. These are mostly situated in the posterior mediastinum along the paravertebral gutter, arising from either the intercostal nerve
or the sympathetic chain. This tumour occurs at any age and is most often benign. When seen in children, there may be a tendency towards
malignancy. Incidence of malignancy is between 10 to 20%. The various neurogenic tumours, which are seen in the mediastinum, are
neurilemmoma, neurofibroma, ganglioneuroma, neuroblastoma and pheochromocytoma.
NF.tJRTI .F.MMOMAS.— These are the most common neurogenic tumours seen in the mediastinum. These arise from the Schwann
cells of the nerve sheath and so are called ‘Schwannomas’. These are well capsulated tumours comprising of elongated fusiform cells. Chest
X-ray shows dense, homogeneous mass in the posterior mediastinum.
NEUROFIBROMAS.— These arise from nerve sheath and nerve fibres. These are poorly encapsulated. Histologically these are
composed of random arrangement of spindle-shaped cells lacking the uniformity of neurilemmoma. This tumour may be present as one
of the mainfestations of generalised neurofibromatosis, known as von Recklinghausen's disease. It is difficult to completely excise this
tumour due to its infiltrating growth nature.
GANGLIONEUROMAS.— These originate from the sympathetic chain and are composed of ganglion cells and nerve fibres. These
tumours are more often seen in children though it may occur at any age. A partially differentiated type, which contains immature cells of
sympathetic nervous system mixed with mature ganglion cells, is called ganglioneuroblastoma. This has malignant potentiality and may
present with wide spread metastases.
NEUROBLASTOMAS.— These are the most poorly differentiated malignant tumours arising from the sympathetic nervous system.
These are highly invasive tumour and 75% occurs in children less than 4 years of age.
The usual presentation is combination of fever, cough, vomiting and diarrhoea. Metastases to the regional lymph nodes, bone and 1 iver
may be present at the time of diagnosis. Direct invasion of the spinal cord with neurologic deficit is not uncommon.
Treatment.— Mediastinal neuroblastomas are often unresectable at the time of diagnosis, due to local invasion and distant metastasis.
However the tumours are usually radiosensitive. Radiotherapy alongwith chemotherapy has made the prognosis much better than
previously.
PHEOCHROMOCYTOMAS.— Less than 1 % of all pheochromocytomas occur in the mediastinum. Clinically these tumours are no
different from intra-abdominal pheochromocytomas.
CYSTS OF THE MEDIASTINUM

Bronchogenic cyst.—
These cysts originate from the ventral foregut that forms the respiratory system. These cysts are located close to the trachea or main
stem bronchi. Rarely there is communication of the cyst with the tracheobronchial tree. Histologically these are composed of ciliated
respiratory epithelium, cartilage, smooth muscle, fibrous tissue and mucous glands.
Clinical features.—These cysts are found most often in young adults and are uncommon in infancy. The usual symptoms are the result
of compression by the cyst e.g. dyspnoea, dysphagia, cough and chest pain.
Chest X-ray shows a smooth density just in front of the trachea or main siem bronchi at the carinal level. When the cyst communicates
with the tracheobronchial tree, air-fluid level may be seen within the cyst.
CT scanning is useful in localising these cysts.
Malignant degeneration has been reported in these cysts on rare occasions.
Enteric cysts.—
These are also called enterogenous cyst, gastric cyst, reduplication cyst or inclusion cyst. These cysts originate from the dorsal division
of the foregut that develops into the gastrointestinal tract. These cysts are smooth walled and are composed of muscular coat and mucosa
which are usually ciliated. It usually contains a clear and colourless mucoid fluid. These cysts are mainly located in the posterior
mediastinum adjacent to the oesophagus. These cysts occasionally may communicate with the oesophagus.
Clinical features.— Approximately 60% occur in infants less than 1 year of age. Symptoms are due to pressure on the oesophagus or
the tracheobronchial tree. As many of these cysts are lined with aberrant gastric mucosa, peptic ulceration, perforation and bleeding are
recognised complications. Very occasionally it may erode into the lung parenchyma to cause lung abscess. Rarely enteric cyst may be
multiple or may be associated with duplication of abdominal portions of the gastrointestinal tract with a communication between the
thoracic and abdominal portions of the duplication through the diaphragm.
Treatment is operative removal of the cyst. Sometimes dissection may be difficult due to previous inflammation and adhesions to the
surrounding structures.
Pericardial cyst.—
This is the most common cyst of the mediastinum. This is a solitary cyst adjacent to the pericardium near the cardiophrenic angle. It
is thought to originate from a failure of fusion of the primitive pericardial lacuni. According to some it develops from abnormal folds in
the embryonic pleura. Such cysts usually contain a clear fluid. It may communicate with the pericardium.
Histologically the cyst wall is composed of a single layer of mesothelial cells.
Clinicalfeatures.— Though congenital in origin, these cysts are usually first detected in adult life. This i s rarely seen in children. These
cysts occasionally produce symptoms and majority are found as incidental finding on routine chest X-ray. It is also characteristically
diagnosed by CT scanning and by echocardiography.
Treatment is surgical excision. Such removal is more indicated to exclude other diagnosis.
THE DIAPHRAGM
Development.— Closure of the pleuroperitoneal opening is caused by a mesodermal partition which separates the thoracic from the
abdominal cavity and forms the Diaphragm in the adult. The diaphragm is developed from composite structures, of which the septum
transversum is the main. The pars diaphragmatica of the septum transversum starts developing in the region of the neck and that is why
the muscles which form the diaphragm is derived principally from the 4th cervical myotome and is innervated by the phrenic nerve (C3,
4 and 5). Besides the septum transversum the diaphragm receives a small contribution dorsilaterally from the pleuroperitoneal membrane.
In front of the oesophageal hiatus a small contribution is received from the gastrohepatic ligament which is derived from the pars
mesenterica of the septum transversum. Between the oesophageal and aortic hiatuses the diaphragm is formed by the dorsal mesentery.
Behind the abdominal aorta and lateral to it the diaphragm is formed by the mesoderm of the dorsal body wall. The most lateral portion
of the diaphragm which is almost attached to the costal wall is formed by the costal portion of the chest wall.
So developmentally, dia
1 phragm is a composite structure
which is formed by (i) the pars
diaphragmatica of the septum
transversum, (ii) pleuroperi
toneal membrane, (iii) gas
trohepatic ligament (pars mesen
terica), (iv) the dorsal mesen
tery, (v) mesoderm of the dorsal
body wall and (vi) costal portion
of the chest wall.
DIAPHRAGMATIC
HERNIA
Basically there are two types
of diaphragmatic hernia — 1.
Congenital hernia and 2. Ac
quired hernia.
The CONGENITAL IIF.R
NIAE occur at certain well rec
ognised points due to failure of
fusion of the various elements
which make up the diaphragm.
Such hernia usually has a well
defined peritoneal sac and adhe
Fig.41.9.— Shows the development of the diaphragm and different congenital defectssions around this type of hernia
(foramina) through which diaphragmatic hernia may occur. S.T. — The portion which are uncommon. There may be
develops from septum transversum. C.P.— The portion develops from costal part. associated other congenital
M.D.— The portion develops from mesoderm of dorsal body wall. P.P. —The portion anomalies.
develops from pleuroperitoneal membrane. 1. Foraman of Morgagni. 2. Oesophageal Congenital hernia may oc
cur through oesophageal hiatus,
hiatus. 3. Foramen of Bochdalek. 4. In the dome of diaphragm.
through foramen of Morgagni
(retrosternal), through foramen of Bochdalek (posterolateral), through failure of development of dorsal part of the diaphragm (posterior
hernia) and eventration or central hernia through the dome of the diaphragm due to atrophy and loss of muscle in one-half of the diaphragm.
ACQUIRED HERNIAE.— These may occur due to trauma or very rarely following operations involving the diaphragm. But
oesophageal hiatus hernia forms the major part in this group and constitutes about 98% of diaphragmatic hemiae.
DIAPHRAGMATIC HERNIA
Congenital Acquired
1. Through oesophageal hiatus. 1. Oesophageal hiatus hemia (98%).
2. Through foramen of Morgagni. 2. Traumatic.
3. Through foramen of Bockdalek. 3. Postoperative.
4. Posterior hemia.
5. Eventration.
Oesophageal hiatus hernia.—This is mainly an acquired condition, which is presented in the middle age and it is considered in detail
in the section of ‘Hiatus Hernia’ in the chapter of ‘The Oesophagus’. I'll 1 s hernia however may occur as a congenital abnormality and is
presented by children or adolescents or young adults. This is extremely rare.
Hernia through the foramen of Morgagni (Retrosternal hernia).— This foramen is a defect between the sternal and costal
attachments of the diaphragm. It is situated anteriorly almost behind and lateral to the sternum. Such hernia is more common on the right
side. The symptoms are due to subacute obstruction and is usually presented by adult patients. It is often the transverse colon which herniates
through the defect. So the obstruction is of chronic nature. More often this condition remains symptom free.
Hernia through the foramen of Bockdalek (Posterolateral hernia).— This foramen is often called pleuroperitoneal canal due to
defect in the development of the pleuroperitoneal membrane. The opening lies on the posterolateral aspect of the dome of the diaphragm.
It provides a free communication between the pleural and abdominal cavities. This hemia usually does not possess a peritoneal sac. It is
usually presented by neonates or children with respiratory difficulty due to herniation of abdominal hollow viscera inside the thoracic cavity
which press on the lungs. Sometimes the case is presented as acute intestinal obstruction, though small intestine or large intestine may
herniate. The condition is more common on the left side.
Eventration (Central hemia).— This condition is due to loss of muscle of a portion of diaphragm which becomes fibrous. The thin
diaphragm gives way to the increased abdominal pressure and the whole dome of the diaphragm with abdominal viscera herniate into the
thoracic cavity. This condition may be due to intrauterine rupture of the pars diaphragmatica of septum transversum which is covered by
fibrous tissue later on. This condition is also more common on the left side. Occasionally respiratory difficulties may be complained of,
though basically this condition remains asymptomatic. It is only discovered during routine X-ray examination by raised and immobile
diaphragm. It is in fact not a true hemia.
TREATMENT.— Surgical repair is the only available treatment in diaphragmatic hemia. It is usually performed through a low
thoracotomy incision. The defect is closed by two rows of non-absorbable sutures. It is always advisable to look for any other associated
congenital abnormalities present. Particularly in neonates there is a chance of presence of mal-rotation of bowel or midgut volvulus. It
should be corrected through separate abdominal incision and is corrected by dividing Ladd’s band and repositioning of the bowel.
Traumatic hernia.—It is a type of acquired hemia. Rupture of the diaphragm may occur due to penetrating injury (by dagger or bullet)
or due to crush injury of the abdomen (traffic accident or fall from a height). Rupture may also occur from crushing injury with the body
flexed (accidents in mines). In case of bursting or crushing injury there occurs a linear tear in the dome of the diaphragm particularly on
the left side (as the right side is well protected by the liver). Through the rent there is herniation of the stomach and transverse colon.
Diagnosis can be established by the history that the patient gets respiratory difficulty during feeding. On examination bowel sounds may
be detected in the chest, unless there is paralytic ileus. X-ray examination is confirmatory as it shows fundal gas or gas of the transverse
colon inside the chest. Basal opacity may confuse the diagnosis and the condition may resemble a pneumothorax. Barium meal X -ray will
be more helpful to diagnose this condition.
Treatment is reduction of hemia and repair of the tear in the diaphragm with non absorbable sutures. The access may be obtained
through lower thoracotomy or thoracoabdominal incision.
657
CHAPTER - 34
THE HEART AND PERICARDIUM
CARDIAC ARREST
Definition.—Cardiac arrest is in fact cardiopulmonary arrest, which is the unexpected cessation of effective
ventilation and circulation in a person.
The heart and lungs should be considered as one unit. Initially one of these may be affected, but its failure
very rapidly involves the other. Thus respiratory failure rapidly leads to cardiac arrest and vice versa.
Incidence.— In civil life cardiac arrest is seen (i) mostly in the operation theatre with major surgical
procedure especially those performed on hearts. But it must be reiterated that cardiac arrest is also seen in mi
operations and even in case of diagnostic procedures.
The other causes are — (ii) electrocution, (iii) drowning, (iv) major trauma and (v) asphyxia.
Pathogenesis.— There are a number of causes of cardiac arrest or ventricular fibrillation. These causes
are:—
1. Anoxia.— (i) Inadequate ventilation and tracheobronchial obstruction either from retained secretions
or from aspirated gastric contents may cause cardiac arrest. This is the commonest cause of cardiac arrest, (ii)
Excessive anaesthesia, overdosage of narcotic or tranquillizer drugs may also cause ventilatory failure, (iii)
Sudden severe fall in blood pressure may produce hypoxia. All these causes will cause myocardial hypoxia
which is the most frequent and important precipitating cause of cardiac arrest.
2. Coronary occlusion.— Occlusion of one or more coronary arteries with resulting myocardial
ischaemia or infarction is the second common cause of cardiac arrest. Such coronary occlusion is often seen
in coronary artery disease affected with atherosclerosis. Coronary occlusion may be brought about by (i)
thrombus, (ii) air, (iii) excessive radiopaque medium injection, (iv) dissection of the wall of the artery or (v)
ligation.
3. Reduced cardiac output may also cause cardiac arrest due to marked decrease of cardiac output and
rapid fall in blood pressure. This condition may be seen in (i) shock, (ii) cardiac tamponade, (iii) arrhythmia,
(iv) cardiac myopathy or (v) myocarditis.
4. Electrolyte abnormalities.— Either deficiency or excess of potassium may cause cardiac fibrillation
and arrest. This is more often caused by hyperkalaemia. The heart muscle is quite sensitive to alteration in its
biochcmical environment, particularly to alteration in the extracellular levels of potassium. The heart is arrest
in diastole in the presence of hyperkalaemia. Such hyperkalaemia may be caused by (i) renal failure, (ii)
excessive potassium administration or (iii) rapid infusion of cold stored blood.
Acidosis may rarely cause cardiac arrest. Such acidosis may be seen in (i) diabetes mellitus, (ii) starvation,
(iii) high intestinal fistula, (iv) hypothermia.
5. Drugs.— A few drugs, when used in excessive amounts, are known to induce ventricular fibrillation
or even cardiac arrest, (i) Most anaesthetic agents induce hypotension and even dysrhythmias. Digitalis is one
of the most prominent in this group. Myocardium becomes more sensitive to digitalis with rise of concentrati
of potassium in the serum, (ii) Inotropic drugs e.g. isoprenaline, adrenalin and dopamine may cause ventricu
dysrhythmia leading to fibrillation, (iii) Quinidine may cause ventricular fibrillation at a normal dosage, (iv)
Beta-blockers and other vasodilators, when used in combination, may cause profound hypotension and asyst
6. Arrhythmias.— Profound bradycardia with a heart rate below 60 beats per minute may progress to
ventricular arrhythmia with either fibrillation or arrest. Ventricular arrhythmias from any cause may progres
to fibrillation. Constant monitoring of the electrocardiogram is an integral part of any postoperative cardiac u
7. Diseased myocardium.—It has less reserve and relatively minor disturbances may cause cardiac arrest
in already diseased myocardium.
8. Reflex stimulation.— With stimulation of vagus nerve, which also supplies the heart, it may lead to
cardiac fibrillation and arrest. Experimentally constant electrical stimulation of the vagus nerve has produced
42
cardiac arrest, but only for a few seconds. It is more probable for already diseased or injured myocardium
go to cardiac arrest with such vagal nerve stimulation. Vagus nerve stimulation may be caused by (i) inser
of a gastric tube, (ii) endotracheal suctioning or (iii) vomiting.
9. Aberrant electric currents.— Electrocautery may induce cardiac arrest following fibrillation. Mal
function of an implanted pacemaker is another rare cause.
Types of cardiac arrest.— The heart may cease to act adequately in one of the following ways :—
1. Ventricular fibrillation is the most common cause which may lead to cardiac arrest. Ventricular
fibrillation is usually associated with diseased heart (myocardial infarction) or with an irritable heart as a r
of manipulation, trauma or drugs. In this condition the myocardium of the ventricles contracts irregularly
feebly, so that the cardiac output is very much depressed and cardiac arrest may occur.
2. Mechanical asystole.— In this condition the heart beat becomes slow and feeble and ultimately stops
The myocardium is often diseased and flabby. The usual causes are severe anoxia and massive coronary
thrombosis.
3. Circulatory obstruction.— This is often caused by massive pulmonary embolism or accidental
occlusion of one of the main vessels.
Pathology.— The central nervous system is the most vulnerable tissue which becomes so readily affecte
by interruption of circulation and oxygenation. Only 4 to 6 minutes of anoxia can be tolerated at normal
temperature before cellular damage becomes irreversible. Following cessation of circulation the pupils beg
to dilate in 30 to 45 seconds. The respiratory drive is lost after approximately 1 minute as the mediulla oblo
becomes depressed. An adult can tolerate only 4 minutes of this sequence.
When the cellular damage is irreversible in the brain, restoration of circulation may be accompanied by
function of other organs in other areas of the body, but with loss of cerebral function. Without cerebral reco
the person is almost considered dead. So diagnosis of cardiac arrest must be made as quickly as possible w
immediate management.
Diagnosis.— The diagnosis of cardiac arrest usually depends on absence of carotid or femoral pulse. The
radial pulse is not a reliable index for making this diagnosis. The additional findings are loss of normal ski
colour, failure of mucous membrane perfusion and loss of cerebral function indicated by dilated pupils an
unconsciousness. While the patient is being operated on, thecolour of blood gives an indication of cardiac
The colour becomes blackish with cardiac arrest.
Electrocardiographic changes cannot be wholly relied upon, as electrical activity can persist long after
cardiac action has become ineffective. Monitoring of the electrocardiogram on an oscilloscope may give
indications of cardiac fibrillation. Direct monitoring of arterial pressure by an indwelling catheter is also
valuable in this respect. This also permits monitoring of arterial blood gases by repetitive sampling. These
the anaesthetist in preventing cardiac arrest and if it does happen early treatment can be instituted.
In nut-shell, diagnosis of cardiac arrest is made by the following findings —
(i) Disappearance of peripheral pulses (by palpating femoral or carotid arteries).
(ii) Auscultation of the chest demonstrates no cardiac sounds.
(iii) Change of colour of the blood.
(iv) Dilatation of pupils.
(v) Loss of consciousness.
Treatment.— Every attempt should be made to diagnose this condition from the first 3 signs, as the last
2 signs are relatively late and should not be allowed to appear. Since irreversible brain damage will develo
following 3 to 4 minutes of cardiac arrest, it is imperative that immediate treatment should be started as so
as this diagnosis is made.
1. VENTILATION.— To provide adequate oxygenation is the prime treatment of cardiac arrest. T
airway of the patient is opened by tilting his head backward as far as possible placing one hand on the fore
and the other behind the neck. This manoeuvre lifts the tongue from the back of the throat where it would
otherwise obstruct the airway. It may also be necessary to displace the jaw further forward to open up the a
THE HEART AND PERICARDIUM 659
either by traction on the lower lip (Fig. 42.1) or by pushing forwards on the angles of the mandible.
Usually the patient cannot begin respiration spontaneously. So artificial respiration must be started using
mouth to mouth or mouth to nose technique. This can be
begun immediately and continued till less laborious meth
ods can be arranged. In hospitals, an oral airway, self inflat
ing bag and face mask are often available. Similarly most
cardiac resuscitation kits include a laryngoscope and an
endotracheal tube, which can be inserted by any physician
with moderate experience. It must be borne in mind that
one of the primary causes of resuscitation failure is at
tempted placement of endotracheal tube by an inexperi
enced person. Using either direct breathing or an anaes
thetic bag for ventilatory resuscitation, inflation should be
provided every 5 seconds and the patient is permitted to
exhale passively. The chest should be seen to expand with
Fig.42.1.— Shows the initial step in resuscitation of ventilation.
cardiac arrest. The airway is kept open by tilting the head 2. CARDIAC MASSAGE.— With the initiation of
back and elevating the jaw to displace the tongue forward ventilation, carotid pulse is palpated. If the pulse is absent,
so that it cannot obstruct the airway. ........................................... ... , , . . ........................ ........ . . . ;__________________ „
circulation is initiated by EXTERNAL CARDIAC
MASSAGE. This is accomplished by intermittent compression of the heart between the sternum and the
vertebral column.
For performing cardiac massage, the patient must be on a firm surface, such as the floor or a board. Certain
points are essential in this technique. The heel of the hand should be placed
over the lower third of the sternum and with the other hand above it depress
the sternum intermittently for 3 to 4 cm. Such sternal compression should
be brisk with depressing the sternum sharply and then releasing it fully to
permit cardiac fdling. The position of placement of the heel of the hand is
highly important as if the hand is placed at a lower level near the xiphoid,
it may injure the liver, whereas if it is placed more superiorly, it may cause
multiple fractures of the ribs. External massage should be maintained at a
rateof 60 per minute. Usually more than one person will be required, since
one person will be fatigued quickly. Simultaneously the other person
should palpate the peripheral pulse —.either carotid or femoral to note the
amount of force applied by the external massage.
Fig.42.2.— Shows the correct method
The time for which external cardiac massage should be continued is not
of external cardiac massage. The hands
are placed one above the other cn the definite. It should be continued so long as cardiac resuscitaion remains
sternum and external massage is per feasible and cerebral function is intact. Though majority of successful
formed by depressing the sternum 1 to 2 cardiac resuscitations are accomplished within a few minutes, on rare
inches with the heels of the hands.
occasions it may be continued for even a few hours.
If the closed cardiac massage fails to bring about adequate resuscitation, open cardiac massage should be
performed through a left lateral thoracotomy through the4th and 5th intercostal space. It is rarely needed, thou
it should be tried if cardiac arrest has occurred during operations on the lungs or heart. Even during abdomin
operations one may do the cardiac massage through the diaphragm.
OPEN CARDIAC MASSAGE.— The indications for open-chest cardiac massage are :
(i) This is performed particularly when the chest has already been opened for an operation.
(ii) When closed cardiac massage fails to provide effective circulation.
(iii) This is particularly required when cardiac tamponade, tension pneumothorax or other internal thoraci
injuries have been suspected.
(iv) It becomes obligatory in patients with chest or spinal deformities including severe emphysema.
Technique.— The chest is opened through the left 5th intercostal space. The incision is made from the
sternum to the axilla. The wound usually does not bleed much. A rib spreader is used to retract the incisio
margins. If this is not available, massage should be started with one hand. For convenience of massage, the
pericardial sac should be opened. Only the ventricles are compressed and not the atria. Massage is efficien
performed with two hands — one placed above and the other below the ventricles. The cardiac massage is
performed with the flat of the hand andfingers, but not with the finger tips. The rate of compression should be
about 50 times per minute. Adequate care must be taken not to damage the myocardium. With the open ch
cardiac massage the tone of the myocardium is improved due to increase of coronary blood flow and simil
the brain also receives more oxygenated blood flow. The arrested heart is flaccid, cyanosed and distended,
gradually becomes firmer, smaller and pinker after the massage. Direct cardiac massage allows visual
assessment of the tone of the heart and presence or absence of ventricular fibrillation. If such fibrillation
continues, defibriller should be used by direct application of electrodes on the heart.
Before closing, it is a good practise to attach chest pacemaker wires to the left ventricle to avoid further
episodes of arrest. The closure of the wound should be performed under sterile conditions.
3. PHARMACOLOGIC THERAPY.— Several drugs may be essential early in the management of
cardiac arrest:—
(i) Epinephrine is one of the most effective drugs used in cardiac resuscitation. The possible ionotropic
effect of epinephrine does not improve the results of resuscitation, so there is less need for intracardiac
administration. But it is the positive chronotropic effect of epinephrine which can convert asystole to sinus
rhythm to improve the rate in bradycardia. It is indicated for all types of cardiac arrest. It is administered i
at the dose of 0.5 mg and repeated at 5 minutes intervals or as an infusion 1 to 2 ml epinephrine in 1 : 10000
dilution directly into a peripheral vein.
(ii) Sodium bicarbonate is required to combat acidosis. The acidosis of the cardiac arrest is well managed
by hyperventilation. But restoration of normal pH often becomes necessary before effective cardiac contrac
tions can be obtained. Sodium bicarbonate is administered as an initial dose of 1 mEq/kg intravenously.
{iii) Calcium chloride is a powerful stimulant of myocardium. In fact it has both positive chronotropic and
inotropic effects. But it increases ventricular irritability and so should be used with caution particularly in
digitalised patients. Usually it is given in the dose of 5 ml of 10% solution at 5 minutes interval. If calcium
gluconate is used, it has less ionizable calcium and the dose should be 10 ml of 10% solution.
(iv) Atropine sulphate reduces vagal tone and enhances A-V conduction, which makes it useful in the
treatment of sinus bradycardia. It should be used when the heart beat is less than 60 per minute or there is
A-V block. A bolus dose of 0.5 mg is administered intravenously, which may be repeated if required.
(v) Lidocaine has antiarrhythmic properties. It elevates fibrillation threshold. It controls multifocal
premature ventricular contractions. It also controls ventricular tachycardia and fibrillation. It is administer
intravenously in the dose of 50 to 100 mg. Procainamide may also be used for this purpose.
(vi) Certain other agents may be used e.g.—
(a) Isoproterenol for complete heart block.
(b) Propranolol-forsuppressionof ventriculararrhythmiasparticularly inpresenceofdigitalis toxicity.
(c) Diuretic agents, l
(d) Corticosteroids. ) To manage cerebral oedema.
(e) Anticonvulsant therapy may be required.
All resuscitated patients should be placed in an intensive care unit. Constant monitoring of electrocardi
gram, urine output, blood gases and vital signs is of extreme importance particularly for first 48 hours.
4. DEFIBRILLATION.— In the presence of ventricular fibrillation, which can be confirmed by direct
inspection in case of open chest cardiac massage or by electrocardiogram, electrical defibrillation should be
performed with defibrillator unit. Generally capacitance discharge(DC) defibrillation is used today. In closed
technique chest electrodes are applied over the base and apex of the heart or one large electrode is applied
posteriorly near the vertebral column and a small electrode anteriorly near the apex of the heart. Defibrillatio
is usually done with either alternating or direct current, though direct current defibrillation is mostly preferr
The cause of failure to defibrillation is anoxia or acidosis. Acidosis is corrected with bicarbonate. Sometimes
injection of epinephrine may be required to increase myocardial tone to facilitate subsequent defibrillation.
Except for a case of coronary thrombosis, it is possible to defibrillate almost all fibrillating heart. Sometimes
the electric current becomes inadequate and in these cases complete defibrillation may not be possible. Cases
of inadequate electric current include low voltage applied, defective electrodes and the manner in which
electrodes are applied to the heart.
5. LATER MANAGEMENT following cardiac resuscitation.— After restoration of normal rhythm of
heart, a careful assessment should be made about damage done to the central nervous system due to cardiac
arrest. The patient may remain in comatose stage. These cases should be treated by mild hypothermia lowering
the body temperature to 33° to 34°C. This temperature should be maintained for 3 to 4 days. Another problem
is cerebral oedema, for which massive dosage of a steroid e.g. 2 to 3 g of prednisone should be given every 8
hours for 1 to 2 days.
Careful monitoring of cardiac rhythm with an oscilloscope is essential as arrhythmias are not uncommon
following restoration of cardiac arrest. In these cases intravenous administration of Lidocaine 1 mg per minu
and procainamide is useful for suppressing cardiac arrhythmias. Periodic measurement of arterial and venou
blood gases is required.
Fluid therapy should not be excessive, as this may increase cerebral oedema. Renal damage is another
complication of cardiac arrest due to less vascular flow to the kidneys. If renal activity is impaired, measures
described under renal anuria should be instituted.
Prognosis.— In one sentence it can be said that without any underlying myocardial defect, cardiac arrest
can be treated effectively. The mechanism of arrest is the major determinant of survival. Various other diseas
such as pneumonia, hypotension, renal failure and cancer when previously exist in these patients, survival ra
obviously will not be encouraging. On the other hand cardiac arrest in an otherwise healthy individual can b
managed effectively as mentioned above.
SPECIAL INVESTIGATIONS FOR HEART DISORDERS
Cardiac surgery has advanced a lot in the last two decades. Precise cardiac surgery has been made possible by detail informations of
the diseased heart through various special investigations. These are described in nut-shell in the following paragraphs —
1. Radiological Investigations.—
(a) STANDARD CHEST X-RAY.— These give informations about the shape and size of the heart. A few special views from
different angles may indicate enlargement of a particular chamber of the heart e.g. left atrial enlargement can be detected from left lateral
view particularly during barium swallow examination of the oesophagus.
Plain X-ray also gives a definite information on pulmonary circulation. This has been described in details under special investigation
of various cardiac conditions later in this chapter.
(b) FLUOROSCOPY.— This indicates more precisely the cardiac borders and contour and size of various cardiac chambers.
Certain amounts of functions of the cardiac chambers may also be assessed with this investigation.
(c) CT SCAN is more helpful in getting informations regarding pericardium and other mediastinal structures surrounding the
heart. Conditions like coarctation of aorta, calcified valves may be detected through this investigation.
2. Angiocardiography.— By injection of radio-opaque solution of 30 to 70 ml of Niopam 370 under high pressure, ordinary
angiocardiography may be obtained with cut films. Cine angiocardiography may be obtained by using cine-film. With this technique
important anatomical examination regarding size and shape of the different heart chambers, presence of a shunt or septal defects and
function of different valves can be obtained. The aorta and the pulmonary artery and its branches are also visualised in detail. Selective
angiocardiography is possible to delineate the anatomy of the coronary arteries in patients with angina. Atherosclerotic plaque in the artery,
its correct size and extent and collateral circulation can be well assessed using Neopam 370 with a dose of 4 to 6 ml per selected coronary
artery.
When the various datas from angiocardiography are manipulated with computer technology fine images can be obtained, which is
known as Digital Subtraction Angiography (DSA).
3. Cardiac catheterisation.—The development of cardiac catheterisation can be separated into 3 majorperiods. In the first period,
methods were developed for inserting catheters into the heart and measuring pressures from various chambers, in the 2nd period, these
techniques were combined with radiographic imaging to produce various important informations regarding function of the various
chambers of the heart. In the 3rd period catheterisation techniques were modified and extended to allow the angiographer to treat cardiac
disease as well as to diagnose it
Access to the vena cava and right heart chambers can be attained either percutaneously or by surgical venotomy. Percutaneous right
heart cannulation is usually done via the femoral vein, whereas venotomy is performed at the antecubital fossa. Right heart catheterisation
can also be done from the internal or external jugular or subclavian veins.
Cannulation of the left heart is performed percutaneously from the femoral artery or by surgical cut down on the brachial artery.
Occasionally the left heart chambers are approached from the right atrium via the right femoral vein using a technique known as transseptal
catheterisation. This procedure involves puncture of the interatrial septum with a special catheter. Most catheters are composed of Woven
Dacron or nylon covered with a radio-opaque plastic coating.
Pressure measurement.— Measurement of intravascular and intracardiac pressure is a major objective of cardiac catheterisation. The
normal haemodynamic values are —
Right atrium — 0 to 8 mm Hg; Right ventricle — 5 to 30 mm Hg (systolic) and 0 to 8 mm Hg (diastolic).
Pulmonary artery — 15 to 30 mm Hg (systolic); 5 to 15 mm Hg (diastolic); Pulmonary artery wedge — 1 to 12 mm Hg.
Left ventricle — 90 to 140 mm Hg (systolic); 2 to 12 mm Hg (diastolic); Aorta — 90 to 140 mm Hg (systolic); 60 to 90 mm Hg
(diastolic). Measurement of cardiac output is also a function of cardiac catheterisation.
A contrast cine angiogram of the left ventricle (contrast left ventriculography) is a routine part of most left heart catheterisation studies.
Left ventriculography may be performed on either a biplane or single plane basis. It permits an evaluation of ventricular function and
chamber size, segmental wall motion, wall thickness and presence and severity of mitral regurgitation. Angiographic assessment of the
severity of a regurgitant vulvular lesion is an important step in determining the proper timing for valve replacement surgery.
Coronary angiography is another investigation which may be performed by cardiac catheterisation and gives a clear delineation not
only of the anatomy of the coronary arteries but also the presence of atherosclerotic plaque, its site and extent. Intracoronary administration
of streptokinase is another part of the new and rapidly evolving field of interventional cardiac catheterisation.
4. Echocardiography or cardiac ultrasound.— Beams of high speed ultrasound waves are directed through heart. When these
waves cross a boundary or interface, the waves will be reflected back to the transmiting source provided the reflecting surface is at right
angles to the original beam. By placing the transmeter, the movements of various walls of the heart including various septa and leaflets
of valves can be recorded with useful informations. Thickening, calcification and mobility of the valve cusps can be clearly demonstrated,
so that necessary operation can be timed properly. It also indicates presence of any atrial tumour or pericardial effusion with certainty.
Recent developments have included investigation of all forms of congenital heart disease by two dimensional and pulsed Doppler
echocardiography. This investigation alone can find out various important informations of the diseased heart, so that cardiac catheterisation
and angiocardiography can be dispensed with.
5. Radionuclcar studies.— Radionuclear imaging has made a major advance in the understanding of myocardial function both
in health and diseased Using a gamma camera one can assess how the ventricles are moving and with Thallium scans one can assess the
blood supply to the heart. If radioactive material is coupled with specific antimyocardial monoclonal antibodies, areas of heart damaged
during heart attack can be defined.
6. Magnetic Resonance Imaging (MRI).— With improvements in equipment technology, faster scan times and software
upgradation, MRI is becoming the investigation of choice of patients with congenital heart disease. MRI studies also give excellent details
particularly by using cardiac gating informations about cardiac chambers, myocardium, septa, valves and great vessels. This is also proving
useful in investigating cases with myocardial infarction, ventricular aneurysm, intracardiac thrombi and tumours.
It also helps both in diagnosis and demonstrating the extent of dissecting aneurysm.
The most impressive recent introduction is cine MRI, which is probably going to replace conventional angiographic procedures to study
the heart and coronary arteries.
TYPES OF CARDIAC SURGERY
The various types of cardiac surgery are as follows :—

1. Extracardiac operations.— Such operations are not performed on the heart itself, but are performed
on the main vessels outside the heart. The examples arepericardiectomy, resection of thoracic aortic aneurysm
systemic-pulmonary anastomosis, ligation of patient ductus and excision of coarctation of aorta. In these
operations cardiac function is not usually disturbed.
2. C losed heart surgery.—These are in fact blind operations and access is obtained into the heart throug
incision on the ventricular or atrial wall. The heart is allowed to work while it is operated on. Mitral valvotom
is probably the only operation which is still performed as a closed intracardiac operation.
3. Open heart surgery.—Majority of the cardiac surgeons will like to operate on an open and motionless
heart. If the heart is made motionless, blood supply to the various tissues will be stopped. This cannot be
accepted. So some alternative arrangement must be made to continue blood supply to the vital organs of the
body, so long as the heart is operated on and kept without its function of pumping blood. The various alternat
arrangements to continue blood supply while the heart is operated on are as follows:—
(i) HEART-LUNG BY-PASS.— In this technique, oxygenated blood is pumped to the vital organs of the body with
a heart-lung machine. This type of machine is now widely available in the market in many commercial models. Basically
the machine consists of an oxygenator (alternative of lungs) and a pump (alternative of the heart). The circulating blood is
diverted from the heart and lungs and is passed through this heart-lung machine, so that the surgeon can operate on the heart
while it is not functioning. By this technique, majority of complicated congenital and acquired cardiac abnormalities are
operated on.
In this technique, a median sternotomy incision is applied. The patient is first heparinised with 3 mg/kg body weight.
The ascending aorta is cannulated with a plastic tube through a purse-string suture placed in the coat of adventitia. Each vena
cava is also cannulated through the right atrial wall. These two cannulae are now connected to the heart-lung machine. So
the deoxygenated blood from the venae cavae are coming to the heart-lung machine, where it is oxygenated and then pumped
into the ascending aorta. This is the procedure, with which the heart and lungs of the patient are made inactivated for
operation on the heart. Before starting the heart lung machine one must be sure that all air bubbles have been eliminated.
After the operation is over, the cannulae are removed, the purse-string sutures are tightened and the heparin is counteracted
with protamine (6 mg/kg body weight). Various methods are adopted for monitoring the extracorporeal circulation. A few
of these are measurement of blood gases, determination of serum potassium and measuring urinary output.
Myocardial preservation is an important part of this extracorporeal circulation. The surgeons prefer a motionless
relaxed heart for a considerable period to operate on. This is achieved by myocardial cooling with a crystalloid solution at
4°C. This solution also contains an elevated concentrationof potassium to make the heart to stop in diastole. As temperature
of the myocardium is considerably reduced, its consumption of oxygen is also dramatically reduced. For this the
myocardium can be kept with safety for 2 to 4 hours.
(ii) LEFT HEART BY-PASS.— This is a miniature form of heart-lung by pass. In this technique the left atrium and
the left femoral artery are cannulated. The blood from the left atrium is diverted through a pump into the left femoral artery.
With this technique the left ventricle continues to pump to send oxygenated blood to the head and upper extremities. The
extracorporeal pump is supplying blood to the lower extremities and the abdominal viscera through the femoral artery. With
this technique the thoracic aorta is made empty for operations to be performed on this region.
(iii) FEMORO-FEMORAL BY-PASS.— In this technique the femoral vein and the artery are cannulated. The blood
is diverted from the femoral vein through an extracorporeal oxygenator and a pump and the blood is sent back into the
femoral artery. This is almost similar to the left heart by-pass, though here an additional oxygenator is used as the lungs are
a'so inactivated by this technique. Its indication is also similar to the heart by-pass. This operation is only performed when
the left atrium is not readily accessible.
(iv) REGIONAL SHUNTS.—In this technique operations like aneurysms or coarctations are operated on by diverting
blood from the aortic arch or the left subclavian artery to the femoral artery. Through this local by-pass system, the
operations on the important arteries are performed without jeopardizing the viability of their supplying organs.
(v) HYPOTHERMIA.— Before advent of the heart-lung machine, this was the technique adopted for performing
small operations on the heart. By cooling the tissues, the metabolic needs of the body can be considerably reduced, so that
these tissues can survive total deprivation of oxygen for a short period of 10 minutes or partial deprivation for longer periods.
Simple cardiac operations e.g. closure of atrial defects or relief of pulmonary stenosis can be performed with this technique.
Hypothermia is usually achieved by either of the two ways —
(a) Surface cooling.— The whole body is immersed in cold water or by application of cool blankets. With this
measure the body temperature can be reduced to 28 to 30°C.
(b) Veno-venous cooling.—The superior and inferior venae cavae are cannulated. Both these cannulae are joined
with a cooling chamber, so that blood from the superior vena cava is diverted into the cooling chamber and the cold blood
is sent back to the inferior vena cava. With this technique the body temperature can be reduced to 15 to 18°C and periods
upto 45 minutes of circulatory arrest may be tolerated. Surgery of congenital heart disease in infants may be carried out with
this method. It should be remembered that ventricular fibrillation may start at a temperature below 25°C particularly in
adults, so cardiopulmonary by-pass is the best technique.
CONGENITAL HEART DISEASES

The scope of cardiac surgery has been increased considerably in the last decade. This has made possible to
operate on both congenital and acquired heart diseases. In this section I shall discuss the important common
congenital heart diseases v/hich are well amenable to cardiac surgery.
About 6 babies in every thousand live births have congenital abnormalities in the heart. These congenital
cardiac abnormalities can be broadly classified into two groups — I. Acyanotic congenital heart disease and
II. Cyanotic congenital heart disease.

I. ACYANOTIC CONGENITAL HEART DISEASES
In this group the arterial oxygen saturation remains normal so the body never becomes cyanotic. In this
the various abnormalities are as follows:—
1. PATENT DUCTUS ARTERIOSUS.—
INCIDENCE.—This is the most common congenital abnormality, which occurs once in about every 4000
births and thus constitutes about 15% of all cases of congenital heart disease.
It is about 2 to 3 times more common in females.
Aetiology.— The patent ductus arterious develops from the 6th left aortic arch and is an important norm
foetal pathway connecting the left pulmonary artery or pulmonary artery at its bifurcation to the aorta just
beyond the origin of the left subclavian artery. Through this channel blood by-passes the collapsed lungs in
embryonic life so that blood flows directly from the pulmonary artery into the aorta by-passing the lungs.
With the birth, the baby starts respiration with expansion of the lungs. The blood in the pulmonary arter
passes to the lungs, so the ductus arteriosus usually closes within a few days and becomes fibrotic, which is
called ligamentum arteriosum. It is said that changes in the oxygen tension of the arterial blood exerts a dire
stimulus on the closure of the ductus.
It is not known, why patency exists in a few babies, but it has been shown that an infusion of prostaglan
(PGE,) may maintain patency of ductus.
Pathology.— As the pressure is higher in the aorta than in the pulmonary artery, blood will flow from th
aorta to the pulmonary artery. In case of a large ductus, the shunt may constitute 50 to 70% of the output of
left ventricle. With this pulmonary blood flow increases to as high as 10 to 15 litres per minute. With this inc
of blood in the lungs the pulmonary vessels become dilated (pulmonary plethora) and their pulsation becom
increased (hilar dance). This additional blood flow to the lungs will cause more blood to the left side of the
resulting in left ventricular hypertrophy.
Clinical features.—The symptomatology is directly proportional to the size of the ductus. Many cases ma
remain asymptomatic, whereas a few with large patent ductus may cause serious heart failure during the fi
year. More definite symptoms of congestive heart failure are usually seen only in adult patients. It often app
during the first pregnancy in females.
Physical signs.— The most important sign of patent ductus is a continuous murmur. It is often described
as a ‘machinery’ murmur. This murmur becomes accentuated in systole and diminished in diastole. It is bes
heard in the 2nd intercostal space maximal in the pulmonary area. With smaller patent ductus, this murmur
becomes audible earlier much before the patient develops cardiac failure. The pulse is collapsing in nature.
wide pulse pressure is found with a large ductus. A thrusting left ventricular apical impulse may be felt.
Chest X-ray may be normal. On fluoroscopy a hilar dance may be observed.
Electrocardiogram is usually normal with a small ductus, but will show left ventricular hypertrophy with
large ductus.
Cardiac catheterisation can readily localise the shunt. With appropriate manipulation the cardiac catheter
can be passed through the patent ductus confirming the diagnosis.
Aortography is the most definite diagnostic method.
Complications.— 1. Cardiac failure. 2. Bacterial endocarditis.
Treatment.— Operation is the treatment of choice. This is usually carried out in babies over 2 to 3 years
of age. The operative risk is low and the results are excellent.
Technique.— Operation is performed through a left posterolateral thoracotomy through the 5th intercosta
space. The lung is retracted. The mediastinal pleura is incised over the aortic arch. The vagus nerve and the
recurrent laryngeal nerve are retracted anteriorly. The ductus arteriosus is cleared. Ligation of the patent du
is performed with multiple nonabsorbable ligatures—two transfixation ligatures one on either end of the du
and two in the middle portion of the ductus. Staples may be used instead of ligatures. A temporary aortic shu
usually a left atriofemoral by-pass may be used to permit temporary occlusion of the aorta above or below th
ductus.
2. COARCTATION OF AORTA.—
INCIDENCE.— It is also a common congenital malformation which is second to the patent ductus
arteriosus. It constitutes 10 to 15% of all congenital heart diseases. It is about twice as frequent in males.
Aetiology.— This condition is nothing but narrowing of the aorta immediately beyond the origin of the left
subclavian artery very near to the position of ligamentum arteriosum. The most popular theory is that coarct
is an extension of the fibrotic process which converts the patent ductus into ligamentum arteriosum.
Pathology.— In most patients the constriction is about 2 to 4 cm in length just below the origin of left
subclavian artery. Usually the lumen becomes 1 to 3 millimetre in the constricted area. Distal to the coarctatio
the aorta is usually dilated. It may rarely develop an aneurysm in older patients. Dilated intercostal arteries
entering the distal aorta provide collateral circulation to by-pass the constricted coarctation of aorta. In older
patients these arteries produce ‘notching’ of the ribs. Rarely they may become aneurysmal and may rupture.
There are two main types of coarctation of aorta —
(i) Past-ductal type or adult coarctation.— This is the usual type of coarctation of aorta as described
above.
(ii) Pre-ductal type or infantile coarctation.— Occasionally coarctation may occur in the aorta above the
joining of patent ductus arteriosus. As the ductus usually remains patent, deoxygenated blood pass from the
pulmonary artery into the aorta distal to the coarctation. So the lower trunk and lower extremities become
cyanosed, whereas the head, neck and upper extremities remain pink. This is known as ‘differential cyanosis’.
These patients may have other cardiac lesions and the mortality rate is high.
Clinical features.— The main feature is that there will be hypertension above the obstruction and
hypotension below the obstruction.
Hypertension will be characterised by headache, dizziness, epistaxis, throbbing and pulsation of arteries o
head and neck and a systolic murmur at the apex. There is a chance of left ventricular failure.
The features of hypotension are weak femoral pulsations, cold lower extremities and intermittent claudica
tion of the legs.
Complications include left ventricular failure, intracranial haemorrhage, intrathoracic haemorrhage and
very rarely rupture of aorta.
Chest radiographs may demonstrate notching of ribs.
Electrocardiogram shows signs of left ventricular hypertrophy.
Cardiac catheterisation and aortography should be performed routinely to locate the site of coarctation and
its extent.
Treatment.— Except for infants with congestive cardiac failure, where operation should be performed
urgendy, the ideal age for operation is between 5 and 7 years. If performed earlier without any definite reason
coarctation may recur as the child grows older.
Operative technique.— The coarctation of aorta is excised and end-to-end anastomosis of the aorta is
performed usually with a graft.
A left posterolateral thoracotomy through the 4th intercostal space is usually preferred. The mediastinal
pleura is incised, after which the vagus nerve is retracted medially. Now the aorta is mobilised both above an
below the constriction taking care not to damage the intercostal vessels. The proximal aorta and the distal aor
are occluded with vascular clamps. The coarctation of the aorta is excised. In children as much as 5 cm of aort
may be excised, whereas in older children upto 3 cm of aorta can be removed. The ligamentum arteriosunvis
also divided. An end-to-end anastomosis is usually possible. This is performed with continuous sutures with
polypropylene (prolene). After anastomosis, the blood pressure should be measured proximal and distal to th
anastomosis. If the difference of blood pressure is more than 4 to 5 mm Hg, a dacron patch is inserted through
a short anterior arteriotomy. This is to widen the lumen of the aorta.

Less than 10% of cases may require vascular grafts. By-pass dacron graft is mostly used.
Postoperatively, antibiotics are given routinely for 3 to 4 days. The results of operation are usually good a
the patients are discharged in 7 to 10 days.
3. ATRIAL SEPTAL DEFECT.—
This is a not uncommon congenital abnormality of the heart. It constitutes about 6% of all congenital cardiac
abnormalities. This defects allows blood to flow from left to right atrium, so that the right side of the heart and lungs become
overfilled, whereas the left side of the heart receives less blood.
Three main types are usually seen —
(i) SECUNDUM DEFECT.— This is the commonest variety. The defect lies in the centre of the septum.
Embryologically this results from failure of complete development of septum secundum. Symptoms are uncommon in the
first few years of life. The most frequent symptoms are fatigue, palpitation and exertional dyspnoea. Gradually signs of
congestic cardiac failure appear. A soft systolic murmur may be heard at the pulmonary area. The second pulmonic sound
is widely split.
Treatment is direct suturing and closure of the defect by continuous suture with prolene. If direct suturing is not possible,
a prosthetic patch of knitted dacron or pericardium may be inserted. This operation is performed with the help of heart-lung
machine.
(ii) OSTIUM PRIMUM DEFECT.— This is relatively infrequent and constitutes only 4 to 5% of patients with atrial
septal defect. This defect is usually associated with incomplete formation of mitral and tricuspid valves.
Treatment.— Operative correction is usually required between 4 to 6 years of age. Operation is performed with the help
of heart-lung machine. Initially the cleft in the mitral valve is closed with interrupted sutures placed from the ventricular
septum out to the free margin of the mitral orifice. After repair of the cleft mitral valve, the septal defect is repaired with
a patch of pericardium inserted with interrupted sutures. A defect in the tricuspid valve is frequent but usually not amenable
to repair by direct suturing.
(iii) ANOMALOUS DRAINAGE OF PULMONARY VEINS.— This is due to failure of incorporation of sinus venosus
into the atrium proper. The right pulmonary veins usually enter the superior vena cava inferior to the point of entry of azygos
vein, or enter into the right atrium or into the inferior vena cava. Left pulmonary vein may also anomalously enter the
superior vena cava.
Treatment.— A single anomalous pulmonary vein may be harmless and does not require treatment. When treatment is
required, the anomalous veins can be corrected by insertion of prosthetic patch so that the defect is closed and the pulmonary
veins are made to enter the left atrium.
4. VENTRICULAR SEPTAL DEFECT.—
INCIDENCE.— It is a common congenital defect and constitutes 20 to 30% of patients in different cardiac clinics. It
may occur as one of the complex anomalies e.g. Fallot's tetralogy.
Pathology.— The defect may be single or multiple. Ventricular defect is mostly situated in the membranous part or
fibrous part of the septum. The membranous septal defects are either located posteriorly or anteriorly in relation to the crista
supraventricularis. The posterior defects are close to the tricuspid valve on the right and the mitral valve on the left. The
bundle of His is located at the posterior and superior rim of the defect. The anterior defect is safely away from the conduction
bundle and its closure is easier than that of the posterior defect.
The septal defect varies from 3 mm to more than 3 cm in size. The defects smaller than 1 cm is called ‘small’ defect
and larger than 1 cm is called ‘large’ defect.
The defect allows passage of blood from the left to the right ventricle resulting in over-filling of the right heart and
pulmonary hypertension.
Clinical features.— Patients with small ventricular septal defect may remain asymptomatic. But those with larger
defects are usually symptomatic and the first and most common symptom is dyspnoea on exertion. Gradually pulmonary
hypertension develops and haemoptysis may result. Severe cardiac failure may develop subsequently.
On Physical examination a loud pansystolic murmur is typically present in the 3rd and 4th intercostal space along the
left sternal border. Sometimes a thrill is palpable. Retardation of growth may be obvious and some cardiac enlargement. is
regularly present. Rales may be present due to chronic pulmonary congestion.
1. Chest X-ray with small ventricular septal defect is usually normal. With large defects, enlargement of both
ventricles may become visible. Enlargement of pulmonary artery and its tributaries and pulmonary congestion may be
visible in X-ray.
2. Electrocardiogram of small defect is usually normal. But with large defect evidence of right ventricular
hypertrophy may be present.
3. Cardiac catheterisation confirms the diagnosis and it also assesses the extent of left to right shunt.
Treatment.— Operation is the treatment of choice and it is usually performed in the 2nd year. If symptoms are not
disabling, the time for operation may be deferred to 4 to 6 years.
Technique.— The operation is performed through a median sternotomy with the help of extracorporeal circulation. A
longitudinal ventriculotomy is performed usually in the infundibular part of the right ventricle and near the anterior
descending coronary artery. The alternate approach is through the right atrium, particularly when pulmonary vascular
resistance is significantly increased. The defect is usually closed with an oval patch of knitted Dacron by mattress sutures
(prolene) posteriorly and continuous suture (prolene) anteriorly.
Postoperatively, Digitalis is usually given, as some degree of right ventricular failure is common. The risk of operation
increases somewhat if pulmonary vascular resistance is increased. Earlier diagnosis and treatment have brought down
operative mortality to as low as 1 to 2%.
II. CYANOTIC CONGENITAL HEART DISEASES

In cyanotic congenital heart diseases, the patients become cyanosed very soon after birth. The most
important and common in this group is Fallot's tetralogy.
1. FALLOT'S TETRALOGY.—
Tetralogy of Fallot was first described in 1671 by Stenson. But little was understood until 1888 when Fallo
described clearly the combination of abnormalities and that is why this condition is called ‘Fallot's tetralogy'.
INCIDENCE.— This condition constitutes over 50% of all cases of cyanotic heart disease.
Pathology.— The 4 features of tetralogy from which the name originates are — (i) pulmonary stenosis
(obstruction of the outflow tract of the right ventricle), (ii) a ventricular septal defect, (iii) dextroposition of th
aorta, which receives blood from both the ventricles and (iv) right ventricular hypertrophy. The right ventric
obstruction increases right ventricular systolic pressure equal to that of the left ventricle. The ventricular sep
defect is large about 2 to 3 cm. The right ventricular obstruction may be an infundibular stenosis or a valvula
stenosis or a combination of the two.
In this condition due to obstruction in the right ventricular outflow and presence of ventricular septal def
the venous blood entering thcright ventricle is shunted direcdy into the aorta to produce cyanosis. This cond
also decreases pulmonary blood flow and thus limits and ability to absorb oxygen. This causes the basis for
severe intolerance to exercise. Due to presence of large ventricular septal defect, right ventricular pressure ca
never exceed left ventricular pressure inspite of presence of pulmonary stenosis. For this reason, cardiac
enlargement and failure are usually not seen.
Severity of anoxia varies with the degree of reduction in pulmonary blood flow. Arterial oxygen saturatio
may come down to 30 to 35%, when the body can walk only a short distance. Very low saturations of 10 to 20
is also seen in rare cases when the infant is not only unable to walk, but also may lose consciousness due to
cerebral anoxia.
Chronic anoxia may produce compensatory polycythemia and eventually clubbing of the extremities.
Polycythemia is seldom seen before 2 years of age. In fact severe cyanosis is visible only after polycythemia
has developed. About l/3rd of patients are cyanotic at birth, these patients often do not survive infancy unle
operation is performed quickly.
Threat to life in the 1st year is cerebral infarction. Brain abscess is another serious complications.
Symptoms.— Almost all patients are symptomatic. Dyspnoea on exertion is the first symptom. Soon
cyanosis develops. After walking a short distance the body squats down to take rest. Walking for short distan
interrupted by squatting, is a pathognomonic symptom of this condition.
Physical examination.— The findings on physical examination are :—
(i) Various degrees of cyanosis.
(ii) Clubbing of digits.
(iii) Heart of normal size.

(iv) A systolic murmur presents at the 3rd or 4th intercostal space along the left sternal border, which m
be accompanied by a thrill in half the patients.
(v) The second pulmonic sound is weak or absent, while the aortic second sound is increased.
(a) Chest X-ray usually shows nothing characteristic except for decreased vascularity in the lung fields.
(b) Electrocardiogram is usually abnormal with right ventricular hypertrophy of varying severity with
right axis deviation.
(c) Cardiac catheterisation demonstrates several features — (i) right to left shunt is detected by arterial
unsaturation, (ii) Right and left ventricular systolic pressures are usually equal, (iii) Pulmonary artery press
is less than normal, (iv) The pulmonary blood flow is decreased.
(d) Selective angiocardiography is of great importance in planning the type of surgery. Any associated
abnormalities in the pulmonary arteries are also noted. Simultaneous opacification of the aorta and pulmon
arteries when the dye is injected into the right ventricle is typical of Fallot's tetralogy.
Treatment.— Operation is the only way to save the child.
LIFE SAVING ANASTOMOTIC PROCEDURE.— Infants with cyanotic spells i.e. eipsodes of sudden increase in
intensity of cyanosis followed by unconsciousness, require urgent operation. Some type of shunt procedure is performed.
The best type of shunt in these critically ill babies, usually under4 months of age is probably Blalock's subclavian-pulmonary
anastomosis. This operation was first performed in 1944 by Blalock. He created an anastomosis between the left subclavian
artery and the left pulmonary artery. In fact the subclavian artery is divided at a distance from its origin and the cut proximal
end of the subclavian artery is then anastomosed to the upper border of the left pulmonary artery which is already mobilised
and doubly clampped for convenience of performing the anastomosis. A continuous thrill is felt over the anastomosis as soon
as the clamps are released. There are a few alternative anastomotic procedures available where Blalock's operation cannot
be performed. A side-to-side anastomosis between the ascending aorta and the right pulmonary artery was advocated by
Waterson. An aorto-pulmonary anastomosis was constructed with a Goretex graft. An anastomosis is made between the
descending aorta and left pulmonary artery (Pott’s). Superior vena cava is sometimes anastomosed with the right pulmonary
artery (Glenn).
CORRECTIVE OPERATION.— This operation is carried out through median sternotomy with the help of extracor-
poreal circulation. A high vertical ventriculotomy is performed which stops near the pulmonary annulus and is limited to
the infundibular portion of the right ventricle. Through this incision the ventricular septal defect is closed with a Dacron
patch. The pulmonary vulvular and infundibular obstruction is also widened with a patch graft of Dacron. This may be
extended when necessary upto the bifurcation of the pulmonary artery. The ventriculotomy is now closed with an
appropriate Dacron patch.
Following closure of the ventriculotomy and removal of air from all cardiac chambers, extracorporeal circulation is
stopped. Now the intracardiac pressure is measured to confirm that the right ventricular systolic pressure is reduced to less
than 60 to 70% of that of the left ventricle. If right ventricular pressure is still elevated, more correction of the ventricular
obstruction becomes necessary.
Prognosis.— The risk of operation varies with the age of the patient and the degree of cyanosis. While the risk is about
10% for smaller children, it is only 2 to 5% in older children.
2. TRANSPOSITION OF GREAT VESSELS.—
INCIDENCE.— It constitutes 30 to 40% of all cyanotic congenital heart diseases and its incidence is 2nd
to Fallot's tetralogy. It is the most common cause of cardiac failure in the new bom.
Pathology.— In this condition the aorta arises from the right ventricle and the pulmonary artery from th
left ventricle. As a result venous blood is ejected through the aorta and the oxygenated blood returning from
the lungs into the left atrium enters the left ventricle and is again pumped through the pulmonary artery to
lungs. This is obviously incompatible with life except for if a communication exists between the pulmonary
systemic circulations in the form of a patent ductus arteriosus, an atrial septal defect or a ventricular septal
defect. One or more of these congenital anomalies must exist for the infant to survive even a few hours after
birth.
Transposition of the great vessels is often associated with other congenital abnormalities e.g. pulmonary
stenosis, coarctation of aorta, dextrocardia etc.
Clinical features.— High percentage of infants are deeply cyanotic at birth (80%). Cyanosis appears in
most other patients in the first year of life. Anoxic spells of unconsciousness are frequent. Cardiac failure is
similarly frequent. Dyspnoea on exertion is always present. The children who survive beyond first 2 years o
life, clubbing and polycythemia appear. Signs of congestive failure are always found with pulmonary
congestion, cardiac enlargement and hepatomegaly.
Treatment.—
EMERGENCY PROCEDURE.— Because of high fatality in the first month of life, some sort of surgical procedure
must be done to create communication between the pulmonary and systemic circulations. The simplest procedure is the
Balloon Septostomy, in which the atrial septal defect already present is enlarged by passing a deflated balloon catheter
through the defect into the left atrium, and after inflating the balloon it is forcefully pulled across the septum to enlarge the
opening. This technique was first developed by Rashkind and it is almost always done at the time of cardiac catheterisation.
If Balloon Septostomy is ineffective, atrial septal defect may be created by the Blalock-Hanlon technique. In this technique
the right atrium and pulmonary vein are parallely incised. A portion of the atrial septum is excised and the two incisions
are now anastomosed.
CORRECTIVE OPERATION.—Total correctionof transposition during the first two years of life should bemade. This
is achieved by switching over the aorta and pulmonary arteries with transposition of the abnormal coronary arteries.
ACQUIRED HEART DISEASE

1. MITRAL STENOSIS —
Aetiology.— This condition is almost always due to rheumatic fever, though a definite history can be
obtained in only 50% of cases. After the initial episode of rheumatic fever, symptoms of mitral stenosis may
not appear for 10 years or more. It is suggested that scarring of the mitral valve due to rheumatic fever cause
turbulent flow of blood which in tum causes more scarring and contraction over many years. Usually severe
mitral stenosis takes about 20 to 30 years to develop after the last known bout of rheumatic fever.
Pathology.— Rheumatic fever produces a widespread manifestation in the heart. It affects all the three
layers. But in fact involvement of the mitral and aortic valves gives surgical importance to rheumatic fever.
Endocarditis produces ulceration of the endocardium along the edges of the valve leaflets where they norma
appose in systole. Tiny 1 to 2 mm nodules of fibrin and platelets accumulate and gradually progress to fusio
of the leaflets at the commissures. The above-mentioned nodules are the Aschoff nodules. Gradually the valv
cusps become more swollen and roughened. Later on organisation with fibrosis and calcification occur. So th
valve leaflets become thickened, rigid and immobile. The various stages from simple fusion of the commissu
to grossly calcified and functionless valve are seen in different patients. Mitral stenosis gradually increases in
severity over many years.
Pathophysiology.— According to the cross sectional area of opening of the mitral valve, it can be classified
into 4 classes — in class I the cross sectional area is reduced to 2.5 cm2 and this is the mildest form of mitral
stenosis, which are often asymptomatic. In class II the cross sectional area is reduced to 1.5 to 2 cm2 and the
patient complains of some symptoms. In class III the area is reduced to 1 to 1.5 cm2. In class IV it is reduced
to less than 1 cm2 and the patients are seriously disabled.
3 significant haemodynamic events result from mitral stenosis — (i) increase in left atrial pressure, (ii)
increase in pulmonary vascular resistance and (iii) decrease in cardiac output.
Two other disabilities which appear with chronic mitral stenosis are atrial fibrillation and systemic
embolisation. Arterial embolism is a serious consequence which may cause death by cerebral embolism in 20
to 25% of patients. The emboli evolve either due to stasis in the dilated left atrium or from the atrial appenda
SYMPTOMS.— (i) The most important symptom is dyspnoea. When left atrial pressure exceeds 30 mm
Hg, it produces significant transudation of fluid into the pulmonary capillaries, which causes pulmonary
oedema and dyspnoea. In the beginning dyspnoea appears with extreme exertion, but with more severe sten
it occurs with lesser degrees of exertion.

(ii) Chronic cough which becomes worse at night in recumbent position due to pulmonary congestion.
(iii) Orthopnea and paroxysmal nocturnal dyspnoea.
(iv) Haemoptysis, which varies from expectoration of blood-tinged sputum to massive bright red blood.
(v) Due to right heart failure, there will be venous distension, peripheral oedema and hepatic enlargem
(vi) Arterial embolism is a constant threat and may manifest in different ways.
(vii) Angina pectoris is seen in 10% of patients, but the basic cause is not clear. The possible mechanism
may be impaired blood flow through the coronary arteries or recurrent small emboli into the coronary arter
PHYSICAL EXAMINATION.— (i) The patients are usually thin and frail with muscular wasting, typical
of suffering from chronic illness.
(ii) Dilated neck veins are often visible due to congestive cardiac failure.
(iii) Rales are frequendy audible over the lung bases.
(iv) The auscultatory findings are increased first heart sound, an opening snap and a diastolic murmur a
the apex. The intensity of the murmur however does not correlate with the severity of the stenosis. A severe
calcified and fibrosed valve may not produce audible murmur due to little mobility of the valve. A short ap
systolic murmur may be heard in patients with pure mitral stenosis without any associated mitral insufficie
(a) Echocardiography is the simplest and most precise method for making the diagnosis.
(b) Only lateral chest radiography exposed during oral administration of barium to outline the
oesophagus may detect left atrial enlargement. The middle-third of the oesophagus will be displaced backw
to form a concave curve.
In the lung fields one may find engorged pulmonary veins. Dilated pulmonary lymphatics become visib
as transverse lines across the lower lung field known as ‘Kerley lines’. This indicates left atrial hypertension.
(c) Electrocardiogram is often normal. The possible change is increased P-wave due to atrial hypertrophy
(d) Cardiac catheterisation is often required to evaluate the class of mitral stenosis. It also indicates if ther
is mitral insufficiency or aortic valvular disease. The left atrial pressure is estimated from the pulmonary
capillary ‘ wedge’ pressure. Coronary arteriography is an important part of evaluation of cardiac catheterisa
particularly in patients over 40 years of age, in whom coronary atherosclerosis may be present
Treatment.— Mitral stenosis as such is first treated by medical means. If this fails, operation is considered
Indications for operation.— (i) Failure of medical treatment.
(ii) If there are indications of peripheral embolism, operation should be performed as soon as the patien
has recovered from embolic episode.
(iii) If the patient's age is between 20 and 50 years, the result of operation is much better.
(iv) In pregnant woman mitral stenosis should be operated on early. But if the condition is diagnosed in
months of pregnancy, it is better to rely on conservative treatment till delivery, after which operation can be
considered.
(v) The most important consideration about the indication of mitral valvotomy is the mobility of the mi
vulve. The more mobile the valve is, the more satisfactory will be the result of operation. A mobile valve wi
produce accentuation of the first heart sound with the presence of opening snap. On the contrary rigidity of
mitral valve will produce poor first heart sound and absence of an opening snap.
The contraindications for operation are —
(i) Evidence of acute rheumatism with fever. Operation should be avoided till the infection is controlled
(ii) Presence of any septic focus, which should be attended first before operation.
(iii) For mitral valvotomy operation, one must be sure that mitral stenosis is the most dominant lesion
before performing this operation, as it may be associated with other valvular diseases.
(iv) Presence of atrial fibrillation increases the operative risk and postoperative results are also inferior to
those without atrial fibrillation.
(v) Persistent congestive cardiac failure is a contraindication to mitral valvotomy.
(vi) If the size of the heart is big particularly the right ventricle, valvotomy cannot produce satisfactory
result.
Types of operations.— The closed mitral valvotomy was one of the earliest and most successful of closed
cardiac operations. But for some years mitral operations are being performed with the heart-lung machine on
a ‘stand by’ basis. A closed mitral valvotomy is first attempted and if it becomes unsatisfactory, open mitral
operation is performed. Gradually for various reasons open operation is being more favoured mainly for two
reasons — (a) the hazard of emboli is much less in open surgery and (b) an effective commissurotomy can be
performed in open surgery.
CLOSED MITRAL VALVOTOMY.— All patients before undergoing mitral valvotomy should be well
checked by a cardiologist. A good preoperative preparation is required for better operative results.
In the operation, after exposing the heart, an incision is made in the left atrium and the surgeon's right
forefinger is introduced through this opening. The opening is now surrounded by a purse-string suture. The
finger within the atrium palpates the valve. Gradually the finger is thrust through the valve to enlarge its ope
Splitting will occur in the line of commissures. If the finger cannot properly dilate the valvular opening, a sma
incision is made on the wall of the left ventricle near the apex. Tubb's dilator is introduced immediately throu
ventricular incision. The right forefinger guides the dilator through the mitral valve opening. The dilator is
gradually opened, so that the mitral valve opening is widened for 3.5 cm to 5 cm. After this the dilator is take
off and the ventricular wound is controlled by pressure with the thumb till the wound is sutured. When the v
is calcified and does not yield to these dilators, it is better to remove the diseased valve and to replace it by a
prosthetic valve, such as Start-Edward shielded ball valve or Shiley's disc prosthesis.
OPEN MITRAL VALVOTOMY.— A median sternotomy incision is applied and cardiopulmonary by
pass machine is applied. Once the by-pass is established, the perfusate temperature is lowered to 20° C, the ao
is clamped and the heart is arrested with cold blood and hyperkalaemia. The left atrium is then opened with a
longitudinal incision in the interatrial groove. Any thrombi or atrial appendages in the atrium are carefully
removed. Atrial appendages are potential source of postoperative emboli and are so routinely excluded from
the atrial cavity. The fused commissures are clearly visualised. The commissures are then carefully separated
with a knife. When the fused commissures are attached to the papillary muscle, this muscle is carefully split w
a knife for as much as 1 cm, carefully preserving the chordae to each leaflet of the valve. Any tear or irregular
of the leaflet mechanism is repaired.
After the operation by-pass is discontinued. Correction of mitral stenosis is confirmed by measuring left
atrial and ventricular pressures by needle puncture. The patients are usually discharged in 10 to 12 days.
MITRAL VALVE REPLACEMENT.—
Indications.— (i) The most important indication of this operation is the presence of both insufficiency and
stenosis in the mitral valve.
(ii) It is frequently needed in case of mitral stenosis with excessive calcification particularly in the
commissures.
Technique.— The valve is excised by incising it a few millimetres from the annulus with a circumferential
incision. The underlying papillary muscles are divided near their apices. Porcine prosthesis has been used in
majority of patients. Bjork disc prosthesis is also being used. The Starr cloth-covered steel ball prosthesis was
previously used and now abandoned because of long term problems.
The valve prosthesis is inserted with a series of 12 to 18 mattress sutures of Dacron. Care should be taken
while inserting sutures in the annulus, as deeper suture may injure thecoronary sinus, the circumflex coronary
artery or the conduction bundle. Removal of air is necessary after the operation.
2. MITRAL INSUFFICIENCY —
Aetiology.— It is usually rheumatic in origin. Other causes are bacterial endocarditis, rupture of chordae
tendineae and papillary muscle dysfunction, which is due to extensive disease of coronary arteries.
Treatment is open valve replacement with the help of cardiopulmonary by-pass. As mentioned in the
section of mitral stenosis, the porcine prosthesis is mostly used. The operation has been described above in the
section of ‘mitral stenosis’.

3. AORTIC STENOSIS.—
It should be remembered that rheumatism has a predilection for the mitral and aortic valves, whereas syphilis for the
aortic valve and aortic wall. Degenerative lesions are often found in the aortic valve, coronary vessels and myocardium.
Aetiology.—
(i) Calcification superimposed on a mild congenital aortic stenosis is probably the most frequent cause.
(ii) Rheumatic fever, the definite history of which is only 30 to 50% of all patients.
Pathophysiology.— Obstruction due to aortic stenosis impedes the forward flow of blood from the left ventricle to the
aorta. This causes left ventricular hypertrophy. Gradually the left atrial pressure is elevated. Due to aortic stenosis the arterial
pulse becomes of low amplitude and it becomes slow rising and sustained, which is known as 'plateau pulse'. The pulse
pressure becomes small. A coarse systolic murmur and thrill are detected in the aortic area.
Effort dyspnoea, syncope and angina pectoris are often complained of. Once angina or syncope appears, the average
life expectancy for the untreated patients is 3 to 4 years.
Treatment.—
Indications for surgery.— (i) Operation is usually indicated when the gradient exceeds 50 mm Hg with cardiac
catheterisation.
(ii) Once syncope, angina or congestive cardiac failure has appeared, operation should be performed immediately.
Technique of operation.— Open surgery is always performed with the help of cardiopulmonary by-pass machine. In
only a small percentage of cases simple fusion of the valve commissures are found, which can be treated by open
commissurotomy. In most cases there is extensive destruction of the valve cusps, so that complete removal and valve
replacement is the only desired method. Usually a porcine valve (prosthetic) of appropriate size is used. If an appropriate
size porcine valve is not available, the Bjork disc prosthesis is used.
4. AORTIC INSUFFICIENCY.—
Aetiology.—
(i) Syphilis was a cause previously seen, but not seen nowadays.
(ii) Bacterial endocarditis.
(iii) Rheumatic fever is again the most common cause.
(iv) A dissecting aneurysm.
(v) Marfan syndrome.
(vi) Congenital.
In aortic insufficiency there is left ventricular dilatation and hypertrophy. The earliest symptom is palpitation due to
forceful contraction of dilated left ventricle. Dyspnoea on exertion and angina pectoris are also seen.
In addition to an aortic systolic murmur, a diastolic murmur is available on the left sternal edge. The pulse is
characteristically water-hammer with high systolic and low diastolic pressure resulting in a large pulse pressure.
Treatment.— Operation is usually advised when symptoms become significant. Aortic valve replacement is the main
operation performed for this condition.
Operative risk is surprisingly small usually in the range of 1 to 3%. It is influenced by the preoperative extent of
congestive cardiac failure, patient's age and associated diseases.
5. ISCHAEMIC HEART DISEASE.—
Aetiology.—
(i) Atherosclerosis is the fundamental cause. It involves males about 4 times more than females. Its
incidence is highest in Finland followed by United States, whereas Japan has the least incidence.
(ii) Disorders of lipid metabolism such as diabetes, hypothyroidism and hypercholesterolaemia are often
associated with coronary atherosclerosis.
Pathology.— The basic pathology is a segmental atherosclerotic plaque often localised within the first 5
cm of the origin of the coronary artery from the aorta. A common pattern is occlusion of the proximal anterior
descending coronary artery with distal 50% remaining patent The significant pathological feature is that the
disease affects segments of coronary arteries larger than 2 mm in diameter. The right coronary artery is
frequently occluded. The circumflex is also often involved.
Diagnosis.— Angina pectoris is the most common manifestation. Patients experience periods of discomfort
particularly appearing with exertion. These symptoms are relieved by sublingual nitroglycerine.
Myocardial infarction is the most familiar complication of coronary disease. In a small percentage of
patients congestive cardiac failure may eventually develop.
Electrocardiogram is done as a routine but it has little prognostic value. The most important is the coronary
angiography and left ventricular angiography to know the function of left ventricle and measure the left
ventricular diastolic pressure. The decision of successful operation depends on the presence of patent distal
arterial segment shown by angiography and on the proper functioning of the left ventricular muscles evaluated
by left ventricular angiography.
Surgical treatments.—
CORONARY BY-PASS OPERATION.—This operation is pathologically based on the fact that atherosclerosis affects
only limited portion of proximal coronary arteries and do not involve distal vessels of 2 mm or less in diameter. This
operation is routinely performed with extra-corporeal circulation. The right coronary artery is usually approached from the
posterior border of the heart near the posterior descending coronary vein. A by-pass graft is inserted between the aorta and
this area. The preferred graft is 5 inches reversed segment of saphenous vein attached proximally to the aorta and distally
to the coronary artery as an end-to-side anastomosis. The distal anastomosis should be performed with a segment of about
more than 1 mm in diameter and free from atherosclerosis. For anastomosis, interrupted or continuous sutures of 6/0 or
7/0 silk is used. Sometimes operative microscope may be required. The anterior descending coronary artery is approached
through apex. The by-pass grafts are done according to the necessity—either a single by-pass graft or double grafts usually
to the anterior descending and the right coronary arteries and in a few patients tripple grafts to all the three major coronary
arteries have been used. These grafts should be separately connected to the aorta.
ARTERIAL IMPLANTS.— The concepts of implanting an artery into the myocardium was developed by Vineberg in
1946. The internal mammary artery is often used as arterial implant. The arterial implant, e.g. internal mammary artery
remains patent in nearly 90% of cases. Patency is due to the presence of myocardial sinusoid and embryonic capillary like
remnants, which provide some immediate run-off of blood from the implanted artery. In addition the rhythmic myocardial
contraction produces an alternating to and fro motion of blood in the implant flowing away from the heart in systole and
towards the heart in diastole. This avoids thrombosis. In the ensuing weeks after implantation, arterial tributarily,
progressively appear around the implant and may connect the regional coronary vessels. With the evolution of these
tributaries, there will be an increase in blood flow through the implant. This requires about 4-6 months to develop. So benefit
after such operation cannot be expected within 4-6 months.
Left ventricular aneurysm.— Following myocardial ischaemia, the dead muscle is healed by scar tissue which easily
stretches to form an aneutysm. Most of these aneurysms are located in the anterior portion of the left ventricle in the area
supplied by the anterior descending coronary artery. Aneurysms of the posterior portion of the ventricle is the area supplied
by the circumflex artery are much less frequent. Aneurysm can impair function of the left ventricle as contraction of it is
dissipated into expanding the wall of the aneurysm. This is recognised by fluoroscopy.
Complication.— Mural thrombi often develop in the aneurysm and may embolise, but this is unusual. The aneurysm
may enlarge and rupture. .
Treatment.— The treatment is mainly operation, in which a subtotal excision of the aneurysm is performed. The wall
of the aneurysm is divided about 2 cm from its junction with the ventricular muscle. After excision the opening is sutured,
the line of which will be through the scar near the junction of the ventricular muscle, thus avoiding interruption of collateral
circulation around the margins of the aneurysm and also avoiding any reduction in size of the ventricular cavity.
If concomitant coronary by-pass grafting is to be done, this should be attached first. Attachment of all grafts may not
be possible until the heart is mobilised and the aneurysm excised.
THE PERICARDIUM
CARDIAC TAMPONADE —
Increase in intrapericardial pressure secondary to accumulation of fluid or blood in the pericardial sac due
to trauma or progressive effusion will yield pressure on the heart, which is known as cardiac tamponade.
It produces a shock-like state and if not relieved immediately may prove fatal.
In majority of cases cardiac tamponade occurs due to trauma either blunt or penetrating injury. It may occur
in almost any type of pericarditis.
On clinical examination, the pathognomonic signs of cardiac tamponade are — (i) increased venous
pressure, (ii) decreased pulse pressure, (iii) pulsus paradoxus, (iv) an enlarged area of cardiac dullness. (v)
43
subsequent development of hypotension and (vi) decreased heart sounds.

Pulsus paradoxus means the pulse becomes weaker on inspiration than on expiration. Aortic systolic
pressure falls more than 10 mm Hg during inspiration. This is due to normal inspiratory fall in the
intrapericardial and right atrial pressure during inspiration.
Treatment.— Emergency treatment includes aspiration of the pericardial sac with an 18-gauze needle
through the xyphicostal angle.
If the cause is cardiac wound, immediate thoracotomy is usually required to repair it.
ACUTE PERICARDITIS.—
In recent years widespread use of antibiotics has made acute pyogenic pericarditis a rare disease. It is the
children who are more often affected nowadays usually younger than 5 years of age. This occurs then as a
mainfestation of generalised infection with lack of resistance. The most common bacteria causing pericarditis
are Stap. aureus, H.influenzae, Neisseria and Streptococci.
In present days acute pericarditis is often idiopathic or viral. It may be secondary to acute myocardial
infarction, trauma, neoplastic infiltration or uraemia.
Pathologic changes in the pericardium consists of an acute inflammation with increased pericardial
vascularity and fibrin deposition. Fibrinous adhesions between the pericardial parietes and exudation of fluids
into the pericardial space are typical features.
Clinical features.— Chest pain is the most frequent symptom. Pain becomes worse while lying supine and
coughing. It is eased while sitting up. Dyspnoea is also a common symptom.
On physical examination the pathognomonic sign is pericardial friction rub.
Chest X-ray is of little diagnostic value unless it is accompanied by a large pleural effusion.
Echocardiogram is probably the most sensitive test for evaluation of pericardial effusion.
Electrocardiogram usually shows characteristic elevation of the ST segments.
Treatment.—
MEDICAL THERAPY is first tried which includes (i) bed rest till pain and fever subside, (ii) Non-steroidal
antiinflammatory agents such as aspirin or indomethacin should be tried to control pain, (iii) Appropriate
parenteal antibiotics is the main therapy, (iv) If pain is not relieved within 48 hours, corticosteroids (60 to 80
mg of prednisone daily) may be given.
SURGICAL TREATMENT.— Pericardial aspiration and instillation of antibiotics is usually necessary if
medical therapy fails. Surgical drainage of the pericardium is required if aspiration proves ineffective in
controlling the disease.
Aspiration Of The Pericardium.— Aspiration is performed with 18-gauze needle along the cos-
toxyphoid angle in the upward and backward direction at an angle of 45° to the skin. The advantage of this site
is that — (i) it does not puncture the pleura, (ii) It aspirates the pericardial cavity through the most dependent
part, (iii) It is less likely to damage any coronary vessel.
Drainage Of The Pericardium.— It is done by making an incision over the 6th intercostal space in the
mid clavicular line. The approach is through the pleural cavity. Once the paricardium is reached a window is
excised of approximately 3 cm2 and this is sent for histological examination (pericardiotomy). Any further
collection of pericardial fluid is drained into the pleural space. The incision is closed after putting a drain in the
pleural cavity.
CHRONIC CONSTRICTIVE PERICARDITIS OR PICK'S DISEASE.—
Aetiology.— (i) The cause is unknown in majority of cases.
(ii) The disease often represents the end stage of an undiagnosed viral pericarditis.
(iii) Tuberculosis was considered to be the most frequent cause but in recent years it is almost unknown.
(iv) Traumatic haemopericardium may evolve to constrictive pericarditis.
(v) It may be a complication of open heart surgery.
Pathology.— The pericardium becomes thickened, fibrosed and calcified. The pericardial cavity is
obliterated by dense scar tissue. The heart is in fact is confined in a rigid inelastic case preventing it from its
proper functioning.
The pathological effect of this condition is that it prevents ventricles from proper filling in diastole. This
causes decreased cardiac output. A compensatory tachycardia'is seen. There is corresponding increase in right
atrial pressure and right ventricular diastolic pressure. There is also elevation of central venous pressure. This
venous hypertension may produce peripheral oedema, hepatic enlargement and ascites.
Clinical features.— The disease is usually seen in 2nd or 3rd decade.
Fatigue and dyspnoea on exertion are common complaints. Gradually the patient complains of oedematous
swelling of the feet and abdominal enlargement due to ascites.
On examination, peripheral oedema, enlargement of liver and ascites should be detected. Dilatation of
peripheral veins are also noticed. The pulse pressure is normally decreased and a paradoxic pulse is found in
a small percentage of cases.
Treatment.— Once the diagnosis is confirmed, pericardiectomy is the treatment of choice. The patient is
prepared with diuretics and aspirations of pleural or ascitic fluid. A sternotomy incision is often preferred
nowadays. The constricting pericardium should be removed from the entire heart, although removal of
pericardium from the ventricles may relieve the diseased condition. Correct plane of dissection should be found
out. If this is identified, bleeding is surprisingly small. It is always the technique to free the left ventricle first
to prevent pulmonary congestion. It is sometimes difficult to remove the adherent pericardium from the
diaphragmatic part of the ventricle. Removal of pericardium from the atria and vena cava is physiologically less
important, though it should be done. Heart-lung machine is sometimes used.
The risk of operation varies with the age of the patient and the severity of the case. An operative mortality of 4 to 6%
is usually seen in various series.
Pericardiotomy and pericardial biopsy.— Open drainage of the pericardium is required in presence of chronic
pericardial effusion or purulent pericarditis. Pericardiotomy or pericardial biopsy may be required for establishing the cause
of pericardial disease.
Post pericardiotomy syndrome is sometimes come across in 10 to 40% of cases by the appearance of fever, pericarditis
and pleuritis. The aetiology seems to be an autoimmune reaction. Anti-heart antibody titres are sometimes raised.
676
CHAPTER - 35
THE OESOPHAGUS
ANATOMY
The oesophagus is a muscular canal of about 25 cm (10 inches) long and extends from pharynx above to stomach below. It begins at
the lower border of the pharynx which is situated opposite 6th cervical vertebra or at the lower border of the cricoid cartilage. It descends
through superior and posterior mediastinum and ends at the cardiac orifice of the stomach at level of the 11th thoracic vertebra. It descends
vertically almost through midline but presents two slight curves to the left. At the commencement it is placed in the midline, as it descends
downwards it slightly inclines to the left upto the root of the neck. It again moves towards the midline as it descends downwards and reaches
the midline at the 5th thoracic vertebra. It follows the midline course till the 7th thoracic vertebra when again it gradually shifts to the left
till it passes through the oesophageal orifice of the diaphragm at the level of the 10th thoracic vertebra. The oesophagus also presents
anteroposterior curvatures following the curvature of the cervical and thoracic portions of the vertebral column. During its course it is
constricted at 4 places — (i) at its commencement, 6 inches from the incisor teeth, which is the narrowest point in the gastointestinal tract
measuring 14 mm in diameter, (ii) where it is crossed by the aortic arch, 9 inches from the incisor teeth; (iii) where it is crossed by the left
main bronchus, 11 inches from the incisors and (iv) where it crosses the diaphragm (the diameter is about 16 to 18 mm), about 16 inches
from the incisors. These constrictions are important clinically during oesophagoscopy. While inserting oesOphagoscope one must be careful
at these constrictions. The uppermost constriction is the most vulnerable part and a common site of perforation during oesophagoscopy.
Oesophagus can be broadly divided into three parts — 1. Cervical part, 2. Thoracic part and 3. Abdominal part.
The cervical part is about 5 to 6 cm in length and ends at the lower border of the 1st thoracic vertebra, where it is continuous with
the thoracic part. The cervical part of the oesophagus is in close relation with the trachea and the recurrent laryngeal nerve on each side
anteriorly; the vertebral column, prevertebral muscles and the prevertebral layer of the deep cervical fascia posteriorly; the common carotid
artery and the posterior part of the lobe of the thyroid gland on each side.
The thoracic part of the oesophagus is at first situated in the superior mediastinum between the trachea and the vertebral column.
Then it passes behind and to the right of the aortic arch and descends into the posterior mediastinum along the right side of the descending
thoracic aorta. After the 7th thoracic vertebra it inclines to the left and crosses in front of the aorta to enter the orifice in the diaphragm meant
for it at the level of the 10th thoracic vertebra to commence the abdominal part. It is in relation, anteriorly (from above downwards) with
the trachea, right pulmonary artery, the left main bronchus and the pericardium. Posteriorly it is in relation with vertebral column, the longus
colli muscles, the right posterior intercostal arteries, the thoracic duct, the azygos veins, terminal parts of the hemiazygos and accessory
hemiazygos veins and in the lower part the thoracic aorta. On the left side the aortic arch, the left subclavian artery, the thoracic duct and
the left pleura and the left recurrent laryngeal nerve runs upwards in the groove between it and the trachea to come in relation with the
oesophagus in the superior mediastinum; whereas in the posterior mediastinum the oesophagus is in relation with descending thoracic aort i
and the left pleura. On the right side the oesophagus is related to the right pleura and the azygos vein while it arches forwards to join the
superior vena cava.
The abdominal part of the oesophagus is in direct relation with the oesophageal groove on the posterior surface on the left lobe of
the liver. This part of the oesophagus is directly related to the left crus of the diaphragm and the left inferior phrenic artery posteriorly.
The left vagus nerve lies on the anterior wall of the oesophagus while the right vagus nerve lies on the posterior wall of the oesophagus.
This is due to embryonic rotation of the stomach.
The diaphragmatic oesophageal hiatus is elliptical in shape and is formed by the splitting of the medial fibres of the right crus.
Sometimes however both the left and right crura contribute to the hiatus. It transmits the oesophagus, the vagus nerve and the oesophageal
branches of the left gastric artery.
The fascia on the undersurface of the diaphragm is continuous with the transversalis fascia and is particularly rich in elastic fibres in
this area. This fascia extends upwards through the oesophageal hiatus in a conical fashion to be attached to the wall of the oesophagus slightly
above this hiatus. This fascial expansion is called thephreno-oesophageal ligament. Some of its elastic fibres penetrate through the muscle
coat of the oesophagus and reach the submucosa. This ligament permits some mobility during the movements of swallowing and respiration,
but at the same timelimits upwards displacement of the oesophagus. It should better be called phreno-oesophageal membrane as it does
not contain the strong fibrous bands to be qualified for the term ‘ligament’.
The precise location of the junction of the oesophagus and stomach is controversial. Three theories have been put forward to locate
this junction exactly. These are—(i) where the oesophageal squamous epithelium turns into gastric columnar epithelium. But unfortunately
the distal part of the oesophagus often contains columnar epithelium, (ii) It is the junction where the tubular oesophagus joins the gastric
pouch. In presence of hiatus hernia this junction is difficult to find out. (iii) The junction of the oesophageal circular muscle layer with the
oblique sling fibres of the stomach is the real junction. This seems to be the most accurate theory and enjoys widespread acceptance. Of
course endoscopically the gastro-oesophageal junction is identified by the presence of columnar red epithelium.
HISTOLOGY.—Oesophagus has four coats from outside in wards—(i) fibrous coat, (ii) muscular coat, (iii) areolar or submucous
coat and (iv) mucous coat. Oesophagus does not possess a serous coat like other abdominal viscera.
1. FIBROUS COAT.—Instead of the serous coat oesophagus has an outer covering of areolar tissue containing many elastic fibres.
2. MUSCULAR COAT.— This is composed of two layers of considerable thickness — an external longitudinal and an internal
circular muscles.
The longitudinal muscles from a complete investment for nearly whole of oesophagus except the posterior portion of the upper most
3 or 4 cm, before which the longitudinal muscles diverge away from the median plane forming two longitudinal muscular fasciculi which
incline upwards and forwards to the front of the tube and pass deep to the inferior constrictor muscle to be attached to the upper part of the
ridge on the posterior surface of the lamina of the cricoid cartilage. The V-shaped interval is covered by circular muscle fibres and the
THE OESOPHAGUS 677
overlapping lower edge of the inferior constrictor.

Circular muscle fibres are continuous superiorly with the inferior constrictormuscle posteriorly and with the two longitudinal fasciculi
anteriorly. Inferiorly the circular muscle fibres are continuous with the oblique fibres of the stomach.
It must be remembered that in the upper two-thirds of the oesophagus striped muscles are present whereas in the lower-third it contains
only unstriped muscle fibres. Between the two muscle layers is a thin connective tissue that contains fine blood vessels and ganglion cells
of Auerbach's plexus.
3. AREOLAR OR SUBMUCOUS COAT is relatively thick and contains fatty and areolar tissue which provide considerable
mobility to the oesophageal mucosa, a point of surgical interest. The submucous coat contains blood vessels, nerves, Meissner’s neural
plexus and extensive lymphatic vessels. The most peculiar feature of this coat is that it contains mucous glands.
4. MUCOUS COAT.—This coat is also quite thick and pale red in colour, it is folded longitudinally in resting phase, so that when
dilated these longitudinal folds disappear. It consists of three layers and from outside inwards, these are — (a) the muscularis mucosae,
a layer of longitudinally arranged unstriped muscle fibres and this layer is absent at the commencement of the oesophagus, (b) A layer
of connective tissue, which projects into the folds of mucosa, (c) A layer of stratified squamous epithelium, which at the distal 1 to 2 cm
may become junctional columnar epithelium. More often the stratified squamous epithelium of the oesophagus is abruptly succeeded by
the simple columnar epithelium of the stomach, the junction of which is clearly visible through oesophagoscopy from pink smooth
oesophageal mucosa to redder mamiUated gastric mucosa. Oesophageal glands are small, compound racemose glands of the mucous type
and are lodged in the submucous coat. The duct of this gland pierces the muscularis mucosa and opens in the mucous coat.
Blood supply.— Oesophagus is supplied by segmental blood supply by a number of arteries. The cervical oesophagus is supplied by
the inferior thyroid artery, branch of thyrocervical trank. The thoracic oesophagus is supplied by 4 to 6 aortic oesophageal arteries,
intercostal arteries and bronchial arteries. The lowerpart of the oesophagus is nourished by the oesophageal branch of the left gastric artery
and from the left inferiorphrenic, branch of abdominal aorta. These arteries anastomose with one another on the outer coat of the oesophagus
and small arteries from this anastomosis supply and penetrate the muscular coat to form another longitudinal anastomosis in the submucous
coat. Oesophagus is notorious for its poor blood supply and how much it is justified is probably not known.
Venous drainage from the cervical part of the oesophagus mainly goes to the inferior thyroid veins. From the thoracic part the veins
mainly drain into the azygos, hemiazygos and accessory hemiazygos veins. The abdominal part is mainly drained into the left gastric vein
which is a tributary of the portal vein. So this is the part of the oesophagus where the anastomosis between the systemic veins and the portal
vein occur. In case of portal hypertension abdominal part of the oesophagus is often involved with varicosity and the patient presents with
fatal haematemesis.
Lymphatic drainage.— Two lymphatic plexuses, one in the mucous and the other in the muscular layer, are usually present. The
mucosal lymphatic capillaries pierce the muscular layer and form a lymphatic plexus with the muscular lymphatics. Lymphatic; from this
plexus pierce the muscular coat and drain into the perioesophageal and paraoesophageal lymph nodes lying adjacent to the oesophagus.The
lymphatics from these glands in the upper two thirds of the oesophagus follow an upward course and drain into the mediastinal nodes,
subcarinal nodes and even the deep cervical nodes. Whereas efferents from the peri- and paraoesophageal lymph nodes of the lower one
third of the oesophagus drain into the lower mediastinal group and even to the perigastric and left gastric lymph nodes.
Nerve supply.— The nerves are derived from both the vagus (parasympathetic) and sympathetic. The cervical part of the oesophagus
receives branches from the recurrent laryngeal nerve and from the cervical sympathetic trunks by means of the plexus around the inferior
thyroid artery. In the thorax the vagus nerves lie on two sides of the oesophagus and supply branches to this part of the oesophagus. The
sympathetic supply of this part of the oesophagus comes from the upper thoracic and splanchnic nerves. The abdominal part of the
oesophagus is supplied by the vagal trunks lying on its anterior and posterior walls. The sympathetic supply comes from the plexus around
the left gastric and inferiorphrenic arteries. The nerves form a plexus in themuscular coat which contains small ganglion cells of Auerbach's
plexus and another plexus is formed in the submucous coat which also contains ganglion cells and is called Meissner’s plexus.
PHYSIOLOGY
The main function of the oesophagus is to propel ingested material from the pharynx to the stomach. The two physiological sphincters
— one at the upper end (upper oesophageal sphincter) and one at the lower end (lower oesophageal sphincter) contract and relax in such
a harmony that the ingested material without any obstruction moves towards the stomach.The upper oesophageal sphincter (UES) is
normally closed with its excessive tone and thus does not allow entry of air into the oesophagus during each inspiration. But as soon as the
swallowed material reaches the pharynx the upper oesophageal sphincter opens up temporarily to allow the swallowed bolus of food to
pass into the oesophagus. This is followed by a postdeglutitive contraction. The intraluminal oesophageal pressure measurements may be
obtained by transmission of pressure changes through the swallowed hollow tubes connected externally to the transducer and recording
system. Usually polyethylene or polyvinyl tubing constantly perfused and having three lumen are mostly used for this purpose. By this
technique the intraluminal oesophageal pressure and pressure in the upper and lower oesophageal sphincters can be easily measured. The
upper oesophageal sphincter is about 3 cm in length and the mean resting pressure within it is about 40 mmHg. During swallowing it relaxes
only for a second and then is closed down for postdeglutitive constriction which lasts for 4 seconds and the pressure within it increases to
80 to 100 mmHg. Thus the bolus of food enters the oesophagus and a primary peristaltic wave is thus initiated.
As the oesophagus is within the thorax, due to the negative intrathoracic pressure its intraluminal pressure ranges from -5 mmHg
(during inspiration) to +5 mmHg (during expiration). But when the peristaltic wave reaches a particular part of oesophagus the intraluminal
pressure in that area increases to about 25 mmHg.
The lower oesophageal sphincter (LES or LOS) also remains closed during rest to prevent reflux of gastric contents into the oesophagus.
The normal resting pressure within LOS is about 20 mmHg. This pressure is abnormally low in patient who is suffering from reflux
oesophagitis. More sensitive test of gastro-oesophageal reflux is the acid reflux test. This is performed by keeping a pH electrode 5 cm
proximal to the LOS. 300 ml of 0.1 N HCL is poured in the stomach. Intragastric pressure is increased by various manoeuvres and the
oesophageal pH is recorded through that electrode. Decrease in pH to less than 4 is considered to be a direct proof of presen
oesophageal reflux. The LOS only relaxes during swallowing and when the peristaltic wave reaches it. It must be confessed th
not the only thing which prevents gastro-oesophageal reflux. The other factors which importantly contribute in preventing gastro-
oesophageal reflux are—(a) oblique angle of entry of oesophagus, (b) mucosal folds at the lower end of the oesophagus, (c) the dia
and (d) the valve-flat mechanism. The basal sphincter pressure of LOS is due to tonic myogenic activity and not due to autono
activity. LOS is also controlled by neural and hormonal influences. The sphincter relaxation is chiefly due to vagal activity. A fe
influence in lowering LOS basal tone. These are excessive ingestion of alcohol, smoking, atropine, beta-adrenergic agents, pregnan
(effect of excessive progesterone) etc. The LOS basal tone can be enhanced by drugs such as metoclopramide, bethanecol (Choline
glucagon, gastrin and gastric neutralisation. When the intragastric pressure increases the normal resting tone of LOS is also i
response is due to vagal activity and can be abolished by vagotomy. This is the most essential feature of a component LOS to
oesophageal reflux.
CONGENITAL OESOPHAGEAL ATRESIA

Congenital atresia of the oesophagus is often associated with tracheoesophageal fistula. Usually 4 types are
noticed. In type I, which occurs in 90% of cases the upper oesophageal segment ends blindly and the lower
portion of the oesophagus is connected with the trachea through tracheoesophageal fistula. The oesophageal
fistula usually joins the trachea at or just above the tracheal bifurcation, admitting inspired air into the stomach,
or in retrograde fashion gastric juice into the lungs. In type //.both upper and lower oesophageal segments end
blindly with a portion of oesophagus in between missing. This occurs in about 8% to 10% of cases. In type III,
the proximal segment of the oesophagus is connected with by tracheoesophageal fistula, while the distal
segment of the oesophagus ends blindly. This occurs in 1 % to 2% of cases. In type IV, both proximal and distal
segments of the oesophagus are connected with the trachea by tracheoesophageal fistulae. This occurs in only
less than 1% of cases.
IB © HD
Flg.43.1.— Four types of congenital oesophageal atresia. A is the commonest type (90%). B is type II according
to the text and is seen in only 8% to 10% of cases. C is type III of the text and is seen in only 1% to 2% of cases.
D is type IV of the text and is extremely rare (less than 1% of cases).
Associated congenital anomalies are quite common and in 20% of babies bom with oesophageal atresia
some variant of congenital heart disease occurs and in 12% of cases there is associated imperforate anus. This
condition is often associated with hydramnios (50%), so in all cases of hydramnios such possibility should be
considered.
Clinical features.—The earliest and most important clinical feature of oesophageal atresia is regurgitation
THE OESOPHAGUS 679
of saliva or feedings. Attempts to feed are met with ‘spitting up’ or frank vomiting. Saliva pours almost
continuously from its mouth. Persistence in feeding may produce aspiration, choking, cyanosis and res
distress.
DIAGNOSIS.— A soft rubber catheter is introduced into the oesophagus through the mouth, which
encounter an obstruction at about 10 cm from the lips. This confirms the diagnosis.
Radiological confirmation may be made by contrast X-ray study in which 1 ml of dionosil is used as co
medium which is instilled down the catheter to demonstrate obstruction. After the radiograph has been
the dionosil should be aspirated.
In straight X-ray air in the stomach confirms the first type of anomaly in which the lower end of the
oesophagus is connected with the trachea.
Treatment.— Surgical intervention should be immediate. The baby should be kept in 30° head-up p
Antibiotic should be started immediately even if aspiration pneumonia is not clinically manifested. Cath
suction of the upper oesophageal pouch is started and intravenous infusion is also started.
Gastrostomy is a useful adjunct in the management of many babies before operative repair of the oe
is undertaken.
Operation.—The approach is made usually through right sided thoracotomy incision at the level of the
intercostal space. The azygos vein is divided between ligatures. The upper segment of the oesophagus is
by the presence of rubber catheter inside it. The lower segment is now dissected out and cleared from
neighbouring structures. The tracheoesophageal fistula is divided between ligatures.Now end-to-end an
mosis is performed between the proximal and distal segments of the oesophagus after excising the sma
portions. Correction of this form of oesophageal anomaly leads to a satisfactory outcome with nearly no
oesophageal function in most patients. The wound is closed with an under-water seal chest drain.
Complications.—
1. Leakage at the anastomosis is a not uncommon complication.
2. Mediastinal infection is occasionally seen with oesophageal disruption. This may require anothe
operation.
3. Gastroesophageal reflux has been sometimes the late complication of this operation.
OESOPHAGEAL PERFORATION
Aetiology.— The absence of serosa in the oesophagus makes it more likely to rupture. During vomitin
the lower oesophagus momentarily increases its diameter by about 5 times. Swallowing of a large bolus
requires a rapid increase in the oesophageal lumen. Combination of (a) the pressure gradient between
intrathoracic negative pressure outside and high positive pressure inside with rapid distension of the o
during vomiting and ingestion and (b) absence of serosa sometimes compels the oesophagus to rupture
is known as spontaneous rupture ( Boerhaave Syndrome).
There are other causes of oesophageal perforation and today the most common cause is oesophagea
instrumentation. THE CAUSES OF OESOPHAGEAL PERFORATION ARE :
A. Instrumental —
(i) Oesophagoscopy;
(ii) Dilatation (bougienage);
(iii) Intubation.
B. Spontaneous rupture ( Boerhaave Syndrome),
C. Traumatic —
(i) Foreign body;
(ii) Penetrating wounds;
(iii) Blunt injury to the chest or abdomen;
(iv) Surgical dissection;
(v) Ingestion of corrosive agents.
D. Pathology in the oesophagus —
(i) Peptic perforation;
(ii) Carcinoma;
(iii) Anastomotic.
Instrumental perforation can occur at any part of the oesophagus, but the sites of normal narrowing o
oesophagus are mostly involved. The most common site is the cervical oesophagus and next is just abo
cardia. In the former case normal narrowing of the oesophagus at its junction with the pharynx and th
impingement of rigid oesophagoscope against the bodies of the hyperextended vertebrae may crush th
This is more so particularly in older patients with osteophytes in the cervical vertebrae. In the latter si
the forward and left lateral bent of the distal oesophagus before it enters the orifice in the diaphragm c
to perforation at the lower end. The incidence of instrumental perforation has been considerably reduce
to introduction of flexible fibreoptic oesophagoscope.
Spontaneous rupture of oesophagus has been explained earlier
and it mostly occurs in the lower third of the oesophagus, more often
the left side than on the right side.
Traumatic perforation from (i) ingestion of foreign bodies may
occur anywhere in the oesophagus where the foreign bodies common
lodge. There are three common places of lodgement of foreign bodies
These are the normal narrowings of the oesophagus —just below the
crico-pharyngeal sphincter, at the level where it is crossed by the aor
arch and the distal oesophagus just above the cardia. Traumatic per
ration from (ii) penetrating wounds are now gradually becoming
commoner. This may result from wounds in the neck, chest or abdo
men. Obviously the level of injury depends upon the location of the
penetrating wound, (iii) Blunt injury to the chest or upper abdomen m
cause rarely rupture of the oesophagus, (iv) During certain operation
which involve dissection around the oesophagus may rarely cause
perforation of the oesophagus. Such occurrence has been recorded
during abdominal vagotomy, repair of hiatus hernia and during ante
spinal fusion when cervical oesophagus has been involved, (v) Inges
tion of corrosive agents especially lye may cause perforation of the
oesophagus in severe cases.
Pathology in the oesohagus may cause in rare cases oesophageal
rig.43.2.— Barium swallow film perforation. The location of which obviously depends on the location
showing perforation of the oesophagus of the pathology, (i) Ectopic gastric mucosa has been noticed in the
following bougienage.
distal oesophagus where peptic peforation may occur. In reflux oeso
phagitis very rarely this type of perforation may occur in the distal oesophagus where metaplasia to co
epithelium has taken place, (ii) Carcinoma of the oesophagus may penetrate full thickness of the oesop
and may cause oesophageal perforation, (iii) Oesophageal perforation may also occur very rarely follow
anastomosis involving oesophagus, so after anastomosis with the oesophagus one must be careful of o
of such incidence.
Symptoms.— (i) Pain, (ii) early collapse and (iii) nausea are the main three symptoms of this condition
PAIN is usually severe and it mimics very much the pain of perforated peptic ulcer, acute pancreatitis,
myocardial infarction and dissecting aneurysm of the aorta. EARLY COLLAPSE will be more elaborately
described under the heading ‘signs’. NAUSEA is quite common complaint, though vomiting is not a de
symptom of this condition. Vomiting may precede the onset of pain in case of spontaneous rupture, bu
spontaneous rupture may occur without prior vomiting. When vomiting follows pain, it often contains
It must be remembered that distal oesophagus is in close relation with the left pleura, whereas midoes
is in direct relation with the right pleura. So perforation in these parts of the oesophagus will obviously
pleural cavity resulting in pneumothorax, pneumohydrothorax and haemothorax. This will cause diffic
respiration (DYSPNOEA).
THE OESOPHAGUS 681
Signs.— There are mainly six signs which are seen in oesophageal perforation and one must be awar
these signs for exclusion and early detection of a case of oesophageal perforation. This is a grave condit
the patients with oesophageal perforation usually die if diagnosis and treatment are not made within 24
of occurrence of such perforation. The six signs are (i) fever, (ii) shock, (iii) tenderness, (iv) crepitus, (v)
Hamman’s sign and (vi) signs of pleural involvement.
(i) Fever develops quickly and the temperature shoots up rapidly almost simultaneously with pain.
(ii) Shock.—The patient rapidly becomes acutely ill and collapses. The vital signs of shock appear .Th
are tachycardia, hypotension, tachypnoea, low blood pressure etc.
(iii) Tenderness.— Local tenderness should arouse suspicion of this condition. Cervical tenderness is a
early and constant feature of cervical oesophageal perforation.
(iv) Crepitus in the neck following mediastinal emphysema is quite diagnostic. Gradually crepitus ma
extend over the chest wall. Whenever there is air in the mediastinum crepitus will be first felt in the nec
(v) Hamman'-s sign.— Air in the mediastinum crackles with each heart beat when the patient holds hi
breath. This is known as mediastinal crunch sound ofHamman.
(vi) When perforation has penetrated ihe pleural cavity the signs include those of pneumothorax, ple
effusion and haemothorax. Absence of breath sounds, dullness on percussion, tracheal shift, limited ex
of the haemothorax all will be apparent.
A few confusing signs such as guarding and tenderness of the upper abdomen may confuse this conditi
with peptic perforation.
1. CHEST X-RAY (anteroposterior and lateral views) in the erect posture is quite diagnostic of this
condition. Mediastinal widening may be prominent in X-ray. Air in the mediastinum may be outlined ag
the left pleural surface. In the erect posture it can exclude peptic perforation. In the lateral view, anterio
displacement of the trachea, widening of the retrovisceral space and air in the tissue spaces may straig
diagnose a cervical oesophageal perforation. Involvement of the pleural cavity in the form of pneumotho
hydropneumothorax, haemothorax and collapse of lung may be obvious in X-ray.
2. CONTRAST RADIOGRAPHY.— Water soluble medium such as gatrografin has been used to loca
the site of perforation. If nothing is detected with gastrografin swallow, examination should be repeated
barium. Even when perforation is obvious in chest X-ray, this contrast study is essential to localise the
perforation and to know the extent of perforation which will help in treatment.
3. OTHER INVESTIGATIONS.— (i) High W.B.C. count and (ii) haemoconcentration due to fluid loss
may be detected, (iii) E.C.G. should be performed to exclude myocardial infarction, (iv) Arterial blood ga
determinations should provide a clue as to the severity of pulmonary dysfunction, (v) Aspiration of pleu
may reveal high amylase level due to swallowed saliva.
4. ENDOSCOPY should be forbidden except when foreign body is suspected as the cause of perfora
Treatment.— In any case of oesophageal perforation treatment consists of (i) intensive antibiotic thera
(ii) eliminating oral feeding, (iii) provision of intravenous elementation with electrolyte correction, (iv)
Cardiorespiratory support and (v) surgery which includes surgical repair of the perforation and drainage
surrounding tissues.
CERVICAL PERFORATION.— Besides medical treatment which has been formulated above, surgical
treatment includes operative drainage and closure of the perforation. When closure of perforation is not
possible, cervical oesophagostomy tube can be inserted through the perforation and led out through a s
wound in the neck to provide drainage and a controlled fistula.
THORACIC PERFORATION.— Here also quick surgical exploration, closure of the oesophageal
perforation and chest drainage are indicated. In case of upper two-thirds of the oesophagus the best ap
is transpleurally through a right mid-thoracotomy. In case of lower third of the oesophagus, a lower left
thoracotomy is indicated. During closure of the oesophageal perforation one may use adjacent pleura or
fundus to reinforce the closure.
If perforation has been discovered promptly in a patient with an intrinsic oesophageal pathology and
surgical treatment is undertaken early, a definite surgical technique for the disease is desirable.This may
necessitate oesophagectomy in case of carcinoma or stricture of the oesophagus. Anti-reflux proce

dure or hiatus hernial repair should be performed in case of perforation in reflux oesophagitis case.
In late perforations of mid-thoracic oesophagus, oesophagectomy with closure of the cardia and a
cervical oesophagostomy may be necessary to control continuing infection in the mediastinum. At a
later stage oesophageal reconstruction by substernal colon interposition is performed.
Following surgical treatment one must keep good watch on the possible COMPLICATIONS which
are serious threat to the patients. These are mediastinitis, empyema, mediastinal abscess, lung ab
scess, subphrenic abscess, breakdown of the oesophageal closure. These must be diagnosed early and
surgically drained promptly. Other serious complications following this condition are aspiration pneu
monia and haemorrhage from the aorta weakened by sepsis and eroded by an adjacent drainage tube.
So one must be careful in providing the drainage tube which should be well away from the aorta.
REFLUX OESOPHAGITIS
Regurgitation of gastric contents into the oesophagus is called gastro-oesophageal reflux.

In the normal subject during waking hours and in the erect posture gastric juices may enter the
oesophagus in only 20 minutes / a day. This occurs during distension of the stomach, belching and
burping. In the supine position the intraluminal pressure of lower oesophageal sphincter (LOS)
rises and this reduces any chance of reflux during this position. Only when reflux occurs more
frequently and at times when the stomach is not distended the gastro-oesophageal reflux is
considered to be pathological. A degree of gastro-oesophageal reflux is normal, particularly after
meals when there is a need to regurgitate swallowed air to maintain comfort. Physiological reflux
mostly occurs during transient lower oesophageal sphincter relaxations (TLOSRs), which are quite
separate from swallow-induced relaxation. In the early stages of GORD (gastro-oesophageal reflux
disease), most of the pathological reflux occurs as a result of an increased number of TLOSRs. In
severe GORD, a greater proportion of reflux occurs across a LOS that has lost its basal tone and has
a shorter length exposed to intra-abdominal pressure. Understanding of the function of the LOS has
been largely elucidated by Dent, who discovered the importance of TLOSRs, and by DeMeester, who
clarified the importance of the basic competence of the LOS, which is governed by basal LOS
pressure, the overall length of the LOS and the length that is exposed to intra-abdominal pressure.
Loss of competence of LOS leads to gastro-oesophageal reflux disease (GORD). The main reasons
of such pathological reflux are (i) the intraluminal tension of the lower oesophageal sphincter is
considerably reduced and (ii) that the length of the intra-abdominal oesophagus is much shorter than
normal.
Aetiology.— Normal competence of the gastro-oesophageal junction is maintained by the LOS.
There has been considerable controversy about the relative importance of the physiology of the LOS
and the anatomy of the cardia. This controversy is not completely resolved, but it is currently ac
cepted that the most important factor in gastro-oesophageal competence is the function of the LOS,
which is augmented by a normally functioning diaphragmatic hiatus.
Loss of the competence of the LOS leads to gastro-oesophageal reflux disease (GORD).
(i) Sliding hiatus hernia has a variable association with GORD. In general, patients with the
more severe stages of GORD tend to have a hernia, but most GORD sufferers do not have a hernia
and many of those with a hernia do not have GORD. It should be noted that rolling or paraoesophagea
hiatus hernia is a quite different and potentially dangerous condition. Reflux oesophagitis is a com
plication of GORD that occurs in a minority of sufferers. It occurs in 40-50% of those referred to
hospital, but in a much lower proportion of those who suffer from symptoms of GORD in the commu
nity as a whole. The majority of the patients with clinically significant gastro-oesophageal reflux
have associated sliding oesophageal hiatal hernia. But the majority of patients with hiatal hernia do
THE OESOPHAGUS 683
not have significant reflux to cause clinical problems.

(ii) Systemic collagen diseases involving oesophagus may cause reflux oesophagitis. In these
cases there is considerable loss of lower oesophageal sphincter tone and oesophageal peristalsis which
may cause such pathological gastro-oesophageal reflux. Scleroderma is the most common disease in
this group which involves the oesophagus.
(iii) Impaired gastric-outlet emptying may give rise to gastro-oesophageal reflux.
(iv) Other causes of gastro-oesophageal reflux include operations which destroy or
by-pass the normal lower oesophageal competence mechanism. These include resection of the
gastro-oesophageal junction, various types of cardioplasties and badly performed myotomy for
achalasia.
(v) In Westernised countries, GORD is by far the most common condition affecting the upper
gastrointestinal tract. This is in part a relative change due to the declining incidence of peptic ulcers
as the incidence of infection with Helicobacter pylori has been reduced due to socioeconomic con
ditions. However, there has almost certainly been an absolute increase in the incidence of GORD in
the last 20-30 years. The cause of the increase is unclear, but may be due in part to increasing obesity
In a curious way, it may also be an effect of the reduced incidence of Helicobacter infection. Some
suggest that the net effect is increased secretion that may increase the incidence of GORD. The
incidence of cancer of the lower oesophagus and cardia is also increasing, possibly as a result of the
changed incidence of GORD.
(vi) It seems increase in obesity may be the cause of increased incidence of GORD in the last few
years.
Acid peptic contents of the gastric juice are mainly responsible for causing reflux oesophagitis.
Bile and pancreatic secretions can also cause such oesophagitis if they are exposed to the lower
oesophagus. The severity of the condition mainly depends on the type and concentration of the secre
tions refluxed into the oesophagus and their contact time with the oesophageal mucosa.
Symptoms.— The symptoms of reflux oesophagitis fall into three groups : (1) Pain, (2) Dysph
agia and (3) Haemorrhage. These symptoms may occur singularly or in combination.
PAIN.— Pain is mostly retrosternal and is often referred to by the patient as ‘heart-bum’. The
peculiarity of such pain is that it is related to posture and the pain increases on lying down or by
stooping or by wearing surgical belt or tight corsets on the abdomen. This pain may radiate down one
or both the arms. This type of pain is considered to come from oesophageal spasm rather than mu
cosal irritation. It mimics angina pectoris. Sometimes the patient may complain of a chronic sensa
tion of a foreign body lodged in the throat. At other times the patient may become unable to initiate
swallowing. This seems to be due to reflux into the upper oesophagus causing irritation and spasm of
cricopharyngeal sphincter.
DYSPHAGIA or difficulty in swallowing may be very slight or complete. This is due to muscle
spasm and motor disorder due to irritation of the oesophageal mucosa. Direct injury to the
oesophageal mucosa may cause oedema, inflammation, spasm, fibrosis and even stricture in
advanced cases. The latter will lead to complete dysphagia. It must be remembered that the squamous
epithelium is mostly suffered. So in Barrett’s oesophagus, the oesophagus may be involved
higher up.
HAEMORRHAGE.— The bleeding from reflux oesophagitis usually presents as occult blood positive
in stool and chronic anaemia. Overt haemorrhage is usually due to an associated deep peptic ulcer. It
must be remembered that an ulcer developing in oesophagus containing gastric epithelium i.e.
columnar epithelium may be quite deep, but ulceration on the squamous epithelium of the
oesophageal mucosa is usually superficial.
OTHER SYMPTOMS.— Flatulent dyspepsia is often an associated symptom in this condition.
Whether this is the cause or effect of reflux oesophagitis is still a controversy. Respiratory
symptoms may be complained of in this condition as chronic aspiration of gastric contents into the
lung may cause recurrent pneumonia, lung abscess, bronchiectasis etc. One must remember
respiratory symptoms may be mere association with this disease rather than being definitely caused
by reflux oesophagitis.
Diagnosis.—
RADIOGRAPHY.— A barium swallow and upper oesophageal radiograph are performed first.
The whole of the oesophagus and stomach are to be examined first to exclude any disorder in the
upper oesophagus or any abnormalities of the stomach including delayed gastric emptying. It must be
remembered that the radiologists must see spontaneous free gastro-oesophageal reflux during the
course of barium swallow examination. Unfortunately only half of the patients who ultimately are
proved to have this disorder reveals reflux during barium swallow examination. So oesophageal functio
tests are to be performed.
OESOPHAGEAL FUNCTION TESTS.— These have been described in the section of ‘physiol
ogy’. Particularly the acid reflux test is more informative in this disease.
OESOPHAGOSCOPY.— It is always indicated to assess the degree of damage to the oesophagus.
Oesophagitis is graded from 0 to 4 according to the severity of changes observed through oesophagosco
Grade I is reddening of the mucosa without ulceration. In grade II there are ulcerations in the oesoph
ageal mucosa. Grade III is characterised by stiffening of the wall of the oesophagus. Grade IV is
characterised by frank stricture which prevents passage of the oesophagoscope into the stomach.
Presence of columnar epithelium more than 3 cm above the gastro-oesophageal junction suggests the
diagnosis of Barrett’s oesophagus. This is due to metaplasia and is known to be precursor of adeno
carcinoma of the distal oesophagus.
Two types of oesophagoscopes are normally used.—
A. RIGID OESOPHAGOSCOPY is now virtually obsolete
though some surgeons still use this traditional instrument. It re
quires skill to introduce rigid oesophagoscope and is not unsafe
in the hands of experts, though there is significant risk of perfo
ration. This instrument is probably better for examination of the
lower pharynx and the cricopharyngeal area, as the view with
flexible endoscope is rather poor in this area. Dilatation of oe
sophageal stricture was undertaken with this rigid instrument
and the classic Chevalier Jackson Bougie for many years, but
now with flexible oesophagoscope the dilators passed over
guidewires are much safer.
B. FLEXIBLE OESOPHAGOSCOPY — has virtually replaced
the rigid instrument for both diagnostic and therapeutic purposes.
First of all it does not require any general anaesthesia and can
be performed as an out-patient method. The quality of magni
fied image is far superior and the instrument is quite safe to pass
through the oesophagus.
Video endoscopy is a more advanced technology. The
stomach, duodenum and oesophagus can be examined
simultaneously.
Endoscopic ultrasonography can be used to assess the
tumour stage alongwith CT Scanning. It provides detailed
images of the layers of the oesophageal wall and also gives Fig 43.3.— Barium swallow X-ray
an idea about involvement of lymph nodes close to the oesopha- showing stricture of the lower
aus. Taking biopsies is quite easy with this instrument and it oesophagus due to oesophagitis
following gastro-oesophageal reflux.
THE OESOPHAGUS 685
even allows fine-needle aspiration samples of lymph nodes nearby to oesophagus.

Complications of gastro-oesophageal reflux.— (i) Bleeding; (ii) Shortening of the oesophagus;
(iii) Stricture of oesophagus; (iv) Barrett’s oesophagus; (v) Oesophageal ulcer penetration or perfo
ration; (vi) Respiratory aspiration; (vii) Contraction ring of lower oesophagus (Schatzki’s ring);
(viii) Adenocarcinoma.
TREATMENT.— Medical treatment is always tried first except a few complications of gastro-
oesophageal reflux when surgery is indicated straightway.
MEDICAL THERAPY.— Medical treatment should be given a sufficient trial of usually 6 months
or more. Medical treatment includes :
(i) The patients are instructed to sleep with the head end of the bed elevated on 6 inches
blocks.
(ii) Not to eat just before bedtime.
(iii) To avoid stooping whenever possible.
(iv) Smoking, excessive consumption of alcohol, tea or coffee should be avoided.
(v) Antacids should be prescribed 1 hour after meals and before bed time. H2 antagonists
were quite effective. But recently proton pump inhibitors (PPIs) e.g. omeprazole, lansoprazole and
pantoprazole are more effective drugs for this condition. This has been a major advance in the
treatment of this condition and oesophagitis heals in majority of cases. Even many strictures respond
well after 1 or 2 dilatations with long term PPI treatment. Some suspicion has been raised whether it
increases incidence of adenocarcinoma of the lower oesophagus and cardia due to long use of these
drugs.
(vi) Drugs such as Metoclopramide may be used to increase oesophageal peristalsis and gastric
emptying.
(vii) The patients should be instructed to reduce weight.
(viii) The patients must take small meal at a time.
(ix) Tight fitting garments and corsets which increase intra-abdominal pressure must be
avoided.
The drugs which should be avoided in this condition are : Muscle relaxants, Anticholinergic drugs
and Tranquillizers.
Surgical treatment.— The indications are :
1. When symptoms are not con
trolled by vigorous medical therapy.
2. If the symptoms recur soon af
ter cessation of medical treatment.
3. Oesophagitis is intractable.
4. Ulceration or stricture formation.
5. High grade dysphagia or metapla
sia to columnar epithelium.
When indications for surgical treatment
are clear, the operation performed^s an
anti-reflux operation. This operation is
aimed at restoration of the intra-abdomi
nal segment of oesophagus and mainte
nance of the distal oesophagus as a tube
like structure. This operation involves
mobilisation of cardia and lower oesopha-
Fig. 43.4.— Nissen fundoplication operation. See the text. 8US> some type of plication of the stom
ach around intra-abdominal oesophagus and narrowing of the oesophageal hiatus to prevent the re
constituted abdominal oesophagus from sliding back into the chest. Three types of anti-reflux opera
tion are commonly practiced. These are — (1) Nissen fundoplication, (2) Belsey Mark IV operation
and (3) Hill posterior gastropexy and calibration of the cardia.
1. NISSEN FUNDOPLICATION.— A vertical midline incision is made to enter the abdomen. A
thorough exploration is done to exclude presence of gallbladder disease, peptic ulcer, pancreatic
pathology and diverticular disease. The oesophageal hiatus is now explored and the size of the
hernia, if at all present, is assessed. The triangular ligament of the left lobe of the liver is divided and
it is retracted to the right. Traction on the stomach is made to reduce the hernia and to facilitate
division of phreno-oesophageal ligaments which constitute the sac of the hernia. Finger dissection
makes the oesophagus completely mobilised. If only too much adhesion of the oesophagus is antici
pated, a thoracic approach is worthwhile.
A rubber sling is used to pull down the mobilised oesophagus. If there is a good gap in the oe
sophageal hiatus, this should be repaired anterior or posteriorly with non-absorbable material. Both
the vagi nerves are preserved. Now the fundus of the stomach is exposed and upper short gastric
vessels are divided. The spleen must be protected with great care. The fundus of the stomach is
brought posteriorly around the oesophagus and sutured. Sutures are placed through the anterior fun
dus, the wall of the oesophagus and the fundus brought posteriorly and sutured. In this way about Wi
inch (3 to 4 cm) of oesophagus is wrapped by the fundus. It must be remembered that the fundus
should be anchored to the intra-abdominal oesophagus securely, lest it should slip down on to the
body of the stomach and cause obstruction to the stomach. This technique involves full 360° plica
tion of stomach around the oesophagus and causes a higher intraluminal pressure in the abdominal
oesophagus which is the sole objective of anti-reflux operation and in this respect this operation
seems to be the most effective of all anti-reflux procedures. The only complication is that it may be
a too tight repair and thus causes oesophageal obstruction. Postoperative barium swallow examination
should be done to exclude such complication.
Fig. 43.5.— Steps of Belsey Mark IV operation. A.— Shows how fundus of stomach is fixed firmly
around 2/3rds of the circumference of the lower most 4 cm of the oesophagus. B.— Shows how
the oesophageal hiatus is narrowed by suturing the crura posteriorly.
THE OESOPHAGUS 687
2. BELSEY MARK IV OPERATION.— This is a trans-thoracic operation through the 6th inter
costal space. The oesophagus is mobilised above upto the aortic arch to allow a sufficient long intra
abdominal oesophagus. The cardia is freed from attachments to the diaphragm. The oesophageal
hiatus is'narrowed by suturing the crura posteriorly. The fundus of the stomach is fixed firmly around
2/3rds of the circumference of the oesophagus along its lower 3 to 5 cm. The posterior segment of the
oesophagus is not included in the wrap. Post-operative barium swallow should demonstrate a 4 cm
segment of intra-abdominal oesophagus.
As it is not a total fundoplication recurrence rate is more in long-term follow up.
3. HILL PROCEDURE.— The main intention of this procedure is to narrow the abdominal oe
sophagus and thus increasing the
intraluminal pressure of the distal
oesophagus. The operation is
done through an abdominal ap
proach. The oesophagus is
mobilised extensively through
the hiatus, but the phreno-oe-
sophageal membranes are kept
intact. After adequate
mobilisation of the.oesophagus,
a rubber sling is used to pull the
abdominal part of the oesopha
gus down. The opening of the
hiatus is narrowed by inserting
sutures anterior to the oesopha
gus, so that only one finger can
be passed
Fig. 43.6.- Hill procedure. A.— Shows the technique. B.— Shows the between the oesopha
appearance at the end of operation. gus and the hiatal margin. The
gastro-oesophageal junction is
anchored to the arcuate ligament. Now the stomach is wrapped around the entrance of the oesopha
gus into stomach by placing sutures on both anterior and posterior aspects of the gastro-oesophageal
junction. These sutures are also passed through the median arcuate ligament for posterior gastropexy.
Manometric pressure readings before, during and after this procedure indicate a rise in sphincter
pressure to a level of 40 to 50 mmHg.
LAPAROSCOPIC FUNDOPLICATION.— Usually 5 Cannulae are inserted for laparoscopic
fundoplication — all in the upper abdomen above the umbilicus. The lower oesophagus and the car
dia are separated from the diaphragmatic hiatus. The short gastric vessels are divided to mobilise the
fundus. The fundus of the stomach is drawn up behind the oesophagus and then sutured in front of the
oesophagus. The diaphragmatic hiatus is now narrowed with sutures placed behind the oesophagus.
In Nissen fundoplication, the fundus is sutured as explained encircling the oesophagus completely.
Now a more popular procedure e.g. Toupet (a surgeon from France) partial fundoplication used in
which the fundus is sutured on each side of the oesophagus, leaving the anterior aspect of oesophagus
exposed. In any case if the laparoscopic method fails, the abdomen is opened with upper midline
incision and the procedure is completed as open operation.
Reflux oesophagitis with stricture (See Fig. 43.3).— This causes shortening of the oesophagus.
It mainly involves the distal oesophagus, but occasionally the middle of oesophagus may be involved
and these are examples of Barrett’s oesophagus when the lower part of the oesophagus has columnar
epithelium. The treatment of reflux oesophagitis with stricture is difficult, so every effort should be
made to prevent such stricture formation and to perform anti-reflux surgery before stricture
develops.
TREATMENT in the beginning should be intensive medical therapy and repeated dilatations. This m
reduce oedema, spasm and inflammation. When No. 40 French Bougie can be passed through the str
the inflamma
tion is reduced
considerably, an
anti-reflux re
pair has a good
chance of suc
cess.
If the stric
ture cannot be
dilated and there
is extensive
shortening of the
oesophagus,
Collis gastro
plasty is ad
vised. In this
operation upper
part of the stom
ach is cut longi
Fig.43.7.— Steps of operation of Collis gastroplasty. A.— Shows upper part of stomach is cut tudinally. The
longitudinally and sutured so that the oesophagus is lengthened.B.— Shows the redundant fundus hasportion with the
been sutured to the newly formed oesophagus by wrapping like other anti-reflux operations i.e. NVsen
fundoplication or Belsey Mark IV repair. lesser curvature
is sutured
around a No. 40 French Bougie so that this part forms the abdominal part of the oesophagus and thus
oesophagus is lengthened. The other sides of the cut surfaces are sutured to form a redundant fundu
redundant fundus is now used for an anti-reflux operation e.g. Nissen fundoplication or Belsey Mark
Post-operative dilatation of the stricture is always necessary. The vagi may be sacrificed in the process
need pyloroplasty to be performed. Pyloroplasty itself gives some symptomatic relief to the patient.
When the stricture has caused too much narrowing of the oesophagus, Thai fundic patch operation
alongwith a fundoplication should be
performed. In this operation the nar
rowed part of the oesophagus is incised
longitudinally across the stricture allow
ing the opening in the oesophagus to
gape widely. This opening is later on
closed with a skin graft. After this the
fundus of the stomach is used for a full
360° degree fundoplication of Nissen
type. Satisfactory results are claimed in
75% of cases.
When recurrence develops after
above-mentioned operations, it is un
likely that further attempts at repair will
be successful. In such cases, resection of
the damaged oesophagus alongwith in
testinal interposition using either jeju
Fig.43.8.— Thai operation. A.— Shows longitudinal cutting across num or left colon should be advised. Use
the stricture. B.— Shows applying the skin graft on the opening and of stomach to reconstitute the oesopha
plicating the adjacent fundus of the stomach around lower end of gus after resection is not advised as inci
oesophagus. dence of reflux is quite high in postop-
THE OESOPHAGUS 689
erative period. To minimise reflux oesophagitis and further stricture formation it is better to interpose an intes
tinal segment from the oesophageal remnant through the diaphragm upto the stomach.
Barrett’s oesophagus.— When in the lower part of the oesophagus there is columnar epithelium instead
of normal squamous epithelium, it is called Barrett’s oesophagus. This abnormal oesophageal lining may extend
upto the level of the aortic arch or above. This columnar epithelium is mainly mucus secreting with only sparse
parietal cells. When the squamous epithelium of the oesophagus is eroded by chronic reflux, replacement may
occur with columnar epithelium. Yet it is very difficult to mention with certainty that all cases of Barrett’s oe
sophagus is due to reflux oesophagitis. A few cases may be congenital — due to cephalad growth of columnar
epithelium from the gastric cardia. Peptic ulcer may develop in such columnar epithelium which is known as
Barrett's ulcer. Stricture may also develop but this stricture is always situated at the junction of columnar and
squamous epithelium which may be in the middle of the oesophagus.
The columnar epithelium of the Barrett’s oesophagus may undergo dysplasia or neoplastic change and the
risk of adenocarcinoma developing in patients with Barrett’s oesophagus is greater than in general population.
TREATMENT.— After the diagnosis has been made, multiple biopsies of the mucosa should be taken to
exclude presence of adenocarcinoma. When this is excluded an anti-reflux operation should be performed. In
such patients long term observation with repeated endoscopy and biopsy should be performed. When associ
ated with stricture,dilatation of the stricture is necessary. Resection of the oesophagus is only indicated when
adenocarcinoma is present.
HIATUS HERNIA
Hiatus hernia is the herniation of stomach into the thorax through oesophageal hiatus in the diaphragm.
There are three types of hiatus hernia — 1. Sliding or axial hiatus hernia, 2. Para-oesophageal or rolling hernia
and 3. Mixed type consisting of both the above types.
1. Sliding or axial hiatus hernia (Type I).— This is by far the commonest type consisting of more than
80% of all cases of hiatus hernia. It is not a true hernia as the phreno-oesophageal membrane is intact. There
is also no typical hemial sac. This hernia may be symptomless, but its symptoms only appear when there is
Fig.43.9.— A.— Sliding hiatus henia. B.— Para-oesophageal hiatus hemia. O.M.— Oesophageal mucosa.
G.M.— Gastric mucosa. P.O.L.— Phreno-oesophageal ligament. D.— Diaphragm. P.— Peritoneum.
T.P.O.L.— Tom phreno-oesophageal ligament.
44
gastro-oesophageal reflux.
DIAGNOSIS is mainly performed by (i) Barium meal X-ray (contrast radiographic study). During the
Fig.43.10.— Barium swallow skiagram showing two types of hiatus hemia. Left figure shows large sliding hiatus
hemia with cardia well above the diaphragm and is incompetent allowing gastric juice to enter the oesophagus.
Right figure shows a large para-oesophageal hemia in which almost the whole stomach has entered the thorax
where it lies upside down.
course of routine barium meal X-ray the patient is turned into a semiprone position on the right side and the table
is tilted to 20°Trendelenburg position. In case of hiatus hemia barium will regurgitate into the hemia without
the aid of any additional abdominal pressure. If the barium does not regurgitate from the hernia into the oesopha
gus, there is usually no symptom and no treatment is required.
(ii) Oesophagoscopy reveals varying degree of oesophagitis which has been discussed under the heading
of gastro-oesophageal reflux.
TREATMENT.— If there is no symptom, no treatment is necessary. Treatment is only required when there
is gastro-oesophageal reflux causing various symptoms. The treatment of this condition is same as gastro-
oesophageal reflux which has been discussed in the previous section.
2. Para-oesophageal or rolling hernia (Type II).— It is rare, compared to the previous variety and
constitutes only 10% of all cases of hiatal hemia. There is a true hernial sac and phreno-oesophageal membrane
is ruptured. So this is a true hemia from all aspects. Hernia of the stomach usually occurs at the left anterolateral
portion of the oesophageal hiatus. In this condition the fundus of the stomach enters the thorax through the
oesophageal hiatus. As it is a typical hemia it increases in size and may be quite big inside the thorax. This type
of hemia may be completely asymptomatic, so much so that it may reach a large size without the patient being
aware of it. The distal oesophagus maintains its normal intra-abdominal location, so it is usually not associated
with gastro-oesophageal reflux.
CLINICAL FEATURES.— As has already been mentioned this hernia may be asymptomatic in large
number of cases. If symptoms do occur, the followings are mostly complained of:
1. Fullness after meals, early satiety, post prandial vomiting and other digestive disturbances.
THE OESOPHAGUS 691
2. Dysphagia is also caused when the big hernia presses on the distal oesophagus.
3. Stasis in the incarcerated gastric pouch may lead to erosion of the gastric mucosa.
4. Acute and chronic gastric ulcer in the pouch is often seen. This ulcer is situated above the diaphragm
and is called ‘riding’ ulcer. This ulcer may cause bleeding and perforation.
5. When the size of hernia is quite big there is an every possibility for gastric volvulus to develop.
This may strangulate to cause sudden death of the patient.
After meals gurgling or splashing noises in the chest may be heard on auscultation.
DIAGNOSIS.— Simple chest X-ray shows an air-fluid level in the mediastinum behind the heart which
is quite diagnostic. This is confirmed by barium swallow examinations. Flexible fibre-optic gastro-oesophago-
scopy should always be performed before operation to detect any abnormality in the oesophagus or stomach.
TREATMENT.— Unlike the type I hiatal hernia where medical treatment is first advised only in patients
with symptoms, the patients harbouring a type II hiatal hernia are always advised surgical operation due to
the risk of sudden catastrophic complications. There is no place of medical treatment in this condition.
Presence of type II hiatal hernia is itself an indication for surgery.
Operation is performed through thoracic or abdominal approach. But majority of the surgeons prefer thoracic
approach as this type of hernia may be adhered to the surrounding structures. The principles of operation are (a)
reduction of hernia, (b) elimination of the sac, (c) repair of the large opening in the hiatus and (d) an anti-reflux
operation to eliminate the risk of post-operative gastro-oesophageal reflux. There is a chance of recurrence due
to attenuation of surrounding tissues and the muscles of the diaphragm due to presence of a large hernia.
ACHALASIA OF THE OESOPHAGUS
This disease though discovered in 1674 by Thomas Willis, yet it was properly described first by Hurst in 1915. He
first described that this disease is due to failure of relaxation of the lower oesophageal sphincter. The term ‘achalasia’
has been derived from a Greek word which means ‘failure of relaxation’. In fact in this condition peristalsis is absent
or feeble in the body of the oesophagus and the lower oesophageal sphincter fails to relax during swallowing.
Aetiopathology.— The physiological abnormalities are incomplete or absent relaxation of lower oesophageal
sphincter and absence of peristalsis in the body of the oesophagus. Oesophagus empties incompletely containing
residual food and fluid. It must be remembered that there is no gas bubble in the stomach as no bolus with accompanying
normal gas bubble can pass through the lower oesophageal sphincter. The oesophagus becomes dilated i.e. megaoesophagus
and tortuous with persistent redemption oesophagitis due to fermentation of food residues. The most important fact is
that there is increased incidence of the carcinoma of the oesophagus in patients with achalasia. Histology of muscle
specimen shows reduction of ganglion cells with variable degree of chronic inflammation. The basic difference between
achalasia and Hirschsprung’s disease of the colon is that the dilated oesophagus usually contains few ganglion cells,
whereas the dilated colon contains normal ganglion cells proximal to the constricted, aganglionic segment.
Pseudoachalasia is usually due to adenocarcinoma of the cardia or by cancers outside the oesophagus constricting
the cardia and lower oesophagus leading to achalasia-like disorder.
Degeneration or absence of the ganglion cells of Auerbach’s plexus throughout the body of the oesophagus is a
definite histological feature. So neurogenic basis is the main cause of this condition. In 30% of cases this degeneration
or absence of ganglion cells is not present, so some extraoesophageal cause has been found out. The defect may be in
the central nuclei or in the vagus nerve itself.
Various causes have been incriminated : (i) Emotional stress, (ii) External compression or trauma, (iii) Chagas’
disease, caused by Trypanosoma Cruzi and (iv) Infection.
Clinical features.— Three main symptoms of the patient are — (a) dysphagia, (b) regurgitation and (c) weight
loss. Men and women are affected with equal frequency though there may be a slight tilt towards women. Though
this condition may occur at any age, yet it is more often seen between the ages of 30 and 50 years.
(a) Dysphagia— Patient mainly complains of obstruction in swallowing at the low retrosternal area. In the
beginning difficulty in swallowing is more obvious with cold than with warm foods. Patient feels obstruction particu
larly in case of liquids, whereas solid seems to pass more easily. Gradually the patients feel difficulty in swallowing
solid as well and show a tendency towards taking water with food so that food can be washed away into the stomach.
(b) Regurgitation.— This is a very characteristic feature of this condition and is particularly obvious
at night when the patient is recumbent. But there is usually no sour taste of the regurgitated material, this
692 A CONCISE TEXTBOOK "OF SURGERY
shows that the regurgitation is not from stomach and not associated with gastro-oesophageal reflux. In late
cases patient may complain of regurgitation of foul-smelling intraoesophageal contents. Regurgitation may
lead to aspiration and development of pulmonary complications.
(c) Weight loss is quite common in this condition, as the patient fails to take food to his satisfaction.
Pain is not a usual symptom of this condition, though retrosternal pain may be complained of occasion
ally in early cases. This pain may even radiate to the interscapular region or even to any of the arms
simulating angina pectoris. Once the oesophagus dilates pain vanishes off. It must be remembered that in 5
to 10% of cases carcinoma may be associated with this condition. It is often considered as a premalignant
condition. This is mainly due to the result of mucosal irritation and subsequent metaplasia induced by the
retention oesophagitis. It must be noted that oesophageal carcinoma in this condition tends to arise in the
middle-third of the organ. This.carcinoma is squamous cell variety.
Diagnosis.— (i) Barium oesophagogram or barium meal X-ray of the oesophagus may help to diagnose this condition
even in the early stage by showing slight dilatation of the oesophagus and obstruction at the cardia. As the disease
progresses the oesophagus becomes dilated and the lower most portion of the oesophagus ends like a ‘bird-beak’ tapering.
(ii) In straight X-ray one may find posterior mediasiinal air-fluid level
on the lateral view and there may be very little or no fundal gas in the stomach.
(iii) Oesophageal manometry is the best possible way to make the firm
diagnosis. It will reveal that the pressure in the body of the oesophagus is
higher than normal and may be equal to the atmospheric pressure. Being a
thoracic organ its pressure should be much below the atmospheric pressure.
This manometric study will also reveal that there is no typical co-ordinated
peristaltic wave of the oesophagus in response to swallowing, instead feeble
and repetitive contractions may occur throughout the oesophagus. The pecu
liarity one may notice that the upper oesophageal sphincter relaxes normally in
the majority of cases, but the lower oesophageal sphincter fails to relax after
swallowing. The intraluminal LOS pressure is increased at rest.
Mecholyl test.— 8 lo 10 mg of methacholine, a vagomimetic drug is
injected intravenously. This produces marked elevation of the intra-oesoph-
ageal pressure and frequency of simultaneous oesophageal contractions
corresponding with complaints of chest pain.
(iv) Oesophagoscopy is indicated (a) to assess presence of retention
oesophagitis and (b) to assess presence of associated carcinoma. One may
Fig. 43.11.— Shows barium meal X-ray
of a typical case of achalasia. Note the be confused to differentiate reflux oesophagitis from retention oesophagitis
characteristic persistent ‘bird-beak’, taper of achalasia. In the former condition the lower oesophagus will look whit
at the oesophago-gastric junction. ish, fibrotic and with superficial ulceration, whereas in the latter condition
of achalasia the oesophageal mucosa will look oedematous and reddish
purple discolouration.
Treatment.— Basically this con
dition is incurable. The treatment is
aimed at relief of the distal oesoph
ageal obstruction. So for symptomatic
relief there are three devices which have
been put forward by their proponents
as the treatment of choice.
(a) MEDICAL TREAT
MENT.— Calcium channel antago
nist was used but its long-term effect
is quite low. Sublingual nifedipine may
be used for transient relief of symp
toms, but hence no place in definitive
treatment. Botulinum toxin has been
Fig. 43.12.— Shows the technique of oesophagocardiomyotomy operation. given by endoscopic injection into the
Interrupted line shows the line of division. lower oesophageal sphincter. It acts by
THE OESOPHAGUS 693
interfering with cholinergic excitatory neural activity at the sphincter. Its effect is also not permanent and the injection
may be repeated after a few months. This is a relatively new form of treatment, whose place is not yet established.
(b) MECHANICAL DILATATION — involves stretching of the cardia with a balloon to disrupt the muscles.
This treatment first described in the Mayo clinic by Plummer. Plummer in fact used hydrostatic bag which became quite
popular. Previously such dilatation was also tried by Hurst-Maloney bougies in the range of 50 to 54 French type. But soon
this became unpopular. Nowadays plastic balloons with precisely controlled external diameter are being used. Balloons of
30-40 mm in diameter are being used and are inserted over a guide wire. This ruptures the circular muscle fibres of the lower
sphincter. The most probable complication of this technique is oesophageal perforation, which is less than 0.5%. The risk is
more with bigger balloons, but these may be used by progressive dilatation over a period of weeks. Nowadays curative
dilatation has been reported in 75% to 85% of cases. The results are better in older group of patients above 45 years.
(c) OESOPHAGOCARDIOMYOTOMY.— This operation was originally described by German surgeon Mr. Heller
in 1914. But he performed the operation transabdominally and oesophagotomy was performed both on the anterior and posterio
walls of the gastro-oesophageal junction. But the modern oesophagomyotomy is a modification of Heller’s operation in which
thoracic approach is preferred and the myotomy is performed only on the anterior wall of the oesophagus.
Preoperatively washing of the dilated oesophagus should be performed for the last 24 hours and the patient should be on
liquid diet. Transthoracic approach through left lower intercostal space is performed. The oesophagus is mobilised. A longi
tudinal incision is made on the anterior wall of the oesophagus 7 to 10 cm in length through all the muscle layers of the distal
oesophagus. The incision must reach well above the constricted portion of the oesophagus proximally and must reach the
stomach within 1 cm distally. The submucosa is exposed. Damage to the vagus nerve and the supporting structures around
the hiatus is avoided. This operation has shown good result in over 90% of cases on 10 years follow-up. So majority of
surgeons believe that this should be the treatment of choice in achalasia of the oesophagus. But others are in the opinion
that as non-operative treatment like hydrostatic dilatation can cure 65% of patients, it is worthwhile trying first and opera
tion should be reserved for those who have failed to show good result by hydrostatic dilatation.
3% of patients treated by oesophagocardiomyotomy ultimately develop gastro-oesophageal reflux. If the incision on the
stomach becomes more than 1 cm, a prophylactic antireflux operation should be performed. The usual practice is to perform a
partial rather than total fundoplication in this situation. So a few surgeons are in the opinion that it is better to perform an anti
reflux procedure alongwith Heller’s operation. But it must be remembered that anti-reflux operations may also fail in a few
cases, so it is not justified to do anti-reflux procedure as a routine. Majority of cases of failure of Heller’s operation is due to
persistent obstruction of the distal oesophagus or persistent achalasia. In such cases it is advised to do re-myotomy operation.
LAPAROSCOPIC HELLER’S MYOTOMY — is now being used quite successfully in more than 90% of cases.
DIFFUSE OESOPHAGEAL SPASM OR CORKSCREW OESOPHAGUS
Some psychic problem seems to be associated with this condition. A history of irritable bowel syndrome, spastic colon, py-
lorospasm or other gastrointestinal conditions e.g. peptic ulcer, gallstones and pancreatitis may be associated with this condition.
Clinical features.— This condition is more common in females. Pain and dysphagia are the two main symptoms of this condition.
Pain is often felt as a discomfort under the lower half of the sternum. It may be severe and colicky. It may radiate through to the back,
to the shoulders and to the arms resembling angina pectoris. The symptoms seem to be greatest during the periods of emotional stress.
Dysphagia is not that significant as pain and the clinician must give the patient a lead to find out this symptom. Regurgitation is quite
rare, but some clever patients may give a history of regurgitation of intra-oesophageal saliva at the time of oesophageal colic.
Diagnosis.— (i) E.C.G.— This is mainly performed to exclude coronary artery disease.
(ii) Contrast study.— Barium meal X-ray usually shows abnormality in less than 50% of cases. The typical abnormality is
'curling' or crock-screw oesophagus caused by segmental contraction of the circular muscle of the oesophagus. There may be 'beak
like' taper or distal oesophagus as an early case of achalasia. There may be oesophageal wall thickness. Occasionally oesophageal
Pulsion diverticulum may be seen.
(iii) Oesophagoscopy should be performed to exclude presence of oesophagitis, stricture or carcinoma.
(iv) Oesophageal manometry seems to be the most important diagnostic tool in this condition. Primary peristaltic wave may
be recognised in the upper half of the oesophagus, but in the lower half it is usually replaced by multiphasic, repititive and high-
amplitude contractions. In contradistinction to achalasia, upper and lower sphincters pressure and relaxation with swallowing are
usually normal, although a hypertensive LOS may be seen.
Treatment.— Medical treatment with sublingual nitroglycerin may be tried, similarly oesophageal dilatation with Hurst-Maloney bougies
may relieve pain and dysphagia for even a few months. Long oesophagomyotomy has been more often tried in this condition with success. Left
thoracic approach is always preferred. The lower limit of the longitudinal incision is same as that of achalasia, but the upper limit should be
extended as high as the aortic arch or above. Oesophagomyotomy has benefited only 75% to 80% of patients in most of the series and it is less
effective than for achalasia. If hiatus hernia is associated with this condition it should be treated by an anti-reflux operation.
THE SCLERODERMA
This is a collagen vascular disease of unknown aetiology. It is characterised by induration of the skin, fibrous replacement of the smooth
694
muscle of internal organs and loss of visceral function. Oesophagus is the most commonly involved in the gastrointestinal tract. The fibrous
replacement of oesophageal smooth muscle disrupts its normal peristalsis and LOS loses its tone. Gastro-oesophageal reflux is quite
common. Dysphagia due to slow emptying of the oesophagus and severe heart burn due to gastro-oesophageal reflux are common
complaints of this condition. Gastro-oesophageal reflux will lead to reflex oesophagitis and even stricture formation in the distal
oesophagus. Diagnosis is mainly performed by contrast radiography, oesophageal manometry, acid-reflux test and oesophagoscopy.
Treatment is mainly aimed at relieving the patient from gatro-oesophageal reflux problems. Death usually comes from cardia
and pulmonary involvement and only half of the patients survive more than 5 years. Medical anti-reflux treatment should be tried
H2 inhibitors e.g. cimetidine or ranitidine. If the symptoms persist anti-reflux operations should be performed. In case of stricture
Collis gastroplasty alongwith Nissen fundoplication should be performed.
OESOPHAGEAL DIVERTICULUM
Oesophageal diverticulum is protrusion of the oesophageal mucous membrane through the oesophageal wall. It may be either (I) 'true ’
variety, when it contains all the layers of the oesophageal wall thatmeans the mucosa, submucosa and the muscle layers or (II) ‘false ’ variety
in which the diverticulum consists of only the mucous and submucous layers. Oesophageal diverticulum can be further classified into (1)
Pulsion diverticulum, in which the diverticulum arises due to elevated intraluminal pressure which forces the mucosa and the submucosa
to herniate through the oesophageal musculature. So it is a ‘false’ divertculum. (2) Traction diverticulttm, which forms as a result of traction
effect by chronically inflamed and granulomatous mediastinal lymph nodes that adhere to the oesophageal wall.
There are mainly three sites where oesophageal diverticulum may be seen — A. Pharyngo-oesophageal — at the junction of the
pharynx and oesophagus, B. Para-bronchial (mid-oesophageal) — near the bifurcation of the trachea and C.Epiphrenic (supradiaphrag
matic) — at the distal oesophagus. Whereas pharyngo-oesophageal and epiphrenic diverticula are Pulsion diverticula and are ‘false’, the
parabronchial diverticulum is a ‘true’ diverticulum and of traction variety. It must be remembered that all the three varieties of oesophageal
diverticula are acquired.
A. Pharyngo-oesophageal diverticulum.— Though this diverticulum was first described 200 years ago,
yet Zenker in 1878 properly narrated its details and clinical features in published paper. Since then this
diverticulum is also known as Zenker’s deverticulum. This is the commonest variety of all the diverticula in
the oesophagus. It is hardly seen before 30 years of age and usually occurs after 50 years of age.
Premature contraction of the cricopharyngeus muscle during swallowing seems to be the cause of this
condition. This increases the intraluminal pressure and the mucous membrane of the pharyngo-oesophageal
junction alongwith submucous coat finds its way posteriorly between the cricopharyngeus muscle inferiorly
and the oblique fibres of the thyropharyngeus muscle superiorly. The muscular gap on the posterior aspect of
the pharyngo-oesophageal junction through which this diverticulum comes out is called Killian’s triangle.
Gradually the diverticulum develops and insinuates itself in the prevertebral space between the oesophagus and
the cervical vertebrae. As the ingested material fills in the diverticulum it develops caudally and may even reach
the superior mediastinum. For more detail description of aetiology, clinical features and treatment see page 630.
CLINICAL FEATURES.— Cervical dysphagia, effortless regurgitation and gurgling sensation in the neck
on swallowing are the main three symptoms of this condition. While the last one appears late when the
diverticulum is quite large, the other two appear quite early, particularly the cervical dysphagia which seems
to be the first symptom of this condition. Weight loss is a noticeable feature and may confuse this condition with
malignancy. Regurgitation is particularly prominent during sleep and this may wake the patient up during sleep.
Due to regurgitation recurrent episodes of airway contamination and aspiration pneumonitis may result.
DIAGNOSIS.— Diagnosis is mainly performed by contrast radiography (barium oesophagogram). There
is hardly any need for oesophagoscopy. One may perform manometric study to find out inco-ordination of
muscles during swallowing.
TREATMENT.— Surgery is the main treatment. If dehydration is present it should be corrected before
operation. Similarly presence of pneumonitis or lung abscess should be dealt with first before surgery of this
condition.
Surgery is always done under endotracheal anaesthesia and rapid sealing of the airway with a cuffed balloon
should always be performed. Oblique left cervical incision parallel to the anterior border to the sternomastoid
muscle is made. The sternomastoid muscle and the carotid sheath with its contents are retracted laterally while
the thyroid and the trachea are retracted medially. The diverticulum is located and gradually dissected off the
surrounding structures. No. 40 to 45 French bougie is passed into the oesophagus and the neck of the
diverticulum is properly identified. Myotomy of the cricopharyngeus muscle is performed (See Fig. 36.3) i.e.
the muscle fibres of the cricopharyngeus are divided. Majority of the small diverticula disappear following
THE OESOPHAGUS 695
cervical oesophagomyotomy. Large diverticulum should be excised using automatic stapler. Where automatic
stapler is not available, the diverticulum is excised very near to the neck and the gap is closed with atraumatic
suture. After completion of myotomy and resection of the diverticulum, a nasogastric tube is inserted by the
anaesthetist into the upper oesophagus. Air and saline are insufflated and the oesophagomyotomy and the suture
line are tested for no mucosal tear.
Cricopharyngeal myotomy, with or without diverticulectomy is the most effective treatment of this condition
and is the treatment of choice. It carries very low mortality and morbidity.
B. Parabronchial (midoesophageal) diverticulum.— This is the least common of all the three diverticula seen in the
oesophagus. Though this diverticulum typically occurs near the bifurcation of the trachea, yet this may occur anywhere particularly in the
middle third of the oesophagus. The diverticulum is always associated with granulomatous infection of the mediastinal lymph nodes,
particularly the subcarinal and parabronchial lymph nodes. Tuberculosis is the most common of the granulomatous disease, though
histoplasmosis may be seen in a few conditions.
CLINICAL FEATURES.— This diverticulum rarely causes symptom and is mainly asymptomatic. Diagnosis is made incidentally
by barium oesophagogram for other condition.
TREATMENT.— When asymptomatic, no surgical treatment is required. Treatment of tuberculosis should be commenced. Only
when a fistulous communication is formed between the oesophagus and the respiratory tract due to necrosis of the granulomatous process,
surgery may be required in the form of division of the fistula, suturing of the mucous membrane of the oesophagus and the respiratory tract
and interposition of adjacent normal tissue.
C. Epiphreilic diverticulum.— It occurs mostly in the distal oesophagus within 10 cm from the cardia. It is the protrusion
of mucosa and submucosa through the oesophageal musculature. It is again due to oesophageal motility disturbance and may be associated
with diffuse spasm, achalasia, oesophageal sliding hiatus hernia, reflux oesophagitis and stricture. Only rarely this diverticulum may exist
without any other associated lesion. Due to mechanical distal obstruction raised intraluminal pressure is responsible to blow out the mucosa
and the submucosa through the muscle of the oesophagus.
CLINICAL FEATURES.— As such this condition is asymptomatic and cases are on record when this diverticulum was diagnosed
through barium oesophagogram for other condition . But as mentioned earlier it is usually associated with other oesophageal lesion like
hiatus hernia, diffuse oesophageal spasm, achalasia, reflux oesophagitis and even carcinoma. Dysphagia and retrosternal pain may be the
only symptoms.
DIAGNOSIS.—Barium oesophagogram is the main tool of its diagnosis. Manometric study and oesophagoscopy should be performed
later on to know more about functional abnormalities of the oesophagus and presence of other associated lesions.
TREATMENT.— Mild symptomatic patients do not require any treatment. When symptoms like severe dysphagia and chest pain are
bothering the patients, operation is justified.
Operation is performed through left thoracotomy. Resection of the diverticulum alongwith a long thoracic oesophagomyotomy from
the level of aortic arch to the oesophagogastric junction should be performed. Presence of other condition should be dealt with properly.
MISCELLANEOUS LESIONS OF THE OESOPHAGUS
PLUMMER VINSON SYNDROME

Plummer and Vinson from United States and Kelly and Paterson from England almost simultaneously (1914
to 1920) described this condition. The main symptom is cervical dysphagia. Iron deficiency anaemia is very
much associated with this condition. So this is often called sideropenic dysphagia.
Typically patients are women and over 40 years of age. They have atrophic oral mucosa, spoon shaped
fingers and brittle nails, long-standing anaemia and cervical dysphagia. A fibrous web partially obstructing the
oesophageal lumen at its upper end a few millimetres below the cricopharyngeus muscles seems to be the cause
of the cervical dysphagia. Dietary deficiency has been incriminated.
Treatment.— Correction of nutritional deficiency and forceful dilatation of the web with oesophageal
bougies are the main modalities of treatment. The only problem is that this condition has been considered as
a pre-malignant lesion and in approximately 10% of patients carcinomas develop in the oral cavity, hypo-
pharynx and oesophagus. So a careful follow-up is very much necessary in this condition.
MALLORY-WEISS SYNDROME
In this condition there is linear mucosal laceration at the oesophagogastric junction. The reason is the sudden
increase in intra-abdominal pressure during vomiting transmitted to the oesophagus against closed glottis. The
similar mechanism also causes spontaneous rupture of oesophagus when the force is too much. A history of
vomiting followed by either melaena or haematemesis suggests the possibility of this syndrome.
Diagnosis.— Though oesophagoscopy is the best diagnostic instrument to find out the site of bleeding, yet
in majority of cases bleeding is so profuse that oesonhagoscopy fails to detect anything. Barium oesophagogram
cannot make the diagnosis as such, but it is helpful
10 cxc'uc^c o
/■' differential diagnosis. Coeliac angiography may at
■ I • :mes demonstrate the site of bleeding when bleed
ing is quite profuse.
mSwlBtdgdik, Treatment.— Nasogastric aspiration and in-
UL travenous blood transfusion should be started im-
Ik mediately. Nothing should be allowed by mouth.
Iced saline gastric lavage may be performed. This
conservative treatment <s usually successful in
■L" stoping the bleeding.
WMSBBBmSk Surgery.— When bleeding becomes continu-
. .■ ■ ■ lip ous or even profuse inspitc of this conservative
Bk treatment, a long proximal gastrotomy should be
performed to inspect the oesophagogastric junc
tion. The blood clots are evacuated from the stom-
K ach and the mucosal tear is oversewn. Surgery is
f :■ quite successful in this condition and recurrence is
almost nil.
SCHATZKI RING
f; It is an oesophageal web in its lower most part.
This web contains only ni ucosa and submucosa. It
■IBBBBi. ■■ is covered with squamous epthelium above and
Fig.43.13.— Barium swallow skiagram showing ‘web’ at columnar epithelium below. So it actually appears
the upper end of oesophagus. at the squamo-columnar junction within 1 to 2 cm
above the oesophagogastric junction. This condition is in majority of cases asymptomatic. Dysphagia only
occurs when the diameter is minimised to less than 15 mm.
Diagnosis.— Barium oesophagogram is most dependable to diagnose this condition. One thing must be
remembered that it usually is associated with sliding hiatus hernia. The web seems to be due to excessive
submucosal fibrosis. It may not be associated with gastro-oesophageal reflux or oesophagitis.
Treatment.— Intermittent oesophageal bougienage is the treatment of choice of this condition. Only when
it is associated with reflux oesophagitis, an anti-reflux operation is justified.
BENIGN STRICTURE
There are certain conditions which may cause benign stricture of the oesophagus. These are: (i) Corrosive
oesophagitis, (ii) Tuberculosis, (iii) Syphilis, (/v) Herpes, (v) Radiation oesophagitis, (vi) Crohn’s disease, (vii)
Secondary to reflux oesophagitis, (viii) Schatzki ring and (ix) Secondary to Plummer Vinson syndrome.
Here only corrosive oesophagitis will be described, since other conditions have already been discussed.
Corrosive oesophagitis.— Ingestion of strong acid or alkali may cause virulent inflammation of the
oesophagus which is known as corrosive oesophagitis. At present this type of oesophagitis is not very common,
only a few stray incidents may be obtained where children have ingested lye, a strong cleaning agent containing
sodium hydroxide and sodium carbonate. Examples of ingesting strong acids may also be seen. In case of acid
ingestion, the oesophagus frequently escapes injury as squamous epithelium is relatively resistant to acid and
as the shrot time the acid is exposed to the oesophageal mucosa. But it usually causes destruction in the stomach
as pylorospasm caused by acid keeps it longer time in the stomach, produces gastritis, necrosis and even
perforation when the acid is quite strong.
THE OESOPHAGUS 697
The pathologic changes in the oesophagus in case of corrosive oesophagitis is more or less
similar to that found in burns in the skin. It may be superficial or deep. It starts with oedema,
congestion and inflammation. It causes thrombosis of the vessels. The superficial layer sloughs out
which is followed by fibrosis and delayed re-epithelialization. In deep burns oesophageal strictures
develop.
CLINICAL FEATURES.— Burns of the lips, tongue and mouth may be obvious. Stridor,
hoarseness of voice may be due to laryngeal oedema. Patient will complain of pain in the mouth
and larynx and may feel nausea and vomiting. In subsequent few days the patient will complain of
painful dysphagia. After 2 or 3 weeks if there is stricture formation, patient will complain of
dysphagia only.
TREATMENT.— Intravenous fluid to make good the blood volume depletion should be started
immediately. Nothing should be permitted by mouth. Early water-soluble contrast radiography should
be performed. Endoscopy may be performed, but upto the upper most area of corrosive oesophagitis.
Under no circumstances the oesophagoscope should be passed into the zone of corrosive oesophagitis.
Steroids have been advocated by a few surgeons, whereas others have avoided it since it may mask
the dreaded symptoms of oesophageal or gastric perforation. Vigorous antibiotic should be started.
During the inflammatory stage bougienage must be avoided. Only when the stage of acute inflam
mation has been subsided and definite stricture has been formed, dilatation by bougie should be
advised.
Dilation Of Strictures.— At present guidewire-directed dilatation of the oesophagus has been
the treatment of choice. Previously the guidewire was passed blindly and the method was not popu
lar. Subsequently the guidewire was passed down the biopsy channel of the endoscope under vision
through the stricture. The endoscope is now withdrawn, leaving the guidewire in place. Then the
dilators are passed over the guidewire. Radiographic screening is required to check that the guidewire
is in satisfactory position and the dilators can be passed safely. With more experience, radiographic
screening is now rarely required only for difficult cases. For normal swallowing, the stricture should
be dilated to at least 16 mm in diameter.
Balloons may be used for dilatation of strictures. These balloons can be passed down the biopsy
channel of the endoscope or may be passed by radiographic screening. But it must be remembered
that balloons are less effective than dilators. To facilitate bougienage one may perform gastrostomy.
This will facilitate feeding as well as retrograde bougienage.
Sems In Benign Oesophageal Diseases.— The use of SEMS in benign oesophageal disease is
controversial, though uncovered metallic stents have been used in patients in long standing peptic
or postsurgical strictures which otherwise require regular dilatation and have failed to respond to
high dose treatment with proton pump inhibitors and who are unfit for surgery. In benign perforation
SEMS should be avoided. In Boerhave’s syndrome, as there is no pre-existing stricture, the stent
fails to occlude perforation and overflow occurs around the upper end of the stent resulting in medi-
astinitis and empyema.
When the above measures fail, and the stricture of the oesophagus does not respond to repeated
bougienage, reconstructive operation should be advocated. Total by-pass of the strictured oesopha
gus by a segment of right or left colon interposed substernally may be advocated. Rarely jejunum or
stomach tube has also been used for by-pass.
TUMOURS OF THE OESOPHAGUS

BENIGN TUMOURS AND CYSTS
Benign tumours of the oesophagus are rare and constitute only 1% to 5% of oesophageal neo
plasms. According to incidence the followings are the benign conditions seen in oesophagus:
(i) Leiomyoma; (ii) Cyst; (iii) Polyp; (iv) Papilloma; (v) Lipoma; (vi) Haemangioma;
(vii) Adenoma; (viii) Granular cell myoblastoma.

Leiomyoma.— This is the most common benign tumour. It is found in patients between 20 and
50 years of age. Approximately in 1/10th of cases it is multiple. Majority of this tumour occur in the
middle and lower third of the oesophagus. Histologically, this tumour consists of interlacing bundles
of smooth muscles.
CLINICAL FEATURES.— This tumour may give rise to symptoms only when it is more than 5
cm in diameter. The symptoms are dysphagia and vague retrosternal pain. Bleeding may occur when
there is malignant transformation to leiomyosarcoma. Multiple leiomyomas are known as leiomyo
matosis.
DIAGNOSIS.— Barium oesophagogram usually diagnoses this condition. Particularly in lateral
view this tumour may be diagnosed by a smooth filling defect with intact mucosa and very definite
border. Oesophagoscopy is indicated more to rule out malignant lesions. Biopsy taking through
oesophagoscopy is not advised as scarring may make subsequent resection difficult.
TREATMENT.— Even asymptomatic leiomyomas should be excised, as ultimately they will grow
larger and will definitely cause symptoms. Further, malignancy can only be ruled out by excision.
Leiomyomas of the middle third of the oesophagus are approached through right thoracotomy inci
sion, whereas those in the distal third are approached through left thoracotomy incision. Only in
case of very big leiomyomas that oesophageal resection may be necessary.
Oesophageal cysts.— This is the second most common benign lesion of the oesophagus. Cyst is
more often seen among infants and children as these arise as diverticula from embryonic foregut.
The epithelium of these cysts is either simple columnar ciliated epithelium or stratified squamous
epithelium. These usually produce symptoms like dysphagia or respiratory difficulty or retrosternal
discomfort by pressing on the adjacent oesophagus or tracheobronchial tree.
On barium oesophagogram oesophageal cyst resembles leiomyomas and this is also seen more
commonly in the lower half of the oesophagus.
The treatment is excision of the cyst. The entire epithelial lining must be removed.
Polyps.— These are usually present in the cervical oesophagus and in old men. These are com
posed of vascular fibroblastic tissue. Intermittent dysphagia, haematemesis or melena are the usual
symptoms. Diagnosis^ mainly performed through barium swallow examination. Oesophagoscopy
is more informative regarding these polyps.
Treatment is excision, rather than electrocoagulating the pedicle through oesophagoscope.
Resection is usually performed through a lateral cervical oesophagotomy and the polyp is resected
under direct vision.
MALIGNANT TUMOURS
Besides carcinoma of the oesophagus which is the most common malignant neoplasm in the
oesophagus, the other malignant lesions are sarcoma, mostly leiomyosarcoma. Carcinosarcoma
and adenoid cystic carcinoma have also been reported to occur in oesophagus. These of course
show better prognosis. Primary malignant melanomas have been reported in the oesophagus.
CARCINOMA OF THE OESOPHAGUS
Though carcinoma is the commonest neoplasm in the oesophagus, yet it is a rare type of cancer
in the alimentary tract. It only accounts for 7% of all gastrointestinal malignancies.
Aetiology.— 1. Age and Sex.— Though oesophageal cancer may occur in young individuals, it
is predominantly a disease of the old. The usual victims are between 45 to 75 years with highest
incidence between 65 to 75 years. Except the cervical oesophagus, where men and women are equally
affected, in thoracic and abdominal oesophagus men are more often affected.
2. Geographical distribution.— The incidence of oesophageal cancer is more common from
the shores of Caspian Sea (in northern Iran) to China. The highest incidence is in Henan province in
THE OESOPHAGUS 699
China, where the incidence is approximately 100 cases per 1 lac of population per annum. The cause
of such high incidence in these areas is not yet determined, but is probably due to fungal contamina
tion of food with the production of a carcinogenic mycotoxin, together with nutritional deficiency in
the population of this area. Supplementation of diet with beta-carotene, vitamin E and selenium has
been shown to reduce the incidence of cancer.
3. Alcohol and tobacco have been incriminated to increase the incidence of this disease. Na
tive alcohol is more dangerous in this respect. Squamous cancer incidence is mostly increased. It is
now accepted that excessive consumption of alcohol and smoking are important aetiological risk
factors in the origin of the carcinoma of the oesophagus, particularly even of adenocarcinoma.
4. Malnutrition, vitamin deficiency, anaemia, poor oral hygiene also increase the incidence of
oesophageal carcinoma. This disease is more often seen in ‘familial keratosis palmaris et plantaris
(dylosis palmaris et plantaris).
5. Plummer Vinson syndrome is a precancerous condition and increased incidence of carci
noma in cervical oesophagus in women is well explained through this.
6. Achalasia.— A direct relation has been seen between achalasia and cancer of oesophagus.
Chance is 10 times more in patients with achalasia than normal individuals. The cancer arising from
achalasia is usually of squamous type and occurs in younger age group. Most unfortunate is that
cancer usually appears in the dilated portion of the oesophagus and remains asymptomatic for long
lime.
Various other oesophageal lesions are believed to be premalignant. These are 7. Hiatus hernia
and reflux oesophagitis, 8. Barrett’s oesophagus, 9. Irradiation oesophagitis, 10. Corrosive oesophagitis
from lye and 11. Oesophageal diverticulum. Adenocarcinoma develops more frequently in patients
with peptic oesophagitis and is strongly associated with Barrett’s oesophagus.
Pathology.— In last two decades incidence of adenocarcinoma has increased by about 8%
per annum. While histologically, more than 95% of oesophageal cancers were squamous cell
carcinoma, at present adenocarcinoma accounts for 60% to 75% of oesophageal cancers in
several countries. The reason for such change is not wholly understood, but usually developed
from (i) Barrett’s oesophagus, (ii) junctional columnar epithelium in the distal oesophagus,
(iii) glandular epithelium or (iv) ectopic gastric mucosa. It must be remembered that the sur
vival rate of such cancer is quite poor, though in a few series of U.K. the rate has been in
creased from 5% to 10% in 5 years. The poor prognosis of the oesophageal cancer is mainly
due to spread of the cancer. Histologically, more than 95% of oesophageal cancers are squa
mous cell carcinoma. Adenocarcinomas, constituting less then 5% of oesophageal cancers, usually
develop from (i) the junctional columnar epithelium in the distal oesophagus, (ii) Barrett’s
mucosa, (iii) Glandular epithelium or (iv) Ectopic gastric mucosa. Grossly oesophageal carci
nomas have either polypoid, infiltrative or ulcerative appearance. The squamous cell carci
noma predominates in the upper and middle thirds of the oesophagus while adenocarcinomas
restrict themselves in the lower third of oesophagus. Adenocarcinomas may extend into the
cardia and even fundus of the stomach. Multiple malignant lesions are seen in 3% to 10% of
patients.
MODES OF SPREAD.— Cancer of oesophagus is of equal malignancy to that encountered in
growths in other parts of the G.I. tract. Adenocarcinomas metastasise more rapidly and extensively
than squamous growths. In lower third of the oesophagus, the prognosis of adenocarcinoma is much
worse. As other carcinomas in the body oesophageal carcinoma also spreads by (i) infiltration,
(ii) lymphatics and (iii) blood.
(i) Local infiltration.— There is a marked tendency of this carcinoma to spread by burrowing
under the mucosa. This occurs both longitudinally and circumferentially, thus producing long stric
ture. This spread may extend upto 1 to 3.5 cm. So considering the elasticity of oesophagus resection
should be performed 6 cm away from the oesophageal growth. The thick compact muscles of the
oesophagus, surprisingly enough does not prevent spread of growth through the oesophageal wall.
Early oesophageal carcinomas are defined when squamous cell carcinoma is limited to the mucosa
or submucosa without lymphatic involvement. Their prognosis is much better than those of more
developed carcinomas. Microscopically, columns of cells may be seen spreading between the muscle
fibres to the surrounding structures thus involvement of trachea, bronchus, aorta and crura of the
diaphragm may be explained.
(ii) Lymphatic spread.— Besides involvement of the regional lymph nodes, there is direct sub
mucous spread through lymphatic permeation and embolism which leads to the formation of satel
lite growths well beyond the apparent upper margin of the tumour. This feature calls for a very wide
excision of the growth to avoid recurrence at the anastomosis. The upper third drains into the wide
spread lymphatic glands in the neck. This feature, alongwith close proximity of vital structures,
precludes the possibility of radical surgery for growths arising in the cervical and supra-aortic seg
ment of the oesophagus. Another interesting feature is that the lymphatic spread is often discontinu
ous — that means the distant regional lymph nodes may be involved when local nodes are free from
tumour. But fortunately enough growths in this area are frequently radiosensitive and are best treated
by radiotherapy. The middle third drains to the gland in the hilum of the lung and to the subcarinal
glands. Radical surgery is difficult and it is in this region that the rival claims of surgery and radio
therapy are not yet settled. In the lower third lymphatic drainage is to the glands around the cardiac
orifice, to the splenic and to the coeliac glands. This is the region where radical surgery is possible
and lower third of the oesophagus together with stomach, spleen, tail of pancreas and the adjacent
omenta can be removed en bloc. Accessibility of growth and the fact that many of the cancers are
adenocarcinomas therefore radioresistant, surgical excision has been regarded as the most suitable
treatment for carcinomas in this region.
(iii) Blood spread.— As other carcinomas in the body, blood spread is late. Considering the fact
that the patients do not survive long and in these cases there is high operative mortality, only few
patients develop blood borne metastasis. Systemic spread is mainly to the liver and lungs, but prac
tically any organ may be involved including the bone, brain and skin.
Clinical features.— The most important symptom, which should raise suspicion, is progressive
dysphagia. Onset is usually insidious and in the beginning nonspecific symptoms like retrosternal
discomfort, indigestion, weight loss, occult mild anaemia may be present. At the initial stage dysph
agia is more felt during ingestion of solids, but gradually swallowing of liquids and saliva become
difficult. Patients may present with rather non-specific dyspeptic symptoms or a vague feeling that
something is obstructing during swallowing.
Hoarseness due to recurrent nerve palsy is a sign of advance and incurable disease. If the lymph
nodes are palpable in the neck, it is also a sign of advanced disease.
Diagnosis.— 1. This can be made with a high degree of accuracy by the usual barium oesophagogram.
One may use air-contrast radiographic techniques to detect small lesions of 10 mm diameter,
(i) Irregular mucosal filling defects, (ii) distortion of the oesophageal lumen, (iii) annular stricture
and (iv) irregular ‘rat-tail’ filling defect of the distal oesophagus may be detected in barium studies.
It must be remembered that irregular filling defect more often signifies malignant lesion rather than
the smooth, tapered stricture which signifies a benign lesion. The other characteristic feature is that
in benign obstructing lesion there is proximal dilatation of the oesophagus of varying degree, but
such dilatation is not seen in malignant lesions.
2. Endoscopy should be performed in all cases of suspected oesophageal cancer. Oesophageal
biopsy and brushing for cytological examination may be performed through oesophagoscopy. Bron
choscopy may be performed when the lesion involves upper oesophagus to detect malignant in
volvement of the adjacent tracheobronchial tree. Additional diagnostic study such as radioactive
phosphorus which is concentrated in the carcinomas is not so popular. Endoscopic ultrasonography
(EUS) is the best method for preoperative staging of the primary lesion and involvement of the
THE OESOPHAGUS 701
regional lymph nodes.

3. CT scanning of the chest and abdomen is mandatory to know the stage of metastasis. CT has
improved greatly in recent years, though is not so accurate for staging lymph nodes.
4. Ultrasonography of the liver is important to exclude metastasis in the liver.
5. Bronchoscopy should be done particularly in lesions of the upper and middle-thirds where
there may be tracheal and bronchial invasion.
6. Mediastinoscopy is important to know involvement of mediastinal group of lymph nodes.
7. Laparoscopy is particularly important in case of adenocarcinoma of the distal oesophagus
to detect transperitoneal spread and liver metastasis. It is quite simple and should be used particu
larly in carcinoma of this region.
8. Scalene node biopsy may be performed to detect lymph node metastasis. Respiratory excur
sions should be noted to exclude phrenic nerve involvement.
9. Respiratory and cardiovascular function are the most important aspects to assess the patients
before operation.
On endoluminal ultrasound (EUS) oesophageal carcinoma is revealed as a mass with a
hypoechoic pattern within or penetrating the oesophageal wall depending on the depth of the
invasion. However in stenosing lesions EUS may be technically impossible in a significant percent
age of patients. In these cases double contrast barium study of the oesophagus is a highly sensitive
modality for diagnosing early and advanced carcinoma of the oesophagus. Barium study may
also reveal a second site of carcinoma in the oesophagus. But barium studies can neither
evaluate the depth of invasive growth nor assess the exact length of tumoural lesion within the
oesophagus.
Staging.— Staging of oesophageal carcinoma is performed by EUS and CT. EUS has the advan
tage of being able to visualise the extent of disruption of the layers of the oesophageal wall. CT is
used to assess the extension and resectability of the lesion as well as to detect lymph node and
distant metastasis. Involvement of the trachea and main stem bronchus should be suspected if an
oesophageal cancer either causes inward bowing of the posterior tracheal or bronchial wall or dis
places the trachea and/or bronchi away from the spine. CT cannot accurately assess tumoural inva
sion of the diaphragm; may be due to oblique orientation of the gastro-oesophageal junction as
compared to the axial orientation of the CT plane. CT also has a low sensitivity for detection of
metastatic lymph nodes in the mediastinum, whereas its sensitivity for visualising involvement of
upper abdominal lymph nodes is rated at about 80%. EUS is now considered as more accurate than
CT in the evaluation of tumour extension and mediastinal lymph node involvement in oesophageal
carcinoma, but CT is more accurate than EUS for detection of infradiaphragmatic lymph node inva
sion and for distant metastasis. MRI probably has the same possibilities and the same limitation as
CT for evaluating the exact extension of oesophageal carcinoma, but MRI may in the future prove to
be more useful because of its multiplanar capabilities.
TREATMENT.— There are mainly two methods of treatment available — radiotherapy and
surgery.
RADIOTHERAPY.— Though squamous cell carcinoma is radiosensitive, yet radiation therapy
has hardly succeeded as the only treatment. The average 5 years survival rate following
radiotherapy is less than 10% and not more than 17% even in the reported series of its strongest
proponent. 5,000 to 6,000 rads over 5 weeks period have been used for cure. Only cervical oesoph
ageal carcinoma should be treated with radiotherapy. Radical radiation therapy is also associated
with complication such as radiation pneumonitis, post radiation stricture, tracheo-oesophageal fis
tula, spinal cord injury, pericardial effusion and constrictive pericarditis.
Palliative low dose radiotherapy (2,000 to 3,000 rads) may be used to alleviate distressing symptoms
such as pain, dysphagia and bleeding.
Preoperative radiation appears to improve resectibility, though its application is yet not popularised.
702
SURGERY.—Radical and curative surgery is only possible for growths of the lower third of the oesophagus.
In case of cancers affecting upper two-thirds of the oesophagus radical surgery is not possible in majority of
cases and surgery is mainly aimed at palliation so that the patient can eat properly during the rest of his life.
Operative mortality is approximately 25% and 3 years survival rate is approximately 25% to 35%.
In cervical growths the treatment of choice still remains radiotherapy and surgery as yet has not made any
appreciable advances.
Cancer of the lower third.— It is only in this part of the oesophagus where curative and radical surgery
should be attempted. Accessibility of the lesion, its lymphatic field and all adjacent structures have made block
dissection of the growth possible. Growth at this part of the oesophagus should be further subdivided into (a)
Infradiaphragmatic cancers and (b) Supradiaphragmatic cancers.
(a) INFRADIAPHRAGMATIC CANCERS.— In case of growths below the diaphragm and those at the
gastro-oesophageal junction the ideal access is through left thoracoabdominal incision. The patient lies on the
right lateral position. Left thoracoabdominal incision along the line of the 7th rib is made. In the beginning only
medial part of the incision is made to know if the tumour is inoperable or not. When the tumour is operable the
whole thoracoabdominal incision is made. The stomach alongwith its whole lymphatic field the spleen, lower
third of oesophagus and even left lobe of the liver are excised. Reconstruction using Roux-en-Y jejunal loop
with jejuno-jejunum anastomosis should be performed. If possible pyloric antrum may be preserved for oeso
phagogastric anastomosis. In that case pyloromyotomy may be performed. Oesophagogastric anastomosis
seems to be better from physiology point of view. In case of oesophago-jejunal anastomosis there is chance of
biliary regurgitation, heart bum and stricture formation.
(b) SUPRADIAPHRAGMATIC CANCERS.— In case of growths in the lower third above the diaphragm
2-stage technique as described by Lewis and Tanner {Lewis-Tanner technique) should be practiced. In this
technique upper left paramedian incision is
made and the stomach is mobilised carefully
to preserve its blood supply from gastroepip
loic arch and the right gastric artery. The left
gastric artery is secured close to its origin
and smaller vessels in the region of the
diaphragmatic hiatus are divided. Peritoneal
reflection and phrenooesophageal ligaments
are divided. Kocher’s manoeuvre is applied
to mobilise the 2nd part of the duodenum.
Pyloromyotomy as performed in Ramstedt’s
operation is carried out since oesophageal
resection will cause complete trunkal vagot
omy and pyloromyotomy will help in proper
emptying of the stomach.
The 2nd stage begins with a right thora
cotomy through the 6th interspace. The right
side is preferred as no important great ves
A B sels intervene in mobilisation of the oe
sophagus. Only the azygos vein lies on the
right wall of the oesophagus. The oesopha
Fig.43.14.— A.—The dotted area is the extent of resection along gus is mobilised and the stomach is pulled
with the tumour. B.— Anastomosis of the oesophagus with the through the oesophageal hiatus of the dia
remnant of the stomach with pyloroplasty, as vagotomy is inevitable
at the time of resection.
phragm into the right chest. Affected seg
ment of the oesophagus together with the
proximal part of the stomach is excised. The distal stomach remnant is stapled. The anastomosis of the
oesophagus to the stomach remnant is made end-to-side. The opening in the stomach being cresentic in shape
on theanterior wall of the stomach adequate distance away from the stapled suture line. The anastomosis is made
THE OESOPHAGUS 703
in two layers — vertical mattress silk sutures interiorly so that the knots are tied in the lumen and a continuous
catgut suture exteriorly.
Cancer of the middle third.— This
part of the oesophagus is not so easily acces
sible due to presence of vital structures of
the hilum of the lung around. This part
should be divided into (a) lower half and (b)
upper half for better description.
(a) LOWER HALF.— In case of can
cers in this region surgical technique is almost
similar to that described for cancers in the
supradiaphragmatic part of the lower third
of the oesophagus.
(b) UPPER HALF.— In this region
excision of the growth and performance of
the anastomosis becomes difficult and the
access becomes narrow. Moreover cardiac,
aortic and pulmonary movements make
accurate insertion of suture difficult and the
anastomosis may be unsound with subse
quent leakage. To avoid the dangers of per
forming anastomosis in the depth of the
thoracic cavity, the method of total oesoph-
Fig.43.15.— A.— Dotted area indicates the extent of resection agectomy has been introduced. While per
alongwith the tumour. B.— Shows anastomosis of the oesophagus
with the fundus of the stomach. forming total oesophagectomy Roux-en-Y
jejunal segment was used to bridge the gap
between the stomach and the cervical oesophagus in front of the sternum in a subcutaneous tunnel. But this
technique did not stand due to fistula formation and non-acceptance of a good anastomosis between the high
columnar epithelium of jejunum and squamous epithelium of upper oesophagus. Subsequently transverse
colon, right colon or even left colon was used in front and behind
sternum to bridge the gap between cervical oesophagus and the
stomach. But again leakage and stricture formation appear to be the
common complications after these types of replacement.
Ultimately three-stage oesophagectomy bringing the stomach
as a whole up into the neck and anastomosing with the cervical
oesophagus was introduced. This technique otherwise became
successful as this is a more physiological approach by making
anastomosis between the oesophagus and the stomach. In this
technique the first two stages are similar to those of Lewis-Tanner
procedure. But in this operation the stomach is however mobilised
with even better care. Each omental branch of the gastroepiploic
arch is ligatured separately and not by bunching. The left gastric
artery is ligatured at its origin from the coeliac axis, so that blood
supply from the right gastric artery is adequate to supply the fundus
of the stomach. The importance of blood supply to the fundus of the
Fig.43 16.—Incision of three stages oesoph- stomach cannot be emphasised strongly since this is the region
agectomy advocated by McKeown. Firststage where anastomosis will be made with the cervical oesophagus,
is abdominal operation through abdominal Qnjy a few short gastric vessels are ligatured just to make mobili-
incision. Second stage is thoracic operation . c . ,, . rr,. , „,
through thoracic incision. Third stage is sation of the stomach adequate enough. The second part of the
cervical operation through neck incision. duodenum and head of the pancreas are mobilised extremely so that
the pylorus can be brought to the midline in the oesophageal hiatus. Pyloromyotomy, same as Ramstedt’s
operation, should always be performed.
In the 2nd stage the entire thoracic oesophagus is mobilised after dividing the vena azygos between
ligatures. The anterior surface of the oesophagus is cleared completely from the trachea and the left recur
rent laryngeal nerve is well preserved.
In the third stage exposure is made through the right side of the neck to avoid damage to the thoracic
duct and the left recurrent laryngeal nerve. The right lobe of the thyroid is retracted forward alongwith the
carotid sheath. The entire oesophagus containing the tumour with the stomach is pulled out through the
cervical incision. The gastro-oesophageal junction is divided and the cardiac opening of the stomach is
stapled and oversewn. The oesophagus is now divided in its cervical part and is anastomosed with a new
crescentic opening in the fundus by two layers suturing as is described in the Lewis-Tanner operation
mentioned above.
In this three stage total oesophagectomy there are various advantages e.g. (i) Wide clearance of the
tumour is achieved; (ii) There is hardly any chance of leakage; (iii) The anastomosis is performed without
tension; (iv) Epithelial union takes place readily between the squamous epithelium of the oesophagus and
mucosa of the gastric fundus; (v) In this technique the gut is not opened inside the abdomen or thoracic
cavity so there is least chance of potential contamination (during colonic replacement, a few anastomoses
are required and the gut is opened in the abdomen and in the thoracic cavity); (vi) The patient can eat
without discomfort; (vii) In case radiotherapy is required, the anastomotic site is well away from the region
of radiotherapy. .
Palliative procedures.— In many cases oesophageal carcinoma may be irresectable. In these cases one
of the palliative procedures may be adopted. In these cases obviously patient does not survive more than 6
months and the palliation is aimed at relieving dysphagia. The various palliative methods are :
1. RESECTION WITH ANASTOMOSIS.— Surgical resection is still the best accepted treatment
providing good palliation and occasionally cure. However, the majority of patients with oesophageal can
cer are unsuitable for surgical treatment due to advanced disease, age or associated medical problems. The
most important symptom is difficulty in swallowing the degree of which varies and eventually progresses to
complete dysphagia. Some form of palliation is a must in these cases. The aim of palliation is the relief
from dysphagia with minimum morbidity and maximum quality of life. This operation is particularly advo
cated in case of adenocarcinomata at the cardio-oesophageal junction as these are radioresistant.
2. INTUBATION.— Oesophageal intubation was the first technique to palliate malignant dysphagia
and remains the most commonly used method. Intubation should
ideally be performed endoscopically and under X-ray screen
ing. Most of the various systems currently available involve
sliding a prosthetic tube, carried on flexible introducer along
a guide wire through the stricture. With experience, success
ful tube placement should be possible in approximately 95%
of cases, but there are certain limitations to use a tube. Gross
angulation of the lumen due to the tumour or inadequate gut
lumen distal to the tube may both impair tube drainage. Tubes
may not be well tolerated and there is a risk of airway com
pression and pulmonary aspiration if placed closed to the
cricopharyngeal sphincter. When placed across the cardia,
gastro-oesophageal reflux can be troublesome. About 1 /4th
of the patients require tube servicing due to food blockage
and in few cases there may be overgrowth of tumour to block
tube ends. All these problems can usually be solved by fur
Fig. 43.17.— Celestin tube is used for intuba ther endoscopic manoeuvres. The major benefits of this intu
tion of inoperable growth of the distal part of
the oesophagus. bation are its inexpensiveness, can be accomplished in one
THE OESOPHAGUS 705
session and provides immediate relief of dysphagia. The major hazard is oesophageal perforation which
occurs in about 10% of cases. Two types of tubes are often used for this purpose — Celestin’s tube and
Souttar’s tube. These tubes are passed through the malignant stricture and left in situ. This will relieve
dysphagia and the patient will be able to take soft food.
The use of intubation has been greatly advanced with the use of flexible endoscope. Atkinson of Naughtimham
has introduced a silastic tube with nylon spiral enforcement with a distal retaining flange to prevent proxi
mal displacement. The tube is inserted over a guide wire with a specially designed introducer. The technol
ogy of intubation has now moved on with invention of various types of expanding metal stents (sems)
which is described below.
Celestin’s tube is a flexible polythene tube with oval cross section and 10 inches in length. For its
introduction a pilot bougie is always used, which is about 24 inches in length. With the aid of an oesophagoscope
the tip of the pilot bougie is passed through the malignant stricture into the stomach. The abdomen is
opened and a small incision is made at the anterior wall of the stomach below the cardia and at the midpoint
between the greater and lesser curvatures. The tip of the pilot bougie is brought out through this opening in
the stomach wall. The upper end of the pilot bougie is anchored securely with the lower end of the Celestin’s
tube. The pilot bougie is now pulled out till the upper funnel-shaped end of the tube impacts against this
stricture. Excess of Celestin’s tube inside the stomach is cut off. Gastrostomy is closed. Abdominal wound
is closed in layers.
Souttar's tube is made up of spirally wound silver wire. This is also introduced through an oesophagoscope
after the malignant stricture has been properly dilated. Celestin’s tube has enjoyed more popularity than
Souttar’s tube.
3. LASER PHOTOCOAGULATION.— Laser recanalisation involves vaporizing tumour using neody
mium yttrium aluminium garnet (Nd : YAG Laser). Exophytic tumours are more suitable for laser therapy.
Sharply angulated tumour at the cardia or near cricopharyngeus and tumours longer than 6 cm in length are
less suitable. Nowadays contact method has been used and a lower power of laser light can be used for
treatment, thus reducing the risk of perforation. Typical power setting ranges from 50 to 100 w and the
energy is delivered in 1-2 second pulses from a distance of about 1 cm from the tumour surface in case of
non-contact method. In case of contact method the power setting is reduced to 10-20 w. The tip of the
instrument is used to burn the tumour. Lasering starts from the distal tumour margin and progresses
circumferentially upto the proximal margin. In this technique the oesophageal lumen is always in view and
should reduce the incidence of perforation. As yet there is no clear advantage between the contact and non
contact methods with respect to the number of treatment sessions, relief of dysphagia or complications. A
delay of upto 1 week between initial treatment and relief of dysphagia is typical. Further treatment is
required in case of regrowth of tumour. Successful palliation is reported in approximately 85% of cases.
Perforation and creation of tracheo-esophageal fistula may occur in 5% to 10% of cases (this is less than
intubation technique). In both laser and intubation there is significant initial improvement in quality of life
which gets deteriorated in the terminal phase of the disease.
4. PHOTODYANAMIC THERAPY (PDT).— In oesophageal cancer the photosensitizer is
haematoporphyrin derivative, which is injected intravenously 48 hours prior to endoscopy. At endoscopy
the tumour is exposed to 6-30 nm wave length (red light) from a tunable argon pumped dyelasar. Necrosis
follows damage to the tumour vasculature by cytotoxic singlet oxygen liberated from the activated pho
tosensitizer. At present PDT is of limited use as it is only effective in the treatment of superficial cancers
involving the mucosa and submucosa. With advanced cancers, tumour necrosis following PDT is incom
plete and may be delayed upto 1 week thus providing poor palliation. There is also a risk of major haemorrhage.
Future developments in PDT are expected when new photosensitizers will be available.
5. ELECTROCOAGULATION WITH DIATHERMY PROBES.— Electrocoagulation using con
tact bipolar diathermy probes may be used to canalise oesophageal cancers as a cheaper alternative to laser
treatment. These probes are inexpensive and a recent comparative trial has shown it to be as efficacious and
safe as laser treatment. This treatment is particularly useful for tumours in the upper-third of the oesopha
45
gus and cardiac sites which would otherwise be a problem to palliate with either tube or laser.
6. GASTROSTOMY.— This operation can be carried out only as a temporary measure when the
obstruction is complete and intubation is impossible. It neither improves patient’s general condition nor
gives any relief to the patient from the distressing complaint, i.e. regurgitation of saliva.
7. RADIOTHERAPY— In contrast to endoscopic methods, radiotherapy offers the possibility of
inhibiting the local progression of the primary cancer. Traditionally radiation is given by external beam
from a linear accelarator or cobalt source. The optimum dose for external beam radiotherapy is unknown,
but the minimum accepted for radical treatment is 5000 cGy; and more than 6000 cGy often leads to
unacceptable side affects. Fractional doses are safer than a single large dose. With a daily dose of 200 cGy
and 5 treatments per week, a full course of treatment lasts for 5 weeks. But many patients cannot complete
the full course of treatment due to poor tolerance. Postirradiation stricture and creation of oesophagorespiratory
fistula are serious complications of this treatment. Debilitating effects of radiotherapy may also deteriorate
the quality of life remaining to the patient. For cancer of cervical oesophagus, radiotherapy is the treat
ment of choice. In fact this gives considerable palliation to squamous carcinoma, though dysphagia may
recur which is commonly due to fibrous stricture rather than the primary tumour. Adenocarcinoma of the
oesophagus has often been considered radioresistant, but there are data showing little difference in survival
rates between patients with adenocarcinoma and squamous carcinoma affecting the cardia treated by radio
therapy.
8. INTRACAVITY IRRADIATION (BRACHYTHERAPY).— A selectron applicator tube is passed
over an endoscopically placed guide wire and positioned across the tumour using fluoroscopy. The applica
tor is fixed at the mouth and the patient is transferred to a protected treatment room and connected to the
Selectron machine. The treatment is timed so that 1500 cGy are given. In this treatment a single high dose
fraction is given to obtain rapid palliation. The great advantage of brachytherapy is that the radiation dose
is highest to the tumour while adjacent normal tissues are almost spared, though some patients develop
troublesome oesophagitis. A combination of a low dose external beam radiotherapy alongwith intracavi
tary treatment is an attractive new development.
9. CHEMOTHERAPY.— Chemotherapy alone has no significant place, but as part of a multimodal
approach combined with either radiotherapy or surgery has been encouraging. Response rate with single
agent chemotherapy has been poor, but a measurable response rate (20% to 30%) has been obtained when
cyclical combination chemotherapy has been used particularly with cisplatin and 5-fluorouracil. Combined
chemotherapy (5-fluorouracil cisplatin x 4 cycles) and radiotherapy (5000 cGy) has been compared with
radiotherapy (6400 cGy) alone in patients with either squamous or adenocarcinoma. It has been seen to
produce considerable shrinkage of the disease in about 60% of the patients. The response is better in
squamous cell carcinoma. A significant improvement in survival and quality of life have been noticed in
combined chemotherapy and radiotherapy group.
10. MULTIMODALITY TREATMENT.— Surgical resection and external beam radiotherapy may be
used for palliation. Surgical bypass is sometimes a major procedure for use in a patient with limited life
expectancy. Randomised prospective studies of preoperative and postoperative radiotherapy have not shown
much improvement in survival. Preoperative or postoperative chemoradiotherapy has shown a problem of
morbidity. At present preoperative chemotherapy may be used as oesophageal cancer is a systemic disease
and this treatment may improve the results still further in coming days.
11. BY-PASS OPERATION.— When thoracotomy reveals the growth to be irremovable, a by-pass
operation can be attempted in the form of oesophago-jejunostomy-en-Y or even oseophago-gastrostomy
above the level of the obstruction.
12. SEMS.— Over the last 5 years self expanding metal stents (SEMS) have become an established
method of treatment for the palliation of malignant dysphagia, the closure of tracheo-oesophageal fistulae
and relief of malignant biliary obstruction. Their uses in the management of benign oesophageal perfora
tion and strictures, relief of pyloric and duodenal obstruction, benign bile duct strictures and obstructing
rectal carcinoma are controversial. It is advised that SEMS should be inserted under fluoroscopic control
THE OESOPHAGUS 707
after crossing the stricture by means of a guide wire inserted either via an endoscope or using fluoroscopic
guidance. It is common practice to predilate the stricture using a balloon before employing the stent. It is
important to leave adequate length of SEMS above and below the stricture as these shorten during expan
sion. SEMS are available in both uncovered and plastic covered versions. When there is no plastic cover
the stent adheres to the full length of the stricture as the surrounding tissues project through the mesh and
minimises migration. These prostheses are prone to occlusion due to tumour ingrowth. Plastic covered
prostheses are protected from ingrowth, but these are more liable to migration.
In malignant oesophageal disease at least 50% of patients will be unfit for or have diseases too ad
vanced for surgery. These patients require effective palliation for dysphagia either by SEMS or by plastic
tubes or by producing tumour necrosis with Laser therapy or by argon beam electrocoagulation. Whereas
intubation is one-stage treatment, but producing tumour necrosis requires repeated treatment at regular
intervals. When compared to plastic tube and Laser photocoagulation, SEMS appear overall to produce
better relief of dysphagia with less complications and reduced hospitalisation. If the patient is being treated
with chemotherapy, SEMS should be avoided and the patient should be treated with Laser, as effective
response to chemotherapy predisposes to stent migration.
CAUSES OF DYSPHAGIA
The term ‘Dysphagia’ means difficulty in swallowing. Another related term ‘Odynophagia’ means painful
swallowing. Dysphagia may be functional mainly due to neurological causes or physical due to pressure
on the lumen or foreign body in the lumen.
A list of causes of dysphagia is given below to help the students in differential diagnosis :
1. In the mouth : Tonsillitis, quinsy, carcinoma of the tongue and paralysis of the soft palate (due to
diphtheria in children and bulbar paralysis in adults) etc.
2. In the pharynx.—
(i) In the lumen — Impaction of foreign body (e.g. coin, tooth and denture).
(ii) In the wall — Acute pharyngitis, malignant growth, hysterical spasm, Paterson-Kelly syndrome,
CNS diseases e.g. cerebrovascular accident, Parkinson’s disease, bulbar poliomyelitis, multiple sclerosis,
amyotrophic lateral sclerosis; odynophagia; muscular diseases e.g. muscular dystrophy, metabolic myopa
thy (thyrotoxicosis, hypothyroidism), myasthenia gravis; miscellaneous e.g. cricopharyngeal spasm.
(iii) Outside the wall — Retropharyngeal abscess, enlarged cervical lymph node, malignant thyroid etc.
3. In the oesophagus.—
(i) In the lumen — Impaction of foreign body.
(ii) In the wall — (a) Benign stricture — may be due to reflux oesophagitis, swallowed corrosives,
tuberculosis, scleroderma, radiotherapy etc.; (b) spasm — Paterson-Kelly syndrome, achalasia, webs and
rings etc.; (c) Diverticulum and cyst; (d) Neoplasms — mainly malignant; (e) Nervous disorders — bulbar
paralysis, post-vagotomy; (f) Miscellaneous — Crohn’s disease.
(iii) Outside the wall — Malignant or any large thyroid swelling; retrosternal goitre, pharyngeal diver
ticulum, aneurysm of the aorta, mediastinal growth, dysphagia lusoria, epiphrenic diverticulum, perioesophagitis
after vagotomy, paraoesophageal hiatus repair.
INVESTIGATION and TREATMENT are discussed in the sections of respective causes.
Odynophagia.— Odynophagia means pain on swallowing. It becomes particularly severe in chemical
injury of the oesophagus. Patients with reflux oesophagitis feel burning retrosternal discomfort as soon as
they swallow hot beverages or alcohol.
708
CHAPTER - 36
THE STOMACH AND DUODENUM I
Embryology.— At the end of 4th or beginning of the 5th week the stomach appears as a fusiform dilatation in the proximal part of
the digestive tube. Just distal to this dilatation the gut is connected with the vitello-intestinal duct which opens into the yolk sac. At this
stage the stomach is placed in the median plane and is connected posteriorly to the body wall by a short dorsal mesentery, termed the
dorsal mesogastrium. Anteriorly the stomach is connected to the distal part of the septum transversum with ventral mesogastrium. Due
to rapid growth of the dorsal border the pyloric end of the stomach is carried ventrally and a concavity appears in the lesser curvature.
Now the stomach is displaced to the left of the median plane and is rotated on its vertical axis so that the right surface is directed dorsally
and the left surface ventrally. Due to this rotation the right vagus becomes the posterior vagus and the left vagus becomes the anterior
vagus. The dorsal mesogastrium increases in length and becomes folded on itself to form the greater omentum. The ventral
mesogastrium becomes the lesser omentum which after the rotation almost lies in the coronal plane rather than the anteroposterior
plane. Due to this rotation the duodenum is carried dorsally and to the right. Approximation of the duodenum to the dorsal abdominal
wall leads first to adhesion of the right layer of its mesentery to the parietal peritoneum and later absorption of both the layers. In this
way the duodenum comes to be retroperitoneal.
ANATOMY
STOMACH
Stomach is the most dilated part of the digestive tube and it is situated between the end of the oesophagus and the beginning of the
small intestine. It lies in the epigastric, left hypochondriac and umbilical regions of the abdomen. Through the cardiac orifice it
communicates with the oesophagus and this orifice is situated behind the 7th costal cartilage and 2.5 cm to the left from its junction with
the sternum. It corresponds to the level of the 11th thoracic vertebra. The left margin of the oesophagus joins the greater curvature of the
stomach at an acute angle, called the cardiac notch. The part of the stomach which lies above and to the left of the level of the cardiac
orifice is known as the fundus of the stomach. Through the pyloric orifice the stomach communicates with the duodenum and its
position is usually indicated by a circular groove on the surface of the organ. It is also identified by the prepyloric vein which runs
vertically along its anterior surface. The pyloric orifice lies 1.2 cm (V2 inch) to the right of the median plane at the transpyloric plane
which corresponds to the lower border of the 1st lumbar vertebra (in the supine position). There are two curvatures or borders in the
stomach — the lesser curvature and the greater curvature. The lesser curvature is continuous above with the right border of the
oesophagus. This curvature runs straight down and then curves to the right below the omental tuberosity of the pancreas to end at the
upper border of the pylorus. The most dependent part of the curve where it forms a notch, is termed the angular notch. The lesser
curvature gives attachment to the lesser omentum. The greater curvature forms the left border of the stomach and gives attachment to
the greater omentum. Directly opposite the angular notch the greater curvature presents a bulge which is the left extremity of the pyloric
part of the stomach. This bulge is limited on the right by a slight groove which indicates the demarcation line between the pyloric
antrum on the left and the pyloric canal on the right. The pyloric canal is 2 to 3 cm in length and terminates at the pyloric orifice.
There are two surfaces of the stomach — anterosuperior and posteroinferior. Anterosuperior surface lies in contact with the
diaphragm, which separates it from the left pleura, the base of the left lung, the pericardium and the 6th, 7th, 8th and 9th ribs and
corresponding intercostal spaces on the left side. The upper and left part of this surface is in contact with the gastric surface of the
spleen. The right half of this surface is in relation with the left lobe and quadrate lobe of the liver and the anterior abdominal wall. The
posteroinferior surface lies on the stomach bed, from which it is separated by the omental bursa. The stomach bed is formed by the
following structures — diaphragm, left kidney and suprarenal gland, splenic artery and vein, pancreas, transverse mesocolon, transverse,
colon and left colic flexure. There is a small triangular area near the cardiac orifice, which is bare and is not covered with peritoneum.
This area is in direct relation with the diaphragm and sometimes with the left suprarenal gland. On the left side of this bare area lies a
short peritoneal fold which is called the gastrophrenic ligament.
The pyloric sphincter is a muscular ring composed of thickened portion of circular muscle. Some of the longitudinal muscles may
turn in and interlace with the fibres of the sphincter.
Histology.— The wall of the stomach consists of four layers : serous, muscular, submucous and mucous layers.
The SEROUS LAYER or the visceral peritoneum covers the entire surface of the organ except (i) along the attachments of the
greater and lesser omenta and (ii) the bare area close to the cardiac orifice.
The MUSCULAR LAYER is separated from the serous layer by subserous areolar tissue. The muscle layer consists of three layers
of unstriped muscle fibres — longitudinal, circular and oblique. The longitudinal fibres are the most superficial and continuous above
with the longitudinal fibres of the oesophagus. These fibres are better developed near the curvatures and end distally to the pyloric
portion. Another set starts from the middle of the body of the stomach and gradually passes to the right becoming more thickly arranged
as they approach the pylorus. The superficial fibres of this set pass on to the duodenum to form the longitudinal muscle fibres there and
the deep fibres of this set dip inwards and interlace with the fibres of the pyloric sphincter.
The circular fibres form a uniform layer over the whole extent of the stomach deep to the longitudinal fibres. The circular fibres of
the stomach are continuous with the circular fibres of the oesophagus but are sharply marked off from the circular fibres of the
duodenum by a connective tissue septum. At the pylorus these fibres are abundant and form a ring which forms the pyloric sphincter.
The oblique fibres, internal to the circular layer, are most developed near the cardiac orifice. They sweep downwards from the
cardiac notch and run more or less parallel to the lesser curvature and they possess a well defined right margin and on the left they blend
THE STOMACH AND DUODENUM 709
with the circular fibres.

The SUBMUCOUS LAYER consists of loose areolar tissue between the muscular layers and the mucous membrane.
MUCOUS MEMBRANE is thick and its surface is smooth and velvety. It is red or reddish brown in colour except at the pyloric end
where it is pinkish. When examined with a lens, the inner surface of the mucous membrane presents a honey-comb appearance due to
small, shallow depression of hexagonal form of about 0.2 mm in diameter. These are gastric pits and at the bottom of each are the
orifices of gastric glands. The surface of the mucous membrane and of the gastric pits are covered with a single layer of columnar
epithelium with occasional goblet cell?. The gastric glands comprise (i) the cardiac glands, (ii) the body glands and (iii) the pyloric
glands. The cardiac glands are few in number and confined to a small area near the cardiac orifice. These are compound racemose
glands and some are simple tubular glands. Mucus secreting cells predominate and oxyntic and zymogenic cells are few and far between.
The body glands in the body and fundus are simple tubes with two or more openings into a single pit. There are six types of cells in these
gastric glands : surface, neck cells, progenitor, chief, parietal and endocrinal cells. The surface epithelial cells contain abundant mucous
granules and are designed to protect the epithelium from gastric acids. These are the source of sodium-rich alkaline secretion. The neck
cells line the entrance of the gastric glands. These also buffer the acid as it enters the gastric pits. The progenitor or stem cells are
concerned with the development of new surface cells and the cells of the gastric glands. Parietal cells or oxyntic cells are larger cells and
secrete hydrochloric acid of the gastric juice. The chief cells or the zymogenic cells are small cuboidal cells containing coarse granules
of pepsinogen. These secrete pepsinogen, which is converted to active pepsin at the pH below 2.5. Endocrine cells exist within the
gastric gland and some cells secrete gastrin and serotonin whereas the function of other cells is still obscure, hi the antral and pyloric
glands one can find epithelial cells and mucous neck cells, but no parietal or chief cells. Gastrin producing G-cells are seen in this region.
In the mucous membrane deep to the glands there is a thin layer of involuntary muscle fibres, known as muscularis mucosae. It
consists of an outer longitudinal layer and an inner circular layer. From the inner layer strands of muscle pass between the glands^
contraction of which probably aids emptying of the glands
Blood supply.— The'left gastric artery, branch of the coeliac artery and the right gastric artery, branch of the common hepatic
artery supply the half of the area of stomach near the lesser curvature. The right gastroepiploic artery, branch of the common hepatic
artery and the left gastroepiploic, branch of the splenic artery supply the half of stomach towards the greater curvature The short gastric
branches of the splenic artery pass through the gastrosplenic ligament and supply the fundus of the stomach. Gastroduodenal artery
sends a few branches to the area of the pylorus. Smaller arterioles from these arteries enter the muscular coat and supply the muscles of
the stomach. They then ramify in the submucous coat and finally distribute to the mucous membrane. In the mucous membrane the
arteries breakup at the deep ends of the gastric glands into a plexus of fine capillaries which runs between the glands anastomosing with
each other. Plexus of larger capillaries also surrounds the mouth of the glands and also the gastric pits. Numerous arteriovenous
anastomoses are present in the mucous coat. From these, veins run straight course between the glands to the submucous coat where they
form a rich plexus. From this the veins drain the muscle and pierce the muscular coat to come to the surface and follow the big venous
channels
VENOUS DRAINAGE. — The left gastric and the right gastric veins are direct tributaries of the portal vein. The short gastric veins
and the left gastroepiploic vein are tributaries of the splenic vein. The right gastroepiploic vein and the pancreaticoduodenal vein are
tributaries of the superior mesenteric vein. The splenic vein and the superior mesenteric vein join behind the neck of the pancreas to form
the portal vein. In one word the veins of the stomach ultimately drain into the portal vein.
Lymphatics.— The lymph vessels of the stomach follow the blood vessels for the most part and are arranged in four sets. The first
set accompany the branches of the left gastric artery, receive tributaries from a large area on both surfaces of the stomach and terminate
in the left gastric lymph nodes. The second set drains the fundus and left portion of the body of the stomach, accompany the short gastric
and left gastroepiploic vessels and end in the pancreatosplenic lymph nodes. Vessels of the third set drain the right part of the body of the
stomach and end in the right gastroepiploic lymph nodes. The fourth set drains the pyloric region and pass to the hepatic, pyloric and left
gastric lymph nodes.
Nerve supply.— The sympathetic supply is mainly from the coeliac plexus through plexuses around the gastric and gastroepiploic
arteries. Branches from the left phrenic plexus pass to the cardiac end of the stomach.
The parasympathetic supply is derived from the vagus nerves. The two main vagal trunks lie on the anterior and posterior surfaces
of the oesophagus. The anterior trunk comprises mainly left vagal fibres whereas the posterior trunk comprises the right vagal fibres.
The left or anterior vagus nerve gives off a hepatic branch and the remaining portion innervates the anterior wall of the stomach The
hepatic branch also sends a few fibres to the pylorus of the stomach. The posterior vagus nerve gives off a large branch to the coeliac
plexus and the remaining nerve supplies the posterior wall of the stomach. Parasympathetic supply of the stomach is concerned with the
secretion of acid and pepsin, stimulates or inhibits release of gastrin and stimulates motility of the stomach.
DUODENUM
The duodenum is the shortest, widest and most fixed part of the small intestine. It has no mesentery and is only partially covered
with peritoneum. It has got four parts. The first part is surgically most important as this is the portion of the duodenum which is most
often affected with peptic ulcer. The second part or the descending part is important as in the middle of this part the bile duct and the
pancreatic duct open through the hepatopancreatic ampulla. So this part is important in biliary and pancreatic surgery.
The first part is about 5 cm in length and its proximal half gives attachment to the lesser omentum and greater omentum and is
covered with peritoneum in both anterior and posterior aspects. The distal half is devoid of peritoneum in its posterior aspect. This first
part of duodenum is in relation in front with the quadrate lobe of liver and the gallbladder, posteriorly with the gastroduodenal artery,
the bile duct and the portal vein; superiorly with the epiploic foramen and inferiorly with the head and neck of the pancreas.
The second part of the duodenum is 8 to 10 cm in length and descends along the right side of the vertebral column upto the lower
border of the body of the third lumbar vertebra. It is in relation in front with the duodenal impression on the right lobe of the liver, the
transverse colon, the root of the transverse mesocolon and the jejunum; posteriorly with the right kidney and the structures at its hilus,
the head of the pancreas and the bile duct; on its lateral side to the right colic flexure and on medial side to the head of the pancreas and
the bile duct The bile duct and the main duct of the pancreas open on the summit of a papilla, termed the major duodenal papilla which
is situated at the junction of the medial and posterior walls of the duodenum at about 8 to 10 cm from the pylorus. Before opening in the
duodenal papilla the two ducts unite to form a dilatation, termed hepatopancreatic ampulla. The accessory pancreatic duct, when
present, opens 2 cm proximal to the major duodenal papilla through a papilla termed minor duodenal papilla.
Blood supply.— The arteries supplying the duodenum are derived from the right gastric, supraduodenal, right gastroepiploic, the
superior and inferior pancreaticoduodenal arteries. There is no anastomosis in the wall between the vessels supplying the stomach and
the vessels supplying the duodenum.
PHYSIOLOGY
Functions of the stomach.— 1. Storage.— The main function of the stomach is to mix and churn the food so that it is delivered
slowly to the duodenum. Swallowed food enters the stomach where it is mixed with gastric juice and changed to a more liquid form. It
brings the food to the same temperature of the body. The storage function of the stomach is mainly performed by receptive relaxation.
The upper portion of the stomach relaxes as the intake of food is anticipated. The solid food settles near the greater curvature of the
fundicarea of the stomach, whereas the liquids pass rapidly along the lesser curve, known asMagenstrasse. So Magenstrasse is exposed
to injurious effect of the hot liquids like tea and coffee. Food particles are reduced in size ►y the grinding action of the antrum. Pylorus
constantly returns ingested material to the proximal stomach to be churned repeatedly until and unless it is ready for delivery to the
duodenum.
2. Digestion.— Small amount of digestion takes place in the stomach, mostly proteolysis. Pepsin, the proteolytic enzyme of the
stomach is active in acid environment (pH below 5). It also secretes mucus which prevents autodigestion of the stomach.
The liquified, churned food which has undergone slightly proteolysis is then delivered slowly into the duodenum. The mixing and
slow emptying of the mixed meal from the stomach is performed by ‘antral pump’. Contraction of the body of the stomach propels
contents into the gastric antrum. As the antrum fills the pylorus opens to allow the escape of some chyme. When contraction wave
reaches the pylorus it closes. The antral contents are now pushed back into the body of the stomach. Thus each contraction wave
produces both the escape of a small quantity of chyme and mixing of the remainder. The amount of chyme passed through the pylorus
with each contraction will depend upon the viscosity and amount of solid in the gastric contents. Fluids are emptied more rapidly.
Starches undergo enzymatic breakdown by low pH, which is favourable for the activity of salivary alpha-amylase. Peptic digestion is
mainly aimed at to start proteolysis and initiate dispersion of fats, proteins and carbohydrates by breaking down cell walls. Gastric
mucosa also secretes a lipase which assists in the early stage of fat digestion.
3. It produces intrinsic factor (by the parietal cells) which is essential for absorption of Vitamin B12 and thus helps haematopoiesis.
4. Sterility of the foregut is mainly maintained by gastric acid. Majority of the bacteria die due to the low gastric pH. Only a few
unusual fusiform bacilli can withstand the gastric acid.
5. Defence mechanism.— Gastric mucosa has got the capacity to protect its surface from harmful ingestants. Rapid mucus release
is the first line of defence. If potentially dangerous material permeate through the mucosa, the lamina propria stands in the way with the
army of mast cells, macrophages and lymphocytes.
6. Heat exchange.— The stomach, due to its abundant mucosal microcirculation, can act as heat exchanger. Due to this mechanism
a stable thermal environment is maintained against too cool or too warm ingestant. This offers protection to the adjacent viscera against
thermal damage.
Regulation of gastric secretion.— Gastric secretion can be classified into (a) spontaneous or interdigestive or basal secretion and
(b) stimulated or prandial secretion following ingestion of food.
Stimulation of gastric secretion occurs through three phases — (i) the cephalic phase, in which the secretion is stimulated by sight,
smell, thinking of food or chewing of food, (ii) the gastric phase, in which the secretion is stimulated by presence of food in the stomach,
(iii) The intestinal phase in which stimulation occurs by presence of food in the small intestine.
CEPHALIC PHASE.— In this phase stimuli (sight or smell of food) activate the vagal nuclei in the medulla. Impulses travel along
the vagus nerves and terminate in the gastric mucosa with the release of acetylcholine from the nerve endings. Release of acetylcholine
in the fundus and body of the stomach directly stimulates acid secretion by the parietal cells and release of pepsinogen by the chief cells.
Release of acetylcholine in the antral mucosa causes discharge of gastrin.
GASTRIC PHASE.— This is stimulated by food in the stomach by direct contact or by distension. Through this gastrin is liberated
from the antral mucosa either due to antral distension or upon contact with polypeptides and small peptides. When the surface pH of the
antral mucosa decreases to 3.5, gastrin output is diminished and when it reaches 1.5, gastrin output is absolutely stopped. So this is a
feed back mechanism in which production of gastrin is inhibited by presence of acid in the antrum of the stomach.
The most remarkable action of gastrin is its ability to stimulate gastric acid secretion. It is 30 times more potent than histamine.
Besides its action on acid secretion, it stimulates pepsin secretion and increases gastric mucosal blood flow. It also stimulates pancreatic
enzyme secretion in man.
INTESTINAL PHASE.— This phase is acted upon by instillation of food particularly proteins or acids into the proximal jejunum.
Distension of jejunum will also stimulate secretion. The nature of the humoral agent has not been fully identified. Cholecystokinin, the
duodenal hormone which acts to stimulate secretion of pancreatic enzymes and stimulate contraction of the gallbladder, also acts like
gastrin. There is also an inhibitory activity noticed in this phase. Duodenal acidification provokes release of hormone which inhibits
gastric acid secretion. When fat is introduced the secretory response of a denervated fundic pouch is inhibited. This inhibition is due to
release of a hormonal factor called enterogastrone from the duodenal and intestinal mucosa. Enterogastrone acts by inhibiting the
release of gastrin from the antrum.
CONGENITAL PYLORIC STENOSIS

This is one of the more common congenital anomalies. It occurs approximately 1 in 350 live births.
Males dominate in the ratio of 4 : 1. It is classically seen in first born male babies. Some familial
incidence has been noticed (6% to 10% of cases).
Aetiology.— The most accepted cause of this condition is failure of the pylorus to relax (achalasia).
In fact the pylorus is often hypertrophied, so it is often called ‘hypertrophic pyloric stenosis’.
Ganglion cell dysfunction almost similar to Hirschsprung’s disease has also been incriminated as
the cause of this condition.
Pathology.— The muscles of the pylorus are always hypertrophied, mainly the circular fibres. At
the pylorus the muscle layer is so thick that the lumen may admit only a fine probe. In fact hypertrophy
begins in the musculature of the pyloric antrum which gradually increases and becomes most at the
pylorus. The hypertrophy terminates abruptly at the end of pylorus and duodenum remains normal
Clinical manifestations.— The most common age of onset of the disease is between 4 and 12
weeks. 7 weeks being the average. The main complaint is that the infant begins to vomit the feedings.
There is absence of bile in the vomitus. This is of clinical significance as it excludes more distal
obstructions. Gradually obstruction becomes more complete, the stomach musculature hypertrophies
and the vomitus becomes more ‘projectile’ in nature within several days to a few weeks. Gradually the
infant will not be able to hold down water and becomes severely dehydrated, showing metabolic
alkalosis, and severe depletion of potassium and chloride ions. Serum potassium however remains
normal even after severe losses. But serum pH becomes high. The infant gradually becomes lethergic.
emaciated and there is considerable loss of weight. Constipation is usually present and the stool is
passed small and dry resembling that of a rabbit.
PHYSICAL EXAMINATIONS -— Careful inspection may show visible peristalsis after the child
has been fed from left to right across the upper abdomen.
The most important clinical finding is discovery of a mobile, smooth mass in the epigastrium,
which is nothing but hypertrophic pylorus and feels ‘cartilaginous like’. It is almost olive shaped. To
detect presence of such a lump, it may be required to decompress the stomach with aspirating tube.
Special Investigations.— Diagnosis is mainly made by clinical examination. Barium meal X-ray is
occasionally required, which shows persistent narrowing and elongation of pyloric canal Rarely
ultrasound may be used to confirm the diagnosis.
Treatment.— Operation is the treatment of choice. But some preoperative preparations are re
quired. Volume deficit and electrolyte imbalance must be corrected preoperatively. 5% dextrose in one-
half of normal saline with 30 mEq KCL per litre should be transfused till dehydration and electrolyte
imbalance is corrected. The general condition of the baby is improved. An antibiotic may be adminis
tered as there is increased risk of postoperative gastro-enteritis.
Only in subacute cases when the patient comes after the age of 2 months one may try medical
treatment in the form of Eumydrin (atropine methylnitrate) 1 : 1000 of water freshly made is given in
the dose of 1 ml to 2ml half an hour before each feed. This occasionally may cure the condition, though
toxic manifestations of this drug should be considered e.g. erythema, hyperpyrexia etc. Small frequent
feeds should be advised.
OPERATION.— Pyloromyotomy described by Ramstedt (Ramstedt’s operation) is the operation
which usually cures this condition. The stomach is washed out with saline for several times and finally
1 hour before operation. Just before the operation gastric aspiration should be performed.
The abdomen is opened by a grid-iron incision in the upper right quadrant of the abdomen. The
stomach is first detected and then hypertrophic pylorus is delivered out of the operation wound. With a
fine scalpel incision is made on the superior surface of the pylorus which is the least vascular part. The
incision is made through the serosa and through the hypertrophied pylorus musculature. After about
half of the thickness of the musculature has been incised, splitting of muscle coats is started by blunt
dissection. Koop’s modification is that this blunt dissection can be performed with the scalpel handle.
The tips of an artery forceps are introduced through the incision and the tips are separated to lay open
the deeper muscie fibres which are now teased apart with the scalpel handle to save the mucosa. The
mucosa automatically bulges as soon as all the muscle fibres are divided. Great care should be taken
not to penetrate the mucosa. To ascertain this some air may be pushed into the stomach and squeezed
through the pylorus and duodenum to see if there is any mucosal leakage or not. If there be any mucosal
perforation it is closed by 3 or 4 interrupted chromic catgut sutures with a wisp of omentum held on
the perforation. Haemostasis must be achieved. The abdominal incision is closed.
Postoperative care.— After a few hours majority of patients will tolerate small volume (not more
than 5 ml) frequent feedings. The volume of feed is gradually increased and normal feedings are started
by 3 to 4 days postoperatively. If the mucosa has been repaired, gastric decompression should be advised
for longer period without feeding. Occasionally, an infant may vomit upto a week postoperatively.
Occasional complications are — (i) postoperative vomiting — this may be treated by repeated
aspiration and intravenous feeding, (ii) postoperative pyrexia, (iii) gastroenteritis — all these can be
treated by antibiotic and tepid sponging with repeated aspirations, and (iv) disruption of wound.
Result.— This is an excellent operation which offers usually 100% cure with almost no mortality,
no morbidiity and no recurrent obstruction.
PEPTIC ULCER
There are two main sites of peptic ulcer — gastric and duodenal. Rare peptic ulcers may be seen
in the (i) cardiac end of oesophagus; (ii) Meckel’s diverticulum (due to presence of ectopic gastric
mucosa); (iii) In any segment of bowel (anastomotic ulcer) which has been surgically anastomosed to
the gastric fundus. Peptic ulcers may be acute ulcers, which are shallow and multiple and chronic ulcers,
which are single, deep and scirrhous.
AETIOLOGY AND PATHOGENESIS
ACUTE PEPTIC ULCERS.— (i) About half the patients give history of ingestion of aspirin or butazolidin.
(ii) Sometimes these acute ulcers may occur following stress, when they are called ‘stress ulcers’. This may occur
following hypotension from haemorrhage, endotoxin shock or cardiac infarction, (iii) Sepsis is an important
aetiologic factor. Undrained pus may be responsible for acute stress ulcers. Upper G.I. bleeding from these ulcers
may be seen in critically ill patient and should be a signal to search for pus. (iv) These acute ulcers may be seen
after cerebral trauma or neurosurgical operations (Cushing’s ulcer). Higher rate of acid secretion and higher gastrin
level suggest that patients with head injury may have increased vagal activity, (v) After major bums acute ulcers
may be seen (Curling’s ulcer). Within first 48 hours multiple acute erosions may develop anywhere in the body
and fundus of the stomach (antrum and duodenum usually escape). During convalescent period of such bum cases,
acute duodenal ulcer may occur which often become chronic, (vi) Patients on steroids may develop acute ulcers,
known as ‘steroid ulcers’.
CHRONIC PEPTIC ULCERS.—
Gastric ulcer.— Gastric ulcer patients secrete either low normal or below normal amounts of acid. Only
5% of patients may demonstrate acid hypersecretion.
1. DIMINISHED MUCOSAL RESISTANCE.— This has been incriminated as the cause of chronic gastric ulcer.
This is due to lowering of the ability to resist the effect of acid pepsin digestion.
2. PYLORODUODENAL REFLUX.— Regurgitated bile and other duodenal juices have been taken to be the
prime cause of preulcerative superficial gastritis. Though such biliary reflux may account for a large number of
gastric ulcer cases, it does not seem possible to explain all of them on this basis. Some gastric ulcers occur in
the fundus or at the cardia where such biliary effects would seem least active.
3. DEFICIENT MUCOUS BARRIER.— A surface layer of mucus protects normally from the digestive effect
of the hydrochloric acid and pepsin. When this mucous barrier becomes deficient gastric ulcer may develop. But it is
a matter of clinical observation that in most cases of gastric ulcer the stomach produces large quantities of mucus.
4. MUCOSAL TRAUMA.— 85% of gastric ulcers occur along the lesser curve. This fact together with the
observation that fluids tend to pass through the lesser curve of the stomach (Magenstrasse) suggests that a mechanical
factor might be involved. This part of the stomach is exposed to injurious effects of heat and trauma.
5. LOCAL ISCHAEMIA.— Microemboli artificially introduced into the gastric circulation of dogs or inter
ference with blood supply by ligation of vessels or omental stripping would cause gastric erosions and ulcers to
develop. Arteriovenous shunts which are present in the submucosa of the stomach are under the control of sympathetic
nervous system and excessive stress and strain may cause diminution of blood supply to the mucous membrane of the
stomach leading to ulcer formation.
6. ANTRAL STASIS.— This usually produces increased acid secretion and it is an accepted fact that the major
ity of patients with gastric ulcers have low acid content in the stomach. But it is seen that nearer the ulcer to the pylorus
more is the acid secretion of the stomach.
As the gastric ulcer patients have low acid content some factor such as injury to the gastric mucosa which renders
it more susceptible to acid peptic damage may lead to ulcer formation. Factors like reflux of bile and pancreatic juice
and pyloric dysfunction are also important in the pathogenesis of gastric ulcer. Bile salts apparently damage the
mucosa which is then attacked by acid peptic digestion. Gastric ulcers invariably occur in areas of gastritis. Gastric
ulcers lie in the achlorohydric zone of mucosa. 95% of gastric ulcers occur on the lesser curvature near the incisura
angularis. Against regurgitation of bile theory it can be said that diverting the route of bile through the stomach by
cholecystogastrostomy does not cause ulceration. Local ischaemia seems to be a valid pathogenic factor.
7. NONSTEROIDAL ANTIINFLAMMATORY DRUGS (NSAIDs).— Ingestion of these drugs in patients suffering
from arthritis as a long term basis is a significant aetiologic factor at present time. The drugs of this group are often called
ulcerogenic drugs. These drugs seem to disrupt the prostaglandin-driven support of the mucosal barrier. These prostaglan
dins are related to the production of mucosal gel layer in the stomach, which provides a protective barrier to the gastric and
duodenal lining. So disruption of this mucosal barrier allows even minimal amount of acid to cause ulceration.
8. HELICOBACTER PYLORI.— It is a spirochaetal bacterium which exists in the deep mucosal layer of the
antrum mainly and duodenum rarely. Association of this bacterium with ulcer disease was first originally described in
1984. Since then lots of papers have been published to indicate its association with ulcer disease. Upto l/5th of normal
population harbours this bacterium. In almost 100% of cases of duodenal ulcer patients H.pylori have been demon
strated. Eradication of this bacteria has led to decreased recurrence rate of ulcer cases. So presence of H.pylori clearly
predisposes to peptic ulceration.
H.pylori is a small curved, gram-negative, microaerophilic rod with multiple polar flagellae. Its normal habitat is
in the stomach, where it remains closely to the gastric mucus secreting cells. The main characteristic feature of H.pylori
is its ability to hydrolise urea resulting in the production of ammonia, which is a strong alkali. This urase activity
protects the bacteria from hydrogen ions in gastric acid juice and provides a source of nitrogen for H.pylori. Besides
its protective role, ammonia may also alter gastric epithelial permeability resulting in mucosal injury. The effect of
ammonia on the antral G-cells is to cause the release of gastrin. This is responsible for the modest hypergastrinaemia
in patients with peptic ulcer disease, which in turn may result in gastric acid hypersecretion. The motility of H.pylori
is due to its spiral shape and presence of 4 to 6 flagellae. This permits the bacterium to penetrate the mucous layer and
migrate to the regions of lower acidity. Adherence of H.pylori to gastric epithelial cells and its capacity to cytotoxin
production are considered virulent factors as they are associated with degenerative changes in epithelial cells. H.pylori
secretes a number of enzymes and chemicals including urease, catalase, mucinase, lipase, phospholipase A2, haemolysins
and alkaline phosphatase some of which reduce the viscosity of mucus. Infection of H.pylori leads to the disruption of
gastric mucous barrier by the enzymes produced by the organism and the inflammation induced in the gastric epithe
lium is the basis of many of the associated disease processes.
Presence of H.pylori appears to be linked to lower socioeconomic status. H.pylori is very much concerned with the
development of chronic gastritis which predominantly affects the antrum. Antral mucosa shows full thickness infiltra
tion of lymphoid follicles. It has been shown that irradication of H.pylori leads to significant improvement in acute
and chronic gastritis alongwith patient’s symptoms.
The relationship between H.pylori and gastric ulcer remains less clear, though it has been shown that gastric ulcer
is associated with H.pylori in over 70% of patients. If drug induced ulcers are excluded, the prevalence of H.pylori
approaches to more than 90%. A weakening of mucosal defence mechanism may render the gastric wall to be suscep
tible to acid-peptic attack. It has been shown that irradication of H.pylori speeds up gastric ulcer healing within 6
weeks. Irradication also diminishes the recurrence rate of gastric ulcer indicating that H.pylori plays an important role
in the aetiology of gastric ulcer disease. A dramatic fall in the incidence of chronic gastric ulcer has been noted in
U.K. which is probably attributed to greater use of antibiotics and higher standard of food hygiene which considerably
reduces or eliminates presence of H.pylori. H.pylori has the ability to split urea with formation of ammonia, which
causes a rise in local pH, this leads to epithelial damage and also increases the secretion of gastrin causing hypergastrinaemia
and hypersecretion of H* ions.
Duodenal ulcer.—
1. ACID HYPERSECRETION.— Pathogenesis of duodenal ulceration is seemingly simplified at first sight by a
clear relationship to over-production of hydrochloric acid by the stomach. In most collected series, the mean basal and
maximal acid output of duodenal ulcer patients is approximately P/2 to 2 times more than those of the control patients.
It has also been shown that the stomachs of duodenal ulcer patients have almost twice the number of parietal cells
(increased parietal cell mass) compared to normal stomachs. Serum group I pepsinogen level is also increased in
duodenal ulcer patients. It has got a direct relationship with the acid secretory potential of the stomach. Duodenal ulcer
patients also show increased gastrin stimulation. They also show an increased rate of gastric emptying. Diminished
acid inhibition of gastrin release is also noticed. Increased vagal excitation has also been assumed to underlie the
duodenal ulcer diathesis.
2. GENETIC FACTORS.— Diminished power of resistance of the mucosa has also been incriminated to cause
duodenal ulcer. In a great number of cases the acid production may be within the high side of the normal range and in
these cases ulceration cannot be explained except the diminished mucosal resistance to normal acid secretion. A
genetic background can be well explained. There is a significant relationship between blood group ‘0’ and the devel
opment of duodenal ulcer. Persons of blood group ‘0’ who do not possess AB antigen are peculiarly apt to develop
duodenal ulcers.
3. ENDOCRINE ORGAN DYSFUNCTION.— In addition to the Zollinger-Ellison syndrome, in which there is
over-production of gastrin by pancreatic tumour tissue with consequent hyperacidity and ulcer formation, other endo
crine adenomata may be associated with duodenal ulcer. In Cushing’s syndrome, the high level of endogenous steroids
may be responsible for duodenal ulcer. In parathyroid tumour hyperacidity may be either due to hypercalcaemia or
other causes have been noticed. Some bronchial carcinomas do produce hyperacidity. Multiple adenoma syndrome,
where adenoma in pituitary, adrenal, parathyroid and pancreas have been noticed, may cause hyperacidity.
4. LIVER DISEASE.— Ulceration of both stomach and duodenum has co-existed with disease of the liver
particularly cirrhosis. It may be due to increase in the blood supply to the gastric mucosa and over-production of
histamine in the stomach wall to stimulate the parietal cells.
5. EMOTIONAL FACTORS.— Anxiety, stress and strain have always been incriminated to cause peptic ulcer.
6. DIET AND SMOKING.— Irregular diet, spicy food and excessive drinking of tea and coffee have always
provoked formation of peptic ulcer. Opinions vary regarding alcohol. Some have found a clear relationship whereas
others could not find any definite relation. Smoking does appear to predispose ulcer formation. Cigarette smoking has
a definite relation with ulcer formation. The exact cause is not yet clearly understood, but it seems that smoking
diminishes mucosal defence mechanism almost similar to NSAIDs.
7. HELICOBACTER PYLORI.— As mentioned in the aetiology of chronic gastric ulcer, H.pylori have been
isolated in 100% of duodenal ulcer cases. Its irradication has definitely led to decrease in recurrence rate and this
clearly indicates its importance in the aetiology of duodenal ulcer. It is difficult to find out a direct relationship
between H.pylori and duodenal ulcer, though prevalence of H.pylori in duodenal ulcer patients has been found to be
between 95% and 100%. The main question in defining the role of H.pylori in duodenal ulcer is how H.pylori in the
stomach can cause local damage in the duodenum. As mentioned above, production of ammonia by H.pylori does
increase the level of circulating gastrin and thus increases acid secretion. However, the difference of gastric acid
secretion between normal subjects and those with duodenal ulcers is considerable and the modest increased acid levels
in patients with helicobactor-associated antral gastritis are insufficient to explain the aetiology of the duodenal ulcer
ation. The explanation can probably be found in the phenomenon of duodenal gastric metaplasia. Gastric metaplasia is
normal response of the duodenal mucosa to excess acidity. This is an attempt by the mucosa to resist injurious stimulus
of the acid. Although normal duodenal mucosa cannot be infected with H.pylori, gastric metaplasia in the duodenum
is more commonly infected and this infection results in the same inflammatory process that is observed in the gastric
mucosa. The result is duodenitis, which is almost certainly the precursor of duodenal ulceration. This can be explained
by the presence of gastric metaplasia in the duodenum in patients with duodenal ulcer disease.
8. DECREASE IN BICARBONATE PRODUCTION— by the stomach and/or duodenum leads to peptic ulcer
ation. It has been clearly noticed after various studies that patients with duodenal ulcer have in fact reduced production
of bicarbonate. Those with decreased bicarbonate production cannot maintain a pH-neutral microlayer between the
mucosal lining below and mucous gel layer above. That is why the drugs which increase bicarbonate production are
being investigated to be used in the treatment of peptic ulcer disease.
PATHOLOGY
Approximately 75% to 80% chronic peptic ulcers occur in duodenum. More than 90% of chronic duodenal
ulcers develop in the first part of the duodenum. Ulcers whether gastric or duodenal tend to occur in alkaline
mucosa. The characteristics of chronic ulcer are : (i) Destruction of mucous and submucous layer to reach the
muscle coat in the centre of the ulcer; (ii) Dense fibrosis in the base; (iii) Adhesion of muscularis mucosae to
the muscle coat at the margin of the crater and (iv) Presence of periarteritis and endarteritis in the surrounding
vessels, (v) The mucous membrane around the ulcer will show the usual proliferative changes with downgrowth
of glandular tissue simulating carcino-
matous change, (vi) There may not be
any nerve in the floor of the ulcer but
many in the edge, the terminations of
t
which are bulbous similar to those in
amputation stumps.
Gastric ulcer.— Gastric ulcers may

be acute or chronic. Approximately 80%-
85% of chronic ulcers are found on or
near the lesser curvature, the great ma
jority of these being closer to the
incisura angularis. Only 10% of chronic
gastric ulcers are found in the antrum,
2% in the pyloric canal, 3% in the cardia
and 5% in the fundus and body of the
stomach. It is rare to find two or more
chronic gastric ulcers in a state of activ
ity at the same time (5%), but combined
gastric and duodenal ulcers are encoun
tered in 10% to 20% of cases. Naked-
eye appearance of gastric ulcer is similar
to that of duodenal ulcer except that the
gastric ulcers are larger, tend to pene
trate deeply and are associated with greater
degree of fibrosis.
During operation presence of a
chronic ulcer should be verified. A chronic
ulcers. 85% of these ulcers are within the first 2 cm of

the duodenum. 10% within the next 3 cm and the
remaining 5% above the ampulla of Vater. Chronic
duodenal ulcers are usually smaller than the chronic
gastric ulcer. Average size is about 1 cm in diameter.
These ulcers vary in shape — circular, oval, cresentric,
pear-shaped or triangular. The ulcer has a punched out
appearance, the margins are overhanging. The granulat
ing base is covered with mucopurulent debris. Though
the muscle coat is always reached, the depth of the
ulcer depends on the degree of penetration. Multiple
duodenal ulcers occur in 10 to 15% of cases. These are
usually seen on the anterior and posterior walls facing
each other (kissing ulcers) and produce considerable
scarring and distortion of the bulb of the duodenum. So
far as the duodenal ulcer is concerned when there is
excessive cicatrisation it may cause pyloric stenosis.
Acute perforation occurs most frequently in ulcers near
the superior surface or anterior wall of the duodenum.
Bleeding is more common in posterior wall ulcers.
Fig. 44.2.— Figure shows two gastric ulcers — one in the
vestibule and the other in the pyloric canal. It also shows two CLINICAL FEATURES.—
duodenal ulcers on the posterior wall in the first part of the SYMPTOMS.—Symptoms of acute peptic ulcers
duodenum. These are causing pyloric obstruction. and the chronic peptic ulcer are different. In case
of acute peptic ulcers symptoms are usually of short duration. Slight attack of dyspepsia may go
unnoticed. These ulcers are more often recognized when they cause haematemesis. Acute peptic ulcer
may be the cause of haematemesis in both sexes in all ages. Occasionally an acute ulcer may perforate
particularly when it occurs in the wall of the duodenum. Acute ulcers may progress to chronic ulceration.
Symptoms of chronic peptic ulcers are different in case of gastric ulcer and duodenal ulcer. The
main symptom is the pain in the upper abdomen. It has got definite relation with food. In case of gastric
ulcer pain is aggravated following intake of food, whereas in case of duodenal ulcer pain appears
approximately 3 hours after food when the stomach is empty and so it is called hunger pain. This pain
is well relieved by food.
The clinical features of chronic gastric ulcer and chronic duodenal ulcer are described below :—
Chronic gastric ulcer Chronic duodenal ulcer
1. Age.— The patients are usually middle aged. 1. Age.— The patients are usually young adult or
mid-adult (25 to 40 years).
2. Sex.— More common in males than in 2. Sex.— Males dominate though not as much as
females. gastric ulcer.
3. Constitution.— The patients are usually thin 3. Constitution.— The patients are healthy males
and anaemic with J-shaped hypotonic stomach. with steer-horn stomach which is high in position.
4. Periodicity is less marked. The attacks last 4. Periodicity is well marked. The attacks also
several weeks followed by intervals of freedom last for several weeks with intervals of freedom
from symptoms for 2 to 6 months. from 2 to 6 months. Attacks usually appear in
the spring and autumn.
5. Pain.— It is strictly epigastric. Pain is boring 5. Pain.— Pain is more severe and spasmodic in
or pricking in nature. When the ulcer pene character.
trates, pain may radiate to the back.
(i) Site.— In gastric ulcer pain is complained (i) Site.— In duodenal ulcer patient complains
of in the midepigastrium or slightly to its of pain on the transpyloric plane about 1
left. inch to the right of the midline.
THE STOMACH AND DUODENUM " .................................................................. 7 1 7
(ii) Relation with food.— Pain occurs almost (ii) Relation with food.— Pain usually starts
immediately or any time upto IV2 hour 2Vi to 3 hours after food when the stomach
after meal as food irritates ulcer. gradually pushes the chyme into duode
num and irritates ulcer.
(iii) Pain is not felt in empty stomach. (iii) Pain is very much felt in empty stomach,
which is called ‘hunger-pain’. Excess acid
is not neutralised by food and irritates
ulcer.
(iv) Food does not relieve pain, on the contrary (iv) Food relieves pain as this dilutes acid.
it aggravates pain.
(v) Pain is not felt at night. (v) Pain at dead of night is very characteristic.
The patient gets up with pain, he takes
biscuits and milk. He is relieved of pain
and goes to sleep.
6. Vomiting.— In more than half the cases vomi 6. Vomiting is rare, unless pyloric stenosis com
ting is a notable symptom. It often occurs after plicates the procedure. More common is regur
food. It relieves the pain and may be self gitation of acidic fluid into the mouth or pain
induced. behind the sternum due to reflux oesophagitis
(‘heart-bum’).
7. Appetite — is good. But the patient is afraid 7. Appetite is quite good and he eats frequently
to eat as this initiates pain. So the patient to avoid pain.
actually complains of ‘does not feel to eat’.
8. Diet.— These patients usually learn to avoid 8. Diet.— As any particular food does not initiate
fried and spicy foods since this initiates pain pain immediately, he usually does not avoid
immediately. anything. Only a few intelligent patients may
avoid fried and spicy foods.
9. Weight.— Some loss of weight is usually present. 9. Weight.— Some gain of weight is expected, as
the patient learns to take food .frequently.
10. Haemorrhage is less common than duodenal 10. Haemorrhage is more common than in gastric
ulcer (approximately 30%). Haematemesis is ulcer. Melaena is more common than haema
more common than melaena. temesis. Haematemesis is only possible when
massive haemorrage forces open the pylorus.
11 .On examination — tenderness can be elicited 11 .On examination — tenderness can be elicited
in the mid-epigastrium or slightly to the left of at the ‘duodenal point’ which is situated on the
it. transpyloric plane 1 inch right to the midline.
SPECIAL INVESTIGATIONS
1. Examination of blood.— Haemoglobin level will be low in patients with chronic blood loss (melaena
and/or haematemesis). A raised E. S. R. in gastric ulcer suggests malignancy.
2. Examination of stool.— Occult blood in the stool may be detectable in all cases of active ulcer due to
oozing of blood from the ulcer as both stomach and duodenum have enormous blood supply. In case of melaena
the stool becomes black and tarry as the blood during its passage through the intestine becomes partially digested
and altered.
3. Gastric function tests.— These tests are performed as first things in the morning and are comprised of
basal secretion and maximum secretion by stimulants such as insulin, histamine and pentagastrin.
The patient should have had nothing to eat or drink from the previous night and should not have taken antacid
or anticholinergic drugs for previous 24 hours. The patient should remove his shoes, jacket and tie and open his
collar. His weight and height are measured. The patient now lies comfortably on a couch and his nostril and throat
are sprayed with a solution of 3 percent lignocaine in isotonic saline. A nasogastric tube, which was Ryle’s tube
previously and now it is a plastic, radio-opaque 125 cm long tube with holes close to the tip is passed to the stomach.
The tube is first well lubricated with liquid paraffin and is passed through the nose. The patient is asked to swallow
repeatedly while the tube is being pushed steadily and rapidly down through the pharynx and oesophagus into the
stomach. A large 20 to SO ml syringe is then fixed to the end of the tube and the stomach is emptied of juice
and air by repeated aspirations. The patient is now taken to the fluoroscopy room and the position of the tube
is adjusted so that its tip lies in the most dependent part of the stomach which is shown to be along the left border
of the spinal column. The tube is now fixed to the face and the end of the tube is connected to a low continuous
suction machine which works at a subatmospheric pressure of 3 to 5 cm Hg. Minor adjustment of tube position
may be necessary to allow satisfactory aspiration. Normally the quantity of this aspiration is less than 70 ml. If
it be more than this, it indicates, presence of duodenal ulcer, pyloric obstruction, pylorospasm or hypersecretion.
Now the time is recorded and one 60-minutes or four 15-minutes aspirates may be collected and labelled with
the times. This is basal secretion.
NIGHT FASTING SECRETION (Dragstedt).— This is actually the night secretion of the stomach in its
interdigestive or resting period. Gastric secretion is aspirated through continuous or intermittent low pressure
suction for the period of 12 hours from 9 P. M. to 9 A. M. Normally this secretion amounts to about 400 ml.
Volumes above this level are suggestive of vagal hyperactivity. In Zollinger-Ellison syndrome this volume may
be more than a litre. The juice is tested for HCL in mEq. In duodenal ulcer this figure is between 40 to 80, in
gastric ulcer it is between 5 to 15, in Zollinger-Ellison syndrome it is between 100 to 300 (normal figure being
between 10 to 20).
BASAL SECRETION.— 12 hours over-night fasting secretion has little diagnostic advantage over the moming
basal secretion. Moreover technically the former is unreliable. The mEq acid per hour of basal secretion in duodenal
ulcer is about 5 mEq/hr, in gastric ulcer 1-2 mEq/hr. (normal figure being 1 mEq/hr). Basal secretion represents
secretion of that portion of the patient’s parietal cell mass which is being excited under the resting condition.
MAXIMUM SECRETION or PEAK OUTPUT.— This can be found out with various stimulants. Whereas Kay’s
augmented histamine test is gradually losing popularity and Hollander’s insulin test has got limited scope of
application, pentagastrin is becoming a popular stimulant and is used more often than any other stimulants
nowadays.
PENTAGASTRIN TEST.— The optimum dose of pentagastrin is 6 microgram per Kg body weight. It is mostly
injected I. M. 15 minutes samples are collected during the next one hour. The term maximum acid output (MAO)
is generally used as the maximum acid output in the whole 60 minutes after injection of pentagastrin is expressed
as m.mol/hr. This test not only has a diagnostic importance but also helps in assessing treatment of the patient
e.g. when the acid status is low operation like vagotomy and drainage procedure is enough; whereas in case of
high acid status individuals operation like vagotomy and antrectomy or partial gastrectomy should be called for.
In gastric carcinoma MAO is very low.
KAY’S AUGMENTED HISTAMINE TEST.— This test determines the total mass of oxyntic cells in the stomach.
At first the fasting stomach contents are collected. Mepyramine maleate is given intramuscularly at the dose of
100 mg to nullify the side effects of histamine except its stimulation of gastric acid. About 30 minutes later
histamine acid phosphate at the dose of 0.04 mg per Kg body weight is injected subcutaneously. The gastric acid
secretion is collected during the next one hour. The average HC1 response in mEq free acid per hour is as follows:
a gastric ulcer - 15; duodenal ulcer - 30 to 40; anastomotic ulcer - 30 to 35.
HOLLANDER’S INSULIN TEST.— This is based on the fact that hypoglycaemia, caused by insulin, induces
direct vagal stimulation on the parietal cell mass. Insulin given to a patient who has had a vagotomy performed
should result in no increase in acid production. This test is of more value to assess the completeness of vagotomy
in the postoperative period. After the fasting stomach contents are aspirated, insulin in the dose of 0.2 unit per
Kg. of body weight is injected intravenously. 2 ml of venous blood is taken just before the introduction of insulin
for estimation of sugar. Eight 15-minutes aspirates are collected and labelled. 2 ml of venous blood is .taken at
30 and 45 minutes after introduction of insulin to estimate the level of blood sugar. It must be remembered that
patient’s comments and appearance should be noted. Dryness and slight impairment of the level of consciousness
should immediately rouse the suspicion of imminent hypoglycaemic coma. Dextrose (50 percent) in the dose of
50 ml should be always kept available during the test and injected immediately intravenously should the said
condition arise. A fall in the blood sugar level below 45 mg per 100 ml will lead to hypersecretion of acid. Maximum
acid output is expected at that time. A rise in concentration of 20 m. mol per litre above the basal level in the
first hour suggests incomplete vagotomy. It must be remembered that a high acid concentration in basal secretion
in the range of more than 20 m. mol free acid per hour is indicative of Zollinger-Ellison syndrome.
4. Radiological Investigations. — BARIUM MEAL X-RAY is often diagnostic in peptic ulcer. In case of
gastric ulcer a niche or ulcer crater will be seen projecting from the smooth outline of the stomach. In some.cases
there will be a constant notch on the greater curvature just opposite the position of the ulcer. This is due to local
spasm of the circular muscles. Barium X-ray also gives a clue to differentiate between benign gastric ulcer and
carcinomatous ulcer. The most important differentiating feature is that in case of benign ulcer the ulcer crater
penetrates beyond the projected line of the wall of the stomach, but in malignant ulcer an erosion into a filling
defect that protrudes into the stomach is detectable. In duodenal ulcer 75% to 80% cases can be diagnosed
accurately by barium meal X-ray. A normal duodenal bulb is rounded and full. In case of ulcer disease, there is
Fig. 44.3.— Shows a large crater projecting into the Fig. 44.4.— Giant ulcer in the lesser curve
lesser curvature (chronic peptic ulcer). shown by arrow.
irritability and the bulb becomes difficult to fill with contrast material. Demonstration of ulcer crater itself is the
positive evidence of an active ulcer. Because ulcer craters are much more commonly located on the anterior or
posterior wall of the duodenal bulb, the crater is more likely to be seen ‘en face’. As the crater has no mucosa
and barium sticks to the bottom of the crater, compression films will show barium, displaced from other areas
of the bulb, while it remains adherent to the crater itself. Secondary radiologic signs are mucosal oedema and
spasm. Mucosal oedema will cause widening radiolucent folds clearly demarcated by barium lying in the crevices.
These folds radiate towards the margin of the ulcer. Ulcer in the bulb frequently gives rise to spasm of the pylorus.
Spasm may result in extremely rapid emptying so that the radiologist is unable to obtain pictures of filled bulb.
Multiple films should always be taken and any constant deformity of the bulb should be noted as indicating presence
of ulcer. This is due to chronic cicatricial process. There may be rugal convergence towards the ulcer site.
Appearance of pyloric stenosis and hour-glass deformity of stomach are also evident of presence of chronic duodenal
ulcer and chronic gastric ulcer respectively.
5. Endoscopy.— Development of fibre-optic panendoscope has greatly facilitated diagnosis of peptic ulcer
disease. Diagnostic accuracy is about 95% or more and the evidence is clear that endoscopy is superior to
radiography in defining presence

of lesion in the oesophagus, stom
ach and duodenum. By endoscopy,
the whole of the interior of the
stomach can be adequately in
spected. The fibreoptic endoscope
is an instrument in which glass-
fibres act as lens. This is a flex
ible instrument so introduction
is easy. By this endoscopy one
can clearly inspect the inside of
oesophagus, stomach and duode
num. Addition of gastro-camera
will allow taking pictures of the
inside views. One can even take
biopsy under direct vision through
this instrument. Inside can also
be visualised by television method.
Fig. 44.5.— Ulcer in the prepyloric Rg. 44.6.— Ulcer at the bulb of Indications.— Endoscopy is
region after evacuation of the the duodenum. valuable (i) in the diagnosis of
barium. shallow gastric or duodenal ul
cer which is not visualised by barium meal X-ray; (ii) In undiagnosed dyspepsia; (iii) In checking results of medical
treatment; (iv) To differentiate chronic peptic ulcer from carcinomatous ulcer; (v) To detect any form of gastritis;
(vi) Examination of stoma in cases of suspected gastrojejunal ulcer; (vii) Its value is perhaps greatest in bleeding
patients, either from oesophageal varices or from ulcers; (viii) In demonstrating acute mucosal erosions.
TREATMENT
Conservative (Medical) Treatment
iii cases of both gastric ulcer and duodenal ulcer a medical trial should always be given. The aim
of treatment for gastric ulcer is the healing of the ulcer, whereas in case of duodenal ulcer is the relief
of symptoms.
Chronic gastric ulcer.— Barium meal X-ray and endoscopic inspection must be performed to
confirm the diagnosis before starting therapy. In doubtful cases one should even take biopsy through
endoscopy to confirm that the lesion is benign. As the aetiology of gastric ulcer is vague, there is no
specific therapy.
THE BASIC GENERAL TREATMENT which should be given to both gastric ulcer and duodenal
ulcer patients are : -
(a) Rest as far as practicable. Anxiety and elements of stress and strain should be given up.
Tranquillizers at night may be helpful particularly during the period of acute exacerbation. Routine use
of sedation should be avoided.
(b) Diets should be regulated. Diets must be taken in time. Spicy foods should be avoided. Bland
diet is advised. In case of duodenal ulcer meals should be taken at 2 hours interval. Milk is widely used
in the treatment of ulcer disease, but there are few data to support its efficacy. Calcium in milk is
known to stimulate release of gastric acid secretion. Alcohol should be prohibited. Smoking should be
stopped.
(c) Now that a host of medications with proven efficacy are available, majority of the patients do
not require surgery. It is only required in less than 5% of patients. The medical management of upper
gut ulceration varies for duodenal and gastric ulcers. Sedatives or tranquillizer should be used. If pain
is not relieved within 24 hours, nasogastric aspiration and intravenous fluid therapy should be started.
MEDICAL THERAPY OF CHRONIC GASTRIC ULCERS.—
Accurate diagnosis is extremely important with endoscopic inspection and biopsy to exclude gastric
cancer. A careful history must be taken whether the patient is taking any ulcerogenic drug e.g. NSAIDs
and corticosteroids. Specimens should be sent forCHO test for Helicobacter pylori. Radiology is similarly
important to assess the size of the ulcer. Once the diagnosis is confirmed as benign ulcer, current recommendation
includes initial therapy with an H2-receptor blockers e.g. cimetidine or ranitidine. Although secretion of
acid is subnormal in majority of cases, yet these drugs heal the ulcer in more than half the cases within a
period of 6 to 8 weeks. All ulcerogenic agents should be stopped immediately e.g. NSAIDs, corticosteroids,
cigarette smoking and alcohol.
H2-receptor antagonist and proton pump inhibitors — have revolutionised the management of peptic ulceration.
Most gastric ulcers and duodenal ulcers can be healed by a few weeks of treatment with these drugs provided they are
taken in time and absorbed. But a few patients may be relatively refractory to conventional doses of H2-receptor
antagonists. In these cases proton-pump inhibitors can be used and majority of ulcers heal within 2 weeks. Relief of
symptoms is quite impressive. Both these drugs are quite safe and with little serious side-effects. The only problem
is the relapse following cessation of therapy.
Six weeks after the institution of treatment, objective evidence of healing must be obtained. A barium meal X-ray
is the simplest test.
Endoscopy should be performed after 6 weeks of treatment and evidence of healing should be achieved. If it is
not obtained, endoscopic 4-quadrant biopsy should be taken of the ulcer and presence of H.pylori should be assessed.
If the latter is found amoxycillin and metronidazole alongwith bismuth tablets should be prescribed for 2 weeks.
The mostly accepted ideal treatment regimen for irradication of H.pylori is the triple therapy with bismuth compounds,
e.g. colloidal bismuth subcitrate 120 mg/qds, in combination with tetracycline 500 mg/tds (or better amoxycillin 500
mg/tds) and metronidazole 400 mg/tds for 2 weeks. With this combination the irradication rate is around 90% but the
problem is the high rate of side effects. Metronidazole resistance is an increasing problem, especially in developing
countries. Nowadays commonly used combination is omeprazole 40 mg/od and amoxycillin 500 mg/qds for 14 days.
The irradication rate of this combination is around 80%. It is better that a proton pump inhibitor and amoxycillin
should be the first line of treatment. An alternative antibiotic is clarithromycin. A combination mostly used in the
present days is clarithromycin 500 mg/bd, lansoprazole 30 mg/bd and tinidazole or metronidazole 400 mg/bd. The
latter combination can irradicate H.pylori in a short period of just 7 days.
Only in case of intractable gastric ulcers which fail to respond to this medical treatment, surgery is indicated
mostly in the form of Billroth 1 gastrectomy.
Chronic duodenal ulcer.— Aetiology of duodenal ulcer is high acid secretion. The pain of duodenal ulcer
arises from contact of acid with the lesion. So in duodenal ulcer legitimate aim is to keep the intragastric pH
about 5.5 so that pepsinogen is not activated. Traditional antacids should be used, but long term use should be
avoided because it may lead to metabolic alkalosis and if associated with increased intake of milk, milk-alkali
syndrome may develop. This is hypercalcaemia, nephrocalcinosis and eventually renal failure. Various antacids
are available in the market either iri the form of liquids or tablets. Those should be prescribed to be taken after
meals and at night before going to bed. Antacids mostly used are aluminium hydroxide, silicate or glycinate
alongwith magnesium hydroxide, carbonate or trisilicate. These are relatively insoluble in water and are long
acting if retained in the stomach. Magnesium salts increase intestinal motility, whereas aluminium decreases
it. So antacids containing former tend to be laxative, whereas those containing latter may be constipating.
Activated dimethicone (Simethicone) either alone or with antacid mixture acts as an antifoaming agent to
reduce flatulence. Antacid-Simethicone combination may be useful for the relief of hiccough. Alginic acid
may be combined with antacids to encourage adherence of the mixture to the mucosa. So this combination
may be used in reflux oesophagitis. If this be associated with oxethazine, it will improve pain relief quality.
Large doses of antacids in the form of 120 ml daily of magnesium hydroxide mixture should be prescribed,
because one has to consider that the aim is to buffer secreted acid. But with this high dosage of antacid there
is a high incidence of diarrhoea, which may not be acceptable to all the patients.
Acid secretion at the parietal cell level is mediated by histamine acting on H2 histamine receptors. H2-blockers
have now been introduced to act on these H2 histamine receptors and thus decreases acid secretion. The first such drug
introduced is Cimetidine. Nowadays Ranitidine is a better drug than cimetidine. Cimetidine tablets (200 mg) are given
after each meal for thrice daily and two tablets (400 mg) are given just before going to bed. This gives maximum plasma
level of cimetidine 2 hours after food which is the time of appearance of pain in duodenal ulcer. The night dose is to
reduce nocturnal basal secretion. Ranitidine acts over a longer period and one tablet twice a day is adequate. This treatment
46
should be continued for six weeks, after which only the night dose may be maintained for 3 months.
Presently Famotidine is being used, which has a longer half-life and requires fewer doses in a day. 40
mg once at bed time or 20 mg twice daily for 4 to 6 weeks is often curative. Roxatidine is also histamine
H2-receptor antagonist and it is a potent and selective inhibitor of basal and stimulated gastric acid
secretion. Total pepsin secretion is also reduced. It is used in the dose of 75 mg in the evening or twice
daily.
Anticholinergic drugs are moderately helpful. Antrenyl is quite effective in this group.
The enzyme H+K+ ATPase present on the secretory surface of the gastric parietal cell is known as
proton pump. Certain drugs inhibit this proton pump and block the final and common step in gastric
acid secretion. Both basal and stimulated acid secretions are inhibited irrespective of the stimulus.
Omeprazole and Lansoprazole are proton pump inhibitors. It is used in case of recurrent or persistent
disease as it is more effective in inhibiting acid secretion. It has a longer half-life and requires only
one dose in a day. It is particularly effective in antral G-cell hyperplasia and Zollinger-Ellison syndrome.
Lansoprazole is used in the dose of 30 mg once daily in the morning for 4 to 8 weeks. Only in refractory
cases and Zollinger-Ellison syndrome daily dose may be increased to 60 mg for 8 to 12 weeks.
Omeprazole is used in the dose of 20 mg/day for 4 to 8 weeks and in Zollinger-Ellison syndrome it
is used in the dose of 60 to 100 mg in two divided doses for 8 to 12 weeks.
It is always essential nowadays to test for presence of H.pylori. If it is present, a course of amoxycillin
and metronidazole with bismuth tablets for 2 to 3 weeks is prescribed. Combination drugs are now
available containing omeprazole 20 mg, amoxycillin 750 mg and tinidazole 500 mg to get rid of H.pylori.
Another combination in the form of lansoprazole 30 mg, clarithromycin 250 mg and tinidazole 400 mg
or 500 mg can also be used to irradicate H.pylori in a very short period of just 7 days.
Relapses mostly respond to the standard drug regime as mentioned above. H2-receptor antagonist
may be used with nocturnal dose only as maintenance therapy to prevent relapse. In case of relapses
one must consider the presence of H.pylori which should be excluded, otherwise treatment should be
given to irradicate H.pylori. Prolonged therapy should be avoided, as it may mask the disease and is
also expensive without any definitive advantage. In case of relapses or continuous symptoms one must
be careful to reassess the diagnosis as there are various diseases which may give rise to similar symptoms
as ulcer cases e.g. chronic cholecystitis, hiatus hernia etc.
THE DURATION OF MEDICAL TREATMENT.— In case of gastric ulcer the case should be
reviewed after 6 weeks by barium meal X-ray and endoscopy. If there is no improvement by proper
medical treatment given for 6 weeks, there is every reason that the medical treatment should be stopped
and surgery is indicated. In case of duodenal ulcer, medical treatment is tried for 6 months. Even if
the symptoms continue after 6 months surgery is indicated.
INDICATIONS FOR SURGERY.—
1. When the ulcer fails to heal after rigid medical treatment for the prescribed period, which is 2
months for gastric ulcer and 6 months for duodenal ulcer operation is required.
2. When the patients want quick relief of their symptoms and do not want to carry on a prolonged
trial of medical treatment surgery is indicated.
3. When the history suggests that the ulcer is present for 5 years, it is unlike that the ulcer will
heal without operation.
4. When repeated pain has made the patient intolerable with frequent loss of work, surgery is
indicated.
5. When ulcer has produced obstruction in the form of hour-glass stomach or pyloric stenosis, surgery
is indicated.
6. When the ulcer is giving rise to haemorrhage in the form of haematemesis or melaena, operation
is indicated.
7. If the ulcer perforates, operation is the only treatment.
8. When the patient gives a history of previous perforation of ulcer, the treatment is straightway
surgery.
THE STOMACH AND DUODENUM
723
9. Suspicion of malignancy is a strong indication of surgery. If after 6 weeks of medical treatment

endoscopy does not show any sign of healing of gastric ulcer, four quadrant biopsy should be taken
through endoscopy. If the report be malignant, treatment is surgery. All gastric ulcers above the age
of 45 years should be considered as suspicious and endoscopic biopsy is a must. Unless a definite
improvement by medical trial is achieved within one month, surgery is indicated.
Surgical Treatment
Choice of operation.—
DUODENAL ULCER.— This ulcer is almost always associated with high level of gastric acid
secretion. So the operation is always aimed at to reduce the level of acid secretion. As the vagus nerve
is responsible for the psychic phase of gastric secretion, its transection i.e.vagotomy will definitely
decrease the level of acid secretion. Vagotomy also decreases the motility of the gastric muscles, hence
hampers gastric emptying. So & drainage procedure should always accompany vagotomy. This drainage
operation can be either pyloroplasty i.e. widening of the pyloric canal or gastro-jejunostomy i.e. to by
pass the pyloric canal by making an anastomosis between the stomach and the jejunum. Antrum is
responsible for producing gastrin — the gastric phase of gastric secretion. Antrectomy i.e. excision of
the antrum and making the anastomosis between remnant of the stomach and the first coil of jejunum
will decrease the gastric acid level considerably. It may or may not be associated with vagotomy. Partial
gastrectomy i.e. excision of distal two-thirds of the stomach leave very little parietal cell mass to secrete
gastric acid. It must be remembered that women patients do not tolerate partial gastrectomy so well and
this operation should better be avoided in their cases.
Pentagastrin test is always performed to assess the gastric acid status of the individual. In duodenal
ulcer, the basal secretion varies generally from 4 to 9 m. mol free acid/hour, whereas maximal secreticr.
varies from 30 to 50 m. mol or more free acid/hour. The operation is selected as follows :— When the
maximal free acid is from 30 to 40 m. mol/hour — vagotomy and drainage operation is performed; from
40 to 50 m. mol/hour, antrectomy is performed and from 50 m. mol/hour onwards — the operation of
choice is either partial gastrectomy or vagotomy and antrectomy.
GASTRIC ULCER.— As the aetiology of gastric ulcer is still vague and as in at least 10% of cases
it is associated with carcinoma, excision is of utmost importance in case of operation of this type of
ulcer. Billroth I partial gastrectomy is still the operation of choice in gastric ulcer. This operation
involves excision of distal two-thirds of the stomach followed by anastomosis between the remnant of
the stomach and duodenum. The resected ulcer is always sent for histological examination.
Vagotomy and Pyloroplasty, associated with frozen section biopsy of the gastric ulcer (if benign),
is gradually gaining popularity.
Highly selective vagotomy or proximal gastric vagotomy with excision of the ulcer is being
performed in some centres. The supporters of this technique claim that it is either equal or even a better
operation than Billroth I gastrectomy, as the gastric physiology is best maintained in this operation.
OPERATIONS
Vagotomy
Indications.—
(1) As has been mentioned earlier, Vagotomy with drainage procedure is probably the most popular operation
for duodenal ulcer.
(2) Vagotomy alone is performed in case of anastomotic ulcer following gastro-jejunostomy or partial
gastrectomy.
Vagotomy can be done through thorax or through abdomen. Transabdominal vagotomy is by far the more
popular operation. Three types of vagotomy are in vogue in surgical practice. These are :
1. Truncal vagotomy i.e. both trunks of the vagus nerves are transected. In fact, about 5 to 7 cm of the nerves
are excised so that this technique can be referred to as ‘Vagectomy’.
2. The selective vagotomy is aimed at removal of all gastric fibres of the vagus nerves, keeping intact the
hepatic and coeliac branches.
3. The proximal gastric vagotomy or highly selective vagotomy is designed to denervate the acid secretory
part of the stomach, keeping the vagal supply to the alkali secreting gastric antrum and other abdominal viscera,
thus motility of the stomach is not hampered and drainage procedure will not be required.
Transabdominal truncal vagotomy
A midline or left paramedian incision is made. The left lobe
of the liver is mobilised by dividing the left triangular ligament.
The position of the oesophagus is guided by the presence of the
nasogastric tube. The peritoneum over the abdominal part of the
oesophagus is transversely incised taking care not to damage the
inferior phrenic vessels. Beneath is the fascia of the phreno-
oesophageal ligament. This is also divided in the same line. If
now, the operator passes his finger through this incision, his
finger will enter the posterior mediastinum. The lowest 3 inches
of the oesophagus is mobilised and retracted downwards. The
assistant is asked to pull the stomach down when the tense
anterior trunk will be seen lying on the anterior surface of the
oesophagus. The main posterior trunk lies some distance separate
from the oesophagus. About 5 to 7 cm of both these trunks are
excised and remaining ends are tied with fine silk. The ligature
pyloroplasty
is made to avoid bleeding from the ascending oesophageal ves
sels, which run up along with the nerves. The horizontal deficien
cy in the hiatus is closed with non-absorbable suture.
COMPLICATIONS.—
1. The most important operative complication is gastric
retention for which drainage operation is performed along with
this operation.
2. Diarrhoea.— This is generally not very troublesome.
Only in 2% of cases it may give trouble to the patient. To avoid
Fig.44.7.— Schematic diagram of Truncal Vagotomy. this complication, selective vagotomy is preferred by some sur
Note that 5 cm of each trunk should be resected.
geons to this operation. This operation is probably contraindicated
to patients already
suffering from severe
diarrhoea.
3. Pseudo
achalasia of the car
dia.
4. Recurrent ul
cer may be seen af
ter vagotomy and
drainage operation.
The reason may be a
few intact vagal fi
bres, which may be
detected by Holland
er’s insulin test and
in this case
reoperation should be
performed to com
plete vagotomy. Only
in rare cases one may
find recurrent ulcer
even after complete
rig. 44.8.— Schematic diagram of Fig. 44.9.— Schematic diagram showing vagotomy. These cas
selactive Vagotomy. highly selective Vagotomy. es may need partial
THE STOMACH AND DUODENUM — — — 7 2 5
Fig. 44.10.— Shows the technique of performing Fig. 44.11.— Shows the technique of performing
anterior highly selective vagotomy. posterior highly selective vagotomy.
gastrectomy. One must keep in mind the possibility of Zollinger-Ellison syndrome in these cases.
Selective vagotomy
Access is same as that of the truncal vagotomy. The hepatic branches of the anterior vagus are identified in the upper part of the
lesser omentum. An incision is made through avascular area below them to reach the lesser sac. The dissection is started along with
the anterior vagus nerve in the lesser omentum downwards to find out all the gastric branches which are ligated and divided one by
one. Now for posterior selective vagotomy, an incision is made through the peritoneum at the angle of His. Right index finger is passed
through the hole to reach behind the gullet and the right thumb is passed through the hole made in the lesser omentum. These two fingers
will meet behind the oesophagus and will only be intervened by the so-called ‘mesentery’ in which will be lying the posterior vagal
trunk. The tissues behind the posterior vagus nerve are burst through and a tube is inserted to include the gullet and the vagi. A good
look is made to the posterior trunk to save its coeliac branches. With the right index finger, the posterior trunk is pushed posteriorly
and tissues in front of the finger are very minutely dissected to secure the gastric branches of the posterior vagus nerve. These are ligated
and divided. The last part of the oesophagus is now thoroughly exposed to clear any additional fibres, which may be left behind. The
whole circumference of the cardia is examined and all residual vagal branches are divided, leaving behind a ring of bare muscles.'
Proximal gastric vagotomy (Highly selective vagotomy)

This operation differs from the previous one only in the point of preservation of the nerves of Latarjet, which run along with the
lesser curvature lying 2 to 5 cm distant from it and supply mainly the antrum and the pylorus. These nerves are preserved and separated
from the proximal gastric branches by passing forceps through the lesser omentum to the left of the nerve of Latarjet close to the gastric
wall about 3 inches (7.5 cm) from the pylorus. It is very convenient to save the posterior nerve of Latarjet through the lesser sac, which
is entered through the greater omentum at the middle part of the greater curvature. The proximal gastric branches are dissected, ligated
and divided and the main nerve, which supplies the antrum and pylorus, is preserved.
Lesser curve seromyotomy.— This operation was first advocated by Taylor. In this operation posterior truncal vagotomy is being
performed alongwith anterior lesser curve seromyotomy. This operation can be performed by using laparoscope. A few surgeons are
performing seromyotomy in both anterior and posterior aspects of the lesser curve. The advantage of this operation is that the disturbance
to the neighbouring structures is least and it can be performed by minimal access procedure also.
Gastrojejunostomy
Indications.— 1. In uncomplicated duodenal ulcer, this operation is often used along with the vagotomy.
2. In gastric ulcer, some surgeons are liking this operation along with vagotomy and the ulcer is biopsied.
3. In pyloric stenosis, this operation is mo?t successful.
4. As Palliative measure this operation can be performed in gastric carcinoma for the relief of pyloric obstruction. In this case mostly
anterior gastrojejunostomy is performed.
Preoperative treatment.—
1. When the general condition of the patient is not good enough to carry out the operation, a long-continued
milk-drip therapy is advisable for fortnight. For this, a Ryle’s tube is passed through the nostril of the patient into
the stomach. The tube is connected with a milk reservoir, hung about 3 feet above the patient’s head. The milk is
allowed to drop into the stomach at such a rate that five pints can be given in 24 hours. Cold milk drip may be used
in case of haematemesis.
In patients with cachexia or upper gastro-intestinal bleeding, blood transfusion will be required. The patient’s
blood is sent for grouping and crossmatching with a requisition of such amount of blood which will be required for
the particular patient. By the time the blood is received, intravenous infusion of glucose-saline should be
administered.
2. Gastric lavage with normal saline or plain sterile water should be carried out by means of a Ryle’s tube 3 or
4 days before operation. The last irrigation should be performed about one hour before premedication. Of course, the
Ryle’s tube is kept in situ as it will be required to deflate the stomach during and after the operation.
3. One should not forget to institute proper doses of vitamins, particularly vitamin C, which is connected for
proper healing of the anastomosis several days before the operation is performed.
Operation.—A posterior retrocolic (i.e. behind transverse colon; if anterior gastro-jejunostomy is made there
will be a loop which will give rise to regurgitant vomiting), isoperistaltic, no loop and no tension, vertical
gastrojejunostomy is usually made. The opening in the stomach is made vertical (Moynihan) for easy evacuation,
though oblique (Mayo) or horizontal (Kocher) opening does not make much difference in emptying.
The steps of operation are :
Upper right paramedian incision is used to explore the abdomen.
The greater omentum, transverse colon and the lower part of the stomach are brought out of the wound and are
turned upward The transverse mesocolon is split vertically through an avascular area to enter the lesser sac. The
posterior wall of the stomach will be seen. With the right hand a vertical fold of the posterior wall of the stomach,
close to the greater curvature is drawn out through the split in the mesocolon. Two pairs of Allis’ tissue forceps are
applied 3 inches apart to the fold of the wall of the stomach. A pair of occlusion clamp may be used to hold this fold
of stomach so that gastric secretion and bleeding from the stomach wall will not disturb the anastomosis.
The transverse colon is lifted upwards and allowed to fall on the upper part of the wound so that the posterior
surface of the transverse mesocolon is exposed. A hand is passed along the under-surface of the transverse mesocolon
to near the hilum of the left kidney just below the tail of the pancreas, where the duodeno-jejunal flexure will be
grasped. The ligament of Treitz, which leads to the duodeno-jejunal junction, also serves as a guide. The first loop
of the jejunum is situated here. It is picked up and placed by the side of the held posterior wall of the stomach. There
should not be any redundant loop of jejunum between the duodeno-jejunal flexure and the anastomosis. In fact the
portion of thejejunum between the duodeno-jejunal flexure and the anastomosis should not be more than 6-9 inches.
The loop of the jejunum, which is kept very close to the posterior wall of the stomach, should be such that the proximal
portion of the jejunum will be lying against the portion of the fold near lesser curvature of the stomach, while the
distal portion of thejejunum will be lying against the portion of the stomach close to the greater curvature. Thus an
isoperistaltic anastomosis is performed. Two Allis forceps are applied to the jejunum about 3 inches apart and an
occlusion clamp may or may not be applied to hold the anastomotic site of the jejunum by the side of that of the
stomach.
The guts are now placed side by side. A piece of swab soaked in warm sterile water is placed between the two
guts just beneath the anastomosing site. All other viscera are returned to the abdomen and covered with two hot moist
mops from both the sides, so that only the two portions of the gut held by occlusion clamps will be exposed.
A continuous sero-muscular suture is passed through the serous and muscular coats of the stomach and jejunum
using No. 00 catgut on an atraumatic curved needle. After completing the first row of posterior sero-muscular
(Lembert) suture, the needle and catgut are left aside in a piece of gauze, so that they can be used again in the 4th
row, i.e. anterior sero-muscular suture. With a knife, the wall of the stomach and the jejunum are incised about 5
mm away from the first row of sero-muscular suture for about 2 ‘/ inches. As soon as the mucous membrane is incised,
the gastric and the jejunal juices should be sucked out so long as the incision ofthe mucous membrane is continued.
This will prevent contamination ofthe surrounding area. The knife, which was used for incision, is discarded. Now
a continuous posterior through-and-through stitch taking all the layers of the stomach and thejejunum is performed.
This is continued as the anterior through-and-through suture (3rd row of suture) till the point, where the posterior
through-and-through suture is reached. The catgut is tied there. The last row of anterior sero-muscular suture is
applied with the needle and catgut used for the posterior sero-muscular suture and continued a little beyond the point
of commencement.
Closure of the opening in the transverse mesocolon.— This is important to prevent subsequent internal
herniation of the coils of small intestine, which may pass through the gap between the anastomosis and the opening
in the mesocolon. The posterior wall of the stomach is sutured to the margin of the gap in the transverse mesocolon
with a few interrupted sero-muscular sutures.
The abdomen is closed in layers as usual without drainage.
Anterior gastro-jejunostomy
This operation is seldom performed because of the possibility of the complication of regurgitant vomiting
Only two conditions, where this operation is performed, are :— (a) Where dense adhesions will prevent access
to the posterior wall of the stomach and (b) As palliative measure in gastric carcinoma, so that the gastro-jejunal
anastomosis is not so easily involved by the extension of the growth.
In this operation, the jejunum is brought round the transverse colon and applied to the anterior wall of the
stomach. So the afferent loop is always kept long enough not to be compressed by the transverse colon. The
anastomosis is made at the most dependent part of the stomach and horizontally. Jejuno-jejunal anastomosis between
the afferent and efferent loops of the jejunum may be made only in case of carcinoma. If it is done in other cases, it
will invariably lead to anastomotic ulcer as the alkaline juices of the duodenum and jejunum will not get an access
to the gastro-jej unal anastomosis, but will be by-passed through the anastomosis between the afferent and the efferent
loops.
Pyloroplasty
This operation is also a type of drainage operation as the preceding one.
Indications.—
1. In uncomplicated duodenal ulcer, this operation along with vagotomy is probably the operation of choice.
Being more physiological and as it maintains the normal anatomical configuration, this operation is gaining more
and more popularity over the gastroenterostomy (gastrojejunostomy).
2. In case of gastric ulcer this operation along with vagotomy may be performed, provided the ulcer is excised
and biopsied.
3. In peptic perforation, when the patient is a known sufferer of duodenal ulcer and when the patient’s condition
is not too grave to perform this operation, pyloroplasty along with vagotomy is not only a life saving measure, but
also a curative operation
This operation is contra-indicated in case of pyloric stenosis and when the pyloroduodenal area is scarred,
fixed and deeply placed in an obese abdomen.
Two types of pyloroplasty are commonly used. They are :—
1. Heinke-Mikulicz pyloroplasty.— The access is made through midline incision to facilitate the vagotomy
operation, which is mostly performed in association with the pyloroplasty. Kocher’s mobilisation of the duodenum
is first performed.
An incision is made through all the coats on the anterior wall of the pyloric canal midway between the greater
and lesser curvatures starting from 3 .5 cm proximal to the pylorus extending upto 2.5 cm distal to the pylorus on the
anterior wall of the duodenum The contents in the stomach and duodenum are aspirated and the inner walls are
inspected to know the position of the ulcer and to ensure that there is no stenosis distal to the incision. If the ulcer
is found very close to the incision, it should be encircled and excised along with the incision. A pair of tissue forceps
is applied to the upper edge and one at the lower edge, both at the midpoints of the incision. These two pairs of forceps
are now pulled apart so that the proximal and the distal ends of the incision approach to each other and the defect
becomes vertical thus widening the pyloric canal. Now the defect is closed using an all-coats suture of 00 chromic
catgut, leaving a vertical suture line. The same catgut is used for seromuscular Lembert stitch.
Weinburg’s modification is to close the defect with an all-coats suture using anon-absorbable suture material
such as silk. Interrupted stitches are used and the needle is so inserted as to prevent invagination of the mucous
membrane. Seromuscular suture, which generally invaginates the walls of the gut thus narrowing the pyloric canal,
is not used.
2. Finney Pyloroplasty.— In this operation, Kocher’s method is used more generously to mobilise the whole of
the second part of the duodenum, so that this part of the duodenum will lie against the greater curvature of the gastric
antrum. A seromuscular Lembert suture is used to unite the greater curvature of the stomach and the desending
duodenum closing the angle below the pylorus. The anterior walls of the stomach and the duodenum are incised about
5 mm away from the suture line along an inverted horse-shoe shaped line. The contents of the stomach and the
duodenum are aspirated. The position of the ulcer is determined. If the ulcer is found very close to the incision, it should
be encircled and excised along with the incision. An

all-coats stitch is used to unite the greater curve edge
of the stomach to the left edge of the duodenal wall
from above downwards. This stitch is continued
around the comer to unite the right edge of the
duodenum to the left edge of the stomach. The
closure is completed with a seromuscular stitch to Partial gastrectomy
invaginate the all-coats suture line.
Partial Gastrectomy
Indications.—
1. For the treatment of duodenal ulcer when
the maximal acid secretion ofthe individual is more
than 50 m.Eq/litre, partial gastrectomy is probably
/
Billroth I
Billroth II
the operation of choice. Polya gastrectomy (Billroth

II) is preferred to Billroth I operation as the duode
nal bulb at times becomes scarred and it may be
difficult to mobilise it to unite with the proximal
stomach.
In patients with duodenal ulcer, with lower acid
secretion, the distal 1 /3rd of the stomach may be
excised. This operation goes by the name oiantrectomy,
which is thus always combined with vagotomy to
prevent recurrence of ulcer.
2. In case of benign gastric ulcer, Billroth I
Fig.44.12.— Diagrammatic representation of two
main types of partial gastrectomy — Billroth I and
Billroth II.
gastrectomy is still the operation of choice. The unscarred

and mobile duodenum can easily be united to the
proximal stomach remnant. In case of high lesser curve
ulcer, it can be excised with a tongue of stomach,
preserving longer greater curvature for the gastro-duoaenal
anastomosis. This operation was described by Schoemaker
This type of high gastric ulcer will also heal if a
hemigastrectomy is performed below the ulcer, fol
lowed by a Polya reconstruction; this i s Kelling-Medlener
operation.
3. When gastric and duodenal ulcers co-exist,
Polya or Billroth I reconstruction give equally good
result. A tongue of lesser curve can be excised to include
a high gastric ulcer using either method. If the duodenal
bulb is scarred, fixed and narrow, Polya reconstruction
is safer.
4. In case of gastroduodenal bleeding, partial
gastrectomy can be performed. The more popular alter
native is to excise or to under-run the bleeding site. If
the bleeding occurs from multiple gastric erosions that
cannot be controlled by local measure such as under-running
the bleeding points, gastric resection may be necessary.
The erosions are usually localised to the distal stomach
and can therefore be dealt with by distal gastrectomy
and a Billroth I reconstruction.
Fig.44.13.— Shows Polya or Billroth II
5. For benign tumours or carcinoma in the
partial gastrectomy.
distal part of the stomach, polya gastrectomy is the
operation of choice. Polya gastrectomy has the theoretical advantage that the full width of the stomach is used for
anastomosis, thus minimising the chance of subsequent stomal obstruction if the growth recurs in the gastric remnant.
Cases are on record that gastric carcinomas often invade the duodenal bulb which should be excised and closed.
Technique of Polya (Billroth II) Gastrectomy

Access is made through a right upper paramedian incision about 20 cm long or through amidline incision skirting
the umbilicus, opening the peritoneum to one or other side of the falciform ligament. The stomach and duodenum are
thoroughly examined to know the exact details of the pathology. After being satisfied with this, the other viscera are
inspected. The stomach is drawn out of the wound and the probable extent of the resection is estimated.
A hole is first made through the gastrocolic omentum in an avascular area to the left of the left gastro-epiploic
vessels. The greater omentum is detached from the stomach by division between successive pairs of artery forceps
applied close to the greater curvature of the stomach. It is an advantage to commence the division from the left side
as adhesions are least at this site. While division is started from the left side, the left gastro-epiploic vessels and one
or two short gastric vessels are divided between ligatures. At this time, care must be taken not to damage the spleen.
Gradually the gastrocolic omentum is detached along the greater curvature towards the right side as far as the end
of the first part of the duodenum. The main right gastro-epiploic vessels as they lie near the inferior border of the
pylorus are divided between ligatures.
Now the operator should switch over to the lesser omentum. The right gastric vessels are first identified, isolated
and divided between ligatures just above the duodenal bulb and pylorus. Now the lesser omentum is detached from
the lesser curvature of the stomach gradually towards the left between the pairs of artery forceps in the same fashion
as done in case of greater omentum.
This detachment operation of the lesser omentum should stop before reaching the left gastric artery. This artery
is divided at a later stage of operation.
The posterior surface of the first part of the duodenum is dissected from the pancreas sharply or bluntly and if
there are vascular adhesions, they have to be divided between ligatures. Duodenum is freed at least 1 cm distal to
the ulcer. At this site, gastro-duodenal artery may have to be ligated, but the common bile duct and the hepatic artery
should be identified and preserved.
Two occlusion clamps are applied side by side at the site of proposed section of the duodenum. The area is now
well separated from the rest of the abdominal contents with mops. Sucker machine is switched on, the duodenum is
divided between the clamps and the opened duodenum is sucked so that no intestinal juice can contaminate the
abdominal contents. The proximal cut end, held in the clamp, is covered with a piece of gauze and turned towards
the left side of the wound. Now attention is drawn to the closure of the duodenal stump. This should be done very
meticulously as the duodenal leakage is a serious postoperative complication. This closure can be done convention
ally by an all-coats through-and- through suture and a seromuscular Lembert suture to invaginate the first layer. Care
must be taken to invaginate the mucous membrane completely.
A second invaginating suture or a purse string is used to invert the stump within it. It is better to cover the stumps
with peritoneum by means of a suture catching the ligated stumps of the right gastric and right gastro-epiploic vessels,
the anterior wall of the duodenum and the peritoneum over the pancreas.
The stomach is now held up with the help of the clamp so that the left gastric vessels are tense. With the fingers
the pulsation of the left gastric artery is felt where it reaches the lesser curvature 2 to 3 cm below the cardia. The vessels
are carefully dissected, doubly clamped, divided and ligated. Select the line for division of the stomach to remove the
distal half, two-thirds or three-quarters according to the circumstances. Loose tissues just above the proposed line of
transection are trimmed off from the greater and the lesser curvatures.
An opening is made in the transverse mesocolon in an avascular area to the left of the middle colic vessels. The
proximal loop of jejunum is brought upwards through this. The loop should be as close to the duodeno-jejunal flexure
as possible and it should not be kinked or tense. This loop should be comfortably placed along-side the stomach so
that the proximal portion will correspond with the lesser curvature and the distal portion to the greater curvature of
the stomach. Two pairs of the tissue forceps are applied to the two ends of the proposed anastomotic segment of the
jejunum. An occlusion clamp is applied across the stomach just proximal to the level of section, while a similar clamp
is applied to the antimesenteric fold of jejunum, raised by the pairs of tissue forceps. Lembert seromuscular suture
is made to unite the adjacent surfaces of the two viscera using 00 atraumatic catgut. A Payer’s crushing clamp is now
applied to the stomach 1.5 cm distal to the suture line. Now all the abdominal contents are pushed inside the abdomen
and covered with two mops. The stomach is divided proximal to the crushing clamp and when whole length stoma
is to be utilised, the jejunum is incised 1 cm away from the suture line. When the insides of the viscera are exposed,
they are well sucked and thus avoid abdominal contamination. After this, classical 4 layer anastomosis is performed.
FINSTERER VALVULAR ANASTOMOSIS.— Some surgeons prefer this type of anastomosis to direct the path
of the food from the stomach to the efferent loop of jejunum easily. In this type of anastomosis, the stomach is divided
as described earlier. The upper portion of the opening in the stomach is closed keeping the lower portion open for
anastomosis. The jejunum is incised not more than 4 to 5 cm i.e. Wi to 2 inches opposite the lower part of the cut-
end of the stomach (towards the greater curvature). The upper part of the cut-end of the stomach is closed by through-
and-through sutures. Seromuscular suture is used for the closed part to unite it with the intact jejunum to reinforce
the closure and this suture is continued downwards as the conventional first and fourth layer sutures for the anastomosis.
At the greater and lesser curvatures the suture is re-inforced with omentum.
CLOSURE OF THE HOLE IN THE TRANSVERSE MESOCOLON.— The anastomosis is now drawn downwards
through the opening in the mesocolon. The margins of the opening in the mesocolon are fixed to the stomach wall
about 1 cm proximal to the anastomosis with interrupted catgut stitches. This is an important step in this operation.
This not only prevents the herniation of small bowel through the gap in the mesocolon, but also prevents kinking of
the jejunum.
Technique of Billroth I Gastrectomy

It goes without saying that this operation can only be performed when the duodenum is wide and mobile and
not scarred, adhered or narrow.
The stomach and the first part of the duodenum are mobilised in the same manner as done in Polya gastrectomy.
Mobilisation of the duodenum is more conveniently done by Kocher’s method, i.e. incising the peritoneum on the
lateral aspect of the duodenum. But the lesser curve is freed of omentum only 2 cm proximal to the ulcer.
The duodenum is divided between clamps, just distal to the pylorus. The distal cut-end of the duodenum is covered
with gauze and kept aside for future anastomosis. The transection of the stomach is carried out with the aid of two
pairs of clamps applied at an angle to each other. The lower clamp is so applied that it covers that portion of the
stomach which anastomoses with the duodenum, while the upper clamp is so placed as to resect upto 2 cm above
the ulcer. Tlie portion of the stomach held by the upper clamp is closed with an over-and-over stitch including the
clamp, the clamp is withdrawn and the stitch is gradually tightened. A sero-muscular stitch is applied to invaginate
this layer. Thus a ‘New lesser curvature’ is made.
ANASTOMOSIS.— Now the distal cut end of the stomach and the cut duodenum are brought together. Make
sure that they come to each other without tension. A seromuscular stitch is applied on the posterior walls of the two
viscera back and forth while the bowel ends lie apart. The stitches are then tightened seriatim to draw the seromuscular
layers in contact. Now join together the stomach and the duodenum using a continuous all-coats suture. First the posterior
walls are joined. Care must be taken at the upper comer where there is the new lesser curvature. This all-coats suture
is continued to unite the anterior walls of the two viscera. The anastomosis is completed by using the seromuscular
stitch for the anterior walls of the two viscera.
WHEN THE ULCER IS ADHERENT TO OR PENETRATING THE PANCREAS — it is carefully dissected from
the pancreas without opening the stomach. If it is suspected that the ulcer can be of malignant variety, a portion of
the pancreas should be excised along with the stomach wall around the ulcer leaving the base in situ. This is then
cauterised and covered with the omentum.
POSTOPERATIVE TREATMENT.— Nasogastric tube is always left in situ. Two hourly suction and intravenous
infusion are continued as discussed under gastrojejunostomy operation. Dietary regime is more or less like postoperative
care of gastrojejunostomy operation. Patients are instructed to take small and frequent meals due to the greatly reduced
size of the stomach. But gradually the stomach attains the normal contour to utter surprise.
COMPLICATIONS AFTER GASTRIC OPERATIONS

These can be classified into — I. General complications and II. Complications specific following these
operations.
I. General complications.— Operations on the stomach are fairly major and the complications (thrombotic,
pulmonary, electrolyte imbalance etc.), which may occur following any major operations, may follow these
operations also.
II. Complications peculiar to gastric operations can be conveniently divided into two groups — (a)
Early, i.e. the complications which develop within one year of operation and (b) Late, which appear later
than one year after operation.
(A) EARLY.—
1. Paralytic ileus.— After gastric operation, this complication is occasionally come across. Generally
it is treated by suction and intravenous infusion methods. Continuous suction may be required in obstinate
cases.
2. Haemorrhage from the suture line.— As the popularity of the use of the occlusion clamps is on
the wane, so is this complication. If at all this complication takes place, continuous gastric lavage with
I ml 1 : 1000 solution of adrenalin usually stops the bleeding. Blood transfusion may be required. If still
the haemorrhage persists the abdomen is reopened, the suture is reinforced with through-and-through catgut.
Only in very odd cases, the haemorrhage may not be stopped yet. In these occasions, the stomach should
be opened and actual bleeding points are under-run.
3. Leakage from the duodenal stump.— This complication is not uncommon. This may occur at
gastroduodenostomy (following Billroth I operation) and also from the duodenal stump following Billroth
II operation (this is more popularly known as duodenal blow out which is described below). So we are
now concentrating on the former condition. Leakage of the suture line is most commonly caused by ischaemia.
It results in peritoneal soilage with gastroduodenal contents and is associated with peritonitis, ileus, sepsis
with a moderately high (10 to 15%) mortality rate. As soon as this condition is suspected, a drain is
immediately inserted upto the gastroduodenal anastomosis alongwith nasogastric aspiration and intravenous
fluid administration. If the condition of the patient worsens immediate operation with conversion of Billroth
I to Billroth II with slight resection of stomach remnant is performed.
4. Stomal obstruction.— Five types of stomal obstructions may occur of which (a) stomal obstruction
due to mucosal oedama at the actual stoma is by far the most common. This occurs more frequently following
gastroduodenal anastomosis. This is generally treated conservatively by nasogastric suction and intravenous
therapy to correct the electrolyte balance. Potassium deficiency is more or less always associated with this
condition and potassium supplementation is of utmost importance, (b) Retrograde jejuno-gastric intussus
ception, in which efferent loop of jejunum enters stomach through gastrojejunostomy stoma, may occur
as early as 3rd day or may delay upto 3rd week. Patient complains of sudden distension and the stomach
fails to empty. Barium meal X-ray will not only diagnose the case, but also may cure it. Gastric lavage
may be tried to cure this condition. If these fail, operation has to be performed and the jejunum is slowly
dragged down to reduce the intussusception. Later on the afferent and efferent loops are sutured seromuscularly
to prevent recurrence, (c) Technical error during operation may cause stomal obstruction e.g. narrowing
of the efferent loop in Billroth II (Polya) gastrectomy. This causes obstruction of the outflow from the stomach,
(d) Stomal obstruction may be caused by oedematous and hypertrophied mucosa of the antrum following
Billroth I operation. In this case the hypertrophied mucosa has to be excised, (e) Apparent stomal obstruction
may be due to lack of muscle tone of the stomach without any organic lesion in the stoma. So in case
of a stomal obstruction if no cause can be found out by barium meal X-ray, one must perform endoscopy
to see if the stoma is widely patent or not. A widely patent stoma with symptoms of stomal obstruction
means atonic stomach.
5. Duodenal blow out.— It is in fact leakage from duodenal stump following Billroth II (Polya)
gastrectomy. It is a serious complication, but fortunately enough this is very rare and mostly due to surgeon’s
fault. The closure of the duodenal stump was not done in copy book fashion. But the present theory is
that this ‘give way’ is due to avascular necrosis from over-distension of the afferent loop of the jejunum.
This complication mostly occurs in the first postoperative week. Sudden intense thoraco-abdominal pain
in the first postoperative week should be thought in the line of duodenal blow out rather than basal pneumonia
with pleurisy.
Prompt action should be taken, otherwise death is the usual sequel. Abdomen is opened, peritoneal
toilet is performed very meticulously. A stab hole is made at the subcostal region to institute suction drainage.
Jejunostomy may be performed and the duodenal discharge is pushed through the jejunostomy tube to maintain
proper electrolyte balance. The external duodenal fistula will be closed automatically.
The students must remember that prevention is more important in this case. This can be prevented
by the following methods — (i) the gastrojejunal stoma should be made in such a fashion that afferent
loop contents should get free access. If the afferent loop is kinked at the anastomosing site, the contents
of this loop (pancreatic juice and biliary secretion) will not get access and will ultimately blow out the
duodenal stump, (ii) A drain should be put down to the duodenal stump if such complication is anticipated,
(iii) The stump should be closed very meticulously through normal duodenal wall and not through ischaemic
duodenal wall caused by the use of crushing clamp, (iv) The surgeon must be careful not to close the stump
through an inflamed duodenal wall or through an active duodenal ulcer.
6. Post cibal (dumping) syndromes.— This term is generally used to describe a rather variable symptom
complex which may occur after any type of operation for peptic ulcer, but is generally seen after gastrectomy.
It is also referred to as “Dumping syndrome” because it has been supposed to result from rapid emptying
of the stomach and consequent distension of the jejunum. This is least seen in valvular small gastrojejunal
stoma. Post-prandial discomfort, giddiness and sweating are common phenomena in early days after
gastrectomy and are expected to disappear with the passage of time. Majority find them nuisance during
first 6 months and may disappear within one year, that is why this group is included in the early complications.
Spontaneous cure or improvement is usual though it may be long delayed. These syndromes can be better
described under three heads — early dumping, late dumping and bilious vomiting.
EARLY DUMPING SYNDROME starts within half an hour after ingestion of meals. This consists of
abdominal colic, nausea, vomiting, fainting, diarrhoea, epigastric discomfort, sweating, pallor and palpitation.
This is due to sudden entry of hyperosmolar foods into the jejunum causing splanchnic hypovolaemia (fall
in the blood volume). There is often pronounced fall in serum potassium associated with T and S-T segments
alterations. Dumping occurs less in case of the valvular anastomosis. The other theories postulated as cause
of this syndrome are — (a) that there is some disorder of carbohydrate metabolism and following ingestion
of carbohydrate diet there is initial transient hyperglycaemia. This causes suppression of absorption of glucose
which is retained in the intestine, causes hyperosmolarity and leads to fluid shift from the blood to the
lumen of the intestine leading to fall of blood volume and increased intestinal activity, (b) Many physicians
find a correlation of the severity of dumping syndrome with symptoms of emotional instability. This is
due to the fact that while almost all post-gastrectomy patients will have minor dumping symptoms, why
is it that only 5% of patients have symptoms severe enough to bring them back to the surgeons.
Management is generally conservative. Meals should be taken small in quantity, dry and frequently.
Milk and carbohydrate meals are avoided. Just after meals the patients should be advised to rest in bed.
Insulin or an oral hypoglycaemic drug may be given before food. Small dose of anticholinergic drug may
help. If still the symptoms persist for 8 months and are becoming more troublesome, operation is justified.
Conversion of Polya gastrectomy to Billroth I is the operation of choice. A small segment of reversed jejunum
(approximately 10 cm) may be placed between stomach and duodenum to impede gastric emptying (Henley
loop).
LATE DUMPING SYNDROME.— This is by far the rarer variety than its previous counterpart. This
occurs 2 hours after meal. The symptoms are nausea, epigastric emptiness, faintness, tremor etc. It is due
to insulin sensitivity. After initial rise of blood sugar, there is rapid fall of the blood sugar to about 50
mg/100 ml or so. This rapid fall is due to increased insulin activity.
Treatment is generally conservative, i.e. taking of food and glucose.
BILIOUS VOMITING.— This is characterised by periodic vomiting of large quantities of bile and
pancreatic juice. This was considered to be due to mechanical obstruction from kinking of the afferent jejunal
loop. Recent theory is that it is due to biliary gastritis, i.e. irritant bile upsets the stomach and hence frequent
vomiting. Conservative treatment often fails and operative treatment is to be resorted. The existing anastomosis
is converted to Roux-en-Y anastomosis. The afferent jejunal loop is divided 2-3 cm from the point where
it joins the stomach. The attached end is closed by invagination and the free end is anastomosed to the
jejunum in an end-to-side fashion well below the gastrectomy stoma. When bilious vomiting occurs after
Billroth I operation, a portion of jejunum is interposed between the duodenum and the stomach to prevent
biliary regurgitation into the stomach remnant.
7. Intestinal obstruction.— Intestinal herniation.— In Polya gastrectomy, a loop of small intestine

may herniate through the gap between the anastomosis and the hole in the transverse mesocolon. Commonly
this occurs between the 6th and 20th postoperative days. The symptoms are more or less similar to any
high intestinal obstruction. The colicky pain may become continuous when the hemia has become strangulated.
The treatment is operation. As soon as this has been suspected, the abdomen is reopened, the hemia
is reduced and if the hemia has become gangrenous, that portion of the bowel should be resected.
8. Acute postoperative pancreatitis.— This complication carries high mortality rate, but fortunately
this occurs very occasionally. Management is same as that of acute pancreatitis.
(B) LATE.—
1. Recurrent ulcer.— Ulcer may recur either in the anastomotic site or in the jejunum slightly distal
to the anastomosis (jejunal ulcer). Gastric ulcer in the remnant of the stomach is rather unusual. It goes
without saying that incidence of recurrent ulcer can be very much reduced by proper case selection and
selection of the ideal operation which will be suited for the particular patient. The acid status of the individual
should be brought down by selecting proper operation. It has already been discussed under the heading
of ‘Choice of Operation’. Some surgeons are in the opinion that application of occlusion clamps predispose
to ulcer formation and better be avoided. That is why the incidence of recurrent ulcer has gone down recently
to less than 2%. One word of caution should be remembered by the students and young doctors that while
performing partial gastrectomy the level of the excision of the stomach should not be as low as to leave
a part of antrum, which will increase the incidence of recurrent ulcer to 40% or should not be as high
as to produce nutritional deficiencies later on.
The symptoms generally appear 2 years after operation and consist of persistent pain ‘burning’ in type,
which becomes worse within half an hour of taking food. This pain generally radiates down to the left
side of the abdomen towards the left iliac fossa. These ulcers may often bleed and produce haematemesis
and/or melaena. Very occasionally they may perforate, which is more fatal than the perforation of a duodenal
ulcer.
When clinically it seems that the patient is suffering from a recurrent ulcer, barium meal X-ray should
be performed. But radiology fails in more than 50% of cases to diagnose. Endoscopy is more valuable
investigation in this case. Maximal acid output is generally increased to about 30 or more m.Eq/litre.
The treatment is operation and conservative management has practically no place.
When the ulcer follows vagotomy and a drainage operation, Hollander test should be performed to know
completeness of the nerve section. If the test reveals incomplete nerve section, operation is re-performed
and a search is made to identify undivided vagal nerve. This is divided. If an intact vagus nerve cannot
be identified or the Hollander’s test does not reveal incomplete nerve section, a Polya gastrectomy should
be performed.
When an anastomotic ulcer is found following Polya gastrectomy, vagotomy should be performed. If
the acid secretion of the individual is low, a high gastrectomy and a fresh anastomosis is performed to
prevent stasis.
An anastomotic ulcer following Billroth I gastrectomy should also be treated by vagotomy. If the ulcer
recurs in the gastric remnant, a higher gastrectomy (Polya type) is performed.
Ir all cases of recurrent ulcers, one should always keep in mind the possibility of presence of Zollinger-
Ellison syndrome.
2. Gastro-jejuno-colic fistula.— Gastro-jejuno-colic fistula is a sequel of the preceding condition. The
ulcer penetrates and erodes the transverse colon, which lies very close to the anastomosis. A patient, who
had undergone gastrojejunostomy operation 2 to 3 years ago, was suffering from pain at the anastomotic
site radiating downwards and to the left for the last few months and now suddenly complains of severe
diarrhoea after every meal and eructation of foul gas, is probably suffering from gastro-jejuno-colic fistula.
The chief factor in rapid deterioration of the patient’s condition is fouling of thejejunum by colonic contents
disturbing the absorbing mechanism. It is never due to the passage of gastric contents directly into the
colon, which the students often make mistake of. The diagnosis is established by a barium enema and
not by a barium meal, as the latter often fails to reveal the fistula in X-ray. The treatment is operation.
The patient is properly resuscitated. The fistula is resected, the colon is repaired and a higher partial
gastrectomy (Polya type) is performed. Vagotomy may be performed as an additional measure against
recurrence.
3. Nutritional deficiency.— Various types of nutritional deficiency may occur following gastrectomies.
To understand the proper mechanism behind these deficiencies one should have a thorough knowledge of
the physiology of gastric and intestinal functions. The maximum absorption takes place in the first 100
cm of small intestine distal to the pylorus. This portion is mainly concerned for absorption of carbohydrate,
fat and protein. Besides this, duodenum is also responsible for absorbing water-soluble vitamins, iron, calcium
and certain other minerals. Folic acid is absorbed all throughout the small intestine, while vitamin B,2 is
absorbed only in the terminal ileum, which is also concerned with absorption of bile salts and fat soluble
vitamins.
From this idea it is obvious that in gastrojejunostomy operation or Polya gastrectomy, where duodenum
and a small proximal portion of jejunum is by-passed, absorption of the main items of the diet will be
affected and the patient will suffer from some sort of nutritional deficiency. In this connection, it may be
mentioned here that pyloroplasty is definitely a more physiological operation than gastrojejunostomy so far
as the drainage procedure is concerned.
DIARRHOEA.— Most patients following gastrectomy will complain of loose stool or increased bowel
habits, but only 5% may complain of troublesome and persistent diarrhoea. It may be related to intestinal
hurry or to steatorrhoea. Loperamide or Diphenoxylate + Atropine is quite helpful.
This complication has increased incidence following vagotomy. Although about 70% of patients report
an increase in the frequency in the bowel movements after vagotomy, this often acts to relieve postoperative
constipation. The incidence of significant postoperative diarrhoea varies in various series from 5 to 20%.
The aetiology of diarrhoea following vagotomy is not well understood. It may be that there is loss of protectiv
action of the hyperacidic stomach with resultant increase in gastroenteritis with change in the composition
of small bowel mucosa causing diarrhoea. Treatment of significant diarrhoea is medicinal and only in
exceptional cases surgery may be required in the form of insertion of a small segment of reversed jejunum
(Henley loop).
STEATORRHOEA.— This means loss in the stool of more than 7% of total amount of fat ingested.
This is due to non-mixing of the pancreatic enzymes with food following gastrojejunostomy or Polya
gastrectomy.
IRON DEFICIENCY ANAEMIA.— If the duodenum is by-passed, the incidence of iron deficiency anaemia
will be as high as 40% after two years of operation. So iron should always be supplemented in these cases.
MEGALOBLASTIC ANAEMIA.— Unlike the previous type of anaemia, this is not so common following
partial gastrectomies. But it may appear about 5 to 10 years after the operation due to gastric mucosal
atrophy rather than anything else. It is however almost invariably seen after several years of total gastrectomy
When this condition appears following partial gastrectomy there is evidence of reduced serum vitamin B12
level. Intramuscular vitamin B)2 (cyanocobalamin) injection 100 ng weekly is given till the blood level comes
to normal.
VITAMIN B DEFICIENCY.— This is common when the duodenum is by-passed and the symptoms
are angular stomatitis, glossitis and peripheral neuritis. A regular supplementation will be required.
CALCIUM DEFICIENCY.— As many as 40% of patients may suffer from this deficiency when the
duodenum is by-passed. This condition is often associated with steatorrhoea. Bone changes (decalcifying
bone diseases) are seen very occasionally and as a rule calcium should be given to all patients after partial
gastrectomy.
WEIGHT LOSS.— This is also very common after total gastrectomy and Polya gastrectomy but not
so after Billroth I. It is obviously due to reduced absorption of carbohydrate, fat, protein and different mineral
from the proximal intestine. It is not a serious complication and in fact is beneficial in certain circumstances
with reduced incidence of coronary diseases following gastrectomy.

4. Intestinal obstruction.— Two types of intestinal obstruction may occur following gastric operations
— (a) Intestinal herniation, which commonly occurs between 6th and 20th postoperative days and hence
described under EARLY complications.
(b) Bolus obstruction.— The pylorus being either by-passed or widened, unmasticated food, mainly
orange pith will get access into the small intestine and may be obstructed at the narrowest part of the small
intestine, i.e. 1 metre proximal to the ileo-caecal valve. This will give rise to intestinal obstruction which
will mimic gallstone ileus. So all postoperative patients should be advised to masticate solid foods properly
and to avoid swallowing of dried fruits and orange piths.
5. Alkaline reflux gastritis.— A small number of patients following partial gastrectomy complain of
severe continuous burning epigastric pain aggravated by meals. This pain is usually not relieved by vomiting.
This condition is caused by bile reflux into the stomach. Gastroscopy reveals beefy red mucosa of the stomach
which is inflamed with multiple superficial gastric erosions. Vomiting is quite common, though it does
not relieve pain nor it indicates any obstruction of the gastric outlet.
Medical treatment with cholestyramine which binds bile salts may be tried, though not effective to
the level of satisfaction. When this treatment fails, surgery is required in the form of diverting the bile
away from the stomach. This is performed in case of Billroth II anastomosis by forming a Roux-en-Y jejunal
loop (see Bilious vomiting); or in case of Billroth I anastomosis by inserting a small segment of reversed
jejunal loop (Henley loop).
6. Tuberculosis.— Patients who had undergone gastrectomies, show a sign of increased susceptibility
to pulmonary tuberculosis. In these patients reactiveness of a latent tuberculous focus is also observed
probably due to malnutrition.
7. Gallstones.— Some increased incidence of gallstones have been recorded following all types of gastric
surgery, mostly vagotomy.
8. Carcinoma.— In various research studies it has been revealed that there is a greater predilection
towards formation of carcinoma in gastric remnant following partial gastrectomy than normal individuals.
Such carcinoma may develop even 15 to 20 years after partial gastrectomy. This may be one reason in
favour of vagotomy and drainage procedure as treatment of gastric ulcer, as carcinoma may develop not
only at the margin of the gastric ulcer, but also in the gastric remnant following partial gastrectomy. But
till today the operation of choice in gastric ulcer is Billroth I operation and if one tries to perform vagotomy
and drainage procedure four quadrants biopsy must be taken from the gastric ulcer to prove it to be benign.
Inference.— After such a big list of complications, one may consider that probably most patients after
gastric surgery will complain of one complication or the other. But it is gratifying to know that over 75%
of patients after gastric surgery remain fully satisfied with the result. Only 20% to 25% of cases remain
unsatisfied with the result of the operation. A feeling of distension after meals, loss of normal appetite,
failure to gain weight etc., are the common complaints the patients may be worried about. But even then
most patients remain content to accept them as cost of their freedom from ulcer pain.
COMPLICATIONS OF PEPTIC ULCER

1. Perforation; 2. Haemorrhage — haematemesis and/or melaena; 3. Stenosis; 4. Penetration into
neighbouring viscera; 5. Carcinoma; 6. Residual abscess.
Perforated Peptic Ulcer
This is a dreaded complication and more commonly complicates the duodenal ulcer rather than gastric
ulcer. Men are much more often affected than females. The ratio is approximately 12 : 1 to 20 : 1 according
to various series. Perforation occurs when an anteriorly and laterally placed ulcer erodes through the full
thickness of the wall of the duodenum into the free peritoneal cavity spilling acid peptic juice, bile and
pancreatic juice into the peritoneal cavity. Much less frequently, ulcer on the anterior surface of the stomach
usually near the lesser curvature or the pyloric antrum may perforate into the greater sac of
peritoneum. More rarely, ulcer on the posterior wall of the stomach may perforate into the lessei sac. Whe
a gastric ulcer perforates, malignancy should be excluded, since it is rare for benign gastric ulcer to
perforate.
Pathology - 1. ACUTE PERFORATION-
Stage 1.— When a peptic ulcer perforates, acid peptic juice, bile and pancreatic juice come out into
the gereral peritoneal cavity.This results in peritoneal irritation. This stage is called the stage of
peritonism. The patient cries out in severe pain.
Stage II.— The resultant chemical injury has been aptly compared to a bum of the peritoneum.
Peritoneum reacts to it by secreting peritoneal fluid copiously and this gives relief of pain for a short time.
The peritoneal fluid is sterile. This is the stage of reaction. This stage lasts for 3 to 6 hours.
Stage III. — At this stage there is diffuse bacterial peritonitis. Acid secretion of the stomach is abolished
reflexly as soon as perforation occurs. Since there is no acid barrier, the bacterial invasion becomes easy.
This is called the stage of peritonitis. This stage only starts after 12 hours of perforation.
2. SUBACUTE PERFORATION.— This so called ‘ leaking peptic ulcer’ occurs when a circumscribed
area of peritoneal cavity becomes contaminated by the leakage. This condition occurs due to various facto
such as (i) small size of perforation, (ii) emptiness of stomach, (iii) adhesions around the ulcer or (iv)
plugging or sealing-off of the opening shortly after perforation either by omentum or a neighbouring
viscus.
3. CHRONIC PERFORATION — When an ulcer perforates but the area is walled off by adhesions or
by viscera e.g. the liver, colon or omentum or when a gastric ulcer perforates into the lesser sac with a seal
omental foramen, a chronic abscess may form and may give rise to considerable confusion in the diagnosi
These patients usually present with an abdominal mass and/or signs of subphrenic abscess.
Clinical features — Males are involved much more frequently than the females in the ratio of 12 :
1 to 20 : 1. Majority of the victims are in the age group of 30 to 50 years. In about 80% of cases a previous
history of peptic ulceration is obtained. Just before perforation the patient is in severe pain. In 20% of cases
there may not be any previous history of peptic ulcer and this is called ‘silent perforationMany of these
patients are on cortisone therapy.
Occasionally peptic perforation may be associated with haemorrhage, when the prognosis is obviously
grave. From the moment of perforation, clinical course can be divided into three stages each of variable
duration.
PRIMARY STAGE OR THE STAGE OF PERITONISM.- Patient feels acute agonising pain in the
epigastrium or right hypochondrium. The patient becomes restless in pain but soon he lies still after
chemical peritonitis sets in. He may or may not vomit. Pain
may radiate along the right paracolic gutter to the right iliac
fossa. This is due to the fact that acid peptic juice after
coming out into the greater sac flows alongthe right paracolic
gutter to gravitate down to the right iliac fossa. This may
simulate symptoms of acute appendicitis.
On examination the patient is pale and anxious. The
tongue is dry. The temperature is slightly subnormal (95° to
96° F). The pulse rate is raised to 90 or so. The abdomen is
held still. Respiration is mainly thoracic without involving
abdomen. The abdomen looks straight and rigid. In a thin
patient it is retracted or scaphoid with the rectus muscles
thrown into prominence.
On palpation there is tenderness all over with board-like
Fig.44.14.— PA view of chest X-ray shows gas rigidity. The rigidity is highest at the epigastric and right
under the right cupula of the diaphragm which is hypochondriac region. ‘Rebound tenderness’ is characteristi
diagnostic of perforated peptic ulcer. cally present. Abdominal percussion is painful all over. Liver
dimness in the midaxillary line is either obliterated or brought down to a lower level as the escaped gas
accumulates under the diaphragm. On auscultation the abdomen is silent and there is definite absence of norm
peristaltic sound of the intestine. This part of examination is very important. Rectal examination will reveal
pelvic tenderness. From the moment of perforation this stage takes about 2 to 6 hours depending on the size
and site of the perforation. If the size is big the patient may pass rapidly to the next stage.
SECONDARY STAGE OR THE STAGE OF REACTION.— This is the stage of illusion or delusion.
At this stage the patient is relieved, and it cannot be more deplorable if the surgeon also gets relief. This
is the stage in which fire continues under the ashes. The pathology of peptic perforation is being continued
and the worst stage of peritonitis is on the way, when it will be difficult to save the patient. At this stage
the pulse continues to be high and the temperature gradually rises to normal and higher. Abdomen becomes
slightly distended. Tenderness and rigidity are slightly less marked. Bowel sounds remain absent.
TERTIARY STAGE OR THE STAGE OF PERITONITIS.—Diffuse peritonitis develops. The patient
looks toxic (facies hippocratica) with pallor, sweating, pinched face, anxious look and bright eyes. The
extremities become cold. Vomiting is now frequent. The patient complains of an insatiable thurst. The
pulse rate is very high, small and thready and the patient is in shock. Respiration is shallow and rapid. The
temperature shoots up. On inspection there is gross distension of the abdomen with the accumulation of
gas and fluid in the paralysed intestine. On palpation abdomen is no longer board-like, but the muscles
still ‘guarded’. Tenderness is still generalised, but the palpating hand is no longer resented. Percussion
is dull. Bowel sounds are absent but occasional ‘obstructive tinkle’ is heard.
Special Investigations — Diagnosis is made mainly on clinical examination, (i) To confirm the
diagnosis a straight X-ray of the abdomen with the patient in the erect or sitting position will show gas
under the right cupula of the diaphragm in 75% of cases. If the patient is not able to sit or stand, a lateral
X-ray film with the patient on one side may show the gas under the diaphragm or the gas bubble has shifted.
It must be emphasised that negative X-ray findings do not exclude the diagnosis of perforation, (ii)
Aspiration of the peritoneal cavity may show bile-stained fluid which is alkaline and indicates perforation
of duodenal ulcer, (iii) Some clinics have used X-ray pictures of the abdomen following injection of 60 ml
of 50% Gastrografm down a nasogastric tube. The dye escapes through the perforation, thus making it
possible to identify its exact site.
Treatment — The treatment of acute perforated ulcer is surgery. Some surgeons use conservative
Fig.44.15.— Shows the technique of dosure of peptic perforation.

47
738 A CONCISE TEXTBOOK OF SURGERV
treatment in selected cases, but as a rule it is adopted only for those patients who are not considered fit
enough to withstand an abdominal operation and in a few cases of leaking perforation where the diagnosi
is not definite.
PRE-OPERATIVE MANAGEMENT — It is mandatory to resuscitate the patient prior to operation,
(i) Rest and sedation with injection of morphine or pethidine (sedatives should not be given until diagnos
is firmly established), (ii) No fluids should be given by mouth and a nasogastric tube is inserted. Hourly
aspiration should be continued, (iii) Intravenous infusion should be started immediately. 0. 18% saline in
4.3% dextrose should be commenced. A specimen of blood is taken for blood count, blood grouping, and
electrolyte estimations. Where shock is severe plasma expanders such as Dextran should be infused.
Amount of fluid infused should replace the daily fluid requirement (approximately 2.5 litres) plus the
amount lost in gastric aspiration, (iv) Broad spectrum antibiotic should be started immediately by
parenteral route, (v) A catheter should be inserted into the urinary bladder. Amount of urine voided shou
be noted and urine should be tested for estimation of sugar, (vi) Blood pressure and pulse rate should be
recorded at '/2 hourly intervals.
Surgery — Simple suture of the perforation remains the standard treatment today. Yet definitive
operation has got a role in the treatment of peptic perforation. Considering the fact that simple suture
treatment has achieved 85% cure rate if the ulcer is acute, but only 25% if the ulcer is chronic, so definitive
surgery is indicated, (i) When the ulcer is chronic with a long history; (ii) When there is history of previous
perforation, (iii) When there is history of previous haemorrhage; (iv) Those who were treated by medicine
(v) Some surgeons prefer to perform definitive operation when the patient comes within 6 hours of
perforation; (vi) Suspicion of malignancy in a perforated gastric ulcer.
It is a well known fact that considering total number of cases both acute and chronic, after simple sutu
operation. 70% of patients continue to complain of symptoms of ulcer and about 50% will require further
surgery.
SIMPLE SUTURE OPER.4TION.-~ The choice of anaesthetic must be left to the expert anaesthetist.
Muscle relaxants have added greatly to the ease of performance of the operation and wound closure.
There is a choice between two types of incision — midline and paramedian. Midline incision is prefer
by many as entry is rapid and closure is easy. Moreover in a potentially infected area, rectus sheath is not
On opening the peritoneal cavity there is often an escape of gas and lots of fluid will be seen in the per
cavity. The edges of the wound are gently retracted. The right lobe of the liver is drawn upwards with a su
retractor and the stomach is brought out of the wound dragging to the left of the patient exposing whole o
lesser curvature of the stomach, the pylorus and the first part of the duodenum. In most cases the perforat
is readily seen. It may be oval or circular and punched out with variable diameter. The gut around the per
is congested and oedematous. In case of chronic ulcers lots of adhesions may be expected around. In case
the stomach the perforation is commonly situated on the anterior aspect of the lesser curvature. If the site
perforation is not obvious, acareful search may reveal a posterior gastric ulcer which has ruptured into the
sac. In case of duodenum perforation mostly lies in the anterior or superior aspect of the first part of the
duodenum. The simplest method of closing the perforation is to introduce three interrupted sutures of No
atraumatic chromic catgut. The first one is at the upper part of the perforation, the second one at the lower
of the perforation and the third one through the middle of the perforation. During application, the ligature
are not tied immediately, but the ends are held separately with artery forceps. A convenient portion of gre
omentum is laid over the perforation and the sutures are then tied gently over the greater omentum. Too m
tension on the sutures may cause them to cut out when the gut wall is oedematous.
Peritoneal toilet should then be carried out. Excess fluid should be sucked out from the peritoneal cav
Particular care is given to mop the following spaces : (i) The right subphrenic space should be revealed by
drawing down the right lobe of the liver; (ii) Rutherford Morison's pouch and the right paracolic gutter ar
exposed and mopped by retracting the intestines medially; (iii) The intestines are drawn up and the fluid i
the pelvis is mopped; (iv) The spleen is retracted medially and the left subphrenic area and the paracolic g
are suckcd out. Swabbing with gauze should be minimal as trauma to the inflamed visceral peritoneum m
encourage formation of adhesions. A specimen of fluid should be taken for bacteriological examination.
Drainage is necessary when the patient comes after 6 hours of perforation and there is frank pus in
the peritoneal cavity. Many surgeons prefer to drain as a routine but its utility is questioned. The drain is
given to the Rutherford Morison’s pouch and/or to the right paracolic gutter. The end of the drain is brought
out through a stab incision in the loin. Corrugated rubber drain or cigarette drain is used. In addition it
is wise to drain the superficial layers of the abdominal incision in obese patient, as peritoneum is more
apt to tackle infection than the abdominal wound. Abdominal incision is closed in layers.
DEFINITIVE OPERATIONS.— Closure of perforation is usually practised in case of perforation of peptic
ulcers. When there is definite indication (discussed earlier), when the surgeon is experienced and the facilities
are available one can go for definitive operation in peptic perforation. This minimises two operations and
two convalescent periods.
In case of perforated gastric ulcer the definitive operation is partial gastrectomy — Billroth I operation
with an end-to-end gastroduodenal anastomosis. A few surgeons often recommend vagotomy plus pyloropla
and closure of perforated gastric ulcer, but particularly in view of high association of carcinoma with this
lesion, Billroth I gastrectomy seems to be more justified. In case of perforated duodenal ulcer the definitive
operation is vagotomy and gastrojejunostomy. A few surgeons prefer to perform pyloroplasty through the
perforated duodenal ulcer. But in majority of cases there is gross induration and oedema of the duodenum
adjacent to the pylorus which is not suitable for pyloroplasty.
LAPAROSCOPIC CLOSURE OF PERFORATION.— As minimally invasive surgery has become the
choice of the day, it is being practised for closure of peptic perforation also. Pneumoperitoneum is being
achieved with carbondioxide and a telescope is inserted through a 10 mm subumbilical port. A colour
T.V. monitor is being used to see through the telescope the intra-abdominal structures. A needle holder
is inserted through a second port of 5 mm diameter and a forceps is inserted through another port of same
diameter. The perforation is closed by simple suturing. The peritoneal cavity is inspected thoroughly and
is washed out properly. The instruments are taken out and the small wounds are closed. Postoperative care
is same as mentioned above. The hospital stay is much less and the patient goes back to work quite early.
Definitive operation should be performed at a later convenient stage.
Management of subacute perforation.— Conservative treatment should be started immediately as
mentioned in the preoperative management of acute perforation. If the patient is improving rapidly one may
continue with this treatment. A close watch must be kept on the patient. If one is not sure of the diagnosis
and if the patient shows any sign of general peritonitis, immediate operation as mentioned in the treatment
of acute perforation is advised. Residual abscess is not uncommon in these cases which may require aspiration
or drainage in the later part of treatment.
Peptic Ulcer Haemorrhage

Peptic ulceration causing haemorrhage may be either an acute or chronic lesion. It commonly occurs
from gastric or duodenal ulcer. But it may also occur from stomal ulcer (following gastrojejunostomy
operation), from ulceration of the oesophagus in association with hiatus hernia or Barrett’s ulcer or it may
occur from ectopic gastric mucosa in a Meckel’s diverticulum.
ACUTE ULCERS.— Acute gastric and duodenal ulcers causing severe bleeding may be difficult to
diagnose and will be missed if too much reliance is placed on extra findings. Such ulcers develop rapidly
and heal without scar within a few weeks. They may only be diagnosed if endoscopy is performed within
a day or two of the bleeding. They may be seen as small, discrete lesions with hyperaemic margin and
sometimes with a large vessel exposed at the base of the ulcer. Such acute ulcers may be gastric or duodenal.
Gastric lesions are often associated with low rate of acid secretion, whereas the duodenal ulcers develop
when there is high rate of acid production. Stress is an important aetiologic factor. Ingestion of Aspirin.
Butazolidine, Cortisone or Salicylates is also important aetiologic factor.
CHRONIC ULCERS.— Any chronic peptic ulcer may be responsible for bleeding. There appears to
be an increased tendency to haemorrhage if the patient is of blood group ‘O’. Onset of bleeding is an indicatio
that active ulceration is taking place and such activity is usually associated with pain.
In case of gastric ulcer bleeding usually occurs from chronic ulcer near lesser curvature. A moderate
size vessel, a branch of left or right gastric artery may be involved.
In case of duodenal ulcer the ulcer is often situated on the posterior wall and bleeding occurs from
a branch of gastroduodenal artery.
The initial haemorrhage is usually not fatal, except when the bleeding vessel is unusually big. It becomes
fatal when — (a) recurrent haemorrhage occurs in a day or within 2 or 3 days, (b) initial repeated small
haemorrhages followed by a sudden severe haemorrhage.
In case of chronic ulcer bleeding may not stop so easily by natural haemostasis. The reasons are —
(i) Extensive fibrosis at the base of the ulcer prevents retraction of the vessel, (ii) Sometimes the branch
of the artery is eroded on its lateral wall and fails to contract as occurs in case of complete cut where the
ends contract, (iii) When the vessel is atherosclerotic particularly in old people where surgery is indicated.
Different causes of haematemesis and melaena.—
(i) Chronic duodenal ulcer 33%;
(ii) Chronic gastric ulcer 17%;
(iii) Acute peptic ulcer and multiple erosion 20%;
(iv) Portal hypertension (gastro-oesophageal varices) 16%;
(v) Postoperative stomal or recurrent ulcer 2%; (vi) Mallory-Weiss syndrome 5%;
(vii) Additional causes — idiopathic, hiatus hemia, Meckel’s diverticulum, carcinoma of stomach,
purpura, haemophilia, pernicious anaemia etc. — 7%.
Clinical features.— Though there is a previous history of ulcer in majority of cases, yet haemorrhage
may be the first manifestation particularly in acute ulcers.
The patient feels a sense of ill being with faintness, sweating and pallor when haemorrhage starts. There
may be abdominal pain or discomfort simultaneously. Later on black tarry stool (melaena) or vomiting of
blood (haematemesis) is complained of. In case of duodenal ulcer the presenting feature of haemorrhage
is melaena. Only when the bleeding is massive and the pylorus is open haematemesis may be complained
of. In case of gastric ulcer haematemesis occurs first and then melaena. A careful drug history must be taken.
Ingestion of NSAIDs or cortisone often is the cause of haematemesis. In these cases withdrawal of these
drugs often cure the condition.
On examination features of haemorrhage may be obtained i.e. rapid and feeble pulse, fall of blood
pressure, cold clammy extremities, sweating and rapid respiration.
No definite clue may be obtained on examining the abdomen, except that a definite tenderness may
be felt on the gastric or the duodenal point. There may be slight distension of the abdomen. When associated
with perforation features of perforation may be noticed.
MANAGEMENT.— In the beginning conservative treatment should be started immediately.
CONSERVATIVE MANAGEMENT.—
1. Reassure the patient. He must be explained that he is bleeding from ulcer and will be cured if blood
is transfused.
2. Absolute bed rest and mental relaxation.
3. Foot end of the bed is raised with two wooden blocks.
4. Sedation with phenobarbitone injection, which is preferred to morphine as this may cause nausea
and vomiting and this may induce more bleeding. Injection pethidine is also good.
5. Blood is drawn for grouping and cross-matching. Intravenous infusion is started immediately.
Estimation of haemoglobin and urea should also be performed. Blood transfusion is started as early as possib
Frequent pulse rate, central venous pressure and blood pressure readings should be taken to know the amou
of blood to be transfused. Even after bleeding has ceased and blood transfusion is discontinued, these readin
will give an idea about any further haemorrhage.
6. Nasogastric tube is introduced. Opinions defer regarding this and a few surgeons believe that this
may initiate bleeding.

7. Ask for hourly blood pressure chart. Measurement of central venous pressure is of great help in the
management.
8. If it is decided that surgery is not required at present, soft diet with milk may be given to the patient.
Cold milk is particularly helpful to minimise bleeding. It must be remembered that diet may initiate bleeding
9. A few tests should be performed to know the cause of haemorrhage : (i) Hess test for capillary
fragility; (ii) Testing for blood coagulation or bleeding defect; (iii) Liver function tests.
10. Oesophagoscopy and gastroduodenoscopy.— Endoscopy with fibreoptic endoscope is almost an
obligatory method to detect the bleeding point. The patient’s pharynx is spread with local anaesthetic and
the patient is slightly sedated with slow intravenous injection of diazepam in the dose of 10 to 20 mg. As the
instrument is introduced through the pharynx into the oesophagus, careful watch should be maintained to
detect bleeding point. The instrument is gradually introduced into the stomach. Acute linear mucosal tear at
the end of the oesophagus indicates Mallory-Weiss syndrome. Presence of oesophageal varix can also be
detected here with bulged dilated vessels at the lower end of the oesophagus. Injection of sclerosant may be
made to the oesophageal varix to stop bleeding. One may find acute erosions in the stomach or a bleeding
ulcer. In case of bleeding ulcer attempt at laser coagulation or injection of a sclerosant (e.g. 98% alcohol or
adrenaline 1 : 10,000) may stop bleeding. If blood is seen coming through the pylorus, there is every
possibility that duodenal ulcer is bleeding. The endoscope is now introduced into the duodenum to detect
the bleeding vessel. Bleeding from the stomach and duodenum can be treated with a number of haemostatic
measures. These include diathermy, heater probes and lasers. These approaches are quite useful in the
treatment of bleeding ulcers.
Gastroduodenoscopy with fibreoptic instrument is essential to find out duodenal bleeding point.
11. If endoscopy does not give any clue to the diagnosis, a barium meal examination should be performe
on the following morning.
A close watch is kept on the patient whether improvement is occurring or not. A decision should be made
within 48 hours of commencement of bleeding, whether surgery should be undertaken or not. Experience ha
shown that when operation is delayed beyond that time the mortality rises sharply. In a few cases operation
should be undertaken quickly after preliminary resuscitation. Indications for immediate operations are :—
(i) Those patients who rebleed after admission to hospitals.
(ii) The patients who are above 45 years of age.
(iii) The patients who require 5 or more units of blood to restore their red cell volume and central
venous pressure.
(iv) In patients where conservative treatment is not doing much good.
(v) If there is possibility of associated perforation of the ulcer.
(vi) When there is history of previous bleeding within a few months.
Choice of operation.—A quick operation is suturing the bleeding point through a transverse pyloroduode
incision and then performing vagotomy and pyloroplasty operation. This can also be applied in case of
bleeding gastric ulcers.
In case of chronic duodenal ulcer the treatment of choice is probably underrunning the bleeding point,
pyloroplasty and vagotomy.
In case of gastric ulcer, gastrotomy and underrunning of the bleeding vessels should be performed. At
this time four-quadrant biopsy of the ulcer should be taken to prove it to be benign. If the bleeding vessel is
near the pylorus, a wide pyloroplasty should be made alongwith direct suturing of the bleeding vessel at the
ulcer base. Vagotomy should be.performed alongwith direct suturing. If no ulcer is found, the gastrotomy is
extended to detect erosions or vascular malformations. These should be tackled with diathermy or direct
suturing. Blind partial gastrectomy should always be avoided. If erosions are found to cover a wide distal
area of the stomach, a Billroth I partial gastrectomy should be performed. Some surgeons prefer Billroth II
operation in these cases.
Diagnosis and finding out of the bleeding vessels are extremely important in case of upper G.I. tract
haemorrhage, which has been discussed in page 860.
Chronic Stenosis
Mainly three types of stenosis are seen as complications of peptic ulcer. These are (I) Pyloric stenosis,
(II) Hour-Glass stomach and (III) Tea-pot stomach.
PYLORIC STENOSIS
This is not due to ulcer at the pylorus of the stomach but mostly due to chronic cicatrization of chronic
duodenal ulcer or juxtapyloric ulcer (very rare). Scar at the chronic duodenal ulcer contracts and gradually
narrows the lumen. After months of intermittent obstruction it may suddenly cause complete obstruction
of the pylorus.
Clinical features.— Pyloric stenosis occurs quite often in women. A long standing history of ulcer
is obtained. The onset is slow and silent. Once obstruction has developed, the following symptoms may
be noticed :
1. Pain.— There are certain changes in the characteristics of pain. It loses periodicity. It loses its
definite relationship with food. Intensity of pain is diminished. More obvious is the sensation of fullness.
It is more pronounced towards evening. Though the patient can usually take breakfast and lunch, yet
rejects afternoon tea and never takes dinner.
2. Vomiting.— This is the classical symptom of pyloric stenosis. If this symptom is not present, the
diagnosis of pyloric stenosis should be reconsidered. Copious, projectile and foul vomitus is characteristic.
This usually takes place in the evening and the vomitus contains undigested particulate matter taken
on that day or one or more days earlier. Vomiting gives considerable relief.
3. Periodicity is lost.
4. Constipation is also complained of if specifically questioned.
5. Loss of weight becomes obvious.
ON EXAMINATION :
1. Visible peristaltic waves passing from left to right is quite characteristically noticed after giving
anything to drink. This peristaltic wave is more clearly seen as the patients are often very thin.
2. A succussion splash is often heard on shaking the patient and keeping the clinician’s ear very
near to the patient’s abdomen. This is due to presence of retained fluid and gas within the stomach.
3. On ausculto-percussion the greater curvature can be delineated and the stomach is found grossly
distended.
Special Investigations.— 1. Gastric function tests will show huge quantity of fasting content due
to stagnation of old food. There is low acid content due to chronic gastritis from fermentation of stagnant
food in the stomach. Absence of bile in all the samples and copious amount of mucus due to chronic
gastritis are detected in aspirated samples.
2. Barium meal examination will show a large and low stomach and presence of barium even after
6 hours. Emptying of stomach is much below normal and in the first plate while the stomach is full
of barium yet the duodenal bulb is not full with barium.
Management.— Because of continuous vomiting and due to massive loss of H+ and Cl', there is
hypochloremic alkalosis alongwith hypocalcaemia. Gastric juice contains 10 mEq/ litre of potassium so
potassium deficiency is also obvious. To replenish this loss, administration of sodium chloride and
potassium chloride solution usually suffice. When a patient with gastric outlet obstruction is admitted
to the hospital, any significant acid base and electrolyte abnormality must be corrected. It is important
to empty the stomach of retained food. Polythene Ryle’s tube or large bore Ewald tube should be
introduced into the stomach. This will permit oedema of the obstruction to subside. The stomach should
be decompressed for 2 to 3 days before operation.
Definitive treatment is SURGERY. Truncal vagotomy either with antrectomy or with gastrojejunostomy
is advised. Due to technical reasons gastrojejunostomy or gastroenterostomy is more preferred to pyloroplast
THE STOMACH AND DUODENUM 74:
Although acid secretion of these patients is low, yet vagotomy is always advised, as soon after the obstructio
is relieved, chronic gastritis will disappear and high acid secretion will start. Since duodenal ulcer is almost
always associated with high acid secretion and this condition is a complication of chronic duodenal ulcer
the treatment should always be vagotomy alongwith antrectomy or more often gastrojejunostomy. Pyloropla
cannot be used as a drainage
procedure alongwith vagotomy
' -a- ./ as pylorus is very much scarred.
|fy ' In very elderly patients only
ft, gastrojejunostomy may he ad-
K h ' , ■ vised.
HOUR-GLASS STOMACH
j This is due to cicatricial
contraction of a saddle-shaped
mw a ulcer at the lesser curvature.
K S j j f c ' , T h e
. i n t o two chambers through
jf . . c h a n n e l which admits barely a
5Clinical features.— This

condition is almost always seen
ifc *in women. Periodicity is lost
k H a n d the symptoms practicall
fplrcontinue without any remission.
Vomiting is quite common,
Fig. 44.16.— Hour-glass stomach as sequel of a large saddle-shaped ulcer. though it is not SO projectile
and foul as in case of pyloric
stenosis. Also it does not give any relief as seen in case of pyloric
stenosis. Weight loss is a feature as seen in pyloric stenosis.
Special Investigations.— 1. Barium meal X-ray is quite char
acteristic and diagnostic. It may be confused with pyloric stenosis
when the second pouch fails to fill with barium.
2. Gastroscopy will reveal the upper chamber and the scarred
channel leading to the lower compartment.
Treatment.— Billroth I gastrectomy with removal of the con
stricted part and second compartment and gastroduodenal anastomo
sis is the treatment of choice. If gastroduodenal anastomosis becomes
difficult Polya gastrectomy is advised.
TEA-POT STOMACH
Longitudinal shortening of the long-standing gastric ulcer at the
lesser curvature will produce tea-pot deformity of the stomach. The
pylorus is pulled up with a long redundant greater curvature. This will
produce stagnation and may mimic in many ways the symptoms of
pyloric stenosis.
Fig. 44.17.— Demonstrates ulcer chang
ing into carcinoma in the skiagram taken Penetration into neighbouring viscera
after evacuation of the barium. Note the
ulcer crater with malignant guide lines Penetration to pancreas from a posteriorly placed gastric or
that no longer run straight and are be duodenal ulcer may take place. In this case pain changes its type. Pain
coming irregularly thickened. radiates to the back. This pain is often aggravated by lying down.
Carcinoma
Incidence of malignant change in gastric ulcer is not very definitely known. Ulcers near the greater
curvature and near the lesser curvature below the angulus are more prone to malignant change. Ulcers
in the characteristic situation near the lesser curvature are very rare to undergo carcinomatous change.
It is due to this prone to malignancy that treatment of gastric ulcer is different from that of duodenal
ulcer. Duodenal ulcer almost never changes to malignancy. Endoscopy and even four quadrant biopsy
will definitely give a clue whether malignant change has involved in an ulcer or not. When periodicity
is lost and vomiting does not relieve pain in gastric ulcer, malignancy may be suspected.
Residual Abscess
Subacute perforation or leaking perforation or chronic perforation may cause residual abscess
formation. This has been discussed under the heading of chronic perforation in page 842.
GASTRIC NEOPLASMS
BENIGN TUMOURS
Benign tumours of the stomach are rare in comparison to malignant tumours and that is why these
are losing importance.
Benign tumours are mostly (i) Polyps, (ii) Leiomyoma, (iii) Lipoma; (iv) Neurofibroma and (v)
Ectopic pancreas.
Polyps.— These are the most common benign tumours of the stomach. There are two types of polyps
— hyperplastic polyp and adenomatous polyp. While the former is an inflammatory lesion and much
more common (20% of benign tumour and 90% of benign polyps), the latter is the true tumour. Besides
the two varieties mentioned above, adenomatous polyps may arise in the stomach in conjunction with
multiple small bowel polyposis (Peutz-Jeghers syndrome) or the familial polyposis of Gardner’s syn
drome.
HYPERPLASTIC POLYP.— These polyps are usually sessile, but may be pedunculated, solitary or
multiple arising mostly in the antrum or fundus of the stomach. These are usually asymptomatic, except
when they are adjacent to the pylorus and prolapse through it causing symptoms of pyloric obstruction
to appear. These polyps are usually associated with atrophic gastritis, megaloblastic anaemia, achlorhy-
dria and intestinalisation of gastric mucosa. Intense interest has existed and conflicting opinions have
been expressed regarding the malignant potentiality of hyperplastic polyp of the stomach. Approximately
30% of these polyps may coexist in stomachs with invasive carcinoma. The possibility may be that
achlorhydric patient with intestinalisation of gastric mucosa are responsible for development of both
cancer and hyperplastic polyp.
ADENOMATOUS POLYP.— This may be sessile or pedunculated, papillary or villous in character.
It is a true neoplasm and is potentially malignant. This adenoma also develops in achlorhydric patients
with atrophic gastritis and intestinalisation of gastric mucosa. Both the polyps may coexist in the stomach.
TREATMENT.— One must exclude by serial radiogram and by endoscopy presence of coexisting
adenocarcinoma. Fibreoptic endoscopy has facilitated the diagnosis and treatment of gastric polyps.
Pedunculated lesions can be totally excised by use of the snare and cautery and the histology of the lesion
is established. Further surgical treatment is indicated (a) when the polyp is more than 2 cm in diameter
and one is not sure from the histological report that the tumour is benign and (b) when the sessile lesion
is more than 2 cm in diameter. A solitary sessile lesion is best removed by wedge excision with a margin
of surrounding gastric wall and submitted for frozen section examination. Further surgical procedure will
depend on the pathological report. If multiple polyps involve the distal stomach a subtotal gastrectomy
is advised. A group of closely aligned polyps in the body of the stomach can be removed by wide local
excision. In case of diffuse polyposis that includes the fundus of the stomach, a total gastrectomy may
be required. If a few polyps remain in the proximal pouch, they are removed by endogastric resection and
submitted for frozen section examination. When 4 to 6 polyps are randomly located in the stomach, gas
trostomy with endogastric resection and frozen section are indicated.
Leiomyoma.— Among benign gastric neoplasms of mesodermal origin, this tumour is the commonest
and represents about 80% of such tumours. This tumour has got little clinical significance until they
enlarge to more than 4 cm in diameter. At an early stage of growth the leiomyoma is intramural. With
expansion the tumour protrudes into the gastric lumen as a submucosal mass. When they become more
than 4 cm in diameter there may be ulceration and proteolytic digestion of the core of the neoplasm. Then
central necrosis occurs and culminates in a massive upper gastrointestinal haemorrhage, which may
require emergency gastric resection. So haematemesis is the most common symptom. However
necrobiosis of the tumour may lead to perforation of the serosal surface with intraperitoneal bleeding
and even perforation of the stomach.
TREATMENT.— Small lesions can be shelled out of the gastric wall or removed by wedge resection.
When large, it is difficult to differentiate from malignant leiomyosarcoma and the treatment is resection
with liberal margin around.
Lipoma.— Lipomas of the stomach arise from the submucous coat. These are usually asymptomatic.
These are usually diagnosed by radiography done for some other purpose. Endoscopy will confirm the
diagnosis by their submucosal position. This tumour usually does not require any treatment.
Neurofibroma.— This lesion is quite rare and usually asymptomatic. When large it may give rise to
symptoms like leiomyoma.
Ectopic pancreas.— This lesion is usually submucous. These are mostly seen in the antrum or prepylori
region. The tumour may project into the lumen of the stomach and may cause pyloric obstruction. This may
require excision when the patients present with unremitting dyspeptic symptoms or pyloric obstruction.
MALIGNANT TUMOURS
Carcinoma of the stomach is by far the commonest lesion in the stomach, yet there are two more
conditions which one should keep in mind. These are — (i) Leiomyosarcoma and (ii) Lymphosarcoma.
CARCINOMA OF THE STOMACH
Incidence.— Gastric carcinoma is one of the major causes of cancer mortality. Though its prognosis
is poor, yet it can be eminently cured provided it is detected at an early stage. It rarely disseminates before
it has involved the lymph nodes.
There is a marked variation in the incidence of this disease. Whereas it is approximately 10 to 15 per
1,00,000 population in a year in U.K. or U.S.A., in Japan it is about 70 per 1,00,000 population per year.
There is a small geographical area in China where the incidence is even double that in Japan. Men are
affected more by the disease than women. The incidence increases with age. It is also interesting to know
that the incidence of this disease is now starting to fall at about 1 % per year. But this reduction is mainly
in the cancer arising in the body and distal stomach, but the incidence is increasing in the proximal stom
ach, particularly the cardia. It is more interesting to know that carcinoma of the body of the stomach and
distal stomach is more common in low socioeconomic group, whereas carcinoma in proximal gastric
cancer affects principally the higher socioeconomic group. The last important fact to be remembered is
that H.pylori infection is more concerned with carcinoma of the body and distal stomach, but never with
the proximal gastric cancer.
Aetiology.— 1. Diet.— As the stomach is in prolonged contact with food, dietary factors should be
considered as aetiology of gastric carcinoma. Gastric cancer has been incriminated to be positively corre
lated with ingestion of starch, pickled vegetables, salted fish, fresh vegetables, Vitamin C and refriger
ation. Increased salt consumption is known to be associated with stomach cancer. Higher average intake
of nitrates is present in populations at high risk for gastric malignancy. An association between cigarette
smoking and gastric carcinoma has now been well established.

2. Environmental.— Incidence of gastric carcinoma varies from country to country. In United States
cancer of stomach is definitely de
creasing. Gastric cancer is particularly
CARDIA prevalent in such countries as Japan,
Iceland, Chile and Hawaii. Japan ranks
second highest in the world with only
FUNDUS Chile outranking it in incidence. Pos
sible contributing factor could be great
consumption of smoked fish and
BODY smoked meat in these countries nota
bly Iceland. Perhaps the process of
smoking meat and fish adds carcino
ANTRUM gens or carcinogenic hydrocarbons to
these foods. Ingestion of peculiar spirits
used in certain pockets of China and
Fig. 44.18.— Shows distribution of the primary gastric carcinoma.
Japan may induce gastritis and in the
long term cancer. Excessive salt in
take and exposure to N-nitroso compounds are also involved in the aetiology of gastric cancer.
3. Age andSe*.—Cancer is rare below 30 years of age. The disease is most frequently seen between
the ages of 50 and 70, the pick age incidence being about 59 for both sexes. Conflicting reports have been
received so far as sex involvement is concerned. In a few reports males are more often affected than the
females even upto the ratio of 3 :1. Whereas in a few reports the sex incidence has been quoted as equal.
4. Heredity.—Certain families show a strong predilection toward the development of carcinoma of the
stomach, though such families are comparatively rare. Blood group A is more frequent in patients with gas
cancers than in controls. First-degree relatives of patients with gastric cancer have about two folds increase
the risk of developing this disease. Gastric malignancy has been reported in monozygotic twins.
5. Helicobacter pylori.— As mentioned earlier that H.pylori may be associated with carcinoma of
the body of the stomach and distal stomach rather than the proximal stomach. This organism is associated
with gastritis, gastric atrophy and intestinal metaplasia, which may result in malignancy in later years.
Predisposing factors.— 1. Chronic atrophic gastritis.— In this condition normal gastric glands are
decreased or absent. Thus these patients are frequently hypo-or achlorhydric. The risk of malignancy is
increased when this atrophic gastritis coexists with intestinal metaplasia, in which the gastric mucosa is
replaced by mucosa closely resembling that of the small intestine. Incidence of chronic atrophic gastritis
with intestinal metaplasia is increased in Japan. Gastric cancer develops in 10% of patients with chronic
gastritis followed up for 20 years, whereas only 0.6% of patients with normal stomachs develop cancer
during the same period.
2. Pernicious anaemia.— Similarly 10% of patients suffering from pernicious anaemia also develop
malignancy. It may be that achlorhydria, which is invariably present in this condition, leads to malignancy
3. Chronic gastric ulcer.— Most authorities are agreed that in a certain proportion of cases cancer
arises in a chronic gastric ulcer. The position of the ulcer in the stomach is of greatest significance as
regards its possible malignancy. A chronic ulcer situated on or within Vi an inch of the greater curvature
should be regarded and treated as malignant. Ulcers occurring in the pyloric segment should always be
viewed with suspicion, as 20% of these are primarily malignant ulcers. Large indolent ulcers occurring on
the posterior wall away from the curvatures show malignant changes in 10% cases.
4. New growths ofthe stomach.— Benign polyps in association with atrophic gastritis may take turn
to malignancy. Adenomatous gastric polyps are also premalignant conditions. Incidence of gastric cancer
has of course been higher in patients with multiple gastric polyps than in those who have single gastric
polyps. Single polyps less than 1 cm in diameter are frequently benign. Incidence of cancer is increased in
THE STOMACH AND DUODENUM ----------------------------------------------------------------------------------------------------------------- 747
polyps larger than 2 cm in diameter. Approxi

mately 20% of patients operated upon, the
polyp was malignant and 80% of these pa
tients were achlorhydric. In 25% of cases ad
enocarcinoma was discovered at the tip of
the polyp without invasion of the stalk sup
porting the malignant potential of this lesion.
5. The patients who had peptic ulcer
surgery, particularly with drainage procedures
are approximately at about 4 times more risk
than average persons to develop carcinoma.
Reflux gastritis is also related to increased
risk of malignancy.
6. Hypertrophic gaslropalhy (Menelrier’s dis
ease) — in which there is gianl hypertrophy of fundic
mucosa with cystic changes in the crypts. Gastric can
cer has been reported to occur in such patients in ap
proximately 10% of cases.
7. Other possible factors.- Smoked Fi9' 44'19
~ Shows cauliflower 9rowth at ,he pyloric antmm-
food, very hot and iced drinks, over smoking, excessive consumption of alcohol, constant nervous strain,
lack of Vitamins (especially Vitamins A and C) and malnutrition are a few factors which have been thought
to predispose cancer of the stomach.
PATHOLOGY.—
SITE.— Gastric adenocarcinoma mostly develops from mucous cells anywhere within the stomach,
although the majority develop in the pyloric and antral regions, particularly along the lesser curvature. So
the commonest site is pyloric and antral regions. Next common is along the lesser curvature. Fundal
carcinoma and carcinoma at the oesophagogastric junction are rare and constitute about 10% to 15% of all
gastric cancers. When carcinoma follows pernicious anaemia, it is more likely to be fundal.
MACROSCOPIC TYPES.— 1. Ulcerative.— Ulcerative carcinoma of the stomach is the most malig
nant and commonest type seen. These growths occur most frequently in the pyloric segment or in the
region of the lesser curvature, though no portion of the stomach is immune. This type infiltrates widely
and rapidly, soon gives rise to metastases of the regional lymph nodes and the liver. The ulcer is usually
oval or circular in shape and has a firm, raised and rolled out edge, the floor of which is often necrotic.
2. Proliferative or cauliflower
type.— This forms bulky, cauliflower
like masses or rounded soft tumours
with broad pedicles which project into
the lumen of the stomach. These usu
ally arise in the body of the stomach
in the region of the greater curvature,
posterior wall and fundus. These are
usually of low grade malignancy. These
are prone to become infected and to
ulcerate. When these complications de
velop, these tumours may bleed and
effects of bleeding become the strik
ing feature. These growths are usually
adenocarcinomas and are composed of
coloumnar epithelial cells. Infiltration
is confined to a limited area and re- F‘9' 44.20.— Cut section of leather-bottle stomach or linitis plastica.
gional lymph nodes are involved late in the course of the disease.
3. Leather-bottle stomach or linitis plastica.— The local form of the disease starts at the pylorus
and spreads slowly in the direction of the cardia and is associated with much fibrosis. It is often called
scirrhous carcinoma of the stomach. Two varieties are usually seen :—
(a) Localised variety which usually involves the pyloric region and produces chronic scirrhous can
cer of the pylorus.
(b) The diffuse form which usually starts at the pyloric region infiltrating the submucosa and subse-
rosa growing slowly around the circumference and along the longitudinal axis of the stomach towards the
cardia. The stomach eventually becomes shortened and contracted and is transformed into a leathery, rigid
tube, incapable of being distended. So this is called Leather-bottle stomach or Linitis plastica. The mu
cous membrane is swollen and markedly rugose. A few shallow ulcers irregular in shape may be present.
The pyloric and cardiac orifices lose sphincteric control. The serosal surface of the stomach is usually of
greyish brown colour. Section of stomach wall shows thickening consists mainly of white fibrous tissue
involving chiefly the submucosa and subserosa. Fragmentation of the muscular layer by fibrous septa is
quite obvious.
4. Colloid or mucoid carcinoma is merely a gelatinous degeneration of one of the above varieties.
5. Ulcer cancer.— This has been described above in predisposing factors.
6. Carcinoid of the stomach.— Only 2% of all carcinoid tumours arise in the stomach as compared
to 70% in the appendix and 20% in the ileum and caecum.
MICROSCOPIC TYPES.— 1. Adenocarcinoma.— This is by far the commonest variety and comprises
about 95% of all gastric cancers. Different types of cells like columnar, cuboidal or round cells may be
present. Tubular or acinar arrangements are common. These are embedded in a fibrous stroma. Colloid or
mucoid tumours are characterised by presence of large amount of mucin. There is also a signet-ring cell typ
of carcinoma with large amount of intracellular mucin. A few tumours may be of undifferentiated type.
2. Squamous cell epithelioma.— Growths situated at the lower end of the oesophagus may also
invade the stomach.
3. A very rare variety gastric carcinoma presents an admixture of glandular and squamous-cell ele
ments and is termed adenoacanthoma.
MOLECULAR PATHOLOGY OF GASTRIC CANCER.— This is less understood than colorectal cancer. Errors in
DNA replication manifesting as microsatellite instability have been demonstrated in approximately 20% of cases. This genetic
phenotype is associated with the inherited cancer syndrome and similarly with hereditary colorectal cancer syndrome — or the
Lynch syndrome. Inactivation of p 53, a tumour-suppressor gene is found in about 30% to 40% of diffuse gastric cancer. Mutation
or loss of heterozygocity in the ape gene or P-catenin is more important and found in even 50% of cases of intestinal type cancer
It must be understood that these genetic changes may be mostly responsible in the familial predisposition to gastric cancer.
Spread.— 1. DIRECT SPREAD.— In the stomach wall.— The spread is usually upward more along
the lesser curvature than along the greater curvature towards the cardia. The growth spreads mainly in the
submucous coat. The infiltration in this coat is usually 5 cm or more in advance of the visible growing
edge. Gradually the cancer involves the muscular coat lying deep to its site of origin. Later on the cancer
cells reach the serosa. When the serosa is breached, cancer cells become detached from the parent growth
and profusely involve the whole of the peritoneal cavity with malignant cells. It must be emphatically
stated that gastric cancers do invade the duodenum, if the gastric lesion lies near the pyloric ring. The
mode of spread is either direct or lymphatic permeation or even combination of the two.
To the adjacent organs.— Growth in the stomach may involve neighbouring viscera by direct spread.
The organs most frequently involved are the colon, pancreas, liver, gallbladder, omentum, spleen and
upper coils of jejunum. This spread often occurs along adhesions.
2. LYMPHATIC SPREAD.— The position and extent of nodal involvement is dependent on the
size, the position, the nature and the grade of the malignant tumour. But it must be remembered that a larg
growth may sometimes present with little or no metastasis in the lymph nodes, while a small ulcerating
carcinoma may be associated with widespread metastases in the lymph nodes.
Lymphatic spread mainly occurs either by embolism or by permeation. Usually the nodes which drain
the particular area of stomach are first involved. So ‘lymphatic drainage of stomach’ must be remembered
and has been described under the same heading in the section of Anatomy. Inflammatory nodes are also
enlarged, but unlike malignant nodes these are soft, elastic and discrete whereas malignant nodes are
irregular, hard and shotty. Besides the regional lymph nodes, lymphatic spread may take place along the
ligamentum teres towards the umbilicus where hard, nodular tumours develop. Invasion of Virchow’s
glands in the left supraclavicular fossa is rather peculiar of stomach cancer. These nodes are involved via
the thoracic duct.
3. BLOOD SPREAD.— Malignant cells enter the blood stream and metastasis may occur in the
draining organs. The veins of the stomach mainly drain into the portal vein to the liver, so the liver is the
most commonly affected organ through this spread. Metastasis in the liver forms large, white, hard, um-
bilicated tumours accompanied by enlargement of the liver and later jaundice and ascites. The other or
gans affected through this spread are the lungs, pleura and bones. Hard subcutaneous nodules may de
velop under the skin from this spread.
4. TRANSPERITONEAL SPREAD.— As already described in the direct spread, when cancer cells
reach the peritoneal surface of the stomach, malignant cells are soon freely discharged into the general
peritoneal cavity and give rise to carcinomatosis peritonei. Malignant cells may gravitate to the pelvis and
form pelvic tumours which may be felt on rectal examination. Bilateral ovarian tumours (Krukenberg’s
tumours) have also developed following gastric cancer in case of premenopausal women. These tumours
are usually the result of transcoelomic implantation. On section, these tumours show involvement of the
medulla and that is why retrograde lymphatic permeation has been more incriminated to be the cause of
this tumour rather than transcoelomic implantation.
SYMPTOMS.— Unfortunately there is rarely any symptom that is attributable to the existence of early
carcinoma of the stomach. Symptoms usually depend on the situation, extent and type of the growth.
Cancers at the inlet or outlet of the stomach are associated with mild dyspeptic symptoms besides obstruc
tive symptoms. Growths occurring in the body of the stomach may be clinically silent or may produce
vague symptoms such as anorexia or epigastric uneasiness. A large polypoid cancer on the greater curva
ture may grow exuberantly
without giving any warning
of its presence. The common
symptoms presented by pa
tients with cancer of the
stomach according to the
order of frequency are as fol
lows : (a) Epigastric pain and
indigestion; (b) Anorexia; (c)
Loss of weight; (d) Vomit
ing and/or haematemesis; (e)
Melaena; (f) Abdominal
mass; (g) Dysphagia; (h)
Diarrhoea.
Followings are the types
of presentation :
Group I.— New Dys
pepsia.— Vague but per
sistent indigestion occurring
in a patient over 40 years of
age should arouse suspicion
Fig. 44.21.— Barium meal X-ray shows malignant ulcer at the pyloric end of the stomach. Stomach cancer. These
patients usually do not give any history of previous stomach trouble. This dyspepsia is more often due to
chronic gastritis and atrophic gastritis with hypochlorhydria or achlorhydria rather than due to cancer
itself.
Fig. 44.22.— Barium meal X-ray showing carcinoma Fig. 44.23.— Barium meal X-ray showing exten-
at the pyloric end of the stomach with irregular filling sive carcinoma of the body of the stomach with gross
defect and gaping pylorus. irregular filling defect and obliteration of folds of mucous
membrane.
Group II.— Insidious onset.— This type is mainly caused by the growth arising from the greater
curvature or the body of the stomach. The early symptoms are epigastric pain and discomfort, anorexia,
nausea and loss of weight. These patients usually bleed either obvious haematemesis and/or melaena or in
the form of invisible loss, so that anaemia becomes the main feature. Anaemia may be of the microcytic
type or rarely of the macrocytic type due to interference with gastric haemopoietic factor.
Group III.— Pain.— This is a common first symptom and has been observed in about 95% of patients
by the time a diagnosis of gastric carcinoma is made. This pain is more or less continuous abdominal pain
or epigastric discomfort, without any periodicity. This is not relieved by food. Substemal or pecordial
pain may be associated with tumours at the cardia. Weight loss is almost always present. Patient may
complain of vomiting, but this does not relieve pain. Vomitus is of coffee-ground character.
Group IV.— Obstructive types.— Carcinoma is more common near the pylorus and pyloric obstruc
tion is not an uncommon feature. This is usually associated with fullness, belching and vomiting. Carci
noma of the cardiac region may present with dysphagia.
Group V.— Lump.— In about 1 /4th of the cases incidental discovery of a lump in the epigastrium
becomes the only presenting feature. Besides vague symptoms like dyspepsia, anorexia and loss of weight
there may not be any specific symptom. Though in majority of cases the lump is the stomach cancer, yet
enlarged lymph nodes, carcinomatous involvement of omentum, liver metastasis may present as lump.
Group VI.— Symptoms from metastasis.— Occasionally the primary disease remains silent, till symp
toms appear due to metastasis. These patients may complain of abdominal swelling from ascites caused by
hepatic or peritoneal metastasis. Pleural effusion and dyspnoea may be caused by pulmonary metastasis.
Patient may present only with jaundice due to enlarged lymph nodes obstructing the porta hepatis. Pa
tients may also present with distant metastasis like Krukenberg’s tumour, enlargement of Virchow’s lymph
nodes in the left supraclavicular fossa (Troisier’s sign), Trousseau’s sign (phlebothrombosis of the super-
ficial veins of the leg) or backache (metastasis to the vertebrae).

PHYSICAL EXAMINATIONS.— A firm non-tender, movable epigastric mass separate from the liver
will suggest cancer of the stomach. Whenever such mass is detected, one should try to exclude metastasis.
Liver should be palpated for any enlargement. If the liver is enlarged, find out its border and consistency.
An irregular hard liver is suggestive of metastatic liver. Lymph nodes at the left supraclavicular fossa
should be felt for enlargement. Sister Mary Joseph node (infiltration of the umbilicus) should be looked
for. The whole abdomen is palpated to exclude carcinomatous peritonei and/or ascites. Rectal examina
tion should be performed to detect metastasis in the pelvis and to exclude Krukenberg’s tumour.
1. ROUTINE BLOOD EXAMINATION will reveal low haemoglobin, low R. B. C. count and a high
sedimentation rate (E. S. R.). High E. S. R. is very common and is present in nearly 80% of patients.
2. ROUTINE STOOL EXAMINATION will reveal presence of occult blood in about 80% of cases.
3. GASTRIC FUNCTION TESTS will reveal gross hypochlorhydria or achlorhydria. Presence of
blood in the basal secretion goes in favour of the diagnosis of cancer stomach.
4. BARIUM MEAL X-RAY.— Though small lesion is liable to escape notice, yet majority of the cases
can be diagnosed by this investigation. When the patients come to the surgeon, carcinomas have grown
enough to be revealed by barium meal X-ray. Only flat growths in the body of the stomach may remain
undetected. Irregular filling defect is the most constant finding in favour of carcinoma. A regular filling
defect is more often a benign lesion and irregular filling defect with short history is mostly cancer of the
stomach.
5. FLEXIBLE ENDOSCOPY.— This has revolutionised the diagnosis of gastric cancer. In early stage
when the patients only complain of dyspepsia, gastroscopy is justified particularly if the patient is above
40 years of age. This will diagnose early case of gastric cancer. Nowadays a solidstate camera is mounted
at the instrument tip. The output is via a monitor which can be seen by the other members of endoscopy
team. This is particularly important to perform interventional techniques and for taking biopsies. It goes
without saying that flexible endoscopy is more advantageous and sensitive than conventional radiology in
the assessment of majority gastroduodenal conditions, particularly in upper gastrointestinal bleeding.
It is a safe investigation, though certain amount of training is required. Morbidity and mortality are
extremely low, though the technique is not without hazard. There may be chance of perforation of the
oesophagus or other part of upper G.I. tract. Similarly an early gastric cancer may be missed. So a higher
index of suspicion for any mucosal abnormalities should be maintained and more biopsies should be
taken. Even spraying the mucosa with dye endoscopically may properly discriminate between normal and
abnormal mucosa.
Such endoscopy is carried out under sedation, which is more important in case of G.I. bleeding. Buscopan
may be used to abolish or to reduce duodenal motility for examinations of the second and third part of the
duodenum. Examinations in this region can be best performed by using side-viewing endoscope which is
used for Endoscopic Retrograde Cholangiopancreatography (ERCP).
Nowadays instruments which allow both endoscopy and endoluminal ultrasound to be performed si
multaneously are more often used.
6. ULTRASONOGRAPHY.— Thickening of the gastric wall in malignancy, assessment of local inva
sion and peritoneal disease can be well investigated by standard ultrasound imaging. But it is less sensi
tive than other investigating procedures. So endoluminal ultrasound and laparoscopic ultrasound are probab
better techniques now available for preoperative staging of gastric cancer. In abdominal ultrasound, 5
layers of the gastric wall can be identified and depth of invasion of the tumour can be assessed to more
than 90% accuracy. Enlarged lymph ntjdes can also be identified to about 80% accuracy. Laparoscopic
ultrasound is also a very sensitive imaging modality and it is the best method to detect liver metastasis
from gastric cancer.
7. CT SCANNING and MAGNETIC RESONANCE IMAGING (MRI).— Gastric wall thickening
associated with carcinoma of any size can be easily detected by CT, but it may miss smaller lesion. Lymph
node enlargement can be detected with reasonable accuracy. However if the lymph nodes are enlarged
even with microscopic tumour deposits this cannot be detected. Detection of small liver metastasis is also
possible. Determination of the extent of disease may assist in making decisions regarding treatment. For
this all patients should undergo computed tomography (CT) scan after the diagnosis of gastric malig
nancy. This correlates closely extragastric extension, accurately demonstration of nodal involvement and
liver metastasis. Thus CT scan can be used to avoid unnecessary surgery in some patients.
Magnetic Resonance Imaging (MRI) has failed to offer any specific advantage in assessing stomach
carcinoma, though it has a higher sensitivity for detection of gastric cancer and liver metastasis than
conventional CT imaging.
8. EXFOLIATIVE CYTOLOGY.— Examination of cells detected by washing of the stomach or gas
tric lavage may diagnose a case of carcinoma. 75% accuracy has been claimed by this technique. Negative
results should not be given much importance, since it does not exclude diagnosis of gastric cancer. Chy-
motrypsin lavage may soften the mucous lining and may extrude more carcinomatous cells in the lavage
for detection.
9. TETRACYCLINE FLUORESCENCE TEST.— Growing cancer cells absorb tetracycline quicker
than normal cells and are stained yellow. When these yellow cells are seen in ultraviolet light they show
yellow fluorescence. These cells can be identified either by gastric lavage or by gastroscopy.
10. SERUM PEPSINOGEN I LEVEL.— This has been suggested as a specific marker for intestinal
metaplasia, a possible precursor of gastric carcinoma. Serum pepsinogen I level would greatly enhance
our ability to identify those at high risk of developing cancer of the stomach.
TREATMENT.— When the diagnosis of gastric carcinoma has been made laparotomy should always
be carried out. Advance in anaesthesia, efficient pre-and postoperative management have definitely in
creased the scope of surgery in gastric carcinoma. More patients who were previously considered unfit for
operation are now becoming operable.
Laparotomy is only contraindicated in patients (a) who are obviously unfit to stand the operation or
(b) in whom there are definite signs to show that the disease has advanced beyond the scope of any
operation. Such signs are (i) the growth is palpably fixed in situ; (ii) Palpable metastasis even in the pelvis
and the peritoneum with or without ascites; (iii) Multiple metastasis in the liver (solitary metastasis may
be resectable); (iv) Palpable metastasis in the left supraclavicular lymph nodes (Troisier’s sign); (v) Jaun
dice and (vi) Evidence of metastasis in lungs or bones.
The disease spreads so fast that only 50% of the cases will be qualified for exploration. Of these, 50%
will not be suitable for radical operation and only palliative measure should be adopted. Only 5% of cases
who will be suitable for radical operation will survive for more than 5 years.
Exploration of the abdomen.— Wherever possible, an abdominal approach is always preferred to an
abdominothoracic one, as the latter carries a greater risk. Only in cases of involvement of the upper one-
third of the stomach, an abdominothoracic approach can be considered. As soon as the abdomen is opened
a definite plan is made out on the extent of the growth. This decision is of profound importance. After this
one should look for the signs which will disqualify radical surgery. So the contraindications to radical
surgery are : (a) Fixation of the growth to the pancreas or posterior abdominal wall; (b) Fixity of the
involved lymph nodes; (c) Presence of secondaries all over the peritoneal cavity; (d) Presence of multiple
secondaries in the liver — the only exception is when there is a solitary resectable nodule. In presence of
such contraindications, radical surgery cannot be performed and only a palliative surgery is indicated.
Radical operations.— Radical operation means resection of the growth with at least 1 inch of the
surrounding healthy wall of the stomach (1 inch outside the palpable margin of the tumour), together with
all the lymph nodes draining the stomach. According to the position of the growth radical gastrectomy
may be either— 1. Total radical gastrectomy or 2. Upper radical partial gastrectomy or 3. Lower radical
partial gastrectomy.
1. TOTAL RADICAL GASTRECTOMY.— This operation is indicated for growths involving the midd
of the stomach or the whole of the stomach (Linitis plastica). In this operation an upper left paramedian
incision is made. The spleen with its hilar lymph nodes, the splenic vessels, the tail and body of the
pancreas are mobilised from left to right en bloc. The operation is retroperitoneal. Now the stomach with
both lesser and greater omenta is resected. The lymph nodes around the coeliac axis are removed before
beginning gastrectomy. In the process the left gastric artery and the right gastric artery should be ligated.
The lymph nodes of the supra- and subpyloric groups are also removed with ligation of the right gastro
epiploic artery. After excision of the whole stomach, the cut edge of pancreas is closed with sutures. The
continuity of the alimentary canal is restored with oesophagojejunostomy (Roux-en-Y type). By this pro
cedure regurgitation of bile and pancreatic juice into the oesophagus is prevented. Before closure a drain
is inserted upto the pancreas and the other end is brought out through a separate stab incision at the
subcostal region. It must be remembered that the mortality of total gastrectomy even in expert hands is as
high as 30% in comparison to that of the partial gastrectomy which is only 5%. So the tendency should go
for partial gastrectomy more and to perform total gastrectomy only in those cases where the surgeon is
very much sure that the local spread of the tumour has definitely gone beyond the domain of partial
gastrectomy.
2. UPPER RADICAL PARTIAL GASTRECTOMY.— It is indicated for growth involving the cardia
and upper third of the stomach. The pyloric end of the stomach is preserved and is anastomosed to the
oesophagus. A pyloroplasty is usually performed to prevent postvagotomy retention.
3. LOWER RADICAL PARTIAL GASTRECTOMY.— This operation is indicated for carcinoma of
the lower one-third of the stomach. The operation is ultimately completed with gastroduodenal anastomo
sis (Billroth I) or if first part of the duodenum has been resected, gastrojejunal anastomosis (Billroth II) is
performed.
4. Quasi-total gastrectomy.— This can be performed when upper l/3rd of the stomach is unaffected to
take the advantage of a small remnant of the stomach to anastomose with jejunum for better anastomosis
than oesophagojejunostomy.
Palliative operations for gastric carcinoma.— It has already been discussed that in quite a good
number of patients after exploration, the growth comes out to be not suitable for radical operations. In
these cases some sort of palliative operation should be performed. Followings are a few varieties of pal
liative operation :—
1. PALLIATIVE RESECTION OF THE GROWTH.— This is by far the best palliative measure, which
can be adopted in gastric carcinoma. Whenever possible, if the malignant mass in the stomach can be
resected together with the healthy margin of a gastric wall, this should be undertaken. Thus foul, necrotic
and sloughing mass of the tumour, which can produce toxaemia and bleeding, is got rid of. Some 30% of
all resections of the stomach for cancer are palliative partial or sub-total gastrectomies, though the post
operative mortality is high, which may vary from 10%-15%. But those who survive palliative resection,
live for more than one or two years with little problem of symptoms.
2. ANTRAL EXCLUSION OPERATION (DEVINE).— For fixed adherent irremovable growth in
volving the distal, antral or pyloric portion of the stomach, which defies resection, antral exclusion com
bined with antecolic gastro-jejunostomy is indicated. A pair of clamps is applied to the healthy portion of
the stomach 5 cm proximal to the edge of the growth. The stomach is transected and the distal end is
securely closed and sealed off. A gastro-jejunostomy is made by bringing the jejunum in front of the
transverse colon and anastomosed with the remaining proximal portion of the stomach. The immediate
results are good as appetite is resorted and the patients return to work very soon. But the majority of
patients die within one year not from the obstruction of the stoma, but from the hepatic metastasis or from
carcinomatosis.
3. GASTRO-JEJUNOSTOMY.— For irremovable malignant lesions of the antrum and pylorus associ
ated with obstructive symptoms, anterior or antecolic gastro-jejunostomy may be indicated. The anterior
operation is preferred as the tumour shows a tendency to invade the omental bursa posteriorly. The opera
tion is simplier and can be rapidly performed.
4. JEJUNOSTOMY.— When the cancer of the stomach invades the stomach wall so extensively that it
48
renders the performance of a gastro-jejunostomy or a gastrostomy impossible, jejunostomy can be tried

for palliation. Jejunostomy is done in the same method as that of Stamm or Witzel. Marwedel jejunos
tomy, in which the rubber catheter is inserted into the cavity of thejejunum following a curved course
through the seromuscular layer, is also preferred and may be tried as a palliative measure for gastric
carcinoma. One thing must be remembered that postoperative duration of life is not proper measure of
palliation in case of incurable cancer. Relief of symptoms, freedom from distress and a sense of well
being outweigh the importance of duration of life and more considered so far as palliation is concerned.
5. GASTROSTOMY.— In case of irremovable cancer of the cardiac end of the stomach in which
oesophago-gastrostOmy or oesophago-jejunostomy is not feasible, gastrostomy may be tried. But the re
sult of gastrostomy as a palliative procedure is never very encouraging.
6. SEMS (SELF EXPANDING METAL STENTS) IN PYLORIC AND DUODENAL DISEASE.—
SEMS can be used to manage strictures of the pylorus and duodenum and offer an alternative to gastroje
junostomy.
Postoperative complications of gastrectomy.— Radical gastrectomy is a major surgery and there is
a larger number of potential complications of the operation :—
(i) Leakage of oesophagojejunostomy, which can often be managed conservatively as Roux-en-Y
reconstruction means that it is mainly saliva and ingested food that leaks.
(ii) A fistula from the wound or drain site. It is a good practise to perform a water-soluble contrast
swallow at 5 to 7 days after operation to determine whether the anastomosis is intact or not.
(iii) Leakage of the duodenal stump can occur.
Long-term complications of Surgery.— After radical surgery long-term complications are not at all
alarming and particularly the young patients do well after such surgery. Only the patients have to eat sma
meals in shorter intervals. It is also interesting to find that there is hardly any functional difference betwee
total gastrectomy and subtotal gastrectomy. Some surgeons try to form a jejunal pouch to be attached to
the oesophagus, but its acceptance has not been great as there is little functional advantage. Nutritional
deficiencies may occur, particularly vitamin B12 deficiency due to loss of the parietal mass and routine
replacement is required. Dumping and diarrhoea are also not so often seen after usual gastric surgery.
Results of Surgery.— Result varies a lot depending on the stage of the disease and the condition of
the patient. If the surgery is performed early with proper clearance of lymph nodes, the result is quite
encouraging. The lymph nodes must be sent for pathological examination. 5-years survival rate varies a
lot between the results of the West and Japan, whereas in case of former it is only 25% to 50%, in Japan it
is about 50% to 70%.
Other modalities of treatment.— This group includes radiotherapy and chemotherapy as the radical
surgery fails to cure advanced gastric cancer.
RADIOTHERAPY.— The role of radiotherapy is rather disappointing in gastric cancer as there are a
number of radiosensitive tissues around, which limits the dose of radiotherapy. However radiotherapy ha
a palliative role in painful bone metastasis.
CHEMOTHERAPY.— This is definitely much more encouraging than radiotherapy and the best result
has been obtained using a combination of cis-platinum, 5-fluorouracil and epirubacin by continuous infu
sion. Yet, chemotherapy so far could not attain the overall popularity due to morbidity associated with thi
regime. In Japan they use mytomycin C-impregnated charcol given by intraperitoneal route. The perito
neal lymphatics take up this chemotherapy and probably yield better result. But overall acceptance of
chemotherapy has been very poor.
SARCOMA OF THE STOMACH
In comparison to carcinoma it is very rare and constitutes only 1 % of gastric malignancy. The various
sarcomas found in stomach are as follows :
1. Lymphosarcoma.— This is the commonest variety of all sarcomas. Unlike lymphosarcoma of the
intestine, it is usually solitary. Treatment is partial gastrectomy alongwith the tumour. Though lymphosar
should respond to radiotherapy, yet gastric lymphosarcoma is not so well treated by radiotheraphy.
2. Leiomyosarcoma — It usually arises as malignant change of leiomyoma, which is the second benign
tumour of the stomach. This tumour is very vascular. The only symptom is massive haematemesis and/or
melaena. Metastasis is quite late, and if detected it is usually the liver which is involved. The treatment is ag
partial gastrectomy and the result is much better than carcinoma (about 50% survive more than 5 years afte
operation).
3. Neurofibrosarcoma and 4. Fibrosarcoma are very' rare malignant tumours of the stomach which are
difficult to diagnose clinically.
ACUTE DILATATION OF THE STOMACH
This condition sometimes develops following abdominal operations or after traumas e.g. fracture shaft
of femur etc.
CLINICAL FEATURES.— Vomiting of small amounts of coffee-ground gastric juice, often associated
with hiccoughs (over-flow vomiting) should arouse suspicion of this condition. Gradually the pulse rate rise
and the patient becomes shocked. Later on effortless vomiting of dark watery fluid is noticed.
TREATMENT — Immediate introduction of nasogastric tube and aspiration of gastric contents should
be started. Large amounts of air and gastric juice are usually recovered by aspiration. Simultaneously fluid
balance should be maintained by intravenous infusion of dextrose saline and normal saline. These patients
usually suffer from hvpopotassaemia and this should be corrected. In very occasional cases massive
haemorrhage or rupture of the stomach may occur requiring immediate operative repair. But this is a grave
condition.
UPPER GASTROINTESTINAL TRACT BLEEDING
Acute upper gastrointestinal tract haemorrhage is a common emergency. The mortality Figures have
remained constant at 10% or more despite advances in methods of diagnosis and treatment. Bv convention,
when the source ofbleeding lies above the duodenojejunal flexure it is referred to as upper G. I. tract bleeding.
Causes.— Causes may be local or general. Causes of upper G. I. tract bleeding are numerous and these
can be classified as follows :
A. Local causes. According to the site of haemorrhage —
1. OESOPHAGUS.-
(i) Gastro-oesophageal varices. - This is a very common cause in this country and probably
constitutes about 20% or more (in a few scries) of upper G. I. tract bleeding.
(ii) Reflux oesophagitis.
(iii) Hiatus hernia.
(iv) Mallory-Weiss syndrome. This may cause mild, moderate or even massive bleeding
contributing about 5 to 15% of upper G. I tract bleeding.
(v) Barrett’s ulcer.
(vi) Polyps and carcinoma.
(vii)Achalasia and foreign bodies.
2. STOMACH AND DUODENUM -
(i) Chronic duodenal ulcer (33%). Haemorrhage usually occurs from ulcers situated
posterior wall of the first part of the duodenum.
(ii) Chronic gastric ulcer (20%). Mostly the ulcers in the lesser curv ature and posterior wall of
the stomach bleed.
(iii) Multiple erosions and acute peptic ulcer (10 to 25%). Erosions are usually multiple. Erosions
may occur in burns (Curling ulcer), in the head injury (Cushing ulcer), CVA, septicaemia, uraemia,
respiratory and liver failure. Drugs and alcohol may also produce erosion.
(iv) Tumours — polyps and carcinoma. Other rare tumours e.g. leiomyoma, lymphoma,
leiomyosarcoma etc. may cause bleeding.
3. SMALL INTESTINE. - Though by convention this group should not be included, yet when these
only produce haematemesis, these may be included as causes of upper G.I. tract bleeding.
(i) Very rarely Meckel’s diverticulum may present with haematemesis.
(ii) Peutz-Jegher’s syndrome.
(iii) Polyps.
(iv) Vascular malformations.
(v) Various tumours.
B. General causes —
1. Haemorrhagic disorders e.g. thrombocytopaenia, purpura, haemophilia, pernicious and other anaem
Ehlers Danlos syndrome, DIC, liver diseases, periarteritis nodosa, amyloidosis. Turner’s syndrome, Kaposi
sarcoma, neurofibromatosis etc.
2. Ingestion of drugs e.g. steroids, non-steroidal antiinflammatory agents etc.
3. Salicylates and alcohol.
Of the various causes mentioned above the common are (i) chronic peptic ulcer, (ii) acute ulcers and
multiple erosions, (iii) oesophageal varices and (iv) Mallory-Weiss syndrome
DIAGNOSIS —
1. Assessment of haemorrhage — It is difficult to assess the degree of blood loss. Patients often over-estimate the
amount lost and the stated volume of haematemesis may be misleading unless the blood is collected and mea
objectvely. The initial haemoglobin value after an acute bleeding is unhelpful because it is many hours befor
occurs and the haemoglobin drops to a representative level. However, when bleeding has occurred over a prol
the haemoglobin value may be a more accurate reflection. If one gets low haemoglobin level immediately afte
bleeding, this probably means that there has been chronic occult loss previously. Probably the degree of shoc
indication with the thready pulse and low blood pressure. Again when the patient is at rest in bed his pulse r
pressure may be reasonably normal despite a fairly large bleeding. However on standing, the pulse rate may r
blood pressure falls.
2. Assessment of the cause — A careful history is highly important to assess the probable cause of bleeding. Such
history must include drug history and intake of alcohol. A history of long standing heavy alcohol intake may
hepatic cirrhosis and a possible variceal bleeding. Dysphagia or discomfort on swallowing suggests either a b
malignant oesophageal lesion or a hiatus hemia with oesophagitis. A Mallory-Weiss tear presents classically a
haematemesis following an episode of prolonged vomiting, frequently caused by alcoholic gastritis. However
instances of the Mallory-Weiss lesion haematemesis may occur with the first vomit and not following prolong
and retching. A previous history of peptic ulcer is also suggestive of bleeding from chronic peptic ulcer.
On examination, epigastric tenderness on palpation will suggest chronic peptic ulceration as a probable ca
bleeding. A palpable mass in the epigastrium may suggest gastric carcinoma and/or splenomegaly may indica
ol'bleeeding as gastrooesophageal varices. It must be cautioned that bleeding may occur from other site despi
detected on clinical examination. As for example a tenderness in the duodenal point may suggest chronic duo
but probably bleeding is coming from a Mallory-Weiss tear or even oesophageal varix.
A careful assessment of the history and a physical examination may yield no definite cause in above 50%
with upper G. I. tract haemorrhage.
INVESTIGATIONS —
1 Endoscopy — Endoscopy has definitely helped in finding out the bleeding point. But it must be remembe
that emergency endoscopy in a bleeding patient is more difficult than routine endoscopy. A little preparation
required before endoscopy apart from starving the patient for at least 4 hours. The necessity for preliminary g
is debatable and has one major disadvantage in that the mucosa of the stomach may be damaged. Gastric lava
avoided by the use of intravenous metoclopramide. It probably helps to empty the stomach of blood and certa
to sufficient peristalsis to interfere with the examination. It is also sensible to render the gastric contents alkal
cimetidine before the examination, although the value of this drug is still to be proved. Treatment with cimeti
however help prevent bleeding from chronic peptic ulcers.
Sedation is difficult since excessive drowsiness increases the risk of inhalation. Some endoscopists ther
use any sedation, but this often leads to a difficult examination. But endoscopy should better be performed un
with intravenous diazepam, which should be administered slowly in anaemic and shocked patients and dose
not to exceed 5 mg. Pharyngeal anaesthesia is quite helpful and this is performed with lignocaine.
Usually blood does not obscure the view. If there is a blood clot in the stomach which is resi stant to me
suction and gastric wash out, it is usually still possible to see the lesser curve, the antrum and the duodenum a
the majority of the patients a diagnosis can be made out. If necessary, the gastroscope can be withdrawn into th
(to stop the tip becoming obscured by blood) and the patient is rolled on to his right side so that the blood clot
the antrum, the fundus can then be seen. If no bleeding point can be found out with a forward-viewing endosc
and third parts of the duodenum and ampulla should be examined using a side-viewing instrument if necessar
Contraindications to endoscopy.— There are a few absolute contraindications —
(i) Rapid bleeding is an indication for surgery and endoscopy merely delays this, since it is extremely d
to see anything during torrential bleeding.
(ii) Endoscopy should not be performed on a patient who is known or suspected to be positive for hepa
antigen.
(iii) Alcoholics or violent patients are difficult to perform endoscopy.
(iv) Chest infections and severe congestic cardiac failure are relative contraindications and these patient
have radiology first. Endoscopy is a good vagal stimulus and can precipitate heart block in these patients.
The ideal time for endoscopy to be performed.— As certain amount of preparation is required for endoscopy,
should not be performed immediately after admission. Moreover the diagnostic rate decreases after 48 hours. S
endoscopy should be performed on all patients between 12 to 48 hours after admission. It should always be pe
experienced endoscopist in the endoscopy room preferably in the operation theatre.
Therapeutic endoscopy.— Oesophageal varices can be injected with a sclerosant via an endoscope.
2. Radiology.—
(i) STRAIGHT X-RAY is almost unhelpful in upper gastrointestinal bleeding. Occasionally indirect poin
source of bleeding may be revealed, for example an enlarged spleen in portal hypertension, a soft tissue mass i
intussusception, a gastric carcinoma calcification or metastasis on the chest radiography.
(ii) CONTRAST STUDIES.— Barium studies in actively bleeding patients are often disappointing since a
examination is technically difficult in the presence of haematemesis or melaena and also the blood clot in the v
examined obscures on gross lesions. The source of active bleeding may remain undetected by barium studies in
patients or even more.
Nevertheless, if endoscopy has proved impossible barium studies are worth attempting. In upper G. I. tra
barium studies may typically show oesophageal varices, a chronic peptic ulcer or a tumour of the stomach.
The accuracy of a barium meal in detecting lesions such as erosions, small ulcers or early tumour is greatl
by the use of the double-contrast technique. This is performed in a fasting patient by the use of hypotonic agen
buscopan or glucagon. The stomach is distended with gas and adequate quoting of the mucosa with barium ca
lesions.
3 Angiography.—There are two main reasons for performing angiography in acute upper G. I. bleeding—(i) t
the source of bleeding when this is unknown and (ii) to stop the bleeding by selective infusion of drugs or emb
into the bleeding territory. Angiography is particularly successful when the blood loss is more than 0.5 ml per m
site of bleeding is revealed by extravasated contrast medium remaining in the bowel in the late films of angiog
It must be remembered that selective study of coeliac axis and superior mesenteric artery should be performed
midstream aortography.
When a bleeding point has been found haemorrhage can be controlled by the selective infusion of vasop
deliberate injection of embolic material such as sterile absorbable gelatin sponge (Sterispon), lyophilized hum
(Lyodura), steel coils, acrylic polymers or detachable balloons.
In case of portal hypertension with bleeding varices, various radiological techniques may be used to asse
disease and to demonstrate the anatomy of the portal venous system prior to any surgery. In this respect spleno
is quite helpful.
4. Isotope studies.— Technetium-lebelledorradiochromium-lebelled red cells ortechnetium-lebelled sulphur c
can be injected intravenously and extravasation into the bowel detected by a scintillation camera. But in most c
not proved to be particularly useful in clinical practice. The other isotope technique that may be useful in the d
ofheterotopic gastric mucosa in a Meckel ’ s diverticulum by the intravenous inj ection of "“T c pertechnetate, w
by the cells of the gastric mucosa.
5. Ultrasound and CT scanning.— These imaging techniques are not very helpful in the investigation of acute upp
G. I. tract bleeding, unless some specific clinical indication for their use exists, for example a palpable abdomin
MANAGEMENT.— Management depends on the cause of bleeding and this has been described in the
appropriate section according to the cause of bleeding.
758
CHAPTER — 37
THE LIVER AND PORTAL HYPERTENSION
ANATOMY
The liver is covered by a fibrous capsule which is called Glisson's capsule. The superior surface of the liver is in direct relation
with the undersurface of the diaphragm. In the adult the normal liver extends in the midclavicular line from approximately the
right 5th intercostal space down to slightly below the costal margin. So it is essentially under the protection of the ribs. The inferior
surface of the liver is in contact with duodenum, the right kidney, the right adrenal gland, the right colic flexure, the oesophagus
and the stomach. The gallbladder lies on the under surface of the liver and its fundus lies on the transpyloric plane. The entire liver
is invested by peritoneum except (i) the ‘bare’ area on the posterior surface adjacent to the inferiorvenacavaand(ii) the gallbladder
fossa where peritoneum reflects from the liver to cover the superficial surface of the gallbladder.
Reflections of the peritoneum from the liver are important, (a) The falciform ligament which extends from the anterior surface
of the liver to the anterior abdominal wall from the diaphragm to the umbilicus. At the inferior border of the falciform ligament
lies the ligamentous teres hapatis, which is the obliterated umbilical vein and the small periumbilical veins, (b) The coronary
ligament is formed by reflection of the peritoneum from the diaphragm to the superior and posterior surfaces of the right lobe.
It consists of an upper and a lower layers which are continuous at the right extremity with the right triangular ligament and enclose
a triangular area of the liver which is not covered with peritoneum and is termed the ‘ bare area ’ of the liver, (c) The right triangular
ligament is formed by approximation of the upper and lower layers of the coronary ligament. This connects the lateral part of the
posterior aspect of the right lobe of the liver to the diaphragm, (d) The left triangular ligament passes from the upper surface of
the left lobe to the undersurface of the diaphragm. It consists of two closely applied layers of peritoneum, whose anterior layer
is continuous with the left layer of falciform ligament. On the left the ligament ends in the free margin, (e) The lesser omentum
is the two folds of peritoneum extends from the lesser curvature of the stomach to the fissure for ligamentum venosum of the liver.
Its anterior layer becomes continuous with the posterior layer of the left triangular ligament and its posterior layer is continuous
with the line of reflection of peritoneum from the upper end of the right border of the caudate lobe (indirectly with the lower layer
of the coronary ligament). So the caudate lobe of the
liver projects into the superior recess of the omental
I VC bursa. This falciform ligament anatomically divides
the liver into the right and left lobes. The lesser
omentum comes down in front of the porta hepatis to
be attached to the lesser curvature of the stomach. The
right border of the lesser omentum forms the anterior
boundary of the epiploic foramen of Winslow. The
foramen is bounded above by caudate process, in front
by the right free margin of the lesser omentum which
contains bile duct on the right side, common hepatic
artery on the leftside and portal vein posterior to these
two structure. This foramen is bounded posteriorly by
the inferior vena cava and inferiorly by the hepatic
artery proper. By putting the index finger into the
foramen of Winslow and thumb in front of the bile duct
one can feel the supraduodenal part of the bile duct to
know its thickness and presence of stone inside it.
Through this foramen of Winslow the lesser sac com
municates with the greater sac of the peritoneum.
SURGICAL LOBES.—Surgically the liver can be
divided into two lobes — the right and left through a
plane connecting the inferior vena cava and the gall
Fig. 45.1.— Diagrammatic representation of the surgical lobes
bladder fossa. The LEFT LOBE is further subdivided
of the liver. The line of demarcation between the right and left
into a medial segment which lies to the right of the
lobes Is represented as a bold line shown by arrow. This line
falciform ligament and contain the quadrate lobe and
stretches from Inferior vena cava to the gallbladder fossa.
Another arrow Indicates Inferior vena cava. the caudate lobe. The lateral segment which lies to the
left of the falciform ligament is further subdivided by
THE LIVER AND PORTAL HYPERTENSION 759
a mid-horizontal line into upper lateral and lower lateral lobes. The caudate lobe is the posterior projection of the liver bounde
on the left by the fissure of the posterior extension of the falciform ligament and the ligamentum venosum and on the right by t
groove for the inferior vena cava. This lobe is also in the medial segment of the left lobe but is in the anatomical right lobe. The
RIGHT LOBE of the liver is also subdivided into an anterior and a posterior segment which is further subdivided by a mid
horizontal line into upper anterior, upper posterior and lower anterior and lower posterior segments. So there are altogether ei
segmental lobes of the liver, four in the right and four in the left lobe. Knowledge of the exact anatomy of the segments of the
liver help in the segmental resection of the liver in case of neoplastic lesions.
Portal vein. — The portal vein carries approximately 75% of the blood supply to the liver. It is formed by the junction of the
superior mesenteric and splenic veins behind the neck of the pancreas. Then it passes upwards posterior to the first part of the
duodenum and passes through the right free margin of the lesser omentum slightly posterior to the common bile duct and the he
artery. Ultimately it divides into right and left branches at the porta hepatis. It is approximately 5 to 8 cm in length. In only 10%
of cases it divides into two right branches going to the right lobe and one to the left lobe.
There are certain areas where there is natural communication between the portal and systemic venous systems. These are :
(1) The left gastric vein and short gastric veins, tributaries of portal vein send oesophageal tributaries and these communicate w
the oesophageal venous plexus, tributaries of superior vena cava at the lower end of the oesophagus. This is the most important
portal-systemic anastomosis and duri ng portal hypertension nature tries to divert blood through this anastomosis into the system
circulation. The result is that the communicating veins become dilated and tortuous and is called oesophageal varix. This varix
may rupture and bleed profusely to cause haematemesis in a patient with portal hypertension. (2) Umbilical vein along the lowe
border of the falciform ligament, which is a tributary of the portal vein communicates with periumbilical veins (systemic veins)
around the umbilicus. These veins when dilated during portal hypertension will result in the formation of caput medusae. (3)
Superior haemorrhoidal vein, the continuation of inferior mesenteric vein (tributary of portal vein) communicates with the midd
rectal and inferior rectal veins (systemic veins) in the anal canal. But it must be remembered that internal haemorrhoid which is
dilatation of the superior haemorrhoidal veins is hardly caused by portal hypertension. (4) Other retroperitoneal communication
between the systemic and portal veins.
Hepatic artery.— The common hepatic artery arises from the coeliac axis and comes down at the superior surface of the first
part of the duodenum, where it gives off the gastroduodenal artery and is then termed the proper hepatic artery. This artery first
forms the floor of epiploic foramen and then moves up through the right free border of the lesser omentum and ends into the rig
and left branches at the porta hepatis. The cystic artery usually arises (i) from the right hepatic artery, although there is some
variability. The most common of which is origination of the cystic artery (ii) from the gastroduodenal artery, the next common
is its origination (iii) from the left or common hepatic artery. There may also be double cystic arteries. Within the liver the right
and left branches subsequently divide into smaller branches corresponding to the portal venous system and segmental anatomy.
Due to abundant collaterals ligation of the hepatic artery proximal to the gastroduodenal artery can be performed without dama
to the liver. Even ligation of the proper hepatic artery can often be performed without serious consequences due to rich collater
extrinsic blood supply from the superior mesenteric and inferior phrenic arteries. Ligation <5f the right or left hepatic artery usu
results in enzymes elevation although with no clinical manifestations.
Hepatic veins.— There are mainly three major hepatic veins — right, middle and left. Short segments of these veins emerge
posteriorly from the liver and drain into the inferior vena cava. The right hepatic vein is the largest of the three and follows the
intersegmental plane between the anterior and posterior segments of the right lobe. It provides the principal drainage for the rig
lobe of the liver. The middle hepatic vein lies in the lobar fissure between the right and the left lobes and drains principally the
medial segment of the left lobe and a variable portion of the anterior segment of the right lobe. It joins the left hepatic vein in 8
of cases. The left hepatic vein drains principally the left lateral segment.
In addition, there are multiple small veins that drain the posterior aspect of the liver directly into inferior vena cava. With
thrombosis of the major hepatic veins, which is known as Budd-Chiari syndrome, the small posterior veins as well as the portal
collateral circulation become more important.
Biliary drainage.— Bile drains from thecanaliculi into intrahepatic ducts that follow the segmental anatomy with the arterial
supply. The anterior and posterior segmental ducts in the right lobe join to form the right hepatic duct. The medial and lateral
segmental ducts in the left lobe join to form the left hepatic duct. The right and left hepatic ducts become extrahepatic and form
the COMMON HEPATIC DUCT just outside the porta hepatis. Hepatic ducts are most anteriorly placed structures in the porta
hepatis. The common hepatic duct descends in the right free margin of the lesser omentum. It is joined on the right side by the
cystic duct draining the gallbladder. The common hepatic duct, the cystic duct and the liver form the cystohepatic triangle ofCalot.
This triangle is surgically important as it usually contains the right hepatic artery and the cystic artery, besides aberrant segment
ducts and arteries. When the common hepatic duct is joined by the cystic duct, it is called the COMMON BILE DUCT. The common
bile duct runs through the right free margin of the lesser omentum (the supraduodenal part), then behind the first part of the
duodenum (retroduodenal part) and then behind the head of the pancreas (infraduodenal part) and joins the major pancreatic duct
(duct of Wirsung) in 90% of cases forming the ampulla of Vater. This ampulla opens through the sphincter of Oddi into
the middle of the second part of the duodenum in its posteromedial aspect.
SPHINCTER OF ODDI has three parts — (i) the sphincter of the bile duct (the circular muscle fibres surrounding the
intramural and submucosal common bile duct); (ii) the ampullaris sphincter, which is a layer of longitudinal fibers and is
concerned with prevention of reflux of intestinal contents into the common bile duct and (iii) the pancreatic sphincter,
which is only present in l/3rd of cases and surround the opening of the major pancreatic duct. Relaxation of ampullaris
sphincter may promote reflux into the pancreatic duct.
The nerves.— Liver derives nerves from both sympathetic and parasympathetic systems. The sympathetic fibres are
derived from the sympathetic ganglion from T1 to T10. The sympathetic fibres are arranged in two plexuses — the ante
rior plexus surrounds the hepatic arteries, whereas the posterior plexus surrounds the portal vein and bile ducts. The
parasympathetic supply is derived from the right and left vagus nerves. The clinical importance of nerve supply of the
liver is not known, but sympathetic system is probably concerned with sensation of pain.
Lymphatics.— The lymphatic fluid starts from the perisinusoidal space of Disse and clefts of Mall. Gradually the
lymphatics join with each other and become larger and follow the blood vessels and bile ducts of the liver. The lymphatics
of the liver drain into the lymph nodes in the porta hepatis, coeliac group of lymph nodes and lymph nodes near the
inferior vena cava.
Functions of the liver.—
1. Secretion of bile.
2. Synthesis of major human plasma proteins. The liver is the only organ that produces serum
albumin and alpha-globulin. Albumin is the major protein in the human serum. Serum albumin level
is decreased in cirrhotic patients. Protein synthesis occurs mainly in the membrane-bound ribo
somes of the rough cndoplasmic reticulum.
3. Liver synthesises most of the urea in the body. Deamination of aminoacids occurs in the
liver with the formation of urea. Removal of ammonia thus takes place from the portal blood.
4. Liver plays an important role in glucose metabolism. It provides a continuous supply of
glucose for the central nervous system and red blood cells. 50% of glucose reaching the liver is
converted into glycogen. Glycogen is stored in the liver. This glycogen is broken down to glucose
which supplies the central venous system, red blood cells and other tissues such as muscle.
5. Fatty acids may also be synthesised from glucose, which are esterified and secreted as
very low density lipoproteins. During fasting fatty acids act as alternative to glucose as the
principal fuel for most tissues. Hepatic glycogen stores become almost nil within 48 hours of
fasting. Glucogenesis then begins using carbons from aminoacids from muscle proteins. En
ergy is also supplied by ketone bodies produced in the liver using fatty acids from the adipose
tissues.
6. So liver plays an important role in providing energy to the body.
7. The liver is the most active site of cholesterol and bile salt synthesis. Bile salt
synthesis is the major catabolic pathway of cholesterol in the liver. 7 a-hydroxylase is the
enzyme for conversion of cholesterol to bile salts. Cholesterol is also eliminated directly into
the bile.
8. Vitamin metabolism.— Liver plays an important role in uptake, storage and mobilisation of
vitamins. Vitamin D activation occurs in the liver where vitamin D3 is converted to 25-
hydroxycholecalciferol. Vitamin A is also stored in the liver. B vitamins pass through the portal
vein into the liver and there riboflavin, nicotinic acid, vitamin B12 and folic acid are preferentially
retained in the liver. Certain forms of B vitamins like thiamine, pyrophosphate and pyridoxin phos
phate are processed by the liver.
Vitamin K, which is essential for blood coagulation, is absorbed through the distal intestine
in presence of bile salts. So bile salt deficiency will result in insufficient absorption of
vitamin K.
9. Blood coagulation.— Liver plays an important role in blood coagulation. It synthesises

fibrinogen (factor I), prothrombin (factor II) and factors V, VII, VIII, IX, X, XI and XII.
The most valuable tests to assess liver-induced coagulation dysfunction is the prothrombin
time.
10. Liver plays an important role in the metabolism of blood and toxins.
11. Liver also plays some part in destruction of bacteria.
IMAGING OF THE LIVER
Over recent years major advances have taken place to improve the safety of liver surgery
and even planning of such surgery through preoperative imaging. The ideal choice of imaging
modality is determined by the likely liver pathology, available equipment and radiological
expertise.
Imaging modalities.— There are a few imaging modalities available for liver pathology —
(i) Ultrasound; (ii) Spiral CT; (iii) MRI including MRCP; (iv) ERCP; (v) PTC; (vi) Angiography;
(vii) Nuclear Medicine; (viii) Laparoscopy and Laparoscopic ultrasound.
ULTRASOUND.— It is the standard first-line investigation due to its safety and
availability. It gives an idea about presence of gallstones, bile duct dilatation and presence of
liver tumour. Doppler ultrasound provides an idea about blood flow in the hepatic artery,
portal vein and hepatic veins. It can be used as a screening test for primary liver tumour in a
high-risk population. Ultrasound can be used in guiding to take percutaneous biopsy from a
liver lesion.
COMPUTERISED TOMOGRAPHY.— Recently a multislice, triple-phase, spiral computerised
tomography is used in liver imaging. This technique provides fine details of liver lesion even in less
than 1 cm in diameter. Oral contrast enhancement allows visualisation of the stomach and duode
num in relation to liver hilum. The early phase of intravenous contrast vascular enhancement is
useful to detect small liver tumours due to the preferential arterial blood supply. Inflammatory liver
lesions exhibit rim enhancement with intravenous contrast, whereas common haemangioma shows
late venous enhancement. These investigations can also provide information about the presence of a
cystic lesion.
MAGNETIC RESONANCE IMAGING.— This is almost as effective as CT in majority of liver
diseases. However it offers several advantages. MRI can be offered to those patients where
contrast CT cannot be performed due to their allergy to the use of iodine-containing intravenous
contrast agent. MAGNETIC RESONANCE CHOLANGIOPANCREATOGRAPHY (MRCP) produces
excellent imaging of the biliary tract. Though it is a non-invasive technique and its image quality is
currently below that available from ERCP or PTC, but its standard is gradually improving. It is
particularly useful when ERCP has failed or is impossible due to previous surgery. Magnetic Reso
nance Angiography (MRA) similarly provides high-quality images of the hepatic artery or portal
vein without the need for arterial cannulation. It is used as an alternative to selective hepatic
angiography.
ENDOSCOPIC RETROGRADE CHOLANGIOPANCREATOGRAPHY (ERCP) — is particularly

performed when there is suggestion of the abnormality of the biliary tract or there is an obstructive
pattern detected from liver function tests. A preoperative check of coagulation is essential alongwith
prophylactic antibiotics. This is due to probable complications which include pancreatitis, cholan
gitis and bleeding or perforation of the duodenum while performing sphincterotomy. Endoluminal
ultrasound of the biliary tract is possible which provides additional information of hilar tumours.
Therapeutic use of ERCP includes balloon dilatation of stricture, endoprosthesis insertion, stone
retrieval and brush cytology of tumours.
PERCUTANEOUS TRANSHEPATIC CHOLANGIOGRAPHY (PTC).— It is indicated
where endoscopic cholangiography has failed or is impossible. It is also required in patients with
hilar bile duct tumours in whom endoscopic cholangiography fails to visualise the intrahepatic bile
duct.
ANGIOGRAPHY.— Selective visceral angiography is required prior to liver resection to visualise
the anatomy of the hepatic artery to the right and left sides of the liver and to confirm the patency of
the portal vein. It also provides information about the nature of a liver nodule, as primary liver
tumours possess a well-developed arterial blood supply. A few therapeutic advantages of angiogra
phy include embolisation of bleeding sites in the liver, in the treatment of liver tumours
(chemoembolisation) and to occlude arteriovenous malformations.
NUCLEAR MEDICINE SCANNING.— Radioisotope scanning provides diagnostic information
which may not be obtained by other imaging modalities. Technetium-99m (99mTc)-labelled radionu
clide which is administered intravenously is removed from the circulation by the liver and excreted
in the bile. Imaging with a gamma camera allows to know its uptake and excretion which is moni
tored in real time. These are required in case of a suspected biliary leak or biliary obstruction. It is
non-invasive screening test. A sulphur colloid liver scan can be particularly useful to confirm the
nature of a liver lesion, adenomas and haemangiomas by detecting Kupffer cell activity.
Fluorodeoxyglucose positron emission tomography (FDG-PET) is a new imaging modality that de
pends on the meagre uptake of glucose by cancerous tissue in comparison with benign or inflamma
tory tissue. At present it is mainly used to determine the nature of a mass lesion demonstrated in
another form of imaging.
LAPAROSCOPY AND LAPAROSCOPIC ULTRASOUND.— This is particularly useful for
staging hepatopancreatobiliary cancers. The lesions which could not be detected by conventional
imaging are mainly peritoneal metastasis and superficial liver tumours. These are well detected by
this investigation. Additional lesions are detected by laparoscopy in the range of 10% to 30%.
Laparoscopic ultrasound may increase this figure and provides additional information about liver
tumours.
INJURIES OF THE LIVER
Liver is the second intra-abdominal organ in frequency which is often involved by Injury. It is
only surpassed by the spleen. Liver injury mostly occurs from trauma either to the lower thoracic
region or to the upper abdomen. Blunt trauma may cause rupture of the liver. Penetrating wound
injuring the liver is gradually decreasing in frequency. Rupture of the liver may occur spontane
ously when it is pathological. Such rupture has been noted with primary carcinoma or with benign
hepatic adenoma. Obviously rupture of liver is gradually increasing in incidence due to increased
traffic accidents. Rupture of the right lobe is much more common than that of the left, as the latter
is more mobile and the former is larger and less mobile. Rupture is mostly seen
on the anterior and superior surfaces of the organ. Injury to liver should always be suspected whenever right
sided lower ribs are fractured.
Pathology. — Injury to liver can be classified into (a) transcapsular injury, (b) subcapsular injury and (c)
central injury, (a) When rupture ofthe liver has involved the Glisson’s capsule, blood and bile are extra vasate
into the peritoneal cavity and this is called a transcapsular injury, (b) When the Glisson’s capsule remains
intact blood is collected deep to the capsule and this is usually found on the superior surface of the organ and
is known as subcapsular injury, (c) Central rupture consists in interruption of the parenchyma of the liver.
Blunt trauma may be associated with hepatic parenchymal emboli to the right heart and lung causing death.
Clinical features.— When the capsule has been ruptured, there is extravasation of blood and bile and this
causes the main symptoms and signs. There is shock and patient may complain of right upper quadrant pain
of the abdomen. ON EXAMINATION one may find nothing abnormal except bruise over the right upper
quadrant of the abdomen. On palpation tenderness and rigidity over the liver area may be detected. Biliary
leakage may lead to bilTary peritonitis and subsequent abscess formation.
When the capsule remains intact, bleeding with in the liver may form a large haematoma. On palpation
tenderness and rigidity may be elicited overthe liverarea. Such haematoma may later become infected to form
an abscess. It may even rupture into the bile duct giving rise to haemobilia. Infarction of liver tissue due to
occlusion of blood supply may occur in blunt injury. Such infarction may also turn into an abscess.
Complications.— Obviously haemorrhage is the most important cause of death in injury to the liver.
Recurrent bleeding may occur secondary to necrosis. Two other conditions which may occur as complications
of injury to the liver. These are :
1. Hepatorenal syndrome.—Damaged livercells released into the circulation may produce a toxin which
has the capability to destroy kidney cells.
2. Haematobilia.— This condition occurs only when a communication has existed between a blood
vessel and the biliary tree. It may occur in subcapsular injury and central injury. This condition may occur
within a few days after injury or more commonly after a period of even a few weeks. This is revealed as
gastrointestinal haemorrhage — melaena is more frequent than haematemesis. Jaundice, either mild or severe
may be present in a few cases.
Abdominal injury and subsequent colicky pain and gastrointestinal haemorrhage in the form of melaena
and/or haematemesis should be suspected to be a case of haematobilia.
Diagnosis is confirmed by angiography.
Treatment is resection of the lesion, debridement and ligation of the communicating artery.
Special Investigations.— 1. BLOOD EXAMINATION.— Increased leucocyte count is almost always
present and even more frequent than reduced haemoglobin. Serum bilirubin level may be increased on 3rd or
4th day.
2. X-RAY.— Straight X-ray ofthe abdomen may reveal evidence of fluid in the peritoneum. Widening
of the gap between the ascending colon and the right peritoneal line indicating blood in the right paracolic
gutter. On screening raised and rather immobile right cupola of the diaphragm is also diagnostic.
3. ULTRASONOGRAPHY may indicate presence of intraperitoneal fluid. This may also indicate
subcapsular haemorrhage in the liver.
4. LIVER SCAN may be helpful in detecting subcapsular haemorrhage.
5. COELIAC ANGIOGRAPHY may precisely define hepatic rupture and in suspected cases will
distinguish between liver rupture and splenic rupture.
6. PARACENTESIS, though useful ifblood canbe detected inaspiration, yet the cause of haemoperitoneum
cannot be assessed. Negative result cannot exclude rupture of liver.
TREATMENT.— Haemorrhagic shock is first corrected with blood and intravenous fluid. The patient
should be taken quickly to the operation theatre for laparotomy.
OPERATION.— The patient is placed for right thoracoabdominal incision. In the beginning only the
abdomen is opened through right paramedian incision. Surgical procedure is directed to control the bleeding
by ligating the vessels in the wall and in the depth of the tear and removal of necrotic devitalised tissue.
Debridement of dead liver tissue is a must since failure of this will favour infection and secondary
haemorrhage.
In case of penetrating wounds there will be simple tear and sutures are introduced parallel to the wound
and then mattress sutures are used to coapt the parallel sutures. This type of liver suturing is also effective i
case of simple nonlacerated liver injury. It is better to use omentum to be incorporated in the sutures, which
will act as a pack.
In case of major liver injury where it is difficult to control haemorrhage, Pringle manoeuvre should be
adopted. In this manoeuvre the vascular inflow to the liver is blocked by occluding the right free margin of
the lesser omentum through which the hepatic artery and portal vein pass. The extensive liver injury requir
sublobar debridement with as much tissue preserved as possible. But all the devitalised tissue should be
removed. With extensive haematoma formation and rupture of liver tissue, hepatic resection may be require
Such resection should be limited to segmental resection.
If it becomes difficult to control bleeding, packs may be used, but it is better to avoid if possible. In these
cases a ‘second look’ operation allows further debridement of nonviable tissues and to control more arterial
bleeding.
External drainage should be carried out in almost all cases to prevent biliary peritonitis, as leakage of bile
occurs from tom ducts. T-tube drainage of the common bile duct does not offer any extra advantage and ma
increase complication rate.
Portal vein or hepatic artery injury is not so dangerous as ligation of hepatic artery does not cause major
hepatic ischaemia or disfunction and collateral supply becomes apparent within 4 hours. Portal vein injury i
rare and can be managed by end-to-end anastomosis or lateral venorrhaphy or graft interposition. But most
dreadful condition is hepatic vein injury. Most of these patients die from uncontrollable haemorrhage either
before operation or in the operation table. Control of bleeding is only possible by occluding the porta hepati
(thus inflow is blocked) and insertinga catheter via either the inferoir vena cava (from below) or the right atr
(from above) in such a fashion that umbilical tapes may be placed above and below the area of the hepatic
veins.
HEPATIC ABSCESSES
Mainly two types of hepatic abscesses are seen — 1. By pyogenic organism c&usingpyogenic absess and
2. By Entamoeba histolytica causing amoebic liver abscess.
PYOGENIC LIVER ABSCESS

Aetiology.— Pyogenic liver abscess may result from : (1) Via portal vein as occurs in appendicitis or
diverticulitis. (2) Via the biliary tree (ascending biliary infection) as in cholangitis. (3) Via hepatic artery as
in sepsis or generalised septicaemia. (4) Via direct extension from infection in the neighbourhood such as
advanced cholecystitis, subhepatic abscess etc. (5) Following hepatic trauma. Nowadays the most frequent
cause has been cholangitis secondary to biliary calculi or some obstruction of the common bile duct (mostly
carcinomatous). The second most common cause is from generalised septicaemia. Liver abscess from portal
venous root is becoming rare. In a few cases no apparent cause of hepatic abscess has been found. These cases
are not very negligible and has been reported in various series from 2 to 20%. These are called cryptogenic
liver abscess.
The most common pathogen discovered from liver abscess is Escherichia coli which accounts for about
l/3rd of causative cultures. The organism is mostly found in abscesses caused by ascending biliary tract
infection and infection along the portal venous route. Staphylococcus aureus and haemolytic streptococcus
have been found mostly from abscesses due to systemic infection. Bacteroids and other anaerobes are gradu
more often seen in pyogenic abscess of liver. Proteus and Klebsiella are found in about 10% of cases.
Pyogenic abscesses may be solitary, multilocular and multiple. Single and multiple abscesses occur in
equal frequency. Single abscess is usually found in the right lobe.
Clinical features.— 1. Fever is the most important and common symptom of this condition. Fever is
usually hectic, showing a ‘picket fence’ type of pattern. Fever is frequently associated with chill and sweating
2. Pain is the second symptom and is rather late in appearance. Continuous pain in the right subcostal
area or in the epigastrium is noted. Pain may radiate to the right flank. Diaphragmatic irritation may lead to
the referral pain to the right shoulder or right side of the neck.
3. Nausea, vomitingand anorexia occur with varied frequency. It is more common in case of large single
abscess. Jaundice may appear though relatively uncommon. On palpation liver enlargement has been noted
in half the cases. Liver tenderness is also present in half the cases.
Special Investigations.— 1. Blood examination. — Leucocytosis is usually present. The white blood count
ranges between 12,000 and 18,000. Blood culture may be positive to find out becteria in approximately l/3rd
of patients. This is usually positive in case of abscesses secondary to systemic septicaemia. Hypoalbuminemia
is also seen. Alkaline phosphatase level is often increased. Transaminases and lactic dehydrogenase (LDH)
are also seen to be elevated in this condition. Bilirubin is normal in 90% of patients.
2. Radiologic Investigation.— Chest X-ray reveals elevation and restriction of movement of the right
cupola of the diaphragm. The right cardiophrenic angle is obliterated. Slight effusion or atelectasis is not
uncommon.
3. Barium enema X-ray may be performed to exclude occult diverticulitis.
4.Ultrasonography.— Echography should be done as the initial test in confusing cases followed by other
imaging technique for accurate localisation of the abscess. Ultrasonography not only diagnoses and indicates
the position of the abscess, but it also indicates the stage of resolution of the abscess with medical therapy.
5. Liver scan.— It has limitations as it fails to
differentiate between solid and cystic structures. It also
cannot detect lesions less than 2 cm in diameter. Yet in
certain series it is claimed to be accurate in 80 to 90%
of cases. Liver scan is an acceptable screening test in
evaluation of a patient with fever of unknown origin.
Computed tomography seems to be better than
radionuclide studies for this purpose.
6. Other radionuclide imaging techniques.—
Gallium scanning, which detects uptake by
inflammatory tissue may be used, but whether it is more
informative than the usual imaging technique is yet to
be proved.
7. Computed tomography (CT scan).— This is
recommended to be the first method for detection of
suspected hepatic abscess. Its accuracy has beenclaimed
to be more than 95%. The abscess may vary in appea ranee
Flg.45.2.— Radioisotope hepatogram showing static from smooth margins, fluid filled cavities to poorly
gamma camera scan 60 minutes after Injection showingdefined masses. A dense rim around the abscess may be
uptake of the Isotope by the normal liver. Excess
concentration In the gallbladder and excretion Into thefound after contrast enhancement. At the end it may be
gut are noticed. said that if the CT scan is normal, liver abscess can be
excluded, but a positive CT scan may not be definite to
diagnose an abscess.
8. Fine needle aspiration biopsy (FNAB).— Its main advantage may be taken by using it in case of CT
diagnosed suspected liver abscess. It is safe. But it should not be used in case of hydatid cyst where there is
risk of anaphylaxis and dissemination. So if the cyst wall is calcified in CTscan or the patient is from the area
where hydatid disease is endemic, aspiration should be deferred.

After aspiration the fluid should be cultured for organisms.
9. Angiography.— CT scan has almost replaced this mode of investigation in diagnosing liver abscess
Its ability remains in only doubtful cases where metastatic disease or vascular lesion cannot be excluded w
certainty.
TREATMENT. — Management of pyogenic liver abscess is based on two principal lines — (a) antibioti
therapy and (b) surgical drainage.
(a) ANTIBIOTIC THERAPY.— This therapy is greatly dependent upon the results of culture obtaine
by percutaneous needle aspiration or at the time of surgical drainage. But antibiotic should be started bef
surgical intervention and it should be directed at commonly encountered pathogens — gram negative bac
and enteric anaerobes. Intravenous administration of aminoglycoside and metronidazole generally cover
organisms. In addition ampicillin or penicillin should be considered in patients with generalised sepsis.
Clindamycin is also quite effective, similarly is the 3rd generation cephalosporin, though these are quite
expensive. Whatever antibiotics are chosen, they should be modified on the basis of the culture results.
How long should be the antibiotic therapy? If a single abscess is drained percutaneously or open surgic
antibiotic treatment should be continued for 4 to 8 weeks. When multiple abscesses are present and have
drained, antibiotics should be given for 6 to 8 weeks. When multiple abscesses could not be drained antib
therapy should be continued for 8 to 12 weeks.
(b) SURGICAL DRAINAGE.— This is particularly indicated for solitary abscess and for large multip
abscesses. The abscesses may be drained percutaneously under ultrasonography or CT control. About 80%
success has been claimed by this technique. This technique should definitely be adoped in whom there is
evidence of biliary tract or gastrointestinal causative factors. In othercases, the safest approach is open surg
drainage.
The route of surgical drainage depends on the positionof the abscess. It may be transthoracic (transpleur
or transabdominal (transperitoneal). The transperitoneal approach has two clear advantages — (i) it gives a
clear view to the liver to detect any unsuspected abscesses and (ii) it gives access to the biliary tree or
gastrointestinal tract to exclude any cause there. The disadvantage of transperitoneal approach is that the
abscesses situated in the superior or posterior surface are difficult to drain.
In the last mentioned cases either extraperitoneal or transpleural technique is the best. Extraperitoneal
approach may be done anteriorly or posteriorly depending on the size of the abscess. If the abscess is in the
anterior or anteroinferior surface of the liver, the incision is made anteriorly just beneath and parallel to th
costal margin. The muscles are incised, so is the transversalis fascia. The parietal peritoneumis reflected d
from the inferior surface of the diaphragm. The abscess is reached and drained extraperitoneally.
If the abscess is posteriorly placed, skin incision is made over the 12th rib. The rib is resected
subperiosteally. A transverse incision is then made through the bed of 12th rib. The parietal peritoneum is
reflected from the inferior surface ofthe diaphragm. Thus the abscess is reached and drained extraperiton
Transpleural approach has been criticised for causing contamination of the pleural cavity and chance of
empyema or other pleuropulmonary complications. Transthoracic approach seems to have no advantage
the extraperitoneal approach for posterior liver abscesses.
Prognosis.—The mortality rate for undrained hepatic abscess may reach 100%. So careful managemen
is absolutely essential. Response to treatment should be closely assessed by clinical, laboratory and radiol
investigations. Prior to stopping antibiotic therapy CT scan should be repeated to confirm resolution of th
abscess. It must be remembered that patient should be observed carefully for 48 hours after cessation of
antibiotics in order to detect recurrent fever.
AMOEBIC ABSCESS
Amoebic abscess is a complication of amoebic dysentery.
Pathology.— Entamoeba histolytica pass from the colonic lesion via the portal vein into the liver. Usuall
the upper and posterior portions of the right lobe are affected. Actually the disease can be divided into two
stages — (1) Amoebic hepatitis and (2) Amoebic abscess.
Amoebic hepatitis is a type of diffuse involvement of the liver characterised by increased lymphocyte,
mononuclear infiltration, fatty changes and lysis of hepatic cells. But the exact pathology of amoebic hepati
has not yet been clear. It is still questioned that whether diffuse hepatitis at all takes place or not.
It therefore seems more or less clear that the only proven amoebic lesion of the liver is the abscess. In the
beginning when Entamoeba enter the liver, liver infection begins with intrahepatic portal thrombosis and
infarction. The cytolytic activity starts and leads to liquefaction of the surrounding stromal and parenchyma
structures. Coalescence of such small necrotic areas results in the formation of a large single abscess. As has
been described earlier the usual location of amoebic abscess is in the right lobe. In 30% of cases there may
be more than one abscess.
Gross appearance.— The liver is usually enlarged and there may be adhesions to the diaphragm. The
liquefied material within the abscess is characteristically viscid and semitransparent. The content is a mixtu
of red blood cells, leucocytes, broken down liver cells and this looks chocolate or reddish-brown coloured.
Such pus of amoebic abscess is variously described as ‘chocolate sauce’ or ‘anchovy sauce’. In early cases
the wall of the abscess is thin with little fibrosis. But in older abscess it has a fibrous capsule which demarca
it from the normal liver. The earlier the stage, more likely that the amoebae will be found. But in later stages
these amoebae are not so easy to be detected. These amoebae are present not in the central necrotic zone but
near the wall adjacent to the fibrous capsule. From aspirated material amoebae are found in only 20% to 40%
of cases.
So microscopically three zones are recognised — a central necrotic zone, a middle zone with destruction
of parenchymal cells and an outer zone which is almost adjacent to the fibrous capsule and in which amoeb
may be demonstrated.
Secondary infection is seen in about half the cases. Staphylococci, Streptococci and Esch. coli have been
indentified in the amoebic pus. Otherwise the pus is sterile.
Complications.— Prognosis of amoebic abscess is much better than pyogenic abscess. However if the
abscess remains untreated, it may burst.
It may burst into (a) right pleural cavity, (b) right lung, (c) peritoneal cavity. The abscess when bursts int
the pleural cavity empyema may result. When it bursts into the lung it may cause bronchohepatic fistula, lu
abscess or pneumonia. Single large abscess of the left lobe may rupture into the peritoneal cavity or even to
the pericardium. Amoebic peritonitis carries a mortality rate of 20% even with early surgical intervention.
Extension of abscess into the pericardium is more dangerous. Amoebic abscess rarely may extend to the
kidney.
Clinical features.—Amoebic abscess develops after an attack of amoebic dysentery. This may occur soon
after the attack or may take a long time to appear after the attack. It had even occurred after many months o
amoebic dysentery and even a few years after an attack of amoebic dysentery. Amoebic abscess mav develop
even in a carrier, who has not shown definite symptoms and signs of amoebic dysentery. Amoebic abscess h
also appeared in persons who had mild diarrhoea not diagnosed as typical amoebic dysentery and conseque
no specific treatment of that condition was given.
Though anaemia and loss of weight are first to appear, yet the typical symptoms of amoebic abscess are
(i) fever and (ii) liver pain.
(i) Fever may shoot upto 39° C or even more particularly at night. But unless complicated by secondary
infection the temperature is usually less than that of pyogenic abscess. Fever is usually accompanied by chill
and sweating.
(ii) Pain is present in nearly 90% of patients. The site ofpainis usually related to the location of the hepat
abscess. Pain is usually felt over the right lower intercostal spaces. There may be slight bulging and pitting
oedema. Superior surface abscesses may cause pain referred to the right shoulder. Abscesses in the bare area
ofthe liver which is not in contact with peritoneum may remain painless forquite sometime. Left lobe absces
present as pain in the epigastric region.
Enlargement of liver may be demonstrated. Tender hepatomegaly is often seen in this condition.
Tenderness and rigidity may be felt just below the right costal margin. In case of left lobe liver there may be
tender swelling in the epigastric region.
Unfortunately only '/2or V3 rd of patients offera history of previous diarrhoea. Clinical jaundice is relativ
rare but may be seen in a few cases. Abnormal pulmonary signs may also be looked for.
Special Investigations.— 1 .Blood examination will reveal leucocytosis in early cases. In chronic cases
anaemia may be revealed.
2. Serological tests to detect antibodies to E.histolytica are essential to evaluate a case of suspected liver
abscess. Indirect haemagglutination and complement fixation tests are useful in this regard. Antibody titres
are higher in patients with amoebic abscess than in those with amoebic dysentery. About 95% accuracy has
been claimed in these tests. One great advantage of such test is that negative serologic tests exclude amoebic
abscess as a diagnostic possibility.
3. Examination of stool for amoebae is not very diagnostic. Though in certain series they found amoebae
in the stool in about 45% of cases, yet these are only found in less than 20% of cases.
4. Liver function tests are also not helpful in establishing the diagnosis.
5.Sigmoidoscopy may reveal characteristic amoebic ulcers which will give a clue to the causative lesion.
6. Radiography often reveals elevation and fixation of the right cupola of the diaphragm.
7. Diagnosis is 100% confirmed by aspiration of the liver abscess. The ‘anchovy sauce’ pus is quite
diagnostic. Occasionally the abscess content may be creamy white even though there is no secondary bacter
infection. Only in these cases definite diagnosis remains in doubt. Amoebae may be demonstrated in the
aspirate in V3rd of the patients.
Treatment.— Management of amoebic abscess is mainly drug therapy with amoebicidal drugs. A few
abscesses, particularly the large ones, may require needle aspiration.
AMOEBICIDAL DRUG should be tried first. Metronidazole which acts on both the intestinal and hepatic
amoebiasis is the drug of choice. The recommended dose of Metronidazole in amoebic liver abscess is 500
mg or 750 mg orally 3 times daily for 5 to 10 days. Alternatives to metronidazole include Emetine,
Dehydroemetine and Chloroquine. Emetine and dehydroemetine are cardiotoxic. Metronidazole has fewer
side effects. In many cases even after a course of metronidazole patients continue to pass cysts in their stools
In these cases diidohydroxyquinolone 600 mg orally daily for 10 days or diloxanide furoate 500 mg orally 3
times daily for 10 days should be given to clear intestinal amoebiasis.
NEEDLE ASPIRATION is only employed inselected cases. Though inareas where amoebiasis is endemic
aspiration of abscess is done as a routine procedure without radiologic imaging. Since most patients respond
to medical management, indications for aspriation are—(i) persistence of clinical features of amoebic abscess
following a course of amoebicidal drugs; (ii) Clinical or radiographic evidence of presence of hepatic abscess
Drug therapy should be instituted several days before aspiration. No drug should be injected directly into th
abscess cavity.
Technique of aspiration.— Aspiration should be conducted in the operation theatre. A long needle with
wide bore is selected. The preferred route is through the 9th or 10th interspace between the anterior and
posterior axillary lines. The needle may better be introduced through the guidance of CT or ultrasound.
Surgical drainage of amoebic abscess carries great morbidity and mortality. It should be avoided. It is onl
indicated (i) when the abscess is secondarily infected as evident by needle aspiration; (ii) Amoebic peritoniti
requires surgical drainage.
IN NUTSHELL the treatment of amoebic liver abscess is mainly drug therapy. Aspiration of the abscess
is only required in case of failures of medical therapy and persistence of such abscess. There is hardly any pl
of open surgical drainage except when the abscess is secondarily infected and that there is amoebic peritonit
CYSTS OF THE LIVER

Cysts of the liver are generally benign. They may be solitary or multiple. They may be unilocular or
multilocular. The various types of cysts seen in the liver are: (i) Hydatid cyst; (ii) Retention cysts—(a) Solitar
cysts and (b) Multiple cysts (polycystic disease); (iii) Lymphatic cysts; (iv) Endothelial cysts ; (v) Blood and
degenerative cyst; (vi) Dermoid cyst; (vii) Cystoadenomas. Cysts of the liver can be classified into two major
groups — A. Parasitic cyst e.g. hydatid cyst and B. Non-parasitic cysts which include the other varieties
described above.
NON-PARASITIC CYSTS
Pathology.— Single nonparasitic cysts are usually situated on the anteroinferior surface of the right lobe
of the liver. The cyst contains a clear watery yellowish brown material. Polycystic disease of the liver shows
a honeycomb appearance with multiple cavities. These may be continued to one lobe or involve the whole of
liver. Polycystic disease of the liver is frequently associated with polycystic disease of the kidney.
Clinical features.— These cysts are usually asymptomatic. Swelling is the only complaint, which is
painless. Only in case of intracystic haemorrhage or intraperitoneal rupture the patient complains of pain.
Jaundice is rare. Physical examination may reveal the lump which is characteristically associated with the
liver. Liver function tests hardly give any indication to diagnosis. CT scan, ultrasonography and angiography
will give clue to the diagnosis.
Treatment.—Though excision of cyst is the treatment of choice, yet one has to be very selective regarding
this. As the cysts are usually
asymptomatic only those cysts should
be excised which are easily approachable
and techniqually possible. Excision of a
large cyst extending deep into the
parenchyma of the liver may be
dangerous. If the cyst contents are sterile
and do not contain bile, unroofing of the
cyst may be justified. If the cyst contains
bile, unroofing should be accompanied
with Roux-en-Y jejunum anastomosis.
Incase of polycystic disease excision
is contraindicated.
HYDATID CYSTS
Pathology.— This condition is
caused by a parasite called Echinococcus
Granulosus. Unilocular cyst is almost
always caused by E.granulosus, while
the alveolar type may be caused by
Echinococcus multilocularis.
Dogs are the chief mediators of hydatid disease. Animals, particularly sheep, are infected by eating contaminated grass (as
eggs of the Echinococcus are discharged through the faeces of the dog and this contaminates the grass). Human being is also alm
similarly affected as the dog either (i) by taking uncooked vegetables contaminated with infected canine faeces or (ii) by direct
handling of the infected dogs or (iii) by allowing the dog to feed from the same dish. Human infection does not occur through
49
contaminated water. This is the mode of infection in case of human being. Animal like sheep, pig, horse or goat are considered
to be intermediate hosts. The eggs of echinococcus after being swallowed by the intermediate hosts behave in the same pattern
as after being swallowed by human beings. The only difference is that once the hydatid cyst is formed in the liver or in the lun
the intermediate hosts are eaten by the definitive host like the dog. The cycle continues. The life cycle of the eggs of echinococc
in the human beings is exactly the same as that occurs in the intermediate hosts. But human being is not designated as the
intermediate host, the reason being that the definitive host like dog does not get an opportunity to eat human being to contin
the cycle. So intermediate host like sheep, pig or cattle is essential to continue the cycle and hence hydatid disease is mainly
in the sheep rearing areas.
Morphology.— Adult worm is a small tape worm measuring 3 to 6 mm in length. It comprises of (i) a head or scolex, (ii) neck
and (iii) strobila consisting of three segments (the first segment is immature, the second one is mature and the last one is grav
The egg is ovoid in shape and contains a hexacanth embryo with three pairs of hooks. The egg is infective to man and the
intermediate hosts like sheep and other herbivorous animals.
Life cycle.— The eggs are discharged with the faeces of the definitive hosts. These are swallowed by the intermediate hosts
and human beings. In the duodenum the hexacanth embryos are hatched out. The embryos bore their ways through the intest
wall and enter the radicles pf the portal vein in about 8 hours. The embryos are carried to the liver by the portal vein and are
in the sinusoidal capillaries (first filter). Some of the embryos may pass through the hepatic capillaries and enter the pulmonar
circulation ( second filter). A few embryos may pass the pulmonary embryos and enter the general blood stream and lodge in t
various other organs.
Wherever the embryo settles, it forms the hydatid cyst. From the inner sideof the cyst, brood capsules with a number of s
are developed. A fully developed scolex is an endproduct and its presence inside the hydatid cyst is a sign of complete biologic
development. These fertile hydatids are eaten by definitive hosts like dog and then infected. The adult worms develop in the
intestine of the definitive host within 6 to 7 weeks. The adult worm discharges eggs through the faeces ofthe definitive host. T
the cycle is repeated.
Hydatid cyst.— This cyst is formed by the embryo. The cyst consists of three layers — (i) Adventitia
consisting of fibrous tissue and is grey in colour, it is blended immediately with the liver; (ii) The laminated
membrane (ectocyst) is formed by the parasitic cells. To the naked eye the ectocyst has the appearance of the
white of a hard boiled egg. It is elastic and when incised or ruptured it curies on itself exposing the inner lay
(iii) Inner germinal layer (endocyst) is cellular and consists of a number of nuclei embedded in a protoplasm
mass. It is very thin. It is the vital layer of the cyst and gives rise to (a) brood capsule with scolices, (b) secret
hydatid fluid and (c) forms the outer layer.
Brood capsules sprout from the germinal layer. It is at first spherical, but soon becomes vacuolated and
transformed into a vesicle. The scolices, numbering 5 to 20 or more develop within these brood capsules. A
fully developed scolex presents the future head of the adult worm. The hydatid cyst when ingested by the
definitive host the scolices fix at the small intestine with success and gradually form into the adult worms in
the intestine of the definitive host.
COMPOSITION OF HYDATID FLUID: It is clear and colourless fluid with specific gravity 1005 to 1010.
The reaction is probably slightly alkaline. It contains sodium chloride, sodium sulphate, sodium phosphate
and sodium and calcium salts of succinic acid. It is antigenic and highly toxic, as it gives rise to anaphylactic
symptoms. It may contain hydatid sand which is nothing but granular deposit and consists of liberated broo
capsules and free scolices.
RATE OF GROWTH OF HYDATID CYST in man is quite slow. At the end of one year it is approximately
5 cm in diameter and at this time the brood capsules and scolices begin to appear.
Clinical features.— Approximately 80% of hydatid cysts are initially single and in the right lobe. In only
l/4th of the cases there are multiple cysts. Hydatid cyst remains symptomless for quite a long time. When
symptoms occur, they are usually caused by pressure to the adjacent organs. A visible and palpable swelling
in the upper abdomen can be discovered on careful examination. Pain is sometimes caused by pressure on th
adjacent organs. Once a palpable mass is detected, it is found to be connected with liver and is cystic. So call
‘hydatid thrill’ and fremitus may be elicited. Jaundice and ascites are uncommon. When complicated with
secondary infection fever with chill may occur. When it ruptures in the biliary tree, biliary colic, jaundice and
urticaria may be noted. Intraperitoneal rupture will cause abdominal and anaphylactic shock. Intrathoracic
iupture may be associated with shoulder pain and cough which contains blood and bile. Expectoration may
contain membranes. Presence of hydatid membrane inthe vomitus (hydatidemesis)orinthe stool (hydatidenter
may occur very rarely.
Alveolar hydatid cyst occurs from ingestion of echinococcus multilocularis. The chief character of the
lesion is the absence of the capsule of the hydatid cyst and that is why it shows tendency to metastasise. Most
of the alveolar hydatid cysts (multilocular hydatid cyst) are sterile.
Complications.— 1. Intrabiliary rupture is the commonest complication and occurs in 5 to 10% of cases.
2. Suppuration is the second commonest complication caused by the bacteria from the biliary tract. This
turns the hydatid cyst into a pyogenic abscess with death of the parasites.
3. Intraperitoneal rupture will cause contamination of peritoneum with hydatid fluid, brood capsule and
scolices. The scolices may survive and produce new cyst (secondary echinococcosis) of the peritoneum.
4. Cyst in the superior portion of the liver
may push into the pleural cavity, with the
formation of empyema and bronchopleural
fistula. It may rupture into the lung. It must be
remembered that lung is also a primary site
of the hydatid cyst. Such secondary invasion
can be determined by presence of bile pigment
inside the cyst.
Special Investigations.— 1. BLOOD
EXAMINATION will reveal eosinophilia of
20 to 25%. Mildly elevated liver function
tests may be noted.
2. Of the SEROLOGIC TESTS the indirect
haemagglutination test, Casoni’s test and
complement fixation will be positive.
Casoni’s test.-— Intradermal injection of
Flg.45.4.— Straight X-ray of the abdomen showing 0.2 ml of fresh sterile hydatid fluid produces
a calcified hydatid cyst.
a wheal of 5 cm in diameter within half an
hour. This is a quite sensitive test and becomes positive in majority of cases. Problems with the Casoni skin
test are that it may cause false positive result and may produce anaphylaxis.
3. RADIOGRAPH YCALLY calcification of the cyst wall may be visualised in 50% of cases.
4. CT SCAN furnishes useful information.
5. ULTRASONOGRAPHY and ARTERIOGRAPHY are also diagnostic of hydatid cyst. The finding
of daughter cyst or hydatid sand on ultrasonography and CT scan help to differentiate this cyst from pyogenic
or amoebic liver abscess. This differentiation is extremely essentia] as percutaneous needle aspiration, which
is the treatment of pyogenic and amoebic liver abscess, will cause spillage and spread of the cyst to cause
disaster.
Treatment.— Treatment is primarily SURGICAL (excision). After exploring the abdomen it is carefully
packed with mops around the cyst to reduce the risk of peritoneal contamination. Chlorhexidine, 80% alcohol
and 0.5% cetrimide may by instilled into the cyst cavity. This will destroy 80% to 90% of scolices. Excision
of the hydatid cyst using the natural cleavage plane which exists between the germinative layer and the
adventitia is carried out. Adventitial layer may also be excised. In case of large and multiple cysts partial
hepatectomy may be performed. When a hepatic cavity remains after excision of the hydatid cyst, it should
be treated by either (i) suturing and closure of the cavity, (ii) omentoplasty or (iii) marsupialization and
drainage. Omentoplasty is the choice of majority surgeons.
Alveolar hydatid cyst by echinococcus multilocularis is fatal though extensive hepatic resection should
be tried and has been successful in a few cases.
NEOPLASMS OF THE LIVER

BENIGN NEOPLASMS
Haemangioma.— This benign tumour is most common among all the benign tumours in the liver. It is
usually a cavernous haemangioma. Liver is the most commonly affected of all the abdominal organs. This
tumour is more commonly seen in females than in males (5:1). Hormonal influence has been incriminated t
explain the difference of sex incidence. Haemangioma is usually solitary. Haemangioma is often associated
with foecal nodular hyperplasia and cysts of liver and pancreas.
Haemangioma is usually symptomless and is only found at necropsy or incidentally at operation. Only
when it becomes large enough, it may cause
a lump. The compressibility of the tumour
and bruit heard on the lump can make the
' -. diagnosis possible. Ultrasonography, CT scan
or hepatic arteriography are helpful to make
IHP*1 diagnosis with confirmation. Obviously
needle biopsy is contraindicated.
COMPLICATIONS.— (i) Major
Vv complication is rupture with intraperitoneal
haemorrhage, which is more often seen in
children and pregnant women. Obviously the
■Hk condition is fatal and the mortality rate is
llk^l jpPpI 9 a^°ut80%.
: ‘ ( i i ) Large tumours in infants may b
associated with arteriovenous shunts which
cause congestive cardiac failure.
. MANAGEMENT.— There is no place of
biopsy lest uncontrollablehaemorrhage may
risk the life of the patient. Large or
Fig. 45.5.—CT scan of the abdomen showing hepatic symptomatic lesion in any age group may
haemangioma A) and pheochromocytoma (B). . . TT,, .. . * .
require resection. When there is congestive
cardiac failure steroids may be tried to regress the swelling. Hepatic artery ligation may help the patient to
reverse the cardiac failure. In case of intraperitoneal rupture the treatment is resection of the tumour. Radia
therapy using 2000 rads in 15 days in adults may significantly reduce the size of the tumour and this is often
tried as the first line of treatment.
Adenomas.— Hepatic adenomas are composed of hepatocytes. These are usually solitary. The main
complications are haemorrhage and necrosis causing rupture. Microscopically the adenomas are composed
of conglomerated cords of hepatocytes that have vacuolated borders. The centres of the adenomas may
undergo degenerative changes. Adenomas are abundantly supplied with blood.
FOCAL NODULAR HYPERPLASIA have often been considered alongwith adenoma. But this lesion
does notproduce symptoms or does not undergo complications such as haemorrhage or ru ptu re. Microsco
this lesion consists ofagglomeration of cells of slightly different in colour and gradually blend with the norm
hepatic parenchyma at the periphery. There is no true capsule. The basic cell structure of this lesion is simil
to that of normal hepatocyte.
Both adenoma and focal nodular hyperplasia occur primarily in young women. Recently these lesions h
brought attention since a possible relationship has been established between oral contraceptives and these
lesions. Conclusive evidence cannot be drawn at this stage that oral contraceptives in fact cause this lesion.
However almost all the patients who present with intraperitoneal haemorrhage as a consequence of ruptur
of hepatic adenoma were taking oral contraceptives. The explanation may be that the patients who stop usi
oral contraceptives and become pregnant are at considerable risk for tumour rupture and haemorrhage.
CLINICAL FEATURES.— Adenomas like other benign tumours of the liver are usually symptomless
until complicated by haemorrhage and rupture. A few patients have complained of pain or a lump in the
abdomen.
SPECIAL INVESTIGATION.— CT scan and arteriography give conclusive proof to the diagnosis.
MANAGEMENT.— Patients who are on contraceptives should be advised to stop taking contraceptives.
Regression of the lesion has been noticed following cessation of contraceptives. If the lesion has not ruptured
operation can be avoided, since there is no evidence that this lesion becomes malignant.
Other benign solid tumours.—The othertumours which are found in liver include hamartomas, fibromas,
leiomyomas, lipomas, myxomas, carcinoid tumour, cystadenomas and teratomas. Mesenchymal hamartomas
are rare but they grow to an extremely large size in infants. Treatment is surgical excision. Carcinoids are also
rare in liverand are usually associated with carcinoid syndromes. Biliary cystadenomas are also rare and may
cause pain and extrahepatic biliary obstruction.
MALIGNANT TUMOURS
In comparison to the metastatic tumours, primary malignant tumours are quite rare. PRIMARY
MALIGNANT TUMOURS are mainly of two varieties — 1. Hepatocarcinoma and 2. Cholangiocarcinoma.
Hepatocarcinoma.— Hepatoma is more commonly seen in south-east Asia, Japan, the Pacific Islands,
Greece and Italy. The disease is rare in Western Europe and North America. Whereas it is quite common in
Africa — particularly in Nigeria and Mozambique and China. Chinese may even be affected after they change
their habitation.
Hepatomas are about eight times more common in men than in women.
AETIOLOGY.— Like other carcinomas aetiology is not clear. However the predisposing factors are —
(i) hepatitis B; (ii) alcoholic cirrhosis (post necrotic cirrhosis) is the type most commonly preceding
hepatocellular carcinoma; cirrhosis is present in 60% of cases. On the other hand hepatoma occurs 5% of
cirrhotic patients; (iii) haemochromatosis; (iv) parasitic infestation with the liver fluke Clonorchis sinensis
(more commonly seen in China and Japan) (this has also been considered a factor in the development of
cholangiocarcinoma); (v) low protein intake; (vi) alpha-antitrypsin deficiency; (vii) blood group B.
The risk of hepatocellular carcinoma with oral contraceptive is not clear, though a number of such tumour
have been reported to have started within benign adenomas in oral contraceptives users.
Alphatoxins, products of the fungus Aspergillus flavus, which is found in wheat, soyabins, corn, oats are
the principal diets of the Africans and Asian communities with high incidence of hepatocellular carcinoma.
Hense alphatoxin has been incriminated as potent carcinogens.
CLINICAL FEATURES.— The most common symptoms are weakness, malaise, upper abdominal pain
and weight loss. These symptoms are present in 80% of cases. AbdominI pain is present in about ha If the case
The pain is dull and persistent. Occasionally due to rupture ofthe tumour or necrotic erosion of a blood vessel
sudden pain may be complained of. Jaundice is present in l/3rd of the cases. Hepatomegaly or enlargement
of the liver is the only diagnostic criteria clinically. The liver is hard, irregular but not tender. Arterial bruit
may be heard over the liver. Splenic enlargement is present in l/3rd the of cases. There may be other signs
of portal hypertension in also about 1/3 rd of cases. Ascites develops in one-half to three-quarters of patients.
The most common presenting symptom is abdominal lump, next is pain and next is weight loss.
SPECIAL INVESTIGATIONS.— 1. Blood examination.— Erythrocytosis has been associated with
hepa tocellular carcinoma. Amongthe liver function tests, BSP and alkaline phosphatase are consistently high.
A high alkaline phosphatase level in absence of bone disease and obstructive jaundice is considered
presumptive evidence of hepatocellular carcinoma. Serum bilirubin level increases if jaundice is present.
Demonstration of Alpha-fetoprotein (AFP) in the serum by immunoelectrophoresis and immunoassy
technique is quite useful in differential diagnosis. This protein is normally present in foetus and disappers
within a few weeks after birth. Patients with hepatocellular carcinoma have significant elevation of AFP in
serum. About 60% to 80% of patients all over the world with hepatocellular carcinoma will show raised level
of AFP in serum. It must be remembered that AFP in the serum will also be high with embryonic tumours of
the ovary and testis. Resection of the tumour makes AFP level low to normal and recurrence of the tumour
will show again high level of AFP in the serum.

2. Straight X-ray will show an enlarged liver, elevated right cupola of the diaphragm and occasional
calcification of the tumour.
3. Ultrasonography is a non-invasive and inexpensive method to visualise a suspected mass in the liver.
4. Radionuclide scans (liver scans) are extremely helpful, but have more false positive results. Lesions
less than 2 or 3 cm in diameter are often not detected by ultrasonography or liver scan.
5. CT scan is more accurate and can detect lesions as small as 1 cm in diameter. It also differentiates
Fig. 45.6.— Liver scan showing normal liver with Flg.45.7.— Liver scan showing complete
symmetrical concentration of the Isotope. replacement of the right lobe and Invasion of the
left lobe by a large mass, which Is nothing but primary
hepatoma.
between cystic and solid lesions. Selective hepatic arteriography has been utilised to demonstrate the tumour
characterised by pooling and increased vascularity- helpful
It i in identifying the number and locations of
multiple lesions.
6. Splenoportography may demonstrate
invasion of the portal vein and intrahepatic spread
of tumour.
7. Laparoscopy to obtain needle biopsy of
the lesion is not accepted widely.
TREATMENT.— The definitive treatment is
surgical excision. But the lesion must be solitary or
localised, must not involve lymph nodes, blood
vessels or bile and should not have distant metastasis
to qualify for excision. According to the position of
the lesion segmental resection or lobar resection
may be performed. Total hepatectomy with liver
transplantation has not been encouraged.
Radiation therapy has not achieved good results.
Extensive radiation causes damage to the liver and
even produces suppurative cholangitis.
Chemotherapy.— Hepatic artery infusion with
Fig. 45.8.— Selective angiography showing 5-fIuorouracil has been used with success to cause
a primary carcinoma of the Uver. 40% response in certain series.
Cholangiocarcinoma.— Cholangiocarcinoma constitutes about 10 to 25% of primary liver cancer.

rcinoma arising from the small ducts or ductules are included in this category, though carcinoma may occur
in major hepatic ducts outside the liver substance.
Right AETIOLOGY.— Cholangiocarcinoma is often
Trisegmenteclomy
associated with (i) cirrhosis, (ii) haemochromatosis,(iii)
\
chronic cholestasis and (iv) congenital cystic disease of
the liver, (v) Infestation of Clonorchis Sinensis is seen
in 90% of cholangiocarcinoma in Hongkong.
Extahepatic cholangiocarcinoma may arise
anywhere in the hepatic ducts or common bile ducts.
PATHOLOGY.— Microscopically the lesion is a
sclerosing adenocarcinoma.
CLINICAL FEATURES.—Women a re more often
affected in the ratio of 2:1. Vague abdominal pain,
fever, pruritus and jaundice are the usual symptoms
Folciform Lig.
with which the patients present. On examination jaundice
is obvious. Slight hepatomegaly is quite common. Only
Middle Hepatic Vein
when there is extrahepatic cholangiocarcinoma,
gallbladder may be palpable.
principal Plane
TREATMENT.—Surgical excision is the treatment
Fig. 45.9.— Types of right lobectomy In case of primary
of choice. If the tumour is not resectable a by-pass by
carcinoma of the liver. an intubation procedure may provide good palliation.
Iridium seeds may be implanted through a biliary
Exlended For mo I drainage tube but its effectivity is still questioned and
Lefl Lefl Left Lateral
how far can it improve the survival rate is not yet
determined. In poor risk patients with unresectable
tumour, percutaneous biliary drainage is the only
available palliative treatment. Intestinal anastomosis
with intrahepatic duct such as Longmire procedure
may be tried if possible in unresected
cholangiocarcinoma.
OTHER PRIMARY MALIGNANT TUMOURS
Besides the twocommon CARCINOMAS described
above, a few malignant tumours may be seen in
liver, though not very common. These are (i)
Hepatoblastoma — an epithelial malignant tumour
occurring primarily in children (60% of cases occur
below 2 years of age). This tumour has a poor prognosis.
Other carcinomas are (ii) Cystadenocarcinoma and
(iii) Squamous cell carcinoma, (iv) Carcinoid and (v)
Fig.45.10.— Types of left lobectomy In case of
primary carcinoma of the liver. Teratomas have also been reported in liver. Among the
SARCOMAS which are often combined with cirrhosis
(i) anogios
leiomyosarcoma, (iii) fibrosarcoma and (iv) mesenchymal sarcoma.
METASTATIC TUMOURS
Pathology.— These are most common malignant tumours of the liver. Liver is the second organ only to
the lymph nodes as the most frequent site of metastatic carcinomas. Bronchogenic carcinoma is the most
common primary carcinoma causing liver metastasis. Next in frequency are colorectal, pancreas, breast and
stomach tumours.
Metastasis in the liver reaches by four routes :— (i) Portal vein, (ii) lymphatic spread, (iii) hepatic artery
and (iv) direct infiltration.
The growth rate ofthe metastatic tumour is more rapid than the original lesion. Metastasis in the liver m
occur (i) before the primary lesion is suspected e.g. carcinoid tumour of the ileum (this is known as precocio
metastasis), (ii) Metastasis may occur when the primary lesion is just detected (this is known as synchronous
metastasis), (iii) Metastasis may occur delayed even after removal of the primary tumour as may occur in
ocular melanoma (this is known as metachronous metastasis).
Secondary tumours in the liver can be divided broadly into four groups — A. Secondary carcinoma, B.
Secondary carcinoid tumour, C. Secondary melanoma and D. Secondary sarcoma.
A. Secondary carcinoma.— Secondary growths in the liver grow very rapidly and due to degeneration
of cells in the centre these are often umbilicated. Majority of these secondary carcinomas are multiple thoug
a few are solitary. When the metastasis in the liver is solitary, it may not preclude radical resection of the
primary tumour followed by resection of that part of the liver containing the solitary metastasis. This often
results in long-lasting survival.
B. Secondary carcinoid tumour.— These secondaries only develop when the primary carcinoid tumour
is in the small intestine or in the bronchus. The lesion is usually multiple in the liver and they often grow to
a large size. Increased urinary excretion of 5-hydroxyindole acetic acid is diagnostic of such secondary
metastasis.
C. Secondary melanoma.— This usually occurs when the primary growth is in the eye. Metastasis in the
liver is often quite late and may take place even years after removal of the primary growth.
D. Secondary sarcoma.— Liver is an uncommon site for secondary deposits in sarcoma. The lungs are
much earlier involved by metastasis from sarcoma. Liver is involved through blood route in case of sarcom
CLINICAL FEATURES.— Weight loss and anorexia are first main symptoms of liver metastasis.
Enlargement of liver, ascites and jaundice are second to appear. On examination, enlargement of the liver i
the only sign of liver metastasis. The liver is firm with nodularity and irregular margin. Friction rub may be
audible in 10% of cases. Sometimes signs of portal hypertension may be noticed. In case of carcinoid tumou
metastasis flushing syndrome will be obvious.
SPECIAL INVESTIGATIONS.— Laboratory
detection can be done early, before the development of
signs and symptoms.
(i) Carcinoembryonic antigen (CEA) assessment
should be performed as routine follow-up in patients
where there are possibilities of liver metastasis e.g.
colorectal cancer, gastric cancer etc.
(ii) Alkaline phosphatase is increased over 80% of
patients.
(iii) The SGOT level is elevated in 70% of patients.
(iv) It should be remembered that serum alpha
fetoprotein is not raised in liver matastasis unlike
hepatocellular carcinoma.
(v) Radionuclide scans (liver scan), computed
Fig. 45.11.— Liver scan showing many filling defects
tr.mography (CT) and angiography define presence,
indicating multiple hepatic metastases. location and operability of these lesions.
Treatment.— Treatment of hepatic metastasis is
only considered when (i) there are no systemic metastasis, (ii) primary tumour has been treated properly an
(iii) patient’s condition will tolerate major operative procedures.
Resection of the segment of the liver containing metastasis has given the patients a resonable long survival
without recurrence. This is particularly true in case of colorectal carcinomas.
So the PRINCIPLES of treatment of liver metastasis are: (a) to investigate to know if there are secondaries
in the liver as soon as the primary tumour has been diagnosed, (b) If the investigation shows that the liver is
not involved, a close follow-up is required to detect as soon as the liver metastasis takes place, (c) In case of
solitary liver metastasis or multiple metastases involving a segment of the liver, segmental resection of the
liver is indicated. Even when one lobe has been involved by metastasis, lobectomy may be performed if the
primary tumour has been treated properly, there is no other secondaries in the body and when the patient’s
condition will approve.
A variety of other treatment modalities may be advocated. Chemotherapeutic agent like 5FU when infused
through the hepatic artery has caused reduction in the size of hepatic metastases. Mitomycin C is another
chemotherapeutic agent which has also been used with some success in liver metastases following colorectal
carcinomas. Recently a percutaneous refillable pump is implanted in the subcutaneous tissue and attached to
the catheter surgically positioned in the hepatic artery. Chemotherapeutic agent is infused intra-arterially in
long term basis.
Chemotherapy combined with hepatic irradiation has provided palliation to a certain extent.
PORTAL HYPERTENSION
Portal hypertension is defined as an increase in portal vein pressure above the normal level of 5 to 10 mm
Hg. In established cases of portal hypertension, direct portal pressure measurement may be elevated to 15 m
Hg or even more.
Portal hypertension is due to obstruction somewhere in the portal vein or its tributaries (pre-hepatic), in
the portal venules and sinusoides in the liver (hepatic) or in the hepatic veins draining into the inferior vena
cava (post-hepatic).
Aetiology.— The various causes of portal hypertension can be classified into : (a) Pre-hepatic causes,
which constitutes about 20% of cases of portal hypertension; (b) Hepatic causes, which constitutes 80% of
cases of portal hypertension and (c) Post-hepatic causes, which are rare and occasionally seen.
A. PRE-HEPATIC CAUSES.— (i) Congenital atresia or hypoplasia, as an extension of the obliterative
process of the umbilical vein and ductus venosus.
(ii) Cavernomatous transformation of the portal vein, which represents thrombosis and recanalisation
within the vessel.
(iii) The most common in this group is portal vein thrombosis associated with sepsis or thrombosis in
neonatal period. Bacteria may be transmitted through a patent umbilical vein, there maybe history of neonat
omphalitis.
(iv) Trauma and extrinsic compression caused by adhesions.
(v) Tumours pressing on the portal vein.
(vi) Isolated splenic vein thrombosis may be caused by alcoholic pancreatitis (in this case splenectomy
only cures portal hypertension).
B. HEPATIC CAUSES.— (i) Nutritional cirrhosis.
(ii) Postnecrotic cirrhosis.
(iii) Biliary cirrhosis.
(iv) Haemochromatosis.
(v) Wilson’s disease.
(vi) Congenital hepatic fibrosis.
(vii) Infiltrative lesions.
(viii) Schistosomiasis, in which there is fibrosis of the terminal portal venous radicles.
Nutritional cirrhosis is the most common cause and in the Western World it is frequently associated with
chronic alcoholism. Postnecrotic cirrhosis represents progression of viral hepatitis or toxic hepatic injury.
Biliary cirrhosis may be due to extrahepatic obstruction. Portal cirrhosis is almost an invariable feature of
haemochromatosis. Wilson’s disease (hepatolenticular degeneration) is characterised by alteration of hepatic
function and structure and mental deterioration. Congenital hepatic fibrosis, an autosomal recessive disease,
is usually characterised by firm consistency of the liver, cholangitis and manifestation of portal hypertensio
C. POST-HEPATIC CAUSES.— (i) Budd Chiari syndrome.
(ii) Failure of the right side of the heart, may be caused by tricuspid valvular incompetence and constrict
pericarditis.
Budd chiari syndrome is obstruction of the hepatic veins, most frequently associated with endophlebitis
of the hepatic veins, which may be isolated or part of the generalised thrombophlebitic process. A web in th
suprahepatic part of the inferior vena cava may cause such syndrome and has been reported from Japan.
Neoplastic encroachment of other organs also accounts for this syndrome. This syndrome is often associated
with polycythemia, clotting diseases and the use of hormones for contraception. The clinical picture may be
acute or more commonly chronic. In acute cases there is sudden and complete obstruction of the outflow and
it is characterised by nausea, vomiting and severe abdominal pain due to rapid enlargement of the liver as a
result of congestion. Death may occur from hypotensive shock.
In chronic cases obstruction to the hepatic venous system appears to be gradual and is characterised by
mild abdominal discomfort and ascites. There may be simultaneous development of oedema of the legs whi
signifies involvement of the inferior vena cava in the occlusive process.
Collateral circulation.— When there is obstruction to the portal veins, nature tries to reduce portal
pressure by diverting blood from portal system to systemic system through a few known collaterals.
When the obstruction ispre-hepatic, collaterals between the portal vein distal to the obstruction and the
portal vein proximal to the obstruction enlarge. Thus the accessory veins of Sappey, the hepatocolic and
hepatorenal veins and veins of the suspensory ligament become enlarged.
When the obstruction is intrahepatic, a few known collaterals between the portal and the systemic systems
become dilated and transfer the blood from the high pressure portal system to low pressure systemic system
These collaterals are :
(i) Collaterals around the lower end of the oesophagus between the oesophageal branches of the left
gastric vein (portal system) and the loweroesophageal veins which drain into theazygosand hemiazygos vei
(systemic veins). Dilatation and tortuosity of these collaterals are called ‘oesophageal varix’, bleeding may
occur from such varices causing haematemesis and is known as variceal bleeding.
(ii)CoIIaterals around the lowerthird ofthe anal canal between the superior haemorrhoidal veins (por
venous system) and the middle and inferior haemorrhoidal veins (systemic venous system). This of course v
rarely dilates and causes haemorrhoids in this disease.
(iii) Collaterals around the umbilicus between the paraumbilical veins, which accompany the ligamentu
teres hepatis (portal venous system) and the superficial veins of the abdominal wall which drain into the
superior and inferior epigastric veins. Dilatation of such collaterals occur in about 20% of patients with port
cirrhosis and is known as the Caput Medusae.
1. BLOOD EXAMINATION.— (i) Anaemia, usually microcytic hypochromic, is almost inevitable in
porta] hypertension. It is usually due to various causes e.g. bleeding, haemolysis and nutritional deficiency.
(ii) Leukopenia and thrombocytopaenia may also occur due to splenomegaly and hypersplenism of porta
hypertension. Anaemia, leukopenia and thrombocytopenia may also be due to bone marrow depression
occurred in alcoholic cirrhotics.
(iii) Coagulation defects are common and mostly due to thrombocytopaenia and impaired synthesis of
coagulation factors by the damaged liver.The liver is responsible for synthesis of prothrombin and factors V
VII and X.
2. LIVER FUNCTION TESTS.— Functional disturbance of the liver indicated by the various tests e.g.
serum albumin estimation, esti ma tionof serum transaminases (SGOTand SGPT), serum alkaline phosphata
estimation, serum bilirubin estimation, bromosulphthalein test and turbidity and flocculation test are not ve
good indices as to the severity of liver damage. The tests may be entirely normal in the presence of establish
cirrhosis. Serum bilirubin is a measure of combined functions of production, hepatocyte uptake and secretio
SGOT (serum glutamic oxaloacetic transaminase) and SGPT(serumglutamicpyruvicacrd transaminase) are
THE UVER AND PORTAL HYPERTENSION 779
markers of hepatocyte injury or necrosis. Elevations of these markers are seen in hepatitis of all aetiologies.
Alkaline phosphatase is raised when there is biliary obstruction. Serum albumin level falls in liver diseases.
3. ENDOSCOPY.— Upper gastrointestinal endoscopy represents the most reliable single technique, a
shows the oesophageal varix and bleeding point. It should be carried out with fibreoptic instrument to visua
the inside of the oesophagus and
stomach. Oesophageal varices
are seen as dilated longitudinal
veins running a zig-zag course.
Such endoscopy is equally
important to exclude peptic ulcer
asa source of bleeding in a patient
with documented varices.
4. RADIOLOGY.— (i)
UPPER GASTROINTESTINAL
BARIUM series may
demonstrate oesophageal varices
as filling defects at the lower end
of the oesophagus. But this
demonstration is present in only
half the patients. This
investigation is even less accurate
inthe diagnosis of gas trie varices.
This examination may detect
other gastroduodenal pathology
e.g. peptic ulcer disease. But it
must be confessed that its role is
limited and has largely been
superseded by endoscopy.
(ii)
has two main advantages — (a)
measurement of portal pressure
Fig. 45.12.— Barium X- Fig. 45.13.— Barium X-ray shows severe and (b) visualisation of abnormal
ray shows dilated varicose oesophageal varices. venous anatomy incase of portal
oesophageal veins. hypertension.
(a) Measurement of portal venous pressure.— This can be performed by direct measurement through
transhepatic portography, umbilical vein catheterisation or splenoportography. These methods also provide
good visualisation of the venous anatomy.
Measurement of portal venous pressure may also be performed by indirect method by means of wedged
hepatic vein pressure. This is performed by wedging a catheter in a peripheral hepatic vein. In case of
intrahepatic portal obstruction measurement of portal blood pressure may be performed by catheterising
hepatic vein. Under local anaesthesia an antecubital vein is opened and a cardiac catheter is passed through
it. The catheter is advanced through the right atrium and inferior vena cava under radiographic control. The
tip is then passed through a hepatic vein until a peripheral radical is occluded. The tip of the catheter should
be in a peripheral position. Pressure recordings are then taken. In established cirrhosis case with oesophagea
varices the portal pressure may rise to 30 mm Hg or more. It must be remembered that the degree of portal
hypertension does not correlate with the risks of variceal haemorrhage or ascites formation, hence its
significance is questioned.
(b) Portal venography or portography.— This is often performed by splenoportography. Under local
infiltration anaesthesia a fine lumbar puncture needle is passed upwards and backwards through the 9th
intercostal space in the left midaxillary line. The needle is pushed into the spleen, which is evident by respir
seen on the needle. The stylet of the needle is removed and blood will be seen coming out through the splee
pressure is recorded which is often closely related to the portal venous pressure. 40 ml of 70% Diodone is inje
a series of X-rays are taken at short intervals. The dye reaches the portal circulation and thus the portal tree
can be seen in X-ray. With this splenoportography one can assess (a) if there is any block in the portal vein (
obstruction); (b) Distortion of intrahepatic radicles of the portal vein, which indicates intrahepatic obstructio
number of portosystemic collateral vessels, particularly the oesophageal varices. It must be remembered tha
splenoportography one should assess the prothrombin time and platelet count to avoid risk of haemorrhage
MANAGEMENT.— When a patient comes with acute variceal bleeding the management is performed
in three stages : 1. Resuscitation, 2. Diagnosis and 3. Specific treatment.
1. Resuscitation.— This is almost similar to all the patients who present with acute upper gastrointestinal
bleeding. Only a few special points which need stress are discussed here :
(i) Blood volume should be maintained by transfusing blood. But over-transfusion should be avoided. Coagu
lation abnormalities require fresh frozen plasma and platelets as indicated.
(ii) Saline should be avoided because of ascites.
(iii) Pulse rate, blood pressure, central venous pressure and urine output should be monitored frequently.
(iv) Sedation should be used with caution as these drugs are usually metabolised in the liver, but the liver is damaged. Bu
an agitated patient runs greater risk of precipitating recurrent haemorrhage and this should be considered against the abuses o
extra sedatives. Valium can be given intravenously. Librium is a good drug in the alcoholics facing withdrawal.
(v) Liver function tests must be performed to know underlying liver disease. A coagulation profile should also
be performed to know about underlying coagulopathy. Coagulation defect, if present, should be corrected. It may
require only vitamin K (10 mg I.V.) or administration of fresh-frozen plasma. There may be associated thrombocy
topenia secondary to hypersplenism due to cirrhosis and this should be treated.
(vi) Rapid clearing of the blood from the bowel should be effected by mild purgatives and enemas. This will
reduce ammonia load and hence encephalopathy.
(vii) Gastric acid secretion should be decreased by cimetidine administration.
(viii) In patients with ascites sodium intake should be minimised. Spironolactone (aldactone) should be used.
Paracentesis is required to reduce intra-abdominal pressure.
In this phase the patient is quickly stabilised so that one can go for proper diagnosis of the case.
2. Diagnosis.— Endoscopy is the main diagnostic stool. If too much bleeding is obscuring the view through
endoscopy, lavage through an Ewaled tube is necessary. If the rate of blood loss prohibits proper endoscopic evaluation,
a Sengstaken-Blakemore tube should be inserted to provide temporary haemostasis. After inserting this tube the gastric
balloon is inflated with air upto 250 ml and retracted to the gastric fundus. Here the oesophagogastric varices are
tamponated by subsequent inflation of oesophageal balloon to 40 mmHg. The other two remaining channels of the tube
allow gastric and oesophageal aspirations. A radiograph may be taken to confirm the position of the tube. The balloons
should be temporarily deflated after 12 hours to prevent pressure necrosis of the oesophagus. Assessment of the size and
extent of the varices is made. One must exclude bleeding from other causes particularly peptic ulcer. It must be remem
bered that bleeding due to gastritis in patients with portal hypertension should be managed as variceal bleeding.
3. Specific Treatment.—
(i) VASOPRESSIN (PITRESSIN).— This is a potent vasoconstrictor and is used to control variceal bleeding
by splanchnic vasoconstriction. Pitressin has a short half life (10 to 15 minutes) and should be given by continuous
infusion after a primary bolus dose. In acute bleeding 20 units in 20 ml of 5% dextrose should be given intravenously
over 20 minutes. This should be followed by a continuous infusion of 0.4 unit per minute. Presently Octreotide, the
long-acting somatostatin analogue is being used equally effectively.
The side effects of pitressin are due to generalised smooth muscle contraction, (a) Cramping abdominal pain,
which may be associated with bowel evacuation, is distressing to the patient, (b) Coronary artery vasoconstriction
may lead to myocardial ischaemia. (c) Peripheral vasoconstriction may cause Raynaud’s syndrome.
Recently propranolol is being used to prevent recurrent bleeding by reducing cardiac output. Isoproterenol may
be given to reduce the haemodynamic hazards of vasopressin. I.V. somatostatin is often used nowadays.
(ii) ENDOSCOPIC VARICEAL SCLEROSIS.—This has revolutionised the treatment of variceal haemorrhage.
This has definitely decreased the mortality rate in such haemorrhage. A sclerosant solution is injected through an
endoscope into the varices. Injection may be para-variceal or intravariceal. In acute bleeding intravariceal injection
is preferred, but to stop recurrence of bleeding para-variceal injection is preferred. Flexible endoscopy is used. There
is wide choice of sclerosant solutions, but 2.5% sodium morrhuate, ethanolamine oleate or butyl cyanoacrylate may
be used. Early rebleed is quite unlikely after such sclerotherapy. Third rebleed is a very rare incidence.
Complications of this method are primarily (a) retrosternal chest pain due to phlebitis, (b) Local microperforation,
though major perforation is rare, (c) Pulmonary complications such as effusion which may be accompanied by fever.
(iii) BALLOON TAMPONADE.— This is a temporary method to control acute bleeding, if the above methods have
failed to control it. The aim should be to use tamponade for as short time as possible. This step may be even omitted in case of
good risk patients where one can think of urgent shunt operation after preliminary trial of pitressin and sclerotherapy.
Sengstaken-Blakemore tube fs usually used for balloon tamponade. Balloons must be checked. The tube is ad
vanced well into the stomach. The gastric balloon is then fully inflated with 300 ml air and appropriate traction must
be applied. The oesophageal balloon should be inflated to 45 mm Hg only if the gastric balloon does not control the
bleeding. Oesophageal suction is continued above the balloons.
Complications are (a) aspiration is common, (b) Ulceration of the gastric and oesophageal mucosa from sustained
pressure can produce more bleeding, (c) Oesophageal rupture from this technique is quite rare, but if occurs, is fatal.
(iv) TRANSHEPATIC VISCERAL EMBOLISATION.— The aim of this treatment is to occlude the feeding vessels as also
to cause thrombosis within the oesophageal varices. At the onset percutaneous transhepatic portal vein puncture is made unde
local anaesthesia. Venous pressure is measured and anatomy of the portal venous tree is visualised. The left gastric vein is usu
the main inflow track. Selective catheterisation is performed. Occlusion of this inflow track is achieved with one of the variety of
agents e.g. gelatin foam, thrombin, spring coil, sodium tetradecyl sulphate and detachable balloons. It is better to sclerose the
varices with 100% alcohol initially, followed by occluding agents into the feeding vessel.
Initial control rate of bleeding from oesophageal varices has been claimed to be 45% to 90%, though there has
been a high rebleeding rate of about 25% to 75% in almost all series within a few days to months. It must be
remembered that the use of transhepatic embolisation is a temporary step in poor risk patients who continue to bleed
following Pitressin therapy, sclerotherapy and tamponade.
TRANSJUGULAR INTRAHEPATIC PORTOSYSTEMIC STENT SHUNTS (TIPSS).— This has helped to im
prove the treatment of variceal haemorrhage which initiated in 1988. Those variceal haemorrhage which did not respond
to either drug treatment or endoscopic therapy, this technique seems to be the best. Under local anaesthesia and analgesia
with sedation, the shunts are introduced under fluoroscopic and ultrasonographic guidance. A guidewire is inserted into
the hepatic vein and ultimately into a branch of the portal vein through internal jugular vein and superior vena cava. The
track of the guidewire is dilated with a balloon catheter. By this time a drop in portal venous pressure with reasonable
control of variceal haemorrhage can be detected. Now a metallic stent is introduced through the expanded channel.
The main complication is perforation of the liver capsule, which may result in fatal intraperitoneal bleeding.
There is also a chance of post-shunt encephalopathy in about 40% of patients, an almost similar incidence found after
surgical shunts. The main longterm complication is stenosis of the shunt which may result in further variceal haemorrhage.
The main contraindication of TIPSS is portal vein occlusion.
Treatment of complications.—
(1) Shock : Sedation with barbiturates. Fresh blood transfusion should be given.
(2) Clotting Problems : It may either be due to prothrombin deficiency from liver damage or thrombo
cytopenia from splenic enlargement. Vitamin K may be administered. Fresh blood transfusion also works he
(3) Encephalopathy : This is prevented by continuous gastric lavage which will prevent absorption
of blood protein. Magnesium sulphate and neomycin should be given through Sangstaken tube. Neomycin
is given 500 mg. in the first hour and then every two hours. High bowel wash also helps in these cases.
(4) Liver failure : Plenty of Carbohydrate should be given by mouth. Fat should very much be reduced in diet.
(5) Ascites: This means severe liver failure and mortality is much higher in these cases. Low salt diet
and diuretics should be given in these cases.
CHOICE OF OPERATION
This requires wise judgement and considerable experience.
Shunt operation is usually done as an elective operation after one bout of haemorrhage. There is no place
of prophylactic shunt operation, as being far from beneficial, it is sometimes deleterious. This operation is
contraindicated in cases of (i) elderly patients, (ii) with severe encephalopathy, (iii) with marked liver failure
i.e. Serum Albumin is less than 2.5 g./lOO ml., the patient is jaundiced, B.S.P is more than 40% etc.
The patients who remain in the contraindication group of the shunt operation should be treated by
one of the emergency operations.
EMERGENCY OPERATIONS
These operations are only temporary measures designed to arrest bleeding. But these do not decrease
the portal vein pressure or prevent subsequent haemorrhages.
(1) Transthoracic Oesophagotomy.— Under general anaesthesia the patient is placed in the right lateral position.
An incision is made along the 8th or 9th rib. The periosteum of the rib is elevated from its outer as well as the inner surface.
The whole rib is then resected and an incision is made on the periosteum as well as the parietal pleura. The lung is retracted
forwards. The parietal pleura lying over the oesophagus is incised very carefully to expose the lower end of the oesophagus.
The oesophagus is now transected transversely and resutured with continuous catgut so that all the bleeding vessels are held
and occluded by the catgut suture. Nowadays circular stapling device is being used which can be quickly applied and the result
is also similar to this operation. This operation gradually lost its popularity as the oesophagus is not a good gut to anastomose
because of its low vascularity. So this type of suturing was almost always followed by leakage. For this reason Boerema-Crile
and Milnes-Walker introduced the operation where the oesophageal musculature was incised longitudinally so that the anasto
motic leakage did not follow. Similarly Tanner introduced subcardiac gastric transection due to high vascularity of the stomach
and anastomosis in this organ is not followed by leakage.
(2) Boerema-Crile Operation.— The access to the lower part of the oesophagus is made through the bed of the 8th or
9th rib. The patient is laid in the right lateral position and a nasogastric tube is pushed into the stomach. The steps of this opera
are more or less similar to those of the previous one till the exposure of the lower end of the oesophagus. The muscles of the
oesophagus are incised longitudinally and the edges are held apart by stay sutures. The columns of varices, usually 3 in numbe
are under-run with continuous catgut sutures. To tackle the gastric varices the diaphragm may require to be incised. But this is
done in presence of ascites. Finally the oesophagus is repaired and the thoracic wound is closed in layers.
Recently sophisticated staplers are being used for oesophageal transection and reanastomosis. The technique
is as follows : For transection of the oesophagus, the peritoneal cavity is entered and the oesophagogastric junction
is exposed. The lower 3 cm of the oesophagus is mobilised and particular care is taken to avoid vagus nerve injury.
The perioesophageal veins are ligated. A vertical incision is made high in the anterior wall of the stomach. EEA
stapler is inserted using the largest size cartridge. The oesophagus is tied over the centre rod 2 cm above the gastric
junction. The instrument is fired. This results in simultaneous transection and reanastomosis of the oesophagus.
(3) Milnes-Walker Operation.— Here the mucous and the submucous coats of the oesophagus are transected
and then resutured to interrupt the communication between the portal and systemic veins at the lower end of oesopha
gus to stop the bleeding. The approach is same as that of the previous operation. The oesophageal musculature is
incised longitudinally. The mucous and the submucous coats of the oesophagus are taken out off the musculature as
a single tube and completely divided across. This is again sutured with the continuous catgut sutures so that the veins
fig._ 2 A ligature is placed around the oeso FIG-3 The ligature is tightened about 2 cm
phagus and the gap between the conical head above the cardia and a flange of full thick
and cylindrical body widened. ness of oesophageal wall invaginated between
the two parts of the gun.
fig. 1 Insertion of gun into lower oesophagus

via a small anterior gastrotomy. The anterior
vagus is protected in a sling.
Fig. 45.14.— bhows steps of using stapler for oesophageal transection and reanastomosis,
responsible for haemorrhage are completely obliterated.
(4) Tanner’s Operation.— In this operation the stomach is transected two inches (5 cm.) below the cardia
and all its vessels having been divided and ligatured is immediately reanastomosed. This operation may be p
when the bleeding varices are mostly in the stomach, otherwise this operation does not prove to be useful.
(5) Oesophageal transection with paraoesophageal devascularisation.— The main components of this tre
ment are (i) oesophageal transection, (ii) splenectomy, (iii) paraoesophageal and gastric devascularisation (th
vessels supplying the distal part of the oesophagus and upper half of the stomach are ligated individually an
selective vagotomy and pyloroplasty. This procedure was advocated by Sugiura and Futagawa. In this techn
sion is maintained which ensures portal venous perfusion and maintenance of liver function, but stops bleed
Fig. 45.15 & 45.16.— Endoscopic scierotherapy. In Fig. 45.15 paravariceal injection is shown. Note that the injec
tion is made by the side of the varices, so that surrounding sclerosis causes constriction of varices. In Fig. 45.
intrauariceal injection is being shown. Injection is made inside the varices, so that intravariceal thrombosis o
leading to cure of the condition. C M.— Circular muscle; M.M.— Muscularis mucosae, O.V.— Oesophageal
formation of new varices. Left thoracotomy is performed for oesophageal transection and paraoesophageal devascularisation.
Laparotomy is then performed for splenectomy, gastric devascularisation, selective vagotomy and pyloroplasty.
The operative mortality in Sugiura’s series was only 2.7% and 5 years survival was 83% and rebleeding rate was
only 2%. But at the hands of other surgeons applying the same technique the mortality rate was higher (20% to 40%)
and 5 years survival was 40% to 70% and rebleeding rate was 20% to 50%. This is a fairly major operation.
(6) Endoscopic sclerotherapy.— The method has already been discussed in the conservative management.
A few surgeons advocate this treatment as a definitive procedure. Predominantly poor risk cirrhotics who are not
even fit for emergency operations, may be given the advantage of this method. It has been reported that about 65% of
cases were alive from 1 to 10 years. The rebleeding rate was 24%. 80% of patients require multiple sclerotherapy
sessions. The benefits of sclerotherapy lie in the preservation of portal perfusion (portal blood flow is maintained)
and maintenance of hepatic function. The complications have also been mentioned in the conservative treatment.
The present role of endoscopic sclerosis in definitive management is undefined. The poor risk patients who will
not tolerate major surgery will mostly be benefited.
SHUNT OPERATIONS
More availability of TIPSS and even liver transplantation, surgical shunt operations have been re
duced to a considerable extent. Moreover morbidity and mortality of these operations in the acute man
agement of variceal haemorrhage is quite high. However surgical shunts are quite effective in preventing
rebleeding from oesophageal and gastric varices as they reduce the pressure in the portal circulation by
diverting the blood into low-pressure systemic circulation.
Surgical shunts may be divided into 2 groups — (i) selective — which includes splenorenal as it
preserves blood flow to the liver while decompressing the left side of the portal circulation which is
responsible for giving rise to the oesophageal and gastric varices. Similarly the selective shunts are asso
ciated with a lower incidence of postsurgical encephalopathy.
(ii) Non-selective — which is portacaval shunt.
There are principally three types of shunt operations :
(i) Portacaval, (ii) Lieno-renal and (iii) Mesenterico-caval. Other shunt operations between portal and
Fig. 45.17.— Slde-to-slde porta-caval Fig. 45.18.— End-to side porta-caval

anastomosis. anastomosis.
unnamed systemic veins are now obsolete.

I. Portacaval Shunt.— This is the first choice shunt operation and used in even failed cases of lien
renal shunt. A right subcostal incision is made. The duodenum and the head of the pancreas are mobilised
the left by Kocher’s manoeuvre to expose the inferior vena cava. A small incision is made on the peritoneum
lying over the inferior vena cava. Now the portal vein is exposed in the posterior part of the free border of t
lesser omentum and is mobilised as far as possible. It is divided at the porta hepatis and the upper stump is
ligated. The lower cut end is
/ brought near the inferior vena
/1 C3Va an<* an el,d-to-side
Jy , /'s, anastomosis is performed after
■ CL-n partially occluding the vena
9 I\\ cava by a special Pott’s clamp
I MJ W/dt (Fig.45.18). Side-to-side
/ L? > anastomosis is also possible
% 1 (Fig.45.17).
1\ /M/ • A îs. ■• II- Lieno-renal Sh-
9 ' \ unt.— This is only performed
\ when there is thrombosis
\\ hi \ ' Vy affecting the portal vein or
---- where splenomegaly deserves
JT \'\ r~\ removal ofthe spleen. But it is
3 ' l~ V-. .- contraindicated if the splenic
Jl Vv Ve’n *S "ess t*lan * cm- 'n
V diameter as shown in
Venography. A left thoraco
abdominal incision is oftenused
Fig. 45.19.— End-to-slde spleno-renal anastomosis as removal of a huge spleen is
after splenectomy. easier through this incision.
When the spleen is not very enlarged one can use

subcostal incision. The spleen is removed as usual
leaving behind as great length of the vein as possible.
The vein is now separated from the body of the
pancreas by ligating and dividing its tributaries.
The left renal vein is dissected out and the
peritoneum over it is carefully incised. A special
clamp is applied to renal vein to partially occlude
it and the splenic vein is anastomosed to the renal
vein in an end-to-side fashion (Fig. 45.19).
DI. Mesenterico-caval Shunt.— This is the
third choice operation and only rarely used when
both the above operations are not possible to per
form. Here the inferior vena cava is divided just
above its lower end. The lower cut end is ligated and
the proximal cut end is joined to the side of the
superior mesenteric vein at the root of mesentery.
Sometimes a dacron graft may be used to connect
the superior mesenteric vein and the inferior vena
cava.
Complications of Shunt operations.—
I. EARLY COMPLICATIONS.—
1. Haemorrhage from suture lines.
2. Occlusion of anastomosis by thrombosis,
which makes the shunt operation a failure. Such
occlusion may occur particularly if the veins of
narrow calibre are used e.g. splenorenal or superior
mesenterico-caval anastomosis.
3. Hepatic coma following liver failure,
n. LATE COMPLICATIONS.—
Portosystemic encephalopathy.— If this shunt
operation is performed in a patient with major liver
failure, such complication may come across. Nor
mally the toxic products of protein break down,
mainly ammonia, enter the liver where they are
detoxicated. After shunt operation these toxic products get direct access into the systemic circulation and
reach the central nervous system particularly the brain causing encephalopathy. It is more often precipitated
after large protein meal or after upper G.I. tract haemorrhage.
The clinical features are disorientation, rigidity of the limbs, flapping tremor of the outstretched hand
and deep coma. Ankle clonus may be elicitated. Some intellectual deterioration and changes in personality
are often noticed. Slurring of speech is also frequently seen.
In electroencephalogram there is marked slowing of the frequency upto the delta range.
Treatment is restriction of protein diet, removal of blood from bowel with enemas or purgation with
magnesium sulphate. Oral lactulose in the dose of 20 to 30 ml 3 to 4 times daily help in clearing protein
or blood in the intestine. Lactulose enemas may also be used. Electrolyte deficiencies must be corrected,
vitamin supplementation is required. One must not use any sedative.
50
786
CHAPTER 38 -
THE BILIARY SYSTEM

The gallbladder, the cystic duct, the hepatic ducts, the common hepatic duct and the common bile
duct form the biliary system.
ANATOMY —
The duct system.— The duct system starts with the hepatic ducts and ends at the opening of the common bile duct in the duodenum.
The right anterior and the right posterior segmental ducts join to form the right hepatic duct.The left lateral and the left medial segmental
ducts form the left hepatic duct. The right hepatic duct joins with the left hepatic duct to form the common hepatic duct. The right hepatic
duct joins with the left with a sharp curve, this is why calculi are less commonly found in the right hepatic duct.
The common hepatic dud— The length of the common hepatic duct is extremely variable. When it is joined with the cystic duct, it
is called the common bile duct. Commonly the common hepatic duct is about 3 to 4 cm in length. It is joined at an acute angle by the cystic
duct to form the common bile duct.
Common bile duct— The common bile duct is approximately 8 to 10 cm in length and 6 to 10 mm in diameter. It can be divided into
four parts : 1. The supraduodenal portion, about 2.5 cm long runs in the right free edge of the lesser omentum, to the right of the hepatic
artery and anterior to the portal vein; 2. The retroduodenal portion, which curves to the right behind the first part of the duodenum and here
it moves away from the hepatic artery and the portal vein; 3.The infraduodenalportion, curves more to the right lying in a groove in the
posterior surface of the head of the pancreas. The right edge of the inferior vena cava lies quite near to this part of the common bile duct; 4.
The intraduodenal portion, passes obliquely through the wall of the second part of the duodenum to open on the summit on the duodenal
papilla, which is surrounded by the sphincter of Oddi. Near its opening it is joined by the main duct of the pancreas (duct of Wirsung) to
form the ampulla of Vater. The union of the bile duct and the main pancreatic duct may follow one of the three patterns, (i) The ducts may
unite outside the duodenum and form the ampulla and traverse the duodenal wall and papilla as a single duct; (ii) The two ducts join within
the duodenal wall arid have a short common terminal portion; (iii) In 25% of cases the two ducts open separately on the papilla.
Blood supply of the common bile duct derives from the superior pancreaticoduodenal, hepatic artery proper, right hepatic artery as
also the cystic artery. Branches from these arteries form a plexus on the bile duct which is joined by axial vessels — the 3 O’clock and 9
O’clock arteries.
Gallbladder.— It is a pear shaped organ of about 7.5 to 12 cm. in length. It has an average capacity of 50 ml, but it is capable of
distension to about 50 folds. The gallbladder lies in the bed of the inferior surface of the liver. It has got four anatomic portions — fundus,
corpus or body, infundibulum and neck.The fundus is the most distal part of the organ, it is the rounded end which normally extends slightly
beyond the inferior margin of the liver. It may be kinked and present the appearance of a ‘Phrygian cap’. The fundus contains most of the
smooth muscle of the organ. The corpus or body, which is the major storage area contains most of the elastic tissues. The body tappers into
the neck, which is funnel shaped and connects with the cystic duct. The neck usually follows a gentle curve and the convexity of the curve
is distended and is known as infundibulum. When this part is dilated it is called Hartmann 's pouch.
STRUCTURE.— The gallbladder has three coats — serous, fibromuscular and mucous.
The serous coat is derived from the peritoneum. It completely invests the fundus, but covers only the undersurface and sides of the
body and neck of the gallbladder. Beneath the serous coat lies an areolar subserous layer.
The fibromuscular coat is a thin layer of fibrous tissue mixed with unstriped muscular fibres, which are mostly longitudinal in
direction, though a few may be circular in arrangement.
The mucous coat is loosely connected with the fibromuscular coat, so it is elevated into minute rugae which give it a honeycomb
appearance. It is yellowish-brown in colour. The epithelium consists of a single layer of columnar cells which vary in size. Electron
microscopy shows presence of microvilli on the apical surface. This feature indicates the capacity of the epithelial cells to absorb water and
solutes from the bile to make it more concentrated. Mucous granules are present in the apical half of some cells, from which mucus is
secreted into the lumen. There are many capillaries lie close to the basement membrane.
BLOOD SUPPLY.— The gallbladder is supplied by the cystic artery which usually is a branch of the right hepatic artery when it is
behind the cystic duct. It passes behind the common hepatic duct and the cystic duct to gain the upper surface of the neck of the gallbladder,
on which it runs downwards and forwards, before dividing into superficial and deep branches. The superficial branches ramify on the
inferior surface and the deep branches on the superior surface of the gallbladder. Occasionally the cystic artery arsies from the hepatic artery
proper or rarely from the gastroduodenal artery. At this time it crosses in front of or behind the bile duct or common hepatic duct to reach the
gallbladder. Accessory cystic artery may sometimes be present and originate from the common artery or one of its branches. The cystic
artery also supplies branches to the hepatic ducts and upper part of the common bile duct.
VENOUS DRAINAGE — is carried out by small veins which enter directly from the gallbladder into the liver. A large cystic vein is
almost always present which follows the cystic artery and drains into the right portal vein.
LYMPHATIC DRAINAGE.— Majority of the lymphatics from the subserosal and submucous coats drain into the cystic lymph node
of Lund (the sentinel lymph node), which lies in the angle created by the junction of the cystic and common hepatic ducts. Efferents from this
lymph node go to the hilum of the liver. Lymphatics from the gallbladder also pass directly into the liver to connect with the subcapsular
lymph channels of the liver. This accounts for the frequent spread of the carcinoma of the gallbladder to the liver. Other lymphatics of the
gallbladder drain into the lymph nodes near the porta hepatis, which are often enlarged in case of carcinoma of the gallbladder and produce
obstructive jaundice.
NERVE SUPPLY.— Gallbladder is supplied by both sympathetic and parasympathetic nervous system. Parasympathetic nerves are
derived from the vagus nerve through the coeliac ganglion. Sympathetic supply comes from the level T8 and T9 and these fibres form plexus
THE BILIARY SYSTEM 787
in the coeliac plexus from where the post-ganglionic fibres supply the gallbladder along the hepatic artery.
Cystic duct— It starts from the gallbladder and drains into the common hepatic duct at an acute angle. It is of variable length,
average is 4 cm. The right branch of the hepatic artery is just behind the cystic duct where it joins the common hepatic duct. Congenital
variations of the cystic duct may be present and have been described in the next section. The cystic duct may be even absent.
The mucous membrane lining its interior is thrown into a series of crescentic folds from 5 to 12 number. Such type of folds is also
found in the neck of the gallbladder. These folds are directed obliquely and are called spiral valve of Heister.
PHYSIOLOGY.— Liver secretes bile at a constant rate of about 40 ml/hour. This bile is composed of 1 to 2% of bile salts and 1%
of bile pigments, cholesterol and fatty acids and the major part i.e. 97% is water. The sphincter of Oddi is usually in contracted position
except during active feeding. So the whole of bile leaving the liver passes into the gallbladder.
The FUNCTIONS ofthe gallbladder are :
1. Storage of bile.— Bile is stored in the gallbladder. When food reaches the duodenum, a hormone known as cholecystokinin is
secreted by the duodenum. This hormore causes contraction of the gallbladder and relaxation of the sphincter of Oddi. With that bile trickles
into the duodenum in small amounts to help digestion of the food.
2. Concentration of bile.— The bile is concentrated in the gallbladder while it is stored. This helps storage of the bile in the
gallbladder. Bile is concentrated 5 to 10 times within the gallbladder. The mucous membrane of the gallbladder absorbs water, sodium,
chloride and bicarbonate. So the concentration of bile salts, bile pigments, cholesterol and calcium increases.
3. Changing the reaction of the bile.— The bile which is excreted by liver is alkaline with pH of about 8.2. In gallbladder the bile
gradually becomes acidic and its pH goes down to 7.4 to 7.0. This is due to selective absorption of various ions by the mucous membrane of
the gallbladder.
4. Secretion of mucin.— It has already been described in the histology of the gallbladder that mucin is secreted by the alveolar glands
lining the infundibulum and neck. About 20 ml of mucin is secreted in a day
5. Cholesterol excretion.— It is still not very definite, yet it seems that gallbladder adds cholesterol to the bile.
CONGENITAL ANOMALIES
Gallbladder.— (i) Absence of the gallbladder.— This is extremely rare. Intrahepatic gallbladder and
left sided gallbladder must be rulled out before making such diagnosis.
(ii) Duplication of the gallbladder with two separate cystic ducts may be present.
(iii) There may be bilobed gallbladder with a single cystic duct.
(iv) Accessory gallbladder may be situated on the left side and its cystic duct may empty' into the left
hepatic duct rather than the common duct Cholelithiasis and cholecystitis may involve one gallbladder
while the other gallbladder remains unaffected.
(v) Phrygian Cap of the fundus as mentioned in the ‘anatomy’ may be responsible for some
pathologies and detected in 5% of cholecystographies.
(vi) ‘Floating gallbladder’ occurs when the organ is almost completely invested by peritoneum.
Normally one-third of the circumference of the gallbladder lies in a shallow bed on the inferior surface of
the liver. Such floating gallbladder may or may not have a mesentery. Occasionally the neck have a mes
entery in which the cystic artery lies. While the fundus and body are free this predisposes torsion of the
gallbladder.
(vii) Gallbladder may be left sided with the cystic duct entering into the left hepatic duct or common
duct.This condition is also known as retrodisplacement, in which the fundus extends backwards in the free
margin of the lesser omentum.
(viii) The gallbladder may be totally intrahepatic. Partial or completely intrahepatic gallbladder is as
sociated with increased chance of cholelithiasis.
Hepatic ducts.— Accessory hepatic ducts are present in approximately 15% of cases, (i) Large duct is
usually single and drains a portion of the right lobe of the liver. It joins the right hepatic duct, common
hepatic duct or infundibulum of the gallbladder, (ii) Small ducts of Luschka (cholecystohepatic ducts) may
drain directly from the Kver into the body of the gallbladder. After cholecystectomy these cause leakage of
bile as they are overlooked during cholecystectomy. This leakage of bile has compelled many surgeons to
drain the hepatorenal pouch routinely following cholecystectomy.
Cystic artery and hepatic artery.— Anomalies of these arteries are not uncommon.
(i) A large accessory left hepatic artery may originate from the left gastric artery.
(ii) The right hepatic artery may originate from the superior mesenteric artery.
(iii) There may be two hepatic arteries — one originating from the common hepatic artery and the
other from the superior mesenteric artery.

(iv) A'Caterpillar hump’ or 'Moymhan’s hump’.— The right hepatic artery is sometimes tortuous
and the cystic artery becomes short. In this case the former is liable to be injured during cholecystectomy.
(v) The right hepatic artery may course a tortuous turn in front of the cystic duct, so that while
clamping the cystic duct the right hepatic artery may be clamped causing accidental liver infarction.
(vi) The cystic arteiy may originate from the left hepatic artery or the junction of the left and right he
(vii) Cystic artery passes in front of the common hepatic duct, rather than to the right or posterior to
duct
(viii) There may be double cystic arteries, both arising from the right hepatic artery or may have abno
(ix) Cystic artery arises from the gastroduodenal artery.
(x) The right hepatic artery is adherent to the cy stic duct and neck of the gallbladder.
Cystic duct.—
(i) Cystic duct may be absent and the gallbaldder is joined to the common hepatic duct. In this case
surgeon must be careful not to clamp the common duct. In this case neck of the gallbladder should be
divided close to the opening in the common duct.
(ii) The cystic duct may be quite long and its union with the common hepatic duct may be as low as
just above the duodenum.
(iii) The cystic duct may be even longer and may join the common hepatic duct behind the duodenu
(iv) Cystic duct is adherent to the common hepatic duct and actual union is quite low. In these cases
the surgeon often leaves the adherent portion of the long cystic duct, which leads to post-cholecystectomy
syndrome.
(v) The junction between the cystic duct and common hepatic duct may be quite high.
(vi) Cystic duct may drain into the right hepatic duct.
(vii) Cystic duct crosses anterior to the common hepatic duct and joins it posteriorly.
(viii) Cystic duct courses posteriorly to the common hepatic duct and joins it anteriorly.
(ix) Cystic duct may drain into the left hepatic duct or right hepatic duct.
CHOLEDOCHAL CYST
Congenital cystic abnormalities may occur throughout the entire biliary system, starting from the
intrahepatic biliary radicles to the end of common bile duct. Here I shall discuss only the extrahepatic cys
dilatations involving the biliary system. Such congenital disease has been classified by Alonzo-Lej et al. In
such classification type A is dilatation of the extrahepatic ducts (commonest and known as "Choledochal
cyst ). Type B is a rare disorder in which cystic dilatation takes the form of a diverticulum and is connecte
with a small stalk to the hepatic duct, gallbladder or the common bile duct. Type C is the choledochocele i
cy stic dilatation involving only intraduodenal portion of the common bile duct and this is the least comm
variety.
Choledochal cyst (Alonzo-Lej type A) is the most common variety of congenital cyst of the extrahepat
biliary tract.There are three major varieties in this group: (a) Cystic dilatation involving the entire commo
bile duct and common hepatic duct with the cystic duct entering the choledochal cyst; (b) Diffuse dilatatio
of the common bile duct and (c) A small cystic dilatation of the distal common bile duct.
Aetiology.— The cause of formation of choledochal cyst is still not known, but there are many
speculations. One such is that the supraduodenal diverticulum results from a localised perforation in the
duct. Another speculation is that fusiform dilatation results from distal obstruction and destruction of the
proximal duct epithelium by pancreatic juice when both bile duct and pancreatic duct open commonly at
ampulla of Vater. Other speculations are not very significant and beyond the scope of this treatise.
Clinical features.— This condition occurs four times more frequently in females. Only l/3rd of cases
are diagnosed in the first decade of life and only half the cases present before the age of 20 years. The cyst
may contain as much as 1 to 2 litres of bile and the cyst wall shows inflammatory changes with absence of
lining epithelium.
The classic triad of this condition is a combination of (i) upper abdominal pain, (ii) obstructive jau
ndice and (iii) fever. Pain and jaundice are frequently intermittent but gradually become severe. Fever is
due to cholangitis from bile stasis and bacterial colonization.
On examination a palpable epigastric mass may be discovered.
Special Investigations.— (i) Intravenous cholangiography often outlines the choledochal cyst.
(ii) Nowadays non-invasive techniques like ultrasonography has been more popular in diagnosing this condition.
(iii) Transhepatic cholangiography is also good in diagnosing this condition preoperatively.
(iv) MRCP (Magnetic Resonance Cholangiopancreatography) is now quite a popular investigation to diagnose
choledochal cyst.
Complications.— If untreated this condition proves fatal. It will lead to complete biliary obstruction, ascending
cholangitis and secondary biliary cirrhosis. It may undergo rupture, which occurs frequently during pregnancy leading to
diffuse peritonitis.
Treatment.—Early operation is the treatment of choice.
Alonzo-Lej type A should be treated by excision of the cyst coupled with Roux-en-Y anastomosis of jejunum to the
proximal normal duct (known as hepaticodocho-jejunostomy). Previously Roux-en-Y anastomosis of thejejunum was
made with the choledochal cyst (this was known as Roux-en-Y cystojejunostomy or choledochocystojejunostomy). But
one-third of these cases develop recurrent pancreatitis and one-fourth of cases develop carcinoma arising from non
excised choledochal cyst. This has led to the advocation of the former treatment (hepaticodocho-jejunostomy) as the
treatment of choice at present.
Alonzo-Lej type B and C are treated by excision of the cyst, if required, followed by anastomosis either
choledochoduodenostomy or choledochojejunostomy.
CONGENITAL BILIARY ATRESIA

Pathology.— The bile ducts first develop as solid structure. Gradually the solid core becomes vacu
olated and the vacuoles coalesce to establish the lumen. Arrest in the solid stage causes biliary atresia. The
obliteric process may involve the common bile duct, one or both hepatic ducts, cystic duct and the
gallbladder in variety of combinations. When there is distal blockade, dilatation of the proximal portion
of the biliary system and the gallbladder may be noted. Liver is usually enlarged and may be diffusely
nodular. The liver turns dark green. Gradually the signs of biliary cirrhosis may be apparent. About l/4th
of the patients will have other coincidental congenital anomalies e.g. imperforated anus, duodenal atresia,
mongolism, congenital heart disease and most commonly urinary tract anomalies.
(a) In 10% of cases there is complete absence of all extrahepatic ducts; (b) In 64% there is partial
obstruction particularly the distal part, so that the proximal part is dilated with signs of obstructive
jaundice; (c) In 11% there is total atresia ofthe hepatic ducts, but associated with normal common bile
ducts; (d) In 5% there is atresia of the intrahepatic bile canaliculi and 7% have atresia of the visible larger
intrahepatic ducts (Caroli’s disease); (e) Rest 3% demonstrate only stenosis.
Clinical features.— Jaundice is the most constant finding in these cases. Either it is present at birth or
shortly thereafter. Jaundice usually does not become deep until the child is about 2 to 3 weeks old. After
that jaundice becomes gradually progressive, urine becomes dark brown. Though the first meconium is
often normal, thereafter the stools are white or clay-coloured. Gradually the liver enlarges and it is easily
felt. The liver feels rather hard. Ascites very rarely appears. Sometimes the spleen becomes enlarged and
evidence of portal hypertension may be present. Petechiae and subcutaneous haemorrhages occur due to
reduction in prothrombin time following vitamin K deficiency.
If unrelieved, the patients usually die within 3 to 6 months.
Neonatal jaundice may appear due to various medical diseases and these should be excluded. There are
hereditary spherocytosis, haemolytic sepsis, erythroblastosis foetalis, congenital syphilis, serum hepatitis
(if the neonates had blood or plasma transfusion), neonatal hepatitis, haemolytic disease, alpha-trypsin
deficiency, Crigler-Najjar syndrome and inspissatated bile syndrome.
Special Investigations.— (i) Blood examination will reveal excess bilirubin and mild anaemia. High
level of alkaline phosphatase is common. Level of SGOT goes up to 400 or 500.
(ii) Urine examination will show excess bile pigments and no urobilinogen.
Treatment.— Early operation should be advised, but patients should be given the privilege of
preoperative management to make it fit for the operation.

Preoperative measures include correction of dehydration, if present. Vitamin K( is always necessary to
combat prothrombin deficiency. Blood transfusion may be required. A broad spectrum antibiotic should b
started in the preoperative period. Amplicillin is good in this regard.
Technique of OPERATION. — A midline incision is made. After opening the abdomen the liver biopsy
should be performed and a frozen section should be examined to rule out intrahepatic bile duct atresia.
Dissection is started at the free edge of the leser omentum to find out the common bile duct. If a
proximal filled common bile duct is discovered, the gallbladder should be looked for. If the gallbladder
contains a lumen, the fundus is opened to determine the colour of the fluid. White bile indicates obstructio
of the cystic duct, while normal bile indicates patency of both hepatic ducts and cystic duct. An operative
cholangiogram should be performed to define anatomy in this situation.
If the gallbladder is not found, the porta hepatis should be explored to detect hepatic duct stump.
If a proximal segment of the extrahepatic biliary system is patent, choledochoduodenostomy,
choledochojejunostomy or hepaticodocho-jejunostomy should be performed according to the circumstanc
When extrahepatic biliary system is not identified and the liver biopsy demonstrates presence of
intrahepatic ducts, transhepatic drainage should be attempted at. Hepatic portoenterostomy with double
Roux-en-Y anastomosis advocated by Kasai is a procedure worth trying. In this technique one loop of
jejunum is taken out externally to prevent ascending cholangitis, which is a common complication after
such type of operation.
In cases where there is atresia of the intrahepatic duct, the only treatment left with is orthotopic total
liver transplantation.
Caroli’s disease (Congenital dilatation of intrahepatic ducts).— In this condition there are multiple, saccular dilatations of the
intrahepatic ducts due to intrahepatic atresia of biliary ducts. Such biliary stasis leads to cholangitis and stone formation. This condition is
presented in childhood and in early adult life. It is non-familial. This condition may be associated with other congenital anomalies e.g.
meduliary sponge kidney, congenital hepatic fibrosis etc. This condition may be complicated with cholangiocarcinoma.
Treatment is antibiotic for cholangitis and removal of calculi. This condition is restricted in one segment or even in one lobe, so
segmental resection or lobectomy should cure this condition.
SPECIAL INVESTIGATIONS
1. Straight X-ray of the abdomen should always be performed in biliary tract disease This diagnoses radio-opaque
stones in 15% of cases. Moreover faintly calcified stones, which may be rendered invisible if contrast radiography is
advised in the beginning, can be diagnosed in first instance. Whether the stone is radio-opaque or not depends on its
calcium content. Bile pigment calculi, which originate from haemolytic disorders, are usually non-radio-opaque.
Similarly pure cholesterol stone is also not radio-opaque,
but calcium carbonate stones are always radio-opaque.
Gallstones which are formed with infection or inflamma
tion are generally mixed stones. Their visibility is depen
dent on the amount of calcium present in the stone. This
investigation also shows rare cases of calcification of the
gallbladder (porcelain gallbladder) and limy bile. Air or
gas in the bile duct system can also be visualised.
2. Oral cholecystography.— This is to visualise
gallbladder by using contrast medium. This was first in
troduced by Graham and Cole in 1924. Successful
visualisation of the gallbladder depends on (i) blood flow
to the liver, (ii) ability of the liver cells to excrete the dye
into the bile, (iii) patency of hepatic and cystic duct sys
tem and (iv) capability of the gallbladder to concentrate
the excreted dye.
Oral cholecystography cannot be helpful in diagnosis
and hence should not be used in (i) acute cholecystitis, (ii)
if the patient is jaundiced with plasma bilirubin level over
3 mg/100 ml (the liver cells are unable to excrete the
contrast medium into the biie> and (iii) when renal function is impaired.
Telepaque is the contrast medium used
most commonly. The patient takes light dinner
of non-fatty meal between 8 to 9 p.m. on the
evening before the radiological examinations.
Patient ingests 6 tablets of Telepaque one at a
time with water, after dinner until bed time. On
the following morning nothing is given by mouth
to the patient till the radiological examinations
are performed. After 2 or 3 films, the patient is
given fatty food which will cause contraction of
the gallbladder. 20 to 40 minutes later again
films are taken to demonstrate if the gallblad
der contracts after fatty stimulus or not Normal
gallbladder contracts after fatty meal and within
40 minutes its size is reduced to 1 /3rd or l/4th
of its normal size. If the gallbladder fails' to
contract in response to fatty meal, it is said to
be ‘dyskinetic gallbladder ’.
Abnormal cholecystogram may demonstrate
poor visualisation or non-visualisation of the
gallbladder. It may also indicate presence of
filling defects for calculi or tumours. Oral
cholecystography with Telepaque is about 98%
accurate based on surgical findings.
Fig.46.2.— A signet-ring gallstone on straight X-ray Non-visualisation of the gallbladder usu
ally suggests that the gallbladder is diseased
and it has lost the concentrating ability of the dye. In other words visualisation of the gallbladder indicates a normal
gallbladder. Non-visualisation of the gallbladder may be caused by failure of absorption of oral contrast medium e.g. in
pyloric obstruction, excessive vomiting, excessive diarrhoea, hepatic dysfunction, hepatic or cystic duct obstruction.
Oral cholecystography is probably the best method to demonstrate gallbladder disease and calculi within it (either by
direct visualisation or by visualisation of filling defects). A few cases may show a normal gallbladder on oral chole
cystography though the patient is suffering from pain in the gallbladder region. In these cases cholecystokinin (CCK)
cholangiography may be used to deifine normal gallbladder contraction. 75 IVY units of CCK is given intravenously
and the normal gallbladder will show reduction of size more than 50% in 20 minutes.
Oral cholecystography still remains the standard procedure for establishing the diagnosis of chronic cholecystitis
and cholelithiasis in non-jaundiced patients. This method is seldom effective if the serum bilirubin is over 2 mg/100 ml
3. Intravenous cholangiography.— This technique is applied when the patients are unable to absorb the orally
administered contrast medium. The technique is probably suitable for visualisation of the bile ducts particularly after
cholecystectomy. This method can be applied to slightly jaundiced patients in whom serum bilirubin is not more than
3.5 mg/100 ml.
20 ml of biligrafin is injected very slowly through a vein taking about 3 minutes. Very soon contrast medium
appears in the bile with a concentration of 50 to 100 times that of the blood. This causes radiological visualisation of the
biliary tract.
Advantages.— For the gallbladder, it is inferior to oral cholecystography (it is only indicated in gallbladder disease
when the patient is unable to absorb the oral dye). Intravenous cholangiography has another advantage that it can
confirm gallbladder affection in acute cholecystitis (where oral cholecystography is contraindicated).
This technique may cause severe allergic reaction (cyanosis, stertorous respirations and inperceptible pulse), so a
test dose is usually given before administering the dye into the vein. If such reaction takes place, treatment is to admi
nister antihistamin drugs, oxygen and assisted respiration. Radionuclide scans are gradually replacing this technique.
4. Operative cholangiography.— In this method contrast dye is directly instilled into the cystic duct during
operation to demonstrate the entire biliary tract.
During operation, before doing cholecystectomy, the cystic duct is isolated and opened. A fine polythene catheter
is passed through the cystic duct into the common bile duct. Two ligatures are tightened — one distal to the opening of
the cystic duct (on the gallbladder side) and one or. the proximal side of the opening of the cystic duct. The latter
ligature is tied 011 the polythene catheter so that there is no leakage of the contrast medium through the opening of the
cystic duct. The catheter is filled with normal saline, so that no air bubble is pushed into the biliary tract which may give
X-ray appearance of a radiolucent gallstone. A cassette is placed beneath the patient so as to include the entire biliary
tract. 25% Hypaque or Urografin is pushed through the catheter and X-ray exposures are taken after momentary
stoppage of respiration (to obviate blurring of picture due to movement of respiration). A normal operative cholangiogram
makes exploration of the common bile duct unnecessary.
This technique should be performed in all cases of cholecystectomy in order to (i) know the congenital abnormali
ties of the cystic duct, hepatic ducts and the common bile duct and (ii) to detect stone in the biliary tract particularly at
the most distal part of the common bile duct which may not be detected by digital palpation and (iii) to know whether
exploration of bile duct is necessary or not (this prevents morbidity due to many unnecessary explorations of common
bile duct).
5. Postoperative cholangiography.— This is performed 10 to 14 days after choledochostomy through the T-tube
which was inserted into the bile duct during choledochostomy. This cholangiography is done prior to removal of the T-
tube to demonstrate (i) patency of the common bile duct, (ii) presence or absence of retained stones and (iii) whether
there is free passage of bile into the duodenum or not. 10 to 15 ml 50% Hypaque is diluted with normal saline to 30 ml
and this is administered slowly through the T-tube.
6. Ultrasonography.— Gallbladder ultrasonography is now very well established as the primary method for
gallstone detection. One recent perspective study has shown little difference in sensitivity between ultrasonography and
oral cholecystography if both are properly performed. Each method has a detection efficiency of more than 95%.
Ultrasonography however remains the technique of choice as it is more innoquous and is capable of providing
Fig.46.3.— Longitudinal scan showing Fig.46.4.— Longitudinal scan showing Fig.46.5.— Ultrasonography showing
normal gallbladder. grossly distended gallbladder. distended gallbladder. L.— Liver.
information about related structures in the right upper quadrant of the abdomen.
Inflammation of the gallbladder is seen as thickening of the layers of the gallbladder wall with mucosal
irregularity. Acute and chronic inflammation are not readily separated but the presence of a pericholecystic collection
or of fluid within the wall of the gallbladder indicates an acute process. Increase in bile density increases its echog-
enisity and reports of sludge within the gallbladder or common bile duct lumen may be detected. This phenomenon is
usually secondary to biliary stasis and is a physiological process. Sludge and pus are very similar in acoustic properties
and are indistinguishable in ultrasonography. Immediately drainage under local anaesthetic with fine needle aspiration
of the gallbadder under ultrasonography can produce spectacular results and greatly improves the condition of the
patient before definitive surgery.
Ultrasonography is less sensitive than scintigraphy in showing cystic duct obstruction but specificities of 99% have
been reported in acute cholecystitis, and the morphological changes shown by ultrasonography are more relevant to
treatment planning.
Ultrasonography reliably demonstrates stones with more than 90% accuracy. Only small calculi and a single stone
impacted in the cystic duct may be missed with this technique. This non-invasive technique is particularly helpful in
patients (i) with pregnancy, (11) with acute cholecystitis, (iii) who cannot absorb contrast medium given orally (oral
cholecystography) and
(iv) in jaundiced patients.
Carcinoma of the gall
bladder can present diag
nostic problems to the
ultrasonologists. Fixed
mucosal polyps of less
than 2 cm in diameter are
rarely of any significance,
but as the size increases
beyond this limit likeli
hood of malignancy in
creases quickly.
For JAUNDICED
PATIENTS ultrason
ography is at its best. As
sessment ofthe biliary tree can be measured accurately. The level of any obstruction can be shown reliably except for the
final few centimetres of the common bile duct (CBD). In good hands it is unusual to miss a bile duct or pancreatic tumour
and even CBD stones. Majority of the failures to find out the cause of an obstructive jaundice now occur with either
transient obstructions due to stones or to the presence of coexisting disease processes e.g. periampullary carcinoma.
Conventional ultrasonography is used widely in the investigation of gallstone disease, but is limited in the detection of bile
duct stones due to poor visualisation. It has been shown that endoscopic ultrasonography clearly visualises the entire
extrahepatic biliary tree and accurately identifies the bile duct stones. Sensitivity of ERCP and endoscopic ultrasonogra
phy in identifying stones was 79% and 88% respectively; specificity was 92% and 96% respectively.
Routine intra-operative cholangiography has been advocated to prevent bile duct injuries after laparoscopic cholecystectomy.
Preoperative intravenous cholangiography (IVC) may be performed routinely and intraoperative cholangiography is reserved for
indeterminate IVC examinations or the need for better anatomical clarification.
7. Computed Tomography (CT Scan).— This non-invasive technique is also helpful in diagnosing biliary cal
culi, but its efficacy is no better than ultrasonography. On the other hand it is more expensive. However it is useful for
those patients in whom ultrasonography is difficult e.g. obese patients and those with excessive bowel gas.
8. Radioisotope scanning (Cholescintigraphy).— A few isotopes have been used which are secreted in the bile
and can define gallbladder function and its pathology. Nowadays wTc"' labelled derivative of iminodi-acetic acid (Techne-
tium-IDA scan) is most often used. This is gamma-emitting agent which has a half life of 6 hours. After intravenous
administration, this material is excreted by the liver into the biliary ductal system. Normally the scan outlines the liver and
extrahepatic biliary tract including the gallbladder and shows the nuclide flowing into the upper small intestine as well.
This technique is the diagnostic choice in acute cholecystitis. In acute cholecystitis, the gallbladder is not seen on the scan,
presumably because the gallbladder outlet or the cystic duct is obstructed. Sensitivity of this test is almost 100%, that
means the test will be positive in all patients who actually suffer from acute cholecystitis. Complete obstruction of the
common bile duct or the common hepatic duct is detectable on the technetium-IDA scan. But choledocholithiasis or other
abnormalities are not so clearly seen as by PTC or ERCP.
9. Radiomanometry.— Bile duct pressure can be measured and this is abnormally raised in a few pathological
conditions. With X-ray image intensifier and TV control a graduated burette containing Hypaque is raised slowly against
a scale to see when the contrast medium starts flowing into the duodenum. The height of the meniscus in the burette at that
point indicates the biliary pressure. Normal pressure is 15 ± 3 cm of the contrast. A constant flow infusion technique may
also be employed to detect the pressure. The normal is about 23 ± 7 ml/min. High pressure is noted (i) where there is stone
in the distal part of the duct, (ii) pancreatitis, (iii) thickened and fibrosed sphincter of Oddi, (iv) underlying functional
change of the sphincter causing dyskinesia.
10. Choledochoscopy.— A choledochoscope inserted into the supraduodenal part of the common bile duct may be
employed to determine presence or absence of calculi there. This technique may be used when the common bile duct is
explored. Choledochoscopy can be used for removal of stones and bile duct tumour and for biopsy.
A few surgeons advocate the use of operative choledochoscopy; either rigid or flexible, in patients following gallstone
removal and regard this as a mandatory part of common bile duct exploration. The major indications remain acute obstruc
tive suppurative cholangitis, acute cholangitis and duct stones after cholecystectomy. There is continuing controversy
with regard to endoscopic removal of common bile duct stones. There is also scope for endoscopic sphincterotomy.
11. Percutaneous transhepatic cholangiography (PTC).— In the recent years by using a 23-gauge thin walled
needle the percentage of successful study has been increased and the incidence of complication has been decreased thus
Fig.46.8.— Cholangiogram showing dilated common bile Fig.46.9.— Cholangiogram showing dilated common bile
ducts (CBD), as a large calculus is obstructing the out- duct most probably due to carcinoma of head of the
flow at the distal end of CBD and another big stone is pancreas,
seen in the gallbladder.
making this an important investigating method. This investigation shows intra- or extrahepatic biliary obstruction due to
various causes. This should be done in the operation theatre keeping everything ready for operation, if be needed. The
prothrombin level should be raised to normal by I.M. injection of vitamin KI. The needle ensheathed by a flexible polypro
pylene tube is pushed through the liver into dilated intrahe-
patic biliary cannalicula. The needle is withdrawn, the
Fig.46.10.— Cholangiogram showing filling defects Fig.46.11.— Percutaneous cholangiogram showing

in the common bile duct due to carcinoma there. dilated intrahepatic ducts due to cholangiocarcinoma
at the hilum.
polypropylene tube is attached to a syringe and by trial and error aspiration of bile will be seen flowing into
the syringe At this time 20 to 40 ml of 45 percent

Hvpaque is injected and X-ray exposures are made At
least three attempts should he made before it is presumed
■
that there is no dilatation of the mtra-hepatic bile duel
Haemorrhage, biliary leakage and sepsis are the three
major complications of this investigation It should be a
routine practice to send some bile for culture and sensitiv
ity test so that if sepsis ultimately develops one can use
the most suitable antibiotic.
It should be confessed that PTC has largely been

replaced by ERCP which has a lower complication rate
and a greater therapeutic potential. Even a simple Chiba
needle study is likely to introduce infection So PTC should
be reserved for failures of endoscopic cannulation or for
delineation of obstructed segments prior to planned percu
taneous drainage.
12 Endoscopic Retrograde Cholangiopancreato
graphy (ERCP).— Nowadays common bile duct and pan
creatic ducts can be cannulated by side viewing fibre-
optic duodenoscope through ampulla of Vater Cannulation
of the papilla of Vater is carried out with the instrument
so positioned as to give an end-on-view of the papilla
from some 1 cm distance A polythene cannula is made
clear of air GALLSTONES
and flushed (CHOLELITHIASIS)
with 60% Urografin ITie Cannula
passed— Gallstones
is Incidence. through are not theuncommon in generaltaking
instrument population. careThese are not rare intothe first two decades
spill
Incidence
contrast gradually medium increasesinto
after 21 years
the and itduodenum
reaches the picksince in the 5th and this 6th decades. Women are
stimulates
peristalsismore often
affected andthan men makesin the ratio of cannulation
4 : 1. It is said that difficult.
gallstone is more Contrast
common in Fat, meFertile
dium
(multiparous), is Forty introduced
and Females i.e. slowly
four F’s. under fluoroscopic control. Both
biliary and pancreatic ductal systems
Composition of gallstone veries considerably. But the majorfill,elements but usually
in gallstone
Fig.46.12.- Endoscopic retrograde cholangiography duct fllls first If the pancreatic duct is filled first contrast
one
are cholesterol, bile
pigment
showing and calcium.
a stricture Gallstone
in the common alsoduct.
hepatic includes iron, carbonates, phosphorus,
medmm more than 2 to 2 5 mJ should nQt be mjerted
proteins, cellular debris, mucus
and carbohydrate. When the pancreatic ductules at the tail are filled injec
Pathogenesis
tion must be stopped of since — Mainly
stoneoverfilling willthere
lead toare four factors
extravasation andwhich contribute
will cause topancreatography
pain. After the formation of thegallastones.
tip of
These are : is1.readjusted
the cannula Metabolic to factor, 2. Reflux
fill the biliary duct. factor,
Now 40 3.
mlStasis factor
of contrast canand 4. Infective
be used factor.25% Hypaque is
and preferably
used1. toMET
preventABOLIC FACTOR.—The
obscuring of the small stones. solubility of the cholesterol
Its main indications are three :depends on—the
(i) Jaundice concentration
Persistent of conjugated
and recurrent
undiagnosed jaundice (cause of obstruction will be revealed); (ii) Biliary tract problems.— Undiagnosed upper
abdominal pain (suspected to be biliary in origin) and postoperative biliary symptoms; (iii) Pancreatic Disease.—
Undiagnosed abdominal or back pain (suspected to be pancreatic in origin), chronic and relapsing pancreatitis
(stricture, irregular dilatations, cysts etc. can be seen). The main complications of this procedure are infection
(including cholangitis and serum hepatitis) and pancreatitis.
bile salts and phospholipids. Lecithin is the predominant phospholipid in the bile. Cholesterol is insoluble i
aqueous solution, but is dissolved by bile acid into micelles alongwith phospholipids. It is maintained in
solution by the creation of micelles having central core of cholesterol surrounded by a hydrophilic shell ma
up of bile salts and lecithin. The normal ratio of bile acid to cholesterol is 25 : 1. But when this ratio falls to
13 : 1 the cholesterol precipitates and thus gallstone forms. The bile acid remains in the bile in the form of b
salts. So the basic defect is decreased bile acid and phospholipid secretion. It may so happen, particularly in
obese subject that cholesterol secretion is greatly increased without any reduction in bile salts and phospho
secretion. Excessive sucrose intake, liver damage, removal of ileum so that absorption of bile salts is
diminished, a Polya type of partial gastrectomy and infection with bacteria or fungi may cause precipitation
of cholesterol. Prolonged administration of progesterone and oestradiol to rabits resulted in the formation o
stones. This may explain frequent relationship of gallstones with multiparity.
Bile pigment stones usually result from excessive haemolysis, which is seen in haemolytic anaemia, sep
haemolysis and malaria. In these disorders there is increased breakdown of haemoglobin and the excess of
pigment excreted in the bile precipitates to form pigment stone. So in this group the liver and not the gallbl
appears to be responsible for producing stones.
2. REFLUX FACTOR.— Pancreatic enzymes have been detected in the gallbladder of patients suffering
from cholelithiasis. Reflux of pancreatic enzymes into the gallbadder is also considered to be the cause of
cholesterol precipitation. Trypsin disturbs colloidal balance and pancreatic phospholipase A may convert
lecithin into toxic lysolecithin.
3. STASIS FACTOR.— Temporary cessation of bile flow into the intestine and stagnation of bile in the
gallbladder has also been incriminated as a major factor in producing gallstones. Interruption of bile flow in
the intestine is associated with interruption of enterohepatic circulation, which in turn is accompanied by a
decrease in the output of bile salts and phospholipids reducing the solubility of cholesterol. Stasis is usual d
pregnancy and this may cause increased incidence of stones in multipara. Stasis may predispose bacterial
invasion and stone formation.
4. INFECTIVE FACTOR.— This factor seems to be the major cause of formation of gallstones. Moy-
nihan’s aphorism that a gallstone is a tomb stone erected in the memory of the organisms within it’ is still
true today. Evidence in favour of infection includes isolation of such organisms asE. coli, Bacterium typhos
and streptococcus from the gallbladder wall as well as from the centres of the stones in majority of gallston
Slow growing actinomyces have also been recovered in over half the gallstones examined in one series. The
organisms reach the gallbladder via the blood stream from a focus of infection elsewhere in the body. The
organisms may reach the gallbladder from the bowel through the lymphatics. Mixed stones are said to be
infective in origin.
Types of gallstones.—Primarily gallstones can be divided into two major groups — 1. Pure stones, which
constitute approximately 10% of all gallstones and 2. Mixed and combined gallstones which account for
approximately 90% of gallstones.
1. Pure stones.—
(i) CHOLESTEROL STONES.— Of the pure stones cholesterol is the commonest type. Majority of the
stones have particularly high content of cholesterol averaging 70%. But pure cholesterol stone which is
discussed here, is not common. This cholesterol stone is usually solitary with smooth surface. It is oval or ro
in shape. It is light in colour. A pure cholesterol stone is pale yellow in colour, but more often bile pigments
are deposited within it. Cholesterol stones are thought to be formed in aseptic static bile. That is why this ty
of stone is more often seen in Hartmann’s pouch. On section a cholesterol stone shows radiating lines which
cross the circular strata. Sometimes a stone starts as a pure cholesterol stone, but ultimately receives mixed
covering of pigment and cholesterol. This is known as combination stone.
(ii) PIGMENT STONES.— Pigment stones may be pure or consist of calcium bilirubinate.
Pure pigment stones are black or dark brown in colour and found almost exclusively in the gallbladder
These are associated with excessive haemolysis e.g. hereditary spherocytosis, sickle cell disease, thalassemi
etc. This is due to excessive breakdown of haemoglobin resulting in formation of excessive bilirubin which
are excreted in the bile and ultimately form pigment stones in the gallbladder. These stones are usually smal
soft, putty-like masses. On section pigment stones are amorphous.
Calcium bilirubinate stones are earthy brown to orange in colour and soft in consistency. These stones ar
more often seen in the bile ducts. These stones are also found within the intra- and extra-hepatic ducts. These
calcium bilirubinate stones contain bilirubin for about 50%. Cholesterol is also present in such stones in
concentration of about 5 to 25%. Calcium bilirubinate stones are often caused by infection. Recurrent pyogen
cholangitis or Oriental cholangiohepatitis often cause to precipitate calcium bilirubinate stones. Parasites and
E. coli often precipitate such stones. Mucin glycoprotein is also present in calcium bilirubinate stones.
(iii) CALCIUM CARBONATE STONES.— This is the rarest type of stone. These are greyish white in
colour with smooth surface. They have articulated surfaces as seen in mixed stones. Increased alkalinity of th
bile may favour precipitation of calcium carbonate with slow build up of stones over the course of a few year
Their sizes vary from sand grains to polyhedral shapes upto 2 cm in diameter
2. Mixed and combined stones.— Mixed gallstones referred to those having varying proportions of all
three of the stones forming constituents of the bile e.g. cholesterol, bile pigment and calcium. Combined
gallstones are those in which either the central core or external layers are pure and the remainder of the stone
is a mixture of constituents. Combined stones are sometimes solitary but mixed gallstones are invariably
multiple, often the gallblader is seen to be literally stuffed with hundreds of stones. These are mixed stones.
Their surfaces are faceted by mutual pressure. These stones may vary in size upto 2 cm in diameter. What wo
be the colour of such stones is determined by the predominence of the stone-forming constituent. When it is
cholesterol, it is yellow, when it is bilirubinate it is black and when it is calcium carbonate it is greyish white.
On section mixed stones look laminated. The central nucleus may contain epithelial debris and bacteria. This
suggests inflammatory origin of these stones. The laminations are composed of cholesterol, calcium bili
rubinate and calcium carbonate. Mixed stones are frequently associated with cholecystitis. In about V2 the ca
bacteria can be cultured from these gallbladders. Presumably the chemical inflammatory changes prepare the
soil for bacterial invasion.
EFFECTS AND COMPLICATIONS OF GALLSTONES
1. In the gallbladder.— (i) Asymptomatic gallstones;
(ii) Hydrops of the gallbladder;
(iii) Flatulent dyspepsia;
(iv) Gallstone colic;
(v) Acute obstructive cholecystitis, which may lead to (a) Mucocele, (b) Empyema, (c) Gangrene, (d)
Perforation and fistula formation;
(vi) Chronic cholecystitis;
(vii) Carcinoma.
2. In the common bile duct.— (i) Obstructive jaundice;
(ii) Liver failure,
(iii) Cholangitis;
(iv) Acute or recurrent pancreatitis.
3. In the pancreas.— (i) Acute pancreatitis;
(ii) Acute relapsing pancreatitis;
(iii) Chronic pancreatitis.
4. In the intestine — Gallstone ileus.
Gallstones may be associated with other diseases in the body.
Saint’s triad.— Gallstones, hiatus hernia and diverticulosis of the colon may coexist. The patient presents
with flatulent dyspepsia. Obesity is often noticed. What is the cause of association of these three conditions
is difficult to elicit. But obesity may be the single common factor which initiate all the three conditions.
Cholecystic heart.—Diseased gallbladder may cause decreased coronary blood flow, arrhythmia or heart
block. This is known as cholecystic heart. But it must be confessed that there must be some disorder ofthe hea
previously which was latent. Cholecystitis only reveals such latent disorder or worsen the condition. It has
been noticed that cholecystectomy often improves the symptoms of such 'cholecystic heart ’. Early cholecys
is advised to avoid operation at a later date when the cardiac condition may be less favourable.
Asymptomatic gallstones.—Liberal use of cholecystography and ultrasongraphy has resulted in the dia
gnosis of asymptomatic gallstones. Such asymptomatic gallstones after a long follow-up 50% has turned
symptomatic and serious complications have occurred in 20% of cases. The most dreaded complication of
asymptomatic gallstone is carcinoma of the gallbladder. Incidence of cancer of gallbladder in patients with
symptomatic gallstones range between 1 and 15%. It is yet to be established what is the real incidence of
carcinoma in asymptomatic cholelithiasis.
TREA TMENT.— Considering high incidence of ultimate development of symptoms and complications
and however small it may be the chance of cancer, the treatment is cholecystectomy.
Hydrops of the gallbladder.— Usually cholesterol type of gallstone may impact in the cystic duct or neck
of the gallbladder resulting in hydrops. The bile is absorbed and the gallbladder becomes filled and distend
with mucus. It is also called mucocele of the gallbladder.
Gallbladder is generally palpable and slightly tender. Slight jaundice may be seen if the oedema cons
equent upon impacted stone may encroach the common bile duct.
T reatment is early cholecystectomy to avoid complications such as infection, perforation of the gallblad
and even gallstone ileus.
Flatulent dyspepsia.— Stones in the gallbladder may cause such symptoms as flatulent dyspepsia. This
symptom includes a feeling of fullness after food, belching and heart bum which becomes worse after a larg
or fatty meal. Such symptom in a patient should arouse suspicion of presence of stone in the gallbladder. O
should exclude oesophageal hiatus hernia and chronic pancreatitis which also give rise to flatulent dyspeps
Gallstone colic.— When small calculi accumulate at the neck or at the entry of the cystic duct, muscles
of the gallbladder contract vigorously to expel those calculi from obstructing its mouth. Such vigorous mus
contraction of gallbladder causes gallstone colic. It usually occurs at night when the patient goes to bed and
in the horizontal position calculi find easier to accumulate at the neck or at the entry of the cystic duct. Such
colic gives rise to excruciating pain at the upper and right quadrant of the abdomen. The pain may shoot to
the back towards the inferior angle of the right scapula or may complain of referred pain at the right should
The patient tosses on the bed in agony to get some relief of pain in different postures, but in vain. Such atta
is often accompanied by nausea and vomiting and even retching This colic lasts for about 2 hours and it pa
off as suddenly as it came with great relief to the patient. Colic may last for longer period with great distres
to the patient. This may repeat later on.
ON EXAMINATION, it is often impossible to examine the abdomen satisfactorily. If the patient is excep
tionally co-operative one may find an enlarged gallbladder on palpation. Jaundice may follow an attack of
ladder colic in 20% of cases due to stone obstructing the common bile duct. Murphy’s sign is usually positiv
SPECIAL INVESTIGATIONS.— Straight X-ray may demonstrate radio-opaque stone in only 10% of
cases. Oral cholecystogram is not advised at the stage of gallstone colic as the liver function is depressed. O
investigations are more or less similar to those performed in acute cholecystitis.
TREA TMENT.— 1. T reatment of gallstone is cholecystectomy, but in acute cases treatment is same as
of acute cholecystitis.
2. If gallstone has migrated into the common bile duct — treatment is cholecystectomy with choled
olithotomy. Gallbladder has to be removed as the main source of stone is the gallbladder. The operation of
choledocholithotomy has been described later in this chapter.
ACUTE CHOLECYSTITIS
In about 90% of cases inflammation of the gallbladder is associated with calculi. Whether the stones are
the cause or the effect is yet to be proved. In about 60% cases of acute cholecystitis bile culture is positive w
shows bacterial cause of cholecystitis.
Pathogenesis.— Pathogenesis of acute cholecystitis can be conveniently described by four factors — (i)
Obstruction or stasis, (ii) Chemical irritation, (iii) Bacterial infection and (iv) Pancreatic reflux.
(i) OBSTRUCTION OR STASIS.— Stones obstructing the cystic duct can be implicated in upto 80% of
cases of acute cholecystitis. Even in the absence of stones at surgery or autopsy, obstructive factor cannot be
excluded since the stones might have passed into the common bile duct and G. I. tract. Kinking of gallbladde
or duct or pressure from anomalous vessel or from adjacent structures may cause non-calculous obstruction.
Oedema or erosion caused by the stone may also cause obstruction of outlet of gallbladder. Obstruction will
cause stasis of bile leading to progressive concentration of bile and chemical irritation of the gallbladder wall
It must be remembered that hydrops of the gallbladder, in which the outlet is obstructed by a stone, produce
marked distension, but acute inflammation does not follow. In animals, ligation of the cystic duct alone does
not produce acute cholecystitis. So simple outlet obstruction cannot cause acute cholecystitis until and unless
it is added with some other factor or factors.
(ii) CHEMICAL IRRIT ATION.— Such other factor may be chemical irritation with concentration ofbile
or erosion of the mucosa by a stone. Such erosion gives access to bile salts into tissue planes. Bile salts are ver
toxic to cells and this causes destruction of cells and chemical cholecystitis.
Venous or lymphatic stasis may play a contributory role in chemical irritations. Stone obstructing the cys
duct also impaires venous return. This causes congestion of the gallbladder. Such extrinsic pressure may
interfere with the blood supply of the gallbladder. This will make the gallbladder a prey to chemical irritation
by the concentrating bile.
(iii) BACTERIAL INFECTION.— In a small number of cases approximately 5 to 10% of all cases only
bacterial infection may be incriminated as the initiating aetiologic agent. There is usually some concomitant
severe infection elsewhere or septicaemia. Bacteria may reach gallbladder through blood, lymphatics, bile
ducts or by direct invasion from neighbouring viscera. The common offending organisms are E. coli. Stre
ptococci, Aerobacter, aerogenes, Klebsiella, Salmonella, Clostridia and Staphylococci. Gallbladder may be
secondarily involved by bacterial invasion which is already affected by interference with blood supply or
chemical injury. Once chemically injured, as mentioned in the earlier section, gallbladders may be prone to
develop secondary bacterial infections. Bacteria have been cultured from the gallbladder wall in 75% of cases
of acute cholecystitis. In acute cholecystitis small arteries may be secondarily occluded by the inflammatory
process. This will lead to gangrenous cholecystitis and subsequent perforation.
(iv) PANCREATIC REFLUX.— Experimentally injection of pancreatic enzymes exercises a definite
inflammatory response. Active lipases, amylases and proteases have been identified in the bile in patients
suffering from acute cholecystitis. Since pressure in the pancreatic duct is generally greater than that of the
billiary tract, presence of a common channel permits entry of pancreatic juice into the gallbladder.
Pathology.— The gallbladder is usually enlarged two to three times. It becomes bright red or violet to
green-black in colour. The serosa is congested, may be covered with a fibrinous exudate and may have areas
of gangrene or necrosis. The wall of the gallbladder becomes oedematous and thickened. The obstructing sto
may be noticed to be impacted in the infundibulum or the cystic duct. Bloody bile or pus may be found withi
the lumen. The mucosa may show sloughing in a few places. When the content exudate is virtually pure pus,
the condition is called Empyema of the Gallbladder. Cystic duct obstruction is essential for development of
empyema. In neglected cases spontaneous drainage of the gallbladder through the abdominal wall may occu
causing Empyema Necessitatis. Gallstones are usually present upto 80% of cases. Often a fine sandy gravel
is mixed with the biliary contents. The gallbladder wall may be thickened upto ten times the normal Oedema
fluid exudate and haemorrhage will flow from the cut surface. The mucosa is hyperaemic and may show nec
rotic surfaces in severe cases. This condition is called Gangrenous Cholecystitis. Certain areas of ischaemia
may be noticed due to thrombosis of the small arteries. Perforation through the site of ischaemic gangrene
may give rise to (a) biliary peritonitis. What is more common is that the omentum and surrounding viscera
and the parietal peritoneum will adhere and confine the area resulting in a (b) localisedpericholecystic abscess
or local abscess. Rarely the gangrenous area of the gallbladder becomes adherent to the wall of the duodenum
or the small intestine. In such case perforation through this gangrenous area may cause a (c) cholecystoenteric
fistula (internal fistula). Gallstone may pass through such fistula into the small intestine. If the stone is
sufficiently large it may be impacted at the distal part of the ileum near ileocaecal valve causing intestinal
obstruction. This is known as gallstone ileus (See Fig.46.13).
MICROSCOPIC PICTURE.— The inflammatory reac

tion consists of the usual pattern of acute inflammation i.e.
oedema, leucocytic infiltration, vascular congestion etc. Poly-
morphonuclears are relatively few and the exudate is thickened
in the outer layers of the wall. The epithelial lining may be
intact even when the inflammation is extremely acute There
may be ulceration in places. Inflammatory oedema is the most
striking feature. It may be observed in the mucosa, but it is
usually most abundant in the serous and subserous layers.
Oedema is responsible for most of the thickening of the wall
Some evidence of chronic cholecystitis may be present such as
hypertrophy of the muscular coat, out pouching of the mucosa
into the deeper layers and varying infiltration of chronic
inflammatory cells including eosinophils. This suggests that
acute cholecystitis has superimposed on chronic cholecystitis.
This is present in about 65%ofcases. These findings show that
acute cholecystitis frequently occurs in patients who have had
previous attacks.
As the acute process resolves, fibrosis of the wall and
chronic inflammatory infiltrate will be noticed.
Fig.46.13.— Straight X-ray of the abdo SYMPTOMS.— Majority attacks of acute cholecystitis
occur in patients who give past history of chronic cholecystitis
men showing gallstone ileus. Note air in
the biliary tree (shown by arrow) which is
and cholelithiasis. Acute cholecystitis can occur at any age but
diagnostic of this condition
the highest incidence is between 4th and 5th decades.
The onset is usually sudden. Often it follows a heavy, fatty meal. This is due to vigorous attempts of th
gallbladder to empty its contents. Acute cholecystitis presents as an acute abdominal emergency . Agonisin
pain is complained of in the right upper quadrant of the abdomen and may be referred back to the inferior
of the right scapula or in the inter-scapular area or to the right shoulder when the diaphragm is irritated b
the inflammatory process. Persistent pain in the area of the gallbladder is present in almost every case. Pain
probably is first caused by gallbladder distension and finally by inflammation of the gallbladder and adja
peritoneal surfaces. Persistence and severity of the pain serve to distinguish acute cholecystitis from gallbl
colic. In case of the former pain may last for several days, but in case of the latter pain rarely lasts for more
than a few hours. Nausea and vomiting are important symptoms and are seen in about 70% of cases. These
are reflex phenomena due to rapid rise in gallbladder pressure. Sometimes patient may induce vomiting i
attempt to gain relief.
SIGNS.— Pyrexia is a regular feature of acute cholecystitis. It may be absent only in the elderly and in
patients who take steroids or nonsteroidal anti-inflammatory drugs
Jaundice is present in only 10% of cases and is usually mild. This is accompanied by cholangitis. Jaundi
may be due to entry of bile pigments into the circulation through the damaged gallbladder mucosa. Jaund
may also occur from choledochal sphincter spasm induced by the adjacent inflammatory process. Concom
choledocholithiasis may also be the cause.
Tenderness in the right upper quadrant is a reliable finding. In about 'A of the patients there may be rig
idity. Rebound tenderness may also be present when the parietal peritoneum is inflammed. Murphy’s sign,
though often present, may not be solely relied upon. During deep palpation of the right upper quadrant, t
patient is asked to take deep breath in and out Patient complains of acute pain during deep inspiration wi
inspiratory arrest when tender inflamed gallbladder comes down and touches the palpating fingers. This
Murphy’s sign. A mass in the region of the gallbladder is palpable in 40% of cases. Gallbladder itself will be
palpable in some patients. In many cases a mass will be palpable because the omentum becomes attached
gallbladder in response to inflammation. There may be pericholecystic abscess which may also cause a mass
in the gallbladder region. Tender mass in the gallbladder area is almost pathognomonic of acute cholecystiti
Boas ’ssign, if present, is diagnostic of acute cholecystitis. This is an area of hyperaesthesia between the
9th and 11th ribs posteriorly on the right side.
Special Investigations.— 1. BLOOD.— Leucocytosis presents in 85% of cases with high polymorpho
nuclear count. There may be elevation of serum bilirubin and serum amylase (in l/3rd of cases). Serum
amylase may be as high as 1000 Somogyi units in acute cholecystitis.
2. E. C. G. should be done in all patients above 40 years of age.
3. STRAIGHT X-RAY of the abdomen in supine and in erect posture and an upright chest X-ray study
are essential. Only 15% of gallstones are radio-opaque. Upright chest X-ray is performed to exclude other
conditions of acute abdomen. Straight X-ray may indicate cholecystoenteric fistula.
4. CHOLECYSTOGRAPHY.— There is no place of oral cholecystography. Intravenous cholangiography
may be performed, but its place is gradually taken over by cholescintigraphy and ultrasonography.
5. CHOLESCINTIGRAPHY.— This is performed with a derivative of ^Technetium-iminodiacetic
acid (Technetium-IDA scan). This is the only specific test for acute cholecystitis. After intravenous inje
ction that contrast material is excreted by the liver into the biliary ductal system even in presence of hyper-
bilirubinaemia. Normally the scan outlines the liver and extrahepatic biliary system including the gallblad
der. In acute cholecystitis the gallbladder is not seen in the scan as the gallbladder outlet or the cystic duct
is obstructed. This test becomes positive in almost all patients who are actually suffering from acute
cholecystitis. Obstruction of the common bile duct or the hepatic duct is also detectable by this scan but
these are more clearly visualised by PTC or ERCP.
6. ULTRASONOGRAPHY can detect calculi within the gallbladder as also right upper quadrant mass
and enlargement of the bile duct and pancreas. One may perform routine ultrasonography in acute cho
lecystitis to confirm presence of gallstones.
Differential diagnosis.— Acute cholecystitis must be differentiated from other acute abdominal con
ditions e.g. perforated or penetrating peptic ulcer, acute pancreatitis, acute high retrocaecal appendicitis,
acute pyelonephritis, gallbladder colic and hepatitis. Acute cholecystitis should also be differentiated from
coronary thrombosis.
Complications.— The main complications of acute cholecystitis are (i) perforation, (ii) pericholecystic
abscess and (iii) internal fistula.
(i) Free perforation is rare. This will cause biliary peritonitis and the mortality rate is quite high.
(ii) Pericholecystic abscess results from perforation of the gallbladder walled-off by omentum and
adjacent organs e.g. stomach, duodenum, colon etc. This is more common than free perforation.
(iii) Internal fistula may form when gallbladder perforates into the G. I tract. Duodenum is the most
common site followed by colon. Cholecystojejunum and cholecystogastric fistulae are rare. Such internal
fistula may occur from Crohn's disease, tuberculosis, trauma and intra-abdominal abscess. Through this
fistula gallstones may pass into the small intestine. A sufficiently large gallstone may be impacted in the
terminal ileum resulting in gallstone ileus. In case of internal fistula air may be seen in the area of
gallbladder and biliary tree in straight X-ray (see Fig.46.13).
TREATMENT.— Though conflicting opinions exist as to whether immediate cholecystectomy should
be performed or not in case of acute cholecystitis, yet majority of surgeons in this region favour conserva
tive treatment followed by elective cholecystectomy at an interval of 6 weeks to 3 months. The believers
of this treatment explain that (i) most cases of acute cholecystitis subside on conservative management
without significant complications; (ii) Acute inflammatory changes obscure the anatomy and lead to
technical errors if the operation is performed early without conservative management; (iii) In early stages
there is vascular congestion and vigorous inflammation and surgery may be injurious by spreading
infection; (iv) Many of the patients with this disease may have associated diseases which should be excluded
and be treated before one ventures for cholecystectomy.
Conservative management aims at creating a situation of functional rest for the gallbladder and upper
51
gastrointestinal tract and relaxing spasm of sphincter of Oddi. This can be achieved by :
1. Nothing is given by mouth. Nasogastric aspiration should be started immediately and should be
continued for at least 3 to 5 days. Intravenous fluid administration should be started. In the beginning 5%
dextrose saline may be started, but subsequently fluids should be changed according to the electrolyte
balance of the patient. Monitoring of haemodynamic parameters and urinary output should influence fluid
administration.
2. Anticholinergic drugs should be given to reduce gastric and pancreatic secretion. This will also relax
the sphincter of Oddi.
3. Analgesics should be given to combat pain. Morphine and pethidine should be avoided as both these
drugs cause spasm of sphincter of Oddi. Though pethidine has got relaxant effect on the smooth muscles of
the G I. tract, yet it does cause spasm of sphincter of Oddi. Small amounts of Demerol may be used.
4. Antibiotics should be started immediately to control inflammatory process. Broad spectrum antibiot
ics are usually preferred. The broadest coverage may be achieved by the combination of ampicillin,
clindamycin and aminoglycoside But the last antibiotic is known for its toxicity. Therefore administration
of second generation cephalosporin is often practised by many surgeons Simple chloramphenical also has
a broad coverage on organisms of acute cholecystitis. But blood examinations should be performed regular
when this drug is used. Antibiotic should be initiated as soon as the diagnosis is made.
When temperature, pulse and other physical signs show that the inflammation is subsided, conservativ
treatment is continued. On the 3rd day suppository is given to empty the bowel. Once the bowel is moved,
tenderness is greatly reduced and there is disappearance of mass in the gallbladder region, gastric aspiratio
tube may be removed and fluids may be given by mouth. Gradually the I. V. drip is removed. After 5 days
soft fat free diet is given and gradually within a few days normal fat free diet can be recommended. An ora!
cholecystogram is advised 3 weeks later. Cholecystectomy is advised 8 to 10 weeks after the acute symptoms
have subsided.
CONSERVATIVE TREATMENT IS STOPPED and early cholecystectomy is advised — (i) if pain
and tenderness spread across the abdomen; (ii) Gallbladder lump becomes obvious and increases in size
alongwith increase in muscle rigidity and rebound tenderness; (iii) If pulse rate continues to rise alongwith
fever inspite of best conservative management and (iv) in the very ill and elderly patients who are not
responding to conservative management as expected (in these patients cholecystostomy is the operation of
choice).
CONSERVATIVE TREATMENT IS NOT ADVISED (i) when the diagnosis is in doubt and condi
tions like acute high retrocaecal appendicitis and peptic perforation have not been excluded; (ii) In case of
typhoid cholecystitis due to frequency of perforation in these cases.
Early and immediate operation is advocated by some surgeons. According to them 5% of patients fail
to respond to conservative management and more than '/2 of the patients who respond well initially expe
rience an exacerbation later on before elective surgery is advised. According to them low mortality rates are
expected from early cholecystectomy. The risk of operation in an area of inflammation is highly exagger
ated There is usually little difficulty in displaying the duct system. If early operation is performed and the
inflammatory process is seen to obscure the structures, cholecystostomy should be carried out. Cholecystosto
is also recommended for extremely ill and old patients. Early cholecystectomy, according to these surgeons
does not carry a mortality range of more than 0 to 5%.
Cholecystectomy.— The steps of this operation performed in case of acute cholecystitis is more or less
similar to the elective cholecystectomy and cholecystectomy performed for chronic cholecystitis and chol
elithiasis Only point is that one must be very careful to identify the junction of cystic duct and common bile
duct as inflammatory adhesions will make dissection at this area difficult. There is also every chance to
injure the ductal system as obscured by inflammatory process. The structures are so friable due to
inflammation that there is every possibility to injure the ductal system and the neighbouring structures.
There will be more bleeding in acute cholecystitis and this will make the operation more problematical.
Indications for exploration of the common bile duct are the same as those during elective cholecystectomy.
Cholecystostomy.— The gallbladder is segregated from other abdominal viscera by hot moist packs. A
wide-bore needle with a syringe is pushed through the fundus of the gallbladder to aspirate some bile from
it. Two pairs of tissue forceps are applied on each side of the needle and they are lifted up. The needle is
withdrawn and immediate incision is made through the puncture of the needle. The remaining contents are
evacuated including small stones. The neck of the gallbladder and cystic duct are carefully palpated. Any
calculi there are milked towards the gallbladder. In case a stone is firmly impacted at the neck of the cystic
duct there may be risk of inflicting severe trauma to dislodge this stones. In this case the surgeon should be
content with simple drainage to relieve the patient of the fulminating infection. Inflammatory oedema will
be subsided later on to loosen the stone, so that it may come out through the drainage opening or down the
duct into the bowel. The importance of removal of the stones cannot be over emphasized, as this will cause
gallbladder symptoms after removal of cholecystostomy tube if a stone is impacted within the infundibulum
or cystic duct. A rubber tube about half an inch in diameter is introduced into the gallbladder through the
incision at its fundus. This is kept in position with catgut stitch at the edge of the opening. The closure of
the incision around the duct is performed by a purse-string suture. The tube is brought out through a
separate stab incision below the right costal margin. A drainage is also provided.
Postoperative treatment.— The tube is connected with a receptacle at the bed side. The tube is taken off
after 7 to 10 days. The fistula closes spontaneously within a few weeks unless there is any obstruction in the
common bile duct. Cholangiography through the tube prior to its removal will identify retained stones,
which can be extracted under fluoroscopic guidance.
CHRONIC CHOLECYSTITIS
Chronic cholecystitis is of two types : One type follows an episode of acute cholecystitis and is known
as secondary chronic cholecystitis and the other type occurs primarily without antecedent acute cholecystitis
and is known as primary chronic cholecystitis.
PATHOLOGY.— The external surface of the gallbladder no longer has an appearance of thinness,
but it becomes opaque and yellow due to accumulation of subserous fat. The gallbladder may be dilated or
contracted depending on the relating balance of obstruction and inflammation If obstruction occurs before
the chronic inflammatory changes have had time to produce thickening, the gallbladder may be dilated and
relatively thin-walled. Otherwise the gallbladder is contracted and its wall is thickened. After opening the
gallbladder, the lumen usually contains fairly clear, greenish-yellow mucoid bile. Stones are present in 90%
of cases. The mucosa may show usual mucosal folds or flattening of the mucosal folds with thinning and
atrophy of the mucosa due to obstruction.
MICROSCOPICALLY the degree of inflammatory reaction is variable. In mild cases only scattered
lymphocytes, plasma cells and macrophages are found beneath the columnar epithelial cells and in the
subserous fibrous tissue. In more developed cases there is increase in fibrous tissue submucosally and
subserosally (numerous fibroblasts ) accompanied by mononuclear cell infiltration. In extreme cases the
wall may be permeated by fibres with considerable obliteration of the smooth musculature.
Rokitansky-Aschoff sinuses are found in 90% cases of chronic cholecystitis. This is due to out pouching
of the mucosa of the gallbladder through the muscularis presumably due to increased intracystic pressure.
Sometimes inflammatory proliferation of the mucosa is noticed with fusion of the mucosal folds giving rise
to buried crypts of epithelium within the gallbladder wall. This is known as cholecystitis glandularis
proliferans.
CLINICAL FEATURES.— Chronic cholecystitis is vague and insiduous to start with. It usually man
ifests itself by intolerance to fatty food, belching, postcibal epigastric distension, nausea and vomiting.
Recurrent attacks of pain in the right upper quadrant or epigastric region are common complaint. Pain
usually follows meals. There may be discomfort and not typical pain. Nausea and vomiting may occur
during the pain and often it is self induced in an attempt to get relief of pain. The discomfort may persist for
several days or only a few hours. There may be variable intervals between the attacks lasting for a month to
several years.
Sometimes the pain may be colicky in nature (gallbladder colic) which results from the temporary
obstruction of the gallbladder outlet by a stone in the cystic duct or the infundibulum Pain after a large m
is explained by gallbladder contraction induced by cholecystokinin against fixed obstniction. The pain
persists so long as the contraction remains and is relieved when the gallbladder relaxes Gallbladder pain
characteristically radiates to the back to inferior angle of the right scapula or inter-scapular region or to th
right shoulder.
PHYSICAL SIGNS.— Right upper quadrant tenderness or epigastric tenderness can only be elicited
during attacks. There is no muscle guarding or rebound tenderness. The gallbladder is also not palpable.I
jaundice is present it is due to choledocholithiasis rather than anything else. Murphy 's sign may be positi
SPECIAL INVESTIGATIONS.—1. Examination of blood does not reveal any specific picture.
2. Oral cholecystography shows non-visualisation of gallbladder and is quite diagnostic. If the liver
function is alright and the serum bilirubin level is normal this is a dependable diagnostic clue
3. Ultrasonography is highly sensitive accurate test for the diagnosis of gallstones. By using real
time grey-scale scanning an accuracy of about 98% has been claimed. It also demonstrates that the stone
moves to the dependent part of the gallbladder when the position of the patient is changed The advantag
of ultrasonography are that it is accurate, safe, does not use radiation and can be performed rapidly witho
preparation. For these reasons it is gradually replacing oral cholecystography in the diagnosis of chronic
cholecystitis.
Differential diagnosis of chronic cholecystitis include peptic ulcer, pancreatitis, oesophageal hiatus
hernia, appendicitis, right pyelonephritis, myocardial infarction, pleuritis. arthritic changes in the thoraci
spine causing radicular pain which radiates to the right upper quadrant and hepatitis.
TREATMENT.— CHOLECYSTECTOMY is the definite treatment for cholecystitis and cholelithiasis.
If the patient presents with biliary colic conservative treatment should be started immediately. This is
discussed later in this chapter.
CHOLECYSTECTOMY
These patients are likely to have some disturbances of liver function So glucose drink — 150 gm. daily
for 3 days should be given by mouth before operation. In cases where oral intake is not allowed. 5% gluco
may be given intravenously. Broad spectrum antibiotics should be started before operation, as cholangiti
may be associated with these conditions. An oral cholecystogram should always be done any time before
operation. When the patient gives history of jaundice with acute pain and fever (Charcot’s triad) during t
present illness the surgeon can ask for I V. Cholangiography.
Technique.— After preliminary exploration and taking the decision that gallbladder has to be remove
the surgeon will now proceed to perform cholecystectomy One wet mop is placed to displace downward
the duodenum, the transverse colon and coils of small intestine and another wet mop is placed slightly to
left of the common bile duct to displace the stomach to the left. These two mops are held by the assistant.
Now the inferior surface of the right lobe of the liver is retracted upwards by a Deaver’s retractor. The
whole of the gallbladder, common bile duct and cystic duct are now well exposed.
There are two principal methods, which can be adopted to remove the gallbladder. One is the 'duct-
first ’ mothod, i.e. the cystic duct and the artery are dissected first and divided, after which the gallbladder
removed. Another method is 'fundus-first' method, in which the dissection is started from the fundus of th
gallbladder and gradually proceeded towards the cystic duct which is divided last of all. But the first met
is popular because of the fact that there is less chance of injury to the common bile duct or to the right
hepatic artery as the dissection of the junction of the cystic duct and common bile duct is done first before
soiling of the part with exudate, haemorrhage or biliary leakage.
THE ‘DUCT-FIRST’ METHOD.— If the gallbladder is very much distended to prevent a good
dissection at its neck and cystic duct, it is better to aspirate the gallbladder first and then to clamp the
aspirating point so as to prevent biliary leakage. A sponge holding forceps is applied to the infundibulum
of the gallbladder and is used to retract the gallbladder to the right so that the cystic duct is made taut. Th
junction of the cystic and the common bile duct is now displayed by snipping the overlying peritoneum a
then by gauze dissection with Lahey’s forceps. If a stone is felt at the cystic duct it is milked towards the
gallbladder. If the stone remains impacted, the stone is removed through a small nick on the cystic duct. The
dissection at the junction of the cystic, common hepatic and common bile duct must be very clear. These
three ducts should be shown to the assistants so that not only the surgeon but also the assistants are satisfied
with the exposure.
This step is very important and the only way to prevent damage to the common bile duct, common
hepatic duct and the right hepatic artery. Moynihan’s cholecystectomy forceps is passed deep to the cystic
duct to bring No. 2 chromic catgut or silk. The ligature is now divided to make two strands of ligature. One
strand is tightened on the cystic duct about 1 cm distal to its junction with the common bile duct. The other
strand is tightened on the cystic duct at its junction /ith the common bile duct.
Operative cholangiography. It is
a good practice to do this X-ray investi
gation as a rule at this stage of opera
tion. This not only explores any con
genital abnormality which may be
present, but also gives a clear indica
tion whether the common bile duct
should be explored or not. Many a time
a small stone becomes impacted at the
ampulla of Vater and cannot be revealed
by palpation of the common bile duct.
Here lies the importance of the Opera
tive Cholangiography which so easily
reveals the stone. To do this cholangi
ography. a small polythene tube or a
ureteric catheter is pushed through a
small nick on the cystic duct just proxi
mal to the tightened ligature on the cys
tic duct nearer the gallbladder and
pushed along the cystic duct towards
the common bile duct and the second
ligature is now tightened over this tube
or catheter. Now a syringe containing
normal saline is fitted with the opposite
end of that tube. Some normal saline is
pushed through this tube to get rid of air bubble from the bile duct. This syringe is now replaced with a
syringe containing 17.5% Diodrast solution. 5 to 7 ml of this solution is pushed at a time through the tube.
An X-ray picture is taken. This is repeated thrice at five minutes interval. The polythene tube is taken out
and the second ligature is made tightened on the cystic duct near the junction with the common bile duct.
A Cholecystectomy forceps is applied just proximal to nick on the cystic duct and this duct is divided
between the second ligature and cholecystectomy forceps. Now the dissection is started to explore the cystic
arteiy which is mostly a branch of the right hepatic artery and lies posteriorly. The cystic artery is divided
between ligatures. The artery must be traced to the gallbladder before applying the ligature, as sometimes
the right hepatic artery is mistaken for cystic artery. The gallbladder is now only attached to the liver with
peritoneum. The cholecystectomy forceps holding the cystic duct is lifted up and the peritoneal reflection on
each side of the gallbladder is divided by scissors. This division is done more towards the gallbladder than
towards the liver so that a fringe of peritoneum can be retained with the liver on each side with which the
gallbladder bed can be covered. Some minute haemorrhagic spots may be seen in the gallbladder bed. This
is arrested by pressure with a hot moist pack or by light coagulation with the diathermy. If an aberrant
hepatocholecystic duct is encountered, it should be secured and ligatured.
It is a good practice to provide drainage after this operation, as there is always a chance of oozing from
the gallbladder bed or leakage of bile. A cigarette drain is commonly used.This drain is inserted through a
separate stab wound below the right costal margin. The inner end of the drain is kept at the hepatorenal
pouch of Morison near the gallbladder bed. This drain is generally taken out after 48 hours.
'FUNDUS-FIRST' METHOD.— This method is only applied when dissection at the region of the
junction of the cystic duct, common hepatic duct and common bile duct becomes difficult due to lots of
adhesions and inflammatory exudates. This operation of the gallbladder is commenced from the fundus.
The peritoneal sheath is divided with scissors on each side of the gallbladder. When the gallbladder is
completely freed from the liver, the cystic duct and the artery are defined as much as practicable. These ar
divided between ligatures. The danger remains of injuring the common bile duct and the right hepatic
artery.
OPERATIVE PROBLEMS
(1) The common bile duct and the right hepatic artery may be injured during the operation of mostly t
fundus-first-method. This can be avoided by clear dissection at the region of the junction of cystic duct and
common bile duct. This must be shown to the assistant. Before ligating the cystic artery, one must follow it
to the gallbladder and make sure that it is the cystic artery and not the right hepatic artery.
(2) An undetected duct may escape and lead to biliary peritonitis. This can be avoided by performing
operative cholangiogram and by looking for the hepatocholecystic duct.
(3) Sometimes the torn cystic artery may be slipped off the ligature and may lead to profuse
haemorrhage. Injudicious attempts to arrest this bleeding by catching the cystic artery with a pair of artery
forceps in pool of blood may lead to damage to the common bile duct, hepatic duct or right hepatic artery.
The ideal procedure is to pack the bleeding area tightly and leave it for five minutes. The packing is now
slowly removed, the bleeding vessel will be seen to spurt a little and it will be rather easy to secure this
vessel. It may sometimes be required to occlude temporarily the hepatic artery- proper at the foramen of
Winslow to minimise the bleeding and to help to catch the bleeding vessel.
(4) A drainage is a must after this operation as there may be biliary leakage from some unknown duct
which may lead to a syndrome known as Waltman-Walter ’s syndrome. This syndrome is manifested by
chest pain or an upper abdominal pain, tachycardia and a low blood pressure. It mimics coronary thro
mbosis. pulmonary embolism etc. This condition is fatal and no time should be wasted to re-explore the
abdomen, once this diagnosis is made.
POSTOPERATIVE TREATMENT.—
The drain is removed after 48 hours. It may be kept for longer period, if the discharge continues. Naso
gastric aspiration and intravenous fluid administration are continued until the peristalsis of the intestine
comes back and the patient passes flatus. At this time aspiration and fluid administration are stopped and
liquid diet is gradually allowed by mouth. Next semi-solid and fat free solid diet are gradually given.
Indications for exploration of the common bile duct.—
(1) When there is a history of intermittent jaundice or biliary colic;
(2) When one or more stones can be palpated within its lumen;
(3) When the bile duct is dilated and thickened and ^
(4) When on aspiration the bile is white’, one should explore the common bile duct.
It should not be considered that exploration of the bile duct can be done as a routine practice along wi
cholecystectomy as this little operation is not without its cost. It also increases the convalescent period.
The role of Operative Cholangiography in this respect cannot be overemphasised. A small stone at the
ampulla of Vater can be missed by all the indications given above but would not be missed by operative
cholangiography. Small soft calculi may be missed by palpating fingers but not by operative cholangiogra
Gallstone dissolution.— Predominantly cholesterol gallstone can be dissolved in some patients by oral
administration of chenodeoxycholic acid (Chenodiol). This is a type of bile acid that will dissolve choles
terol stone. In various studies it is proved that the therapy for 2 years resulted in complete dissolution in
14% and partial dissolution in 40% of cases. Dissolution is more common in female patients with small
floating stones and those with serum cholesterol level above 250 mg/100 ml. This drug therapy must be
continued even after dissolution to prevent recurrence of stones. The side effects of this drug is mild
diarrhoea and elevated serum transaminase level. Ursodeoxycholic acid has been used with similar success
and with little side effects. At present this drug therapy should be reserved for elderly patients or young
individuals who have other associated diseases that pose a high operative risk.
ALTERNATIVES TO CHOLECYSTECTOMY FOR GALLSTONES.—

Surgeons have always tried to cause less discomfort to the patient and to minimise hospital stay after
cholecystectomy. The benefits of early ambulation after surgery are now well established. Nasogastric tubes
can often be omitted or removed soon after surgery and early postoperative feeding has been instituted to
minimise hospital stay. The necessity of draining the subhepatic space following cholecystectomy is no
longer accepted as routine and may indeed lead to more complications and prolonged hospital stay.
Mini cholecystectomy.—
Short subcostal muscle splitting incision has been made for quick wound healing and short hospital
stay. The incision is slightly longer than appendicectomy incision and basically the same muscle splitting
type. This can give an adequate exposure for safe biliary surgery particularly if the surgeon uses modern
fixed retraction system. During cholecystectomy fundus to neck method has been adopted to shorter the
period of operation.
Laparoscopic cholecystectomy.—
The effort to reduce cholecystectomy to its least invasive form has laid to the recent development of
laparoscopic cholecystectomy. The rationale for laparoscopic cholecystectomy is based on good cosmetic
result, rapid healing of the operative wound, reduction of hospital stay and ability to return to work soon
after surgery.
Technique.— Numerous descriptions of the technique of this operation have appeared recently. Some
surgeons position the patient in the lithotomy position. But the standard procedure is that the surgeon stand
on the patient’s left side with the monitor level with the patient’s right shoulder. A second monitor may be
placed on the left of the patient for the benefit of the assistants. A 10 mm cannula is introduced into the
umbilicus for carrying the laparoscope. A second 10 mm cannula is inserted just to the right of the midline
below the xyphoid process and to the right of the falciform ligament to introduce operating instruments
Two 5 mm cannulas are inserted under laparoscopic vision into the right upper quadrant of the abdomen —
one in the midclavicular line close to the costal margin and a second low down on the anterior axillary line
These will be used to carry ratracting forceps held by the assistant.
After the fundus of the gallbladder has been grasped and retracted up and over the liver, any adhesions
are taken down by blunt dissection, or divided with scissors as appropriate. The second grasping forceps is
placed on the neck of the gaflbladder and the cystic duct and artery are displayed by blunt dissection with
curved dissecting forceps or with a hooked diathermy dissector. After demonstration of the anatomy of the
structures in Calot’s triangle, the cystic duct is nicked and may be cannulated for an operative cholangiogram
The operation proceeds are exactly same as in traditional cholecystectomy with division of the cystic duct
and artery and dissection of the gallbladder from its bed. Freeing of the gallbladder from the liver may be
performed using an electrocautary probe of laser dissection for haemostasis. Irrigation and suction are used
to wash away blood, and haemostasis is achieved as the dissection progresses. After the gallbladder is freed,
it is grasped at the cystic duct remnant and withdrawn into one of the 10 mm cannulas. When part of the
gallbladder appears on the surface of the abdomen, the gallbladder is opened and its contents evacuated
prior to the delivery of the remainder of the gallbladder through the wound. If the gallbladder is performed
during dissection leakage of the bile may be controlled either by repositioning the grasping forceps or by
application of a ligature to the gallbladder. An acutely inflamed friable gallbladder may be removed
piece-meal, in which case the fragments of the gallbladder and the gallstones are placed in an Espiner bag
(Ethicon) introduced for this purpose.
A video camera may be attached to or incorporated into the laparoscope and is manipulated by an
8(18 A CONCISE TEXTBOOK OF SURGERY
assistant. This frees the surgeon’s hand for manipulating the dissecting instruments while allowing the surg
and all the assistants an excellent view of the operative field.
Its advocates are excited by its early promise and suggests that over 90% of patients coming to cholecyst
tomy are suitable for this operation. Intravenous cholangiography should be performed preoperatively in al
patients and if choledocholithiasis is confirmed then a formal open operation is performed. Alternatively, if
duct stones are found at the laparoscopic operation on cholangiography, then either this procedure is aband
an ERCP and stone removal can be carried out at a later date. As open operation might be required at any ti
during the laparoscopic procedure, this should always be performed by the biliary surgeons.
Major operative complications of this procedure are — (i) bile leakage in 4% of cases, (ii) bile duct injury in 1% of cases, (iii)
perforation of viscus e.g. jejunum, (iv) pancreatitis, (v) bleeding etc. As experience grows and operative expertise improves, it is
possible, that such complications may become less frequent.
Operative results are extremely encouraging with more than 90% success rate. The complication rate appears to be low, although
operating time is longer. Hospital stay is extremely short. Indeed in some centres the procedure is performed on a day-case basis, though
in majority of cases postoperative stay is usually 1 to 2 days. 2/3rds of patients return to work within 14 days, though quite a number of
patients return to full employment within 1 week.
Needlescopic cholecystectomy.—
Several studies have been reported regarding the feasibility of using needlescopic instruments with a diameter of less than
3 mm in minimally invasive surgery. Patients with this surgery had less pain and obviously smaller scars than conventional
laparoscopic cholecystectomy. In this surgery the patients require fewer intramuscular pethidine injections. So needlescopic
cholecystectomy resulted in less postoperative pain and a smaller surgical scar than laparoscopic cholecystectomy. For
needlescopic procedure, the ports are 10 mm, 2 mm, 3 mm and 2 mm in the umbilicus, right lateral abdomen, right hypochon-
drium and epigastrium respectively. The gallbladder fundus is held with a 2 mm grasper, Hartmann’s pouch is held with 3 mm
grasper and dissection is performed using a 1.7 mm ball-tipped coagulator. The camera is charged to a 3 mm needlescope for
clipping of the cystic artery and cystic duct and subsequently changed back to the 10 mm instrument for division of the cystic
structures using a pair of 2 mm scissors. The combined lengths of the incisions are measured and dressings are the same in
both categories of patients. All patients receive a standard analgesic protocol with oral naproxen 375 mg twice daily and
intramuscular pethidine 1 mg/kg every 6 hours according to individual need. It must be remembered that the conversion rate
is around 10% when the author is writing this article mostly to conventional laparoscopic cholecystectomy or rarely to an open
operation. Patients after needlescopic cholecystectomy usually have less postoperative pain and intramuscular pethidine injec
tion requirements is fewer than the laparoscopic group. Post-operative stay in hospital is usually 2 days. The operating time
may be slightly longer, but due to reduction in scar size the need for postoperative analgesia is less.
Needlescopic instruments may be used to perform other operations such as appendicectomy, fundoplication, adrena
lectomy, inguinal herniorrhaphy etc.
The benefits to the patients have to be weighed against the additional expenses involved in the use of needlescopic
instruments. Non thickened and relatively less inflammed gallbladders should be selected for needlescopic surgery, other
wise conversion to laparoscopic cholecystectomy may be more. It must be remembered that dissection to identify the
cystic structures are done safely using 10 mm laparoscope. The view is changed to 3 mm needlescope only for clipping
and not for division of the cystic artery and duct.
Extracorporeal shock wave lithotripsy (ESWL).—
This technique has become quite successful for renal calculi. Renal calculi pass spontaneously after fragmentation,
but the biliary tract does not provide such a simple passage for fragment stones. The cystic duct is not an easy channel to
pass for fragmented calculi. This new technique has been greeted with perhaps exaggerated enthusiasm. This technique
however may be used as an adjunct to pharmacological dissolution therapy.
Oral dissolution therapy.— About 80% of gallstones are predominantly composed of cholesterol. These cholesterol stones
are amenable to dissolution therapy. These cholesterol stones form as the patients secrete bile which is saturated in cholestero
due to reduced bile acids in bile. If bile acids are given therapeutically, this not only increases concentration of bile acids in the
bile, but also decrease cholesterol saturation in bile. Chenodeoxycholic acid and ursodeoxycholic acid are two naturally occur
ring bile acids that may be given orally for gallstone dissolution. These bile acids reduce cholesterol saturation in bile and
dissolve gallstones. Chenodeoxycholic acid also reduces HMG-CoA reductase activity thus reducing the synthesis and secretio
of cholesterol. Moreover bile acid synthesis from cholesterol in the liver may be increased by ursodeoxycholic acid.
Both these drugs have been widely used in clinical practice and appear to be safe. Chenodeoxycholic acid may cause
diarrhoea and it also causes minor lipid alterations and carries a small theoretical risk of promoting atherosclerosis. It may
also cause minor reversible elevations in serum liver enzymes. Ursodeoxycholic acid on the other hand does not have any
adverse effect and is therefore more preferred in treating gallstones, though it is more expensive. Any of these drugs is
used at a dose of approximately 15 mg/kg per day. When used together each drug is given 7 mg/kg/day. The latter only
THE BILIARY SYSTEM S09
reduces cost and side effects.

Rowachol is a non-bile acid compound and when administered orally dissolve gallstones in human beings. It has 6 cyclic
monoterpene oils including menthol. It depresses HMG-CoA reductase and possibly inhibits nucleation of crystals in bile. It has
choleretic antispasmodic properties with minimal side effects. It is not very expensive.
It should be remembered that patients should have functioning gallbladders if these dissolving drugs are to be used.
The stones should be radiolucent and less than 15 mm in size. Small floating and radiolucent stones on oral cholecystog
raphy are usually rich in cholesterol and are particularly suitable for dissolution therapy. Success rate has been quoted as
90%. Radio-opaque stones or pigment stones with non-functioning gallbladder are contraindications for this therapy.
Stones of 5 to 10 mm in diameter usually dissolve within 1 to 2 years. Smaller stones require shorter time. Patients
should be monitored for stone size during treatment. The symptoms may continue during therapy, though the risk of
complications is not apprehending.
This therapy however has not become popular. Only less than 20% of patients with gallstones fulfill the requirements for diss
tion therapy. Even when the cases are suitable, success rate is 60% in neutral studies and the duration of treatment is about 18
months. However it remains as a safe alternative to those who are unwilling or unfit for surgery.
Direct contact gallstone dissolution therapy.—The main disadvantage of oral dissolution therapy is the length of time required
for complete gallstones clearance. In direct contact method, a 5-french pigtail polyethylene catheter is introduced transcutaneou
through the liver into the gallbladder using local anaesthesia and under a combination of fluoroscopic and ultrasound control. 5 to
of MTBE (Methyl tert-butyl ether) is repeatedly instilled and aspirated through the catheter thus agitating the gallbladder contents
MTBE rapidly dissolves cholesterol gallstones and these stones can be cleared in a matter of hours, though some stones may ta
3 days, particularly if the stones are multiple.
There are notable drawbacks, firstly, difficulty in inserting the catheter. Secondly, stones with calcium will not be
dissolved. Thirdly, the toxicity of MTBE is a cause for anxiety with the side effects e.g. nausea, vomiting, duodenal
erosion etc. It is also highly inflammable and explosive. Calcium solvents, e.g. ethylene diamine tetra-acetic acid (EDTA)
have not been proved successful.
Contact gallstone dissolution therapy with MTBE is unlikely at present to have a wide role in clinical practice.
Alternatively, combined treatments using dissolution together with ESWL may find an application.
GALLSTONE RECURRENCE has never been much studied, as cholecystectomy was the treatment of choice for
gallstone. After advent of ESWL and more enthusiasm in oral dissolution therapy, there has been a study about gallstone
recurrence. The recurrence rate in 2 to 12 years after confirmed complete gallstone dissolution is between 30 and 60%. In
fact in 1st five years the recurrence rate is about 30 to 50%. Only one word I would like to mention regarding prevention
of recurrence is that non-steroidal antiinflammatory drugs (e.g. aspirin) are known to reduce the incidence of recurrence of
gallstone. Probably this drug inhibits prostaglandin-mediated stimulation of mucin secretion by the gallbladder and in fact
mucin acts as a nucleating agent.
POSTCHOLECYSTECTOMY SYMPTOMS
Majority of the patients are relieved of symptoms after cholecystectomy. Unfortunately in 15% of cases the
same symptoms persist following cholecystectomy. For these cases sometimes the term ‘postcholecystectomy
syndrome’ is often used wrongly. Actually the patients suffer from the same symptoms as previously so the
better nomenclature is ‘postcholecystectomy symptoms’. The causes may be (a) extrabiliary disorders or (b)
disorders of the extrahepatic biliary tract.
(a) Extrabiliary disorders.— A few conditions of the abdomen give rise to similar symptoms as cholelithiasis and
during investigations if gallstones are detected, cholecystectomy is performed. But the main disease remains causing the
same symptoms as previous to cholecystectomy. These conditions are hiatus hernia, peptic ulcer and chronic pancreatitis.
(b) Disorders of the biliary tract.— The common disorders which give rise to symptoms after chole
cystectomy are (i) residual stone in the common duct, (ii) stricture of the bile duct (often caused by trauma
during cholecystectomy), (iii) cystic duct syndrome and (iv) biliary dyskinesia.
(i) Residual stone in the common duct.— So far as the residual stone in the common duct is concerned,
operative cholangiography has gone a long way to prevent this. Further, postoperative T-tube cholangiogram
has also reduced incidence of this condition.
(ii) Stricture of the bile duct.— This is discussed later in this chapter.
(iii) Cystic duct syndrome.—A comparatively long stump of cystic duct may cause symptoms suggestive
of calculous cholecystitis. Excision of such stump in the 2nd operation has mostly cured the condition. Some
times the long cystic duct stump may be dilated resembling a miniature gallbladder. Stones may form
in such dilated cystic duct. Operative cholangiography has also helped to detect such condition and give
warning to the surgeons so that he also removes the cystic duct stump during cholecystectomy. Sometimes
the cystic duct joins with the common bile duct lower than usual and after dissecting that region the
surgeons may miss this condition. This is again revealed by operative cholangiogram.
(iv) Bilary dyskinesia.— Fibrosis and stenosis of the sphincter of Oddi and/or of the papilla of Vater
a clinical entity and is often responsible for intermittent or continuous attacks of pain in the right upper
quadrant of abdomen, with or without associated jaundice. The concept of biliary distension as a result of
spasm of the sphincter of Oddi in the absence of such organic changes in the ampulla may be developed in
many patients This stenosis of sphincter of Oddi is commoner in females than in males in the ratio of 3 : 1
The condition may be revealed at any age, but more frequently observ ed between 50 to 70 years of age.
ACUTE ACALCULOUS CHOLECYSTITIS
Acute inflammation of the gallbladder may occur in absence of gallstones in approximately 8% of
cases. This condition is more common in males at the ratio of 1.5 : 1.
Aetiology.— Three major factors have been incriminated to cause this condition. These are (i) Stasis,
(ii) Sepsis and (iii) Ischaemia.
(i) Stasis.— In absence of stone, stasis may be caused by absence of release of cholecystokinin (which
causes regular contraction of the gallbladder), a hormone released by certain products of digestion in the u
small intestine. With extraction of water from the gallbladder, bile is reduced to a viscid material known as
sludge’. Such viscid bile may cause functional obstruction of the gallbladder leading to oedema, venous an
layniphaticobstruction, necrosisetc. Stasiswill alsorenderitmoresusceptibletocolonizationofbacteria. Such
stasis has been caused by lack of oral nutrient intake, trauma, major operative procedures, serious debilitat
diseases and administration of narcotics. These are the conditions in which acalculous cholecystitis may oc
(ii) Sepsis.— Injection of E.coli endotoxin into dogs causes acute cholecystitis. So sepsis plays an
important role in the development of acalculous cholecystitis.
(iii) Ischaemia.— Brief or prolonged periods of hypotension is not uncommon during major opera
tions, trauma, burns and in sepsis. Decreased blood flow to the gallbladder epithelium may cause ulcers in
the mucous membrane through which concentrated bile acid gets access to the gallbladder wall. This being
toxic to the tissues, will cause acute cholecystitis. But again acalculous cholecystitis is a rare consequence o
hypotension, so question remains how far ischaemia or hypotension causes acalculous cholecystitis. Throm
of the arterioles of cystic artery may also cause ischaemia and acute acalculous cholecystitis,
(iv) A few other causes have also been incriminated to cause such acalculous cholecystitis. These are
(a) spasm of the sphincter of Oddi, (b) specific infections such as typhoid fever and actinomycosis and (c)
wide variety of febrile illnesses in young children.
Pathology.— Pathology of acute acalculous cholecystitis is almost similar to that of calculous cholecystit
only difference is that the acalculous variety is more prone to gangrene and perforation. Whether this is du
to delayed diagnosis and treatment remains to be found out. Acute acalculous cholecystitis is often caused
recent trauma, major surgery, bacterial sepsis, cardiovascular disease, diabetes, debilitating diseases,
prolonged illness, multiple transfusions and administration of total parenteral nutrition. This itself in
creases higher mortality rate and late diagnosis of acute cholecystitis.
Clinical features.— Symptoms are identical to those of acute calculous cholecystitis, though they may
be masked by symptoms of precedent conditions.
The most significant physical findings are fever and tenderness in the right upper quadrant of the
abdomen. Jaundice is less frequent. Slight abdominal distension and absent bowel sounds may be present
'Ath of the cases.
Special Investigations.— Elevated W.B.C. count, high alkaline phosphatase and SGOT level give
some clue to the diagnosis.
Cholescintigraphy, which is the best investigative procedure in case of acute calculous cholecystitis is
also accurate in about 85% of these cases. Higher incidence of false positive scans have been reported, as
radionuclide may not be able to enter the otherwise normal gallbladder if the bile is viscid.
Ultrasonography may be helpful by showing distension and thickening of the gallbladder.

Treatment.— Emergency cholecystectomy is the treatment of choice, though conservative treatment
and delayed operation is indicated for acute calculous cholecystitis. This is due to more chance of gangrene
and perforation in this condition. During operation, if possible operative cholangiography may be per
formed to exclude possibility of passage of single gallstone into the common bile duct. In difficult cases one
may perform cholecystostomy It must be remembered that mortality rate of acute acalculous cholecystitis i
more than acute calculous cholecystitis because of the antecedent and concomitant conditions.
CHRONIC ACALCULOUS CHOLECYSTITIS
In comparison to acute acalculous cholecystitis, the entity of chronic acalculous cholecystitis is
doubtful. Anyway symptoms of chronic cholecystitis when present with absence of stone in the gallbladder
found out by repeated ultrasonography, is a condition known as chronic acalculous cholecystitis. This is
often associated with cholesterosis and adenofnyomatosis. The treatment is again confusing, though
cholecystectomy has been reported to relieve the symptoms.
CHOLESTEROSIS (SYN. STRAWBERRY GALLBLADDER)
This condition was first described by Moynihan and later on McCarty gave the name starwberry
gallbladder’. In this condition the red mucosa of the gallbladder is studded with tiny yellow flecks giving a
typical picture of ripe strawberry. Sometimes the entire gallbladder may be involved and other times only
one portion is involved.
This condition represents a local disturbance in cholesterol metabolism and not associated with
disturbance of the cholesterol level in the blood. A few views have been put forward to explain this conditi
-— (a) excessive abnormal absorption of cholesterol from the bile by the epithelial cells of the gallbladder
causes this condition; (b) Lymphatic and venous stasis predispose to the accumulation of cholesterol
absorbed from the bile contents; (c) Failure of the mucosa to secrete cholesterol results in an abnormal
deposition of cholesterol within the mucosa and submucosa.
PATHOLOGY.— The main pathology is that the mucosa of the gallbladder is studded with minute
yellow flecks.
Histologically there is distension of the mucosal folds with aggregation of round and polyhedral
histiocytes within these mucosal folds. These histiocytes have fat-laden cytoplasm and small, dark, promin
nuclei. When the deposits become more massive these cells die with release of lipids giving rise to precipita
of cholesterol crystals in the subepithelial region. The yellow material is sometimes confined to the summit
of the ridges and sometimes it can be traced down into the depth of the recesses. In severe cases the distribu
is widespread. Cholesterol content of the mucosa of strawberry gallbladder is enormously in excess to that
in the normal organ. Occasionally focal collections of lipid-laden histiocytes may take the form of polyp
formation, which are known as cholesterol polyps. These are obviously not true neoplasms, but focal forms
of cholesterosis.
Some inflammatory reaction with presence of white cells, giant cells and fibroblasts may be seen aroun
Clinical features.— This condition is asymptomatic and is only discovered incidentally at surgery or
in postmortem. When symptoms are present they are usually due to associated cholecystitis or gallstones. O
or more cholesterol stones may be present, supposedly derived from the deposits in the mucous membrane
Oral cholecystography will show gallbladder with dense contrast medium and slightly blurred edge of
gallbladder.
CHOLEDOCHOLITHIASIS (STONES IN THE COMMON BILE DUCT)
In about 10% of cases of cholelithiasis, stones are found in the common bile duct. In majority of cases
stones migrate from the gallbladder. These are known as secondary bile duct stones. It may happen that the
stones found in the common bile duct are larger than the diameter of the cystic duct. This is due to the fact
that the stones grow bigger within the bile duct system.
Stones may form within the bile ducts. These stones are called primary bile duct stones. These are
usually made up of calcium bilirubinate and are usually associated with bile duct obstruction. The
pathogenesis of such stones is thought to be precipitation of unconjugated bilirubin as the calcium salt.
Normally bilirubin is conjugated as glucuronide. This is soluble form of bilirubin. When this soluble
bilirubin glucuronide is deconjugated by beta-glucuronidase, an enzyme produced by the epithelium of the
biliary tract and by bacteria such as E. Coli, insoluble unconjugated bilirubin is formed to precipitate with
calcium. Some sort of biliary obstruction e.g. post-traumatic biliary stricture, stenosis of the sphincter of
Oddi, sclerosing cholangitis, Oriental cholangiohepatitis and narrowed biliary-enteric anastomosis are
the usual causes.
(i) Common bile duct calculi may rarely be asymptomatic. Occasionally stones may lie dormant for many
years in the bile duct giving rise to only vague indigestion
(ii) Pain.— Typically biliary colic is caused by stone in the common bile duct This biliary colic is more
or less similar to the gallbladder colic. Biliary colic is characterised by right hypochonodrial pain, ill localised
and with variable radiation to the back (to the inferior angle of the right scapula) or to right shoulder. The pa
is often not truely colicky; it is more obstructive in nature, of gradual onset, rising to a pick which is sustained
for some hours or even a day or two and gradually subsiding. Systemic upset is minimal, although reflex nau
and vomiting may occur. The pain is sometimes merely a discomfort, while in other cases it is excruciating.
This latter type is often called colic’. Fatty foods often precipitate it.
'Gallstone colic ’ is a severe pain caused by spasm of the gallbladder as it tries to force down a stone in the
cystic duct. This is described in the section of Cholelithiasis’. This gallbladder colic and biliary colic are in
fact not typical colics. As the pain is intermittent and sometimes excruciating, they are often called colics. But
the character of the pain is usually not griping. The ‘biliary colic’ is even less common as there is very little
smooth muscle in the wall of the common bile duct.
(iii) Jaundice.— Within 48 hours the pain isfollowed by jaundice. The tinge of jaundice ranges from pale
lemon to bright orange. The urine becomes yellow with bile and the faeces become pale. Jaundice will be inte
mittent if the obstruction is partial, or it may be progressive if the stone becomes impacted in the distal duct.
The skin becomes itching and this sometimes becomes intolerable. With the jaundice, patient loses weight.
(iv) Fever.— Chills and fever are usually associated with abdominal pain. Rise of temperature is often due
to cholangitis. Sometimes in late cases symptoms of cholangitis are accompanied by shock and confusion.
Fluctuating jaundice, pain in the right upper quadrant of the abdomen and fever with rigors constitute
CHARCOT’S TRIAD. This is classically seen in case of stone in the common bile duct. In the beginning the
stone remains floating in the bile duct and later on it gets impacted. When the proximal duct dilates the
stone again becomes loose, but subsequently impacts again. Stones may be impacted anywhere in the com
mon bile duct. But the commonest site is in the supraduodenal part just above the upper margin of the first
part of the duodenum. The second common site is the retroduodenal part and the third common site is in the
ampulla of Vater.
PHYSICAL EXAMINATION.— Tenderness in the right upper quadrant or in the epigastrium is the usua
finding. Obviously jaundice and fever may be present. No definite finding is usually detected on abdominal
examination. As a rule the gallbladder is impalpable. This is according to COURVOISIER 'S LAW. This law
states that if in a jaundiced patient the gallbladder is enlarged and palpable, it is probably not a case of stone
in the common bile duct, because in that case previous cholecystitis has already made the gallbladder fibrotic
and small (when gallbladder is palpably enlarged in a case of jaundice, it is probably due to neoplastic
obstruction in the distal part ofthe bile duct either Cancer at ampulla of Vater or Cancer at the head of pancre
There are however a few exceptions of the law, where gallbladder may be enlarged not due to cancer of the
head of the pancreas. These are:— (a) Double impaction of stones i.e. one in the cystic duct and the other in
the common bile duct; (b) Oriental cholangiohepatitis and (c) A pancreatic calculus obstructing the ampulla
of Vater.
Special Investigations.— The W.B C. count is usually elevated when cholangitis is present, otherwise
it is normal In case of obstructive jaundice the alkaline phosphatase level is quite high, similarly serum
bilirubin will also be high. Serum amylase level is only elevated when there is associated pancreatitis.
Ultrasonography should be done to detect presence or absence of gallstone and dilatation of the bile
ducts This is not reliable in the detection of common duct stones.
ERCP (Endoscopic Retrograde Cholangiopancreatography) is indicated in jaundiced patients. PTC
(Percutaneous Transhepatic Cholangiography) is also helpful to detect cause of the jaundice. ERCP has
added advantage to visualise the other portions of the gastrointestinal tract and pancreatography which ma
be more informative. ERCP has therapeutic advantage that sphincterotomy or papillotomy can be performe
through it when indicated. See Special Investigations in page 869.
Complications.— 1. Suppurative Cholangitis.— Stasis of bile may initiate colonization of bacteria, which
may cause suppurative cholangitis in late cases. This is a dangerous condition which will cause liver failure
and even death if timely surgical intervention and antibiotic therapy are not initiated.
2. Impairment of liver function.— Sometimes above the impaction of bile duct stone, the bile looks
white. This is known as ‘white bile’. This is noticed when the liver function becomes seriously depressed
usually after 4 weeks of impaction of stones. The ‘white bile’ or ‘surgical bile’ is nothing but mucus
secreted from the glands lining the bile duct. Some amount of cholesterol and trace of bile salts may be
added to this. So the white bile is not bile in the true sense as it is not secreted by the liver. This is only seen
after cellular damage of the liver due to mounting pressure within the bile duct.
3. Hydro-hepatosis.— This rare condition means gross dilatation of the intrahepatic biliary canaliculi,
which are filled up with white bile. This is one stage ahead of white bile in the common bile duct and more
commonly seen in cases of obstructive due to carcinoma of head of pancreas rather than due to stone in the
common bile duct.
4. Stone may ulcerate through the common bile duct to cause biliary peritonitis. But this is extremely
rare Stone may pass to the retroperitoneal tissue and the perforation may be too small to be detected on
opening the abdomen. Treatment is obviously to drain the common bile duct and also the peritoneal cavity
or the retroperitoneal tissue as the case may be
5. Rarely stone may ulcerate through the bile duct into the duodenum to cause natural cure.
6. Acute pancreatitis.
TREATMENT —
PREOPERATIVE PREPARATION.— When a patient is admitted with typical Charcot’s triad and
with the diagnosis of stone impacted in the common bile duct, the patient will be jaundiced and the
following conservative management is required.
1. Antibiotic.— A broad spectrum antibiotic should be started immediately to prevent cholangitis
2. Analgesics.— As discussed in page 876.
3. A relaxant of sphincter of Oddi (anticholinergic drug).— As discussed in page 876.
4 Vitamin K1 should be given parenterally for several days before operation in the dose of 10 m
daily i.m or i.v. This is required to raise the prothrombin level in the blood. Due to deficiency of bile salts
in the distal ileum, Vitamin K is not absorbed properly and this leads to prothrombin deficiency.
5. Glucose drink is advised to combat liver failure by forming excessive glycogen in the liver. Before
operation I. V. Glucose 25% in 100 ml should be administered.
6. High carbohydrate, low protein and no fat rich in calorie should be given. Adequate Vitamins,
particularly Vitamin B complex and Vitamin C should be offered.
7. Blood transfusion, particularly fresh blood should be kept at hand to be used during operation if
required. This also reverts the coagulation defect due to prothrombin deficiency.
8. Mannitol may be given intravenously to promote diuresis and to prevent renal failure which is
often seen in jaundiced patients.
If the jaundice gradually subsides, one should wait for complete clearance when the operation should b
performed. If the jaundice is persistent or even increasing and is not responding to conservative manage
ment, operation may be justified and it should be restricted to only drainage of the bile duct and removing
stones as quickly as possible.
Surgery — When jaundice is not present, cholecystectomy is advised along with operative chol
angiography. If this suggests stone in the common bile duct or if there are other indications of choledochoto
one should perform this operation. The indications for common duct exploration are :
(i) When there is history of intermittent jaundice or biliary colic.
(ii) One or more stones can be palpated within its lumen.
(iii) When the bile duct is dilated and thickened.
(iv) When on aspiration the bile is 'white'.
(v) Previous history of pancreatitis.
(vi) A dilated cystic duct.
The role of operative cholangiography in this respect cannot be over emphasized. A small stone at the
ampulla of Vater can be missed by all the indications given above, but would not be missed by operative
cholangiography. Moreover small soft calculi may be missed by palpating fingers but not by operative
cholangiography In addition it also restricts unnecessary negative common duct exploration. It must be
remembered that the addition of common duct exploration increases the mortality, morbidity and expense
cholecystectomy.
Supra-duodenal choledochotomy.— The supra-duodenal part of the duct which lies in the right free border ofthe
lesser omentum is relatively accessible.
The packs are arranged in the same manner as those used in cholecystectomy. The overlying peritoneum is snipped
and the duct is exposed by blunt dissection. If one is not sure whether this is the duct or not it is better to aspirate with
a fine aspiratory needle. Bile will come out if it be the common bile duct Hie wall of this duct is steadied with stay
sutures on the sides of the proposed incision. These stay sutures are lifted up and a small longitudinal incision is made
on the wall ofthe duct through the aspirating puncture point. Escaping bile is immediately sucked out. A flexible probe
is then passed upwards and downwards. The hepatic duct will be entered in the upward direction and the duodenum
will be entered in the downward direction. If a stone is palpated in the supra-duodenal part, a direct incision is made
over the stone and it is scooped out. If a stone is located in the lower part, it should be milked up towards more
accessible part of the duct. It is steadied between the thumb and the fingers. An incision is made over it and the stone
is taken out.
If the stones are not palpable in the supra-duodenal part, through the incision on the duct, as has been described
earlier, a pair of Desjardins' choledocholithotomy forceps is introduced to the lower part ofthe duct for search of stones
and their removal. After these stones have been removed, an ordinary rubber catheter is introduced through the incision
of the duct downwards through the papilla into the duodenum and some normal saline solution is pushed through this
catheter to determine patency of the duct and to dilate the sphincter of Oddi slightly. This catheter is also passed
upwards towards the liver and thus the patency of the hepatic ducts is confirmed. Small arms of a T-tube is now pushed
through the incision ofthe common bile duct and the wound is closed above and below the long arm of the T-tube with
a few interrupted catgut sutures. Now the long arm of the T-tube is taken out through the same wound as the drainage.
This arm of the T-tube is fixed to the skin edge with a silk suture.
Retroduodenal choledochotomy.— This operation is indicated, though rarely, when the stone is impacted in this
segment or a little below it The descending part of the duodenum is mobilised by incising the peritoneum on its lateral
side (Kocher’s method). This part of the duodenum along with the head ofthe pancreas is turned medially so that the
posterior aspect of the duct is exposed. It is now possible to milk the stone up to the more accessible part of the duct
If not possible, a direct incision is made on it. The opening in the duct is closed with interrupted catgut sutures. The
retroduodenal space is now drained in the same fashion as the drainage of Morison's pouch. If continuous drainage of
the bile duct is at all required, it should be done through the supra-duodenal part.
Transduodenal choledochotomy.— This operation is employed when the stone is impacted at or just above the
ampulla of Vater. The second part ofthe duodenum is incised longitudinally on its anterior wall. Now the papilla and
the stone can be seen and palpated on the posterior wall of the duodenum. An incision is made directly over the stone
downwards upto the papilla. The stone is removed but the incision is not sutured.The incision on the anterior wall of
the duodenum is sutured longitudinally or better transversely with two layers of sutures.
Postoperative treatment.— The end of the long arm of the T-tube is kept in a receptacle at the bed side. The bile
is continuously drained at this receptacle. This bile should be examined daily noting its colour and its quantity. If the
bile was ‘white bile’ just after the operation it will gradually retain its normal colour within 2 days. The quantity of the
draining bile will gradually be decreased. Usually the tube is kept for 7 to 10 days. At the end of this period one should
be sure that there is no obstruction in the bile duct before the tube is taken off. This is ascertained by noting the colour
THE BILIARY SYSTEM----------- . 815
ol the faeces, which will be pale or white if there is obstruction and of normal yellow hue when there is no obstruction.
The arm of the tube is clamped off and see if the patient complains of pain in the gallbladder region This indicates
presence of obstruction. If the patient does not complain of pain, that means he is not having any obstruction in the bile
duct. Lastly the patency of the duct is determined by postoperative cholangiography, which means injecting 'hypaque'
down the T-tube and the skiagram is taken. If the dye is seen flowing freely into the duodenum, it is assumed that there
is no obstruction in the bile duct. The small silk suture at the edge of the wound is severed and the T-tube is pulled out.
The resulting external biliary fistula will heal within a week.
Nowadays choledochoscopy is used routinely. The flexible choledochoscope is more manoeuvrable but visualisation
is better with rigid instrument. Choledochoscopy is required to exclude
intraductal papillary tumours and occult carcinoma.
When stone is impacted in the distal part of the duet and is rather
impossible to leniove Ironi above, duodenotomv and sphmctcnUomv ate > . 1 , • -v;'; ■
necessary.
In some situations sphincteroplasty is more efficacious I his is
particularly the
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Fig 46.15.—T-tube cholangiography a.—Shows retained Fig. 46.16.—T- tube cholangiography
drainage proce
stones in CBD b.— Shows after removal of the stone. showing very dearly a stone as filling
dure of the com defect in the distal CBD
mon bile duct.
After choledocholithotomy, T-tube cholangiography (postoperative cholangiography) must be performed before
the T-tube is removed. A technique of percutaneous extraction of calculi may be tried through the passage of T-tube
when stones are present indicated by T-tube cholangiography. The T-tube should be left in place for about 6 weeks and
the T-Tube cholangiogram is repeated. After location of the retained stone, the T-tube is withdrawn. A steerable
catheter is guided into the bile duct through the sinus tract of the T-tube. Its movable tip is advanced beyond the
retained stone. The basket is inserted through the steerable catheter beyond the retained stone The catheter is
withdrawn.The basket is opened. Tlie open basket is withdrawn in order to remove the stone. But this technique is still
to be popularised.
BILE DUCT STRICTURE

Bile duct stricture can be broadly classified into two groups — A. Benign strictures and B. Malignant
strictures.
A. Benign stricture can be further classified into :
(a) TRAUMATIC STRICTURE (mainly Iatrogenic following cholecystectomy or bile duct surgery);
(b) INFLAMMATORY STRICTURES (i) due to accumulation of bile around the common bile duct
when the cystic duct is not properly ligated during the operation of cholecystectomy or there is presence of
cholecystohepatic duct which escaped surgeon’s notice, (ii) It may occur in stenosing cholangitis (sclerosin
cholangitis) in which there is fibrosis of the submucosal and serosal layers of the wall of the duct with
marked narrowing of its lumen. The involved segment may be small or local or may be large or diffuse
involving the major portion of the common duct and even the right and left hepatic ducts. The primary type
is of unknown aetiology and is very rare. The secondary type is associated with a few diseases. These are
pancreatitis, chronic ulcerative colitis, fibrous retroperitonitis, Crohn’s disease, Riedel’s thyroiditis and
Banti’s syndrome, (iii) Asiatic cholangiohepatitis. (iv) Cholangitis of various aetiology.
(c) FIBROSIS OF SPHINCTER OF ODDI.
B. Malignant stricture from BILE DUCT CARCINOMA.
TRAUMATIC STRICTURE.—
More than 90% of bile duct strictures are due to iatrogenic injury during cholecystectomy or bile duct
surgery. Over 80% of bile duct strictures follow cholecystectomy and are due to inadvertant injury to the
common hepatic or common bile duct. The remainder 10% result from abdominal trauma, chronic
pancreatitis or impaction of a calculus within the common bile duct. Stricture of the distal common bile du
usually results from injuries by dilators during exploration of common duct or by extensive scarring and
fibrosis due to damage to the blood supply of the bile duct.
During cholecystectomy or bile duct surgery the followings may lead to stricture of duct system : —
(a) When cystic artery bleeds the common mistakes a surgeon may do is to apply a haemostat blindly
The haemostat may be applied to the common hepatic duct and this will cause injury and subsequent
stricture formation of the common hepatic duct. To prevent this the best way is to control bleeding by
inserting the index finger into the foramen of Winslow and press the free edge of the lesser omentum
between index finger behind and thumb in front. This will minimise the bleeding and will help to ligate th
bleeding vessel accurately. This is known as Hogarth Pringle’s manoeuvre.
(b) When dissection becomes difficult near the junction of cystic duct and common hepatic duct
surgeon may start dissection from the fundus. This is known as fundus-first operation. When the gallbladd
has been freed from the bed and the cystic duct is to be clamped, an excessive pull to the gallbladder may
lead to clamping of both common hepatic and common bile duct. This will cause ultimately stricture.
(c) There may be some anatomical anomalies of the cystic duct and bile duct. Ignorance of such
anomalies may inflict trauma to the common hepatic duct or common bile duct.
(d) Distal bile duct injury may be caused by dilators used for exploration of stones or to dilate
sphincter of Oddi.
(e) A small percentage of cases of stricture of the duct system may occur after partial gastrectomy In
this case the retroduodenal part of the bile duct is often injured.
Clinical features.— Symptoms may be manifested in the immediate postoperative period or many
years later. In the early postoperative period jaundice and leakage of bile from the drain will give indicatio
to the injury of the duct system. When occurs late, recurrent cholangitis is the commonest symptom. Here
also intermittent jaundice and recurrent pain will give indication to the biliary stricture. The ultimate
threats to life posed by a bile duct stricture are (i) sepsis from cholangitis, (ii) development of cirrhosis, (iii)
rarely portal hypertension and (iv) haemorrhage from oesophageal varices.
Special Investigations.— Elevated serum bilirubin and alkaline phosphatase give indication to ob
struction. Leakage of bile may be detected by paracentesis and confirmed by "Technetium-ED A scan. PTC
is more useful than ERCP as the former gives better information about the proximal extent of the lesion an
this only determines the type of repair to be undertaken and technical difficulties one has to face during
operation.
Treatment.— The main moto is to reconstruct the bile duct after excising the strictured portion.
IMMEDIATE REPAIR.— When injury to the common bile duct is discovered during the operation it
should be immediately repaired by end-to-end suture and T-tube drainage. The long arm of the T-tube is
taken out through a separate small incision on the duct and not through the end-to-end suture. Interrupted
sutures of fine catgut is used to do this end-to-end suture.

LATE REPAIR.— It depends on the type of traumatic stricture affecting the common bile duct. If the strict
very small one affecting the supraduodenal portion of the duct an end-to-end choledochostomy is performed
stricture is long, but the upper portion of the bile duct is quite patent, it is a good practice to do choledochodu
But to perform this operation the duodenum has to be mobilised. Sometimes the duodenum cannot be taken u
patent portion of the common bile duct. At this time choledochojejunostomy (Roux-en-Y) operation is perform
When the stricture affects the upper part of the duct so that no portion of the common bile duct is available fo
anastomosis, a hepaticodocho-jejunostomy is advised. The Roux-en-Y limb of the jejunum is anastomosed to the
common hepatic duct with interrupted sutures of fine chromic catgut passed through all the layers of thejejun
the wall of the common hepatic duct. This anastomosis may be made over some type of prosthesis. Such pros
not required if the hepatoenteric stoma is of adequate calibre. Simple T-tube may be employed as prosthesis a
inserted through the limb of thejejunum. The one limb of the T-tube should be passed through the anastomos
Sometimes the stricture may affect the common hepatic duct and the right and left hepatic ducts so that no
portion of even the hepatic ducts is available for anastomosis. In this case Longmire’s operation can be perfor
only when the surgeon is certain that there is good communication between the intrahepatic duct of the left
lobe with that of the right. In this operation the left lobe of the liver is mobilised and its lateral 2/3rds are
removed. The largest branch of the left hepatic duct is isolated and is anastomosed to a Roux-en-Y jejunal
loop. An indwelling latex tube splints the anastomosis.
SEMS (SELF EXPANDING METAL STENTS) are useful in selected cases of benign strictures which have not responded to
repeated dilatation. Sometimes stent can be used for short term in case of bile duct leaks after laparoscopic cholecystectomy. In these
cases SEMS are ideal as they can be removed endoscopically after the hole has sealed.
In short strictures of the pancreatic duct adjacent to the sphincter of Oddi, SEMS can be used to reduce pancreatic duct pressure.
FIBROSIS OF SPHINCTER OF ODDI.—
Fibrosis or stenosis of the sphincter of Oddi is a clinical entity and is often responsible for intermittent and continuous attacks of pain
in the right hypochondrium and in the epigastric region with or without jaundice. It has been maintained that fibrosis takes place only w
inflammatory reaction has been associated with an impacted calculus in the ampulla or papilla, or when the end of the common bile duct
been injured during dilatation with probes, sounds, scoops etc. Otherwise obstruction in this region is caused by spasm.
Stenosis of the sphincter of Oddi is commoner in females than in male* in the ratio of 3 : 1. The condition may reveal itself at any
age but is most frequently observed between the ages of 50 and 70 year?.
Symptoms are usually pain, which may be continuous or intermittent or even in the form of colic. Jaundice is present in about 50%
of patients. Other symptoms include nausea, anorexia, indigestion, epigastric fullness after fatty food, vomiting and pruritus.
Intravenous cholangiography or percutaneous cholangiography (PTC) or ERCP will diagnose this condition.
Treatment.— Surgery is the only treatment available in this condition. Transduoderuxl sphincterotomy is often performed in these
cases. The common bile duct is dissected out and is opened anteriorly after introducing two stay sutures on either side of the incision.
The bile duct is explored. If 3 mm dilator cannot be passed through the papilla, it is obviously stenosed or fibrosed. In this case the
anterior wall of the duodenum is incised, duodenal contents are aspirated, small retractors are inserted and the papilla is visualised.
Babcock’s forceps are applied on either side of the papilla to elevate the posterior side of the duodenum. The dilator through the
choledochotomy is lifted up to make the papilla prominent. Papillotomy — simple longitudinal division of the papilla of Vater, followed
by sphincterotomy should be performed for such lesions.
Following sphincterotomy a short-guttered T-tube is used for drainage of the ductal system through choledochotomy incision.
Duodenum is closed and the choledochotomy incision is closed by the side of the emerging T-tube. Choledochoduodenostomy mav be
performed in difficult cases.
CARCINOMA OFTHE GALLBLADDER
Though carcinoma of the gallbladder is the most common malignant lesion in the biliary tree, yet it constit
only 5% of all cancers found in body. More than 90% of patients are over 50 years of age. Women are effected
3 to 4 times more than men (cf. bile duct carcinoma, where men are more affected).
Associated conditions.— (i) It is a well established fact that carcinoma of the gallbladder is often associated
with gallstones. About 70% of patients with this cancer are associated with gallstones. Whether single stones
or multiple stones are more prone to cause gallbladder cancer is not known, but the size of the stone has a
direct relationship with development of carcinoma. The risk for developing carcinoma in a patient with 3 cm
gallstone is 10 times that for someone with a stone less than 1 cm in diameter.
There are three other conditions which are presumably associated with the development of carcinoma of
the gallbladder.
(ii) Cholecystoenteric fistula may cause gallbladder carcinoma, as 15% incidence of carcinoma of
52
gallbladder has developed in patients with cholecystoenteric fistula.

(iii) Porcelain gallbladder is also seen to be associated with gallbladder carcinoma and such associa
tion ranges from 15 to 60%. But both these conditions are associated with gallstones, so whether these
conditions de novo or gallstones are responsible for such association is to be questioned.
(iv) Ulcerative colitis has a well known association with biliary tract malignancy. Although the
majority of neoplasms involve the bile duct about 15% originate in the gallbladder.
It is still controversial which factor plays a major role in malignant transformation — whether (a)
gallstones, (b) bacteria or (c) carcinogens associated with gallstones.
Pathology — About 90% of the carcinoma of the gallbladder is adenocarcinoma. Adenocarcinoma
may be in the form of scirrhous, papillary or mucinous. 7% is undifferentiated carcinoma. 3% is squamous
cell carcinoma and 1% or less is constituted by mixed carcinoma or adenoacanthoma.
A few sarcomas are also found in gallbladder, though they are quite rare. These are lymphosarcoma,
rhabdomyosarcoma, fibrosarcoma and reticulum cell sarcoma.
Two other tumours, though may occur, are also rare in gallbladder. These are melanoma and carcinoi
tumour.
Spread of carcinoma.— As carcinoma elsewhere in the body the main routes of spread are — (a)
direct infiltration, (b) lymphatic spread, (c) vascular spread, (d) intraductal spread and (e) intraperitoneal
seedling.
(a) DIRECT INFILTRATION.— Spread to adjacent organs occurs with some frequency and usually
involves the liver, stomach, duodenum, hepatic flexure of colon and abdominal wall at the site of previou
cholecystectomy Invovement of liver is of importance in gallbladder carcinoma. Liver is involved quite
early in this disease. Direct infiltration is the first mode of involvement. The second is through lymphatics
Sometimes wide nodular hepatic involvement may occur from vascular metastasis. Involvement of liver c
occur in absence of lymph node metastasis.
(b) LYMPHATIC SPREAD.— Majority of the lymphatics draining the right side of the gallbladder
drain into the pericholedochal nodes lying to the right of the common duct in the right free margin of the
lesser omentum. Most of the lymphatics draining the left side of the gallbladder terminate into the cystic
lymph nodes
(c) VASCULAR SPREAD.— Cholecystic veins draining the gallbladder terminate in the quadrate lobe
both from the deep surface and from the superficial surface of the gallbladder
(d) INTRADUCTAL SPREAD.— The tumour may spread along the cystic duct into the common
hepatic duct or bile duct. Such spread is more often seen in papillary adenocarcinoma.
Clinical features.— Symptoms of gallbladder carcinoma are not specific. Sometimes the patients
complain of weight loss or anorexia or a mass in the right upper quadrant or sometimes simply pain in th
right upper quadrant of the abdomen. Pain is of nagging in nature and is continuous. It is more of a
discomfort rather than anything else. Sometimes jaundice is the only presenting symptom.
ON EXAMINATION one may detect a lump in the upper quadrant of the abdomen There may be
enlargement of liver with irregular and hard margin. The gallbladder may be palpable. Jaundice is often t
only sign available. Jaundice may be due to invasion of the common duct or compression of the common
duct by involved pericholedochal lymph nodes. Jaundice may be due to involvement of liver or rarely du
to concurrent stone in the biliary tract. In gallbladder carcinoma jaundice is often accompanied by pain an
this is the distinguishing feature from periampullary carcinoma, which is usually painless
Diagnosis is mainly confirmed by computed tomographic scan, sonography and angiography. Upper
G I. tract barium study may show compression of the first part of the duodenal area.
TREATMENT.— In this type of malignant disease not many cases come in early stage, where radical
resection is possible. So most often the surgeon has to be content with palliative procedure to relieve the
obstructive jaundice.
Even when the carcinoma is detected in very early stage i.e., it is still localised within the wall of the
gallbladder, simple cholecystectomy is not the operation of choice, as only a very few patients after this
operation survive more than a year. The choice lies between (i) extended cholecystectomy and (ii) extended
right hepatic lobectomy depending on the age of the patient, spread of the disease and capability of the
surgeon so far as hepatic resection is concerned. First operation is radical surgery and this involves excision
of the gallbladder in continuity with the hepatic bed and regional lymph nodes. In the second operation
besides excision of regional lymph nodes right hepatic lobectomy is performed through a right
thoraco-abdominal approach.
It is difficult to prove whether radical excision has been able to increase survival. These cases which
after cholecystectomy have revealed carcinoma found histologically have not shown better prognosis after
reoperation and radical surgeiy.
Palliative treatment.— When the carcinoma of gallbladder has infiltrated the porta-hepatis, which is
mostly encountered by a surgeon, palliative T-tube intubation is the operation of choice. In this operation
the contrated empty common bile duct is opened and probes of various sizes are used to dilate the obstructe
common hepatic duct into the dilated intra-hepatic duct system. When the bile drains out, a portion should
be sent for culture and sensitivity tests. These conditions are mostly associated with pyogenic cholangitis
due to stasis of bile within the liver. After dilating the malignant stricture properly a Cattell T-tube of the
largest possible size is introduced through the opening in the common bile duct, so that its upper limb
reaches well beyond the stricture into the dilated ductules. The abdomen is closed in layers.
Some palliation may also be achieved by removing the gallbladder, when visible, in the hope of
delaying obstruction of surrounding structures.
Chemotherapy could not add hope for better survival in these cases.
Prognosis — In one sentence the prognosis is poor in malignancy of the gallbladder. About 90% of
patients die within one year. If operation is performed when the tumour is confined to the mucosa and
muscularis patients may survive for 5 years, but with serosal (or adventitial) involvement only 7% will live
upto 5 years.
BILE DUCT CARCINOMA
Bile duct carcinoma is an uncommon neoplasm appearing in 0.4% of all carcinoma cases. This
condition is usually recognised late and because of the location i.e. close proximity to the liver, hepatic
artery and portal vein, this is often not resectable. On the other hand these tumours do not show great
tendency towards metastasis. So palliation is possible for quite a long time.
Pathology.— This tumour can occur throughout the biliary tree, but about 50 to 75% occur in the upper
third of the biliary tree which extends from the undersurface of the liver to the joining of the cystic duct.
Approximately 15 to 25% of this tumour occur in the middle third of the biliary tree which extends from the
cystic duct to the superior border of the pancreas. 10 to 20% of these cases occur in the lower third of the
biliary tree which extends from the superior border of the pancreas to the ampulla.
Bile duct carcinoma usually occurs as solitary lesion, though in a few patients there may be multiple
lesions. This carcinoma is invariably adenocarcinoma, although occasionally squamous cell carcinoma is
seen. The growth pattern of this carcinoma is local extension and infiltration and the process is usually
slow. A few carcinomas may show aggressive proliferation with widespread metastasis. The gross appear
ance of this carcinoma may be (a) polypoid lesion or (b) scirrhous lesion. The latter is more common with
dense fibrosis in the area of the tumour.
ASSOCIATIONS.— Bile duct carcinoma appears to be associated with other gastrointestinal disease.
About half the patients have a previous history of biliary calculi. A varying number of patients may have
chronic ulcerative colitis. Those with this association, are usually younger. Colectomy does not affect the
potential for development of bile duct cancer. Patients with sclerosing cholangitis have shown an increased
tendency to the formation of bile duct cancer. Other conditions in which incidence of bile duct cancer is
increased include chronic typhoid carrier state and choledochal cyst.
Clinical features.— The mean age of presentation is between 60 and 65 years, though cases are seen
above 30 years of age. Males and females are equally affected though there is a slight tilt towards the male
Growth of this tumour is most often silent until it obstructs the flow of the bile. Nearly all patients
present with obstructive jaundice. Half the patients complain of epigastric pain and significant weight loss.
Pruritus is frequent. Sometimes the condition may present with cholangitis — manifested by abdominal
pain, chills, fever and jaundice.
Physical examination may reveal an enlarged tender liver. Gallbladder may be palpable if the lesion lie
distal to the entrance of the cystic duct. Ascites and splenomegaly indicate portal obstruction and implies
grave prognosis.
Special Investigations.— Elevation of bilirubin and alkaline phosphatase indicates obstructive jaun
dice Percutaneous transhepatic cholangiogram (PTC) is the most helpful study, since it outlines the
proximal end of the carcinoma. In addition a catheter can be left in place for decompression of the biliary
tree. Bile duct cancers can also be visualised with angiography, ultrasonography and ERCP, but these
studies usually do not add significantly to the information gained from PTC. Computerised axial tomograp
(CAT) scans will outline extraductal extensions of the tumour, liver metastasis and subhepatic masses. This
will improve operative planning. If this scan raises the question of metastatic disease, barium studies of the
upper G.I. tract and the colon and sigmoidoscopy are indicated.
TREATMENT.— The most desirable treatment of bile duct carcinoma is complete excision of the
lesion. Unfortunately this approach is possible in less than half the cases. For convenience of description
biliary tree can be divided into three parts —
PROXIMAL THIRD.— Carcinoma in this region of the biliary tree should be treated by excision of the
lesion which may require resection of both the right and the left hepatic ducts. Reconstruction should be
done by Roux-en-Y hepaticojejunostomy, splinted by silastic tubes that are brought out through the liver an
skin proximally. This tube can be changed under fluoroscopic guidance.
When cancer in this region involves the liver and the branches of the hepatic artery and portal vein,
rescction is not advisable, palliation is affected by biliary drainage through an external catheter placed at th
time of doing PTC. Once the bile ducts are cannulated in this fashion larger tube can be passed to provide
egress of bile. Now the indwelling tube is passed through the neoplasm into the distal common duct and
duodenum and two holes are made in the tube above and below the tumour to provide internal drainage o
bile. The patient himself can irrigate the tube every other day to reduce encrustation. Once a tract has been
formed the tube can be changed with relative ease.
In institutions where such elaborate procedure is not possible the bile flow may be restored by passage
of one limb of the T-tube through the tumour. As blie encrustation obstructs these tubes, periodic changes
are only possible through laparotomy. Radiation therapy may be helpful in prolonging life.
MIDDLE THIRD.— Lesions in this region, if resectable, should be resected and reconstitution is
performed by Roux-en-Y hepaticojejunostomy. An indwelling splint may be necessary particularly if
radiation therapy is required as bile duct epithelium is often damaged by radiation.
Palliation is performed in the same manner as the lesion of the proximal third.
DISTAL THIRD.— Carcinomas in this region of the bile duct is in fact a pancreatic lesion as bile duct
passes behind the head of the pancreas and lies in a groove in that region. It is difficult to differentiate bile
duct lesion from pancreatic cancers in this region. Whipple procedure (pancreaticoduodenectomy) is the
RADIATION THERAPY.— The role of radiation therapy in bile duct carcinoma is not clear. In the absence of data
to the contrary, it is reasonable to consider radiating the primary tumour in patients who are provided with effective
by-pass of their biliary obstruction.
CHEMOTHERAPY.— As with most carcinomas of the G.I. tract the only anti-cancer drug with established record
of activitv is 5-fluorouracil. But response of this drug in biliary duct carcinoma is limited. However an attempt to treat
metastatic disease with 5-fluorouracil is reasonable. If this treatment is responded with by reduction of symptoms, the
treatment may be continued. If there is no obvious improvement, this treatment should be discontinued.
Prognosis.— Overall prognosis is poor. Average survival is about a few months. Less than 10% of patients may
survive 3 to 5 years. Prognosis is worst in proximal third cancers, a little better (about 10% survive 3 to 5 years) in
middle third cancers and is best in the lower third cancers (approximately 25% survive 3 to 5 years).
821
CHAPTER- 39
THE SPLEEN
ANATOMY —
The spleen is principally situated in the left hypochondriac region of the abdomen, but its posterior end extends into
the epigastric region. It lies between the fundus of the stomach and the diaphragm. The spleen is almost entirely surrounded
by peritoneum, which is firmly adherent to its capsule. To perform operations on the spleen one must have a clear conception
of the peritoneal folds, which are related to the spleen. The spleen develops in the upper part of the dorsal mesogastrium
and remains connected with the stomach and the posterior abdominal wall by two folds of peritoneum. The latter, termed
lienorenal ligament, is composed of two layers of peritoneum where the wall of the general peritoneal cavity comes in
contact with the omental bursa between the left kidney and spleen. The splenic vessels and sometimes a portion of the
tail of the pancreas lie between its two layers. The former fold, termed gastrosplenic ligament, also consists of two layers
and is also formed by the meeting of the walls of the greater sac and omental bursa between the stomach and the spleen.
The short gastric and left gastroepiploic vessels run between its two layers. The lateral end of the spleen is in contact
with phrenico-colic ligament. Accessory Spleen (Splenunculi).— These are small encapsulated nodules of splenic tissue,
which are developmentally segregated from the main spleen and are found mostly (i) in contact with the spleen near
its hilum, (ii) in gastro-splenic ligament, (iii) in lienorenal ligament in relation with the splenic vessels and (iv) in the
greater omentum, mesentery, mesocolon and near left testis or ovary. These are functionally similar to the spleen and
while performing splenectomy for blood dyscrasias removal of these accessory spleens are obligatory, otherwise there
always remains a chance of recurrence.
PHYSIOLOGY.—
Spleen is an organ of mystery and till today we know very little about spleen. Its main functions, so far have been
understood, are as follows :—
1. In early embryonic life, the spleen contributes actively to the production of both red cells and white cells which
enter the circulation. From 5th month onwards the spleen gradually loses its haemopoietic function, but retains the capability
throughout life.
2. Abnormal and aged erythrocytes, abnormal granulocytes, normal and abnormal platelets and cellular debris are cleared
by the spleen. The abnormally shaped or rigid red cells are destroyed by culling. Culling refers to filtering and phagocyiosis
of old red blood cells which have either been damaged or are abnormally shaped or contain abnormal inclusions e.g.
nuclei, nuclear remnants (Howell-Jolly bodies). It also removes spherocytes, siderocytes and target cells. Normal red cells
usually traverse the splenic circulation and may undergo ‘repair’ by having surface abnormalities such as pits or spurs
removed. Reticulocytes pass through the spleen more slowly than mature red cells and lose nuclear membranes and excess
membrane before entering the circulation as mature red cells. Spleen also removes certian inclusions by ‘pitting’. Such
inclusions may be red cell nuclei or malarial parasites without destroying the red cells. These ‘cleaned’ red cells ultimately
pass through the splenic circulation and re-enter the blood stream. Only the aged red cells (more than 120 days) that
have lost membrane plasticity and enzymatic activity are destroyed in the spleen. Blood cells coated with immunoglobulin
G (IgG) are destroyed by the splenic monocytes. As the spleen removes cells coated with IgG or IgM, it is the site of
destruction in diseases e.g. autoimmune haemolytic anaemia, idiopathic thrombocytopaenic purpura or probably Felty’s
syndrome. Overactivity of splenic function leading to accelerated removal of any or all of the circulating cellular elements
of the blood, which may result anaemia, leucopenia, or thrombocytopenia, is known as hypersplenism. The normal red
cell possesses a life span of approximately 120 days which is not prolonged after splenectomy. That means there are
other sites of red cell destruction.
3. The neutrophil is removed from the circulation with a half life of about 6 hours. Though the role of the spleen
in the destruction of neutrophils is not clearly known, yet in some hypersplenic conditions there is excessive destruction
of neutrophils leading to neutropenia.
4. The platelets or thrombocytes under normal conditions survive about 10 days in the circulation. ‘/3rd of the total
platelet pool is normally sequestered in the spleen. With splenomegaly a larger proportion of platelets (upto 80%) is sequestered
in the spleen. The role of spleen in the final removal of normal platelets is not precisely known. Tlie accelerated platelet
destruction in the spleen may account for thrombocytopenia. Splenectomy results in an increase in platelets to levels even
greater than 1 million cells per cubic mm.
5. The spleen is involved in specificand nonspecific immune responses. Propadine, an luiniuuugiubuhn, lixes complement
to bacterial or fungal surface prior to phagocytosis. This and tuftsin, which are synthesised in the spleen, are in fact opsonins.
Tuftsin binds to granulocytes to promote phagocytosis. Because these opsonin proteins are also produced by other organs,
the loss of the splenic contribution to their synthesis is probably small. However serum levels of propadine and tuftsin
are beiow normal after splenectomy. As a response to antigenic challenge there is proliferation of T-lymphocytes within
the lymphatic sheaths and antibody-forming B-lymphocytes within the lymphatic nodules. This causes an increase in the
production of humoral immune factors of both B and T cell origin.
6. Macrophages and histiocytes of the spleen remove bacteria and foreign cells. When radioactively labelled bacteria
are administered to animals, the liver clears most of the well opsonized micro-organisms and the spleen removes (hose
which are poorly opsonized. When specific antibody is lacking to facilitate bacterial removal by the liver, the spleen
becomes the main organ for clearance of such bacteria. Encapsulated bacteria, which resist antibody binding, are also
removed by the spleen.
7. Phagocytosis of foreign substances is also performed by reticuloendothelial macrophages of the spleen. Experimentally
it has been shown that there is an uptake of radio-opaque thorium into the spleen following administration of the contrast
material thorotrast which was once used in arteriography and cerebral ventriculography. Particulate matter, bacteria, fungi
and protrozoa are also removed from the circulation by these macrophages. Phagocytosis of abnormal lipoids is the cause
of splenic enlargement in lipoid dystrophies.
8. A very important immune function of the spleen is the production of specific antibody, especially immunoglobulin
M (IgM). Particulate antigens i.e. salmonella flagella, lodge in the splenic red pulp and are transported by macrophages
into the germinal centres where the IgM response is presumed to occur. In splenectomised individuals IgM levels fall
and the antibody response to a blood-borne antigen diminishes.
9. The role of spleen in removing malignant tumour cells is not sufficiently estimated. Micrometastases to the spleen
occur frequently. In one series 50% of spleens from patients with solid tumours contained neoplastic cells. From this
study conclusion can be drawn that intense destruction of malignant cells in the spleen limits the incidence of clinically
apparent metastases.
CONGENITAL ABNORMALITIES
Congenital abnormalities of the spleen are quite rare. These are:—
1. Splenunculi.— Single or multiple accessory spleens are sometimes present and if left behind during splenectomy,
they may undergo hyperplasia and lead to recurrence of the disorder for which splenectomy was performed. 50% of these
accessory spleens are found near the hilum of the spleen. 30% of these accessory spleens are found behind the body
and tail of the pancreas in close relation to the splenic vessels. A few accessory spleens are seen in the splenic ligaments
and mesocolon.
2. Absence of spleen is extremely rare. This condition may be associated with other congenital abnormalities particularly
of the heart. These patients are often liable to fatal infection.
3. Splenic cysts.— Congenital cysts are mainly true cysts formed from embryonal rests. False cysts may also occur
resulting from trauma which contains serous or haemorrhagic fluid.
4. Hamartomas.— Occasionally these are found in the spleen at autopsy or during splenectomy. There are two varieties
of hamartomas — lymphoid hamartomas, resembling white pulp and vascular hamartomas resembling the red pulp. These
hamartomas vary in size from a small swelling less than 1 cm diameter to a large mass to cause abdominal swelling.
RUPTURE OF THE SPLEEN

AETIOLOGY.—
The spleen is the most common intra-abdominal organ injured in blunt trauma. Only occasionally there
may be spontaneous rupture. In majority of cases rupture of the spleen occurs from penetrating trauma,
nonpenetrating trauma and operative trauma.
(a) Penetrating Trauma.— Gun-shot wounds, missiles and stabings may cause splenic rupture. The
penetration may occur through the anterior abdominal wall, through the flank or transthoracically piercin
the pleural space, the lung and the diaphragm. Surrounding organs may be injured, of which the stomach,
the left kidney, the pancreas and the root of the mesentery are important.
(b) Non-penetrating Trauma.— Automobile accidents, bicycle injuries, blows and during various contact
sports injury to the spleen may occur. In blunt trauma other organs besides spleen may be injured, of whic
the liver, the kidneys, the chest (rib fractures), the lungs, the small intestine, the colon and the stomach are
important.
(c) Operative Trauma.— Spleen is injured in about 2% of operations involving viscera of the left upper
quadrant Injury may also occur from retractors placed against this organ to get exposure to the depth in
various operations.
(d) Spontaneous Rupture .— Spontaneous ruptures may only occur when the spleen is pathologic. Such
rupture may occur from minor trauma. Spleen ruptures more easily when it is enlarged in infectious mono
or malaria. In infectious mononucleosis, this complication occurs most frequently in the 2nd to 4th weeks
of the disease. In other pathologic conditions also splenic rupture has been reported e.g. sarcoidosis, acute
and chronic leukaemia, congestive splenomegaly, haemolytic anaemia and polycythemia vera.
PATHOLOGY.—
Splenic injuries vary from simple transverse tear of the parenchyma to transverse crack of the hilus. The
may be subcapsular haematomas only in minor cases or there may be complete disruption of the organ and
its vessels in the fulminating injuries. Majority of the injuries result in transverse rupture of the parenchym
the direction of rupture is determined by the internal architecture of the organ which is arranged in transve
THE SPLEEN 823
fashion in spleen.
Mainly 3 types of rupture are seen in spleen —
1. ACUTE RUPTURE which occurs mostly due to blunt trauma and is featured by immediate intraperiton
bleeding. In this variety two types are seen — in one type the patient succumbs rapidly giving no chance
to initiate proper treatment. In the 2nd type there is initial shock, from where the patient recovers by treatme
revealing signs of ruptured spleen. Fortunately the 2nd type is much more common.
2. DELAYED RUPTURE.— In this type after an interval of a few days to weeks after injury, sudden
intraperitoneal bleeding starts. This delayed rupture is reported in 10 to 15% of the cases of blunt trauma.
In about half of these cases bleeding occurs within 7 days and in 75% of cases bleeding starts within 2 weeks
of the accident. Such delayed type of rupture is probably due to (a) blood clot, temporarily sealing the rent,
becomes lysed by the enzymes of the lacerated tail of the pancreas; (b) slowly enlarging subcapsular haemato
which eventually ruptures or (c) the greater omentum, which shuts off the injured site initially, gradually
moves off.
3. OCCULT SPLENIC RUPTURE.— The term is applied when traumatic pseudocyst of the spleen is
diagnosed though injury to the organ previously has not been diagnosed. This type is seen in less than 1%
of patients sustaining injury to the spleen. It is caused by organisation of intrasplenic or parasplenic haemato
Another condition related to splenic injury is known as splenosis. It is due to autotransplantation of fragmen
of ruptured spleen on to the peritoneal surface. This condition is usually asymptomatic, but patients may
present with intestinal obstruction later on due to adhesions.
The clinical course of an isolated splenic injury is variable depending on severity and rapidity of
intra-abdominal haemorrhage. Laceration through the body of the spleen can extend into the splenic pedicle
causing extensive and continued haemorrhage with haemoperitoneum and acute shock. An adhesion betwee
the spleen and its ligaments or diaphragm may seal the capsular avulsion with cessation of haemorrhage afte
an initial blood loss of not more than 500 ml. If injury is limited to the capsule or pulp and does not involve
the major splenic vasculature, the patient may remain haemodynamically stable. However subcapsular
haematomas have potentiality to rupture later producing ‘delayed rupture’ of the spleen.
If a splenic injury is suspected, admission to the hospital for monitoring is mandatory. A careful history
should be obtained regarding mechanism of the injury. Injury to the left upper abdomen, more so with associ
fractured ribs, may cause injury to spleen.
The signs and symptoms of injury to the spleen depend on severity and rapidity of intra-abdom inal haemo
as also on presence of other organ injuries.
(i) Some degree of shock due to hypovolaemia, characterised by tachycardia, low blood pressure,
restlessness, increasing pallor and sighing respiration may be seen in majority of cases.
(ii) Local bruising and tenderness in the left upper quadrant of the abdomen is often seen.
(iii) Patient usually complains of generalised upper abdominal pain, which in V3rd ofthe cases is localise
to the upper left quadrant.
(iv) Pain may be referred to the tip of the left shoulder, which is known as Kehr’s sign. This sign is
inconstant and varies in incidence from 15% to 75%. Kehr’s sign can be elicited by bimanual compression
of the left upper quadrant after the patient has been in Trendelenburg’s position for about 10 minutes prior
to the manoeuvre. There may be hyperaesthesia on the left shoulder. Kehr’s sign is due to irritation of the
undersurface of the diaphragm with blood and the pain is referred to the shoulder through the affected fibres
of the phrenic nerve (C4 and C5).
(v) On rare occasions a palpable tender mass can be felt in the left upper quadrant with persistent dullne
This is known as Ballance’s sign. This sign is due to extracapsular or subcapsular haematoma which is guarded
by omentum or by early coagulation of splenic blood.
(vi) Tenderness and rigidity of the left upper quadrant is a frequent and reliable physical sign.
(vii) Shifting dullness may be detected on the right side due to intraperitoneal haemorrhage.
(viii) Diagnostic peritoneal lavage is a useful and inexpensive manoeuvre which may reveal intraperitonea
haemorrhage.
1. Haematocrit value may be reduced if there is major bleeding, but initial readings may be normal. Increase
in W.B.C. count (moderate leukocytosis) is noticed in many cases.
2. Routine STRAIGHT X-RAY of the abdomen often gives confirmatory evidence regarding diagnosis.
This investigation is extremely helpful in places where sophisticated investigations are not possible. The p
findings in X-ray in case of splenic rupture are:—
(a) Obliteration of the splenic outline, (b) An enlarged splenic shadow, (c) Obliteration of the psoa
shadow, (d) Indentation of the left side of the gastric shadow, (e) Widening of the space between the splen
flexure and the properitoneal pad of fat. (f) Elevation of the left side of the diaphragm, (g) Free fluid betwe
gas filled intestinal coils, (h) Fracture of one or more lower ribs on the left side.
A normal well outlined spleen indicates intact spleen on straight X-ray.
3. SPLENIC ANGIOGRAPHY can demonstrate splenic injury. But its use has been limited by greater
accuracy of simple investigation like peritoneal lavage and more availability of various non-invasive imag
techniques.
4. ULTRASONOGRAPHY of the spleen will show haematoma surrounding the splenic capsule with
reasonable accuracy. This has become the investigation of choice in diagnosis of splenic rupture. Even seri
examinations may show change in splenic size which indicate enlarging subcapsular haemorrhage.
5. ISOTOPE SCANS (with the use of "mTc sulphur colloid) are popular in many centres for diagnosis
of splenic rupture in acute cases. The diagnostic accuracy rate has been quoted to exceed 90%.
6. CT SCAN is probably the most accurate method available for diagnosis of splenic injury.
TREATMENT —
Immediate laparotomy and splenectomy is the life saving procedure and is still the standard treatment.
The peritoneal cavity should be well toileted. Injury to other viscera should be excluded and the abdomen
is then closed. Blood transfusion is mandatory in almost all cases.
When the organ is damaged by a stab wound or penetrating missile through the left pleural cavity, acce
should be made through the thoracic wound and by enlarging the opening in the diaphragm.
In children if there be parenchymal rupture defined by scans, operative intervention may be avoided in
majority of patients. The patients should be carefully observed for 10 to 14 days if delayed rupture occurs
or not. But this is not a safe procedure as interpretation of scans must be made by very competent radiologist
to venture this technique.
OPERATIVE TECHNIQUE for splenectomy in ruptured spleen.— An upper midline incision is generally
preferred due to its rapidity and its extensibility if other organ in the abdomen is found injured. After ente
the abdomen the spleen is lifted forward and the splenic pedicle is approached from behind. Manual comp
to the splenic pedicle will control bleeding and facilitate the operation. If lacerations are small, they can be
sutured over omentum or oxidised cellulose or oxycel. But this is usually not performed. The splenic vesse
are tied individually and splenectomy is performed as described later in this chapter.
Operative mortality for ruptured spleen alone ranges from 5% to 15%. When it is associated with other
visceral injury, the mortality rate goes upto 20% to 40%.
Changing concepts in the treatment of ruptured spleen.— Considering spleen’s important role in cellular
and humoral immunity and considering the danger of severe bacterial infection in asplenic patients, conse
is now adopted in many centres. Repairing of injured spleens by use of sutures have been reported for man
years. Nowadays partial splenectomy, splenorrhaphy and capsular repair have been used in many centres
In case of partial splenectomy, after resecting the lacerated portion of the spleen, the portion of the spleen
which is left behind is compressed between the 4 fingers on one side and the thumb on the other side to
minimise bleeding from the incised surface. Now sutures are applied with heavy catgut in the form of mat
sutures to control bleeding from the raw surface.
ANAEMIA FOR WHICH SPLENECTOMY IS REQUIRED.—

1. Hereditary Spherocytosis.—
This is transmitted as an autosomal dominant trait This condition is not uncommon and is the most com
of the symptomatic familial haemolytic anaemias.
The main defect lies in the erythrocyte membrane in which there is deficiency in spectrin, a major comp
of the red cell membrane, which is responsible for strength of the membrane and the shape of the red cell.
This leads to abnormality of the shape of red cells. The normal red cell is a flexible biconcave disc. But
in this condition the red cell turns into a small and spherical one. These abnormal cells show increased osm
fragility. Lacking adequate deformability to traverse the splenic microcirculation, these spherocytes are tra
in the splenic red pulp and are eventually destroyed by the reticuloendothelial cells.
THE SPLEEN 825
CLINICAL FEATURES.— The main signs and symptoms are anaemia, jaundice, splenomegaly and
reticulocytosis. The severity of these vary with the severity of the disease. The disease may be so severe
that even repeated blood transfusion may fail to maintain a functional haemoglobin level, or it may be so
mild as to go unnoticed in childhood only becoming manifested in adult life with the development of symp
cholelithiasis. Jaundice usually parallels the severity of the anaemia. Periodic and sudden increase in intensi
of the anaemia and jaundice may occur. Cholelithiasis e.g. gallstones of pigmented variety has been reported
in 30 to 50% of patients and is uncommon before age of 10 years. Moderate splenomegaly is a characteristic
finding. Chronic ulcers of the leg may be present though rare in adults. Sometimes liver may be enlarged.
SPECIAL INVESTIGATIONS.— Diagnosis is established by the presence of spherocytes in the periphera
blood with osmotic fragility and negative Coombs’ test. Reticulocytosis is present in 20% of cases.
(i) Fragility test.— Normal erythrocytes begin to haemolyse in 0.47% saline solution. In this condition
haemolysis occurs in 0.6% or even in stronger solutions.
(ii) The reticulocyte count.— The reticulocytes are immature red cells which are discharged by the
bone marrow to compensate for the loss of erythrocytes by haemolysis. For demonstration of these reticuloc
in the blood films vital stains are required. This reticulocyte count is greatly increased after a crisis.
(iii) Excess red cell destruction can be demonstrated by labelling patient’s red cells with 51Cr. This
can be particularly demonstrated by daily scanning over the spleen which is the main organ in which the
red cells are lysed or destroyed. If radioactivity over the spleen is increased, splenectomy will be of value.
(iv) Faecal urobilinogen will also be increased.
TREATMENT.— The only treatment available for this condition is splenectomy. The reason of splenectomy
lies in the fact that the spleen will not allow the red cells to survive long. It is generally recommended that
operation should be performed after 6 years of age, though it can be advised in younger patients if the sever
of anaemia is quite high and there is need for repeated transfusions. Though the membrane abnormality of
the red cells persists and osmotic fragility of the cells are not altered, yet haemolysis virtually ceases in vivo
and erythrocytes achieve normal life span with disappearance of jaundice following splenectomy. It is alway
advisable to do gallbladder ultrasonography or oral cholecystogram prior to splenectomy. During operation
gallbladder should always be examined to exclude presence of gallstones there. If gallstones are present,
cholecystectomy should be performed alongwith splenectomy. Due to absence of adhesions, the operation
is comparatively easy, which accounts for low operative mortality. In fact splenectomy is never more succes
than in this case.
2. Acquired Autoimmune Haemolytic Anaemia (AIHA).—
The aetiology is formation of an antibody produced by the body against its own red cells. Probably spleen
may serve as a source of antibody. Both ‘warm’ and ‘cold’ antibodies have been described. Majority of these
antibodies are haemagglutinins rather than haemolysins. Ultimately the reticuloendothelial system traps and
destroys the immunologically altered red cells. Various studies have proved that this process occurs primari
in the skin. The anti-red cell antibodies are classified as ‘warm’ and ‘cold’ antibodies dependig on whether
they bind to red cells at 37°C or less than that. ‘Warm’ antibodies are usually IgG. ‘Cold’ antibodies are
usually IgM and bind to the red cells mainly in the peripheral circulation where blood temperature is lowere
Cold antibodies cause immediate intravascular haemolysis and destruction of sensitised red cells by the live
These patients usually suffer from chronic haemolysis that is worsened by exposure to ‘cold’ and show
acrocyanosis (Raynaud’s phenomenon) due to intracapillary red cell agglutination.
CLINICAL FEATURES.— Though this condition may develop at any age, yet it occurs more frequently
over 50 years and it is twice as common in female than males. Mild jaundice is often present. Spleen is
enlaiged in half the cases. The extent of anaemia varies and in some patients it may be fulminating. Severe
haemolysis may produce haemoglobinuria and acute tubular necrosis. Usually the disease is chronic with va
degrees of severity of months or years.
SPECIAL INVESTIGATIONS.— The diagnosis depends on demonstration of positive direct Coombs’
test, though it may not be present in all the cases. Anaemia with reticulocytosis is often detected. Products
of red cell destruction are found in the blood, urine and stool.
TREATMENT.— Corticosteroid and blood transfusions are the main treatment of this condition. Splenectom
is usually performed (i) when steroids are ineffective, (ii) when complications preclude the use of steroids,
(iii) if toxic manifestations of steroid become apparent, (iv) if steroids are contraindicated for some reason
or the other or (v) in case of ‘warm’ antibody haemolytic anaemias.
Excessive splenic sequestration of 51Cr-tagged red cells offers a guide for selection of patients who may
require splenectomy. In addition to removing the primary site for destruction of sensitised RBCs, splenectom
significantly reduces production of anti-red cell antibody as the spleen is the major site of IgG antibody
production.
About 80% of patients selected for splenectomy show favourable responses after splenectomy. Even patien
without prominent spleen sequestration may respond to splenectomy.
3. Idiopathic Thrombocytopenic Purpura (ITT).—
Aetiology is not very clear. Many cases may represent the results of autoimmunity which damage the patien
own platelets. Transfused platelets also have a short survival time. The term ITP is reserved for a haeinonhag
disorder characterised by subnormal platelet count in presence of bone marrow containing normal or increas
megakaryocytes and in absence of any systemic disease. The spleen is often implicated either as the major
sequestrating site for sensitised platelets or as a source of antibody production.
CLINICAL FEATURES.— This condition is more often seen in females in the ratio of 3 : 1. The most
common presenting signs are the petechiae and/or purpuric patches or ecchymoses in the skin and mucous
membranes. There is also a tendency to spontaneous bleeding revealed by bleeding gum, epistaxis, gastroint
haemorrhage, haematuria, haemarthrosis and menorrhagia in women. Incidence of central nervous system
bleeding is only 2 to 4% and may be the cause of death. Spleen is palpable in only 10% of cases and its
huge enlargement should evoke suspicion about the diagnosis of ITP.
SPECIAL INVESTIGATIONS.— A platelet count in the peripheral blood is generally reduced to 50,000
or less. The bleeding time is often prolonged, though the clotting time remains normal. Anaemia is not of
significance. Platelet survival time is also short.
Bone marrow examination reveals megakaryocytes either normal or increased in number. Qualitatively th
is degranulation of the cytoplasm, rounding of cytoplasmic edges, appearance of vacuoles in cytoplasm and
disappearance of usual pseudopodia of platelets are seen.
TREATMENT.— The behaviour of ITP is different in children and adult.
In children under 16 years of age about 80% of patients make complete and permanent recovery without
specific therapy. A short course of prednisone therapy may be prescribed.
In adult cases there are still debates about relative advantages and disadvantages of steroid therapy and
splenectomy. However in majority of series the results achieved by splenectomy are clearly more impressive
than those of the steroids. Steroid is given in the form of prednisone 1 mg/kg/day, An increase in platelet
count occurs within 3 to 7 days in most patients. Occasionally azathioprine has been used with some success
Splenectomy is obviously a definite indication for severe cases which do not response to steroid therapy and
for the girls approaching menarche. About 75% of total number of patients subjected to splenectomy respond
permanently and require no further steroid therapy. In most cases the platelet count rises to over 1 lac within
7 days after operation, though sometimes return to normal level may take months.
Splenectomy however is contraindicated in acute phase of ITP.
At present the generally accepted management for ITP cases is initial 6 weeks to months period of steroid
therapy. If the patient does not respond with elevation of platelet count, splenectomy is performed. If the
patient responds to steroid therapy, it is gradually tailed off. However if thrombocytopenia recurs, splenecto
is carried out. Manifestations suggestive of intracranial bleeding demand emergency splenectomy. For patien
with almost nil platelet count platelet packs should be administered following removal of spleen who continu
to bleed.
4. Thalassaemia or Cooley’s Anaemia or Mediterranean Anaemia.—
It is transmitted as a dominant trait. The main defect is in haemoglobin polypeptide chain synthesis. Specif
pairs of genes are responsible for synthesis of Alpha, Beta, Gamma and Delta chains of the haemoglobin
molecules and deficiency of synthesis of one of these chains will lead to thalassaemia. Beta-thalassaemia
is most common type in which there is quantitative reduction in the rate of Beta chain synthesis. When abnor
genes are inherited from both parents (homozygous), thalassaemia major results. Heterozygous patients show
mild anaemia and termed thalassaemia minor.
In thalassaemia major, reduction in the rate of Beta chain synthesis produces marked decrease in the amou
of normal adult haemoglobin (HbA) and compensatory increase in foetal haemoglobin (HbF). Homozygous
Alpha thalassaemia is incompatible with life and these infants are either stillborn or die shortly after birth.
In thalassaemia major, deficiency of beta-chain synthesis results in relative over-production of Alpha chain
which form insoluble inclusions in bone marrow erythroid precursors. These inclusion-bearing red cells are
detained in the spleen and are ultimately destroyed.
THE SPLEEN 827
CLINICAL FEATURES.— Thalassaemia major, is usually manifested in the first year of life. There
is pallor, retarded body growth and enlargement of the head with typical ‘thalassaemic fades’. There is usua
splenomegaly and hepatomegaly. Intractable leg ulcers, intercurrent infections and gallstones may be seen
in certain cases. Intense erythroid hyperplasia in the bone marrow results in expansion of the medullary cav
and attenuation of the cortex producing bony abnormalities, which may predispose fractures.
Thalassaemia minor patients lead normal lives, though a few show severe expression of the disease (these
cases are known as thalassaemia intermedia). These cases may present with mild anaemia, mild jaundice
and moderate splenomegaly.
SPECIAL INVESTIGATIONS.— Diagnosis of thalassaemia major is established by smear revealing
hypochromic microcytic anaemia with markedly distorted red cells of various sizes and shapes. Nucleated
red cells almost always present and may outnumber the leucocytes. The reticulocyte count is elevated, so
is the W.B.C. count. Haemoglobin electrophoresis in thalassaemia major reveals almost complete absence
of HbA and presence of large amount of HbF
TREATMENT.— It is only recommended in case of symptomatic patients. Repeated transfusions are
usually required at regular intervals, which should be directed to maintain haemoglobin at the level of
10 g. per 100 ml. Splenectomy peculiarly helps in curing the condition. Though splenectomy does not influen
the basic haematologic disorder, yet there is considerable decrease of blood transfusion requirements after
splenectomy and it also relieves discomfort from splenomegaly.
Minor thalassaemias do not require treatment. Though there is a trend to offer therapeutic iron to these
cases, it should be avoided as there is risk of iron overload.
5. Sickle Cell Anaemia.—
This condition is also a hereditary haemolytic anaemia seen predominantly in blacks. This disease is
characterised by presence of sickle and crescent shaped erythrocytes. The normal HbA is replaced by abnorm
sickle haemoglobin (HbS). HbS defers from normal adult haemoglobin (HbA) in the substitution of valine
for glutamic acid in the 6th position of the beta chain. Presence of HbS imparts the sickle shape to deoxygena
red cells which is responsible for this disease. In the homozygous state HbA is totally lacking and the red
cells contain mainly HbS.
Under reduced oxygen tension, HbS molecules undergo crystalisation within the red cell, which elongates
and distorts the cells. The sickle cells themselves contribute to increased blood viscosity and circulatory stasi
The consequence is thrombosis which may lead to ischaemia.
CLINICAL FEATURES.— Anaemia is the most common sign. Sickle cell trait occurs in approximately
9% of the black population. In majority of patients the disease remains asymptomatic. Manifestations of this
disease may be both acute or episodic (crisis) and chronic or progressive.
Patients with sickle cell crisis complain of severe abdominal pain and cramps due to visceral arterial stasi
simulating an acute abdomen. Depending on the vessels involved the patient may have bone and joint pain,
haematuria, priapism, neurological manifestations or ulcers over the malleoli. The incidence of pigment galls
increases with age and are present in approximately 70% of adult patients. Thrombosis of splenic vessels
may result in an unusual complication of splenic abscess manifested by splenomegaly, pain and fever.
Chronic features of sickle cell anaemia include retarded growth and development of bone and joint disea
pulmonary, hepatobiliary, genitourinary and neurologic manifestations and ulcerations over the malleoli afte
the first decade. Pigment gallstones appear later in life.
The role of spleen in this disorder is not clear. In the early stage splenomegaly occurs. But later on this
spleen undergoes infarction and marked contraction with eventual autosplenectomy.
Majority of patients with this disease die in the first decade of life, though a few may survive upto 5th
decade. Death may result from intercurrent infections, cardiac or renal failure.
SPECIAL INVESTIGATIONS.— Diagnosis is confirmed by presence of characteristic sickle cells on
blood smear and haemoglobin electrophoresis showing predominantly HbS and variable amounts of HbF an
no HbA.
Leucocytosis is often noticed alongwith increased number of platelets.
There may be some elevation of serum bilirubin.
TREATMENT.— Conservative treatment should be tried first. Sodium cyanate is used to prevent sickling
of HbS. Transfusions are required to maintain adequate haemoglobin level. Partial exchange transfusion and
adequate hydration are helpful during crisis.
Splenectomy should be performed in a few patients in whom excessive splenic sequestration of red cells
can be demonstrated.
MISCELLANEOUS DISEASES WHICH MAY BE BENEFITTED BY SPLENECTOMY.—

Myeloid Metaplasia.—
This condition is a proliferative disease manifested by connective tissue proliferation of bone marrow, liver, spleen
and lymph nodes. Continued fibroblastic proliferation impairs normal haematopoiesis and ultimately produces sclerosis
of the bone marrow and myelofibrosis. This condition is closely related to polycythemia vera, myelotic leukaemia and
idiopathic thrombocytosis, all these conditions together constitute a disease spectrum known as myeloproliferative disorders.
AETIOLOGY of this condition is not much known. The characteristic features of this condition are (i) progressive
fibrosis of the bone marrow, (ii) extramedullary haematopoiesis, (iii) presence of immature erythroid and granulocytes
precursors in the peripheral blood and (iv) massive splenomegaly.
CLINICAL FEATTJRES.— Manifestations of this disease are seen in middle age and old individuals. The symptoms
are usually related to anaemia and increasing splenomegaly. Generalised abdominal discomfort, feeling of fullness after
meals and intermittent pain of splenic infarction are often seen. Other symptoms include malaise, dyspnoea, weight-loss,
spontaneous bleeding, bone pain, pruritis etc.
The most common physical findings are pallor and splenomegaly. Splenomegaly is due to extramedullary haematopoiesis
and myeloid metaplasia. Hepatomegaly is present in 50 to 70% of cases.
SPECIAL INVESTIGATIONS.— The peripheral blood smear characteristically shows immature red cells, poikilocytosis,
anisocytosis with numerous tear drop and elongated shape. The anaemia is of normochromic variety.
The white cell count is usually less than normal in majority of cases. Immature granulocyte forms are present.
A normal platelet count is present in 'Ath of cases, though thrombocytopenia occurs in ‘/3rd of cases and thrombocytosis
in ‘Ath of cases. The serum alkaline phosphatase is usually high.
Hyperuricemia is present frequently and should be anticipated to avoid episode of gout and renal calculi.
Bone marrow biopsy shows varying degrees of fibrosis with scattered foci of haemopoietic elements.
TREATMENT.— This is mainly directed at the anaemia and splenomegaly. Blood transfusions, corticosteroids and
androgen therapy may be of value in this condition. Alkylating agents may be effective in reducing splenic size and transfusion
requirements. Busulfan is the most commonly used alkylating agent, but cyclophosphamide may also be used in
thrombocytopenic patients as it is less likely to suppress platelet production. Some patients do respond to chemotherapy,
but this drug should be used with caution.
Splenectomy has been effective in controlling anaemia and relieving symptoms due to splenomegaly. It also controls
thrombocytopenia. In patients with oesophagogastric varices portal pressures should be determined before and after
splenectomy.
Felty’s Syndrome.—
This syndrome consists of the triad of rheumatoid arthritis, splenomegaly and neutropenia. It may occur in patients
with long history of rheumatoid arthritis as these patients cannot show granulocytosis in response to infection. So recurrent,
persistent and severe infections may occur. Mild anaemia and/or thrombocytopenia are detected in a few patients. Moderate
splenomegaly is common due to expansion of the red pulp.
TREATMENT.— Splenectomy is quite effective in this syndrome. This is particularly performed in those patients
with recurrent infections and chronic leg ulcers. The granulocyte response is immediate and majority of patients will have
resolution of granulocytopenia within 48 to 72 hours after splenectomy. Sometimes corticosteroids have been used to
reverse neutropenia to reduce susceptibility to infection.
Gaucher’s Disease.—
This is a familial disorder of lipid metabolism characterised by abnormal storage or retention of glycolipid cerebrosides
in reticuloendothelial cells. Proliferation and enlargement of these cells produce enlargement of the spleen, the liver and
lymph nodes.
CLINICAL FEATURES.— This disease mainly manifests itself in childhood, though it may become evident only
in late adult life.
Progressive enlargement of the abdomen occurs primarily due to splenomegaly and to lesser extent by hepatomegaly.
Bone pain is common due to bone destruction and pathological fractures or collapse of vertebral bodies may develop
in long standing cases. Many patients show haematologic manifestations of hypersplenism. Moderate thrombocytopenia
and normocytic anaemia with mild leukopenia are not uncommon.
TREATMENT.— Splenectomy is almost always carried out in patients with splenomegaly. It does have beneficial
effect in correcting the haematological disorder. There is no evidence to show that splenectomy influences the basic course
of the disease.
Sarcoidosis.—
The disease is mostly seen among young adults. This condition starts with constitutional symptoms, but fever is unusual.
Cough, shortness of breath and night sweats are often seen mostly due to mediastinal or pulmonary involvement. Generalised
lymphadenopathy is quite frequent and skin lesions are seen in 50% of patients. In 25% of cases hepatomegaly and
splenomegaly are come across. In l/sth of cases hypersplenism is seen with haemolytic anaemia, neutropenia, pancytopenia
and thrombocytopenic purpura. Spontaneous splenic rupture has also been detected in this condition.
THE SPLEEN 829
TREATMENT.— Spontaneous recovery is the rule in majority of cases and there is no specific treatment. If there
be splenomegaly with hypersplenism, splenectomy should be considered as correction of haematologic abnormalities is
always seen following splenectomy.
CYSTS AND TUMOURS OF THE SPLEEN

Cysts are unusual in the spleen and can be broadly classified into 2 groups — (a) Parasitic and (b) Nonpara
cysts.
(a) PARASITIC CYSTS are almost exclusively due to echinococcal disease. This type accounts for 70%
of splenic cysts in countries (Australia, South America and Greece) where hydatid disease is endemic.
(b) NONPARASITIC CYSTS are more often encountered in countries where echinococcal disease is
rare. These cysts can be further classified into 2 groups — (i) primary or true cysts which have an epithelial
lining and (ii) pseudocysts, (i) True cysts can be of dermoid, epidermoid and epithelial varieties and may
also include cystic haemangiomas and cystic lymphangiomas, (ii) Pseudocysts are more common and result
from liquefaction of old haematomas, areas of infarction and inflammation.
CLINICAL FEATURES of splenic cysts are vague. The symptoms are usually due to the presence of
mass and compression of adjacent viscera and due to diaphragmatic irritation.
TREATMENT is usually splenectomy, though selected nonparasitic cysts may be treated by aspiration
alone. In case of very large cysts, intraoperative drainage may facilitate splenectomy.
TUMOURS —
Primary tumours are rare in the spleen. Majority ofthe primary tumours are malignant — either sarcoma,
angiosarcoma or splenic lymphoma. In case of lymphoma every effort should be made to exclude lymphoma
in the bone marrow, lymph nodes and liver. Benign splenic tumours are uncommon and if present usually
include haemangiomas, lymphangiomas and hamartomas.
Metastatic tumours are rare in the spleen. Though spleen is an effective filter and frequently show malignan
cells, yet metastatic deposits are rare. Experimentally it has been proved in rodents that metastatic tumours
rarely develop in the spleen following injection of the tumour cells into the splenic artery. It is probably
due to splenic immune mechanism. Only in cases of Hodgkin’s disease and non-Hodgkin’s lymphomas that
metastasis in the spleen is noticed.
ABSCESSES —
Splenic abscesses are also uncommon. Such splenic abscess may occur front thrombosis of the splenic,
vessels with infarction of the spleen which may later on be infected to cause splenic abscess. It may also
be caused from infected splenic embolus. These are examples of primary abscesses. Secondary or metastatic
abscesses ofthe spleen may occur from osteomyelitis, puerperal sepsis, otitis media and typhoid or paratypho
fever. Sometimes abscess of the upper pole of the spleen may rupture to form left subdiaphragmatic abscess.
Occasionally abscess in the lower pole may rupture to cause diffuse peritonitis.
Clinical manifestations include chills, fever and rigor, splenomegaly and left upper quadrant tenderness.
Diagnosis is confirmed by scan or angiography.
Treatment is romoval of spleen. Very often there is so much adhesion that splenectomy becomes difficult
and in these cases splenotomy and drainage of abscess are required. Splenectomy is only undertaken when
the condition has settled and the patient’s condition has improved.
Splenic vein thrombosis.—
Pancreatitis is the cause of splenic vein thrombosis in more than V2 the cases. Other causes are pancreatic
carcinoma, pseudopancreatic cyst, penetrating gastric ulcer and retroperitoneal fibrosis.
With thrombosis of splenic vein, venous collaterals develop particularly involving the short gastric veins
to the submucosal venous plexus of the stomach, which leads to gastric varices at the cardia and fundus.
Splenic vein thrombosis should be suspected in case of upper G.I. bleeding which reveals isolated gastric
varices on endoscopy. This is more confirmed when there is history of pancreatitis or pancreatic carcinoma.
Splenomegaly is often present with anaemia and normal liver function tests. Diagnosis is confirmed by
coeliac angiography which demonstrates absence of splenic vein.
Splenectomy is the treatment of choice, which also cures gastric varices.
HYPERSPLENISM
Hypersplenism is a concept which refers to increased splenic function with peripheral cytopenias and a
reactive bone marrow. Usually four criteria have been laid down for diagnosis are — (i) anaemia, leukopen
thrombocytopenia or combinations thereof; (ii) Compensatory bone marrow hyperplasia; (iii) Splenomegal
and (iv) improvement following splenectomy. Platelets and granulocytes are most frequently and severely
affected.
Hypersplenism is classified broadly into 2 groups — (a) primary hypersplenism, where an underlying di
cannot be identified to account for the exaggerated splenic function and (b) secondary hypersplenism wher
an underlying disease is identified.
(a) PRIMARY HYPERSPLENISM.— This is extremely rare condition. With invention of sophisticated
diagnostic tools many patients who were previously diagnosed as primary hypersplenism are now conside
as suffering from secondary hypeisplenism.
Majority of patients with primary hypersplenism are females. The clinical features depend on the type
of depressed cells. Fever, frequent and recurring infections and oral ulcerations are noted with neutropenia
Petechiae and ecchymoses are seen with thrombocytopenia. Pallor is a feature of red cells depression. The
bone marrow reveals pancellular hyperplasia. In the peripheral blood smear there should not be any eviden
of leukaemia or myeloproliferative disorders. Primary hypersplenism is a diagnosis of exclusion and an ex
search should be made for a specific aetiology of hypersplenism. Only after such search has been unreward
that a diagnosis of primary hypersplenism can be made.
Treatment.— Corticosteroids seldom work in this condition. Splenectomy is the only answer and should
be carried out once this diagnosis is made. Splenectomy brings about marked haeinatologic improvement
in almost all patients. Occasionally patients followed for long periods have subsequently developed leukae
histiocytic lymphoma or reticulum sarcoma.
(b) SECONDARY HYPERSPLENISM.— Secondary hypersplenism includes a number of diseases sharin
the common feature of splenomegaly. The mechanisms producing splenic enlargement are work hypertroph
from immune response e.g. infectious mononucleosis, Felty’s syndrome etc.; Work hypertrophy from red cell
destruction e.g. spherocytosis, thalassaemia major etc.; Venous congestion e.g. portal hypertension, splenic
vein thrombosis; Myeloproliferation e.g. myeloid metaplasia, chronic myelocytic leukaemia; Infiltration e.g.
Gaucher’s disease, sarcoidosis, amyloidosis etc.; Neoplastic proliferation e.g. lymphoma, chronic lymphocytic
leukaemia, metastatic cancer and hairy cell leukaemia. Diverse pathophysiologic mechanisms are involved
in the resulting hypersplenism. In both primary and secondary hypersplenism, the degree of splenomegaly
does not correlate closely with the severity of clinical symptoms or the degree of depression of formed elem
of the blood.
SPLENOMEGALY
Enlargement of spleen occurs in a variety of conditions which may be medical or surgical. A short list
is given below keeping emphasis on surgical diseases.
1. Blood disorders.—
Hereditary spherocytosis.
Autoimmune haemolytic anaemia.
Idiopathic thrombocytopenic purpura.
Thalassaemia.
Sickle-cell anaemia.
Acute leukaemia.
Chronic leukaemia (lymphocytic and myelocytic).
2. Infective.—
(a) Bacterial.—
Typhoid and paratyphoid.
Tuberculosis.
Septicaemia.
Anthrax.
(b) Viral.—
Infectious mononucleosis.
Psittacosis.
(c) Protozoal and parasitic.—
Malaria.
Schistosomiasis (Egyptian splenomegaly).
THE SPLEEN 831
Kala-azar.
Hydatid cyst.
Tropical splenomegaly.
3. Neoplastic.—
Tumours of the spleen.
Hodgkin’s lymphoma.
Non-Hodgkin’s lymphoma.
Reticulum cell sarcoma.
4. Circulatory disorders.—
Infarcts (bacterial endocarditis or mitral stenosis).
Portal hypertension.
Splenic vein thrombosis.
5. Cysts of the spleen.
6. Miscellaneous diseases.—
Felty’s syndrome.
Sarcoidosis.
Gaucher’s disease.
Porphyria erythropoietica.
Myeloid metaplasia.
Hodgkin’s disease.—The students are referred to the chapter 17 ‘Diseases Of The Lymphatic System’
for elaborate description of this disease.
Non-Hodgkin’s Lymphomas (NHL).—
These constitute a group of primary malignancies of lympho-reticular tissue. Though microscopically this
group is divided into 4 major histologic types viz. lymphocyte predominants, nodular sclerosis, mixed cellul
and lymphocyte depletion, yet for prognostic and therapeutic purposes NHL is classified into nodular (favo
and diffuse (unfavourable) varieties.
CLINICAL FEATURES.— In 25% of patients the onset of NHL occurs in an extra-nodal site. NHL is
found initially as an abdominal mass or as hepatic and/or splenic enlargement. In contrast to Hodgkin’s dis
only about -fcrd of patients with NHL initially have asymptomatic lymphadenopathy. Constitutional sympt
e.g. fever, weight loss and night sweats are frequently present. The mode of spread is unpredictable and man
patients have disseminated disease at the time of presentation. Progression of NHL arising in extranodal are
may occur through local invasion of adjacent structures, extension to regional lymph nodes and/or dissemin
to non-contiguous lymph nodes or distant extra-nodal sites.
Usually at the time of diagnosis the patients are about 50 years of age without any sex preference. If the
disease is diagnosed before the age of 35 or after the age of 65 it is mostly a diffuse variety.
TREATMENT.— As with Hodgkin’s disease chemotherapy and/or radiation therapy are the primary form
of treatment. The type of treatment is based on the histopathologic type of lymphoma and the stage of the
disease. As majority of patients with NHL have disseminated disease at the time of presentation, staging
laparotomy is seldom required. However it is indicated in patients with limited disease in whom laparotomy
findings may influence selection of therapy.
Splenectomy in this condition is considered for 3 reasons — to improve haematologic depression, to reliev
symptomatic splenomegaly and to prevent from recurrent splenic infarctions. Severity of cytopenia may requ
withholding of chemotherapy and radiotherapy. In these cases red blood cell transfusions and splenectomy
improve the condition. Almost all patients undergoing splenectomy for hypersplenism will require red cell
and platelet transfusions preoperatively. In about 80% to 90% of patients significant therapeutic benefit may
be achieved by splenectomy. However the prognosis is more favourable for the nodular than for the diffuse
forms of NHL.
Chronic lymphocytic leukaemia.—
It is a lymphoproliferative abnormality that occurs primarily in the elderly. Majority of the patients are
in the 6th decade of life and males predominate in the ratio of 2 : 1.
Proliferation and accumulation of abnormal lymphocytes in the lymphatic tissues result in lymphadenopa
splenomegaly and lymphocytosis in the peripheral blood.
The most constant abnormality is lymph node enlargement. Splenomegaly is present in most patients and
it is progressive. Hepatomegaly is also a common finding. Lymphocytic infiltration is also seen in the skin,
G.I. tract and respiratory tracts as the disease progresses.

Diagnosis is based on increase in total leucocyte count. There is large number of abnormal, small, immatur
lymphocytes. Bone marrow examination reveals variable degree of infiltration of abnormal lymphocytes.
TREATMENT.— The management of this condition includes chemotherapeutic agents, corticosteroids,
irradiation and splenectomy. Though this disease is not curable, yet effective palliation can be achieved. As
with non-Hodgkin’s lymphoma, splenectomy in this condition is performed for haematologic depression
seccondary to hypersplenism and for palliation of symptomatic splenomegaly. Significant haematologic
improvement follows splenectomy in 80 to 90% of patients, though natural course of the disease remains
unchanged.
Chronic myeloid (granulocytic, myelocytic) leukaemia.—
It is a myeloproliferative abnormality characterised by marked elevation of leukocyte count due to excess
myeloid cells in all stages of maturation and by neoplastic overgrowth of granulocytes in the bone marrow.
This condition is also more common in males in the ratio of 3 : 2. Splenomegaly is the most common
finding alongwith lymphadenopathy, hepatomegaly and sternal tenderness. A peculiar chromosomal abnor
called as the Philadelphia chromosome (Ph) occurs in 90% of cases. Patients who are Ph-negative possess
poorer prognosis.
TREATMENT consists of chemotherapy, irradiation, radioactive phosphorus and extraperitoneal irradiat
of the blood. Busulfan is the mostly used chemotherapeutic agent Splenectomy has less effective result than
the previous condition. It may be of benefit in selected patients during chronic stage to palliate massive
splenomegaly, to relieve pain from splenic infarctions and to palliate severe thrombocytopenia and/or anaem
Schistosomiasis.—
Schistosoma mansoni in 3Ath of cases and schistosoma haematobium in 'Ath of cases are responsible for
Egyptian splenomegaly. This condition is mostly seen in Africa, Asia and South America. Enlargement of
spleen occurs due to hyperplasia which is induced by phagocytosis of disintegrated worms and toxins. This
infestation also produces hepatic fibrosis which in turn causes portal hypertension and splenic enlargement.
Splenomegaly from this condition may occur at any age and males are more often affected. Splenic enlarge
may be massive. The condition is confirmed by finding ova of Schistosoma in the urine and faeces. Liver
function tests usually reveal varying degrees of hepatic impairment. Hypochromic anaemia is often present.
TREATMENT is removal of spleen. If ascites is present, portosystemic shunt should be combined with
splenectomy.
Tropical splenomegaly.—
Spleen may be enlarged to an enormous size due to malaria, kala-azar and schistosomiasis. One type of
splenomegaly is often seen in Africa and New Guinea and it is difficult to find out any cause as mentioned
above. This is often known as ‘tropical splenomegaly’. Probably an abnormal immune response to malaria
or some unknown species of plasmodia is the cause of this type of splenomegaly.
The spleen is often enormously enlarged in this condition. Anaemia and thrombocytopenia often accompa
TREATMENT is splenectomy which should be followed by anti-malarial chemotherapy in the form of
100 mg proguanil daily.
Hypersplenism due to portal hypertension.—
In portal hypertension there is not only splenomegaly but there is associated anaemia, thrombocytopenia
and leukopenia. Portal hypertension may be due to intrahepatic or extrahepatic portal obstruction. Splenome
with engorgement of vascular spaces leads to accelerated destruction of the circulating cells within the spleen
This hypersplenism associated with portal hypertension secondary to cirrhosis seldom requires splenectomy
Cytopenias are usually improved after shunt operation between the portal and systemic circulations presum
due to relief of congestive splenomegaly.
SPLENECTOMY
Indications.— The diseases which have been described above are in fact indications for splenectomy. The
effectivity of splenectomy is not equal for all diseases and this is also described alongwith each disease. In
nutshell the conditions in which splenectomy is beneficial is mentioned below:
1. Blood disorders.—
Hereditary spherocytosis.
Autoimmune haemolytic anaemia.
833
THE SPLEEN
Idiopathic thrombocytopenic purpura.

Thalassaemia.
Sickle-cell anaemia.
Acute leukaemia.
Chronic leukaemia (lymphocytic and myelocytic).
2. Infective.—
(a) Bacterial.—
Typhoid and paratyphoid.
Tuberculosis.
Septicaemia.
Anthrax.
(b) Viral.—
Infectious mononucleosis.
Psittacosis.
(c) Protozoal and parasitic.—
Malaria.
Schistosomiasis (Egyptian splenomegaly).
Kala-azar.
Hydatid cyst.
Tropical splenomegaly.
3. Neoplastic.—
Tumours of the spleen.
Hodgkin’s lymphoma.
Non-Hodgkin’s lymphoma.
Reticulum cell sarcoma.
4. Circulatory disorders.—
Infarcts (bacterial endocarditis or mitral stenosis).
Portal hypertension.
Splenic vein thrombosis.
5. Cysts of the spleen.
6. Miscellaneous diseases.—
Felty’s syndrome.
Sarcoidosis.
Gaucher’s disease.
Porphyria erythropoietica.
Myeloid metaplasia.
PREOPERATIVE MANAGEMENT.— Before elective splenectomy is performed for haematologic disorder
a few important considerations should be made. Blood should be administered at room temperature in cases
of leukaemia and malignant lymphoma. In cases of acquired haemolytic anaemia and thalassaemia grouping
and cross matching may be difficult and sufficient time is required to accumulate the blood which may be
required during the operation. In idiopathic thrombocytopenic purpura (l l'P) platelet packs are not administ
preoperatively as these platelets are destroyed by the spleen and hence become ineffective. However platelet
should be kept in hand to be used after removal of spleen.
Nasogastric tube is inserted after endotracheal intubation of decompression of the stomach to facil ita te ha
of the short gastric veins within the gastrosplenic ligament.
Technique of operation.—
Incision.— Splenectomy can be performed by using one of several standard abdominal incisions. A midlin
incision is probably ideal for ruptured spleen. The left subcostal incision is preferred for elective splenectomy
Left upper paramedian incision may be used with division of the outer fibres of the left rectal muscle. It
is rarely necessary to use a thoracoabdominal incision even to remove a massively enlarged spleen.
Mobilisation of the spleen.— The left margin of the wound is retracted laterally by the assistant. The
surgeon puts his hand on the lateral side of the spleen and brings it medially, so that the lateral layer of
the lieno-renal ligament will be made taut. This is incised and the fascia beneath it is carefully dissected,
so that the splenic vessels will be under view. If there is too much adhesions, these adhesions should be
divided between artery forceps under vision. After this, a pack is inserted on the posterior surface of the
spleen and attention is directed to the anterior surface where lies the gastro-splenic ligament.
Division of gastrosplenic ligament.— This fold carries short gastric vessels and left gastroepiploic vessels.
This fold is clamped from below and divided serially. These are later ligatured. At this stage care must be
taken not to injure the stomach. If compromise of blood supply to the fundic portion of the greater curvat
of the stomach is a concern, enfolding of this area should be performed to prevent development of a gastr
fistula.
Usually the technique of dividing splenic ligaments and mobilisation of the spleen toward the midline
prior to securing the hilar vessels is adopted in case of normal sized of slightly enlarged spleens and for
ruptured spleens. But in case of massive splenomegaly initial ligation of the splenic artery and vein along
the upper edge of the pancreas before splenic mobilisation is a very useful technique as it controls major
portion of vascular supply to the spleen and allows safer mobilisation of the spleen and dissection of its h
branches.
Division of the splenic vessels.— The attention is again directed posteriorly. The spleen is mobilised forw
and medially. The pancreatic tail is dissected off the splenic vessels, which are now seen distinctly. The ar
and the vein are ligated separately, the artery being ligated first so that blood in the spleen will get a chan
to be drained through the vein before ligation thus restoring the normal blood volume. The artery is doub
ligated before division. The vessels are then divided. Gentle handling is of utmost importance, otherwise t
vessels of the spleen may be tom.
Technique adopted in case of ruptured spleen.— In this case time does not permit to dissect the vessels
separately. Firstly the tail of the pancreas is dissected off and then the vascular pedicle is clamped and div
from below in small segments. While applying the clamps care must be taken not to injure the neighbouri
viscera and for this the clamps should be applied as close to the hilum of the spleen as possible.
Excision of accessory spleens.— This is a very important step when the splenectomy is being done for
blood dyscrasias. If this step is omitted recurrence of the disease is almost inevitable. The probable situatio
as has been discussed in Anatomy, should be explored. If present, the pedicles are clamped, divided and
ligated to excise these accessory spleens.
Inspection of the wound and closure.— After splenectomy the ligature of the vessels of the spleen and
at the gastrosplenic ligament are checked. If any small oozing is seen this should be tackled by re-ligature
The tail of the pancreas should be carefully inspected. If it is lacerated, there remains a possibility of woun
disruption.
Whether drainage should be given or not ? — When there is no oozing inside the wound and the tail
of the pancreas is not injured, drainage is not necessary. Otherwise it will be required.
POSTOPERATIVE COURSE.—
Following splenectomy, Howell-Jolly bodies are present in almost all the patients. Generally leukocytos
and increased platelet counts are observed. In ITP cases the platelet count return to normal within 2 days,
but pick level may not be reached for 2 weeks. The white blood cell count is also elevated on the first day
and it may remain persistently elevated for several months.
Postoperative complications.—
1. Haemorrhage.— Oozing of blood may be persistent and troublesome after removal of a large and adherent spleen.
Bleeding from raw splenic bed is best controlled by hot packs. Haemostasis can be greatly improved by approximating
the cut edges of the lienorenal and gastrosplenic ligaments with a continuous suture of fine catgut as the last step of
operation.
2. Left lower lobe atelectasis is a frequent complication. It may or may not be associated with pleural effusion. This
is mostly due to irritation or damage to the left hemidiaphragm or due to presence of subphrenic abscess.
3. Gastric dilatation may be noticed in the early postoperative days if proper nasogastric aspiration is not carried
out during operation and in early postoperative days.
4. Haematemesis may occasionally occur due to mucosal damage to the stomach during ligation of the short gastric
vessels.
5 Damage to the tail of the pancreas during dissection for hilar vessels may occur if particular care is not taken.
This may lead to abdominal wound dehiscence, peritoneal effusion and localised abscess. If the area has been drained,
a pancreatic fistula may result.
6. Thrombosis.— Rise in the platelet count after splenectomy carries a theoretical risk of postopera live venous thrombosis.
Such thrombosis may occur in portal, hepatic or systemic veins. However practically this complication is not seen so
frequently as is expected.
7. Gastric fistula may occur due to compromise in vascular supply to the fundus and greater curvature of the stomach
THE SPLEEN 835
due to ligation of the short gastric vessels. However this type of fistula may also occur due to damage to the greater
curvature while ligating the short gastric vessels.
8. Infection.— There is some evidence that splenectomy in young children may be followed by an increased susceptibility
and a decreased resistance to acute bacterial or viral infections. In adults also there is chance of increased susceptibility
to infection. The reason has been elaborately described in the section of physiology of the spleen in the beginning of
this chapter. The spleen phagocytes bacteria and it takes part in antibody production. It has been revealed after elaborate
study that deaths from sepsis in splenectomised patients are 200 times as prevalent as in the population at large. However
fulminant post-splenectomy infection is very rare. It has been shown that splenectomy results in a variety of immunologic
defects, including a poor response to intravenous immunisation with particulate antigens, a deficiency in phagocytosis-promo
ting peptide, a decreased serum IgM and decreased propadin.
The organisms most frequently isolated from septic splenectomised children are those of diplococcus pneumonia and
H-infiuenzae. However other bacteria e.g. N-meningitidis, Str. pneumoniae have also been detected to cause septicaemia
in splenectomised children. It is therefore reasonable to delay splenectomy for haematologic disorders in very young children
especially those under the age of 2 years. The risk of infection becomes greater when splenectomised patients are treated
with cytotoxic chemotherapy or radiation.
So it is the practice to give pneumococcal antitoxin and antibiotic cover until 18 years of age. Polyvalent pneumococcal
vaccine should be given to all patients preoperatively (pneumova 05 ml), particularly those undergoing splenectomy which
will be followed by chemotherapy and radiation. Splenectomised patients in our country should receive antimalarial
prophylaxis.
836
CHAPTER - 40
THE PANCREAS
EMBRYOLOGY
The pancreas is developed in two parts — a dorsal and a ventral parts. The DORSAL PART arises in the second half of the 4th week as
a diverticulum from the dorsal wall of the duodenum a short distance proximal to the hepatic diverticulum. This dorsal part gradually grows
dorsally and slight proximaliy in the mesoduodenum. This part forms the whole ofthe neck, body, tail and a portion ofthe head ofthe pancreas,
that means the major portion of the pancreas
The VENTRAL PART arises in the form of a diverticulum from the primitive bile duct at the point where it opens into the duodenum
This diverticulum grows round the gut and enters into the mesoduodenum where it enlarges to form the remainder of the head of the pancreas.
The duct of this part ultimately forms the main pancreatic duct and joins with the duct of the dorsal part at the neck ofthe gland. The proximal
part of the dorsal part lying in the head ofthe pancreas usually disappears. In case it persists it forms the accessory pancreatic duct and opens
directly into the duodenum. Early in the ^th week the two parts of the pancreas fuse and a communication is established between their ducts.
At first the body of the pancreas is directed dorsally and proximaliy between the two layers of the dorsal mesoduodenum. During rotation
of the gut this part of the mesoduodenum fuses with the dorsal parietal peritoneum and the gland becomes retro-peritoneal.
ANATOMY
Pancreas is a soft lobulated yellow-pink gland lying transverselly in the posterior abdominal wall behind the stomach extending from the
duodenum to the spleen. It lies obliquely to the left and slightly upwards in the epigastric and left hypochondriac regions. It is divided into four
parts — the head, neck, body and tail.
The head is lodged within the curve of the duodenum. Its superior border is overlapped by the first part of the duodenum and the other
borders are grooved to receive the adjacent margin of the duodenum. From the lower and left part of the head there is a prolongation named the
uncinate process which projects upwards and to the left behind the superior mesenteric vessels. In the groove between the duodenum and the
right lateral border of the head lies the anastomosis between the superior and inferior pancreaticoduodenal arteries. On the anterior surface the
boundary between the head and neck is determined by a groove for the gastroduodenal artery and on the posterior surface the same boundary
is demarkated by union of the superior mesenteric and splenic veins to form the portal vein. The major portion ofthe middle of the anterior surface
of the head is in relation with the transverse colon only areolar tissue intervening. The upper and lower parts of the anterior surface are covered
with peritoneum.
The neck is about 2 cm in length and its anterior surface is covered with peritoneum and supports the pylorus with the omental bursa
intervening. The gastroduodenal artery descends in front of the neck near the junction with head, while its posterior surface is in relation with
the superior mesenteric vein and the beginning of the portal vein.
The body ofthe pancreas has three surface — anterior, posterior and inferior. The anterior surface is covered with peritoneum and forms
a part ofthe stomach bed and is separated from the stomach by the omental bursa. The posterior surface is devoid of peritoneum and is in contact
with the aorta and origin of the superior mesenteric artery, the left crus of the diaphragm, the left suprarenal gland and the left kidney and its
vessels. It is intimately related to the splenic vein which separates it from the structures mentioned. The inferior surface is covered with
peritoneum derived from the lower layer ofthe transverse mesocolon ?nd it lies upon the duodenojejunal flexure and some coils of thejejunum.
Its left extremity rests on the left colic flexure.
The tall is narrow and is contained within the two layers of the lienorenal ligament together with the splenic vessels.
The pancreatic duct (Main duct of Wirsung) traverses the pancreas from left to right lying nearer its posterior than its anterior surface.
It begins in the tail of the pancreas and gradually increases in size as it passes to the right. After it reaches the neck it turns downdards, backwards
arid to the right and comes in relation with the bile duct. This part is developed from the ventral part of the pancreas whereas the major distal
part ofthe duct develops from the dorsal part. The bile duct and the pancreatic duct together pass obliquely into the wall ofthe descending part
of the duodenum and they unite to form a short dilated duct named the hepatopancreatic ampulla( or ampulla of the bile duct). The constricted
distal end of this ampulla opens on the summit ofthe major duodenal papilla which is situated in the second part ofthe duodenum at the junction
of its medial and posterior walls 8 to 10 cm distal to the pylorus. The ducts may not unite till they approach very close to the opening of the
major duodenal papilla. Sometimes the two ducts may open separately into the duodenum.
Frequently there is an additional duct known as the accessory pancreatic duct (duct of Santorini). This duct runs upwards and in front
of the main pancreatic duct to which it is connected by a communicating duct at the neck of the pancreas. This duct represents continuation
ofthe duct ofthe embryologically dorsal part of the pancreas. This duct opens into the duodenum about 2 cm above slightly ventral to the major
duodenal papilla.
Vessels and nerve supply.— Arteries to the pancreas are derived from the splenic artery and from the pancreaticoduodenal artery. Its
veins drain into the portal, splenic and superior mesenteric veins.
The NERVES are derived from both parasympathetic (vagus nerves) and sympathetic. The parasympathetic nerves are derived from vagi
and are mainly secretory fibres. Sympathetic nerves are derived from greater, lesser and least splanchnic nerves (T5 to T10) carrying pain fibres.
PHYSIOLOGY
Exocrine Activity.— The human pancreas secretes daily 1,500 to 2.500 ml of colourless, odourless fluid at pH 8.00. This exocrine
secretion is mainly secreted by the centroacinar cells and ductal cells in response to stimulation. The bicarbomate secretion is mainly under the
influence of secretin, whereas the enzymes are secreted under the influence of parasympathetic supply. So there are two separate components
in pancreatic exocrine secretion.—
THE PANCREAS 837
The FIRST — water and electrolyte secretion which is iso-osmotic with the plasma and its osmolarity is independent of the rate of flow
both in health and disease. Bicarbonate is the main ion and its concentration varies directly with the rate of flow. Chloride ion varies inversely
with bicarbonate. The sum of the concentrations of bicarbonate and chloride is constant under all conditions. The sum of the concentrations
of the sodium and potassium is approximately to that found in the plasma and remains independent of the rate of flow of pancreatic secretion.
Regulation of this part of the pancreatic secretion is mainly performed by secretin, the hormone which is released from the duodenal mu
cosa in the presence of hydrochloric acid, proteolytic byproducts, fatty acids and aminoacids. Secretin stimulates the flow of pancreatic juice
which contains large amounts of bicarbonate. Vasoactive intestinal peptide (VIP) also stimulates water and bicarbonate secretion from the
pancreas. This VIP is thought to be associated with nervous element and it stimulates bicarbonate secretion by stimulation of the cyclic AMP.
Insulin seems to be necessary for the normal release of bicarbonate. Conversely the flow of the pancreatic juice and the concentration of the
bicarbonate are reduced by glucagon, somatostatin (pancreatic endocrine secretion) and antidiuretic hormone.
The OTHER COMPONENT of exocrine function of pancreas consists ofthe elaboration and secretion of small volumes of fluid with rich
enzymatic activity. Digestive enzymes are synthesised on polysomes attached to the endoplasmic reticulum. The secretory proteins are formed
on the ribosomes and then transferred across the membranes of the rough endoplasmic reticulum. The protein-rich fluid of high specific gravity
contains the inactive forms of the enzymes trypsin, chymotrypsin A and B, carboxypeptidase A and B and active forms of ribonuclease,
deoxyribonuclease, amylase and lipase. So some ofthe digestive enzymes are secreted in their active forms (e.g. amylase, lipase) while others,
particularly the proteolytic enzymes (trypsin, chymotrypsin, carboxypeptidase A and B) are released as inactive forms. The enzymes of this
latter group are activated within the duodenum where enterokinase converts t*ypsinogen to trypsin and trypsin activates chymotrypsinogen and
carboxypeptidases. Pancreatic juice also contains ribonuclease and deoxyribonuclease. Within the intestine the pancreatic proteolytic enzymes
split proteins into peptides and aminoacids, lipase breaks fat into glycerol and fatty acids and amylase degrades starches to disaccharides.
The major stimulants to enzyme secretion of pancreas are cholecystokinin and pancreozymin (CCK-PZ), gastrin and the vagus nerves.
CCK-PZ is peptide hormone released from the mucosa ofthe duodenum and jejunum by the presence offatty acids. The neural secretory effects
are mediated by the vagus nerve. It also distributes motor fibres to the smooth muscles of the major ducts. Both trunks of the vagus nerve app
ear to be involved. Stimulation of the vagus nerve provokes secretory response of pancreatic juice with rich in enzymes. Injection of CCK-PZ
also provokes same type of pancreatic secretion. Both CCK-PZ and vagal stimulated secretion requires presence of calcium as a second
messenger. Depletion of intracellular calcium inhibits secretion.
Exocrine secretion of pancreas occurs in four phases—cephalic phase, gastric phase, intestinal phase and postcibal phase. The cephalic
phase of pancreatic secretion is mediated by vagal stimulation. The sight and smell of food initiates this stage and vagal stimulation results in
the secretion of low volume and enzyme-rich juice. Vagal stimulation also results in gastrin release from the stomach and circulating gastrin
stimulates pancreatic enzyme stimulation. Gastric phase starts when the meal reaches the stomach to cause gastric distension and presence of
protein in the stomach causes release of gastrin which stimulates enzyme secretion by the pancreas as well as acid secretion by the stomach.
Intestinal phase starts when acid enters the duodenum. It stimulates release of secretin which stimulates pancreatic fluid and bicarbonate
secretion. Peptides, aminoacids and fatty acids within the duodenum and jejunum will release the peptide hormone CCK-PZ. This hormone
causes a slow but sustained increase in the rate of enzyme secretion by the pancreas. The postcibal phase is characterised by inhibition of the
pancreatic secretion. Intravenous infusions of glucose or protein hydrolysate and presence of fat in the distal intestine will inhibit pancreatic
secretion.
Endocrine secretion.—The internal secretions ofthe pancrease are derived from the islets of Langerhans. These islets are approximately
1 million in number. The individual islet is 100 to 150 nm in diameter. This islet consists of beta (B) cells (about 75%), alpha (A) cells (about
20%), delta (D) cells (about 5%) and a small number of PP cells. The alpha cells constitute the outermost layer, delta cells the intermediate layer
and the beta cells form the central layer. Alpha cells are the source of glucagon, beta cells are the source of insulin and delta cells produce
somatostatin and gastrin. The PP cells have small dark granules and are present not only in islets but also scattered in the exocrine pancreas.
They secrete pancreatic polypeptide, vasoactive intestinal peptide (VIP) and gastrointestinal inhibitor peptide (GIP). These exert a number of
gastrointestinal effects causing diarrhoea, hypermotility and hypochlorhydria. Tumour of these cells cause WDHA syndrome.
Glucagon stimulates hyperglycaemia by promoting breakdown of liver glycogen with consequent release of glucose into the circulation.
This effect on blood sugar provides release of insulin. This glucagon also inhibits exocrine secretion ofthe pancreas and for this it is often used
in acute pancreatitis. It also inhibits gastric acid secretion, inhibits gastric and intestinal motility, stimulates the flow of bile and stimulates
intestinal secretion. Glucagon is also secreted by the intestinal mucosa.
Insulin is the product of beta cells within the islets of Langerhans. The granules of these beta cells represent the storage form of the hor
mone. Release of insulin from the beta cells is controlled by alterations in the concentration of blood sugar. An increase in the concentration of
sugar will cause an increase in circulating insulin. In addition the. hormone secretin also causes the release of insulin. Stimulation of vagus nerve
has been shown to cause insulin release. This action is presumably the result of the effect of vagal stimulation on acid secretion and in turn
stimulation ofsecretin release by acid in the duodenum. Somatostatin interferes with insulin release. Various hormones which increase the blood
sugar, such as growth hormone, glucocorticoids, thyroid hormone and epinephrine may secondarily increase the secretion of insulin. Insulin
promotes the transfer of glucose and other sugars across cell membranes. The transfer of sugars into muscle cells, fibroblasts and adipose tissue
requires insulin. In the absence of glucose fat is utilised with the resultant ketosis and acidosis. Aminoacids may be oxidised to provide energy
and may cause a negative nitrogen balance when glucose is not being used properly. Insulin plays a major role in the conversion of glucose to
glycogen in the liver.
Pancreatic polypeptide is released by vagal stimulation. It provides an important inhibitory control of exocrine secretion of pancreas.
Annular pancreas.— It is a rare congenital abnormality and results when two parts of the congenital pancreatic
tissue which have been named as dorsal and ventral parts encircle the second part of the duodenum due to inc
rotation ofthe ventral part of the gland. So a collar of pancreatic tissue surrounds the duodenum.
CLINICAL FEATURES.— A variable degree of duodenal obstruction occurs in this case. There may be c
atresia of the duodenum in a few cases. In majority of cases the condition remains asymptomatic. When sym
they include abdominal pain, nausea and vomiting. About '/3rd of the cases appear with symptoms before t
birthday. But symptoms may appear at any age.
SPECIAL INVESTIGATION.— In case of complete atresia there may be ‘double bubble’ appearance in s
ray. Partial duodenal obstruction with indentation of the right lateral wall can be seen on barium meal X-ray
of cases.
TREATMENT.—Duodenoj ejunostomy is the most effective way of relieving the obstruction. Duodenod
is sometimes possible in adults and is physiologically ideal. But in majority of cases it is technically difficult
Partial resection of the annular portion of the gland is frequently followed by pancreatic fistula.
Ectopic pancreas.— Pancreatic tissue is sometimes found in other organs in the abdomen. This is called
pancreas or heterotopic (accessory) pancreas. This is most commonly found in the submucosa of the stomac
small intestine or Meckel’s diverticulum. This is also detected in the wall of the gallbladder, in the hilum of
or within the liver. In the stomach ectopic pancreas may be confused with leiomyoma or gastric ulcer. This m
cystic degeneration. Most gastric lesions are on the greater curvature of the antrum. Ectopic pancreas in the
intestine may be the starting point of intussusception. This condition usually does not produce any other sy
Congenital cystic condition of the pancreas.—This is extremely rare and may occur in association with c
cystic disease of the liver and kidneys.
FIBROCYSTIC DISEASE OF THE PANCREAS
This is an hereditary congenital abnormality of all mucus-secreting glands particularly those of the
pancreas and bronchioles. In this disease abnormally viscid mucus is secreted. This causes obstruction of the
pancreatic ducts and retention of pancreatic secretions. This results in distension of the alveoli and
subsequently rupture. Pancreatic enzymes escape and pancreatitis results with subsequent fibrosis. The othe
abnormality is that the meconium becomes abnormally viscid and it causes obstruction of the intestine more
frequently at the distal ileum. Viscid mucus into the bronchioles causes bronchiolar obstruction predisposes
to respiratory infection. Sweat glands produce sweat containing four times more sodium chloride than norm
So exocrine glands are also involved. See also page 924 under the heading of ‘True Cysts of the pancreas’.
Clinical features.—The condition may manifest itself at any age — either at birth during infancy, in older
children and in adults. The main presentation is so follows
AT BIRTH.— The infant is bom with meconium intestinal obstruction or even rarely meconium
peritonitis from perforation of the intestine.
IN INFANTS.— The respiratory system is more often affected and bronchiolitis develops. Patients
complain of dyspnoea with inspiratory indrawing of the lower chest and suprasternal notch. There may be
bronchiectasis. Due to fibrocystic disease of the pancreas patients present with steatorrhoea and the stools a
pale in colour, greasy and with bad odour. Though the appetite is much, yet the infant is cachectic with dist
abdomen.
IN OLDER CHILDREN steatorrhoea and wasting are the main features. Attacks of respiratory infection
are noticed. Cirrhosis of the liver with portal hypertension is often noticed.
IN ADULTS — main presentation is steatorrhoea and long-standing pulmonary infection. Opacity in th
vitreous humour in the eye may cause choroiditis. There may be bilateral enlargement of submaxillary saliv
glands. Excessive loss of salts through sweat is a problem for maintenance of the electrolyte balance ofthe
patient.
Special Investigations.— These mainly are based on chemical test of sweat. Normal content of sodium
is 70 mEq/litre, chloride is 60 mEq/litre and potassium 20 mEq/litre. In all patients suffering from this dise
these figures are greatly exceeded. Trypsin in the duodenum is often low or even absent.
Treatment.— Except meconium ileus, which may require operation, majority of these cases are treated
conservatively. In case of streatorrhoea fat intake should be drastically reduced and extraprotein should be
given. Enteric coated capsules of pancreatin (5 to lOg) are given before meals to supplement deficiency of
pancreatic enzymes in the duodenum 200 units of vitamin D and 10,000 units of Vitamin A are given daily.
THE PANCREAS 839
Respiratory infection must be controlled by antibiotics.
PANCREATITIS
There are four types of pancreatitis, according to the classification of Marseilles (1963):
I. Acute pancreatitis — a single episode of pancreatitis in a previously normal gland.
II. Acute relapsing pancreatitis— recurrent attacks of acute pancreatitis with normalcy in the intervals
between attacks and without permanent functional damage of the pancreas.
III. Chronic pancreatitis — irreversible destruction of pancreatic function with constant pain.
IV Chronic relapsing pancreatitis— recurrent attacks of pain with frequent pain-intervals with
progressive functional damage of the pancreas.
ACUTE AND ACUTE RELAPSING PANCREATITIS
'Acute pancreatitis’ means acute inflammation superimposed on a normal gland and when such several
episodes occur ‘acute relapsing pancreatitis’ is said to exist.
Pathogenesis.—
1 GALLSTONES AND CHOLEDOCHOLITHIASIS.— Gallstones and alcohol are the two major
conditions which can give aetiological explanation of no less than nearly 90% of cases of acute pancreatitis.
Gallstones have been detected in 2/,rds of the cases in private nursing homes whereas '/3rd of cases in
government institutions among low income groups Just reverse is the incidence of alcoholic pancreatitis,
which is more (approximately V^rds) in government institutions among low income groups.
The mechanism by which gallstones result pancreatitis is not very clearly known, (a) For quite a long tim
common channel theory ’ has given much importance in which bile reflux into the pancreatic duct as the two
ducts join together to form the common channel before they open into the duodenum. But unfortunately
bidirectional reflux i.e bile flowing into the pancreatic duct and pancreatic juice into the bile duct has been
observed in humans without pancreatitis. Active perfusion of normal bile into pancreatic duct at normal
pressure does not cause pancreatitis. Moreover pressure in the pancreatic duct system is consistently higher
than that in the bile duct system and that is why one cannot expect that bile will perfuse the pancreatic ducts,
(b) Transient obstruction of the pancreatic duct by gallstones can result in pancreatitis. Transampullary
migration of biliary calculi appears to be well established as an important cause of acute and acute relapsing
pancreatitis. Several studies have indicated that choledocholithiasis can lead to the development of acute
pancreatitis even in the absence of a common biliary-pancreatic channel. Presumably the presence of an
ampullary stone or oedema at the papilla can obstruct pancreatic duct outflow and thus results increase in
pressure within the pancreatic duct system.
2. ALCOHOL.—The exact mechanism is also not known how alcohol can induce pancreatitis, (a) A direct
toxic effect of alcohol on the pancreatic parenchyma has been postulated but could not find a solid base, (b)
With prolonged alcohol intake protein is precipitated in pancreatic juice within the ductules leading to ductu
obstruction and increased pressure within the ductules, (c) Duodenal inflammation induced by alcohol may
produce some degree of duct obstruction, (d) Persistent vomiting may cause regurgitation of duodenal conten
into the pancreatic ducts Two mechanisms seen to give reasonable explanation how alcohol may cause acute
pancreatitis — (e) alcohol stimulates pancreatic secretion by way of acid-induced secretion release, (f) Alcoho
increases sphincteric tone at the ampullary region. So alcohol increases secretion against an unyielding
sphincter. This seems to be the most reasonable explanation of how alcohol causes acute pancreatitis.
3. OBSTRUCTION.— It is obvious that some sort of obstruction of the pancreatic duct is required to
produce acute pancreatitis But deliberate ligation of the major pancreatic duct in the treatment of chronic
relapsing pancreatitis has not caused acute disease So duct obstruction must be associated with stimulation
of pancreatic secretion.
Closed-loop duodenal obstruction with biliary exclusion is followed by fulminating type of acute
pancreatitis. Obstructed duodenum may elaborate factors that may provoke pancreatic inflammation
4. METABOLIC FACTORS.— (a) Hyperlipidaemia has got some relation with acute pancreatitis. Some
patients with a genetic predisposition to hyperlipidaemia and pancreatitis are often diagnosed in childhood
second variety of hyperlipidaemia which causes pancreatitis is often diagnosed as idiopathic variety. In this
case neutral fats are usually increased immediately before the onset of abdominal symptoms and return to
normal when attack is over. Dietary-induced hypertriglyceridaemia may cause attacks of acute pancreatitis
alcoholic patients. It seems that conversion of triglycerides to toxic free acids within the pancreatic parenchy
by pancreatic lipase may be the cause of pancreatitis in hyperlipidaemia. Fat emboli may cause obstruction
the pancreatic duct and may cause pancreatitis.
(b) Hypercalcaemia and pancreatitis are often associated with. Hyperparathyroidism may reveal itself b
repeated attacks of acute pancreatitis. Precipitation of calcium phosphate in the pancreatic duct will lead to
obstruction alongwith increased pancreatic secretion to cause pancreatitis. Parathyroid function should alw
be investigated in any patient with pancreatitis of obscure cause.
(c) Haemochromatosis has been thought to produce pancreatic fibrosis and atrophy due to irritating
property of deposited iron in the pancreas.
5. VASCULAR FACTORS.— Pancreatitis may be induced by injection of microspheres of various sizes
into the pancreaticoduodenal arteries in animals. These particles occlude the terminal arterial supply and
produce local ischaemia. Sometimes in older patients who have widespread vascular obstruction from
atherosclerosis and patients who have undergone cardiopulmonary bypass are sometimes seen with severe
haemorrhagic pancreatitis.
6. POSTOPERATIVE PANCREATITIS.— Following certain intra-abdominal operations pancreatitis
may occur. These operations are mainly on the stomach or on the biliary tract. After Billroth II partial
gastrectomy afferent loop obstruction may cause pancreatitis. After common bile duct exploration, specially
if a long-armed T-tube has been placed through the sphincter of Oddi pancreatitis may follow. Even after
exploration of the common bile duct while passing dilator through the sphincter of Oddi one may injure the
papilla causing oedematous swelling and even pancreatic duct injury, which will all cause pancreatitis. Dur
gastrectomy when the region of the head of the pancreas is being dissected injuiy will cause pancreatitis. Af
splenectomy pancreatitis may result following operative injury to the tail of the pancreas. It must be
remembered that mortality rate of postoperative pancreatitis is quite high reaching about 50%.
7. MISCELLANEOUS.— A wide variety of seemingly unrelated factors have been associated with the
development of pancreatitis.
Certain toxins such as methyl alcohol, zinc oxide, cholinesterase inhibitors have been known to produce
pancreatitis by pancreatic injury.
A few viral diseases e.g. mumps, echovirus infection, coxsackie virus infections, mononucleosis have
been incriminated to cause pancreatitis.
A few drugs e.g. corticosteroids, phenformim. azathioprin, chlorothiazide, frusemide etc. have been hel
responsible to cause pancreatitis.
A certain im'estigative procedures particularly ERCP may cause pancreatitis.
Trauma. scorpion sting, porphyria, shock, vasculitis are a few factors which have some direct relation w
pancreatitis. Autodigestion by activated intrapancreatic enzymes may lead to such pancreatitis.
Pathology.— The basic process in acute pancreatitis is one of autodigestion following activation of
trypsinogen. Activated phospholipase A and elastase are also held responsible to cause acute pancreatitis.
The various pathological changes can be described under two heads, (a) The PERITONEAL CAVITY
contains blood stained exudates. The omental and subperitoneal fats show areas of fat necrosis. Fat necrosis
are duly opaque and yellow-white areas. These are mostly seen around the pancreas. In the greater omentu
and in the mesentery such fat necrosis are abundantly seen This fat necrosis consists of small island of
saponification caused by liberation of lipase which splits fat into fatty acids and glecerol. Fatty acids combin
with calcium to form fat necrosis.
(b) THE PANCREAS.— A precise classification of acute pancreatitis based on histologic examinatio
of the gland would be of considerable value. A cute pancreatitis can be classified as oedematous, necrotising,
haemorrhagic and gangrenous. Perhaps the most characteristic histologic alteration of acute pancreatitis is
THE PANCREAS 841
focal areas of fat necrosis that occur in the stromal, peripancreatic fat and throughout the abdominal cavity.
the oedematous stage, which is the wildest form the whole or part of the organ becomes oedematous. In
necrotic and haemorrhagic varieties one may find haemorrhages and areas of necrosis in the gland. The retro
peritoneal tissues around the pancreas are engorged with blood-stained fluid.
Sometimes fluid may accumulate in the lesser sac and when the condition gradually resolves fibrosis oc
curs which walls off such collection of fluid within the lesser sac. This is called pseudocyst ofthe pancreas.
This occurs in about 12% of cases of acute pancreatitis. With migration of bacteria into such fluid collection,
the condition may turn into abscess formation.
In 1993 a Consencious Conference at Atlanta evolved what is currently known as ‘Atlanta classification’,
which is widely accepted — 1. Acute oedematous pancreatitis (AOP) is the milder form of the disease, ac
counting for 80% of the cases. The pathological feature is oedematous gland without significant necrosis. Th
disease runs a short course with a favourable outcome and hospital mortality is less than 1%.
2. Acute necrotising pancreatitis (ANP), accounts for 20% of the cases and is characterised by pancreat
and peripancreatic necrosis (the latter being usually more extensive). Pancreatic duct or its major branches a
disrupted partially or completely in 30% to 50/% of the cases. The disease usually runs a strong course, with
hospital mortality 5% to 15%. Local complications include pseudocyst (after4 weeks with a lining of granula
tion tissue), infected pancreatic necrosis (before 28 days) and pancreatic abscess (after 28 days).
Clinical features.— The signs and symptoms of acute pancreatitis vary according to the degree of the disea
different varieties of acute pancreatitis have been described as (a) acute oedematous type, (b) haemorrhagic p
and (c) necrotic pancreatitis.
SYMPTOMS.— The main symptom of oedematous pancreatitis is penetrating upper abdominal pain whic
follows heavy meal. The pain is frequently located in the midepigastrium and often radiates to the back or ev
flanks. The patient’s discomfort is often improved by sitting up and gets aggravated by lying down. In haemor
necrotic pancreatitis the pain is cramp in nature and excruciating in degree. The distressing pain is a very ch
symptom of acute pancreatitis. Pain is sometimes felt in the right or left upper quadrant due to severe involv
head or the tail of the pancreas respectively. Pain is agonising and Moynihan described it as ‘illimitable agon
Persistent and repeated vomiting with nausea is another characteristic symptom of acute pancreatitis. Retc
common. Vomiting may even occur in empty stomach.
PHYSICAL EXAMINATION usually reveals a low grade fever and epigastric tenderness. There may be guar
involuntary rigidity of the epigastric region. Signs of shock are quite common including sweating, tachycardia
sion. Abdominal distension is sometimes evident due to paralytic ileus and free fluid within the peritoneal cav
usually due to loss of fluid and blood in the peritoneal cavity and retroperitoneal tissue as well as fluid loss t
vomiting. Moreover a myocardial depressant factor (MDF) is often released from the pancreas during pancre
also contributes to the shock. The shock may be partly due to circulating ‘kinins’ which are formed by the ac
the plasma proteins. Mild jaundice may occur in Vath of the cases and this is partly due to swelling of the head
and excessive haemolysis of red blood cells which become more fragile in acute pancreatitis. Cyanosis may be
a regular feature. Hypocalcaemia is a feature of this disease. Whether it is due to hypoalbuminaemia or unresp
the end-organ to parathormone or stimulation of thyrocalcitonin is something to be predicted. Some excess s
glucagon is also noticed during pancreatitis and this also contributes to the hypocalcaemia. Lot of calcium is
formation of fat necrosis. Very occasionally patient may show carpopedal spasm from severe hypocalcaemia.
Paralytic ileus is limited in the beginning to the duodenum and proximal jejunum. The gas-filled solitary l
proximal jejunum may be seen on straight X-ray as ‘Sentinel loop’. Unless nasogastric aspiration is started, a
dominal distension may be evident after 12 hours.
Discolouration of the skin is a characteristic finding of acute pancreatitis, though not a regular feature. Disco
skin around the umbilicus is known as Cullen s sign. Such discolouration of skin varies from slate blue to mo
brown colour due to ecchymosis and extravasated blood. It may be seen in the loins, when it is called Grey T
At the end of the 2nd week approximately 10 days after the onset of the disease, a tender palpable mass m
the epigastrium. This is the pseudocyst ofthe pancreas. If the mass appears after 3rd week, it is due to abscess for
1. ELEVATED SERUM AMYLASE is a well established feature of acute pancreatitis. Although it may
stated that the higher the serum amylase level, the greater is the probability of acute pancreatitis, it is impos
sible to predict with accuracy either the diagnosis of acute pancreatitis or severity of an individual episode
using only the level of serum amylase. Normal serum amylase level is 80 to 150 Somogyi units. 400 units or
above is suggestive of acute pancreatitis and a level of 1,000 units or above more clearly speaks in favour
of acute pancreatitis. The highest level is attained within 1 hour after the onset of symptoms. After that,
the level gradually decreases and reaches normal level within 3 to 5 days. Persistent hyperamylasemia beyond
the initial week of illness may indicate the development of complications e.g. pancreatic pseudocyst, phlegmo
or abscess or may indicate on growing acute pancreatic inflammation. Apart from acute pancreatitis there
are a few conditions which will also lead to high level of serum amylase. These are : acute cholecystitis,
common duct stone with or without cholangitis, alcoholism in absence of pancreatitis, intestinal obstruction,
perforated peptic ulcer, intestinal gangrene, intracranial bleeding, ectopic pregnancy, carcinoma of pancreas,
renal failure and mumps. After the use of drugs such as meperidine (Demerol) or morphine serum amylase
level is also increased. Increase in the level of serum amylase is observed in about 90% of patients subsequentl
proved to have acute pancreatitis. So, absence of hyperamylasemia does not exclude the diagnosis of acute
pancreatitis. There are many possibilities for the absence of elevated serum amylase level e.g. brief
hyperamylasemia, extensive pancreatic necrosis or an already chronically diseased gland which fails to
elaborate sufficient circulating amylase at the time of acute inflammation and patients with hyperlipidaemia
usually show normal level of serum amylase.
2. The rate of URINARY AMYLASE EXCRETION has been found to reflect the amount of amylase
released from the pancreas into the blood. Quantification of the urinary amylase in addition to serum amylase
determination will increase diagnostic accuracy for acute pancreatitis. Moreover urinary amylase remains
elevated for longer periods. Estimation of total amount of amylase in a 24-hour urine sample is more accurate
than the concentration of the enzyme in one sample of urine. The number of positive diagnosis of pancreatitis
is doubled when the amylase output in the urine exceeds 300 units in 1 hour.
3. Elevation in the SERUM AND URINARY LIPASE activities is also associated with acute pancreatitis.
Elevated serum lipase alongwith elevated serum amylase is more diagnostic. Elevation of serum lipase is
a more accurate indicator of acute pancreatitis than is the elevation of serum amylase due to the fact that
lipase is solely of pancreatic origin. Moreover the duration of hyperlipasemia often exceeds that of
hyperamylasemia. However elevation of serum lipase is also not entirely specific of acute pancreatitis, but
is observed in other diseases e.g. acute cholecystitis, perforated peptic ulcer and intestinal ischaemia.
4. The measurement of renal clearance of amylase improves the accuracy of the diagnosis of acute
pancreatitis. The amylase-creatinine clearance ratio is considered to be more consistent in diagnosing acute
pancreatitis. This ratio is as follows —
Urine amylase Serum creatinine
_________ _____ x ____________________xlOO
Serum amylase Urine creatinine
This ratio normally varies from 1% to 4%. A ratio of greater than 6% is diagnostic of acute pancreatitis.
When this ratio increases to more than 15%, the condition is considered to be a case of very severe pancreatitis
However it must be remembered that a normal clearance ratio does not exclude the diagnosis of acute
pancreatitis absolutely.
5. The finding of SERUM LACTESCENCE is a specific indicator of acute pancreatitis. This is observed
when the circulating triglyceride values exceed 500 mg/100 ml. It is interesting to note that patients with
lactescent serum usually have falsely normal serum amylase level making it a valuable diagnostic indicator
of acute pancreatitis.
6. An elevated white blood cell count above 10,000 cells per cu. mm is typical of this condition.
7. HYPERGLYCEMIA is often noticed, probably due to relative hypoinsulinaemia.
8. HYPOCALCAEMIA is often associated with more virulent type of pancreatitis and in fact value
less than 7.5 mg/100 ml indicates poor prognosis. Explanation of low serum calcium in virulent acute
pancreatitis includes (a) deposition of calcium in the peripancreatic retroperitoneal tissues, (b) a loss of serum
albumin, (c) inadequate parathormone response at the bone level, (d) excess calcitonin secretion and (e)
due to hyperglucagonaemia of pancreatitis. Hypocalcaemia may persist for many days.
9. ABNORMALITIES OF LIVER FUNCTION TEST may be seen in gallstone associated pancreatitis.
THE PANCREAS 843
Elevated bilirubin, alkaline phosphatase, y-glutamyl transferase and alanine aminotransferase indicate
some obstruction to the free flow of bile through the ampulla of Vater.
10. In a small number of patients arterial blood gas abnormalities may be seen. In case of severe
attacks pulmonary dysfunction marked by dramatic hypoxemia and hyperventilation may occur.
11. PARACENTESIS is sometimes utilised to confirm the diagnosis of acute pancreatitis. Increased
amylase and lipase in the aspirated fluid may be detected when their respective serum levels are normal.
However diagnostic paracentesis is not an ideal test for the confirmation of the diagnosis due to its poten
tial complications and lack of specificity.
12. E.C.G. ABNORMALITIES are also noticed in acute pancreatitis and may be due to electrolyte
disturbances. Such abnormality includes varying degrees of depression of ST segment, prolongation of
QT interval and flattening of T waves. But normal E.C.G. does not preclude the diagnosis of acute pancre
atitis.
13. CERTAIN SERUM ENZYMES are found to be increased in acute pancreatitis.
Deoxyribonuclease /values are markedly elevated in the blood only in pancreatic necrosis. In oedema
of the pancreas the value remains normal. So increased concentration of this enzyme in the serum will
reflect the presence of pancreatic disease, but its sensitivity is less than the values of serum amylase.
Leucine Aminopeptidase (Lap).— A raised level of this enzyme is considered sensitive and reasonably
specific index of hepatobiliary disease and pancreas, but differentiation is not possible.
Lecithinase A.— This enzyme has a greater concentration in the pancreas and this is concerned in
converting lecithin to lysolecithin and cephalin to lysocephalin with release of fatty acids. Elevation of
this enzyme in the serum correlates well with acute pancreatitis in the same manner as increased level of
serum amylase and lipase.
14. STRAIGHT X-RAY of the abdomen may reveal pancreatic or biliary calcification, (i) A
single dilated paralytic loop of jejunum adjacent to the pancreatic bed known as ‘Sentinel loop sign’
only provides contributory evidence to the diagnosis, (ii) Distension of the duodenum of moderate
degree may be revealed in this investigation. Occasionally air-fluid level may be detected in severe
cases, (iii) There is often mild distension of the transverse colon due to vicinity of this organ to the
inflamed pancreas, which may be revealed in straight X-ray. The descending colon is usually col
lapsed. So air-fluid distended transverse colon is seen to be cut-off suddenly and this is known as
the ‘cut-off sign’, (iv) Other possible findings are gallstones in the gallbladder and obliteration of
the psoas margin due to retroperitoneal oedema.
15. CHEST X-RAY may show left basal atelectasis, elevation of the left hemidiaphragm and left
pleural effusion. These findings may support the diagnosis of acute pancreatitis and eliminate other
diagnoses.
16. BARIUM X-RAY of the upper G.I. tract, if the patient’s condition permits, may show an enlarged
‘C - Loop’ of the duodenum due to swelling of the head of the pancreas. On lateral films, the stomach may
be seen displaced forward due to extensive peripancreatic oedema. Such anterior displacement is more
obvious due to accumulation of fluid in the lesser sac.
17. ULTRASOUND and COMPUTED TOMOGRAPHY often give conclusive evidence as to the di
agnosis of this disease. It must be remembered that neither USG nor CT scan is very useful in the early
diagnosis. In acute pancreatitis, swelling of the gland, loss of internal echoes and loss of the cleavage
plane between the splenic vein and the pancreas may occur. Ultrasonography is the method of choice for
diagnosing and following pseudocyst. Cysts as small as 1 cm can be found by this study. Ultrasonography
determines whether or not the bile duct is dilated with or without coexistence of gallstones.
Computed tomography also gives an indication to acute pancreatitis by changes in the size or shape of
the organ, decreased density, loss of sharp peripancreatic soft tissue planes due to extension of the inflam
matory process into the adjacent retroperitoneum. Appearance of pseudocyst can be easily diagnosed by
this technique. Currently the most widely accepted method used to confirm the diagnosis of acute pancre
atitis is CT. Accuracy of CT Scanning has been improved with both oral and intravenous contrast en
hancement. Almost all patients with acute pancreatitis have some abnormalities on CT Scan with pancre
atic and peripancreatic changes. Pancreatic changes are enlargement, oedema or necrosis with liquefac
tion. Peripancreatic changes include thickening of the surrounding tissue planes, presence of fluid collec
tions and blurring. An almost definite correlation exists between the degree of CT abnormality and sever
ity of acute pancreatitis. The complications of acute pancreatitis e.g. pseudocyst, pancreatic abscess and
necrosis are also finely demonstrated in CT Scan. Currently contrast-enhanced CT is the gold standard for
identifying and quantifying necrosis. Peripancreatic necrosis is usually more than pancreatic as the pan
creas does not have a complete fibrous capsule and hence extravasation of pancreatic secretion into
retroperitoneum and related areas occurs early. The overall accuracy of CT scan is more than 90%. Necro
sis is best diagnosed after 48 to 72 hours.
18. MAGNETIC RESONANCE IMAGING (MRI) offers a more accurate sophisticated method to
diagnose acute pancreatitis. Currently CT and MRI provide equivalent informations to come to a definite
diagnosis.
Diagnosis And Assessment.— The diagnosis requires detection of elevated pancreatic enzymes in
plasma or serum together with an appropriate clinical picture. The cut-off value for diagnosing acute
pancreatitis is three times the upper limit of the laboratory normal range for amylase or twice normal for
lipase. About 5% of patients can have imaging evidence of acute pancreatitis in the absence of raised
amylase levels. The most effective investigation in this circumstance is abdominal Computed Tomogra
phy (CT). CT is relatively unreliable in the first day of admission and is not recommended, as there is no
evidence to support its use at this stage of the illness. After the patient has been stabilised and is perhaps
failing to improve 7 to 10 days after admission, CT becomes useful to diagnose necrosis and to define its
extent.
TREATMENT.— Surgery is always deferred in acute pancreatitis and the treatment of choice is
conservative management. Any attempt to operate will carry a mortality rate more than 50%. It is now
generally agreed that immediate operation is unwise, provided other acute surgical emergencies can be
excluded.
Acute pancreatitis is a disease with wide spectrum of severity. 80% of attacks are mild with rapid
recovery on conservative treatment alone. The remaining 20% of attacks are severe with a pro
tracted course and a mortality rate of 50%. The severe group needs more vigorous resuscitation and
monitoring including intensive care facilities. Aggressive treatment such as early surgery, perito
neal lavage or endoscopic sphincterotomy might be justified in patients with a poor outlook. Unfor
tunately in no other abdominal condition is the outcome so unpredictable at the outset. So a multi
factor prognostic scoring system (Ranson) has been used to detect the severity of the condition. 9
factors are being considered e.g. (i) Age — above 55 years; (ii) Serum transaminase more than 200
units per litre; (iii) White cell count (x 109/L) more than 15; (iv) Blood glucose — more than 200
mg /100 ml; (v) Arterial oxygen saturation (kPa) — less than 8; (vi) Serum calcium — less than 2
mmol/L; (vii) Serum albumin — less than 32g/L; (viii) Serum lactate dehydrogenase more than 600
units/L and (ix) Serum urea — more than 16 mmol/L. 0-2 adverse factors predict mild disease and 3
or more adverse factors predict severe disease. Ranson’s clinicopathological criteria are widely
used. Prognosis worsens with each positive criterion beyond three. Drawbacks of Ranson’s system
are — (i) it requires 48 hours observation period, (ii) usually ‘one time’ assessment is necessary,
(iii) some laboratory tests are not routinely performed, (iv) it has not taken into consideration obe
sity which is an adverse factor.
Similarly the Apache II scoring system may also be used. A score of 9 or more indicates a severe
attack. An Apache score of 6 or more may indicate chance of development of complications in almost
95% of cases.
CONSERVATIVE MANAGEMENT.— 1. MANAGEMENT OF SHOCK AND ELECTROLYTE
IMBALANCE.— The most urgent requirement of the acutely ill patients is the prevention of shock
and its treatment. Intravenous fluid is started immediately. The amount of fluid required is detected
THE PANCREAS 845
by the degree of severity. Careful monitoring of fluid balance by central venous pressure and hourly
measurement of urinary volume assists accurate replacement. About 1 /3rd of the circulating blood
volume may be sequestered as a result of acute pancreatitis. Plasma and dextran may be infused so
long as the blood is not available. Blood transfusions are required when the haemoglobin concentra
tion drops. Nothing is permitted by mouth so gastric aspiration should also be added alongwith
invisible water loss through lungs and skin and estimated fluid loss from the disease should be
considered totally. The adequacy of volume replacement is assessed by the response of the heart
rate, blood pressure and urinary output. In patients with pre-existing cardiac or pulmonary disease
or in patients with severe pancreatitis, invasive monitoring including urethral catheterisation, cen
tral venous pressure measurement, measurement of cardiac output and cardiac filling pressures via
a Swan-Ganz catheter is necessary. Shock in acute pancreatitis is mainly due to massive fluid se
questration and accumulation of fluid within bowel lumen secondary to paralytic ileus and due to
marked oedema in the peripancreatic region. External fluid losses may occur due to severe vomit
ing. So generous fluid replacement is highly essential. Crystalloid solutions are generally used.
Although haemorrhagic pancreatitis requires blood transfusion. Colloid therapy has little advanta
geous role. When there is hypocalcaemia calcium gluconate will need to be added to the parenteral
fluid. Similarly potassium may be supplemented when hypokalaemia is detected. Hypomagnesemia
may also be observed and should be corrected as this may hasten the normalisation of serum ionised
calcium. Mild hyperglycemia is usually corrected with volume replacement. However marked hy
perglycemia may require cautious insulin administration.
Enteral nutrition.— For many years it was believed necessary to ‘rest the pancreas’ in order to prevent
worsening of pancreatic tissue damage. This now appears to be false, and indeed it seems that depriving
the gut lumen of nutrients is likely to impair gut mucosal barrier function and exacerbate the problem of
translocation. In clinical trials it is shown that patients with severe acute pancreatitis can tolerate enteral
nutrition delivered either by oral intake or by nasoenteric tube feeding with no adverse effect. Indeed
there appears to be a reduction in infective complications. There was reduced ITU stay, a reduced require
ment of surgical treatment and a reduced hospital stay.
2. RELIEF OF PAIN.— As soon as the diagnosis is confirmed and the course of treatment is deter
mined, the patient should be given relief of pain. Pain is very severe and agonising in acute pancreatitis, so
it should be relieved as soon as possible. Moreover pain is frequently accompanied by vasoconstriction
which may be harmful to the myocardium and may reduce the blood supply to the pancreas to convert
simple oedema to necrosis. Morphine, which is quite effective in relieving severe pain, cannot be given in
acute pancreatitis as this causes spasm of sphincter of Oddi. Moreover, administration of morphine is
frequently followed by nausea and vomiting. Demerol (Meperidine hydrochloride) in a dose of 50 to 100
mg every 4 hours is considered to be the analgesic of choice because of its anticholinergic action. It may
be used in combination with Papaverine (100 mg intravenously) or Nitroglycerine. One of the barbiturates
or paraldehyde may be used. In only extreme cases bilateral paravertebral splanchnic block or epidural
block may be necessary.
3. SUPPRESSION OF PANCREATIC SECRETIONS.— This has a great beneficial effect in the
treatment of acute pancreatitis. This can be performed (i) by stopping everything by mouth, (ii) by
nasogastric aspiration and (iii) by non-absorbable liquid antacid (preferably a combination of mag
nesium trisilicate and aluminium hydroxide as a liquid gel). All these act by curtailing secreting
stimulus. H2 receptor antagonist should be used e.g. cimetidine, ranitidine, famotidine etc. Cimetidine
may be effective as an antacid, (iv) An adequate dose of anticholinergic drug such as probanthine 30
mg every 8 hours or atropine sulphate 0.4 to 0.8 mg every 4 hours intravenously is effective in
reducing pancreatic secretion by decreasing vagal stimulus, (v) Acetazolamine (Diamox) has been
found to reduce the volume of pancreatic exocrine secretion and bicarbonate concentration. A dose
of 250 to 500 mg may be administered twice daily without any untoward effects, (vi) Glucagon is
known to reduce exocrine pancreatic secretion and has been claimed by some surgeons to reduce the
mortality rate. But its general acceptances is still awaited, (vii) Calcitonin also suppresses pancre
atic exocrine and gastric acid secretion, so this drug can also be used. Aprotinin is a specific drug
which is being used in this condition with improved prognosis, (viii) Somatostatin is a potent in
hibitor of pancreatic exocrine secretion and gastric acid output. This can only be used by continu
ous intravenous infusion as its circulating half-life in the blood is less than 3 minutes. Octreotide is
a long-acting octapeptide that is now available for clinical use. Though this drug has been effective
in reducing mortality from bile-induced pancreatitis in animal models, however multicentre clinical
trials have failed to produce reduction in mortality rate in patients with acute pancreatitis, (ix) Chole-
cystokinin-receptor antagonist proglumide has also been proved efficacious in animal models and
its use is being investigated in human beings.
However recent trials have failed to show any detectable improvement in this condition by using this
group of drugs.
4. ANTIENZYME PREPARATIONS.— Theoretically inhibition of proteolytic activity might
affect the course of pancreatitis. Some of the deleterious effects of acute pancreatitis are caused by
activation of pancreatic proteolytic enzymes and to liberation of biologically active polypeptides
similar to bradykinin. The release of trypsin from the affected gland is capable of activating pancre
atic Kallikrein another proteolytic enzyme which splits to vasoactive decapeptide Kallidin from a
globulin. This peptide is a potent vasodilator and hypotensive agent. An antienzyme preparation
shown to be effective toward trypsin and Kallikrein in both experimental and human acute pancre
atitis is Trasylol (Aprotinin). This has been extracted from bovine parotid glands. This agent inhib
its trypsin, chymotrypsin, Kallikrein and plasmin. But it should be remembered that once the ne
crotic process is well established Trasylol becomes ineffective. So Trasylol has to be used at the
earliest possible opportunity in a massive dose (1,00,000 units or more daily intravenously). Recent
studies however have failed to show any significant improvement in the condition of patients with
acute pancreatitis by using this group of drugs. Calcium disodium-EDTA has also failed to produce
any decrease in morbidity or mortality in human acute pancreatitis. Although the initial study of
aprotonin showed evidence of benefit, several subsequent randomised studies have failed to con
firm this. Similarly there are conflicting results of the value of gabexate. Studies of therapy aimed at
inhibiting pancreatic secretion with anticholinergic agents or inhibitory hormones such as glucagon,
somatostatin or somatostatin analogues, have all yielded negative findings. There is in fact nothing
to demonstrate any effect of octreotide in over 400 patients.
5. ANTIBIOTICS.— Early antibiotic prophylaxis is strongly advocated as the initially sterile
necrosed tissue (pancreatic and peripancreatic) is vulnerable to infection. The incidence of infec
tion is 20% in first week, 40% in second week and 60% in the 3rd week. Infection dramatically
worsens the prognosis. Currently majority of deaths in ANP are associated with infection. The or
ganisms responsible for infection traverse by translocation from intact gut and are the enteric flora
mostly coliform, with 20 to 30% anaerobes. Imipenem is the antibiotic of choice, as (i) it has the
maximum blood-pancreas diffusion and (ii) it has widest spectrum against organisms of enteric
flora and anaerobes. The next best choice is quinolone (especially ofloxacilin) as the previous drug
is quite expensive. It may be used in combination with anti-anaerobes. Imipenem is administered
intravenously thrice a day for 2 weeks. This may be supplemented with norfloxacin or amphotericin.
Use of these prophylactic antibiotics have significantly reduced the incidence of pancreatic sepsis.
Its effectivity is certainly more in acute fulminating pancreatitis. It will counteract superimposed
infection, prevent widespread peritonitis and suppurative complications. Third generation Cepha
losporin has also been claimed to be highly successful in fulmination pancreatitis. It is definite that
antibiotic is quite effective against the infective complications of acute pancreatitis. What is not
known is the most appropriate antibiotic to be used, and the appropriate duration of therapy. The
organisms which infect pancreatic necrosis are usually enteric bacteria and in this respect cefuroxime
is a relatively inexpensive, widely available and safe antibiotic which can destroy this bacteria. This
THE PANCREAS
should be given for 7 days and after this time, antibiotic treatment should be discontinued or altered
on the basis of culture report.
6. OXYGEN-DERIVED FREE RADICALS.— Systemic hypotension in this condition alongwith em
boli to mesenteric vessels may cause relative pancreatic ischaemia with resultant subsequent necrosis.
Attempts to improve pancreatic perfusion with dextran have proved certain beneficial effect in experi
mental animals, though not in human beings. Free radical scavengers e.g. superoxide dismutase or xan
thine oxidase inhibitors such as allopurinol though have been successful in arresting the disease process in
animal models, have been failed to produce any benefit in the treatment of established acute pancreatitis
in human beings.
7. ANTACID THERAPY.— If there is upper G.I. bleeding, H2 blockers or proton-pump inhibitors are
usually beneficial. However routine use of antacids should be avoided.
8. PERITONEAL LAVAGE.— Peritoneal lavage is quite effective in limiting the number of early
deaths in severe acute pancreatitis, but is probably not capable of preventing late local sequel of pancre
atic necrosis. It removes the toxic products of pancreatic inflammation. Its use is limited to those who
continue to deteriorate inspite of the best conservative treatment and when the diagnosis is absolutely
confirmed. A lower midline or left lower quadrant incision is used and the peritoneal lavage catheter is
introduced by making a nick through the abdominal muscles. 2 Litres of standard peritoneal dialysis
solution containing 1.5 g/100 ml glucose, 4 mEq. of potassium per litre and 500 USP units of heparin are
run in gravity during 30 minutes period. This fluid is then drained out by lowering the bottle to the floor in
the next 90 minutes. The cycle is repeated every 2 hours for 72 hours. Cardiovascular and respiratory
monitoring are imperative as introduction of this fluid into the abdominal cavity may have adverse effects
on the cardiac output and pulmonary compliance. Various studies have suggested that peritoneal lavage
may be of benefit in reducing the early systemic complication of severe pancreatitis, though further study
is required to know specifically the advantage of peritoneal lavage.
9. LEXIPAFANT.— The proposed mechanism of organ failure and tissue damage in acute pan
creatitis invokes the activation of the immune system. The key role of platelet activating factor
(PAF) in these pathways is evident. So there is considerable interest in the development of PAF
antagonist for the treatment of acute pancreatitis, because PAF appears to be involved in the causa
tion of local damage as a result of pancreatic injury and subsequently in the generation of the sys
temic inflammatory response syndrome (SIRS). Clinical trials using a synthetic PAF antagonist,
lexipafant, have shown very encouraging results. Use of this drug can reduce the severity of organ
failure and also reduce the numbers of patient with local complications. It has shown a significant
reduction in mortality rate in the lexipafant treated group.
Future therapy.— As TNF is one of the principal mediators of endotoxin medeated injury, it seems
logical to explore TNF receptor antagonist as the drug of choice in acute pancreatitis. Interleukin 10 is an
inflammatory cytokine which regulates down the response. There is some experimental evidence which
suggests that Interleukin 10 can diminish the severity of acute pancreatitis. This offers exciting prospects
for further clinical development.
SURGICAL TREATMENT.— Acute pancreatitis is mainly treated by conservative management and
the role of surgery is extremely limited. INDICATIONS OF SURGERY are mainly five :—
1. The main indication is uncertain diagnosis. Many conditions of acute abdomen resemble acute
pancreatitis and some of them require immediate operation. So doubt in the diagnosis is the first indica
tion of surgery in acute pancreatitis. Some conditions very much mimic acute pancreatitis — these are
perforated viscus and acute mesenteric ischaemia. In these cases opening of abdomen is obligatory. How
ever with widespread availability of abdominal CT scan, cases of uncertainty of clinical diagnosis are
becoming less frequent. As soon as the abdomen is opened, any ascitic fluid, if present, is sampled for
amylase, lipase, cell counts, aerobic and anaerobic culture. The abdomen should be explored to exclude
any extra-pancreatic disease. If this is not detected, the gastrocolic omentum is opened to fully expose the
body and tail of the pancreas. If uncomplicated acute pancreatitis is diagnosed, no manipulation is re
quired and the abdomen is closed. In case of severe pancreatitis with large amount of peritoneal fluid
exudate peritoneal dialysis catheter is placed, the abdomen is closed and postoperative lavage is contin
ued. If cholelithiasis with presumed gallstone-associated pancreatitis is present, definitive biliary surgery
including cholecystectomy and intraoperative cholangiography is only performed if the patient’s condi
tion permits.
2. Deterioration of clinical condition of the patient inspite of good supportive treatment is an indica
tion for operative intervention. If there is presence of necrotising pancreatitis by clinical and CT scan,
local debridement of obviously necrotic tissue i.e. necrosectomy should be performed. Some surgeons
prefer an early intervention when the patient’s condition deteriorates, however controversy still exists.
But it is an accepted fact that after adequate trial of medical treatment, if the patient’s condition deterio
rates, surgical intervention is required.
At operation, a retroperitoneal approach has been advocated by some surgeons. The claim is that
it minimises intestinal injury. The aim of surgery is to carry out digital, near total sloughectomy,
complete ablation being impossible as the necrosed tissue is often adherent to vital structures like
blood vessels, spleen, intestine etc. The density of adhesions of the necrosed tissue to these struc
tures is directly related to the time interval between the onset of ANP and necrosectomy. All pock
ets of pus/infected fluid should be opened and drained. The retroperitoneum must be deroofed over
all the necrotic tissue. The peritoneal cavity is thoroughly irrigated with copious quantity of normal
saline with or without antibiotics. A feeding jejunostomy is quite helpful, but recently nasojejunal
tube is more advocated for early enteral feeding. Cholecystectomy is performed if the ANP (Acute
Necrotising Pancreatitis) is of biliary aetiology.
After the whole procedure the abdomen is closed conventionally with multiple wide bore drains. It
must be remembered that mortality of this procedure is about 20% to 50% and the incidence of recurrent
infection is about 30% requiring reoperation. This is because necrosis is an ongoing process even postop
eratively perhaps due to disruption of main pancreatic duct as evidenced by rich quantity of active en
zymes/toxins in the drainage fluid. So recently continuously lavage of lesser sac with 10 litres of fluid per
day via two large bored tubes has reduced the mortality to around 20%. This method is called ‘closure
with continuous lavage’. The peritoneum is kept open with special non-adherent packs, so the patient can
be managed with scheduled reoperations to debride the recurrent necrosed tissue. The mortality with this
approach is even less.
3. Correction of associated biliary tract disease.— When the diagnosis of gallstone-associated pan
creatitis is confirmed, it was the practice to defer the definitive biliary surgery upto 8 weeks after the acute
episodes. However, 50% of patients awaiting deferred elective operation experience a recurrence of gall
stone-associated pancreatitis. If the CT scan shows multiple peripancreatic fluid collection with marked
ileus wifh abdominal distension, a delay in electing operation should be advised and nonoperative man
agement is followed as long as clinical improvement persists thereby allowing resolution of pancreatic
and peripancreatic inflammation. 2 to 4 weeks should be allowed in these cases between hospitalisation
for acute pancreatitis and readmission for definitive biliary tract surgery. Another treatment action is an
early operative intervention within first 72 hours after the onset of the disease. The rationality for such
early intervention is to eliminate ampullary obstruction by common duct calculus to reduce the severity of
the episode of pancreatitis. But it seems early surgical therapy does not offer any advantage in majority of
patients, since most patients improve with standard supportive measures. Thus the current recommenda
tion favours initial supportive therapy followed by delayed biliary operation.
Only in case of deteriorating clinical course with supportive therapy, the use of Endoscopic
Retrograde Cholangiopancreatography (ERCP) and Endoscopic Sphincterotomy (ES) should be
considered. In randomised trial it has been found that such patients treated with ERCP and ES
versus conventional therapy, the former group shows significantly fewer complications and signifi
cantly less mortality rate. Moreover the stay in hospital was also shorter. So in patients with severe
attacks of gallstone pancreatitis, the use of early ERCP combined with ES in presence of common
THE PANCREAS 849
bile duct stones seems rational.

4. Secondary pancreatic infections, which include pancreatic abscess, infected pancreatic ne
crosis and infected pancreatic pseudocyst, are life threatening complications and occur in about 5%
of all cases. More is the severity of the case, more is the possibility of these septic complications.
The organisms which are related to such infection appear from transmural migration from the gut or
from haematogenous source. Polymicrobial infection is common in which enteric organisms pre
dominate. Such septic complication should be suspected when there is clinical deterioration after
the first week and in patients in whom pancreatitis fails to resolve within 10 days. Clinical manifes
tations include abdominal pain, fever, abdominal distension and there may or may not be a palpable
abdominal mass. Plain X-ray of the abdomen may show retroperitoneal air, typically known us soap-
bubble sign. CT scan also suggests pancreatic sepsis. One may use contrast-enhanced CT scan for
better detection.
Treatment of such condition is vigorous antibiotic therapy with prompt drainage. Local debride
ment is necessary to remove paste-like collection of necrotic material, which is known as necrosectomy.
This is followed by wide sump drainage or open packing. Anterior transperitoneal approach is made.
The gastrocolic omentum is divided. Necrosectomy is carried out. The peripancreatic region is co
piously irrigated with saline and topical antibiotic solutions. This is followed by either a sump
drainage or open packing. Sump drainage means placement of multiple large-bore drains in depen
dent positions to drain the infected area. In case of open packing, the abdominal fascia is not closed
and multiple packing changes are required in the early postoperative period in intensive care unit.
The latter method seems to work better.
5. In case of local complications such as pseudopancreatic cyst or pancreatic abscess there is a defi
nite role of surgery.
COMPLICATIONS OF ACUTE PANCREATITIS
1. Massive haemorrhage may account for fatality initially.

2. Development of pseudocyst occurs in about 12% of cases. Pseudocyst rarely appears before the 2nd
week of the disease. Formation of a pseudocyst requires about 4 weeks or more from the onset of acute
pancreatitis. It is a collection of pancreatic juice enclosed in a wall of fibrous or granulation tissue which
develops following an attack of acute pancreatitis.
Development of pseudocyst occurs in about 10% of patients with acute pancreatitis and 25% to 40% of
patients with ANP. It must be remembered that about 40% of these pseudocysts, especially those without
ductal communication and those which are less than 5 to 6 cm in diameter resolve spontaneously. Pseudocyst
rarely appears before 2nd week of the disease. A pseudocyst leading to pressure effects before at least 6
weeks from the onset of ANP is best treated by an initial percutaneous USG/CT guided theiapeutic aspi
ration. Drainage instead of aspiration has a higher risk of post-procedure infection. The aspiration or
drainage is followed by ERCP and if pancreatic ductal leak is demonstrated, the duct is stented. If these
procedures fail, the cyst is drained to exterior by conventional or laparoscopic surgery. Before 6 weeks or
when the cyst wall is immature to hold suture the cyst should not be anastomosed to any part of gas
trointestinal tract.
An infected cyst is in reality a pancreatic abscess and should be treated as such.
Observation beyond 6 weeks (for uncomplicated cases) permits maturation of the cyst wall. At this
point of time several treatment options are available. A cyst less than 5 cm in diameter, is just observed.
For other cysts, the first preferred step is ERCP and if ductal communication is seen, the main pancreatic
duct is stented. With a successful stenting 1 or 2 aspirations may only be required to cure the cyst. If
ERCP and stenting are unsuccessful and if no communication with the pancreatic duct is demonstrated,
the cyst is drained into thejejunum, stomach or duodenum depending on local anatomy. For this internal
drainage laparoscopic surgery is more being used than conventional surgery. A current non-surgical op
tion is endoscopic transgastric or transduodenal stenting of the cyst. With this resolution has been achieved
54
in 60% of cases. Complications were bleeding and infection. Cyst recurrence was about 12% after 3 years.
However this technique is only recommended if there is minimal or no debris which is first confirmed by
a pre-procedure CECT Scan (Contrast-enhanced CT scan). Endoscopic ultrasound (EUS) is a good guide
to know the anatomy and for fusion of the cyst wall to gastric wall and to ensure a relatively avascular are
for stent introduction.
3. Pancreatic fistula.— This is come across in 25% to 50% of cases and is due to disruption of main
pancreatic duct or its branches, which occurs in 40% to 50% of patients with ANP. Supportive therapy
often suffices to lead to spontaneous healing. Recently endoscopic stenting of the pancreatic duct is being
performed to expedite healing. However successful stenting may be defeated by severe oedema, ductal
disruption at multiple sites or sticture.
Octreotide reduces incidence of magnitude of pancreatic fistula following effective surgery for cancer
of pancreas and chronic pancreatitis. Many surgeons have used octreotide in patients undergoing surgery
for infected pancreatic necrosis.
4. Pancreatic necrosis indicates a focal or diffuse non-viable parenchyma which is typically associ
ated with peripancreatic fat necrosis. Infection often results in this necrosis which increases the mortality
rate to considerable degree.
5. Pancreatic abscess (PA).— Pancreatic abscess formation is a fatal complication, the mortality rate
of which is quite high approaching 100%. Clostridial organisms are the cause of infection. Such abscess
usually does not appear before the 3rd week. Gradually a swelling appears in the epigastric region or in
the left flank. This alongwith swinging temperature should arouse suspicion of abscess formation. An
abscess should be drained retroperitoneally.
Currently the treatment of choice for this case is percutaneous guided aspiration and drainage by one
or more sump drains. But in nearly 50% of cases this may not be possible or fail due to considerable
necrosis, multilocularity or severely ill patient. Two conditions are often near each other — one is IPN or
infected pancreatic necrosis, another is PA or pancreatic abscess. IPN usually starts before 28 days, wherea
PA appears after 28 days. In case of IPN the necrosis is considerable and adherent to vital structures with
multiple small pockets of pus and fluid. In case of PA necrosis is less and is usually loose with few large
pockets of pus and fluid. In case of IPN multiple organ dysfunction syndrome is around 50%, but in case
of PA this is around 5% only. Mortality is 20% to 50% in case of IPN, whereas only 5% to 10% in case of
PA.
6. Extraintestinal bleeding.— The incidence is about 3% to 6%. Bleeding usually reflects a severe
necrotic form of the disease with a mortality of even more than 50%. DSA (Digital subtraction angiogra
phy) and embolisation is ideal for arresting the bleeding.
7. Multiple organ dysfunction syndrome (MODS).— Patients with IPN have a higher incidence of
MODS rather than those with sterile necrosis. About 50% of patients with IPN ultimately suffered from
MODS.
8. Gastrointestinal fistula.— This occurs in about 15% of cases and is due to autodigestive necrotic
process. Upper left colon is the most frequent site. This is best managed by diversion loop ileostomy, as
transverse mesocolon is usually severely oedematous and shortened. Sometimes the fistulae are multiple.
9. Recurrent infection.— This is seen in 30% to 50% of cases. The ideal treatment is percutaneous
CT/USG guided sump drainage. Failure of this drainage is due to multiple pockets or very thick pus.
Success rate is around 50%. 20% to 30% of cases may require revision surgery.
10. It may cause obstruction of the common bile duct and even duodenum.
11. Collection of blood in the lesser sac though rare, is a dreaded complication. Sudden appearance of
an epigastric swelling should be suspected in this line. This will require surgery and the clot should be
evacuated immediately.
12. Acute renal failure is also a fatal complication of this disease. Presence of progressive azotemia
and persistent oliguria, despite the correction of hypotension and dehydration, should be suspected as a
case of acute renal failure and treatment as acute renal insufficiency should be instituted.
THE PANCREAS 851
13. Haematemesis and melaena may sometimes complicate this condition. It is often a complication of
alcoholic pancreatitis. It carries bad prognosis.
14. Pancreatic ascites may be seen. There is generalised peritoneal effusion which may be associated
with pancreatic duct disruption. Such effusion is obviously enzyme-rich. This may also be due to cirrhosis
following alcoholism.
15. Diabetes mellitus may occur as a sequel of acute pancreatitis. The frequency of diabetes increases
with the number of attacks.
16. Acute psychosis is also a complication associated with acute pancreatitis among alcoholics.
17. Pseudoaneurysm of major peripancreatic vessel may be associated with infection. Recurrent bleeding
may occur from this and may culminate in fatal haemorrhage.
18. Chronic pancreatitis may develop as an aftermath of acute pancreatitis due to damage to the pan
creatic tissue. This is a quiet progressive fibrosis leading to pancreatic insufficiency, which gives rise to
steatorrhoea, nutritional deficiency and at times diabetes.
Management of local complications.— The main role in the management is a conservative approach.
If there is any fluid collection, percutaneous or transgastric drainage should be performed.
The main indication for operative intervention after local complications in acute pancreatitis is the
presence of an abscess or necrosis in or around the pancreas, which is called infected pancreatic necrosis.
Such necrosis can even be managed conservatively by percutaneous drainage with a rigid scope and all
the pancreatic debris is removed. A CT scan is the best investigation to know whether a necrotic fluid or
an infected fluid has been formed or not. Under CT guidance a needle is passed into the necrotic area
without traversing any hollow viscus. If the aspirate is infected and the patient’s condition is deteriorating,
only then a laparotomy with debridment of the dead tissue around the pancreas should be performed.
Unfortunately this process is progressive and further necrotic tissue may be formed. So either the necrotic
cavity is drained and flushed with proper fluid or repeated laparotomies can be performed till there is
clean granulating cavity. This laparotomic removal of necrotic tissue is called 'necrosectomy'.
Subsequent treatment is nutritional support, even parenteral nutrition is required. Once peristalsis is
resumed, feeding may be commenced via jejunostomy, which is performed during laparotomy.
Prognosis of acute pancreatitis.— This mainly depends upon the stage of the disease. In acute mild
episode, the mortality should not be more than 1%. In severe group this mortality rate goes upto about
25%. In case of pancreatic necrosis, the mortality even goes upto 50%. After recovery of acute pancreati
tis after an interval of 1 month patients should be thoroughly investigated for presence of biliary tract
disease. Operation must be performed to cure such biliary diseases. This should be cholecystectomy for
gallstones, exploration of bile duct for biliary calculi and sphincteroplasty. One may perform
choledochoduodenostomy if there is chance of any remnant stones. Failure to remove the predisposing
factor may lead to further attack of pancreatitis which is usually fatal.
Prognosis.— Acute necrotising pancreatitis still has an overall mortality of around 10%. Early deaths
are due to MODS. Severity and incidence of MODS is related to the severity of the disease and to infec
tion. Mortality of infected pancreatic necrosis ranges from 20% to 50% or even more. Mortality of pan
creatic abscess is around 5% to 10%.
CHRONIC AND CHRONIC RELAPSING PANCREATITIS

The distinction between chronic pancreatitis and chronic relapsing pancreatitis is wholly clinical. In
chronic relapsing pancreatitis inspite of progressive destruction of the gland, there may be asymptomatic
periods of varying duration. In chronic pancreatitis there is no such asymptomatic peripd and the abdomi
nal pain is continuous and unrelenting.
Though acute pancreatitis may turn into chronic pancreatitis, yet chronic pancreatitis should be con
sidered as a separate disease entity from acute pancreatitis. In majority of cases chronic pancreatitis de
velops de novo without previous acute disease and the average age of patients with chronic pancreatitis is
10 years less than the average age of the patients with acute pancreatitis.
Pathogenesis.—
1. Chronic alcoholism is the most frequent cause of this condition. It is often believed that the obstruc
tion at the ampulla of Vater is a factor common to biliary tract disease and alcoholism. Alcohol presum
ably causes oedema and inflammation of the papilla of Vater by its local effects.
2. Biliary tract disease.— Cholecystitis, calculous cholecystitis, choledocholithiasis, dysfunction or
fibrosis of the sphincter of Oddi, benign and malignant growths of the ampulla of Vater are important
aetiological factors.
3. The common channel theory. — Many believe that the obstruction of the ampulla of Vater is the main
cause of pancreatitis. So transduodenal sphincterotomy became one of the important treatments of this
condition.
4. Hyperparathyroidism has often been associated with chronic pancreatitis.
5. Hyperlipidemia has often been seen in chronic pancreatitis.
6. Intrapancreatic duct obstruction at one or more sites can be demonstrated in many instances of
chronic pancreatitis. Whether this represents a cause or an effect is to be found out. Due to alcoholism
both in man and in experimental animal plugs of protein has been precipitated and often calcified in the
ductal system of pancreas.
7. Hereditary pancreatitis, malnutrition and a large unexplained idiopathic group form the rest of the
causes. When heredity is the cause, pancreatitis begins at younger age associated with high incidence of
diabetes mellitus and stone formation. There is also an increased
risk of development of pancreatic cancer, particularly if the patient
smokes tobacco heavily.
Pathology.— Histologically lobules of functional acinar and
islet tissue are surrounded by thick band of fibrous tissue. Alter
nating areas of stricture and dilatation of the main ductal system is
a regular feature. Calcification occurs in later stages. It is almost
always intraductal and may be interstitial. Calcification and ductal
distortion are common features of familial or genetic chronic pan
creatitis.
Clinical features of chronic pancreatitis.— The patients are
usually in their late thirties or early forties. A past history of chronic
alcoholism and repeated attacks of pancreatitis may be received.
Pain is the most outstanding symptom in majority of patients. The
site of pain depends on the site of the disease. If the disease is atFig. 48.1.— Straight X-ray of the abdomen
the head of the pancreas, the pain is epigastric or right subcostal.showing calcification in the pancreatic
When the disease is in the body or tail, pain is limited to the left region.
subcostal area or even back pain. Pain changes from intermittent to persistent and continuous. It is usually
located in the epigastrium and characteristically radiates to the back. The pain is aggravated by lying
down and is relieved to certain extent by sitting and stooping forward. Pain may radiate to the left shoul
der. Nausea is quite common during attacks. Anorexia and weight loss are quite common. Steatorrhoea
and malabsorption syndrome are also characteristic. In steatorrhoea the stools become greasy, bulky and
foul smelling. Diabetes is a common accompaniment due to failure of internal secretion. Strangely, cir
rhosis of the liver may present with this condition. Jaundice, often mild, may be apparent.
Clinical features of chronic relapsing pancreatitis.— Recurrent attacks of pain in the epigastrium
is the main symptom of this condition. This pain also radiates to the back and characteristically similar to
that of chronic pancreatitis. But the only difference is the duration of pain. It usually stays for 2 to 3 days.
This is followed by a period of remission. In the period of remission the patients are not absolutely pain
less as happens in acute relapsing pancreatitis. The pains may appear as quickly as once in a week or as
infrequent as twice or thrice a year. With the passage of time the attacks of pain become more frequent.
Weakness or fatigue is common and often heralds an oncoming attack.
THE PANCREAS 853
Vomiting occurs in half of the patients.

Jaundice is rare and when present is mild. It is due to pressure
on the distal part of the common bile duct.
Special Investigations.— 1. Decreased pancreatic secretions
have been found out by decrease of pancreatic polypeptide level in
response to secretin and diminished trypsin value following CCK-
PZ stimulation.
Lundh test.— In this test a test meal is given orally and the
duodenal juice is collected for 2 hours after the meal by aspiration
through a carefully positioned tube. Trypsin is normally more than
9 pEq/min./ml. In chronic pancreatitis it will be reduced to ap
proximately 2|0.Eq/min./ml.
2. Straight X-ray often shows pancreatic calcification. Such
calcification may be intraductal or diffusely scattered within the
pancreatic parenchyma.
3. Barium meal study of the Upper G.I. tract will show enlarge
ment of the C-loop of the duodenum. Hypotonic duodenography
will show more elaborately the subtle changes in the pancreati
coduodenal anatomy.
4. Recently ultrasonography and computed tomography (CT)
have been helpful in demonstrating pancreatic microcalcification pig 48.2.— Endoscopic retrograde
or dilated pancreatic ducts. pancreatography showing a short length of
CT scan of the abdomen is useful to evaluate both parenchymal dilated duct with no distal filling,
and ductal disease. The size and texture of the gland can be assessed, similarly calcification, nodularity
and inhomogeneous density can be detected.
5. MRI is quite a good investigation which will show the outline of the gland as also the texture of the
gland. MR cholangiogram may show presence of biliary obstruction and MR pancreatogram shows the
state of the pancreatic duct.
6. The most definite diagnostic stool available at present is pancreatography through ERCP. It has
proved to be both remarkably safe and informative regarding
macroscopic pancreatic ductal system. Endoscopic Retrograde
Cholangiopancreatography (ERCP) shows ductal dilatations, ductal
strictures and calculi. The characteristic chain of lakes represent
ductal dilatation with ductal strictures, which is a classical sign
of chronic pancreatitis. Sometimes uniform ductal dilatation can
be detected. A normal pancreatogram can safely eliminate the
diagnosis of chronic pancreatitis.
TREATMENT.—
Medical treatment.— Medical management is mainly aimed
at (a) to control abdominal pain, (b) treatment of exocrine insuffi
Fig. 48.3.— Endoscopic pancreatography
ciency and (c) treatment of endocrine insufficiency. showing dilated distal duct system which
(a) Abdominal pain is a major problem. In case of alcohol is suitable for longitudinal pancreatico-
related chronic pancreatitis, total abstinence from alcohol often jejunostomy (See treatment).
helps. Dietary manipulation in the form of small volumes of frequent low fat meals is recommended. High
dose of exogenous pancreatic enzyme, when given, may reduce pain by decreasing pancreatic secretion.
Often non-narcotic analgesic is tried followed later by narcotic analgesic. Octreotide has been used with
modest improvement. Abdominal pain is sometimes the sole indication for operative intervention. Ulti
mately splanchnic nerve block may be required to bring about relief.
(b) Treatment of exocrine insufficiency.— Patients often suffer from steatorrhoea and malabsorption
syndrome due to enzyme deficiency of the pancreas. Exogenous pancreatic enzyme supplementation in
the form of 30,000 I.U. of lipase and 10,000 I.U. of trypsin in the postprandial period is quite effective. If
malabsorption still persists, H2-receptor antagonist may help by diminishing gastric acid induced degra
dation of exogenous enzyme preparations.
(c) Treatment of endocrine insufficiency.— Insulin therapy is particularly required in chronic pan
creatitis-associated diabetes. Hypoglycaemia must be avoided, which is liable to be produced secondary
to malabsorption.
Vitamin supplementation is required in the form of multivitamin capsules.
SURGICAL TREATMENT.— The primary goal of surgical treatment is to relieve pain and the sec
ondary goal is to preserve endocrine and exocrine functions of pancreas as far as practicable. To decide
which operation will help most, two investigations are important — (i) CT scan and (ii) Endoscopic
Retrograde Pancreatography to know the pancreatic ductal condition. The surgical treatment of chronic
pancieatitis is usually one of the following three groups — (a) ampullary dilatations, (b) drainage proce
dures of the pancreatic duct and (c) excisional procedures.
(a) Ampullary dilatations.— Sphincteroplasty of the ampulla of Vater was first successfully carried
out by Doubilet and Mulholland in 1956. The procedure was designed to eliminate pancreatitis by pre
venting bile reflux into the pancreatic duct due to presence of common channel between the pancreatic
duct and the distal common bile duct. 75% to 80% success was claimed by various surgeons through this
operation in chronic pancreatitis. But in the recent past its result has not been favourable. This procedure
is only limited in case of focal obstruction at the ampullary orifice, which is a rare finding and also due to
relative stenosis of the minor duct papilla. Previously it was thought that the commonest site of obstruc
tion in the pancreatic duct in chronic pancreatitis is at the junction of the two pancreatic ducts in the head
of the pancreas. Transduodenal sphincteroplasty is performed to keep the ampulla wide open and there is
no chance of recurrent obstruction. In case of stenosis of the minor pancreatic duct papilla, transduodenal
minor sphincteroplasty or papilloplasty is performed. But in reality since this type of pathology is rare, the
chance of success of this operation is also rare. It must be remembered that sphincteroplasty should al
ways be combined with exploration of the pancreatic duct and its dilatation. Recently therapeutic endo
scopic stenting of the major or minor pancreatic duct is being performed, the result of which is yet to be
evaluated.
(b) Drainage procedures of the pancreatic duct.— In this group, 2 operations are usually
performed — (i) Duval’s pancreatojejunostomy and (ii) Peustow’s longitudinal pancreatojejunostomy.
(i) DUVAL'S PANCREATOJEJUNOSTOMY.— In this operation a limited distal pancreatectomy is
performed alongwith end-to-end anastomosis of the Roux-en-Y loop of jejunum with cut end of the pan
creatic duct to decompress the pancreatic duct in a retrograde manner. Pancreatojejunal anastomosis is
accomplished with a series of all coats interrupted sutures of chromic catgut so that the mucosa of the duct
is approximated to the mucosa of jejunum. The anastomosis is splinted with a polythene tube which is
subsequently passed into the small intestine by means of jejunal peristalsis. The result of this operation
has not been very encouraging as it is only suitable if there is single proximal obstruction in the head of
the gland. But usually as knowledge of pancreatic ductal pathology reveals there is more widespread
ductal disease. This operation may be performed alongwith splenectomy.
(ii) PEUSTOW'S LONGITUDINAL PANCREATOJEJUNOSTOMY.— In most of the patients with
primary chronic pancreatitis multiple strictures of the pancreatic duct wijh dilated pockets are noticed.
Pancreatic secretions into these pockets build up considerable pressure which is responsible for the pain
in this disease. So this procedure is now more widely accepted with success rate of approximately 60% to
80%, as it decompresses nearly the entire pancreatic duct. It is particularly recommended when the dilated
pancreatic duct is more than 1 cm in diameter and in case of presence of pancreatic calcifications. A
defunctioned limb of jejunum is anastomosed with the pancreatic duct side-to-side longitudinally and
intestinal continuity is reestablished by a Roux-en-Y jejunojejunostomy. This operation can be performed
with splenectomy or without splenectomy. Ductal drainage however does not improve established pancre
THE PANCREAS 855
atic exocrine or endocrine dysfunction.

(c) Excisional procedures.— Three types of excisional procedures can be performed —
(i) Pancreaticoduodenectomy (modified Whipple operation) when the parenchymal disease is limited
to the head of the gland, (ii) distal subtotal pancreatectomy when the parenchymal disease is limited in
the body and tail of the pancreas and (iii) total pancreatectomy when the pain continues after lesser
resection.
(i) PANCREATICODUODENECTOMY (MODIFIED WHIPPLE OPERATION).— When the disease
is localised to the head of the pancreas without any distal ductal dilatation, this operation is justified
which involves resection of the head of the pancreas and duodenum alongwith a portion of distal bile duct.
Usually the pylorus of the stomach is preserved and that is why it is called modified Whipple operation.
This ablative procedure preserves a substantial mass of islet cell tissue in the body and tail of the pan
creas, so endocrine function is adequately restored.
(ii) DISTAL SUBTOTAL PANCREATECTOMY.— When the parenchymal disease involves the body
and tail of the pancreas, often secondary to trauma and when the whole of the pancreatic duct system
alongwith its final tributaries is choaked with calculi, there is no way but to perform distal subtotal pan
createctomy. In this operation the pancreas is mobilised from its bed. The splenic vessels are ligated and
divided alongwith removal of the spleen. The dissection proceeds further to the right to reach the neck of
the pancreas where the superior mesenteric vessels and the portal vein are saved. The dissection is ex
tended beyond the pancreatic neck to the level of the intrapancreatic portion of the common bile duct. The
gastroduodenal artery is ligated. The pancreas is now divided securing the common bile duct and the
arterial loop of pancreaticoduodenal arteries. The anterior and posterior walls of the pancreas are sutured
but no ductal anastomosis is necessary. The abdomen is closed with a drain placed down to the pancreatic
fragment.
Postoperative leakage of the pancreatic juice takes place, though the external fistula heals by itself.
This operation has a nearly universal risk of postoperative insulin-dependent diabetes mellitus. The suc
cess rate is claimed in the range of 60% to 80%.
(iii) TOTAL PANCREATECTOMY.— This operation combined with necessary duodenal resection is
only performed in patients with refractory pain after lesser ablative procedures. However insulin depen
dent diabetes mellitus, excessive diarrhoea, steatorrhoea and weight loss have restricted this procedure to
only a few carefully selected patients.
A few newer surgical procedures have been performed in this disease. The pancreatic head is resected
preserving duodenum, combined with denervation of the body and tail of the pancreas.
Pancreatic autotransplantation has been performed following major resection of the pancreas to pre
serve endocrine function. But the result of this operation has not been very encouraging.
Prognosis.— Relief of symptoms can be achieved in about 3/4th of cases by choosing correct
surgery. Aetiological factor must be removed. There is a chance of pancreatic cancer to develop when the
disease is present for more than 20 years. A careful follow-up is required to know the development of
cancer.
CYSTS OF THE PANCREAS

Cysts of the pancreas can be broadly classified into two groups — A. Pseudocyst, which is by far the
commoner and constitutes about 80% of all cysts and B. True cysts, which constitute only 20%.
PSEUDOCYST OF THE PANCREAS (PSEUDOPANCREATIC CYST)

A pseudocyst is caused by encapsulation of fluid or blood in the lesser sac of peritoneum or in the
peripancreatic cellular tissue.
Aetiology.— (i) A pseudocyst may develop from trauma — a severe blow to the epigastrium may cause
laceration of the pancreas. Pancreatic secretion and blood escape into the lesser sac and the foramen of
Winslow is sealed by inflammatory exudate. This causes encapsulation of the effusion.

(ii) It may follow an attack or repeated attacks of acute pancreatitis.
(iii) Following a few operations, such pseudocyst may develop e.g. pancreatolithotomy, caudal
pancreatectomy, pancreatoduodenectomy, partial gastrectomy particularly when the peptic ulcer is firmly
adherent to the pancreas or for malignant lesion in the stomach.
The fluid contained in this cyst is alkaline in reaction, of medium or low specific gravity and contains
albumin, mucin, cholesterin, blood cells and necrotic tissue. It may be clear or light brown or pale green
in colour. Sometimes it may be cloudy with pus cells. One or more pancreatic enzymes may be present,
but in longstanding cysts such enzyme may not be present.
Pseudocysts are most frequently found in the region of body and tail of the gland. A pseudocyst may
bulge between the stomach and the transverse colon, between the stomach and the liver or behind or below
the transverse colon stripping through the leaves of the mesocolon.
Clinical features.— Epigastric swelling is the main symptom of the pseudocyst. Although a few patients
may be essentially asymptomatic, in majority of patients there is upper abdominal pain suggesting recurrent
pancreatitis. There may be anorexia and weight loss. Kehr’s sign may be positive indicating irritation of
the diaphragm. Dyspepsia, nausea and vomiting are commonly noted. Sometimes the mass consists of the
oedematous pancreas and peripancreatic swelling of the omental and retroperitoneal tissues and this is called
pseudopseudocyst.
Special Investigations.— (i) Serum amylase level may or not be elevated and it is of little value to
establish the diagnosis of pseudocyst.
(ii) Straight X-ray of the abdomen may show calcification of the wall of the pseudocyst. Such
Fig. 48.4.— Barium meal films showing displacements of the stomach due to presence
of pseudopancreatic cyst. a.— Shows anterior displacement of the stomach in lateral
radiograph, b.— Shows lateral displacement towards left on PA view.
THE PANCREAS 857
calcification is more common in case of cystadenoma of the pancreas.

(iii) Barium meal X-ray of the upper G.I. tract is quite helpful and will show widened C-shaped
duodenal loop, a filling defect, distortion and indentation of the stomach, duodenum or transverse colon
by the cyst. On lateral X-ray the width between the vertebral column and the stomach is increased due to
the presence of pseudocyst behind the stomach.
(iv) Diagnostic ultrasound has been of great assistance in distinguishing between pseudocyst and
massive peripancreatic oedema.
(v) Computed tomography is probably more accurate than sonography and both these techniques are
popular as they are noninvasive, reliable and safe.
COMPLICATIONS.— The main complications which may appear in a pseudocyst are (i) infection
leading to abscess formation; (ii) Rupture into the peritoneal cavity, pleural cavity or into adjacent organs;
(iii) Haemorrhage — mainly intracystic, though bleeding from varices secondary to portal obstruction or
mucosal haemorrhage from G.I. tract may occur; (iv) Obstruction of the G.I. tract such as the stomach,
duodenum, jejunum or colon may rarely come across; (v) Most lethal complication is haemorrhage from
rupture of a pseudoaneurysm associated with pseudocyst. This can be diagnosed by the angiography.
TREATMENT.— Pseudocyst may be classified into acute and chronic pseudocyst. ACUTE
PSEUDOCYST commonly arises after severe attack of pancreatitis and half of these cysts usually resolve
without any treatment.
So no treatment should be given during the first few weeks. Serial ultrasonic measurements may be
made to know the progress of the cyst.
The management of patient with pseudocyst is guided by the natural history.
The indications of surgery in pancreatic pseudocyst are — (i) presumed duration of more than 6 weeks
without resolution, (ii) size of the pseudocyst is greater than 5 to 6 cm, (iii) evidence of secondary infection
and (iv) development of any other complications.
Serial CT scans or ultrasound studies obtained at monthly intervals are essential to assess condition
of the pseudocyst, its enlargement or resolution. It must be remembered that if any significant symptoms
exist, surgical intervention is indicated if one assumes that pseudocyst wall maturation has already occurred
Surgical treatment.—
(i) INTERNAL DRAINAGE.— The most preferred surgical management in uncomplicated pseudocyst
is internal drainage. The three options are — cystojejunostomy in which a defunctionalized Roux-en-
Y jejunal limb is used for drainage of the pseudocyst; cystogastrostomy — drainage into the stomach; and
cystoduodenostomy — drainage into the duodenum. The anatomical basis of selecting one of the 3 options
depends on the location of the pseudocyst. The drainage must be dependent. Cystojejunostomy is the most
preferred technique and it is particularly appropriate when the pseudocyst presents at the base of the transv
mesocolon and it is not adherent to the posterior gastric wall. Cystogastrostomy is used when the pseudocys
is adherent to the posterior wall of the stomach. It is faster, easier to operate and according to the position
of the pseudocyst this operation is most commonly performed. When the pseudocyst is limited to the head
of the pancreas near the duodenum, cystoduodenostomy is performed. This operation is least performed,
as the position of the pseudocyst is usually not favourable for this operation and there is also chance of
a potential duodenal fistula.
Currently endoscopic approaches are being used to drain the pseudocyst into the stomach or duodenum
by placement of an endoprosthesis using flexible upper G.I. tract endoscopy.
(ii) EXCISION OF PSEUDOCYST is hardly required and is usually limited to the pseudocyst involving
the tail of the pancreas. Distal pancreatectomy with or without splenectomy is performed in this case. This
operation may be associated with drainage of the pancreatic duct if any proximal obstruction is suspected
in the form of Roux-en-Y pancreaticojejunostomy.
(iii) EXTERNAL DRAINAGE of pseudocyst is only required when it is associated with gross infection
in an otherwise grave patient in whom any complex operation is impossible. It is also occasionally used
in case of immature pseudocyst with thin wall. The external pancreaticocutaneous fistula heals by itself.
However persistent fistulas may require operative closure.
Non-operative approach using percutaneous catheter drainage is currently used. A tendem trocar catheter
insertion technique or Seldinger technique is being used. The catheters of 7 to 16 French sizes are being
used. Once the catheter has entered the pseudocyst, the fluid is aspirated and the cyst is irrigated with small
amounts of saline several times a day. The duration of catheter drainage varies from several days to several
months. Though short-term efficacy of this percutaneous drainage procedure is almost similar to open
technique, but long term efficacy has been poorly documented.
The indications of surgery in pancreatic pseudocyst are (i) presumed duration of 6 weeks without
resolution, (ii) evidence of secondary infection and (iii) development of any complication.
A CHRONIC PSEUDOCYST indicates maturity of the cyst wall and this is usually attained at about
4 to 6 weeks. Elective surgical management of chronic pseudocyst is one of the three methods — (i) excision,
(ii) external drainage and (iii) internal drainage.
(i) EXCISION.— This should be reserved for small cyst of the body or the tail of the pancreas with
minimal adhesions to the surrounding structures. This is not a safe procedure and has not been generally
accepted.
(ii) EXTERNAL DRAINAGE.— This is still preferred for infected cysts and abscesses, otherwise internal
drainage is the treatment of choice.
(iii) INTERNAL DRAINAGE.— It is now the most popular method of treatment. The anatomical basis
is that (a) anastomosis must be made to a mature fibrous cyst wall, (b) selection of the organ depends on
the size and location of the pseudocyst and (c) dependent drainage is mostly considered. Of the several
methods of internal drainage the most frequently used method is transgastric cystogastrostomy or
cystojejunostomy to a Roux-en-Y loop of jejunum.
CYSTOGASTROSTOMY.— The anterior wall of the stomach is incised. An incision of no less than
7 cm in length is made on the posterior wall of the stomach into the cystic cavity. The wall of the incision
is sutured along with the cyst wall with catgut running suture. This will act as haemostasis. Now the contents
of the cyst will drain into the stomach. The anterior wall of the stomach is closed in layers. The abdomen
is closed. See Fig. 28.1 in page 359 of Author’s ‘A PRACTICAL GUIDE TO OPERATIVE SURGERY’.
TRUE CYSTS OF THE PANCREAS

True cysts of the pancreas can be classified as follows :—
A. Congenital.—
1. Single or multiple cysts within the pancreas.
2. Simple cysts of the pancreas associated with polycystic disease.
3. Fibrocystic disease (mucoviscidosis).
4. Dermoid cyst.
B. Acquired.—
1. Retention cyst.
2. Parasitic cyst (hydatid cyst).
3. Neoplastic cyst — Cystadenoma, cystadenocarcinoma, cystic teratoma and unusual secondary cav
itation of solid tumour e.g. adenocarcinoma, leiomyosarcoma and lymphoma.
Of the congenital cysts fibrocystic disease is important and has already been described. See page 940.
Retention cysts.— These cysts may be unilocular or multilocular and they have communications with
the ducts. Such cyst is due to ductal obstruction by chronic pancreatitis, stone or tumour. These start within
the pancreas and gradually extend beyond the glands. Majority of these cysts contain relatively clear pancreati
juice in which all the pancreatic enzymes can be detected. This type of cyst possesses a lining of epithelial
cells unless high intracystic pressure has resulted in flattening out of these cells. The wall of the cyst contains
THE PANCREAS 859
encrustation of pancreatic substance due to fibrotic degeneration of the surrounding parenchymal tissues.
Parasitic cyst (hydatid cyst).— Hydatid cyst of pancreas is rare. If present, this is treated by enudeation.
When the cyst is large and involves the tail or body of the pancreas, distal pancreatectomy with splenectom
Neoplastic cysts.— These cysts account for 15% of all cysts of the gland. Cysts from cystadenoma
are usually multiple and lie in adenomatous mass. These often have narrow attachment to pancreas. Excisio
is therefore easy.
CLINICAL FEATURES.— Epigastric discomfort is the main presenting symptom. Sometimes swelling
may be complained of. Such swelling is difficult to differentiate from a renal swelling.
TREATMENT.— Except when the cyst is situated at the tail of the pancreas, when distal pancreatectomy
is the treatment of choice, otherwise internal drainage is preferred. A large cyst at the head of the pancreas
is usually treated by cystoduodenostomy. A similar large cyst in the body is treated by cystogastrostomy.
NEOPLASMS OF THE PANCREAS

Neoplasms of the pancreas can be broadly classified into two groups — A. Carcinoma of the pancreas
and B. Neoplasms of the islet cells which are concerned with endocrine secretion of the pancreas.
CARCINOMA OF THE PANCREAS

Though it seems that more than 3/4th of cases are adenocarcinomas of duct cell origin, yet most of
the carcinomas arise from primitive stem cells which ultimately differentiate into both duct cells and acinar
cells. Only 1% of carcinomas originate from the acini.
The average age of the patient is about 60 years, but for carcinoma of the ampulla the average age
is about 5 years less. Males are more frequently affected. There is no special racial predilection.
Pathogenesis.— Incidence of carcinoma of the pancreas has risen steadily over the past 10 years. There
are some factors which can be considered as initiating or provoking carcinoma of the pancreas. These are
(i) Cigarette smoking (and not cigars); (ii) Consumption of coffee; (iii) Diet rich in fat; (iv) Certain chemical
agents such as B-naphthylamine and Benzidine; (v) Diabetes; (vi) Carcinogens in duodenal contents refluxin
into the pancreatic ducts; and (vii) Alcohol ingestion. Controversies are there and many pathologists believe
that intake of alcohol does not increase incidence of carcinoma of pancreas.
Pathology.— There is fairly standard distribution of the carcinomas of the pancreas. In the head 60
to 80% (2/3rd in the head proper and l/3rd in the periampullary region); In the body 15 to 30% and in
the tail 5 to 10%. Carcinomas of the head of the pancreas differ strikingly from those of the body and tail
from the standpoints of their clinical significance and manner of spread. The lesions of the head of the
pancreas tend to be discovered while still small and before widespread metastasis has occurred, as they reve
themselves through jaundice by obstructing the distal portion of the common bile ducts. In contrast, cancers
of the body and tail may grow silently for long periods and become manifest only by extension to adjacent
structures and by metastatic dissemination.
(a) CARCINOMA OF THE HEAD PROPER.— Adenocarcinoma is the predominant lesion, often
accompanied by extreme fibrous connective tissue stromal proliferation. The tumours may be mucinous or
nonmucin secreting. Only 10% assume either an adenosquamous pattern or the uncommon pattern of extreme
anaplasia with giant cell formation, numerous mitoses and bizarre pleomorphism. Only 0.5% arise in cyst
and are termed cystadenocarcinoma. The lesion is often small with increased consistency and irregular
nodularity. The carcinoma looks greyish white scirrhous or homogeneous tumour which replaces the usual
yellow lobular structure of the pancreas. A considerable desmoblastic response is seen. In some areas there
are only a few isolated clusters of tumour cells widely separated by bands of collagen. Sometimes one may
find carcinoma in situ in the ducts adjacent to the cancer, which suggests ultimate multicentric nature of
this tumour. These tumours compress the pancreatic and common bile ducts and at times extend directly
through the wall of the duodenum to produce a small fungating lesion within the duodenal lumen. As a
consequence of obstruction of the common bile duct, the bile duct proximal to the obstruction becomes
distended alongwith the gallbladder and thus the gallbladder is often distended and palpable in cancer head
of the pancreas according to Courvoisier’s law. On the other hand the inflammatory fibrosis of cholecystitis
and cholelithiasis will cause constriction of the gallbladder and hence not palpable. Regional lymph node
metastasis is present in 90% of cases. Cystadenocarcinomas are rare lesions of the pancreas and show
predilection for females.
CARCINOMAS OF THE AMPULLA OF VATER are columnar cell adenocarcinomas. While 80% of
carcinoma of pancreas arise from the head of the pancreas, less than 10% represent ampullary carcinoma.
This neoplasm arises in the duodenal papilla, in the ampulla of Vater or in the duodenal mucosa adjacent
to the papilla. There may be an area of pancreatitis in the head of the pancreas. The primary lesion is so
small that it is difficult to palpate. In such carcinoma jaundice may not be progressive as recurrent sloughing
of the central portion of the tumour will relieve obstruction of the bile duct and the jaundice becomes
intermittent. The pattern of metastatic spread is similar to that of carcinoma of the head of the pancreas.
(b) CARCINOMA OF THE BODY AND TAIL.— These tumours are usually large, hard and irregular
masses that may sometimes wipe out virtually the entire tail and body of the pancreas. These carcinomas
frequently extend more widely than those of the head. They impinge upon the adjacent vertebral column,
extend through the retroperitoneal space upwards and downwards and may sometimes invade the spleen
or the adrenal. They may extend into the transverse colon or stomach. Lymph node metastasis is present
in 90% of cases. The liver is involved in 80% of cases. The liver metastasis will cause hepatic enlargement
with tumour nodules. Such massive hepatic metastases are characteristic of carcinoma of body and tail and
may to certain extent due to involvement of the splenic vein giving rise to portal hypertension.
Spread.— Local spread has already been described above.
Lymphatic spread from the head first involves the pancreaticoduodenal group and then the lymph nodes
at the porta hepatis and hepatic group of lymph nodes along the hepatic artery. From the body and tail
of the pancreas, coeliac, gastric, mesenteric and para-aortic group of lymph nodes are involved. The left
supraclavicular lymph nodes (Virchow’s) are less commonly affected than in case of carcinoma of the
stomach.
Vascular spread is extremely uncommon in case of cancer of the head of the pancreas. Liver is mostly
affected through such spread from the body and tail of the pancreas.
Peritoneal implantation resulting in ascites is rarely seen in cancer of the body and tail of the pancreas.
Clinical features.— Two types of presentation are usually seen :
A. Painless Progressive Obstructive Jaundice.— Carcinoma of the head of the pancreas usually presents
this type of feature. Cancers of the body and tail may present with this type of clinical feature only when
there is lymph node enlargement at the porta hepatis. Progressive jaundice is usually associated with pruritus
due to presence of bile salts in the blood. The jaundice usually progresses steadily until the patient is almost
green in colour. In case of periampullary carcinoma jaundice may be intermittent. Pain is not a marked
feature. When carefully enquired for, the patient may complain of dull and aching pain in the epigastrium.
Radiation to the back is frequent and occasionally it may radiate of both lower quadrants. Pain is often relieved
by sitting in hunched position and is aggravated by supine position. Eating may aggravate pain. Weight
loss is the single most common symptom of carcinoma of the pancreas irrespective of the location of the
tumour. Anorexia is almost always present. Diarrhoea with pale and foul smelling stool is sometimes a
feature of periampullary carcinoma. There may be steatorrhoea due to enzyme deficiency.
On examination, jaundice is the main sign. A palpable distended gallbladder is detected in 60% of cases
(according to Courvoisier’s law). Enlargement of the liver is found in slightly more than half of the cases.
In carcinoma of the head of the pancreas it is often due to biliary obstruction. In cancer of the body of
the pancreas it is mostly due to metastasis. Virchow’s nodes are less frequently enlarged.
B. Intractable Pain Without Jaundice.— Such pain is often noticed in case of cancer of the body and
THE PANCREAS 861
tail of the pancreas. Pain is intractable and mostly referred to the epigastric region with radiation to the
back. The pain gets aggravated on lying down and is slightly relieved in sitting posture and leaning forward
Loss of weight, anorexia and diarrhoea are often accompanied. Chills and fever, though rare, may occur.
‘Thrombophlebitis migrans’ is often accompanied with tumours of the body of the pancreas. This appears
spontaneously and may affect any superficial vein. It is called Trousseau's sign. It also occurs in other types
of abdominal carcinoma.
Diabetes mellitus is often accompanied with carcinoma of the pancreas. Approximately 10% of patients
with carcinoma of the pancreas are obviously diabetic. On the other hand pancreatic malignancy occurs at
least twice as frequently in diabetics as in nondiabetic patients. So any patient over 40 years of age with
diabetes and complains of sudden weight loss should arouse the suspicion of pancreatic malignancy.
On examination, there is generalised wasting. The liver is palpable in about half the cases. Very occasionall
particularly in thin individuals, carcinoma of the body of the pancreas may be palpable and may transmit
the aortic pulsation. Splenomegaly may be detected in 1/10th of cases due to splenic vein thrombosis.
CARCINOMA OF AMPULLA OF VATER shows a few peculiar symptoms and signs. Pain is less frequent
in this condition, but when present it is apt to be more colicky in nature. Jaundice is often intermittent.
Chills and fever are not uncommon in this condition probably due to associated cholangitis.
Special Investigations.— 1. Tests for obstructive jaundice should be performed. The serum bilirubin
almost never rises above 30 to 35 mg/100 ml in pancreatic cancer. Higher level may be seen in acute
hepatic necrosis. Alkaline phosphatase is almost always increased, even before the onset of jaundice. Faecal
urobilinogen estimation is valuable. Figure below 5 mg of urobilinogen per 24 hours is diagnostic. Serum
transaminase estimation will rule out hepatitis, and in biliary obstruction its value should not exceed 500.
Serologic markers for pancreatic carcinoma have been evaluated including carcinoembryonic antigen (CE
alpha-fetoprotein (AFP), pancreatic oncofetal antigen (POA), carbohydrate antigen 19-9 (CA 19-9) and
DU-PAN-2. However no currently available serologic test is completely accurate for diagnosis. At present,
CA 19-9 is used most frequently to assist in the diagnosis and follow-up.
2. RADIOGRAPHY.— Barium meal X-ray of the upper G.I. tract will show some distortion of the
pattern of gastric antrum and duodenum. Sometimes the barium filled C of the duodenum will be widened
in cancer head of the pancreas. This is known as ‘Pad’ sign. Sometimes in periampullary carcinoma a
filling defect may be seen in the duodenum in the appearance of a reversed 3 (e sign). Hypotonic duodenography
in which 20 to 40 ml of liquid barium solution is run into the duodenum and 4 mg of antrenyl is given
intravenously to make the bowel atonic. Air is then insufflated to distend the duodenum. This will give a
clear outline of the duodenum. Any distortion of the wall of the duodenum will be obvious in this contrast
radiography.
3. Recent improvement in ULTRASONIC techniques and COMPUTERISED TOMOGRAPHY (CT)
have revolutionised the diagnosis of pancreatic malignancy. Both these tests must be performed if this
disease is suspected particularly in case of malignancy of the body and tail of the pancreas. Ultrasonography
is a useful screening examination particularly in patients less than 40 years of age. Pancreatic enlargement
with cysts and dilated ducts are nicely demonstrated.
CT scanning is an essential procedure particularly in older patients. Thin-section and contrast-enhanced
CT scanning are superior to sonography in that it allows visualisation of the entire pancreas without distortio
from overlying bowel gas. It also provides better accuracy in detecting hepatic metastasis and determining
the size of the periampullary tumour. MRI, particularly in this disease, appears to offer no advantage over
CT. Contrast-enhanced helical CT scan is now very specific for the pancreas. It shows more clearly the
lesion even if it is small.
4. ENDOSCOPIC RETROGRADE CHOLANGIOPANCREATOGRAPHY (ERCP).— Duodenoscopy
can reveal ampullary carcinoma and it can be biopsied at the same time. The ampulla of Vater can be
cannulated using a side-viewing fibreoptic duodenoscope. 65% angiografin is used to delineate the biliary
and pancreatic ducts. In pancreatic carcinoma the main pancreatic duct is narrowed and completely obstruct
at the site of the tumour with dilatation of the distal part. Cytological examination of the pancreatic juice
may be performed through this technique. Cholangiography can suggest the site of tumour origin and is
essential in planning successful resection. ERCP is particularly valuable in the diagnosis of duodenal or
ampullary carcinoma, where diagnostic tissue can be obtained by endoscopic biopsy. Another therapeutic
advantage of ERCP is that biliary endoprosthesis may be placed at the time of ERCP as a short or long
term manoeuvre to palliate biliary obstruction and to allow for reduction in the degree of jaundice.
5. PERCUTANEOUS CHOLANGIOGRAPHY (PTC) may be performed in case of obstructive jaundice
to know the cause of obstruction.
6. Percutaneous FINE NEEDLE ASPIRATION BIOPSY (FNAB) of pancreatic tumours has recently
been shown to be safe and accurate in about 70% of cases. Even then as exploration is often justified in
such cases intraoperative fine needle aspiration is preferred to percutaneous technique.
7. Selective coeliac and mesenteric angiography, combined with the evaluation of portal venous
anatomy can be used for deliniation of major arterial and venous anatomy and for staging for resectability.
8. Laparoscopy is now advocated as a means of improving staging and to detect unsuspected liver
metastasis and peritoneal implants.
TREATMENT —
Treatment of carcinoma of the head of pancreas.— Once the diagnosis is established, the treatment
is early operation. Delay will cause further deterioration of hepatic function and will increase operative risk
as the patient continues to lose weight. Adequate nutrition and correction of anaemia should be accomplished
as early as possible. Preoperative evaluation of renal function is necessary, as postoperative renal failure
is not uncommon in these cases. Preliminary transhepatic biliary drainage for 7 to 10 days may be of some
value in deeply jaundiced patients.
Conservative management for jaundice has been discussed in page 915, Chapter 46.
Clinically if there is no contraindication to surgery, one should explore the abdomen. This is mostly
performed through right paramedian incision which starts at the right costal margin lateral to xiphoid proces
and extends downwards to a point to the right of the umbilicus. A few regional nodes are removed and
biopsied. One can even use Vim-Silvermann needle to biopsy the tumour itself of the pancreas. Once the
diagnosis is established the next step is to determine the feasibility of radical excision. When the distant
lymph nodes are not involved, when the tumour is not fixed and when the liver is free from metastasis,
one can go for radical surgery. Tumours less than 3 cm in diameter are usually resectable, whereas those
greater than 5 cm are not resectable. Resectable tumours are most frequently situated near the ampulla, while
the tumours in the body of the pancreas are mostly unresectable. So when resection is possible, the area
resected is the head and neck of the pancreas together with the duodenum, which is known as
pancreaticoduodenectomy or Whipple’s operation. But unfortunately only 5% of pancreatic cancer fall into
this category.
Pancreaticoduodenectomy (Whipple’s operation).—
PREOPERATIVE PREPARATION includes (i) assessment and supplementation of nutrition, (ii) Assess
ment of coagulation status with correction of prolonged prothrombin time by supplementation of vitamin
K. (iii) Intravenous prophylactic antibiotics to reduce the possibility of wound infection, (iv) Consideration
of placement of a percutaneous transhepatic catheter or endoscopic placement of an endoprosthesis for
drainage of biliary tree, particularly in case of cholangitis with high grade biliary obstruction. This reduces
operative mortality.
Pancreaticoduodenectomy (Whipple’s operation).— This is the operation chosen for radical surgery
in this condition. An incision is made on the transverse mesocolon to free the hepatic flexure and right
half of the transverse mesocolon as far as the middle colic vessels. This portion of the colon is now displaced
below to expose the duodenum and anterior surface of the pancreas. The duodenum with the head of the
pancreas is mobilised medially by dividing the peritoneum on the lateral side of the duodenum (Kocher’s
manoeuvre). This process is continued till the inferior vena cava is reached. It is made clear that superior
mesenteric vessels and the portal vein are not involved in cancer. The gastrohepatic omentum is incised,
THE PANCREAS
863
the right gastric artery is ligated and divided. It is followed and the gastroduodenal artery is also identified,
ligated and divided keeping safe the hepatic artery. The common bile duct is now dissected. The index finge
of the left hand can then be passed behind the neck of the pancreas and in front of the portal vein so as
to emerge below the body of the gland in front of the superior mesenteric vein. This is an excellent method
of ascertaining that the portal and superior mesenteric vein are not adherent to the growth. The common
bile duct is now doubly clamped, transected above the duodenum and the distal end is ligated with stout
silk.
The left gastric artery is isolated, ligated and divided between ligatures about an inch from the cardia.
The left gastroepiploic vessels are similarly secured and divided close to the power pole of the spleen. Two
occlusion clamps are placed on the body of the stomach at the junction of the upper and middle thirds.
The stomach is transected with a knife between these two clamps. The distal end of the stomach is caught
with a large Payr’s clamp which acts as a retractor.
The pancreas is divided at the neck and haemorrhage is controlled with Babcock forceps. The duct of
Wirsung is identified and dissected out before division and is allowed to project from the cut surface of
the body of the pancreas. The distal raw surface of the pancreas is closed with a series of interrupted mattres
sutures of silk leaving the duct of Wirsung projecting.
The transverse colon is lifted up and the jejunum is divided between two clamps about 6 inches from
the duodenojejunal flexure. The distal portion of the duodenum and short segment of the proximal jejunum
are freed by blunt dissection and drawn out beneath the superior mesenteric vessels.
Some surgeons prefer to excise the gallbladder and the cystic duct along with the common bile duct
leaving only the common hepatic duct for anastomosis.
Now the reconstruction is started with the distal limb of the jejunum bringing in front of the transverse
colon and the transverse mesocolon towards the common bile duct or the common hepatic duct as the case
may be. The end is anastomosed to the common bile duct in an end-to-end fashion. The duct of Wirsung
is anastomosed to the jejunum in an end-to-side fashion. Mucosa-to-mucosa suture is accomplished. An
indwelling tube or splint is required to maintain patency of the anastomosis. A small seromuscular incision
is made on the antimesenteric surface of the bowel, which is sutured to the margins of the pancreas with
interrupted silk sutures. Now the remnant of the stomach is anastomosed to the jejunum in an antecolic
Billroth-II fashion with a valve similar to Finsterer type to direct the food materials into the distal loop
of the jejunum.
The abdomen is closed in layers as usual but the areas of biliary and pancreatic anastomoses must be
drained.
The mortality of this operation in the experienced hand is approximately 5% in present days. A
modification of the standard Whipple operation, the pylorus-preserving pancreaticoduodenectomy, is gainin
popularity. This modification eliminates gastric resection and leaves a 2 cm cuff of duodenum for enteric
reconstruction of duodenojejunostomy. Thus postgastrectomy complications are got rid of. Moreover post
prandial release of gastrin and secretin are nearly normal.
At present the overall 5-year survival rate for all patients with resected periampullary carcinoma is
approximately 15% to 25%. The most important determinant factor of survival is the site of origin of the
tumour. Whereas cancers of the distal bile duct, ampulla and the duodenum are associated with high surviva
rates of 40% to 60% in 5-year, resectable carcinoma of the head of the pancreas is associated with a survival
rate of only 5% to 20% in 5-years.
Other operations.— Formerly total pancreatectomy was proposed in the idea that there is a consid
erable incidence of multifocality of pancreatic cancer. It now appears that this is absolutely theoretical and
no advantage can be gathered following total pancreatectomy in comparison to Whipple operation. On the
contrary total pancreatectomy removes all exocrine and endocrine function of pancreas.
Regional pancreatectomy.— When the superior mesenteric vein is involved by the growth, the condition
is considered to be not fit for radical resection. But Fortner first showed that involvement of this vein adjacen
to the uncinate process is not a contraindication. In this case the involved superior mesenteric vein segment
is excised and an end-to-end anastomosis to the portal vein is performed. This operation should be accom
panied with wider lymphatic clearance and this procedure is called regional pancreatectomy.
Total pancreatectomy is only considered when the growth seems to be multicentric.
PALLIATIVE SURGERY.— It must be remembered that 95% of all cases of pancreatic carcinoma are
treated palliatively. The reason is that in over 80% of cases the disease has spread beyond surgical resec
tion at the time of presentation. It has spread to the mesenteric and para-aortic lymph nodes, to the superio
mesenteric vein and hepatic metastases. Moreover advanced age and limited cardiopulmonary reserve pro
hibit resectional surgery.
Palliative surgery is mainly aimed at to alleviate (i) tumour associated pain, (ii) biliary obstruction and
(iii) rare duodenal obstruction.
(i) Pain is controlled with strong analgesics, mainly pethidine. In case of intractable pain chemical
splanchnicectomy using 50% alcohol should be performed. Dilated pancreatic duct may be anastomosed to
the back of the stomach side-to-side, which is often advocated to relieve pain due to ductal obstruction.
(ii) Jaundice produced by biliary obstruction should require some form of biliary by-pass. This is
required in about 80% of all patients with pancreatic cancer. Choledochoduodenostomy is the most physi
ological method, but cholecystojejunostomy is more often practised due to its simplicity. But the latter
operation has fallen into disrepute due to the fact that the cystic duct through which drainage occurs is qui
narrow. Endoscopic insertion of endoprosthesis is now being used by ERCP, but its use is limited by pros
thetic migration and side hole obstruction by biliary sludge which demands repeat endoscopy for replace
ment or manipulation. Such endoprosthesis or stent requires changing every 5 months. Newer metallic
endoprosthesis has certain advantages and can be used. This process is particularly useful for the elderly
with a limited life expectancy. Surgery is ideal for younger group with better outlook.
(iii) In about 10% of cases there may be duodenal obstruction which may be seen in even l/3rd of
patients with unresectable tumours. Gastrojejunostomy is usually performed as palliative measure to alle
viate duodenal obstruction. Gastrojejunostomy is also performed prophylactically at the time of biliary by
pass and this does not add to the morbidity or mortality in these cases.
(iv) SEMS (SELF EXPANDING METAL STENTS).— The advent of ERCP and plastic stent insertion has
rendered the need for surgical decompression of the biliary tree due to advanced carcinoma of the head of the pancreas
and cholangiocarcinoma largely obsolete. In most cases life expectancy is short and the patient succumbs before the
plastic stent occludes. If occlusion does occur, the stent needs replacement by further ERCP.
ADJUVANT THERAPY— Chemotherapy alone does not have any definite role to prolong survival following
curative resection or palliative surgery. Single drug has practically no response, although combination drug therapy
appears to improve response rates in carefully selected patients.
However combination of chemotherapy and radiation has been shown to prolong survival rate following Whipple’s
operation. 40 Gy external beam radiation therapy (EBRT) and weekly intravenous injection of 5-fluorouracil follow
ing Whipple’s operation demonstrated a significantly longer survival in the range of about 20 months compared to
those without any adjuvant therapy. However in case of unresectable tumours the effect of the combination of chemo
therapy and radiation is not that much. In an effort to boost the radiation dose delivered directly to unresectable
tumours intraoperative radiation therapy (IORT) in the form of radioactive implantation with l25I seeds has been
undertaken. However this has failed to improve survival rate, moreover it increases perioperative complications. How
ever if IORT is combined with EBRT with or without chemotherapy, there is some improvement in long term survival.
Carcinoma of the body and tail of the pancreas.— Adenocarcinoma involving these areas represents
about 30% of all cases of pancreatic carcinoma. The peculiarity of cancer of this region is that it grows
silently to a large size before the development of any symptom.
CLINICAL FEATURES generally involve weight loss and pain. Only less than 10% of patients present
with jaundice. On physical examination, vague abdominal tenderness is usually present. An abdominal
mass may or may not be palpable. Evidence of metastatic dissemination includes hepatomegaly, ascites or
lymph node metastasis to Virchow’s nodes.
INVESTIGATIONS include serum tests to detect tumour markers — either CEA or CA 19-9. Negative
result does not exclude the disease.
Abdominal CT scan is the best investigation to demonstrate primary tumour in the pancreas. It also
THE PANCREAS 865
detects liver metastasis, involvement of adjacent viscera or vessels or lymph node metastasis. ERCP may
only detect pancreatic duct abnormality in the form of a cut off representing obstruction to the flow of cont
material by the neoplasm. When the proximal pancreatic duct is absolutely normal, finding of sudden sten
in the region of the body or tail of the pancreas is highly suggestive of pancreatic tumour.
Visceral arteriography of the coeliac axis, splenic artery and vein and superior mesenteric artery may
be evaluated. However tumour involvement of these vessels indicate nonresectability.
Pathologic evaluation is only possible after laparotomy or by laparoscopy. Percutaneous needle aspirat
of the primary tumour will give an idea about the histopathologic nature of the tumour.
TREATMENT.— The resectability rate of the carcinoma of the body and tail of the pancreas is even
less than 6%. The prognosis is very grave with mean survival of only 5 to 6 months. Only a few may surviv
5-years following resection and in majority of these cases the tumours are discovered accidentally during
evaluation of other intra-abdominal pathology.
Subtotal pancreatectomy keeping only a portion of pancreas right to the bile duct alongwith duodenum
is the treatment of choice if the growth has no metastasis and is well resectable without involving any vesse
Obviously replacement of endocrine and exocrine secretions of the pancreas is required for the rest of the
life. Many surgeons nowadays prefer only distal pancreatectomy with splenectomy in case of resectable
adenocarcinoma as the treatment of choice.
In the majority of patients palliative surgery is only required. If the disease is considered nonresectable
at laparotomy, intraoperative chemical splanchnicectomy is performed to relieve pain. In most of the patien
biliary by-pass or duodenal by-pass is not required. However in a few cases the tumour may encroach the
duodenojejunal junction and in these cases palliative gastrojejunostomy is indicated.
Adjuvant chemotherapy and postoperative EBRT following resection of adenocarcinoma of the body
and tail of the pancreas may benefit the patients, though confirmatory information is still lacking.
Nonresectable tumours usually do not respond to chemotherapy and radiation.
ENDOCRINE NEOPLASMS
INSULINOMA.— Insulin-producing adenoma of the Beta cells is the most common islet cell tumour.
Due to excessive secretion of insulin from the Beta cell lesions there will be (i) attacks of hypoglycaemia,
with blood sugar level below 50mg/100 ml, (ii) the attacks consist principally of confusion, stupor and loss
of consciousness and are related to fasting or exercise and (iii) the attacks are promptly relieved by feeding
or parenteral administration of glucose. This is the classical Whipple’s triad and very much characteristic
of insulinoma.
PATHOLOGY.— About 70% are solitary adenomas, approximately 10% are multiple adenomas, 10%
are metastasising tumours that must be interpreted as carcinomas and the remainder are a mixed group of
diffuse hyperplasia of islets. The insulinomas vary in size from minute lesions difficult to find to huge mass
These are usually encapsulated, firm, yellow-brown nodules, that by expansile growth compress the
surrounding pancreatic substances. Microscopically, insulinomas are composed of cords and nests of well
differentiated Beta cells. Rupture of the capsule and extension into the surrrounding pancreatic substance
are not reliable criteria of malignancy and the diagnosis of carcinoma should not be made in the absence
of unmistakable evidence of metastasis or local invasion beyond the substance of the pancreas.
CLINICAL FEATURES.— Majority of the patients are in the 4th to 7th decades of life. Sex incidence
is approximately equal.
If the blood sugar falls rapidly, the primary symptoms may be referable to the release of epinephrine
caused by hypoglycaemia. Sweating, weakness, tachycardia, hunger and trembling result from this. A slow
decrease in the blood sugar produces cerebral symptoms such as headache, mental confusion, visual
disturbances, convulsions and coma. Symptoms may last for a few weeks or a few years. Bizarre neurologic
or psychiatric disorders are not uncommon in this condition.
TREATMENT.— The only permanent cure of this condition is excision of the tumour or tumours.
55
Preoperative management consists of adequate quantities of glucose usually in the form of 10% dextrose
solution. ACTH and Cortisone may be given to prevent hyperthermia during or immediately after operation,
but these drugs, if not given, won’t do any harm. Diazoxide may be given to inhibit insulin release from
Beta cells and thus to control hypolycaemia preoperatively. This drug inhibits insulin release directly, causes
release of glucose from the liver and interferes with peripheral utilisation of sugar. Streptozotocin, a broad
spectrum antibiotic is a powerful agent for control of the symptoms of insulinoma.
In operation every portion of the pancreas must be carefully examined. Both the anterior surface and
the posterior surface as also the inferior surface should be inspected properly. The head of the pancreas
must be completely mobilised by Kocher manoeuvre. Sometimes insulinoma may be seen in the stomach,
duodenum, jejunum, ileum, mesentery and omentum. These are ectopic sites. Simple excision is sufficient
in most of the cases as majority of these tumours are benign. One must thoroughly explore the pancreas
even when a solitary lesion has been detected, as multiple lesions may be present.
The problem comes in when after thorough examination the tumour cannot be detected. In these cases
a distal subtotal pancreatectomy to the left of the mesenteric vessels should be performed. Another group
of surgeons advocate pancreaticoduodenal resection with preservation of the tail of the pancreas, when
thorough exploration fails to detect the pancreatic tumour. These surgeons believe that small tumours are
much more easily overlooked in the head and uncinate process than in the tail or body. But the latter operation
carries higher morbidity or mortality. So the former operation is more popular and this can be extended
to a 90% resection or more if necessary.
A marked increase in blood sugar level within 30 minutes of removal of the lesion is confirmatory
evidence that the lesion has been removed.
Streptozotocin, a potent antibiotic which destroys islets, is useful in treating patients with far advanced
metastatic islet cell carcinoma, but one should be cautious about its toxic side effects.
ZOLLINGER-ELLISON SYNDROME (GASTRINOMA).— In 1955 Doctors Zollinger and Ellison
from Ohio State University first defined this disease in 2 patients who presented with bleeding peptic ulcer
and non-beta-cell tumours in the pancreas. Delta cells (D cells) of the iselts of Langerhan secrete somatostatin
and gastrin. The latter hormone is also found in G cells of the gastric mucosa. Somatostatinomas are rare
tumours associated with a diabetic glucose tolerance curve and steatorrhoea. Gastrinomas are much more
common and is the subject of discussion of this section.
In this condition peptic ulcers develop for high acid secretion of the stomach due to stimulation by gastrin
which is being secreted by this tumour known as gastrinoma. Gastrin has been demonstrated in these tumours
by radioimmunoassay and has been elaborated in cultures of tumours cells. Although common in the pancreas
yet 12% of gastrinomas have been found in the duodenum.
PATHOLOGY.— About 60% of these tumours are malignant and 2/3rds have already metastasised
when detected. 40% are benign. Among the benign lesions 30% are adenomas and 10% are hyperplasia
of islets.
Associated endocrine disease has been found in 20% of cases with Zollinger-Ellison syndrome. This
usually consists of adenomas of other endocrine glands, such as pituitary, pancreatic islets (Beta cells),
parathyroid and adrenal cortex. MEA-I (multiple endocrine adenomatosis) in which 90% of patients have
hyperparathyroidism usually caused by hyperplasia of parathyroids, 70% have gastrinomas, 40% have
adrenocortical hyperplasia and 30% have pituitary adenomas. This is not a familial disease. But another
condition with polyendocrine adenomas and peptic ulceration often have giant gastric rugae. This is known
aS Menetrier's disease which is carried by an abnormal gene — autosomal dominant gene with high degree
of penetrance.
CLINICAL FEATURES.— This condition is slightly more common in males. Majority of the patients
are in the 3rd and 4th decade of life. These patients show an ulcerogenic diathesis. 75% of the ulcers occur
in the usual sites within the stomach or more often in the first and second parts of the duodenum. Abnormally
located peptic ulcers in the distal portions of the duodenum and jejunum occur in 25% of cases. In 10%
THE PANCREAS 867
of cases there are multiple ulcerations. Today most patients present with peptic ulcer disease and/or diarrhoe
Diarrhoea is often caused by high volume of acid alongwith neutralization of pancreatic enzymes causing
steatorrhoea-type diarrhoea.
About 2 to 3 litres of fluid is found in 12-hour nocturnal secretion. The overnight resting secretion
often contains 200 to 300 mEq of free hydrochloric acid. Another important feature is that the secretory
rate is already close to its maximum and further stimulation with histamine generally produces very little
response, that means basal secretion is quite high almost reaching the maximal secretion. A ratio of basal
acid output to maximal output (histamine-stimulated) is greater than 60% and this is almost diagnostic of
Zollinger-Ellison syndrome.
Gastric hypersecretion is associated with distressing watery diarrhoea in about l/3rd of cases. About
2 to 8 litres of liquid stool daily has been reported and may precede the onset of peptic ulceration. Steatorrhoea
may also occur, either due to inactivation of pancreatic enzymes in abnormally acid environment in duodenum
or due to irritative action of acid on the mucosa of the small bowel.
Diagnosis of gastrinoma is mainly by suspicion and by measurement of serum gastrin. When the serum
gastrin level is not elevated to a great extent, the case may be diagnosed by gastric pH analysis followed
by a secretin test. This test is accomplished by measuring basal serum gastrin level and then injecting 2
units of secretin per Kg of body weight followed by measurements of serum gastrin level at various periods
upto 1 hour. Patients with this disease will show an abnormal elevation of serum gastrin level whereas normal
patients should have no change or a reduction in serum gastrin level following intravenous secretin injection.
TREATMENT.— Medical therapy is particularly indicated for patients who have gastrinoma associated
with MEA or MEN syndrome and in patients who have metastatic gastrinoma.
Medical management consists of high dose of H2 antagonist or omeprazol to control the ulcer disease.
Diarrhoea is automatically relieved to a great extent.
Surgical management.— Metastatic disease must be ruled out by CT scanning. The patient must not
have MEA or MEN syndrome and must not have evidence of metastatic disease to be qualified for surgery.
Localisation of the tumour can be performed by Magnetic Resonance Imaging. Partial venous sampling for
gastrin is occasionally successful to localise intraoperatively the gastrinoma. Majority of the gastrinomas
exist in the head of the pancreas in the gastrinoma triangle formed by an apex is at the cystic duct-common
duct junction and base is formed by the third part of the duodenum. Almost 70% of gastrinomas exist in
this area (Triangle).
After opening the abdomen the transverse colon is completely mobilised to expose the entire surface
of the pancreas. Kocher’s manoeuvre is performed to mobilise the duodenum and to facilitate the palpation
of the pancreas. Intraoperative ultrasonography may be used at this stage to localise the lesion particularly
in the head of the pancreas. The lymph nodes around should be biopsied, as solitary gastrinomas are sometime
found in these lymph nodes. If ultrasonography fails to detect the gastrinoma, a pyloroplasty is made and
the duodenal wall is palpated through the lumen to localise isolated duodenal gastrinomas. Gastrinomas
in the duodenal wall or in the pancreas should be shelled out. Solitary lesions in the tail can be treated
by tail resection. Only in case of multiple lesions in the head of the pancreas, a Whipple resection
(Pancreaticoduodenectomy) is necessary.
If no lesion is detected, or in whom the disease is multicentric or metastatic, a palliative ulcer operation
in the form of truncal vagotomy and pyloroplasty should be performed. The patient may be maintained
on omeprazol after ulcer operation. Some surgeons even prefer to do highly selective vagotomy, but scarring
at the lesser curvature following this operation may lead to difficulty in performing subsequent gastrectomy.
Only on rare occasions total gastrectomy is required, who do not respond to medical therapy and in
whom proper localisation of tumour is not possible.
WDHA SYNDROME.— This is a syndrome which refers to watery diarrhoea, hypocalcaemia and gastric anacidity
or hypochlorhydria and WDHA represents the first letters of each of these. Middle aged females are most frequently
involved. Diarrhoea is usually profuse averaging 4 to 5 litres per day and contains 200 to 400 mEq of potassium daily.
This condition is often called ‘pancreatic cholera’. Symptoms of severe hypocalcaemia are common. Hypercalcaemia
occurs in l/3rd of cases though the parathyroid glands are normal. The most likely explanation for the sym
the secretion of vasoactive intestinal peptide, pancreatic polypeptide, gastrointestinal inhibitor peptide and
three hormones are secreted by PP cells of the islets and neoplasm affecting these cells of the islets will cau
syndrome.
About 40% are benign tumours, 40% are malignant tumours usually with metastases and 20% are hype
of these cells of the islets.
Treatment is resection of these tumours.
869
CHAPTER-41
__________ THE SMALL INTESTINE__________
TUBERCULOSIS OF THE INTESTINE
Tuberculosis of the small intestine occurs in two forms. Primary infection is usually due to Bovine strain
Mycobacterium tuberculosis and results from ingesting infected milk. In India the human strain may also cause
such primary tuberculosis. This produces hyperplastic tuberculosis and occurs most commonly in the ileo-caeca
region, although solitary or multiple lesions of the lower ileum may be present.
The more common form ulcerative tuberculosis is secondary to pulmonary tuberculosis and arises as a resu
of swallowing tubercle bacilli.
HYPERPLASTIC ILEO-CAECAL TUBERCULOSIS
Pathology.—It occurs in a patient who has already developed resistance against mycobacterium tuberculos
In Western Countries all cases are due to ingestion of mycobacterium tuberculosis bovis, whereas in Eastern
Countries, like India, Pakistan, Bangladesh etc. human strain may be responsible for a few cases. Terminal tw
inches of ileum and the caecum are usually affected. Infection first starts in the lymphoid follicles and spreads
the submucous and subserous planes. Chronic inflammation sets in and the intestinal wall becomes thickened
thickening is partly due to tubercular granulation tissue and oedema, but is mostly due to excess fibrous tissu
causes narrowing of the affected segment. Regional lymph nodes are involved early in the disease and may case
Unlike the ulcerative variety, there is no ulceration and unlike regional ileitis abscess formation and fistula are
seen. The regional mesentery also becomes thickened and oedematous.
Microscopically, tubercular lesions are seen as usual with more lymphocytes and more fibrosis.
If untreated, subacute or acute intestinal obstruction may occur. This is due to narrowing of the lumen of
involved segment and sometimes enterolith may impact within the narrowed segment to cause acute intestina
obstruction.
Clinical features.— 1. Attacks of abdominal pain off and on due to subacute intestinal obstruction are often
the first symptom. This may be associated with intermittent diarrhoea (alternate constipation with pain and
diarrhoea).
2. Features of blind-loop syndrome’ may develop due to stasis, distension and chronic infection in the segm
of ileum proximal to obstruction. Anaemia(due to vitamin B12 deficiency), loss of weight and steatorrhoea are
features of ‘blind-loop syndrome’.
3. A mass in the right iliac fossa. This is rather confusing as one must exclude Crohn’s disease, actinomyco
and carcinoma of the caecum.
Special Investigations.— No other investigation is very suggestive of this condition but barium meal X-
ray. 1. Barium meal radiography will reveal (i) persistent narrowing of the affected segment i.e. the terminal
ileum and the caecum, (ii) The caecum is pulled up and may become subhepatic. (iii) As the caecum is pulled
up. the ileo-caecal angle is widened. Normal ileo-caecal angle is about 90°. In ileocaecal tuberculosis this angle
may increase upto 180°. The ileum may drop down almost vertically from the caecum to make the ileo-caecal
angle about 180°.
2. Stool examination may reveal blood and mucus occasionally.
3 . E.S.R is usually not high.
4. Chest X-ray is negative in most of the cases.
Treatment— (a) When the diagnosis is definite and there is no intestinal obstruction the treatment is
antitubercular chemotherapy with sanitary regime.
(b) If obstruction is present, surgery is advised under cover of antitubercular treatment. Right hemicol
with removal of the diseased segment is the treatment of choice.
•(c) In case of acute obstruction and when the patient’s general condition is poor, a defunctioning
ileocolostomy is recommended to bypass the diseased segment. If necessary, resection is undertaken later
Resection of the involved segment is necessary as there always remains the chance of further recrudescence
of the disease and even involvement of the by-pass anastomosis.

ULCERATIVE TUBERCULOSIS
Pathology.— It is usually secondary to pulmonary tuberculosis and results from swallowing of tubercl
bacilli. In the terminal ileum there are multiple ulcers, the long axes of which lie transversally (cf. typhoid
which is longitudinally placed) along the lymphatic vessels. These ulcers are shallow with undermining e
The overlying serous coat is injected, thickened with multiple tiny tubercles Fibrosis is very characteristic
surrounding the ulcers which prevents perforation of the ulcers. Due to this fibrosis and transverse dispos
single or multiple strictures of the ileum are not infrequent.
Clinical features.— This type of tuberculosis starts with diarrhoea as the main symptom. Stools contain
pus and have a bad odour with occult blood (bleeding from ulcer). The patients gradually lose weight. Th
patients are often known as tubercular patients.
Special Investigations.— 1. Stool examination is very important. It contains occult blood, pus and even
tubercle bacilli.
2. Routine blood examination reveals high lymphocyte count and high E.S.R.
3. Chest X-ray reveals pulmonary tuberculosis.
4. Barium meal examination fails to detect any abnormality in the lower ileum as the meal passes quic
through this segment due to hypermotility of the affected segment of the ileum. It may fail to show the dis
ileum, caecum and even most of the ascending colon.
Treatment.— (a) Conservative treatment in the form of antitubercular chemotherapy and sanitary regi
usually cures this conditions if detected early.
(b) Only in very late cases when strictures have developed in the terminal ileum surgery will be requir
to bypass the strictured segment.
(c) In rare incident of perforation immediate surgical intervention is required.
Difference between hyperplastic ileocaecal tuberculosis and ulcerative tuberculosis are as follows :—
Hyperplastic ileo-caecal tuberculosis Ulcerative tuberculosis

1. It isusually primary and there is no pulmonary 1 It is usually secondary to pulmonary tubercu
tuberculosis. losis and results from swallowing tubercle
bacilli in the sputum.
2. It is mostly caused by bovine type of bacillus, 2. It is almost always caused by human strain of
though in eastern countries human strain may tubercle bacillus.
be responsible. But the bacilli are usually of
less virulent variety.
3. Majority of the patients have already acquired 3. It occurs in patients with low resistance so cas
immunity against tuberculosis, that is why the eation and breakdown of tissues are quite co
response is excess fibrous tissue formation. mmon.
4. It affects ileocaecal region that means termi 4. Usually longer part of the terminal ileum is af
nal 2 inches of ileum and caecum are affected. fected.
5. Barium meal radiography is the most impor 5. Barium meal X-ray is not very suggestive as
tant investigation and is diagnostic in majority the barium meal passes quickly through the af
of cases. fected segment due to hypermotility.
6. Chest X-ray is often negative. 6. Chest X-ray often reveals pulmonary tubercu
losis as this condition is usually secondary to
pulmonary tuberculosis.
7. E.S.R. may not be high. 7. E.R.S. is almost always high.
8. Stool examination is often not rewarding, but 8. Stool examination is important as it often con
sometimes it may contain mucus or even blood tains pus, occult blood and even tubercle bac
illi.
THE SMALL INTESTINE 871
CROHN’S DISEASE
In 1932 Crohn described this disease as ‘terminal ileitis’. Gradually it was recognised that the disease, tho
most frequent in the terminal ileum, may affect any part of the intestine and hence the term ‘regional ileitis’
It is now universally accepted that the disease also involves colon, infact it may involve any portion of the G
from mouth to anus. Two commonest sites which are involved, are the terminal ileum and the anal canal. Th
particular predisposing factors at these sites are not known with certainty, but could be related to the distrib
excessive lymphoid tissue at these sites or to relative stasis of the bowel contents that could occur in these sit
Pathogenesis and Aetiology.— In one sentence, pathogenesis and aetiology of this disease are unknown. (1) Crohn in
his original paper proposed that terminal ileitis may have a specific infectious causative agent. But despite countless investigatio
no infectious agent could be discovered. (2) Inoculation of tissue homogenates obtained from patient with Crohn’s disease
could produce granulomatous changes in the foot pads of CBA mice. A small virus, probably of the RNA type, has been
identified. (3) It was also thought to be a variant of sarcoidosis. (4) A few different types of aetiologies have also been
incriminated such as (a) trauma, (b) lymphatic obstruction, (c) absorption of toxic substances from food, (d) inherited metabolic
defects, (e) predisposing genetic defect such as Turner’s syndrome, (0 imbalance between sympathetic and parasympathetic
nerve activity etc. (5) There is considerable evidence that Crohn’s disease is associated with immunologic disturbances (immune
mechanism). Cell-mediated immune function seems to be defective in patients with Crohn’s disease. Presence of granulomas
and systemic manifestations such as elevation of gamma globulin, erythema nodosum, iritis, eczema etc. go in favour of this
theory. Moreover favourable response to corticosteroids and azathioprine also supports this theory. (6) Smoking seems to have
some influence as it increases the risk threefold. (7) There is an association with ankylosing spondylytis. (8) Many clinicians
feel that emotional stress is important in the initiation and perpetuation of inflammatory bowel disease. Above all, Crohn’s
statement that ‘the actual aetiology is completely unknown’ is still very much true even today.
Pathology.— MACROSCOPIC APPEARANCE.— Crohn’s disease particularly involves the ileum accounting for about
60% of cases. 30% of cases are limited to large intestine. Remainders are seen with ileal disease alone or more proximal small
bowel involvement. It must be remembered that though Crohn’s disease is uncommon in oesophagus, stomach and duodenum,
anal lesions are quite common. Diseased segments are dull purple-red thickened two or three times normal diameter and
covered with strands and patches of thick greyish white exudate. All layers of the bowel wall are involved in a transmural
inflammatory process. The lumen becomes narrow and the diseased portion of the bowel is thickened by fibrosis, oedema and
cellular infiltration. Mesenteric fat tends to grow over the serosa so that it nearly encompasses the bowel. Involved segments
are often adherent to adjacent loops or other viscera. The thick mesentery nursing and draining the diseased bowel contains
numerous enlarged lymph nodes. The serosa is opaque, granular and engorged with distended lymphatics. Due to this intense
serosal reaction affected loops adhere to the neighbouring structures. Abscesses develop in between the loops and fistulas may
originate with the diseased bowei to penetrate into any organ within the abdominal cavity (internal fistula) or may open outside
on the abdominal wall (external fistula). The most characteristic feature is that the segments of diseased bowel are separated by
apparently normal bowel to form characteristic ‘skip lesions’. The mucosal surface may vary from grossly normal to slightly
oedematous and hyperaemic. Serpiginous ulcers may develop. Long ‘snail-track’ ulcers may be produced from coalescence of
the previous ulcers. These transverse ulcers intensify ‘cobblestone’ appearance of the mucosa as these ulcers intervene betwee
the elevated mucosa caused by submucosal thickening. These ulcers penetrate deep into the muscle layers of the gut distinguis
Crohn’s disease from other inflammatory diseases of the bowel such as ulcerative colitis or ischaemic colitis. Infection gains
access to the muscle layers through these ulcers and transmural inflammatory reaction sets in. This gives rise to characteristic
thickening of the wall of the gut and later fibrotic stenosis. It is the ulceration penetrating through the muscle to the serosal
layer of the gut that is responsible for the complications of perforation, abscess and fistula. Fissures may develop from the
mucosal ulcers and extend a variable distance into the bowel wall. The anal lesions consist of fissures, fistulas, perianal
abscesses and/or spreading superficial ulcerations.
MICROSCOPIC APPEARANCE.— The most striking finding in the early phase is marked oedema of the entire bowel
wall, specially the submucosa. Mucosa is essentially normal except for an increase in the proportion of goblet cells.
Fibrinopurulent exudate is invariably present on the serosal surface. Granulomas are not found in the early phase. In the
intermediate p/iasethickening of the bowel is more attributable to fibrosis of submucosa and subserosa. Small focal ulcers that
rarely penetrate the muscularis mucosa develop numerous in the mucosa. The lamina propria is infiltrated with lymphocytes,
plasma cells and variable number of eosinophils. In the later stage, in the submucosa, the extensive fibrosis is accompanied by
diffuse infiltration of mononuclear cells and prominent hypertrophy and hyperplasia of lymphoid follicles. Granulomas may
be present in the submucosa, serosa or regional lymph nodes. They resemble the epithelioid giant cell granulomas of tuberculos
but do not caseate and do not contain tubercle bacilli. These are called sarcoid like granulomas. Mucosal ulcers become
deeper to involve the muscle coat.
CLINICAL FEATURES.— ACUTE ILEITIS.— In about 10% of patients, particularly in the young, the
onset is acute. It mimics acute appendicitis. There is midabdominal or right lower quadrant pain, low grade
leucocytosis, often nausea and vomiting and occasionally diarrhoea. On examination, localised tenderness is p
in the right iliac fossa. Diagnosis is extremely difficult, but probably diarrhoea from the very beginning of th
disease gives a clue to distinguish this condition from acute appendicitis where constipation is more commo
early stage. Very rarely there can be free perforation of the small intestine resulting in a local or diffuse perit
Similarly in colon there may be toxic megacolon, but is much less common than in ulcerative colitis.
CHRONIC ILEITIS.— In majority of the patients the onset is insidious, the course is protracted and
slowly progressive. Symptomatic periods are intervened by symptom-free periods. Symptomatic periods
gradually become more frequent. PAIN is the most frequent symptom of this disease. This is due to partial
obstruction of the lumen and increase in motility proximal to the site of obstruction. A second type of pain is
constant aching usually implies advanced disease. Tenderness and a palpable mass nearly always accompan
ihis type of pain. DIARRHOEA is the second most frequent symptom and is present in about 85% of patients.
The frequency of stool is not so great as compared to ulcerative colitis and the stools rarely contain mucus, p
or blood as in ulcerative colitis. Frothy and foul smelling stools characteristic of steatorrhoea represent an
advance stage of illness. FEVER is present in about l/3rd of these patients. Fever can reflect the development
of intramural or abdominal abscesses or may be a systemic sign produced by unknown toxins. Malnutrition
manifested by weight loss, anaemia, hypoproteinaemia and vitamins and mineral deficiencies is quite comm
A type of blind-loop syndrome is seen in Crohn’s disease. Extra-intestinal manifestations in the form of (i)
skin (erythema nodosum, pyoderma gangrenosum), (ii) eye (uveitis, iritis), (iii) joint (arthritis, ankylosing
spondylitis), (iv) mouth (aphthous stomatitis), (v) kidney (nephrolithiasis, hydronephrosis, amyloidosis), an
(vi) hepatobiliary (cholelithiasis, sclerosing cholangitis) etc. may be seen in one way or the other in late cases
Anal lesions may herald the onset of the disease by many years. Though anal lesions invariably present
when the large bowel is involved, yet these lesions may be seen less frequently with disease of the small bow
The most common lesion is anal fissure. It is a broad, shallow ulcer rather than a crack and it may occur
anteriorly and laterally as often as posteriorly. It is often painless. Anal ulcers, frequently multiple, are seen
advanced disease. They involve perianal skin, external genitalia and the groin. Fistula-in-ano, ischiorectal
abscess and a simple fissure are also common anal lesions. The anal pathology may be considered as a form
‘skip lesion’ because the proximal rectal mucosa is usually normal.
In nutshell chronic regional ileitis manifests in three stages :
In 1ST STAGE patients present with diarrhoea, abdominal pain, fever, anaemia and loss of weight. An ill
defined tender lump may be present at the right iliac fossa. Perianal abscess may be present in this stage.
2ND STAGE is characterised by symptoms of acute or chronic intestinal obstruction.
3RD STAGE is the stage of formation of adhesions, abscess and fistulas. Fistula may be internal, with
pelvic colon (enterocolic) or urinary bladder (enterovesical). External fistula develops in the right iliac fossa.
It must be remembered that any patient who presents with a history of the triad of colicky abdominal pai
diarrhoea and weight loss, the patient should be suspected to be suffering from Crohn’s disease. The clinical
manifestations are so variable that diagnosis is often made quite late.
SPECIAL INVESTIGATIONS.— There is no specific laboratory test for Crohn’s disease. The diagnosis rests
on clinical evaluations supported by endoscopy, biopsy and radiology.
1. Radiology.— Barium study of the bowel is vital to the diagnosis of Crohn’s disease. Usually barium enema is used
to diagnose this condition. Involvement of the colon and rectum becomes more evident in barium enema examination. The
earliest mucosal changes and aphthous ulceration are visualised by meticulous attention with double contrast barium
technique. After submucosal infiltration and oedema develop, barium study demonstrates thickening and distortion of the
mucosa. Both longitudinal and transverse mucosal ulcers or fissures present as ‘spicules’ in profile views. Radiologically,
cases can be divided into nonstenosing and stenosing stages —
A. IN THE NON-STENOSING STAGE — ulcers combined with submucosal oedema produce a coarse nodularity or
‘cobblestone’ pattern, which becomes obvious. There may be straightening of valvulae conniventes. Ulceration tends to
take the form of sharp ‘fissures’ passing from the lumen into the bowel wall shown as ‘spikes’ (‘Raspberry thorns’ or
‘Rose thorns’). Nodularity of the lumen due to oedema may appear as filling defects. Filling defects may also be due to
hyperplastic lymph follicles, which may be the first indication of a ‘neoplastic’ consequence of a chronic disorder. At
times the mucosa may be completely denuded, giving the radiologic appearance of a nonpliable, nondistensible, rigid, cast
like tube. One hallmark of the disease is the presence of ‘skip lesions’, with apparently normal intervening bowel that may
measure a few inches to several feet in length.

B. IN THE STENOSING STAGE the affected bowel looks like a rigid tube. In case of terminal ileum the classical ‘string
sign’ of Kantor will be seen. There is gross irregular narrowing of the terminal ileum in this case. It is usually due to acute
transmural inflammation and oedema with spasm, but it could be the end result of fibrosis leading to stricture formation.
2. Endoscopy.— Colonoscopy is mainly performed in this condition. Direct visualisation of the pathology of Crohn’s
disease is very helpful in diagnosis of this condition. It is more possible in case of colonic affection. It must be remembered
that in Crohn’s disease there will be areas of normal colon or rectum. In between these areas one can find inflamed mucosa
which are irregular and ulcerated with mucopurulent exudate. In the beginning small ulcers surrounded by ring of erythematous
mucosa can be detected. Gradually these become larger and deeper. In colonic disease there may be stricture, when malignanc
should be excluded. Endoscopy provides a mean to follow and record the course of the disease and response to therapy.
3. Biopsy.— A rectal biopsy is frequently of value in establishing the diagnosis. Biopsy may be obtained from the
sigmoid colon or descending colon through colonoscopy. If non-caseating sarcoid granulomas are seen in the mucosa or
submucosa, the diagnosis of Crohn’s disease is hardly in doubt.
4. CT Scan — is mainly used to find out if there are intraabdominal abscesses or to exclude other complications of
this condition.
5. Magnetic Resonance Imaging (MRI) — is mainly useful in assessing perianal disease.
TREATMENT.— Unfortunately Crohn’s disease is hardly curative — either by medical or surgical
treatment. Medical therapy is mainly symptomatic and is directed to relieve abdominal pain, infection, contro
diarrhoea and correcting deficiencies in protein, haemoglobin, electrolytes and vitamins. It is usual that Crohn
disease should be treated with medical treatment in the beginning.
Medical treatment includes the followings :
1. GENERAL TREATMENT.— It consists of rest in bed, high protein diet with vitamin supplementation.
Particularly important is the correction of haematological and biochemical deficiencies with appropriate iron
therapy, folate, vitamin B12, other vitamins and electrolyte supplements. Symptomatic therapy is also import
Antidiarrhoeal agents are helpful, but codeine phosphate is best avoided in patients with Crohn’s colitis.
Steatorrhoea may be greatly improved by low fat diets.
SPECIFIC THERAPY includes the followings :
2. Steroids.— Short term steroid therapy has an important place in the management of patients with non
obstructive active small bowel disease. Prednisolone about 40 mg orally daily alongwith 5-ASA (5-Amino
Salicylic Acid) compounds particularly in patients with colonic involvement are advised. It is best to avoid
long term steroid therapy whenever possible. Topical steroid enemas are useful in patients with Crohn’s proc
or who have had a previous ileorectal anastomosis.
3. Sulphasalazine (Salazopyrin).— This drug has been effective particularly when the colon is the sole site
of the disease. It is also considered to be the drug of choice of previously untreated patients. Both prednisolon
and sulphasalazine are effective when the disease involves the colon as well as the ileum. Prednisolone is mo
effective in case of small bowel disease. But these drugs are not that effective in maintenance of remission.
4. Azathioprine.— This immunosuppressive drug is yet in the experimental stage. It may require
administration for 3 toS weeks before its effectiveness becomes apparent. Its most effective application may
be in combination with corticosteroid when continuous therapy is required to control the disease. Its limitatio
are mainly its side effects (e.g. leucopenia, gastric intolerance and pancreatitis) for which the physicians are
reluctant to prescribe this drug.
5. Antibiotics.— These are particularly helpful in acute stage. In this case gentamicin and metronidazole
are proved effective.
In short, till today no drug has been found to work efficiently in this disease.
Nutritional support is very much necessary. Anaemia, hypoproteinaemia, vitamin deficiency and electroly
imbalance are often seen in these cases. Nasogastric feeding is enough, but in severely ill patients intravenous
feeding should be prescribed.
Surgical treatment.— Large majority of patients with Crohn’s disease will ultimately need surgical treat
ment. About 55% of patients come to operation within 2 years of onset of symptoms and 94% within 10 years.
In a few series only 5% had not undergone surgery. It is not always easy to decide at what stage of the disease
the patient should have operation. THE MAIN INDICATIONS FOR SURGERY ARE (i) Failure of medical
treatment to control the disease — this means persistence of poor health or debilitating symptoms inspite of
medical treatment.
(ii) Development of complications of which the most important are obstruction, perforation, formation
abscess and internalfistulae. Acute intestinal obstruction is rare, but obstruction with colic and distension shou
require surgery. Free perforation into general peritoneal cavity is rare but this has occurred particularly as
complication of steroid therapy requiring emergency operation.
It must be remembered that the surgeon must distinguish the diagnosis of acute appendicitis from Croh
disease involving distal ileum. In case while doing appendicectomy for acute appendicitis, one finds that the
diagnosis was wrong and it is a case of Crohn’s disease, the surgeon should come out without performing
appendicectomy, to avoid a faecal fistula to be developed.
CHOICE OF OPERATION.— Resection with immediate anastomosis is the operation of choice advocated
by most of the surgeons. Only when the involved bowel is severely inflamed and adherent to important stru
with gross mesenteric oedema, resection may be hazardous. In such circumstances it is porobably safer and
to avoid the inflamed area and to carry out a bypass operation. Most patients will improve after this procedur
resection should be required later on, when it can be done with greater safety.
Surgical techniques.— As mentioned above resection of the involved bowel with immediate anastomosis
is the treatment of choice. The question is how much length of the bowel should be removed. There is ample
evidence that inadequate excision leads to a higher recurrence rate and Crohn himself advised a proximal an
distal clearance of 12 inches of apparently normal bowel. Many surgeons believe that it is too radical. Regard
this, frozen section of the divided bowel at the time of operation has been practised in certain institutions. Bu
it could not be a very successfiil method as often the pathologists may miss slight affection of a part of the bo
and report it as normal bowel
1. For ileo-caecal Crohn’s disease, a right hemicolectomy with end-to-end or end-to-side ileotransverse
anastomosis is the most popular method. Many surgeons have considered this to be a very radical approach
advised to save a large part of the ascending colon, which may be anastomosed with the ileum with similar
In acute cases with unprepared bowel a defunctioning ileo-transverse by-pass operation should be performe
2. For colonicCrohn’s disease, segmental colectomy should be performed. When a considerable large portio
of the colon has been involved or colon has been generally involved, total colectomy with ileorectal anastom
is adviced. The main problem is that anal canal is often affected which still remains. So far this pancolectomy
ileostomy may be preferred.
3. In case of local small bowel involvement, segmental resection should be performed.
4. When a large segment ofbowel is involved by multiple strictures, strictureplasty may be performed in
strictures to avoid excess bowel resection. But there is a good chance of recurrence in these cases of stricture
When a patient has had previous surgery for Crohn’s disease and another operation becomes necessary
surgeon should be conservative as many patients are however greatly benefitted by limited resections The a
this type of salvage surgery’ should be minimal resection and restoration of intestinal anatomy to as near no
as possible.
Recurrence.— A patient who has had Crohn’s disease, whether treated medically or surgically is believe
to remain liable to recurrence of the disease indefinitely. In many series after a first resection for chronic regi
ileitis, symptomatic recurrence was found in about V3rd of patients at 5 years and a little over half at 10 year
factors influencing the recurrence rate are :
(i) Type of operation.— It is generally agreed that resection and anastomosis should be done if possible
as this procedure gives the best chance of cure. Bypass operations show more recurrence rate.
(ii) Length of involved segment.— Longer the segment of ileum diseased, the greater is the probability
of recurrence.
(iii) Length of history before operation.— Those with a short duration of symptoms before surgery have
higher recurrence rate than those with a long history.
(iv) Age.— Recurrence rate is higher in those under 30 years of age.
TRAUMATIC RUPTURE OF THE INTESTINE
Injury to the small instestine may occur from A. PENETRATING INJURY, which becomes obvious from
THE SMALL INTESTINE
875
outside and treatment is carried out immediately.

B. NON-PENETRATING INJURIES are more dangerous as in these cases rupture of the intestine m
be overlooked and this may cause fatal consequences, (i) Runover accident usually involves duodenojejunal
flexure, as this is the junction of the mobile part and fixed part of the small intestine. This may cause
retroperitoneal rupture which is more easily overlooked, (ii) Blow on the abdomen may cause rupture of the
small intestine as it crushes against the sacral promontory, (iii) Seat-belt injury from car accident when the
whole body thrusts forward and the seat-belt in the abdomen crushes the small intestine against the sacrum
promontory, (iv) Irreducible hemia or strangulated hemia may rupture.
Laceration of mesentery may occur from non-penetration and penetrating injuries.
CLINICAL FEATURES are similar to peptic perforation. It is extremely essential to diagnose as early as
possible, as in late cases it is difficult to save the patient even after operation.
TREATMENT.— Immediate operation is the treatment of choice. The approach is more or less like pepti
perforation. Peritoneal toileting is done. If there is single perforation it should be closed with atraumatic catg
If there are multiple perforations in a small segment of bowel, excision of that segment of the bowel and end
to-end anastomosis should be performed. When the mesentery is lacerated, the involved segment of the bow
should be resected and end-to-end anastomosis is carried out.
DIVERTICULA OF SMALL INTESTINE

Meckel’s Diverticulum
Meckel’s diverticulum is present in 2% of cases, 2 feet proximal to the ileocaecal valve, it is usually 2
inches in length and is found on the antimesenteric border of the ileum. It possesses a mesentery like meso-
appendix through which its blood supply is maintained. It contains all the layers of the small intestine and i
many respects it is similar to appendix. In '/5th of cases it contains heterotopic epithelium like gastric, colon
or rarely pancreatic tissue. This heterotopic epithelium usually lies in the proximal end of the diverticulum
and not infrequently it also extends for a short distance into the nearby ileum.
Importance of Meckel’s diverticulum lies in the fact that it may produce a few complications which are
dangerous and should be diagnosed as early as possible. But it must be remembered that many of these
diverticula are accidental findings at laparotomy and are asymptomatic. Clinically important manifestations
are found primarily in children, over 60% occurring before the age of 10 years.
Clinical features.— Meckel’s diverticulum occurs in equal frequency in both the sexes, though
symptomatic cases are mostly seen in males
Presence of Meckel’s diverticulum can only be detected when some complication occurs in it. Without
complications Meckel’s diverticulum remains silent.
SILENT MECKEL’S DIVERTICULUM.— As mentioned above Meckel’s diverticulum may remain
symptomless throughout life and is only detected at necropsy. It may also be detected during abdominal
operation, performed for some other purpose. It is usual practise to look for Meckel’s diverticulum at its usu
position during appendicectomy.
The IMPORTANT COMPLICATIONS which may occur in a Meckel’s diverticulum are :—
1. Intestinal obstruction.— (a) In adults this is probably the most common complication. Intestinal
obstruction may occur around a band running from the tip of the diverticulum to the umbilicus. Intestinal
obstruction may result from volvulus or kinking around this band
(b) Intestinal obstruction may also be caused by intussusception due to swollen, inflamed heterotopic
epithelium at the mouth of the diverticulum and not due to inversion of the diverticulum.
2. Bleeding is also a common manifestation. This is due to peptic ulceration produced by secretion of
acid-pepsin by the ectopic gastric mucosa in the diverticulum. Melaena is usual, but frank hemorrhage with
passage of dark red clots may occur per rectum. Perforation from such ulceration is rare. Patient also vomits
but vomitus does not contain blood. When the abdomen has been explored with the diagnosis of peptic
ulceration haemorrhage and no peptic ulcer can be detected in the stomach or duodenum, it is wise to look f
Meckel’s diverticulum and ulceration there.

3. Meckel’s diverticulitis is the third complication in the adult. Inflammation in Meckel’s diverticulum
occurs due to lodgement of food residues within it. Symptoms are very much akin to appendicitis. About 50
of cases there may be perforation and general peritonitis. It is the usual practice to look for Meckel’s divertic
after performing appendicectomy, as the patient might have been suffering from Meckel’s diverticulitis, whe
the diagnosis of appendicitis was made.
4. Chronic peptic ulceration — may occur when there is ectopic gastric mucosa in the diverticulum.
Patient mainly complains of pain around the umbilicus (typical ‘hunger pain’). Pain relating to Meckel’s
diverticulum is always felt around the umbilicus as it is a part of the midgut.
5. Exceptionally Meckel’s diverticulum may be found in an inguinal or femoral hernia, when it is called
Littre's hernia.
Diagnosis.— 1. RADIOGRAPHY.— Barium meal radiography is not very significant in detecting presence
of Meckel’s diverticulum, as often the entrance of the diverticulum is blocked by oedema. Small bowel enem
would be a better proposition.
2. TECHNETIUM (99Tcm) SCANNING — is helpful particularly during haemorrhage taking place from
the diverticulum. 30 to 100(iCi "Tcra is injected intravenously and the uptake of the isotope by heterotopic
gastric mucosa in Meckel’s diverticulum is detected by using gamma camera on the abdomen. Diagnostic
accuracy is about 90% and uptake of the isotope by the ectopic gastric mucosa may be enhanced by injecting
pentagastrin in the dose of 0.6 M-g/kg given subcutaneously.
Treatment.— Whenever Meckel’s diverticulum is associated with any complication, treatment is excision
of the Meckel’s diverticulum. It must be remembered that during excision of Meckel’s diverticulum, the base
of the diverticulum should be included in the resection, lest heterotopic epithelium is left behind. End-to-end
anastomosis of the intestine is then performed.
The question is what should be done when
Meckel’s diverticulum is found during laparotomy for
some other reason. When the patient is below 5 years
of age excision of the diverticulum is justified, as
Meckel’s diverticulum is often involved in compli
cations after that age. But when this diverticulum is
detected after 30 years of age, it is better to leave it,
as morbidity of incidental removal outweighs the
potential disease prophylaxis.
Diverticulum of the Small Intestine
There are two varieties of diverticulum of small
intestine — A. Congenital — which contains att the three
coats of the bowel. Meckel’s diverticulum is an example
of such congenital diverticulum. B. Acquired— which con
tains only mucous and submucous coats, but not the
muscular coat. This usually occurs due to increased
intraluminal pressure and the mucosa herniates through the
point of entrance of blood vessel. So these diverticula
usually arise on the mesenteric border of the intestine.
Duodenal diverticulum.— There are two types of
duodenal diverticulum — primary and secondary.
(i) Primary.— This is same as acquired diverticu
lum and is usually found on the inner wall of the 2nd and
3rd parts of the duodenum. These usually do not produce
Fig. 49.1.— Barium meal radiograph illustrating two duode symptom and are accidentally discovered by barium meal
nal diverticula — one at the junction of 2nd and 3rd parts and X-ray.
another in the third part. Note that the third part of the duode (ii) Secondary.— This diverticulum is usually sec
num is displaced downwards. ondary to scarring of peptic ulcer and is usually seen in the
duodenal cap.
Jejunal diverticulum.— These diverticula are usually multiple. Majority are found in thejejunum. These also lie
on the mesenteric border often projecting between the leaves of the mesentery. Like acquired diverticula these contain
only mucosa and submucosa.
Clinically these are often (a) symptomless. Occasionally (b) there may be small intestine obstruction from a distended
or inflamed diverticulum or by adhesions from the diverticulum to the surrounding viscera, (c) Acute diverticulitis and
haemorrhage have also been reported, (d) Malabsorption syndrome, consisting of anaemia, hypoproteinaemia, avitaminosis
and steatorrhoea may be seen when these cause ‘blind-loop syndrome’.
Treatment.— Asymptomatic diverticula require no treatment. When diverticula cause complications, the affected
length of the bowel should be resected and end-to-end anastomosis should be performed.
BLIND-LOOP SYNDROME
When there is stagnation of small intestinal contents by stricture, stenosis, blind-pouch formation or diverticula, the
bacterial flora in the stagnant area are altered both in number and in kind. These produce a symptom complex such as
anaemia, hypoproteinaemia, steatorrhoea etc. This is called ‘blind-loop syndrome When this blind-loop occurs in the
distal part ofthe small intestine the abnormal bacterial flora compete for Vitamin B12 producing Vitamin B12 deficiency
and megaloblastic anaemia. This blind-loop when involves the upper part of the small intestine, bacteria deconjugate bile
salts causing disruption of micellar solubility of fats. This produces steatorrhoea. This bacterial flora also disturbs
absorption of protein and other vitamins to cause hypoproteinaemia and avitaminosis. This leads to weight loss.
Neurological disorders may develop from deficiency of vitamin B1 and B6.
Treatment.— Though tetracycline and vitamin supplements can improve the condition of the patient, but this is a
temporary cure. Surgical correction of the condition which is causing stagnation is the actual treatment of this condition
for permanent cure.
SHORT BOWEL SYNDROME
Massive resection of small bowel will produce this syndrome. Mesenteric occlusion, volvulus, traumatic disruption
of the superior mesenteric vessel and sometimes in recurrent Crohn’s disease, this type of massive small intestinal
resection may be needed. If the lower ileum and ileocaecal valve can be preserved even 70% of resection can be tolerated
Otherwise nutrition can be severely impaired by even 50% of small bowel resection.
In short bowel syndrome there are mainly problems of absorption of fat, water, electrolytes and vitamin B12. Fat is
least efficiently absorbed in normal individuals and it is absorbed in both jejunum and ileum. Absorption of bile salts
mainly occurs in the ileum and help in fat absorption. If ileum is missing there will be bile salt deficiency and a defect
in the intraluminal phase of fat absorption will occur. Massive intestinal resection also causes gastric hypersecretion and
a low pH in the small intestine interferes with digestion of fat. Vitamin B12 is mainly absorbed from the distal part of the
ileum and if this is missing vitamin B12 deficiency will occur. Hypoproteinaemia, water and electrolyte depletion, all
vitamin deficiency to certain extent will also be come across in this syndrome.
Treatment.— Drugs such as lomotil or codeine will slow intestinal motility and will help more absorption. Oral
calcium carbonate will decrease diarrhoea by neutralizing hydrochloric acid. Dietary fat is restricted to 30 to 50 g daily
to minimise steatorrhoea. Cholestyramine, an agent that sequesters bile acids, is often helpful in these patients. Electrolyte
depletion should be made of good particularly sodium and potassium.
Certain surgical procedures may be tried. These are reversal of a segment of intestine, vagotomy-pyloroplasty etc.
The hope of future is probably allotransplantation of a segment of intestine.
TYPHOID ENTERITIS
Typhoid is mainly a medical disease which is caused by Salmonella typhi. The main concern of the surgeons is that in this disease there
is hyperplasia and ulceration of Peyer’spatches ofthe intestine, mesenteric lymphadenopathy and to less extent parenchymal changes in the liver
and splenomegaly. Confirmation ofdiagnosis is obtained by culturing S. typhi from blood or faeces or by finding a high titre ofagglutinins against
the O and H antigens of the organism.
The followings are the complications of this disease which the surgeon is concerned with.
(i) Intestinal haemorrhage occurs in 10% 20% ofhospitalised patients. This occurs from multiple ulcers and the bowel is extremely
friable. Usually blood transfusion with antityphoid drugs cures this condition. Only in rare cases a laparotomy may be needed to control life
threatening haemorrhage.
(ii) Perforation ofthe typhoid ulcer is seen in only 2% of cases. This usually occurs during the third week. It occurs through ulcerated
Payer’s patches in the terminal ileum. It must be remembered that these ulcers are longitudinal (cf. tuberculous ulcer, which is transverse because
it follows lymphatic channels). Operation is only the treatment of choice to close the perforation.
(iii) Paralytic ileus is probably the commonest complication of typhoid and is associated with distension ofthe abdomen. Conservative
treatment is justified.
(iv) Cholecystitis.— Chronic typhoid cholecystitis may result in the patient becoming a typhoid carrier. Gallstones will contain S. typhi
bacilli. Acute cholecystitis from this disease is also not uncommon. The main danger is that this type of cholecystitis often perforates.
(v) Joints.— Mild effusion to suppuration may complicate this disease.
(vi) Bone.— Typhoid osteomyelitis though rare is sometimes come across.
(vii) Genitourinary complications.— Typhoid pyelitis, cystitis and epididymo-orchitis may occur.
NEOPLASMS
T umours of the small intestine are uncommon. Colonic neoplasms occur forty times as frequently as small intestinal
neoplasms. But the peculiarity of small intestinal tumours is that benign and malignant neoplasms occur with equal
frequency. The two interesting clinical syndromes associated with small intestinal neoplasms are : (a) Peutz-Jegher’s
syndrome and (b) carcinoid syndrome.
BENIGN NEOPLASMS
The benign tumours which are found in the small intestine are leiomyoma, lipoma, adenoma, polyp, haemangioma,
fibroma, neurogenic tumours, fibromyoma, myxomas etc. according to the order of frequency.
Only 15% of benign neoplasms are found in the duodenum, about 25% in the jejunum (particularly in its proximal
one-third) and majority of these tumours (60%) are found in the ileum particularly in its distal one-third. No age is exempt,
and most of the victims are between 40 to 50 years of age.
Clinical features.— A good number of small bowel benign tumours apparently cause no serious symptoms. The two
most common clinical manifestations of small bowel tumours are bleeding and obstruction. More commonly bleeding is
occult and intermittent giving rise to iron deficiency anaemia and positive occult blood test in the stools. Leiomyomas and
haemangiomas are the lesions that most oflen bleed. About one-third of the patients with benign tumours present with
bleeding. Only rarely bleeding may be severe.
Intestinal obstruction may be produced either by encroachment of the tumour into the lumen or by intussusception
with the tumour acting as the intussusceptum. In fact about 40% of cases of adult intussusception are due to benign
neoplasms of the small intestine. Occasionally perforation of the small bowel may occur from benign neoplasm resulting
in abscess formation, peritonitis, pneumatosis cystoides intestinalis (multiple gas cysts of the intestinal wall) and internal
fistula formation.
Special Investigations.— Small bowel barium meal studies are the only investigating tool available to detect benign
neoplasms preoperatively. Accuracy of diagnosis varies from 50% to 90% depending on the nature of the lesion. Selective
angiography has also been successful to detect these neoplasms.
Treatment— Surgical removal is the treatment of choice. Lest these neoplasms should cause complications which
may be life threatening total excision of the tumour is always advised. Segmental resection with primary anastomosis is
usually required. The entire bowel should be searched for other lesions, since these are often multiple. Excised specimen
should be sent for histopathological report as benignity can only be confirmed through this study.
Peutz-Jeghers syndrome.— This condition was first reported by Peutz in 1921 and Jeghers rediscovered it with
greater details in 1949. This syndrome consists of (a) multiple intestinal polyposis and (b) melanin spots in the oral mucosa,
lips, palms of the hands and soles of the feet. This is an hereditary disease and inheritance is through a simple Mendelian
dominant gene. There may be polyposis without pigmentation or pigmentation without polyposis. Polyps are mostly seen
in the jejunum and next in the ileum. Colon and rectum have been involved in ‘/3rd of cases, whereas stomach in about
‘/4th of cases. These polyps were initially thought to be adenomas, but are now confirmed to be Hamartomas. So these are
without malignant potentiality.
CLINICAL FEATURES.— Recurrent abdominal colicky pain caused by transient intussusception is the most
frequent symptom. Sometimes a palpable mass may be present alongwith abdominal pain. Haemorrhage occurs less
frequently. Besides the sites described above melanin spots may be seen on the digits and even in the perianal region
TREATMENT.— As malignant transformation is uncommon, excision is only indicated if polyposis are associated
with complication such as intussusception and/or bleeding. Polypectomy or minimal resection of the intestine is advised.
Though there are multiple polyposis extending almost all over the small and large bowel, yet excision should be restricted
to the polyps, which are concerned with complications.
MALIGNANT NEOPLASMS
Malignant neoplasms of the small intestine are extremely rare and comprise only 2% of gastrointestinal malignant
tumours. Adenocarcinoma is the commonest, followed by carcinoid tumour, lymphoma and sarcoma (principally
leiomyosarcoma). While other tumours affect predominantly ileum, it is the commonest adenocarcinoma which occurs with
equal frequency in duodenum, jejunum and ileum.

Adenocarcinoma.— This occurs at the age of above 40 years. Jejunum is only slightly more involved than ileum.
CLINICAL FEATURES..— There are mainly three groups of clinical manifestations — (a) obstruction with
abdominal pain, nausea and vomiting, (b) Diarrhoea with excessive amounts of mucus and tenesmus, (c) Chronic blood-
loss with melaena and anaemia.
Lymphosarcoma.— This tumour occurs more commonly between 30 to40 years of age. The cell type is most frequently
histiocytic lymphoma (formerly called reticulum cell sarcoma), followed by Hodgkin’s sarcoma and mixed cell lymphoma.
Malabsorption with steatorrhoea, loss of weight and anaemia are the chief symptoms. The affected part of intestine turns into
a rigid tube. Perforation into the peritoneal cavity may occur.
TREATMENT.— Wide resection including regional lymph nodes is the treatment of choice. If spread of the disease
precludes radical excision, by-pass operation should be performed. 5 years survival in case of adenocarcinoma is 25%,
lymphosarcoma is 35% and leiomyosarcoma is 40%. Postoperative irradiation is of value in case of lymphomas.
Carcinoids.— These tumours originate from the Kultschitzsky cells (argentaffin cells or enterochromaffin cells)
which show affinity for silver. Cytoplasm of these cells contain granules rich in 5-hydroxytryptamine. Carcinoids are also
known as argentaffin tumours. These tumours are also endocrine in nature. Carcinoid tumour can occur anywhere in the
gastrointestinal tract from the stomach to the anus. The appendix is most frequently involved (50%), followed by ileum
(25%) and rectum (15%). Outside G.I. tract carcinoid tumour is found in the bronchus, in ovarian teratoma and
sacrococcygeal teratoma.
Malignant potentiality of this tumour depends on the site of origin and size of the primary. While only 3% of
appendicular carcinoid tumours metastasise, 25% of ileal carcinoids usually metastasise. Majority of these tumours are
below 1 cm in diameter and only 2% of this group metastasises, whereas more than 2 cm in diameter tumours (which are
very rare, approximately 5%) metastasise in 80% to 90% of cases. Appendicular carcinoids are usually solitary tumours,
but '/3rd of the intestinal carcinoids are multiple.
Carcinoid tumours usually present as elevated, smooth, rounded yellow-grey nodules. The mucosa over carcinoids is
usually intact but occasionally may ulcerate.
MALIGNANT CARCINOID SYNDROME.— Clinical syndrome of functioning malignant carcinoid is due to
overproduction of serotonin. This serotonin is broken down in the liver to 5-hydroxyindole acetic acid (5 HIAA) which
is excreted in the urine. Release of serotonin into the systemic circulation occurs most frequently with carcinoid metastasis
in the liver, but hardly with metastasis in other sites. Functioning carcinoids, in addition to serotonin, produce 5-
hydroxytryptophan, kallikrein, histamine, epinephrine, nor-epinephrine, dopamine, prostaglandin and ACTH. Carcinoids
are thus apudomas. ‘Apudoma’ is a tumour arising from APUD cells which are distributed widely in the body and
synthesise variety of polypeptides and amines. The APUD cell derives its name from the initial letters of 3 of its most
important properties. These are (i) a high content of amine, (ii) the capacity for amine precursor uptake and (iii) presence
of aminoacid decarboxylase for the conversion of aminoacid precursors to amines.
CLINICAL FEATURES.— The most frequent and characteristic feature of malignant carcinoid syndrome is
cutaneous phenomenon. Flushing is the commonest early symptom. The face, neck, arms and upper trunks show a dusky red
hyperaemia. This may be accompanied by oedema, sweating, pruritus and vasomotor collapse. Flushing is precipitated by
emotional stress,ingestion offood or alcohol. Gradually permanent reddening ofthe skin may occur. Diarrhoea is a significant
complaint. This is characterised by audible borborygmi, cramping abdominal pain, watery but not bloody stool. Peripheral
oedema is also a frequent sign. This is due to increase in venous pressure during flushing and anti diuretic effect of serotonin.
Asthmatic attacks usually concurrent with flushing attacks are also common. Cardiac involvement is a late development in
the syndrome and occurs in about V* the cases. It is a peculiar form of valvular disease affecting primarily the tricuspid and
pulmonary valves. The valve cusps are thickened and shortened producing stenosis of the pulmonary or tricusoid valve.
SPECIAL INVESTIGATIONS.— The most important laboratory test is determination of urinary 5 HIAA. Normal
excretion is less than 5 mg per day, whereas patient? with this syndrome will excrete more than 40 mg/day.
TREATMENT.— If the primary tumour is less than 1 cm in diameter and no extension or metastasis is demonstrable,
local excision is advised. In case of lesions more than 1 cm in diameter wide resection is advised. A radical operation in the
form of right hemicolectomy is advised in distal ileum tumours alongwith removal of regional node bearing tissues. For lesions
in the rectum abdominoperineal resection is advised. Solitary metastasis in the liver should be excised. Ligation of hepatic
artery or gelfoam embolisation in the hepatic artery has been proved effective to deprive the metastasis of the blood suRply
and hence amelioration of symptoms of carcinoid syndrome. Antiserotonin agent like methysergide has been helpful in
controlling the bowel symptoms but not flushing. Flushing attacks are ameliorated by phenothiazines or by alpha-adrenergic
blocking agents such as phentolamine. Corticosteroid therapy may also be tried. Cancer chemotherapy with the combination
of 5-fluorouracil and streptozotocin has yielded some palliation of the syndrome.
880
CHAPTER 42 -
INTESTIN4L OBSTRUCIIOM
When there is pathological interference with the normal progression of the intestinal luminal content
distally, the condition is called intestinal obstruction. Such obstruction may be due to mechanical obstructi
of the intestine when it is called mechanical obstruction. It may also occur from paralysis of the intestinal
muscle so that the peristalsis of the intestine is lost, so is the progression of the intestinal contents. This is
paralytic ileus.
AETIOLOGY
A. Mechanical Obstruction.— This includes :
1. OBSTRUCTION IN THE LUMEN may be caused by (i) meconium, (ii) Bezoars which may be
trichobezoar (hair) or phytobezoar (fruit and vegetable fibres), (iii) gallstones, (iv) polypoid tumour of the
bowel, (v) intussusception, (vi) impaction of barium or worms.
2. LESIONS OF THE BOWEL WALL also cause intestinal obstruction These can be classified into —
(a) Congenital.—This includes (i) Atresia and stenosis; (ii) Megacolon (Hirschsprung’s disease), (iii)
Meckel’s diverticulum; (iv) Imperforate anus; (v) Diverticuli.
(b) Traumatic.
(c) Inflammatory.— (i) Crohn’s disease; (ii) Ulcerative colitis (rare); (iii) Diverticulitis (rare).
(d) Neoplastic.— Various tumours of the small intestine and large instestine also cause obstruction.
(e) Miscellaneous.— (i) Radiation therapy; (ii) Iatrogenic stricture following intestinal anastomosis;
(iii) Potassium induced stricture.
3. LESIONS EXTRINSIC TO THE BOWEL are important causes of intestinal obstruction. These are :
(a) Adhesive band constriction or angulation by adhesion.— This is a leading cause of small intestinal
obstruction. This may follow previous surgery or inflammation. Adhesions may produce kinking or angu
of the intestine or create bands of tissue that compress the bowel.
(b) External hernia is the second common cause of mechanical small intestinal obstruction. Inguinal,
femoral, umbilical and incisional hernia are important causes of bowel obstruction.
(c) Volvulus.— This is a separate entity.
(d) Extrinsic masses e.g. (i) Haematomas and abscess may press on the bowel and cause obstruction (
Neoplasms outside the bowel can also press on it to cause obstruction, (iii) Annular pancreas, (iv) Abnorm
vessels may cause such obstruction, which of course is extremely rare.
B. Paralytic ileus.—The causes of paralytic ileus can be divided into two categories; (a) Abdomi nal cau
and (b) Systemic causes.
(a) Abdominal causes include (i) intestinal distension, (ii) peritonitis and (iii) retroperitoneal lesion
retroperitoneal haemorrhage, retroperitoneal sarcoma, distension of the ureter etc.
(b) Systemic causes include (i) electrolyte imbalance particularly hypokalaemia and (ii) toxaemias.
CLASSIFICATION of intestinal obstruction can also be made as follows :
1. Simple mechanical obstruction in which there is obstruction but blood supply to the intestine remains
intact.
2. Strangulated obstruction, in which the mesenteric vessels are occluded besides the usual mechanical
obstruction. This is a dangerous condition and should be operated on without delay.
3. Closed loop obstruction when both limbs of the loop are obstructed so that there is neither progressio
nor regurgitation.
. Intestinal obstruction can be further classified into : (i) A cute obstruction, which is an obstruction to the
small bowel and is characterised by central abdominal pain, early vomiting, central abdominal destension
constipation, (ii) Chronic obstruction, when obstruction is confined to the large bowel and is characterised
lower abdominal colic, absolute constipation and later on distension, (iii )Acute-on-chronJc obstruction, wh
starts in the large bowel but gradually involves the small intestine. Early pain and constipation are the
symptoms to starts with but when the small intestine is involved it is characterised by vomiting and gene
INTESTINAL OBSTRUCTION 881
abdominal distension.
PATHOLOGY.— BOWEL MOTILITY.— When the intestine is obstructed, the part of the intestine
above the obstruction shows vigorous peristalsis to overcome the obstruction. This continues from 2 to 6 days.
The more distal is the obstruction, the more vigorous is the peristalsis and longer does it remain. If the
obstruction is not relieved, increasing distension of the intestine ensues and a time comes when peristalsis
ceases and the obstructed intestine remains flaccid and paralysed.
For a few hours the intestine below the obstruction shows normal peristalsis and absorption. This will
empty its contents and later on it becomes immobile, contracted and pale.
DISTENSION.— In case of intestinal obstruction accumulation of fluid and gas proximal to the
obstruction occurs. This produces distension of the intestine proximal to the obstruction. Ingested fluid,
digestive secretion and intestinal gas play the major role to form this distension.
Fluid and electrolyte imbalance.— Large volume of saliva, gastric secretion, bile and pancreatic juice
enter the gut daily. These are mainly absorbed in the small intestine. Distension increases intestinal secretion
and decreases absorption. This phenomenon results in increased fluid accumulation in the bowel proximal
to the obstruction. Besides ingestion of fluid, various digestive juices comprise about 8000 ml/day. Saliva 150
ml, gastric juice 2500 ml, bile and pancreatic juice 1000 ml. and intestinal juice 3000 ml. Accumulation of
such huge amount of fluid alongwith repeated vomiting causes severe metabolic disturbances. Particularly in
proximal obstruction there is relatively more vomiting and this leads to losses of water, sodium, chloride,
hydrogen and potassium ions producing dehydration with hypochloraemia, hypokalaemia and metabolic
alkalosis. Distal small bowel obstruction may cause loss of large quantities of fluid, but the abnormalities of
serum electrolyte values are less dramatic, probably because of hydrochloric acid losses are less.
With dehydration the-e will be oliguria, haemoconcentration and azotemia. If dehydration continues,
there will be reduced cardiac output, low central venous pressure, hypotension and hypovolaemic shock.
Distension of the abdomen will lead to elevation of the diaphragm to impair proper ventilation.
Intestinal gas.— Much of the distension is caused by gas accumulation in the intestine proximal to the
obstruction. This mainly consists of (i) gas swallowed from the atmospheric air, (ii) diffusion from blood into
the bowel lumen (carbondioxide from neutralisation of bicarbonate) and (iii) organic gases (hydrogen sulph
ide, ammonia, amines and hydrogen) from bacterial fermentation (10%). Swallowed air is the most important
source of gas in causing intestinal distension. While the oxygen and carbondioxide are absorbed, nitrogen is
not absorbed by intestinal mucosa. So nitrogen content is very high in intestinal gas. On the other hand
carbondioxide diffuses very rapidly, as the partial pressure of carbondioxide is high in the intestine and
intermediate in the plasma Thai is why though carbondioxide is produced in large amounts in the intestine,
it contributes little to gaseous distension ofthe intestine due to its rapid diffusibility. So composition of the
intestinal gas. which contributes a lot to the distension in intestinal obstruction, is nitrogen (70%),
oxvgen(12%) and carbondioxidc(8%) and remaining 10% is composed of organic gases — hydrogen
sulphide(5%). ammonia and amines(4%) and hydrogen(l%).
BACTERIAL PROLIFERATION.— During intestinal obstruction there is rapid proliferation of intes
tinal bacteria. Normally the small intestine contains very small quantity of bacteria and may be considered as
almost sterile. Normal peristalsis with continued progression of luminal content minimises small intestinal
bacterial flora. But during small intestinal obstruction, whatever may be the cause, bacteria proliferate rapidly.
That is why, intestinal contents become faeculent’ during obstruction. As the bacteria or bacterial toxins
cannot cross normal intestinal mucosa the bacteria in the small intestine probably play no role in the ill effects
of simple mechanical small intestinal obstruction.
Strangulated obstruction.— Strangulation develops when the circulation to the obstructed intestine is
impaired. This frequently occurs secondary to (i) adhesive band obstruction, (ii) hemia, (iii) volvulus or (iv)
intussusception. If the obstructed distending bowel is held by unyielding adhesive bands or hernial rings
strangulation may occur. Similarly in volvulus or intussusception, the mesenteric vessels are occluded by
twisting of the mesentery. In strangulated obstruction the patient suffers from all the ill effects of simple
obstruction plus to the effects of strangulation.
56
Distension.— Distension in case of strangulated obstruction is different from simple obstruction. Unlike
non-strangulated obstruction, early distension of the proximal intestine is absent. In fact for a few minutes
several hours the proximal intestine contracts. After this, vigorous peristalsis occurs in the proximal segme
without any distension. When gangrene is imminent, retrograde thrombosis of the related tributaries of th
mesenteric vein will cause distension of both the proximal and distal segments of the strangulated intestin
For a considerable time the strangulated segment alone distends. The greatest distension occurs when the
venous return is completely impaired and the arterial supply continues uninterrupted.
The onset of gangrene.— Gangrene does not occur till the venous return is completely occluded. At this
time the colour of the intestine changes from purple to black. Gradually the arterial supply is also impeded
Now the serous coat loses its glistening appearance, the mucous membrane becomes ulcerated and thus w
gangrene develops.
Loss of blood volume. — In addition to the accumulation of fluid and gas in the obstructed loops, blockag
of venous outflow from the strangulated segment will cause extravasation of bloody fluid into the bowel. S
strangulation causes loss of blood and plasma. This loss of blood and plasma will cause shock particularly
the patient is already dehydrated. The amount of loss of blood volume will depend upon the length of the
strangulated segment. If strangulation produces gangrene, peritonitis with its sequelae will occur. Rupture
perforation of strangulated segment is possible.
Transmigration of bacteria and toxin.— In addition to the loss of blood volume, another important fac
tor in strangulated obstruction is production of toxic material in the strangulated bowel. As mentioned abo
the bacteria proliferate and produce toxic meterial within the strangulated segment. When the intestinal
mucous membrane is normal this toxic material is not absorbed, but when the wall of the intestine become
partly devitalised, both bacterial toxin and the products of tissue autolysis pass through the wall of intestin
into the peritoneal cavity, whence these are absorbed into the circulation. So if the strangulation is external
it is far less dangerous than intraperitoneal strangulation.
Closed-loop obstruction.— When both afferent and efferent limbs of a loop of bowel are obstructed, it
is called closed-loop obstruction. It is dangerous as this type of obstruction very rapidly becomes strangula
even before the usual manifestations of intestinal obstruction. Obstruction to blood supply occurs either fr
the same mechanism which produces such obstruction or by the twist of the bowel on the mesentery.
Development of distension and onset of gangrene are almost same as strangulated obstruction described a
Colon obstruction.— In general, effects of colon obstruction is usually much less dramatic than the effec
of small bowel obstruction. If the ileocaecal valve is competent colon obstruction will lead to closed-loop
obstruction (described above). In this case pressure within the caecum becomes quite high to compress blo
vessels within its wall. Stercoral ulcers develop, followed by even perforation. If the ileocaecal valve is
incompetent, signs of small bowel distension may accompany colon obstruction.
Otherwise colon obstruction is less dangerous as it produces less fluid and electrolyte imbalance than s
bowel obstruction. Further colon obstruction usually does not strangulate except cases of volvulus.
CLINICAL FEATURES.— The important symptoms of simple mechanical intestinal obstruction are:
(i) Abdominal pain, (ii) Vomiting, (iii) Failure to pass gas (flatus) or faeces per rectum and (iv) abdominal
distension.
(i) Abdominal Pain.— This is the first symptom and usually starts suddenly. The pain is typically cra
like. This cramping pain is felt synchronously with hyperperistalsis. The pain is represented by severe cram
with intervals of 4 to 5 minutes in proximal intestinal obstruction and with more intervals (15 to 20 minute
in distal obstruction. In between attacks the patient is often free from pain. The pain is diffuse, poorly local
and is felt across the upper abdomen in high obstruction, at the level of the umbilicus in low ileal obstructi
in the lower abdomen in colon obstruction and in the perineum in case of rectosigmoid obstruction. When
obstruction is not relieved the characteristic abdominal colicky pain may stop by itself and will be replaced
steady generalised abdominal discomfort. It must be remembered that continuous severe pain without any
quiescent period is usually indicative of strangulation. In paralytic ileus there is no typical colicky pain of
mechanical obstruction, but there may be steady generalised abdominal discomfort.
(ii) Vomiting.— There may be early vomiting which is ‘reflex’ and is followed by a quiescent period
of variable length before ‘actual’ vomiting starts. This interval depends on the site of obstruction and is short
in high obstruction and long (evena day or two) in low small bowel obstruction. With high obstruction vomitin
is more frequent and copious and may cause some relief by decompressing the obstructed bowel. With lew
small bowel obstruction vomiting is less frequent and does not cause any relief. In this case vomiting may be
‘faeculent’ because of large bacterial population of distal small bowel. In acute small intestinal obstruction,
the character of the vomitus alters. Initially it contains partly digested food next it becomes yellow or green
from regurgitation of bowel and finally it becomes faeculent. This is important and must be remembered. In
colon obstruction reflex vomiting is absent and vomiting does not occur until due to incompetent valve the sm
bowel is retrogradely involved. When the ileocaecal valve is competent vomiting is absent in colon obstruction
(iii) Constipation.—Failure to pass gas (flatus) or faeces through the rectum is an important symptom
of intestinal obstruction. But it must be remembered that it becomes evident only after the bowel distal to the
obstruction has been evacuated. So there may be one or two natural actions of bowel after the onset of attack
before constipation develops.
It should be remembered that in a few conditions of intestinal obstruction there may not be constipation
e.g. Richter’s hemia, mesenteric vascular occlusion and intestinal obstruction with pelvic abscess.
(iv) Distension.— In early case of small intestinal obstruction there may not be any abdominal
distension. Distension is much less in high small bowel obstruction. In low small bowel obstruction centrally
placed distension becomes evident but late. Visible peristalsis may be present, if the abdomen is inspected very
carefully. This is evident in the proximal loops. Borborygmi may be quite loud and may not require a
stethoscope to hear it. In auscultation, sound of hyperperistalsis coinciding with attack of colic is definite
evidence of intestinal obstruction.
PHYSICAL EXAMINATION.— A thorough examination must be done with particular attention to a
few points.
Tachycardia and hypotension indicate severe dehydration and/or peritonitis. The degree of dehydration
is estimated by examination of the skin turgor and moisture of the mucous membrane. Fever suggests
strangulation. It must be remembered that simple mechanical obstruction within first 24 hours yield surp
risingly few abdominal signs. In strangulated obstruction patient appears very ill during this early period.
Inspection.— In early stage visible peristalsis may be the only sign present particularly in these
individuals with long standing obstruction. One must look for surgical scars, indicative of previous surgery
(which indicates adhesion or cancer). Abdominal distension is a late sign of intestinal obstruction. But one must
exclude distension due to ascites. In the latter case there will be fluid thrill, shifting dullness and fullness in
the flanks. All hernial orifices must be inspected. This will diagnose many obscure hernias (even strangulated)
to be the cause of intestinal obstruction.
Palpation— During colic there may be muscle guarding. Slight tenderness may be present between
attacks of pain. Tenderness and rigidity at the site of obstruction usually indicate strangulation. Rebound
tenderness suggests peritonitis and likelihood of strangulation. Abdomen should be thoroughly palpated to
exclude presence of mass (lump) which may be present in intussusception, neoplasms and abscesses Again
all the hernial orifices should be palpated to exclude presence of hernia (impulse on coughing should be tried)
Percussion.— Tenderness on light percussion suggests strangulation.
Auscultation.— It is of great value. In simple mechanical obstruction — during attacks of colic the
bowel sounds become loud, high-pitched and metallic. In paralytic ileus occasional isolated bowel sound may
be heard. In presence of strangulation, bowel sound is completely absent at that region.
Rectal Examination should be performed in all cases of intestinal obstruction. Presenceof masson rectal
examination within or outside the lumen will give a clue to the diagnosis. Most of rectal cancers are within
the reach of the rectal examination finger. It should be noted presence or absence of faeces in the rectum.
Absence of faeces means the obstruction is higher up. If present, it should be studied for presence of occult bloo
which indicates mucosal lesion e.g. cancer, intussusception or infarction.
Sigmoidoscopy examination should be done if colonic obstruction is suspected.
1. BLOOD EXAMINATION.— The haematocrit rises roughly in proportion to the fluid loss. In the e
is little change in the concentration of sodium, potassium and chloride in the plasma. White blood cell count is useful
to differentiate various types of obstruction. While a normal or slight rise in W.B.C. count indicates
obstruction, a moderate increase in W.B.C. count (15000 to 20000) with marked polymorphonucle
indicates strangulation and very high W.B.C. count (30000 to 40000) suggests primary mesenteric
Serum amylase level is often elevated in intestinal obstruction due to entry of amylase into the blood by re
the pancreas because of back pressure in the duodenum. Serum amylase level also increases in str
peritoneal absorption of amylase after leakage of this enzyme into the peritoneal cavity through the
be slight change in the pH and C02 to indicate metabolic alkalosis seen in upper intestinal obstruction due
loss of acid gastric juice. Metabolic acidosis due to combined effects of dehydration, ketosis and loss of a
is very common in distal intestinal obstruction.
2. RADIOLOGICAL EXAMINATIONS.— This is in fact the most important diagnostic procedure to confi
clinical diagnosis and to locate the site of obstruction accurately.
STRAIGHT X-RAY of the abdomen should be done as soon as the patient is admitted. These film
in the supine and upright positions with AP and lateral views of the chest. If the patient is unable t
demonstrate air under the diaphragm) a left lateral decubitus film may suffice. Gas-fluid levels are the m
criteria of diagnosis of intestinal obstruction. In small bowel gas is normally not visible (except in in
air passes very rapidly through the intestine. But if there is intestinal obstruction gas collects along
intestinal fluid and produces gas-fluid levels which are best seen in the upright film of the abdome
highly suggestive of intestinal obstruction including paralytic ileus (in gastroenteritis and severe co
be gas-fluid levels demonstrated in straight X-ray).
Gas shadows.—Abnormally large quantities of gas in the bowel can be demonstrated in straight X-r
the level of intestinal obstruction. In straight X-ray gas in the jejunum outlines the val vulae conniv
the entire transverse diameter of the bowel image. Typically the small bowel gas occupies central p
while the colon gas is seen on the periphery on the abdominal films or in the pelvis. Colonic haustr
seen in a portion of the transverse diameter of the bowel due to presence of gas within the colon. H
valvulae conniventes are spaced irregularly and the indentations are not placed opposite one anoth
is seen as a straight pipe without any valvulae conniventes or haustral folds. This is typically descr
In colonic obstruction gas shadow will be seen in the caecum as well as in the colon proximal to th
Fluid levels.— Films are taken in the upright or lateral decubitus position. In patients with mechan
obstruction the films usually show multiple gas-fluid levels with distended bowel. Normally infants
may show a few fluid levels in the small intestine. In case of paralytic ileus fluid levels are more nu
obvious. It takes sometime for the gas to separate from the fluid. So fluid levels appear later than gas shadows. B
time fluid levels become apparent, obstruction is advanced. The number of fluid levels is proportion
obstruction and to the site of obstruction (the more distal is the small bowel obstruction, the more
levels). In colonic obstruction fluid levels are only seen if the ileocaecal valve is incompetent and th
involved the ascending colon.
BARIUM ENEMA, is indicated when the clinical picture and straightX-ray suggest colonic obstr
indicated if there is no clear evidence of obstruction on straight X-ray. It is also indicated in suspec
strangulated intussusception. The dangers of barium enema are : (i) possibility of changing a partia
to a complete one and (ii) possibility of perforation in an inflammatory lesion and strangulation.
Intravenous urography may be indicated to exclude presence of ureteric calculi (which has not been v
straight X-ray), which may cause marked paralytic ileus.
MANAGEMENT.— Principle of treatment of intestinal obstruction includes : (a) fluid and electrolyte
therapy, (b) decompression of the bowel and (c) timed surgical intervention to relieve the obstruction.
Of these three, operative treatment to relieve the obstruction is by far the most important and in fact
the patients, except in the immediate postoperative period, with mechanical intestinal obstruction should
operated upon. The question is when to operate. The optimal time for a particular patient must be found o
The first two principles (a) & (b) are actually preoperative treatment.
When the operation is performed within 24 hours of the commencement of the disease, extensive
preoperative preparation is not needed, as water and electrolyte depletion has not been so serious. Intrav
fluid and nasogastric suction should be started and on the way to operation theatre chest and abdominal
rays are done The mortality rate is considerably low if the patient is operated on within 24 hours of
commencement of the disease.

If the obstruction has been present for more than 24 hours when the patient is first seen, a period of
preparation is required before the patient is operated upon to relieve the obstruction. The only exceptions to
this rule are (i) strangulation and (ii) closed-loop obstruction, where operation should be performed as soon
as possible. Otherwise longer the obstruction is there, the longer it will take the patient to ready for operation
(a) Fluid and electrolyte therapy.— A plastic venous catheter is threaded into the superior vena cava
for frequent measurements of central venous pressure and rapid administration of fluid. An indwelling cathet
is inserted into the bladder for accurate measurement of urinary output. Haematocrit reading may be used to
estimate the extent of fluid loss and to assess the fluid volume necessary to restore normalcy. In case of acid
gastric juice losses, ordinary normal saline solution should be used. Otherwise lactated Ringer’s solution and
5% dextrose in water in about equal proportions should be used to replace fluid loss. Potassium chloride may
be necessary to replace lost potassium, but it should be given with due caution as high potassium level in the
blood is even more dangerous and it should not be given if the urinary output is not satisfactory.
Patients with bowel obstruction are likely to be depleted of water, sodium, chloride and potassium. So
intravenous therapy with an isotonic sodium chloride solution should be started. Firstly the aim is to replace
the loss and about 3.5 litres of fluid should be given intravenously if the patient shows sign of severe
dehydration. Subsequently daily requirement is about 2.5 litres plus the amount aspirated through nasogastric
suction (considering normal urine output). Potassium chloride should be added only when there is adequate
urine formation Administration of blood, plasma or both should be considered if strangulation is suspected.
The rate of fluid administration is best controlled by monitoring the central venous pressure (C.V.P).
Fluid should be given rapidly so long as the C.V.P. remains below 10 to 12 cm of water. Volume replacement
will be indicated by sudden rise in C.V.P. Other guides are hourly rate of urine production and return of skin
turgor.
When strangulation exists, preoperative treatment with fluid and electrolytes to normalcy is not possible
or advisable Vigorous preparation with fluid and electrolytes and massive antibiotics with nasogastric suction
should be done to make the patient safe for an early operation. Operation in this condition must be performed
as early as possible.
Antibiotics should be given particularly if strangulation is suspected. The choice of antibiotics is a matter
of individual preference. Ampicillin alone is a quite competent antibiotic in this respect. Metronidazole has
been used alongwith one antibiotic successfully. Sophisticated antibiotics like gentamicin, clindamycin or
third generation cephalosporin may also be tried in bad cases of strangulation.
(b) Decompression of the bowel (Nasogastric aspiration). — Two types oftubes are available — short’
tube for gastric aspiration and ‘long’ tube for aspiration of the small intestine. The Levin tube is the most
popular among the short tubes. Complete decompression is not possible as only gas and fluid from the upper
intestine may regurgitate into the stomach for aspiration. But this tube is quite efficient in reducing the hazard
of pulmonary aspiration of vomitus as well as minimising further intestinal distension from swallowed air.
Among the ‘long’ intestinal tubes Miller-Abbott is quite popular. This tube is passed through the nostril
to the pyloric antrum. The patient lies on his right side with feet slightly elevated so that gravity will help to
pull the tube through the pylorus. Now fluoroscopically the position of the tip of the tube can be judged and
slowly passed through the pylorus into the duodenum. The mercury-containing balloon or small bag at the dis
end of the tube is inflated while in the small intestine. The balloon is carried distally by peristalsis. The purpos
of mercury is to get the tube through the pylorus.
If strangulation can be definitely ruled out, it is well justified to decompress the bowel sufficiently before
the patient is taken to the operation theatre.
(c) Operative treatment for intestinal obstruction.— Operation for intestinal obstruction should be
performed under general anaesthesia administered through an endotracheal tube. The particular risk in
operating these patients is vomiting and tracheobronchial aspiration of the vomitus during operation.
In absence of external hemia in patients with small bowel obstruction, abdominal exploration should be
performed through a midline vertical incision. On opening the peritoneum, presence or absence of free
peritoneal fluid should be noted and its colour. Clear straw-coloured fluid is found in simple obstruction a
bloody fluid denotes strangulation. The point of obstruction is best found by looking at the caecum. If caec
is grossly distended, the obstruction is in the colon. If caecum is collapsed, the collapsed small bowel is fou
and is followed back to the point of obstruction. The distended proximal loops of intestine are then not tak
out from the abdomen at this preliminary stage.
It is often difficult to determine whether the affected segment of intestine is viable or not. The three crite
determine viability of the bowel are (i) Colour, (ii) Motility and (iii) Arterial pulsation. If in doubt, the segme
intestine should be completely released and placed in saline moistened swab for 10 minutes and then re-e
If normal colour has returned and peristalsis is evident, it is safe to retain the bowel. If there is doubt of bo
viability as the normal colour is not returned and peristalsis has also not returned, it should be resected. B
problem remains if a long segment of intestine is affected. In this case the border line intestinal loop shoul
returned back to the abdomen and the patient is observed very closely for progressive toxicity to develop.
develops, re-operation and resection of the bowel should be performed.
Decompression of grossly distended intestine during operation is sometimes necessary. An effective sa
method of decompression is by passing a tube with wide lumen (Baker tube) through a proximal jejunosto
The tube is advanced by manipulation through the entire distended bowel to the obstructed segment. The
whole length of the distended intestine is thus pleated on this long tube.
The obstructed point can be located by following distended bowel distally unit collapsed intestine is fo
Manipulation of distended bowel is easier if the intestine has been decompressed preoperatively. During o
eration an intestinal tube may be passed into the distended bowel and aspiration through this should be d
The approach to colon obstruction is somewhere different from small bowel obstruction. If there is ob
structive lesion of the right colon, right colectomy with ileotransverse colostomy or if resection is not poss
a simple ileotransverse colostomy is performed to give a chance of later elective resection of the right colon
The simple bypass operation is reserved for poor-risk patients and in those where the growth is irremovab
In case of obstruction of the left colon three stages operation is performed — (i) proximal defunctioning
colostomy, (ii) removal of the diseased segmental colon and anastomosis and (iii) closure of the colostomy
when healing of the anastomosis is complete.
PARALYTIC ILEUS.— This can be defined as failure of transmission of peristaltic waves due to neuromuscular failure.
There are two nerve plexuses in the wall of the intestine — myenteric plexus between longitudinal and circular muscle layers and
one in the submucous coat which is known as submucous plexus or Meissner’s plexus. This failure of transmission of peristaltic
waves leads to accumulation of intestinal fluid and gas inside the lumen which results in abdominal distension. The main feature of
this condition is absence of bowel sounds, which is loud and high piched in case of mechanical obstruction. Vomiting and absolute
constipation alongwith abdominal distension are the features of this condition which is similar to those of mechanical obstruction.
Types of paralytic ileus.— Basically 4 types of paralytic ileus are found in clinical practice —
1. Postoperative paralytic ileus.— This is almost always seen after abdominal operation for a limited period of 24 to
72 hours. Gradually the bowel sounds come back and this state passes away. Only during presence of peritonitis or
metabolic abnormalities (hypoproteinaemia, hypokalaemia and uraemia) this stage may continue for quite sometime.
2. Peritonitis.— Intra-abdominal sepsis may produce localised or generalised paralytic ileus. To start with it is neuro
genic. Later on mechanical obstruction may develop due to resultant adhesions.
3. Metabolic paralytic ileus.— When the patient is suffering from uraemia, hypoproteinaemia and hypocalaemia,
paralytic ileus may be precipitated.
4. Reflex paralytic ileus.— This may occur following retroperitoneal haemorrhage, fractures of the spine or ribs or
even by the application of a plaster jacket.
CLINICAL FEATURES.— The characteristic feature of paralytic ileus is absence of bowel sound on auscultation.
Another important feature is absence of pain. Effortless vomiting, abdominal distension and no passage of flatus are the
features almost similar to those found in mechanical obstruction.
Straight X-ray of the abdomen shows gas-filled loops of intestine with multiple fluid levels.
TREATMENT.— This condition is primarily treated by conservative means with an intension to prevent this condi
tion. This is performed by nasogastric suction and intravenous fluid administration. Correction of electrolyte imbalance,
particularly hypokalaemia is important. In some cases where there is too much distension, long intestinal tube should be
used for intestinal decompression. If mechanical obstruction or intra-abdominal sepsis can be clearly ruled out, a
parasympathomimatic drug such as neostigmine (prostigmin) may be used.
If paralytic ileus continues for sometime after surgery, one must rule out two possibilities — (i) intra-abdominal sepsis
and (ii) mechanical obstruction for which abdominal exploration may be necessary.
ACUTE INTUSSUSCEPTION
When one portion of the gut invaginates into the immediately adjacent loop, the condition is called intussusception.
Usually proximal loop is invaginated into the distal bowel. But rarely the distal loop may invaginate into the proximal loop
and this condition is called retrograde intussusception (e.g. jejunogastric intussusception following gastrojejunostomy).
Sometimes the mass of intussusception may again invaginate into the distal bowel and this condition is called com
pound or double intussusception.
Intussusception is usually single but very occasionally one may find more than one intussusception at different levels.
This is called multiple intussusceptions.
Intussusception is usually acute, but rarely chronic intussusception may persist for months or years. Intussusception
may recur and this is called recurrent intussusception.
AETIOLOGY.— Broadly speaking there are two varieties of intussusception — I. Where there is definite cause of intussusception
— Secondary intussusception and 2. Where there is no definite cause for intussusception — Primary or idiopathic intussusception.
1. SECONDARY INTUSSUSCETION.— Polyp, papilliferous carcinoma, lymphoma, hamartoma, submucous lipoma, stump of appendix,
an inverted Meckel’s diverticulum etc. may cause intussusception. This type of intussusception, which is caused by some pathology, is known
as secondary intussusception. This type of intussusception may occur at any age. Secondary intussusception usually occurs in the ileum.
Sometimes intussusception may occur in the early postoperative period due to
inco-ordinale peristalsis in the small intestine.
2. PRIMARY OR IDIOPATHIC INTUSSUSCEPTION.— The majority
of the intussusceptions belong to this group. This type of intussusception usually
occurs in children between 6 to 9 months of age. Various theories have been
put forward to account for such intussusception. These theories are —
(i) When there is a change in diet, i.e. when the infant is weaned
(breast milk is stopped) or some different cereals are added in infant’s food.
(ii) Intussusception often follows an attack of upper respiratory tract
infection. Even antibodies to certain viruses have been isolated.
(iii) Idiopathic intussusception usually commences in the last 50 cm of
the small intestine. Some structural peculiarity of this part of the intestine may
play some role — (a) mobile intestine terminating into immobile caecum, (b)
oblique entrance of ileum into the caecum and (c) excessive lymphoid tissue.
(iv) A peculiar defect in the neuromuscular co-ordination of the distal
part of the intestine has been incriminated. The constricted segment is pushed
into the adjacent passive dilated loop of the gut and then by peristalsis
intussusception occurs. This occurs as the inhibitory nervous mechanism
appears late in children and at this age it starts appearing, so some aberrant
contractions cause such intussusception.
(v) The lower part of the intestine contains maximum aggregation of
Peyer's patches. Hypertrophy of these Peyer’s patches may cause
intussusception. Elevation of Peyer's patch will make a protrusion into the
intestinal lumen which will act in the same principle as a polyp to initiate
intussusception. Hypertrophy of Peyer’s patches will be caused by (a) change
in diet which will bring about a change in bacterial flora of the intestine and
will cause inflammation of the Peyer’s patch, (b) Inflammation of Peyer’s
patch may occur secondary to upper respiratory tract infection.
(vi) Occasional intussusception has been recorded in Muslims after
Ramjan fast.
Various types.— There are various types of intussusception, but the
commonest variety is ileocolic and ileocaecal. Next common are ileo-ileo-colic
and ileo-ileal and least common are colocolic and multiple intussusceptions.
In ileocolic, the starting point is the terminal part of the intestine. So it is ileo-
ileal to start with and then passes through ileocaecal valve to make it ileocolic.
Fig.50.1.— Gross features of acute intussusception
PATHOLOGY.— An intussusception is composed of three parts
of ileocaecal region.
— (i) the entering or inner tube, (ii) the returning or the middle tube
and (iii) the sheath or the outer tube.
The entering or inner tube and the returning tube are together called intussusceptum. The ensheathing tube or outer tube is called
intussuscipiens. The starting point ofthe intussusception is called the apex. It is the junction of the entering and returning tubes. It
is the fixed point of intussusception and intussusception progresses at the cost of the ensheathing tube or the outer tube. The site
where the retuning layer and the ensheathing layer meet is called the neck and this point varies as the intussusception progresses.
Intussusception is a type of intestinal obstruction which often accompanies strangulation.
As the intussusception progresses, the mesentery of the entering and returning tubes is dragged alongwith the gut
through the neck of the intussusception. Gradually the mass of the intussusception by the pull of the mesentery becomes
sausage-shaped with concavity towards the umbilicus (approximately the point of attachment of the mese
the mesentery becomes compressed between the entering and returning tubes. In the beginning the
mesentery become constricted and severe venous engorgement and oedema of the wall of the intussu
oedematous intussusceptum may cause total intestinal obstruction. Such oedema will also discharge blood a
from its wall and this will be discharged per rectum. Such mixture of blood and mucus is called 'Red-c
If the mesentery is quite long intussusception can even present through the rectum at the anal c
pull on the mesentery becomes sufficient enough to occlude the arteries. This causes onset of gangre
gangrene is dependent upon the tightness of the invagination and it often occurs in ileocolic intussus
ileocaecal valve exerts pressure on the mesentery. The returning layer near the apex is the first site t
gangrene. Gangrene may cause perforation and ultimately peritonitis.The ensheathingtube is hardly aff
In rare instances gross adhesion may develop at the neck between intussusceptum and intussuscip
develops in such case, the whole mass of intussusceptum becomes necrosed and sloughs out. This bri
cure.
CLINICAL FEATURES.— Healthy male children between 6 and 9 months of age are mostly affected.
Onset is usually sudden. The child screams with abdominal pain, which is colicky in nature. Alongwit
the pain the child draws up his legs. During the attack the child may vomit. But remember that vomiting i
a late feature and usually does not appear before 24 hours of the onset of the disease. Such attacks are also
accompained by facial pallor. The attacks usually last for a few minutes and recur every 15 minutes. In bet
the attacks the child lies motionless and looks very drawn. Patient may pass a few normal motions before
currant jelly’ stool is passed.
Fig.50.3.— Barium enema showing crescentic ridge

variation of pitch fork sign'
Fig.50.2.— Not frequently straight X-ray of the In long continued and untreated cases pain becomes
abdomen is diagnostic in a case of intussuscep- continuous. After 2 or 3 days, the abdomen gradually starts
tion. In this film arrows show apex of the intus- i*•*•.
susception with gas filled transverse colon and distending. Vomiting becomes copious. Absolute intestinal
coils of small intestine obstruction occurs and death is the ultimate result from
intestinal obstruction alone or peritonitis following gan
grene and perforation.
PHYSICAL SIGNS.— No typical feature is usually revealed on physical examination, the abdomen
becomes voluntarily contracted during paroxysms of pain. In early cases distension is not noticed. Distensio
only appears after 2 or 3 days of the commencement of the disease. If the abdomen is carefully palpated betw
the attacks one may feel a lump under the right or left
ju. | costal margin. This lump is a sausage-shaped lump
with concavity towards the umbilicus. Right iliac
■ fossa is peculiarly empty on palpatio
called Signe-de-Dance. This is due to the fact that the
If terminal part of ileum and caecum do not remain m
right iliac fossa, but arc involved in intussusception
and arc tclcscopcd through the ascending colon,
transverse colon and descending colon according to
V the various stages.
M '' ' RECTAL EXAMINATION should always be
jt, « performed One may feel the intussusceptum if it has
MM reached the rectum. It will feel verymuch like cervix
uteri in the vagina. In majority of cases the apex of the
H intussusception cannot be felt per rectum but the
mm. S*oved finger will be smeared by blood-stained mu
m cusThis will give a definite clue to the diagnosis. In
pi j&XBKm very occasional cases intussusception may actually

prolrude through the anus when the patient possesses
K. ■BBHi an unusually long mesentery. In this case it looks like
a prolapse.
Fig.50.4.— Barium enema film showing 'pitch fork sign’ SPECIAL INVESTIGATIONS__
of instussusception. I X-ray of the abdomen shows absence of
caecal gas shadow and incresed gas shadows in the small intestine.
2. Barium Enema Radiography is very diagnostic when
the intussusception has passed distally through
ileocaecal valve. When the intussusception has reached at least the ascending colon the barium will sto
intussusceptum and there it will show a ‘pincer-shaped ’ or ‘colied-spring ’ (Fig. 50.5) deformity or ‘pitch fork
50 3 & 50 4 )
1 Barium enema has got a therapeutic value, in the
K
Jggf WjBB sense that the pressure of the barium enema may cause
tSPJM spontaneous reduction ofthe intussusception.

: * ip TREATMENT.—
,.«# W PREOPERATIVE MANAGEMENT— Intra-
| venous fluid administration should be started im-
y > mediately and appropriate fluid resuscitation should
be begun. Decompression of the small intestine
through nasogastric suction is similarly important.
J• El. Prophylactic antibiotics should be given if symp-
r‘ toms have been present for more than 24 hours.
h‘ HYDROSTATIC REDUCTION.— When m
; is,. fants present with less than 24 hours of symptoms.
..> '. hydrostatic reduction is a successful treatment in 60
to 70% of patients Barium enema can be used for
^ hydrostatic reduction of intussusception The en
ema bag is suspended more than 1 metre above the
entry ofbarium enema into small bowel loops is characteristic of successful reduction. The patient also becom
abruptly well. Only after seeing these signs it can be assumed that the intussusception is reduced. Glucagon
can be injected intravenously to produce relaxation of the smooth muscle of the intestine and thus facilitates
reduction by hydrostatic method. This has been used with success in different institutions.
If the hydrostatic reduction is successful, the infant is kept on intravenous fluid for 2 days and then oral
fluids are started. If hydrostatic method fails to reduce intussusception everything should be made ready for
immediate operation
Contraindications to hydrostatic reduction(i) When symptoms are existing for more than 24 hours;
(ii) There are evidence of intestinal obstruction (straight X-ray finding); (iii) Tenderness of abdomen; (iv)
Peritonitis; (v) Intestinal performation.
OPERATIVE TREATMENT.— Exploration is carried out through right lower paramedian incision.
Reduction is started by squeezing the most distal part of the intussusception proximally. Slowly the
intussusception will be reduced. The last part of the intussusception is the most difficult part to reduce. The
part should be taken out of the abdomen and is covered with warm saline-soaked pack. This will reduce the
oedema. After 5 minutes the apex of intussusception is squeezed through the ileocaecal valve to the terminal
ileum. After reduction it is found that the caecum and appendix are often congested and oedematous. If the
blood supply to the appendix is seen compromised, appendicectomy should be performed.
In difficult cases, the following methods are tried :
1. Cope's methodThe little finger is inserted into the neck of the intussusception and all adhesions
between the intussusceptum and intussuscipiens should be divided. Manipulative method of reduction is ag
attempted at.
2. The thumb in front and four fingers behind are placed at the apex of the intussusceptum and gradually
the pressure is increased. This will squeeze the oedema out from that region and will help to push the
intussusceptum through the ileo-caecal valve.
Due to earlier diagnosis the number of irreducible intussusception is decreasing very' fast.
RESECTION.— The indications of resection are :— (i) If the intussusception cannot be reduced by
manipulative procedures, resection of the intussusception should be performed, (ii) A frankly gangernous
bowel should be resected without attempting reduction of the intussusception, (iii) When there is polyp, a
tumour or Meckel’s diverticulum, it should be resected.
The whole intussusception is resected with primary ileocolostomy. The ileum is cut proximal to the
intussusception and the proximal end is anastomosed end-to-side with the transverse colon distal to the
intussusception The whole mass is brought out of the abdominal wound by mobilisation. The abdominal
wound is closed around the colon. Actual resection of the colon is done extra-peritoneally and the colon is
drained by means of a large rubber tube. This drainage will relieve tension at the suture line. Later on, the co
is closed in layers and remains extra-peritoneally over which the abdominal wound is sutured.
POSTOPERATIVE C ARE.—Fluid support, antibiotics and intestinal decompression are continued. If the
is seriously toxic he may require full intensive care support, even mechanical ventilation. Intravenous fluid s
continued till peristalsis returns.
Prognosis.— If properly treated, the postoperative course is usually short and uneventful. Recurrence wit
hydrostatic or operative reduction is about 3% (1 to 10% in various series). Previously it was thought that rec
should be operated on straightway. But this is not true nowadays and hydrostatic reduction may be tried in t
there is no specific contraindication to hydrostatic reduction.
DUODENAL ATRESIA
The common area of blockage is just below the ampulla of Vater. Duodenal obstruction may be complete a
duodenal atresia or partial as in (i) duodenal web or (ii) stenosis, (iii) annular pancreas and (iv) malrotation o
Clinical features.— Obviously vomiting is the most common and early manifestation of this condition. I
of cases it is bilious vomiting as the obstruction in the duodenum is below the opening of the common bile d
may not be bilious and it may contain only clear gastric contents if the obstruction is above the opening of th
bile duct. Generalised abdominal distension alongwith bilious vomiting is mainly caused by malrotation and
volvulus. The new bom with upper G.I. tract obstruction may or may not pass meconium
Straight X-ray ofthe abdomen or more particularly air-contrast upper gastrointestinal series will show dou
deformity.
Treatment—The duodenum can be adequately decompressed via nasogastric tube, so surgical treatmen
urgent. A careful search should be made to exclude other congenital abnormalities such as cardiac and the c
abnormalities (since 30% of these cases have trisomy-21). On the other hand surgery is immediately necessa
malrotation and midgut volvulus. So the diagnosis must be perfect that it is a case of duodenal atresia and n
Atresia, stenosis and annular pancreas should be by-passed by duodeno-duodenostomy or duodeno-jejuno
anastomosis is performed between the most dependent portion of the proximal distended duodenum and t
below the obstruction. Duodeno-duodenostomy is usually performed by end-to-end anastomosis and duod
is performed by end-to-side anastomosis. Between these two operations duodeno-jejunostomy is more popu
presence of bile duct, portal vein, pancreas makes duodeno-duodenostomy a rather risky operation. There i
gastrojejunostomy as it is a potentially ulcerogenic operation and is not physiological..
Webs can be excised through a vertical duodenal incision, which is closed horizontally.
Gastrostomy should be performed routinely for proper decompression of the anastomosis. A tube is pa
the gastrostomy and through the anastomosis for decompression in the early postoperative days.
MIDGUT VOLVULUS
This condition is due to defect in the rotation of midgut, which takes place during the intrauterine life a
is bom with volvulus of the midgut.
Pathology.— FIRST STAGE OF ROTATION.— During foetal life, around the 6th week, the midgut is so e
ated that it cannot be accommodated inside the abdominal cavity. So the physiological hernia occurs and the m
the umbilical cord with a rotation of 90°. Hence the proximal limb (the limb nearer to the stomach) lies to th
the distal limb to the left. This relative position is maintained so long as the hernia persists, but during this t
which forms the small intestine becomes elongated and coiled, but the colic part of the hernia elongates less
has no tendency to become coiled. At the 10th week, when the foetus has attained a length of 40 mm, the pe
has enlarged sufficiently to accommodate all the abdominal viscera and the hemia undergoes rapid reductio
SECOND STAGE OF ROTATION.— The manner in which reduction of physiological hemia occurs is im
as at this stage the gut undergoes a further process of rotation. As the gut re-enters the abdominal cavity the
intestine, which return first, enter to the right of the dorsal mesentery and they thrust it over to the left passi
the superior mesenteric artery and thus the superior mesenteric a
runs in front of the horizontal part (3rd part) of the duodenum in
adult. The caecum is the last part to re-enter the abdomen and it i
carried dorsally and to the right, where it lies in contact with the
caudal aspect of the liver. The portion of the colon which adjoins
caecum (the transverse colon) now lies ventral to the duodenum a
rotation of the gut is completed. The mesentery of the descending
colon is thrust against the dorsal abdominal wall by the coils of sm
intestine. In this way the descending colon loses its mesentery an
becomes retroperitoneal. The transverse colon now lies in front of
coils of small intestine and fuses with that part of the dorsal
mesentery which becomes the greater omentum. Its mesocolon
persists.
THIRD STAGE OF ROTATION.— During the later months
of the foetal life the caecum descends to the right iliac fossa and the
ascending colon is thus formed.
Developmental abnormality.— If there is incomplete
second stage and third stage rotations, the duodenum lies to the r
of the superior mesenteric artery and the caecum remains in the r
upper quadrant. The bands (Ladd’s bands atttempting to fix the
caecum to the abdominal wall strangle the duodenum and may
obstruct it. The entire midgut and its vessels are therefore suspen
on a narrow pedicle which may twist. Thus midgut volvulus result
in high intestinal obstruction and may cause midgut ischaemia if
Fig.50.6.— Diagrammatic representation of superior mesenteric blood supply is cut off.
midgut volvulus (Volvulus neonatorum). Clinical features.— Irritability and bilious vomiting are
symptoms. There may be mild upper abdominal distension and tenderness. If blood supply is at stake, there
stools and features of peritonitis and septic shock may set in.
Straight X-rays will show little gas throughout the intestine and a few scattered gas-fluid levels. A barium
may show displaced caecum and gives a clue to the abnormality in the rotation.
Treatment.— Early operation is the treatment of choice to prevent strangulation of the gut. The whole of s
intestine is taken out from the abdominal cavity and base of the mesentery must be inspected. The volvulus
and the bands are divided particularly the Ladd’s bands. Then Ladd procedure is performed. In this procedur
duodenum and upper jejunum is repositioned on the right side of the abdomen. Appendicectomy is perform
caecum and the ascending colon are placed on the left side of the abdomen. This is done to spread out the ba
mesentery. Any obviously necrotic bowel resulting from delayed treatment should be resected and primary
is done to restore continuity. It is not necessary to place any holding suture in the caecum and the whole duo
bands are fully divided. When the viability of the midgut is doubtful the volvulus is reduced and returned t
After 24 to 36 hours a ‘ second look’ has to be made to see the condition of viability ofthe bowel. Any necroti
be resected and primary anastomosis should be made to restore continuity.
MECONIUM ILEUS
This is a condition of intestinal obstruction caused by impaction of meconium in the distal ileum. This co
usually associated with cystic fibrosis and lack of pancreatic enzymes which leads to viscosity of the meconi
is usually small, beaded and relatively empty containing only dry mucus.
Clinical features.— Infant may bom with distended abdomen due to intestinal obstruction. Occasionally
be ascites either due to inflammatory response to the ischaemic over distended small intestine or to meconiu
from perforation. If distension is absent at birth, it develops rapidly with failure of passage of meconium. Vo
follows and it is usually bilious. Rectum is small and empty.
STRAIGHT ABDOMINAL X-RAY in upright position will show enormously distended small bowel wit
fluid levels. Small bubbles of gas are trapped in the inspissated meconium in the terminal ileum and thus pr
characteristic ‘ground glass’ appearance. Occasionally meconium spillage is identified by intraperitoneal cal
A Contrast enema preferably with gastrografin will show a microcolon and terminal ileum filled with pel
meconium.
Treatment.— Gastrografin contrast enema is the first line of treatment of meconium ileus. Dilute gastrog
passed through the colon under fluoroscopic control into the meconium filled ileum. Since gastrografin is hy
and acts by absorbing fluid from the interstitial fluid into the intestinal lumen maintaining adequate hydrati
meconium will be soft and will be rejected naturally. The enema may be repeated at 12 hour intervals over s
until all the meconium is evacuated pier rectum. Large volumes of intravenous balanced salt solutions are n
the fluid loss.
If this technique fails resection of the distended terminal ileum is performed and the distal bowel is flash
N-acetyl cysteine. This will again dissolve meconium pellets. Now this can be performed by Bishop-Koop an
In this technique the affected segment is resected. The distal segment is brought out through the abdominal
ileostomy. The proximal segment is anastomosed to the distal segment in end-to-side fashion just within the
One should not attempt at ‘milking’ the meconium at the time of operation lest this should damage the bow
the ileostomy wash out of inspissated meconium should be carried out with Gastrografin or Mucomyst.
893
CHAPTER-43
THE PERITONEUM,OMENTUM AND

MESENTERY
THE PERITONEUM
The peritoneal cavity is a potential space containing the abdominal viscera. The peritoneum provides a friction-less surface over which
the abdominal viscera can freely move, and the mesothelial lining secretes fluid that serves to lubricate the peritonea] surfaces. The
peritoneum covers the inner side of the parietes, which is known as parietal peritoneum. Peritoneum also covers the outer surface of
the abdominal viscera which is known as visceral peritoneum. Between these two layers lies the potential space, which is known as
peritoneal cavity. Normally, there is about 100 ml of clear straw-coloured fluid in the adult. The quality and quantity of this fluid may
change with various pathological conditions.
STRUCTURE.—The peritoneum is a single layer of flat mesothelial cells resting on a layer of fibroelastic tissue containing macrophages,
fat cells and some collagen and elast-c fibres. Beneath the peritoneum, supported by a small amount of areolar tissue, lies a network
of lymphatic vessels and reach plexus of capillary blood vessels from which absorption and exudation occur. The parietal peritoneum
is reinforced by the transversalis (endoabdominal) fascia which lies external to it. The visceral peritoneum is identical with the serosa
or capsule of the intra-abdominal organs. It must be remembered that peritoneal cavity is a completely closed sac except the ends of
the fallopian tubes in case of females through which it is communicated with the exterior. The peritoneal cavity is divided into the
greater sac and the lesser sac. The lesser sac lies behind the stomach and lesser omentum, whereas the greater sac covers the whole
of the abdomen including the pelvic cavity.
PHYSIOLOGY.— There is great ability of the peritoneum to absorb substances — fluid, electrolytes and blood. This absorption
occurs primarily through fenestrated lymphatic channels on the undersurface of the diaphragm. There is a tendency that the peritoneal
fluid moves upward probably due to decreased intra-abdominal pressure, the upward movement of the diaphragm duing expiration and
by capillary attraction. In a few minutes coloured particles which are left in the peritoneal cavity reach the lymph vessels underneath
the diaphragm. This upward movement of peritoneal fluids is responsible for the subphrenic collection of many intra-abdominal infections.
The surface area of the peritoneum is about 2 m2, which is approximately identical to the area of the skin. The peritoneum acts as
a semipermealile membrane and permits transport ofwater, electrolytes and peptides in both directions according to theosmotic concentration.
Absorption from the peritoneal cavity of particulate matter takes place when the size is less then 10 (im. Such particulate matters may
include bacteria, formed blood elements, proteins etc. Such absorption takes place through stomata to the lymphatic channels. These
lymphatic channels are also responsible for the appearance of the so-called sympathetic pleural effusions whenever transabdominal
inflammatory process takes place as invariably subdiaphragmatic lymphatic plexus is involved early.
The bi-directional transfer property of the peritoneum is used in peritoneal dialysis. By adjusting the composition of the dialysate,
excess water, sodium, potassium and products of metabolism can be removed from the blood stream. A variety of drugs can be removed
by peritoneal dialysis.
The peritoneum heals very rapidly following injury. Even large defects can be restored in a matter of hours. The majority of cells
involved in healing of the peritoneal wound are derived by differentiation of stem cells present within the subperitoneal tissues in the
surrounding area. Growth of mesothelial cells occur from margins of the defect. If normal peritonea] healing is delayed or incomplete,
adhesions form. The adhesions may be transient, eventually resolving as delyed healing becomes complete or they may be permanent
in nature. Fibrins elaborated from the inflamed peritoneal mesothelium are the scaffold upon which adhesions are built. Formation of
adhesions is a protective response helping to localise the peritonea] insult and is also an adaptive healing response which helps to bring
additional blood supply to the ischaemic injured areas of the peritoneum. The beneficial effects of adhesions should always be remembered.
NERVE SUPPLY.— The parietal peritoneum is innervated by both somatic and visceral afferent nerves and so it is quite sensitive
same as the skin. The anterior parietal peritoneum is most sensitive, while the pelvic peritoneum is the least sensitive. Local injury
or inflammation of parietal peritoneum leads to protective voluntary muscular guarding and later on to reflex muscular spasm, the signs
which are indicative of such insult. Perception of pain is indicated as localised tenderness and rebound tenderness.
In contrast to the parietal peritoneum, the visceral peritoneum receives afferent innervation only from the autonomic nervous system
and hence is insensitive. However visceral afferent nerves respond well to traction or distension and less to pressure, but no receptors
for pain or temperature.
PERITONITIS
Peritonitis is inflammation of the peritoneum either a portion or all of the parietal and visceral, surfaces
of the peritoneal cavity. Peritonitis may be either septic or aseptic, bacterial or viral, primary or secondary,
acute or chronic. Most surgical peritonitis is secondary to bacterial contamination from the gastrointestinal
tract. So when a suigeon refers to ‘peritonitis’ without qualification, the clinical situation is acute suppurativ
bacterial peritonitis.
Primary peritonitis refers to inflammation of the peritoneal cavity without a documented source of
contamination.
894
Routes of bacterial invasion.— 1. Direct invasion either due to (i) penetrating injury of the abdomen
or (ii) due to perforation of some part of the gastrointestinal tract or (iii) due to insertion of foreign material,
drain, dialysis tube etc.
2. Local extension from (i) a neighbourhood inflamed organ e.g. cholecystitis, appendicitis etc. or (ii)
migration through the devitalised gut wall e.g. strangulated hemia or (iii) via the fallopian tubes.
3. Through blood stream e.g. general septicaemia.
Natural factors which prevent general peritonitis.—
1. Peritoneal cavity is divided into various compartments, so that the pus cannot go to the other compartm
unless the involved compartment has been filled with pus. Firstly the peritoneal cavity is divided into the
greater sac and the lesser sac. The greater sac is again divided into abdominal cavity and pelvic cavity. The
abdominal cavity is again divided into supracolic and infracol ic compartments by transverse colon and mes
So if supracolic compartment is involved due to perforation of peptic ulcer, pus can only reach the infracolic
compartment either by overflowing the supracolic compartment over the colon or by way of the right paraco
gutter to the right iliac fossa and from there to the pelvis.
2. Adhesions usually form around the affected organ as flakes of fibrin appear from the exudate from
the inflamed peritoneum. This also causes adherence ofthe coils of intestine around the inflamed organ. Mor
the greater omentum also envelops the inflamed oigan or area so as to localise the peritonitis as far as possib
Peristalsis also becomes sluggish to help in localisation of peritonitis.
3. Postoperative drains also helps to drain the pus from the local collection instead of allowing it to spread
all over the abdomen.
There are certain FACTORS WHICH CAUSE DIFFUSE PERITONITIS. These are —
(a) Ingestion of food or even water stimulates peristaltic activity which helps in spreading of the peritonit
Administration of purgative or enema also helps in the similar fashion.
(b) Sometimes a hollow viscus suddenly perforate without giving an opportunity to the nature to localise
peritonitis. Such cases are seen in case of peptic ulcer perforation or perforation of inflamed appendix.
(c) When the virulence of the organism is so great that localisation becomes impossible.
(d) In children localisation is less evident due to small omentum, which cannot reach any part of the
abdomen to wrap up the inflamed organ.
(e) Rough handling helps in spreading peritonitis.
(f) When there is deficiency of the immune mechanism e.g. in Acquired Immune Deficiency Syndrome
(AIDS) or when the patient is on steroids.
Causing organisms.— A mixed or polymicrobial bacterial flora usually is present in patients suffering
from suppurative peritonitis. The most common offending organisms are E. coli, anaerobic bacteroides, anae
and aerobic streptococci, enterococci and ciostridia. Less frequently staphylococci and Klebsiella pneumonia
may be seen.
CLINICAL FEATURES.
Localised peritonitis.— The signs and symptoms of the causative lesion are the main features. There will
be complaint of pain at or near the causative lesion. As the pain increases, vomiting is often complained
of.
On examination, the most important feature is localised tenderness. As soon as the local peritoneum is
involved there will be guarding and rigidity of the abdominal wall with rebound tenderness. The pulse rate
will rise alongwith the body temperature.
If the pelvic peritoneum is involved due to salpingitis or inflamed appendix in the pelvic position, abdom
signs will be minimal, but tenderness will be elicited in rectal and vaginal examinations.
With conservative treatment majority of the localised peritonitis cases resolve. In only ‘/s th of cases abscess
may follow. Very occasionally localised peritonitis may become diffuse peritonitis mainly in untreated cases.
DIFFUSE OR GENERALISED PERITONITIS.—
The clinical feature of this condition can be conveniently described under 3 stages.
1. The FIRST STAGE is known as peritonism i.e. irritation of the peritoneum. This is due to irritation
of the peritoneum caused by perforation or inflamed viscus near about TTie pain is severe and is made worse
by breathing and movement. It is first experienced at the site of the lesion and gradually spreads all over
the abdomen. The patient may or may not vomit.
On examination, the patient usually lies still. There is little change in the pulse and temperature. Tendernes
THE PERITONEUM, OMENTUM AND MESENTERY 895
rigidity and muscle guard are constantly present over the site of the lesion. It must be remembered, in this
context, that in case of pelvic peritonitis or peritonitis of the lesser sac there is hardly any tenderness or rigidi
of the anterior abdominal wall. So rectal and vaginal examination alongwith palpation of the flanks are highl
important. Infrequent bowel sounds will be heard as the paralytic ileus has not set in.
Diagnosis should be made at this stage, as if the condition is allowed to continue the chance of survival
of the patient will be minimised. Two features are important for diagnosis at this stage viz. onset of pain
with dramatic suddenness and presence of muscle guard and rebound tenderness.
2. The SECOND STAGE is known as the stage of reaction. At this stage the irritant fluid becomes diluted
with the peritoneal exudate. The intensity of the symptoms dwindles, although the fire is still burning under
the ashes. The patient feels comfortable and nothing is more diplorable than the attending doctor sharing
the patient’s comfort.
On examination muscle rigidity continues to be present though it may be softer the other two new features
at this stage are obliteration of liver dullness and appearance of shifting dullness. Paralytic ileus sets in with
silent abdomen on auscultation. Rectal examination will still elicit tenderness in case of pelvic peritonitis in
the rectovesical or rectouterine pouch.
At this stage straight X-ray in sitting posture will reveal gas under the diaphragm in 70% of cases.
3. The THIRD STAGE is the stage of diffuse peritonitis. At this stage the patient has gone a step further
towards the grave. The pinched and anxious face, shunken eyes and hollow cheeks — the so called facies
hippocratica is quite characteristic of this condition.
On examination the pulse rate rises and becomes low in volume. There is persistent vomiting. The abdome
becomes silent and increasingly distended. There is board-like rigidity of the abdomen. The patient finally
collapses into unconsciousness.
1. Serum amylase estimation may show raised level in case of peritonitis due to perforated duodenal ulcer,
acute pancreatitis etc. There will be high leucocyte count.
2. Examination of peritoneal aspirate is not always necessary, though it may be helpful in certain cases
of peritonitis. Presence of pus indicates bacterial peritonitis. Bile stained fluid indicates perforated duodenal
cancer. Blood in the aspirate indicates intraperitoneal bleeding or acute pancreatitis. In latter case there will
be high amylase level.
3. Straiglu X-ray of the abdomen in sitting posture demonstrates free gas under the diaphragm in about
70% of cases. If the patient is too ill to be seated, a lateral decubitus film is also useful. In late cases there
may be dilated gas-filled loof * of bowel with multiple fluid levels in third stage, which indicates paralytic
ileus.
MANAGEMENT.— The management includes both therapeutic and diagnostic efforts. While therapeutic
efforts are directed to resuscitate the patient, diagnostic efforts should be continued to find out the exact cause
of peritonitis.
Conservative treatment—This in fact is the preoperative preparation which includes (1) fluid resuscitation
and correction of electrolyte imbalance, (2) Nasogastric intubation for decompression, (3) Antibiotics and
(4) Ventilatory support.
1. FLUID RESUSCITATION.— The patients are usually hypovolaemic with disturbed electrolytes. Large
volumes of fluid may be needed very rapidly till blood volume and urine output are restored. Till the central
venous pressure (CVP) reaches the level of 10 cm of water, fluid administration should be at a rapid rate.
The most frequent mistake made is that the rate of initial fluid administration is too slow. The slow rate
is undertaken for fear of precipitating congestive cardiac failure. If CVP is monitored, there is no chance
of occurrence of congestive cardiac failure. A central venous catheter should be placed through the subclavian
or internal jugular vein to assess intravenous replacement. Fluid administered must include crystalloid to rep
water and electrolytes. Colloids (albumin or plasma) should also be given to restore an effective volume quick
Plasma protein depletion needs correction as inflamed peritoneum leaks protein continuously. Whole blood
or packed red blood cells are administered, if needed, to correct anaemia and to maintain an adequate red
cell mass.
2. NASOGASTRIC INTUBATION.— Decompression is performed by nasogastric intubation to evacuate
the stomach and reduce accumulation of additional air in the paralysed bowel. Urinary catheterisation is also
important to monitor urinary output. Oral feeding is absolutely prohibited till the bowel sounds return, tende
disappears and the abdomen becomes soft following resolution of peritonitis.

Vital signs such as temperature, blood pressure, pulse and respiration rate are recorded every 4 hours
or more often if needed. Biochemical evaluation which includes measurements of serum electrolytes, gluc
creatinine and alkaline phosphatase and a urinalysis should be performed as required.
3. ANTIBIOTICS.— Antibiotics that are known to be effective against the full spectrum of aerobic and
anaerobic gastrointestinal bacteria should started as soon as possible, as the acutal organism may not be k
Antibiotics that are effective against E. coli are mostly used. These are cephalosporins, aminoglycosides,
cefainycin and chloramphenicol.Tetracyclineand ampicillin are also active against many coliforms. The dr
effective against bacteroids are clindamycin, chloramphenicol, metronidazole and the newer cephalospori
4. VENTILATORY SUPPORT.— Oxygen is administered to help the response to the increased metabol
demands of peritonitis which are so often associated with impairment of pulmonary ventilatory function
mild hypoxia. A nasal catheter supplying oxygen at about 5 litres per minute is sufficient prior to inductio
of anaesthesia. Assessment of respiratory function should be made clinically noting the work of breathing
and apparent tidal volume. If impairment is suspected, measurement of ventilatory volume and arterial b
gases are indicated. When the patient’s arterial oxygen tension falls below 70 mm Hg, ventilatory support
with inspired gas concentration of 40% oxygen should be given.
VASOACTIVE DRUGS.— Administration of these drugs has not been very effective. Only when
staphylococcus aureus, an exotoxing-producing organism is the causative agent, combination of phentolam
and propranolol significantly improves the condition of the patients. Drugs with alpha-adrenergic effects
of limited value as this artificial attempt to maintain blood pressure by inducing vasoconstriction is poten
harmful.
STEROIDS.— Recent clinical studies support the idea that large doses of steroids reduce the mortality
risk in suppurative peritonitis. Steroids are needed in most of the cases. An initial intravenous dose of 30
mg/kg methylprednisolone or 5 mg/kg dexamethazone is given over 5 to 10 minutes shows a beneficial r
and no additional injection is usually needed. If no response is seen after two doses in the interval of 3 to
4 hours, continued administration is of no use.
ANALGESICS should not be administered to patients until diagnosis is made. Analgesia may obscure
abdominal findings and gives rise to difficulty in establishing a firm diagnosis. Once a decision on diagno
and operation has been made, pain may be relieved with potent narcotics e.g. morphine intravenously.
Operative management.— Operation is mainly aimed at to correct the underlying cause. Every attempt
should be made to perform the operation as soon as possible.
The incision of choice is midline vertical incision, though some surgeons prefer right paramedian incisi
or even transverse incision for better healing of the wound. Transverse incisions are particularly better in
children below 2 years ofage due to more susceptibility of these patients towards postoperative wound de
In case of localised peritonitis however incision is made over the region involved.
As mentioned above the aim behind surgery is to correct the underlying cause. In case of perforated
appendicitis, appendicectomy should be made, only in rare cases however appendicular abscess may be d
only. In case of acute perforated diverticulitis with generalised peritonitis resection of the involved segmen
of sigmoid colon should be performed followed by end-to-end suturing or temporary end colostomy. In ca
of ulcerative colitis, total proctocolectomy with ileostomy is the treatment of choice, though in occasional
grave cases only terminal ileostomy may be made. In case of perforated peptic ulcer, either suturing of the
peptic ulcer or definitive operation of the peptic ulcer is performed if the patient is fit for that. In case of
gangrenous cholecystitis, cholecystectomy should be the treatment of choice, though in occasional grave ca
only cholecystostomy may be performed. Only in case of acute pancreatitis, conservative treatment is the
As soon as the abdomen is opened, odour of the peritoneal fluid is of signiGcance. In case of lower sma
intestinal perforation the odour is faeculous, whereas in case of upper G.I. tract perforation above the
duodenojejunal flexure, the peritoneal fluid is almost odourless. So a preliminary diagnosis can be made ju
after opening the abdomen. Odour also depends on the type of infecting organism. In case of E. coli, usual
no odour is detected, whereas in case of infection by anaerobic streptococci or bacteroids or Clostridium a
penetrating foul odour can be detected. The general rule is that aerobic infections do not produce marked
odour, whereas anaerobes do.
PERITONEAL TOILET.— All peritoneal pus, pseudomembranes, losely adherent fibrins and other exud
should be completely removed. Contents of any localised collections orabscesses should be completely evac
This is called ‘debridement of exudate' or ‘peritoneal debridement’.
This should be followed by irrigation with saline solution of all parts of the peritoneal cavity until the
effluent is clear. It has been noticed that if peritoneal lavage is made with antibiotic solution using kanamyc
or bacitracin solution, the incidence of wound infection and general mortality is considerably reduced. Even
postoperative peritoneal lavage with an antibiotic solution has been proved successful in patients with seve
peritonitis who fail to improve despite correction of source of infection and adequate fluid therapy and syst
antibiotics. The irrigation catheters are placed during operation if postoperative antibiotic lavage is anticipa
DRAINAGE.— The drains, particularly sump-suction drains are highly important in these cases. But rece
lots of controversial reports have been published and it has been shown that placement of drains in case of
non-localised, generalised peritonitis is of no benefit In fact, presence of drains in such cases is harmful
since it not only interferes with peritoneal defence mechanism, but also provides access for exogenous bacte
contamination. However drains are undoubtedly of great help in cases of localised peritoneal fluid collectio
CLOSURE.— In case of midline sutures the linea alba are sutured as a single layer with polypropylene
or nylon taking generous bites of tissues on either side. In case of right paramedian or transverse incision,
the closure is performed in the usual fashion. The skin and subcutaneous layers of the wound usually should
be left open. A few layers of fine gauze soaked in antibiotic solutions are used to cover the subcutaneous
tissue. Dry gauze dressings are then placed to cover the wound. All dressings including those within the
wound are removed after 48 hours and are replaced with similar coverings. Delayed primary closure of the
skin can be performed after 4 to 5 days if the wound remains healthy.
A few surgeons are in the opinion of treating generalised peritonitis by leaving the abdomen completely
open. The major difficulties with this technique are evisceration and poor efficacy of the subsequent healing
wound. It also requires a quite aseptic ward to treat, which is often not possible.
POSTOPERATIVE MANAGEMENT.— Intravenous fluids, nasogastric aspirations and antibiotics are
continued. Urine output, pulse, blood pressure, temperature and blood gases are monitored frequently. Whe
the results of antibiotic sensitivity of the peritoneal pus are available, due consideration should be given to
change the antibiotic therapy to the most specific and least toxic of the sensitive drugs.
Complications.—
1. Paralytic ileus.—Paralytic ileus is not uncommon following generalised peritonitis. The peculiar feature
is that pain is conspicuous by absence and there is distension of the abdomen. The bowel sounds are irregula
or almost absent. Straight X-ray shows multiple gas-filled loops with fluid levels.
2. Intestinal obstructions due to peritoneal adhesion.— This complication is quite common following
peritonitis. When a patient complains of a central colicky abdominal pain following history of peritonitis,
this complication should be thought of. It is more common following localised peritonitis, X-ray may reveal
gas-filled small intestine with fluid levels.
3. Residual abscesses.— Two places are quite common for residual abscesses. These are pelvic abscess
and subphrenic abscess following generalised peritonitis. These are discussed below.
SUBPHRENIC ABSCESS
Surgical anatomy.— There are five subphrenic spaces in the upper abdomen between the diaphragm and the liver by
disposition of various peritoneal folds. Of these five spaces four are intraperitoneal and only one is extraperitoneal.
1. RIGHT ANTERIOR INTRAPERITONEAL SPACE.— This space lies in front and above the right lobe of the liver. It is bounded
posteriorly by the upper layer of the coronary ligament and the right triangular ligament, and to the left by the falciform ligament. The
common causes of abscess in this space are perforated duodenal ulcer, perforating cholecystitis, duodenal stump ‘blow out' and very
rarely appendicitis.
2. RIGHT POSTERIOR IN 1KAPERTTONEUM SPACE (Rutherford Morison's hepatorenal pouch).— This space lies beneath the
right lobe of the liver and in front of the right kidney. It is bounded above by the lower layer of the coronary ligament, in front by
the inferior surface of the right lobe of the liver and behind by the diaphragm and anterior surface of the right kidney. In recumbent
position this is the lower most space of the body, so pus often accumulates in this space. Abscess in this space is caused by cholecystitis,
perforated duodenal ulcer, appendicitis or following upper abdominal surgery.
3. LEFT ANTERIOR INTRAPERITONEAL SPACE.— This space is bounded behind by the left triangular ligament and lefl lobe
of the liver, lesser omentum and anterior surface of the stomach; to the right by the falciform ligament and to the left by the spleen,
gastrosplenic ligament and diaphragm. The common causes of abscess formation in this space is following operations on the stomach,
the spleen or the splenic flexure of the colon.
4. LEFT POSTERIOR INTRAPERITONEAL (Lesser sac).— It is bounded in front by the lesser omentum and posterior surface
of the stomach and greater omentum and behind by the structures forming the stomach bed e.g. the left kidney and suprarenal, pancreas,
transverse mesocolon, transverse colon and the diaphragm. The lesser sac is communicated on the right through the forearm of Winslow
with the greater sac.
5. THE MEDIAN EXTRAPERITONEAL SPACE (Bare area of the liver).— This space is bounded above by the upper layer of
the coronary ligament and below by the lower layer of the coronary ligament and on the left by the inferior vena cava. Abscess in
this space usually develops from amoebic hepatitis or pyogenic liver abscess.
Causative organisms.-— Bacteriology of the subphrenic abscess is almost similar to the bacteriology of gen
peritonitis, though anaerobic organisms slightly dominate.
Clinical features.— The symptoms and signs of subphrenic abscess are very elusive. That is why an old
adage still holds good today — ‘pus somewhere, pus no where detected, that means under the diaphragm’
SYMPTOMS.— Often there is a past history of localised or generalised peritonitis of the abdomen or
some infective focus in the abdomen. The patient was doing good, except recently he is again feeling indisp
with recurring or persistent fever. Fever is typically intermittent or spiking in character in the beginning, th
it becomes progressively more persistent as the abscess matures. The fever is often accompanied with chills
and tachycardia. These are the result of transient episodes of blood stream invasion from the abscess. The
condition of the patient steadily deteriorates, with wasting and anorexia. The patients sometimes complain
of pain in the epigastric region or referred pain to the shoulder of the affected side due to irritation of the
sensory fibres of the phrenic nerve at the diaphragm which is referred along the descending branches of th
cervical plexus (C3, 4 and 5).
Intensity of symptoms may be modified by administration of antibiotics, which suppresses the infection
although it fails to cure the abscess. So it is often preferable to discontinue antibiotic therapy when presenc
of subphrenic abscess is suspected.
LOCAL EXAMINATION.— If the abscess has involved the anterior spaces, abdominal examination ma
reveal tenderness and rigidity. Occasionally a swelling may be palpable. Examination of the chest is always
important, as in majority of cases there may be evidence of basal effusion or empyema.
1. BLOOD EXAMINATION.— Invariably the patients with subphrenic abscess will show absolute
leucocytosis. The E.S.R. is always elevated. Blood cultures may document septicaemia and may identify the
organisms involved in the abscess.
2. STRAIGHT X-RAY of the abdomen may demonstrate presence of gas under the diaphragm or air-flui
level under the diaphragm. On screening, the diaphragm is often seen elevated with impaired movements.
Chest X-ray may show pleural effusion.
3. CT SCAN is quite helpful, particularly in obese patients.
4. ULTRASOUND EXAMINATIONS are also helpful in diagnosing subphrenic abscess.
5. Scans using gallium (67Ga) have been used and have proved successful in localising subphrenic absce
Radio-gallium collects in the areas of inflammation and in intra-abdominal abscesses. But it must be remem
that there is limitation of using this scan by the fact that this radioisotope is excreted through the colon and
the colon content must be fully evacuated before localising accurately the abscess collection.
Management— When suppuration and abscess have formed, surgical intervention is indicated to drain
the abscess. The essential feature of surgical management is to establish adequate drainage. As many patien
are nutritionally depleted and septic, urgent preparation with attention to fluid resuscitation, parenteral nu
administration of antibiotics and appropriate monitoring measures should be instituted preoperatively. Ext
toneal approach is preferred.
PERCUTANEOUS DRAINAGE.— Percutaneous needle aspiration and closed catheter drainage have be
proposed as an alternative to operative drainage. Usually computerised tomography is used to localise the
abscess and to find the ‘window’ for needle and catheter insertion. The ‘window’ is that portion of the absc
which is in contact with the abdominal wall without any intervening viscera. Ultrasound is then used to gu
the percutaneous needle, guide wire and ultimately the catheter. The success rate of this method is about
80%.
Operative drainage.—Right subphrenic abscesses are preferably drained using a lateral subcostal incision
The incision is made from the tip of the 11th rib and carried obliquely and anteriorly parallel to the costal
margin. The dissection is largely extraperitoneal until the abscess cavity either anteriorly or posteriorly loca
is approached.
A left subphrenic abscess is best drained through posterior extraserous approach through the bed of the
12th rib after removal of the outer part of the 12th rib. In this posterior approach the pleura must not be
opened. If the abscess is situated anteriorly on the left side, a similar subcostal incision may be employed
as performed for the right subphrenic abscess. It is important in approaching the left subphrenic abscess to
avoid injury to the spleen.
If a swelling is detected in the subcostal region or in the loin indicating subphrenic abscess, an incision
should be made over the site of maximum tenderness or over the area where oedema is maximum. Through
this region it is possible to reach the abscess cavity without opening or contaminating the general peritoneal
cavity.
PELVIC ABSCESS
Pelvic abscess is quite common and probably the commonest site of intra-abdominal abscesses. Pelvic absce
often follows a ruptured appendix (pelvic position), infected fallopian tube, ruptured colonic diverticulum
and other pelvic inflammatory diseases.
Clinical features.— Pus may accumulate in pelvic cavity with serious constitutional disturbances. The
patient may complain of poorly localised, dull and lower abdominal pain. Irritation of the urinary bladder
and/or the rectum producing urgency and frequency or diarrhoea and tenesmus may be only symptoms rece
in a few cases.
EXAMINATION.— Unless the abscess involves the anterior abdominal wall no physical sign will be
present on examination of the abdomen. However the abscess usually can be palpated directly by rectal or
vaginal examination. The typical pelvic abscess bulges as a tender mass into the anterior rectal wall. This
is usually soft cystic. If left untreated pelvic abscess may finally rupture into the rectum and the patient recove
spontaneously. In women, the swelling, which is soft and cystic, is palpated in the posterior fornix.
Treatment— As abscess anywhere in the body the pus should be drained by incision either through the
rectum (in case of males) or through the vagina (in case of females). Incision for drainage should be delayed
until formation of the pyogenic membrane or a definite abscess to exclude injury to the small bowel or other
intraabdominal viscera. In fact when the most prominent part of the abscess presenting rectally or vaginally
begins to soften, the condition is now ready for drainage. Using a speculum or a proctoscope, the abscess
should be exposed. The presence of pus is confirmed by needle aspiration. The needle is placed in situ as
a guide and a sharp incision with a fine bladed knife is made into the abscess cavity. The cavity should
be explored with a finger. Loculations should be broken down and the cavity is thoroughly irrigated. It is
difficult to retain drain in the pelvic abscess cavity. To ensure proper drainage, daily dilatation of the tract
is made digitally or with an instrument till the abscess cavity becomes obliterated in a few days.
TUBERCULOUS PERITONITIS
The incidence of tuberculous peritonitis has declined over the past several decades. This is now a rare
disease. It usually occurs in patients who are malnourished or have cirrhosis.
In majority of cases it is the secondary involvement and there is some primary focus elsewhere in the
body. Though sometimes the primary focus remains obscure, almost always it is later demonstrated to be
in the lung. The various possible sites of primary are — (i) pulmonary tuberculosis, (ii) tuberculous mesenteric
lymph nodes, (iii) tuberculous ileocaecal region, (iv) tuberculous kidney and (v) tuberculous pyosalpinx. Majo
of cases are due to reactivation of latent peritoneal tuberculosis which had developed by haematogenous sprea
from a pulmonary focus.
Acute tuberculous peritonitis.— Sometimes tuberculous peritonitis presents as acute peritonitis and often
the abdomen is opened. Straw-coloured fluid with tubercles scattered althroughout the peritoneum and greate
omentum is found inside the abdomen. Immediately the fluid is evacuated and a portion is sent for bacteriolog
study. A portion of the diseased omentum is removed for histological study. The wound should be closed
without drainage. This type of presentation is quite rare.
Chronic tuberculous peritonitis.— This is more common form of presentation. The onset is insidious,
presenting with fever, anorexia, weakness and weight loss. Four forms are usually seen —
1. ASCITIC FORM.— Ascites is almost always present in more than half of the cases. There is diffuse
abdominal pain.
On examination dilated subcutaneous veins will be obvious. The abdomen is very slightly tender and
the feel is typically described as ‘doughy abdomen’. Shifting dullness can be elicited readily. Rarely one
can feel a transverse solid mass in the upper abdomen which is nothing but rolled-up greater omentum in
with tubercles.
Clinical manifestations of generalised tuberculosis are seen in Yard of patients which includes anorexia
weight loss and night sweats.
Special Investigations.—(i) A chest X-ray should always be performed to exclude presence of tuberculosi
of the chest
(ii) Tuberculous organisms can be found out in 80% of cases from ascitic fluid if more than 1 litre
of fluid is cultured. The ascitic fluid has increased protein content, there is lymphocytosis and a glucose
concentration below 30 mg per dl. Blind peritoneal biopsy is positive in only 60% of cases.
If these measures do not establish the diagnosis, peritoneoscopy and guided direct biopsy of the perito
are recommended. As a last resort exploratory laparotomy with peritoneal biopsy may be undertaken to e
the diagnosis.
2. Encysted form.— In this form only part of the abdominal cavity is affected. The affected portion
presents as an intra-abdominal swelling. When the swelling is in the pelvis, an ovarian cyst is often diagno
3. Fibrinous form is characterised by fibrinous deposits in the abdomen which cause adhesions of the
coils of intestine. The coils become dilated and act as blind loop giving rise to wasting, abdominal pain and
steatorrhoea.
These cases may require operation in the form of plication or excision of strictured portion of the ileum
as sometimes the adhesions are accompanied by fibrous stricture of the ileum as well. Usually conservativ
treatment with antitubercular drugs after adequate surgery rapidly cures this condition.
4. Purulent form occurs only when it is secondary to tuberculous salpingitis. Usually the tuberculous
pus is surrounded by adherent intestine and omentum. Sometimes the cold abscess points towards the sur
near the umbilicus.
Usually general treatment of tuberculosis is enough to cure this condition, though occasionally surgery
may be required to evacuate cold abscess or to relieve intestinal obstruction.
On the whole tuberculous peritonitis is no more a dangerous condition due to advent of proper antitub
drugs. Usually after 1 year of treatment the patients become asymptomatic. But tuberculous peritonitis oft
heals with formation of dense fibrous adhesions which often liable to the future development of intestinal
obstruction. Treatment with prednisone during the initial months of antituberculous drug therapy reduce
incidence of adhesion formation and subsequent development of obstruction.
Pneumococcal peritonitis.—This disease is presented as one of the two forms — 1. Primary and 2. Seconda
1. Primary pneumococcal peritonitis is much more common. The patient is often a malnourished girl in the first
decade. In these cases pneumococci have got access through the vagina and fallopian tubes into the peritoneal cavity.
It must be remembered that after 10 years pneumococcal peritonitis is most unusual.
2. Secondary pneumococcal peritonitis is usually secondary to the pneumococcal infection of the upper respiratory
tract or the middle ear. The peritonitis occurs due to blood borne infection.
CLINICAL FEATURES.— The onset is usually sudden. Pain is complained of mostly in the lower half of the abdomen.
Associated rise of temperature and frequent vomiting and diarrhoea are almost characteristic. Increased frequency of
micturition is complained of due to pelvic peritonitis. On examination there is lower abdominal rigidity. In case of secondary
peritonitis there is often high respiratory rate.
TREATMENT.— Conservative treatment of general peritonitis with antibiotic particularly effective against pneumococci
is often successful. Only when diagnosis is not very certain, laparotomy becomes necessary to exclude other conditions
and to take a little peritoneal fluid for culture and sensitivity test. Odourless and sticky exudate is almost diagnostic of
pneumococcal peritonitis found on exploration of the abdomen.
Bile peritonitis.— The common causes of biliary peritonitis are (1) Following perforation of the gallbladder, (2) Leakage
of choledochal cyst; (3) Following biliary surgery — damage to the common bile duct, slipping of ligature of the cystic
duct, divided cholecystohepatic duct, divided accessory bile ducts; (4) Following gastrointestinal surgery — Anastomotic
leakage of the jejunum, duodenal stump blow out in case of Polya type partial gastrectomy.
The case is presented with signs of diffuse peritonitis with a degree of shock. Slight jaundice may or may not be present.
Infected bile is more dangerous than sterile bile.
TREATMENT is according to the condition. Early surgical intervention is very much essential as soon as the patient
is resuscitated to a respectable level.
Postoperative peritonitis.— Such peritonitis may occur following leakage from suture line. The most important feature
of this type of peritonitis is the problem to diagnose. As there is no abdominal pain associated with this condition and
tenderness being masked by presence of a recent wound, diagnosis becomes difficult. Failure of expected betterment of
the patient’s condition following operation is probably the most important guide to diagnose. The patient becomes ill with
rise in pulse rate and peripheral circulatory failure. This is often wrongly attributed to be due to pulmonary collapse.
TREATMENT is usually a second operation.
THE GREATER OMENTUM

Structure.— The greater omentum consists of double sheet of flattened epithelium, within which there are epiploic
vessels, lymphatics and nerves in areolar tissue with variable amount of fat. The structure hangs in a double fold from
the greater curvature of the stomach down to almost pelvis and then folds on itself and moves up in front of the transverse
colon and mingles with the transverse mesocolon to end at the anterior border of the pancreas. The right border is attached
to the pylorus and first portion of the duodenum while the left border forms the gastrosplenic ligament. The right side
is usually longer and heavier and may possess tongue-like process extending into the pelvis. The omentum in infants
is usually underdeveloped. With growth, there is elongation and thickening of the omentum due to deposition of fat within
its layers.
Rutherford Morison called the greater omentum as ‘policeman of the abdomen’. Whenever there is any pathology
within the abdomen, the greater omentum attempts to limit the infective process. In case of acute appendicitis, it has
often been found to wrap the appendix to prevent its rupture and general peritonitis. The greater omentum has also been
seen trying to seal the perforated peptic ulcer. It has also been seen to plug the neck of the hernial sac to prevent coils
of intestine to move into the hernial sac. In case of tuberculous peritonitis or carcinomatosis peritonei, the greater omentum
becomes rolled on itself to produce an upper abdominal lump. It has often been questioned how the omentum can act
as ‘policeman of the abdomen’. It has no spontaneous or ameboid activity. But the displacement probably occurs as a
result of postural changes of the individual, diaphragmatic excurtions and intestinal peristalsis and ultimately the omentum
becomes fixed to the inflamed structure by the fibrous exudate. The usefulness of the omentum in inflammatory processes
is also related to its bectericidal and absorptive properties.
Torsion of the omentum.— It is a condition in which the greater omentum twists on its long axis to an extent causing
vascular obstruction. This may vary from mild vascular constriction producing oedema to complete strangulation leading
to infarction of the distal part.
Torsion may be primary or idiopathic when cause is not known and this is rare, though a few predisposing factors
have been suggested e.g. bulky omentum, accessory omentum, tongue-like projection of omentum, irregular distribution
of fat within the omentum and a few precipitating factors e.g. heavy exertion, coughing, straining, overeating causing
hyperperistalsis and sudden change in body position, are incriminated.
Omental torsion may be secondary when it is associated with intra-abdominal localised inflammation, post-surgical
scarring, cysts or tumours at the free end of the omentum or presence of internal or external hemiae. Secondary omental
torsion is more common.
PATHOLOGY.— Omental torsion usually occurs in clockwise direction, either the whole omentum or more often
a small portion undergoes torsion. In the distal omentum there is oedema and congestion. There may be haemorrhagic
extravasation into the peritoneal cavity. If not excised, the torsioned omentum becomes atrophic and fibrotic and may
be autoamputated.
CLINICAL FEATURES.— Omental torsion is more commonly seen in the 4th or 5th decade of life and males dominate
in the ratio of 2:1. Pain is the most important symptom, which is usually sudden with gradual increase in intensity. The
pain is mostly periumbilical or may be localised to the right lower quadrant of the abdomen. Nausea and vomiting occur
in less than half the patients.
On examination tenderness is usually present. Occasionally a mass may be palpable.
TREATMENT consists of resection of the distal part of involved omentum. In secondary torsion the cause should
be corrected.
Cysts of the omentum.— These are rare. True cysts are mainly lymphatic cysts either by the growth of congenitally
misplaced lymphatic tissue or by obstruction of the lymphatic channels. Pseudocysts result from fat necrosis, haematoma
or foreign body reaction.
CLINICAL FEATURES.— True omental cysts are usually found in children or young adults, though the aged people
have also been involved.
These may be asymptomatic and only large cysts become palpable and produce symptoms like heaviness or pain or
torsion.
Solid tumours of the omentum are extremely rare. The most common is the metastatic carcinoma, the primary source
of which is usually in the stomach or colon or pancreas or ovaries.
Other benign tumours may occur e.g. lipomas, fibromas, neurofibromas and leiomyomas.
Surgical resection is the only treatment. Incase of benign tumours local excision is enough. In case of metastatic carcinoma,
removal of the primary as well as total omentectomy may be performed if the other organs are not involved.
THE MESENTERY
The wound ofthe mesentery.— Mesentery may be injured by either penetrating or non-penetrating abdominal trauma. Most penetrating
injuries are due to stabbing or gun-shot wound. In these circumstances injury to other organ is frequent. Isolated injury to the mesentery
and mesenteric vessels following blunt abdominal trauma is rare and in 60% of cases it is associated with rupture of intestine.
CLINICAL FEATURES.— There is no special clinical manifestation of this condition. Depending on rapidity of the haemorrhage,
varying degrees of shock are noticed. Abdominal pain, tenderness, rigidity are almost always seen. Straight X-ray of the abdomen is
not helpful in diagnosis.
TREATMENT.— Injury to the mesentery and small intestine should always call for an immediate exploration of the abdomen.
Basically treatment consists of controlling the bleeding vessels. If the tear in the mesentery is a large one and particularly transverse,
the blood supply to that part of the intestine is cut off. So that portion of the small intestine should be resected with end-to-end anastomosis.
Small tear in the long axis of the mesentery without any damage to the vascular supply of the any part of the small intestine may
be only sutured. It must be remembered before securing any bleeding vessel in the mesentery that this vessel supplies a part of small
intestine. So ligature of that vessel means that part of the intestine has to be resected followed by end-to-end anastomosis. If long segments
of small intestine are of doubtful viability, it is best to leave in place to be re-examined at a second operation 24 hours later. If a small
segment of small intestine is of doubtful viability that segment may be exteriorized to see later on whether it remains viable or not.
If it remains viable, the segment is returned to the abdomen, whereas if it loses viability, that portion of small intestine should be resected.
NON-SPECIFIC MESENTERIC LYMPHADENITIS

This condition is one of the common causes of acute abdominal pain in children. Its true incidence is no
known, as it can only be accurately diagnosed at laparotomy and as it is a self-limiting disease. It is still
considered to be the most common cause of inflammatory enlargement of the abdominal lymph glands. T
disease is important because of its clinical similarity to several acute adbominal conditions which require
immediate surgical intervention, particularly acute appendicitis.
Aetiology.— The cause of this disease is not known. Virus has been blamed to cause this disease. Respira
infection often precedes an attack of non-specific mesenteric lymphadenitis. Sometimes appendicitis has b
incriminated to cause this condition, though in majority of these cases the appendix is found absolutely n
However appendicectomy reduces the incidence of further attack. It seems likely that this condition repre
a reaction of some type of material absorbed from the small intestine, probably a hypersensitive reaction
to a foreign protein.
Pathology.—Mostly the ileocaecal mesenteric lymph nodes are enlarged. This may be due to the concent
of mesenteric nodes in this area and because of abundant lymphatic drainage of the intestinal tract from th
distal ileum. Moreover stasis of intestinal content in the terminal ileum favours absorption of bacterial pro
or toxins from the bowel lumen.
In the beginning the para-ileal or juxta-intestinal glands are mainly affected. Later on there is involveme
of the intermediate and central groups of lymph nodes. The lymph nodes remain discrete, firm and enlarg
The gross appearance of the intestine and appendix remains normal. Small amount of clear serous fluid is
frequently present within the peritoneal cavity. The nodes and free peritoneal fluid are usually sterile on c
The nodes which are nearer the attachment of the mesentery are usually the larger.
Occasionally specific mesenteric adenitis due to beta haemolytic streptococci may occur. In these instanc
there is acute febrile illness with signs of peritoneal involvement.
Clinical features.— Patients are usually children, before they reach puberty. There is no sex predilection.
The ratio between this condition and acute appendicitis is 1:10.
Very often there is a history of upper respiratory tract infection or sore throat. Pain is usually the first
symptom. It varies in intensity from mild ache to severe colic. The initial pain is usually in the upper abdo
though eventually the pain localises to the slight lower quadrant. The patient often cannot indicate the exa
site of pain. Nausea and vomiting occur in ‘Ard of cases. On examination, there may be slight tenderness
ill the right lower quadrant of the abdomen, slightly higher and more medial and less in intensity than tha
of acute appendicitis. Voluntary guarding is sometimes present, though true muscle rigidity is rare. Early
in attack, the temperature is moderately elevated, though often the temperature may be normal. Shifting te
is a valuable sign, which clearly differentiates this condition from acute appendicitis. If the patient is laid
on the left side for 5 minutes, the maximum tenderness will move towards the left than the original site,
but in case of acute appendicitis tenderness remains in the same spot
In 20% of cases there may be lymphadenopathy elsewhere, most often in the cervical region. So the neck
axillae and groins should be palpated for large lymph nodes.
On rectal examination there may be tenderness on the right side of the pelvis, which is also a very charact
sign.
Leucocyte count is often over 10,000 per cubic mm.
Treatment—As the prognosis is excellentand complete recovery is almost assured without specific treatme
so no specific treatment is required except assurance and bed rest. Only when it is difficult to exclude acute
appendicitis, exploration is justified and it is safer to perform appendicectomy.
In about *A th of cases patients will have fitrther bouts of abdominal pain during childhood.
Tuberculosis of mesenteric lymph nodes.— Tuberculosis of mesenteric lymph nodes is a rare entity, even much rarer tha.i non-specific
mesenteric lymphadenitis. Affection of mesenteric lymph nodes is usually through Peyer’s patches and mesenteric lymphatics to the
lymph nodes and the causative organism is often bovine tubercle bacilli. This condition is extremely uncommon nowadays and due
to pasturisation of milk presence of bovine tubercle bacilli in the milk has also been reduced considerably. So quite a few cases may
be due to human tubercle bacilli due to ingestion of sputum in case of pulmonary tuberculosis.
CLINICAL FEATURES.— These cases are usually presented in one of the following six forms
1. With abdominal pain.— These cases are often presented with abdominal pain and on examination there is tenderness to the right
of the umbilicus. Occasionally firm discrete tender lymph nodes may be palpable.
2. With general symptoms.—Often these cases are presen ted with loss of appetite, evening rise of temperature etc. i.e. general symptoms
of tuberculosis.
3. With radiological demonstration.— Occasionally these cases are presented only when straight X-ray of the abdomen is performed
for some other reason. Calcified tuberculous lymph nodes are seen on straight X-ray.
4. With features almost similar to those of appendicitis.— Sometimes these cases are presented with abdominal pain and vomiting,
tenderness and rigidity in the right iliac fossa, the features which are usually come across in cases of subacute appendicitis. Straight
X-ray may show calcified lymph nodes.
5. With intestinal obstruction.—Caseating mesenteric lymph nodes may cause adherence of coils of small intestine leading to intestinal
obstruction.
6. With mesenteric cysts.—Tuberculous lymph nodes may caseate and ultimately a cold abscess may develop which remains confined
between the leaves of the mesentery giving rise to a cystic swelling of the mesentery almost simulating a mesenteric cyst.
TREATMENT.— General conservative treatment of tuberculosis which has been described in detail in thechapter of ‘Special Infections'
is usually enough to cure this condition. Only when intestinal obstruction or a cyst develops which is not cured or resolved by such
general treatment requires surgical intervention. In case of intestinal obstruction, the adhesions and caseating nodes are dissected oul.
In case of cyst the cyst is excised. A vigorous postoperative antitubercular regime is continued.
MESENTERIC CYSTS
Mesenteric cyst is also a rare entity and is occasionally come across by a surgeon. The main three types of cysts which are seen
in the mesentery are — 1. Lymphatic cyst, 2. Enterogenous cysl and 3. Dermoid teratomatous cyst.
1. Lymphatic cyst.— This is the commonest variety and arises from the congenitally misplaced lymphatic tissue that has no efferent
communication with the lymphatic system. The cyst is thin walled and composed of connective tissue lined by flat endothelium. The
fluid inside the cyst is the clear lymph, occasionally there may be chyle of varying consistency.
2. Enterogenous cyst is developed from a diverticulum at the mesenteric border of the intestine which has become detached from
the intestinal canal during embryonic life. This may also develop from duplication of the intestine. The cyst is lined by muscle and
mucous membrane and the content of the cyst is yellowish-brown or colourless mucin. This cyst usually derives blood supply in common
with the portion of the small bowel it develops from, so during excision of the cyst while ligating the blood vessel it may be required
to resect that portion of the bowel supplied by the same artery.
3. Dermoid teratomatous cyst.— This is extremely rare in the mesentery. This cyst contains structures derived from entoderm,
mesoderm and ectoderm. It is more often found as a retroperitoneal cyst.
Clinical features.— Mesenteric cyst is most often seen in the 2nd decade of life. It is usually presented as : (a) Recurrent attacks
of abdominal pain and on examination a lump is detected in the umbilical region, (b) A painless abdominal swelling near the umbilicus
which is cystic in nature and moves freely in a plane right angle to the attachment of the mesentery but does not move along the line
of attachment. Occasionally (c) an acute abdomen with torsion of the mesentery containing the cyst giving rise to intestinal obstruction
or rupture of the cyst giving rise to haemoperitoneum and shock or haemorrhage into the cyst giving rise to acute abdominal pain.
Special Investigations.— Barium meal X-ray is often diagnostic as the coils of small intestine will be found displaced by the cyst
or some portion of the lumen of the small intestine may be narrowed.
CT scan and ultrasound are helpful in diagnosing this condition. Ultrasound is particularly helpful in case of painless enlargemenl
of the cyst.
Treatment— If the case is as a painless abdominal swelling, exploration of the abdomen and enucleation of the cyst without disturbing
the blood supply to the small intestine, is the treatment of choice.
When the case is presented as torsion of the mesentery and intestinal obstruction, the mesentery is derotated and if the small intestine
is completely viable, enucleation of the cyst is enough.
If there is loss of viability of the small intestine, that portion of the intestine should be resected, the cyst is excised and end-to-end
anastomosis of the small intestine is performed.
904
CHAPTER - 44
'TITR’ WPMTFOPM
A XjLEj V HiJtvlVilJr A PPPMTITY
UxviVI Jt JBixN UJL2v
ANATOMY
Embryological ly, the appendix is a continuation of the caecum from its inferior tip and the appendix is shaped like an inverted pyramid.
The caecum is bilaterally sacculated in early childhood with the appendix still at the inferior tip. Further growth of the caecum is unequal.
Rapid growth of the right side and anterior aspects of the caecum rotate the appendix to its adult position on the posteromedial aspect below
the ileocaecal valve. As the appendix varies considerably in length, the relation of the base of the appendix to the caecum is essentially
constant. The base of the appendix can be marked on the surface as the McBurney's point which is situated at the junction of the lateral
V,rd and medial 2/,rds of the line joining the anterior superior iliac spine and the umbilicus. McBumey’s point is the classical site of
tenderness in appendicitis.
The vermiform appendix is present only in human beings and certain anthropoid apes. In many herbivorous animals there is a big caecal
diverticulum in which bacteriolytic break down of cellulose takes place. Presence of lymphoid tissue in wall of the appendix is characteristic
of human vermiform appendix.
Appendix varies in length, but the average length is about 10 cm in adult. On longitudinal section the irregular lumen of the appendix
is encroached upon by multiple longitudinal fold of mucous membrane.
Structure.— From without inwards the structure of appendix is as follows :
(i) A serous coat is composed of peritoneal coat, which covers the whole of the appendix except along the narrow line of
attachment of the mesoappendix.
(ii) Muscle coat — it consists of outer longitudinal muscles and inner circular muscles as seen in case of small intestine. The
longitudinal muscle is formed by coalescence of the three taeniae coli at the junction of the caecum and appendix. Thus the taeniae,
particularly the anterior taenia may be used as a guide to locate an elusive appendix. The inner circular muscle is continuation of the same
muscle in the caecum. The peculiarity of the musculature of the appendix is that there are a few gaps in the muscular layer called ‘hiatus
niuscularis'. Through this infection from the submucous coat directly comes to peritoneum and regional peritonitis occurs. Through these
hiatus muscularis appendix may perforate when there is a rise in tension inside the organ.
(iii) Submucosa.—The submucous coat of the appendix is very rich in lymphoid tissue. It contains lymphoid follicles which are
known as abdominal tonsil’. The number of submucosal lymphoid follicles are few at birth. This number gradually increases to a pick of
approximately 200 follicles between the ages of 12 and 20. After that the number is gradually reduced and reaches to about half at the age
of 50 years and almost absence of lymphoid tissue at the age of 60 years.
(iv) The mucous coat resembles that of large intestine, but crypts of Lieberkuhn are less frequent.
The mesoappendix passes behind the terminal ileum and joins with the mesentery of the small intestine. The appendicular artery runs
in the free border of the mesoappendix. In early childhood the mesoappendix is very transparent and blood vessels may be seen through
it. In adults it becomes laden with fat in the same proportion as the mesentery of the ileum.
Blood supply of the appendix.—The APPENDICULAR ARTERY is the main arterial supply to the appendix. It is a branch of the
lower division of ileocolic artery and passes behind the terminal ileum to enter the mesoappendix a short distance from the base of the
appendix. It then comes to the free border of mesoapppendix. The mesoappendix often does not continue upto the tip of the appendix. In
this case the artery lies in direct contact with the tip of the appendix. It must be remembered that the appendicular artery is an end artery.
Inflammation of the appendix will cause thrombosis of the artery. This precipitates gangrene of the tip of the appendix and ultimate
perforation.
Accessory appendicular artery supplies the base of the appendix and this artery should be properly ligated otherwise haemorrhage will
continue after appendicectomy. This is a branch of the posterior caecal artery.
The APPENDICULAR VEIN, which follows the appendicular artery along the free border of the mesoappendix, drains into the ileo
colic vein which is a tributary of the inferior mesenteric vein i.e. the portal venous system. Inflammatory thrombus may cause suppurative
pylephlebitis in case of a gangrenous appendicitis.
Lymphatic vessels draining the appendix travel along the mesoappendix to drain into the ileocaecal lymph nodes.
Various anatomical positions.— (i) Retrocaecal position (commonest position—70%)— the appendix lies behind the caecum
although in majority of cases in an intraperitoneal location. Peritoneum reflects from the posterior surface of the caecum to the parietis at
variable level of the caecum but usual|y opposite the ileocaecal junction. Only in case of long retrocaecal appendix the tip of the appendix
remains in the retroperitoneal tissue close to the ureter.
(ii) Pelvic position (second most common position —25%).— The appendix hangs from the caecum and tip lies near the beam of
the pelvis.
(iii) Subcaecal (2%).
(iv) Splenic (I %) — that means the tip of the appendix is towards the spleen. Which may be either pre-or post-ileal i.e. lying in front
or behind the terminal part of the ileum.
(v) Paracaecal (1%).
(vi) Paracolic (1 %) — by the side of the ascending colon on the right or left side (behind the terminal part of ileum.) The tip if often
THE VERMIFORM APPENDIX 905
in the extraperitoneal tissue.

Functions of appendix.— The question comes in as surgeons often take appendicectomy not seriously and even perform while
doing other operations like cholecystectomy or operations for peptic ulcer. It should be appreciated that it is not a vestigeal organ
and it does play a useful role in the defence mechanism of the body.
(i) The lymphoid follicles present in the appendix act for maturation of B lymphocytes.
(ii) The appendix participates in the secretory immune mechanism in the gut. Appendix forms an integral part of the 'gut
associated lymphoid tissues’ (GALT) and forms globulin for immune mechanism. Yet appendix is not indispensable in this regard
and removal of the appendix produces no detectable defect in the functioning of the immunoglobulin system.
(iii) In 1960s it was shown that carcinoma of colon was found to he higher in incidence following appendicectomy than in
comparable control groups. But subsequent studies could not prove its soundness.
These are quite rare. These may occur in the form of (i) agenesis, (ii) duplication, (iii) diverticula
and (iv) left sided appendix.
(i) Agenesis.— The vermiform appendix is absent. Occasionally appendix may not be seen dur
ing appendicectomy following acute appendicitis. This is due to sloughing of the appendix.
(ii) Duplication.— A few cases have been reported where there are double appendix.
(iii) Diverticula are very rarely seen in appendix.
(iv) Left sided appendix.— In case of situs inversus viscerum there may be transposition of the
thoracic and abdominal viscera. In that case appendix with caecum will be seen on the left side. In
certain cases of non-rotation of the midgut the caecum and appendix may be seen as midline structure
or on the left side.
APPENDICITIS
There are four types of appendicitis : (i) Acute appendicitis; (ii) Subacute appendicitis; (iii) Re
current appendicitis and (iv) Chronic appendicitis.
ACUTE APPENDICITIS
Incidence.— Acute appendicitis is the most common acute surgical condition of the abdo
men. Acute appendicitis may occur at all ages, but is most commonly seen in the second and
third decades of life. It must be noted that there is some relation between the amount of lym
phoid tissue in the appendix and incidence of acute appendicitis. Both are pick in the middle of
the second decade. In children, appendicitis is not common as the configuration of the appendix
makes obstruction of the lumen unlikely. After middle age the risk of developing appendicitis
in future is quite small.
There is hardly any difference of sex incidence, but this condition seems to be more commonly
seen in teenaged girls.
Aetiology and Pathogenesis.—
1 .OBSTRUCTION OF THE LUMEN seems to be the dominant factor in production of acute
appendicitis. This may occur due to obstruction of the lumen, obstruction in the wall or obstruction
from outside the wall.
(a) In the lumen faecolith and hyperplasia of submucosal lymphoid follicle are the major causes
of obstruction. Other causes are intestinal worms e.g. round worm, thread worm etc., vegetables,
fruit seeds, inspissated faeces or barium from previous X-rays. A faecolith is composed of inspis
sated faecal material, epithelial debris, bacteria and calcium phosphates. Sometimes a foreign body
may be incorporated into the mass. Presence of a faecolith is so important that it even provides an
indication for prophylactic appendicectomy.
(b) In the wall, stricture (due to fibrosis from earlier inflammation) or neoplasms of which carci
noid is the commonest are the main causes. A stricture in the appendix usually indicates previous
appendicitis which has resolved without surgery. Presence of carcinoma or carcinoid may be sus
pected when acute appendicitis occurs in the middle age or the elderly people.
(c) Outside the wall adhesions and kinks are common in this group.
2. DIET.— Diet plays an important part in producing appendicitis. Rise in incidence of appendi
citis amongst the highly civilised society is mostly due to diet which is relatively rich with fish and
meat and departure from simple diet rich in cellulose and high residue.
3. SOCIAL STATUS.— This disease has been considered to be the disease of aristocratic fami
lies. This is more often seen in individuals of social classes I and II rather than class IV.
4. FAMILIAL SUSCEPTIBILITY.— In certain families this disease is more often seen than at
large. May be, it is due to the peculiar position of the organ which predisposes to infection.
PATHOLOGY.— Acute appendicitis may be of obstructive variety or non-obstructive
variety.
Obstructive acute appendicitis.— Obstruction is the major factor in the production of acute
appendicitis. In many cases of early appendicitis the appendix lumen is patent despite the presence of
mucosal inflammation and lymphoid hyperplasia. Lymphoid hyperplasia ultimately narrows the
lumen of the appendix leading to luminal obstruction. Obstruction increases the severity of the
inflammatory process. The sequence of events following obstruction of the appendix is probably as
follows :
A closed loop obstruction is produced continuing normal secretion of the appendicular mu
cosa rapidly produces dis
tension. The luminal capac
ity of the appendix is very
small — 0.1 ml. Secretion
of as little as 0.5 ml distal
to the block raises the in
traluminal pressure to about
50 cm of water. Unfortu-
- nately enough, appendicu-
’■ 'VWflB lar mucous membrane is ca-
' jHHnBPM pable of secreting at high
^ pressure. Such distension
stimulates visceral nerve
endings concerned with
pain. This produces vague,
| dull and diffuse pain in the
Jp umbilical and lower epigas-
..■ffSiMir ‘-^SH lr'c region according to
1 ; 7'|£9p nerve supply of the appen-
© v" dix (T10) (Referred pain).
Peristalsis is also stimulated
■
Sjtt by such sudden distension,
Wfc. | which produces cramping
m Pam superimposed on the
dull, visceral pain charac
teristic in early appendi
citis. Such distension of
appendix with mucus is
known as ‘mucocele of appendix’.
Rapid multiplication of the resident bacteria of the appendix also increases distension. Con
tinued mucous secretion and inflammatory exudation increase intraluminal pressure, obstruct
ing lymphatic drainage. Oedema and mucosal ulceration may gradually develop, so that the
bacteria may pass into the submucous layer. Resolution may occur at this stage either in the
response to antibiotic therapy or spontaneously. If the intraluminal pressure increases further
venules and capillaries are occluded, but arteriolar inflow continues resulting in engorgement
and vascular congestion of the appendix. At this stage of distension, reflex nausea and vomit
ing start, the visceral pain also becomes severe. Pressure within the organ increases so much
that it exceeds venous pressure. Gradually the serosa is involved, more due to presence of hia
tus muscularis and local peritonitis ensues. As soon as this develops there is shifting of pain to
the right lower quadrant. At this stage the greater omentum and loops of small bowel become
adherent to the inflamed appendix preventing the spread of peritoneal contamination. This re
sults in a phlegmonous mass or appendicular abscess. Sometimes or very rarely appendicular
inflammation may resolve before causing local peritonitis, leaving a distended mucus-filled
appendix, known as a mucocele of the appendix.
When this bacterial invasion occurs to the deeper coats, fever, tachycardia and leucocytosis
develop as a consequence of absorption of bacterial toxin and dead tissue products. Distension of
appendix with pus is known as ‘empyema of the appendix’. Gradually distension increases and
arteriolar pressure is exceeded. This occurs in localised areas particularly those areas with poorest
blood supply. Ellipsoidal infarcts develop more commonly in the tip, antimesenteric border and at
the site of impaction of faecolith. Perforation may occur through such infarcts. Peritonitis is the
greatest threat of acute appendicitis, which occurs as a result of free migration of bacteria through
the ischaemic appendicular wall or through frank perforation. Factors which promote this process
include extremes of age, obstruction of the appendicular lumen, a free-lying pelvic appendix and
diabetes mellitus.
BACTERIOLOGY.— The bacteriology flora, customarily found in acute appendicitis, is a mixed
colonic flora with both aerobic and anaerobic organisms. Most frequently seen organisms are Esch.
coli, enterococci, bacteroides (gram-negative rod), non-haemolytic streptococci, anaerobic strepto
cocci and Cl. Welchii.
It must be remembered that the sequence described above is not inevitable. Some episodes of
acute appendicitis apparently subside spontaneously before they reach the acute stage. This is called
subacute appendicitis. This condition may recur. Presumably obstruction of the lumen due to lym
phoid hypertrophy or soft faecolith may spontaneously be relieved allowing subsidence of appen
dicular inflammation and its attendant symptoms.
If a full-blown appendicitis does not ensue, the appendix may turn into a ‘grumbler’
precipitating recurrent attacks. This is known as recurrent appendicitis. These attacks are
usually milder. The patients remain symptom-free between attacks and physical examination is
normal. Barium enema X-ray often shows normal filling of the appendix due to disappearance of
obstruction.
Sometimes pathological examination of the appendix may reveal thickening and scarring
suggesting old, healed acute inflammation. This is chronic appendicitis. Patients with such
appendicitis often complain of persistent right lower abdominal pain. It must be remembered that
the resected appendix must show fibrosis of the appendicular wall, evidence of old mucosal
ulceration and scarring and infiltration by chronic inflammatory cells to be designated as chronic
appendicitis.
Non obstructive acute appendicitis.— This is a less dangerous condition. Inflammation com
mences in the mucous membrane or in the lymph follicles. Gradually inflammation spreads to the
submucosa. The appendix becomes red and congested. The end artery, if involved in such inflamma
tion, its lumen will be thrombosed and localised gangrene will appear. As there is no obstruction
there is not much distension, but when the serosa is involved localised peritonitis develops and the
patient complains of pain in the right iliac fossa. Such inflammation terminates either by (i) suppura
tion, (ii) gangrene, (iii) fibrosis or (iv) resolution. Many of the subacute appendicitis, recurrent ap
pendicitis and chronic appendicitis develop from this variety.
CLINICAL FEATURES.— Symptoms.— (i) Pain is present in all patients with appendicitis.
The initial typical pain is diffuse and dull and is situated in the umbilical or lower epigastric region.
Sometimes the pain is moderately severe. Intermittent cramping may superimpose on such pain. Gradually
the pain is localised in the right lower quadrant. It takes about 1 to 12 hours for such localisation. In
some patients the pain of appendicitis begins in the right lower quadrant and remains there. Variation
in the anatomical position of the appendix will account for variation of the principal site of the pain.
In case of retrocaecal appendix, pain may be complained of more in the flank. In case of pelvic
appendicitis, pain may be referred to the suprapubic region. Malrotation of the appendix will lead to
more confusion of the site of pain.
(ii) Anorexia.— Nearly always anorexia is complained of in case of appendicitis. This symptom
is so constant that the diagnosis should be questioned if the patient is not anorectic.
(iii) Nausea, at least of some degree, is present in 9 out of 10 patients with appendicitis. Vomit
ing is variable — children and teenagers frequently vomit but vomiting may be entirely absent in
adult. Most patients vomit only once or twice. Vomiting is usually not persistent. Vomiting appears
after the onset of pain. Typically pain, vomiting and temperature constitutes Murphy’s triad of this
condition. If vomiting precedes pain the diagnosis should be questioned.
(iv) The character of bowel function is of little diagnostic value. Many patients give
history of constipation before the onset of abdominal pain. A few voluntarily submit that
defaecation relieves their pain. To the contrary diarrhoea occurs in some patients, particularly in
young children.
The sequence of symptom appearance has great diagnostic value. In over 95% of patients
anorexia is the first symptom, followed by abdominal pain and this is followed by nausea and
vomiting.
Physical signs.— (i) Temperature.— Appendicitis may cause rise of temperature, but
higher temperature is unusual with uncomplicated appendicitis. Temperature elevation is usually
restricted to 99° or 100° F (39°C). Normal temperature is often present even with advanced
appendicitis. In case of generalised peritonitis following rupture of appendicitis temperature may
shoot upto 40°C.
(ii) Pulse rate.— The pulse rate is usually normal or slightly elevated. High pulse rate should
question the diagnosis. Pulse rate increases in proportion with the temperature of the patient. In case
of spreading peritonitis following rupture pulse rate may rise upto 100 per minute.
INSPECTION.— The patient looks anxious in pain and the tongue is dry. On careful inspection,
in very acute condition, it may disclose some limitation of the respiratory movement of the lower half
of the abdomen.
PALPATION.— Presence of peritoneal inflammation can be suspected if cough or percussion on
the abdominal wall elicits pain.
(i) Systemic gentle palpation will detect an area of maximum tenderness that corresponds to the
position of the appendix (see above) and is usually located in the right lower quadrant at or near
McBurney’s point. -
(ii) Muscle guarding or resistance to palpation roughly parallel to the severity of the
inflammatory process. Early in the disease resistance, if present, consists mainly of voluntary
guarding. As peritoneal irritation progresses, voluntary muscle guarding increases and is eventually
replaced by reflex involuntary rigidity. One must try to differentiate voluntary guarding as opposed
to involuntary rigidity. Involuntary rigidity does not diminish during expiration as is seen in
voluntary guarding.
(iii) Cutaneous hyperaesthesia can be found out by light stroking of the skin of the right and left
side of the abdomen. In acute appendicitis hyperaesthesia is found over Sherren’s triangle (formed by
the anterior superior iliac spine, the symphysis pubis and the umbilicus). This ordinarily is unpleas
ant and is not a very reliable sign.
(iv) Rebound tenderness.— The classic method of demonstrating peritoneal inflammation is re
bound tenderness. In this case gentle pressure is exerted on the inflamed area and sudden release of
the hand will cause extreme pain of the patient at the inflamed area. This is called rebound tender
ness. The finding of rebound tenderness may be elicited in only half the cases.
(v) Rovsing's sign.— Pain in the right lower quadrant is complained of when palpation pressure
is exerted in the left lower quadrant. It is also called ‘referred rebound tenderness’ and when present
is quite helpful in supporting the diagnosis. Retrograde displacement of the colonic gas strikes the
base of inflamed appendix or displacement of the ilial loops to the right side of the abdomen to
irritate the inflamed appendix is the probable explanation of this sign.
(vi) Psoas sign.— This test is performed by having the patient lie on his left side. The examiner
then slowly extends the patient’s right thigh, thus stretching the iliopsoas muscle. This will produce
pain to make the sign positive. This indicates presence of irritative inflamed appendix in close prox
imity to the psoas muscle. This is possible in retrocaecal appendicitis.
(vii) Obturator test.— Passive internal rotation of flexed right thigh with the patient in supine
position will elicit pain. This positive obturator sign is diagnostic of pelvic appendicitis.
(viii) Percussion.— Light percussion on McBurney’s point will elicit pain in case of early appen
dicitis.
(ix) Auscultation of the abdomen will reveal meagre or no bowel movement on the right iliac
fossa. In spreading peritonitis following rupture of appendix abdomen remains absolutely silent and
no bowel sound can be heard.
(x) Rectal examination.— This is important and should be performed in every patient suspected
of suffering from appendicitis. Its primary function is to exclude any pelvic lesion particularly in
females. Its secondary purpose is to elicit tenderness in cases of pelvic appendicitis. In case of pelvic
appendicitis there may not be any tenderness on the anterior abdominal wall, so rectal examination is
very essential to exclude such appendicitis. When inflamed appendix lies in the pelvis, presence of a
mass or tenderness will be present on the right side of the fornix.
It must be remembered that the diagnosis of acute appendicitis is essentially clinical. It is said
that it is better to remove a normal appendix than to delay diagnosis and end-up with complications.
But one must be very rational to avoid removal of normal appendix also. There are a number of
clinical and laboratory-based scoring systems, of which Alvarado score is most widely used. It is as
follows :—
Symptoms Score
Anorexia 1
Nausea and vomiting 1
Migratory RIF pain 1
Signs Score
Raised temperature 1
Tenderness in RIF 1
Rebound tenderness 2
Tests Score
Leucocytosis 2
Shift to left (segmented neutrophils) 1
Total: 10
When the score is 7 or more it is a case of acute appendicitis and immediate operation is required.
When the score is 5 to 6, these are borderline cases, where further investigation is required to reduce
normal appendicectomy.
Special Investigation.— 1. Blood examination will reveal moderate leucocytosis ranging from
about 10,000 to 18,000 per cubic mm. with polymorphonuclear predominance. It must be remem
bered that in case of normal total and differential W.B.C. count, the diagnosis of appendicitis should
be questioned. In case of perforated appendicitis the total white cell count may rise above 18,000.
In dehydrated patients serum electrolytes and urea are to be estimated and normalised by proper
fluid therapy.
2. Urine examination.— Except for high specific gravity due to dehydration, routine urine
examination will usually reveal normal result in case of appendicitis. Only when the inflamed
appendix lies near the ureter or bladder, white cells and even red cells may be seen in the
urine.
3. X-ray examination.— There is no pathognomonic sign of appendicitis in X-ray examination.
Plain films may show a faecolith at the appendicular region (see Fig. 52.1). A distended loop of
small bowel in the right lower quadrant may be seen. Less often a distended caecum or a gas-filled
appendix may be detected. In late complicated acute appendicitis straight X-ray may reveal absence
of right psoas shadow or absence of small bowel gas in the right lower quadrant.
4. Barium enema examination.— This procedure is obviously unnecessary in most cases of acute
appendicitis in which the diagnosis is reasonably clear on clinical grounds. The positive findings to
be sought during barium enema examination are non-filling or partial filling of the appendix and
extrinsic pressure defect on the caecum producing a picture of ‘reverse 3’ on the caecum and mucosal
irregularities of the terminal ileum.
5. Chest films may be performed to exclude any disease of the base of the right lung as disease in
this area may irritate the spinal nerve to simulate the symptoms of appendicitis.
6. Ultrasonography.— As there is no specific diagnostic tool to diagnose such a common
condition as acute appendicitis and delay in diagnosis may lead to significant morbidity
and mortality, timely surgical intervention is the key treatment of this condition. Abdominal
ultrasonography has shown promise for accurate diagnosis in the management of acute right lower
quadrant pain. There are many conditions which give rise to pain at the right lower abdomen e.g.
small bowel obstruction, right sided inguinal hernia, infection of Meckel’s diverticulum,
gynaecological conditions in females e.g. twisted ovarian cyst/tumour, ectopic pregnancy,
salpingitis etc. Urological conditions e.g. ureterolithiasis, mesenteric lymphadenitis may also
cause pain in the right illiac fossa. In a study out of 100 cases of lower abdominal pain 70 were
diagnosed to have appendicular pathology by USG and of which 65 cases were confirmed to have the
pathology after laparotomy and histopathological report. All the patients with gynaecological
conditions were diagnosed accurately by ultrasonography. The overall specificity of USG in
diagnosing appendicular pathology is more than 90%, indicating ultrasonography as the most signifi
cant tool in the diagnosis of appendicitis. So this can be recommended in all cases of right lower
quardrant abdominal pain. It is also helpful to diagnose appendicular mass and even appendicular
abscess.
7. CT Scan is not required to diagnose a case of simple appendicitis, but to detect appendicular
mass, appendicular abscess or pelvic abscess this investigation is of great help. Contrast-enhanced
CT scan may be used when there is diagnostic uncertainty even after ultrasonography. Intravenous
contrast highlights inflammation surrounding the appendix and also shows faecolith and distended
appendix. But regular use of this investigation should be restricted.
CLINICAL FEATURES MODIFIED according to various anatomical positions of the
appendix.—
RETROCAECAL APPENDICITIS.— Rigidity and tenderness may not be so obvious on the ante
rior abdomen. This is because of the fact that caecum is in front of the inflamed appendix which may
be retroperitoneal and is not in contact with the parietal peritoneum of the anterior abdominal wall.
Tenderness may be present near the loin. There may be rigidity of the quadratus lumborum. ‘Cope’s
psoas test’ may be positive in this type of appendicitis. Inflamed appendix may lie in close relation
with the ureter and may cause slight pyorrhoea or haematuria.
PELVIC APPENDICITIS.— When the appendix is entirely within the pelvis there may be
complete absence of rigidity and tenderness on the right iliac fossa. Rectal examination is
helpful to detect such appendicitis. Tenderness will be present on the right side of the rectovesical
pouch or pouch of Douglas. In case of such appendicitis patient may complain of tenesmus and
diarrhoea. Cope’s obturator test is usually positive in this type of appendicitis. This is due to the
fact that inflamed appendix is in contact with the obturator internus muscle. Passive internal
rotation of the hip will cause pain in the hypogastric region. Inflamed appendix may lie in contact
with the urinary bladder and may cause frequency of micturition and a little bit of pyorrhoea and
haematuria.
PREILEAL AND POSTILEAL APPENDICITIS.— Continued irritation of the ileum will lead to
nausea and vomifing. This symptom becomes very prominent. Tenderness instead of lying on the
McBurney’s point is elicited more medially near the umbilicus. As inflamed appendix lies near the
ileum it may cause slight diarrhoea.
SUBHEPATIC APPENDICITIS.— When the caecum is higher up than its normal position and the
appendix is retrocaecal and reaches the subhepatic position, such appendicitis may give rise to diffi
culty in diagnosis. The case is often diagnosed as acute cholecystitis. In case of such recurrent ap
pendicitis or subacute appendicitis the diagnosis is made of peptic ulcer. So one must be careful and
should keep in mind such position of the appendix.
COMPLICATIONS of acute appendicitis.— 1. APPENDICULAR RUPTURE.— It must be
remembered that the use of antibiotic therapy in an attempt to avoid or postpone operation is danger
ous and is never advised. In these cases if the obstruction persists the pathology will continue to
make the appendix gangrenous and will cause rupture of the appendix. Rupture of the appendix takes
place distal to the obstruction or rarely at the place of obstruction. Contents of the distended appen
dix spill through the necrotic rent into the peritoneal cavity. General peritonitis from ruptured appen
dix is dangerous.
2. APPENDICULAR MASS (PHLEGMON).— In majority of cases as soon as the appendix be
comes gangrenous, omentum and coils of small intestine cover the inflamed appendix all around.
There is no discrete collection of pus inside. This is an attempt of the nature to prevent general
peritonitis even if rupture of the appendix occurs. Usually such appendicular mass develops on the
3rd day after the commencement of an attack of acute appendicitis. This is a tender mass on the right
iliac fossa. This mass usually resolves by conservative treatment. In untreated cases or when the
patient does not react to the conservative treatment such appendicular mass may turn into an appen
dicular abscess and becomes larger in size.
3. APPENDICULAR ABSCESS.— A progressive suppurative process in an appendicular mass
forms an appendicular abscess walled off by the omentum, inflamed caecum and coils of small intes
tine. Such abscess may follow rupture of the appendix with the expulsion of small content of the
appendix distal to the obstruction. The caecal contents cannot come out due to the occluding faecolith.
In such appendicular abscess there may be variable pyrexia and slight increase in the pulse rate.
There is definite increase of the leucocyte count with relative increase of polymorphonuclear cells.
The commonest site of the abscess is in the lateral part of the iliac fossa (from retrocaecal appendici
tis). The second common position is in the pelvis. In untreated cases lethal form of peritonitis is
produced by secoridary rupture of appendicular abscess.
4. SUPPURATIVE PYLEPHLEBITIS.— Ascending septic thrombophlebitis of the portal venous system
(pylethrombophlebitis) is a grave but rare complication of gangrenous appendicitis. Septic clots from involved
mesenteric veins produce multiple pyogenic abscess in the liver. It is heralded by chills, spiking fever, right
upper quadrant pain and jaundice.
In infants and young children, in young women, during pregnancy and in the elderly appendicitis has got
distinctive clinical settings with some peculiarities which will influence management of such cases of
appendicitis. So these cases and their peculiarities are mentioned herewith.
Appendicitis in infants and young children.— Firstly these patients are not capable of giving accurate
history and so diagnosis becomes difficult. As the diagnosis is difficult, the treatment is delayed and
complications develop. To make the condition even worse in these patients, the disease progresses more ra
than in adults — gangrene and rupture occur earlier in the course of acute appendicitis. In pre-school child
incidence of rupture rate varies from 50 to 80%. This is because of the fact that the walling-off process is les
efficient because of the small and incompletely developed greater omentum. Another problem is diarrhoea
which is not normally seen in adult appendicitis but is quite common in children. Because of diarrhoea, vom
and vague abdominal pain these patients are often admitted in the medical ward. So ‘beware of diarrhoea i
a child who complains of abdominal pain in the beginning’— these cases should be suspected to be append
and this diagnosis must be excluded.
Appendicitis in young women.— In women of 20 to 30 years of age misdiagnosis of acute appendicitis
is often made. Pain and discomfort associated with ovulation (mittelschmerz), diseases of the ovary, ruptur
ectopic gestation, salpingitis, diseases of uterus, infections and other disorders of the urinary system are oft
misdiagnosed as appendicitis. While taking history and physical examination one must be careful to exclud
these possibilities. Even in these cases role of laparoscopy has not been clearly justified. Probably in these
cases when symptoms and signs do not progress for several hours, one can exclude the diagnosis of append
by doing barium enema examination. If this visualises the appendix diagnosis of appendicitis may be ruled
out. But it must be remembered that negative exploration is to be preferred to miss a diagnosis of acute
appendicitis.
Appendicitis during pregnancy.— Appendicitis is the most common extrauterine condition requiring an
abdominal operation during pregnancy. Appendicitis occurs more frequently during the first two trimester
During first 6 months of pregnancy symptoms of appendicitis do not differ much from those in the non-pre
women. Appendicectomy should be performed in these cases as if the pregnancy is not present. Appendice
at this stage often does not disturb the pregnancy if performed before rupture of appendix, though there is
chance of miscarriage particularly in the first trimester.
During the third trimester, the problem is more, since mortality is about 20% —10 times greater than that
in the first and second trimesters. The clinical picture is also altered because of upward and lateral displacem
of the caecum and appendix as a result of enlargement of uterus. Pain becomes higher and more lateral and
diagnosis of pyelonephritis must be excluded by urine examination. Microscopical examination of urine wil
solve the problem. In addition, appendicitis in this last trimester tends to be more serious as delay in the dia
leads to increased incidence of perforation. Displaced omentum is unable to wrap up the inflamed appendi
Rupture usually follows generalised peritonitis. Appendicitis in this trimester may lead to premature delive
in '/2 of the patients.
Moreover acute pyelitis and torsion of the ovarian cyst during pregnancy can be difficult to distinguish fr
appendicitis. Early appendicectomy is the treatment of choice for appendicitis in all stages of pregnancy.
Appendicitis in the elderly.— Classic symptoms of pain, anorexia and nausea are also present in most old
patients but in less pronounced form. Pain in the right lower quadrant is often very mild and causes little in
concern. So diagnosis at early stage becomes a problem. Rigidity of the right lower quadrant is not so
pronounced in elderly patients due to lax abdominal wall. Even the case may be wrongly diagnosed as suba
intestinal obstruction. To worsen the condition enemas may be given.
Impaired blood supply and structural weakness of appendix are said to produce early perforation in thes
patients. But important than this is the delay in diagnosis. In these patients early appendicectomy should be
carried out. It must be remembered that elderly patients die because surgeons do not operate in doubtful ca
than due to misdiagnoses and removal of normal appendices.
DIFFERENTIAL DIAGNOSIS OF ACUTE APPENDICITIS

A. Abdominal causes.—
1. Acute cholecystitis.
2. Perforated, peptic ulcer.
3. Cyclical vomiting — mostly seen in children. Acetone is found in the urine and rigidity is absent.
4. Enterocolitis.— There is intestinal colic with diarrhoea and vomiting. Localised tenderness is absent.
Only pre- and post-ileal appendicitis may mimic this condition.
5. Non-specific mesenteric lymphadenitis.— The patient is usually a child below 10 years of age. This
is almost invariably associated with upper respiratory tract infection. The pain is usually diffuse less in inten
and tenderness is not sharply localised. True involuntary rigidity is rare. There is shifting tenderness, that m
if there is tenderness on the right iliac fossa the patient is turned to left for a few minutes and the tenderness
be noted to be shifted to the midline. Generalised lymphadenopathy including cervical lymph nodes often
noticed. Patient is free from pain between attacks. Examination of the blood reveals relative lymphocytosis. I
differentiation is difficult, immediate operation is a safe course, as appendicectomy often helps in resolution
the lymph nodes.
6. Intestinal obstruction.
7. Crohn's disease.
8. Carcinoma ofthe caecum.
9. Amoebic colitis.
10. Meckel’s diverticulitis.
11. Acute pancreatitis.
12. Mesenteric vascular occlusion.
B. Gynaecological disorders.—
1. Salpingitis.
2. Ectopic gestation.
3. Ruptured ovarian follicle (mittelschmerz).— It usually occurs halfway between menstrual periods i.e.
about 14th to 16th day of the menstrual period. It occurs in young girls. Ovulation results of spill of sufficient
blood and follicular fluid to produce such mild lower abdominal pain. If the right ovary is affected appendici
may be simulated. Pain and tenderness are rather diffuse. Leucocytosis and fever are absent. There is no histo
of missed period.
4. Twisted right ovarian cyst.
C. Retroperitoneal causes.—
1. Right ureteric colic.
2. Right sided acute pyelonephritis.
3. Torsion of testis — either descended or undescended testis.
4. Haematoma in the retroperitoneal tissue.
D. Thoracic diseases.—
Basal pneumonia and pleurisy.
E. Other causes.—
1. Henoch-Schoenlein purpura — usually occurs due to bleeding into appendicular and related struc
tures, which can result from blood dyscrasias. Abdominal pain may be prominent, but joint pains, nephritis a
purpura are almost always present. Purpuric manifestations should be looked for in these cases.
2. Porphyria;
3. Diabetic abdomen — indicates abdominal pain and vomiting which sometimes may precede coma.
TREATMENT.— Acute appendicitis.— Immediate appendicectomy is the treatment of choice in acute
appendicitis without rupture. Immediate appendicectomy should be performed to obviate possibility of rupture
of appendix and spreading peritonitis.
PREOPERATIVE PREPARATION.— No patient with acute appendicitis should be taken directly to operation theatre
on admission. All patients require a preoperative preparation which rarely requires more than 3 or 4 hpurs or at least 1 hour
58
before the patient is taken to operation theatre. This is more important in case of patients in whom perforation and peritonitis
are suspected.
Nasogastric aspiration is helpful in all patients with appendicitis, particularly in those with peritonitis. Intravenous fluid
replacement should be started immediately to establish a good urinary output and to replenish the loss through nasogastric
aspiration. High temperature is sometime a problem in case of children. Temperature should be brought down and it is better
that anaesthesia should not be induced in patients whose temperature is over 39°C.
Antibiotics are started immediately. Although prophylactic administration of antibiotics is a matter of controversy, the
evidence in various reports in the past decade is clearly in favour of antibiotic administration. Antibiotics are of minor benefit
unless the appendix is gangrenous or has perforated. But in cases of gangrenous appendix or perforated appendix antibiotics
play a major role in reducing the incidence of wound infection if started preoperatively.
Operation.— After the patient is anaesthetised, the abdomen is again thoroughly palpated. This will give a clear idea
regarding the size of the mass. Position of the caecum is ascertained to choose the right incision close to the appendix.
INCISION.—When the diagnosis is confirmed McBurney’s grid-iron incision is made. When diagnosis is in doubt right lower
paramedian incision is preferred. Lanz’s transverse incision is very cosmetic and should be applied in cosmetically conscious patients.
Rutherford Morison's incision and Battle’s incision are hardly used and have fallen into oblivion.
McBurney ’s grid-iron incision.— This is an oblique incision through the McBumey’s point perpendicular to the spinoumbilical line at
its junction between lateral j rd and medial | rd Though this is the classical McBumey’s incision, yet the surgeon should try to feel the
caecum and position the incision accordingly, as sometimes caecum may be abnormally placed (even sub-hepatic). The skin, fascia of
Camper and fascia of Scarpa are divided along the line of incision. The fibres of the external oblique aponeurosis are split along the line of
incision and retracted. The muscle fibres of internal oblique are now seen running perpendicular to the line of incision. These fibres and the
fibres of the transversus abdominis are separated by inserting the tip of the artery forceps and opening it. The fingers are now introduced
and these muscle fibres are retracted to expose the peritoneum. The peritoneum is picked up by two artery forceps and incised to enter the
abdominal cavity.
Lanz’.i transverse incision.— This incision is made at a level 2 to 3 cm below the umbilicus and is centred on the midciavicular-
midinguinal line. The aponeurosis and the muscles of the abdominal wall are split or incised in the direction of the skin incision. This incision
lies in the direction of skin wrinkle lines and is a better cosmetic incision than the McBumey incision. The only disadvantage of this incision
is that the rectal sheath is opened at the medial end of the wound.
Paramedian incision.— A vertical incision is made from 2.5 cm below the umbilicus 1.25 to 2.5 cm to the right of the midline and ends
just above the pubis. Skin, superficial fascia and fasciaof Scarpa are incised along the line of incision. The anterior rectus sheath is also incised
along the line of the incision. The rectus muscle is retracted laterally. The posterior rectus sheath, transversalis fascia and peritoneum are
incised in one layer with the help of two pairs of artery forceps and the abdominal cavity is entered. Its advantage is that it can be extended
above or below according to necessity. The disadvantage is that (i) the incision is not on appendicular region and lot of retraction is required
for appendicectomy. (ii) This incision is also more likely to be infected and (iii) chance of wound dehiscence is more.
Rutherford Morison 's incision.— It is similar to McBumey’s incision but it is muscle-cutting i.e. external aponeurosis, internal oblique
and transversus are cut instead of splitting the muscle fibres, thus extending the incision. All the muscles are cut along the line of incision.
So there remains chance of wound infection and wound dehiscence and subsequent hemia due to nerve injury.
Battle‘s pararectal incision.— This incision is hardly used now-a-days. There is chance of damage to the intercostal nerves supplying
the rectus muscle over and above wound infection and wound dehiscence. Enthusiastic students are referred to page no. 209 ofthe Author’s
‘A Practical Guide To Operative Surgery’ for details of this operation.
Technique of operation :
ISOLATION OF THE APPENDIX.— After opening the peritoneal cavity, the two fingers are introduced to get hold of
the caecum. Coils of ileum, which has got no taeniae coil, may be taken out. Sometimes sigmoid colon, which has got a
mesocolon is taken out. In a visceroptotic cases the transverse colon, which has got omentum attached to it, is withdrawn.
Caecum is best withdrawn by following the peritoneum on the lateral side of the abdomen and it reaches the caecum which
is relatively fixed because the ascending colon has got no peritoneum in its posterior surface. The caecum, which is relatively
whitish, which has got taenia coli and no omentum and mesocolon, is taken out of the abdomen with the aid of a pair of
Babcock’s tissue forceps. Now the anterior taenia coli is followed downwards to reach the vermiform appendix. Sometimes
it is very easy to find out the appendix, when the appendix is more or less exposed as soon as the peritoneum is incised to
ask the surgeon ‘How do you do’, so it is called ‘How do you do’ appendix. In other cases, it may be very difficult to find
the appendix out which may be fixed in the retroperitoneal tissue behind the caecum. In this case the peritoneum on the lateral
side of the caecum has to be incised to lift the caecum and appendix with it.
DIVISION OF THE MESOAPPENDIX.— All other portions of bowel are reinserted into the abdominal cavity except
the caecum and the appendix which are surrounded by a wet mop to separate them from the abdominal wound. A pair of
tissue forceps is applied to the tip of the mesoappendix. The appendix is lifted up with this tissue forceps. The mesoappendix
is pierced at its base with a mosquito artery forceps and the appendicular artery is secured with a ligature through this hole.
The mesoappendix is now divided close to the appendix till the caecum is reached. One must be careful about the presence
of accessory appendicular artery which should be held with ligature. If the appendix is kinkfcd with firm adhesions, this
division of the mesoappendix should be done in segments.

REMOVAL OF THE APPENDIX.— The base of the appendix is crushed with a pair of strong artery forceps. By this process only
the mucous and the muscular coats are crushed and curled inwards to occlude the lumen but the peritoneal coat remains unaffected. A
ligature is tied around the crushed area. A seromuscular purse-string or figure of N-suture is inserted in the caecal wall around the base
of the appendix. A pair of artery forceps is applied to the appendix 5 mm distal the ligature. The intervening lumen is emptied before
hand by momentary pressure with an artery forceps. A swab is placed beneath the base of the appendix and the appendix is divided close
to the forceps. The stump is cauterised with pure carbolic acid and is invaginated while the purse-string suture is tightened.
The appendix, the knife, the swab and other instruments which have come in contact with the contaminated mucosa of the appendix
are placed in a bowl and removed from the field of operation.
The ligature to mesoappendix is re-examined and make sure that it is not oozing. The terminal ileum is drawn out of the wound and
inspected for one metre or so to exclude the presence of kinking band of Lane, Crohn's disease, Meckel’s diverticulum etc. In female the
right uterine tube and right ovary are also palpated. Thus completing the operation, abdominal wound is sutured in layers as usual.
Treatment of appendicular mass (phlegmon).— In these cases conservative treatment (Ochsner-Sherren regimen) should be
started immediately. Nature has already localised the lesion and it is better not to disturb such localisation. Surgery at this stage is
difficult and dangerous as it is difficult to find appendix due to adhesions and ultimately faecal fistula may form. When 48 hours have
passed since commencement of the disease, presence of lump may be felt on careful palpation. With a skin pencil the lump is demar
cated.
CONSERVATIVE TREATMENT includes:
(i) Intravenous fluid with dextrose saline and Ringer solution as and when required.
(ii) Hourly nasogastric aspiration.
(iii) An intake and output chart.
(iv) Diet.— Mouth washes may be given. Otherwise nothing should be given by mouth.
(v) Antibiotic therapy.— A broad spectrum antibiotic should be given intramuscularly. Metronidazole may be given intrave
nously.
A close watch is kept on the patient while he undergoes the conservative treatment. The followings are the conditions which should
stop the conservative treatment and immediate appendicectomy should be carried out. This means, the nature is failing to control the
disease and there is a chance that the appendix may perforate any moment The conditions in favour of stopping the conservative
treatment are:
(a) A rising pulse rate; (b) Vomiting or increase in gastric aspiration; (c) Increase in the abdominal pain — suggesting an impending
spreading peritonitis; (d) Increase in the size of the lump.
Conservative treatment should make the patient better by decreasing the pain, decreasing the amount of gastric aspiration (which
indicates the return of peristalsis), temperature is lowering down and pulse rate is becoming normal and the size of the lump is reducing
considerably and ultimately disappears. About 90% of cases resolve without any problem. The patient is kept under observation for
further 4 to 5 days after resolution of the lump. Before the patient is discharged he should take normal diet. He is instructed to have
appendicectomy done (interval appendicectomy) 6 to 8 weeks after his discharge.
Treatment of appendicular abscess.— Immediate drainage under antibiotic cover is the treatment of choice. The incision for drainage is
made just medial to the anterior superior iliac spine at the level of the most prominent portion of the appendicular abscess. The muscles are split
and the lateral edge of the peritoneum is exposed. The peritoneum is pushed medially so that the mass surrounding the appendix is approached
from its lateral peritoneal aspect. If the pus is under pressure, the abscess will rupture automatically. Otherwise a finger should be slowly
introduced into the abscess and its loculations are broken down by blunt dissection. Care is taken not to breakdown adhesions walling-off the
medial aspect of the abscess mass. This technique is mainly adopted for the commonest retrocaecal appendix.
If the appendicular abscess is situated more medially the same incision for appendicectomy is made. When after opening the
peritoneum one sees appendicular abscess, it is better to drain the abscess and come out.
Appendicectomy is usually avoided during draining of the abscess, lest a faecal fistula may result due to injury to the inflamed
caecum and inflamed coils of small intestine. Appendicectomy is only performed in case of infants, if it becomes very easy, as there is
a chance of continued drainage of faeces from caecum through perforation of the appendix due to broad lumen of the appendix in infant.
A sump drainage tube should be inserted into the appendix cavity. The subcutaneous tissue and skin incision are kept open as
should be done in case of gangrenous appendicectomy to avoid wound infection. So long as the drainage continues the tube is kept in
position. When the drainage has been stopped a sinogram may be performed to know that the abscess cavity has been obliterated. The
drainage tube is removed. Systemic antibiotics are continued for 5 days postoperatively. Rectal examination should be made almost
daily to detect developing pelvic abscess.
A pelvic abscess may be drained in the female into the vagina and in the male into the rectum.
If the appendix is not removed when the abscess is drained, interval appendicectomy should be done 6 to 8 weeks after the wound
has healed.
Management of subacute, recurrent and chronic appendicitis.— The treatment of choice is early
appendicectomy.
COMPLICATIONS OF APPENDICECTOMY.— 1. Wound infection.— Infection of the subcutaneous tissue is the most
common complication following appendicectomy.
2. Pelvic. Subphrenic or intra-abdominal abscess — may occur following gangrenous or perforated appendicitis.
3. Faecal fistula may occur if a ligature slips from a tied but noninverted appendiceal stump, too tight suturing of the base of the
appendix or purse string suture, necrosis from a periappendiceal mass encroaching on to the caecum, erosion of the wall of caecum by
drain, Crohn’s disease etc. Faecal fistulas usually close spontaneously. All that is required is to ensure that the tract remains open until
the drainage ceases, (i) If the bowel beyond the fistula is obstructed or (ii) the mucous membrane of (he gut is continuous with the skin,
closure of the fistula will require an operation.
4 Pylephlebitis or portal pyemia may result which is characterised by jaundice, high fever and chills.
5. Intestinal obstruction, initially paralytic but occasionally may go on to true mechanical obstruction may occur with slowly
resolving peritonitis. Intestinal obstruction due to adhesion formation is not uncommon after 2 months of operation.
6. Right inguinal hemia — is said to be more common following the gridiron incision for appendicitis due to injury to the
iliohypogastric nerve.
LAPAROSCOPIC APPENDICECTOMY.— Laparoscopic appendicectomy is not as popular as laparoscopic cholecystectomy
due to the fact that conventional appendicectomy is performed through a small incision and the hospital stay is also short. The greatest
advantage of laparoscopic appendicectomy is probably to confirm the diagnosis before appendicectomy.
Many surgeons use open technique to establish pneumoperitoneum rather than using a Verress needle for greater safety. A moderate
trendelenburg tilt of the operating table is made to keep the loops of small bowel away from pelvis for better visualisation of the
appendix. The surgeon stands on the left side of the patient and faces the video monitor placed at patient’s right foot. The operating ports
are placed according to surgeon’s choice depending on previous abdominal scars.
The appendix is searched out by identifying the caecal taeniae. Laparoscopic tissue holding forceps is used to catch hold of the
appendix, which is lifted to display the mesoappendix. A dissecting forceps is used to create a window in the mesoappendix and the
appendicular vessels are ligated or coagulated. The appendix is made free from its mesoappendix and its base is now ligated with an
absorbable loop ligature. The base of the appendix is divided and the appendix is removed through one of the ports. It is not always
practicable to invert the stump of the appendix. Subcuticular sutures are used for the ports.
It probably requires a longer operating time than conventional appendicectomy, but the stay in hospital is slightly shorter.
At present a question has cropped up whether needlescopic approach is better than laparoscopic appendicectomy. For LA (laparoscopic
approach) 3 trocars are used — one 12 mm subumbilicat trocar for introducing telescope attached to an endocamera, one 12 mm trocar
in the left iliac fossa and one 5 mm trocar in the right lower abdomen. The mesoappendix is divided with clips or with stapler or
coagulated using monopolar/bipolar energy. The appendix is divided with linear cutter stapler and removed after applying endoloops at
the base. The appendix is extracted through the subumbilical port.
In case of needlescopic approach (NA), apart from 10 mm port in the infraumbilical area for camera, there are two 2 mm ports —
I in the suprapubic region and the other in the middle third of the lower abdomen. After a diagnostic laparoscopy using a 10 mm
laparoscope, the 2 mm needlescope is shifted to the suprapubic port. The other 2 ports are used for a 5 mm dissector and 2 mm
instruments to expose the appendix. The rest of the procedure is similar to LA. Laparoscopic appendicectomy could not become as
popular as it could not establish itself as a procedure of choice in complicated or perforated appendicitis as it was felt that CO,
pneumoperitoneum may enhance the incidence of bacteraemia and plasma endotoxin concentration. But it must be confessed that
laparoscopy reduces the rate of unnecessary appendicectomy and improves diagnosis in fertile women. Moreover the major advantages
of LA are fewer wound complications and improved cosmesis. The decrease in wound infection after LA is due to the fact that the
appendix is extracted through a trocar or inside a bag without contaminating the wound. In case of complicated appendicitis e.g.
perforation, abscess formation or peritonitis the abdominal wall complication rate is fewer in case of LA than open surgery, though
conversion to open surgery is more frequent in these cases as compared to simple cases.
Readers are referred to Chapter 22 of Author’s ‘A Practical Guide To Operative Surgery’.
NEOPLASMS
Neoplasms of the appendix are extremely uncommon and are usually diagnosed at operation or autopsy. MALIGNANT
tumours are : (i) Carcinoid tumour; (ii) Adenocarcinoma; (iii) Malignant mucocele.
Carcinoid.— About 40% of all carcinoid tumours of G.I. tract have been reported to be found in appendix. But true
incidence is more as majority of these tumours are without symptoms.
Carcinoids of appendix are typically small, firm, yellowish brown tumours. Majority of these tumours occur at the
distal third of the appendix and only less than 10% oscur at the base. These are without symptoms and are usually
discovered at the time of operation. Only less than 3% of appendiceal carcinoids metastasise.
Treatment is appendicectomy with excision of mesoappendix. If nodal metastasis is demonstrated, right hemicolectomy
with excision of the nodes bearing mesentery is indicated.
Adenocarcinoma.— By all means this is similar to colonic adenocarcinoma. Preoperative diagnosis can only be
confirmed by visualisation of extra-caecal mass on barium enema. Majority of these cases are diagnosed during
appendicectomy. In a few instances the lesion is even missed during appendicectomy and is only detected on histopathologic
report ofthe appendicectomy specimen.
Treatment is right hemicolectomy.
Malignant mucocele.— Benign mucocele may occur in the process of acute appendicitis and has been described
in section of ‘Pathology’ of acute appendicitis. Malignant mucocele is a mucous papillary adenocarcinoma (Grade I). This
is a cystic dilatation of the appendix containing mucoid material.
Treatment is simple appendicectomy. Care must be taken to avoid rupture of mucous-filled appendix, as there is a
chance of pseudomyxoma peritonei to develop.
917
CHAPTER — 45
MEGACOLON
Megacolon is of two types — (1) Congenital megacolon or primary megacolon (Hirschsprung’s disease or
congenital aganglionic megacolon) and (2) Secondary or acquired megacolon.
PRIMARY MEGACOLON (HIRSCHSPRUNG’S DISEASE)
The disease was first described by Hirschsprung in 1888 who found in the autopsies of two children the
massive dilatation and hypertrophy of the colon.
Aetiology and Pathogenesis.— It is caused by absence of ganglionic cells of the pelvic parasympathetic
system in both Auerbach’s plexus between the circular and longitudinal muscle layers of the colon and Meiss
plexus in the submucosa. It is believed to be the result of failure of migration of neuroblasts into the gut from
nerve trunks. It usually occurs at the end of the first trimestar of foetal life. Aganglionosis may result if there
cessation of migration of neuroblasts, which migrate from the primitive node along the alimentary track dista
wise. The internal anal sphincter is aganglionic in every case of Hirschsprung’s disease. This aganglionosis ex
proximaliy to variable distance according to the failure of descent of the neuroblasts. Approximately 80% of c
involve the rectosigmoid junction and 15% have aganglionic segment extending as far proximaliy as the hepa
flexure. The former condition is called ‘short segment aganglionosis’ and the latter condition is called ‘long se
aganglionosis’. There are some cases where aganglionosis occurs in skip areas, these are known as ‘segmenta
aganglionosis’. There is absence of peristalsis in the aganglionic segments thus producing adynamic intestina
obstruction. Lack of peristalsis in the aganglionic segment and failure of relaxation of the internal anal sphinc
produce varying degrees of intestinal obstruction found in this disease.
Pathology.— The bowel proximal to the aganglionic segment becomes gradually dilated and hypertrophied
for a variable length as the peristaltic waves try to propel stools through the obstructing aganglionic segment
There is a visible transition zone, usually 1 to 5 cm in length between the dilated bowel which contains
ganglionic cells on the proximal side and normal sized aganglionic segment of bowel on the distal side. All
layers of the dilated intestine show gross pathological changes. The mucous lining is chronically inflamed and
frequently ulcerated. The pelvic mesocolon is elongated and thickened and its blood vessels are large and
prominent. As in majority of cases the aganglionic segment stops proximaliy at sigmoid colon, the grossly
dilated portion mostly involves the upper sigmoid colon and lower descending colon.
Clinical features.— This condition is more common in males and it shows familial tendency. The symptoms
appear within 3 days of birth and the presenting features are as follows :
(i) Constipation.—The new born child fails to pass meconium within first 2 or 3 days. If the little finger
is introduced into the rectum meconium is passed in inadequate amount and toothpaste like.
(ii) Abdominal distension.— This becomes obvious by the 3rd day. Gradually the distension progresses
and the colon is involved in distension. Visible peristalsis may be seen with loud borborygmi.
In some babies the symptoms may suggest mildgastroenteritis or a feeding problem associated with mild
constipation. As the condition becomes more chronic the baby fails to gain weight, becomes hypoproteinaemi
and suffers from intermittent episodes of severe constipation and diarrhoea. Eventually enterocolitis may
develop, a lethal complication of Hirschsprung’s disease. The clinical picture includes fever, vomiting, watery
or bloody diarrhoea, septic shock and finally death. Enterocolitis develops due to invasion of bacteria from th
dilated colon through erosion and ulceration in the mucosa into the wall of the colon. Immediate vigorous
management is indicated.
Rectal examination — reveals that the rectum is empty and the anus is free from any pathology.
Special Investigations.— 1. BARIUM ENEMA EXAMINATION.— This should be done in unprepared
bowel as wash-outs may minimise the dilatation of the gut above the obstruction. Barium enema should be
prepared with normal saline and not with water, as magacolon absorbs water much more rapidly than norma
bowel and may result in water intoxication. This examination will demonstrate dilated colon followed by
narrow aganglionic segment. The diagnosis becomes difficult if the child has a very short segment involve
or if the entire colon is aganglionic. In infants the proximal non-affected colon may not become very much
dilated, but in these cases the retention of barium after 24 hours is quite diagnostic. It is always essential th
both anteroposterior and lateral views should be taken as narrow short segments may be overlapped by di
proximal colon in one of the views.
2. RECTAL BIOPSY will demonstrate absence of ganglionic cells in the intramural and submucous
plexuses. Biopsy should be taken at least 2 cm above the dentate line. An attempt should be made to take f
thickness wall for biopsy, as superficial biopsy cannot confirm presence or absence of ganglion cells in the
intramural plexus.
3. MANOMETRIC STUDIES can be done easily in the older children and absence of relaxation of the
internal anal sphincter will confirm the diagnosis.
Treatment.— The main curative treatment of this disease is excision of the entire aganglionic segment
(the cause of functional obstruction) and continuity is restored with normal sphincteric control of the anus
The upper limit of resection must include the transitional zone and a little of the healthy dilated colon abov
it. The lower limit should be so designed as to preserve the anal canal with its sphincters.
COLOSTOMY.— Prompt colostomy should be performed in neonate with this disease. If the infant has
enterocolitis and is septic, he must be treated quickly and aggressively to control the sepsis, dehydration an
hypoproteinaemia. While the sepsis is being treated by vigorous antibiotics, decompression should be don
by nasogastric suction and dilatation of the anal sphincter. Rectal tube may be inserted through the anus an
wash-outs can be made in the distal colon, but adequate care is required as it may perforate the bowel.
When the condition of the child is stable colostomy should be performed. Usually two stage operation is
performed in this condition. But only in case of patients above 2 years of age with slight dilatation of the co
and in moderately fair health, one may go for one stage operation, i.e. without colostomy.
Two types of colostomy can be performed — (i) right transverse colostomy and (ii) loop colostomy plac
just above the transition zone. If one wants to protect the anastomosis right transverse colostomy is better,
it requires a third operation, i.e. closure of the colostomy. In case of the loop colostomy above the transition
zone, at the time of second operation i.e. resection and anastomosis, the loop colostomy is included in the
resection. So the anastomosis is not protected by a defunctioning colostomy. Right transverse colostomy is
better than the left transverse colostomy as more bowel can be used if a greater segment is to be resected. I
the aganglionic segment extends higher than usual i.e. to mid-descending colon, right sided colostomy ma
be inadvisable resulting in too short a length of colon to reach the perineum. In this case again loop colosto
is advised.
Definitive operation is postponed till the child becomes at least 1 year of age and of normal weight.
Operative procedures.— 1. SWENSON’S OPERATION.— The patient is placed in semilithotomy
position. A suitable incision is made on the abdomen. The rectum, the contracted aganglionic part and the
commencement of the normal dilated portion are freed from their attachments as far down as towards the
canal. The dissection must be kept immediately outside the fascia propria. The pelvic nerves to the bladder
are protected. All surrounding structures should be carefully preserved. Now the level of resection is judge
One may go for frozen section biopsy to know that he is above the transition zone. The colon is transected
through the normal dilated portion well above the transitional zone. The distal end is closed by purse-strin
suture. The mobilised aganglionic segment with purse-string suture is now everted through the anus. The
anterior half of the junction of the inverted rectum with the anal canal is incised transversely and through t
the proximal colon is pulled through. End-to-end anastomosis between the colon and the anal canal is carri
out. The everted aganglionic segment is removed. The anastomosis of the normal to the remaining rectum
not be higher than twice the width of the internal sphincter. If more than this length of aganglionic rectum
is retained, i.e. more than 1.5 cm above the anus, there can be recurrence of all symptoms.
Complications include stricture, leaks, abscesses and neurogenic bladder.
THE COLON 919
2. MODIFIED SWENSON’S OPERATION.— In this operation the anastomosis is made obliquely instead
transversely (as performed in Swenson’s operation). 2 cm of anal canal remains anteriorly and 1 cm posterio
to obviate the tightness of the sphincter. It also includes resection of a portion of internal sphincter and ther
the tightness.
3. DUHAMEL’S OPERATION.— In Swenson’s operation as there is absence of rectum after operation no
rectal sensation is lost and defaecation reflex is disturbed. The aganglionic segment is removed upto the rec
upper end of rectum is closed. The normal colon is brought down behind the rectum through the sacral holl
is widely stretched and a transverse incision is made in the posterior wall just above the sphincter. Through
the colon lying behind the rectum is brought down to the anal opening. The colon is then fixed to the rectum
catgut stitches to make a colorectal anastomosis. A special crushing clamp is introduced to include the poste
the rectum and anterior wall of the colon between its blades. The clamp is tightened and left in situ till the s
A IB ©
Fig. 53.1.— Operations for Hirschsprung’s disease. A.— Swenson’s operation. B.— Duhamel's
operation. C.— Soave’s operation. Aganglionic rectal segment is shown as white. Ganglionic normal
colon is indicated as dotted (Dots represent ganglia) and striped wall.
and the clump becomes loose, so that it can be removed. The faecal content from the colon comes into the co
junction so that the rectal sensation remains intact so is its reflex defaecation.
4. SOAVE’S OPERATIONS.— Soave presented his procedure in 1961. Through the abdomen aganglionic
above the rectum is removed. The mucosa of the rectum is excised upto the anus. The normal proximal colo
through the muscular sleeve of rectum. It is brought out through the anus for a distance of several centimetr
through colon is anastomosed directly to the anus (Boley modification). In this operation it preserves rectal
yet avoids the blind rectal loop because the sphincter is not damaged, many patients have recurrence of thei
and require repeated dilatations or sphincterotomies. Other complications include stricture of the anastomo
and abscesses.
5. COLOANAL ANASTOMOSIS.— This operation only be performed in older children, teenagers or in a
The rectum is fully mobilised as mentioned above and transected just above the level of the pelvic floor whi
be normal. This normal colon is now joined to the top of the anal canal with stapling technique. A sleeve tec
also be applied following mucosectomy of the rectum and upper anal canal.
ACQUIRED OR SECONDARY MEGACOLON
Aetiology and Pathogenesis.— 1. Chagas’ disease is caused by infection with Trypanosoma cruzi, en
demic in south and central America. Megacolon is one of the complications of the chronic form of this
disease. This is due to widespread destruction of the intramural nervous system. Subtotal colectomy with
ileoproctostomy is probably the treatment of choice. Depending of the amount of involvement one can even
perform rectosigmoidectomy.
2. There are certain conditions which may give rise to mechanical obstruction in the rectum and anal
canal. These are lymphogranuloma venereum, endometriosis, radiation proctitis and anorectal injury.
3. Neurogenic disorders such as paraplegia or poliomyelitis may cause megacolon.

4. Adynamic obstruction due to septic shock or diabetes may produce symptoms as mega colon due to a
dilatation of colon.
5. Megacolon is often seen in psychotic patients due to extreme inactivity and perhaps voluntary inhibitio
of defaecation.
6. Faecal impaction in old patients may give rise to this condition.
7. Acute painful lesions ofthe anus e.g. fissures, fistulas, thrombosed external haemorrhoids may also lead
to this condition due to faulty bowel habit.
TREATMENT depends on the cause of the condition.
ULCERATIVE COLITIS
Aetiology.— The cause is unknown, but several theories have been put forward of which the main ones
are infective, nutritional, psychosomatic and immunological.
(i) Infective.— Extensive studies into the infective hypothesis have failed to demonstrate a pathogen
organism as the agent directly responsible. Scattered reports suggesting that Chlamydia, cytomegalo virus,
Clostridial toxin or RNA virus is responsible for producing ulcerative colitis. Yet no definite proof could be
elicited. Bacterial allergens may be involved in some of the immunological disturbances occurring in the
disease.
(ii) Nutritional.— Attempts to identify a nutritional cause have likewise proved fruitless.
(iii) Psychosomatic.— Psychologic factors have long been thought to play a critical role in exacerbations
of the disease. Various investigations have suggested that the subjects who develop ulcerative colitis have a
characteristic personality and those personality factors are present long before the onset of colitis. Further
more, colectomy is usually followed by a marked improvement in pre-existing morbid psychologic tests suc
as depression or social estrangement. However, in most recent full scale psychological study, most of the
subjects with ulcerative colitis were assessed as psychologically normal, though an emotional disturbance ju
before the onset of illness was not unusual.
(iv) Immunological.— At the present time, a great deal of interest is attached in various immunological
disturbances in the disease. Lymphocytes may be rendered cytotoxic to colonic epithelium by incubation wit
serum from patients with ulcerative colitis. These patients have also been found to have alteration of their T
and B cell lymphocyte populations. In case of ulcerative colitis patient while total lymphocyte and T-cell
lymphocyte count are normal, thymosine-dependent T-lymphocyte response may be abnormal suggesting a
immune deficient state. It has also been shown that IgGantibodies may play a role in the chronicity of the
disease, but may not be involved in its onset. The patients with ulcerative colitis frequently have high titres
of circulating antibodies to cow’s milk proteins and a controlled dietary trial has shown that a few patients
benefit from milk-free diet.
The possibility that ulcerative colitis is an autoimmune disease has received much attention in recent yea
Autoantibodies to colon in the disease has been demonstrated and it has been confirmed by many workers u
a variety of technique. But these autoantibodies do not correlate with the severity or course of the disease,
which suggests that they may be a response to the damaged epithelium rather than a prime cause of the dise
Another immunological feature of potential importance is the cross-reaction between colonic epithelium and
some ofthe colonic bacteria, notably E. coli. This raises the possibility that an intestinal infection may set up
immunological processes which themselves may damage the colonic epithelium.
Pathology.— Ulcerative colitis is a disease confined to the mucosal and submucosal layers of the colonic
wall. The rectum is the most frequently involved portion (90% to 95%) of the bowel. It is the earliest site of
involvement from where the disease spreads proximally. In more than % the cases, the entire colon is disease
In only 10% of cases terminal ileum may be involved due to back washing from the colon when the ileocaeca
valve is incompetent and is known as back-wash ileitis. It must be remembered that disease is always in
continuity and there is no ‘skip lesion’ as seen in Crohn’s disease.
THE COLON 921
MACROSCOPICALLY, the disease involves the mucosa and submucosa mainly, so the serosal surface
remains normal fora longtime. The mucosal surface demonstrates superficial fissures and small and regular
pseudopolyps. Irregular, shallow, linear anastomosing ulcers intersperse between islands of swollen mucosa
—pseudopolyps, which is a characteristic feature of this disease. Bloody pus may cover the ragged ulcerative
surface of the mucosa. The serosa of the affected bowel remains normal for quite a long time. Only in very
advanced cases the bowel becomes greatly shortened. The serosa becomes dull and greyish with little or no
exudate unless perforation has occurred. The mesentery is contracted, oedematous and slightly thickened, bu
less marked than what is seen in Crohn’s colitis. Large lymph node masses are conspicuous by their absence
in ulcerative colitis. There may be abscess formation in areas of localised perforation. In fulminating acute
ulcerative colitis, the entire bowel wall is very friable with numerous areas of necrosis. Fistulas, except
perianal, are rare in ulcerative colitis compared to Crohn’s colitis.
MICROSCOPICALLY, the disease can be diagnosed through biopsies. The earliest lesion starts in the
bases of the crypts of Lieberkuhn, where neutrophils pass between the lining cells to accumulate inside the
crypt lumen forming ‘crypt abscesses’ alongwith eosinophils, serum and red-blood cells. These crypt
abscesses ultimately rupture through the mucosal surface forming tiny ulcers or may rupture into the
submucosa. Gradually more and more crypts of Lieberkuhn are affected and larger areas of mucosa breakdo
producing bigger ulcers. As the disease becomes chronic, lymphocytes, plasma cells and macrophages
infiltrate both mucosa and submucosa. Eosinophils and mast cells also appear. In between these ulcers norm
mucosa becomes inflamed and oedematous with proliferation of granulation tissue. This is known as
pseudopolyp. In fulminating ulcerative colitis and toxic megacolon lesions may penetrate through the full
thickness of the bowel wall and may lead to perforation.
Clinical features.— Ulcerative colitis can be divided into three forms according to its clinical features.
These are : (i) Chronic and continuous; (ii) Chronic-relapsing-remitting and (iii) Acute fulminant.
The onset of the disease is usually highest in the third decade, though second and fourth decades are oft
involved. A slight female predominance has been reported. The first symptom is watery diarrhoea. Abdomin
pain is the next symptom and rectal discharge of mucus, sometimes blood and sometime pus is not uncomm
1. CHRONIC AND CONTINUOUS.— The onset is usually gradual in this case, the diarrhoea gradually
becomes worse for a considerable period. Lower abdominal cramp is almost always present in the earlier
phases, but when the bowel becomes thickened and shortened, cramping is less marked. Cramping is usually
followed by urgency and tenesmus and painful passage of small watery stool consisting of stool, mucus, bloo
and pus. Later on cramping may not be present to warn of impending defaecation. At this stage defaecation
occurs unexpectedly and the patient becomes insecured. Gradually there is weight loss and malnutrition.
2. CHRONIC-RELAPSING-REMITTING.—This is the commonest form seen in ulcerative colitis. The
course is variable and characterised by almost unpredictable exacerbations and remissions. Recurrences are
often associated with emotional stress and other acute illness and in women during menstruation and
pregnancy. Bloody diarrhoea is the predominant symptom which occurs during relapses. Diarrhoea and
abdominal pain more or less occur in the same fashion as the chronic variety, only difference is that in the
remitting stage patient is almost free from disease.
3. ACUTE FULMINANT.— Sometimes the onset is very acute and fulminant colitis may superimpose
as an exacerbation upon the chronic form. Unrelenting diarrhoea, preceded by severe lower abdominal cramp
takes place day and night. Tenesmus and urgency are marked. Number of stools are about 30 to 40 per day.
They consist of small amount of watery stool, mucus, blood and pus. Systemic toxicity is the main feature of
this type. Fever goes upto 39° to 40°C. Extreme dehydration, hypocalcaemia, anaemia, hypoproteinaemia and
marked weight loss are features of this form. The facies are gaunt with shunken eyeballs. Colonic perforation,
haemorrhage and toxic megacolon always threaten this condition. Mortality of this form is about 20%.
Physical findings.— On inspection, typical facies of acute colitis should be detected. Pallor and weight
loss of chronic disease should not be missed. Tenderness on the affected colon may be revealed. Physical
examination is more important in acute fulminant type. High temperature should be noted. Abdominal
tenderness, with distension is very characteristic of toxic megacolon. Certain amount of rigidity is also
noticed in toxic megacolon and in cases with perforation. With perforation, features of general peritonitis
will be obvious. Rectal examination may reveal perianal inflammation in the form of fissure, abscess or
fistula-in-ano, though these are much more common in Crohn’s disease. Examinations of the skin, tongue
joints and eyes are important to exclude general complications of this disease, which are described after
special investigations.
Special Investigations.— 1. BARIUM ENEMA.— It should be given with caution particularly during
acute exacerbation. Extensive preparation is notsrequired and only bowel wash out with physiological
saline may be done in the X-ray department shortly before the radiological procedure is carried out. Oral
laxatives should not be given. When the patient is ill, preliminary plain X-rays are required to show if ther
is colonic dilatation, where barium studies may be judged to be contraindicated. In straight X-ray toxic
megacolon will be seen as remarkable dilatation of the colon with air inside it. Free air in the peritoneal
cavity suggests perforation of the colon.
Barium enema examination, usually with air contrast, can be performed safely in most cases and is
extremely helpful in identifying the extent and severity of the disease. Barium enema findings in this dis
ease are (i) loss of haustration. This is an early finding and is thought to be due to paralysis of the muscu-
laris mucosa, (ii) Irregularities of colon wall
represent small ulcerations. As the disease
progresses, pseudopolyps become a promi
nent finding, (iv) In advanced cases the co
lon assumes the appearance of a rigid con
tracted tube due to the scar that forms with
repair. In all patients with ulcerative colitis a
barium view of the whole of colon should be
taken at a convenient time to exclude malig
nancy. As the incidence of malignancy is strik
ingly high specially after 10 years of the dis
ease, it is appropriate to obtain a yearly barium
examination and colonoscopy.
2.
ally flexible sigmoidoscope or colonoscope
is used. It is a helpful and specific diagnostic
aid, as ulcerative colitis involves rectum in
90% to 95% of cases. Mucosa of both the
rectum and sigmoid colon is usually erythema
tous and granular. Superficial ulceration may
be seen. The mucosa is friable. With more
severe cases, diffuse haemorrhagic inflamma
tion is obvious with patches of exudate and
macroscopic ulcers. Cobblestoning and deep
linear ulceration which are common in Crohn’s
disease are unusual in ulcerative colitis. Ul
cers may be surrounded by heaped-up areas
of granulation tissue and oedematous mucosa which may assume polypoid appearance —pseudopolyposis.
Mucosal bridging may also be found. In chronic advanced disease the lumen of the rectosigmoid is remar
ably contracted. The use of flexible sigmoidoscopy has improved diagnostic accuracy and patient’s accept
ability. Colonoscopic examination is of value in determining the extent and activity of the disease. Colonoscop
is more helpful in diagnosing carcinoma in association with ulcerative colitis. These tumours are more
evenly distributed throughout the colon with approximately 50% being found proximal to splenic flexure.
THE COLON 923
The biopsy specimen may be taken with a surgical biopsy forceps or with suction type of instrument.
3. COMPUTERISED TOMOGRAPHY — is particularly helpful in diagnosis of acute diverticulitis.
This not only demonstrates the diverticula, but also any associated pericolic abscess. So barium enemas
and endoscopy can be reserved for patients who have recovered from an attack of acute diverticulitis. This
is to protect against perforation or peritonitis.
Complications of ulcerative colitis.— The complications of ulcerative colitis are numerous. These
can be divided into two main groups — local complications and systemic or remote complications.
LOCAL COMPLICATIONS.—(i) Haemorrhage, (ii)
H
Perforation either free producing peritonitis or confined
with abscess or fistula formation, (iii) Stricture formation
with partial obstruction, (iv) Perianal and perirectal
abscesses and fistulas, (v) Toxic megacolon and (vi)
Carcinoma of the colon. Of these, two complications
deserve special mention :
Toxic Megacolon.— It is a manifestation of

fulminant colitis and usually occurs with the initial acute
episode, less frequently during a relapse of the remitting
type of ulcerative colitis. The cause of toxic dilatation
is not known. Necrotising inflammation of the smooth
muscle of the bowel due to deep ulcers and at times
damage to the myenteric plexus seems to be the main
cause. Other factors which may play role in this condition
are hypocalcaemia, hypoproteinaemia, anticholinergic
drugs etc.
Diagnosis should be immediately suspected in any
patient with acute colitis in whom number of stools
suddenly decreases with bloody rectal discharge and
the patient is obviously very toxic and febrile with
progressive abdominal distension and absent bowel
sound. Plain abdominal X-ray will show marked gaseous
distension particularly of the transverse colon.
Treatment consists of antibiotics, intestinal
decompression, correction of electrolyte deficits, blood,
starts before the age of 25 years the risk of cancer is about twice as great as in those in whom the disease
starts later.
Carcinomatous growths following ulcerative colitis are usually multiple, flat and infiltrating with poorly
differentiated mucus-secreting types. Prognosis is poor. These cancers may develop anywhere in the colon
and does not show predilection towards rectum as the original disease shows. It must be remembered that
pseudopolyps usually do not turn malignant.
No specific symptom of cancer has been detected, yet excessive diarrhoea with abdominal pain, rectal
bleeding and weight loss are suggestive.
The only preventive measure which can be adopted is to advise total colectomy with ileostomy for any
patient who is suffering from active total colitis for more than 10 years. It is very difficult to say which
patients will develop carcinoma. Even carcinoembryonic antigen is of no value in this regard.
GENERAL COMPLICATIONS.— Systemic complications include (i) Macrocytic anaemia, (ii)
Hypoproteinaemia, (iii) Avitaminosis, (iv) Amenorrhoea, (v) Amyloidosis, (vi) Osteoporosis, (vii) Retarded
sexual development and retarded growths. This disease produces complications in certain specific organs
such as (a) eyes — conjunctivitis, iritis, choroiditis, even ulcerative panophthalmitis, (b) Joints — arthralgias
(swelling, pain, redness with migratory involvement) mainly affecting lower limb joints, ankylosing spondy
sacroilitis. (c) Bones — different forms of inflammatory disease, (d) Skin — Erythema nodosum, pyoderma
gangrenosum, clubbing of fingers, aphthous stomatitis, (e) Liver and gallbladder — fatty liver, hepatitis,
pericholangitis, cirrhosis, gallstones, carcinoma of the bile duct, (f) Urinary system — pyelonephritis and
urolithiasis, (g) Interstitial pancreatitis, (h) Peripheral neuropathy, (i) Vascular thrombosis.
TREATMENT.— Primary treatment of ulcerative colitis is medical. As the aetiology is not known
there is no specific treatment. The components of therapy are (i) antidiarrhoeal, (ii) antibiotics, (iii) corticoste
(iv) diet, (v) vitamin, (vi) minerals and (vii) general support.
(i) Antidiarrhoeal agents, though definitely helpful, may induce toxic megacolon. Most frequently
lomotil (diphenoxylate hydrochloride with atropine) or codeine is used.
(ii) Sulphasalazine (Azulfitine or Salazopyrin), has enjoyed widespread acceptance in chronic cases
of ulcerative colitis as antimicrobial agent. This may inhibit mucosal prostaglandin synthesis to produce
such a good response in this disease. This drug seems to be of lesser efficacy in acute ulcerative colitis.
This is an oral non-absorbable sulphonamide.
(iii) Corticosteroids seem to be quite helpful in this disease. But if the patients require surgery later on
this drug is quite harmful. Moreover Cushing’s syndrome may be produced on long term therapy. In seriou
ill patients intravenous ACTH 40 I.U. every 12 hours or continuous intravenous prednisolone 100 mg per
day is advised. If remission is achieved, oral prednisolone can be used after a few days. If there is no
significant improvement in 7 to 10 days, surgery should be seriously considered. Maintenance steroid
therapy is with oral prednisolone starting at 60 mg daily in dividing doses and taperring as rapidly as
possible to 15 mg or less. Longterm steroid therapy is not justified and operation should be advised. Retenti
enemas with water soluble corticosteroids are often beneficial in patients with disease limited to rectum
and sigmoid colon. 5-ASA (5-Amino Salicylic Acid) agents can be used both systematically and topically.
The main function of these agents is to maintain remission rather than treating an acute attack. Nowadays
prednisolone 20 to 40 mg per day alongwith sulfasalazine 1 g thrice a day or one of the newer 5-ASA agents
given for 3 to 4 weeks period is the accepted treatment.
(iv) Rigid dietary restrictions have not done much good to the patients. A balanced milk-free diet
should be given and too hot or too cold food should be rejected.
(v) & (vi) Vitamins A, C, B and D with supplements of iron and potassium should be given.
In nutshell medical management for mild and moderate attack should be as follows :
Prednisolone 5 mg four times a day, sulphasalazine 0.5 g. four times a day and predsol retention enema
at night should be continued. If the patient improves on this therapy it should be continued. If sudden
relapse breaks out during this therapy medical management for severe attack should be adopted.
Medical management for severe attack is as follows :
THE COLON 925
Intravenous fluids to overcome dehydration and electrolyte losses, blood transfusion to correct anaemia
vitamin supplement and maintenance of nutrition through parenteral feeding are advised.
Nothing by mouth except water, prednisolone 60 mg a day in divided doses in I.V. drip. Hydrocortison
sodium succinate 100 mg in approximately 120 ml saline administered by rectal drip twice a day. Parentera
feeding by aminosol with fructose or ethanol or some equivalent preparation and parentrovite are prescrib
Broad spectrum antibiotics should be given by mouth. Metronidazol may be given by mouth or intravenou
drip. Morphine or lomotil may be used as antidiarrhoeal agent.
With this regime patient usually responds within 5 days. After this the patient is converted to oral
management. Feeding is resumed, prednisolone is given 40 to 60 mg a day in divided doses. After a week
or so the steroid doses are reduced and sulphasalazine is added. Patient is discharged with the treatment o
prednisolone 5 mg 4 times a day, sulphasalazine 0.5 g. 4 times a day and predsol enema at bedtime once a
day.
Prevention of recurrences is mainly performed by sulphasalazine 0.5 g. 4 times a day. Corticosteroids
have not been successful to prevent recurrences.
Immunosuppressive drug like azathioprine should do good in this disease as it has got some autoimmu
background. The drug is yet to achieve wide acceptability. It has been used in the dose of 2 to 2.5 mg per
kg. body weight and 25% of patients have shown clinical improvement.
Surgical treatment.— In contradistinction to Crohn’s disease, 75% to 80% of patients with ulcerative
colitis are satisfactorily managed by medical treatment. Only 10% will need surgery.
INDICATIONS/or emergency surgery are: (i) massive and unrelenting haemorrhage, (ii) toxic magacolon
with impending perforation and (iii) fulminating acute ulcerative colitis which is not responding to medica
treatment.
INDICATIONS/or elective surgery are : (i) Partial intestinal obstruction, (ii) confined perforation with
abscess formation, (iii) chronic disease not responding to medical management, (iv) pararectal complication
such as fistulae and abscesses, (v) serious systemic or distant complications not responding to medical
treatment and (vi) in long continued colitis which carries higher risk of colonic cancer.
Main surgical treatment is single staged total proctocolectomy.
This procedure is performed through midline incision. After the abdomen has been opened, a full explo
made with particular attention to the state of the liver and of the biliary tract, as gallstones are not uncomm
The colon is examined carefully with particular reference to any adhesion to any neighbouring structure
might have sealed-off perforation. If so, care must be taken to mobilise the colon lest spillage of faeces shou
the peritoneal cavity. The ascending and descending colons are mobilised. The greater omentum is separate
colon. The ureters are identified at the pelvic brim and a nylon tape is passed round each one, so that the su
dissection of the rectum can be carried out without risk of damaging them. The blood vessels to the ascendi
and descending colons are ligated with catgut and divided.
The dissection of the rectum is a very important part of operation. The tissue, surrounding the rectum, is d
by injection of a solution of 1 : 200,000 noradrenalin in normal saline. This serves to define the muscular lay
reduces haemorrhage. The perineal surgeon, after a concentric dissection of anal sphincters, concentrates on
anteriorly until the pouch of peritoneum in front of the rectum is opened. The posterior dissection is carried
surgeon working in the abdomen. He follows the plane of cleavage just behind the rectum without entering
space, where he can injure the autonomic nerves. He follows this plane of cleavage right upto the tip of the
where he meets the surgeon from the perineum. The lateral ligaments of the rectum are divided close to its
wall.
The small intestine is divided 8 inches above the ileocaecal valve. The proximal end is closed with a purs
suture, the ends of which are held with a pair of artery forceps. The colon and rectum are now removed. Th
in the pelvis is sutured without tension. The perineal skin is also sutured with nylon with a pelvic drain in t
of the perineal wound. Now the attention is directed to make the ileostomy opening. A disc of skin and subcu
tissue, 3 cm in diameter is cut from the anterior abdominal wall from the site previously marked. A cruciate
made on the rectal sheath. A disc of the underlying rectal muscles and the posterior sheath is removed. The
purse-string suture of the ileum are used to pull the ileum out through this hole in the abdominal wall until
about 3 inches, thus ensuring that the finished ileostomy will be a spout of at least \Vi inches in length. The
between the parietal peritoneum and the divided mesentery is closed with catgut taking care not to damage
vessels in the mesentery. This is to prevent internal hernia. The ileum is anchored to the posterior rectal sheat
number of interrupted sutures to prevent prolapse.
At this stage of operation, a drain from the pelvic floor is brought out through a stab wound in the left ilia
The purse-string suture on the end of the ileum is removed. The cut edge of the ileum is freshened. The ile
turned inside out and the edge of the mucosa is anchored to the edge of the skin with interrupted catgut sutu
suitable ileostomy appliance is immediately fixed and the operation is completed.
Early postoperative care.— The ileostomy begins to work from the 2nd to 4th postoperative day and the nasogastri
tube can then be removed. On the 5th day, the pelvic and the abdominal drains are removed. Similarly the ur
is also removed on the same day. After the ileostomy has worked for 2 or 3 days, a permanent appliance is fit
as ileostomy has started working, the patient can take ordinary light diet which can be increased gradually.
Sometimes ileostomy alone may be performed in gravely ill patients, who are not suitable for total colectomy
should always be made not to do this operation as the diseased colon, which is often toxic and may easily per
in the abdomen. Total colectomy is not a very difficult operation and if required an experienced surgeon shou
for to do this operation. Moreover, in subsequent stage when the patient has recovered to certain extent and a
colectomy is being planned, the surgeon may face adhesions due to previous ileostomy operation.
Total proctocolectomy with ileoanal pouch.— In this operation two loops of terminal ileum are sutured side-by-
side to form a pouch before anastomosing with the anal canal. This pouch substitutes the rectum for normal d
This pouch may need to be irrigated by the patient to achieve evacuation. This technique is only applied at a f
special colo-proctological centres.
Care of ileostomy. — Nowadays, immediately after operation special ileostomy bag is fitted to the ileostomy ‘sp
Such bag is supported by a waist strap and also is adhered to the skin by special adhesive plaster. Care must
that the lower rim of the bag does not press on the lower margin of the ileostomy spout. During the first few p
days, liquid stool comes out and fluid and electrolyte balance should be well maintained. If soreness or excor
the skin occurs, a paste of aluminium 10 parts and zinc oxide 90 parts should be applied on the skin. A paste o
gum may also be used as both protective and adhesive before applying the ileostomy bag. After a few weeks
gradually becomes thickened and semisolid, so ileostomy care becomes easier. Occasionally there may be bol
or stenosis of the stoma, which requires digital dilatation.
Continent ileostomy (Koch) (See Fig. 53.4).— According to Nils Koch, an ileostomy reservoir is made
from which the terminal ileum opens to the surface by one-way valve. This type of ileostomy requires no bag or
appliance and can be emptied by the patient at a time he desires to do it. That is why the ileostomy is called ‘continent’.
It is made in such a fashion that ileal content cannot escape through the ileostomy until the patient passes a catheter for
emptying of the ileal pouch. It is a difficult operation to perform and many cases may fail to work properly. Probably
ileoanal pouch as mentioned above is a more satisfactory alternative.
End Ileostomy (Brooke).— In majority of cases of permanent ileostomy, every effort should be made to
achieve good functional result. The ileum is brought out through the lateral edge of the rectus abdominis mus
spout of ileum is made to project about 4 cm from the skin surface. A disposable appliance can be placed over
ileostomy so that the surrounding skin remains healthy.
Ileostomy care.— In the first few postoperative days the fluid and electrolyte balance must be adjusted with gre
care, as the fluid loss can amount to 4 or 5 litres a day due to the loss of colon. The stools gradually thicken in
weeks and become semisolid in a few months. It is better to take the advise of the stoma care nursing speciali
Modern appliances are also available to get a better stoma care with almost no skin problem.
Complications of ileostomy are prolapse, retraction, stenosis, bleeding and paraileostomy hernia.
Postoperative complications.—Besides the usual complications, which may follow any major abdominal operations
such as pulmonary collapse, infection, wound abscess, deep-vein thrombosis, pulmonary embolism, haemorr
certain specific complications may follow this operation. This list includes :
n.— A Gram-negative septicaemia may follow this operation which is tackled by intravenous tetracycline.
Paralytic ileus, a sequel of intra-peritoneal infection or hypokalaemia, is treated by conservative treatment.
(iii) Intestinal obstruction — due to adhesions to the colonic bed or pelvic floor or from internal hernia.
(iv) A persistent perineal sinus.
(v) Ileostomy prolapse.
(vi) Skin problems.
Other possible alternative operation is subtotal colectomy with ileorectal anastomosis. One advantage
of the operation is that it eliminates abdominal ileostomy. The disadvantage is that the operation does not
eliminate proctitis. Rectum is often involved in this disease which remains in situ and not excised. Another
THE COLON 927
problem is that risk of developing carcinoma in the rectal remnant remains. This procedure may be tried in
patients who have refused ileostomy or if the rectal segment is not severely diseased or strictured or there is
Fig. 53.4.— Stages In the construction of continent Ileostomy reservoir by Kock.
no perianal infection and the sphincter function is normal. Some patients suffer from continuing severe
ulcerative proctitis who will require total colectomy with ileostomy later on.
The third alternative is colectomy, mucosal proctectomy and endorectal ileoanal anastomosis. As the
disease is mostly confined to the mucosa and submucosa, mucosal proctectomy will get rid of the disease so
chance of developing ulcerative colitis in the remnant rectum is minimal.
CROHN’S DISEASE
Besides ‘terminal ileitis’ which Crohn described in 1932, this disease involves the large bowel as well.
About 30% to 60% (according to various reports) of cases of Crohn’s colitis are associated with disease of the
ileum also.
Pathology.— Unlike ulcerative colitis total involvement of colon is less frequent in this disease. In case
of partial involvement this disease involves right colon more often. Rectal involvement is seen in only 50%
of cases (cf. ulcerative colitis where rectal involvement is 95%). This disease is peculiar to have skip lesions
unlike ulcerative colitis. The small bowel is involved in approximately 50% of cases of Crohn’s colitis
(considering various series), whereas in ulcerative colitis small bowel is involved in only 10% of cases as
‘back-wash ileitis’. Macroscopical and microscopical features have been described under the heading of
‘Crohn’s disease’ in the chapter of ‘Small Intestine’.
Clinical features.—The common symptoms of large bowel Crohn’s disease are diarrhoea, loss of weight
and abdominal pain. Bloody stool is rarely seen in Crohn’s colitis. On examination, there may be slight fever.
Slight tenderness may be detected on the affected colon. Loss of weight is also quite obvious. A lump may
be palpated due to pericolonic thickening or infection. Only in very severe forms of Crohn’s disease or toxic
928 ------------------------------------------------------------------------------------------------------ A CONCISE TEXTBOOK OF SURGERY
dilatation of colon there^may be distension of the abdomen.

External fistula or internal fistula may be detected. Perianal
Fig. 53.6.— Barium enema showing

Irregularity and spiky ulceration of sigmoid
colon suggesting Crohn's colitis.
mucosa to be more oedem-
' small petechiae and scat-
• ' xj \ of normal mucosa may be

* seen. Rectal palpation will
reveal
~ palpable lumpy
thickening of the rectal
wall with narrowing.
2. Radiology.—
Barium enema X-ray will reveal partial obliteration of haustration.
Segmental involvement may be noticed with intervening normal segments.
The involved portion shows rigid wall with stenotic lumen. Fissures may
be seen from the lumen into the bowel wall due to deep ulceration.
Nodula rity of the mucosa due to oedema may be seen and if these nodules
are separated by linearulcers, ‘cobblestone’ appearance is produced. In
Crohn’s disease small intestine may be involved and such a lesion is
shown radiologically.
Treatment.—A. MEDICALTREATMENT.— It is same as Crohn’s
disease described in the chapter of‘Small Intestine’. Corticosteroids are
less effective in Crohn’s disease and azathioprine may be tried in
postoperative patients to prevent recurrence.
B. SURGICAL TREATMENT.— (i) With total involvement of the
colon including rectum—total proctocolectomy and permanent ileostomy
should be the operation of choice. Even two ileostomy procedure without
resection of colon has been successful to make the disease quiescent. In
this procedure the terminal ileum is transected and both ends are brought
out, the proximal as a functioning ileostomy and the distal as a Fig. 53.7.— Barium enema showing
defunctioning ileostomy. But resection has always yielded better result a region of constant narrowing of
in Crohn’s disease, but to avoid mortality and morbidity of such a big ascending colon suggestive of
Crohn’s disease.
THE COLON 929
operation, this procedure may be justified, (ii) When whole of colon is extensively diseased but without rectal
_ ,m ......... ....... involvement—total colectomy and ileoproctostomyis
!( < * Jj justified. But unfortunately the recurrence rate after
.~ ■ ileoproctostomy for Crohn’s disease is about 50%. So
C * many surgeons are gradually favouring total
• ' proctocolectomy and permanent ileostomy, (iii) In
. segmental colonic involvement — treatment of choice
; I is segmental resection with primary anastomosis. If the
. Ejjr J disease involves right colon, right hemicolectomy is
Br* m justified. In case of left colon involvement, left
jM hemicolectomy has not produced good result, so total
j. JHR ;j::; proctocolectomy and ileostomy is becoming more
rational.
Evenaftersuch radical resection, long-term outlook
af*er definitive surgery in Crohn’s colitis is less
favourable than in ulcerative colitis.
ISCHAEMIC COLITIS
There are three variety of ischaemic colitis — (i) Transient
ischaemic colitis, (ii) Stricture ischaemic colitis and (iii) Gangre
nous ischaemiccolitis. The splenic flexure is the most vulnerable
segment as this is the junction of the supply of superior mesenteric
and inferior mesenteric arteries and in this area marginal artery of
Fig. 53.8.— Double-contrast barium enema Illustrating Drummond is at its greatest distance from the bowel wall. But
Crohn's Involvement of the rectum, though remaining ischaemic colitis can affect any segment of colon.
colon remains normal. Clinical features.— Majority of patients are very old and it
is rarely seen below the age of 45 years. Some medical problems are often associated with e.g. cardiovascular disease, diabetes
etc. The onesi is usually acute with mild to moderate generalised or lower abdominal cramp followed by passage of blood per
rectum. Vomiting is rare. Further symptoms depend on which of the three types of ischaemic colitis is developing.
(i) In transient or reversible form symptoms are mild and lasts only 2 to 4 days, (ii) Instricturing ischaemiccolitis pateinl's
symptoms do not progress and neither disappear. Mild to moderate abdominal pain continues. Rectal bleeding also continues but
in small quantity. Gradually symptoms of partial intestinal obstruction develop, (iii) In gangrenous type the abdominal pain
becomes severe. Abdominal tenderness becomes generalised. Abdomen becomes rigid with involuntary spasm. Bowel sounds are
hyperactive in the early stages, but gradually cease. Gradually features of spreading bacterial peritonitis and septic shock develop
Special Investigations.— 1. Radiography.— Barium enema is contraindicated in gangrenous ischaemic colitis and straight
X-ray of the abdomen is often confirmatory. It reveals paralytic ileus and gaseous distension of the involved segment. Occasionally
small bubbles of gas may be detected in the wall of the infarct bowel.
Barium enema is diagnostic in (a) stricturingcolitis. Marginal 'thumb printing' may be seen due to submucosal haemorrhage
and pericolic fat inflammation. Later on spasm and stricturing become obvious, (b) In transient ischaemic colitis barium enema
will reveal similar 'thumb printing'or superficial ulceration if done promptly otherwise these usually revert to normal in no time.
2. Endoscopy.— Sigmoidoscopy does not reveal any characteristic feature but it excludes other diagnosis. Sigmoidoscopy
will show normal rectal mucosa and blood will be seen coming from above. Only when the rectosigmoid junction becomes
ischaemic one can see blue black mucosa with sloughing and blood is oozing from such mucosa. Colonoscopy is helpful.
3. Angiography, particularly selective superior and inferior mesenteric angiographies will reveal the site of block as the cause
of ischaemia.
Treatment— (i) In case of transient ischaemic colitis no specific therapy is necessary, (ii) In stricturing ischaemic colitis,
conservative therapy is indicated and one can expect self cure, as the condition is reversible. Anticoagulants should be avoided.
Only when the colon becomes strictured, the segment should be resected with primary anastomosis, (iii) In gangrenous type no
time should be wasted in various sophisticated investigations such as angiography. Barium enema is contraindicated and straight
X-ray of the abdomen is only required to establish the diagnosis. Conservative treatment with I. V. fl uid and nasogastric aspiration
is started. Emergency operation should be performed as soon as the patient's condition is stabilised. The involved segment is
resected and primary anastomosis is performed. If the condition of the patient does not allow such operation exteriorization of
the involved segment should be performed.
AMOEBIASIS
This is an infective disease due to infestation with Entamoeba histolytica.
Pathogenesis.—Transmissionof E. histolytica is effected through its encysted stage and infection occurs
through ingestion of these cysts. In man the incubation period varies a great deal but is generally 4 to 5 days
E. histolytica passes through three stages — (i) trophozoite (growingstage), (ii) precystic stage and (iii) cysti
stage. After ingestion of cyst through contaminated food or drink, the cyst passes through the stomach into
the small intestine. The cyst wall is resistant to the action of the gastric juice but is digested by the action of
trypsin inthe intestine. Excystation occurs in the lower part of the ileumand each cyst liberates a single amoe
with four nuclei (tetranucleate amoeba) which divides and forms eight trophozoites by the division of four
nuclei. So there is hardly any chance for affection of the G. I. tract above ileocaecal valve. Caecum is the first
part to be affected. The trophozoite phase is responsible for producing the characteristic lesion of amoebiasi
Pathology.— This may be described under two heads :
1. PRIMARY OR INTESTINAL LESIONS —which are mainly the concern of this chapter and will be
described below.
2. SECONDARY OR METASTATIC LESIONS, which appear mainly in the liver, but may be seen in
the lungs and brain. Cutaneous amoebiasis may be found over the region adjoining a visceral lesion such as
in the area of drainage of liver abscess or colostomy wound, in the sites of ruptured appendicular and peri
colic abscesses. Extensive necrosis and sloughing of the skin and subcutaneous tissues are caused by the
trophozoites of E. histolytica in these areas. Besides this granulomatous ulceration, a granulomatous mass
simulating an epithelioma may be seen in the perianal region.
1. INTESTINAL LESIONS.— Trophozoites enter through the crypts of Lieberkuhn and penetrate
directly through the columnar epithelium by their amoeboid activity and by dissolving intestinal epithelial
cells with a proteolytic ferment they secrete. They gradually burrow into the submucous coat and form colo
there. With destruction of tissues around the colonies ulcers develop. These ulcers are confined to the large
gut. Though the whole large gut may be involved, yet there are mainly two places which show predilection
to such ulcer formation — these are the caecum and the sigmoid colon. Caecum is more often affected than
the sigmoid colon. Amoebic ulcers are ragged undermined ulcers, which are flask-shaped on vertical section
These ulcers are usually round or oval and become transverse when these ulcers coalesce.
Complications.— (i) Local peritonitis, (ii) haemorrhage, (iii) perforation and general peritonitis, (iv)
pcricaecal or pericolic abscess, (v) fibrous stricture, (vi) intestinal obstruction, (vii) amoeboma, (viii)
sloughing and gangrene of the large gut.
Complications are rare. Perforation may occur in the caecum and rectosigmoid junction. Usually
perforation occurs in a confined place where adhesions have previously formed. So local peritonitis develop
followed by abscess formation, which eventually needs draining. General peritonitis from perforation is
extremely rare. Healing of extensive ulcers may lead to stricture formation and intestinal obstruction may
result. This may also follow adhesions associated with pericolitis. An uncommon complication of chronic
amoebic colitis is the amoeboma, a mass of granulation tissue in the colon. A tender sausage-shaped swellin
is often palpable. Partial obstruction may result. Granulomas are most frequent in the caecum which may be
confused with carcinoma, tuberculosis or actinomycosis.
Clinical features.— This may be divided into acute amoebic dysentery and chronic amoebic dysentery.
Acute amoebic dysentery.— This is rare and is due to massive contamination of the water supply. Onset
is abrupt with high fever, abdominal cramps and profuse bloody diarrhoea and tenesmus. Serological tests f
E.histolytica antibodies may be used to confirm the diagnosis. Trophozoites can usually be found in warm
saline preparations of fresh stools. Extensive ulceration of the rectum may be seen on sigmoidoscopy. This
condition must be differentiated from ulcerative colitis and Crohn’s colitis. Perforation may result which has
been discussed earlier.
Chronic amoebic dysentery.— It is the common form of this disease. Onset is gradual. There is intermittent
diarrhoea with 2 to 4 foul smellingstoolsdaily. There is vague abdominal pain. Stool may contain blood. Peri
of relapse is followed by a period of remission lasting for many weeks or months. Diagnosis may be difficult
as cyst or trophozoite may not be detected in the stool. E. histolytica antibodies may be detected in the serum
THE COLON 931
in majority of the patients.

Treatment.— Acute amoebic dysentery should be treated by metronidazole 750 mg 3 times daily for 10
days. Alternatively emetine-and tetracycline injection should be given initially to control symptoms followed
by a course of metronidazole. Chronic amoebic dysentery may be treated by diiodohydroxyquin 650 mg 3
times daily for 20 days. Diloxanide furoate 500 mg 3 times daily for 10 days is also successful in cases where
the previous drug is not so effective. One of the dreaded complications of diiodohydroxyquin is optic neuritis.
Tetracycline improves results probably by coping with superadded infection.
Amoebic abscess of the liver is the most common complication of amoebic colitis. Hepatic abscesses may
rupture into the pleura, pericardium or peritoneum.
ACTINOMYCOSIS
Actinomycosis is an uncommon suppurative infection produced by anaerobic fungus Actinomyces Israeli. These reside in the
mouth and invade whenever there is a breach in the mucous membrane. The cervico-facial area is the most commonly involved site
followed by thoracic and abdominal involvement.
In the abdomen, caecum is the most frequently involved site of actinomycosis. An indurated pericaecal mass sometimes develops.
This often follows appendicectomy. This fungus normally remains quiescent, after trauma it becomes virulent and infection results.
Gradually secondary infection sets in and an abscess develops. This abscess bursts and forms indolent external sinuses. At any stage of
the disease if pus is collected and allowed to trickle down the side of a test tube, sulphur granules may be discovered. The pus should be
sent for immediate bacteriological examination. Actinomycosis rarely gives rise to obstructive symptoms as the intestinal lumen is not
narrowed.
Treatment.— Actinomyces are usually sensitive to penicillin, tetracycline, lincomycin etc. A prolonged intensive course of penicillin
(10 megaunits daily) is quite effective.
Angiodysplasia (Vascular anomalies).—

The main pathology of this condition is capillary or cavernous haemangiomas present in the colon at any age.
Angiodysplasias occur mainly on the right side of the colon particularly in the ascending colon and caecum. Elderly
patients over the age of 60 years are mainly affected. The anomaly is in fact dilated tortuous submucosal veins. In severe
cases the mucosa may be replaced by massive dilated deformed vessels. Actual pathology lies in the vessels which are thin
walled, distorted and with scanty muscles in their walls.
The lesions may pass undetected at endoscopy, as the mucosa may look normal. The lesions may be seen on careful
inspection, as of a few millimetres in size and reddish raised areas. It is even more difficult to diagnose at laparotomy as
these cannot be felt nor seen from outside of the colon.
The aetiology of this disease is unknown.
The patient presents with chronic, intermediate or severe bleeding. It must be remembered that the common finding
however is obscure gastrointestinal bleeding and these are diagnosed when investigated for occult bleeding. The percentage
of the cases presented with occult bleeding is almost 50% or even more.
This condition is best diagnosed by colonoscopy and angiography. Before the advent of these two investigating
armamenterium, this condition was not known. Barium enema has no role to diagnose this condition and should better be
avoided. The effectivity of colonoscopy has been discussed above. The most reliable technique for demonstrating these
lesions is undoubtedly the selective mesenteric angiography. These will show the site and extent of the lesion with a blush.
In case of failure one can try using technetium-99m ("Tc) — labelled red cells, which will confirm the diagnosis.
Treatment.— Colonoscopic diathermy is sufficient for small lesions. When the bleeding is brisk, a catheter is introduced
through the appendix stump and the colon is irrigated with saline. Preoperative colonoscopy is carried out to detect the site of
bleeding. Electrocautary laser ablasion, injection sclerotherpy or argon beam ablation may be used to stop acute haemorrhage.
When the lesion is a big one or there are multiple lesions in a localised part of the colon, that part of the colon has to be resected w
end-to-end anastomosis to maintain continuity of the bowel. If there are multiple lesions involving other parts of the colon or it is
still not clear exactly which segment of the colon is involved, the treatment is total colectomy with ileorectal anastomosis.
DIVERTICULAR DISEASE
Two types of diverticula of colon are recognised — (i) multiple false diverticula of the left colon, which is
known as diverticulosis and (ii) rare true single diverticulum of the caecum or ascending colon. We shall now
discuss multiple false diverticula of the colon which is known as diverticulosis coli.
DIVERTICULOSIS COLI
Aetiology and Pathogenesis.— Diverticula ofthe colon are acquired herniations of mucosa and submucosa
through the circular muscle layer at the points where blood vessels penetrate the colonic wall. Diverticul
to occur in rows on either side of the colon between mesenteric and the respective antimesenteric taeniae
the penetrating vessel is in close relation to the neck ofthe diverticulum. The proximity of this vessel presumably
accounts for the propensity of diverticula to bleed. The mechanism how these diverticula are produced is
controversial. The followings are usually incriminated —
(a) Abnormal contraction rings form in the sigmoid colon. With contraction of the colonic muscles
intraluminal pressure goes upto at least 90 mm Hg. Contraction of these closed segments force the mucos
herniate through the weakest spot in the muscles.
(b) Chronic constipation with age and obesity and inherited predisposition may account for this con
(c) Hypertrophy of bowel musculature is often demonstrable in diverticular disease.
(d) Diet — a low residue diet definitely predisposes this condition. This is very rare in Asian countri
whereas it is a common disease in Western countries.
Sigmoid colon is the main site involved. Sigmoid colon plus descending colon are involved in 80% of
Sigmoid plus other colonic sites are involved in 95% of cases. Rectum and ascending colon are involved i
each cases. In about 5% of cases this disease may be associated with gallstones and hiatus hemia (Saint’s tr
Diverticulosis itself is an asymptomatic condition. Its main two complications are bleeding and inflamm
(diverticulitis).
Bleeding.— Two-thirds of all cases of massive lower G. I. bleeding are due to diverticulosis. Colorectal
carcinoma is the next cause of rectal bleeding, but this bleeding is nearly always mild or moderate. As the
diverticuli come out through the gap of the arteries in the muscle coat of the colon, bleeding is quite obvi
due to close proximity of the diverticuli to the arteries of the colon. Bleeding dye to diverticular disease is
characteristically sudden, unexpected and profuse from the onset. This characteristically occurs in old ind
viduals with atherosclerosis and/or hypertensive cardiovascular disease.
Treatment— Majority of the patients will stop bleeding spontaneously with adequate transfusion and
supportive therapy. A safe non-operative method of controlling diverticular bleeding is the selective infu
of vasoconstrictive substances such as vasopressin into the visceral artery supplying the bleeding site afte
identification by selective angiography. In some patients the bleeding is controlled and does not recur. Si
barium enema may be used as therapy for massive diverticular bleeding and in many patients bleeding w
arrested. If bleeding continues after correction of hypovolaemia at a rate of more than 500 ml per 8 hours
immediate operation is indicated.
Emergency operation for massive bleeding is rather difficult. The main problem is to find out the site from
where the bleeding occurs. After exploration, the whole colon will be seen distended with blood. Colosto
with operative endoscopy may not be able to locate the site of bleeding. In that case one can milk the who
colon to evacuate all blood clots through a rectal tube. Several occlusion clamps are applied to isolate diff
segments of colon. If active bleeding is present that segment of colon will fill up with blood. This portion
should be resected with primary anastomosis. Where bleeding point cannot be located properly, total abd
nal colectomy with ileoproctostomy is gaining favour as the procedure of choice.
DIVERTICULITIS
Inflammation is the commonest complication of diverticulosis coli. The chance increases as the age ad
vances. This condition is hardly seen below the age of 40 years. Diverticulitis is more common in patients
widespread diverticulosis.
Pathogenesis.— Diverticula remain filled with colonic contents. If an inspissated faecal plug obstructs the neck of
the diverticulum, proliferation of ever present bacteria produces inflammation within the diverticulum. If the obstructing
plug moves away the content of the diverticulum is discharged into the colon and inflammation subsides. If the obstructing
plug remains in place, inflammation spreads to the peridiverticular tissues. Extension occurs longitudinally. In the begin
ning diverticulitis starts in a single diverticulum and gradually spreads to the others.
Clinical features.— Clinical presentation may be ‘acute' or ‘chronic ’. The clinical picture of sigmoid diver
ticulitis very much resembles that of appendicitis and is often called left-sided appendicitis. While diverticul
mostly an asymptomatic condition, usually appearance of symptoms suggests that diverticulosis has pro
THE COLON 933
diverticulitis. Pain is the most important symptom. It is mild to moderate and is felt deep in the left lower qua
or suprapubic region. It is usually dull, continuous and aching, occasionally it may be intermittent and cramp
This is simply due to increased intraluminal pressure in an isolated segment of colon. Anorexia and mild naus
common, but vomiting is rare. Some change of bowel habit is noted — either diarrhoea or constipation. Low g
fever and mild leucocytosis are not uncommon. On examination, tenderness on the left lower quadrant is quite
diagnostic. A tender mass representing the inflamed faeces-filled colon may be palpable.
Special Investigations.— 1. Sigmoidoscopy — should be done immediately once this condition is suspected. This
is the only special investigation which can be done even in the acute stage. Mucosal oedema and erythema may be seen. It
is difficult or rather impossible to introduce the sigmoidoscope beyond 15 cm (rectosigmoid junction) due to immobility
to the bowel and fixed angulation at this point. It is more important to exclude other conditions.
2. Barium enema.— When acute stage has been subsided, barium enema may be performed. In the beginning small
saw-tooth projections from the contour of the colon may be seen. These projections are either necks of the diverticula or
they represent the filling of crevices between the folds of redundant mucosa. Large saw tooth or accordion-pleated outline
indicates more advanced stage of the condition. In the early stage this diverticula may have wide necks, but later the necks
become narrow and elongated. The so called ‘champagne glass’ sign indicates partial filling of a diverticulum which is
occupied by a stercolith.
Treatment.—
PREVENTIVE.— It is now obvious that diverticulitis is primarily due to over-use of low-residue diet. In
the early stage it seems possible that the condition may be reversed by adaptation of a high residue diet,
supplemented by bulk-producing laxatives such as Normacol or Isogel. It is only when the condition has been
organically irreversible that a bulk producing diet will become ineffective.
MEDICAL TREATMENT.—Medical treatment should be tried in all cases of first attacks of uncomplicated
diverticulitis. This treatment includes (i) admission to hospital, (ii) parenteral fluids, (iii) nasogastric suction,
(iv) broad spectrum antibiotic, (v) drugs such as Pentazocine to relieve pain, but morphine is not used as it
increases intracolonic pressure. Pethidine is quite effective drug in this condition, probanthine may also be
used as it relaxes colonic muscles.
Significant improvement of all symptom and signs is expected within 48 hours. Once the acute symptoms
have been relieved some form of therapy should be given to avoid constipation. Bulk laxatives are given to
keep the stool soft and bulky.
SURGICAL TREATMENT.— Indications of surgical therapy are: (a) If the patient does not respond prompt
to medical treatment; (b) Recurrent acute diverticulitis; (c) Diverticulitis with complications and (d) when
carcinoma cannot be ruled out.
When the disease is not associated with any complication which may require resective surgery, the elective
treatment of this condition is sigmoid myotomy. Muscle coats of the sigmoid colon are longitudinally incised
between the two antimesenteric teniae. This operation is technically similar to Heller’s operation done for
achalasia of the cardia or Ramstedt’s operation done for congenita! pyloric stenosis.
Operation.— A lower midline incision is preferred. The sigmoid colon must be carefully separated from the
left pelvic wall dividing peritoneal adhesions through a blood-less plane, so that the bowel may be held out th
the wound. A preliminary incision is made with a scalpel starting from the rectosigmoid junction and proceed
upwards on the exact antimesenteric border of the colon over the thickened bowel between the two antimesen
teniae. The incision is carried on proximaliy for 8 to 12 inches till normal unthickened bowel is reached and th
for an inch or so further. It may be necessary to incise upto 24 inches. It is important that the bowel should be h
straight, so that the incision is on the relatively blood-less midline. If bleeding occurs, a wet swab should be ap
while the other part of the incision is deepened. It may be of assistance to inject saline with or without adrenal
along the line of incision. Diathermy or ligation should be avoided. After preliminary incision, the cut is deepe
by snipping the circular fibres with the fine scissors till the mucosa bulges throughout the length of the wound
better to be too conservative than too drastic. Accuracy of division is assisted by maintaining gentle retraction
the lips of the incision by pairs of fine tissue forceps. Perforation of mucosa should be rare if meticulous dissec
is carried out. If it occurs, all that is necessary is to suture the mucosa with fine atraumatic catgut. A drain shou
inserted as a precaution after closing the rent. The sigmoid colon is now replaced inside the abdomen and the
incision on the left pelvic wall is closed. The abdomen is now closed.
Presence of pus or active peritonitis found on laparotomy is an absolute contraindication-far this opera
Complications of diverticulitis.—
1. PERFORATION and PERITONITIS.— The inflammation is usually localised to the area adjacent to t
perforation, thus forming a pericolic abscess. This abscess may in turn burrow into one of the viscera whic
contributed to the walling-off process and thus an internal fistula develops. Only occasionally the pericoli
may burst into the free peritoneal cavity producing purulent peritonitis. Also rare is that the initial perfora
not been walled-off, so that free perforation occurs with a chance of generalised faecal peritonitis.
Treatment.— With localised peritonitis medical treatment is justified with careful watch. When acute inflammation
has completely subsided, elective operation should be called for. In case of acute generalised peritonitis emergency opera
tion becomes mandatory. Operative procedure is as follows : —
Operative procedure.— In this case proximal diverting colostomy, closure of perforation and drainage should be
performed. In more infective cases, the diseased bowel is resected, end-to-end anastomosis is performed with a proximal
decompressing colostomy. Another procedure may be adopted in which the diseased bowel is mobilised and resected. The
proximal bowel is brought out as an end colostomy. The distal bowel is either brought out as a mucous fistula or the end
is closed and left in situ (Hartmann procedure). The peritoneal cavity is obviously irrigated with antibiotics and drains are
placed. After 2 to 3 months continuity is established by end-to-end anastomosis.
2. OBSTRUCTION.— Sometimes a patient will present when natural defences have localised the infection in the
pelvis and the patient is not seen by the surgeon till symptoms of intestinal obstruction have occurred. Partial obstruction
may be due to inflammation, spasm and oedema with an element of paralytic ileus. Complete obstrjetion may occur due
to repeated episodes of diverticulitis with fibrosis and stenosis. Straight X-ray of the abdomen is valuable to differentiate
between small and large bowel obstructions.
Treatment.— After exploration one should first attempt to find out whether or not a carcinoma is present and to do this it
may be necessary to mobilise the mass. The main treatment of obstruction with diverticulitis is diverting transverse colostomy
and primary resection of the bowel with anastomosis. In some cases when proximal distension is much, immediate transvers
colostomy is performed and an interval of about 3 months is allowed before resection is carried out. If carcinoma is suspected
primary resection is more justified, but in hazardous cases one may resort to resection 2 to 3 weeks after colostomy.
3. FISTULA.— Internal fistulas may be seen in 5% of cases between the involved segment of colon and adjacent
organs e.g. urinary bladder, ileum, uterus, vagina and ureter. Colocutaneous fistulas (external fistula) rarely occur sponta
neously, but are common postoperative complications through the incision or drainage site. Pneumaturia (air in the urine)
and Faecaluria (faeces in the urine) are diagnostic of colo-vesical or colo-ureteric fistulas. Fever is also common. Sigmoi
doscopy cannot demonstrate fistula, barium enema may sometimes demonstrate the fistula. But cystoscopy and cystogra
phy are more useful.
Treatment.— With proper preoperative preparation one stage operation may be possible. Fistula in the bladder is
dissected out and the bladder wall is closed. The diseased colon is resected with primary anastomosis. Suprapubic drain
age is given. In case of colouterine fistula, histerectomy with resection of involved colon is performed. Similarly in case
of coloenteric fistula segment of ileum and diseased bowel resected. When inflammatory process is extensive, operation
performed in two stages. The diseased bowel is resected and the proximal colon is brought out as end colostomy. The
distal portion is closed. Later on anastomosis is performed. Sometimes proximal to the diseased colon is incised, the
proximal colon is brought out as an end colostomy and the distal portion is sutured. When the inflammation has subsided
adequate resection is performed and end-to-end anastomosis is done.
VOLVULUS
Volvulus means rotation of a segment of bowel around its mesenteric axis. Partial or complete obstruct
the bowel occurs. Varying degrees of circulatory impairment may occur to the involved bowel by twisting
root of the mesentery. Volvulus can occur only in that part of the intestine which is freely mobile. In the co
volvulus in most frequently seen in the sigmoid colon (90%) and is occasionally seen (10%) in the caecum
is more mobile. Volvulus of transverse colon is extremely rare so is volvulus of the small intestine.
SIGMOID VOLVULUS
Aetiology.— (i) A redundant sigmoid loop attached by a narrow mesenteric root may cause sigmoid
volvulus, (ii) Severe chronic constipation is a frequent cause of sigmoid volvulus. Dilatation and lengthen
of chronically distended colon is responsible for volvulus. This mainly occurs in patients with severe
THE COLON 935
psychiatric or neurologic diseases or elderly people with cardiovascular and pulmonary diseases. It is quite
uncommon for sigmoid volvulus to occur in a person who leads an active life and has no serious mental or
physical illness, (iii) Congenital megacolon may be present in subclinical form throughout life. This probabl
accounts for only a small percentage of cases of sigmoid volvulus, (iv) It may occur in acquired megacolon,
a complication of Chagas’ disease.
Pathology.— Sometimes the sigmoid loop rotates for
half a turn and spontaneous rectification may occur. When
the sigmoid loop has rotated 1V2 turns the veins a re compresse
and the loop becomes greatly congested. If the sigmoid loop
has turned more than 1V2 turns, arterial supply is also cutoff
and the loop soon becomes gangrenous. It must be
remembered that sigmoid colon turns in anticlockwise
direction for volvulus to occur.
Clinical features.— Usually the patients are middle-
aged or elderly. Males are more commonly affected than
females. Sometimes a previous history of acute abdominal
pain on the left lower quadrant may be felt due to partial
volvulus. This volvulus untwists itself and is followed by
passage of large quantities of flatus and stool with relief of
Flg.53.9.— barium enema showing 'Bird’s beak- pain and distension. Onset of volvulus of the pelvic colon
deformity of sigmoid volvulus. as a rule sudden and is characterised by severe abdominal
cramp. This may occur when the patient is straining at stool. This is soon followed by progressive marked
abdominal distension with complete constipation and absence of passage of flatus. In the beginning the
distension is only in the left lower quadrant, but soon involves the whole abdomen. Hiccough and retching
may occur early, but nausea, vomiting and dehydration occur after several hours.
Special Investigations.— (i) Straight X-ray of the abdomen almost always shows a distended single loop
occupying the left lower half of the abdomen with both ends in the pelvis, called ‘bent inner-tube’ or ‘Omeg
loop’ sign. Variable distension of colon proximal to the obstruction and of the small bowel may be shown
dependingon the duration of obstruction, (ii) Barium enema radiography is usually not necessary. Only whe
the straight X-ray is atypical, barium enema radiography may be requited. Barium column ends at the level
of the distal sigmoid torsion ir. a characteristic ‘twisted bird's beak’ or ‘ace of spade’ deformity. Barium enem
is contraindicated when gangrene is suspected.
Treatment.— Sigmoidoscopy is carried out to visualise the site of distal sigmoid obstruction. If frank
mucosal ulceration or dark blood is seen strangulation of the involved bowel is probable and emergency
operative intervention is indicated. If no signs of strangulation are seen, a well lubricated rectal tube is passed
via the sigmoidoscope through the obstructing twist into the distended loop of volvulus. Deflation of the
volvulus occurs and the tube is secured in place by taping it to the buttock and left in place for 2 to 3 days un
bowel function resumes. Patient should be closely watched for signs of gangrenous bowel. There is a small
chance of perforating the weakened sigmoid colon. This tube deflation is usually successful in 75% to 80%
of cases.
If tube deflation fails, immediate laparotomy is mandatory. If the segment is viable at exploration, simple
derotation (or detorsion) should be performed.
When strangulation is suspected, the strangulated bowel must be resected and the proximal end is broug
out as a colostomy. The distal loop is closed as done in Hartmann procedure. Later on when the patient’s
condition approves end-to-end anastomosis is performed. Mukulicz exteriorization may be performed as an
alternative procedure followed by resection when the patient’s condition permits. A few authors have
advocated primary resection and anastomosis for all patients with volvulus requiring emergency operation.
The mortality rate of this emergency operation is about 50%.
Following successful nonoperative reduction (tube deflation), patients should probably undergo elective
resection, as the risk of recurrence is very high (55%). Resection with primary anastomosis should be
performed with prior preparation of the patient for 1 week.
VOLVULUS OF THE CAECUM
Aetiology.— There is only one definite aetiology of caecal volvulus — that is when there is hypofixation
of the caecum and proximal ascending colon and this portion becomes congenitally mobile, volvulus of
caecum may occur.
Pathology.— Volvulus of caecum occurs in a clockwise direction. The first twist obstructs the ascending
colon and the 2nd twist obstructs the ileum.
Clinical features.— Volvulus of caecum may be seen at all ages, but is most frequent between 25 to 35
years of age. The clinical manifestations are those of acute small bowel obstruction. Onset is rapid and
characterised by midabdominal colicky pain, followed by abdominal distension, nausea and vomiting. Pain
is intermittent in the beginning, but soon becomes constant severe burning pain within a few hours. In the
beginning some faeces and flatus may be passed as the existing content of the colon, but soon absolute
constipation and absence of passage of flatus ensue. On examination, the abdomen is distended and
hyperresonant on percussion particularly in the right lower quadrant. Rigidity, tenderness and rebound
tenderness indicate strangulation of the bowel.
Special Investigations.— (i) Straight X-ray of the abdomen is again diagnostic. Volvulus becomes
obvious by presence of massive distension of the caecum and distended small intestine loops. There may be
air-fluid level in the caecum. It must be remembered that distension may not be obvious in the right lower
quadrant, as the caecum is mobile and distension may become apparent in the middle or even in the left sid
of the abdomen. There is relatively empty large intestine, (ii) Barium enema is usually not helpful, except th
it may indicate the location of obstruction. It also excludes possibility of sigmoid volvulus.
Treatment.— Operation should always be performed. The volvulus is derotated and the mobile caecum
should be fixed by suturing to its original place (caecopexy). Sometimes untwisting is not possible unless th
distended caecum is deflated by insertion of a needle. In this case untwisting should be followed by
caecostomy, which prevents recurrence and relieve distension. If strangulation is present, right haemicolecto
with ileotransverse colostomy should be performed. Only in moribund cases, exteriorisation of the strangula
bowel is justified.
NEOPLASMS OF THE COLON

Broadly, neoplasms of the colon and rectum can be classified into two groups — A. Polyps and B.
Carcinoma.
A. POLYPS
Any circumscribed mass of tissue that arises from mucosa and protrudes into the lumen of the G.I. tract
is called a polyp. This is a purely clinical term and this term does not signify anything histopithologically.
Polyps of the colon are classified as follows :
(a) INFLAMMATORY —
(i) Benign lymphoid polyps;
(ii) Pseudopolyps (Ulcerative colitis).
(b) HAMARTOMAS —
(i) Juvenile polyp;
(ii) Peutz-Jegher’s polyp.
(c) HYPERPLASTIC POLYPS.
(d) NEOPLASTIC —
(i) Tubular adenoma (adenomatous polyp);
THE COLON 937
(ii) Villous adenoma (papilloma);

(iii) Familial polyposis coli.
INFLAMMA TORY POLYPS
In this group there are (i) benign lymphoid polyp and (ii) inflammatory polyposis.
The benign lymphoid polyp is most frequently found in the rectum and terminal ileum. As the name
suggests, it is composed of normal lymphoid tissue, but devoid of sinuses. Sometimes diffuse benign lympho
polyposis occurs when the whole of colon and rectum show hypertrophy of these lymphoid aggregates. Ben
lymphoid polyp is more common in children. Only excisional biopsy can diagnose this condition with
certainty.
Inflammatory polyposis is associated with ulcerative colitis or Crohn’s disease. It is not these pseudopolyps
or inflammatory polyps which are precancerous, but the flat mucosa in between these pseudopolyps turn int
malignancy in long standing cases of chronic ulcerative colitis.
HAMARTOMAS
JUVENILE POLYPS —
As the name suggests this polyp principally occurs in children in the first decade of life. But it must be
remembered that this condition does appear in adult also. These are uncommon after 15 years of age and
extremely rare after 30 years. The highest incidence is at age of 5 yrs. These polyps are single in 70% of patien
Even when these are multiple, these are only 3 or 4 in number. In extremely rare instances this polyp may be
so numerous as may simulate familial polyposis. Familial incidence has been noted and inheritance is throug
autosomal dominant gene.
PATHOLOGY.— Macroscopically these polyps are usually oval in shape, some are nearly spherical and
almost always pedunculated. This lesion is approximately 3 to 10mm in diameter, smooth, reddish brown an
covered with mucous membrane. Microscopically, there is proliferation of glandular and stromal elements
with marked vascularity and infiltration with lymphocytes, polymorphs, plasma cells and eosinophils. The
slender stalk is covered with normal colonic mucosa continuous with the adjacent mucosa. The bulbous porti
is covered by a single layer of goblet cells, which may become ulcerated and chronically inflamed.
As to its pathogenesis, it is controversial. Retained secretions have often been incriminated and so it is also
called ‘retention polyp’. Hereditary, inflammatory, allergic and congenital theories have also been put
forward. This polyp is not neoplastic.
CLINICAL FEATURES.— The most important symptom is streaks of blood on the stool. Occasionally
rectal bleeding is also complained of. Repeated bleeding will make the patient anaemic. Rectal polyp may
protrude through the anus and the patient will complain of something coming out during defaecation. Very
rarely a colonic polyp may initiate intussusception. Rectal examination is very important as majority of these
polyps are seen in rectum and may well be reached by the index finger. Sigmoidoscopy will help to visualise
when the polyp is higher up. Colonoscopy will diagnose this condition in case of polyp even higher up. Bariu
enema, particularly air-contrast type, will help in the diagnosis of this condition.
TREATMENT.— As this neoplasm is without malignant potentiality, treatment is excision biopsy. This
excision can be done easily when the polyp is within the reach of the finger during rectal examination. When
it is beyond the reach of the finger, excision is performed either through sigmoidoscope or colonoscope by
cold biopsy forceps orelectrothermic snare. Only occasionally transabdominal approach may be required and
polypectomy may be performed through colotomy.Shortsegmental resection of the colonisvery rarely needed
when the polyp has a broad base or almost sessile. These polyps do not recur after excision. But new polyps
may appear in other place in about 10% cases after polypectomy.
POLYPS ASSOCIATED WITH PEUTZ-JEGHER’S SYNDROME.— These polyps are usually
situated in the small intestine. However these can occur in colon or rectum and may be multiple. These polyp
are also not precancerous but cancer may be associated with this condition.
HYPERPLASTIC POLYPS
Tbese are mostly of academic interest as these usually do not produce any symptom. These small
plaque-like polyps are usually encountered at proctosigmoidoscopy or colonoscopy. These are usually sess
and less than 1 cm in diameter. These are frequently multiple. These are seen in all ages, but more frequent
i bove 40 years of age
■- , minor imbalances between cell divisionand metaplasia.
So these are often called‘metaplastic polyps’.
If detected accidentally, excision is indicated only
mP for histological diagnosis.
NEOPLASTIC
■' - A T U B U L A R ADENOMA.—
:■ H m j W ff I lt k
is also called adenomatous polyp and its
:1"; incidence in the colon and rectum is approximately 5
~ TL ..' nl- to 10% ofthe general population. It is much commoner
i ' ^ K .jr than villous adenoma (8 : 1). It is the most common
■■ "i;• ’ ■ v r j B t - " jjHgineoplasm of the colon and rectum. This condition is
^ rare in patients under 20 years of age (except familial
j polyposis). Its incidence increases as age advances and
\A majority of patients are in the 6th decade.
v Distribution of this tumour is variable, but about
70% occur in rectum, rectosigmoid and lower sigmoid
r, rr, „ . , . . . , colon within the reach of the sigmoidoscope. 20
r % in
Fig. 53.10.— Pedunculated adenomatous polyp. °
the upper and middle sigmoid colon. 3% in the
descending colon and only 2% each in transverse and ascending colon. Its incidence is currently shifting more
to the right colon and recent series show more than 2% incidence in the ascending colon.
PATHOLOGY.—These are usually pedunculated,
’ H,______ firm in consistency, vary in size from 1 mm to several
centimetres in diameter. The bulb is pink It' red m
■ •*' colour and is usually irregularly lobulated. If it is
*' ulcerated the polyp is generally malignant.
Microscopically in the beginning one can see
* / J* ' replacement of some of the lining cells of the crypts by
/\ M cells that are taller, more slender and more
hyperchromatic. The nuclei stain darkly and there are
—- * III a few vacuoles indicative of mucin secretion. Mitotic
r - f figures are abundant. As it grows the stalk represents
vascular connective tissue covered by mucosa and the

;: muscularis mucosae which has extended from the
gi normal adjacent mucosa. This suggests that the stalk is
h i not a part of neoplasm and is pulled out by peristaltic
i - t r a c t i o n . The head of the polyp consists of glands with
' . considerable variability in size and shape. Not
infrequently circumscribed areas of tubular adenomas
may demonstrate the cytologic criteria of malignancy
Fig. 53.11.— Barium enema showing . ...
pedunculated polyp. ,e'marked pleomorphismand atypical glands and cells
with frequent mitoses and hyperchromatism. This is
THE COLON 939
carcinoma in situ. Truely invasive carcinoma can be diagnosed only if there is definite invasion beneath the
muscularis mucosae.
CLINICAL FEATURES.— Majority of the tubular
adenomas are asymptomatic and are discovered on routine
■ proctosigmoidoscopy or barium enema performed lor so
other reason. When these become symptomatic, the most common
, symptom is modest degree of rectal haemorrhage. Mucus
discharge per rectum and something coming out through anus
arc other symptoms which may be complained of. Anaemia of
unknown cause may be the presenting feature. Occasionally
’.. v abdominal pain maybe the only complaint. Intestinal obstruction
■ Treatment.-— It is described alongwith the treatment of

villous adenoma.
VILLOUS ADENOMA.—
It is also called papillary adenoma as it consists of pointed
or blunt finger-like processes of lamina propria covered by
epithelium that shows branching. This type is often sessile than
Fig. 53.12.— Benign polyp outlined In pedunculated. Majority of this lesion is more than 1 cm in size
barium-filled colon. ancj jn fact of villous adenoma are over 2 cm in diameter.
It is much rarer than tubular adenoma and in fact its incidence is ‘/gth that of tubular adenoma. About 60%
villous adenoma arise in the rectum, 20% in the rectosigmoid junction, 10% in the sigmoid colon and 10%
in all segments of the colon. While majority of the victims of tubular adenoma are in the 6th decade, villous
_______ adenoma is more common in the 7th decadc and this is
j PATHOLOGY.— Grossly, villous tumours arc

' Bfer Sail bulky,sessileandpoorlydemarkated.Theyaresmooth,
soft a ltd velvety, so difficult to detect by palpation. That
is the reason why though majority of these tumours
arise in the rectum and may be within the palpable reach
. of the finger, yet it is often missed by the clinicians.
\ ,* >• Areas of Firmness represent malignancy. The colour is
^ almost similar to the adjacent mucosa or it may be bit
. ■. '| v» j? more pale. Numerous lrond-like processes may be
Microscopically, these arc numerous long villous

projections with narrow stroma covered by a single
layer of cylindrical epithelial cells. The cells are
' elongated with nuclei compressed and situated in the
’ basal portion. When malignant transformation is seen
- ’JsP* ; nd the diagnosis of invasive villous adenocarcinoma
invasion.
Fig. 53.13.— Gross appearance of sessile villous Clinical features.— Two-thirds of patients will
adenoma showing shaggy surface due to thousands present with bright red rectal bleeding. Discharge
of flnger-llke processes. mucus and watery diarrhoea are also common
complaints. Weight loss is seen in about */2 the cases. About l/2 the patients will present with obstruction,
constipation and lower abdominal colic. This tumour is liable to secrete a large quantity (about 3 litres/day)
of electrolyte-rich mucus. So hypokalaemia (as much as 200 mEq of K* per day may be required, as 25 to 35
mEq pe. litre is lost), hyponatraemia (100 to 150 mEq per litre is lost), hypochloraemia and uraemia are not
uncommon.
Diagnosis is mainly performed by sigmoidoscopy and biopsy. To know whether invasive cancer is present
or not, biopsy should be taken from the junction of normal colon with the base of the tumour. The tumours
which are above the reach of sigmoidoscopy, barium enema is the diagnostic tool available. Irregular filling
Fig. 53.14.— Barium contrast film showing Fig. 53.15.— Barium enema film showing villous
benign sessile polyp. adenoma causing a filling defect.
defect with wrinkled margin is the usual barium enema picture of this tumour. Colonoscopy can a Iso diagnose
this tumour with added advantage of biopsy.
Treatment.— (i) In case of small tumours without invasive malignancy above the peritoneal reflexion,
colonoscopic removal by cautery snare is justified. All polypoid lesions greater than 1 cm diameter should
be removed totally and submitted for histologic examination, (ii) Large tumours with invasive malignancy
located above 7.5 cm from the dentate line, anterior resection is indicated, (iii) When the similar lesion lies
less than 7.5 cm above the dentate, combined abdominoperineal resection should be performed, (iv) When
invasive cancer is not demonstrable on biopsy, the lesion is completely excised after wide dilatation or division
of the anal sphincter. The entire specimen is now examined histologically. If invasive malignancy is not
detected, no further treatment is necessary. If invasive malignancy is detected, immediate abdominoperineal
resection should be carried out.
It is always advisable to do follow-up proctoscopy at regular intervals, as recurrence is common even
though the lesion is histologically benign.
FAMILIAL POLYPOSIS COLI —
Multiple adenomas ofthe colon are now recognised as a Mendelian dominant inherited disease, that will
eventually develop into adenocarcinoma. Carcinoma of the colorectuni will develop in essentially 100% of
patients with familial polyposis unless treated or death from another cause supervenes. This is a rare condition
Males and females are equally affected and either may transmit the disease. These usually start at the age of
about 13 years in the distal segments ofthe colon and rectum. More and more polyps gradually appear till the
THE COLON 941
age of about 20 years when the entire colon and

rectum are involved. The small bowel is not involved.
Though this is the usual presentation, yet polyposis may
start even earlier. Cancer associated with this disease is
often multiple. If untreated, majority die of carcinoma
before the age of 50 years.
Pathology.—Microscopically, the polyps are tubula r
adenomas, absolutely similar to that of solitary tubular
adenoma seen in adult. These may be mixed with
villous adenoma. Though potentiality of single polyp to
develop into cancer is negligible, yet conglomeration of
thousands of polyps increase potentiality to transform
into carcinoma to a great extent.
Fig. 53.16.— Familial polyposis. Large pedunculated Clinical features.— This condition also does not
lesions have the structure of papillary adenomas. The smallproduce prominent symptoms so that the disease can be
tumours are early adenomatous polyps.
diagnosed early. The symptoms may be absent or slight
intermittent abdominal discomfort may be the only symptom present. Passage of loose stool, blood-stained
stool with mucus and frequent bouts of abdominal pain are quite common. Anaemia, weight loss and gene
debility appear alongwith carcinoma. In certain cases the symptom is only revealed when rectal cancer has
developed. Occasionally large polyps may prolapse through the anus or cause intestinal obstruction by
initiating intussusception.
Special Investigations.— (i) Air contrast barium enema will determine the extent of the disease and will
almost confirm the diagnosis.
(ii) Sigmoidoscopy or colonoscopy will visualise the lesion and added advantage will be biopsy o
lesion. Any lesion, particularly in the distal colon and rectum, suspected to be malignant should also be bi
Treatment.— Total abdominal colectomy, abdominoperineal resection of rectum and anus and terminal
ileostomy should be the treatment of choice. This is the only way to get rid of all polyps and discard any ch
of malignant transformation.
To avoid ileostomy some surgeons would prefer to do a subtotal colectomy with an ileorectal anastomosis.
There remains a chance of developing cancer in the retained rectum, which is claimed as 5% in 5 years.
Obviously regular follow-up proctoscopy should be performed to assess such condition ill early stage. The
are also reports of spontaneous regression of rectal polyps after ileoproctostomy. So if close follow-up is
performed this procedure can be adopted in patients who have no polyp in the rectum.
Another alternative is subtotal colectomy with endorectal ileoanal anastomosis. In this technique the
neoplasia-borne rectal mucosa is removed and the ileum is anastomosed with the anal canal through the re
Disadvantage is that bowel control is not as normal.
GARDNER’S SYNDROME.—
This isa syndrome in which multiple polyposis is associated with bony tumours (osteomas or exostoses principally of the skull,
mandible and sinuses and even fibrosarcoma of the ribs) and soft tissue tumours (sebaceous cysts, fibrous, desmoid tumours in
abdominal incisions and postoperative mesenteric fibromatosis).
Multiple polyposis is not similar as familiar polyposis coli in the sense that (i) polyps are also present in the small bowel
(duodenum, jejunum and ileum), (ii) polyps do not appear before the age of 30 or even 40 years and (iii) colorectal cancer is found
in */3rd of cases.
This isalsoan inherited disease transmitted by autosomal dominantgene, but different from that determiningfaniilial polyposis.
There is another syndrome known as Turcot syndrome which includes polyposis coli and central nervous system tumours.
B. CARCINOMA
Cancer of the colon and rectum compete with only the lung as the leading site of cancer in countries like
U.K. and U.S.A. Its incidence is probably lower in Indian subcontinent. Females are slightly more affected
than males. It is a disease of old individuals, yet this carcinoma is seen below 40 years of age and even befo
the age of 20 years when it is in association with familial polyposis. Its peak incidence is in the 7th decade.
The distribution of colorectal cancer is such that rectum is the most affected part, next comes sigmoid colon
and after that is the caecum. Ascending, transverse and descending colons are after caecum in order of
frequency, while hepatic and splenic flexures are the last to be involved by this disease.
Aetiology.— (a) There are a few conditions which are considered to be precarcinogenic. These are (i)
villous adenoma, (ii) familial polyposis, (iii) Gardner’s syndrome and (iv) chronic ulcerative colitis. But this
accounts for only a small number of carcinomas seen in practice.
(b) Genetic factors have been suggested as incidence of this disease is often found in families.
(c) Contribution of adenomatous polyp is still speculative.
(d) Diet is probably the most important aetiologic factor in this disease. Colorectal carcinoma is more
frequently seen in Western countries. Those who eat a diet of raw fruits and vegetables and unrefined grains
and produce large bulky stools with a rapid transit time are much less affected by this cancer, polyps and
diverticulosis. The rate of colonic cancer is directly proportional to the level of animal fat, particularly beef,
in the diet. High fat diet changes the composition of intestinal flora, with an increase in the species able to
chemically alterprimary bile acids and sterols. Primary bile acids are converted to secondary bile acids such
as deoxycholic and lithocholic acids, a step in the formation of carcinogenic polycyclic aromatic compounds.
(e) Bile acid intestinal flora hypothesis of colonic cancer is more firmly based by the fact that
cholecystectomy increases the risk of colonic cancer by about two times. Absence of gallbladder will lead to
continuous flow of bile salts and prolonged exposure of bile acids to intestinal flora which will change the
primary bile acid to secondary bile acids.
PATHOLOGY.— Previously, as described earlier, 75% of colorectal cancers were within the reach of
the examining finger or sigmoidoscope and only 20% were seen in the caecum and ascending colon. But
gradually there is a shift to the right colon and now only 40% are claimed to be within the reach of
sigmoidoscope and nearing 30% are seen in the caecum and ascending colon.
GROSSLY colorectal carcinomas can be divided into four types, (i) Cauliflower or polypoid variety, (ii)
Ulcerative type, (iii) Tubular variety or scirrhous type and (iv) Annular type.
Cauliflower variety is least malignant and commences as a benign adenoma. The annular variety which
is more often seen in the sigmoid colon and rectum carries a relatively better prognosis, not because the growth
is of low-grade malignancy, but because it gives rise to early obstructive symptoms and is extirpated early
before it metastasises.
MICROSCOPICALLY, it is a columnar celled carcinoma arising from the epithelial cells or in the crypts
of Lieberkuhn. In well differentiated tumours the cells are grouped inacinar clusters simulatingnormal glands.
In poorly differentia ted or anaplastic tumours, cells are dispersed in irregularsheetsor cords with no suggestio
of gland formation. The tumour cells also show no resemblance with colonic mucosa cells. Malignant cells
are characterised by pleomorphism, hyperchromatism, large vesicular nuclei of various sizes and shape with
frequent mitoses. Broder ’s classification grading system indicates whether the tumour is a well differentiated
type or anaplastic type to predict biologic behaviour of the tumour.
Spread.— I. LOCAL SPREAD.— The growth is limited to the bowel for a considerable time. It first
spreads circularly round the intestinal wall and to certain extent longitudinally. So it can cause intestinal
obstruction early before penetrating into adjacent structures. Only in case of ulcerative variety there is more
penetration into the bowel wall and to the serous coat, ultimately adjacent structures are invaded. Thus interna
tistula may result. Such penetration will also lead to local abscess formation and external fistula.
II. LYMPHATIC SPREAD.— The lymph nodes draining the colon are classified as follows :
(a) Epicolic lymph nodes, situated on the bowel wall.
(b) Paracolic lymph nodes, lying in relation with the. straight arteries arising from the marginal artery
to supply the colon.
(c) Intermediate lymph nodes, lying close to the main arteries to the colon e.g. the right colic,
ileocolic, middle colic, left colic and the sigmoid colic arteries.
THE COLON 943
(d) The main lymph nodes, which are grouped around the origin of superior mesenteric or inferior
mesenteric artery.
Regional lymph node involvement is the most common form of metastasis in colorectal carcinoma. Even
when the lesion is confined to the bowel wall, incidence of positive nodes is about 45%. To perform radical
excision of colon, the affected lymph nodes should be removed en masse and to perform this, the arteries
alongwith the lymph nodes are clamped and a long segment of bowel has to be excised.
III. BLOOD SPREAD.— This is rather late in colorectal carcinomas. Haematogenous metastasis only
occuis when tumour cells invade veins. The usual route is via the portal system and the liver is most commo
affected. Lungs and bones are the next common sites and the cells reach there by passage through the liver
into the inferior vena cava or by extension of the tumour into the tissues drained by systemic veins.
IV. COELOMIC SPREAD.— When carcinoma has penetrated the serosa, cells may become detached
and seeded to distant points in the peritoneal cavity and eventually peritoneal carcinomatosis results. Early
sites of involvement are the omentum and rectovesical or rectouterine pouch. Another frequent site is the ova
resulting in large bilateral Krukenberg’s tumour and bilateral oophorectomy may be needed unless there is
definite contraindication.
DUKE’S CLASSIFICATION.—
Stage A. — The growth is limited to the bowel; prognosis is exellent.
Stage B. — The carcinoma has spread by direct continuity into the adjoining structures, but without
lymphatic metastasis; prognosis is relatively good after surgical treatment.
Stage C.— When the malignant growth has given rise to lymphatic metastases.
CLINICAL FEATURES.—CARCINOMA OF THE RIGHT COLON.—The faecal content of the
right colon is fluid, moreover it is about 2 ‘/2times broader than the left colon, so obstructive symptoms are
unusual here. Cauliflower or polypoid tumour is the most common type in this region.
(i) Anaemia of varying degree is very common in case of carcinoma at this region, (ii) Dull, nagging pa
in the right lower quad rant of the abdomen is sometimes come across, (iii) Pallor, easy fatiguability, weaknes
dizziness, dyspnoea on exertion may be the only symptoms, (iv) Anorexia, indigestion and weight loss are
often the presenting complaints, (v) Palpable mass in the right lower quadrant helps a lot in the diagnosis of
this condition. In only 10% of cases this is the first sign of disease. Sometimes the patient will complain of
above symptoms only and on careful palpation the mass may be discovered, (vi) Severe symptoms such as
cachexia, jaundice and hepatomegaly will obviously group this tumour as an advanced one.
CARCINOMA OF THE LEFT COLON.— Majority carcinomas arise in this part of colon. The calibre
of the lumen is smaller and the faecal content is more solid. Obviously obstructive symptoms predominate.
Cancers in this region are usually of annular or scirrhous type.
(i) A change in bowel habit is often the first symptom. The patient often states that he is facing difficulty
in getting the bowels to move, so he has to take increasing doses of purgatives. Because of drastic purgation
and irritation by the scybala above the neoplasm, excessive mucus is secreted and diarrhoea follows. So
constipation followed by diarrhoea is a very suggestive symptom, (ii) Pain may be of constant ache, which
suggests pericolitis or cramping type due to obstruction, (iii) Palpable lump is often not the growth but
impacted faeces above it. Only in case of pelvic colon tumour a movable swelling may be felt. Rectal
examination will also feel such lump in the rectovesical pouch, (iv) Distension may be present above the
growth, as obstruction is a very common feature of cancer in this region, (v) Blood and mucus in the stool ma
be complained of. (vi) Anaemia is uncommon, but if present indicates poor prognosis, (vii) Tumour at the
splenic flexure tends to invade adjacent structures and gives rise to various symptoms. With gastric
involvement gastrocolic fistula may result, (viii) Complete intestinal obstruction may be the presenting featur
in some patients.
CARCINOMA OF THE SIGMOID COLON.— Though tubular variety is often seen in the rectosigmoid
junction, annular or cauliflower growths may be seen in the sigmoid colon.
(i) Papilliferous growth in the sigmoid colon may give rise to feeling of the need of evacuation, which
may result in ‘tenesmus’ accompanied by passage of mucus and blood. This particularly occurs in the ea
morning, (ii) A mass may be felt as described above, (iii) Pain in the form of colic, may be present, thoug
not common, (iv) Bladder symptoms are not unusual. They indicate irritation of the bladder or may hera
colovesical fistula.
CARCINOMA OF THE TRANSVERSE COLON.— Pain or palpable lump are the two main modes of
presentation. Pain, if present, is usually of colic type. Palpable mass often makes difficulty to differentiate
stomach cancer.
... Associated anaemia,
■kL. '' anorexia, lassitude are
Hf.-'; 'jjSS almostalwayspresenl.
■fe SPECIAL IN
I! . JtaQSRT % VESTIGATIONS.—
, 1. Sigmoidosco
py.. py.— Whenever in
^ doubt sigmoidoscopy
J
ft. should be performed
!r': "m*. to exclude carcinoma
in the rectum a nd low
er sigmoid colon. It
must be remembered
that nearly 70%ofcan-
cers are within the
reach of sigmoido
scope. Biopsy must be
taken if a lesion is sus-
WJ jtt pected to be carcino
ma.
|F <► 2. Radiography.—
Barium enema X-ray
^ i i M should always be
performed even when
Kat i sigmoidoscopy has
.JH revealed a growth.
This is to exclude any
fiSTl^r lesion above the reach
\-; of the sigmoidoscope.
^ A carcinoma is
visualised as a
constant, irregular
filling defect. Negative
Hg. 53.17.— Air contrast enema examination Is quite helpful In finding out any growth X-ray finding cannot
Ir. the colon — be It benign or malignant. This Is such a film of normal colon.
exclude presence of a
growth.
Air contrast enema is the investigating technique in which the barium emulsion is partly evacuated and
air is injected into the colon. By this technique the neoplasm that fails to alter the contour of the barium fill
colon may be demonstrated. Small neoplasms involvingonly the mucous membrane may be demonstrated
this technique.
A tumour of the caecum is more likely to be discovered by barium meal X-ray. Otherwise it is better to
THE COLON 945
avoid barium meal X-ray as it may

precipitate intestinal obstruction.
3. Colonoscopy.— Since barium
enema was introduced there has been no
practical diagnostic method in the colon
after X-ray and before the surgeon’s knife.
With the advent of fibreopticcolonoscope,
the whole of the colon upto the caecum can
be viewed for practical purposes. This
instrument is preferred to sigmoidoscope
by majority of the patients.
The key to pleasant and successful
colonoscopy lies in achieving a clean bowel
before hand. Colonoscopy is never done
under general anaesthesia, but it may be
done aftersatisfactory analgesia by injecting
intravenously diazepam (Valium) 5-20 mg
and pethidine 25 to 75 mg. It is extremely
important for the endoscopist to pay
attention to any pain being experienced
because of excessive stress on the bowel
wall or on the attachments of the colon.
Colonoscopy and the contrast enema
are complementary procedures. When the
barium enema report is at hand, the strong
indications of a diagnostic endoscopic
examination following the contrast study
are listed below : (i) X-ray study negative,
but the symptoms persist including occult
Fig. 53.18.— Shows how fibreoptic colonscope can bloodandanaemia;(ii)X-raystudy positive
be used to see Inside of the colon upto caecum. yet for confirmation; (iii) X-ray study
positive for cancer, but for taking biopsy;
(iv) X-ray study positive for cancer yet to exclude synchronous cancer or associated polyps; (v) X-ray study positive for polyp,
but to exclude malignant change or for additional polyps, (vi) X-ray study positive for inflammatory disease, but to know the extent
of disease and for biopsy.
Perforation is the most frequently reported complication. There are certain clinical conditions in which an attempt at
endoscopic examination appears unwise. These are (i) acute toxic dilatation of the colon, (ii) acute severe ulcerative colitis, (iii)
acute diverticulitis, (iv) radiation necrosis, (v) recent bowel anastomosis and (vi) in uncooperative patients.
BIOPSY.—Biopsy can be taken under direct vision through colonoscope from any point in the colon and even from the tjistal
ileum into which the colonoscope can be introduced. Flexible biopsy forceps are supplied by the manufacturer for this purpose.
This is a safe procedure and hardly gives rise to any complication. The biopsy bite is rather superficial and thus may fail to obtain
a suitable diagnostic tissue specimen. In inflammatory disease, the site of biopsy should be carefully selected. In case of polyps,
one or more biopsies may not be representative of the whole lesion and a locus of cancerous change may be missed. The only wa
to be entirely certain about presence or absence of cancer in a polyp is to remove the entire polyp and study it under the microsco
In case of obvious cancerous lesions endoscopic biopsy has definitely been successful.
CYTOLOGIC STUDIES.— Wash specimens or brushing may be obtained by colonoscope for cytological study. This is
particularly useful where a biopsy cannot be obtained or there is luminal constriction or acute angulation preventing advancement
of the instrument.
COLONIC CANCER.—Colonoscopy has definitely facilitated discovery of colorectal cancer at an early and more favourable
stage of the disease. It has also introduced an opportunity for cancer prophylaxis by removal of premalignant lesions e.g. polyps.
Colonic cancer lends itself to cure by surgery when the tumour is confined to the bowel wall and does not involve the serosa (Duke
classification A). Here the cure rate is about 90% or more. Even cancers can be discovered by colonoscopy when contrast enema
are negative. There is good reason to believe that regular endoscopic reexamination is desirable in patients at high risk for
developing colorectal cancer. Sometimes cancers of the colon may be multiple either synchronously or metachronously.
Metachronous lesions have been discovered within 3 years of the date of original surgery.
INFLAMMATORY DISEASES. —A number of inflammatory ...ditions of the colon can be diagnosed readily and more
accurately by colonoscopy than by other available methods. Chronic ulcerative colitis is a disease that waxes and wanes in
intensity. Contrast enema frequently fails to reveal the true severity and extent of the disease. Colonoscopy can assess the situatio
with greater accuracy. It also affords the opportunity of taking biopsy to exclude presence of carcinoma. Crohn’s disease is also
60
more accurately diagnosed by colonoscopy particularly the skip lesions. It also provides an opportunity to take biopsy. One ca
even see the distal ileum through colonoscope where this condition more commonly involves. Colonoscopy has also a value t
disclose recurrences in distal ileum following ileocolic anastomosis. In case of ischaemic colitis colonoscopy also confirms the
diagnosis and extent of the disease. But some endoscopists believe that colonoscopy is contraindicated in this condition.
Deverticulitisshould not be studied colonoscopically during the acute phase mainly due to fear of perforation. In chronic phase
this condition can be diagnosed endoscopically.
COLORECTAL POLYPS.—Polypectomy via colonoscope is now an established procedure and is widely practised. In this
way colonoscopy provides prophylactic treatment of colonic cancer as there is a rapid accumulating body of evidence indicatin
that most, if not all, colonic cancers develop from polyps.
LOWER GJ. TRACT HAEMORRHAGE.—When such haemorrhage is mild colonoscpy is quite successful in pointing out the
site and cause of haemorrhage. However in case of massive haemorrhage colonoscopy may fail to detect the site and cause o
haemorrhage.
CONCLUSION.—In short, colonoscopy has brought about revolution in the diagnosis of many colorectal conditions which
were difficult to diagnose previously. Particularly in detecting early cancer and treatment of highly placed polyps by polypectom
it has proved itself an indispensible equipment available to surgeons in diagnosis and treatment of colon pathologies.
4. Computed Tomography Scanning (CT SCAN) is emerging as a sensitive, nan-invasive method of
evaluating the extent of the disease particularly in the pelvis. Lymph node metastasis may be detected by t
technique.
5. Intravenous urography is done whenever a lesion is suspected to have involved the urinary tract.
TREATMENT.— Surgical removal is the only acceptable curative therapy for colonic cancer. If the
lesioncauses obstruction, it may be necessary to relieve the obstruction before a definitive operative proced
is performed. Removal of the primary lesion is not necessarily contraindicated by the presence of metastasi
Removal of the primary tumour is the best palliative procedure as it eliminates or diminishes the possibilit
of bleeding, perforation, fistula formation, infection and continuous discharge of foul material per rectum.
PREOPERATIVE PREPARATION.— To correct anaemia, blood transfusion may be needed. A high
calorie and low residue diet should be started once a decision for operation has been taken. Bowel preparatio
is the most important preoperative management before colectomy. It is done in two ways—by (a) Mecha ni
means and (b) Chemotherapy, (a) Mechanical means.— The patient is placed on a liquid diet for 3 days befor
operation. The patient is given a strong oral purgative on each of the three mornings before the operation. S
enema is given at night before opera tionand in the early morning on the day of ope ration. (Jo) Chemotherap
Efficacy of antibiotic prophylaxis in minimising septic complications of colonsurgery is now well establishe
Oral non-absorbable chemotherapy in the form of succinyl sulphathiazole2 g 4 hourly for 5 days alongwith
neomycin 1 g 6 hourly for 5 days should be given before operation. Absorbable broad spectrum antibiotics
are also used to prevent secondary infection around the anastomotic region. But these antibiotics cannot cla
wide acceptance as they may change the bacterial flora and produce resistance of virulent organisms. Yet
ampicillin 0.5 g 6 hourly or metronidazole 750 mg thrice daily may be used alongwith the previous
chemotherapy.
If defunctioning colostomy has been made the lavage should be given through the distal colostomy ope
Operation.— The abdomen is opened through a short paramedian incision, which is extended if the
growth is removable, (i) The tumour is examined to ascertain if it is freely mobile or fixed. If the tumour is
mobile and it is resectable, excision is the best treatment. Now one has to assess whether radical surgery is
possible or not. If the tumour has already metastasised to distant organs, radical surgery is not possible. Th
only exception is when there is a solitary metastasis in the liver, which is resectable. Extent of resection for
radical surgery depends on the lymph node involvement. When epicolic nodes are only affected, segmenta
resection is enough. On the other hand if the central group of lymph nodes are affected around the origin o
superior mesenteric or inferior mesenteric artery extent of resection should include whole length of colon
supplied by the said artery which has to be clamped at the time of radical surgery, (ii) The liver is palpated
for metastasis, the presence of which will obviously contraindicate radical surgery. The only exception is w
the solitary liver metastasis is also resectable. Otherwise palliative surgery in the form of excision of carcino
THE COLON 947
of colon is justified, (iii) The peritoneumis palpated all

throughout, particularly the pelvic peritoneum for
neoplastic implantations. This precludes radical surgery.
(iv) Various groups of lymph nodes are palpated from
the colonic tumour to the origin of the superior or
inferior mesenteric artery. Remember, simple
enlargement of lymph nodes does not mean secondary
involvement. Secondary inflammation also causes
lymph node enlargement. On palpation a hard and
irregular lymph node means metastatic lymph node.
Extent of resection and choice of operation.—
1. FOR CANCERS ARISING IN THE CAECUM,
ASCENDING COLON OR HEPATIC FLEXURE —
right hemicolectomy with ileotransverse anastomosis
performed inone stage is the operation of choice. Right
hemicolectomy involves removal of terminal 8 inches
of the ileum, the caecum, the ascending colon and
proximal ‘/3rd of the transverse colon, that means the
portion of the bowel supplied by the ilieocolic a nd right
colic branches of the superior mesenteric artery. This
will remove the lymph nodes lying close to those
Fig. 53.19.— Shows the extent of resection for arteries which may have been involved in carcinoma.
carcinoma of the transverse colon. Unless the obstruction is advanced, resection with
primary anastomosis on the right side is quite a safe
procedure. This is due to the fact that the anastomosis is performed between well vascularised small intestine
and transverse colon. In very advanced cases of obstruction, one may have to perform ileo-transverse
colostomy first, to be followed by hemicolectomy in the second stage.
In case of inoperable growth of the right half of the colon, a palliative ileo-transverse colostomy should
be performed to obviate the possibility of intestinal obstruction.
II. FOR GROWTHS IN THETRANS VERSE COLON.— It is enough to remove the growth together with
3 inches of healthy bowel on each side with a wedge of mesocolon containing the middle colic artery. This
is followed by end-to-end anastomosis of the two ends. Mostly the growths in the transverse colon occur in
its middle V3rd and the affected lymph nodes lie by the side ofthe middle colic artery, so this simple resection
with primary anastomosis is the operation of choice.
When the growth is inoperable, proximal transverse colostomy should be done to obviate the obstruction.
III. FOR GROWTHS IN THE SPLENIC FLEXURE, DESCENDING AND PELVIC COLON — though
limited resection would have sufficed due to the fact that mostly the epicolic and the paracolic glands are
involved, yet a wide resection is advised to avoid any gland which may be missed lying along the course of
the inferior mesenteric artery. A left hemicolectomy is advised which means resection of the distal third of
the transverse colon, the whole of the descending colon, the pelvic colon and upper part of the rectum. But
if at all it is found that the glands related to the inferior mesenteric artery are involved, this artery is ligated
and divided at its origin from the aorta. The blood supply of the colon is maintained through ‘marginal
anastomosis’, which is supplied by the middle colic artery from above and may well feed the colon right upto
the middle ofthe pelvic colon. So after division of the inferior mesenteric artery, one should look for viability
of the colon and the viable colon either upper part of the pelvic colon or the distal part of the transverse colon
is anastomosed to the lower half of the rectum.
In case of inoperable growths in this region either a permanent colostomy ora transverse-pelvic colostomy
\/
Fig. 53.20.— Shows the extent of resection for carcinoma Fig. 53.21.— Shows the extent of resection
of the descending colon. The terminal bifurcation of the for carcinoma of the sigmoid colon. The left
Inferior mesenteric artery Is retained. colic artery is retained.
may be performed.
IV. FOR GROWTH OF THE PELVIC COLON — the growth along with 3 inches of healthy colon on
both sides is removed and primary anastomosis is made.
For inoperable growths, a permanent transverse colostomy should be performed.
Carcinoma of colon with obstruction.— Although a few surgeons are doing emergency primary
resection, majority would prefer to resect the lesion and bring both cut ends of the colon out — the proxim
as an end colostomy, the distal as mucous fistula. In case of sigmoid colon cancer, it may not be possible to
bring the distal cut end out and in this case the distal cut end is closed by suturing, so a Hartmann procedu
is used. Proximal diverting colostomy alone is the procedure of choice for obstruction in poor risk patients.
Palliative operations.— If the liver metastasis is unresectable or other organs are involved by metastasis,
a palliative resection of the primary tumour should be done if the growth is resectable. Liver involvement is
found in 10 to 15% of patients at the time of initial operation. If the primary lesion is locally unresectable, a
short-circuiting anastomosis around the tumouroffers worthwhile palliation. The type of palliative operation
to be performed incase of growth indifferent regions of colon has been described in separate paragraphs un
the heading of ‘Extent of resection and choice of operation.’
Cancer chemotherapy is recommended for the patient who have inoperable, recurrent or metastatic
colonic cancer. The most frequently used drug is 5-fluorouracil. Though chemotherapy has been used in
conjunction with surgical therapy, yet no current evidence suggests that any benefit may result from this ty
of therapy.
949
CHAPTER - 46
THE RECTUM AND ANAL CANAL
ANATOMY
RECTUM.— It is continuous above with the sigmoid colon and below with the anal canal. The rectosigmoid junction
lies at the level of 3rd sacral vertebra, hence it passes downwards and backwards, then downwards and finally downwards
and forward. This anteroposterior curvature is known as ‘sacral flexure’. Below, the rectum is continuous with the anal canal
by passing through the pelvic diaphragm, from where the anal canal passes downwards and backwards — this is known as
‘perineal flexure’. Besides the anteroposterior curvature, the rectum has got 3 lateral curves. The upper one is convex to the
right, the middle one (which is the most prominent) bulges to the left and the lower one is convex to the right. The beginning
and the end of the rectum lie in the median plane. The peritoneum is related to the rectum in its upper l/3rd in front and on
two sides, in its middle l/3rd in front only. The lowest 3rd of the rectum is devoid of peritoneum. The peritoneum is reflected
from the anterior wall of the rectum to the bladder in the male forming the rectovesical pouch of peritoneum and on to the
posterior wall of the vagina in female forming the recto-uterine pouch. The rectovesical pouch, in case of male, lies 3 inches
above the anus, while in case of females, the recto-uterine pouch lies 2 inches above the anus. The peritoneum is loosely
attached to the muscles of the rectum being intervened by fatty tissue, thus allows considerable expansion of this part of the
gut.
The three taeniae coli of the sigmoid colon fuse together about 5 cm above the rectosigmoid junction to form two thick
bands of longitudinal muscles which descend in front and behind the rectum. There are three transverse folds of semilunar
shape, mostly marked when the rectum is distended. These consist of mucous membrane, submucous coat and circular
muscle fibres. The upper one is situated just below the recto-sigmoid junction. The middle one is the largest and contains
a few longitudinal muscle fibres as well. It lies at the level where the peritoneum is reflected from the anterior surface of
the rectum. The lowest one lies about 1 inch below the middle one.
Relations.— POSTERIORLY, the rectum is related to the 3 sacral vertebrae, the coccyx, the median sacral vessels, the
superior rectal vessels, the left piriformis muscle and the anterior rami of the left three sacral and coccygeal nerves.
ANTERIORLY, it is related in the male to the upper of the bare surface of the bladder, the seminal vesicles, the prostate
and the recto-vesical pouch of peritoneum with its contents e.g. terminal coils of ileum and sigmoid colon. The rectum is
related anteriorly in the females to the uterus, the upper part of the vagina, the recto-uterine pouch of peritoneum with its
contents e.g. terminal coils of ileum and sigmoid colon and the lower part of the vagina. LATERALLY, the upper part of
the rectum is related to the pararectal fossa of the peritoneum containing lower part of ileum and sigmoid colon. The lower
part of the rectum is related to the pelvic sympathetic plexuses, the levator ani and a few branches of the superior rectal
vessels.
The arterial supply of the rectum comes from four arteries.— The superior, middle and inferior rectal arteries and
the middle sacral artery. The superior rectal artery is the continuation of the inferior mesenteric artery. It divides into left
and right branches which break up into smaller branches. These branches pierce the muscular wall of the rectum and run
down through each column of Morgagni. The middle recal artery arises from the internal iliac artery and runs through the
lateral ligament of rectum. The inferior rectal artery, a branch of the internal pudendal artery, crosses the ischiorectal fossa
and supplies the lower part of the rectum. The middle sacral artery, morphologically a continuation of the aorta, arises from
the back of the aorta just above its bifurcation and supplies the posterior parts of the rectum and anal canal. The veins from
the rectum accompany the arteries. The superior rectal vein commences at the internal venous plexus of the rectum. Several
collecting veins pass upwards in the submucosa and pierce the rectal musculature about 7.5 cm above the anus. These veins
unite to form the superior rectal vein, which is continued upwards as inferior mesenteric vein. Dilatation and tortuosity of
these veins are called the internal haemorrhoids (Piles). This possibly occurs due to (a) absence of valves in these veins,
(b) internal pressure from faecal impaction, (c) external pressure from a loaded pelvic colon, gravid uterus, fibroid etc. or
(d) straining at stool specially during constipation (as the veins pass through the rectal muscle). The middle rectal veins
chiefly drain the rectal muscles and end in the internal iliac veins. The inferior rectal veins drain the anal canal and external
haemorrhoidal plexus. They join the internal pudendal veins in the Alcock’s canal.
The lymphatics of the rectum — follow the veins draining the rectum and are also divided into 3 groups. The superior
outflow exactly follows the superior haemorrhoidal veins. The middle group follows the middle rectal vein and drains into
the internal iliac nodes. Lymphatics of the lower part of the rectum follow the inferior rectal vein and drain into the internal
iliac nodes following the internal pudendal vein.
Nerve supply of the rectum — is derived from both the sympathetic and parasympathetic systems. The parasympa
thetic supply is derived from 2nd, 3rd and 4th sacral segments. The rectal mucosa above the pectinate line is insensitive.
Fasciae around the rectum.—(1) The visceral layer of the pelvic fascia invests the rectum and is called fascia propria
ofthe rectum. So long as the carcinoma remains confined within this fascia, excision is easy and little possibility remains
for local recurrence to occur after excision. (2) Fascia of Waldeyer is a strong layer of parietal pelvic fascia and is situated
behind the rectum. It starts from the anorectal junction and passes upwards to be attached to the periosteum of sacrum. Dur
perineal excision of the rectum, after disarticulation of the coccyx and division of the levator ani, this fascia is come across.
It must be divided transversely and completely before exerting a downward pull upon the rectum. (3) Lateral ligaments or
rectal stalks are nothing but columns of condensed parietal pelvic fascia. These extend from the posterolateral walls of the
rectum to the third piece of the sacrum. The middle rectal vessels pass through these ligaments.
ANAL CANAL.— It is about one and half inches long in adult and in empty condition its lumen has the form of an
anteroposterior slit. In front, it is in relation with the perineal body, which separates it from the membranous part of the
urethra and the bulb of the penis in the male and from the lower part of the vagina in the female. Laterally, it is related to
the ischiorectal fossae. Behind, it is inrelation with the anococcygeal ligament, which separates it from the tip of the coccyx.
For the whole length, it is surrounded by sphincter muscles, which in tone keeps it closed.
The upper half of the anal canal is lined by mucous membrane and is plum-coloured owing to the blood in the subjacent
internal venous plexus. The epithelium in this region is variable — it may be stratified squamous with patches of stratified
columnar and a single layer of simple columnar cells like those lining the rectum. In this upper part of the canal, the mucous
membrane presents 6 to 10 vertical folds, known as anal columns of Morgagni, which are better marked in the children than
in adults. Each column contains the terminal radicle of the superior rectal artery and vein. The left lateral, the right anterior
and right posterior columns (3'0 Clock, TO Clock & 1 l'O Clock positions) contain largest radicles and are the most common
sites of primary internal haemorrhoids (Piles). The lower
ends of these columns join together by small crescentic
valve-like folds of mucous membrane, known as anal
valves, above which there are small recesses, known as
anal sinuses. The sinuses are deepest in the posterior wall
of the canal and in these may lodge foreign matter to
become infected very soon forming abscess in the wall of
the anal canal. These anal valves in the posterior segment
are more liable to be tom by hard faeces, producing an
anal fissure. In the region of anal sinuses, anal glands
extend upwards and downwards in the submucosa or may
even penetrate deeply into the internal sphincter. Anal
glands are vesitigial structures, lined by stratified, mucus
secreting columnar epithelium and squamous epithe
lium. Normally there are 6 to 10 glands in the circumfer
ence of the anus. Each gland has a duct and opens into the
anal canal, where this forms small depression in the lining
of the anal canal known as anal crypts at the dentate line.
These are also known as the crypts of Morgagni. From the
Fig.54.1.— Schematic diagram of coronal section of above description it is clear that the anal glands are deeply
the anal canal showing ischiorectal fossa and situated. The glands are usually situated deep to the
pararectal space. internal sphincter near the longitudinal conjoined fibres,
but not into the external sphincter complex. These glands are discharged by the anal ducts which are mainly lined columnar
epithelium. These glands can be considered as diverticula of the anal canal like diverticula in any part of the alimentary track
As the duct passes through the internal sphincter, this may not be able to discharge the contents of the gland so readily as
the muscle tone will tend to compress their lumen. Cystic dilatation and abscess formation is not uncommon due to stasis
and secondary infection. So such abscesses are always deep to the internal sphincter muscle in the intersphincteric zone.
These glands may become infected with the result that an abscess or subsequently a fistula may be developed. The imagina
line along which the anal valves are situated is popularly known as pectinate line (dentate line). It indicates the site at which
the anal membrane is situated in foetus and is thus the junction of the entodermal part and the ectodermal part. Sometimes
small epithelial projections known as anal papillae are present on the edges of the anal valves. These are considered to be
remnants of the anal membrane. The pectinate or dentate line is an important landmark for surgeons. The epithelium above
this line is supplied by sensory fibres from autonomic nervous system and therefore insensitive to painful stimuli such as
cutting or cauterization. The epithelium below this line is innervated by spinal nerves and has somatic sensation.
The succeeding portion of the anal canal extends for about 1.5 cm and is known as transitional zone or pecten. Its
THE RECTUM AND ANAL CANAL 951
epithelium is stratified and is intermediate in thickness between the mucous membrane above and the mucous membrane
below. Submucosa contains fairly tough connective tissue which anchors the lining of the pecten to the muscle coat firmly.
The line below the transitional zone is known as White line of Hilton, which according to some, is the junction of the
entoderm and the ectoderm.
Anal canal musculature.— The muscular junction between the rectum and anal canal can be felt with the finger as
a thickened ridge — the ‘anorectal ring’.
The internal sphincter is the thickened continuation of the circular muscle coat of the rectum. This is an involuntary
muscle and continuous above with the circular muscle of rectum through the pelvic diaphragm. It surrounds the upper 3
quarters of the anal canal (3 cm). It ends below at the Hilton’s line (White line). The internal anal sphincter is 3 cm long
and 2 to 5 mm thick. When exposed, it is pearly white in colour and its transversely placed fibres can be seen clearly. Spasm
and contracture of this muscle play a major part in formation of fissure and other anal conditions.
The longitudinal muscle is the continuation of the longitudinal muscle coat of rectum. At the anorectal junction, the
puborectalis fibres of the levator ani fuse with the longitudinal unstriped muscle coat of the rectum to form a conjoined
longitudinal muscle coat for anal canal between the internal and external sphincters. Distally, this conjoined coat becomes
increasingly fibroelastic and at the level of the ‘White line’ it breaks up into a number (9 to 12) of fibroelastic septa which
spread out fanwise and pass mainly through the subcutaneous part of the external sphincter to become attached to the corium
of the skin around the anus. This is called ‘corrugator cutis ani of Ellis’. These septa mainly consist of yellow elastic fibres
and the most lateral septum passes between the subcutaneous and superficial parts of the external sphincter and becomes
lost in the fat of the ischiorectal fossa.
The sphincter ani externus — surrounds the whole length of the anal canal. It is usually divided into 3 parts — the
subcutaneous part, the superficial part and the deep part. The deep part of this sphincter is a thick annular band which
surrounds the upper part of the internal sphincter. Its deep fibres are fused with the puborectalis muscle. Posteriorly its some
fibres are attached to the anococcygeal ligament. In front, its fibres decussate and become continuous with the superficial
transverse perineal muscles. The superficial part is attached posteriorly to the terminal piece of the coccyx, the only bony
attachment of this sphincter. Anteriorly, it is chiefly inserted to the perineal body. The subcutaneous part surrounds the
lowest part of the anal canal and itlies below the lower border of the internal sphincter and Hilton’s line. Anteriorly, its fibres
are attached to the perineal body and posteriorly to the anococcygeal ligament.
Lymphatic drainage of anal canal.—The lymphatics from the upperpart of the anal canal upto this ‘White line’ follow
the inferior rectal veins across the ischiorectal fossae to be continuous with the lymphatics following the internal pudendal
vessels to end in the internal iliac nodes. Lymphatics from the lower end of the anal canal, which is developed from the
proctoderm, are drained into the superficial inguinal group of lymph nodes of both sides.
Nerve supply of the anal canal.— The nerve supply of the upper part of the anal canal, which is developed from the
hindgut, is supplied by the same sympathetic and parasympathetic supply as the rectum. The lower part of the anal canal
which is developed from the proctodeum, is sensitive and is supplied by the inferiorrectal nerve, a somatic nerve. This nerve
also supplies the external sphincter and sphincter urethrae and so any irritation of the lower part of the anal canal will cause
these sphincters to go into spasm.
The spaces on the lateral side of the anal canal and rectum.— There are 3 spaces lying one above the another at th
region. From below upwards they are (1) The perineal space.— It contains the external haemorrhoidal plexus and the
subcutaneous part of the external sphincter. (2) The ischiorectal space.— It is more important because it is often the site
of abscess formation. It is a pyramidal space, whose apex is directed upwards and the base which is formed by the septum
of the ischiorectal fossa is directed downwards. Its outer wall is vertical and is formed by the obturator intemus muscle and
the fascia covering it. About l’/2 inches above the lower border of the ischial tuberosity in this fascia covering obturator
intemus lies the Alcock’s canal (pudendal canal) containing the internal pudendal vessels and the pudendal nerve. Its inner
wall is oblique and formed by the levator ani muscle and the deep and superficial parts of the external sphincter muscle.
Anteriorly, it is bounded by the base of urogenital diaphragm and transverse perineal muscles. Posteriorly, it is bounded
by the lower margin of the gluteus maximus muscle and the sacrotuberous ligament. It is now obvious from the concept of
the boundaries of the fossa that the pus from one ischiorectal fossa can pass to the opposite fossa breaking the attachment
of the levator ani to the anococcygeal ligament. In this way a horse-shoe shaped fistula is developed. (3) Pelvi-rectal
space.— It is situated above the levator ani. Pus from this space may make its way to the ischiorectal fossa through the hiatus
of Schwalbe, a gap between the obturator fascia to the attachment of the levator ani muscle. The pus from the ischiorectal
fossa can also go up through this hiatus to the pelvi-rectal space resulting in a high fistula.
CONGENITAL ABNORMALITIES are discussed at the end of this chapter.

PROLAPSE OF THE RECTUM

This can be differentiated into (1) Partial prolapse and (2) Complete prolapse.
PARTIAL PROLAPSE
When only the mucosa and submucosa of the rectum come out through the anus it is called partial prola
The length of such prolapse is never more than 3.75 cm. If this prolapsed mass is palpated with one finger i
the anus and the thumb on the outside of the mass, it will be evident that it is composed of two layers of m
membrane with submucosa in between.
Aetiopathogenesis.—This condition occurs more often in extremes of life—children below 3 years of age
and elderly people. IN INFANTS (i) as the sacral curve of the rectum has not yet developed, the direct dow
course of the rectum predisposes to this condition, (ii) Due to diminished tone of the anal musculature this
condition may develop.
IN CHILDREN (i) faulty bowel habit is often the predisposing factor (ii) Straining such as attack of
diarrhoea or whooping cough may cause partial prolapse, (iii) Loss of weight and diminution of pararcctal
may causc prolapse in malnutrition child.
IN ADULTS (i) some loss of tone of anal sphincter may cause partial prolapse, (ii) Third degree
haemorrhoid may be associated with partial prolapse, (iii) In female, tom perineum may cause partial prola
(iv) Excessive straining due to urethral obstruction from enlarged prostate or excessive coughing from
bronchitis may cause partial prolapse, (v) Partial prolapse may also complicate operations for fistula-in-ano
fissure-in-ano. If a large portion of muscle is divided or if excessive stretching of anal sphincter is done, it m
cause such prolapse. Such prolapse is usually localised to the affected quadrant and usually heal by itself.
Any aetiological factor of complete prolapse may cause partial prolapse in the beginning before it turns
complete prolapse.
Treatment.—
CONSERVATIVE TREATMENT.— (a) Digital reposition of the partial prolapse may help a lot. The
mother is taught how to replace the protruded bowel through the anal sphincter. By the index finger the
protrusion is pushed up through the anal canal and the finger is gradually withdrawn. The finger may be
1 ubricated before using it. Attention of bowel habit, avoiding straining at stools, control of diarrhoea
adjustments in case of malnutrition are supportive treatments to be followed.
(b) Submucous injection with 5% phenol in almond oil is carried out under general anaesthesia. This
tried in children only after digital reposition fails for 6 weeks trial. This submucous injection treatment may als
be tried in adults in early partial prolapse. The apex of the prolapse is injected circularly and the tip of the ne
should reach the submucosa. The base of the prolapse should also be injected similarly and the needle mus
the submucosa. 10 ml of such solution may be injected in one sitting. Aseptic inflammation following these
injections will lead to fibrosis and the mucous membrane becomes fixed to the muscular coat and is drawn
OPERATIVE TREATMENT.— (a) Thiersch's operation.— When the conservative measures fail, this
single operation is almost certain to succeed in partial prolapse. Patients of any age may be tried. Two smal
midline incisions are made one in front and the another behind the anal opening about V2 inch away from i
A long curved needle is passed from the posterior incision and is passed round ‘/2 of the anus emerging thr
the anterior incision. A piece of silver wire or stainless steel wire 20 gauze is threaded through the eye of th
needle. The needle is brought out through the anterior incision and now the wire traverses V2 of the
circumference of the anus. The needle is taken out. The needle is reinserted through the same incision behin
the anus and passed round the opposite side of the anus to emerge through the incision in front of the anus
other end of the wire is threaded and the needle is withdrawn through the anterior incision. The index finge
the surgeon is introduced through the anus (the little fing.er has to be introduced in case of children) and th
assistant is asked to twist the two ends of the wire so as to tight the knot. The surgeon appreciates the tightn
of the ring. When the finger can be just sufficiently passed through the anus, the twisted wire ends are cut s
The anterior and posterior incisions are closed with stitches.
In this operation the suture material is passed through the substance of the internal sphincter. This gives
only a mechanical support but also a chemical support by the fibrous deposits around the anal canal. The wi
can be taken out after 3 months if required. In children the stitch must be removed as otherwise anal stenosis
will result. In this case strong chromic catgut may be used instead of silver or stainless steel wire.
The main complication of this operation is that the wound may be complicated with the result of a
discharging sinus. In this case the wire must be removed and usually by that time fibrosis has occurred to pr
further prolapse. In case prolapse recurs, one may repeat this operation in future.
(b) Excision ofprolapsed mucosa.— This can only be performed when partial prolapse has involved onl
a part of the circumference. The base of the prolapse is ligated by Goodsall’s ligature. By this the base of the
prolapse is transfixed twice and the ligature is then tightened. Now the redundant mucosa is excised and if
required the cut margins are sutured interruptedly. This technique may be adopted in case of partial prolaps
associated with 3rd degree haemorrhoid.
COMPLETE PROLAPSE (PROCIDENTIA)

In this condition the rectum comes out through the anus and the protrusion consists of all the layers of th
rectal wall. It is a descending sliding hemia. It is always more than 3.75 cm in length and usually about 10 cm
in length. If palpated between a finger and the thumb, double thickness of the entire wall of the wall of the re
can be palpated. It must be remembered that a complete prolapse usually contains a pouch of peritoneum
anteriorly between its walls. When the prolapse is a very large one this peritoneal cavity contains even coils o
small intestine.
Complete prolapse is rare in children. It may occur at any age but is more common in the elderly. Women
are affected five times more than men. It is often accompanied with prolapse of the uterus.
Aetiological factors.—
(i) Bowel habit.— It is generally accepted that complete prolapse is associated with a long history of
difficulty with defaecation. In about two-third of cases this type of history can be elicited.
(ii) Laxity ofthe anal sphincters is the most obvious abnormality found apart from the prolapse itself.
Sphincteric response to voluntary contraction is also poor. Even if the prolapse is not apparent on inspection
it can be readily induced by asking the patient to strain.
(iii) Sliding hernia.— As has been mentioned earlier there may be the peritoneal pouch on the anterior
aspect of the prolapse. This is same as a sliding hemia where the hemia forms the posterior wall of the perito
pouch. That is why a complete prolapse is often considered to be a type of sliding hemia.
(iv) Lack of rectal fixation.— Muscles of pelvic floor are weak. The rectum is more mobile. It is also not
fixed posteriorly to the sacrum. All these combine together to cause complete prolapse.
(v) Rectal intussusception.— According to this view the rectum folds on itself and passes through the
pelvic diaphragm and ultimately comes out of the anus. The cause of such intussusception is not known. Thi
theory has now been widely accepted. The apex of the intussusception is generally 6 to 8 cm above the anus
probably at the level of the peritoneal reflexion.
(vi) Disordered function of the pelvic floor muscles.— Patients with complete rectal prolapse may have
marked laxity of the whole pelvic floor and anal sphincter mechanism. During straining it has been noted tha
there may be descent of the floor and gaping of the anus. Whether this is the cause or the effect is not known
A few patients, even after rectopexy, show persistence of incontinence. These patients have probably disorde
function of the pelvic floor muscles.
TREATMENT.— There are various operations designed by various surgeons for complete prolapse of
rectum. The more commonly practised operations are mentioned below.
1. Fixation Operations.— (a) IVALON SPONGE WARP OPERATION (WELLS).— Wells described
this operation in 1959. Abdominal approach is made. The rectum is fully mobilised. The rectum is fully
mobilised posteriorly to the pelvic floor. Part of the lateral stocks are divided to permit adequate posterior
mobilisation. A rectangular sheet of Ivalon sponge (polyvinyl alcohol) is then sutured to the presacral fascia
and periosteum of the sacrum. The mobilised rectum is drawn up to make it taut. The Ivalon sheet is wrapped
over it and sutured. The anterior surface of the rectum is left uncovered to prevent constriction of the lumen.
Ivalon sponge will initiate fibrosis and fix the rectum in place.
(b) RECTOPEXY (LOCKHART-MUM-
I.S. MERY) OPERATION.— The incision and
preliminary steps are similar to the previous operation.
A curved incision about 2 inches in length is made
midway between the anus and tip of the coccyx. The
incision is deepened and through it the fibres of the
external sphincter muscle and the anococcygeal
ligaments are cut. The incision is further deepened
and the fascia of Waldeyer is transversely incised.
The rectum is stripped off from the anterior surface
of the sacrum upto the third sacral vertebra. The
resulting cavity is packed with long strips of gauze of
polyvinyl alcohol sponge. This is attached to the fascia
in front of the sacrum by 3 or 4 sutures. The effect of
this sponge is to provoke vigorous fibrous reaction
which will anchor the rectum against the sacrum.
(c) RECTAL SLING OPERATION.— This
operation was introduced by Ripstein in 1965.
Abdominal approach is made. The rectum is mobilised
down to the tip of the coccyx. The lateral peritoneal
folds are opened and the rectum is freed from the
sacrum. The rectum is pulled-up taut, a 5 cm band of
Fig 54.2.— Shows Ivalon sponge wrap operation. A sheet of teflon is placed around ihe rectum. The free ends of
Ivalon sponge is sutured to the presacral fascia, then wrapped this band of teflon are sutured to the presacral fascia
over the rectum and sutured. I.S. — Ivalon sponge. and periosteum of the sacrum 5 cm below the
promontory of the sacrum. The sling must be loose enough to allow one finger to pass between the rectum and the sacrum.
(d) PERINEAL APPROACH (DELORME’S OPERATION).—The collapsed rectum is pulled down as far as
possible. The whole of rectal mucosa is removed from the prolapsed rectum except 0.5 cm strips at its proximal end and
at the tip of the prolapse. A series of chromic catgut sutures are used to imbricate the underlying muscle. When these are
tied the rectal muscle is pulled up towards the anal canal. The anal canal mucous membrane is now sutured to the rectal
mucosa which remains at the tip of the prolapse. So the prolapse is reduced and a ring of muscle surrounds the anal canal
which narrows its orifice. This prevents recurrence.
(e) LAHAUT’S OPERATION.— The whole of rectum and lower sigmoid colon are mobilised. This is now held up
and stitched with the rectus sheath. This operation has lost its popularity.
2. Resection Operations.— (a) ANTERIOR RESECTION OFTHE RECTUM.—The technique is essentially
similar to anterior resection of rectum for carcinoma. Only difference is that the dissection should be close to the
rectum to prevent injury to the nerve supply of the bladder and to prevent impotence in males. The rectum just
above the anterior peritoneal reflexion, which is considered to be the starting point of the intussusception is resected.
The proximal line of resection should be at a convenient point at the rectosigmoid junction or in the sigmoid colon
so that the redundancy is removed. The anastomosis must be done without tension.
(b) PERINEAL RECTOSIGMOIDECTOMY.— This is a technique in which the redundant rectosigmoid
colon is excised through the prolapse itself. The patient is placed in Trendelenburg position or prone jack-knife
position. A circular incision is made through the outer layer of the prolapse 2 cm proximal to the dentate line.
Anteriorly as this incision is deepened the peritoneal cavity will be opened transversely. The pelvic colon should be
pulled down as far as possible until it becomes taut from above. The peritoneum is now sutured to the side of the
pelvic colon as high as possible. The pelvic mesocolon with the vascular pedicle is ligated Vi inch below the
proposed level of section of the pelvic colon. The sigmoid colon is completely divided below the anus in such a
way that there is a greater length posteriorly. The two cut-ends of the bowel — the anal cuff externally and pelvic
colon internally, are now sutured by a series of interrupted suture. The sutured stump is now pushed into the anal
canal and a rubber tube is inserted. The result of the operation is not very encouraging as there is
both recurrence of prolapse and anal incontinence, probably due to the short anorectal stump.
(c) OPERATIONS ON THE PELVIC FLOOR AND PERINEUM.— This operation is Goligher’s
modification of Roscoe Graham operation. With this operation the rectum is mobilised and pulled-up. The
levator ani muscles are approximated anterior to the rectum. The peritoneal pouches are obliterated. Parks
advocated suturing the pelvic floor behind the rectum to restore the anorectal angle. He also used Ivalon
rectopexy as the primary treatment and post-anal repair to improve pelvic floor and sphincter function.
Despite a successful operation to treat rectal prolapse and careful management with the regulation of th
bowel habit, a small proportion of patients will have persistence of symptoms. These are mainly varying d
of incontinence due to anal sphincter dysfunction. The simplest method for trying to improve sphincter fu
is by exercising the pelvic floor muscle and by applying faradic stimulation.
ANORECTAL ABSCESSES
Abscesses around lower rectum and anal canal are known as anorectal abscesses. These are important a
this often culminates in fistula-in-ano.
The causative organism is usually Esch. Coli, less commonly Staphylococcus aureus, bacteroids, Strepto
coccus, B. Proteus etc. In 90% of cases the abscess starts as an infection of an anal gland. In remaining 10%
of cases infection may come from blood borne infection e.g. extension of a cutaneous boil etc.
Classification.— Followings are the types of anorectal abscesses— 1. Perianal, 2. Ischiorectal, 3. Submu
cous and 4. Pelvi-rectal. Of these perianal (60%)
and ischiorectal (30%) are the common abscesses.
1. Perianal abscesses.—
Cause.— (i) Majority of these abscesses arise
from acute inflammation of anal gland. The pus
collects within the internal sphincter and gradu
ally paves its way between the internal sphincter
and conjoined longitudinal muscle to tract down
and comes superficial in the perianal region, (ii)
Infection of a thrombosed external pile may also
result perianal abscess.
CLINICAL FEATURES.— Patient com
plains of throbbing pain around anus. This pain
becomes exaggerated during defaecation. Some
constitutional symptoms such as fever, headache
may be associated with this condition. On inspec
tion, an acute angry lump may be seen at the anal
margin. Sometimes this may not be obviously
seen, but felt by finger in the anal canal just below
the dentate line. It is a very tender cystic lump.
TREATMENT.— Treatment is incision and
drainage of the pus. This should be done immedi
ately under antibiotic cover. An inadequate and
defective incision will lead to anal fistula. The
cruciate incision is placed on the most prominent
part of the swelling preferably under general
Fig.54.3.— Various locations of anorectal abscesses are shown anaeslhesia. The incision must be bold and should
to spread from the primary locus in the intersphincteric zone at . .
the level of the anal valves. Pubo-rectalis muscle has been cross- Open the abscess Cavity adequately. The SinuS
hatched for easy recognition. forceps is passed into the abscess cavity, the
blade of the forceps are opened to break the loculi and is brought out with the open blades for adequate drain
A finger should then be passed into the abscess cavity and all loculi should be broken. The internal sphincter
is separated from the mucosa and the lower part of the internal sphincter should be incised to prevent fistula
formation. The skin edges are incised to keep the wound wide open. The cavity is packed and healing will sta
by granulation tissue.
Sequelae.— If untreated, perianal abscess may (i) rupture into the anal canal, (ii) may rupture to the exterio
causing fistula-in-ano, (iii) may pass laterally through the external sphincter to form ischiorectal abscess.
2. Ischiorectal abscess.—
Cause.— (i) The commonest cause is extension of anal gland inflammation laterally through the external
sphincter, (ii) Infection may be through blood or lymph, (iii) Penetrating injury causing direct infection from
outside, (iv) Extension from pelvi-rectal abscess through hiatus of Schwalbe.
PATHOPHYSIOLOGY.— Ischiorectal fossa is full of fat and poorly vascularised, so infection continues
for a long time and gradually the whole fossa becomes involved. The ischiorectal fossa is connected to the oth
side posterior to the anal sphincter. So ischiorectal abscess may spread to the opposite side if not treated early
CLINICAL FEATURES.— Patient presents with acute pain by the side of the anus. Pain becomes
exuberant during defaecation. Constitutional symptoms and fever may be present. On examination, a tender
brawny indurated swelling is seen and felt superficial to the ischiorectal fossa on one side of the anus.
TREATMENT.— Under general anaesthesia early incision and drainage of the abscess is the main theme
of treatment. A cruciate incision is made on the most prominent part of the swelling. The incisions should exte
more than the edge of the swelling. Adequate portion of the skin which forms the roof of the abscess should b
excised. The cavity is explored with afinger. Septa are divided with the finger and necrotic tissue lining the w
of the abscess cavity is removed by the finger wrapped with gauze. An attempt should be made to find out
whether the abscess has come from perianal abscess or from pelvirectal abscess above. If it is an extension from
a perianal abscess, the treatment should be passage of a probe into the anal canal through that opening and
sphincterotomy right upto the probe to lay open the track as performed in case of fistula-in-ano. If the abscess
has extended from pelvirectal abscess, the hiatus of Schwalbe is enlarged for better drainage and the abscess
cavity above is curetted. The whole cavity is lightly packed with gauze wrung out in any weak antiseptic
solution. A T-bandage is applied. The wound will heal by granulation tissue from the depth.
3. Submucous abscess.—This abscess is situated just deep to the mucous membrane of the anal canal above
the dentate line. It occurs usually from spread of infection from the anal gland or even after injection of
haemorrhoids. This is drained by a small incision either by stretching the anus or by a proctoscope.
4. Pelvi-rectal abscess.— This is situated above the levator ani (pelvic floor) and below the pelvic
peritoneum. It is a simple pelvic abscess which may occur from appendicitis, diverticulitis, salpingitis and
parametritis. It may occur from below by extension of ischiorectal abscess. This is due to overenthusiastic
attempts to drain ischiorectal abscess and may push a probe or a curette through the attachment of the pelvic
floor.
Sequelae.— If untreated, pelvirectal abscess may burst into the rectum or may pass through the hiatus of
the Schwalbe to the ischiorectal fossa causing ischiorectal abscess.
TREATMENT is drainage of the pelvi-rectal abscess either through fornix of the vagina or through anterio
wall of the rectum. When ischiorectal abscess has formed following this condition, the ischiorectal abscess is
drained and the opening in the levator ani is widened for better drainage.
FISTULA-IN-ANO
Fistula-in-ano is an inflammatory track which has an external opening (secondary opening) in the perianal
skin and an internal opening (primary opening) in the anal canal or rectum. This track is lined by unhealthy
granulation tissue and fibrous tissue.
CAUSE.— (a) The fistula usually originates from a perianal abscess ip the intersphincteric space of the ana
canal from infection of the anal gland. As the anal gland is situated deep to the internal sphincter its duct pass
through the internal sphincter to open in the crypts of Morgagni situated on the dentate line. Due to the to
the internal sphincter the duct cannot aptly discharge the contents of the gland. Stasis and secondary infec
lead to abscess formation from the anal gland in the intersphincteric region. From here the internal openin
traverse through the internal sphincter to open into the anal canal and the abscess usually tracks down and
in the perianal skin externally thus fistula-in-ano is formed. Several other disorders must be considered which
may cause fistula-in-ano. These are :
(b) Ulcerative colitis, (c) Crohn’s disease, (d) Tuberculosis and (e) Colloid carcinoma of the rectum.
CLASSIFICATION.— Broadly, anal fistula can be divided into two groups — (I) low fistula and (II) hig
fistula depending on whether the internal opening is below or above the anorectal ring respectively.
(I) Low level fistula.— These fistulae open into the anal canal below the anorectal ring. These can be
further subdivided into (i) subcutaneous type, (ii) submucous type, (iii) intersphincteric type, (iv) transphin
type and (v) suprasphincteric
type.
(II) High level fistula.—
These fistulae open into the
anal canal at or above the an
orectal ring. These can be fur
ther subdivided into (i) extras-
phincteric or supralevator type,
(ii) transphincteric type (which
may be seen in low variety also)
and (iii) pelvi-rectal fistula.
The importance of decid
ing whether a fistula is a low or
a high level type is that a low
level fistula can be laid open
without fear of permanent in-
Fig.54.4.— Various types of fistulae are shown on the left side. On the right side continence as the anorectal ring
various locations of abscesses are shown. See the text for details. or gjjf-jg jg disturbed
Whereas in case of high level fistula one must diagnose the case before operation and it is usually treated b
stages, lest damage to the anorectal ring may cause permanent incontinence.
A fistula may be single or multiple. When there is more than one external opening it is called a multiple an
fistula. In this case there may be one or more internal openings.
Clinical features.— Usually a past history of perianal abscess can be received. The abscess formed and
ruptured by itself, the condition healed leaving a tiny discharging sinus. After a few month, again abscess
formed, ruptured by itself and a discharging opening is left. After a few recurrent attacks the discharging f
fails to heal and continues to discharge. This condition also develops when after abscess formation an
inadequate incision is made for drainage. Similarly new abscesses may form to cause multiple fistulae.
Tuberculosis is a very common cause of multiple fistulae in this country. More common is solitary fistula w
an external opening within 3.7 cm of the anus. Granulation tissue may be seen pouting out from the mouth
the fistula. There is much induration of the skin and subcutaneous tissue around the fistula. When fistula fo
secondary to ischiorectal abscess, both the ischiorectal fossae may be involved (see ischiorectal abscess und
the heading of ‘Anorectal abscesses’). An external opening for each side of the ischiorectal fossa may be see
with intercommunicating track lying posterior to the anus. This is called horse-shoe fistula.
GOODSALL'S RULE.— This rule relates the location of the internal opening to the external opening. If
the external opening is anterior to an imaginary line drawn-across the midpoint of the anus, the fistula run
straight directly into the anal canal. If the external opening is situated posterior to that line, the track usuall
curve and the internal opening will be on the midline posterior of the anal canal. An exception to this rule i
the external opening is anterior to this imaginary line but is situated more than 1V2 inches (3.75 cm) away from
the anus. In this case the track will curve posteriorly and end in the posterior midline.
RECTAL EXAMINATION.— This is extremely impor
A
tant. The internal opening must be felt by digital examination.
If it is above the anorectal ring it is a high fistula and the
treatment is different from low fistula. Number of internal
openings must be noted. Even if there are multiple external
fistulae there may be one internal opening.
PROCTOSCOPY — is sometimes necessary to visualise
internal opening of the fistula.
LIPIODOL INJECTION—into the eternal opening prior
to radiography will show the track of fistula-in-ano. But its
utility is in doubt as it seldom gives more information and on
the contrary it causes a recrudescence of inflammation.
Fig.54.5.— Schematic diagram showing Goodsall’s CHEST X-RAY to exclude tuberculosis is important as
rule. AB - Transverse anal line. F - Anococcygeal
ligament. G - Coccyx.
fistula-in-ano is often associated with tuberculosis in this
country. If the surrounding skin of the fistula is discoloured
and the discharge is watery, it strongly suggests a tuberculous origin. In this case, induration around the Fistula
is lacking and the opening is irregular with undermined edge.
If any doubt regarding cause of fistula-in-ano, the following conditions must be excluded. These are : (a)
Tuberculous proctitis, (b) Ulcerative colitis, (c) Crohn’s disease, (d) Bilharziasis, (e) Lymphogranuloma
inguinale and (f) Colloid carcinoma of the rectum.
TREATMENT-
LOW level fistula.—Fistula track must be laid open. The patient is placed in lithotomy position. The bidigital
examination is made under anaesthesia to reveal cord like induration representing the track. A probe is inserted
through the Fistula track. Care must be taken not to create a false passage. A propointed director is now
introduced through the external opening and its tip comes out through the internal opening. With a knife the tr
is now opened on the director. If there are multiple fistulae the probe-pointed director is passed through
individual external opening and brought out through the internal opening and the corresponding track is laid
open with the knife. After the Fistula track has been laid open, (i) either the unhealthy granulation tissue on the
wall of the fistula is scraped off with a Volkmann spoon or (ii) the whole track with the fibrous tissue is excised
The cavity is packed with roller gauze wrung with weak antiseptic lotion. Healing will take place by granulatio
tissue from the depth.
Some surgeons have advocated split skin graft of the wound resulting from fistulotomy. The grafts are taken
from the inner aspect of the thigh and applied to the anal wound by stitching to the skin edges. However this
is not advised as a routine practice.
High level fistula.—
(i) Supralevator fistula is mostly secondary to Crohn’s disease or ulcerative colitis or carcinoma or foreign
body. This requires treatment of the primary condition and the fistula is ignored. Any attempt to lay open the
fistula will cause incontinence.
(ii) Transphincteric fistula with a perforating secondary track.— In this case there is almost always a low
fistula and if care is not taken while inserting the probe-pointed director, the director will go into the high
secondary track and if passed hard will open into the rectum above the anorectal ring transforming the conditio
into a high fistula. So in this type of fistula the lower track is opened as usual and the upper track opening is ma
wide with scraping the high fistula with Volkmann spoon. The upper track will heal by itself alongwith the low
fistula.
Alternatively the lower part of the track is treated by Fistulotomy. Then a seton of heavy black silk or a rubb
band is passed round the deeper part of the track. This will include intact fibres of the sphincter and the anal ca
mucous membrane. The silk is tied loosely outside and kept in situ for two weeks. This stimulates fibrosis
adjacent to the sphincter muscle. In the
second stage, after 6 weeks, the remaining
part of the track including the fibres of the
sphincter muscles incorporated within the
tie is excised. Fibrosis, from the previous
operation, prevents retraction of the freshly
cut sphincteric fibres. So incontinence which
is the most serious complication of this
operation is avoided. This operation is known
as Gabriel's two-stage operation.
Instead of passing the silk, a stainless
steel wire may be passed round the deeper
part of the track. After two weeks, the knot
is gradually tightened during subsequent
dressings. The wire cuts through the
Fig.54.6.-Shows use of Seton in case of high fistula. See the text. sphincteric musclebut the Sphincter will not
gape as fibrosis has already developed. Healing occurs in parts as the new portion is cut and the old portion
(iii) High intersphincteric fistula.— It is also treated in the similar fashion as described in the previous
section.
Horse-shoe fistula is usually not treated by radical unroofing procedure (fistulotomy). Instead a posterior
midline internal sphincterotomy combined with laying open the deep part of the fistula track is performed.
lateral tracks are excised. This has proved effective. This is Wanley operation.
HAEMORRHOIDS (PILES)
These are dilated veins within the anal canal in the subepithelial region formed by radicles of the superio
middle and inferior rectal veins.
Haemorrhoids are clearly divided into two categories — internal and external haemorrhoids. Internal
haemorrhoid means it is within the anal canal and internal to the anal orifice. It is covered with mucous
membrane and it is bright red or purple in colour. It usually commences at the anorectal ring and ends at the
dentate line.
The external haemorrhoid is situated outside the anal orifice and is covered by skin. The two varieties may
coexist and the condition is called intero-external haemorrhoids. There are two peculiar conditions which are
associated with external haemorrhoid — (i) Dilatation ofthe veins at the anal verge is sometimes seen in persons
of sedentary life particularly during straining, (ii) Perianal haematoma or thrombosed external haemorrhoid.—
A small clot in the perianal subcutaneous tissue can be seen superficial to the corrugator cutis ani muscle. Th
condition is due to back pressure on the anal venule consequent upon straining at stool, coughing or lifting h
weight. The condition appears suddenly and is very painful. It may be seen lateral to the anal margin as tens
and tender swelling. If untreated, it may resolve by itself or may suppurate or may fibrose giving rise to a
cutaneous tag or may burst giving rise to bleeding.
Treatment.— Whenever a thrombosed external haemorrhoid is suspected, the treatment is to incise the
haemorrhoid under local anaesthesia. The two halves of the haemorrhoid are excised. The opening in the ski
is packed with gauze wrung in light antiseptic solution to allow the wound to heal by granulation tissue. Th
more problem appears in cases of anteriorly or posteriorly placed perianal haematoma. These are treated
conservatively since skin wound may become an anal fissure.
Remember that a ‘sentinelpile' is not associated with haemorrhoid, but associated with fissure-in-ano. This
is described in page 1026.
Aetiology of Internal Haemorrhoids.— (i) Hereditary.— It is often seen in members of the same family.
(ii) Anatomical.— It has long been suggested that internal pile is a natural consequence of adaptation of
erect posture by mankind, (a) Absence of valves in the superior haemorrhoidal veins, (b) The veins pass thro
the rectal musculature 10 cm above the anus will cause occlusion of the veins and congestion during defaeca
(c) The radicles of superior rectal vein lie unsupported in loose submucous connective tissue of the rectum.
(iii) Exciting causes.— Parks suggested straining to expel constipated stool caused dilatation of the venous
plexus. Once dilatation of the venous plexus as well as partial prolapse would occur with each bowel movem
it would stretch the mucosal suspensory ligament. Over purgation and diarrhoea of colitis, dysentery, enteri
etc. aggravate latent haemorrhoids.
(iv) Physiological cause.— Some surgeons more recently have regarded the extensive venous plexus of the
upper anal canal as physiological. The pathology of the so called haemorrhoidal plexus is in fact a corpus
cavemosum with direct arteriovenous communication. This plexus is termed corpus cavernosum rectum, which
is a normal constituent in the upper third of the anal canal. Hyperplasia of the corpus cavemosum rectum m
result from failure of mechanism controlling the arteriovenous shunts producing superior haemorrhoidal ve
varicosity and haemorrhoids.
(v) Diet.— Low roughage ‘Western’ diet may excite haemorrhoid formation. Whereas adding bulk or
bulk-forming compounds can prevent haemorrhoid formation.
Secondary haemorrhoids.— Haemorrhoids may be secondary to a few conditions, which must be
excluded before one treats a case of haemorrhoid. These are:—
(a) Carcinoma of the rectum — compresses on the superior rectal veins and gives rise to haemorrhoid.
(b) Pregnancy — compresses superior rectal vein as also causes secondary laxity of smooth muscle of the
veins. Uterine tumours may similarly compress the superior rectal vein.
(c) Chronic constipation — and its cause should be excluded, otherwise the condition will recur.
(d) Difficulty in micturition—stricture of urethra or enlarged prostate will cause increase intra-abdomina
pressure and will raise the venous pressure in the superior haemorrhoidal veins to cause haemorrhoids.
(e) Portal hypertension has hardly ever caused haemorrhoid, though it is the junction of portal and syste
veins.
Pathology.— Through a proctoscope the internal haemorrhoids are well visualised and can be divided in
three parts — (i) pedicle, (ii) body of internal haemorrhoid and (iii) associated external haemorrhoid.
(i) Each internal haemorrhoid has a pedicle in the rectum just above the anorectal ring. The pedicle is
covered vyith pale pink mucosa and through it a large tributary of the superior rectal vein can be seen.
Occasionally a pulsating artery may be felt at the pedicle.
(ii) After the pedicle, the body of the internal haemonrhoid continues distally and ends at the dentate line
The body is covered by bright red or purple mocous membrane.
(iii) Associated external haemorrhoid lies between the dentate line and the anal margin and is covered by
skin. The blue veins can be seen through the skin. Associated external haemorrhoid is present in long continu
cases of internal haemorrhoid.
Each primary internal haemorrhoid contains main terminal divisions of superior rectal artery and vein.
There are three main terminal divisions of such superior rectal vessels arranged in the lefrlateral, right anteri
and right posterior positions. In lithotomy position these correspond with the 3,7 and 11 O'clock positions.
Besides these three primary haemorrhoids, there may be small secondary haemorrhoids in between.
Clinical features.— The principal and earliest symptom is bleeding.
1. BLEEDING is bright red, painless and occurs alongwith defaecation. The patient complains that it
splashes in the pan as the stool comes out (cf. fissure-in-ano, where streak of blood may be seen on the stool)
This may continue for months or even years. As the veins become larger and heavier, partial prolapse will oc
with each bowel movement gradually stretching the mucosal suspensory ligament at the dentate line until th
3rd degree haemorrhoid results.
Alongwith this many surgeons believe that haemorrhoids can be divided into two main types: (i) Vascular
haemorrhoid, which has been described and (ii) mucosal haemorrhoid in which the thickened mucous
membrane slides downwards. This mucosal haemorrhoid alongwith the prolonged dilatation of internal
haemorrhoid may also cause 3rd degree
or prolapsed haemorrhoids.
2. PROLAPSE — is a later symp
tom. In the beginning prolapse is mini
mal. According to prolapse, haemor
rhoids can be divided into four degrees.
FIRST DEGREE — Haemorrhoid
does not come out of the anus.
SECOND DEGREE — Haemor
rhoids come out only during defaecation
and is reduced spontaneously after de
faecation.
THIRD DEGREE — Haemorrhoids
come out only during defaecation and do
not return by themselves, but need to be
replaced manually and then they stay
Fig.54.7.— 2nd degree haemorrhoids — well exposed. reduced
FOURTH DEGREE — The haemorrhoids that are permanently prolapse. At this stage great discomfort is
complained of with a feeling of heaviness in the rectum.
3. PAIN is not characteristic of haemorrhoid unless there is associated thrombosis or there is associated
fissure-in-ano.
4. MUCOUS DISCHARGE is a particular symptom of prolapsed haemorrhoids, which softens and
excoriates the skin at the anus. This mucous discharge is due to engorged mucous membrane. Pruritus ani wil
be caused by such mucous discharge.
5. ANAEMIA is often seen in long standing eases of haemorrhoids due to persistent and profuse bleeding.
ON INSPECTION, internal haemorrhoid without prolapse will not show any abnormal feature. During
second and third degree haemorrhoid, internal haemorrhoids may be seen only when patient strains and that
transiently and the prolapse disappears after the straining is over. During fourth degree the prolapsed piles c
be seen in 3,7 and 11 O'clock positions.
DIGITAL EXAMINATION cannot feel an uncomplicated internal pile unless it is thrombosed.
PROCTOSCOPY will reveal the internal pile as described in ‘Pathology’. The proctoscope is introduced
as far as it does. The obturator is then removed and with an illuminator the inside of the anal canal is visualise
The proctoscope is now withdrawn slowly and the internal haemorrhoid will be seen bulging into the
proctoscope.
Complications.— The two main complications of haemorrhoids are excessive bleeding and thrombosis.
Besides these there are a few complication which may occur in a haemorrhoid and are described below.
(i) Bleeding.— This is the main symptom of haemorrhoid particularly in the first degree and early stage
of the second degree. In fourth degree bleeding is not that profuse. A patient, with first degree haemorrhoid fo
quite a long time will become anaemic. Bleeding usually occurs externally. Only when a bleeding haemorrhoi
is retracted, it may bleed internally into the rectum.
(ii) THROMBOSIS.— External anal thrombosis is common and is often seen in patients who have no other
stigmata of haemorrhoids. The patient notices an acute swelling at the anal verge which is extremely painful.
This possibly occurs due to high venous pressure during excessive straining efforts.
Thrombosis of the internal haemorrhoid is comparatively rare. The affected haemorrhoid becomes dark
purple or black and feel solid. The anal margin becomes oedematous and there is severe anal pain. Pain may
continue for a week or so until the oedema subsides and the thrombosis is absorbed. Treatment is conservative
61
in the beginning consisting of analgesic to relieve pain and mild laxatives to prevent constipation. Icepacks
of doubtful effect. If symptoms continue even after conservative management, surgery may be needed. Sur
is haemorrhoidectomy.
(iii) Strangulation.— Second degree haemorrhoids are more often affected by this condition. When the
internal haemorrhoid prolapses and becomes gripped by the external sphincter, further congestion occurs a
venous return becomes impeded and strangulation occurs. Strangulation is associated with considerable pa
and it is often called ‘acute attack of piles’. Unless the internal haemorrhoid is reduced immediately
strangulation is followed by thrombosis.
(iv) Gangrene only occurs when the arterial supply of the haemorrhoid is somehow or other constricted.
Sloughing occurs which is usually superficial, but occasionally the whole haemorrhoid may slough off leav
an ulcer which gradually heals by itself. Very occasionally massive gangrene may initiate spreading anaero
infection and portal pyaemia.
(v) FIBROSIS usually follows thrombosis of the internal haemorrhoid. Fibrosis also follows transient
strangulation. Fibrosis of external haemorrhoid is much more common than that of an internal haemorrhoid
In the beginning, the fibrosed pile is sessile, but by repeated traction during defaecation it becomes
pedunculated. Then it should be differentiated from adenoma by its white colour.
(vi) Suppuration is very rare and only occurs as a result of infection of thrombosed haemorrhoid.
Throbbing pain with perianal swelling is the feature. Perianal or submucous abscess may follow.
(vii) Pylephlebitis (portal pyaemia).— This is a theoretical entity and with the advent of antibiotics this
has considerably been reduced. This usually follows infection and suppuration of the haemorrhoid, which
ultimately causes portal pyaemia and liver abscesses.
TREATMENT.— Before treatment of haemorrhoid is undertaken the surgeon must exclude any serious
disease in the rectum or colon. Therefore any haemorrhoid treatment must be preceded by sigmoidoscopy and
barium enema. Occult blood test of the stool is also necessary. Conditions such as Crohn's disease and
Ulcerative colitis must be excluded. Associated fissure-in-ano should also be excluded and if present should
be treated first. Treatment of haemorrhoid should start with bowel regulation which has a prophylactive eff
but once the haemorrhoid is established there is no evidence that the process is readily irreversible. So in th
first degree of piles bowel regulation is a must.
Bowel Regulation.— Many haemorrhoidal symptoms can be relieved,by avoiding excessive defaecation
straining. This can be done by advising high residue diet and mild laxatives.
Topical ointments for local applications may do good by reducing oedema and pruritus. During an attac
of piles some relief of discomfort may be obtained by use of suppositories. Patients are very much relieved b
these simple conservative means.
The treatment of haemorrhoid depends on its degree. Manual dilatation of the anus is frequently success
in relieving symptoms probably by preventing congestion of haemorrhoidal veins. Anal dilators may be use
in this respect.
Definitive Treatment.—
INJECTION THERAPY.— Sclerosant injection has been the method of treatment of small vascular
haemorrhoids and indeed is used to control all cases of first degree haemorrhoids whatever may be the
presenting symptoms. The most commonly used sclerosant is 5% phenol in almond or arachis oil with 140 m
of menthol to make 30 ml solution (Albright solution). This solution is injected into the submucosa around t
pedicle of the haemorrhoid with two objects in view. Firstly to produce a chemical thrombosis in the interna
haemorrhoidal plexus and secondly to produce a fibrous reaction in the submucous layer which will fix the
redundant mucous membrane to the inner muscle layer and draw up the pile so that it no longer prolapses
is grasped by the sphincters. Good sclerosis can often be obtained by a single injection of 5 ml into each prim
haemorrhoid. If the injection is given slowly around the base of the pile above the anorectal ring very little
discomfort is experienced. If subsequent injections are required the sclerosed mucosa will not usually take s
a volume and 2 or 3 ml are then injected 1 cm below the initial injection site. The patient is examined 4 to 6 w
after the initial injection and in case of first degree haemorrhoids further treatment may not be necessary. In ca
of large second degree haemorrhoids 2 or 3 injections may be required at intervals of 6 weeks in order to obtai
maximum fibrosis.
Advantages are that (i) this method is quick, (ii) relatively painless, (iii) comparatively free from compli
cations and (iv) in first degree haemorrhoid results in a high percentage of cure. If injection therapy is done fo
treatment of first and small second degree haemorrhoids, the cure rate is in the order of 95% and recurrence m
take place in about 15% of cases within 3 years.
The disadvantages are : (i) It is contraindicated in prolapsed piles, in arterial piles and in presence of
infection, (ii) Faulty technique may lead to sloughing, which is dangerous.
RUBBER BAND LIGATION.— Surgeons for years had been searching for a simple method of ligating
haemorrhoids without the need for a general anaesthetic or admission to hospital. Rubber banding is the idea
method of treatment of treating large first degree and second degree internal haemorrhoid in absence of
associated tags or external haemorrhoidal component. Each haemorrhoid is visualised through a proctoscope.
The upper part of the mucocutaneous line is grasped by an instrument and a small elastic band slipped over it
A recent modification uses a modified proctoscope with bands stretched over the inner drum and pushed off
by advancing the outer drum of the proctoscope over it. The tissue distal to the elastic band undergoes necros
and excess mucosa in the anal canal is removed. The lower anal mucosa is drawn up by the ensuing fibrosis,
which also causes adherence of the mucosa to the underlying muscle. The advantages are that (i) the whole
operation can be done without assistance and (ii) the band can be placed over larger piles. Care must be taken
to insert the band so that it occludes the base of the haemorrhoid at least 1 cm above the dentate line. Should
the dentate line be included in the ligating band considerable pain will result. 2 bands are simultaneously inse
over each haemorrhoid as this reduces the risk of secondary haemorrhage. The ligated haemorrhoid will necro
in 24 to 48 hours and slough off in about 7 days. The main disadvantage is that (i) it is associated with pain,
which is more or less always experienced for the first 24 to 48 hours and sometimes pain is very severe, (ii)
Secondary haemorrhage is another problem.
One or two haemorrhoids may be banded at a time and three large haemorrhoids should not be banded at
a time lest subsequent ulceration covers a large area resulting in stenosis. In absence of complications the patie
should be reviewed 1 month later and any further haemorrhoid is banded or injected as seems most appropria
CRYOSURGERY.— Both elastic band ligation and cryotherapy may welcome to occupy a midposition
between injection therapy and surgical excision. The new form of cryotherapy involves freezing the tissues of
the haemorrhoid for a sufficient time to cause necrosis. If carefully used and applied only to the upper part of
the haemorrhoidal area at the anorectal junction, it achieves a similar result to elastic band but there is no pain
The effectiveness of cryosurgery is at present evaluated. Cryosurgical probe using liquid nitrogen at a
temperature of-160°C is used at the pedicle of the haemorrhoid for 3 minutes each. The patient remains in left
lateral position. When the cryo-probe is placed on the tissue, an ice ball forms as a visible white area which wi
eventually slough. The procedure usually takes 10 to 15 minutes and the patient is obseved for 30 minutes befo
he leaves.
The great advantage of this method is that it is completely without pain. The main disadvantage is the
profuse watery discharge which starts within 3 hours of the procedure and lasts for 2 to 4 weeks. The discharg
contains large amount of protein and potassium. This requires wearing of surgical pads for 2 to 3 weeks and
healing is complete in 4 to 6 weeks.
In the advanced case when there is prolapse of haemorrhoid this technique has little efficacy. So cryosurger
and elastic band ligation are unlikely to replace surgfery, but nevertheless be valuable additions to conservativ
therapy.
MAXIMAL ANAL DILATATION (LORD’S PROCEDURE).— Tightness of the internal sphincter has
been made responsible for many symptoms of haemorrhoids. Maximal anal dilatation was introduced in an
attempt to disrupt this tight band. The whole of the anal canal and lower rectum are slowly and uniformly dila
with the fingers until 3 fingers of both hands are inserted. Tight bands, which Lord called ‘pecten’ are broken
out and irregularities in the anal canal are ironed out. It is important to realise that the pecten bands canno
normally be felt by the fingers of one hand. To feel the pecten band the index finger of the left hand is place
well inside the anal canal and lifted upwards, while the right index finger is inserted into the rectum pressi
downwards. The pecten band will be felt to roll under the finger. Once the bands have been felt they must
stretched until they give way. It is important to avoid tearing so that the dilatation must be gentle and com
with a rotating movement. Although Lord suggested that this method is best reserved for patients with thi
degree or large second degree haemorrhoids, yet many surgeons who have adopted this procedure regard
an ideal method for treating many anal conditions particularly fissure-in-ano. However it does not elimina
redundant tissue and there is significant incidence of incontinence particularly in the elderly with pelvic flo
problems. This treatment is now a more recognised treatment of fissure-in-ano and in selected cases of earl
stage of haemorrhoids.
Haemorrhoidectomy.— For large third de
gree haemorrhoids particularly with associated
tags and an external haemorrhoidal plexus haem-
orhoidectomy is the treatment of choice and is the
only method to give lasting relief in such cases.
Many patients are reluctant to submit to haemor
rhoidectomy because the operation has become
notorious of being associated with a great deal of
postoperative pain and it also has the considerable
economic disadvantage that the patient has to live
in hospital for several days postoperatively and a
further period away from work.
LIGATURE AND EXCISION METHOD.—
This is the most widely used operation nowadays.
Fig.54.8 - Three primary piles are well exposed After being anaesthetised, the patient is kept in the
and held with Kochers torceps.
lithotomy position. A dry swab is pushed into the
rectum and then partially withdrawn. This will allow the haemorrhoids to prolapse along side the swab. Th
are picked up individually with artery forceps. Anal sphincter is now dilated with two index fingers. A V-s
cut is made on the skin adjacent to the primary pile,
so that the base of this V is directed towards the
primary pile and the apex away from the centre of
the anus. The limbs of the V should not extend
beyond the mucocutaneous junction. A little dis
section will now expose the subcutaneous part of
the external sphincter. The haemorrhoids are now
further dissected upwards so that they are now
fixed by the mucosal suspensory ligament. This
newly formed pedicle is now transfixed with a
stout ligature (silk or catgut). If there is any exter
nal piles, it should be included wihtin this V. At this
time too much pull should not be exerted on the
Fig.54.9.— Shows applying ligature at the pedicle of haemorrhoids lest they should be tom at the
right anterior primary internal pile. pedicle. The haemorrhoids distal to the ligatures
are excised.lt will be seen that between each haemorrhoidal wound a bridge of anal mucosa remains in
continuity with the parianal skin. These mucous membranes can be sutured to prevent postoperative steno
of the anus. But this may not be done.
At the conclusion of the operation a proctoscope is passed to make certain that there is no bleeding from the
pedicles and at th§. upper anal canal has not been narrowed by including too large a bridge of tissue into the
pedicle ligatures. A flat moistened dressing is applied to the anus and the patient is encouraged to open his
bowel on the 3rd day. The use of anal dilator is not normally required in the postoperative management of th
form of haemorrhoidectomy but if the patient is apprehensive or there is spasm or narrowing of the anal can
which is examined digitally on the 7th postoperative day, the use of an anal dilator is recommended for 2 to 3
weeks. In this way any degree of permanent stenosis can be avoided. Approximately 25% of patients may
require the use of dilators postoperatively.
CLOSED HAEMORRHOIDECTOMY.— This operation is more practiced in United States. The external
and internal components of haemorrhoids are excised and the wound is closed completely from the high
ligation of the pedicle to the anal margin skin with a continuous catgut suture. The objective of this type of
haemorrhoidectomy is the complete removal of the haemorrhoids with relining of the upper 2/3rds of the an
canal. The proponents of this method claim that the wounds heal quickly by primary intention with less pain
than in the open ligation and excision method. The whole concept of this operation with excision of the
haemorrhoid and overlying mucosa and the drawing together of the mucosal edges with sutures appears inc
If all haemorrhoidal tissue is removed, suturing can only be accomplished by causing marked stenosis of the
anus, otherwise only very early haemorrhoids were treated. Considerable narrowing of the anal canal was al
noticed when digital examinations were carried out on the 3rd and 6th postoperative days.
SUBMUCOUS HAEMORRHOIDECTOMY (PARK’S).— Though this technique was much to recom
mend, yet a number of drawbacks have prevented its wider adoption. The operation is carried out in lithotom
position with a special self-retaining retractor. The submucous plane is infiltrated with saline and adrenalin
which controls bleeding and helps dissection. A vertical incision is made through the mucosa over the
haemorrhoid from the top of the anal canal to the anal margin where any skin tag or external haemorrhoidal
component is removed. The mucosal flaps are lifted on both sides so that the haemorrhoid is completely
exposed. It is then dissected away from the underlying internal sphincter muscle. The pedicle is transfixed,
ligated and excised. The mucosal flaps are allowed to pull back in place and are approximated with several
interrupted catgut sutures. Prolapse of mucosa must be prevented by including part of the underlying intern
sphincter muscle in the suture. The disadvantages of submucous haemorrhoidectomy are that (i) it is a difficult
operation to perform, (ii) takes considerable longer time, (iii) there is often considerable haemorrhage and (i v
a recurrence rate of over 14% at 6 months have been recorded after submucous haemorrhoidectomy. The
advantages of this operation are that (i) it does seem to reduce immediate postoperative pain, (ii) less chance
of postoperative stenosis and (iii) does not require passage of a dilator or a finger as the anal canal is covered
with mucous membrane and anal canal heals by primary intention.
Circular stapled haemorrhoidectomy.— Under general or spinal anaesthesia patients are placed in
lithotomy position. After painting and draping of the part, a proctoscopic examination is performed to confir
findings. The anal verge is held at 3 points where anoderm is slightly everted. Keeping this as counter tractio
the circular anal dilator (CAD 33) is introduced in such a way that the prolapsed anoderm gets reduced. The
dilator is then fixed to the skin by stay sutures at 3 or 4 places. Now the purse-string anoscope is introduced
through the dilator. A purse-string suture using 2/0 prolene about 5 cm above the dentate line is then applied
rotating the anoscope around the entire anal circumference. The haemorrhoidal circular stapler (HCS 33) is
now inserted into the dilator. The head is passed beyond the purse-string and the string is tightened and the
ends of the purse-string suture are pulled out through the lateral holes of the stapler. The entire casing of the
stapler is then introduced into the anal canal, a slight traction is given on the purse-string suture to draw the
prolapse membrane into the casing. The instrument is now tightened and fired to staple. After this the stapler
is held closed for about 30 seconds to act as a tamponade. After this the stapler is opened, withdrawn and the
staple line is examined for haemostasis.
The average duration of procedure is about 15 minutes. There is significantly low postoperative pain. The
patients may be discharged within 36 hours after operation ensuring a smooth and painless passage of stool
postoperatively. First follow-up is performed at 1 week, followed by follow-ups at 2 weeks and 6 weeks.
Usually there is no incidence of postoperative bleeding or incontinence. This circular stapling device acts by
excising a circumferential column of mucosa and submucosa above the dentate line to interrupt the termin
branches of the haemorrhoidal artery, thus reducing flow to the subepithelial space and mucous prolapse.
The main problem of this technique is that the cost of the stapler is minimum Rs. 18,000/- or more.
Complications may occur due to application of a low purse-string suture being close to the dentate line wh
may cause postoperative pain. Second complication is very rarely pelvic sepsis may occur and extreme rare
rectovaginal fistula has been recorded after this procedure. Incontinence is almost unknown after this proc
only if the underlying sphincter is included in the purse-string suture this may occur. Bleeding from suture
should always be looked for and is easily tackled by a simple haemostatic suture over the staple line. This
technique is mostly suitable in grade III and grade IV cases, but it can be used in earlier grades also.
ENDOSTAPLING TECHNIQUE.— This is a recently introduced technique in which a stapling gun is
being used. This is introduced through the anus. A strip of mucosa and submucosa just above the dentate l
is excised circumferentially. The veins leading to the haemorrhoids are incorporated in this excision. The gu
is now activated which repairs the cut mucosa and submucosa by stapling the edges together. This techniq
less painful and less traumatic than conventional haemorrhoidectomy. Its long term result is still to be know
Choice of treatment.— Sclerosing injection method remains the first choice in first degree and early
second degree haemorrhoid. Large haemorrhoids particularly those which are prolapsing are suitable for e
band ligation, but it is a painful method. Cryotherapy is also effective for the same group of patients, but is
more expensive and causes considerable discharge and loss of work than elastic band ligation. Lord’s dilata
has a place in the treatment of acute thrombosed prolapsed piles, but find little place for routine manageme
of haemorrhoids. For large third degree and fourth degree piles particularly with skin tags and external pil
haemorrhoidectomy remains the only form of treatment which can guarantee lasting results.
FISSURE-IN-ANO
Fissure-in-ano is a very common and painful condition. Fissures occur most commonly in the midline
posteriorly, the least protected part of the anal canal. In males fissures usually occur in the midline posterio
(90%) and much less commonly anteriorly (10%). In females fissures on the midline posteriorly are slightly
commoner than anteriorly (60 : 40). The relative frequency of the anterior fissures in the females may be
explained by the trauma caused by the foetal head on the anterior wall of the anal canal during delivery.
Aetiology.— The predominantly posterior midline location of fissures has been explained by (a) posterio
angulation of the anal canal, (b) relative fixation of the anal canal posteriorly, (c) divergence of the fibres of
external sphincter muscle posteriorly and (d) the elliptical shape of the anal canal. 1. Constipation has been
most common aetiological factor. 2. Spasm of the internal sphincter has also been incriminated to cause fiss
in-ano. 3. When too much skin has been removed during operation for haemorrhoids, anal stenosis may re
in which anal fissure may develop when hard motion passes through such stricture.
Secondary causes of anal fissures must be remembered. These are : (i) Ulcerative colitis, (ii) Crohn’s
disease, (iii) Syphilis and (iv) Tuberculosis.
Pathology.— Fissure starts proximally at the dentate line. So whole of the anal fissure lies in the sensitive
skin of the anal canal and that is why pain is the most prominent symptom.
There are two types of fissure-in-ano — (i) acute and (ii) chronic. Acute fissure-in-ano is a tear of the skin
of the lower half of the anal canal. There is hardly any inflammatory induration or oedema of its edges. An
sphincter muscle spasm is always present.
Chronic fissure-in-ano is a deep canoe-shaped ulcer with thick oedematous margins. At the upper end o
the ulcer there is hypertrophied papilla. At the lower end of the ulcer there is a skin tag known as ‘sentinel
(sentinel because it guards the anal fissure). There is characteristic inflammation and induration at the marg
Base consists of scar tissue and internal sphincter muscle. Spasm of the internal sphincter is always present
Sometimes infection may lead to abscess formation. Chronic fissure-in-ano may have a specific cause e.g.
Crohn’s disease, ulcerative colitis, tuberculosis and syphilis, so during operation biopsy must be taken from
chronic fissure to exclude secondary cause mentioned above.
Clinical features.— This condition is more common in women. It is mostly seen between 30 and 50 years
of age. It occurs sometimes in children and may cause acquired megacolon. But it is rare in the aged due to
muscular atony. Constipated hard stool while passes through the anal canal in patients where there is spasm
internal sphincter and hypertrophied anal papilla an acute tear of the anal canal will occur. This ACUTE
FISSURE will cause spasm, pain of the defaecation and passage of bright streaks of blood along with the stool
or will be seen in the tissue paper. If the acute fissure fails to heal, it will gradually develop into a deep
undermined ulcer. This is termed CHRONIC FISSURE-in-ano. A typical chronic fissure-in-ano will have in
its upper end a hypertrophied anal papilla. At its lower end a tag of hypertrophic skin, which is called a sentin
pile and canoe-shaped ulcer in between the upper and lower ends.
Pain and bleeding are the two main symptoms of this condition. Pain starting with and following defaecat
(usually following an hour or more) has been variously described as sharp, biting, burning etc. Pain is someti
intolerable and pain is the main symptom of fissure-in-ano. Haemorrhoids may be associated with fissure-in
ano and it must be remembered that uncomplicated haemorrhoid in first and second degrees are usually with
pain. After the pain goes off the sufferer remains comfortable till the next action of bowel. The bleeding of anal
fissure is variable, but usually occurs as streaks on the outside of the stool or spots noted on toilet tissue (cf.
bleeding in haemorrhoid). Slight discharge may accompany a fully established chronic fissure. Pruritus ani
may be another symptom of this condition.
ON EXAMINATION.— A tightly closed puckered anus is almost pathognomonic of this condition. Sentin
skin tag may or may not be present. If the margins of the anus are gently separated, the lower end of the anal
fissure may be inspected. Because of intense pain digital examination may not be possible. If allowed, a
chronic fissure is easily palpable by digital examination. When the patient does not allow digital examination
a surface anaesthetic such as 5% xylocaine ointment may be applied on the anus and digital examination may
be tried after 5 minutes. In more difficult cases, digital examination and proctoscopy may not be possible
without general anaesthesia. Acute fissure is not palpable. But in chronic fissure, the characteristic crater of th
vertical fissure may be felt.
Differential diagnosis.— 1. MULTIPLE FISSURES in the perianal region are seen as a complication of
skin disease, inflammatory bowel disease or anorectal sexually transmitted disease such as herpes. HIV test
should always be performed as these patients may have acquired immuno deficiency syndrome (AIDS).
2. CARCINOMA OFTHE ANUS in very early stage may simulate a fissure-in-ano. If on recta! examination
there is any doubt, the lesion must be excised under general anaesthesia and submitted to histological examin
3. TUBERCULOUS ULCER may look like a fissure-in-ano, but will have undermined edge.
4. PROCTALGIA FUGAX — which is characterised by severe pain arising from the rectum and occurs at
irregular intervals. The pain is cramp-like, lasts for a few minutes and disappears spontaneously. It often
occurs at night. It may even follow straining at stool or ejaculation. The pain may be unbearable and possibly
due to segmental cramp of the pubococcygeus muscle. It is said to be seen more commonly in patients who ar
in undue stress or anxiety. A more chronic form of the disease has been termed the ‘levator syndrome’ and m
be associated with severe constipation.
It fortunately gradually subsides and requires no treatment. A few enthutiastic surgeons have tried to seve
the puborectalis muscle, but this should not be done, as it causes incontinence.
Treatment.—
A. Acute ulcers with short history usually heals with conservative treatment. Conservative treatment includ
(a) oral pain medication, which may be taken before any anticipated bowel movement, (b) Stool softner may
be used to make the stool soft enough to be passed without anal spasm. Weak bulk laxative or cathartics is bes
in this condition, (c) Nitric oxide is a neurotransmitter which induces relaxation of the internal sphincter.
Glyceryl trinitrate is a nitric acid donor and is applied as an ointment to the anal canal to produce the relaxatio
of the internal sphincter. This heals the anal fissure in majority of patients. Moreover glyceryl trinitrate improv
blood flow to the area which further helps in healing of the fissure. But glyceryl trinitrate has a few side effect
of which severe headache is of main concern. So later on calcium channel blocker e.g. diltiazem is now being
used, (d) Soothing ointments may be applied with doubtful efficacy. 5% xylocaine ointment may be introduce
with a fine nozzle into the anal canal, (e) Self dilatation is highly important as this will relax the anal muscu
and resolves with healing of the fissures. After 5 minutes of application of 5% xylocaine ointment a small a
dilator (St. Marks) should be passed into the anal canal. Anal dilators are commonly made in 3 sizes. Grad
dilatation of the anal canal is advised by using larger dilators. This technique of using xylocaine lubricant a
then dilating the anal canal with dilator should be practiced twice a day for a month. By this time the anal
fissure may be healed, (f) Injection of long acting anaesthetic solutions promotes little relief and has signifi
complications.
B.Chronic ulcers.— Though in these cases conservative treatment may be tried, yet in majority of cases
this treatment fails and surgical management should be called for.
1. ANAL DILATATION.— Lord’s procedure of anal dilatation is the simplest method to dilate the sphi
of the anal canal. Under general anaesthesia and the patient in lithotomy position the index and the middle
fingers of each hand are inserted simultaneously into the anus and pulled apart to give maximal anal dilat
Any constricted bands should be well stretched and the fibrosis around the fissure should be ironed out. T
patient can go home the same day, but should be warned that there may be some faecal incontinent for 10
When the chronic fissure is with excessive fibrosis and skin tag, there is every chance that anal dilatation w
be a failure. In these cases operation is justified.
2. POSTERIOR SPHINCTEROTOMY AND FISSURECTOMY.— The patient remains in lithotomy
position and general anaesthetised. A well greased Sim’s speculum is introduced. A good view of the fissu
now possible. The fibres of the internal sphincter will be seen running transversely in its floor. The transve
fibres are divided and the floor of the fissure is made smooth. If the ulcer is deep with fibrotic edges the ul
should be excised. If sentinel pile is present, it should be excised. It must be remembered that only superfic
fibres of the internal sphincters are divided and not the entire thickness of the internal sphincter. The ends
the divided muscle are retracted and the wound remains smooth. Postoperative treatment includes liquid
for 2 days and the bowel is moved on 3rd day. After moving bowel a daily hip bath and passage of an anal
dilator are required till the wound is absolutely healed. The only disadvantage of this operation is a prolon
convalescent period of 7 to 10 days and in occasional cases there may be persistent mucous discharge.
3. LATERAL ANAL SPHINCTEROTOMY.— In this operation the internal sphincter is divided away
from the fissure either on the right or left lateral position. Though it is said that the convalescent period is l
in this operation, yet this operation is handicapped in the sense that excision of the ulcer or biopsy cannot
performed in one go. So this operation is more appropriate for early cases. Moreover haematoma formatio
and abscess formation has also been reported. 10% to 12% of patients will suffer from anal swelling or imp
control of stool. Recurrent ulcers have also been reported. But in this operation the convalescent period is l
similarly hospital stay may be even 4 days.
4. EXCISION OF ANAL ULCER alongwith skin graft to limit the convalescent period has not been
successful. Even anal skin has been lifted up to cover the defect of the anal canal following excision of the
ulcer. This is called ‘V-Y anoplasty’. This has also been unsuccessful.
5. ANAL ADVANCEMENT FLAP.— In this technique the edges of the fissure are excised and mobilise
as full thickness anal skin flap. These flaps are slid over the fissure and sutured in place. This technique ha
become popular recently as there is little risk of damage to the underlying internal sphincter, so there is no
chance of incontinence.
NEOPLASMS OF THE RECTUM AND ANAL CANAL

Benign Neoplasms.— The rectum shares the same types of polyps as the colon. This has been described
in detail in chapter 53 of The Colon.
Only treatment of a few polyps which are more often seen in the rectum is described below.
1. Juvenile polyp.— It is the common rectal polyp of the children. Usually it possesses a long pedicl
the tumour can be delivered through the anus. In this case the pedicle is ligated and the polyp is excised. If
tumour is high up in the rectum or the pedicle is short, a snare may be used.
2. Adenomatous polyp.— Lots of controversies exist regarding its malignant potentiality. But it is now
assumed that this tumour rarely gives origin to biologic cancer. Yet when an adenomatous polyp is detected
should be removed, however little chance of malignant transformation there may be.
When there is a long pedicle and the polyp can be delivered through the anus, the pedicle is transfixed an
the tumour is excised. When the-growth has small pedicle or is higher up, the tumour is removed with a sna
through sigmoidoscope. In case of sessile adenoma the tumour can be removed either by submucous dissect
per annum or the tumour may be fulgurated with an insulated electrode passed through a sigmoidoscope.
3. Villous adenoma.— This tumour is often of very large size and rarely may even fill the entire rectum.
This tumour is a precursor of carcinoma. The larger the tumour, the more is the tendency to become maligna
This is a well accepted fact. The malignant change can be assessed by palpation with the finger — any hard
area should be assumed to be malignant and should be biopsied. Characteristically this tumour has a frond-
appearance. This tumour discharges mucus and rarely it is so profuse, which is high in potassium, as to caus
electrolyte imbalance and fluid loss. Presence of such tumour should call for excision. Small tumours may be
excised by submucous dissection per annum or by sleeve resection from above. In case of large growth excis
of the rectum is required. When malignant change has occurred rectal excision is required. Transanal endoscopic
microsurgery (TEM) has recently been introduced and is very helpful for local removal of villous adenoma
through the anal canal. In this method a large operating sigmoidoscope is introduced, the rectum is distende
with C02 (carbon dioxide) insufflation. The image of the operation field can be displayed on a monitor throu
a camera inserted via the sigmoidoscope. The lesion is excised with specially designed instrument observing
the monitor screen. This is a highly specialised technique.
Only a few tumours described below are rather peculiar to occur in rectum. These are :
(i) Benign Lymphoma.— It is essentially a submucosal lesion, but appears as a nodule, which is firm
and rather mobile. The colour is pink to greyish white. No age is exempted and it involves both sexes almost
equally. Treatment is local excision.
(ii) Endometrioma.— It usually involves females of 20 to 40 years of age and occasionally at the
menopause. It is also a submucous tumour which appears as a constricting lesion at the rectosigmoid junctio
Diagnosis is not difficult as dysmenorrhoea with rectal bleeding is the only peculiar symptom of this conditi
On sigmoidoscopy the lesion is seen at the rectosigmoid junction as reddish projection into the lumen with t
mucous membrane intact. Treatment is contraceptive pill which inhibits ovulation and amelioration of symptom
If this fails bilateral oophorectomy will cause regression of the lesion. Local resection is usually not necessary
(iii) Haemangioma.— This uncommon tumour is usually localised in the lower part of the rectum or
upper part of the anal canal. Bleeding per rectum is the only symptom. Treatment is extensive excision of the
rectum and anal canal bearing the lesion. Anterior resection or sphincter conserving operation is well suited
this purpose.
CARCINOMA OF THE RECTUM

PATHOLOGY.—
Precancerous conditions — (i) villous papilloma; (ii) Adenomas; (iii) Familial polyposis.
MACROSCOPIC TYPES — (i) proliferative variety — which is common in rectal ampulla, (ii) Ulcerative
variety — it is also seen in the ampulla of rectum, (iii) Annular or tubular variety which is more often seen at
the pelvirectal junction or anorectal junction.
MICROSCOPIC VARIETIES.— Microscopically, all rectal carcinomas are (a) basically columnar cell
adenocarcinoma. Three varieties of adenocarcinoma can be seen according to their differentiation, (i) Well
differentiated variety, (ii) averagely differentiated variety and (iii) anaplastic or undifferentiated variety.
(b) In only small percentage of cases colloid carcinoma may be seen in rectum. It may appear either from
mucoid degeneration of adenocarcinoma or as a primary mucoid carcinoma. The mucus lies within the cell
displacing the nucleus to the periphery like a signet ring appearance. Primary colloid carcinoma grows rapid
metastasises early and possesses a poor prognosis. It may cause fistula-in-ano.
(c) Squamous cell carcinoma, when seen in the rectum, is

usually due to invasion of anal carcinoma extending up into the
rectum.
Spread.— LOCAL SPREAD.— The peculiarity of direct
infiltration of rectal carcinoma is that it usually occurs
circumferentially. Longitudinal spread is restricted to a few
centimetres except in anaplastic tumours. Circumferentially the
spread involves mucous and submucous coats. It takes about 6
months to involve1A th of the circumference and about 1 Vi to 2
years to involve the whole circumference of the rectum.
Gradually the growth spreads deeply to the muscular coat. Then
the spread involves the full thickness of the rectum but is still
limited by the fascia propria (perirectal fascia). Growth takes a
long time to penetrate fascia propria and it is rare before 18
months from the commencement of the disease. Once the fascia
propria is penetrated, the growth is liable to involve the adjoining structures which are as follows :
Anteriorly — in males the prostate, seminal vesicles and the
bladder; in females the vagina and the uterus.
Laterally— the ureter may be involved in either sex causing
secondary hydronephrosis.
Posteriorly — the sacrum and the sacral plexus of nerves
may be involved.
LYMPHATIC SPREAD.— Like carcinoma anywhere in the
body lymphatic spread is quite early. As soon as the muscles of
the rectum are involved, there is chance of lymphatic spread. It
must be remembered that enlargement of the draining lymph
nodes does not mean that it is secondarily involved. Enlargement
of lymph nodes may occur from secondary infection which is
not infrequent.
There are such nodes as epicolic nodes on the wall of the
rectum. Next lymph nodes to be affected are the pararectal nodes
of Gerota (same as paracolic nodes). The intermediate nodes
are situated along the lower part of the superior rectal artery
and the main nodes are at the origin of the inferior mesenteric
artery.
The peculiarity of the lymphatic spread of rectal carcinoma
is that the spread is mainly upwards as the lymphatics move mainly in that direction.
A. Carcinoma ofthe rectum above the peritoneal reflection spreads in an upward direction first involving
the intermediate nodes and then the main nodes.
B. Carcinoma below the peritoneal reflection to within 1 to 2 cm ofthe anal orifice spreads mainly in the
upward direction but the first nodes involved are the pararectal nodes of Gerota, then the intermediate node
and lastly the main nodes.
Carcinoma between 4 to 8 cm from the anus spreads mainly in the lateral direction along the lymphatics
that accompany the middle rectal vein, as this portion of the rectum is supplied by the middle rectal artery.
C. Carcinoma involving 1 to 2 cm of the anal orifice usually spreads downwards to the inguinal group of
lymph nodes as the area of anal canal below the dentate line is drained into the inguinal group of lymph no
Widespread and atypical lymphatic permeation may occur in case of anaplastic carcinoma.
VENOUS SPREAD.— Like other carcinomas of the body spread through blood occurs late, except in case
of carcinoma affecting that part of the anal canal where the mucous membrane is firmly adherent to the dee
structures (pecten). Only anaplastic carcinoma and rapidly growing tumours in younger patients are liable t
spread via blood. The first organ to be affected by venous spread is the liver through inferior mesenteric vei
Occasionally spread may occur through systemic veins like middle rectal or inferior rectal veins and may
metastasise to the lungs, spines, adrenals etc.
TRANSPERITONEAL SPREAD.— In case of rectal carcinoma situated high up in the rectum above the
peritoneal reflection peritoneal metastasis may occur.
Staging of carcinoma.— Like other carcinomas, clinical staging of rectal carcinoma is important to find
out how far has the disease progressed and what should be the line of treatment. Probably more important i
histological grading which will indicate the type of cancer by examining biopsy specimen under microscope
A highly malignant tumour even if detected in early stage will carry worse prognosis than a well differentia
tumour in rather late clinical stage. There are two types of clinical staging — Duke’s classification and TNM
system.
Clinical Staging.—
DUKE’S CLASSIFICATION.—
Stage A — The growth is limited to rectal wall.
Stage B — The growth has extended beyond the rectal wall but no involvement of regional lymph nodes.
Stage C — The growth has extended beyond the rectal wall and the regional lymph nodes are involved.
This stage can be further subdivided into Stage Cl where the local pararectal lymph nodes are only involved
and Stage C2 where intermediate and main nodes are involved.
TNM SYSTEM.—
T1S: Carcinoma-in-Situ.
T1 : Involvement of the mucous and submucous coat but the muscular wall is not involved.
T2 : Involvement of muscular wall, judged by induration on palpation.
T3 : Involvement of all layers of the colonic wall including serosa, which is judged by irregularity.
T4 : Extension to adjacent structures.
NO : No lymph node metastasis; N1 : Regional lymph node involvement.
MO ; No distant metastasis; Ml : Distant metastasis is present.
Histological grading (Broder’s classification).— The more nearly the tumour cells approach normal
texture and shape, the less malignant is the tumour. Conversely the greater the percentage of cells of embryo
nature with lots of mitoses the tumour is of undifferentiated variety and virulently malignant.
Stage I: Low grade (well differentiated) — good prognosis.
Stage II: Average grade — fair prognosis.
Stage III: High grade (anaplastic tumours) — poor prognosis.
CLINICAL FEATURES.— As other carcinomas in the body, rectal carcinoma is a disease of old age. If
it occurs in younger age the prognosis is poor. The patient usually does not come to a doctor before 6 month
of commencement of the disease.
SYMPTOMS.— 1. The main symptom is bleeding per rectum. This is the most constant and earliest
symptom. There may be mucus alongwith bleeding. The bleeding is usually slight in amount and occurs wit
the stool or at the end of defaecation. It is sometimes seen as spot in tissue paper or may stain the under
clothing. If a careful history is taken one may differentiate between bleeding from internal pile and bleeding
due to cancer. It must be noted that it is a painless bleeding like an uncomplicated internal pile.
2 .Alteration to bowel habitis a very common symptom. Either it may be an increasing constipation or it
in the form of early morning diarrhoea. In case of annular carcinoma at the pelvirectal junction the patient
suffers from increasing constipation. Instead of taking advice from his doctor the patient prefers to take incre
dose of laxatives. Ultimately, with the use of laxatives he shows a tendency towards diarrhoea for a limited
period, which is again followed by constipation once the patient stops taking laxative. This is called alteratio
in bowel habit.
The other symptom is early morning diarrhoea. The patient gets up from bed to rush to the toilet. The
patient passes lots of blood and mucus in addition to faeces. This is a particular symptom seen in case of
cauliflower growth at the ampulla of rectum.

3. Sense of incomplete defaecation is quite common when a papilliferous or proliferative growth is situ
at the lower half of the rectum. Every time the patient opens his bowel, he feels that more faeces are to be
passed. So he visits the toilet frequently (spurious diarrhoea or false diarrhoea). But he fails to pass formed
stool, instead he passes flatus and a little blood stained mucus (bloody slime).
4. The intestinal obstruction may be the presenting symptom in case of stenosing growth.
5. Pain is a late symptom. Only with intestinal obstruction due to stenosing growth of the rectosigmoid
junction one may suffer from colicky pain from intestinal obstruction. When the growth has come out of the
rectum and fascia propria the surrounding structures are involved and the patient complains of pain. Sciatic
may be complained of when the growth has invaded the sacral plexus.
6. A few patients may present with bizarre symptoms like loss of weight, slight pain and symptoms associa
with distant metastases. These are palpable lump of liver metastasis, yellowness of jaundice and abdominal
distension from ascites.
Physical examinations.—
Abdominal examination may be negative. Only in case of intestinal obstruction due to stenosing lesion at
[he rectosigmoid junction one may palpate distended large bowel filled with stools. In late cases one may ge
enlarged liver from liver metastasis, ascites and secondary deposits in the peritoneum.
RECTAL EXAMINATION is very important and 90% of rectal carcinoma can be felt digitally. So all case
of slight rectal problem should be examined by digital examination to exclude carcinoma. Typical indurated
feel is noticed in case of carcinoma. Even in case of higher growths, bimanual palpation may feel the carcino
even at the rectosigmoid junction. One finger in the rectum and another on the lower part of the abdomen ca
feel such carcinoma. In case of females one finger in the rectum another in the vagina will give a good idea
about the degree of infiltration. After rectal examination one must look at the gloved finger whether it is
smeared with mucus and blood. If present, the diagnosis is almost certain of cancer.
Special Investigations.— 1. Proctosigmoidoscopy will reveal the growth and may help in taking
biopsy.
2. Biopsy.— Whenever a growth is detected through proctoscope or sigmoidoscope a biopsy must be
taken from the edge of the tumour and also from the central part of the tumour. Histological diagnosis is
more important and it will also detect the histological grading which is essential to know the prognosis.
3. Barium enema.— It should always be performed even when a carcinoma is detected in the lower
part of the rectum. When sigmoidoscope fails to visualise the growth because of the spasm of the bowel
below it, barium enema X-ray is the only easily available diagnostic tool in the hand of surgeon. When
carcinoma has been diagnosed by digital examination or by sigmoidoscopy, even then barium examination
should be performed to exclude multiple adenomatous polyposis and other synchronous carcinomas
higher up in the colon.
4. ENDORECTAL ULTRASOUND IN RECTAL CARCINOMA.— Endorectal ultrasonography (ERUS)
has revolutionised the management of rectal cancer. It is now a powerful tool for preoperative staging of
rectal cancer. The accuracy of digital examination is highly subjective and varies from 60% to 80%. CT
and MRI are not as accurate as this technique in assessing depth of local invasion and involvement of
mesorectal lymph nodes. CT and MRI may detect extension of the tumour beyond rectal wall or the
involvement of adjacent structures, but they do not provide much clue about involvement of different
layers of the rectal wall. Endorectal ultrasonography is also useful to identify patients with locally
advanced disease, who may be considered for primary radiotherapy to down-stage the disease. ERUS
has also been used to follow patients who have undergone sphincter-saving rectal resection to detect
local recurrence without any symptoms.
Position of patient.—ERUS may be performed either in the left lateral position or in the lithotomy position
Whereas left lateral position is commonly used for unsedated patients, but lithotomy position is more often
used for patients under anaesthesia or when ultrasound guided biopsy is required.
Examination.— A careful digital examination is always carried out. A 20 cm sigmoidoscope is then
passed into the rectum to inspect and to note the distance of the tumour from the anal verge. The assembled
endoprobe is then passed through the sigmoidoscope to a position above the lesion. Following the insertion
of the probe, the latex balloon is filled with degassed water. The sigmoidoscope is then withdrawn
slowly and the transducer is activated so that a 360° scan of the rectal wall and the surrounding tissues
are displayed on the screen. The probe can be moved gently and the volume of water in the balloon can
be adjusted to bring a particular feature into the optimal focal range of the transducer. Video recording
of the examination is provided with for record.
The main problem is that it is difficult to examine the high lesions as it is difficult to manoeuvre the prob
through the lesion and there is a potential risk of perforation' The second problem is that it is difficult to do
investigation when the stenotic lesion has a lumen of less than 25 mm.
The probe should be cleansed with spirit before using again. The instrument is disassembled and soaked
glutaraldehyde for 30 minutes.
Endorectal ultrasonography is the best method for preoperative assessment of the depth of infiltration of
rectal cancer.
The accuracy of ERUS in assessing lymph node involvement is in the range of 60% to 85% in
different series. The possibilities of over-staging and under-staging are there. The involved nodes appear
as circular or oval echo-poor lesions. Other parameters concerning the internal structure of the node
have been described as lobulation, inhomogeneity, presence of echo-poor rim, presence of hilar reflection
etc. Metastatic involvement of mesorectal lymph nodes is a major prognostic factor. Presence of more
than 3 nodes is associated with poor prognosis. The detection of lateral lymphatic involvement is equally
important as these nodes may be involved in the absence of mesorectal involvement. Such patients need
wide lateral clearance. The published data support that ERUS is superior to CT or MRI in assessing
perirectal lymph node involvement.
5. Colonoscopy, which is only available in a few specialised units, is definitely the best method to exclu
any lesion higher up in the colon.
TREATMENT.— Like cancers anywhere in the body, radical resection is the only curative treatment
available for carcinoma of the rectum. Such radical excision means excision of the rectum with its
sheath alongwith all nodes lying on the wall with 5 cm normal tissue above and below the growth and all
involved regional lymph nodes. Obviously if the main nodes are involved the only way to do radical
surgery is to ligate inferior mesenteric artery at its origin from the aorta (flush ligation). But this requires
excessive resection of the bowel. So the surgeon usually prefers to ligate inferior mesenteric artery
below the origin of 1 or 2 branches.
The type of resection which should be employed in a particular case depends on the situation of the carci
For this, rectum has been divided into three parts, (a) The proximal third extends from the junction with the
sigmoid colon which is 15 or 16 cm above the anus down to about 11 cm. (b) The middle-third extends from
11 cm down to the lowest portion of the anterior peritoneal reflexion (pouch of Douglas) which is at 6 to 7 cm
in females and 7 to 8 cm in males above the anus, (c) The distal third of rectum is entirely extraperitoneal and
includes the anal canal.
(a) Proximal rectal carcinomas.— Cancers with the lower margin at or above 11 cm can always be
removed by low anterior resection and primary anastomosis conserving the sphincter mechanism. Tempora
proximal defunctioning colostomy may be advisable to secure anastomosis. In young subjects in whom canc
grow rapidly, probably it will be better to do abdomino-perineal resection instead of anterior resection to av
recurrence.
(b) Midrectal carcinomas.—In these cases it is rather difficult to do anterior resection conserving sphincte
mechanism as this is almost invariably followed by recurrence as if a typical 5 cm normal rectum has to be
removed distal to the growth there is hardly any space to do the anastomosis. In these cases (i) abdomino
perineal resection will be the safest, (ii) If the permanent colostomy has to be avoided one may perform
abdomino-perineal pull through operation and making the anastomosis outside the anus to avoid the proble
of doing an anastomosis deep in the pelvis. After resection of the lesion by the abdominal approach the prox
colon is drawn to the anorectal stump and is sutured to the inverted anorectal stump outside the anal canal
drawback is that some patients do not regain faecal continence, (iii) There is now available a stapling instru
E. E. A. stapler, that creates an inverting end-to-end anastomosis. This has made it technically possible to res
carcinomas down to the distal limit and to restore continuity by a safe end-to-end anastomosis.
(c) Distal rectal carcinomas.— In these cases abdomino-perineal resection (Miles) or perineo-abdominal
resection (Gabrial) is the method of choice.
Preoperative preparation.— Colon and rec
tum should be prepared preoperatively so that these
portions should be devoid of any faecal matter and
bacteria as far as possible. This is usually achieved
by a combination of mechanical cleansing and anti
biotic treatment. The mechanical cleansing is per
formed by purgatives, enemas or whole-gut irriga
tion. The antibiotics must be active against both aero
bic and anaerobic organisms. Nowadays cefuroxime
750 mg plus metronidazole 500 mg are given 1 hour
before surgery. Two further doses are given of the
same drugs at 6 and 12 hours after the operation. If
the carcinoma is obstructive it is preferable to do a
temporary colostomy a few days before the opera
tion to do proper cleansing of colon on both sides of
colostomy. In case surgery is necessary immediately,
perioperative washout of the loaded colon is
Fig.54.12.— Sphincter conserving operation using E.E.A. possible if the rest of the operative wound is scru
stapler for anastomosis after resection of mid-rectal pulously protected.
carcinomas.
Electrolyte imbalance, if present, should be
corrected before operation. An indwelling catheter is introduced into the bladder before the patient is sent t
the operation theatre.
Abdomino-perineal resection.— This is a radical operation and was advocated by Miles in 1910. In his
original description, one surgeon operates the abdominal part and then he moves to the lower end of the table and performs
the perineal part. But in 1938, Lloyd-Davies advocated the synchronised operation, in which one surgeon does the
abdominal part of the operation, while the other surgeon performs the perineal part simultaneously. This is widely prac
tised nowadays for the simple reason that it saves lot of time and causes much less shock to the patient.
Essentially, the bowel with the growth along with surrounding healthy tissue and involved lymph nodes are removed.
To do this, the following structures should be removed: (i) The anal canal, external sphincter muscle with a wide area of
the perianal skin, (ii) the whole of the rectum with its surrounding fasciae and epi- and pararectal groups of lymph nodes,
(iii) adjoining part of the pelvic floor and peritoneum and (iv) three quarters of the pelvic colon along with its lymph nodes
at the mesocolon.
TECHNIQUE.— The patient is anaesthetised and placed in the lithotomy-Trendelenburg position. The foot of the
operating table is removed. The buttock of the patient lies at the foot-end of the table. The legs are widely separated and
flexed to 30° at the hips and 45° at the knees. The calves are supported with Lloyd-Davies leg rests. The patient is
catheterised and the catheter is strapped to one thigh.
ABDOMINAL OPERATION.— The abdomen is opened by a long right paramedian incision from the umbilicus tc
2 cm below the pubic crest.
It is noted if there is any free fluid in the abdomen. The coils of the small intestine are packed off into the upper
abdomen. The left wall of the wound is retracted and the adhesions between the sigmoid colon and the posterior abdomi
nal wall are divided. The descending colon is pulled to the right and the peritoneum at its lateral border is cut from the
splenic flexure to the sigmoid colon. The left of the pelvic mesocolon is incised well clear off any malignant infiltration.
The left ureter and the left gonadal vessels are protected.
At this stage, one must assess where to ligate the inferior mesenteric artery. That means the lymph nodes in the sigmoid
mesocolon and by the sides of the inferior mesenteric artery are studied. Normally, the inferior mesenteric artery is ligatured and
divided just below the point where it gives off its first lower left colic (upper sigmoid) branch. If the glands are found to be
involved around the origin of the inferior mesenteric artery, the artery should be tied and divided flush with the aorta. From this
point of division of the main vessels, the peritoneum is incised vertically downwards to reach the right side of the rectum. This
incision is carried forwards over the front of the rectum to join the incision down to the left side of the rectum.
The rectum is lifted forwards from the front of the sacrum. By gentle dissection with the fingers, the rectum is gradually
freed posteriorly as far down as the sacrococcygeal joint, where it meets the perineal operator, who by this time has excised the
last piece of the coccyx. While doing this, one has to incise the fascia of Waldeyer a little away from the rectum.
The rectum is now pushed backwards into the hollow of the sacrum and dissection started at the plane of cleavage
lying between the rectum and the base of the bladder until it reaches the seminal vesicles. The rectum is separated from the
seminal vesicles and from the prostate gland, care being taken not to injure the vas deferens.
In the female, the rectum is separated from the posterior vaginal wall.
As the rectum is freed anteriorly and posteriorly, it is now attached to the sides with the lateral ligaments. The lower
ends of the ureters are defined and their relations with the lateral ligaments of the rectum are assessed. The rectum is drawn
over to one side putting the opposite lateral ligament under stretch. This ligament is secured and divided keeping the ureter
of that side in view. The manoeuvre is repeated on the other side.
Now the level of division of the colon is assessed. As the main artery has already been ligated, the ischaemic areas will
become obvious. The bowel is divided between the crushing clamps. The distal end is covered with a sterile glove, so that
it can be taken out easily through the perineal wound. The whole mass of the rectum and colon are taken out through the
perineal wound.
The abdominal surgeon closes the pelvic floor muscles. The edges of the peritoneum are picked up, mobilised and
sutured with interrupted sutures. It may be sutured with continuous catgut suture, but the ureter must be protected. Thus
peritoneum covers the pelvic floor.
Fashioning the terminal colostomy.— A disc of skin 3 cm in diameter, half way between the umbilicus and the left
anterior superior iliac spine, is excised. The external oblique aponeurosis is incised in a cruciate manner and the underly
ing muscles are split along the line of the fibres. Finally, the peritoneum is opened. The proximal end of the bowel is
brought out through this opening. One must make sure that it is producing no tension on its vessels. The bowel is brought
out for no less than 2 inches. The mesocolon is fixed to the external oblique aponeurosis with a stitch. The peritoneal space
lateral to the colostomy bowel is closed by continuous or interrupted sutures to prevent internal herniation at a later stage.
Extraperitoneal method (Goligher) — is sometimes practised to bring the cut-end of the colon for colostomy
extraperitoneally. For this the lateral cut-edge of the peritoneum is picked up and a tunnel behind the peritoneum is made
for the colon to pass through. This obviates the necessity to close the peritoneal gap on the lateral side of the colon.
Closure.— The packs holding the coils of small intestine out of the way are taken off. A final check is made that
everything is alright. The abdominal wound is now closed in layers.
The end of the protruding colon, which has been crushed by the crushing clamp is cut off. The mucous membrane of
the bowel is now sutured to the skin edge with interrupted chromic catgut sutures. A plastic disposable colostomy bag is
now fitted to the colostomy.
PERINEAL OPERATION.— This part of operation is started when the abdominal exploration has been completed and
the surgeons have taken decision that this type of operation they are going to perform. The surgeon sits on his stool at the
end of the table. A dry swab is inserted into the anal orifice and the anus is closed by a stout purse-string suture introduced
subcutaneously.
Incision.— An elliptical incision is made around the anus. The posterior end of this incision is carried more posteri
orly to one or other side of the midline as far as the middle of the sacrum.
The posterior part of the incision is first deepened until the coccyx is reached. The coccyx is cleared from its attach
ments on both sides and disarticulated from sacrum. At this stage, the middle sacral artery may be injured, which must be
secured to stop bleeding. The fascia of Waldeyer, which is now exposed, is incised transversely to reach the rectum. A
finger is inserted through this incision and the ileococcygeal parts of the levator ani muscles are felt.
Now the attention is drawn to the lateral sides of the anal canal, where the incisions are deepened and the ischiorectal
fossae are reached. Care is taken to secure the inferior rectal vessels which cross these fossae and are liable to be injured.
A finger is insinuated on the upper surface of the levator ani muscle, which acts as a guide. By a pair of scissors, this
muscle is divided on both sides keeping a good margin attached to the rectum. In front, the incision is deepened and it
divides the superficial and deep transverse perinei muscles and puborectalis. At this time the bulb of the urethra is exposed
and gently separated forwards by gauze dissection. The rectum is now attached to the membranous part of the urethra by
the recto-urethralis muscle. This muscle should be divided after defining the prostate gland properly.
Now the perineal surgeon comes in contact with the abdominal surgeon and the whole of the anal canal, rectum and
colon are taken out through the perineal wound.
Closure.— All the bleeding vessels are ligated. The wound is closed keeping a suction drainage. A corrugated rubber
sheet drainage can be used as an adjunct to the suction drainage if oozing continues, so that the debris will have a good acces
Postoperative treatment.— For the first few days the patient is kept with the footend of the bed raised to relieve
pressure on the pelvic floor. The colostomy wound should be inspected daily to look for its viability. Similarly the perineal
drainage should also be looked at. The corrugated rubber sheet drain should be removed after 48 hours. The suction
drainage should be continued for further one or two days. Urethral catheter is kept in situ for 5 days. Some sort of urinary
antiseptic should be prescribed. The colostomy starts moving from 3rd day onwards. Perineal wound heals by granulation
tissue, which takes no less than 4 weeks.
Laparoscopic abdominoperineal excision.— Nowadays abdominoperineal excision is possible
laparoscopically. The rectum is mobilised from above abdominally using the laparoscope. A circular perine
incision is made around the anal canal. The anal canal is mobilised and moved up to reach the mobilised
rectum. The colon is now divided abdominally with Endo GIA instrument. The specimen containing carcin
matous rectum is delivered through the perineal wound. An incision is made in the left iliac fossa from the
abdominal cavity and the sigmoid colon is brought out to form the end colostomy.
The concern of this laparoscopic procedure is the degree of clearance, which is not as curative as the stan
‘open’ technique. The cancer cells may be disseminated in the peritoneal cavity and may be implanted at th
The usual advantages of laparoscopic procedure that the postoperative pain is less and the hospital stay is a
than those of ‘open’ technique, yet its success rate should be assessed before recommendation.
Anterior resection.— This operation is only possible when the lower margin of the growth is about 10
cm or more above the anus i.e. above the reach of the examining finger.
Considering the fact that carcinoma at this region of the rectum spreads by upward direction and that it
does not spread downwards for more than 2 cm has compelled the surgeons to conserve the sphincter mecha
nism of the anal canal and avoid colostomy. Though one may think that after this operation normal defecation
is possible, yet one should keep in mind that normal defecation does not depend on the sphincter only, but
on the presence of at least a portion of the rectum, whose distension will give rise to urge for defecation.
Another point should be considered before performing this operation, is that the growth is not an anaplastic
growth, which is a contraindication to this operation. On the contrary, a well differentiated carcinoma above
10 cm from the anus is very much suitable for this operation.
Technique.— The patient is placed in the lithotomy-Trendelenburg position. A gauze piece is inserted into the anus.
The abdomen is opened through the same incision as has been described in abdominoperineal resection. The pelvic colon
and the rectum are mobilised as mentioned in that operation. Inferior mesenteric artery is ligated at a level according to die
lymph node involvement along its axis. The splenic flexure and the descending colon are always mobilised to minimise
tension at the suture line following resection. The rectum is pulled forwards and it is separated posteriorly from the sacral
promontory and presacral fascia as far down as the tip of the coccyx and the pelvic floor muscles. The areolar tissue behind th
rectum covered by peritoneum on both sides contain lymph nodes which are often involved. This is called rectal mesocolon
and’the whole of this mesocolon must be removed including all the lymph nodes within it. At this time one must be careful to
visualise and preserve the presacral sympathetic nerves. Now attention is drawn towards anterior dissection of the rectum,
where the seminal vesicles are pushed forward with St. Mark’s retractor and dissection is carried out between the vesicles and
the rectum to find out Denonvillier’s fascia. This fascia is incised transversely and dissection is further carried down between
this fascia and the rectum as far distally as the pelvic floor. In case of female, this dissection is carried out between the rectum
and the vagina. The rectum is pulled to one side and the other to identify and divide the lateral ligaments after ligation close to
the lateral pelvic wall. The middle rectal vessels run through this ligament. The rectum is now pulled upwards and the tumour
is also drawn upwards to choose a suitable site for division of the rectum. A 5 cm clearance below the lower edge of the
carcinoma is the site of choice, though at least 2 cm clearance must be present. Before division of the rectum, the superior
rectal artery and the vein are ligated. A clamp is applied at the site of division of rectum and a crushing clamp is applied
just above this clamp. The bowel is divided between these 2 clamps. The remaining rectum and anal canal should be
irrigated with tumouricidal agent e.g. providone iodine prior to transection of the rectum. This prevents seeding of exfo
liated tumour cells and prevents recurrence. This is particularly required when stapled anastomosis is being used.
A suitable level well above the tumour and depending on the level of lymph node involvement is decided on pelvic
colon for division. The pelvic colon is divided just above placing a crushing Parker-Kerr clamp. The upper cut end of the
colon is held with babcock’s forceps or an occluding clamp, so that the lumen can be swabbed out. Now the anastomosis
between the pelvic colon and the remnant of the rectum can be performed either by suturing or by stapling.
Sutured anastomosis.— This anastomosis can be sutured in 1 or 2 layers depending upon the surgeon’s choice. A high
anastomosis is usually sutured by 2 layers, whereas a low anastomosis is best sutured using single layer of non-absorbable
suture material with end-to-end inverted anastomosis. The posterior row of sutures is inserted prior to approximation of
the gut ends. These are vertical mattress sutures, the ends of which are held in artery forceps until all of them have been
inserted. The sutures are now held tight so that the pelvic colon is pushed down till its posterior edge comes in contact with
the rectum. These sutures are tied with the knots inside the lumen. The two lateral sutures are held, whereas the others are
cut. The anterior layer is also sutured using interrupted all-coat vertical mattress stitches.
Stapled anastomosis.— This technique is more often used nowadays, as it is often technically difficult to suture a low
anastomosis. EEA circular stapling device is mainly used to carry out this anastomosis. The EEA gun is introduced through
the anus. The lower cut end of the rectum is tied with a purse string suture as tightly as possible around the shaft of the
instrument above the cartridge. The pelvic colon is now manipulated over the top of the anvil and is also tied with a purse
string suture as tightly as possible. The assistant is now asked to approximate the anvil to the cartridge. Care must be taken to
see that no other structure is being caught between the anvil and the cartridge even the appendices epiploicae. The staple gun
is fired to create the anastomosis. The gun is now opened to separate the anvil from the cartridge. It is twisted to make sure that
the anastomosis is lying free. It is gently rocked and pulled out free from the anus. It must be remembered that the stapler
removes an extra 8 mm of rectum and this must be kept in mind while estimating the distal clearance below the tumour.
The ‘doughnut’s’ of the colon and rectum are removed from the gun. These should be complete. If there is break in the
circumference it should be repaired with interrupted sutures. The distal doughnut is sent for histological examination. The
anastomosis should be checked either digitally or sigmoidoscopically. Some fluid is placed in the pelvis and air is blown
through the sigmoidoscope. If no bubbles appear in the fluid, the anastomosis is satisfactory.
The peritoneum is sutured to the pelvic colon well above the line of anastomosis. A drain is inserted through a stab
wound at the left iliac fossa into the presacral space down the lateral side of the peritoneum. The abdomen is closed in
layers. To prevent spillage of cancer cells into the remnant of the rectum and anal canal, one can wash this part with 1 : 500
perchloride of mercury. The drain is usually removed after 48 hours.
Laparoscopic anterior resection.—This technique is now being used in certain institutions. The operative technique
is almost the same as the standard procedure, which is performed through the abdomen using various ports according to
the choice of the surgeon. After anterior resection, the anastomosis is a rather difficult task and mostly performed
intraperitoneally using a modified circular stapling gun. Nowadays reports are coming up where laparoscopic anastomosis
are being performed below the peritoneal reflection. But this is more difficult. The problem of efficacy of this procedure
remains as there is risk of implanting of cancer cells.
Radiotherapy.— The usefulness of combined radiation therapy with surgery is an attempt to improve results. With
modem techniques some adenocarcinomas now respond to radiotherapy. Some large cancer may shrink to make removal
easier. Preoperative radiotherapy, 2,000 rads in 2 weeks may be given. If the lesion is within 8 cm of the anus an additional 500
rads may be given through the perineal route. The result shows some improvement after surgery. Intracavitary radiotherapy
may be administered directly through a sigmoidoscope like device. High doses of radiation 9,000 to 15,000 rads are precisely
delivered. Small cancers may be treated like this. Electrocoagulation and intracavitary irradiations may be considered as
curative therapy for early and well differentiated cancers.
Chemotherapy.— The efficacy of chemotherapy is very much questioned. A variety of drugs has been tried both as an
adjuvant therapy and for the treatment of disseminated disease. But the results are disappointing. The most frequently used drug
5-fluorouracil (5 FU), which has recently been infused into the portal vein during and immediately after the primary operation. Such
adjuvant therapy should prevent formation of metastasis following operative manipulation of the tumour. Initial results are encoura
to reduce the incidence of metastasis subsequently and to prolong survival. Systemic folinic acid (leucovorin) may be used in
combination with 5 FU. From various studies world-wide the combination of 5 FU and folinic acid offer the best result.
Recent clinical trial data indicate that adjuvant chemotherapy may be effective in patients with stage II as well as stage 111 co
cancer. The combination of 5-FU + leucovorin may slightly improve survival compared with the standard 5-FU + levamisole
combination. The 3 drug regimen (5-Fu + levamisole + leucovorin) is more toxic with no superior effect on survival.
Immunotherapy.— This has arouse an interest particularly in the treatment of disseminated colorectal cancer. Various
monoclonal antibodies to carcinoembryonic antigen have been used to destroy the cancerous cells. These antibodies are
also conjugated to cancericidal agents to have the same effect. But these antibodies are not sufficiently specific and they
also damage normal tissues. Immune therapies with agents such as interferon-aIpha-2a, monoclonal antibody 17-1A and
autologus tumour vaccines can further improve survival.
Hartmann’s operation.— This is an excellent procedure in old man and inept persons who may not
stand an abdominoperineal resection. Through an abdominal incision the rectum is excised like radical
resection. The remnant of the rectum is closed by suturing and the peritoneum is oversewn. The pelvic defect
is covered in the usual way. The cavity below can be drained through anus which is divided posteriorly. The
62
proximal end is taken out as permanent colostomy. As cancers in these patients spread slowly this operat
works well.
Extensive Operations.— When carcinoma of the rectum has spread to adjacent organs, the radical op
can often be extended to remove these structures, (i) IN THE MALES total cystectomy and resection ofthe re
may be performed. Urinary diversion in the form of ileal conduit is made, (ii) IN THE FEMALE a total hyste
may be performed alongwith excision of the rectum. Pelvic evisceration (Brunschwig’s operation)—the p
in lithotomy-Trendelenburg position. All the pelvic viscera together with internal iliac and obturator gro
nodes are removed. In the process internal iliac arteries are ligated. Some form of urinary diversion is per
Results.— In specialised centres overall 5-year survival rate after surgery is approximately 50%. In th
centres resectability rate is as high as 95% and operative mortality is less than 5%. Histological grade very
much influences the outcome. One point should arouse interest that with the more frequent use of sphinc
saving resection compared with abdominoperineal excision, survival has not been affected.
SEMS (SELF EXPANDING METAL STENTS) IN THE LARGE BOWEL AND RECTUM.— Carci
noma of the rectum not infrequently presents with large bowel obstruction as an emergency. In such case
emergency treatment requires formation of a stoma either to decompress the colon prior to definite surge
as part of Hartmann’s operation. In these cases, the patient requires a second operation to restore intersti
continuity. Recently SEMS have been used to relieve such acute obstruction. The patients can then under
elective surgery when fully resuscitated and prepared.
In benign stricture of rectum after gynaecological radiotherapy, the SEMS have been used. Such use m
result in delayed perforation and pelvic abscess formation. Thus SEMS has attained less popularity in the
cases.
CARCINOID TUMOUR
This tumour has been described earlier. It usually remains in the submucous coat and the mucous me
brane over it remains intact. It appears as a small plaque-like elevation. Though carcinoid tumour here is
common than in small intestine and appendix, yet one should always keep in mind this tumour when an
mal tumour in rectum is come across. Incidence of malignancy is about 10% and it is more than appendic
carcinoid tumour but much less than carcinoid tumour of small intestine. Majority of this tumour is slow
progression and very late in metastasis. Treatment is excision of rectum. Even when metastasis is present
resection prolongs life.
IMPERFORATE ANUS
This is a not uncommon congenital abnormality in which there is imperfect fusion between the post-a
toic gut (hindgut) and proctodeum (which forms lower part of the anal canal below the dentate line). Th
abnormality can be broadly classified into the low anomaly and high anomaly depending on whether the
termination of the bowel is below or above the pelvic floor respectively.
Low anomalies.— These anomalies are minor developmental errors and sphincter mechanism of the
is almost normal. There are 4 varieties of such anomaly.
(a) Membraneous stenosis (Imperforate anal membrane). In this condition anal canal is narrowed and
covered with a thin membrane. On examination the membrane will be seen bulged out with retained me
nium. Treatment is a cruciate incision on the membrane and regular anal dilatation.
(b) Covered anus.— The anus is covered by skin so that the anal opening is not situated in its normal
position. A thin track runs forward under cover of that skin so that the anal opening is somewhere in fro
perineal raphe. The treatment is to open the track with scissors upto the normal position of the anus follo
by regular dilatation of the anus.
(c) Stenosed anus (Anal stenosis).— More or less the whole anal canal is slightly narrowed and the anus is
microscopic with a minute opening. Patients usually present a bit late as he or she can pass meconium. T
ment is regular dilatation of the anus.
Fig.54.13.— Shows low abnormalities of the anus. A.— Anal stenosis.

B.— Imperforate anal membrane. C.— Anal agenesis.
(d) Ectopic anus.— In this condition the anus is not situated in its normal position but is placed more
anteriorly in the perineum of the boys or near the vulva in case of girls. In this case the anal canal is nonnally
developed but a thick skin covers the
normal anal opening. The treatment is
‘plastic cut back’ operation.
(e) Anal agenesis — is compara
tively rare.
High anomalies.— In these cases
rectum ends above the pelvic floor and
there is often a fistulous connection be
tween the blind rectal stump and the
bladder (in case of male) or vagina (in
case of female). The followings are the
types of anomalies seen :
(a)
Fig.54.14.— Shows high abnormalities. D.— Rectal agenesis. This may tion the anal canal is normal but ends
have fistulous connections e.g. recto-urethral fistula or rectovaginal fistula. proximally just below the level of the
E.— Rectal atresia.
pelvic floor. The rectum ends below
blindly above the pelvic floor. This anomaly is rare and is usually not associated with fistulous connection.
Treatment is mobilisation of the rectum, an opening is made through the pelvic floor and end-to-end anastom
sis is performed with the anal canal.
(b) Anorectal agenesis.— This is commoner malformation than the previous variety. The rectum ends
above the pelvic floor and is usually connected with the bladder or with the posterior fornix of the vagina
through fistulous communication. The anal canal is not developed.
(c) Cloaca.— This is very rare type of anomaly only seen in females. In this condition the hind gut, urinary
bladder and genital tract all open into a common wide cavity.
Clinical features.— Failure of passage of meconium is the main complaint of the parents. On examination
in high anomalies there is no proper anal canal in anorectal agenesis. Instead a spake of meconium may be se
in the penis or in the vulva. Particularly in the female there may not be any intestinal obstruction as meconiu
is passing through the vagina.
In low anomaly the complaint is same that is failure of passage of meconium. On careful examination one
can find out the variety of anomaly which is present in this particular case.
X-ray examination.— To know whether the anomaly is of high variety or low variety, X-ray examination
with the infant held upside down is essential. It takes about six hours after birth to collect sufficient air in the
large intestine. With a metal button or a coin strapped at the site of the anus or a metal bougie inserted into t
blind anal canal the infant is held upside down. After 3 or 4 minutes radiographs are taken in inverted posit
By that time gas will reach the end of the rectum and one can see the distance between the end of the gas sha
and the metal indicator. If the distance between these two is more than 2.5 cm the abnormality is high. The o
fallacy is that a plug of meconium in the rectum may show an increased gap between these two. It must be
remembered that one has to wait till the rectal gas appears and sometimes it takes about a day or more for re
gas to appear.
TREATMENT.— Low anomalies.— Treatment of these conditions have already been described under
the various varieties.
High anomalies.— The treatment of the common anorectal agenesis with fistula formation is described
below. If the intestinal obstruction is the main feature a preliminary transverse colostomy may be performed
Otherwise treatment of such anomaly can be done in the one stage as the infant can tolerate operation quite
A laparotomy is performed. The rectum is mobilised. If there is any fistula, it should be divided after both en
are closed. A passage is made exactly in the midline between the two halves of the pelvic foor. The passage i
further prolonged downwards through the sphincters of the anal canal. An incision is made at the site of nor
anus. A forceps is pushed up through the passage formed by the dissection and the lower end of the rectum
held and brought out through the anus. The blind bowel loop is opened and the margins are sutured to the s
margins of the anal incision to make the anus. This operation is essentially similar to that of abdominoperine
pull-through operation.
If there is no fistulous communication and the case is one of anorectal agenesis the treatment is prelimina
transverse colostomy followed by abdomino-perineal pull-through operation at the age of 6 to 12 months. W
there is fistulous communication in anorectal agenesis operation should be performed at the age of 6 months
if there is no prior problem of intestinal obstruction.
In case of rectal atresia one may perform the operation in one stage if the gap between the blind rectum a
anal canal is not much. Otherwise preliminary colostomy may be performed.
SACROCOCCYGEAL TERATOMA
As the name suggests it is a teratoma at the sacrococcygeal region. This is probably the most common tum
seen in a neonatal baby. Sacrococcygeal region is the site of the ‘primitive knot’, a group of totipotent cells w
possess potentiality to form various types of cells and that is the reason why teratoma is seen at this region. T
tumour is actually situated between the rectum and the sacrum. It is firmly attached to the coccyx and
occasionally to the last piece of the sacrum. It usually presents as a big swelling and may contain rudimentar
limbs such as hands or feet. It may become malignant.
Treatment.— Excision of the tumour should be performed as soon as the diagnosis is made. Excision is
indicated to avoid fatal ulceration, secondary infection, rectal obstruction and last but not the least malignan
change. Technique.— A longitudinal elliptical incision is made. The skin and subcutaneous tissue are lifted
and the whole tumour is separated from the surrounding structures. The coccyx and the part of sacrum attac
to the tumour must also be removed. Care must be taken during the anterior dissection not to inflict injury to
the rectum. Sometimes there is a fistulous connection with the rectum. This should be excised and the openin
in the rectum is carefully closed. Colostomy may not be required. After excision of the tumour, the dead spa
should be drained and the skin is closed. The pressure bandage is applied.
POST ANAL DERMOID
This may be regarded as a type of the previous condition. The dermoid cyst is situated behind the anal ca
and rectum and in front of the coccyx and sacrum. The main difference with the previous condition is that th
soft anal cystic swelling may be hidden in the hollow of the sacrum without any symptom for quite a long ti
The condition may be presented in adult life when the cyst has become infected with the formation of a sinu
in the exterior. It may present as difficulty in defaecation. Rectal examination is very important to diagnose t
condition.
Treatment.— Complete excision of the cyst alongwith the sinus if present is the treatment.
PILONIDAL SINUS
This is an acquired condition and seen in adult males. This is hardly seen in females. While sitting the
buttocks move and hairs broken off by friction and collect in the cleft. When the toilet paper is used hair
entangled in foecal matter will also be swept into the cleft. Such loose hairs travel down the intergluteal furro
to penetrate the soft and moistened skin at that region or enter the open mouth of a sudoriferous gland. After
the initial entry dermatitis and inflammation start around the loose hairs and once the sinus is formed,
intermittent negative pressure of the area may suck other loose hairs into the pit
This type of sinus is lined by stratified squamous epithelium. The sinus extends into the subcutaneous tiss
Tuft of hair is always seen within such sinus embedded in granulation tissue.
OTHER PLACES WHERE PILONIDAL SINUS MAY BE FOUND ARE : (i) Interdigital cleft of men's
hair-dresser. In this case customer's hairs find access through the interdigital cleft; (ii) The axilla; (iii) The
umbilicus; (iv) Interdigital web of the foot of a worker in hair mattress factory; (v) Face.
Pathology.—
The sinus extends into the subcutaneous tissue from the surface of the skin. The sinus passes upwards and
forwards towards the sacrum. It ends blindly and does not reach the bone. It may possess branching side
channels. It may have as many as six openings strictly in the midline between the level of the sacrococcygeal
joints and the tip of the coccyx. It is an infected track.
Lining ofthe track — is usually granulation tissue. Towards the mouth of the sinus there may be stratified
squamous epithelium lining.
Contents.— These are mainly — (i) Hairs, (ii) Granulation tissue, (iii) Epithelial scales and debris.
The hairs are usually dead and are found
(a) lying loose in the sinus, (b) embedded in
the granulation tissue or (c) burried deep in
the mature scar tissue at the depth.
MICROSCOPICALLY one will find for
eign body giant cells.
Pilonidal sinus is usually presented by
males during third decade. It is rarely seen in
Fig.54.15.— Shows how suction force is developed to suck loose people over 40 years of age. It is more com
hairs to enter the open mouths of sudoriferous glands to produce mon in males than females in the ratio of
pilonidal sinus. approximately 6 : 1 .
This condition is more often seen in Jeep drivers and so pilonidal sinus is often referred to as ‘Jeep disease'.
As mentioned earlier pilonidal sinus is also seen in the webs between fingers of men's hair dressers and also i
the interdigital web of the foot of worker in hair mattress factory.
Typically the patient presents with a chronic sinus about the level of the first piece of coccyx. A tuft of hair
projects from its mouth. The patient complains of blood-stained foul discharge from this sinus. There may be
secondary openings on either side of the middle or a little away from the main sinus. Pain and tenderness are
often associated with due to recurrent infection.
Complications.—
1. Abscess formation.
2. Recurrent inflammation.
3. Recurrence of sinus formation.— This is mostly due to inadequate excision of the sinus or entry of hair
to the scar of the skin. Selection of inappropriate operation and inadequate postoperative care are the main
causes of recurrence. Hairs growing into the healing wounds is probably the most common cause of recurrenc
of pilonidal disease.
4. Very rarely malignant degeneration may occur in this lesion.

Treatment.—
Pilonidal sinus should be excised alongwith the secondary openings. But such excision must be performed
after controlling infection. Local cleansing, local antiseptic dressing, administration of broad spectrum
antibiotic alongwith rest should be given to control infection.
OPERATION.— The treatment of pilonidal sinus is excision of all the sinuses with ramifications in
quiescent stage,
since these si
nuses may have
ramifications,
which may be
left behind. It is
a good practice
to push meth
ylene blue
through the si
nuses. In case,
Fig.54.16.— Steps of wide excision with primary suture for pilonidal sinus. any ramification
of this sinus is cut through it will be obvious by staining of the tissues. An elliptical incision is made to include
all sinus openings. This incision is deepened vertically upto the fascia covering the sacrum and coccyx. If any
of the ramifications has been cut, wider incision should be advised to include the whole of the ramifications
within the excised mass.
If there is any lateral sinus opening, after excision of the mass, a sinus forceps is pushed down the lateral
track and widened. Now this sinus has to be curetted and no hair should be left behind. 1 or 2 cm of the sinus
from the external opening should be excised. If the pilonidal sinus was not infected, one can attempt primary
suture of the wound. A big bite should be taken from both the margins and the needle should pass through the
fascia covering the floor of the wound. The ends of the sutures are tied over a roll of gauze for continual pressure
Fig.54.17.— Steps of Z-plasty operation after wide excision of pilonidal sinus.
on the wound. The advantage of the primary closure is that convalescence will be quick.
OPEN OPERATION.— The problem with the primary suture is recurrence. It is for this reason, that the
surgeons prefer to leave the wound wide open packed with gauze impregnated with petroleum jelly. The pack
is removed after 5 days. Daily cleansing and irrigation of the wound should be done with sitz bath to be followed
by dressing and after each dressing, a T-bandage is applied. Healing is expected in 3 to 4 weeks.
After excision of the pilonidal sinus some surgeons prefer to close primarily by Z-plasty (Fig. 54.17). This
is done for better wound healing and good cosmetic result.
MARSUPIALIZATION.— In this technique the sinus tracks are excised may not be to the whole extent
upto the sacrococcygeal fascial. The edges of the skin are now sutured to the margins of the remnant membrane
which forms the deep part of the sinuses. Haemostasis is maintained and a pressure bandage is applied.
The postoperative care is similar to that of the open technique.
Marsupialization, though not used commonly, has been claimed to give good resultboth as a first operation
and as a procedure for management of recurrent disease after other operations.
Pilonidal abscess.— This should be drained by excising an ellipse, where the pits of the sinuses might be.
These pits will be surrounded by oedema and redness. After the wound has become free from infection by
repeated cleansing, administration of systemic antibiotics and dressing, one should attempt proper excision of
the sinus and its ramifications.
INJURIES OF THE RECTUM AND ANAL CANAL

(i) The commonest cause of such injury is fall in sitting posture on a stick-like thing, sharp or blunt, (ii) Stab
injury isalsocommon. (iii) Occasionally rectum may be injured by rigid sigmoidoscope particularly when there
is ulcerative proctitis or amoebic dysentery or (iv) inadvertent administration of enema.
Clinical features.— Bleeding per rectum is the main symptom. Abdomen must be carefully palpated to
exclude rigidity or tenderness, which indicates intraperitoneal rupture of rectum. Rectal examination must be
made with proper care. With an appropriate speculum the rectum is inspected to note the type and extent of
injury.
Treatment.— If intraperitoneal rupture can be definitely excluded, that means when the rectal injury is
limited to below the pelvic floor, wide drainage is indicated. The wound is properly ’dcbridcd’, bleeding vessels
arc ligated, rectal injury is closed with fine sutures and a protective colostomy is advisable. Broad spectrum
antibiotics must be started immediately.
When intraperitoneal injury is suspcctcd, the abdomen is opened, the perforation is closed by sutures.
Careful peritoneal toileting is performed. Bladder is inspected carefully to exclude any injury there. A left iliac
protective colostomy is performed through separate grid-iron incision on the left iliac fossa. Abdomen is closed
as usual.
PROCTITIS
Inflammation of the rectal mucosa is known as proctitis. It may be associated with similar disease of the colon when
the condition is called proctocolitis. Proctitis may be acute or chronic.
Clinical features.—The typical symptom of proctitis is tenesmus. This is an intense desire to defaecate, but the amount
of faeces passed is small; instead blood, mucus and even pus are passed. Acute proctitis is associated with prodromal
symptoms such as fever, malaise etc.
On rectal examination the mucosa of the rectum is swollen and tender. On the glove of the finger one may find blood
smear.
Sigmoidoscopy will reveal red oedematous inflamed mucosa with small ulcers of the rectum.
Smear taking from the rectal mucosa should be sent for bacteriological report. One may do culture of the stool. Swabs
may be taken from the ulcers for bacteriological report. Biopsy may be necessary to exclude carcinoma.
Causes.— (i) Idiopathic non-specific proctitis is the most common variety and its aetiology is still unknown.
(ii) Ulcerative proctitis, as a part of ulcerative colitis is quite common.
(iii) Bacillary dysentery may cause even acute purulent proctitis with multiple small shallow ulcers.
(iv) Amoebic dysentery produces chronic proctitis with appearance of amoebic ulcer described on page 990. Sometime
amoebic granuloma may present as a short mass in the rectosigmoid junction which may simulate a carcinoma.
Sigmoidoscopy reveals ulcerated surface without much induration in the base.
(v) Tuberculous proctitis is always secondary to active pulmonary tuberculosis. Tuberculous fistula-in-ano may be
associated with. Tuberculous proctitis is more often of ulcerative variety. But hypertrophic type of tuberculous proctitis
may be seen in association with tuberculous peritonitis or tuberculous salpingitis.
(vi) Gonococcal proctitis occurs from rectal coitus. It occurs in both sexes. It may lead to acute proctitis. Diagnosis
can be readily established by bacteriological examination.
(vii) Lymphogranuloma inguinale is also the result from rectal coitus, but in the female infection may spread from
cervix uteri via lymphatics to the pararectal lymph nodes. Strictures of rectum may be seen from such spread of infection
in females. Frei's intradermal test is positive in 95% of cases. Complement-fixation test is positive in 100% of cases.
(viii) Syphilitic proctitis.— Primary chancre may occur inside the anus. Spirochaeta vincenti and basillus fusiformis
may cause infection from rectosigmoid junction to produce strawberry lesion.
(ix) Rectal bilharziasis is caused by infestation of Schistosoma mansoni in tropical and subtropical countries.
PRURITUS ANI
It is not an uncommon problem. It means intractable itching around the anus. There are various causes of pruritus ani.
But here I shall discuss mainly the surgical conditions which can give rise to this symptom. The surgical causes are :
(i) Prolapsing haemorrhoid; (ii) Anal fissure; (iii) Fistula-in-ano; (iv) Ectropion; (v) Condyloma acuminata; (vi)
Colloid carcinoma of the rectum ; (vii) Carcinoma of the anal canal; (viii) Basal cell carcinoma of the anal canal; (ix)
Malignant melanoma of the anal canal.
Other causes are :—
(i) Dermatitis; (ii) Diabetes mellitus; (iii) Jaundice; (iv) Diarrhoea; (v) Leukorrhea; (vi) Parasitic causes (thread worms
particularly in children); (vii) Monilial infection; (viii) Allergy; (ix) Psychoneurosis; (x) Idiopathic which constitutes a large
group.
Treatment.— Treatment depends on the cause. Idiopathic pruritus ani requires hygienic measures to keep anus and
perianal region clean and dry .Hydrocortisone 0.5% preparation applied locally gives temporary relief. Topical fungicides
may also be used for symptomatic control of pruritus ani. Straping the buttocks apart play a considerable role in idiopathic
pruritus ani to keep the perianal region dry.
TUMOURS OF THE ANAL CANAL

BENIGN LESIONS
Condyloma acuminata or Warts are the only benign lesions seen around the anus. The anus and perianal
region are affected. These are caused by filterable virus and are infectious. The extent of the disease varies to
a few small warts to an extensive mass occluding the anal canal. Bleeding, itching and pruritus ani are common
symptoms. On examination soft papillary appearance becomes obvious without any induration. Multiple
biopsies and histological examination (these are papillomata with central core of connective tissue covered with
epithelium) should be done to exclude associated squamous cell carcinoma.
Treatment.— Small warts can be destroyed by 25% podophyllin solution or bichloracetic acid. Extensive
warts in the perianal region or in the anal canal require excision. Close follow-up is necessary as recurrence
rate is about 60%. Immunotherapy using autogenous wart-tissue vaccine may be used in conjunction with
excision to reduce recurrent rate.
MALIGNANT LESIONS
Mainly three types of malignant neoplasms are seen at the anus — (i) Squamous cell carcinoma
(commonest), (ii) Basal-cell carcinoma (next common) and (iii) melanoma (least common).
Epidermoid carcinoma.— This includes two varieties — squamous cell carcinoma arising below the
dentate line and transitional cell carcinoma arising from the transitional zone above the dentate line. Ulcerative
variety is mostly seen as indurated ulcer or ulcerated nodule. Rectal bleeding is the main symptom alongw'ith
pruritus ani. Early diagnosis can be made by careful examination and biopsy. One must exclude carcinoma of
the rectum and colon.
TREATMENT.— Local Excision.— This is reserved for small and well differentiated tumours which
have not invaded the muscular layer. A wide margin of at least 2.5 cm of normal tissue all around should be
excised with the tumour. Close follow-up is performed to exclude recurrence and to detect secondaries in the
inguinal nodes which will require block dissection with removal of glands.
Abdomino-Perineal Resection.— In the majority of patients abdomino-perineal resection with wide
excision of the perineal tissue is the treatment of choice. In case of women a portion of posterior vagina wall
should also be excised. If the inguinal nodes become involved radical dissection of the groin should be carried
out alongwith the actual resection of the tumour.
RADIOTHERAPY.— Interstitial radiation with gold radon seed may be suitable for small lesions. Low
voltage contact X-rays may also be applied in these cases.
COMBINED THERAPY.— Preoperative combination of chemotherapy and irradiation followed by
abdomino-perineal resection have been more successful than only operation. A single dose mitomycin C is
given intravenously at a dose of 15 mg/sq. metre on day one. Irradiation therapy is also started from the same
day at 1000 rads per week for three weeks. On 28th and 31st days 5 FU in a dose of 1000 mg/sq. metre per 24
hours is repeated. Operation is performed 4 to 6 weeks following completion of irradiation therapy. This method
has been very successful.
Basal-cell carcinoma.— This tumour usually starts near the dentate line. This is relatively low malignant
than epidermoid carcinoma. Lymph nodes are usually not involved.
TREATMENT.—Small tumour may be given irradiation therapy, but large tumour requires excision in the
form of abdomino-perineal resection.
Malignant melanoma.— Melanoma of the anal canal represents the 3rd most common site of melanomas,
preceded only by the skin and eyes. Almost all the tumours arise from the epidermoid lining of the anal canal
adjacent to the dentate line.
Rectal bleeding is the most common symptom. Majority of the tumours are however lightly pigmented or
non-pigmented, in which cases these are often misdiagnosed as epidermoid carcinoma or condyloma
acuminata. Even tissue biopsy may be misdiagnosed as undifferentiated epidermoid carcinoma. When
pigmented this tumour appears as bluish-black soft mass which may be confused with thrombotic pile.
Anal canal melanomas spread submucosally into the rectum. Adjacent organs are rarely invaded. Inguinal
nodes may not be involved, instead lymphatic spread may occur to inferior mesenteric nodes through rectal
lymphatics. Haematogenous spread to the liver and lungs are relatively early and usually accounts for most of
the deaths.
Treatment.— Radical excision is the treatment of choice in malignant melanoma. Abdomino-perineal
resection is the operation to be performed. Malignant melanoma is radioresistant and does not respond well to
chemotherapy and immunotherapy. Prognosis is poor. 5 years survival rate is not more than 15% in best
institutions.
LOWER GASTROINTESTINAL TRACT BLEEDING

When the source of bleeding lies below the duodenojejunal flexure, it is referred to as lower gastrointes
tinal tract bleeding. The bleeding may befresh, altered or occult. Lower G. I. tract bleeding can be divided into
3 groups—(a) patients with minor bleeding (occult), (b) patients with slow bleeding (moderate) and (c) patients
with rapid bleeding (severe).
(a) Occult blood loss is that which is detected by routine chemical tests of the stool with or without systemic
evidence of chronic blood loss. About 10 ml blood loss per day is necessary to have stool occult blood test
positive.
(b) Slow bleeding is manifested by recognizable blood loss either altered or fresh per anum in a stable
patient. This patient may become anaemic with or without systemic changes.
(c) Rapid or severe bleeding is defined as rapid blood loss per anum which is reflected by haemodynamic
instability, if left uncorrected. The loss of blood requires 2 units or more of blood for transfusion to bring about
haemodynamic stability.
Causes.— Causes may be divided into two main groups — local causes and general causes.
A. Local causes.—
1. ANAL CAUSES.—
(i) Haemorrhoides; (ii) Anal fissure; (iii) Mucosal prolapse; (iv) Ulceration (Crohn's disease); (v)
Carcinoma; (vi) Fistula-in-ano.
2. PERIANAL.—
(i) Prolapsed rectum and piles; (ii) Ruptured perianal haematoma; (iii) Ruptured anorectal abscess; (iv)
Injury; (v) Condylomata; (vi) Carcinoma; (vii) Skin excoriation.
3. COLORECTAL.—
(i) Diverticular diseases (very common in western countries, though it is quite rare in this country); (ii)
Various types of polyps; (iii) Villous adenoma; (iv) Carcinoma; (v) Ulcerative colitis; (vi) Angiodysplasia; (vii)
Inflammatory bowel diseases; (viii) Endometriosis; (ix) Crohn's disease; (x) Haemangioma.
4. SMALL INTESTINE.—
(i) Intussusception; (ii) Crohn's disease; (iii) Meckel’s diverticulum; (iv) Tumours.
B. General Causes.—
(i) Blood dyscrasias (discussed in upper G. I. tract bleeding in Chapter 44); (ii) Drugs (discussed in upper
G. I. tract bleeding); (iii) Liver failure; (iv) Renal failure.
Clinical examination.—
HISTORY.— Enquiry must be made regarding the amount of bleeding, the colour of the blood lost—bright
red (coming from the rectum or anal canal), dark red (coming from the ascending, transverse, descending or
sigmoid colon) or black i.e. melaena (from the small intestine or higher up). Relation of bleeding to defaecation
must be enquired — whether during or independent of the act. When bleeding occurs at the time of passing hard
stool and the amount is not much, acute fissure-in-ano is the most probable diagnosis. A streak of fresh blood
may be frequently noticed on the side of the stool in both acute and chronic fissure-in-ano. When bleeding occurs
at the time of passing stool or just after defaecation and the blood is bright red and spatters allover the pan,
diagnosis of internal piles can be made with certainty. Bleeding occurring at times other than during defaecation
may be due to prolapsed piles, polyps, carcinoma, diverticulosis, ulcerative colitis, Crohn’s disease, angiod
ysplasia etc. When a child comes with bleeding per anum, a diagnosis of rectal polyp should be made until this
is excluded by rectal examination.
Enquiry should also be made whether it is the blood alone or blood with mucus or blood mixed with stool
or blood streaked on stool. Blood alone is seen in polyps, villous adenoma and diverticular disease. Blood with
mucus is noticed in ulcerative colitis, Crohn's disease, intussusception, ischaemic colon etc. Soiling of clothes
with purulent discharge coming from a sinus is the constant complaint of a patient with fistula-in-ano. In
ulcerative carcinoma of the rectum the patient often passes considerable quantity of blood stained, purulent and
offensive discharge at the time of defaecation.
Enquiry must be made regarding presence or absence of pain. While pain is very much associated with
fissure-in-ano particularly the chronic type as also perianal abscess, pain is absent in haemorrhage from
carcinomatous conditions and polyps. In fact all pathological conditions below the Hilton's line are painful
except carcinoma, but above this line all conditions are painless.
An enquiry should be made regarding abnormality of the bowel habit.
Abdominal examination may reveal a lump in case of carcinoma or intussusception. In case of intussuscep
tion there may be emptiness in the right iliac fossa which is known as sign-dc-dance. In ulcerative colitis there
may be distension of the abdomen. So careful abdominal examination is necessary to find out cause of bleeding
per anum.
Rectal examination is highly important. All anal, perianal and majority of rectal conditions can be diagnosed
through this examination.
INVESTIGATIONS —
1. Endoscopy.— Proctoscopy, sigmoidoscopy and ultimately colonoscopy are of immense value to
diagnose the cause qf lower G. I. tract bleeding. The key to pleasant and successful colonoscopy lies in achieving
a clean bowel before hand. Colonoscopy is never performed under general anaesthesia, but may be carried out after
satisfactory analgesia by injecting intravenous diazepam 5 to 20 mg and pethidine 25 to 75 mg. It must be remembered
that presence of anorectal or distal colonic lesions do not necessarily rule out the presence of a more proximal
source of bleeding. Accurate localisation of lesion is possible in about 95% of cases with endoscopy.
Another method of colonoscopy called virtual colonoscopy (includes CT and MR colography) seems
promising to detect early cancer. There are several methods to stop bleeding through colonoscopy e.g.
electrocautery, laser ablation, injection of sclerotherapy, haemoclip, argon beam etc.
2. Radiological examination.— Where there is not much scope for colonoscopy barium enema examination is very helpful
when the diagnosis has not been made by sigmoidoscopy. The diagnostic accuracy of the barium enema has also been greatly increased
by the use of the double contrast technique provided the bowel has been adequately prepared. Lesions such as inflammatory erosions,
very small polyps can be demonstrated. Particularly in intussusception the role of barium enema is immense and this has been described
in the section of ‘intussusception’.
When colonoscopy is non-diagnostic and barium enema has not been informative, the small bowel lesion should be considered and
a small bowel barium meal follow-through is necessary.
3. Neuclear scintigraphy.— IWm Tc-radiolabelled red blood cell scanning has a high diagnostic value. The long intravascular
half-life of labelled red cells allows repeat scanning and increases the probability of isolating those lesions that bleed intermittently.
»"'Tc-radiolabelled sulphur colloid does not localise the exact bleeding site, but can detect active bleeding as low as 0.1 to 0.5 ml per
minute. The advantages of this technique are accuracy, safety, its non-invasive character, freedom from contrast-related problems and its
low cost. At present radioisotope scanning is limited to screening prior to angiography, but it has no therapeutic value.
4. Angiography.— As mentioned in the upper G.I. tract bleeding the success rate of selective visceral studies is high when the
blood loss is at the minimum rate of 0.5 ml per minute. Selective angiography is necessary through superior mesenteric or inferior
mesenteric artery. The site of bleeding is revealed by extravasated contrast medium remaining in the bowel in the late films of angiographic
series. Haemorrhage can also be controlled by selective infusion of vasopressin or by deliberate injection of embolic material as described
in detail in upper G.I. tract bleeding (page-875). Preoperative localisation of bleeding may facilitate minimal access surgery — for
example laparoscopically assisted colectomy or Meckel’s diverticolectomy.
MANAGEMENT.— This includes general management and local management.
General management includes the measures to resuscitate the patient from shock and at the same time to
give blood transfusion to replenish the blood loss.
Local management depends, on the cause of bleeding. These have been discussed in the respective sec
tions. Only angiodysplasia has not been discussed earlier.
Angiodysplasia (Vascular anomalies).— The various causes of lower G.I. tract bleeding are described in appropriate
chapters. Only one condition is to be discussed here and that is angiodysplasia (see page 1049).
Approximately 15% of patients are amenable to colonoscopic treatment as mentioned above. Bipolar coagulation is safer
than monopolar electrocoagulation. Colonoscopic therapy is often not a definitive treatment modality, it merely tides over the
critical period so that definitive surgical treatment can be undertaken when the patient is in a relatively stable condition.
Treatment alongwith the use of angiography (as mentioned above) is on the rise in the management of lower G.I. bleeding.
Haemostasis can be achieved with embolisation in about 70% of patients and only in 10% the bleeding cannot be controlled.
The procedure may not be technically feasible in about 20% of cases. Vasopressin therapy has not been compared with
embolisation, though angiographic embolisation is usually for patients with continuing bleeding prior to a surgical intervention
so as to allow the patients to be in a better general condition. Surgery is reserved for those who continue to bleed or rebleed
after initial cessation. At operation the identifiable lesions such as carcinoma or Meckel’s diverticulum should be resected. For
patients with continuing bleeding from an unidentified source, a blind subtotal colectomy should be performed.
Diverticulosis.— Diverticuli are usually found in distal colon and 90% of cases are confined to the sigmoid colon only. 50% of
the patients are above 60 years. Bleeding is often self limited, but about 20% of cases rebleed. Endoscopic therapy, as mentioned
above, has a high success rate. Sometimes ‘rebleed’ cases may require surgery which may be segmental or subtotal colectomy.
Neoplasia.— Endoscopic electrocoagulation has been attempted in case of colorectal cancer particularly when bleeding comes
below the peritoneal reflection. Laser ablation is also useful. External radiotherapy at a reduced dose may be tried. Even laser or
bipolar electrocoagulation may be used to control bleeding. But ultimately definitive surgery for neoplasia must be performed.
Obscure bleeding.— A few cases will be there where the reason of lower G.I. tract bleeding cannot be established.
Pan-endoscopy, radiological studies, radio-labelled RBC scan, selective visceral angiography may be performed and only
a few cases may escape detection even through these investigations. An approach being advocated recently, is the use of
anticoagulants, vasodilators or thrombolytic agents to reactivate or augment the bleeding followed by a nuclear scan or
angiography. Only a very small number of cases may even bleed inspite of multiple attempts at preoperative localisation
have failed. These cases will require surgery as the final diagnostic and therapeutic step.
988
CHAPTER -47
UMBILICUS AND ABDOMINAL WALL

Embryology.—
Prior to the formation of the tail fold the caudal end of the embryonic area is anchored to the trophoblast by a connecting stalk. The
formation of the tail fold carries the connecting stalk on to the ventral aspect of the embryo, so that it now assumes the permanent position
of the umbilical cord. Prior to the formation of the tail fold a diverticulum arises from the dorsicaudal portion of the yolk sac and grows
into the mesoderm of the connecting stalk. This outgrowth constitutes the allanto-enteric diverticulum. Gradually the proximal part of this
diverticulum becomes incorporated in the hind gut and its distal portion persists as the allantoic canal or the allantois, which then
communicates directly with the ventral surface of the hind gut. The portion of the hind gut which lies caudal to this communication forms
the entodermal cloaca.
Between the head fold and the tail fold the embryo becomes constricted by right and left lateral folds. The intervening dorsal portion
of the yolk sac which these folds threaten to cut off constitutes the midgut. At first the midgut communicates freely on its ventral surface
with the rest of yolk sac, but the continued growth of the folds results in narrowing ofthe connection, which becomes drawn out as the vitello-
intestinal duct.
As a consequence of the continued expansion of the amnion, the extra-embryonic coelom which was surrounding the embryo is
gradually obliterated. The mesoderm covered surfaces of the head, tail and lateral folds converge on the region of the connecting stalk and
the vitello-intestinal duct. Thus the umbilical cord is formed. The mesoderm of the folds, mentioned earlier, which converge to form the
umbilical cord.forms the abdominal wall surrounding the umbilicus. The umbilical cord consists of an outer covering of amnion, containing
in its interior the vitello-intestinal duct, remains of the extra-embryonic coelom, the allantoic canal and umbilical vessels embedded in a
mass of primary mesoderm. The part of the extra-embryonic coelom included in the umbilical cord acts as the sac for the physiological
umbilical hermia which characterises the embryo between the 6th and the 10th weeks. After the disappearance of this hemia, the remains
of the extra-embryonic coelom normally obliterate.
At the end of pregnancy the umbilical cord is about 50 cm in length. The umbilical vessels, particularly the arteries are provided with
a strong muscular coat, which when contracts produces thickening of the media, infolding of the interna and considerable narrowing of
the lumen. Thus the vessels are obliterated
ANOMALIES OF DEVELOPMENT.—
A. The vitello-intestinal d uct may persist completely or partially to give rise 10 the following conditions.
1. When it is patent althroughout, it gives rise to intestinal fistula, which discharges mucus and
occasionally faeces (then it is termed faecal fistula). Such discharge is usually noticed in the first few months
of life.
2. Sometimes the major part of the duct obliterates, only a small part near the umbilicus remains patent.
This gives rise to a sinus, which discharges mucus. The epithelial lining of such sinus may become everted to
form a Raspberry tumour or adenoma.
3. Sometimes the intestinal end of the vitello-intestinal duct remains patent to form the Meckel's
diverticulum. The tip of this diverticulum may or may not be attached to the umbilicus with a fibrous cord which
represents the obliterated portion of the vitello-intestinal duct. This cord may be the potential danger for
intestinal obstruction.
When a vitello-intestinal cord connected to Meckel's diverticulum, but not attached to the umbilicus, may
become adherent to or knotted around another loop of small intestine to cause intestinal obstruction.
4. Occasionally both the umbilical and the intestinal ends become obliterated, but the central portion
remains patent. Due to accumulation of the secretion of the patent portion of the duct an intra-abdominal cyst
develops, which is known as enterocystoma.
5. Sometimes the whole of the vitello-intestinal duct becomes obliterated but a band persists, which is a
potential danger for intestinal obstruction as the small intestine may become twisted around the band. This is
known as vitello-intestinal cord.
6. Very rarely a cord-like structure may stretch from the umbilicus across the ileum to end in the
mesentery. This is an obliterated vitelline artery and not a vitello-intestinal cord.
B. Urachus.—
1. Only occasionally the urachus, which represents portion of the allantois, may remain patent, so that a
fistula exists between the apex of the urinary bladder and the umbilicus. This is urinary fistula of the umbilicus.
Though this is congenital, yet this is only manifested in the adult or even old age.
2. Another rare condition is a urachal cyst. This is due to patent mid-portion of the urachus with
UMBILICUS AND ABDOMINAL WALL 989
obliterated umbilical and vesical sides.

3. Occasionally the umbilical end of the urachus does not obliterate giving rise to urachal sinus of the
umbilicus. Such sinuses discharge small amounts of mucus from the umbilicus. These may become infected.
Broadly the DISEASES OF THE UMBILICUS can be classified under the following heads :
1. UMBILICAL HERNIAS (described in the chapter 56 of ‘Hernias’).
2. INFLAMMATIONS .—
(i) Infection of the stump of the umbilical cord (omphalitis).
(ii) Umbilical granuloma.
(iii) Umbilical dermatitis.
(iv) Pilonidal sinus.
3. FISTULAE.—
(i) Faecal fistula—(a) Patent vitello-intestinal duct, (b) from tuberculous peritonitis and (c) transverse
colonic neoplasm ulcerating through the umbilicus.
(ii) Urinary fistula — patent urachus.
(iii) Biliary fistula (extremely rare).
4. ANOMALIES OF VITELLO-INTESTINAL DUCT.
5. ANOMALIES OF THE URACHUS.
6. NEOPLASMS.—
(a) Benign neoplasms.—
(i) Adenoma or raspberry tumour.
(ii) Endometrioma.
(b) Malignant neoplasms.—
(i) Primary carcinoma.'
(ii) Secondary carcinoma from the stomach, colon, breast, ovary and uterus.
7. UMBILICAL CALCULUS.
8. EVERSION OF UMBILICUS (mostly due to ascites).
OMPHALITIS
Infection of the umbilicus may occur in babies and adults. It is generally a disease which results from poor
hygiene.
True omphalitis is infection of the stump of the umbilical cord. It results due to improper and inadequate
care of the umbilical stump. Bacterial infection occurs in the stump of the umbilical cord. In more than 50%
of cases the causative organism is the Staphylococcus. Less commonly Streptococci, Esch. coli and even Cl.
tetani have been isolated from infected stump of the umbilical cord.
In omphalitis one can see exuberant granulation tissues with inflammation of the surrounding abdomen. The
clinical importance of such infection is its liability to spread along the defunct hypogastric arteries or umbilical
vein to cause the following complications —
(i) Abscess of the abdominal wall.— A localised deep abscess is formed around the umbilicus. If
pressure is exerted below or above the umbilicus, beads of pus will be seen extruding through the umbilicus.
Such abscess must be opened. A probe pointed director is passed into the sinus and the overlying tissues are
incised in the midline. Systemic antibiotic should always be prescribed.
(ii) Septicaemia.— When organisms enter the blood stream through the umbilical vein, septicaemia
may occur. Jaundice is often the first sign.
(iii) Portal vein thrombosis.— It is a serious sequel of this condition. This may lead to subsequently
portal hypertension.
(iv) Jaundice may occur due to infection reaching the liver via the umbilical vein. Intrahepatic
cholangitis occurs in 3 to 6 weeks. This is a serious condition.
(v) Extensive ulceration of the abdominal wall may occur due to synergic infection almost like post
operative subcutaneous gangrene of the abdominal wall.
TREATMENT.— Prophylaxis is the main treatment, as once it happens, it is a dreadful condition. The
reason is that it spreads very quickly through the defunct hypogastric arteries and umbilical vein. 0.1%
chlorhexidine should be applied daily to the stump of the umbilical cord for a few days. Strict asepsis should
be maintained at the time of cutting the umbilical cord.
Omphalitis in adults is not uncommon. It is also associated with poor hygiene and deeply placed umbilicus
in obese individuals. The patient complains of umbilical discharge which is seropurulent with unpleasant smell.
Pain is very common symptom. Soreness is also associated with. On examination one may find red and tender
umbilicus.
If the infection spreads into the subcutaneous tissues and the opening of the umbilicus becomes narrowed
by oedema, the whole umbilicus can turn into an abscess. This is known as umbilical abscess. Umbilical abscess
may be associated with omphalitis or umbilical calculus. In this condition patient complains of a swollen
umbilicus which discharges pus with throbbing pain at the umbilicus. Clinical diagnosis is based on finding of
a red hot tender swelling in and around the umbilicus which exudes pus.
Treatment is umbilectomy.
UMBILICAL GRANULOMA
If chronic inflammatory process affects the stump of the umbilical cord following severence such condition
may develop. Excess granulation tissue is formed at the stump which prevents the raw area to become
epithelialise. This continues for weeks.
The baby presents with a pouting umbilicus covered with bright red, moist, friable hemispherical mass of
bleeding granulation tissue. In many respects this condition is similar to the pyogenic granuloma in other parts
of the skin.
TREATMENT is destruction of the umbilical granuloma by application of silver nitrate stick followed by
dry dressings.
The important differential diagnosis is umbilical adenoma, which soon recurs inspite of this treatment.
UMBILICAL DERMATITIS
This condition may be seen at any age. Such dermatitis may occur due to discharge from the umbilicus or
due to fungus or parasitic infection.
PILONIDAL SINUS
Pilonidal sinus, though more often seen at the post-anal region in the buttock, in the interdigital cleft in case
of barbers, this is also sometimes encountered in the umbilicus. Diagnosis is made by seeing a sheaf of hairs
in a sinus in the umbilicus.
TREATMENT is excision.
UMBILICAL FISTULA
Besides umbilical vein and arteries, there are two more structures which pass through the umbilicus during
foetal development. These are the vitello-intestinal duct and the urachus. Both these structures normally
obliterate and disappear. Only in rare cases developmental anomalies may affect these structures and cause
various conditions affecting the umbilicus. These have been discussed under the heading of ‘Anomalies of de
velopment’ earlier in this chapter.
TYPES OF FISTULA :
1. A patent vitello-intestinal duct discharges mainly mucus and rarely faeces through the umbilicus,
which may be noticed in the first few months of life. This is a very rare abnormality and is a type of faecal fistula
of the umbilicus.
TREATMENT.—
A patent vitello-intestinal duct should be excised together with the Meckel's diverticulum. During such
excision one must excise the base of the Meckel's diverticulum with end-to-end anastomosis of the small
intestine.
2. A patent urachus permits leak of urine through the umbilicus. But this condition does not reveal itself
until adult life or even old age. The reason is that the contractions of the bladder start at the apex of the organ
and pass towards the base. As the urachus opens at the apex of the bladder, it is closed during contractions of
the bladder and urine does not come out through the patent urachus.
Urinary leakage through the umbilicus becomes only symptomatic when there is some urinary obstruction
at the lower urinary tract.
TREATMENT.—
Since urinary leakage due to patent urachus is not possible without an obstruction in the lower down the
passage, the treatment is directed to get rid of such obstruction. If still the leak continues, the treatment is
excision of the umbilicus with excision of the urachus down to the apex of the bladder with closure of the urinary
bladder.
Besides the developmental anomalies e.g. patent vitello-intestinal duct, patent urachus etc., fistula of the
umbilicus is also seen in other conditions.
3. Sometimes an enlarged inflamed gallbladder perforates at its fundus and may discharge gallstones and
bile through the umbilicus(biliary fistula).
4. Due to presence of foreign body e.g. a gauze piece during operation, there may be discharge through
the umbilicus.
5. Carcinoma of the colon may ulcerate through the umbilicus and cause faecal fistula of the umbilicus.
ANOMALIES OF VITELLO-INTESTINAL DUCT

These have been discussed under the heading of ‘Anomalies of development’ earlier in this chapter.
Vitello-intestinal duct cyst or enterocystoma is a small spherical, mobile swelling deep to the umbilicus.
Through a band it is fixed to the umbilicus and to the small bowel.
TREATMENT.— Treatment of such cyst is excision.
Vitello-intestinal band causing acute intestinal obstruction should also be excised. It is customary to bury
the cut end of the band with purse-string suture.
ANOMALIES OF THE URACHUS

A patent urachus has already been described under the section of ‘Umbilical fistulae’. Other varieties of
anomalies of the urachus have been described under the heading of ‘Anomalies of development’ earlier in this
chapter.
Urachal cyst is an immobile swelling, in the hypogastrium deep to the abdominal muscles.
TREATMENT of urachal cyst is excision.
Abscess in a urachal remnant may cause persistent umbilical discharge and dermatitis. The treatment is also
excision of the urachal remnant.
NEOPLASMS OF THE UMBILICUS

Umbilical adenoma or Raspberry tumour or Enteroteratoma.— It is not a typical tumour. It is due to
a partially or occasionally a completely unobliterated vitello-intestinal duct. Usually the duct near the umbilicus
remains patent and the rest of the duct becomes obliterated. The mucosa of the patent duct prolapses through
the umbilicus and gives rise to a raspberry-like tumour, which is a soft pink tumour moist with mucus. It often
tends to bleed. Intestinal obstruction may occur if there be a vitello-intestinal band. There may also be associated
Meckel's diverticulum, which should always be excluded by barium meal, since its treatment is different.
It is commonly seen in infants, but occasionally it is presented later in life.

Histological picture shows columnar epithelium rich in goblet cells.
TREATMENT.
(i) If the tumour is pedunculated, a ligature may be tied around its base, so that the polyp may fall off within
a few days. But this may recur.
(ii) The actual treatment is umbilectomy with excision of the vitello-intestinal duct. One should always
explore the abdomen. Sometimes one may find Meckel's diverticulum associated with this condition. In that
case the Meckel's diverticulum and the attached cord or duct should be excised alongwith umbilectomy.
Endometrioma.— Sometimes ectopic patch of endometrial glands may be seen in the umbilicus. It is
usually seen in the dermis as the sudoriferous glands open on to the surface of the skin.
Women between the ages of 20 and 45 years usually present with endometrioma. The umbilicus becomes
enlarged, painful and it discharges blood at the sametime as the patient menstruates. On examination, a small
fleshy tumour may be seen in the umbilicus. This condition may be associated with endometriomas in the ovary
or in the uterus.
TREATMENT is umbilectomy alongwith the endometrioma.
Secondary carcinoma.— This condition in the umbilicus is manifestation of late stage of intra-abdominal
malignancies. When umbilicus is secondarily involved, the primary malignancy is often situated in the stomach,
colon, small intestine, ovary or uterus. Primary may even be situated in the breast.
1. Tumour cells reach the umbilicus mainly via lymphatic route. When tumour cells invade the
lymphatics of the ligamentum teres hepatis at the free lower margin of the falciform ligament, umbilicus may
be affected. Umbilicus may be affected with multiple peritoneal metastasis which affect the skin of the
abdominal wall.
Umbilical metastasis is present as a nodule at the umbilicus. Such metastatic nodule may ulcerate and bleed.
2. A condition known as Sister Mary Joseph's nodule, in which a nodule of metastatic carcinoma bulges
through the umbilicus may sometime be seen. It is often considered to be the metastatic lymph node in the
umbilicus as a manifestation of intra-abdominal malignancy, probably with the same diagnostic significance
as Virchow's node in the neck. Such nodule causes serosanguineous discharge.
3. Carcinoma of the colon or small intestine may be adherent to the parietal peritoneum deep to the
umbilicus and may gradually invade the umbilicus. Ultimately an intestinal or faecal fistula may form.
OMPHALITH OR UMBILICAL CALCULUS

Desquamated epithelium from the umbilicus, its sebaceous secretions, mixed with hairs and fluff from
clothings — all these are sucked into the umbilicus and if not properly cleaned, may form a hard stone, which
is known as umbilical calculus or omphalith.
This condition is seen in those who are obese with very deep and narrow umbilicus and in those who do not
keep themselves clean. What is more common are small concretions which give no trouble.
When an umbilical calculus is formed, it may give rise to inflammation and umbilical abscess. Such
infection may spread through the skin causing periumbilical cellulitis.
Diagnosis is made on inspection of the dark or greyish brown stone. On palpation the whole umbilicus feels
hard and swollen.
TREATMENT is to dilate the umbilical orifice and to extract the calculus:
If umbilical abscess is formed, to prevent recurrence it is better to exicise the umbilicus under antibiotic
cover.
CAUSES OF DISCHARGE FROM THE UMBILICUS
CONGENITAL.—
(i) Intestinal fistula (through patent vitello-intestinal duct).
(ii) Patent urachus.
(iii) Umbilical adenoma or raspberry tumour (partially unobliterated vitello-intestinal duct).

ACQUIRED.—
(i) Umbilical dermatitis.
(ii) Umbilical granuloma.
(iii) Umbilical calculus or omphalith.
(iv) Endometrioma.
(v) Umbilical abscess.
(vi) Pilonidal sinus.
(vii) Secondary carcinoma.
(viii) Sister Mary Joseph's nodule.
(ix) Acquired intestinal fistula in Crohn's disease.
(x) Tuberculous peritonitis may give rise to serous discharge.
(xi) Acquired intestinal fistula from secondary carcinoma.
UMBILICAL FISTULA
Causes.—
1. Faecal or intestinal fistula.—
(a) Patent vitello-intestinal duct.
(b) Crohn's disease.
(c) Malignancy of the small or large bowel invading the umbilicus leading to intestinal fistula.
2. Urinary fistula.— Due to patent urachus.
3. Biliary fistula.— Enlarged inflamed gallbladder perforating at its fundus may discharge gallstones
through the umbilicus.
4. Iatrogenic.— If a piece of gauze or an instrument is left behind during abdominal operation, a fistula at
the umbilicus may form discharging pus continuously.
DISCOLOURATION OF THE UMBILICUS

Sometimes discolouration of the umbilicus may give a clue as to the intra-abdominal diagnosis. These signs
are:—
(i) Caput medusae — is a collection of distended veins around the umbilicus often seen in portal
hypertension.
(ii) Spider angiomas may be seen in chronic liver disease.
(iii) Smallpetechiae may be seen in thrombocytopaenia or fat emboli.
(iv) Cullen's sign is the bluish hue around the umbilicus, which is sometimes seen in late cases of acute
haemorrhagic pancreatitis and with extensive destruction of the pancreas.
(v) A few striae may be seen in Cushing's disease.
(vi) Bruising at the umbilicus may be seen in long standing haemoperitoneum e.g. ruptured ectopic
pregnancy.
NEOPLASMS OF THE ABDOMINAL WALL
BENIGN TUMOURS.—
Benign tumours of the abdominal wall may arise from any of the elements contained in it. Lipomas are not
uncommon and are treated by simple excision. Benign fibromas, neurofibromas and haemangiomas may be
seen. These are treated in the same line as in other locations.
The most important benign tumour is the desmoid tumour of the abdominal wall.
DESMOID TUMOUR
This is a benign fibrous tumour which arises in the musculo-aponeurotic abdominal wall especially below
63
the level of the umbilicus. It is more often seen in relation with the sheath of the rectus abdominis muscle.
Though it is benign, it is known for its recurrence. That is why it is also called ‘Recurrent Fibroid of Paget’.
AETIOLOGY.—
(a) It is more common in women (about 80%), particularly in multiparae, probably due to stretching of the
muscles of the abdomen during pregnancy.
(b) Trauma, stretching of the muscle fibres and haematoma of the abdominal wall are aetiological factors.
(c) In certain cases of familial polyposis coli (Gardner's syndrome) this condition may appear.
PATHOLOGY.— This tumour presents as firm, slow growing mass. It is non-encapsulated and is locally
invasive.
Microscopically it is composed of fibrous tissue containing multinucleated plasmodial masses resembling
foreign body giant cell. It may undergo myxomatous degeneration. In this case it increases in size rapidly.
This tumour does not have a propensity towards metastasis. Unlike fibroma elsewhere, sarcomatous change
is hardly seen in this tumour.
Middle-aged women are most often affected. This tumour usually occurs in the rectus sheath or in the
external oblique aponeurosis. Occasionally it may occur in other sites as the plantar fascia of the foot or the
palmar fascia in the hand.
On examination, the mass is firm to hard in consistency, with irregular surface. With leg-raising test, it is
confirmed that the swelling is parietal. The diagnosis is confirmed by biopsy.
TREATMENT.—
Due to its tendency to recur, this tumour is widely excised with a surrounding margin of at least 2.5 cm of
healthy tissue. The defect, after excision, in the abdominal wall is made good by tantalum gauze or nylon mesh.
This tumour is moderately radiosensitive.
MALIGNANT TUMOURS.— Primary malignancies of the abdominal wall are extremely uncommon.
However rarely one may come across fibrosarcoma of the abdominal wall.
Fibrosarcoma.— The characteristics of fibrosarcoma of the abdominal wall arc same as those anywhere
in the body. It is a firm, well vascularised fast growing tumour (unlike desmoid tumour). Soon the mass becomcs
fixed. Diagnosis is confirmed by biopsy.
Blood-borne metastasis, though occur (unlike desmoid tumour), is usually late.
Treatment.— This tumour is resistant to radiotherapy.
Wide excision is the only treatment, followed by tantalum gauze repair of the defect.
995
CHAPTER 48 -
HERNIAS
A hemia is an abnormal protrusion of a part or whole of viscus through an abnormal opening in the wall of
the cavity which contains it In this chapter we are only concerned with the external abdominal hemia. An
external abdominal hernia is protrusion of abdominal viscus through a weak spot in the abdominal wall.
The common external hemiae are:
1. Inguinal — about 73%;
2. Femoral — about 17%;
3. Umbilical — about 8.5%;
4. Incisional — its incidence is not included.
Other 1.5% cases are rare hemiae e.g.
(i) Epigastric;
(ii) Lumbar;
(iii) Spigelian;
(iv) Obturator;
(v) Gluteal.
AETIOLOGY —
Mainly 2 factors play in causing a hemia :—
1. Weakness of the abdominal muscles and
2. Increased abdominal pressure which forces the content out through the normal abdominal musculature.
1. Weakness of the abdominal musculature can be either (a) congenital or (b) acquired.
(a) CONGENITAL WEAKNESS —
(i) Persistence of processus vaginalis — this causes indirect complete inguinal hamia. It is a sort of
preformed sac through which the contents herniate.
(ii) Similarly patent canal of Nuck in female causes indirect inguinal hemia.
(iii) Incomplete obliteration of umbilicus may lead to infantile umbilical hemia.
(b) ACQUIRED WEAKNESS —
(i) Excessive fat in the abdomen causes weakness of the abdominal musculature. Fat separates muscle
fibres and thus causes weakness. This causes the appearance of direct inguinal hemia, paraumbilical hemia or
hiatus hemia.
(ii) Muscle weakness may follow repeated pregnancy.
(iii) Surgical incisions may lead to division of nerve fibres and thus causes muscle weakness. Example
of this is that a direct hemia may develop following appendicectomy due to division of ilio-inguinal nerve. See
Fig. 534 of ‘A Manual On Clinical Surgery’ by Dr. S. Das.
(iv) Incisional hemia develops through weakened abdominal muscle following a previous operation.
Mostly infection in the early postoperative period or excessive fat in the abdominal wall predisposes incisional
hemia.
2. Increased abdominal pressure e.g.
(i) Whooping cough in children.
(ii) Chronic cough in bronchitis, tuberculosis etc.
(iii) Bladder neck obstruction or urethral stricture.
(iv) Enlarged prostate causing dysuria.
(v) Powerful muscular effort or straining during lifting heavy weight.
(vi) Vomiting.
(vii) Repeated pregnancy.
(viii) Constipation.
PATHOLOGY.—
A hemia consists of 3 parts — (i) the sac, (ii) the contents of the sac and (iii) the coverings of the sac.
(i) The sac is a pouch of peritoneum which comes out through the abdominal musculature. This sac
contains abdominal viscus and it has coverings starting from the skin to the sac itself. This sac can be divided
into four parts—(a) the mouth i.e. the opening of the sac through which the contents enter the sac, (b) the neck
of the sac, which is the most constricted part and it is this part which passes through the abdominal musculature,
(c) the body, which is the main portion of the sac and (d) thefundus which is the most redundant part of the sac.
In children the sac is quite delicate, whereas in adults in longstanding cases the sac is comparatively thick.
(ii) The contents.— The viscus which lies within the sac of a hemia is called the content of a hemia.
Depending on the content, the hemia is variously named e.g.
(a) When the content is omentum, the hemia is called an omentocele or epiplocele.
(b) When the content is a loop of intestine, the hemia is called enterocele.
(c) When the content is a portion of the circumference of the intestine, it is called Richter's hemia.
(d) A portion of the bladder is sometimes present in a direct inguinal or sliding inguinal or a femoral hemia.
(e) Ovary may be the content with or without the fallopian tube.
(f) When the content is Meckel's diverticulum, it is called Littre's hemia.
(g) When two loops of small intestine remain in the manner of ‘W\ it is known as Maydl’s hemia.
(h) Fluid—slight fluid is almost always present, but it is more when it is associated with ascites. Such fluid
may be blood-stained when the hemia is strangulated.
(iii) Coverings are the layers of the abdominal wall which cover the hernial sac. This includes the skin and
muscles of the abdomen.
CLASSIFICATION.—
A hemia, irrespective of its site may be either —
(i) Reducible or (ii) Irreducible, (iii) Obstructed or incarcerated or (iv) Strangulated or (v) Inflamed.
Reducible hernia.— When a hemia reduces itself as the patient lies down or can be reduced by the patient
or by the surgeon, it is called a reducible hemia. One of the 2 most characteristic features of the hemia is its
reducibility. The second characteristic feature is impulse on coughing. When the hemia is an enterocele i.e. the
content is small intestine, it gurgles on reduction and the first portion is difficult to reduce. Once reduction is
commenced it is easily reduced particularly the last portion. In case of omentocele the first portion is easy to
reduce but it is difficult to reduce the last portion. An uncomplicated hemia is usually a reducible hemia.
Irreducible hernia.— When the contents of the hemia cannot be returned back to the abdomen it is called
an irreducible hemia. There are various causes of irreducibility :—
(i) Adhesion of its contents to each other;
(ii) Adhesion of its contents with the sac;
(iii) Adhesion of one part of the sac to the other part;
(iv) Sliding hernia;
(v) Narrowing of the neck of the sac due to fibrosis following continued use of the truss;
(vi) Presence of omentum in the sac often causes irreducibility;
(vii) When the content is the large intestine which becomes obstructed (incarcerated);
(viii) When there is massive hemia inside the scrotum (scrotal abdomenJ it often becomes irreducible.
Femoral and umbilical hemiae are often irreducible. Irreducible hemia is dangerous and may lead to
strangulation.
Obstructed or Incarcerated hernia.— It is irreducibility plus intestinal obstruction. An obstructed hemia
means that the hemia is associated with intestinal obstruction due to occlusion of the lumen of the bowel. The
term ‘incarcerated hemia’ is often used as an alternative to obstructed hemia, but to be more precise it indicates
that a portion of colon is the content of the sac and is blocked with faeces. It can be ascertained by indenting
with the finger like putty.
The features of obstructed hernia are —
(i) Expansile coughing impulse is not present;
HERNIAS 997
(ii) The hemia is irreducible;

(iii) Patient does not complain of pain;
(iv) The hemia is lax and not tender,
(v) Features of intestinal obstruction.
One must be very careful to make this diagnosis as against strangulated hemia. It also possesses two of its
features i.e. irreducibility and intestinal abstruction. Of course the 3rd and the most important feature of a
strangulated hemia is missing in this hemia i.e. interference with the blood supply of the intestine. So it is a
dangerous venture to diagnose obstructed hemia when strangulation may be the real state of affairs and thus
valuable time will be wasted until it becomes too late to save the patient’s life.
Strangulated hernia (irreducibility + obstruction + arrest of blood supply to the contents).— A hemia is
said to be strangulated when the blood supply of its contents is seriously impaired. Ultimately the content
becomes gangrenous. This condition develops when the neck of the sac is very much constricted. When the
intestine is the content, intestinal obstruction obviously takes place, but intestinal obstruction may not be present
in case of omentocele, Richter’s hemia and Littre’s hemia. Although inguinal hemia is 4 times more common
than femoral hemia, yet a femoral hemia is more likely to strangulate as the femoral ring is quite tough in
comparison to the superficial inguinal ring.
PATHOLOGY.— When the mouth of the sac is very much constricted, intestinal obstruction first ensues
and the intestine within the sac starts dilating. In case of enterocele the venous return is first impeded. The
intestine becomes congested and bright red. Serous fluid is seen oozing out into the sac. As venous stasis
increases, the arterial supply is also impaired. Ecchymoses appear in the serosa. Blood comes out into the lumen
of the intestine as also into the fluid of the sac, so the fluid in the sac becomes blood stained. The serous layer
loses its shining character and gradually becomes dull and covered with fibrinous exudate.
Gradually the intestine loses its tone and it feels flabby. The vitality of the intestine diminishes and this
favours migration of bacteria through the intestinal wall and the fluid within the sac becomes full of bacteria
and toxins.
The mesentery within the sac becomes congested and haemorrhagic. Thrombosis of its vessels occurs.
Gangrene first appears at the place of constriction and at the antimesenteric border of the intestine. In the
places of gangrene the colour changes from purple to black and ultimately to green. Gangrene may start as early
as 5 to 6 hours after the onset of first symptom of strangulation.
Internal strangulation is more dangerous since spreading peritonitis sets in from the sac.
CLINICAL FEATURES.—Patient first complains of pain and vomiting. Pain is particularly located at the
hernial site. In case of internal strangulation it is located at the umbilicus. Soon pain spreads all over the abdomen
and vomiting becomes forcible and frequent. If the strangulation is not relieved the paroxysm of pain continues.
Such pain will only cease with the onset of gangrene and paralytic ileus. So in case of strangulated hemia
spontaneous cessation of pain is an ominous symptom.
On examination patient is seriously ill. The hemia is tense and tender. Obviously the hemia is irreducible
and there is no impulse on coughing. There are also features of acute intestinal obstruction in case of enterocele.
STRANGULATED OMENTOCELE.— The initial symptoms are more or less similar to those of strangu
lated enterocele. Vomiting is not so prominent feature, similarly the abdominal pain. The pain is localised to
the hernia but recurrent attacks of generalised abdominal pain are absent. Similarly there will be no feature of
intestinal obstruction. Omentum can withstand meagre blood supply for quite a long time, so onset of gangrene
is usually delayed. It first occurs in the most distal part of the omentum. Once the gangrene sets in the mass gets
infected and it becomes an inflamed hemia alongwith strangulation. In case of inguinal hemia such infection
may even cause scrotal abscess.
STRANGULATED RICHTER'S HERNIA.— When a portion of the circumference of the intestine becomes
the content of the sac it is called Richter’s hemia. Strangulation of such a hemia often complicates a femoral
hemia and rarely obturator hemia.
Clinical features mimic gastroenteritis and diagnosis becomes difficult. Vomiting if present is not that
frequent. Unless '/2 of the circumference of the bowel is involved intestinal obstruction may not be present.
Intestinal colic may occur but the bowels are opened normally and there may be even diarrhoea. Absolute
constipation may develop when paralytic ileus supervenes and this often is very much delayed.
For the above reasons diagnosis becomes delayed and operation is performed late. So during operation the
knuckle of bowel in the sac is often gangrenous and peritonitis has set in.
Maydl’s hernia (HERNIA-EN-W) or Retrograde strangulation.— In this condition 2 loops of bowel
remain in the sac and the connecting loop remains within the abdomen and often becomes strangulated. The
loops of intestine look like ‘W’. The loop within the abdomen becomes first strangulated and can only be
suspected when tenderness is elicited above the inguinal ligament and with the presence of intestinal
obstruction. The fallacy of this condition is thateven on opening the sac the coils of intestine look normal. Only
on traction of these loops one can find the strangulated loop inside the abdomen. Since the strangulated loop
is inside the abdomen generalised peritonitis may set in early.
Inflamed hernia.— When a hemia becomes inflamed it is called an inflamed hemia. Inflammation can
occur from outside i.e. from an abrasion or an ill-fitting truss or can occur from inside e.g. when its content is
an inflamed appendix or Meckel’s diverticulum or a salpinx. The diagnosis is made by the presence of
constitutional disturbances associated with local signs of inflammation — overlying skin becomes red and
oedematous. The hemia becomes painful, swollen and tender. The only differentiating feature from a
strangulated hemia is that this hemia is not tense and is not associated with intestinal obstruction.
INGUINAL HERNIA
An inguinal hemia is the protrusion of part of the contents of the abdomen through the inguinal region of
the abdominal wall. This inguinal region is a weak part of the abdominal wall by the presence of the inguinal
canal, the deep inguinal ring and the superficial inguinal ring.
The inguinal canal.—The inguinal canal is a triangular slit almost horizontal in direction which lies just above the inner
half of the inguinal ligament. It commences at the deep inguinal ring and ends at the superficial inguinal ring. In infants the
superficial and deep inguinal rings are almost superimposed and the obliquity of this canal is slight. In adults the inguinal
canal is about 3.75 cm (1 '/2 inch) long and is directed downwards and medially from the deep to the superficial inguinal ring.
This canal has been developed due to descent of testis in the embryonic life.
The deep inguinal ring.— It is an opening in the fascia transversalis 1.25 cm (V2 inch) above the mid-inguinal point
i.e. midpoint between the symphysis pubis and the anterior superior iliac spine. It is of an oval shape, the long axis being
vertical. It varies in size in different individuals and is much larger in the male than in the female. At its margins the fascia
direct hernia transversalis is condensed. Medially it
is related to the inferior epigastric ves
sels. It transmits the spermatic cord in
the male and the round ligament of the
uterus in the female.
The superficial inguinal ring.— It
is an interval in the aponeurosis of the
external oblique muscle. It is situated
just above and lateral to the crest of the
pubis. The aperture is somewhat trian
gular with its long axis oblique corre
sponding to the course of the fibres of
the aponeurosis. It is smaller in the fe
male. Its base is formed by the crest of
the pubis and its sides by the margins of
femoral ring the opening of the aponeurosis which
and septum are called the crura of the ring. The
Fig.56.1.— Right inguinal region is shown from inside. The lateral crus of the ring is stronger. There
inguinal internal ring and femoral ring are shown. are some fibres which course at right
HERNIAS 999
angles to the fibres of the aponeurosis. Some of these fibres may arch over the superficial inguinal ring and are called the
intercrural fibres. The superficial inguinal ring gives passage to the spermatic cord and ilio-inguinal nerve in the male and
to the round ligament of the uterus and the ilio-inguinal nerve in case of females.
Boundaries of the inguinal canal.—
Anteriorly — throughout its whole length there are skin, the superficial fascia and the aponeurosis of the
external oblique and in its lateral l/3rd there are the fleshy fibres of the origin of the internal oblique.
Posteriorly — the transversalis fascia along the whole length of the canal separates it from the extraperi
toneal connective tissue and the peritoneum. In the medial half there are the conjoined tendon (combination of
internal oblique and transversus muscles) and reflected part of the inguinal ligament.
Above — there are arched fibres of the internal oblique and transversus abdominis before they fuse to form
the conjoined tendon.
Below or floor — is formed by the grooved upper surface of the inguinal ligament and its union with the
fascia transversalis. At its medial end there is lacunar ligament.
Presence of the canal weakens the lower part of the anterior abdominal wall. But obliquity of the canal to
some extent compensates, as increase in intra-abdominal pressure will cause approximation of the posterior wall
to the anterior wall of the canal. The posterior wall is strengthened by the conjoined tendon and the reflected
part of the inguinal ligament precisely behind the superficial inguinal ring and the fleshy fibres of the internal
oblique strengthens the anterior wall of the canal in front of the deep inguinal ring.
Contents of the inguinal canal.—
1. Ilioinguinal nerve in both the sexes and is particularly seen in the medial part of the canal. It pierces
the internal oblique muscle distributing filaments to it and then enters the inguinal canal in its midway and lies
below the spermatic cord to accompany it through the superficial inguinal ring.
2. In case of male the spermatic cord and its coverings, the vestigial remnant of the processus vaginalis
(it is the prolongation of the peritoneum, which accompanies descent of testis into the scrotum).
3. In case of female the round ligament of the uterus and the remnant of processus vaginalis.
COVERINGS OFTHE SPERMATIC CORD.—When the testis descends through the abdominal wall into
the scrotum it drags its vessels and nerves alongwith its ductus deferens. These structures meet at the deep
inguinal ring and form the spermatic cord, which extends from the deep inguinal ring to the posterior border
of the testis.
In passing through the inguinal canal the spermatic cord acquires coverings from the different layers of the
abdominal wall and these coverings from within outwards are —
(i) The internal spermatic fascia is derived from the fascia transversalis at the deep inguinal ring.
(ii) Cremasteric fascia which consists of a number of muscular fasciculi derived from the internal oblique
muscle. The muscular fasciculi constitute the Cremaster.
(iii) The external spermaticfascia is a thin fibrous membrane continuous above with the aponeurosis of the
obliquus extemus abdominis at the superficial ring.
STRUCTURES OF THE SPERMATIC CORD.—
(i) The main constituent is the vas deferens.
(ii) Arteries of the spermatic cord are — testicular artery, artery of the vas deferens and artery to the
cremaster.
(iii) Pampiniform plexus of testicular veins.
(iv) Lymph vessels of the testis.
(v) Nerves — testicular plexus of sympathetic nerves which accompany the testicular artery and the artery
of the ductus deferens and the genital branch of the genitofemoral nerve.
Hesselbach’s triangle.— It is a weak spot of the anterior abdominal wall through which direct inguinal
hemia protrudes.
It is a triangle which is bounded —
(i) Medially — by the outer border of the rectus abdominis muscle.
(ii) Laterally — by the inferior epigastric vessels.

(iii) Below — by the medial part of the inguinal ligament.
The floor of this triangle is formed by fascia transversalis. This triangle is bisected by the medial umbilical
fold which is formed by the obliterated umbilical artery. Through this Hesselbach’s triangle direct inguinal
hemia comes out.
Mechanisms which prevent hernia in the inguinal region.— Though inguinal region is a weak spot in
the abdominal musculature, rise in intra-abdominal pressure would have caused inguinal hemia in every
individual. So there must be some defensive mechanisms which prevent hernia to occur. These are :—
1. Obliquity of the inguinal canal — when there is rise in intra-abdominal pressure the posterior wall is
apposed to the anterior wall and thus prevents coming out of abdominal content through inguinal canal.
2. Shutter mechanism of the arched fibres of the internal oblique and transversus abdominis will bring
down these muscles towards the floor when they are contracted during rise of intra-abdominal pressure.
3. Ball-valve action ofthe cremaster muscle which pulls up the spermatic cord into the canal and plug
it during rise in intra-abdominal pressure.
4. In front of the deep inguinal ring there are strong fibres of the internal oblique. This prevents entry of
any abdominal content through the deep inguinal ring.
5. Strong conjoined tendon is there in front of Hesselbach’s triangle to prevent direct inguinal hemia.
INDIRECT OR OBLIQUE INGUINAL HERNIA
In indirect inguinal hernia the contents of the abdomen enter the deep inguinal ring and traverse the whole
length of the inguinal canal to come out through the superficial inguinal ring. This is much more common than
direct inguinal hemia. This hernia usually occurs when there is a preformed sac of partially or completely patent
processus vaginalis. Shortly after birth this processus vaginalis becomes obliterated in normal individuals. Such
obliteration occurs first at the deep inguinal ring, then just above the testis and finally the remaining portion
between the deep inguinal ring and the upper pole of the testis is obliterated to a fibrous cord.
Indirect inguinal hemia is more commonly seen on the right side, though 1/3rd of the cases of the hemia is
or will be bilateral. Particularly in children hernia is more common on the right side due to later descent of the
right testis.
According to the extent of the hemia, it can be divided into 3 groups :
1. Bubonocele.— In this case the hernia is limited in the inguinal canal and the processus vaginalis is
closed at the superficial inguinal ring. This hemia presents as an inguinal swelling. The history is usually short
and majority of the victims are young adults.
2. Funicular hernia.— Here the processus vaginalis is closed at its lower end just above the epididymis.
So the contents of the hernia can be felt separately from the testis and the testis lies below the hemia. Most of
this hernia occurs in adults. A long standing history is usually received in these cases.
3. Complete or vaginal or scrotal hernia.— Here the processus vaginalis is patent throughout. The
hernial sac is continuous with the tunica vaginalis of the testis. In this case the hernia descends down to the
bottom of the scrotum lying in front and at the sides of the testis. The testis can be felt posterior to the hemial
sac with great difficulty. Though it is a congenital hemia and commonly encountered in children, yet may not
appear until adolescent or adult life.
COVERINGS OF INDIRECT INGUINAL HERNIA.— From inside outwards the hemial sac is covered
by the following structures :
(i) Peritoneum;
(ii) Extraperitoneal fat;
(iii) Internal spermatic fascia (derived from the fascia transversalis at the deep inguinal ring);
(iv) Cremasteric fascia and muscles (derived from internal oblique and transversus abdominis), the
muscular fasciculae being separated by areolar tissue;
(v) External spermatic fascia (derived from the intcrcrural fibres at the superficial inguinal ring);
HERNIAS 1001
(vi) Superficial fascia. When the hemia is a complete one the dartos muscle of the scrotum comes in this
layer;
(vii) The skin.
DIRECT INGUINAL HERNIA
A direct inguinal hemia protrudes through the posterior wall of the inguinal canal medial to the inferior
epigastric vessels i.e. through Hesselbach’s triangle. Such hemia lies outside the spermatic cord, either behind
or above or below the cord. So during operation the most important differentiating feature is that the neck of
the direct hernia lies medial to the inferior epigastric vessels, whereas the neck of the indirect hernia lies lateral
to the inferior epigastric vessels.
A direct hemia is acquired with the sole exception of a rare type in which there is a small rigid circular orifice
in the conjoined tendon just lateral to where it inserts with the rectus sheath (Ogilvie hemia).
Direct hemia is much rare and constitutes 15% of all cases. More than */2 the cases are bilateral.
Direct hemia is always an acquired type except the Ogilvie hemia and occurs in elderly persons. It occurs
in individuals with poor abdominal musculature as shown by presence of elongated Malgaigne’s bulges. Direct
hemia almost always occurs in men. Women particularly never develop such hernia.
Direct inguinal hemia rarely attains a large size. Even if it comes out through the superficial inguinal ring
it never descends into the scrotum. As the neck of a direct hemial sac is wide, it rarely gets strangulated.
DIFFERENTIATING FEATURES BETWEEN INDIRECT AND DIRECT INGUINAL HERNIA
Indirect Direct
1. It can occur at any age, but more common in 1. Elderly individuals are usually affected.
children and young adults.
2. Males are affected 20 times more commonly 2. Females are not affected.
than females.
3. In 2/3rds of cases it is unilateral, only in l/3rd of 3. More than 1/2 the cases are bilateral. Such
cases both the sides are involved. It is commoner hemia is usually caused by poor abdominal
on the right side particularly in children due to musculature, evident by presence of long
later descent of the right testis. Malgaigne’s bulges.
4. Frequently, the hemia is complete and in this 4. This hemia is always incomplete and it is of
case it is of pyriform shape. When it is incom spherical shape.
plete it is of oval shape.
5. This hemia descends obliquely downwards and 5. This hernia appears as a forward bulge.
medially.
6. This hemia has to be reduced by the patient or 6. It automatically reduces when the patient lies
the doctor and it does not reduce by itself. down.
1, Impulse on coughing.— Clinician puts his index 7. If an impulse is felt on the middle finger it is a
finger over the deep inguinal ring (l'/2) inch direct hemia.
above the midinguinal point and the middle
finger over the superficial inguinal ring. The
patient is asked to cough or to hold the nose and
blow (Zieman’s technique). If an impulse is felt
on the index finger it is an indirect hemia.
8. Invagination test (see the text below).— When 8. When the little finger goes directly backwards,
the little finger enters the ring if it goes upwards, it is a direct hemia. Moreover when the patient
backwards and outwards it is an indirect hemia coughs, impulse is felt on the pulp of the finger.
and if the impulse is felt on the tip of the finger
it is an indirect hemia.
9. Ring occlusion test (see the text below).— In 9. A direct hemia will show a bulge medial to the
this test indirect hemia will not bulge out. occluding finger.
HISTORY.—
(i) Age.— Inguinal hemia can occur at any age. Indirect inguinal hemia occurs in children in the first few
months of life, in the late teens and young adults. A direct hemia is mostly seen in older subjects.
(ii) Occupation.— Strenuous work is often responsible for development of hemia. Heavy work, especially
lifting weights, puts a great strain on the abdominal muscles. If there is an underlying weakness already present,
hemia may develop. The patient may be able to relate the onset of the hemia to a particular event e.g. lifting
a heavy weight.
SYMPTOMS.—
(i) PAIN.— The commonest symptom of hemia is discomfort or pain. Patient complains of a dragging or
aching type of pain in the groin which gets worse as the day passes. This is often noticed when there is a
‘tendency to hemia’. So pain may appear long before the lump is noticed. Pain continues so long as the hemia
is progressing, but ceases when it is fully formed. In well formed hemia, there is a sense of heaviness or weight.
Pull on the mesentery may cause pain in the epigastric region. The patient may complain of pain allover the
abdomen due to drag on the mesentery and omentum.
When the hemia becomes very painful and tender, it is probably strangulated.
(ii) LUMP.— Many hemiae may cause no pain and he has noticed only a swelling in the groin. But this
is rare and some sort of discomfort is almost always present.
(iii) SYSTEMIC SYMPTOMS.— If the hemia is obstructing the lumen of the bowel (incarcerated hemia)
cardinal symptoms of intestinal obstruction will appear. These are colicky abdominal pain, vomiting,
abdominal distension and absolute constipation. If the patient is vomiting, note the character of the vomitus —
whether bilious or faecal. Faecal smelling vomitus heralds ominous sign.
(iv) OTHER COMPLAINTS.— The cause of hemia must be enquired into. Persistent coughing of
whooping cough or chronic bronchitis, constipation, dysuria due to benign enlargement of prostate or stricture
urethra may show other symptoms which the patient deliberately do not mention considering them to be
irrelevant. Leading questions should be asked to find out these symptoms.
(v) PAST HISTORY.— Whether the patient had any operation or not ? During appendicectomy division
of subcostal or ilioinguinal nerve may lead to weakness of the abdominal muscles at the inguinal region. This
may cause subsequent direct inguinal hemia. Many a patient gives a previous history of hemia repair on the same
side (recurrent hemia) or on the opposite side (right sided hemia generally precedes that of the left side).
LOCAL EXAMINATIONS—The patient should be first examined in the standing position and then in the
supine position. Majority of the hemiae are better examined in the standing position.
Two classical signs of an uncomplicated hernia are — (i) Impulse on coughing and (ii) reducibility.
Sometime must be spent for inspection. Impulse on coughing can be detected by inspection alone.
1. POSITION AND EXTENT.— If the swelling descends into the scrotum or labia majora it is obviously
an inguinal hemia. When it is confined to the groin, it should be differentiated from a femoral hemia. Two
anatomical structures are to be considered in this respect—(a) the pubic tubercle and (b) the inguinal ligament.
An inguinal hemia is positioned above the inguinal ligament and medial to the pubic tubercle, whereas a femoral
hemia lies below the inguinal ligament and lateral to the pubic tubercle.
2. TO GET ABOVE THE SWELLING.— This examination differentiates a scrotal swelling from an
inguinoscrotal swelling. The root of the scrotum is held between the thumb in front and other fingers behind
in an attempt to reach above the swelling. In case of inguinal hernia one cannot get above the swelling, whereas
in case of pure scrotal swelling e.g. vaginal hydrocele one can get above the swelling.
3. CONSISTENCY.— If the inguinal hemia contains omentum (omentocele or epiplocele) the swelling
feels doughy and granular. If it contains intestine (enterocele) it feels elastic. A strangulated hernia feels tense
and tender.
HERNIAS 1003
4. IMPULSE ON COUGHING.—When there is no swelling, a finger is placed on the superficial inguinal

ring and the patient is asked to cough. The root of the scrotum can also be held between the index finger and
thumb and the patient is asked to cough. An expansile impulse on coughing can be felt as the contents of the
hemia will be forced out through the superficial inguinal ring and will separate the thumb from the index finger.
When hemia is already present it becomes larger and more tense on coughing. Impulse on coughing will be
absent in case of strangulated hernia, irreducible hernia and obstructed hernia.
5. REDUCIBILITY.— The patient is first instructed to lie down on the bed. In many instances the hemia
reduces itself when the patient lies down (direct hemia). The patient himself can often reduce the hemia. In the
remaining cases the surgeon should try to reduce the hemia. The patient is then asked to flex the thigh of the
affected side, to adduct and rotate it internally. This will not only relax the pillars of the superficial ring but also
the oblique muscles of the abdomen. The fundus of the sac is gently held with one hand and even pressure is
applied to squeeze the contents into the abdomen while the other hand will guide the contents through the
superficial inguinal ring. This is known as ‘Taxis'.
6. INVAGINATION TEST.— After reduction of the hernia one can perform this *est to know the gap in
the superficial inguinal ring. Little finger should be used. Invaginate the skin from the bottom of the scrotum,
the little finger is gradually pushed up and then rotated to enter the superficial inguinal ring. Normally the
superficial is a triangular slit which admits only the tip of the little finger. When the patient coughs the examining
finger will be squeezed by the approximation of the two pillars. A palpable impulse will confirm the diagnosis.
For convenience of the clinician one may use the index finger, but utmost gentleness is expected.
7. RING OCCLUSION TEST.—The hemia must be reduced first. A thumb is pressed on the deep inguinal
ring i.e. 1/2 inch above the mid-inguinal point. The patient is asked to cough. A direct hemia will show a bulge
medial to the occluding finger but an indirect hernia will not find access, so no bulge.
A hernia can be classified into :
1. CONGENIT AL—when a preformed sac was present congenitally i.e. presence of partly or completely
unobliterated processus vaginalis.
2. ACQUIRED — when there was no preformed sac and the sac has acquired later in life.
A hernia is whether congenital or acquired can sometimes be confirmed by the history alone. A congenital
hemia becomes complete within a short period of its appearance, whereas an acquired hemia progresses
gradually and usually fails to be complete.
All direct hemiae are acquired. Many surgeons believe that all indirect hemiae are congenital. Though the
sac was present since birth, the hemia may not appear until adult life. But other surgeons believe that some of
the indirect hemia are acquired.
According to the contents ofthe sac a hernia can be classified into :
1. Enterocele — when the sac contains intestine.
2. Omentocele — when the sac contains omentum.
3. Entero-omentocele — when the sac contains both intestine and omentum.
4. Cystocele — when a part of the urinary bladder is inside the sac, this usually occurs in a direct hernia or
in sliding hemia. It is suspected when the patient gives the history that the hernia gets enlarged just before
micturition and smaller after the micturition. Moreover pressure on this hemia induces a desire for micturition
particularly when it is distended.
Difference between enterocele and omentocele are :
Enterocele Omentocele
1. On inspection one may see visible peristalsis in 1. Peristalsis is never seen.
this case.
2. Consistency of the hemia is elastic. 2. Consistency is doughy and granular.
3. Reduction.— (i) This hemia reduces easily. 3. (i) Reduction in general is difficult. Its first
Comparatively the first part is more difficult to part goes in easily but the last part resents to be
reduce than the last part which slips in easily. reduced.
(ii) While reduction a gurgling sound can be (ii) No gurgling sound is heard,
heard.
4. Percussion — may produce a resonant note. 4. Percussion reveals dull note.
5. In auscultation one may hear peristaltic sound. 5. No peristaltic sound can be heard.
RARE VARIETIES OF INGUINAL HERNIA

1. Sliding hernia (Syn. Hernia-en-Glissade).— It is a hemia in which a piece of extraperitoneal bowel may
slide down into the inguinal canal pulling a sac of peritoneum with it. In such a hemia the caecum on the right
side, the pelvic colon on the left side or the urinary bladder on either side may slide down. There may be the
usual contents in the sac. The peculiarity is that the posterior wall of the hernial sac is not formed by the
peritoneum alone but by a viscus which lies behind the peritoneum. It may occur with both direct and indirect
hemiae.
This type of hemia is usually seen in older men. Sliding hemia may be suspected by the s’ow way in which
it reappears after reduction. When a large globular hemia descends into the scrotum this condition is suspected.
This condition may be associated with strangulation of small intestine within the sac or a strangulated large
intestine outside the sac.
2. Interstitial hernia.— In this hemia, the hernial sac lies in between the muscle layers of the abdominal
wall. The hemia is usually incomplete. It is commonly associated with an undescended testis. According to the
position of the hernial sac such hemia can be classified into :—
(a) Preperitoneal or intraparietal.— In this type thehemial sac lies between the peritoneum and the fascia
transversalis.
(b)Interparietal.— In this type the hernial sac lies between internal oblique muscle and the external oblique
aponeurosis.
(c) Extraparietal.—The hernial sac lies outside the external oblique aponeurosis in the subcutaneous tissue.
3. Richter’s hernia.—In this condition only a portion of the circum
ference of the bowel becomes strangulated. This condition often compli
cates a femoral hemia and rarely an obturator hemia. It is particularly
dangerous as operation is frequently delayed because the clinical features
resemble gastroenteritis. Intestinal obstruction may not be present until
and unless half of the circumference of the bowel is involved. The patient
may or may not vomit. Intestinal colic is present but the bowels are opened
normally. There may be even diarrhoea. Absolute constipation is delayed
until paralytic ileus supervenes.
4. Littre’s hernia.— In this condition Meckel’s diverticulum is a
content of the hemial sac.
5.MaydI’s hernia (Hernia-en-W) or retrograde strangulation.— In
this condition two loops of bowel remain in the sac and the connecting
loop remains within the abdomen and becomes strangulated. The loops
of the hemia look like a.‘W\ The loop within the abdomen becomes
first strangulated and can onfy be suspected when tenderness is
elicited above the inguinal ligament along with presence of intestinal
obstruction.
DIFFERENTIAL DIAGNOSIS
A long list of differential diagnosis is not required since diagnosis of

an inguinal hemia is relatively easy. Yet when the hemia is incomplete
Fig.56.2.— Maydl’s hemia. and it is almost a groin swelling there are a few conditions which should
HERNIAS 1005
be differentiated. When the inguinal hemia is complete (inguinoscrotal swelling) diagnosis is relatively easier
but a few conditions should be kept in mind.
A. DIFFERENTIAL DIAGNOSIS OF INGUINOSCROTAL SWELLINGS :
1. Encysted hydrocele of the cord.— When a portion of the funicular process persists and remains patent, but shut off
from the tunica vaginalis below and the peritoneal cavity above, it eventually becomes distended with fluid and presents
a cystic swelling either in the inguinal or inguinoscrotal region or in the scrotum. Fluctuation test and translucency test will
be positive. One can very well ‘get above the swelling’. If the swelling is held at its upper limit and the patient is asked to
cough there will be no impulse on coughing. This shows that it has no connection with hemia nor with the peritoneal cavity.
If the testis is pulled down the swelling will also come down and become immobile. This is the traction test. The testis can
be felt apart from the swelling.
2. Varicocele.— It is a condition in which the veins of the pampiniform plexus become dilated and tortuous. Usually
the left side is affected, probably because (i) the left spermatic vein is longer than the right, (ii) the left spermatic vein enters
the left renal vein at a right angle, (iii) at times the left testicular artery arches over the left renal vein at a right angle, (iii)
at times the left testicular artery arches over the left renal vein to compress it and (iv) the left colon when loaded may press
on the left testicular vein. In the beginning the patient will experience aching or dragging pain particularly after prolonged
standing. The swelling appears when the patient stands and disappears when he lies down with the scrotum elevated. The
impulse on coughing is more like a thrill. On palpation it feels like a ‘bag of worms’. After occluding the superficial inguinal
ring with a thumb if the patient is asked to stand up the varicocele fills from below. It must be remembered that a rapid onset
of varicocele on the left side suggests carcinoma of the kidney. Early vascular metastasis is characteristic of this disease.
So the renal vein is often involved earlier by permeation, which may block the opening of the left spermatic vein and thus
causes a quick formation of varicocele on the left side. On the right side the inferior venacava, into which the right spermatic
vein drains, is affected later by permeation and that is why onset of varicocele due to carcinoma of the kidney is rarer on
the right side.
3. Lymph Varix or lymphangiectasis.— It is a condition in which the lymphatic vessels of the cord become dilated
and tortuous caused by obstruction due to filariasis. Past history of periodic attacks of fever with simultaneous development
of pain and swelling of the cord are the main symptoms of this condition. The swelling appears on standing and disappears
spontaneously on lying down, although slower than in case of varicocele. The impulse on coughing is thrill-like and not the
typical expansile impulse found in a case of hemia. On palpation it feels soft, cystic and doughy. Presence of eosinophilia
and living microfilariae in the blood drawn at night are very much diagnostic.
4. Funiculitis.— Besides gonococcal infection funiculitis may be caused by filariasis particularly in this country.
Aching in the groin with variable degree of fever are the presenting symptoms in majority of cases. Initial symptoms may
be those of acute prostatitis. The inguinal and inguinoscrotal regions are inflamed and the skin becomes red, oedematous
and shiny. It is sometimes very difficult to differentiate from a small strangulated hemia. While the former condition is
mainly treated by conservative means, immediate operative intervention is the only life saving measure for the latter
condition. So differentiation is imperative. Palpation just above the deep inguinal ring is of great help in differentiating these
two conditions. In a strangulated hemia the abdominal contents can be felt as they enter the deep inguinal ring whereas in
funiculitis no such structure can be felt.
5. Diffuse lipoma of the cord.— This is a very rare condition. The cord feels soft and lobulated. The swelling is
irreducible having no impulse on coughing.
6. Inflammatory thickening of the cord (extending upwards from the testis and epididymis).— Tuberculosis often
gives rise to this condition. Slight ache in the testis with generalised symptoms of tuberculosis often ushers this condition.
Indurated and slightly tender nodular thickcning of the cord can be felt. Epididymis is obviously tender, enlarged and
nodular. Rectal examination may reveal indurated seminal vesicle of the corresponding side and sometimes of the
contralateral side. In late cases cold abscess develops in the lower and posterior aspect of the scrotum which may discharge
itself resulting in formation of a sinus. About two-thirds of the cases active tuberculosis of the renal tract may be evident.
7. Malignant extension of the testis.— This can be easily diagnosed by presence of malignant growth in the testis. The
cord feels hard and nodular. There may be secondary deposits in the pre- and para-aortic and the even left supraclavicular
lymph nodes.
8. Torsion of the testis.— It is mainly a cause of the swelling of scrotum but an undescended testis may frequently
undergo torsion which is a subject matter of this chapter. This condition mimics a strangulated hemia. It will give rise to
a tense and tender swelling without an impulse on coughing. Absence of testis in the scrotum should arouse suspicion of
this condition. Slight fever, no constipation and dullness on percussion will go in favour of torsion.
9. Retractile testis.— This condition is quite common in children and is often diagnosed as ectopic testis due to the fact
that in majority of cases the testis lies in the superficial inguinal pouch. Strong contraction of the cremaster muscle may pull
the testis up from the scrotum into the superficial inguinal pouch. The testis is usually well developed, the scrotum is also
normally developed and the testis can be brought down to the bottom of the scrotum.
B. DIFFERENTIAL DIAGNOSIS OF GROIN SWELLINGS :
1. Femora) hernia.
2. Saphena varix.— It is a saccular enlargement of the termination of the long saphenous vein. This swelling usually
disappears completely when the patient lies down. The so called impulse on coughing is present in this condition as well,
but it is actually a fluid thrill and not an expansile impulse to the examining fingers. Varicosity of the long saphenous vein
is usually associated with.
Percussion on varicosities of the long saphenous vein will transmit an impulse upwards to the saphenous varix felt by
the fingers of the other hand — Schwartz's test. Sometimes a venous hum can be heard when the stethoscope is applied over
the saphenous varix.
3. Enlarged lymph nodes.— A search for a possible focus of infection should be made in the drainage area which
extends from the umbilicus down to the toes including the terminal portions of the anal canal, urethra and vagina (i.e. portions
developed from the ectoderm). For causes of enlargement of lymph nodes the students are referred to chapter 17. The gland
of Cloquet lying within the femoral canal may be enlarged and simulates exacdy an irreducible femoral hemia. If any focus
cannot be found out or any cause of enlargement of lymph nodes cannot be detected, the nature of the lump remains a matter
of opinion which is best settled urgently in the operation theatre.
4. Psoas abscess.—This is usually acold abscess tracking down from pott’s disease. It is areducible swelling and gives
rise to impulse on coughing. It is a painless swelling and if the pulsation of the femoral artery can be palpated it will be
appreciated that the swelling is lateral to the artery (cf. femoral hemia which is medial to the femoral artery). Sometimes
there is an iliac part of the abscess which is determined by cross-fluctuation. Examination of the back and corresponding
iliac fossa including X-rays clarifies the diagnosis.
5. An enlarged psoas bursa.— This bursa lies in front of the hip joint and under the psoas major muscle. It often
communicates with the hip joint. In osteoarthritis of the hip joint this bursa becomes enlarged and produces a tense and cystic
swelling below the inguinal ligament. This swelling diminishes in size when the hip joint is flexed. Presence of osteoarthritis
in the hip joint, a cystic swelling, absence of impulse on coughing and that the swelling diminishes in size during flexion
of the hip joint are the diagnostic points in favour of this condition.
6. Undescended and ectopic testes.— An undescended testis is one which is arrested at any point along its normal path
of descent. An ectopic testis is one which has deviated from its usual path of descent. In both these conditions the scrotum
of the same side will be empty. If the swelling is within the inguinal canal it is probably an undescended testis. The testis
is recognized by its shape, feel and ‘testicular sensation’. Ascertain whether the testis is lying superficial or deep to the
abdominal muscles by the ‘rising test’. The commonest site of the ectopic testis, is just above and lateral to the superficial
inguinal ring and superficial to the external oblique aponeurosis. It must be remembered that the undescended testis is
always smaller and less developed than its fellow in the scrotum but an ectopic testis is usually well developed. Sometimes
an undescended testis may be associated with an inguinal or an interstitial hemia.
Though the commonest position of ectopic testis is at the superficial inguinal pouch, yet ectopic testis may be found (i)
at the root of the penis (pubic type), (ii) at the perineum (perineal type) and (iii) rarely at the upper and medial part of the
femoral triangle (femoral type).
7. Lipoma.— The diagnostic points in favour of this condition are discussed in Chapter 10 of ‘CommonTumours And
Miscellaneous Lesions Of The Skin’.
8. Hydrocele of a femoral hernial sac.— This is an extremely rare condition in which the neck of the sac becomes
plugged with omentum or by adhesions. The hydrocele of the sac is thus produced by the secretion of the peritoneum.
9. Femoral aneurysm.— Expansile pulsation is the pathognomonic feature of this condition.
TREATMENT OF INGUINAL HERNIA.—
Operation is undoubtedly the treatment of choice in a case of inguinal hernia.
For complete description of the treatment it can be divided into two groups — A. Conservative and B.
Operative.
A. Conservative Treatment.—
1. NO TREATMENT.— This is indicated in a patient (i) with severe general ill-health, (ii) with a short life
expectancy and (iii) in those who refuse operation.
In modern anaesthesia, surgery can be safely undertaken in all ages, only those old patients who are suffering
from chronic bronchitis and not particularly cured by medicinal treatment may be considered unsuitable for
operation.
HERNIAS 1007
2. TRUSS.— A truss does not cure a hemia, with the sole exception of the newborn infants. A truss is used
to prevent hemia to come out of the superficial inguinal ring.
The requirements are : (i) that the hemia should be easily reducible; and (ii) that the patient should be
reasonably intelligent.
The indications are:
(i) Those who refuse operation. They must be informed about the complications of using a truss.
(ii) In old patients suffering from diseases like chronic bronchitis, enlarged prostate, constipation etc.,
where surgery even if performed runs the risk of recurrence. Moreover severe cardiorespiratory disorder may
be to certain extent dangerous for general anaesthesia. In those whose life expectancy is very limited a truss may
be indicated.
(iii) In children a truss if properly used continuously for 2 years without allowing the hemia to descend even
once during this period, the hemia may be cured by causing adhesions. But it must be remembered that a truss
is contraindicated if there is an associated undescended testis. Early operation is indicated in such cases.
Contraindications.— The truss is contraindicated —
(i) When the hemia is irreducible.
(ii) When the patient docs strenuous job or suffers from chronic bronchitis.
(iii) When the hemia is associated with an undescended testis.
(iv) If there is an associated huge hydrocele.
(v) If the patient is not intelligent enough to position the truss properly and to clean the hernial area.
Mode of action.—
(i) A truss acts by pressing the anterior wall against the posterior wall. It also presses on the deep inguinal
ring and prevents the hernia to come out.
(ii) Adhesions gradually develop in the inguinal canal so that the hernia may not find access to come out.
DANGERS OF USING TRUSS.— As a rule use of truss should be condemned.
(i) It causes pressure atrophy of the muscles of the inguinal region and considerably reduces the chance
of successful operation at a later date.
(ii) Improper use can lead to obstruction or even strangulation of the hemia.
(iii) If it is not used after complete reduction of the hernia it may induce damage to the hemial contents e.g.
bowel.
(iv) Improper cleanliness of the inguinal region will produce an unhealthy skin which may lead to difficulty
in wound healing if operation is undertaken later on. Other skin problems may also appear which will force the
patient to reject truss.
(v) Adhesions may develop between the hernial sac and the inguinal canal which is also not good for
subsequent operation if required.
(vi) Above all as the chance of strangulation remains there, use of truss should always be condemned.
Method of use.— (i) A truss should be used in lying down position after reducing the hernia completely.
(ii) Truss should be used allhroughout the day, except at night. It should be worn again before getting out
of the bed.
B. Operative Treatment.—
Three types of operation are usually performed for inguinal hemia — (i) herniotomy, (ii) herniorrhaphy and
(iii) hemioplasty.
1. HERNIOTOMY.— In this operation the neck of the sac is transfixed and ligated and then the hernial sac
is excised. No repair of the inguinal canal is performed. It is indicated —
(a) In infants and children in whom there is a preformed sac.
(b) In case of young adults with very good inguinal musculature.
2. HERNIORRHAPHY.— It consists of herniotomy + repair of the posterior wall of the inguinal canal
by apposing the conjoined tendon to the inguinal ligament. The suture material which is used for such repair
is usually non-absorbable material e.g. proline or silk. Some surgeons still favour a thick chromicized catgut.
The repair is usually done behind the spermatic cord which is known as Bassini's operation. It is indicated —
(i) In all cases of indirect hemia except in children.
(ii) In adult patients whose muscle tone is quite good.
3. HERNIOPLASTY.— This means herniotomy + reinforced repair of the posterior wall of the inguinal
canal by filling the gap between the conjoined tendon and inguinal ligament by (a) autogenous material or (b)
by heterogenous material.
(a) Autogenous materials mean patient’s own tissues. The materials used are :
(i) Strip of fascia lata from the lateral side of the thigh. This is obtained either by a long incision on
the lateral side of the thigh or by small incisions with the help of a fasciatome. In case of long incision the gap
in the fascia lata is closed.
(ii) A strip of the external oblique aponeurosis.
(iii) A flap of the anterior rectus sheath which is turned down to cover the inguinal canal.
(iv) Skin flap may be used in two ways — an elliptical portion of the skin is tensely sutured to the
conjoined tendon and inguinal ligament to cover the posterior wall (dermoplasty) or the skin is made into a
ribbon (skin ribbon) which is now used as a strip same as fascia lata or external oblique aponeurosis.
The strip of fascia lata or skin or external oblique aponeurosis is threaded into a Gallie’s needle. This is a
wide cutting needle with a big eye. Now the suture material is used to ‘dam’ between the conjoined tendon and
the inguinal ligament.
(b) Heterogenous material.— Prolene or a stainless steel wire has been used for darning. Prolene mesh or
stainless steel mesh has also been used. S uch mesh has been used to cover the gap between the conjoined tendon
and the inguinal ligament with a suture ligament.
Indications of hernioplasty are —
(i) Cases of indirect hemia — in patients with poor muscle tone.
(ii) All cases of direct hemia.
(iii) All cases of recurrent hemia.
(iv) Patients who do strenuous jobs or suffering from chronic bronchitis, enlarged prostate etc.
OPERATIONS
HERNIOTOMY.— The incision is
made V2 inch above and parallel to the medial
2/ rds of the inguinal ligament i.e. almost on
3
the inguinal canal. The subcutaneous tissue
is cut along the line of skin incision. The
superficial tissue has 2 layers in this area —
fascia of Camper, the fatty layer and the
fascia of Scarpa, the membranous layer.
Before the fascia of Scarpa is reached the two
named vessels are come across — the.super-
ficial epigastric and the superficial external
pudendal. These vessels are ligated and di
vided. The fascia of Scarpa and the aponeu
rosis of the external oblique are cut in the
same line. The external oblique aponeurosis
is cut upto the superficial inguinal ring so that
the whole of the inguinal canal is exposed.
An incision is made on the cremasteric
Fig.56.3.— The inguinal canal is shown after incision and reflecting
fascia and the internal spermatic fascia. After
the external oblique aponeurosis. White string in the figure is the
ilioinguinal nerve. separating the margins of these fasciae, the
HERNIAS 1009
white wall of the sac will come into view. The sac wall is held by a pair of forceps and is gradually separated
from the spermatic cord by blunt dissections with a piece of gauze to minimise trauma to the structures of the
spermatic cord. This separation should
i, be started from the fundus and gradually
J\H extended towards the neck of the sac.
/- The neck of the sac is identified by :
ImsT"" W (*) "ê constr'ct'on °f the neck
.* (ii) The collar of extraperitoneal

/ r a p ; f a t wall be seen when the mouth of the
sac widens out to be continuous with the
, (iii) The inferior epigastric ves-

\ \1 sels will be seen just medial to the neck
- • '.'wf/.J of the sac in case of indirect hemia and
"7 1k lateral to it in case of direct hemia.
- The sac is now opened and the con
tents are reduced. To make sure a finger
/ Vw * ‘ *s introduced into the sac to see that no
/ WW. r^SVr \ contents are adherent to the neck. The
/ f I /v*" "JP \ \ neck of the sac is secured by means of a
fy\j t transfixion suture i.e. the needle is first
/ p ./ '7 \\ ■% ( passed through the neck of the sac, tied
on one side and then again tied on the
other side, so that the ligature does not
Fig.56.4. The hemial sac is dissected bluntly off the spermatic cord . ^ The sac js abovc ^ Uam_
fixion ligature. The stump will disappear under the arched fibres of the internal oblique.
Closure of the wound is now started. The spermatic cord is allowed to fall back to its normal position. The
external oblique aponeurosis is sutured in
ijk front of the cord by continuous catgut sutures.
The most medial portion is kept open so that
a new superficial inguinal ring is constructed
through which the structures of the spermatic
cord emerges. The skin is closed as usual
either with silk or nylon or Michel’s clip.
HERNIORRHAPHY— This means
repair of the posterior wall of the inguinal
canal in addition to a herniotomy operation.
The steps of operation are same as herni
otomy upto the excision of the sac.
Before proceeding for repair of the poste
rior wall, it is often advised to plicate the
fascia transversalis to narrow the deep ingui
nal ring which often becomes stretched due to
/jr* presence of indirect hemia. Three vertical
Jy/f • nterruptcd sutures are applied on the fascia
cr- tu u i • u • .. u . transversalis
Fig.56.5.— The hernial sac is being twisted after the contents are
C picking up
, ortwo
roo
points giving a
squeezed into the abdomen before transfixion suture is applied. Of I\ inch in between. The most lateral
suture displaces the cord laterally and

narrows the deep inguinal ring to even
less than the tip of the little finger. These
sutures are tied. While suturing care must
be taken not to injure the inferior epigas
tric vessels.
Though some surgeons have advo
cated repair of the transversalis fascia,
yet its effectivity is still questioned.
Bassini’s repair.— The main aim is
to strengthen the posterior wall of the
inguinal canal by stitching the lower
margin of the muscles (internal oblique
and transversus) and the conjoined ten
don to the inner margin of the inguinal
ligament behind the cord. 3 to 5 inter
rupted stitches are applied between the
conjoined muscle and tendon on one
side and the inner margin of the inguinal
ligament on the other side. The most
Fig.56.6.— Bassini's repair. Note how the sutures are applied through
medial suture should be passed through
the conjoined tendon and the inner margin of the inguinal ligament.
the periosteum of the pubic tubercle in
stead of passing
through the ingui
nal ligamentas this
is the part through
which most recur
rences occur.
Whileapplyingthe
middle suture one
must be careful
while biting the
inguinal ligament
not to injure the
external iliac or
femoral vein
which lies just
deep to the ingui
nal ligament. The
most lateral suture
is placed to narrow
the deep inguinal
ring and care must
be taken not to
exert undue con
striction on the
spermatic cord at
Fig.56.7.— Strip of fascia lata is being used as Gallie's method of hernioplasty.
the deep inguinal
HERNIAS
1011
ring. The suture material used for such Bassini’s repair depends mostly on the surgeon’s choice, but
it is preferable to use a non-absorbable suture material e.g. silk, cotton, nylon or prolene.
Care must be taken to apply the suture so that no undue tension is there. This will lead to failure
of purpose of operation. When there is a wide gap between the inferior margin of the internal oblique
and the inguinal ligament, tension on the suture line is almost inevitable. In this case Tanner’s muscle
slide operation may be applied. In this technique the upper leaf of the external oblique aponeurosis
is lifted up, the internal oblique muscle will be seen becoming aponeurotic and fused with the aponeurosis
of the transversus muscle to form the anterior rectus sheath. A curved incision is made on the aponeurosis
of the internal oblique and transversus and the lateral leaf of the incision at once retracts and makes
the tense internal oblique loose.
Once repair of the posterior wall of the inguinal canal has been performed, the spermatic cord is
placed in its position and the external aponeurosis is sutured as mentioned in herniotomy operation.
Overlapping of external oblique aponeurosis is often advocated by many surgeons. This will increase
the strength of the anterior wall. For this the upper leaf of the external oblique aponeurosis is sutured
to the inner side of the lower leaf of the same aponeurosis as much below as possible. Now the margin
of the lower leaf is sutured over the upper leaf like a double-breast coat.
Other techniques which are used in herniorrhaphy are —
(i) Shouldice repair.— This is now a standard technique which is used in most indirect inguinal
hernias. See Figs. 33.7, 33.8 & 33.9 in page 426 of Author’s ‘A Practical Guide To Operative Surgery’.
In this technique the transversalis fascia is incised from the deep inguinal ring to medially as far as
possible near pubic tubercle. The deep inferior epigastric vessels are safe guarded and the fascia is
carefully separated from the extraperitoneal fat. The fascia is now sutured by overlapping (‘double
breasting’), in which the upper flap is placed over the lower flap. The repair is performed using
monofilament continuous suture mostly polypropylene or Dexon. Tension must be avoided. The posterior
wall of the inguinal canal is repaired according to Bassini’s technique. Proponents of Shouldice repair
report a very low recurrence rate in a large series of patients.
(ii) If the deep inguinal ring is weak and stretched, simple Lytle’s method can be used. The cord
is laterally displaced, the inferior epigastric vessels are carefully retracted and the transversalis fascia
around the deep inguinal ring is sutured to narrow the ring.
(iii) Dacron or other mesh implant.— Lichten Stein’s tension-free repair is often used as it is a
relatively easy operation with less stay in the hospital. It may be performed with local anaesthesia. A
Marlex mesh patch is sutured to the aponeurotic tissue overlying the pubic bone and conjoined tendon
above and inguinal ligament below. The lateral edge of the mesh is slipped to allow passage of the
spermatic cord between the split limbs of the mesh. The two tails of the lateral aspect of the mesh are
sutured together. Superiorly, this should extend approximately 2 cm above the internal oblique edge. For
this the external oblique aponeurosis is separated from the underlying internal oblique muscle high
enough. The medial aspect of the mesh should overlap the pubic bone by approximately 2 cm. A running
suture of non-absorbable monofilament material is used. Inferiorly, the inferior edge of the mesh is
sutured to the inner shelving edge of the inguinal ligament. The spermatic cord structures are placed
within the inguinal canal overlying the mesh. The external oblique aponeurosis is closed over the
spermatic cord. Controversy still surrounds the ideal material — Polypropylene, Dacron, Prolene and
Expanded Polytetrafluoroethylene being some of the products currently in use. Using the above-mentioned
materials problem of mesh rejection has been solved and wound infection rates have been minimised.
With this technique the recurrence rate is less than 1% and patients recover rapidly with minimum
postoperative pain. In this technique Expanded Polytetrafluoroethylene mesh has been used for external
approach and preperitoneal approach with good results. But the main limitations are its expense and
its lack of incorporation into the tissue by fibroblasts and collagen proliferation. It is for these reasons
that it is perhaps an ideal material for only large abdominal incisional hernias.
Extraperitoneal repair with mesh is useful when the abdominal wall is very weak and recurrence
is to be expected. Bilateral
——— -n - | _ hernias, combined inguinal and
\ ion suture. In such case it is

better to excise the redundant
Fig. 56.8.— Stainless steel mesh is being used for hernioplasty. . . ., .
3 part and to suture the perito
neum by continuous catgut suture. When the sac is no more than a slight bulge, it should be ignored
and the whole sac is pushed in and the attention is directed more towards proper repair of the muscular
defect to avoid recurrence.
Reconstructive methods.— Due to weakness of the conjoined muscles, there remains a big gap
between them and the inguinal ligament, so simple Bassini’s repair is unlikely to be successful. The defect
has to be closed either by repairing the defect by ‘darning’ with some non-absorbable material such as
fascia lata (Gallie’s operation), a strip of skin (Mair’s operation), silk-ribbon (Gosset’s operation) or
braided nylon. Some surgeons prefer to use a strip of external oblique aponeurosis taken from the upper
and lower margins of the same aponeurosis. But nowadays, Tantalum gauze or a polypropylene mesh
is often used to cover the defect.
LAPAROSCOPIC REPAIR OF HERNIA.— The use of laparoscope or minimal access surgery
has become the trend of the day and it has added an exciting and highly controversial dimension to
herniorrhaphy. The laparoscope allows the surgeon to visualise the hernial defect and surrounding
anatomy with enhanced clarity and magnification. Either of these two techniques is being used — the
transabdominal
preperitoneal repair
(TAPP) or totally
extraperitoneal ap
proach (TEPA). The
main hernia repair
technique is same in
both these methods,
the difference lies in
the manner in which
access to the
preperitoneal space
is achieved. In TAPP
intraperiperitoneal Fig. 56.9.— Bloodgood’s rectus sheath fold is being used for hernioplasty.
HERNIAS
- 1013
approach is made and the peritoneal flap over the posterior inguinal area is incised to reach the
preperitoneal space. In TEPA the preperitoneal space is reached without entering the peritoneal cavity.
In the latter technique the skin incision is made in the periumbilical region and dissection is carried
to the level of the rectus sheath. The rectus sheath is entered and a balloon dissector is placed along
the anterior surface of the posterior rectus sheath and it is advanced to the level of the pubis. The
balloon is now inflated creating an optical cavity in the preperitoneal space, which allows additional
trocars to be placed in this cavity without entering into the peritoneum. A prosthetic mesh is now placed
in the preperitoneal space behind the posterior wall of the inguinal canal and is secured to the posterior
inguinal wall. The prosthetic mesh is secured to the posterior rectus musculature, Cooper’s ligament,
Lacunar ligament, the transversus abdominis aponeurotic arch, and laterally to the lateral extension of
this arch and the superior edge of the iliopubic tract. The mesh is placed across the back of the inguinal
canal to cover the hernial defect completely. It extends laterally beyond the deep inguinal ring and
medially beyond the pubic tubercle. Though majority of surgeons fix this mesh in place with staples
but the common view is that it is unnecessary. When staples are used, none should be placed beneath
or lateral to the deep inguinal ring which may cause injury to the iliac vessels or cutaneous nerves of
the thigh respectively. The mesh should be placed without any crease. Once the mesh is correctly placed,
the peritoneal pocket is closed. Staples are usually used for fixation, but should not be placed below
the iateral iliopubic tract due to potential injury to the genitofemoral nerve and lateral femoral
cutaneous nerve. The staples are also avoided in the triangular area inferior to the deep inguinal
ring, known as the ‘triangle of doom’. The apex of the triangle is at the level of the deep inguinal
ring. The triangle is bordered by the ductus deferens medially and the spermatic vessels in the male
laterally. Inside the triangle are the external iliac vessels and the femoral nerve. The obturator artery
is situated medial to the triangle of doom and should be safe guarded when securing the mesh to Cooper’s:
ligament. .
Various modifications of the TAPP and TEPA techniques have been introduced recently. The
majority of these modifications are related primarily to the size or configuration of the mesh prosthesis.
One innovative and popular method, which has been introduced, particularly in recurrent hernias — is
the double-buttress laparoscopic herniorrhaphy. In this technique a 10 cm x 6 cm sheet of polypropylene
mesh is first placed which is slit to surround the spermatic cord structures. After securing this mesh
with staples, a larger 15 cm x 15 cm sheet of mesh is secured with staples overlying the initial prosthesis.
This ensures adequate closure of the deep inguinal ring and adequate strength of the entire posterior
wall.
Proponents of this laparoscopic technique indicate that excellent visualisation provides adequate
repair, minimal postoperative pain and rapid return to work besides small incisions with less wound
infection and better cosmesis. The critics of laparoscopic technique emphasise high operative cost,
necessity of general anaesthesia, entry into the peritoneal cavity (in TAPP repair) and lack of long term
follow-up results. However it is definitely a viable alternative for the repair of recurrent inguinal hernia
and for simultaneous repair of bilateral inguinal hernia.
Majority of the patients can be discharged after an overnight stay. Return to work is possible after
12 days and to normal domestic activity after 3 to 5 days. Complications are minor in approximately
15% of cases — in the form of fluid collection at the repair site. Major complications are only come
across in less than 2% of cases in the form of retention of urine, small bowel obstruction, mesh
infection etc.
A recent analysis of the cost of laparoscopic hernioplasty showed that the per hour cost in the
operation theatre was 37% more than that of open repair. The mean operating time was 90 minutes
against 55 minutes for an open repair. This resulted in the actual cost for laparoscopic repair being 50%
higher than that for an open repair. Presently the laparoscopic operation is evolving rapidly and w i l l
require further study and better understanding of the anatomy. As techniques and technology improve
this operation may find its way into the general armamenterium of the hernia surgeon. At the present
situation the surgeons should not be pushed prematurely to the mass utilisation of this yet unproven
technique.
Orchidectomy in the operation for inguinal hernia.— While preserving the spermatic cord, there
is no doubt that we are allowing some weakness in the inguinal region e.g. the deep inguinal ring and
the superficial inguinal ring remain, however narrow they may be. Hence orchidectomy should be
considered when function of testis is no more required and it can be sacrificed to give complete strength
to the inguinal region to prevent recurrence. These cases are elderly patients, with very weak inguinal
musculature, with very big hernia, or recurrent hemia. The permission for orchidectomy should be taken
before the operation.
RECURRENT INGUINAL HERNIA.—
In approximately 10% of cases inguinal hernia may recur. Though recurrence rate is more common
in direct hernia, yet due to increased incidence of indirect hemia incidence of recurrence is more in case
of indirect hernia. There are various causes of recurrence of a hemia. The causes can be classified as
follows :—
1. TYPES OF HERNIA —
(i) Sliding hemia;
(ii) Very large and longstanding hernia;
(iii) Large direct hernia.
2. TYPES OF PATIENTS —
(i) Patients with chronic straining e.g. chronic bronchitis, chronic dysuria and chronic constipation.
(ii) Patients with weak inguinal muscles e.g. presence of long Malgaigne’s bulgings.
3. PREOPERATIVE PREPARATION —
Straining factor has not been corrected properly by medicine before operation.
4. OPERATIVE FAULTS —
(i) Failure to ligate the sac at the neck.
(ii) Tension in the stitches in Bassini’s repair so that the portions of muscles held in stitches become
devitalised and replaced by fibrous tissue which yields.
(iii) Use of absorbable sutures in the repair of inguinal canal.
(iv) Imperfect haemostasis predisposing to infection.
(v) Fault in the selection of operation. Herniotomy has been performed when herniorrhaphy should
have been the treatment of choice, or herniorrhaphy has been conducted in place of hernioplasty.
5. POSTOPERATIVE CARE —
(i) Infection of the wound which seems to be the commonest cause.
(ii) Lifting of heavy weights within 3 months after herniorrhaphy.
(iii) Persistent cough, urethral obstruction and straining at defaecation.
6. APPEARANCE OF A NEW HERNIA —
Sometimes a recurrent hernia is in fact not a recurrence but appearance of a new hemia. After
satisfactory repair of indirect hemia, a direct hernia may appear later on.
It must be remembered that majority cases of recurrence take place within 1 year of operation.
TREATMENT OF STRANGULATED INGUINAL HERNIA —
Emergency operation is the treatment of choice to save the patient’s life. As soon as the patient is
admitted, he should be properly resuscitated, at the same time an attempt should be made to reduce the
hernia as gently as possible.
(i) Footend of the bed should be raised (to take advantage of gravity for reduction of hernia).
(ii) Ice bag is applied locally to reduce congestion and oedema of the tissues and at the same time
by lowering the temperature of the content chance of gangrene is delayed.
HERNIAS 1015
(iii) A nasogastric tube is introduced for gastric aspiration, since intestinal obstruction is always associated
with.
(iv) Intravenous fluid administration is essential for the same reason.
(v) Injection pethidine and atrophine is given to relax the abdominal muscles to help reduction.
(vi) Parenteral antibiotics should be started immediately.
(vii) An attempt should now be made to reduce the hemia. The patient’s thigh of the corresponding side is
flexed, adducted and internally rotated. With the right hand the fundus of the sac is very gently squeezed and
with the other hand the contents of the sac are directed through the superficial inguinal ring. It cannot be
emphasised too hard that utmost gentleness is expected from the surgeon. Otherwise following complications
may take place —
(a) Contusion or rupture of the intestinal wall.
(b) Reduction-en-masse i.e. the sac together with its contents is squeezed into the abdomen, but the coils
of intestine within the sac remain strangulated. The symptoms are not relieved.
(c) Reduction into a loculus of the sac.
(d) The sac may rupture at its neck and the contents are reduced not into the peritoneal cavity, but
extraperitoneally.
Operation.—
Anaesthesia.— If the patient’s condition permits, general anaesthesia is the best. If the general anaesthesia
is contraindicated, the patient may even be operated on by local anaesthesia either infiltrating along the line of
the incision or by a field-block by local anaesthetic 1 inch medial to the anterior superior iliac spine to
anaesthetise the ilio-hypogastric and ilio-inguinal nerves supplying the part.
The preliminary steps are similar to those of simple herniotomy. When the hernial sac is reached it is
advisable to open at its fundus before the constriction is relieved. This is done to avoid the risk of contaminating
the peritoneal cavity with highly toxic fluid swarming with the organisms in the sac containing devitalised
bowel. Another advantage is that the contents of the sac will not get opportunity to slip inside the abdomen
before they are thoroughly examined.
The constriction is now divided. A grooved director and a hemia bistoury may be used for division of the
constriction ring. In case of an inguinal hemia the constriction ring is situated (a) at the superficial inguinal ring
or (b) midway between the superficial and the deep inguinal ring, (c) at the deep inguinal ring or (d) anywhere
along the sac.
It must be remembered that if the constriction ring is situated at the deep inguinal ring, the inferior epigastric
vessels are in danger of being damaged during division of the constriction ring. In this case the constriction ring
is divided parallel to the inferior epigastric vessels i.e. upwards and inwards with a grooved director.
Once the constriction ring is divided, the bowel must be drawn out in order to examine the constricted area
and the loop proximal to it. In strangulated Maydl’s hemia (hernia-en-W) the loop inside the abdomen is more
affected than the loops in the sac. If the loops of intestine slip back immediately after the constriction have been
divided, the affected loops of bowel should be sought for within the peritoneal cavity, which fortunately remains
near about and should be brought out with a pair of Babcock’s tissue forceps for proper inspection.
Viability of the bowel is the main thing to be considered in this type of operation. The following points go
against viability that means the loop of bowel is non-viable —
(a) The gut becomes greenish or blackish in colour.
(b) The gut becomes flaccid and lustreless with thrombosis of the mesenteric vessel.
(c) There is no peristalsis in the gut.
(d) When the fluid of the sac is blood-stained and foul-smelling, there is every possibility that the gut has
turned non-viable.
It is always advisable that hot wet mops are placed on the involved loops of bowel for at least 10 minutes.
The loops of bowel are again inspected whether the viability has returned or not. If the loop is gently pinched
with a pair of non-toothed forceps peristaltic movements start. This shows viability. Sim ilarly returning of pink
colour and peristalsis also indicate returning of viability.

When the involved bowel is viable, it should be pushed into the peritoneal cavity. The sac is ligated at the
neck and excised and the operation is concluded as herniorrhaphy as described above. No form of hernioplasty
should be tried.
If the bowel is non-viable.— (i) A linear patch of gangrene at the constriction ring is best treated by
invaginating it by means of Lembert’s sutures, (ii) When the whole loop of the small intestine is gangrenous,
further procedure will depend upon the general condition of the patient. If the condition of the patient permits
and if the bowel above the strangulation is not much distended, resection and end-to-end anastomosis should
be performed then and there. If on the contrary the general condition of the patient is poor and the anaesthetist
is disagreeable and the bowel above the strangulation is grossly distended, it is better to exteriorize the bowel.
Restoration of continuity should be attempted as soon as the patient becomes fit. (iii) If the non-viable bowel
is the large intestine, the best procedure will be exteriorization to be followed by resection (Paul-Mikulicz’s
operation), (iv) When the omentum is strangulated, the healthy portion above should be transfixed and the
affected part is excised.
FEMORAL HERNIA
In this type of hernia abdominal contents pass through the femoral ring, traverses the femoral can
comes out through the saphenous opening.
Femoral hernia is the 3rd according to frequency, after inguinal and incisional hemia. It is more common
in females and accounts for 20% of cases of hernia. Only 5% of cases of hemia in males are femoral hernia.
Femoral hernia is most liable to gel strangulated.
SURGICAL ANATOMY —
Femoral ring is an oval opening ‘/2 inch in diameter (larger in women than in men). It is normally closed
by the femoral septum, which is nothing but thickened extraperitoneal tissue. It is bounded —
In front by the inguinal ligament.
Behind by the pectineus muscle covered by its fascia and the pectineal ligament of Cooper, a thickened
band running along the iliopcctineal line.
Medially by the free margin of Gimbemat’s ligament (Lacunar ligament). Sometimes the pubic branch of
the inferior epigastric artery takes the place of the obturator artery and is known as abnormal obturator artery.
This artery often curves round the medial margin of the femoral ring and is liable to be injured while cutting
the medial margin of the lacunar ligament to relieve the strangulated femoral hernia.
Laterally by a septum which separates it from the femoral vein.
Femoral canal is the innermost compartment of the 3 compartments of the femoral sheath. It is about 2 cm
in length and is funnel shaped. The middle compartment of
this sheath carries the femoral vein, while the outer
compartment carries the femoral artery. The femoral canal
contains areolar tissue, fat, lymphatic vessels and the
lymph node of Cloquet. It is closed above by the femoral
septum at the femoral ring. The femoral sheath is formed
by two fascial layers. The anterior layer is the prolongation
downwards of the fascia transversalis behind the inguinal
ligament and in front of the femoral vessels. The posterior
layer is the downward prolongation of the fascia iliaca
behind the femoral vessels. Posteriorly, the femoral sheath
rests on the pectineus and adductor longus muscles medi
ally and the psoas major and iliacus muscles laterally. Thus
the femoral canal lies in front of the pectineus muscle.
Fig.56.10.— A schematic diagram to show the Femoral canal is closed above by the femoral septum
anatomy of the femoral hernial orifice. which is pierced by lymphatic vessels.The femoral canal is
HERNIAS 1017
closed downwards by the cribriform fascia which covers the saphenous opening.
The saphenous opening (or fossa ovalis) is an opening in the fascia lata situated 4 cm below and lateral to
the pubic tubercle. The upper and outer margins of the saphenous opening are thickened and sharp — known
as falciform process. This process turns the femoral hernia upwards once it has come out of the saphenous
opening. The saphenous opening is covered by loose areolar tissue called a cribriform fascia. This opening is
traversed by the long saphenous vein and lymphatic vessels. The fascia of scarpa, the membranous layer of the
superficial fascia of the abdomen is attached to the fascia lata just below the saphenous opening.
Course of a femoral hernia.— Femoral hernia comes out through the femoral ring, passes through the
femoral canal and comes out through the saphenous opening. After this it progresses upwards in the subcuta
neous tissue of the thigh and may even reach above the inguinal ligament. A fully distended femoral hernia
assumes the shape of a retort with its bulbous extremity looking upwards. The tendency of the femoral hernia
to move upwards after it has come out of the saphenous opening is attributed to the following factors :
(a) Firm unyielding falciform pro
cess turns the hernia upwards.
(b) Attachment of fascia of scarpa
to the fascia lata just below the saphen
ous opening gives it no chance for the
femoral hernia to move downwards, so
it has to move upwards.
(c) Repeated flexion of the thigh
may to certain extent help to push the her
nia up.
Coverings of the sac of the femo
ral hernia.— From outside inwards
these are —
(i) The skin.
(ii) The superficial fascia.
(iii) The cribriform fascia.
(iv) The anterior layer of the femo
ral sheath.
(v) The fatty content of the femo
ral canal.
(vi) The femoral septum.
(vii) The peritoneum.
Rare types of femoral herniae.—
Fig. 56.11.— Note the course of a fully developed femoral hernia. Though majority of the femoral herniae
pass through the femoral canal, a few rare types may be seen as below :
1. Prevascular hernia.— In this case hernia passes in front of the femoral artery and behind the inguinal
ligament and is sometimes associated with congenital dislocation of the hip when there is lack of posterior
support to the femoral hernia (Narath’s hernia).
2. Pectineal hemia.—In this case hernia passes behind the femoral vessels between the pectineus muscle
and its fascia (Cloquet’s hernia). Strangulation of such hernia is very much likely.
3. External femoral hemia.— In this case hemia passes lateral to the femoral artery (Hesselbach’s hernia).
4. Langier’s femoral hernia (Lacunar hernia).— This hernia occurs through a gap in the Lacunar
(Gimbernat’s) ligament. It is diagnosed by the unusual medial position of a small femoral hernia. This hernia,
when diagnosed, is almost always strangulated.
HISTORY.—
(i) Age.— Femoral hernia is uncommon in children. It is rarely seen before late middle age i.e. below 50
years. Majority are seen between 60 to 80 years.

(ii) Sex.— Femoral hemia is much more common in females than males. Remember that even in females
the commonest hernia in the groin is the inguinal hernia. Multiparous women are often affected.
(iii) Side.— The right side is affected twice as often as the left. In 20% of cases it is bilateral.
SYMPTOMS.—
Symptoms can be divided into two groups — local symptoms and general symptoms.
Local symptoms.—
(i) Pain.—- Femoral hemia gives rise to less complaint than inguinal hemia. In fact a small femoral hemia
may be unnoticed by the patients for years till it get strangulated. Adherence of the greater omentum sometimes
leads to a dragging pain.
(ii) Swelling.—This is the usual presenting symptom. It is usually a small globular swelling situated below
and lateral to the pubic tubercle. Such a swelling is more apparent on standing and on straining. It may disappear
on lying down.
General symptoms.— If femoral hemia causes obstruction — abdominal colic, vomiting, abdominal
distension and constipation may be complained of. Femoral hemia is notorious due to its ability to strangulate
quite often. Even a part of the circumference of the bowel may be strangulated — Richter's hemia.
In case of strangulation patient suddenly gets pain at the local site which immediately spreads allover the
abdomen with vomiting.
1. Position.— Femoral hemia is seen below and lateral to the pubic tubercle, and below the inguinal
ligament, whereas inguinal hemia is positioned above the inguinal ligament and medial to the pubic tubercle.
In obese patients it is difficult to feel the pubic tubercle. In this case one may follow the tendon of adductor longus
upwards to reach the pubic tubercle.
2. Size and shape.— It is mostly a globular swelling. Majority of the femoral hemiae are small. If they
become large thery adopt a size of a retort in which the bulbous portion looks upwards and may reach above
the inguinal ligament.
3. Two important signs of a hemia are (a) impulse on coughing and (b) reducibility.
But these signs are relatively less reliable in case of femoral hemia due to (i) adherence of the contents and
(ii) narrowness of the neck of the sac. This makes the differential diagnosis very difficult.
4. Consistency.— Majority of the femoral hemiae feel firm and dull to percussion, as the contents are
mostly omentum or some amount of extraperitoneal fatty tissue surrounding the sac. Rarely the content may
be the urinary bladder.
5. To differentiate from inguinal hernia.—
(a) Impulse on coughing by Zieman's technique the index finger is put over the deep inguinal ring, the
middle finger over the superficial inguinal ring and the ring finger over the saphenous opening. The patient is
asked to hold the nose and blow or to cough. When impulse is felt on the index finger it is the indirect inguinal
hemia, when on the middle finger it is direct inguinal hemia and when on the ring finger it is the femoral hemia.
(b) By invagination test one can detect that the inguinal canal is empty.
(c) Ring occlusion test.— When the hemia is reduced, pressure is exerted over the femoral canal and the
patient is asked to cough, the hernia does not come out.
(d) Position.— This is by far the most important point. The neck of the hemial sac lies below the inguinal
ligament and lateral to the pubic tubercle, whereas an inguinal hemia is always above the inguinal ligament and
medial to the pubic tubercle.
DIFFERENTIAL DIAGNOSIS
This has been discussed above under the heading of ‘Differential Diagnosis of Groin Swellings’.
TREATMENT —
There is no place for conservative treatment and surgery should be performed in all cases of femoral hemia.
The reasons are mainly two: (i) there is always a risk of strangulation, (ii) no truss can be fitted to control femoral
hemia as it becomes displaced with the flexion of the thigh.
HERNIAS 1019
SURGERY.—
Three types of operation are performed in case of femoral hemia and basically these operations are
herniorrhaphy, but the approaches are different.
1. High operation of McEvedy’s operation — approach is made mainly above the inguinal canal but also
below it.
2. Lotheissen’s operation — the approach is through the inguinal canal.
3. Lockwood operation — the approach is below the inguinal ligament via a groin-crease incision.
DESCRIPTION OF OPERATIONS
High operation of McEvedy.—This operation gives a much better access than the ‘low’ operation. This operation
is considered to be the best in strangulated hemia. It allows the sac to be dealt at the fundus as well as at the neck. It is a
more time consuming operation than its ’low’ counterpart.
A vertical incision is made over the femoral canal extending upwards above the inguinal ligament for about 3 inches.
The upper part of the incision lies '/2 inch medial to the linea semilunaris. This part of the incision is deepened, the anterior
rectus sheath is incised and the rectus muscle is retracted medially. The fascia transversalis is divided and by working
downwards the sac entering the femoral canal is identified. In most cases the sac remains empty and is drawn upwards.
The neck of the sac is ligatured and the sac is excised. In irreducible or strangulated hernia, the lower part of the incision
is deepened first till the fundus of the sac is reached. The sac is then opened, its contents are dealt with, after which the upper
part of the incision is deepened in the similar way as has been described earlier and the neck of the sac is drawn upwards
through the canal and ligatured. The repair is now effected by suturing the conjoined tendon with the ligament of Cooper.
Inguinal operation (Lotlieissen’s).— This operation is widely practised, the advantage being that the sac can be
removed flush with the parietal peritoneum.
The incision is made similar to that used for inguinal hemia, except for the fact that it is placed nearer to the inguinal
ligament. The external aponeurosis is incised and the inguinal canal is opened. The spermatic cord or the round ligament
is retracted upwards. The conjoined muscles arc also drawn upwards. The fascia transversalis is divided more or less in the
same plane of incision. This incision should not be extended laterally upto the midinguinal point to avoid injury to the in
ferior epigastric vessels. The inferior margin of the wound is also retracted downwards and the extra-peritoneal fat is pushed
aside by gauze to expose the hernial sac entering the femoral canal. If the sac is empty and is not adherent to the surround
ing structures, it should be drawn up, the
neck is ligatured and the rest of the sac is ex -
cised. Sometimes the sac remains adherent
and the urinary bladder may adhere to the
medial side of the sac. These have to be
carefully dissected off. To dear the fundus
of the sac properly, the lower margin of the
wound has to be retracted downwards.
The femoral ring is now obliterated by
stitching the conjoined tendon or the ingui
nal ligament down to the pectineal ligament.
This suturing is done by three sutures of the
non-absorbable suture material.While the
sutures are being applied, care must be taken
to protect the femoral vein by pushing it lat
erally with a finger. When the femoral ring
is very much widened and flabby, one can
even use a fascial strip from external
oblique aponeurosis to ‘dam’ the opening.
Now the weakness in the posterior wall of
the inguinal canal has to be repaired. The
cord or the round ligament of the uterus are
. _. placed in their positions and the external
Fig.56.12.— Lotheissen s operation for femoral hemia. A.— Transver- ... . . , ,
sals fascia. B.-Inguinal ligament C— Conjoined tendon. D.-Neck obllclue ^neurosis is sutured as usual.
of the sac. Finally the skin is sutured.

1020 ------------------------------------------------------------------------ ------------------------------- A CONCISE TEXTBOOK OF SURGERY
Fig. 56.13.— Last stage of Lotheissen’s operation. The neck of the sac Fig. 56.14.— Best incision for strangulated
is ligatured. Stitches are passed through the conjoined tendon and femoral hernia, which gives simultaneous
pectineal ligament for closure. A.— Transversalis fascia. B.— Inguinal exposure of the neck and fundus of the sac.
ligament. C.— Conjoined tendon. D.— Peritoneum with stump of the
sac. E.— Pectineal ligament. F. — Femoral vein.
Low operation of Lockwood.— This operation is less time consuming. But the main problem of this operation is that
the neck of the sac cannot be reached properly, so proper repair of the femoral ring is not possible and this may well give rise to recurrence.
The incision is made along the groin-crease about Vi inch below the inguinal ligament. The various fatty layers are incised including
the thinned-out cribriform fascia to expose the fundus of the sac. It is freed by gauze dissection as high up as to its neck, if possible.
The fundus ofthe sac is opened and any contents therein, are pushed into the abdominal cavity. If greater omentum remains attached
to the sac, this portion has to be excised. After holding the opened sac by 2 or 3 pairs of artery forceps, a transfixation ligature is applied
to the sac as high as possible. The sac is now resected a little below the ligature. The stump will automatically retract and will disappear.
The closure is made by 2 or 3 stitches which pick up the fasciae forming the floor and the lateral margin of saphenous opening.
Care must be taken not to injure the femoral vein which is protected by a finger placed on it.
Laparoscopic repair.— As mentioned in the inguinal hernia laparoscopic procedure provides

excellent visualisation and access. The femoral space is covered with mesh. The preperitoneal staple
repair is performed. The advantage of this operation is that it can cover both femoral and inguinal areas
simultaneously.
Strangulated femoral hernia.— The high operation of McEvedy is always preferable. The incision
is extended below vertically over the femoral hernia (Fig. 56.14). At first, the sac is cleared and the
fundus is opened. The contents are inspected. The femoral ring is now exposed above the inguinal
ligament and the constriction is investigated. This may be due to narrowness of the sac itself or from
the tough boundaries of the femoral ring. In the latter case, first the lacunar ligament should be incised.
Even if an abnormal obturator artery be present, it will be seen from above and can be avoided. Sometimes
the inguinal ligament has to be cut to relieve the constriction. No harm is done by cutting the inguinal
ligament as it can be sutured afterwards. The neck of the sac is divided against a grooved director. The
contents are now drawn above the inguinal ligament and are dealt with accordingly. The hernia is of
Richter’s type, when a portion of the circumference of the bowel herniates through the femoral ring and
may be strangulated. After the contents of the sac have been dealt with properly, the closure is done
as has been described in non-strangulated type of operation.
HERNIAS 1021
UMBILICAL HERNIA
Three types of umbilical hernia are seen in surgical practice : —
1. EXOMPHALOS — is a developmental anomaly due to failure of whole or part of the midgut
to return to the abdominal cavity during early foetal life. So the abdominal organs remain protruded being
covered by a membrane — which consists of an outer layer of amniotic membrane, a middle layer of
Wharton’s Jelly and an inner layer of peritoneum. Two types of exomphalos can be seen —
(a) EXOMPHALOS MINOR — where the sac is relatively small and to its summit is attached the
umbilical cord.
Treatment.— Sometimes just a twist to the cord may reduce the contents of the sac into the peritoneal
cavity and this is retained by strapping applied firmly. Under no circumstances must this strapping be
removed within fortnight.
(b) EXOMPHALOS MAJOR — in which the umbilical cord is attached to the inferior aspect of
a large swelling containing small and large intestine and a portion of the liver.
Treatment.— Operation should be contemplated as an emergency, otherwise the sac may burst. The
infant should not be fed and an intravenous blood transfusion and fluid therapy is advisable. Broad
spectrum antibiotic should be administered immediately.
Flaps of skin are created on both sides of the swelling by undermining the subcutaneous tissue. The
flaps are attempted to bring over the sac of the swelling. If necessary, relaxing incision may be made
on the flanks. Postoperatively, gastric suction is continued to prevent distension. A second operation
may be required to bring the muscles over the peritoneal sac for closure in layers.
2. UMBILICAL HERNIA IN INFANTS AND CHILDREN.— This is a hernia through a weak
umbilical scar, may be following neonatal sepsis. The hernia is usually symptomless and increases in
size during crying. This hernia occurs more often in males than in females at the ratio of 2 : 1. Small
herniae are spherical in size but when they increase in size they tend to assume a conical shape.
Strangulation is extremely rare in this type of hernia.
TREATMENT.— As 90% of cases are spontaneously cured within 12 to 18 months, reassurance
to the parents is all that is required.
To hasten disappearance of the hernia conservative treatment may be tried. The protrusion is kept
reduced continuously by a pad or a big coin or a round piece of metal on the umbilicus and this is kept
in position by a pad of adhesive plaster which is applied by pulling the skin and abdominal musculature
together. This prevents the hernia to come out and will obliterate the sac by adhesion.
Operation is only justified when the hernia fails to disappear after 18 months or so.
Operation.— It is desirable that the umbilicus should be preserved, so that the child may not be
psychologically handicapped. A small curved incision is made immediately below the umbilicus. The
incision is deepened till the neck of the sac is approached. After making sure that the sac is empty of
its contents, the neck of the sac is incised and closed by ligature. The gap in the linea alba is closed
with nonabsorbable sutures. The skin flap is replaced in position and sutured.
3. PARAUMBILICAL HERNIA OF ADULTS.— In adults the hernia does not protrude through
the umbilical cicatrix. It is a protrusion through the linea alba just above the umbilicus (supraumbilical)
or occasionally below the umbilicus (infraumbilical). That is why it is called paraumbilical.
The contents of the hernia are usually greater omentum often accompanied by small intestine or by
a portion of the transverse colon. In majority of cases the sac becomes loculated due to adherence of
the omentum to its fundus. That is why paraumbilical hernia is seldom reducible.
CLINICAL FEATURES.— Women are by far the major victims and are affected 5 times more
frequently than men. Obese patients are mainly involved and they are usually above 40 years of age.
Obesity, flabbiness of the abdominal muscles and repeated pregnancy are the predisposing factors.
Symptoms.— Pain and swelling are the main symptoms.
1022 - A CONCISE TEXTBOOK OF SURGERY
Some sort of discomfort or pain is often complained of when the hemia is quite small. Such pain
gets worse by prolonged standing or heavy exercise. Pull on the omentum often gives rise to gastrointes
tinal symptoms. Transient attacks of intestinal colic may be present as there may be subacute intestinal
obstruction.
Swelling obviously attracts patient’s notice when there is not much pain. Gradually the swelling
increases and often attains a big size.
On examination.—
(i) Position.— The main bulge of the hernia is mostly just above the umbilicus through the linea
alba or occasionally below the umbilicus through the midline.
(ii) Consistency.— The lump is firm as it contains mostly omentum. On percussion it is dull. If
it contains small bowel, it may be resonant.
(iii) When the contents are not adherent this hernia becomes reducible and expansile cough impulse
becomes also evident but unfortunately in many herniae the contents are adherent so the herniae become
irreducible and impulse on coughing is absent.
TREATMENT.— Operation is the treatment of choice. Gradually, as time goes on, the hemia
becomes irreducible and eventually strangulation may occur. So no attempt should be made for
conservative treatment. If the hemia is symptomless and the patient is obese, it is advisable to reduce
the weight and the operation can be postponed for sometime till the weight has been reduced to a
respectable order.
Mayo’s operation is usually practised. A practical point to be remembered in connection with this
type of hernia is that there are adhesions between the sac and the contents (coils of intestine or omentum)
mostly at the fundus. The neck of the sac remains free from adhesions. This makes the principle of the
operation that the hernial sac is reached at the neck first.
MAYO’S OPERATION.— A transverse elliptical incision is made around the umbilicus. The subcu
taneous tissues are dissected off the rectus she&th to expose the neck of the sac. The sac is opened at its
neck as adhesions are least here. The contents are freed from adhesions at the fundus of the sac and returned
to the abdomen. Sometimes adherent omentum cannot be freed from the fundus of the sac. In that case
the omentum is ligated and removed with the sac. The whole circumference of the neck is gradually incised.
The fundus of the sac alongwith the redundant skin is removed. The peritoneum of the neck of the sac
is closed with catgut stitches. The gap in the linea alba is extended laterally for one inch or more for sufficient
overlapping. Now a row of mattress sutures are tied so that the lower margin is lifted up deep to the upper
margin for about 2 inches and the upper margin of the linea alba is made to lie over the lower margin
of the linea alba. The upper margin of the linea alba is now sutured over the lower flap by interrupted silk
sutures. In fat patients, who ooze blood and liquid fat, a drain may be provided with at the end of the wound.
The subcutaneous tissue and the skin are approximated as usual.
Postoperatively one must care to relieve the patient of cough or from other causes of increased intra
abdominal pressure.
EPIGASTRIC HERNIA (SYN. FATTY HERNIA OF THE LINEA ALBA)

When a hernia protrudes in the midline through the interlacing fibres of the linea alba anywhere
between umbilicus and xiphisternum, it is called an epigastric hernia. Majority of cases occur midway
between umbilicus and xiphisternum. It occurs through the same opening where the linea alba is pierced
by small blood vessel. Such type of hernia begins as a protrusion of extraperitoneal fat and that is why
it is also called ‘fatty hernia of the linea alba’.
As the hernia grows bigger, it drags a pouch of peritoneum after it and it becomes a true epigastric
hemia. The mouth of the hernial sac is usually quite narrow and it does not permit any viscus to enter
the hernial sac, only a small portion of greater omentum may enter it.
HERNIAS 1023
Aetiology.— It seems that sudden strain helps to bring out such hernia. Such strain will lead to
tearing of the interlacing fibres of the linea alba. That is why this hemia is mostly restricted to young
muscular men majority of whom are manual workers.
Clinical features.— Epigastric hernia usually presents itself in one of the three clinical types.
(i) Symptomless.— Epigastric hernia is often symptomless and may be discovered by the patient
only as a swelling during washing his own body.
(ii) Painful swelling.— Sometimes patient with epigastric hernia complains of a localised pain
exactly at the site of the hernia. Pain often gets worse on physical exertion. Occasionally the fatty content
may be pressed upon by the tight margins of the gap in the linea alba to produce partial strangulation.
In these cases the swelling will be tender and patients will feel pain on wearing tight clothings.
(iii) Referred dyspepsia.— Patients with epigastric hernia may give symptoms which mimic peptic
ulcer, though there is actually no such ulcer. Patient might not have noticed the swelling even. Peptic
ulcer may be present in cases of epigastric hernia and such ulcer must be excluded. Patient may complain
of pain after eating possibly due to epigastric distension. Such dyspepsia may also be due to epigastric
hernia.
PHYSICAL EXAMINATION.— Epigastric hernia feels firm and does not usually have a cough
impulse and cannot be reduced. For this, it becomes difficult to distinguish epigastric hernia from lipoma.
Only occasionally when a sac is present, expansile impulse and reducibility may be noticed.
Treatment.— Operation is only justified if the hernia is giving rise to symptoms.
OPERATION.— A long midline vertical or transverse incision is made over the swelling. The
incision must be adequate as the gap in the linea alba must be viewed properly. The incision is deepened
till the fatty protrusion of hemia is detected. '
The protruding extraperitoneal fat is dissected clear from the hernial orifice by gauze dissection.
The pedicle is ligated and the fat distal to the ligation is excised. The gap in the linea alba is repaired
with nonabsorbable suture.
If a small peritoneal sac is present, it is opened to see if there is any content or not. If a small portion
of omentum is the content, it is dragged out and examined to exclude partial strangulation. If partial
strangulation is there the portion of omentum is excised after ligation. If the portion of omentum is healthy
it is pushed back into the peritoneal cavity. The sac is ligated and excised. The gap in the linea alba
is repaired with nonabsorbable suture.
If the gap in the linea alba is big, it should be repaired by overlapping transversally (as Mayo’s
operation) or longitudinally. Skin is closed as usual.
BURST ABDOMEN AND INCISIONAL HERNIA

BURST ABDOMEN (Abdominal dehiscence).—
When an abdominal wound gapes open or disrupts, the condition is called burst abdomen. The
incidence of burst abdomen following abdominal operation is approximately 1% to 2%. This is usually
seen between the 6th and 9th day after operation. But disruption of the wound occurs earlier in the
deeper layers. So in case of partial disruption, where only deeper layers gape, the superficial layers remain
apposed even after removal of sutures, there is a possibility of developing incisional hernia.
THE FACTORS WHICH ARE INCRIMINATED TO CAUSE BURST ABDOMEN ARE :
A. Factors relating to the patients —
(i) Obesity.— This is a single important factor in the development of burst abdomen and incisional
hernia. Fatty omentum and excessive subcutaneous tissue provide increased strain on the operative wound
during early healing. The muscle mass and muscle tone of these individuals are often inadequate with
fat encroaching between the muscle fibres. This causes inadequate strain of the muscle and fascia to
compensate for the added strain. An attempt at weight reduction is often recommended prior to operation.
Moreover there are increased potential for pulmonary complications and wound infection.
(ii) Advanced age is also an important factor in both burst abdomen and incisional hernia. The
tone of the muscle decreases considerably with age which seems to be the reason to form this
complication.
(iii) Multiparity, (iv) Malnutrition, (v) Peritoneal dialysis, (vi) Jaundice, (vii) Hypoproteinaemia,
(viii) Anaemia, (ix) Malignant disease — are all important factors which contribute to the development
of burst abdomen and incisional hernia.
(x) Coughing and vomiting in the early postoperative period followed by removal of the endotra
cheal tube and suction of the laryngopharynx impose tremendous strain on the sutures. Overzealous
ventilation in the early postoperative period in sedated patient may also lead to wound disruption.
(xi) Certain medications have been demonstrated to lead to poor wound healing. Steroids and
chemotherapy are two important drugs in this group, which impair and delay the normal healing process
to cause burst abdomen and incisional hernia. So drug history is important and must not be missed.
B. Faults of the surgeon.—
(i) Choice of incision.— Midline and vertical incisions tend to heal slowly and are liable to disrupt
more than transverse incisions.
(ii) The type of operation.— Operations on pancreas and peritonitis are liable to cause burst
abdomen or develop subsequent incisional hemia. The surgeon must keep this in mind while closing
the abdominal wound and through-and-through tension suture should be applied.
(iii) Method of closure.— Interrupted and through-and-through suturing of the abdominal wall has
low incidence of burst abdomen than continuous suturing of layers. Interrupted far and near single layer
mass closures are particularly recommended in peritonitis cases, operations on pancreas, obese patients
who are vulnerable to burst abdomen and subsequent incisional hernia.
(iv) Choice of suture material.— Obviously use of non-absorbable suture material lessens the chance
of burst abdomen than that in case of use of absorbable suture material. Nowadays polypropylene or
polyamide sutures are quite competent to prevent burst abdomen.
(v) Drainage through the main abdominal wound often causes burst abdomen. So when drainage
is required, it should be employed through a separate stab incision.
Clinical features.— It is twice as common in men than in women. It is more often seen in patients
over 60 years of age. As a rule this condition occurs suddenly. The surgeon is often summoned hastily.
In many cases there is no warning of this catastrophe, but patients may have complained of ‘something
has given way’ or unusual soakage of the abdominal dressing with serosanguineous fluid. It is the most
pathognomonic sign of this condition and it signifies that some intraperitoneal contents are lying
extraperitoneally and the muscle sutures have already given way. This usually occurs between the 6th
and 10th postoperative days. Wound dehiscence actually starts a few days earlier, as at this stage the
sutures of the deep layers have already given way. The patients may present with shock, rise in pulse
rate and temperature. There may be signs of gross dehydration. These usually occur if an occult
dehiscence has been overlooked for more than 24 hours. Alternatively a boggy swelling may be noticed
in the abdominal wound in case of such occult dehiscence. There may be even symptoms and signs of
intestinal obstruction in late cases.
Management.— Burst abdomen is a case of surgical emergency and the nurse in-charge of the
operation theatre should be immediately informed to make the theatre ready for the operation. The
anaesthetist is called for immediately. The abdominal wound should be immediately covered with a sterile
towel wrung out of warm saline. This in turn is covered with cotton wool and firm binder. A nasogastric
tube should be inserted to decompress the stomach and intravenous fluid therapy should be started
immediately. While resuscitating the patient, he should be taken to the operation theatre. Once the
anaesthetist approves and the patient’s condition becomes stable immediate operation should be undertaken.
OPERATION.— Under general anaesthesia the sterile pack is removed. The abdominal wound is
covered with sterile packs and the surrounding skin is cleansed and painted with antiseptic solution. The
HERNIAS 1025
abdomen is draped. The sutures are taken away. Any protruding contents of the abdomen are gently
washed with normal saline and pushed into the abdomen with warm wet mop. The anaesthetist is asked
to relax the abdominal muscles by giving muscle relaxants. Now the abdominal wound is resutured. All
layers of the abdominal wound are approximated by through-and-through interrupted sutures of braided
nylon or polypropylene passed through, a soft rubber tube or plastic tube. The sutures are started about
an inch (2 to 3 cm) away from the edge of the wound. Mattress sutures are used and passed through
soft rubber or plastic tubes before tying, so that these sutures cannot cut out through the skin and to
minimise tension on the suture line. One must be very careful to see that no portion of the bowel is
being trapped in the wound and then these sutures are tightened. The usual technique is to apply all
the sutures first and then they are tied one after another from above downwards. The wound margins
are then apposed with interrupted silk or nylon sutures. There must be a gap between the skin sutures
to allow drainage to come out. The abdomen is dressed with thick pad of gauze pieces and an abdominal
binder. Very occasionally there may be gross abdominal distension and it will be difficult to appose the
wound margins. In these cases decompression of the bowel by retrograde milking of the intestinal contents
into the stomach and nasogastric aspiration may ease the process of closure of the wound. After the
abdominal wound is sutured, it is supported by strips of adhesive plaster covering about anterior 2/3rds
of the circumference of the abdomen. Parenteral antibiotic therapy is started immediately. The sutures
are kept for longer period of approximately a fortnight. Gastric decompression and intravenous fluids
are rigidly continued until the peristalsis of bowel can be properly heard. Early ambulation is not much
encouraged after this operation, but movements of the legs are encouraged.
After closure of abdominal dehiscence, it produces a stronger wound. Healing is usually satisfactory,
which seems to be due to improvement in collagen metabolism. Chance of second dehiscence is extremely
rare. Incisional hernia may occur as a late sequel.
The prognosis of wound dehiscence is grave and becomes worse with advancing age. The outcome
is better if it is detected earlier and treated immediately, while the wound is still clean and prolapse
of intestine has not occurred. Prognosis worsens due to delay in diagnosis.
INCISIONAL HERNIA (SYN. Ventral Hemia or Postoperative Hemia)

An incisional hernia is one which occurs through an acquired scar in the abdominal wall caused
by a previous surgical operation, or an accidental trauma. Scar tissue is inelastic and can be stretched
easily if subjected to constant strain.
Aetiology.—
1. Defect with the patient.—
(i) Obese individuals with lax muscles.
(ii) Patients suffering from chronic cough, which may continue in the early postoperative period
and will lead to incisional hernia.
(iii) Undue abdominal distension in the early postoperative period.
(iv) Malnutrition — patients with severe anaemia, hypoproteinaemia or Vitamin C deficiency may
predispose to incisional hernia.
2. Fault during operation.—
(i) Injury to the motor nerves supplying the area. Certain incisions are vulnerable to cause nerve
injury e.g. Kocher’s subcostal incision for cholecystectomy often inflicts injury to the 8th, 9th and 10th
intercostal nerves; Battle’s pararectal incision for appendicectomy; McBurney’s incision for appendicectomy
may injure the subcostal or ilioinguinal nerve.
(ii) Particular care was not taken during closure of the wound particularly the deeper layers.
(iii) Haemostasis was not perfect or the tissues were manhandled, so that early postoperative
infection was the result.
(iv) Tube drainage through the laparotomy wound.
65
(v) Certain incisions are more liable to cause incisional hemia e.g. midline infraumbilical incision
for caesarean section.
3. Postoperative causes.—
(i) Infection.— This seems to be the commonest cause.
(ii) Postoperative cough and distension.
(iii) Postoperative peritonitis due to more chance of wound infection.
(iv) Too early removal of sutures.
(v) Steroid therapy in the postoperative period.
Pathology.—
(a) Often the incisional hernia starts unnoticed and symptomless with partial disruption of the deeper
layers of a laparotomy wound during very early postoperative period. So careful closure of the wound
is extremely important to prevent incisional hernia. There may be some oozing of serosanguineous
discharge through the laparotomy wound, but this is more of a signal of wound dehiscence or burst
abdomen rather than of incisional hernia.
(b) Wound infection often causes disruption of sutures thus the muscles are separated by weak scar
tissue. A portion of the muscles may also be destroyed by infection which are resolved afterwards by
fibrosis. This also causes weak scar. Through this weak scar incisional hernia occurs.
HISTORY.—
A previous operation or a trauma is often noticed. Patient may give a history of wound infection.
Age.— Incisional hernia may occur at any age, but more common in fatty elderly females.
SYMPTOMS.—
The commonest symptoms are the swelling and the pain. Sometimes attacks of subacute intestinal
obstruction may occur leading to abdominal colic, vomiting, constipation and distension of the abdomen.
Strangulation, though uncommon, is liable to occur at the neck of a small sac or in a locule of a large
hernia.
ON EXAMINATION.—
The old scar is seen with the swelling. The hernia may occur through a small portion of the scar,
often the lower end. Often a diffuse bulge may occur involving the whole of the scar. Usually the swelling
is reducible and an expansile cough impulse is present. The defect in the abdominal wall is often palpable.
It may so happen that the hernia is irreducible. Such cases become difficult to diagnose. These cases
must be differentiated with (differential diagnosis) :
(i) A deposit of tumour.
(ii) An old abscess.
(iii) A haematoma.
(iv) A foreign body granuloma.
Types of incisional hernia.— Two distinct types of incisional hernia should be recognized, as the
principles of treatment are different in these two cases.
(a) IN TYPE I, this hernia is situated in the upper abdomen or in the midline of the lower abdomen.
There is a wide gap in the musculature which is easily recognized and whose margin is smooth and
regular. This hernia reduces spontaneously as soon as the patient lies down. So mostly it is a reducible
hernia. This type of hernia takes the form of a diffuse bulge. Risk of strangulation is almost negligible.
These herniae can be treated by simple abdominal corsets.
(b) IN TYPE II, this hernia is situated in the lateral part of the abdomen. The defect in the
musculature is relatively small and irregular. The contents are normally both bowel and omentum. These
are usually matted together and are adherent to loculated peritoneal sac. There are usually multiple loculi.
So this hernia is partially or wholly irreducible. As the muscular defect is small, risk of strangulation
is high.
HERNIAS 1027
Treatment.—
1. PREVENTIVE TREATMENT.— A few preoperative measures should be carefully adopted to
lessen the chance of incisional hernia. These are :
(a) If the patient is obese, weight should be reduced by dieting if an elective operation has to be
performed.
(b) If the patient has a tendency of chronic bronchitis, it should be treated first.
(c) During operation one must be very careful in closure of the abdomen. Deeper layers must be
sutured with due respect.
(d) All precautions should be adopted to prevent immediate postoperative wound infection.
2. CONSERVATIVE TREATMENT.— There is hardly any scope for conservative treatment in cases
of incisional hernia. Conservative method may be only tried in type I cases if they are reducible. This
method cannot be adopted if the hernia is irreducible. After reducing the hernia a belt is fitted with a
suitable pad so that the hernia does not get an opportunity to come out. If such treatment is continued
for a long time without giving a chance of hernia to come out, there is a possibility of cure. Moreover
this treatment may be applied to those type I cases where operation is contraindicated due to the general
condition of the patient.
3. OPERATIVE TREATMENT.— This is always indicated in type II cases and irreducible type
I cases. Operative treatment is also justified when conservative method has failed. In fact majority of
the cases of incisional hernia need operation sometime or the other.
OPERATION.— An elliptical incision is made enclosing the area of unhealthy skin. The outer edges a
undermined. Now the incision is deepened to the aponeurosis. The unhealthy skin is gradually dissected
sac, which is nothing but a redundancy of peritoneum. The sac is not opened. If the sac is loculated and
it is better to open the sac around its neck. The contents are freed. Adherent omentum may be ligated an
alongwith the sac. Any adhesions involving the bowel should be separated as far as practicable before th
contents are returned to the abdomen.
Repair of the hemia depends on the type of hemia and its size. Followings are the different methods o
which may be applied :—
1. ANATOMICAL RESTORATION.— This is suited for small herniae with minimal scar. The edges of th
defect are carefully dissected and each layer e.g. the peritoneum, the muscle layers or the aponeurosis is
sufficiently. These layers are sutured individually without tension with non-absorbable sutures.
2. APPROXIMATION OF THE RECTUS SHEATH.— This is only performed in case of midline herniae,
particularly below the umbilicus. Here also each layer is separated individually. The peritoneum is first s
The anterior rectus sheaths are now freed from the underlying rectus muscles. The rectus muscles of bot
are sutured in The midline. Some overlapping may be done. Now the anterior rectus sheath is sutured in
if possible by overlapping. To reduce tension one may have to make release incision vertically on the late
of the rectus sheath.
3. KEEL OPERATION.— In this operation the hemial sac is not opened but is pushed back into the ab
With non-absorbable sutures it is pleated so that it projects into the abdominal cavity. A few layers of su
applied one after the other till the healthy margins of the muscles and aponeurosis are brought close. No
margins of the healthy muscles and aponeurosis are sutured to each other. As in this operation the hern
pushed into the peritoneal cavity in a pattern which on cross-section looks like the ‘keel’ of a ship, this o
is called ‘keel operation’.
4. CATTELL’S OPERATION.— In this operation the hemial sac is dissected out with equal care as has
described in the earlier operations. But the sac is opened. The viscera are reduced after freeing the contents
the sac. The peritoneum is repaired. The edges of the abdominal wall are now approximated and are sutu
thick chromic catgut or better with non-absorbable suture material layer by layer. After the surrounding
has been sutured, an incision is made half inch away from the suture line. The medial edges of this incis
sutured over the previous line of suture and the lateral margins are now sutured over this medial layer o
This is continued till the edges of the healthy aponeurosis are brought together firmly.
5. REPAIR BY FASCIAL SUTURES OR SKIN RIBBON.— This operation is more or less similar to
hemioplasty. This type of repair is necessary when the muscular defect is considerable and cannot be clo
tension. The peritoneum is freed and is sutured. The other layers in the margin are separated particularl
layers. The defect is closed with the fascial sutures in an interlacing manner from muscles of one side to the muscles
of the other side. The interlacing suture is made in the form of Lattice work or ‘dam’.
6. MESH CLOSURES.— These are becoming increasingly popular. The incision and the sac are dealt with
similarly as done in the previous operations. The deficiency in the abdominal wall is easily made good without
tension by laying and stitching a sheet of Tantalum gauze or a Mesh made of Dacron or marlex or polypropylene
to the surrounding aponeurosis. Polypropylene mesh and expanded polytetrafluoroethylene (PTFE) are mostly used
nowadays successfully in the repair of incisional hernias. Repair with synthetic mesh is only advised when the
defect is very large and cannot be closed effectively by autogenous tissue. It cannot be used routinely as there is
increased chance of infection. Collection of oozing fluid inside the wound acts as a good nidus of infection. The
following points should be considered whenever a synthetic mesh is used :
(i) Asepsis should be maintained at all costs.
(ii) Too much handling of the tissues should be minimised.
(iii) Haemostasis must be carefully maintained.
(iv) Even the pre-sterilized mesh should be handled as little as possible.
(v) The extra mesh may be used in another patient only after autoclaving. Not more than two autoclavings
should be advised.
(vi) The mesh should be placed as deeply as possible. It should be used as an onlay on the sutured peritoneum.
Under no circumstance the intestine should be allowed to come in contact with the mesh lest dense adhesions should
form. The recti muscles and anterior rectus sheath should then cover the mesh completely. The mesh should not
be used just under the skin.
(vii) The mesh should be sutured all round with fine prolene sutures.
(viii) A suction drainage in the form of Redivac should always be used to aspirate the oozing fluid and thus
to prevent infection.
(ix) Local antibiotics and postoperative parenteral antibiotics should be used.
(x) Nasogastric decompression and intravenous fluid should be continued postoperatively. Nothing by mouth
is allowed till bowel sounds are heard.
(xi) Early ambulation is not encouraged, but ijiovements of the legs and exercises of the legs are encouraged.
(xii) Patient must not resume work or strenuous exercise for 6 months.
After mesh repair recurrence rate is considerably low in these hemiae upto 10% in comparison to 45% after
direct suture or by using autogenous tissue. These are becoming increasingly popular. Tantalum gauze is now
replaced with materials such as Marlex or Mersilene. PTFE is quite expensive. Two points should be borne in mind
— (a) the prosthesis should be implanted deep to the muscles of the abdominal wall on top of the posterior rectus
sheath or fascia transversalis; and (b) the prosthesis should extend far beyond the borders of myoaponeurotic defect.
7. MUSCLE PEDICLE FLAPS.— Defect in the lower abdominal wall below the umbilicus may be reconstruc
ed using active and viable muscle belly. Two muscles are particularly suitable for this purpose. These are the tensor
fascia lata and the rectus femoris.
Postoperative care.— Gastric decompression and intravenous fluid are the key points in postoperative care.
Nothing should be given by mouth till the peristalsis returns. Early ambulation is not much encouraged, though
leg movements are advised. The patient should not do any strenuous exercise for 6 months.
DIVARICATION OF RECTI
This condition means that the two recti muscles separate from each other and a good gap exists
between the two recti muscles.
Causes.—
(i) Multiple pregnancies.
_(ii) Repeated midline abdominal operations, in which the linea alba may stretch.
Anatomical pathology.— The two recti are inserted to the pubis close to each other, but their
origins are quite apart from the anterolateral aspects of the lower ribs. When the recti contract the
upper portions tend to move apart from each other. Moreover contraction of the oblique and transverse
abdominal muscles is added to this. So it is not surprising that the recti can separate a few inches
from each other if the linea alba is weak.
HERNIAS 1029
Clinical features.— This condition is principally seen in elderly multiparae.

During straining, abdominal contents bulge through the gap between the two recti muscles.
On examination one can easily detect the gap between the two recti, through which fingers can
be introduced.
A similar condition of divarication of recti may be seen in babies particularly above the umbilicus.
Treatment.— As this condition is usually symptomless and there is hardly any danger of
obstruction or strangulation, operation is usually not advised.
An abdominal belt should be advised.
In case of children also no treatment is required as spontaneous cure is almost inevitable as the
child grows.
LUMBAR HERNIA
There are three types of lumbar hernia. The first two are primary lumbar herniae which come
out through the superior lumbar triangle and the inferior lumbar triangle. The 3rd one is an acquired
lumbar hernia and is better called an ‘incisional lumbar hernia’.
1. Superior lumbar hernia.— This is rarer than the inferior lumbar hernia. Superior lumbar
hernia is protrusion of abdominal contents through the superior lumbar triangle, which is bounded
above by the 12th rib, medially by the sacrospinalis and laterally by the posterior border of the obliquus
internus abdominis.
2. Inferior lumbar hernia is more common than the superior one and the hernia protrudes
through the inferior lumbar triangle or lumbar triangle of Petit. This triangle is bounded below by
the crest of the ilium, medially by the anterior border of the latissimus dorsi and laterally by the
posterior border of the obliquus externus abdominis.
3. Incisional lumbar hernia may occur in the lumbar region — (a) following an operation or
an infected kidney or drainage of lumbar abscess, in which the wound gets infected post-operatively
OR
(b) Following paralysis of the muscles of the lumbar region either due to injury of the nerve
supplying these muscles or due to poliomyelitis. This is also known as phantom hernia.
Clinical features.— Patient complains of a swelling in the typical lumbar region.
On examination there is soft swelling which corresponds to the superior or inferior lumbar
triangle. The swelling is reducible. It may be reduced by itself when the patient lies down. Impulse
on coughing is also present.
When there is reducibility and impulse on coughing diagnosis may not be difficult, yet the
following conditions should be kept in mind.
(i) Lipoma.— It is a firm or soft swelling, which moves easily over the taut muscles. It is not
reducible and there is no impulse on coughing. On moving the swelling, one will see puckering of
the skin.
(ii) Cold abscess pointing to this region.— Paravertebral cold abscess may become superficial
through the lumbar triangle. This condition very much mimics lumbar hernia. It gives rise to a soft
cystic swelling. Fluctuation test is positive. This swelling is not reducible. But cough impulse may
be present. X-ray of the thoracic and lumbar spine is confirmatory.
(iii) Phantom hernia due to local muscular paralysis — discussed above.
Treatment.— Primary lumbar hernia is treated by herniotomy and repair of the gap i.e.
herniorrhaphy.
Incisional hernia or phantom hernia is treated as incisional hernia (discussed earlier).
OBTURATOR HERNIA
It is an extremely rare condition. It means hernia occurs through the obturator foramen traversed by the
obturator vessels and nerve. This obturator foramen is wider in females and that is why it is about 6 times more
common in women.
Clinical features.— Most of the patients are old women above 60 years of age who have lost considerable
fat.
The condition is difficult to diagnose, since the swelling is covered by the pectineus and no definite swelling
can be seen even in the Scarpa’s triangle. The hemia becomes only apparent when the limb is flexed, abducted
and rotated outwards. The patient usually keeps the limb in the semiflexed position and movements increase pain.
Obturator hernia often gets strangulated as it comes out through an opening surrounded by osseoaponeurosis.
In about Vi the cases of strangulation, pain is referred along the obturator nerve to the knee joint of the corresponding
side by its articulate branch.
Only rectal or vaginal examination can detect the tender swelling in the region of the obturator foramen.
Richter’s hemia is quite common.
Treatment.— Operation should always be performed as strangulation is very common.
Abdominal approach is usually preferred by lower paramedian incision as the condition is often discovered
only after laparotomy which has been performed for intestinal obstruction. The obturator foramen is widened and
the hernia is pulled in after the abdomen has been properly mopped to prevent contamination from the toxic fluid
of the hernial sac. The obturator vessels are always vulnerable of being injured. If the hemia cannot be released
from the abdomen or the diagnosis has been made before operation, the femoral approach may be employed.
Femoral approach.— A vertical incision is made extending downwards from the inguinal ligament 2 cm medial
to the femoral vessels. The adductor longus is retracted medially. The pectineus muscle is separated or divided
to expose the obturator extemus. The hernial sac is usually found lying on the surface of this muscle having emerged
along its superior border. The sac and the contents are dealt with in the similar manner as strangulated hemia and
herniorrhaphy is performed by repairing the gap in the obturator foramen.
OTHER UNIMPORTANT RARE HERNIAE

Gluteal hernia.— This hernia extrudes out through the greater sciatic foramen either above or below the
piriformis muscle.
Sciatic hernia.— This hernia occurs through the lesser sciatic foramen. In the differential diagnosis of
gluteal and sciatic herniae one should remember (i) a cold abcsess, (ii) a lipoma, (iii) a gluteal aneurysm,
(iv) fibrosarcoma beneath the gluteus maximus.
Spigelian hernia.— It is a type of interparietal hernia occurring at the level of the arcuate line just lateral
to the rectus muscle.
The extraperitoneal fat alongwith the hernial sac lies just deep to the internal oblique muscle or may advance
to reach the gap between the external and internal oblique muscles. Only a slight swelling can be detected.
Treatment.— Operation is the treatment. Incision is made on the swelling just lateral to the rectus muscle.
After incising skin and subcutaneous tissue, external aponeurosis is split to expose the hernial sac. The sac is
isolated and the contents are reduced. The sac is ligated and excised. The transversus and oblique muscles are
repaired.
Perineal herniae.— In this case hernia occurs through the pelvic floor. It is extremely rare and occasionally
seen in —
(i) Postoperative hernia through the perineal scar following excision of rectum.
(ii) Pudendal hernia when the hernia occurs as a swelling of the labium majus.
(iii) Ischiorectal hernia, in which the hernia passes through the levator ani into the ischiorectal fossa
through hiatus of Schwalbe.
1031
CHAPTER - 49
THE KIDNEY AND URETER
EMBRYOLOGY.— Kidney develops as a part of development of urogenital organs. Three organs — 1. Pronephros, 2.
Mesonephros and 3. Metanephros develop one after another in time and space to form the excretory system.
(1) Pronephros.— This cannot be distinguished as a separate organ in man. The earliest and most cranially situated nephric tubules
are considered to be the pronephros in human being. These nephric tubules are rudimentary and transient. The pronephros merges caudally into
the mesonephros without a clear line of demarcation. The pronephros disappears completely by the 4th week of embryonic life.
(2) Mesonephros.— Mesonephros develops into mature excretory organ in higher fish and amphibians. It is the principal excretory
organ during the 4th to 8th week of embryonic life. In early stage it consists of nephric tubules which extend to the third lumbar segment. By
the end of the 6th week the mesonephros forms an elongated spindle-shaped organ which projects into the coelomic cavity on each side ofthe
dorsal mesentery. At this time it extends from the septum transversum to the third lumbar segment. This organ is called mesonephric ridge or
wolffian body. The cephalic end of the mesonephros atrophies and disappears, it only exists in the first three lumbar segments. The nephric
tubules of the mesonephros end into a primary excretory duct which is known as mesonephric duct or wolffian duct. This mesonephric duct
runs distally in the lateral part of the mesonephric ridge and then approaches the urogenital sinus to open into the ventral part ofthe cloaca which
forms the vesico-urethral portion. The mesonephric duct itself becomes the canal of epididymis, the ductus deferens and the ejaculatory duct
in the male and in the female it becomes a vestigious organ and forms the longitudinal duct of the epoophoron.
The mesonephros also does not play role in the development of kidney. In fact it atrophies and disappears except a few upper tubules
which may persist as the superior aberrant ductules or the appendix of the epididymis. A few lower tubules may also persist as the paradidymis
in the male and paroophoron in the female.
When the embryo is of 5 mm in length an outgrowth takes place from the dorsimedial aspect ofthe mesonephric duct near the point where
it opens into the cloaca. This outgrowth is known as ureteric diverticulum. It gradually grows dorsally and upwards.
(3) Metanephros.— Blind extremity ofthe ureteric diverticulum grows into the caudal end ofthe metanephros which condenses around
it and forms the metanephrogenic cap. So metanephros is the mass of tissue which is situated below the wolffian body into which projects the
ureteric diverticulum. The presence of the ureteric diverticulum is important for differentiation of the mesoderm of the metanephros to form the
metanephrogenic cap. So in case of agenesis of kidney there will be no ureter, as ureteric diverticulum is developed first and which stimulates
the metanephrogenic cap to form the secretory part of the kidney.
The stalk of the ureteric diverticulum becomes the ureter and its expanded end forms the pelvis of the kidney, the calyces and the
collecting tubules of the kidney. The upper blind end of the ureteric diverticulum expands to form the renal pelvis. As this primitive renal pelvis
comes in contact with the metanephrogenic cap it branches into primary tubules that in tum branch to form secondary tubules. The secondary
tubules then form tertiary tubules, and the branching goes on until approximately 12 generations of tubules are found. The primary tubules
develop into major calices of adult kidney, the tubules of the 2nd to 4th generation fuse to form minor calyces. Those of the 5th generation form
the papillary ducts and the higher orders form the several generation of collecting tubules. The metanephrogenic cap forms the renal corpuscles,
the secreting and convoluted tubules. So human kidney develops from two different organs — its excretory part is formed by the dilated upper
extremity of the ureteric diverticulum, which is in fact a mesonephrogenic origin and its secretory part is formed by the metanephrogenic cap
or from metanephros. Some surgeons believe that failure of fusion between these two parts may lead to the development of congenital polycystic
kidney (theory of Hildebrandt).
In the early stage the kidney is a lobulated organ and in each lobule there is a separate secretory and excretory unit. Such lobulated
appearance persists throughout the foetal life, but disappears in the first year of life by moulding. If lobulated appearance persists, the condition
is called foetal lobulation.
ROTATION OF KIDNEY.— As the kidney moves upwards, it undergoes a rotation, so that the renal pelvis which in the embryo looks
anteriorly, comes to face medially with major calyces projecting laterally. Occasionally such rotation may fail to occur to cause congenital
anomaly of the kidney.
ASCENT OF KIDNEY.— As development of embryo proceeds, the testis descends, but the kidney ascends. When the kidney first appears,
by the junction of expanded upper extremity of the ureteric diverticulum and the metanephrogenic cap, it is in the pelvis. The urteric diverticulum
gradually lengthens and grows upwards, so that the kidney reaches the second lumbar vertebra when the length of the embryo is about 15 mm.
As the kidney ascends it receives blood supply from arteries in its immediate neighbourhood e.g. middle sacral, common iliac arteries and
abdominal aorta. It is not before the 3rd month that it receives the definitive arterial supply from the renal artery from the lower pail of the
suprarenal arteries which constitutes a lateral splanchnic artery. The whole process signifies that there may be additional arteries to the kidney
besides the renal artery. They may enter the hilum of the kidney or at the upper or lower pole of the kidney.
Development of ureter.— The ureteric diverticulum forms as an outgrowth from the dorsimedial aspect of the mesonephric duct. Due
totiifference in rates of growth, the ureteric diverticulum gradually comes to the lateral aspect ofthe mesonephric duct. The whole ofthe ureter
is formed by the upward growth of the ureteric diverticulum. After it has completed its upward extension, two portions of ureter show a little
bit of distension — lumbar distension and pelvic distension. The lumbar distension appears during the 5th month, whereas the pelvic distension
develops in the 9th month. In between the distensions there is a constricted part of the ureter as it crosses the brim of the pelvis. There is another
constriction at its upper end at the pel viureteric junction. There is one more most constant constriction at its lower end where it enters the bladder
wall. So the three constrictions in the ureter are — (i) at its upper end at the pelviureteric junction, (ii) where it crosses the pelvic brim and (iii)
at its lower end where it passes through the bladder wall. The caudal ends of the ureteric diverticula of both sides become incorporated in the
developing bladder and form the trigone ofthe bladder. The openings of the ureters become separated from each other. There is also absorption
of the mesonephric ducts, so that the openings of these ducts are shifted further distally to take the final position at the prostatic urethra. The
two ureters open into the upper lateral angle ofthe trigone of the bladder. But the mesonephric ducts open into that part of the urogenital sinus
which subsequently becomes the prostatic urethra.
CONGENITAL ANOMALIES OF THE KIDNEY AND URETER
A CONGENITAL ANOMALIES OF THE KIDNEY.—

1. Agenesis of kidney.— Absence of kidney on one side is often associated with absence of ureter. This
will be revealed by pyelography that one kidney is absent and cystoscopy will reveal absence of one ureteric
orifice. Occasionally ureter and pelvis may be present but the kidney is absent. In both these cases the present
single kidney becomes hypertrophied and functions almost double the normal to make good the absence of one
kidney.
2. Hypoplasia and dysplasia.— When the metanephrogenic cap fails to develop properly, such
condition may develop when one kidney becomes small and less functioning.
Dysplasia is the term used when the secretory part of the kidney develops abnormally to form different
types of tissues including cartilage and small cysts.
3. Supernumerary kidney.— There may be more than one kidney on one or both sides.
4. Duplex kidney and ureter.
5. Foetal lobulation.— This has been described above (in Embryology — Metanephros).
6. Defcct in the position of kidney or ectopic kidney.—The left kidney is more often seen to be ectopic
than the right one
(i) PELVIC KIDNEY.— This is due to failure of ascent of kidney. It is usually detected by chance
and hardly requires any treatment. Occasionally such kidney may be associated with hydronephrosis, when
treatment will be required. Such pelvic kidneys usually derive segmental arterial supply from common iliac
artery, internal iliac artery and abdominal aorta Usually the opposite kidney lies in normal position.
(ii) CROSSED RENAL ECTOPIA.— Both kidneys are situated in one loin and they become fused.
The kidney which has crossed to the opposite side carries its own blood vessels. Its ureter usually crosses the
midline and opens into the bladder in normal position. Generally the upper pole of the crossed kidney fuses
with the lower pole of the normally placed kidney. Sometimes the ureter of the ectopic kidney may open into
the same side of the bladder as the normal one and then there is often chance of reflux of urine leading to
hydroureter and hydronephrosis of the crossed kidney. Sometimes the pelvis of the crossed kidney faces
laterally giving rise to unilateral S-shaped kidney.
(iii) ROTATED KIDNEY.— Thekidney may rotate abnormally so that its pelvis faces forwards instead
of medially. It does not produce any symptom as such, but a confusing radiographic appearance may elude the
clinician.
7 Fused kidney.— Three types are found :—
(i) Horse-shoe kidney is caused by fusion of lower poles of both kidneys with a bridge.
(ii) Unilateral fused kidney or crossed renal ectopia — This has been described under crossed renal
ectopia.
(iii) S-shaped kidney.
8. Cystic disorders of the kidney.— Not all cysts of the kidney are of congenital origin. Cysts are quite
common in the kidney. They arise from the collecting tubules by dilatation, obstruction or as outpouches or
diverticula. Followings are the different types :—
(i) Polycystic kidney — bilateral condition.
(ii) Medullary sponge kidney.
(iii) Unilateral multicystic kidney.
(iv) Solitary renal cyst.
9. Congenital hydronephrosis — see under hydronephrosis.
10. Aberrant renal vessels.— From the development of kidney it is clear that there may be an aberrant
renal artery supplying the kidney. Such aberrant artery is usually small and insignificant, but occasionally it
may be large and become significant due to the fact that it supplies a segment of the kidney. Such artery is more
THE KIDNEY AND URETER 1033
often seen supplying the lower pole of the kidney. This artery may be associated with hydronephrosis, whether
it causes hydronephrosis by compressing the pelviureteric junction or it simply accompanies it, is a point of
debate. One must be very careful in dividing such aberrant artery as it may cause infarction ofthe corresponding
segment of the renal tissue if it be the only arterial supply to that region.
Aberrant renal artery is more often seen on the left side and it is more common in females.
There may be aberrant renal vein but its significance is much less than aberrant renal artery and it is also
less common. Moreover due to venous collateral circulation its importance is insignificant.
11. Renal arteriovenous fistula may be congenital in 25% of cases.
12. Congenital disorders of functions of the renal tubules.—
(a) PROXIMAL TUBULAR DISORDERS —
(i) Cystinuria.— This is a mendelian autosomal recessive disorder in which four aminoacids —
cystine, ornithine, arginine and lysine (‘COAL’) are excessively excreted in the urine. About 500 mg to 1
g. of cystine is excreted in the urine daily by these patients. These patients are prone to develop cystine stones
which are radio-opaque due to sulphur content.
(ii) Fanconi's syndrome.— In this condition there is failure of absorption of a cluster of aminoacids
as well as phosphate which results in proteinurea and acidosis.
(iii) Vitamin-D resistant rickets.— Here the proximal tubules fail to reabsorb phosphate from the
glomerular filtrate, this results in rickets which cannot be cured by simple administration of Vitamin D
(b) DISTAL TUBULAR DISORDERS —
(i) Renal tubular acidosis.— In this condition the distal tubule is unable to reabsorb water and to
secrete ammonia. Instead it excretes large amounts of water containing sodium, potassium and calcium. There
is marked disturbance in the acid-base mechanism with severe loss of bicarbonate and corresponding retention
of chlorides. There is excessive mobilisation of calcium from bone in response to acidosis. Calcium is
precipitated in the tubules causing speckled calcification in the renal medulla which is known as
nephrocalcinosis’. Due to excessive loss of calcium and phosphate osteomalacia develops. The treatment is
to give potassium bicarbonate to replenish additional loss of postassium. Vitamin D should also be prescribed
to combat calcium loss. Additional calcium in the form of calcium chloride can also be given.
(ii) Nephrogenic diabetes insipidus.— In this condition the distal tubules fail to respond to
antidiuretic hormone (ADH). There is excessive diabetes and the patient becomes dehydrated, which affects
children very much.
B CONGENITAL ANOMALIES OF THE URETER—
1. Absence of one ureter.— It is also associated with absence of the kidney of that side It is due to failure
of development of the ureteric diverticulum.
2. Duplication.—
(i) Duplication of renal pelvis.— In this condition the ureter is divided at its upper part to form two
renal pelves. This anomally is quite common and this is also more often found on the left side. The upper renal
pelvis is smaller and only drains the upper group of calyces, whereas the lower renal pelvis is bigger in size
and drains the middle and lower groups of calyces.
(ii) A ureter may be double in its entire length except in its lower-third where they fuse to form a single
ureter. In that case cystoscopy reveals only one ureteric opening on that side.
(iii) The ureter may be double in its entire length with two separate openings in the bladder on that side
This is less common than the previous anomaly. The peculiarity of this condition is that the ureter which drains
the upper pelvis crosses its fellow and opens below and medial to it. The lower opening may be in an ectopic
position — in the posterior urethra, vagina or vulva.
3. Ectopic ureteric orifice.— This condition occurs when a second ureteric diverticulum comes out
from the mesonephric duct later than the usual time and lower than the usual position. It is almost always
associated with complete double ureters. The ectopic ureteric orifice usually drains the upper part of the pelvis.
It is described later in this section.
4. Congential megaureter.— This is a peculiar condition in which the ureter is not only dilated but its
1034
wall is also thickened. The lower end of the ureter and orifice appear normal. Reflux is also very negligible.
Two peculiar abnormalities noted in this condition are — vigorous peristaltic activity in the dilated segment
ofthe ureter and marked delay in emptying of the pelvis and ureter.
This condition is seen more often in males. Other congenital abnormalities may be present. This
condition is often symptomless. This is only revealed if infection supervenes this congenital anomaly.
Treatment. — This is only required when the case has been infected. Nephrostomy is first performed to
control infection. This is followed by reimplantation of the ureter into a fresh portion of the bladder by
tunnelling to prevent reflux. If the kidney has been grossly damaged by infection, nephroureterectomy should
be performed. It should be remembered that this condition may be bilateral In this case cutaneous ureterostomy
5. Stenosis or atresia of the ureter.— Valves or folds may also cause obstruction to urine in the ureter.
6. Retrocaval ureter.
7. Ureterocele.— This condition is a cystic enlargement of the intramural portion of the ureter caused
by congenital atresia of the ureteric orifice. Another theory is that the medial part of the wolffian duct is not
completely absorbed into the trigone and remains as a thick balloon-like covering for a ureter. This constitutes
ureterocele. The wall of the cyst is usually composed of mucous membrane only, but occasionally muscle coat
may be present.
This condition is more often seen in adult life although occasionally it may be found in children. This
condition is mainly unilateral but in about l/10th of cases it may be bilateral. Females are more often affected
than males.
This condition is usually presented as a case of urinary obstruction. Ureterocele presses on the ureteric
orifice and causes such obstruction. Urinary obstruction leads to stone formation and recurrent ascending
infection. Intravenous urography will reveal typical adder-headed appearance of the lower ureter. Sometimes
simple obstruction of the ureteric orifice will be evident in I. V.P. Cystoscopic examination will reveal a typical
translucent cyst at the ureteric orifice over which blood vessels will be seen to radiate. Occasionally cyst may
be opaque when it contains muscle layer in the wall. With each reflux of urine through the ureteric orifice the
swelling will be seen to enlarge and then the swelling will gradually reduce in size. Occasionally ureterocele
may prolapse through the urethra to cause acute retention of urine
Treatment.— Only when this condition is associated with hydronephrosis, stone formation or recurrent
infection, treatment is necessary. Incision of the ureterocele with a diathermy electrode is first performed.
Micturating cystogram is performed after 3 months to see if there is any urinary reflux. If reflux is present then
the ureter has to be reimplanted into another portion of the bladder by tunnelling. Only in advanced unilateral
cases where the kidney is almost destroyed by recurrent infection, hydro or pyonephrosis, nephroureterectomy
A few conditions ofcongenital anomalies require special mention and elaborate description. These are:—
HORSE-SHOE KIDNEY
About 1 out of 1,000 individuals has some type of renal fusion, of which the most common is horse
Aetiology.— Fusion of the two metanephroi occurs early in embryonic life when the kidneys lie low in
For this reason horse-shoe kidney cannot ascend to the high position of normal kidneys. In fact, horse
move above the origin of the inferior mesenteric artery. Usually the bridge joining the lower poles lies in
lumbar vertebra. Occasionally it may remain in the true pelvis.
Pathology.— Fusion usually occurs when the embryo is about 30 to 40 days old when the metaneph
both sides lie very close to each other. As the fusion occurs quite early, normal rotation of the kidney c
each pelvis lies on the anterior surface of the organ. The ureter rides over the isthmus to traverse the a
the fused portion. Some degree of ureteral obstruction is inevitable. There may be aberrant renal vessels. Due
two factors, incidence of hydronephrosis is high. Infection of the kidney is also very high. Tuberculosis has a
more often in horse-shoe kidney than normal. Calculus formation of the kidney is also common in this co
It must be remembered that the isthmus usually joins the lower pole of each kidney of horse-shoe
rare occasions the upper poles may be fused.
Symptoms.— (i) Majority of patients with fused kidneys have no symptom.

(ii) A few however develop ureteral obstruction.
(iii) Infection, hydronephrosis, calculus formations in the kidney may also give rise to various coi
(iv) Gastro-intestinal symptoms mimicking peptic ulcer, cholelithiasis or appendicitis have been
be due to renodigestive reflex.
Physical signs.— These are usually negative, except a lowly placed renal mass may be felt. In majori
such mass is usually felt in front of the 4th lumbar vertebra.
Special Investigations.— Except excretory urography, no other special investigations can diagnose this
positively.
Excretory urogram shows good renal function.
(i) The renal pelvis lies on the anterior surface of its respective kidney mass, whereas in normal
lies medial to the kidney mass. This is due to defect in normal rotation of the kidney. In urography thi
by superimposition of the shadow of the renal pelvis on that of the calyces.
(ii) The most valuable clue to the diagnosis of this condition is the presence of calyces in the low
points medially (towards the vertebral column). Sometimes majority of the calyces may direct medially
calyces look laterally.
In majority of cases the ureters curve like a flower-vase.
Tomograms will clearly outline the renal mass.
Renal scanning will also delineate the renal mass as sonography will do.
COMPLICATIONS.—
(i) Ureteral obstruction.
(ii) Hydronephrosis.
(iii) Calculus formation.
(iv) Infection, including tuberculosis.
Treatment.— No treatment is necessary unless complication forces it. Drainage of a horse-shoe kidn
improved by dividing the isthmus. If there is stone formation, treatment is directed towards that line.
horse-shoe kidney is badly damaged due to infection or tuberculosis, which is not curable by medicine
surgical excision or partial nephrectomy. Such operation may be needed in case of stag-hom calculus
UNILATERAL MULTICYSTIC KIDNEY

This condition is mainly seen in new bom babies and in contradistinction to much common condit
kidney, it is unilateral. More than half the patients are belowthe age of 5 years. It is non-hereditary an
by irregularly lobulated mass of cysts. The ureter is usually absent or atretic in the affected side.
It may develop due to faulty union of the nephron and the collecting system.
The only finding is the discovery of an irregular mass in the flank.
Urography does not reveal anything characteristic to help in the diagnosis. The cystic nature of th
revealed by sonography. Even this condition can be diagnosed in uterus by ultrasonography.
POLYCYSTIC KIDNEY
It is an hereditary disease and almost always bilateral (95%). The disease does not manifest itself before
40 years of age. The disease encountered in infancy is different from this condition, as this one is an autosomal
recessive condition and life expectancy is short. Whereas polycystic kidney is an autosomal dominant
condition.
This condition is often associated with cysts of the liver, spleen and pancreas.
Aetiology and pathogenesis.— This condition occurs due to defect in the mechanism of joining between
the uriniferous tubules and the collecting tubules. This is the junction-failure theory of Hildebrandt. The blind
secretory tubules which are connected to functioning glomeruli become cystic. As these cysts enlarge, they
compress adjacent tissues and gradually occlude normal tubules.
The upper expanded portion of the ureteric diverticulum divide for a few generations to form collecting
tubules. Some urologists believe that the primary set of collecting tubules may become degenerated and cystic
to form polycystic kidney.
Pathology.—
1036
(i) This is mostly a bilateral condition (95%), although one side may be more advanced than the other.
(ii) The kidney is enlarged to 3 or 4 times the normal size.
(iii) The kidney is studded all over with cysts. The cysts are thin walled and the yellowish or red coloured
contents may be seen through it.
(iv) On section the cysts vary considerably in size. Although occasionally they may open one another,
but they do not open into the renal pelvis unless the wall of a cyst has been destroyed.
(v) The content of the cyst varies — it may be thin or thick or viscid. The colour is yellowish, amber
coloured or dark brown due to haemorrhage.
(vi) Although the content is not urine, yet it may occasionally contain uric acid and other organic
constituents of the urine.
Microscopically, the lining of the cysts consists of a single layer of cells, which are flattened in case of
large cyst, whereas these are cubical or even columnar in case of small cysts. The intervening kidney tissue
shows changes like chronic interstitial nephritis with peritubular fibrosis.
I. IN THE FOETUS huge abdominal lump may be so great as to cause normal delivery almost
impossible.
II. IN CHILDREN.— Occasionally children with this condition are stilborn or die of uraemia soon
alter birth. This condition usually becomes evident within one or two years with bilateral renal swellings, which
has to be differentiated from Wilms’ tumour and congenital hydronephrosis.
III. IN ADULTS.—In majority of cases the patients remain well until the 4th or 5th decade after which
symptoms then develop and bring the patient to the surgeon.
(i) Swelling.— Often the patient presents with complaints of swelling of the abdomen or he discovers
a mass in the abdomen. This he may complain on one side only, probably the side with bigger kidney. It must
be remembered that a bigger kidney does not necessarily mean that the kidney is pathological. It may be that
the other kidney is pathological, which is non-palpable and the palpable large kidney is nothing but
compensatory hypertrophy as the other kidney is non-functioning.
(ii) Pain.— Pain over one or both kidneys may occur due to drag on the vascular pedicles by the heavy
kidneys. Such pain is a type of dull ache, felt in the loin. Tension on the renal capsule by the enlarging cysts
may also cause dull ache in the loin. Rarely this condition may be presented with colicky pain due to stone
formation or clot retention. Three types of pain may be complained of in this condition — (a) dull ache pain,
(b) colicky abdominal pain and (c) an acute abdominal pain due to rupture of a large cyst on the surface of the
kidney.
(iii) Haematuria.— In l/4th of the cases haematuria is noticed. This may occur as the cysts rupture into
the renal pelvis. Haematuria may be severe, which is not uncommon and lasts for a few days or maybe moderate
(iv) Hypertension.— In about 3/4th of cases hypertension has been noticed. The actual cause of this
hypertension is not yet known.
(v) Infection.— This is quite common in this condition. This is often revealed by chills, fever and renal
pain Vesical irritability may be the first complaint. Repeated attacks of pyelonephritis is quite common in this
condition.
(vi) Uraemia.— When renal insufficiency ensues, headache, anorexia, nausea and vomiting may be
complained of. Drowsiness and weakness are also noticed. It may be that no other symptoms were complained
of before till the signs of uraemia suddenly start developing after 40 years.
PHYSICAL SIGNS —
In general examination, hypertension is noticed in about 70% of cases. Anaemia, loss of weight and
evidence of uraemia may be detected.
Local examination only reveals palpably large one or both kidneys. The palpable kidneys feel nodular.
If infected, they may be tender.
1. Blood.— Anaemia is often detected. N.P.N. and urea level may be high in cases of uraemia.
2. Urine.— A high output of urine is very characteristic with low specific gravity(1.010 or less). Urine
may contain a slight trace of albumin. A considerable delay in the excretion of indigocarmine is noticed
Haematuria and proteinuria are not uncommon. Pus cells and bacteria are found when infection has
supervened
3. X-RAY.—
Straight X-ray.— Both renal shadows are enlarged as much as 5 times the normal size in plain film.
Excretory urography.— It is the best investigation to diagnose this condition.
(a) There is considerable delay in excretion of the dye. Infusion urograms with tomography are more
helpful
(b) The renal masses are usually enlarged in all directions.
(c) The renal pelvis is elongated and compressed. The calyces are enlarged and stretched over the cysts,
which look like legs of a spider, hence called ‘spider-leg deformity’. Such urographic picture is also noticed
in space occupying lesion of the kidneys e.g. tumours, but in these cases the spider-legs or the stretched calyces
are irregular and often abruptly cut. But in polycystic kidney the outlines of stretched calyces and elongated
renal pelvis are smooth.
Retrograde urography may be required if excretory urography fails to show clear picture.
Angiography is not that important but may reveal bending of small vessels around the cysts and
non-vascular ‘negative’ shadows of the cysts.
4. Ultrasonography appears to be superior to excretory urography in diagnosing this condition. Presence
of multiple renal cysts becomes visible, some of which may contain fluid or altered blood.
5. Isotope scanning will reveal multiple cold’ avascular spots in large renal shadows.
Complications.—
(i) Pyelonephritis is a very common complication of polycystic kidney. It may be asymptomatic, pus
Cells may be few or even absent in the urine. Gallium67 citrate scan will reveal the sites of infection including
abscess.
(ii) Infection of cysts is usually associated with pain and tenderness over kidney. There may be various
types of febrile response.
(iii) Haematuria may be brisk and persistent to endanger life.
(iv) Hypertension is present in about 70% to 80% of cases. The actual cause is not known. It may be due
to a separate genetic factor which is linked with polycystic kidney.
(v) Renal insufficiency and uraemia.
Treatment.—
If there be no unusual complications which may require surgery, the general treatment is conservative.
A. CONSERVATIVE TREATMENT.— The patient is placed on a low protein diet and is forced to take
large quantities of fluid (3,000 ml or more per day). Strenuous activities should be stopped. Iron may be
prescribed to prevent anaemia and antibiotics to prevent infection. When the patient is in state of absolute renal
insufficiency, treat for uraemia.
B. SURGERY —
Rovsing's operation.— There is no definite evidence that excision or decompression of cysts improves
renal fimction. But if a large cyst is found to be compressing the upper ureter, it may resected or aspirated.
Some surgeons claim that by incising the cysts, the renal luction improves a lot. Rovsing’ s operation is designed
to expose the cysts and they are incised with a narrow bladed scalpel. First the cysts on the convex border of
the kidney are incised, followed by cysts on the posterior surface and finally the cysts on the anterior surface.
One kidney is operated on first followed by the other in the same sitting.
Treatment of complications.— If bleeding from kidney is severe as to threaten life, nephrectomy or
embolisation of the renal or one segmental artery should be considered.
Pyelonephritis is vigorously treated with antibiotics. Care must be taken to prevent renal damage.
Infection of cysts requires surgical drainage.
When renal insufficiency becomes life-threatening, chronic dialysis or renal transplantation may be
required.
Prognosis — When the disease affects children, it has a very poor prognosis.
In case of adult, prognosis is somewhat more favourable. But these patients usually do not live longer than
5 to 10 years after the diagnosis is made, unless dialysis or renal transplantation is made available.
SOLITARY RENAL CYST

Simple solitary cyst of the kidney is unilateral condition. Though called ‘solitary’, there may be a fe
present in the kidney. It is also a disease of adult life and usually occurs over the age of 40 years.
Aetiology and Pathogenesis.— Whether this cyst is congenital or acquired is not very clear. A few theori
be put forward.— (i) Congenital theory.— The origin of this cyst, according to this theory, is very much similar
of congenital polycystic kidney.
(ii) Retention cyst.— According to some pathologists it is a retention cyst either due to interstitial nephr
to blockage of a tubule by infection. The age at which this condition is mostly seen probably favours th
(iii) Traumatic theory.— This has of course lowest number of advocates. This condition may arise from b
trauma or a haematoma may be converted into a cyst.
Pathology.— In majority of cases such cysts usually involve the lower pole of the kidney. The cyst usu
a clear amber fluid which is serous in nature and contains albumin and salts, rarely urea. In about 5%
be haemorrhagic and about half of these patients have papillary cancers on their walls. So haemorrhag
cyst should be taken as suspicious of malignant condition. The wall of the cyst is quite thin. Occasiona
the cyst may be seen.
Simple cysts are usually superficial but may be deeply situated. When it is deeply situated, the cys
to the pelvis or calyces, but the cyst does not communicate with the renal pelvis.
Adjacent renal tissue is compressed and fibrosed.
COMPLICATIONS —
(i) A solitary cyst may be so placed as to compress the upper ureter causing progressive hydrone
(ii) Infection of the cyst is not unusual.
(iii) Haemorrhage into the cyst occasionally occurs.
(i v) The cyst compresses and gradually destroys the surrounding renal parenchyma. But rarely a
of renal tissue may be destroyed to cause renal insufficiency and uraemia.
SYMPTOMS.— (i) Solitary cyst may remain small and asymptomatic.
(ii) Pain in the flank or back in the form of a dull ache is not uncommon. The pain may be severe o
is bleeding inside the cyst causing distension of the cyst wall. The cyst may become infected when the p
of pain in the loin with malaise and fever.
(iii) Swelling.— The patient occasionally discovers a lump in the flank or loin,although cyst of this siz
(iv) Cyst may press on the upper ureter or pelviureteric junction to cause urinary symptoms.
(v) Gastrointestinal symptoms are frequently noted like those of peptic ulcer or gallbladder diseas
PHYSICAL SIGNS.— These are usually normal except a mass in the region of the kidney may be pa
percussed. Tenderness in the kidney region is only noted if the cyst is infected.
RADIOLOGY.— (i) Straight X-ray may show expansion of a portion of kidney shadow. Streaks of calcium
seen on the cyst wall.
(ii) Excretory urography shows filling defect with one or more calyces stretched over the space occu
The pelvis may be indented or bent around the cyst. If the cyst is in the lower pole, the upper part of th
more medially. The space occupying filling defect is seen with smooth border in contradistinction to a s
lesion due to renal neoplasm in which the filling defect will be seen irregular.
Computed tomography.— This appears to be accurate in differentiating renal cyst from tumour.
Renal sonography is also of high value in diagnosing renal cyst.
Treatment.—
Percutaneous needle aspiration of the cyst should be done under fluoroscopic or sonographic control. Clear fl
from aspiration is probably not dangerous, yet it should be subjected to cytologic examination. Now the
is aspirated and it is replaced with a radio-opaque fluid. Films are taken in the various positions to see
wall is smooth or not. Any excrescences may mean presence of tumour. Now 3 ml of pantopaque (iodop
into the cystic cavity. This will decrease the chance of reaccumulation of fluid.
If aspirate reveals blood, immediate nephrectomy or partial nephrectomy (in case of papilliferous ne
be considered as in majority of cases blood means presence of malignant growth.

Kirwin’s method.— If the aspirate is clear fluid, exploration is hardly required. But Kirwin’s method
technique in which recurrence of cyst is impossible. The kidney is explored, the portion of the cyst wall
kidney surface is excised. The cyst cavity is now filled with perinephric fat and the cut edges of the cys
The wound is closed with a corrugated drain.
MEDULLARY SPONGE KIDNEY

It is an hereditary disease carried by autosomal recessive gene.
The basic pathology is widening of the distal collecting tubules causing cystic dilatation of the rena
tubules. It is usually a bilateral condition, but occasionally it may be unilateral.
Clinical features.—The condition itself is asymptomatic, but symptoms are seen when the condition is
by infection and stone formation.
Excretory urogram is highly diagnostic. Though the pelvis and calyces are normal, yet dilated tubules ma
lateral to them. The dilated tubules may contain round masses of radio-opaque material. If stones are p
be revealed in plain film.
(i) Tuberculosis.
(ii) Papillary necrosis.
(iii) Nephrocalcinosis from hyperparathyroidism or renal tubular acidosis.
COMPLICATIONS —
(i) Infection.
(ii) Calculi formation due to urinary stasis in the tubules.
TREATMENT —
Medullary sponge kidney as such requires no treatment. Treatment is only required if it is infected
calculi.The overall prognosis is good.
ECTOPIC URETERIC ORIFICE.— In rare instances the ureter opens at a part other than the normal u
orifice. This is usually due to the fact that a second ureteric diverticulum arises from the mesonephric
than usual. Such ectopic orifice may be present in different places in both sexes.
IN CASE OF FEMALES.— In females the ectopic orifice usually opens distal to the external sphincte
dribbling and incontinence are almost inevitable.The diagnosis can be made from history, in which a gi
history that she is dribbling since childhood (as long as she can remember), yet she has a desire to void
The diagnosis can be established by giving intravenous injection of indigocarmine and placing a swab in
another in the vagina. The positions of ectopic orifice in females are —
(a) Into the urethra just below the sphincter urethrae.
(b) Into the vagina.
(c) Into the apex of the trigone (extremely rare).
IN CASE OF MALES.— In males the ectopic ureteric orifice is usually situated above the sphincter u
the patients are usually continent. Posterior urethroscopy or intravenous injection of indigocarmine is h
ectopic ureter. The usual positions of ectopic ureteric orifice in male are —
(a) Apex of trigone.
(b) Posterior urethra.
(c) Seminal vesicle.
(d) Ejaculatory duct.
(e) Rectum (very rarely).
Treatment.—
In females, where incontinence is almost always associated with this condition, treatment is to resect lo
portion of the ureter and to reimplant it into the urinary bladder. However if the affected portion of the
by ectopic ureter is hydronephrotic and chronically infected to cause severe parenchymal damage, that
kidney has to be excised.
In males, no treatment is needed if the kidney is not damaged. Partial nephrectomy orheminephrectom
of the affected part of the kidney is only required if hydronephrosis or chronic urinary infection has cau
parenchymal damage.
SPECIAL INVESTIGATIONS OF THE URINARY TRACT
A. LABORATORY EXAMINATIONS.—
1. Blood count— (a) Hypochromic anaemia may occur in association with chronic pyelonephritis
(b) Leucocytosis, particularly polymorpholeucocytosis, is a feature of majority pyogenic infections o
tuberculosis of the kidney there will be increased lymphocytes in the blood and there will be increased
(c) Erythrocytosis has been seen in association with a few renal diseases e.g. carcinoma, simple cys
rosis. The erythropoietin level in the plasma is increased. After curative surgery the erythropoietin leve
return to normal. Again if metastasis occurs the red cell count increases.
2. Examination of the urine.— PROPER COLLECTION OF URINE.— In both men and women,
bacteria and a few pus cells. So urine specimen taken casually will be contaminated with normal uret
In men, ‘midstream’ specimen should be taken. For this he should retract the prepuce, cleanse the gla
urination into the urinal. First part of urination is supposed to properly cleanse the urethra, the next
sterile glass test-tube. Thus a midstream specimen is taken.
In women, a nurse should assist the patient to collect the midstream urine. The patient lies in the lith
The labia are held apart and the vulva and labia are cleansed properly with antiseptic solution. After t
urine has been rejected, the midstream is collected in a sterile container. Catheterisation is very helpf
specimen of urine in case of women.
(a) MICROSCOPIC EXAMINATION — of the sediment may reveal white cells, red cells, pus cells, cry
casts.
Staining of the sediment is helpful to detect organisms present in urine. Finding of bacteria in a st
there are at least 10,000 organisms per ml and this is pathognomonic of infection.
For pyogenic organism, tripple-strenglh methylene blue stain is used. Gram’s stain is of limited value in th
urinary infection.
For acid-fast bacilli Ziehl-Neelsen test is the best. It reveals tubercle bacilli in 70% to 80% of cases.
remembered that if urine contains pus. but reveals no bacteria on staining, that means ‘sterile pyuria
tuberculosis of the urinary tract.
(b) CULTURES FOR BACTERIA.— Culture and sensitivity test is significant not only to know the typ
but also to know the sensitivity of the bacteria to particular antibiotic. This helps a lot in treatment of
urinary infection. Culture of tubercle bacilli is a lime consuming procedure, but it is a definite proof o
tuberculosis.
(c) BIOCHEMICAL EXAMINATIONS — for electrolytes, glucose, bilirubin and haemoglobin are essen
sis of 24-hours specimen of urine is especially useful in the investigation of calculus disease to find ou
tion of oxalate, uric acid, calcium and other products of metabolism.
(d) OTHER TESTS OF THE URINE.—
(i) Urinaiy pH.— Normal kidneys contribute to the control of body pH by excreting urine in the pH
7.5. The figure 4.5 is typical of diabetic acidosis, readings above 7.5 mean the presence of urea-splitti
are causing renal alkalosis.
(ii) Cytologic examination by papanicolaou technique is quite effective to find out transitional cell neopla
renal pelvis or ureter or bladder.
(iii) Hormone test.— This also helps to detect various diseases. Estimation of chorionic gonadotrophin
testicular tumour assists to detect presence or absence of particular type of testicular tumour. Presen
various hormones in the urine also indicate prognosis of breast cancer. Determination of the amounts
oestrogen, corticosteroids, pituitary gonadotrophins in the urine is helpful to detect certain endocrine
(e) DIPSTICKS.— Nowadays various dipsticks (multistix or labstix) impregnated with chemicals are
these sticks change colour in presence of sugar, protein, nitrites etc. If the urine is macroscopically cl
dipstick testing, the chance of finding of these elements in urine is negligible.
RENAL FUNCTION TESTS.— It must be remembered that about 75% of the kidney function should
following tests to become positive. So renal damage must be considerable before changes occur in blo
Renal damage is mainly of 3 types, which are rellected in the renal tests. These are — (I) Reduction of
as found in renal artery stenosis or severe hypertension. (II) Destruction of glomeruli which becomes e
cortical necrosis or glomerulonephritis. (Ill) Impairment of tubular function as evident in pyelonephrit
nephropathy, back pressure on renal parenchyma causes all these 3 types of damages.
(i) Urine specific gravity— This is a simple and significant test of renal function. Normal kidneys can
urine to 1.040 at the age of 40 years and 1.030 at the age of 50 years. Fluid is withheld for 12 hours a
gravity of the first two morning specimens should be about 1.020 to 1.025. A litre of water is given by mo
hours the specific gravity of urine will come down to 1.002. A fixed specific gravity of 1.010 in both these
indicate impaired function of distal renal tubules.
(ii) Blood urea level is normally between 3 to 6.5 m mol/1 or 15 to 40 mg/100 ml of blood. When urinar
normal and unobstructed, the plasma urea : creatinine ratio is 10 : 1. If this ratio rises to 20 or above, it
stasis and diminished renal blood flow. So this ratio is a good screening test to detect kidney function. In
limits of blood creatinine is 1.4 mg/ 100 ml. Blood creatinine level is a sensitive test of renal function.
(iii) Endogenous creatinine clearance.—The creatinine clearance is roughly equal to twice the excretion of th
the first Vi an hour. Endogenous creatinine clearance approximates the glomerular filtration rate and its
between 90 to 140 ml/minute. Creatinine clearance gives an idea about glomerular filtration rate, but th
accurate. To assess glomerular function, clearance of chromium-51-labelled ethylenediaminetetra-acetic
(iv) PSP TEST.— The patient is instructed to pass urine. 1 ml of phenolsulfonaphthalein (containing 6
is given intravenously. The patient should drink no more than 200 ml of water during each of the 2 subs
periods. Urine specimens are collected after Vi an hour the average amount of dye normally recovered in
specimen is 50 to 60% and in 2nd Vi hour speciincn is about 10 to 15%. The normal total is about 60 to
normal PSP excretion in children is aboul 5 to 10% higher than in the adult. The PSP test is a test of ren
tubular function.
(v) Serum electrolytes.— Estimation of various serum electrolytes gives suggestion as to the status of ren
B. ROENTGENOGRAPH1C EXAMINATIONS (RADIOLOGY).—
1. Straight X-ray.—
Preparation of the patient.— No food or fluids should be given to the patient for at least 6 hours before X-
examination. A purgative is given at the night before. Enema is sometimes prescribed but it is probably l
Plain film of the abdomen is taken ofthe kidney, ureter and bladder region (KUB region).
It gives a clue to the diagnosis if properly studied.
(a) KIDNEY — size can be assessed from this film. Congenital absence or unascended kidneys can be d
Similarly an enlarged kidney from hydronephrosis, polycystic disease or renal cancer can be diagnosed. A
extends from the top of the 1st to the bottom of the 3rd or middle of the 4th lumbar vertebra. In 90% of c
kidney is lower than the left because of displacement by the liver. Localised swelling as may be caused by
tubercular cyst, a simple cyst or a tumour can be diagnosed.
(b) STONES.— Majority of the urinary calculi are radio-opaque except the pure uric acid stone which i
It is very difficult to assess the exact position of the radio-opaque stone in straight X-ray of the abdomen.
visualisation of the urinary tract with radio-opaque dye is necessary. Numerous small calcific bodies in t
the kidney may suggest tuberculosis or medullaiy sponge kidney or nephro-calcinosis caused by hyperpa
About 7% of malignant renal tumours contain some calcification. A renal calculus has to be differentiated
gallstone, (ii) calcified lymph nodes, (iii) calcified costal cartilage, (iv) phlebolith, (v) calcified aneurysm of
nal aorta or renal artery and (vi) small calcific bodies in the substance of a kidney as discussed above. A
appendix or a faecolith in the colon may be confused with a stone in the ureter. It must be remembered that f
diagnosis of a stone either in the kidney, ureter or bladder, a straight film is all that is required and not a urogram. Even
dense round shadows in urogram may not be due to stone. They are often caused by the depth of the dye
calyces (i.e. those directed anteriorly or posteriorly).
The characteristics of a renal stone are : (i) That a renal calculus moves with respiration which can be verifi
taking two exposures, one at full inspiration and the other at full expiration, (ii) Density of a renal stone i
whereas gallstones are less dense in the centre, (iii) Renal stones take the shape of the renal pelvis and c
solitary gallstone may be round and multiple gallstones are squeezed into the gallbladder and become fac
lateral view the renal stone lies superimposed on the shadow of the vertebral column, whereas gallstones
of the vertebral bodies.
Ureteric stone is usually oval and lies in the line of the ureter. It is an imaginary line passing along the
transverse processes of the lumbar vertebrae, over the sacro-iliac joint, down to the ischial spine from wh
deviates medially. VesicaI calculi are seen just above the symphysis pubis. The prostatic calculi appear as sm
behind the symphysis pubis.
(c) PSOAS SHADOWS are normally seen quite distinctly. Obscure psoas shadows mean perinephric ha
abscess or cold abscess.
(d) BONES should be carefully noticed to detect any arthritic change or presence of metastases (either
commonly seen in a renal carcinoma or osteoblastic — commonly seen in prostatic carcinoma). Arthritic
well lead to radicular pain which may mimic a renal pain.
66
(e) TOMOGRAPHY will enhance the renal and psoas outlines thus clarifying renal size and sha
zones of calcification invisible in the plain film. A space-occupying lesion of the renal pelvis revealed
urogram may show a faint opaque body compatible with stone but not tumour in the tomogram stu
2. Excretory urograms.—
This is probably a better nomenclature than intravenous pyelography (IVP), since this does not o
of the pelvis of the kidney, but also ofthe kidney, calyces, ureters and the urinary bladder.
Preparation of the patient has been described earlier in this section. A straight X-ray of the abd
KUB region) is first taken. Then the radio-opaque fluid is injected intravenously. Generally Hypaque
or Urografin is injected. Adult dose is about 20-25 ml. Injection is made slowly. Preliminary test of h
always performed. Subcutaneous injection of 0.1 nil ofthe contrast medium is made. If induration a
promptly the test is positive. If symptoms and signs of hypersensitivity appear during injection, it s
immediately. Warning signs are respiratory difficulty, itching, urticaria, nausea, vomiting and fainti
of oxygen and intravenous dextrose for shock, intravenous injection of antihistaminic drug and intr
barbiturates for convulsion.
Routine radiograms are taken at 10 seconds for nephrogram effect and at 5, 10 and 15 minutes
supine position. For hypertensive patients films should be taken 2 and 3 minutes after the schedul
concentration of dye in one kidney may suggest decreased renal blood flow and function. At 25 min
erect posture to note the efficiency with which the renal pelvis and ureters drain, ureterograms and
kidneys. All films should incl tide kidneys, ureters and bladder areas, as fine changes in the ureters
of vesico-ureteral reflux may be detected. It is advisable to inject additional radio-opaque medium if
concentration in the initial films.
In infants and children the films should be taken at 3,5,8 and 12 minutes as their kidneys excr
than do those of the adult.
X-ray of the bladder region after voiding should be routine in all urologic patients. At the conclu
study, the patient is instructed to pass urine and a film of the bladder area is taken immediately. T
presence or absence of residual urine.
Excretory urogram is contraindicated in (i) allergic patients, (ii) multiple myeloma (the dye makes insoluble
with Bence-Jones protein and precipitate in the renal tubules), (iii) congenital adrenal hyperplasia,
primaiy hyperparathyroidism.
Excretory urogram is a physiological as
as an anatomical test since it not only deter
the function of the kidney but also clearly
demonstrates the contour of the renal pelvis
calyces.
NEPHROTOMOGRAPHY.— Accurate
visualisation of the kidney and pelvicalycea
system is possible by this technique. The
overlying gas and faecal material in the bow
can be eliminated in this method. Slices of k
are seen beginning from posteriorly and
gradually advancing anteriorly. Fat and cys
more readily identified by lucent areas. Thu
poorly prepared patients can be investigated
this technique.
3. Retrograde urograms.—
INDICATIONS.— (i) Inadequate excretoiy
urograms which have failed to demonstrate the
renal pelvis, calyces and the ureters adequa
this investigation will be required, (ii) Impaired
renal function which has failed to show the pelv
and calyces, this test is needed, (iii) Sensitivity
intravenous contrast medium is the definite
indication for this test, (iv) If pyuria is present
cadieterization of the ureters may be needed
obtain separate specimens from each kidne
bacteriological study and then retrograde urograms may be performed, (v) Since in intravenous urogram
may not be sufficient for oblique and lateral radiograms, retrograde urogram may be required.
PROCEDURE.— (a) Preparation of the patient is similar to that of excretory urogram except for the
may be allowed to take fluids unless general anaesthesia is to be employed, (b) Cystoscopy and uretera
performed, (c) Preliminary straight X-ray of the abdomen is taken to know the positions of the catheters
already discussed earlier, (d) 25%sodium diatrizoate (Hypaque) is used as the contrast medium and 3 to
to delineate normal size pelvis. For hydronephrosis more amount of medium is required, (e) Supine uro
and viewed. If filling is not complete, more dye is instilled before further X-rays are taken, (f) Oblique, la
radiograms are taken as indicated, (g) Pneumopyelography.— To differentiate between a non-opaque st
tumour of the renal pelvis, 4-6 ml of air is instilled into the catheters. A stone may show some opacifica
not, but both these will cause a filling defect in the pelvis or calyx in excretory urogram.
4. Antegrade urogram.—
The clinical indication for this test is inadequate information from intravenous urogram with an un
impossible retrograde examination. Under fluoroscopic or ultrasonic control an 18-gauge needle, 15 cm
passed into a dilated calyx or pelvis. Radio-opaque dye should then be instilled and appropriate films a
to pass the needle into a dilated calyx rather than pelvis as there will be a better seal round the needle
of puncturing large hilar vessels. Temporary drainage can also be provided with by a small plastic cath
through the needle, which will be subsequently removed. The tube now acts as nephrostomy tube.
FINDINGS.— All urograms, be it excretory, retrograde or antegrade are read in the following manne
A. Nephrogram.— From the soft tissue shadow of the kidney, various congenital deformities can be d
tumour or cyst can be suspected. The position and size can be assessed.
B. Calyces — A normal calyx looks like a cup due to projection of the apices of the papillae into the c
calyces are directed outwards. Inward directed calyces suggest congenital abnormality such as horse-s
C. Pelvis.— The size, shape and position of the pelvis are noted. The lower border of the pelvis
with the lower calyx. The right pelviureteric junction is situated opposite the transverse process of the s
vertebra whereas the left is slightly higher up. The most important is the shape of the pelvis and the stu
normal shape of the pelvis.
D. The ureter.— Usually the upper portion of the ureter is visualised. If the whole of the ureter is seen
obstruction further down. Note the shape — whether dilated or not. Dilated ureter indicates obstruction
reflux. Also look at the position of the ureter, whether it is kinking or not and whether there is any cong
5.Cystograms.—
(a) Excretory cystograms can be obtained as later films of excretory urograms. If these are not satisfact
clearly the pathological conditions of the bladder, retrograde cystogram may be required.
(b)Retrograde cystograms are performed by instilling radio-opaque fluid into the bladder through a cat
outline the bladder-wall including the diverticula. Besides these, this test has a diagnostic value in rup
and recurrent infection (vesico-ureteral reflux is the commonest cause of perpetuation of infection).
(c) Voiding cystourethrograms are essential as increased intravesical pressure generated at the time of
show ureteral reflux when cystogram has failed to detect it. This will also reveal function of the bladder
posterior urethral valves or urethral stricture.
6.Renal angiography.—
Although renal angiogram can be performed by direct lumbar needle puncture of the aorta, yet this
superseded by percutaneous femoral angiography. A catheter is passed to the level of the renal arteries
control. It is also possible to do the catheterisation through the brachial or axillary artery. 12 to 24 ml o
suitable for intravenous urography is injected and 10 exposures are taken in 10 seconds time.
Selective renal angiography is accomplished by passing a femoral catheter into one of the renal arteries
fluoroscopic control. About 8 ml of the contrast medium is injected and 16 exposures are taken within
technique gives detail demonstration of the arterial pattern in the kidney and thus differentiates efficien
cyst and tumour. If this technique fails to differentiate in case of small lesion or becomes obscured by o
epinephrine can first be injected into the catheter followed by instillation of radio-opaque medium. This
spasm of normal vessels but has no effect on arteries in tumours.
Embolisation of renal tumour deprives a tumour of its major blood supply so as to cause infarct and sh
tumour. This can be used preoperatively to minimise blood loss during subsequent nephrectomy partic
vascular tumours. This will also reduce showering of tumour cells into systemic circulation at the time
Such preoperative embolisation is also of value to avert severe haematuria from adenocarcinoma of kid
is unfit for surgery. Thus operation may be delayed till the patient becomes fit.
Palliative embolisation may be required in case of patients with inoperable tumours who because of pain or
haemorrhage require some palliative treatment.
Methods.— Embolisation of a renal tumour is performed by injecting thrombogenic emboli into the renal artery
through an angiographic catheter. A midstream aortogram and selective renal arteriogram should always precede
embolisation. The catheter should have a single end hole and should be positioned as selectively as possible to avoid
the problem of overspill of emboli and distal complications.
Various forms of thrombogenic emboli have been used. Embolisation with autologus blood clot is the simplest and
safest, which becomes lysed within a few days. Blood clot treated with epsikapron lasts longer and may be used as
preoperative embolus. Sterisponge is a versatile agent, which is nothing but sterile absorbable gelatine sponge, which
is easy to prepare and small pieces of these are injected through the catheter. It also does not cause permanent block
and recanalisation occurs after a few weeks. If permanent occlusion is required, a small steel coil may be passed
through the catheter. Embolisation takes time and requires patience. Small quantities of embolic material is injected,
followed by check radiographs made with contrast to assess the flow and distribution. This can be ideally recorded on
a video tape. The major complication of therapeutic embolisation is inadvertent embolisation of normal tissue.
Digital Subtraction Arteriography (DSA) offers more clarification in radiological imaging thus satisfactory
imaging of renal vascular anatomy can be obtained. This has almost eliminated the need for translumbar aortography.
DSA can be performed by intravenous or intraarterial injection of contrast medium, though intra-arterial techniques
offer better clarification.
7. Vesical angiography.— A seldinger catheter is passed to the bifurcation of the aorta and 30 ml of 90% contrast
medium is injected. Alternatively each hypogastric artery is selectively catheterized and 10 ml of radio-opaque fluid is
injected. Films are rapidly exposed in first 8 seconds. The series is repeated in oblique position to give tangential view
of the tumour. This technique is occasionally required to judge the size and depth of penetration of the vesical neoplasms.
8. Lymphangiography.— A lymphatic vessel in the foot is cannulated and oily contrast medium is injected. This
leads to opacification of the inguinal, pelvic, aortic groups and supraclavicular lymph nodes. Metastatic infiltration
can be demonstrated in regional lymph nodes by filling defect in malignant tumours of the testis, prostate, bladder and
penis.
9. Angionephrotomograms (Intravenous renal angiogram).— In this investigation a bolus of radio-opaque medium
(30-50 ml of 90% Hypaque) is injected inside a vein (antecubital vein) rapidly. 4-6 tomograms are taken. Space
occupied by a cyst or abscess fails to opacity, whereas a malignant tumour shows a normal or increased opacification.
Renal angiography is however better.
C. ULTRASOUND.— With the static B scanner, the transducer is moved at a constant speed in a single sweep
along the skin overlying the organ to be imaged. Conventional static B scan and real time instruments also visualise
the bladder and prostate with the patient supine. Any change of renal outline and displacement or fragmentation of the
collecting system of echoes is of pathological significance.
(i) With ultrasound, agenesis, hypoplasia, duplex or ectopic kidney can be diagnosed.
(ii) In the evaluation of renal masses, which are found at excretion urography, ultrasound is firmly established as
the next investigation. The majority of such lesions are simple cysts. Grey-scale ultrasound not only demonstrates
smaller cysts, but also gives more information on the renal anatomy and nature of solid lesions. Cysts can be differentiated
from renal carcinomas. In case of haematuria, even if the intravenous urogram is normal, ultrasound can detect a
peripheral lesion that does not deform the calyceal system or renal outline. Renal sonography should follow urography
in evaluation of a renal mass. Renal sonography should be followed by percutaneous puncture (under sonographic
visualisation). If aspiration reveals clear fluid and the area is smooth-walled as demonstrated in X-ray following
injection of a contrast medium, no further investigation is required. If sonogram shows the pattern of solid mass,
arteriography is advised. Sonography is about 95% accurate in distinguishing between solid and cystic renal masses.
(iii) Large renal calculi can be diagnosed. Even exact position of a small calculus can be determined at operation
by the application of a transducer direct to the kidney surface. A small needle can be passed through a slot guide of the
probe to the stone. Radiolucent urinary calculi can be demonstrated by ultrasound, which cannot be seen in straight
X-rfcy. Early nephrocalcinosis, which cannot be seen radiologically, becomes evident with ultrasound.
(iv) One of the most important applications of ultrasound is in renal failure. Diagnosis of obstruction as cause of
renal failure can be made with confidence by demonstrating dilatation of pelvicalyceal system. Normal sized kidneys
with collapsed pelvicalyceal system would suggest acute renal failure.
(v) Ultrasonography has gained particular importance in paediatric urography as it is simple, non-invasive and
painless. It may be repeated frequently without radiation hazards.
(vi) In staging renal tumours ultrasound is of great help. It can demonstrate a patent renal vein and vena cava
which is of great value to the surgeon. Para-aortic lymphadenopathy can also be demonstrated.
THE KIDNEY AND URETER - ! 045
(vii) Staging of bladder tumour is also possible by ultrasound, but this becomes difficult in a patient with shrunken
bladder. B scanning of the bladder has been used to evaluate the intravesical extent of tumours. The transrectal approach
is useful in detecting early asymptomatic tumours of the prostate and in accurately staging local disease of the prostate.
(viii) To follow up transplanted kidney ultrasound is the best. Obstruction is indicated by showing dilatation of
pelvicalyceal system. Urine leak may be demonstrated by showing fluid collection around the kidney or bladder. It can
also demonstrate a swollen kidney as measured longitudinally and transversely.
D. TRANSRECTAL ULTRASONOGRAPHY.—
This mode of investigation is now very commonly used in cases of suspected carcinoma of prostate and sometimes in
benign hyperplasia of prostate. The main indication of using this investigation is either a raised prostate-specific antigen
or an abnormality of the texture of prostate 011 digital rectal examination. One can also take transrectal needle biopsy while
performing this investigation.
E. COMPUTED TOMOGRAPHY (C.T. SCAN).—
Preparation of the patient.— Diluted oral Gastrografin is given at least half an hour before scanning to differentiate
G.I. tract from other soft tissues of similar density. Peristalsis, which can produce artefacts, is reduced by intravenous or
intramuscular injection of 20 to 40 mg Buscopan just before scanning. While scanning the pelvis, Gastrografin is intro
duced per rectum to outline distal large bowel. A full bladder displaces the small intestine out of the pelvis making it easier
to identify pelvic anatomy. In female patients a tampon is inserted to identify the vaginal vault. In this examination the
detector system is usually a scintillation phototube or gas-filled ionization chamber and not the X-ray film as in conven
tional radiography. The X-ray tube and the detector system are on opposite sides of the patient and during scan they rotate
around the patient recording informations about the internal structure of the thin transverse cross-sections through which
the X-ray beam is passing. Through a complex series of mathematical manipulations the computer ‘reconstructs’ and
displays it as an integrated picture on a television monitor.
(i) A swelling in and around kidney is well determined by CT scan. It allows the distinction of a renal cyst from a
solid tumour. The outline of a cyst is sharp and has a well defined thin wall. Tumours are well determined by CT scan, only
small tumours may be missed unless they distort the outline of the kidney.
In this examination, a renal mass is considered to be a simple benign cyst if it has a homogeneous density similar to that
of water and has a very thin wall thickness that is virtually unmeasurable. A renal cancer has density similar to or slightly
higher than that of normal renal parenchyma but has a thick wall which is more significant. Extrarenal spread of tumour may
be seen breaking through the Gerota's fascia and invading the pararenal fat. Involvement of hilar and para-aortic lymph nodes
may also be demonstrated. Tumour invasion of renal vein is difficult to detect, although gross invasion of the vena cava may
be shown by outlining the lumen with contrast medium injected into a peripheral vein just before scanning. C.T. is accurate in
finding out recurrence of tumours in patients who had radical nephrectomy for renal carcinoma.
It is customary that if urography demonstrates a solitary renal mass, it has to be evaluated by diagnostic ultrasound. If
ultrasound demonstrates all the findings of a simple benign cyst, there is no reason to perform any other diagnostic
imaging examination. Only if ultrasound fails to show any convincing result, CT offers an accurate and non-invasive
method of evaluating the lesion. The most frequent causes of indeterminate results from ultrasound are (a) a mass in the
upper pole of the kidney, (b) a mass in the region of the renal pelvis, (c) presence of multiple renal masses and (d)
markedly obese patients. CT is as accurate as angiography in determining the local extent of the cancer, presence of
enlarged lymph nodes and presence of tumour thrombus within the renal vein and inferior vena cava.
(ii) Renal calculi are readily demonstrated, may they be non-opaque calculi. The calculus may be localised preop
eratively to a specific calyceal system.
(iii) Hydronephrosis can be seen if gross. Minor degrees of obstruction cannot be diagnosed as the calyces are
poorly shown.
(iv) Pararenal masses are also finely demonstrated, particularly their relationship to the kidney. The loss of thin
plane of fat between the lesion and the kidney strongly suggests renal involvement.
(v) Lymph nodes between renal hilum and the diaphragm are not adequately visualised by lymphography, but are
usually well delineated by C.T. With the advance in technology in C.T., lymphangiography should be reserved for sus
pected metastasis in normal-size lymph nodes. C.T. is accurate for staging of bladder cancer. Value of C.T. in the staging
of prostatic cancer has not been adequately evaluated.
(vi) Staging of bladder tumours, the degree of muscle invasion by carcinoma of the bladder has an important prog
nostic significance. Cystoscopy, biopsy and bimanual examination under general anaesthesia are recognised to be some
what inaccurate. C.T. is being used as a method of staging with some accuracy. In obese patients bimanual examination
can be extremely difficult, while C.T. scans are more accurate. Extension outside the bladder wall obliterate the distinct
planes of fat separating adjacent organs from the bladder.
F. RADIOISOTOPE RENOGRAPHY.—
100 CiofI131 -labelled hippuran is injected. I.V. and radioactivity is measured over each kidney with a pair of scintillation
detector. The tracing is in direc segments — segment A (vascular phase) with a steep rise lasting 20-30 seconds due to the
arrival of radioisotopes in the vascular bed; segment B (secretory phase) lasting for 2-5 mins. due to accumulation by the
kidney and its subsequent secretion; segment C (excretory phase) indicates gradual tubular excretion. In renal hypertension
the rise is too little (segment A) and prolongation of third phase. In obstruction, the third phase is abnormally prolonged. It is
the actual pattern of tracing which is more important. Function of kidney is very well assessed with this technique.
Technetium 99"' labelled DMSA is often used nowadays. This when injected intravenously and scanned by gamma
camera will provide more information regarding renal plasma flow. This is now more often used than mI hippuran.
Similarly 99m DTPA is excreted earlier and gives a good image of the renal outline. By this technique one can also perform
an antegrade pressure perfusion test devised by Whitaker, in which method a fine needle puncture of the collecting system
is performed and thus inflow and continuous monitoring of intrapelvic pressure are assessed.
G. RENAL SCINTISCAN.—
This consists of measuring the rate of accumulation of l97Hg- labelled neohydrin using an external detector up to 1
hour after injection. This test is not so efficient to determine the function of kidney as the previous test, but in injury, it
shows the portion of kidney affected and supersedes the previous test to determine the type of operation to be required.
H. MAGNETIC RESONANCE IMAGING (MRI).—
The principles of MRI has been discussed in the chapter 31 —■ ‘The Head’. It is agreed that MRI is potentially the
powerful and versatile imaging technique in medicine. There are many ADVANTAGES of MRI. (i) It uses no ionizing
radiation, so no harmful genetic or somatic effects, (ii) No bowel preparation with fluid and food restriction is necessary.
(iii) Contrast media are not required to distinguish the gastrointestinal tract or vascular structures, (iv) Paramagnetic
contrast agent are now being developed that should enhance the advantages of MRI in near future, (v) It offers great
flexibility for imaging in many planes e.g. sagittal, coronal and axial planes, (vi) The images produced are superior to that
obtained from ultrasound, (vii) It gives better information about soft tissues than any other imaging methods.
There are however a few DISADVANTAGES of MRI, which are: (i) It has a low sensitivity for calcified lesions, (ii)
Image acquisition takes longer time than CT scanning. So the patient has to halt respiration which may not be possible for
all and there may be some blurring of images especially in the upper abdomen, (iii) The apparatus is large and expensive.
(iv) As strong magnetic field is used, strict security measurements are needed to prevent injury due to loose metallic
objects being drawn to the magnetic field, (v) Pacemakers cannot be exposed to the powerful magnetic field used in MRI.
One must be veiy careful to select the type of investigation he would require in a particular case. For example,
ultrasonography, CT scanning and MRI are usually ineffective in demonstrating a small uroepithelial tumour, whereas an
excretory urogram is the study of choice for such lesion. Sonography is an excellent non-invasive selectively inexpensive
method for differentiating simple cysts from other mass lesions in the kidney, but is much less effective in imaging the
retroperitoneum than CT scanning. Angiography can delineate the source and extent of vessels supplying renal tumours,
but the examination is relatively expensive, commonly requiring a hospital stay. CT scanning produces excellent images
and is currently the available way to image the retroperitoneum and the adrenal glands. Above all MRI is still in its early
development and already rivals CT scanning in imaging capability. For certain structures e.g. the brain and the spinal cord
it is the best method.
INSTRUMENTAL EXAMINATION OF THE URINARY TRACT
Endoscopy.— Endoscopy has revolutionised investigating method of lower urinary tract.
Preparation.— The external genitalia, scrotum, groin and upper parts of the thighs are first swabbed with
tincture iodine. Now particularly the external genitalia with retracted prepuce is cleansed with a soapy antis
tic solution. 1% lignocaine with 0.25% chlorhexidine jelly is pushed into the urethra to provide anaesthesia
and lubrication. The urethra is milked and 5 to 10 minutes should be given for action of the drug.
Cystoscopy.— Previously rigid cystoscopies were used, though recently fibreoptic cystoscopies have ma
the procedure more comfortable. This instrument is introduced through the urethra in the similar fashion as
bougie. Cystoscope is mainly used to visualise inside ofthe bladder, though ureteric catheters may be intro
duced through the ureteric orifices retrogradely to perform retrograde urography. Systemic inspections of t
inside of the bladder is extremely important to exclude any pathology there. Use of a telescope with a wider
field of vision may be required.
After the cystoscope has been introduced into the bladder, sterile water is instilled into the bladder to
distend it. By pushing the instrument, withdrawing it a little and by rotating it the whole of inside of the bla
can be inspected except a small area at the neck. The ureteric openings are usually situated at 4 O’clock and
8 O’clock positions indicated by a knob on the handle. Cystoscopes can be used in 3 types —
(a) Visualising cystoscope.
(b) Operating cystoscope, e.g. excision of a small polyp or tumour, cauterisation of tumour and for taking
biopsies from the tumour.
(c) Catheterising cystoscope, by which ureteric catheters can be introduced through ureteric opening.
Ureteric catheterisation.— The ureteric catheters are long, narrow, graduated gum elastic tubes with
stellates. The catheters are passed through the cystoscope into the ureteric orifices. Ureteric catheterisation is
performed for —
#
(i) To collect specimen of urine from individual kid-
(ii) To perform retrograde pyelography.
(iii) To locate the level of obstruction within the ureter,

Fig.57.2.— Shows introduction of ureteric (iv) The catheter may be pushed above the impacted
catheter into a ureteric orifice.
stone for drainage as well as to instil lubricants so that the
stone may be passed out through the bladder.
(v) To relieve ureteric obstruction in case of calculous
Where proper X-ray facilities are not available, informa

tion about renal fuction can be obtained by injecting 7 ml of
0 4% (adult dose) of indigocarmine intravenously. Appear
ance of dye will be noticed at each ureteric orifice after a few
minutes. This is known as chromocystoscopy. Delay on one
side is indicative of obstruction or disease on that side.
Nowadays more sophisticated endoscopes have been
introduced to inspect the inside of the ureter (ureteroscope)
and inside of the kidney (nephroscope).
U reth roscopy.— There are two types of urethroscopy —
(a) anterior urethroscopy, which means inspection of penile
urethra and (b) posterior urethroscopy, which means inspec
Fig.57.3.— Chromocystoscopy. Indigocarmine tion of membranous and prostatic urethra.
ejecting out from right ureteric orifice.
(a) Anterior urethroscopy— is mainly used in case of
urethral stricture or chronic urethritis. Even infected urethral
crypt or a granuloma may be excluded.
(b) Posterior urethroscopy — is mainly performed
with an end-viewing optical instrument. Mainly the
verumontanum, which INJURIES is TOan THE KIDNEY
eminence AND URETER
in the posterior midline
of About
the 10% prostatic
of all injuries urethra and department
seen in casualty sinus pocularis
involve the on its
genitourinary summit
system. with
the ejaculatory ducts opening of either side are inspected
carefully. Red and enlarged verumontanum is an indication of
chronic vesiculitis. In case of chronic prostatitis one may
notice pus exuding through the numerous prostatic ducts.
INJURIES TO THE KIDNEY

Renal injuries are the most common injuries of the urinary system. The kidney is well protected by rib
vertebral bodies, lumbar muscles and the viscera. Blows, or falls on the loin and crushing road traffic acci
are the usual causes of injury to the kidney. Fractured ribs and transverse vertebral processes may penetr
the renal parenchyma. It must be remembered that kidneys with existing pathologies e.g. hydronephrosis
tuberculosis or malignant tumours are more readily ruptured following minor trauma.
Aetiology.—
(i) Blunt trauma to the abdomen, flank or back is the most common mechanism of renal injuries. Th
accounts for 85% of all renal injuries. Such trauma may occur in motor accidents, fights, falls or in contact
sports.
(ii) Gun-shot and knife wounds may cause penetrating injuries to the kidney. Any such injury in th
back or in the flank should be well examined to exclude renal injury. Associated abdominal visceral injuri
are present in majority (80%) of such penetrating wounds.
(iii) Sudden break in high speed vehicle may result in major vascular injury of the kidney.
Pathology and classification —
Blunt trauma usually causes laceration of the kidney in the transverse plane. Tears of the renal parenc
usually follow the lines of the collecting tubules. The pathologic classification of renal injuries is as follow
(a) MINOR RENAL INJURY.— Renal contusion or bruising of the parenchyma is the most commo
lesion. This minor renal trauma in fact constitutes majority (85%of cases) of renal injuries. Under this head
three types arc commonly seen —
(i) Subcapsular haematoma in association with contusion.
(ii) Superficial cortical lacerations.
(iii) Incomplete fissure or tear of the capsule and renal parenchyma with perirenal haematoma but
without any extravasation.
(b) MAJOR RENAL INJURY.— This means deep corticomedullary lacerations which extend int
pelvis to causc extravasation of urine in the perirenal space . This constitutes only 14% of cases or slightly
more. The various types in this category are :—
(i) Complete fissure or tear of the renal parenchyma and pelvis to cause gross haematuria.
(ii) Deep laceration of the kidney which causes large retroperitoneal and perinephric haematomas.
(iii) Multiple lacerations causing complete destruction of the kidney.
(iv) Laccration of the renal pelvis or ureter causing urinary extravasation.
A B C D E
Fig. 57.4.— Diagrammatic representation of various types of renal injuries. A.- Superficial cortical laceration.
B. - Complete fissure or tear of the renal parenchyma and pelvis. C.- Deep laceration of the kidney. D.-
Laceration of the renal pelvis causing urinary extravasation. E.- Total avulsion of the renal artery and vein.
In major renal injuries blood and urine usually collect extraperitoneally except in children in whom th
is little perinephric fat and the peritoneum is intimately fixed to the kidney. In these cases blood and urine
escape into the peritoneal cavity.
(c) VASCULAR INJURYVascular injury of the renal pedicle is rare but may occur due to blunt tr
or sudden break in motor car accident. The vascular injury is rare and constitutes only 1% or less of all rena
injuries. Various types of injury in this category are :—
(i) Stretch on the main renal artery without avulsion may cause renal artery thrombosis.
(ii) There may be partial avulsion of the segmental branch of the renal artery
(iii) Total avulsion of the renal artery or vein.
The most important feature of vascular injuries is that it is difficult to diagnose and if this is not mad
quickly, it results in total destruction of the kidney.
LATE PATHOLOGIES.— If the patient survives, late pathologies may develop from various types of
kidney injuries.These are :—
1. Hydronephrosis.— Haematomas and urinary extravasation in the extraperitoneal tissue may result in
perinephric hydrosis leading to obstruction of the ureteropelvic junction. This leads to hydronephrosis. Thi
can be easily diagnosed by excretory urography after all major renal injuries.
2. Urinoma.— Persistent urinary extravasation from deep lacerations which were not repaired may resu
in large perinephric renal mass which may become infected to cause abscess formation. This large perineph
renal mass is called urinoma.
3. Renal hypertension. — Fibrosis around renal artery may constrict it to cause renal hypertension. Blood
flow in non-viable tissue due to injury is compromised, which also results in renal hypertension.
4. Arteriovenous fistula.— This only results after penetrating injury involving renal artery and vein.
The history should include detail description of the accident. In case of penetrating injuries, the type of
weapon should be interrogated and assessed. In case of gun-shot wounds, the type of gun should be questi
as high velocity bullets cause much more extensive damage than low velocity ones.
Microscopic or gross haematuria following trauma to the abdomen or loin indicates injury to the kidne
The degree of renal injury does not correspond to the degree of haematuria. Gross haematuria may occur in
minor renal injury, whereas mild haematuria can occur in major trauma. Presence of haematuria should no
be taken lightly and it demands full evaluation of injury to the kidney. About '/,rd of cases of renal vascula
injury are not associated with haematuria. These cases are usually due to sudden breaks in motor car accide
A. SYMPTOMS.— The most common complaints are pain and haematuria following trauma.
1. Pain.— Pain may be localised to one flank or over the whole abdomen. Pain may be due to fractured
ribs or pelvic fractures and due to injury to other abdominal viscera.
2. Haematuria.— As mentioned above this is an important feature of kidney injury. The patient often
complains of haematuria following accident Haematuria may occur just after the accident, or may appear s
hours after the accident, or it may be as delayed as between 3rd day to 3rd week after the accident. So when
kidney injury has been suspected, the patient must be followed up carefully. Such delayed haematuria is us
due to dislodgement of a clot. When haematuria is profuse, the patient may complain of clot colic, which is
almost similar to ureteric colic due to calculus.
3. General abdominal distension may be complained of after one or two days of injury This generalised
abdominal distension is called ‘metcrorism’. This is caused by retroperitoneal haematoma involving the
splanchnic nerves.
4. Patient may present with a swelling in the loin after injury. This is due to perinephric haematoma or
extravasation of urine. Normal concavity of the loin disappears.
B. PHYSICAL SIGNS — ^
In general examinations hypovolaemic shock or signs of high blood loss may be noted.
In local examinations there may be ecchymosis or bruise in the loin or upper part of the abdomen or in
the back. Fracture of lower ribs may be evident. Abdominal examination may reveal tenderness in the loin o
there may be diffuse tenderness. A large palpable mass represent large retroperitoneal haematoma or
extravasation of urine. Occasionally if the peritoneum is ruptured blood or urine may enter the peritoneal cav
causing distension of the abdomen. Bowel sounds may then be absent.
1. Urine examination.— Microscopic or gross haematuria is revealed in urine examination.
2. Straight X-ray ofthe abdomen will disclose fracture of lower ribs or vertebral body or transverse process
fracture. An increased soft tissue opacity in the renal area and obscuring the psoas shadow are the features
of extravasation of blood and urine. Extent of haematoma may be judged by displacement of colon and stoma
and there may be small bowel dilatation due to ileus if there be extensive retroperitoneal haemorrhage.
3. Excretory urography is performed as soon as the intravenous lines are established and resuscitation
has begun. It is mandatory to demonstrate first and foremost an intact functional kidney on the other side.
This urogram will clearly define the renal outlines, cortical borders and ureters. Sometimes there may be spas
of the renal vasculature with no visualisation of the kidney on the affected side. Yet after 2 or 3 days normal
form and function may be apparent on repeated X-rays. In severe cases a line of laceration may be seen with
extravasation of contrast medium into the perirenal space.
4. Nephrotomography is indicated if excretory urogram does not provide with the necessary informations.
Tomograms will establish presence of cortical lacerations, intrarenal haematomas and areas of poor vascular
perfusion. Excretory urography alongwith tomography will determine the type of renal injury in 85% of cases
5. Ultrasonography and retrograde urography are of little use initially in theevaluation of renal injuries.
6. Computed tomography (CTscan) is also proving to be an affective mean for staging renal trauma. This
defines more clearly parenchymal laceration, extravasation and extension of perirenal haematoma.
7. Radionuclide renal scans are being used in staging renal trauma. However in emergency this technique
is less sensitive than CT scan and nephrotomography.
8. Arteriography determines major arterial or branch injuries. Arterial thrombosis and avulsion of the
renal pedicle are best diagnosed by this means. In these conditions the kidney is not visualised with excretory
urogram. It must be remembered that the major causes of non-visualisation on excretory urogram are (i) arter
thrombosis, (ii) total pedicle avulsion and (iii) severe contusion causing vascular spasm, besides (iv) absence
of the kidney. Angiography reveals also the rate of blood loss which may be an important indication for
operation. It also demonstrates traumatic arteriovenous fistula. But it is fair to say that angiography in acute
trauma is of little importance in this country.
TREATMENT.—
A. Emergency measures.— The objectives of this are to treat shock and haemorrhage. The measures
consist of —
(i) The patient must be hospitalised and lie flat in bed. Movement is disallowed.
(ii) A sedative is immediately given in the form of injection pethidine or morphine, which is also pain
killer.
(iii) An appropriate antibiotic is started at the same time to prevent infection of the haematoma.
(iv) Intravenous infusion is started which should be followed by blood transfusion. Hourly pulse and
blood pressure charts should be maintained.
(v) Samples of urine are sent for examination. Microscopic or macroscopic presence of blood is also
noted.
(vi) Once the central venous pressure (CVP) has been normal, excretory urography (I. V.P) should be
done urgently to know that the other kidney is normally functioning.
B Local management.—
1. BLUNT INJURIES.— (a) As mentioned earlier MINOR RENAL INJURIES constitute 85% of cases.
These usually do not require any operation. Bleeding stops spontaneously with emergency measures. The
patient should be in bed rest for about 1 week till macroscopic haematuria has been absent. Further activities
are also reduced for 1 month.
(b) In case of MAJOR RENAL INJURIES there is persistent retroperitoneal bleeding, urinary
extravasation and evidence of non-viable renal parenchyma, for which operation is justified. The clinical
signs are :— (i) Signs of progressive blood loss (rising pulse rate and low blood pressure inspite of blood
transfusion), (ii) Swelling develops in the loin which indicates retroperitoneal bleeding or urinary extravasati
In sophisticated centres renal angiogram may be performed in these cases to know the exact site of injury and
to locate the bleeding vessel. Embolisation may be performed to stop bleeding. In a few centres there may not
be facilities of urgent urography, in these cases one may perform chromocystoscopy to find that the kidney of
the other side is functioning normally.
When operation is justified, intraperitoneal exposure is usually applied to exclude damage to other organs
and to be doubly sure that the other kidney is normal and uninjured. Now the injury of the kdiney is assessed
If there are transverse tears, these can be sutured over oxycel or a piece of detached muscle to promote
haemostasis. A transverse single laceration through the middle of the kidney can be sutured over oxycel but
if haemostasis cannot be achieved properly it is better to perform nephrostomy through the transv erse tear in
the middle of the kidney and suturing the kidney around the tube. If one pole of the kidney is lacerated, parti
nephrectomy should be performed.
When the kidney is found to be reptured in several places or the kidney pedicle is damaged, nephrectomy
When there is injury to the only existing kidney and it is not responding to the emergency measures,
exploration is justified. The tears are sutured over oxycel. Even if it continues to bleed, it is controlled with
gauze pack in the hope that bleeding will be controlled by this method.
Injury to the other viscera of the abdomen are always assessed carefully. Rupture of spleen is often
associated with left kidney injury. In case of major renal injury, simultaneous splenectomy and left
nephrectomy has been carried out successfully. It must be confessed that injury to the liver or hollow organs
alongwith injury to the kidney increases mortality to great extent.
2. PENETRA TING INJURIES.—These injuries require more often surgical interventions, as other orga
are often injured. More than 80% of cases there is associated other organ injury. Access is usually made throug
the penetrating injuries, though sometimes fresh incisions may be required if penetrating wound is
inconveniently placed.
INJURIES TO THE URETER

Ureteral injury is rare. It may occur in stabbing and gun-shot injuries, but in majority of cases ureter is
injured by the surgeons (iatrogenic).
Surgically ureter may be injured while operating for cancers in the cervix and uterus, for endometriosis
and for inflammatory and malignant diseases of the sigmoid colon. The ureter is also rarely injured in those
surgeries where speed is of paramount importance. Ureter may be injured in operations e.g. emergency
caesarean section or for ruptured ectopic pregnancy. Extensive lymph node dissection may also injure ureter.
Endoscopic manipulation of a ureteral calculus with a stone basket may result in ureteral perforation.
Passage of a ureteral catheter beyond an area of obstruction may perforate ureter.
If the ureter has been ligated inadvertently during operation, the postoperative course is usually marked
by temperature of 101° - 102° F as well as flank or lower quadrant pain. The patient may also complain of
nausea, vomiting and distension of abdomen due to paralytic ileus. Sometimes ureterovaginal or cutaneous
urinary fistula develops, which usually appears within first 10 days after operation. It must be remembered th
bilateral ureteral injury or ligation is manifested by postoperative anuria.
If there is stab or gun-shot wound in the loin, penetrating injury to the ureter should be suspected This
usually takes place in the midportion of the ureter.
1. Microscopic haematuria is noticed in 90% of cases.
2. Straight X-ray is not of much help except it may demonstrate a large area of increased density in the
pelvis or in the retroperitoneal tissue which may arouse suspicion.
3. Excretory urography is more valuable as it may show a diffuse shadow below the kidney on the injure
side. It may show hydronephrosis and delayed excretion. If one ureter has been tied inadvertently non
visualisation of kidney of that side may occur due to transient failure of function.
4. Ultrasonography may outline urinary extravasation. It will also outline hydroureter due to ligation of
the ureter. It is a fairly useful means to detect ureteral injury in the post-operative cases.
Treatment.—
A. All cases of penetrating injury demands exploration.
B. Cases of surgical injury may be discussed in two groups —
GROUP.— I. When the injury is recognised at the time of surgery.— In this case an attempt is made
to restore continuity. If the ureter has been partially clamped or included in a ligature, the clamp is immedi
removed or the ligature is quickly cut. This is followed by cystoscopic catheterisation of the ureter and the
catheter is passed beyond the point of injury. The distal end of the ureteric catheter is brought out per ureth
and secured to a small indewelling Foley catheter. It should be removed after 1 week.
If the viability of the ureter is in question, the damaged segment is excised and the ends are mobilise
for end-to-end anastomosis with interrupted 4/0 Dexon. A defect upto 2 cm may be repaired in this way. A
splinting catheter is always used in these cases which is removed endoscopically after 1 week.
When ureteric injury is low, simple restoration may not be practicable. In such case the ureter is
reimplanted into the bladder. If there is fear of tension on the anastomosis, a few techniques may be adopte
Firstly the superior pedicles of the bladder and if needed the inferior pedicles are divided to mobilise the b
up. This allows the fundus of the bladder to be brought up about 2 inch above the pelvis, where it is ancho
to the psoas sheath. If this technique fails, a Boari flap is created. This tubularisation of the bladder will allo
3 inches of extra length for a tension free implantation of the ureter. If this also fails ileal interposition may
be used In all cases a reflux preventing reimplantation of the ureter into the bladder should be performed.
submucous tunnel is created into which the ureter is implanted obliquely through the muscles of the bladd
A splinting catheter may be used and bladder drainage is also used for 10 days.
In case of upper ureteral injuries, if ureteral anastomosis is not possible, ureteroureterostomy is
performed by swinging the proximal ureter across to the ureter of the other side for anastomosis.
GROUP.— II. Ureteral injury is recognised after surgery.—As mentioned earlier these cases are often
recognised by continuous complain of aching in the loinand continuous fever for the early postoperative p
Sometimes urinary leaks develop per vaginum or through abdominal wall usually between 6th and 10th
postoperative days.
If the case is detected within 48 hours of surgery, re-exploration is indicated. Often however the
surgeons may face stiff resistance from the patients as they have already undergone extensive surgery very
recently. But even then if these patients can be convinced re-exploration is justified. At this stage if the end
are clean cut and no length is lost, end-to-end anastomosis should be performed. In case of low down injur
the ureter is reimplanted into the bladder. In upper ureteral injuries either end-to-end anastomosis or urete
ureterostomy should be performed.
If for whatever reason the patient cannot be reoperated within 3 days, it is wise to wait for as many
months as possible. It is unwise to re-explore on the 10th day or within 1 month, as the reparative processes
are in full swing with hyperaemia, tissue oedema and new capillary loops formation It will be unwise to en
this field, as nothing can be seen or done due to excessive haemorrhage from the new capillary loops. If at a
one has to re-explore at this time, then ureteroureterostomy should be carried out leaving the initial operat
field undisturbed.
If surgery is undertaken after an interval of 3 months, then any of the techniques described in Group
I may be adopted.
HYDRONEPHROSIS
Hydronephrosis means dilatation of renal pelvis and calyces with accompanying destruction of the kid
parenchyma. It is usually caused by partial obstruction to the outflow of urine. Complete block usually pro
acute renal atrophy without significant pelvicalyceal dilatation. For the result of complete block the students
are referred to the section of ‘Acute renal Failure’, later in this chapter.
Hydronephrosis may occur at any age.
Aetiology.—
Hydronephrosis may be congenital or acquired. Congential hydronephrosis means it is caused by
obstruction which developed congenitally e.g. pin-hole meatus, valves and folds in the urethra. Majority of th
congential hydronephrosis are bilateral.
Hydronephrosis may be unilateral or bilateral. Unilateral hydronephrosis occurs when the obstruction is
somewhere in the ureter, above the level of the urinary bladder. Bilateral hydronephrosis occurs when the
obstruction is below the level of the urinary bladder e.g. stricture of the urethra, benign enlargement of the
prostate or neuromuscular dysfunction of the internal sphincter. However bilateral hydronephrosis may occu
due to bilateral ureteric obstruction.
When there is a definite detectable cause of hydronephrosis, it is called secondary hydronephrosis. When
no cause can be detected, it is called primary or idiopathic hydronephrosis.
Causes of secondary hydronephrosis.—
I. Unilateral hydronephrosis.—
Obviously the cause is in the ureter and mostly it is at the pelviureteric junction. The causes can be
classified into — A. Extramural causes, i.e. the cause lies outside the ureter; B. Intramural causes, when the
cause lies in the wall of the ureter and C. Intraluminal, when the cause lies within the lumen of the ureter.
A. EXTRAMURAL CAUSES —
1. Pressure on the ureter by loaded sigmoid colon, gravid uterus, uterine tumours and ovarian tumour
2. Involvement ofthe ureter by malignant neoplasm outside it e.g. carcinoma of the cervix and uterus,
carcinoma of the colon or caecum, carcinoma of the rectum and carcinoma of the prostate.
3. Aberrant renal vessels.— These are usually seen at the junction of the pelvis and ureter. Arteries
are more important in this respect. It is often a lower polar artery which supplies the inferior segment of the
kidney. Such artery may not arise from the renal artery but instead from aorta, common iliac artery or sperma
or ovarian artery. Such aberrant vessel may cause hydronephrosis in children and may be considered as
congenital hydronephrosis. Often this displaced vessel may cause rapid increase in the size of hydronephrosi
but may not be a cause of it. The hydronephrosis might have been an idiopathic’ variety or due to
neuromuscular imbalance at the pelviureteric junction and this so called aberrant vessel’ may have just
increased the size of the hydronephrosis or is a simple coincident.
4. Idiopathic retroperitoneal fibrosis.
5. A moveable kidney may cause kinking of the ureter to seldom cause hydronephrosis.
B. INTRAMURAL CAUSES.—
1 Unilateral congenital hydronephrosis is mostly caused by intramural causes. These causes are
congenital stenosis or achalasia at the pelvi-ureteric junction.
2. Ureterocele and congenital atretic ureteric orifice also cause congenital hydronephrosis
3. There are certain acquired intramural causes which may lead to unilateral hydronephrosis. These
are inflammatory stricture of the ureter mostly due to tuberculosis or following removal of an impacted stone
Stricture of ureter may follow trauma to the ureter during other operations in the pelvis or may follow
ureteroureterostomy.
4. Neoplasm of the ureter (mostly papilloma of the ureter) is rare and may cause unilateral
hydronephrosis. What is more common is a malignant neoplasm of the bladder involving one ureteric orifice
C. INTRALUMINAL CAUSES.—
1. Calculus in the ureter is not only the most common in this group, but also the most common
of unilateral hydronephrosis. This usually causes intermittent hydronephrosis (described below).
2. Congenital folds at the upper end of the ureter may cause congenital unilateral hydronephros
is more often seen on the right side than on the left side.
II. Bilateral hydronephrosis.—
The causes of bilateral hydronephrosis can

be best classified into causes in the urethra and
causes in the bladder.
A. Causes in the urethra.—
1. Pin-hole meatus is a congenital cause.
Very rarely phimosis may cause congenital
hydronephrosis.
2. Congenital valves are more commonly
seen in the posterior urethra and these cause
bilateral congenital hydronephrosis, although
one side hydronephrosis may be bigger than the
other side. It is usually accompanied by
hydroureter.
3. Benign prostatic enlargement and pros
tatic carcinoma are very common causes ofbilat-
eral hydronephrosis with hydroureter.
4. Inflammatory stricture of the urethra is
the commonest cause of acquired bilateral
hydronephrosis in the young and young adults.
Traumatic urethral stricture may rarely cause
hydronephrosis.
5. Carcinoma of the cervix and uterus and
carcinoma of the rectum may sometimes involve
the urethra or neck of the bladder or even both
ureters to cause bilateral hydronephrosis.
B Causes in the bladder.—
D .j j i .j . , , . ,
hg.o/.o.— Hydronephrosis due to calculus in renal pelvis.
i 1. A calculus in the urinary bladder Jmav
act as a ball valve to cause obstruction at the
urethral meatus to cause intermittent bilateral hydronephrosis.
2. Internal sphincter of the bladder may be unable to open due to neuromuscular dysfunction e. g. in
dorsalis or injury to the spinal cord.
3. Neoplasm of the bladder may involve both ureteric orifices to cause bilateral hydronephrosis.
4. Malignant neoplasms of adjacent organs may involve urinary bladder orboth ureters to cause bilat
hydronephrosis.
Primary hydronephrosis.—
There remain however a certain number of cases which have to be labelled as ‘ idiopathic' or 'primary'
hydronephrosis, as no organic cause can be detected. These are mostly encountered in children and the
obstruction lies at the pelviureteric junction or at ureterovesical junction. The obstruction is regarded as bei
neuromuscular in majority of cases. Neuromuscular inco-ordination due to imbalance of the sympathetic a
parasympathetic control of the muscles of the ureter. There are two layers of muscles of the ureter, but unli
G.I tract, the muscles are inner longitudinal and outer circular. In the lower part of the ureter a third layer
of outer longitudinal coat appears which becomes continuous with the longitudinal muscle coat of the trigo
Rhythmic contraction of these muscles forces the urine to pass through the pelvis into the ureter and down
ureter through the ureteric orifice into the urinary bladder. The contraction starts at the papillae of the caly
w here there are more circular muscle fibres. There are also excess circular muscle fibres at the pelviureteri
junction, (i) Due to defect in the co-ordination of the muscular peristalsis, obstruction to the passage of urin
develops to cause hydronephrosis, (ii) There may be spasmodic segment of the circular muscles at the
pelviurcteric junction to cause such obstruction.
PATHOLOGY.—
The essential change in hydronephrosis is dilatation of the renal pelvis and calyces. The normal pelvis ha
an average capacity of 7 to 10 CC (ml) of urine. The dilatation of the pelvicalyceal system may contain 300
ml to 500 ml of urine. The cases which show great dilatation are mostly idiopathic.
ST A GES of hydronephrosis. —
1. Open hydronephrosis.— In this condition the hydronephrosis sac is openly communicated with the
lower urinary tract, as the obstruction is incomplete.
2. Intermittent hydronephrosis.— Here the hydronephrotic sac intermittently communicates with the
lower urinary tract, as the obstruction is complete intermittently. That means when the obstruction is comp
there is oliguria with enlargement of the hydronephrotic sac and the patient complains of pain in the loin o
the same side. After sometimes the obstruction passes off. there is polyuria and diminution in the size of th
sac.
3. Closed hydronephrosis.— In this condition the hydronephrotic sac is completely closed from the lower
urinary tract.
TYPES of hydronephrosis.— Three types are usually recognised depending on whether the kidney has an
extrarenal or intrarenal or mixed type of pelvis.
1. Pelvic type.— When the kidney has extrarenal (the major part of the pelvis lies outside the kidney
substance) pelvis, the renal pelvis becomes grossly dilated in hydronephrosis with minimum dilatation of t
calyces This type is usually seen in idiopathic form and in this type there is greatest dilatation likely to occu
Renal damage is much less as there is little distension of the calyces. It must be remembered that when
hydronephrosis is due to a stone at the upper end of the ureter, accompanying inflammation causes fibrosi
and thickening of the pelvis so as to unable it to dilate much. The principle is almost same as Courvoisier’s
law in case of gallbladder.
2. Renal type.— When the pelvis is intrarenal (that means the major pait of the pelvis remains inside
the kidney substance) there is not much dilatation of the renal pelvis but the calyces are more dilated. This
causes early renal destruction owing to more dilatation of the calyces. This type is more often seen in case o
calculous obstruction.
3. Pelvirenal type.— This is perhaps the most common form, in which both the pelvis and the calyces
are equally dilated.
MACROSCOPIC changes.— In the process of dilatation, first the pyramids of the medulla of the kidne
are suffered. Later on the cortex of the kidney becomes involved. The calyces are blunted and gradually the
distend to destroy the substance of the kidney. On section a typical hydronephrosis kidney looks like a hug
lobulated bag of fluid in which there are vestiges of the interlobular septa. The cortex is thinned to a mere s
The fluid which occupies the hydronephrotic sac is clear and watery and contains urea, uric acid and low
quantity of salts. If infection occurs in hydronephrosis, the clear fluid gradually changes into pus and then
kidney becomes a bag of pus. This condition is known as pyonephrosis.
MICROSCOPICALLY, there is great atrophy of the tubules. In early stages the tubules are dilated, whic
gradually become atrophied in later stages. The glomeruli remain comparatively intact and they appear mo
in number than normal due to parenchymal atrophy of kidney. Later on the glomeruli also become hyaliniz
and gradually fibrosed. The renal cortex remains only a few millimetres thick in a full developed case of
hydronephrosis
The FLUID of hydronephrosis is not stagnant, but it is continuously undergoing changes due to secreti
of fresh fluid and reabsorption of existing fluid. Secretion of fluid is mainly through the glomerulus, where
absorption of fluid occurs through various paths These paths are as follows :—
(i) Pyelovenous back-flow, in which absorption occurs through veins which lie in the wall of the pel
(ii) Pyelotubular back-flow, in which absorption occurs by way of the renal tubules into which the fl
flows back from the hydronephrotic sac.
(iii) Pyelolymphatic back-flow in which hydronephrotic fluid is absorbed by the lymphatics which lie
in the wall of the pelvis.
The effect to the other kidney in unilateral case of hydronephrosis is important. It has been shown that
after the ureter has been obstructed, the other kidney starts hypertrophying in about 3 weeks time and assum
additional function to compensate failure of the affected kidney. After 3 weeks of complete obstruction, the
affected kidney’s function becomes tremendously deteriorated, so much so that even if the obstruction is
removed it cannot get its function to normal level.
1. Unilateral hydronephrosis.— The females are usually more often affected. Curiously enough right
side is more commonly affected than the left side.
Two type are usually seen :—
TYPE I — in which the causes of hydronephrosis are the main presenting features e.g. renal colic and
haematuria in calculous obstruction etc.
TYPE II— in which clinical features of hydronephrosis are the main presenting features. In these cases
onset is insidious. There is dull ache and sense of weight on the affected side of the loin. This becomes exces
after excessive fluid intake and alcohol. On examination one can find an enlarged kidney on the affected sid
2. Intermittent hydronephrosis.— In this type patient first complains of an acute pain which is
followed by a swelling in the loin. A few hours later or even on the next day there is suddenly excess voidin
of urine (polyuria), the pain is relieved and the swelling also disappears. This is known as Dietl’s crisis’.
3 Bilateral hydronephrosis.— In this condi
tion also two types are seen :—
TYPE I — There are symptoms of causes of
hydronephrosis e.g. symptoms of benign enlarge
ment of prostate or carcinoma of prostate or neoplasm
of the bladder and there is hardly any symptom of
hydronephrosis. Hydronephrosis is only revealed by
special investigation.
TYPE II — Bilateral renal swelling is firstly
complained of but this is much rare in comparison to
the unilateral hydronephrosis
1. STRAIGHT X-RA Y of the abdomen may
show enlarged renal shadow and radio-opaque stones
Fig.57.6.— Excretory urography showing as cause of hydronephrosis.
hydronephrosis on the right side. 2. EXCRETOR Y UROGRAPHY (I. VP.).—The
diagnosis is mainly confirmed by this investigation. This is only contraindicated during pregnancy. The
findings in the early stages of hydronephrosis differ according to the type of hydronephrosis.
(a) In The Pelvic Type —
(i) Dilatation of renal pelvis.
(ii) The next change is decreasing concavity and then flattening of the minor calyces with dilatation
of major calyces.
(iii) The pelviureteric junction is no longer the lowermost part of the pelvis and it moves up a little.
A portion of the pelvis becomes more dependent part below the level of the pelviureteric junction.
(b) In The Renal Type —
(i) The earliest change is decreasing concavity and flattening of the minor calyces, which later
become convex, this is known as clubbing’ of minor calyces. It is associated with progressive dilatation of th
major calyces.
(ii) In advanced cases when there is extreme dilatation of renal pelvis and calyces, the urographic
shadow may be very faint or absent This is due to poor excretion of the dye by the grossly damaged kidney.
This is also due to dilution of the excreted dye by the huge quantity of fluid in the sac. In these doubtful case
perfusion urography may be used to visualise the kidney. A fine needle puncture of the kidney through the
is made and the kidney is perfused with radio-opaque medium at a constant rate of 10 ml per minute. Intrap
pressure is monitored. This is a type of antegrade urography and is known as Whitaker test.
3. RETROGRADE UROGRAPHY.— When excretory urography picture is inconclusive, this is a simple
method which may be performed by
B
general surgeons. With this tech
nique one can assess the changes of
the pelvis and calyces in a better
way.
4. ULTRASOUND can easily

Fig.57.7.— Retrograde urography showing dilatation of the pelvis
and calyces. It is a primary hydronephrosis
The indications for operation are —

(i) Increasing renal pain.
(ii) Increasing renal pelvis and calyces.
(iii) When hydronephrosis is complicated by secondary infection, operation is justified following
antibiotic therapy.
Recently, the operation used for hydronephrosis, is mostly conservative e.g. some sort of plastic
operation. But it must be remembered that this type of surgery is only suitable when hydronephrosis is
extrarenal.
NEPHRECTOMY.— When hydronephrosis is intrarenal, dilatation of the calyces occurs earlier at the
expense of the renal parenchyma. When there is extensive damage to the renal parenchyma, nephrectomy is
justified provided the other kidney is functioning normal. Again one point should be very much considered
that hydronephrosis, whose aetiology is still obscure, is often a bilateral condition and affects the other kidney
sometimes later in the process. So nephrectomy should be avoided as far as practicable.
67
PLASTIC OPERATIONS (PYELOPLASTY) FOR HYDRONEPHROSIS.— Three principles are

followed during pyeloplasty operations — (i) to reduce the size ofthe renal pelvis, (ii) to excise the pelviur
junction as this may be the area of failure of muscular co-ordination and to avoid subsequent stricture form
and (iii) the ureter is attached to the most dependent part of the pelvis.
Types of operations.— The conventional method which is commonly practised is as follows — the kidney is exposed through t
lumbar approach The pelvis is cleared off fat by gauze
■ Jgmm dissection The ureter is divided just below the pelvi
ureteric junction or any constricted part there about The
• redundant part of the pelvis is divided m a line parallel
to the hilum. The upper part of the remnant of the pelvis
. ,
w rmamM
** Wk till
is closed by closely spaced interrupted suture with 4/0
catgut The posterior aspect of the divided ureter is slit
; 4gMj downwards to about I inch The oblique opening in the
-4%mk upper part of the ureter is anastomosed to the lower part
v’*1- " o f the remnant of the pelvis
. A N D E R S O N - H Y N E S PYELOPLASTY - It is
,'l’l mostly applied when the ureter, after excising from pelvi-
.'■■l • IRft -.fT?, ureteric junction becomes too short to anastomose with
. '■ 'y. the remnant of the pelvis The renal pelvis is excised in
'' B j k ; . a v'shaPc‘J manner The lower flap is then turned
'-•if';' * -Ift * IB downwards and anastomosed obliquclv with the meter

j. > '•].' ' jJBr when the upper flap is closed as usual
;^..v . Splinting of the anastomosis by means of an
fl’v. ' " f ’■K indwelling catheter, is not much beneficial, on the
S. - contrary it may promote infection
■" CULP PYELOPLASTY—This is performed m
- : : V „ - ■ cases of moderate hydronephrosis from the pelvis The
-JjfV'V’ OPI’fiw • renal pelvis and the upper part of the ureter are cleared
■if properly A vertical incision is made across the
•;,i;' r.; *•? ] 'H pelviureteric junction from 2 cm above the junction in
; 1 the pelvis to 2 cm below the junction in the ureter The
K1 JK*' upper pan of the incision which is lying m the pelvis is

earned laterally and then downwards to the bottom ofthe
■ »*up . I renal pelvis in an inverted U-faslu
sOHs' ‘ pelvis is now turned downwards and sutured in the gap
’S . f.' between the margins of the ureteric incision The renal
' pelvic defect is closed by interrupted sutures. It is wise to
drain the kidney by a nephrostomy tube for 10 days.
FOLEY PYELOPLASTY.— This operation is best
suitable for small hydronephrosis. The renal pelvis and
the upper end of the ureter is again exposed and dissecte
clearly. A vertical incision is made from just above the pelvi-ureteric junction along the ureter for 2 cm. From the upper end
incision, two incisions are made to diverge from each other so the whole incision has now become a Y-shaped one The apex
gradually pulled down and sutured to the lower end of the ureteric incision to give it a V-shape. The sides of the opening are
interrupted sutures This is again drained with a nephrostomy tube for 10 days.
The lumbar incision is closed with a drainage. There always remains a problem of prolonged leakage of urine, but they g
stop by themselves.
ENDOSCOPIC PYELOLYSIS.— Idiopathic pelviureteric junction obstruction is now treated by disruption of the junction wi
specially designed balloon passed up the ureter in specialised centres. The distension in balloon is made under radiographic
Long term benefit of this technique is still to be assessed.
RENAL PEDICLE SYMPATHECTOMY.— This operation has fallen into disrepute presently. Only a handful of surgeons may s
advocate this operation on the belief that this may cure the spasm at the pelviureteric junction due to sympathetic overacti
operation the renal pedicle is exposed through the typical renal exposure. The renal artery, vein and the pelvis are preserve
soft tissues lying outside these structures in the renal pedicle are stripped off. The sympathetic nerve fibres which form a pl
renal vessels to supply the kidney is thus sacrificed. This operation probably plays a significant role in relieving pain associat
hydronephrosis. This has a bad effect that the patient, thus relieved of pain, ignores hydronephrosis which is steadily dilatin
NON-SPECIFIC INFECTIONS OF THE KIDNEY
Non-specific infections of the kidney are those which are not caused by ‘specific organisms’ which cause clinically
unique disease e.g. tuberculosis.

Pathogenesis.—
It is not always possible to truce the mode of entry of the bacteria into the kidney. 4 major possibilities ar
1. Ascending infection.— When there is urinary stasis due to stricture of urethra or enlargement of prostate,
readily make their way from the bladder to the kidney. There is increasing evidence that ascending infection
of all. It is the common mode of infection in chi Idren before the age of 10 years. Great majority of women are
by this route of infection. The high incidence in females appears to be related to their short urethra which ofte
urinary pathogens which migrate from neighbouring perineum to the vaginal vestibule. This mode of infectio
in males above 60 years of age in which benign enlargement of prostate is common. These data strongly supp
is the most common route of infection. Vesico-ureteral reflux also contributes to this type of involvement.
Theoretically ascending infection may occur by three routes : (i) Through the lumen of the ureter; (ii) By p
the lymphatics in the wall of the ureter; (iii) By blood stream. Many pathologists believe that intraureteral spr
common. They are more in favour of the lymphatic spread. The mucosa and submucosa of the urinary bladd
with an extensive network of lymphatics which pass up along the wall of the ureter to the kidney. Bacteria pl
urethral mucosa pass into the lymphatics and up the walls of the bladder and ureter. So route of election in a
infection is by lymphatics.
2. Haematogenous spread.— It is probable that haematogenous infection of the kidney is not infrequent. Bac
from infected tonsils, carious teeth, cutaneous infections particularly boils and curbuncles may affect the kidn
kidney is one of the main filters of the body and any bacteria gaining access to the blood stream are obviously
by this route and thus coming in contact with the kidneys. The bacteria first lodge in the glomeruli where the
large masses readily seen under microscope. Gradually suppuration is produced. Escherichia coli lodge in th
portion of the kidney, although later infection may spread into the cortex . The urine gradually becomes load
and becomes strongly acid in reaction. Pathogenicity of E. Coli is lower than that of pathogenic cocci and a ch
infection may linger for years in Ihe renal pelvis.
In experimental animals, intravenous injections of urinary pathogens lead to pyelonephritis only if the ur
temporarily obstructed or the kidney is trauma! iscd. So it seems that urinary obstruction or vesicoureteral re
to the kidney may prepare the ground for haematogenous infection.
The most obvious examples of renal infection via haematogenous route are tuberculosis and renal curbun
metastasis from skin infections).
3. Lymphogenous spread.— There is firm evidence that infection can spread to the kidney through lymphati
channels. It has been discussed above in ‘ascending infection’ how lymphatics play a prominent role in ascen
Infections may spread from the large bowel to the kidney through lymphatics. Cervicitis also causes vescial a
infection via periureteral lymphatics.
4. Direct extension.— It is true that direct extension from a neighbouring focus of infection may occasionally
Bacteria may be introduced from exterior by penetrating wounds. But these are rare occurrences in clinical pr
Bacteriology.— By far the most common invaders are the gram negative bacteria, particularly E. coli. Oth
group are Enterobacter aerogenes. Proteus vulgaris, Proteus mirabilis and Pseudomonas aeruginosa.
A few cocci may also be responsible e.g. Streptococcus faecalis and Staphylococcus aureus. Stre. faecalis,
present, is usually associated with another organism.
In E.coli and Streptococcal infections the urine becomes acid in reaction. In Proteus and Staphylococcal in
the urine becomes alkaline in reaction, as these organisms split urea into ammonia. These organisms are also
for stone formation.
ACUTE PYELONEPHRITIS
The term ‘pyelonephritis’ means inflammation of the kidney and renal pelvis. The term ‘pyelitis’ means
inflammation of the renal pelvis only, but it is doubtful whether such condition can exist alone or not.
Pathogenesis.— In this condition bacteria reach the kidney either through the blood stream or by ascendin
infection. The latter mechanism is by far more common.
ASCENDING INFECTION.— In majority of cases acute pyelonephritis develops from infection in the
bladder through the mechanism of vesicoureteral reflux. It has been shown that vesicoureteral reflux may
occur during acute cystitis, but ceases when the infection has been cured. Prone to this reflux causes recurring
of infections. Acute pyelonephritis is quite common after marriage (‘Honey-moon pyelitis’) and during
pregnancy. In about 1 /3 rd of such cases of pyelonephritis will exhibit reflux. After termination of pregnancy
reflux disappears.
HAEMATOGENOUS INFECTION.— Pyogenic cocci are more often seen in haematogenous infections
though E.coli is the commonest infecting organism in all cases of pyelonephritis. In case of haematogenous
infection element of obstruction is of greatest importance. If colon bacilli are injected intravenously into rab
in which one ureter had been partially ligated, acute pyelonephritis develops in the obstructed kidney in 7
of cases, but never in the unobstructed kidney. Release of obstruction after a few days induces healing.
Pathology.—
MACROSCOPIC FEATURES.— The affected kidney is usually swollen and congested and the pelvis
is bright red with pus inside. The surface of the kidney becomes dull. Under the capsule there are numerou
yellow spots representing areas of suppuration.
On cut surface the sharp demarcation between the cortex and the medulla is lost. Patchy areas of
suppuration are seen which are spherical in the cortex and linear in the pyramids. Wedge shaped areas of
size are suggestive of infarcts, and represent upward extension of infection. If suppuration is progressive,
abscess cavities ftre formed with destruction of renal tissue. Multiple small abscesses may also be seen. Th
outline of the calyces is destroyed and the resulting distortion is seen in X-ray film, which is an important
feature of diagnosis.
MICROSCOPIC FEATURES.— There are many small abscesses with widespread interstitial infiltration
with polymorphonuclear leucocytes. There is diffuse or spoty inflammation characterised by oedema and
haemorrhagic areas. There are also linear round cell infiltration with admixture of polymorphonuclears. It
the renal tubules which bear the major brunt. There is destruction of the renal tubules with gradual replace
by scar tissue. Many tubules are filled with pus cells. The pathological process is characteristically patchy w
intervening areas of the tubules which are either normal or dilated filled with pink staining colloid like
material. The glomeruli, in contradistinction, are much less involved. In fact they are peculiarly immune to
inflammatory change, though there may be some periglomerular fibrosis.
In the renal pelvis there is round cell infiltration and fibrosis. The arteries show two types of changes —
(a) endarteritis obliterans, a fibrous thickening of the intima with narrowing of the lumen and (b) thickenin
and hyalinization of all layers of the arterioles, which may cause renal hypertension.
As mentioned earlier acute pyelonephritis is more common in females particularly during pregnancy a
soon after marriage, Which is popularly known as ‘honeymoon pyelitis’. Peculiarly enough this condition
affects right side more often than the left but it may be bilateral.
SYMPTOMS —
(i) Constant ache over one or both kidneys is the most frequent complaint. This is mainly caused by
distension of the renal capsule due to oedema. The pain may radiate to the lower abdomen or to the groin
mimicking ureteric colic.
(ii) Children often complain of vague abdominal discomfort instead of localised renal pain.
(iii) Increased frequency of micturition, urgency, nocturia and burning sensation on urination are th
complaints due to cystitis which is often accompanied with.
(iv) Prodromal symptoms e.g. headache, lassittude, nausea, vomiting and prostration are often
complained of.
(v) Rigor alongwith high temperature is quite common.
PHYSICAL SIGNS —
(i) Among general signs increased temperature, which often shoots upto 104° F, increased pulse rate
(which may vary according to the type of infecting organism; In E.coli infection the pulse rate may be only
90/min. In Staphylococcal infection pulse rate may be as high as 140/min ).
(ii) In local examination, tenderness at the renal angle (the angle between last rib and lateral border
ofsacrospinalis) in the back and over the affected kidney in front can be elicited. Sometimes anterior tende
is not so easily palpable due to muscle spasm
(iii) Percussion over the renal angle may be painful.
(iv) Abdominal distension with quiet intestine revealed by auscultation can be elicited in acute cases
Rebound tenderness may also be elicited if there is intraperitoneal infection.

1. BLOOD EXAMINATION — reveals high neutrophil count. The E.S.R is increased. Serial blood
cultures should be done on any patient with high fever, chills and rigor as bacteraemia is not uncommon.
2. URINE is usually scanty and highly concentrated. It is usually cloudy. Protein content becomes high
Urine contains large amounts of pus and bacteria. A few red cells may be noted in the urine. Renal function
as measured by specific gravity or PSP will be slightly affected unless there is overwhelming sepsis.
Bacteriological examination of the urine.— Midstream specimen should be collected in sterile test tube.
The urine is centrifuged and the sediment is examined microscopically. In the beginning the pus cells remain
scanty, though there are many bacteria. When the condition is present for more than a day, the number of pu
cells increases. Quantitative estimations of pus cells and bacteria are important in finding out the severity of
the case. The sediment should be stained as mentioned earlier by Gram’s method. Culture of the specimen
and sensitivity of the organism to antibiotics are highly important to find out proper chemotherapeutic agent
3. X-RAY.— Straight X-ray of the abdomen may not be decisive except some obliteration of the renal
shadow due to oedema of the kidney and perinephric fat.
Excretory urography shows slight diminution of function in acute stage. The pelvis and calyces on the
affected side may be smaller, may be due to secretion of small volume of urine in the affected side. Presence
of obstruction or vesicoureteral reflux should be noted. When infection is severe, it shows less concentration
of dye on the affected side, which returns to normal after appropriate therapy.
It should be borne in mind that excretory urography should not be used to diagnose this condition, neit
her cystography should be performed for diagnosis. These investigations however can be used when the
infection is controlled.
4. Radionuclide imaging.— Imaging the kidneys with Gallium 67 may be used to localise the site of
infection. 85% accuracy has been claimed, though false positive and false negative results have been
encountered.
Complications.—
1. If diagnosis is delayed and treatment is inadequate, the condition may turn to be chronic. This is mor
common when vesicoureteral reflux is present. Such chronic form is not easy to diagnose as not only this
condition is silent, but also there is few or no pus cell in the urine, however bacteria may be detected with
difficulty. Such chronic form may gradually lead to (i) renal insufficiency, (ii) renal ischaemia and
hypertension.
2. In fulminating pyelonephritis bacteraemia or septicaemia may be present. Metastatic abscesses may
develop in other organs. Bacteraemic shock may be seen particularly when gram negative rods are the infecti
organisms
1. Acute appendicitis.
2. Acute cholecystitis.
3. Acute diverticulitis mimicking left sided acute pyelonephritis. However change of bowel habit,
normal urine and characteristic changes in barium enema will diagnose this condition.
4. Pancreatitis.— High serum amylase and absence of pyuria are the diagnostic points in favour of this
condition.
5. Basal pneumonia.— Examination of the chest is important if diagnosis of pyelonephritis is doubtful.
6. Herpes Zoster affecting somatic segments D12 and LI may simulate renal pain. Skin hypersensit
ivity and absence of pyuria are diagnostic points in its favour
Treatment.—
A. GENERAL MEASURES.— While urine should be promptly sent for microscopy, culture and sens
itivity test, some general treatments should be instituted.
1. Pain should be relieved with antispasmodics such as belladonna or phenobarbital. Morphine o
pethidine may be prescribed in intractable cases.
2. Bed rest is highly important as it is required in all cases of infection. Patient shoud be instruc
drink large quantities of bland fluid, at least 3 litres a day. Adequate urinary output should be maintained
severe cases with vomiting and dehydration, intravenous dextrose saline may be required.
3 . If the urine is acid, which is common in coliform infections, alkalisation of the urine is benefi
to relieve symptoms. This will minimise vesical irritability. Potassium citrate with hyoscyamus in the form
of mixture given 4 times a day is very useful treatment in this regard.
B. SPECIFIC TREATMENT.— Antibiotic should be started immediately even when the culture and
sensitivity reports have not arrived. Preferably the antibiotic chosen should reach a high concentration in u
and renal tissue. Such antibiotics are tetracycline, ampicillin, cotrimoxazole, polymyxin B, gentamicin.
kanamycin and amoxycillin.
Once the culture and sensitivity reports are in hand, the proper antibiotic should be started in high do
for at least 10 days, till the urine is rendered sterile. It is better to administer another antibiotic of similar
sensitivity for a further 10 days and again urine examination is performed. Urine must be sterile before sto
all antibiotic treatment.
A few recently available antibiotics are quite effective and these are carbenicillin, cephalosporins (1st
generation — cephalexin. 2nd generation — cefoxitin and 3rd generation — cefotaxine (claforan) ),
ciprofloxacin (cifran), norfloxacin (norbactin) and pefloxacin.
C. FAILURE OF RESPONSE.— If no clinical improvement occurs in 2 to 3 days after offering above
treatment, excretory urograms should be advised to detect any obstruction or vesicoureteral reflux. Obstru
may necessitate surgical treatment e.g. removal of a ureteral stone.
CHRONIC PYELONEPHRITIS
Pathogenesis.—
The term chronic pyelonephritis’ means persistent presence of bacteria in the kidney.
I. Ascending infection.— In majority of these cases the source of bacteria comes from the bladd
ascending infection. In case of females it often comes from the urethra. If ureterovesical junction is grossly
abnormal bacteria in the bladder reach the kidney and true chronic pyelonephritis continues. If the vesical
is kept sterile, pyelonephritis is prevented.
II. Haematogenous infection.— When there is no ureterovesical reflux, haematogenous infection
causing chronic pyelonephritis is possible. But this usually occurs secondary to some ureteral obstruction
ureteral stone. So treatment should be considered in this direction if permanent relief is to be obtained.
Pathology.—
MACROSCOPIC ALL Y, the kidney is of normal size or smaller depending on duration of the disease
capsule becomes pale, yet it cannot be stripped easily. Some areas of the surface of the kidney are pitted an
depressed due to scarring.
The cut surface shows fair demarcation between the cortex and the medulla, but the kidney tissue is p
and fibrotic. The pelvic mucosa is also pale and fibrotic.
MICROSCOPICALLY, the kidney parenchyma is diffusely infiltrated with plasma cells and lymphocy
The renal tubules are mostly affected and these are atrophic, dilated and cystic. Many of these become des
and disappear in the scar tissue The glomeruli however remain normal until late in the disease, when they
may be hyalinized and fibrotic. Considerable thickening of the arteries and arterioles is evident and this is
cause of renal hypertension which is seen in half the cases.
This condition is more common in females (3:1). While majority of the females are below 40 years of ag
majority of the males affected are above 40 years of age.
SYMPTOMS.— It must be confessed that chronic pyelonephritis may remain asymptomatic until rena
insufficiency takes place.
(i) Mild discomfort or dull pain over the kidney is complained of in majority of cases.
(ii) Vesical irritability in the form of increased frequency, urgency and dysuria may be noticed.
(iii) Hypertension is seen in half the cases. It gradually develops and becomes evident in long standing
cases. It is characteristically common in younger patients.
(iv) Vague gastro-intestinal complaints are often seen.
(v) Constitutional symptoms e.g. lassitude, headache, malaise, nausea and anorexia are seen in 40%
of cases. Often the disease is not diagnosed foryears. Anaemia is a very common accompaniment of this diseas
(vi) Pyrexia is not very important, yet this is seen in about 10 to 20% of cases.
PHYSICAL SIGNS.—
1. Hypertension is discovered in half the cases.
2. Some degree of localised renal tenderness may be elicited.
1. BLOOD EXAMINATION shows slight leucocytosis. Anaemia is present in almost all cases
2. URINE EXAMINATION shows decreased protein content.
Urinary sediment may or may not contain numerous white cells, but some bacteria are always present
Renal function tests should always be performed.
3. X-RAY.— Straight X-ray may show small atrophic kidney.
Excretory urograms may be either normal or show changes suggesting scarring e.g. indentations of the
lateral borders, roughening and deformity of the calyces. It may show dilatation of the ureter or vesicoureter
reflux.
Voiding cystourethrography should be performed which demonstrates vesicoureteral reflux in at least
half the cases.
4. CYSTOSCOPY may reveal evidence of chronic infection in the bladder. Reflux at the ureteric orifices
may be detected.
T reat ment.—
Utmost effort is made to detect cause of chronicity.
1.MEDICAL TREATMENT.— Intensive chemotherapeutic and antibiotic treatment is required. The ch
oice of drug depends on sensitivity test. The drug should be given for 2 to 3 weeks. Suitable drugs include —
Mandelic acid and its salts are quite effective against coliform organisms and Strept. faecalis. Ammonium
chloride of about 2 g may be given together with the previous drug 6 hourly. The urine should be kept acid.
In about half the cases infection is by one organism, though after treatment with antibiotic it may be replaced
by another organism. Sulphonamides e.g. urolucosil. septran (sulphonamide mixed with trimethoprim) are
quite effective in controlling E.coli infection and some strains of Proteus and Ps. aeruginosa Furadantin
(nitrofurantoin) is a synthetic antibacterial agent which is particularly effective against E.coli. A.aerogenes
and Proteus. It has proved lethel to even antibiotic resistant strains of these organisms. The dose is about 5 to
7 mg per kg. of body weight, administered three or four times daily after food
Co-trimoxazole (Bactrim or Septran) is a combination of trimethoprim and sulphamethoxazole which
together block two steps in the bacterial synthesis of folic acid
Nalidixic acid is active against E.coli, Proteus. Klebsiella. Enterobacter and some strains of Pseudom-
onas. Alkalising agents provide symptomatic relief by raising the pH of urine. Phenazopyridine hcl. is helpfu
in relieving pain during urinary infection (urinary tract analgesic).
2. SURGICAL TREATMENT —
(i) If any obstruction is detected, this should be removed surgically.
(ii) If vesicoureteral reflux has been demonstrated and is considered to be the cause of lingering
chronicity, repair of the ureterovesical junction should be considered.
(iii) If one kidney is badly damaged, nephrectomy should be considered.
(iv) When the hypertension has become malignant type and the cause is chronic pyelonephritis, if the oth
kidney is normal, nephrectomy of the affected kidney is curative
(v) Partial nephrectomy of a badly damaged portion of the kidney may be necessary.
(vi) When this condition affects both the kidneys badly with uncontrolled hypertension, transplantation
of kidney or recurrent dialysis should be considered
NECROSING PYELITIS
In this condition the papillae in both kidneys become yellow and necrotic, the ducts of Bellini are block
ses renal failure and uraemia. This is a rare and usually fatal condition. It needs only passing mention as it
ordinarily lead itself to surgical treatment.
Pathogenesis and pathology.—
When pyelonephritis is associated with diabetes, ischaemic infarcts result to cause this condition. It res
interstitial inflammation which leads to pressure necrosis of the papillae.
SYMPTOMS.—
At first patient complains of renal pain. Oliguria and uraemic coma develop rapidly which may become fatal.
(ii) Of course in majority of cases symptoms mimic exacerbation of pyelonephritis with symptoms o
irritation. Recurrent renal colic is complained of as sloughed papillae are passed through the ureter.
(iii) Presence of vesicoureteric reflux, diabetes, cirrhosis, sickle cell anaemia or a history of prolonged
analgesics may be detected.
PHYSICAL SIGNS —
(i) High fever and prostration are very characteristics.
(ii) Renal tenderness is usually well marked.
1. Blood examination shows high white cell count. Blood cultures are usually positive. Blood sugar may
Anaemia is almost always present.
2. Urine examination reveals pyuria and bacteriuria. Glycosuria and acidosis are common in diabetic p
Renal function test shows poor function of kidneys. PSP excretion may be as low as 30% in 1 hour.
3. Excretory urography may not reveal any definite clue to the diagnosis, except that satisfactory excret
may not be present. Infusion of increased amount of radio-opaque material also may not show any abnorm
is ulceration of central portion of the papilla cavities may be detected. Filling defect due to sloughed out pa
detected in a few cases.
Treatment.—
A. MEDICAL TREATMENT.— Immediate intensive treatment with appropriate antibiotic is essential,
results may be disappointing. Diabetes, cirrhosis, if present, should be treated properly. Patient must stop
drugs.
B. SURGICAL TREATMENT.— Only when the disease is unilateral and fulminating, whereas the othe
normal, nephrectomy can bring about quick relief. But this operation should be undertaken with caution a
is liable to be involved later on.
PYONEPHROSIS
‘Pyonephrosis’ means dilatation of the pelvis and calyces which are filled with thick creamy pus Thou
the nomenclature is restricted to the pelvis and calyces, yet there is always great destruction of the renal
parenchyma.
Aetiology and pathogenesis.—
This condition may develop (i) from infection of a hydronephrosis, (ii) from acute pyelonephritis or (iii
as a complication of renal calculus, which is known as calculous pyonephrosis.
Pathology.—
Macroscopically, the kidney is much enlarged. The fibrofatty tissue around the kidney becomes more
fibrosed and adherent due to inflammatory process. The surface becomes irregular and lobulated which
contains bag of pus. The renal tissue becomes thinned, but the pelvis and calyces become distended with p
This pus does not contain any living bacteria.
Microscopically, hardly one can find kidney structure. Kidney is full of pus and inflammatory processes
Occasionally a few tubules and glomeruli can be made out.
As a rule the condition is unilateral.
Clinical features.— SYMPTOMS.—
(i) Patients may present as a swelling in the loin.
(ii) High fever and prodromal symptoms may be associated with.
(iii) Patient may complain of simple pain in the renal region ignoring the swelling.
(iv) Symptoms of cystitis and bladder irritation e.g. increased frequency, urgency and nocturia may b
present.
PHYSICAL SIGNS.—
(i) Pyrexia and anaemia are noticed.
(ii) Renal tenderness is always elicited.
1. Straight X-ray may reveal calculus causing obstruction to the urinaiy flow.
2. Excretory urography may show advanced hydronephrosis. Excretion of dye may be delayed.
3. Cystoscopy reveals cystitis and purulent efflux through ureteric orifice.
Treatment.—
The role of surgery is extremely significant in obstructed cases of pyonephrosis. This should be treated
immediately. Percutaneous nephrostomy should be performed under the cover of antibiotics. Even open
nephrostomy may be necessary. The stone should be removed through nephrostomy.
If most of the renal substance has been destroyed and the other kidney is functionally normal, nephrect
should be considered. If the capsule of the kidney is so adhered to the surrounding structures, subscapsular
nephrectomy should be considered.
When the condition is bilateral or the only remaining kidney has been pyonephrotic, permanent
nephrostomy is the best treatment. A few urosurgeons may consider ‘ileal conduit’ as permanent drainage
RENAL ABSCESS OR CARBUNCLE OF THE KIDNEY
Aetiology.— The causative organism of this condition is usually Staphylococcus aureus. This organism
is released from cutaneous lesions such as boil, carbuncle, abscess of the breast, whitiow etc. Injury to the ki
often predisposes this condition, which forms small haematoma which acts as a good nidus for the growth o
the organisms. Nowadays abscesses of the kidney are seen, where the infecting organisms are E. coli.
Pathogenesis and pathology.— Haematogenous spread is the main route of infection. In the beginning
multiple cortical abscesses develop, which coalesce to form multilocular abscess. If this condition remains
untreated, such abscess may rupture into the pelvicalyceal system or into the perinephric space. While in ca
of the former pyuria and bacteriuria are quite evident, in the latter case urine culture will remain sterile.
A few cases of renal abscess may develop from long standing renal infection caused by ureteral obstruc
more commonly due to calculus. In children such abscess may develop as a complication of vesicoureteral
reflux. Of course the infecting organisms in this category are mostly coliform organisms
It must be remembered that l/3rd of cases of renal abscess are diabetics.
SYMPTOMS.—
(i) Patients usually present with persistent pyrexia, chills and renal pain.
(ii) Symptoms of vesical irritability are almost unknown.
(iii) A few cases may give previous history of renal calculus.
PHYSICAL SIGNS.—
(i) Extreme tenderness over the affected kidney is the main physical sign available.
(ii) The kidney may be palpable and tender, though adequate muscle spasm may stand in the way of
better palpation.
I BLOOD EXAMINATION usually reveals elevated white cell count with increase in polymorpho
nuclear neutrophils. A diagnosis of diabetes mellitus can be made in '/3rd of cases with high sugar in the blo
It is wise to perform blood cultures which may reveal infecting organism.
2. URINE — In the early stage urinalysis is negative. Urine only shows pus cells and bacteria if the a
ruptures into the renal pelvis. When renal abscess is secondary to early renal infection or calculous disease,
grain negative rods may be detected in the urine.
3. X-RAY —
(i) Straight X-ray may show enlarged kidney with perinephric oedema which may obliterate the
outline. The psoas shadow is usually indistinct. Scoliosis of spine may be observed when the abscess has ru
tured into the perinephric space. Renal stone may be detected.
(ii) Excretory urography usually demonstrates a space-occupying lesion obliterating or compressing
a group of calyces and/or a part of the pelvis of the ureter.
(iii) Angiography may reveal a space-occupying lesion in which the vessels are displaced. There may
be increased number of vessels around the area of abscess.
4. CT SCAN.— It may not be very easy to diagnose renal abscess on CT scans as the features of necrot
neoplasm are almost indistinguishable.
5. ISOTOPE SCANNING.— Gallium-67 localises inflammatory tissue and abscess. It may detect an
abscess even when excretory urograms fail.
Treatment.—
A. MEDICAL TREATMENT.— Antibiotics do cure early cases. But if the disease has been present for
sometime or when the disease is secondary to some kind of urinary obstruction, surgical treatment is necess
B. SURGICAL TREATMENT.— When response to antibiotic therapy is not satisfactory, surgical
operation in the form of drainage of abscess is required. After drainage, haemorrhage is controlled by press
with a moist warm pack. A drainage tube is passed down to the kidney. The wound is closed around the dr
tube. Antibiotics are continued for at least 10 days.
Heminephrectomy or even nephrectomy should be considered when a portion or whole of the kidney h
been damaged by curbuncle. of course when the other kidney is normal.
When there is definite urinary obstruction which has lead to the formation of renal abscess, initial drain
in the form of nephrostomy should be considered. Attempt should be made to remove the stone through
nephrostomy.
PERINEPHRIC ABSCESS
Aetiology.— Perinephric abscess may be primary or secondary.
Primary.— Primary form is mostly haematogenous. The infection is carried from distant foci e.g. boil, to
Such primary infection is precipitated due to lack of body resistance of the individual as may occur in certa
like scarlet fever. The usual causative organisms are Staphylococci and Streptococci.
Secondary.— The secondary form occurs as the infection travels from the neighbouring organs. The com
of course the kidney (renal abscess or carbuncle due to staphylococcal infection or from advanced non-spec
infection). The other organs from where perinephric tissue may be involved are the gallbladder, the append
organs. In these cases the causative organism is E. coli. Occasionally perinephric tissue may be involved by
ascending upwards through periureteral lymphatics.
Infection of a perirenal haematoma may also cause perinephric abscess. Delay in treatment of pyoneph
carbuncle may burst into the perinephric space to cause abscess. Cold perinephric abscess from tuberculosi
from tuberculous kidney or tuberculosis of a nearby vertebra.
Pathology.— Perinephric abscess lies between the renal capsule and the perirenal fascia of Gerota. Accor
cause of perinephric abscess the different organs may be affected accordingly. Perinephric abscess may bec
and may point through Petit's triangle just above the iliac crest. Occasionally the pus may pass up and form
abscess or may be pass down into the pelvis.
Clinical features.— This condition is more often seen in males
SYMPTOMS.— A history of prolonged urinary infection may be elicited. With the advent of perinephri
temperature increases and patient complains of pain in the flank with varying degree of malaise
PHYSICAL SIGNS —
(i) Increased temperature is almost always present. Marked tenderness over the kidney is usually fo
suppuration is confined to the upper portion of the perinephric fat, tenderness lies just beneath the lower ri
suppuration involves the lower part of the perinephric fat local physical signs become more prominent, e.g
swelling, oedema etc. become evident.
(ii) Scoliosis of the spine with its convexity towards the affected side is usually seen. This is due to sp
psoas muscle.
(iii) Corresponding side of the chest should be examined as ipsilateral pleural effusion is not uncommo
1.BLOOD EXAMINATION almost always reveals leucocytosis. Anaemia may be found. E.S.R. is usuall
2. URINE EXAMINATION may show pyuria and bacteriuria in 50% of cases. In majority of cases the or
is staphylococcus.
3. X-RAY EXAMINATIONS.— (i) Straight X-ray shows some obliteration of renal and psoas shadows d
perinephric oedema. Scoliosis of the spine as mentioned above may also be noticed. Occasionally a localised
of gas formed by the gas forming organisms (coliform) may be observed in the perirenal area.
(ii) Excretory urograms may show delayed visualisation. Space-occupying lesions due to carbuncles ma
evident as the primary cause.
Mathe's sign.— Lack of mobility of the kidney in the erect posture or with respiration strongly suggests
perinephritis.
(iii) A chest film may demonstrate an elevated diaphragm on the affected side with fixation on respirati
free fluid in the pleural cavity may also detected on the affected side.
4. ISOTOPE SCANNING.— Gallium-67 localises inflammatory tissue in the perinephric space.
Treatment.—
A. MEDICAL TREATMENT —
(i) Bed rest and local heat are the general measures which may help the patient. Bed rest accelerates h
(ii) Proper antibiotics should be started immediately.
B. SURGICAL TREATMENT.— When a frank abscess is present, surgical drainage through the flank sh
performed under antibiotic cover. The inicision must be large enough to open up all the pockets above and b
kidney. The surface of the kidney is carefully palpated to detect any unruptured cortical abscess, which shou
and drained. A specimen of pus should always be sent for bacteriological examination, culture and sensitivit
If the condition is secondary to renal disease like calculous pyonephrosis or infected hydronephrosis w
damage to the kidney parenchyma and while the other kidney is normal, nephrectomy should be considered
TUBERCULOSIS OF THE KIDNEY
Renal tuberculosis is never a primary condition. Tubercle bacilli invade kidney through blood from a
distant focus either lungs, lymph nodes or bones. Sometimes it is almost impossible to demonstrate with
certainty the active primary focus. The infecting organism is mycobacterium tuberculosis.
When any part of the body is affected by tuberculosis a shower of tubercle bacilli hit the renal cortex. The
organisms may be destroyed by normal tissue resistance. Minute tuberculous lesions in the kidney can be
detected in every case in which there were tubercle bacilli in the urine. As a rule, however, these minute lesio
heal completely. Evidence of this in the form of only scars in the kidneys may be seen in autopsies of persons
who have died of tuberculosis. However if enough bacteria of sufficient virulence become lodged in the kidn
a clinical infection is established.
Kidney tuberculosis is almost always unilateral at the commencement and may remain so for a remarkab
long time. Eventually however the other kidney may become involved. Tuberculosis of kidney progresses
slowly and it may take 15 to 20 years to destroy a kidney in a patient having good resistance. Usually no clin
disturbance appears till the lesion has involved the calyces or the pelvis, at which time pus and organisms ar
discharged through the urine. The real clinical criterion of active renal tuberculosis is the presence ofpus
and red cells in the urine alongwith tubercle bacilli and not just the presence of tubercle bacilli alone.
Pathology.—
MACROSCOPICALLY, the primary renal lesion usually involves either upper or lower pole. First the
infecting agent passes through the kidney filter and settles down in the collecting tubules. Then by a retrogra
process passes up the lymphatics to infect the cortex. The pathological process is first noticed in one of the
positions — (a) at the base of a pyramid or (b) at the apex of a papilla.
The appearance of a tuberculous kidney varies greatly with the extent of the lesion. In early stage small
lesion may be observed at the base of the pyramid or in one of the papillae. Soft, yellowish cheesy material m
be seen at the site of destruction.
In later stage there is progressive destruction of renal tissue with cavity formation. The kidney becomes
enlarged and on its surface distinct tubercles or larger bosses denoting cavity formation from within may be
detected. The pelvis is gradually involved comparatively early in the process. The pelvic mucosa becomes
roughened and the sides of the papillae become ulcerated.
So the cut surface of a tuberculous kidney shows (i) caseous yellowish tuberculous masses at the base of
the pyramids at one or both poles, (ii) Cavities of varying size with rough walls containing thick creamy che
material are seen, (iii) Extension ulceration and dilatation of the pelvis with destruction of the papillae are
noted, (iv) Thickening and dilatation of the ureter, although in some cases there may be tuberculous stricture
In thefinal stage thekidney becomes a functionless mass of tuberculous tissue. The kidney may be enlarge
due to pyonephrosis or may be shrunken and atrophic.
Sometimes kidney, in the process of tuberculosis, becomes shut off from the rest of the urinary tract due
to sealing-off of the renal pelvis or ureter. The disease process continues in the kidney to complete destructio
though there is no urinary symptom. This is known as closed renal tuberculosis.
MICROSCOPICALLY, the picture depends on the stage of the disease. The early lesion is that of miliary
tubercle. As the disease continues the surrounding kidney is affected and a typical tuberculous lesion is very
soon detected. Such lesion from outside inwards show fibrosis, small round cell and plasma cell infiltration.
Within this fibrosis are epitheloid and foreign body giant-cell typical of tuberculosis, inside which is the cas
eous material seen as an amorphous mass. Acid fast stain will usually demonstrate the organisms in the tissu
The OTHER KIDNEY.—Renal tuberculosis first affects one kidney. Sooner or later however it may becom
bilateral. Tuberculous infection from one kidney passes down the ureter infecting the bladder and then pass
up the other ureter to infect the other kidney. The other kidney may also be involved through haematogenou
route.
URETER.— Tuberculosis of the ureter is secondary to tuberculosis of the kidney. The infection passes
down in the submucous coat of the ureter, in which definite tubercles may be seen This is followed by ulcera
of the mucosa. The muscular coat and serous coat become infiltrated and thickened. It is the upper and lowe
thirds of the ureter which are more often affected than the middle-third. Thus the ureter is gradually convert
into a thick, rigid and dilated tube. Only occasionally scar formation may give rise to localised stricture of th
ureter.
Renal tuberculosis is a disease of early adult life, being commonest between the ages of 15 and 40 years
Males are affected twice as females. Peculiarly enough the right kidney is somewhat more commonly affecte
than the left.
A. SYMPTOMS — In fact there is no classic symptoms of renal tuberculosis. Majority' of symptom
are seen in advanced stage and are vesical in origin.
(i) Generalised malaise, fatigue, continuous loss of weight, low grade evening rise of temperature an
night sweats are some of the non-specific complaints.
(ii) On very careful interrogations one may get complaints of active tuberculosis elsewhere in the bod
in less than half the cases.
(iii) Renal pain is often absent, but on occasions patient may complain of dull ache in the loin.
(iv) In a few cases painless haematuria may occur from ulcer at the renal papilla. The passage of blood
clot may cause ureteric colic.
(v) Very rarely the presenting symptom may be a painless mass in the abdomen.
(vi) Vesical involvement.— The early symptoms of renal tuberculosis arise from secondary vesical
involvement, (a) Increased frequency of micturition is often the earliest and only symptom. It occurs both bv
day and night and it increases over a period of months. Though it is mostly due to patchy tuberculous cystit
yet it may be occasionally due to polyuria as a result of renal tubular inflammation, (b) Burning sensation at
the time of urination is another very frequent symptom. Gradually micturition becomes painful. This is due
to tuberculous cystitis. lust after micturition patient complains of pain at the tip of the penis or vulva, which
is a referred pain (c) Haematuria may be of vesical origin. A few drops of blood at the end of micturition is
particularly due to tuberculous cystitis, (d) If ulceration in the urinary bladder occurs patient often complain
of suprapubic pain, particularly when the bladder is full.
(vii) Pyuria is often complained of when the lesion has drained into the pelvis. Presence of pus
without organisms in acid urine in ordinary staining is very much suggestive of tuberculous affection of kidn
B. PHYSICAL SIGNS.—
(i) Kidney is usually not enlarged and not palpable. In fact when on careful examination a kidney
becomes palpably enlarged it is often the normal kidney which has undergone compensatory hypertrophy.
(ii) The prostate, seminal vesicles and epididymis and the vas deferens are carefully palpated to
exclude any thickening or nodules in those structures to exclude tuberculous affection of those structures.
1. BLOOD EXAMINATION may show lymphocytosis. Anaemia may be detectd in advanced case.
E.S.R is always raised.
2. TUBERCULIN TEST, though insignificant when positive, but is highly significant when negative,
as it almost excludes tuberculosis.
3. URINE EXAMINATION is most important.
(i) Persistent pyuria without organisms stained with methylene blue means tuberculosis unless prove
otherwise. Acid fast stains should be done on the concentrated sediment from 24 hours specimen, which is
usually positive in 70% of cases.
(ii) Culture for tubercle bacilli from urine are positive in more than 90%of cases. Guineapig inoculation
test is also successful in more than 90% of cases.
4. X-RAY EXAMINATIONS.— (a) Straight X-Ray may show calcification of the healing foci. Such
calcification may rarely be seen at lower end of the ureter, but more often seen in seminal vesicles.
(b) Excretory urograms can be diagnostic if the lesion is moderately advanced. The findings are —
(i) Irregular density in the nephrogram.
(ii) Loss or dysfunction of one or more calyces.
> Comparatively early changes.
(iii) Spasm or oedema may obliterate calyceal neck.
(iv) Hydrocalyx.
(v) ‘Moth-Eaten’ appearance of the involved calyces.
(vi) Obliteration of one or more calyces.
(vii) Abscess cavities that connect with calyces.
(viii) Space occupying lesion displacing calyces and pelvis.
(ix) Single or multiple ureteral strictures.
(x) Shortening and dilatation of ureter.
(xi) Absence of functions of the kidney.
(xii) Loss of natural curves of the ureter which becomes straighter, shorter and dilated.
(xiii) Spasm or flattening of the urinary bladder due to ulceration.
(xiv) Contralateral ureter may become dilated due to cicatricial obstruction of the ureter at its
intramural course.
(c) Retrograde urogram is usually not required, but may be necessary if excretory urogram fails to re
veal pathology.
(d) Chest film should always be performed to exclude tuberculosis of the lungs.
5. CYSTOSCOPY— This will clearly demonstrate the extent of disease in the urinary bladder.
(i) Typical tubercles or ulcers of tuberculosis may be visualised around ureteric orifice. Cloudy efflux
of urine may be seen through ureteric orifice.
(ii) Occasionally there may be absence of efflux on the affected side with no pathological changes in
the bladder. These are examples of closed ureter leading to autonephrectomy.
(iii) Pallor around the affected ureteric orifice due to oedema is the earliest vesical involvement.
Tubercles gradually appear usually lateral to the affected ureteric orifice and later on in the dome of the same
half of the bladder.
(iv) These tubercles coalesce to form tuberculous ulcer with irregular margin.
(v) In late cases due to shortening of the ureter, the ureteric orifice is pulled upwards and it looks like
a golf-hole, that is why it is called ‘golf-hole’ ureteric orifice.

(vi) Due to cicatrisation of the ulcers there is severe contracture of the bladder, in which the capacity
the bladder steadily diminishes. This is also a cause of increased frequency of micturition.
TREATMENT.— It must be remembered that renal tuberculosis is a part of generalised disease. So
general treatment of tuberculosis should be the prime treatment.
A. GENERAL TREATMENT.—
(i) Various combination of antitubercular drugs should be given. Previously injection Streptomycin,
Isoniazide and PAS were given for at least 1 Vi years. Nowadays more active antitubercular drugs are avai
which may be given for less period. Rifampicin 600 mg, Isoniazid 300 mg, Pyrazinamide 1 g and vitamin C
daily for 2 months followed by Rifampicin 900 mg, Pyrazinamide 1.5 g and vitamin C 1 g twice a week for
months is quite effective. Ethambutol 800 mg may be given in combination with Refampicin and Isoniazid.
(ii) Sanitarium regime is highly important with good protein rich diet and vitamins. Iron supplements
or even blood transfusion may be required in extreme anaemic cases.
B. SURGICAL TREATMENT.— Some tuberculous lesions of kidney are surrounded by fibrous tissue
so that antitubercular agents cannot reach the lesion in sufficient concentrations to kill the organisms.
These cases require operative treatment. The optimum time for operative treatment is after 6 to 12 weeks of
antitubercular treatment, which has failed to bring about certain improvement of the condition.
The main aim is conservative surgery and to preserve as much renal tissue as possible. An obstructed
lower pole calyx may be drained into the upper ureter. A strictured renal pelvis will need pyeloplasty.
Ureteric shortening or stenosis may require bowel interposition or Boari operation depending on the level
and extent of the fibrosis.
1. Renal cavernostomy by Hanley.— After exposing the kidney through usual approach, the abscess
is aspirated with wide-bore needle. The roof of the abscess is removed and the caseous contents are
swabbed out till healthy granulation
tissue is reached. The cut edges are
sutured by fine catgut to stop bleed
ing. The wound is closed without
drainage, as there is no chance of
leakage of urine, because the pelvis
or calyces is not opened.
2. Nephrectomy.— If after 3
months of medical treatment, the culture
of urine is still positive and there is
gross involvement of the affected
kidney radiologically, nephrectomy
If one or the other pole is grossly
damaged while the other parts of the
kidney are almost disease free, partial
nephrectomy should be considered.
3. Nephroureterectomy.— This
operation should be considered when
the ureter has also been grossly
involved. By a separate hypogastric
incision the ureter is ligated and divided
at its entrance into the bladder. After
that lumbar nephrectomy is performed
Fig. 57.9 — Nephroureterectomy. Ureter is exposed through a sepa- alongwith the removal ofthe ureter.
rate hypogastric incision and is about to be divided between ligatures. .. ..,,
The kidney is dissected off the lumbar incision. removing the ureter alongwith the
kidney, chance of postoperative wound infection is minimised, similarly continued source of infection to the
bladder is also curtailed.
4. When the bladder is extremely contracted, which is known as systolic bladder, it is better to inc
the capacity of the bladder by performing ileocystoplasty (Hanley) in which 15 cm of terminal ileum is isolat
and is incised at the antimesenteric border and is sutured to the remaining portion of the bladder, after excis
the scarred tissue from the dome of the bladder. Continuity of the ileum is restored by end-to-end suturing a
isolating the 15 cm loop.
RENAL CALCULUS
Renal stone or calculus or lithiasis is one of the most common diseases of the urinary tract. It occurs mor
frequently in men than in women and in whites than in blacks. It is rare in children. It shows a familial
predisposition.
Urinary calculus is a stone-like body composed of urinary salts bound together by a colloid matrix of
organic materials. It consists of a nucleus around which concentric layers of urinaiy salts are deposited.
Aetiology.—
The cause of renal stone formation is not yet fully understood but in majority of cases multiple factors ar
involved. The important factors which influence the formation and growth of uroliths are as follows:—
A. HYPEREXCRETION OF RELATIVELY INSOLUBLE URINARY CONSTITUENTS —
1. Oxalate.— Though oxalate is the major component of 70% of all renal stones, yet hyperoxaluria as
a cause of formation of such stone is relatively rare Cabbage, rhubarb, spinach, tomatoes, black tea and cocoa
contain large amount of oxalate. Ingestion of excessive amounts of ascorbic acid and orange juice also increa
urinary oxalate excretion. But dietary oxalate is usually poorly absorbed and does not play a major role in
formation of oxalate stones. In fact restriction of these foods has limited effect in prevention of oxalate stones
Primary hyperoxaluria is a rare genetic disorder affecting the metabolism of glyoxylic acid, which forms
oxalate rather than other soluble end products. It is an important cause of nephrolithiasis in children. Acquir
forms of hyperoxaluria include pyridoxine deficiency, ethylene glycol poisoning small bowel disease with
hyperabsorption of dietary oxalate and methoxyflurane anaesthesia.
2. Calcium.—On regular diets normal urinary excretion of calcium ranges between 200 mg to 300 mg
per day. The major calcium in foods are in milk and cheese. Milk and dietary protein also cause increased
absorptionof calcium from the gut. In a few conditions e.g. prolonged immobilisation and certain bone disea
(e.g. myeloma, Paget’s disease and metastatic cancer) there is hypercalciuria. In these cases calcium excretion
may increase upto 450 mg or more per day Primary hyperparathyroidism also causes hypercalciuria. 2/3rd o
these patients may produce renal stones. There is a condition which is called ‘idiopathic hypercalciuria’ in
which males excrete more calcium though the serum calcium is normal and serum phosphorus is decreased.
This may be due to defective renal tubular reabsorption of calcium. Hypervitaminosis D may also cause
hypercalciuria. Renal tubular acidosis also causes hypercalciuria. But inspite of this long list majority of the
above conditions do not produce renal stones.
3. Uric acid.— Many patients with gout form uric acid calculi particularly when under treatment. If the
urine is made alkaline and diluted while treating this disease chance of uric acid stone formation is Jess.
Administration of allopurinol also decreases stone formation. Many uric acid stone formers have normal seru
and urinary uric acid levels but show a consistently low urinary pH.
4. Cystine.— Cystinuria is an hereditary disease which is more common in infants and children. Only
a small percentage of patients with cystinuria form stones.
5. Drug induced stones.— In rare cases, the long term use of magnesium trisilicate in the treatment of
peptic ulcer has produced radio-opaque silicon stones.
B. PHYSICAL CHANGES IN THE URINE —
1. Urinary pH.— The mean urinary pH is 5.85. It is influenced by diet and medicines. If the urin
becomes infected with urea splitting bacteria e.g. proteus mirabilis, it makes the urine strongly alkaline by
liberating ammonia. The inorganic salts which are less soluble in alkaline medium e.g. calcium phosphate an
1072
magnesium ammonium phosphate (triple phosphate) will form urinary stones.

2.Colloid content.— As mentioned above it has long been claimed that the colloids in the urine allow
the crystalloids to be held in a supersaturated state. But the importance of this theory has been questioned
recently.
3. Decreased concentration of crystalloids.— This may be due to low fluid intake, excessive water
losses in febrile disease and in hot climates, due to excessive perspiration or due to excessive water loss from
vomiting and diarrhoea.
4. Urinary magnesium/calcium ratio.— This probably has notable influence on stone
formation. Acetazolamide (Diamox ) causes hypercalciuria and a decrease in the ratio — this is related to
increased incidence of stone formation. The thiazides, which have tremendous influence in preventing
recurrence of stone formation, increase this ratio.
C. ALTERED URINARY CRYSTALLOIDS AND COLLOIDS —
In urine there are quite a number of crystalloids of different types. These crystalloids are kept in solutio
by the presence of colloids in the urine by the process of absorption. Urinary crystalloids are discussed below
e.g. oxalate, calcium cystine, uricacidetc. Urinary colloids are mucin and chondroitin sulphuric acid, (a) When
there is imbalance in the crystalloid-colloid ratio — either there is an increase in the crystalloid level or a fall
in the colloid level, urinary stones may be formed, (b) If there is any modification of the colloids e.g. they lose
their solvent action or adhesive property, urinary stones may develop.
D. DECREASED URINARY OUTPUT OF CITRATE.—
Presence of citrate in the urine keeps relatively insoluble calcium phosphate and carbonate in solution.
The normal citrate concentration in urine is 300 to 900 mg per day. Excretion of citrate depends on certain
hormones. It is decreased during menstruation.
E. VITAMIN A DEFICIENCY —
Deficiency of Vitamin A in the food tends to induce stone formation in animals. Stone formation is mor
common in northern parts of India and Egypt probably due to this. Deficiency of Vitamin A causes
desquamation of the epithelium. The desquamated cells form nidus for stone formation. This is more applica
to bladder stones.
F URINARY INFECTION —
Association of stone with infection is very intimate. In about 80% of cases there is infection of the urinar
tract. But it is difficult to say whether it is the cause or result of such infection, (a) Infection disturbs the colloi
content of the urine, so there is more chance of stone formation, (b) Infection also causes abnormality in the
colloids which may cause the crystalloid to be precipitated, (c) Infection also changes urinary pH which help
in stone formation, (d) Infection also causes increase in concentration of crystalloids, which may under some
circumstances produce stone.
G. URINARY STASIS.—
It goes without saying that stones are more prone to occur when there is obstruction to the free passage
of urine, (a) Urinary stasis provides a fertile field for bacterial growth, (b) It also causes a shift of the pH of
the urine to the alkaline side, (c) Stasis also predisposes urinary infection, (d) It allows the crystalloids to
precipitate.
H. HYPERPARATHYROIDISM —
Though this condition is seen in only 2% to 5% of cases of renal stone, yet its potentiality to form urinary
calculus cannot be underestimated. In cases of multiple or recurrent urinary calculi this cause should be
eliminated. Due to overproduction of parathormone the bones become decalcified and calcium concentration
in the urine is increased. This extracalcium may be deposited in the renal tubules or in the pelvis to form rena
calculus. Peculiarly enough renal calculi are more likely to develop when hyperparathyroidism is mild and
prolonged without much skeletal lesion.
I. NIDUS OR NUCLEUS OF STONE FORMATION (Including Randall’s plaque).—
Randall observed that the initial lesion in formation of renal calculus is erosion at the apex of one of the
renal papillae. Calcific plaques are seen on these renal papillae, which were known as Randall’s plaques. He
believed that this erosion developed as a result of injury secondary to infection Randall postulated that whe
the overlying mucosa is ulcerated, the calcification acts as a nidus on to which insoluble crystals deposit to f
stones.
Many investigators subsequently believed that most stones develop by precipitation of crystals e.g. calc
oxalate on an organic matrix formed of aminoacids and carbohydrates. Even blood clots,clumps of epithelia
cells, bacteria or even pus cells may form nidus. Necrotic ischaemic tissue and foreign bodies may form nidu
and encourage stone formation. Such tissues may be caused by neoplasms, necrotic papillae or ulcerated mu
membrane from infection.
Types of renal calculi.— Basically the renal stones can be divided into two major groups — I. Primary
stones and II. Secondary stones.
PRIMARY STONES are those which appear in apparently healthy urinary tract without any antecedent
inflammation. These stones are usually formed in acid urine. These stones usually consist of calcium oxalate,
uric acid, urates, cystine, xanthine or calcium carbonate.
SECONDARY STONES are usually formed as the result of inflammation. The urine is usually alkaline,
as urea splitting organisms are most often the causative organisms. Secondary stones are mostly composed
calcium ammonium-magnesium phosphate (the so-called triple phosphates). Amorphous phosphates and
ammonium urate may enter into the composition of secondary stones. Majority of the secondary stones are
phosphate stones.
I PRIMARY STONES —
1. Oxalate calculus (calcium oxalate).— This type of stone is usually single and is extremely hard. It
is dark in colour due to staining with altered blood precipitated on its surface. It is spiky that means it is cov
with sharp projections, which cause bleeding due to injury to the adjacent tissues. This stone is popularly kn
as Mulberry stone. On section it shows wavy concentric laminae that means it is formed by deposition of lay
of calcium oxalate on a nidus.
The peculiarities of this stone are :—
(i) It is often impacted in the ureter.
(ii) It causes bleeding due to its rough surface.
(iii) There may be deposits of secondary phosphate on its surface caused by infection leading to
formation of ‘mixed stone’.
(iv) Due to high calcium content it casts an exceptionally good shadow radiologically (radio-opaque).
The rough surface may also be evident in X-ray.
2. Uric acid and urate calculi.— Pure uric acid calculi are rare and are not visible in X-ray (not radio
opaque). The majority contains urates and enough calcium oxalate to render such calculi radio-opaque. Thes
stones usually occur in multiples and so are typically faceted. The stones are of moderate hardness. Their co
varies from yellow to dark brown. On section the stones display wavy concentric markings. The surfaces of
these stones are usually smooth. These stones usually occur in acid urine.
In children, stones of ammonium and sodium urate are sometimes found. These stones are yellow, sof
and friable. But unfortunately if these do not contain some impurities like calcium oxalate, they do not becom
radio-opaque, so may not be visible on straight X-ray.
3. Cystine calculi.—These stones usually appear in patients with cystinuria. Such cystinuria sometimes
occurs in young girls. Cystine is an aminoacid rich in sulphur. Cystine calculi usually occur in multiple. The
calculi are soft and yellow or pink in colour. When these are exposed outside the hue gradually changes to g
Pure cystine calculi are not radio-opaque, but as they contain sulphur they are usually radio-opaque. Such st
also occur in acid urine.
Cystinuria has been discussed above. It is usually caused by diminished resorption of cystine by the re
tubules. Sometimes excessive cystine appears in urine due to inborn error in metabolism. The condition is of
familial and such cystine is not converted into sulphate. Cystine crystals which are found in urine in cystin
uria are usually hexagonal, white and translucent. These usually appear in acid urine.
4. Xanthine calculi.— These are extremely rare. These are smooth, round and brick red in colour. On
68
cut surface it shows lamellar appearance.

5. Indigo calculi are so uncommon that these are merely academic curiosities. These are blue in co
and are derived from indican, formed by decomposition of tryptophan in the intestine and found in the urin
II. SECONDARY STONES —
1. Phosphate calculus.— Majority of these stones are composed of calcium phosphate, though a few
are composed of ammonium magnesium phosphate, known as ‘triple phosphate’. Such calculus is usually
smooth, soft and friable. It is usually dirty white in colour. This type of calculus usually occurs in infected ur
and so is a secondary calculus. Urine is often alkaline. Such stone enlarges rapidly and gradually fills up pel
and renal calyces to take up the shape of ‘ staghom calculus ’. As this stone gives little symptom due to its sm
surface, it enlarges rapidly. Triple phosphate usually results from liberation of ammonium carbonate from u
brought about by urea splitting organisms. While majority of such stones are made up of calcium phosphate
a few are made up of mixture of calcium phosphate and triple phosphate.
On cut section it shows laminated appearance as the crystalloid are deposited in layers.
These stones are usually radio-opaque as these contain calcium. But it is also due to its large size rathe
than density that it is radio-opaque.
2. Mixed stones.— Phosphate stone may occur as covering of a primary stone. Such stones are known
as ‘mixed stones’. The primary stone is often the calcium oxalate stone. When the urine becomes infected
deposits of phosphate occur on the rough surface of calcium oxalate stones. Such stones also occur in alkalin
urine.
EFFECTS OF STONE :—
The size and position of the stone usually govern the development of secondary pathologic changes in t
urinary tract.
A. SAME KIDNEY —
1. Obstruction.—
(i) A stone lodged at the ureteropelvic junction or in the ureter may cause hydronephrosis if t
obstruction is intermittent or incomplete.
(ii) When the obstruction is complete it may slowly destroy the kidney.
2. Infection.— This is a common complication due to stasis of urine caused by the stone and due to its
presence as foreign body. Such infection may cause pyelitis, pyelonephritis perinephric adhesion and even
perinephric abscess. When infection has been superimposed on hydronephrosis, pyonephrosis may result.
3. The epithelium of the pelvis and calyces in relation to the stone gradually loses lustre, becomes roug
and thickened. Parenchymal ischaemia may be caused by local pressure due to stone.
4. Sometimes due to presence of stone the lining epithelium of the renal pelvis may undergo metaplasi
(from normal transitional variety to squamous variety) which may instigate to initiate malignancy of epid
ermoid nature (epithelioma).
B. OPPOSITE KIDNEY —
1. Compensatory hypertrophy may occur when the affected kidney has lost function due to complete
obstruction with stone.
2. Stone formation may be bilateral.
3. Infection of the opposite kidney may result from ascending infection from the urinary bladder when
urine becomes infected due to presence of stone.
4. Calculus anuria.—Reflex cessation of function of the opposite kidney occurs due to reno-renal reflex
caused by complete obstruction of the affected kidney with calculus.
SYMPTOMS.— Symptomwise cases can be divided into 4 groups :—
1 Quiescent calculus.— A few stones, particularly the phosphate stones, may lie dormant for quite
long period During this time the stones gradually increase in size with destruction of renal parenchyma. Suc
stones may be discovered accidentally in X-ray performed for some other reason or is first revealed with ren
failure and uraemia. Sometimes such stones are also discovered due to symptoms of urinary infection.
When the stone is still in the submucosal stage (Randall’s plaque ) or adherent to the parenchyma, it
may be symptomless. Even ‘staghorn calculus’ may be asymptomatic. Vague gastrointestinal symptoms whic
simulate peptic ulcer or gallbladder disease or enteric syndromes may be found in a few cases.
2. Pain.— Pain is the leading symptom of renal calculus in majority of cases (80%). Three types of pain
are usually noticed viz. fixed renal pain, ureteric colic and referred pain, of which the last is very rare.
(a) Fixed renal pain.— If the stone is free and obstructs a calyx or ureteropelvic junction, there will be
dull flank pain due to capsular and parenchymal distension. Dull aching or boring type of pain is also
experienced in case of big phosphate calculus. The pain is situated in the renal angle posteriorly and in the
corresponding hypochondrium anteriorly. This pain characteristically gets worse on movement particularly
walking up the stairs and during jolting.
(b) Ureteric colic. — This occurs when the stone attempts to pass down the ureter or temporarily blocks
the pelviureteric junction. It is an agonising pain which radiates from the loin to the groin. The pain comes
on suddenly during which the patient rolls about drawing up his knees towards the chest, tossing on the bed
in agony. This colic is often accompanied by profuse sweating, nausea and vomiting. The pulse quickens and
the temperature goes down below normal. The typical radiation of the colicky pain is due to reflex pain which
takes place along the course of the iliohypogastric and ilioinguinal nerves which are the somatic nerves of the
same segments which supply the autonomic nervous system to the ureter (T11,12 and L1). Sometimes the pain
is referred to the scrotum or labium major and to the innerside of the thigh along the distribution of the
genitofemoral nerve when the stone is in the lower part of the ureter. When the stone is in the intramural part
of the ureter ‘strangury’ may occur. ‘Strangury’ means painful straining at urination in vain, with passage of
a few drops of blood-stained urine.
The colicky pain persists for a variable period usually 6 to 8 hours, and passes off as suddenly as it cam
Ureteric colic may pass off with compensatory polyuria or passage of stone in the urine.
(c) Referred pain.— This is quite rare and is sometimes referred to all over the abdomen. Such pain
may simulate peptic ulcer or gallbladder disease. Sometimes pain may be referred to the opposite kidney, wh
is known as renorenal reflex.
3. Hydronephrosis.— Sometimes patient complains of a lump in the loin and a dull ache, which are
due to hydronephrosis caused by renal stone.
4. Occasionally haematuria is the leading and only symptom. Haematuria usually occurs in small
amount to make the urine dirty or smoky during or after an attack of pain.
Infection of the kidney may occur due to stone which is relatively symptomless. Patient presents with
pus in the urine in varying amounts or opalescent urine.
PHYSICAL SIGNS.—In majority of cases characteristic physical signs are not present. The signs which
may be present and should be looked for are :
(i) Tenderness.— This is mostly present at the ‘renal angle’ posteriorly. This angle is between the
lower border of the 12th rib and the lateral border of the erector spinae muscles. Anteriorly such tenderness
may be elicited about an inch below and medial to the tip of the 9th costal cartilage, which is known as the
renal point’.
Tenderness is more a constant feature when renal calculus is associated with infection.
(ii) Muscle rigidity over the kidney may be found in a few cases. Rebound tenderness anteriorly can
also be elicited, particularly if acute infection is associated with.
(iii) Swelling.— When there is hydronephrosis or pyonephrosis associated with renal calculus, a
swelling may be felt in the flank.
The characteristics of a renal swelling are :—
(a) It is oval or reniform in shape.
(b) The swelling is almost fixed and cannot be moved as it is a retroperitoneal swelling.
(c) A kidney lump is ballotable. which is described in ‘A Manual On Clinical Surgery’.
(d) The swelling slightly moves up and down with respiration, but much less than a liver swelling.
(e) Fingers can be insinuated between the lump and the costal margin (which is not possible in sple
nic or liver swelling).

(f) A band of resonance can be elicited anteriorly on percussion, due to presence of colon, duoden
and coils of small intestine in front of the kidney according to the side (but such resonance is absent in sp
and liver swellings).
(iv) Abdominal distension and diminished peristalsis may accompany ureteric colic.
1 Blood examination.— This hardly reveals any specific abnormality, but an increased white blood cel
count may be seen when associated with infection. Anaemia may be found if renal function is not adequa
Renal function must be assessed by estimating blood urea, N.P.N. and creatinine.
If serum proteins are decreased but total calcium is normal, an increase in ionised calcium is indicate
Hypercalcaemia with hypophosphataemia strongly suggests primary hyperparathyroidism, though norm
serum phosphate is found in 60% of patients. Estimation of serum chloride concentration is helpful in thi
respect as when it is above 102 mEq/L it is a case of hyperparathyroidism and when it is below this figur
may be due to hypercalcaemia from other causes.
Serum hypercalcaemia is very much associated with calculus disease, though it is commonly associa
with osteolytic and disseminated malignant diseases e.g. cancers of the breast, lungs, multiple myeloma,
leukaemia etc. It is also seen in sarcoidosis. But these conditions rarely cause renal stones.
Elevated serum uric acid level is found in 50% of uric acid stone carriers.
2 Urinalysis.—
(i) Physical examination may show smoky urine due to slight haematuria or opalescent due to pres
of pus.
(ii) Chemical examination may show presence of protein due to haematuria and blood in the urine.
pH of the urine is higher than 7.6, presence of urea-splitting organisms is assured. This also denotes that
stone is probably of triple phosphate Consistently low pH is a common cause of formation of uric acid ca
A simple chemical test for cystine may be performed by
making the urine alkaline with ammonium hydroxide and then
2 ml of 5% sodium cyanide is added and the urine is allowed to
standfor 5 minutes A few drops of fresh 5% sodium nitroprussi
is added. A deep purplish-red colour means cystinuria.
(iii) Microscopic examination of urine may show
R.B.C., pus cells and casts. Different crystals may be seen in the
sediment to give a clue as to the type of stone present Uric acid
and cystine crystals may be precipitated by adding a few drops
of glacial acetic acid, which lowers the urinary pH to about 4
The test tube of urine is then refrigerated. Uric acid crystals are
shown amber-brown, whereas cystine crystals look like benzen
rings.
(iv) Bacteriological examination of urine is highly
important including culture and sensitivity tests.
(v) Renal function tests should always be perfo
in calculus cases. The PSP may be normal even in presence of
bilateral staghorn calculi. But it may be depressed to 2/,rds of
normal in acute obstruction at the ureteropelvic junction
3 . Radiography.—
A. STRAIGHT X-RA
KUB region (both kidneys, ureters and bladder), the bowels
must be made empty by giving laxative
Fig.57.10— Straight X-ray shows At least 90% of renal stones are radio-opaque and are easily
branched renal calculus in right kidney. visible in a plane film of KUB region unless they are very small
or overlie bones. A staghom calculus can be easily diagnosed and there is no confusion with other radio
opaque shadows.
It is necessary to differentiate renal stone from other structures and pathologies which may produce
radio-opaque shadow on straight X-ray similar to a renal calculus. These structures and pathologies are as
follows :
(i) Phleboliths.
(ii) Ossified tip of the 12th rib.
(iii) A calcified lumbar or mesenteric lymph nodes.
(iv) Gallstones.
(v) A chip fracture of the transverse process of a lumbar vertebra.
(vi) A calcified tuberculous lesion of the kidney.
(vii) A calcified suprarenal gland.
(viii) A few drugs e.g. fersolate or foreign bodies in the G.I. tract.
The characteristic features of renal stone are :
(a) Exposures are made during full inspiration and full expiration. If the opaque material moves with the
kidney as measured from the lower pole of the kidney, it is probably a renal stone.
(b) Renal stone is usually equal in density (whereas gallstones are usually ring shaped with a radiolucent
centre).
(c) In a doubtful case a lateral radiograph should be taken. If the opaque material is seen in front of the
bodies of the vertebrae, it is not a renal stone. A renal stone is superimposed on the bodies of the vertebrae.
B. EXCRETORY UROGRAM is necessaiy to
accurately localise the calcific shadow in relation
to the kidney. It also reveals the functions of the
other kidney. If the stone is non-opaque, excretoiy
urography will show filling defect or negative
shadow.
Retrograde urogram may be needed if excretoiy
urography fails to show the kidney due to poor func
tion.
4. Ultrasonography.— This is helpful to dis
tinguish between opaque and non-opaque stones. It
is also of value in locating the stones for treatment
with extracorporeal shock wave therapy.
5. Computed tomography.— This is partic
ularly helpful in the diagnosis ofnon-opaque stones.
6. Renal Scan.— If excretoiy urogram shows
poor renal function, isotope studies may indicate
further about renal function. Such findings by dif
ferent isotopes may indicate the need for nephrec
tomy rather than nephrolithotomy.
7. Instrumental examination.—
Cystoscopy.— Renal stone as such does not
require cystoscopy for diagnosis. It may be required
to locate the stone in the ureter by ureteral
catheterisation or by measuring renal function bv
Fig.57.11.- Bilateral renal calculi on straight X-ray. catheterisation. This also can determine if
Stag-horn calculus on right side.
the affected kidney has been infected or nol. Cystoscopy diagnoses urethral stricture or prostatic obstructi
the cause of stone formation. Such studies in conjunction with retrograde urograms may be the deciding fa
in choosing between pyelolithotomy and nephrectomy.
8. Examination of the stone.— 1 f a stone is passed previously, crystalographic examination is requir
establishing the type of stone and cause of stone formation.
TREATMENT.—
1. PREVENTION.— This part should have been described at the end of treatment, as the patients w
have already undergone treatment for renal stones should be managed prophylactically in an attempt to p
vent recurrence. With more knowledge of stone formation, responsibilities lie on the surgeons to prevent
further stone formation and cannot be left solely to God to prevent recurrence or to fully cure the patient.
Recurrence may be classified into two varieties — False recurrence and True recurrence.
A. False recurrence, which means a tiny stone was overlooked at the time of operation.
B. True recurrence.— A patient with renal stone is usually liable to produce further stone subsequently
attempt should always be made to prevent such recurrence. The various measures which should be adopt
prevent such recurrence are divided into two categories — (I) General measures and (II) Specific measures
(I) General measures.— I fa stone is available it must be analysed chemically to know its composition. If
a stone is unavailable for analysis the following data should be carefully noted :—
(i) X-ray density, (ii) types of crystals found in the urine, (iii) chemical test for cystine crystals an
abnormalities in blood chemistry (excess of calcium, phosphorus or uric acid).
The general measures or advises which should be given to the patient regardless of the type of stone a
(a) Fluid intake should he high at all limes. Fluids should be taken at bed time so that nocturia will occur
This will prevent dehydration.
(b) Avoidance of milk, cheese and great deal of calcium should be advised. If renal function is satisfac
tory sodium cellulose phosphate 5 g T.D.S. with meals should be prescribed to reduce calcium absorption.
(c) Urine should be kept acid all the time. Alkalies should be prohibited or used in less quantities in t
patients who are suffering from peptic ulcer.
(d) Vitamin D should be stopped or used in very low quantity.
(II) Specific measures.—
(i) Calcium stone disease.—
Non-idiopalhic.— Here a definite underlying cause related to a metabolic defect in calcium (e.g.
hyperparathyroidism, increased vitamin D, sarcoidosis) or oxalate (primary hyperoxaluria or acquired dis
secondary to enteric disorder) is detected. The specific treatment of these disorders is beyond the scope of
book.
Idiopathic.— Most idiopathic stones are composed of calcium oxalate (70%) as the mono-or dihy
drate. Calcium phosphate is present in half such stones which are rarely homogeneous and also contain 10
uric acid. Crystal formation in urine depends on a balance between those forces promoting solute precipit
— urinary oxalate, urinary uric acid, urinary pH and urinary calcium (in decreasing order of risk) — and t
inhibiting it — urinary citrate, urinary magnesium, urinary macromolecules and urinary pyrophosphate (
decreasing order of influence). Inorganic inhibitors act to increase the solubility of calcium and oxalate wh
macromolecules act in concert with them by preventing the aggregation and increase in size of crystals alr
present (Ryall et al 1991). So low urinary volume, hypercalciuria, hyperoxaluria, hyperuricosuria and
hypocitraturia and low urinary magnesium are all responsible for stone formation.
Fluid intake.— A low urinary volume will increase the risk of crystal formation. The aim should be
to maintain the urine volume at a minimum of 1.5 to 2 litres/day.
Diet.— Western diet with increased intake of animal protein and carbohydrate is associated with
increased urinary calcium, oxalate, phosphate and hypocitraturia compared with controls and thus repres
a potent risk of stone formation. So patients should be advised to restrict this type of diet. Dietary intake of
calcium should also be restricted. However it has been shown that calcium binds oxalate in the gut preventin
its uptake, so low calcium intake will increase the amount of oxalate available for absorption creating an
increased risk of oxalate crystallisation. So in mild hyperoxaluria, a high calcium diet is required, together wi
a diet avoiding oxalate-rich foods (e.g. tea and chocholate). A mega dose of vitamin C should be avoided. No
excess stone risk has been shown related to dietary intake of sodium, sucrose or cola.
Citrate.— Value of citrate therapy in calcium oxalate stone prevention has been questioned. Many
urologists have found no difference in stone recurrence rates in randomized trials. Orange juice acts in a
similar way to oral citrate in that it increases both urinary pH and citrate and reduces urinary uric acid. How
ever whilst oral citrate reduces urinary oxalate and calcium, orange juice increases oxalate and has no effect o
calcium.
Cellulose phosphate and thiazide diuretics.— These agents are used in the treatment of hypercalciuria.
When the case is one of diet independent hypercalciuria, best treatment is cellulose phosphate which binds
calcium in the gut limiting its availability. When the primary defect is a failure of tubular calcium reabsorptio
thiazide diuretics can be prescribed, which increase calcium absorption in both poximal and distal convolute
tubules. When there is increased gut absorption of calcium, dietary calcium restriction is the appropriate.
(ii) Infection stones. — Brown (1901) proposed the theory that the splitting of urea by bacteria resulted
ammoniacal urine, alkalinization and stone formation. In general, infection stones consist of magnesium
ammonium phosphate (Struvite) with varying admixtures of calcium phosphate (apatite). Struvite stones ma
partially dissolve in the presence of sterile urine, so long term low-dose treatment with antibiotics is appro
priate even when urine culture is initially sterile. Particularly in the latter case the use of antibiotics active
against Ureaplasma and/or Corynebacterium (e.g. tetracycline and erythromycin) may be beneficial. Many
bacteria other than Proteus produce urease,, e.g. Klebsiella, Providentia and Staphylococci. The ammonia
produced promotes stone formation. Another effective approach to complement existing treatment for
infection stones involves the use of derivatives of hydroxamic acid which inhibit bacterial urease.
(iii) Oxalate stone.— Foods high in oxalate should be eliminated from the diet. These are rhubarb,
strawberrys, plums, spinach, asparagus etc. These may be used in low quantities or with milk or cream, in
which case the oxalates are precipitated as insoluble calcium salts in the intestine and are not absorbed. Pyri-
doxine in large doses may be helpful. Thiazides are useful agents which decrease both urinary' calcium and
oxalate.
Administration of magnesium oxide 150 mg 3 times a day may control recurrence of oxalate stones as
magnesium combines with oxalate to form a more soluble complex.
(iv) Phosphate calculi.— Urine acidifier should be used to keep the urine in the acid side. Sodium or
potassium acid phosphate 4 to 6 g daily is effective (potassium salts are preferable). Ammonium chloride
should also be used as another urinary acidifier. Phosphates in the diet should also be restricted. Aluminium
gel 40 ml T.D.S. and at bed time is also very useful to reduce recurrence of phosphate calculi.
(v) Uric acid calculi.— A low-purine diet should be prescribed for the uric acid stone former. Red me
fish and liver are rich in purine. The urine should be kept at a higher pH level (7.0 or higher) thereby increasi
the solubility of urates to 100%. 50% sodium citrate solution 1 to 2 tea-spoon full 4 times daily is needed. A
mixture of sodium and potassium bicarbonate is also good in this respect. The patient himself can know this
urinary pH with paper indicators. Allopurinol is also essential in patients with high serum uric acid. The
combined use of thiazides and allopurinol seems to be more rational but the toxicity of the agents are enhanc
a little bit.
(vi) Cystine calculi.— Sulphur containing proteins such as meat, fish and eggs should be restricted.
Carbohydrates and fats may be increased in the diet alongwith low sulphur content proteins. Intake of fluids
must be increased to dilute cystine in the urine. Fluid must be taken at night just before going to bed. Urine
should be kept alkaline. Penicillamine may be prescribed to prevent recurrence of cystine calculi. This prepa
ration should be given in the dose of 30 mg/kg daily in divided doses. This usually reduces the amount of
cystine in the urine. Pyridoxine 50 mg daily should also be given. This not only ceases stone formation but
may also dissolve some stones.
(vii)Indomethacin 20 mg T.D.S. has been found to reduce calcium secretion. This may help in preventin
further stone formation.
2. CONSERVATIVE MEASURES.— Not all patients with renal stones require surgery.
(i) When the stones are sufficiently small, these can be naturally eliminated and expectant policy is be
adopted in these cases.
(ii) In the elderly, poor risk patients a coralliform stone is best left alone unless it causes significant
symptoms.
(iii) Chemical dissolution of renal stones requires indwelling ureteral catheters for constant through an
through irrigation with Renacidin or with G solution. Sometimes stone fragments occlude the ureteral cath
eters and cause acute obstruction. With the advent of percutaneous extracorporeal shock wave lithotripsy
(ESWL), this method has mostly become obsolete.
3. PERCUTANEOUS METHODS.— The development of extracorporeal shock wave lithotripsy (ESWL),
percutaneous nephrolithotomy (PCNL) and ureteroscopy (URS) have changed the treatment of stones to th
extent that open surgery is now required in less than 1% to 2% of cases. Sterile urine is desirable prior to an
stone treatment. Preoperative urine cultures are used to guide antibiotic choice but prophylaxis should be
provided in any case with intravenous gentamycin given immediately prior to treatment and oral antibioti
(Norfloxacin, Co-amoxiclav) continued postoperatively.
Percutaneous nephrolithotmy (PCNL).—
First described in 1976, PCNL is a technique which allows safely and reliably the removal of stones from
the pelvicalyceal system and upper ureter. The later development of ESWL has however considerably
decreased its use. With the patient in the prone/oblique position, access to the pelvicalyceal system is secu
by a nephrostomy tract directed through a suitably placed calyx. This tract is then dilated to allow the pass
of instruments used for stone removal. First of all the stone is visualised. If the stone is quite small it can be
extracted through the nephroscope. If the stone is quite large, it is broken with an ultrasonic lithotriptor.
Following this, a 20-22 Fr. nephrostomy tube is inserted to drain the kidney and allow the passage of any
residual fragment or clot. A nephrostogram 48 hours postoperatively confirms the absence of extravasation
and free passage of contrast to the bladder allowing the removal of the nephrostomy tube. In the event of
retained fragment, the nephrostomy tube can be left in situ to allow further PCNL or irrigation chemolysis
required.
Removal of fragments may take quite a long time if the calculus is large. When the operation is finished
nephrostomy tube is left to drain the kidney. It facilitates repeated access if stone particles remain. This
technique of percutaneous nephrolithotripsy may be combined with extracorporeal shock wave lithotripsy
(ESWL) to treat complex big staghom calculus. While the central part of this stone is removed by percutane
ous method, the peripheral portions are removed by ESWL.
Complications.— (i) Haemorrhage from punctured renal cortex is the most common complication, which
may be profuse and difficult to control.
(ii) Sometimes the needle may perforate the colon or pleural cavity and cause disaster.
Bleeding.— Bleeding related to PCNL can be alarming but it is usually controlled by the placement of a
nephrostomy tube or balloon catheter to tamponade the tract. If bleeding continues, the drainage tube is cl
allowing the pelvicalyceal system to tamponade the bleeding vessel. If bleeding still continues or the patie
haemodynamically unstable, open surgery and exploration may be required. Persistent bleeding may be
corrected with angiography and embolization.
Stone fragmentation.— Stones less than 12 mm may be removed intact, but large stones will require
fragmentation. This can be achieved in a variety of ways —
Ultrasonic Lithotripsy (USL).— The tip of such a rod when placed in contact with the stone will rub sm
fragments off its surface and the hollow probe allows suction of the fragments thus produced. This makes its
usefulness in the treatment of friable (staghom) calculi.
Electrohydraulic lithotripsy (EHL).— In this technique stone fragmentation is achieved in a similar fash
ion to that described in ESWL. The EHL probe is flexible, but is traumatic to the urothelium and may cause
perforation if placed in direct contact with it. It utilises the generation of a shock wave by high tension dis
charge across the conducting elements of a co-axial electrode. Nevertheless it is an effective and fast way to
fragment large calculi.
Laser lithotripsy (LL).— A pulsed dye laser with transmission down a > 200 micron fiber can effectively
fragment calculi. The emitted light is absorbed by the stone and a gaseous plasma forms on its surface. Plasm
absorbs more light and expands generating a shock wave which fragments the stone.
Pneumatic lithotripsy (PL).— In this technique compressed air is driven with a metal pellet within a
hollow metal probe. It is very effective to break even hard stones.
Patient selection.— PCNL is mostly indicated in those situations where ESWL is inappropriate or may
give rise to high retreatment rate. These situations are : (i) Large stones — bigger than 3 cm; (ii) staghom
calculus; (iii) Hard stones e.g. cystine; (iv) Anatomic abnormality e.g. obesity, scoliosis etc; (v) Stones
unresponsive to ESWL and (vi) coexisting obstructive uropathy.
The only true contraindication to PCNL is bleeding diathesis.
ESWL (Extracorporeal Shock Wave Lithotripsy).— In this technique the stone is removed with shock
wave without the need for instrumental penetration of the body. The stone in the kidney is fragmented by
repeated shock waves which are focussed towards the kidney stone. The fragments are made so small that th
are automatically passed through the urine. In some instances a ureteroscope may be required for the passag
of fragments. Occasionally these may cause ureteric colic and even obstruction in the ureter which may need
temporary nephrostomy.
This method is gradually replacing operative methods of removal of renal calculi.
The treatment of renal and ureteral stones has undergone dramatic changes following the advent of extra
corporeal shock wave lithotripsy (ESWL). Domier-HM lithotriptor was previously used. Very recently the
second generation lithotriptor.— ‘Lithostar’ is being used with reasonable success. At various institutions thi
is being used in India also.
The urinary calculus is bombarded with shock waves of sufficient energy so that it disintegrates into frag
ments. In the original Domier machine the shock waves were generated by an electrical discharge placed at
one focus of an ellipsoid mirror. The patient is so positioned under radiographic control and by placing a
second mirror in such a position that its focus corresponds to the position of the calculus and the full force of
the shock waves are subjected to the calculus. Both the patient and the shock wave generators are immersed
a bath of water. In present days water bath is not used and the fluid is confined to the path of shock waves. T
shocks may be generated by the discharge of an array of pietzoelectric cells and they may be aimed by
ultrasonography.
Patients are admitted on the day of ESWL and are usually discharged the next morning. All patients are
routinely covered with some antibiotic parenterally starting from the previous night and continuing till the t
of discharge.
The second generation lithotriptor — ‘The Lithostar’ has many advantages over the previous Domier
instrument. These are (i) Stone localisation is done by biplaner fluoroscopy and not by ultrasound. There is
provision to vary the brightness and contrast in the images of the stones to make localisation of the stone eas
(ii) There is no bath tub, that is why the machine is relatively lighter and easy to handle, (iii) The table on wh
the patient is placed is an almost ordinary table with facilities for doing cystoscopy, uretero-renoscopy, PCN
etc. (iv) This unit has two shock head generators one on each side, so that the patient’s position is not altered
(v) This instalment works on electromagnetic generation of impulses and does not require costly electrodes
which need frequent replacements, (vi) This instrument is such that the shock waves hit on kidney only in
expiratory phase of respiration, thus avoiding any wastage of shocks.
Injection pentazocin 15 to 30 mg and injection diazepam 5 to 10 mg i.v. are required before the operation
General anaesthesia is only required in children and non-cooperative patients.
Stones in the renal pelvis and calyces are in ideal location for this treatment as these are surrounded by
fluid. Fragmentation rate is about 93 to 97% in this group.
Shock wave effects.—
Solids.— Shock waves encountering brittle solids in a fluid medium give rise to tensile and contralateral
forces at the fluid/solid interface resulting in stone fragmentation.
Bio effects.— Shock waves cause blunt trauma to the renal parenchyma resulting in haematuria which is
almost universally seen following ESWL. However, clinically significant haematuria or subcapsular/perire
haematoma is rare. The risk is increased with pre-existing hypertension or aspirin use. Lung tissue is sensit
to shock waves and needs to be out of the blast path or shielded prior to treatment. Pancreatitis is reported
rare.
The COMPLICATIONS of this treatment are mainly two — (i) ureteric colic, when the stone fragments
pass through the ureter. An analgesic in the form of non-steroidal anti-inflammatory drug e.g. diclofenac m
be used preliminary followed by spasmoproxyvon. A self retaining stent may be placed in the ureter so tha
fragments of stone can pass without obstruction. Occasionally impacted fragments may require ureteroscop
removal.
(ii) Infection is the second main complication as the calculus contains bacteria which are released. Tha
why prophylactic antibiotic should always be used starting before ESWL and continued in the first few
postoperative days.
Patient selection.— More than 80% of patients will be suitable for ESWL monotherapy. The only excep
tions are pregnant women, abdominal aortic aneurysms and uncorrectable coagulation disorders. Patients w
pacemakers may be treated successfully. Relative contraindications are cystine and matrix stones which do
fragment well with ESWL and stones in poorly draining hydronephrotic kidneys. Any distal obstruction m
be treated prior to ESWL. Ultimately the response to ESWL depends on the site, size and chemistry of the
stone. ,
Long-term effects and safety.— There have been concerns that ESWL may be associated with a late risk of
increased hypertension. However in long-term follow-ups such risk is not found out. There seems to be no
term effects on renal function or glomerular filtration rate. The mortality rate is extremely low in the range
0.02%.
Future developments.— The original HM3 lithotriptor required general anaesthesia. The second genera
tion machines with wide apertures and reduced power have made anaesthesia free ESWL possible. Indeed
HM3 is still considered by many to be the gold standard against which other lithotriptors should be compa
Second generation machines are considered by some to be less effective than the HM3. Third generation
machines, with improvements in shock wave energy range and integration of the shock wave source and
imaging are now available, but the main advantages seem to be economic and in ease of use. It seems unlik
that there will be major improvements in ESWL technology in near future.
Ureteroscopy (URS).—
In performing ureteroscopy, preliminary cystoscopy in the lithotomy position is carried out and a guide
is passed to the appropriate ureter. The ureteric orifice is then dilated with a co-axial dilator. Following dila
tion the bladder is emptied and the ureteroscope is passed through the ureteric orifice guided by the presen
of a previously placed guidewire. The ureteroscope is passed to the stone, which can either be snared in a
basket and removed intact or fragmented using USL, EHL, LL or PL (see above).
Two types of ureteroscope are available — rigid or flexible. Rigid instrumentation allows for better irrig
tion with the instrument in situ. However flexible ureteroscopy allows better access to the proximal ureter
kidney where rigid instruments are unable to negotiate.
The morbidity with rigid instruments relates to mucosal injury (35%), perforation (15%) and bleeding
(10%). These complications can be managed by temporary insertion of a JJ ureteric stent. Later stricture
formation is also an uncommon complication (less than 5%) and can be managed by balloon dilatation.
STONE IN PREGNANCY.— Urolithiasis complicating pregnancy is rare and about 2/3rds of stones pas
spontaneously. Majority of the stones (90%) present during 2nd or 3rd trimester. Ultrasound is the preferred
imaging modality. IVU may be required and after first trimester offers little risk to the foetus.
Obstruction may be required to be relieved with persistent symptoms and infections. This is best achieve
with percutaneous nephrostomy tube drainage or llie insertion of a JJ ureteric stent. Definitive stone treatme
can then be deferred to the postpartum period. If at all a definitive treatment is required, open surgery is
probably the best option and ESWL is contraindicated.
4. SURGICAL METHODS.—
OPEN SURGERY.— Conventional open surgery is now performed in less than 2% of all stone cases.
Choice of technique.—
Kidney stone.— Non-staghorn calculi which are non-cystine stones less than 3 cm in diameter are best
treated with ESWL. The main complication is ureteric obstruction secondary to the passage of stone frag
ments. This problem can be reduced by pre-treatment insertion of a JJ ureteric stent when the stone size is m
than 2 cm.
Staghom calculi require combination of PCNL and ESWL rather than a monotherapy. This approach
yields stone free rates equivalent to open surgery (almost 80%). If staghom calculi are asymptomatic and the
general health of the patient is poor with a good second kidney, conservative treatment can be adopted unle
there is sepsis, pain or loss of function.
Removal of stone is indicated when it is presumed that it cannot be naturally eliminated and may cause
obstruction and progressive renal damage. Unnecessary delay should be avoided. The different operations
may be performed in cases of renal calculus are —
(a) Pyelolithotomy, i.e. removal of the stone through an incision on the pelvis of the kidney when the
stone lies within the pelvis. It may be applied to dislodge stone from one of the calyces through the pelvis.
(b) Nephrolithotomy, i.e. removal of the stone through renal parenchyma is practised when the pelvis is
mostly intrarenal or when the kidney cannot be mobilised sufficiently to expose the pelvis.
(c) Pyelonephrolithotomy, i.e. removal of the stone through both the pelvis of the kidney and through the
renal parenchyma. This may be required when a stone in the calyx is so much impacted that it cannot be
removed through the pyelotomy incision, so a second incision through the renal parenchyma may be necess
(d) Partial nephrectomy.— The indications of this operation in renal calculi are discussed below under
the heading of this operation.
(e) Nephrectomy, i.e. removal of the whole kidney, is indicated in case of hydronephrotic and grossly
infected kidney containing stones, provided of course, the opposite kidney is healthy.
(f) Nephrostomy, i.e. simple drainage of kidney with removal of calculi, should be the operation of
choice in grossly infected cases and when the patient is too ill. It is also indicated in calculus anuria.
Staghom calculus is often silent and better be left alone if the kidney function has already become zero.
When the function of the kidney is still good, an attempt may be made to remove this calculus which is very
difficult and may require Gigli saw to break the calculus and remove it through pyelo- and nephrolithotom
incisions.
(1) Pyelolithotomy.— The lumbar approach is made. The kidney is well mobilised and drawn toward
the wound margin, so that its posterior surface is well exposed. The posterior surface of the pelvis is dissect
free from surrounding fat. The kidney is grasped in the left hand, so that the tips of the index and middle fin
lie beneath the renal pelvis and the thumb above it which prevents the stone from slipping into one of the
calyces. The area is surrounded widi gauze packs and an incision is made on the posterior wall of the pelvis
directly over the stone in the long axis of the renal pelvis. The incision should be long enough to remove the
slone or stones without injuring the margins of the

renal pelvis. The incision should not be extended
to the pelvi-ureteric junction lest a stricture may
cause subsequent obstruction. The stone is removed
with suitable forceps or scoops without bruising the
surrounding tissue.
All the stones, which were radiologically
apparent, should be removed. These stones which
were removed, should be inspected for their
intactness. If they are broken, one should look for
the remaining pieces inside the pelvis. After this, a
catheter may be introduced into the pelvis and a
forceful stream of normal saline is injected to wash
out any stone debris which might be present within
the pelvis.
If pyelography showed a stone in a calyx, the
stone should be located by the little finger intro
duced into the renal pelvis. If possible, it should be
removed through this route by grasping with
suitable forceps. In this process, one must take
Fig.57.12.- The operation of pyelolithotomy is being shown. utmost care not t0 lacerate neck ofthe calyx, since
serious hemorrhage may start from this laceration. If the stone cannot be removed through the incision in th
renal pelvis, a small cortical incision is made over the stone which is steadied by the little finger within the
pelvis. This stone is taken out with a suitable forceps again taking care not to damage the neck of calyx. Thus
pyelolithotomy operation is added with nephrolithotomy to remove stones from the renal calyces. After this
the cortical incision is closed with an interrupted fine catgut suture, not too tight to cut the renal cortex.
A bougie is introduced through the renal pelvis into the pelvi-ureteric junction, to be sure that there is n
obstruction hereabout.
If the kidney is not infected, this incision in the renal pelvis is closed with interrupted sutures of fine
catgut. If the kidney is grossly infected, a nephrostomy is performed before closing the incision in the renal
pelvis.
The problem remains for very large renal calculi. In these cases, the lower end of the incision on the renal
pelvis may be extended along the medial border of the kidney for wider exposure. Still wider exposure has
been advocated by Gilvernet who dissected the posterior wall of the renal pelvis into the renal sinus at a plan
between the pelvis and calyces on one side and the branches of renal vessels on the other side. This plane of
cleavage can be extended upto the neck of the calyces. The incision is now possible to be continued into the
neck of the calyces for a direct view into the calyx and to facilitate the removal of large stones. This techniqu
can be performed with ease and taking time when local hypothermia of the kidney is brought forth either by
ice-chips in polythene bag or liquid nitrogen circulating through coils placed on the kidney.
(2) Nephrolithotomy.— This operation is performed by making an incision through the renal paren
chyma along a line 5 mm behind and parallel to the convex border of the kidney (Brodel’s line). This line
actually demarcates between the areas supplied by the anterior and posterior branches of the renal artery —
this is a relatively avascular line. If the stone is palpable, the incision is made directly over the stone. Even if
the stone is not palpable, the incision is placed according to the position determined by radiography. Again
care must be taken not to incise at the neck of the calyx to prevent excessive haemorrhage. The length of the
incision should be such that it should not be too long or should not be too small to bruise the surrounding ti
during the removal of the stone. When all stones have been removed, the cavity of the kidney is washed wit
normal saline in order to remove any debris which may be left behind. Now any bleeding point should be
under-run with 000 chromic catgut. The edges of the opened calyx should be closed. The renal cortical inci
sion is closed by interrupted catgut sutures which are tied not too tightly to cut out the cortex. If the surgeo
anticipates chance of bleeding even after suturing the cortex, the sutures should be tied over a piece of mus
graft or oxycel. If there is gross infection present within the kidney, a nephrostomy should be carried out by
pushing a self-retaining catheter through this incision into the renal pelvis. This incision is then closed on
either side of the catheter.
(3) Partial nephrectomy.— The indications for this operation are :—
(i) When stone is located at one pole ofthe kidney (either in the upper most or in the lower most calyx
without much affecting the other part of the kidney.
(ii) When removal of stone may damage the calyx to such an extent that it may encourage further ston
formation. This is particularly the case in case of stone in the lower most calyx (lower pole).
(iii) In case of stone impacted in Ihe lower most calyx many surgeons prefer to perform lower partial
nephrectomy with the idea that simple removal of stone may cause recurrence as this calyx is drained again
gravity.
(4) Nephrectomy.— The indications of this operation are —
(i) Stone with gross infected kidney or pyonephrosis.
(ii) Stone with gross hydronephrosis with non-functioning kidney.
(iii) Multiple stones scattered in the kidney substance and in different calyces.
(iv) Branched staghom calculi occupying the whole of pelvis as well as the calyces with poor renal
function. If the renal function is good this stone may be removed by pyelonephrolithotomy. But these calcu
are notorious for recurring, so nephrectomy is often the best treatment.
(v) Stone with malignancy particularly epidermoid carcinoma.
It must be remembered that ihe contralateral kidney must be proved healthy before considering this
operation.
Occasionally nephrectomy may be called for not as a primary operation. These cases are —
(a) During pyelolithotomy if the renal artery is injured and the torrential bleeding cannot be controlled
nephrectomy may be considered. Similarly after nephrolithotomy if haemorrhage cannot be controlled or if
secondary haemorrhage starts after a few days of operation, nephrectomy may be considered.
(b) In a few cases of persistent urinary fistula following pyelolithotomy, nephrectomy may be consid
ered.
“Exposure of kidney” for various above operations is described below.
(5) Nephrostomy.— In this operation the renal pelvis or renal parenchyma is drained to the exterior in
the loin with or without removal of calculi. The indications of such operation are —
(i) Stone with pyonephrosis when the patient is too ill to stand any other operation.
(ii) In calculus anuria nephrostomy is indicated when ureteric catheter cannot be passed above the ob
struction and the kidney should be relieved immediately.
This operation has been described in detail in ‘A Practical Guide to Operative Surgery’.
Bilateral calculi.— Not uncommonly this condition is come across in surgical practice. Usually the
kidney with the better function is operated on first and the operation on the contralateral side is postponed
no less than 2 months to allow adequate time for the first kidney to recover. Only two exceptions are there t
this rule. These are (i) if the patient complains of pain on one side, that side should be operated on first
considering the fact that pain signifies that the stone is obstructing the outflow of urine, so that kidney of th
side must be functioning; (ii) if one kidney is grossly infected resulting in pyonephrosis, it should be treated
first and nephrectomy or, if the patient's condition is poor, nephrostomy should be carried out.
Bilateral staghom calculi are rather uncommon. If the kidneys are without infection or without any sym
tom and particularly, if the patient is elderly it is probably better to avoid any operation.
EXPOSURE OF THE KIDNEY

All operations on the urinary tract should be performed extra-peritoneally, otherwise the peritoneal cavity is
likely to be infected with urine.
Lumbar approach.— This approach is most generally employed nowadays, as it gives a direct access to th
kidney. The main disadvantage is that the access is limited being bounded above by the last rib and below b
crest. So it is not suitable for operations on large renal tumours.
Position of the patient — The patient lies on his sound side with its back brought well over towards the ed
table. The loin overlies the bridge of the table, which can be screwed up to increase the space between the co
and the iliac crest. To maintain the stability of this position, the lower hip and the knee are kept flexed and t
leg is extended over them. Sand-bags are kept in position with a wide strapping to prevent the patient from
The lower arm is pulled forward so that the patient does not lie on it. The upper arm is supported on an arm
prevent the shoulder from sagging forwards and to relieve the chest of compression by the weight of the arm
Incision.— The incision is an oblique one, commencing just above the angle between the 12th rib and late
border of erector spinae muscle and is carried downwards and forwards towards the anterior superior iliac
terminates 2 inches above the said spine. In case of obese patients or when a large kidney has to be operated
incision can be extended forwards as far as the lateral border of the rectus muscle. The skin and the subcuta
are incised through this incision. The lower fibres of the latissimus dorsi are cut along the line of the incision
this incision is extended forwards, it cuts the most superficial i.e. external oblique muscle, of the three musc
lateral abdominal wall. The incision is now deepened at its highest part cutting another muscle — serratus p
inferior, to expose the lateral border of the quadratus lumborum with the lumbar fascia starting from its late
The anterior part of the incision is now deepened and one of the two muscles internal oblique cut along the
incision to protect the peritoneum from being incised. The neurovascular bundle comprising the 12th thorac
accompanying subcostal vessels are found passing downwards and forwards within the deeper layers of th
oblique at right angle to its fibres. These are retracted to save these. The lumbar fascia is now incised just in
lateral border of the quadratus muscle to expose the retro-peritoneal fat. Two fingers are inserted through th
and used to separate the peritoneum from the under-surface of the transversus muscle. As this separation co
one hand, the transversus muscle is divided with a pair of scissors throughout the extent of the incision. So
are incised for this exposure :— Latissimus dorsi and serratus posterior-inferior posteriorly and the three lat
muscles of the abdominal wall anteriorly. Some more room may be obtained by excising the 12th rib. To do
quadratus lumborum and associated fascia are detached form its lower border. The whole or part of the rib
excised subperiosteally. Care being taken not to injure the pleura.
Exposure of the kidney.— The cut muscles are now retracted to expose the loose retro-peritoneal fatty tissu
a little gauze dissection, the renal fascia is identified in the posterior part of the wound. This is incised betw
to expose the kidney. This incision on the fascia is extended anteriorly as fas as required but care should be
safeguard the peritoneum in the anterior part of the wound. In the upper pole, the kidney may be anchored
bands which traverse from the capsule of the kidney to the diaphragm. These are divided between ligatures
gland is carefully separated by the dissecting finger from the kidney. On the anterior surface of the kidney t
peritoneum is adherent and must be detached with care. Other adhesions, if there be any, should be looked
divided to mobilise the kidney properly.
Closure of the incision.— Before closing the incision, one must be sure that the ‘kidney bridge’ has been lo
down. The muscles are repaired in two layers. Care should be taken to include all the muscles which have b
Drainage of the retro-peritoneal space should be provided either by a corrugated rubber sheet or by a suctio
(Redi-vac).
Approach through the bed of the 12th rib.— This approach is advocated by some surgeons to give a better
exposure to the upper part of the kidney. Care should always be taken not to injure the pleura. In case it hap
water-seal drainage should be introduced through the 10th inter space and the pleura is closed.
The incision starts a little medial to the lateral border of the erector spinae muscle at the level of the 12th
incision is carried forwards along the line of the 12th rib and is continued beyond its tip as far as required. T
Latissimus dorsi and serratus posterior-inferior are come across in the medial part of the wound and these a
An incision is made on the periosteum of the 12th rib. The periosteum is lifted from both the surfaces of the
raspatory. The rib is then cut off as close to the spinal attachment as possible. The bed of the rib comprising
periosteum and the fibres of the diaphragm are cautiously incised to get into the retro-peritoneal space. The
reflection of the pleura is identified at the medial part of this incision and is carefully pushed upwards. Late
incision is carried through the three flat muscles of the abdomen in the same way as has been described in th
approach to protect the peritoneum. The renal fascia is divided and the kidney is exposed.
Nagamatsu Incision.— Here the 12th rib is removed as far back as possible. The incision along the 12th rib
carried forward into the loin, while the medial end of this incision is extended upwards vertically upto just ab
neck of the 10th rib. Thus the incision is made in a hockey-stick fashion. The upper vertical portion is deepen
to 3 cm segments ofthe 11th and 10th rib are excised. The diaphragm has to be separated from its lateral attac
This approach will give a very wide exposure, highly suitable for upper pole tumours.
The trans-peritoneal approach.— There are two main conditions in which this approach is preferred — in c
of ruptured kidney and while removing a hypernephroma. In case of hypernephroma, intra-peritoneal appro
preferred as the extent of the growth along the renal vein to the inferior vena cava is assessed and the renal v
ligated before the hypernephroma is mobilised. A long upper paramedian incision with a transverse extensio
level ofthe umbilicus, dividing the rectus and the lateral abdominal muscles is mostly employed. The small b
are pushed towards the other side of the abdomen. The peritoneum on the posterior wall is incised along the
of the flexure of the colon. The colon is then mobilised and displaced medially to expose the anterior surface
kidney and its vessels.
At the end of the operation the peritoneum which was incised is sutured back and the retro-peritoneal sp
drained through the loin.
URETERAL STONE
Ureteral stone usually originates in the kidney. Gravity and peristalsis both contribute to spontaneous
passage into and down the ureter.
Nature of the stone.—
Majority of the ureteral stones are calcium oxalate stones. Due to spiky surface, oxalate stone is easily
caught in the ureter. Stones with other composition have smooth surfaces and are often passed through the
ureter without being impacted.
When a renal stone enters the ureter it is rounded or oval in shape. As it passes down the ureter it
gradually becomes elongated and enlarged. In almost all the cases it is a solitary calculus.
Pathological changes.—
If a renal stone passes to the urinary bladder through ureter without any event, it is not detected. A
ureteral stone is only detected when it causes some symptoms due to its presence in the ureter or any
pathological changes to the kidney or ureter. The probable pathological changes are :—
1. Obstruction.— Ureteral stones are seldom completely obstructive, so that urine can flow around
them, (a) Partial obstruction is usually present, but it may cause dilatation of the ureter proximal to the
stone and renal pelvis. If the stone passes within a few days there is no evidence of renal damage. But if the
stone remains, gradually hydronephrosis may develop. If the stone remains for weeks or months irrepa
rable damage to the renal parenchyma may occur. There are 3 sites of anatomical narrowing of the ureter
where a stone may be arrested. These are — (i) pelviureteral junction, (ii) when the ureter crosses the iliac
artery and (iii) where it enters through the bladder wall.
(b) Complete obstruction is unusual and it may cause calculus anuria or atrophy of the kidney.
2. Impaction.— When the ureteral stone gets impacted attacks of ureteric colic pass off. Such
impaction usually occurs in the pelvic portion of the ureter. Occasionally a stone may remain lodged in a
ureter for many months without harming the kidney. When the stone has impacted patient may complain of
dull ache which gets worse during walking and exercise.
3. Infection may complicate ureteral stone. This usually occurs when there is urinary stasis. Infection
causes further renal damage. Pyelitis, pyelonephritis and pyonephrosis (from hydronephrosis) may occur
due to infection.
4. Ulceration.— Mucosal ulceration may occur in the ureter due to impaction of the stone. Such
ulceration may later on lead to stricture formation.
5. Diverticulum in the wall of the ureter may occur when the stone gets impacted and ulcerates the
epithelium of the ureter. Diverticulum occurs due to pressure necrosis and it may lead to even perforation
1088
with extravasation of urine which is extremely rare. With the formation of diverticulum pain totally goes o
with false belief of the patient that the stone has passed away.
SYMPTOMS.— 1. PAIN.— There are two types of pain :—
(i) Ureteric colic.— When a stone enters the ureter and descends along it there is an attack of
ureteric colic due to hyperperistalsis of smooth muscles of the ureter, pelvis and calyces. The pain starts
abruptly and becomes severe within minutes. It is repeated at longer or shorter intervals till the stone is
ejected into the bladder or becomes impacted in the ureter. This colic becomes severe when the stone
becomes arrested at the anatomical narrowings of the ureter. In case of ureteric colic there is radiation of
pain the position of which suggests the position of arrest of stone in the ureter. When the stone is arrested
high in the ureter the pain passes from the loin to the groin along the distribution of the iliohypogastric and
ilioinguinal nerves. When the calculus is in the lower-third of the ureter, colic starts at a lower level and
radiates to the testicle in the male or labium majus in the female and to the medial aspect of the thigh as the
pain is referred along the two branches of the genitofemoral nerve. This is due to common segment of
innervation of the lower ureter and the genitofemoral nerve. In this case the testis becomes retracted by
spasm of the cremaster.
When the stone enters the intramural part of the ureter, the pain is referred to the tip of the penis in
the male and strangury’ in both sexes.
(ii) Fixed pain.— When the ureteric calculus gets impacted, ureteric colic passes off and is replaced
by a dull ache. The position of this dull ache depends on the position of impaction of the ureteric calculus
Such pain is due to capsular tension and distension of the renal pelvis. This pain is aggravated by exercise,
movement and jolting and is relieved by rest. This pain also varies in intensity. The ureteric stone often get
impacted in the pelvic part of the ureter and at that time dull ache is complained of at the iliac fossa.
When this pain passes off, it is due to the stone has formed a false diverticulum due to pressure
necrosis at the point of impaction. When the pain becomes gradually severe for 1 or 2 days and then
gradually subsides, it suggests complete obstruction of the ureter by the stone. This may lead to loss of
function and complete atrophy of the kidney later on.
2. HAEMATURIA.— Some amount of haematuria, however small it may be, usually occurs after an
attack of ureteric colic. It may last for a few hours to a day. At times it is so slight that it requires micr
oscopic identification, but in '/3rd of cases gross haematuria is observed, even small clots may be passed.
3. Even in the absence of infection symptoms of urgency and frequency of urination may be complained
of when the stone is very near the bladder.
4. Gastrointestinal symptoms are sometimes associated with ureteric stone. Nausea and vomiting are
often complained of. Abdominal distension due to paralytic ileus may also be present. These symptoms m
sometimes overshadow the renal and ureteric pain. This may mimic intraperitoneal pathologies like peptic
ulcer, cholelithiasis or acute appendicitis.
PHYSICAL SIGNS.— The patient usually tosses on the bed (in contradistinction to lying quiet in bed
in patients with peritonitis) as if nothing affords him relief
(i) The skin is cold and clammy and there may be other signs of mild shock.
(ii) Tenderness is marked over the part of the ureter where the ureteric calculus lies. This often gives
difficulty in differentiating this condition from acute appendicitis when the right ureter is involved.
(iii) Muscular rigidity due to spasm of abdominal muscles is felt in the same region of tenderness
(iv) When the stone is in lower end of the ureter, it may be felt by rectal or vaginal examination.
(v) Percussion on the renal angle posteriorly gives rise to pain with marked tenderness.
(vi) The abdomen may be distended and quiet on auscultation (bowel sounds less prominent).
(vii) The corresponding scrotal skin may be hyperaesthetic if the stone lies in the lower part of the ure
1. Examination of blood. 1
2. Urinalysis. J Same as for Renal Stone
3. STRAIGHT X-RAY — A plain film ofthe

KUB region may demonstrate a calcific body in the
line of the ureter. This of course is a presumptive
ground for diagnosis. On many cases no radio
opaque stone may be seen due to its small size or
presence of intestinal gas shadows in front of the
stone. Sometimes the shadow may be of phlebolith
or some other intra-abdominal calcification and not
of ureteric calculus.
It must be remembered that ureter starts at the
level between the first and second lumbar vertebrae,
somewhat higher on the left side and traverses in
front of the tips of the transverse processes of the
lumbar vertebrae. It then runs in front of the sacro
iliac joint and then in front of the tip of the ischial
spine after which it turns medially and forwards to
enter into the bladder.
4 INT
Rg 57 13 — Straight X-ray showing right ureteric 0f immense value, but on occasion no dye may be
calculus and two phleboliths. excreted at the time of or some hours after ureteric
colic. But even in these cases a nephrogram may be seen without a good visualisation of renal pelvis or
ureter. This also indicates ureteric obstruction with good reasonable renal function In excretory urography
the following findings help in the diagnosis :—
(a) The stone lies in the ureter with some dilatation of the ureter above the stone. It also reveals the
degree of ureteric obstruction.
(b) A non-opaque stone forms a filling defect in the ureter. This arises difficulty to differentiate it
from ureteral tumour or blood clot within the ureter.
(c) Non-excretion of the dye with a stone in the ureteric line may indicate non-functioning kidney due
to obstruction. At the same time the function of the other kidney can be assessed.
(d) If excretory urography shows normal excretion of dye after an attack of colic without any positive
or negative shadow of ureteric stone, the patient is probably not suffering from ureteric calculus.
5. CYSTOSCOPY.— Cystoscopy and ureteral catheterisation are seldom needed for the diagnosis of
ureteral stone. In fact this should be avoided unless the diagnosis cannot be established by the above means,
as instrumentation always carries bacteria from the urethra into the upper urinary tract.
Cystoscopy does not reveal any abnormality when the calculus is in the upper part or middle part of the
ureter. When the stone has reached the lower third of the ureter, the ureteric orifice looks patulous with
minute petechial haemorrhages around the affected ureteric orifice. As the calculus descends and comes
near the intramural portion, this petechial haemorrhages coalesce to form larger haemorrhagic spot.
When the stone has entered the intramural portion, the ureteric orifice becomes grossly oedematous.
When the calculus has reached the ureteric orifice it will be seen peeping through the orifice.
6. RETROGRADE PYELOGRAPHY.— This is seldom required for diagnosis and should be avoided
as far as possible for fear of introduction of infection. There are only two places where this examination
should be required :— (a) When a shadow is suspected to be of ureteric calculus on straight X-ray. but
excretory urography shows no excretion of dye.
(b) To display the presence of a non-opaque ureteric calculus (this is more required when excretion
dye is minimum in excretory urography).
TREATMENT.—
During the attack of colic, sedatives like pethidine or morphine may be required. To eliviate spasm a
dose of probanthin may be required, but repeated doses should be avoided as it may produce retention of
69
urine by paralysing the detrusor muscle of the bladder. Atropine 0.8 mg subcutaneously is also an effective
antispasmodic drug. Pain of so called, ‘renal colic’ is due to increased upper tract pressure with increasing
tension in the wall of the renal pelvis. Non-steroidal anti-inflammatories (NSAID) provide a dose depende
decrease in ureteric wave frequency and amplitude. Whether such drug acts in this way or by decreasing r
blood flow is not clear, but these drugs are quite effective.
A. Conservative Treatment.— About 80% of ureteral stones pass spontaneously without much compli
cations. Antispasmodics are helpful. Fluid intake must be high. The stone should be small and urine should
sterile. Progress of the stone should be observed with straight X-ray every 6 weeks. A few excretory urogra
phies may be required to see the function of the kidney.
Removal of stone is only required :—
(i) When the stone in the first instance is seen to be large enough to pass spontaneously.
(ii) When there are repeated attacks of colic without much advance of the stone through the ureter.
(iii) By repeated straight X-rays it is seen that the size of the stone is increasing and it is not moving
distally.
(iv) When the urine is becoming infected.
(v) When there are signs of obstruction with hydronephrosis and diminution of function of kidney du
back pressure as demonstrated by excretory urography.
B. Removal of stone.—
I. PERCUTANEOUS METHOD.—
Both ESWL and URS can be used to treat ureteric stone. Stone size is an important factor and calculi les
than 4 to 5 mm in diameter have a spontaneous passage rate of 40 to 90% and should be treated expectantl
However persistent obstruction, pain failing to respond to analgesia, infection andfailure ofprogression are
all indications for intervention. The stones in the upper third of the ureter are successfully treated by ESWL.
Lower third calculi should be managed by ureteroscopic extraction which is more successful than ESWL.
Nevertheless, some urologists would prefer a preliminary trial ofESWL as it is less invasive than ureterosc
However ESWL is more expensive. Mid-ureteric stones can be treated at the discretion of the operator and
patient — ureteroscopy is generally preferred to ESWL as imaging in this situation can be difficult. Stones
which cannot be extracted intact with URS, can be fragmented using USL, LL or PL (see pages 1174 and
1175). PL would appear to be more effective and less expensive than LL or USL. Residual fragments follow
ing ureteroscopic lithotripsy can be left to pass spontaneously, but removing them with stone basket impro
stone-free rates. Following ureteroscopy, no JJ ureteric stent need be left in the absence of complications, bu
when stone extraction has been traumatic or where there is any uncertainity about the possibility of injury
probably wise to leave a JJ stent. This can be removed 2 to 3 weeks later.
II. INSTRUMENTAL REMOVAL.—
1. Ureteric catheterisation.— When the stone is small, about 14 centimeter or less in diameter and is
arrested in any part of the ureter, usually passes off after ureteric catheterisation. The ureteric catheter is p
beyond the stone and 1 ml of liquid paraffin is injected through the catheter. It is then withdrawn. The ston
usually passes off within a few hours or days.
2. Dormia basket.— This method is particularly used when the calculus is in the lower third of the
ureter. This dormia basket is passed through a cystoscope into the ureter and passed above the stone. The
basket is now opened and it is gradually withdrawn. The opened basket will catch the stone and will grad
be taken out through the ureteric orifice into the bladder.
3. Ureteric meatotomy.— The ureteric orifice is the narrowest part of the ureter and if this opening is
enlarged by cutting the orifice in an upward and lateral direction with a diathermy electrode, the stone ma
easily pass out. The disadvantage of this procedure is that it invariably leads to urinary reflux later on.
4. Intraureteric extraction.— By rigid ureteroscope the whole length of ureter can be inspected and the
stone is removed by forceps or by dormia basket under direct vision.
5. By proximal pushing — It may be easier to push the ureteric stone proximaliy as the proximal part o
the ureter is most of the time more dilated. The ureteric calculus is now gradually pushed upwards into th
pelvis of the ureter, where the calculus is fragmented by ESWL method.

III. OPERATIVE TREATMENT (URETEROLITHOTOMY).— Removal of stone from the ureter by
operation is known as ‘Ureterolithotomy’. When the ureteric stone is so situated that any of the above instru
mental methods cannot be applied for its removal ureterolithotomy is applied.
The basic indications for operative removal are same as ‘REMOVAL OF THE STONE’ as indicated
above. These are — (i) when the stone is too large to pass through the ureter by natural means; (ii) when the
presence of stone is causing repeated attacks of colic without much advance in the passage of the stone; (iii)
when the stone is gradually increasing in size; (iv) when there is evidence of obstruction due to presence of
stone in the ureter and (v) when the urine has become infected due to presence of ureteric calculus.
Operation.— Incision for exposure of the ureter varies according to which part of the ureter has to be expo
case of upper 1/3 rd of the ureter, the incision and approach is same as described under ‘Exposure of the kidney’
1180).
For the middle \/3rd of the ureter incision is made 1 inch above and parallel to the anterior part of the iliac cr
is continued along the same line for a short distance in the anterior abdominal wall. The skin, subcutaneous tis
three flat muscles of the abdomen are divided along the line of the incision. The peritoneum is gently reached a
gradually moved forwards and medially till the posterior abdominal wall is reached. The ureter is often seen b
alongwith the peritoneum near the crossing of the bifurcation of the common iliac arteries. The ureter is now s
from the peritoneum.
For exposure of lower M3rd of the ureter, a low paramedian incision is made. The skin, subcutaneous tissue
anterior rectus sheath are incised along the line of the incision. The rectus muscle is retracted laterally. Below t
between the umbilicus and the symphysis pubis the posterior rectus sheath is absent. So at this place the fascia
lis is exposed. This is incised with caution and the peritoneum is gently raised from the bladder and the side w
pelvis. It is better to distend the bladder first before making the incision. The peritoneum is gradually raised til
part of the ureter is reached.
It should be noted that in all three exposures the ureter is exposed extraperitoneally without opening the perit
Technique of extraction of stone after the ureter has been exposed.— It is most desirable that the patient shoul
submined to radiography just prior to the operation in order to confirm the position of the stone. After the con
of the ureter has been exposed by one of the methods mentioned above, a sling of tape is passed round the ure
to the stone. This will not only assist in handling the ureter, but also will prevent the stone from slipping upwa
more dilated portion. The stone is now milked slightly upwards or downwards to a rather healthy portion of th
longitudinal incision is made directly over the stone. The stone is removed with a suitable forceps or a scoop w
bruising the margins of the ureteric incision. After the stone has been removed from the ureter, closure of the u
incision may or may not be required. Controversy exists on this point. Some surgeons prefer to close the incisio
4/0 catgut or silk suture passing through the muscular wall of the ureter without penetrating the mucous mem
prevent further stone formation. While the other group of surgeons prefer to leave the ureter unsutured for fea
quent stricture formation. The ureteric incision heals by itself provided there is no distal obstruction. The incisi
exposure is now closed by layers with a drainage down to the ureteric incision.
NEOPLASMS OF THE KIDNEY
Classification.— Tumours of the kidney may be divided into ‘tumours ofthe kidney proper' and ‘tumours
of the renal pelvis
TUMOURS OF THE KIDNEY PROPER
These are further subdivided into benign neoplasms and malignant neoplasms.
BENIGN TUMOURS.— From the clinical standpoint benign tumours of the kidney are rare. These tumours
occur in the epithelial tissue, connective tissue and in the perinephric tissue.
Benign tumours are (i) adenoma, (ii) haemangioma, (iii) carcinoid tumours, (iv) fibromas, (v) lipoma, (vi) m
(vii) neurofibromas, (viii) angiomyolipoma (hamartoma) and (ix) endometriosis.
Most of these tumours are 1 to 2 cm in diameter.
Of these tumours adenoma requires special mention.
Adenoma.— This is probably the most common benign tumour of the kidney. It is 3 times more common in
women. These are small yellow nodules frequently multiple. These are usually encapsulated and about 1
Such adenomas may occur in any part of the cortex, although they are commonly seen close to the surface
give rise to no symptom and are only of academic interest.
Angiomyolipoma (Hamartoma).— Obviously it is a very rare tumour of the kidney. The tumour has got a
elements like excessive blood vessels, muscle elements and excessive fat. It is very easily diagnosed on CT
to note that ‘A th of this tumour may turn malignant and may lead to metastasis.
Angioma.— This tumour usually occurs in young adults. The main complaint is profuse haematuria. O
diagnose this condition by renal angiography.
MALIGNANT NEOPLASMS (tumours).— There are mainly two varieties of these tumours :—
1. Adenocarcinoma, which occurs in adults usually above the age of 40 years and constitutes 4/5ths of a
renal neoplasms.
2. Nephroblastoma, which is exclusively a tumour of children, mostly occurs under 4 years of age, avera
1 to 7 years. Between the ages of 7 years and 40 years malignant neoplasms of kidney are unusual.
3. An unusual variety — sarcoma of the kidney is extremely rare.
ADENOCARCINOMA (RENAL CELL CARCINOMA)
It is the commonest tumour of the kidney and constitutes almost 80% of all the tumours.
Nomenclature.— This tumour was previously more popularly known as hypernephroma or Grawitz’s t
Grawitz considered this tumour to arise from ‘adrenal cortical rest’, which may sometimes be present in t
kidney. He came to this view as the microscopic appearance of the tumour closely resembles that of the zo
of the adrenal cortex. Subsequently this view has been cancelled from the facts :— (i) That hypernephrom
in other sites e.g. broad ligament of the uterus, retroperitoneal tissues and bare area of the liver where the
rests are often seen, (ii) If it be adrenal cortical tumour some sort of endocrine effects in the form of electro
or Cushing’s syndrome type or disturbance in sex characters may be noticed. But such changes are never
tumour. At present this tumour is more often called renal cell carcinoma.
Aetiology.— Though there were controversies over the origin of adenocarcinomas previously and as m
above that Grawitz thought that these tumours arose from intrarenal adrenal rests yet the unanimous opi
that this tumour arises from the cells of the renal tubules or from the benign adenomas. This theory is bas
findings. Some of these tumours secrete hormones e.g. gonadotrophins, ACTH, parathyroid-like hormone
prolactin, insulin-like activity and prostaglandin A.
The aetiology of renal cell carcinoma is still uncertain, although a number of factors have been recogni
increase the risk of developing this carcinoma. These are —
(a) Cigarette smoking; (b) Obesity and (c) use of the drug phenacetin.
(d) A number of occupations have been incriminated. These are —
Shoe workers; Workers exposed to cadmium, particularly if they smoke; Leather tanners; Those who a
contrast medium thorotrast; those exposed to petroleum products.
(e) A few chemical carcinogens have been identified — these are dimethyl nitrosamine, diethylnigrosoam
additive potassium bomate. Chronic administration of oestrogen to males in animal models have induced
(f) A few acquired conditions of kidney have been associated with more incidence of renal cell carcinoma
disease of the kidney.
Renal cell carcinoma is not a typical familial disease, though it has been found to affect more than 1 mem
Autosomal dominant von Hippel-Lindau syndrome (cerebelloretinal haemangioblastomatosis) is conside
risk in developing this disease, which occurs at an earlier age than usual and is often bilateral. Most of the
abnormalities which have been described in spontaneous renal cell carcinoma involve deletions in the sho
Pathogenesis and Pathology.— Adenocarcinoma usually arises in one of the renal poles. As the tumour
gradually grows in size, it compresses adjacent renal tissues and displaces calyces and the pelvis. Multipl
adenocarcinomas are found in patients suffering from Lindau’s disease. This tumour is more common in
upper pole than lower pole, but are rarely found in other parts of the kidney.
MACROSCOPICALLY, the tumour forms a round or lobulated mass whose margins appear intact wit
false impression of having a well defined fibrous capsule. On cut surface the two chief characteristic featu
are its yellow colour and remarkable variegated appearance. There are areas of haemorrhage or necrosis.
of varying size are often seen. Some of which contain clear serous or jelly-like material and others contain
blood. Areas of calcification may develop and this may be visible on X-ray.
MICROSCOPICALLY, varying pattern of cells in the same tumour is the most characteristic feature. The
tumour cells may be (i) large with clear abundant cytoplasm with small eccentric nuclei, which are known as
clear cells, (ii) small and compacl with cytoplasm containing basophilic granules, which are known as granu
lar cells (dark cells), (iii) large and eosinophilic cells known as oncocytic cells and (iv) anaplastic cells. The
clear cells are large and peculiarly clear owing to the presence of abundant lipids and glycogen. The arrange
ment of the cells is also variable. They may show solid alveoli or tubular or papillary structure of solid sheets.
The majority are clear cell type, whereas the dark cell type is usually less common. The microscopic appear
ance is very much similar to renal adenoma, from which many of these tumours arise. A particular type which
is known as papillary cystadenocarcinoma is mainly composed of large eosinophilic cells (oncocytes), which
are cystic with papillary arrangements. The anaplastic cells extremely vary in size and shape which may be
polygonal or fusiform.
The peculiar feature of such tumour is that the stroma is scanty. The blood vessels are large and thin-
walled. This probably accounts for haemorrhages inside the tumour and great tendency of the tumour for bloo
spread.
Spread.—
1. Local invasion.— The tumour gradually invades the adjacent parts of the medulla inwards and the renal
capsule outwards. After the renal capsule has been penetrated, the surrounding perinephric fat is gradually
invaded. Later on the tumour may involve the neighbouring viscera e.g. colon, pancreas, liver, duodenum etc.
2. Lymphatic spread.— The peculiar feature of this tumour is that the lymphatic spread is not that impor
tant. When the tumour penetrates through the renal capsule and invades the perirenal fat, it then metastasises
the lymph nodes in relation to the hiluni of the kidney and from there to the paraaortic group of lymph nodes.
Involvement of regional lymph nodes is reported in only 20% of cases undergoing radical surgery.
3. Blood spread.— As mentioned above, due to numerous large thin walled blood vessels which are
present in the tumour, blood spread is by far the most important. In no other carcinoma it is seen at such a gre
degree. Blood spread occurs in two ways — (i) by embolism, in which pieces of growth become detached and
are swept into the venous circulation to become first arrested in the lungs. In the lungs the metastasis produce
‘cannon-ball’ deposits which are revealed in X-ray as round opaque metastases in the lungs and later on furthe
small pieces may enter into arterial circulation and may be deposited in the bones.
(ii) By permeation, in which the tumour pushes into the vein lumen as a polypoid projection. Eventually
the vein is distended by tumour thrombus. First the renal vein is involved and later on the inferior vena cava i
involved. Thus the tumour may extend through the inferior vena cava into the right atrium keeping continuity
with the parent tumour. Sometimes the solid columns of tumour tissue inside the renal vein may cause obstru
tion to the testicular vein particularly on the left side, in which side the testicular vein drains into the renal vein
Obstruction of drainage of the testicular vein may cause varicocele on the left side. So sudden left sided
varicocele in an old man should arouse suspicion of adenocarcinoma affecting the left kidney.
Through blood spread multiple metastases are common, though occasionally one may find solitary me
tastasis only in the lung. The lungs and the bones are the principal sites of metastatic lesions. In X-ray film the
secondary deposits in the lung often present round appearance with a clean-cut circumscribed outline, to whic
the name cannon-ball appearance has been applied. In the bone the tumour is remarkably destructive or
osteolytic so that it may cause pathological fracture later on. A solitary metastasis in the bone occurs more
frequently in this than in any other tumour. The bones which are commonly involved are the long bones e.g.
femur, humerus etc., the vertebrae and skull. Secondary metastasis in the brain and liver is not uncommon in
this tumour. It is the third tumour surpassed only by lung and breast to involve brain by metastasis.
Staging of the tumour.— The tumour has been staged clinically to know the prognosis of the case.
Stage I.— Tumour is confined to the kidney.
Stage II.— Perirenal spread is confined within the perirenal fascia.
Stage III.— (i) Renal vein or inferior vena cava has been involved or (ii) local lymph nodes have been
involved.
Stage IV.— Advanced disease with distant metastases.

Use of ultrasonography, CT scanning and measurement of levels of tumour markers have significantly
increased the accuracy of staging of the tumour preoperatively.
CLINICAL FEATURES.— Renal cell carcinoma is relatively rare before the age of 50 years. Its maxi
mum incidence, which constitutes about l/3rd of cases, is in the 6th decade.
It is twice as common in men as in women. The right and left kidneys are affected with equal frequen
SYMPTOMS.—
(i) Painless haematuria is the earliest and most important symptom of this condition. Such haematuri
may be gross or microscopic. As mentioned, bleeding is painless unless accompanied by renal colic due t
passage of blood clots.
(ii) Pain in the loin due to stretching of the renal capsule may appear. This is dull ache in character an
felt in the back. Haemorrhage into the tumour may also cause such pain. But unfortunately this is often
ignored. In this section clot colic should be remembered as another type of pain.
(iii) Swelling.— Occasionally a patient may discover a swelling in the flank in the absence of other sym
toms.
(iv) Persistent pyrexia is the only symptom in a few cases, the explanation of which becomes difficult.
Such low grade pyrexia is often due to absorption of blood and necrotic material from the tumour itself. T
type of pyrexia usually disappears after nephrectomy, but if it persists, it indicates presence of metastasis
(v) Hypertension is associated with 40% of cases of adenocarcinoma. It is presumably due to renin
secreted by the tumour.
(vi) General symptoms like lassitude, anaemia, lethargy, apathy to work are some symptoms which are
not uncommon in this tumour. Anaemia is often present as it is due to haematuria.
(vii) Metastatic symptoms.— In about V* th of cases the primary growth remains silent and the patients
present with symptoms due to metastasis. Such symptoms are :—
(a) In case of lung metastasis — persistent cough, haemoptysis, chest pain and dyspnoea.
(b) In case of bone metastasis — painful enlargement of bone, pathological fracture etc.
(c) In liver metastasis — Jaundice, ascites etc.
(d) In brain metastasis — persistent headache, nausea and vomiting.
(e) Neck gland and swelling in the form of left supraclavicular lymph node (Virchow’s nodes)
metastasis.
PHYSICAL SIGNS.—
LOCAL EXAMINATION.— A palpable renal tumour is often a late sign and by this time the patient
nearly always has metastasis elsewhere. A fixed renal tumour is an even more late sign.
GENERAL EXAMINATION.— (i) Development of dilated veins on the abdominal wall may be seen
to involvement of the inferior vena cava by tumour permeation.
(ii) A left sided sudden varicocele is often due to occlusion of the left testicular vein as it drains into
left renal vein which is occluded with tumour permeation in case of left sided renal cell carcinoma.
(iii) Arteriovenous fistula is occasionally observed in association with renal cell carcinoma. This is du
diastolic hypertension which often accompanies this condition. Hypertension is caused by renin secreted
the tumour.
(iv) Metastatic signs may be seen late in the disease — a palpable swelling in the left supraclavicular
region is due to metastatic involvement of Virchow’s nodes. Tenderness or a palpable mass may be foun
bone due to metastasis. Later on bony irregularity is due to pathological fracture. Oedema of the legs ma
occasionally seen which is secondary to neoplastic involvement of the inferior vena cava. Physical exami
tion of the chest may not reveal any definite sign, though metastasis is present. Liver is a common site of
metastasis, in which case it becomes enlarged and nodular. Ascites may be found.
(v) Loss of weight is another general sign which is quite frequent in this condition.
Early diagnosis.— Every effort should be made to diagnose renal cell carcinoma as early as possible, a
late diagnosis may be only of academic interest and the patient cannot be survived by any means. When
patient presents with haematuria, pain and a palpable

renal tumour, it is rather a late case.
Haematuria is the earliest symptom and all cases
of haematuria should be investigated with utmost care
to exclude malignant tumour in the urinary tract. He
should be examined cystoscopically, while he is still
bleeding. If blood is seen coming through one ure
teric orifice and clear urine through the other orifice,
probably he is having an adenocarcinoma or a papil
loma in that kidney. Excretory urography and other
investigations as mentioned below should be per
formed quickly to exclude adenocarcinoma of the
kidney.
1. Blood examination.— Erythrocytosis with an
increased plasma erythropoietin level occurs in 3%
to 4% of patients. Anaemia is noted in advanced cases.
E.S.R. is often high. Hypercalcaemia is sometimes
seen as a few tumours are known to secrete parathor
mone. A few tumours have been found to secrete
ACTH which may lead to Cushinoid appearance.
2. Urine examination may reveal presence of
blood.
3 .X-RAY.—
(a) Straight X-ray may show (i) definite bulge
when the outline of the kidney is followed, (ii) The
psoas margin may be obscured if the solid tumour
Fig.57.14.— Urogram showing adenocarcinoma of right
kidney with marked deformity of the upper lobe calyces.
overlies the muscle, (iii) Some irregular calcification
is seen in 7% of cases, (iv) Osteolytic metastasis

may be noted in the vertebrae.
(b) Excretory Urogram.— Early diagnosis of
ten rests on this investigation, but it may be in
conclusive due to lack of proper excretion of the
dye and delineation of the calyces and pelvis.
(i) Filling defect is seen in majority of
cases. Calyces may be bent, elongated or distorted
or even amputated or absent due to the presence
of the tumour.
(ii) Elongation and distortion of the caly
ces are commonly seen in excretory urography
which look like spider legs. Such deformity is clas
sically known as 'spider leg’deformity. This con
dition is also seen in polycystic kidney, but the
differentiating features are that polycystic kidney
is often a bilateral condition and the spider legs in
this condition are smoother in outline in compari
Fig.57.15.— Urogram showing renal cell carcinoma of left kid
son to adenocarcinoma in which the outlinesney. are Note how the pelvis is compressed and the calyces are more
irregular due to the irregular margin of the tumour. or less obliterated.
(iii) When the' tumour has in

vaded the pelvis, a definite spacc occupy
ing lesion is seen in the pelvis of the kid
ney. The unaffected calyces pass upwards
or downwards according to the situation
of the tumour.
(iv) On rare occasion the ureter
may be compressed and hydronephrosis
may develop.
(c) Tomography, during the
nephrogram phase is helpful in outlining
the periphery of the tumour.
(d) Renal Angiography, particularly
the selective type shows the tumour with Fig.57.16.— Ultrasonography to show how it is helpful in differentiating
great vascularity and pooling of the dye a tumour from a cyst.
a.— Shows longitudinal scan on the left and transverse scan on the right.
within the tumour. Some tumours are rela In the left scan an enlarged kidney is visible which on the right transverse
tively avascular and diagnosis becomes scan shows abnormal echoes from tumour tissue.
difficult. In these cases infusion of epi- b.— Shows also longitudinal scan on the left and transverse scan on the
nephrin just before instilling the radio right side, both of which show cyst in the upper pole of the kidney without
any echo.
opaque material will cause marked spasm
of the arterioles of the normal renal tissue but not ofthe vessels of the tumour.
(e) Infusion Angionephrolomograms,
_______________ almost always reveal increased opacifica
tion of the tumour due to increased vas
cularity.
(f) A Chest Film is particularly im
portant to demonstrate metastasis in the
lungs, though negative finding does not
exclude metastasis in the lungs.
(g) Skeletal Survey, particularly of the
long bones may demonstrate osteolytic
metastasis or even pathological fractures.
It must be remembered that skeletal me
tastasis is only recognised in 50% of cases
by X-ray. 50% of bone minerals must be
lysed before it becomes evident on X-ray.
4. ULTRASONOGRAPHY— B-scan
sonography diagnoses tumour with 95%
accuracy.
------------ 5. COMPUTED TOMOGRAPHY
c „ . . ... . . .. , (CT scan).—As the tumour has a slightly
Fig.57.17.— CT scan showing renal cell carcinoma in the left . ,,. ,,,_,
kidney marked as C. increased density comparable to that of the
kidney it is often helpful in the diagnosis.
6. ISOTOPE SCANNING.— A rectilinear scan using 203 Hg will reveal a cold area at the place of cyst or
a tumour. "mTc when used in scanning shows tumour which has got more vasculature.
7. BONE SCAN is obviously much better in early diagnosis of skeletal metastasis. It reveals metastasis
even when the X-rays fail to show it.
8. URINARY CYTOLOGY— Papanicolaou technique when applied to the urinary sediment, may detect
carcinomatous cells of adenocarcinoma. This method has not been very helpful in the diagnosis of this tum
9. TUMOUR MARKERS.— Effectivity of tumour markers in the diagnosis of renal cell carcinoma hav
not been very successful. Elevation of renin is found in 35% of cases. Elevation of serum erythropoietin is
present in 65% of cases. Both these tests have significant numbers of false negative. Carcinoembryonic anti
gen is also raised in certain cases.
TREATMENT.—The definitive treatment for primary renal cell carcinoma is radical nephrectomy. The
place of adjuvant lymph node dissection remains controversial, as is the place of adjuvant radiotherapy com
bined with nephrectomy. The cases can be divided into four groups :—
GROUP I — includes cases where there is no demonstrable metastasis. These cases are suitable for
radical nephrectomy including removal of perirenal fat and regional lymph nodes. Levels of erythropoietin,
renin and carcinoembryonic antigen will fall to normal level after such radical nephrectomy.
GROUP II — includes cases where there are no demonstrable metastases and the tumour is too fixed to
allow nephrectomy to be performed (inoperable cases). Treatment of these cases is palliative X-ray therapy
with or without chemotherapy. Most authorities feel that X-ray therapy or radiotherapy does not work appre
ciably in adenocarcinoma of kidney and its metastasis, so its effectivity either pre- or post-operatively have
been disagreed by majority of the urosurgeons. But in this group as operation is almost impossible, this is the
only form of treatment available. Chemotherapy has also not been very successful in this type of cancer.
GROUP III — this group includes adenocarcinoma of kidney which is resectable with a solitary metasta
sis. The treatment of this group is radical nephrectomy with excision of the solitary metastasis, be it lobectom
or pneumonectomy for lung metastasis or amputation for a bone metastasis.
GROUP IV — in a few cases there may be bilateral tumours or adenocarcinoma in only remaining kidney
In these cases partial nephrectomy should be considered with removal of adjacent perirenal fat and regional
lymph nodes.
Radical nephrectomy for renal cell carcinoma.— As the objective is to gain a wide exposure for radi
cal nephrectomy and to see the renal vessels as also inferior vena cava, abdominal approach is mostly pre
ferred — either a long paramedian incision or a transverse incision is applied.
After opening the abdomen the surgeon should carefully assess the resectability of the tumour. Once it is determined
that the tumour is resectable, the tumour is not further handled and the surgeon puts all attention to the renal pedicle.
Before manipulating the kidney it is advisable to deal with the renal pedicle to prevent further blood borne metastasis due
to handling of the tumour. The renal vein and artery are separated at the renal pedicle. The renal vein is then ligated and
divided. The inferior vena cava should be palpated carefully to detect any tumour thrombus within it. If it be felt it should
be opened and tumour thrombus should be removed. Al the time of dissecting the renal vein, if tumour thrombus is
detected it should be opened and the tumour thrombus is removed. The renal vein is ligated almost flush with the inferior
vena cava. Now the renal artery is ligated and divided and the ureter is ligated and divided as low as possible.
The perinephric fat and fascia are gradually separated from the surrounding tissues from outside inwards. While
the dissection is proceeding inward, all the regional lymph nodes are included within the kidney mass. Ultimately the
tumour with the whole kidney, perirenal fat and regional lymph nodes are removed.
Many urosurgeons now recommend transcatheter renal arterial embolisation 1 to 7 days before nephrectomy
which facilitates operation. Blood loss is decreased and secondary perinephric oedema is reduced. By this technique
tumour cell dissemination during the operation is also prevented to certain extent. This technique should also be
considered in case of life threatening gross haematuria.
A course of post-operative radiotherapy may be applied but its effectivity has been seriously questioned. Even the
leading urosurgeons are now not in favour of such radiotherapy. In one series 5-year survival in the postoperative
radiotherapy group was even lower with a high complication rate due to the radiotherapy, which was mainly gastrointestinal
and in some cases fatal.
Laparoscopic radical nephrectomy is described in page 1221 -
CHEMOTHERAPY.— With recent improvements in chemotherapy this has proved to be beneficial to some extent.
The single drug vinblastine has been used and showed an overall response rate of about 24%. It is to some extent dose-
dependent and it should be at least 0.2-0.3 mg/kg per week, whereas below this dose the response rate is almost half.
Recently there has been considerable interesl in the use of fluorodeoxyuridine (FUDR), which has produced almost
same response rate as vinblastine. Attempts to improve the response rate by combining cytotoxic agents have not been
very successful. However vinblastine + bleomycin + high dose of methotrexate have produced a response rate of 30%.
The duration of remissions to chemotherapy is short and measured in months. This disease seems to be inherently
chemoresistant, the reason is that it derives from renal tubular epithelium, which possesses the multidrug-resistant gene
— MDRI63.
HORMONE THERAPY.— Medroxyprogesterone Acetate (MPA) is proved to be the standard hormonal treatment
for advanced renal cell carcinoma. The drug is given at a dose of 300 mg/day (Bloom’s report). Progesterones other
than MPA seem to be less active. Tamoxifen at a low dose appears to be virtually inactive, but if given at high dose
— 800 mg/day it has shown some response. Combination of hormones with chemotherapy does not seem to have
anything to add to the response rate.
Interferons.— Combination therapy with different types of interferon has shown an overall response rate of 20%,
though complete remission rate is only 3%. The duration of remission to interferon-alpha varies from patient to patient,
however median durations have been reported as from 5 to 16 months, which do not defer with interferon-beta or
gamma. Unlike chemotherapy, where response occurs within weeks or even days, the time taken to respond to interferon
varies widely from 3 to 11 months. It must be noted that combination of interferon-alpha with MPA or chemotherapy
does not increase its efficacy.
Immunotherapy.— Interleukin-2 is a cytokine which was first identified as a T-cell growth factor, but has since
been shown to have a variety of effects including stimulation of macrophage cytotoxicity, stimulation of B-cell growth
and production of other cytokines, lnterleukin-2-stimulated T-cells (LAK) has been used as immunotherapy combined
with intravenous interleukin-2. The overall response rate by continuous infusion or bolus intravenous injection is about
29%. This is an immunotherapy, which has also been used by taking tumour-infiltrating lymphocytes at operation or
by using peripheral blood lymphocytes stimulated by means other than interleukin-2. A number of groups have also
attempted to combine interferon-alpha with interleukin-2 given either subcutaneously. intravenously or as a combination
of the two. The cumulative data suggests that 28% of patients respond to this combination with 8% complete remission
rate.
In conclusion it may be said that metastatic renal cell carcinoma is an incurable condition, but 10% to
20% of patients remain alive for 2 to 4 years.
Radical nephrectomy is the treatment of choice for primary lesions and there is no evidence that
postoperative radiotherapy improves survival. Nephrectomy may be indicated in patients with metastati
disease, but only for specific reasons— usually for local palliation. Standard systemic treatment lies betwe
MPA, interferon and interleukin-2. The response rates seem to be more with interferon-alpha compared t
MPA, but this needs to be confirmed in randomised studies. The place of interleukin-2 remains controver
and cumulative data do not suggest an improvement in response rate over interferon-alpha.
NEPHROBLASTOMA (WILMS’ TUMOUR)
The tumour was first described by Ranee in 1815 in London and then in Scotland by Gairdner in 1828
Wilms first gave a comprehensive description ofthe tumour in 1899 but suggested that the tumour arises
embryologically from undifferentiated cells in the Wolffian ridge. This tumour is also called embryoma or
adenomyosarcoma.
Incidence.— It is a highly malignant mixed tumour. It is almost exclusively a disease of children unde
4 years of age. The incidence is approximately one case per 2 lacs of children bom per year. It occurs in
all parts of the world and is unaffected by race, climate or environment. The disease is occasionally famili
As mentioned earlier the maximum incidence occurs in the first 4 years with a pick incidence at the age o
3 years. After the age of 5 yrs. this tumour is infrequent although rarely met with in adults.
The condition is more ctVimon in males. The tumour is occasionally bilateral.
Aetiology.— The general agreement is that the tumour arises from immature renal blastema, so that it
may be regarded to arise from cells of developing kidney which may be of metanephros in origin. The
complexity of tissues this tumour contains suggests this aetiology. The association of nephroblastoma wit
congenital abnormalities and its familial occurrence imply that there may be genetic factors which play in
the development of this tumour.
Pathology.— This tumour may develop in any part of the kidney. The majority present as a single
expanding tumour surrounded by a pseudocapsule of connective tissue. Sometimes the tumour may app
juxtarenal but it is usually attached to the kidney with a small pedicle. Occasionally the tumour may be
multiple separated nodules spread throughout the renal parenchyma.
GROSS APPEARANCE of the tumour is either solid or cystic and its surface may be smooth or nodula
Rapid increase in size is the rule, but the renal pelvis is not invaded until later in the disease, a fact which
may account for the absence of haematuria. The consistency is soft and the colour is grey or yellowish.
On section, the tumour is fleshy with a lobular appearance separated by fibrous septa. But it looks
comparatively uniform in contrast to the variegated appearance of renal cell carcinoma. But the tissue is
heterogeneous with usually myxomatous areas with haemorrhagic and cystic areas.
MICROSCOPICALLY, the majority of tissues are of connective tissue origin e.g. muscle, cartilage,
bone, myxomatous or lipomatous tissue. The epithelial elements often form abortive or embryonic glomeru
tubular structures and are surrounded by interstitial tissues. As the tumour consists of mixture of two type
of cells, it is often called ‘adenomyosarcoma’.
Spread.—
1. Direct invasion.— This is the major type of spread of this tumour. The tumour gradually invades the
kidney and later on the neighbouring organs such as the liver, spleen, colon, adrenal glands, diaphragm an
posterior abdominal muscles. Renal capsule however remains intact for a long time, so that invasion of the
neighbouring structures are comparatively late.
2. Lymph spread.— This is comparatively rare. Though regional lymph nodes are frequently enlarged
at operation, these glands on section usually show simple hyperplasia without evidence of secondary tumo
3. Blood spread.— Metastases by the blood stream are not frequent. Though blood spread to the lungs
is the commonest site; this spread may occur to the vertebrae, liver and to the opposite kidney.
Prognosis mainly depends on histological appearance of the tumour. The tumour which contains more
mature tissue, shows better prognosis. When the tumour spreads beyond kidney, the prognosis is relativel
worse.
Clinical staging of the tumour :—
STAGE I.— Tumour is restricted to the kidney.
STAGE II.— Tumour extends beyond kidney but within perinephric tissue and it is resectable.
STAGE III.— The tumour spreads beyond perinephric tissue and is not completely resectable.
STAGE IV — with haematogenous metastasis.
STAGE V — bilateral tumour.
SYMPTOMS.—
(i) The most common presentation is a palpable mass in the flank usually discovered by the child’s
parents.
(ii) Abdominal pain which is rather vague and ill-defined may be seen in 2/3rds of cases.
(iii) Haematuria.— In fact no haematuria is seen in 70% of cases. Microscopic haematuria occurs in
only l/3rd of cases. It denotes that the tumour has burst into renal pelvis and indicates bad prognosis. In fa
majority of patients with Wilms’ tumour who complain of haematuria die within 1 year.
(iv) Pyrexia is seen in 20% of cases. Pyrexia is presumably related to liberation of toxins into the blood
stream. Pyrexia may be associated with general malaise, weakness and loss of weight.
(v) Hypertension is present in 15% of cases. It is not very prominent and the precise cause is also
uncertain. It may be due to renal ischaemia. But this tumour with hypertension usually shows a poor progn
PHYSICAL SIGNS.— The lump has to be examined carefully and the diagnosis should be made by
palpation alone. In case of suspicion following special investigations should be performed.
1. Blood examination.— Polycythemia may also be associated with this tumour presumably due to
raised erythropoietin level.
2. X-RA Y.— (a) Straight X-ray.— An enlarged renal shadow is usually evident on straight X-ray of the
abdomen. There may be a rim of calcification around the periphery of the tumour. The bowel as demonstra
by gas inside it is usually displaced.
(b) Excretory urograms usually show distortion of calyceal system in 90% of patients. It may also
show displacement of renal pelvis or proximal ureter. No excretion of the dye may sometimes occur due to
renal vein thrombosis caused by the tumour, but this is more due to polycystic kidney or giant hydronephro
When excretion of the dye is minimum or absent, a retrograde urogram is needed. Excretory urography also
yields essential information about the opposite kidney e.g. its function or presence of bilateral tumour.
(c) Chest film may disclose metastasis in the lungs.
(d) Inferior venacavogram may be helpful in demonstrating displacement caused by extension of the
tumour into the retroperitoneal tissue or protrusion of the tumour into the vena cava to the extent of obstruc
ting it.
(e) Selective angiography may be useful if the diagnosis is still in doubt after excretory urography.
3. ULTRASONOGRAPHY and CT SCAN are helpful in diagnosing this tumour.
4. RADIOISOTOPE SCANS are being increasingly used in the investigation of Wilms’ tumour.
Bone scan may reveal bony metastasis, similarly hepatic scan may show tumour deposits in the liver.
5. TUMOUR MARKERS.— There is not very specific tumour marker for nephroblastoma, but raised
erythropoietin level, high urinary lactate dehydrogenase level are quite helpful.
TREATMENT.— It has been generally accepted that nephroblastoma requires a combined programme
of surgery, radiotherapy and chemotherapy which is modified to the specific needs of different groups of
children.
Surgery.— Surgical treatment of this condition is radical nephrectomy with excision of perirenal fascia
and regional lymph nodes. No child should be rushed to the operation theatre without proper clinical evalua
Blood should be cross-matched lo cover any loss during surgery or to cover preoperative anaemia.
An adequate exposure is made by transperitoneal or thoracoabdominal incision. Some surgeons prefer
paramedian incision or transverse incision. On opening the peritoneum, the liver and para-aortic lymph
nodes are examined for evidence of metastasis. Before palpating the main tumour mass, at least its resectabil
is confirmed and then the renal pedicle is desected free. The renal vein is first dealt with to prevent tumour
emboli escaping into the circulation. After ligation of the vessels, the ureter is identified and tied. There is
no need to excise a long length but the usual point of division is at the pelvic brim. The kidney is now
removed en bloc including perinephric fat, fascia and regional lymph nodes.
Solitary pulmonary metastasis may be resected following resection of the primary tumour.
Postoperative recovery is usually rapid and satisfactory.
Radiotherapy.— Only when it is judged that the tumour is too large to allow nephrectomy to be
performed, preoperative irradiation should be administered. Doses of 500 to 1,500 rads are given to patients
which have considerably reduced the bulk of the tumour.
The purpose of postoperative radiotherapy is irradiation of residual tumour. This is particularly given
when the tumour is invasive and there are lymph node metastasis.
The dosage of radiation depends on the equipment. If cobalt 60 is used, this is given in 5 or 6 fractions
a’week to a dose of 1000 to 1200 rads per week.
Pulmonary metastases are treated by whole lung irradiation including the apices and intradiaphragmati
portion of the lungs. The field extends from the clavicles to about LI level. A dose of 1400 to 2000 rads
is given either simultaneously with or before irradiation to the renal bed.
Hepatic metastases are also irradiated with combination of chemotherapy.
Secondary deposits elsewhere are usually treated with chemotherapy and with 3000 rads in 3 weeks.
Chemotherapy.— The primaiy role of chemotherapy is to destroy disseminated disease. Chemotherapy
may be given preoperatively to shrink a massive tumour to a resectable size.
Chemotherapy has an important role to play in palliation when radical nephrectomy is not possible and
a portion may be left behind. The two most effective drugs commonly used against nephroblastoma are
actinomycin D and vincristine. Recently the tumour has been proved to be quite sensitive to dactinomycin
which should be started a few days before surgery and continued daily for 1 week and then at weekly
intervals. Multiple courses of dactinomycin may be given to control subsequent pulmonary metastasis.
Palliative measures.— 1 f metastases are widespread, particularly affecting the bone or the brain — the
prognosis appears to be hopeless, yet radiotherapy and chemotherapy should be applied. Vincristine has
been found useful in these circumstances. Usefulness of radiotherapy has been discussed in radiotherapy
section. For cerebral metastases the entire calvarium is included in the fields of irradiation. For skeletal
metastasis also the affected bone is irradiated.
TUMOURS OF THE RENAL PELVIS AND URETER

Tumours of the renal pelvis are usually epithelial tumours and can be divided into three groups — 1.
Transitional cell carcinoma, 2. Squamous cell carcinoma and 3. Adenocarcinoma.
As transitional epithelium (urothelium) lines the renal pelvis, by far majority of the tumours are transiti
cell carcinoma. Squamous cell and adenocarcinoma only develop after metaplasia of the transitional epithel
T umours of the renal pelvis constitute about 10 to 15% of all the tumours of the kidney. 80% are transitiona
cell tumours, which occur commonly in men. Squamous cell carcinoma constitutes just less than 15%,
which are more common in women. Adenocarcinomas are rare. The highest incidence of pelvic tumour is
in 5th and 6th decades.
PAPILLOMA AND PAPILLARY CARCINOMA
Though basically papilloma is a benign tumour, yet papilloma of the pelvis and ureter should not be
considered as a typical benign tumour and in fact majority of the urosurgeons regard them as first stage of
malignant lesion. Distinction should be drawn between benign and malignant lesions so far as these tumou
are concerned.
The papilloma has got a peculiar tendency to produce seedlings in the lower urinary tract i.e. the ureter
and the bladder. These tend to recur after local excision. Clinically it is often difficult to differentiate
between the two.
Aetiology.— The cause of these tumours is not known, but their tendency to ‘seed’ in the ureter and
biadder suggests that the urothelium generally is susceptible to formation of this tumour. The metabolites
of tryptophan (alpha-amino-phenols) are
carcinogenic agents. Phenacetin is also a
carcinogenic agent. It seems that some
carcinogenic agents act to stimulate such
growth.
Pathology.— The papillary tumours '
are frequently multiple. The wall o f t h e ^ ,
pelvis may be covered with such tumours. Î
These tumours are very friable and . -=
extremely vascular, so haemorrhage readily ’
occurs. That is why haematuria is the earliest Mef
and most important symptom of this
condition. Such tumour may cause
obstruction to the flow of urine. "
Microscopically, this tumour shows a ' "i’-
central core of connective tissue which is
covered by transitional epithelium. Invasion !
ofthe mucosa is sometimes seen. Mitosis ■'
is often seen in many cells which is a distinct ,
evidence of malignancy.
Spread.—
1. By seedlings.— Seeds from the
primary tumour or pieces of tumour get Fig.57.18 — Urography showing papilloma of the renal pelvis
causing distortion of the pelvis and upper calyces.
detached from the parent tumour and are implanted in the lower urinary tract. This seems to be the main ty
of spread of these tumours.
2. Lymphatic spread.— These tumours do spread through perineural lymphatics, but such spread is not
common.
3. Blood spread is extremely rare.
Clinical staging.—
STAGE I — submucosal infiltration only.
STAGE II — muscular invasion without extension outside the wall of the pelvis or ureter.
STAGE III — invasion outside the wall of the pelvis and ureter involving the perinephric or periuretera
fat.
STAGE IV — extension into adjacent organs, regional lymph nodes and distant metastasis.
(i) Painless haematuria, which is profuse and progressive seems to be the only symptom of this condition.
Bleeding is at times quite profuse.
(ii) Pain.— Flank pain due to ureteral obstruction by the tumour is at times complained of. Clot is also
quite common as blood clot may obstruct the passage of urine in the ureter and cause colicky pain.
PHYSICAL SIGNS.— Examination usually reveals no abnormality. Slight tenderness may be found on
the affected kidney particularly if there is ureteral obstruction or if infection has supervened. An enlarged
kidney is unusual except when there is secondary hydronephrosis due to obstruction by the tumour.
1. Blood examination.— Anaemia is often present as haematuria is a common symptom. Other blood
examinations should be performed to know the function of the kidney.
2. Urine examination.—
(i) Red cells may be seen due to haematuria.
(ii) Pus and bacteria may be found in the urine.
(iii) Sometimes detached villi of the tumour may be seen in the urine.
3.X-RAY.—
(a) Plain film of the abdomen is not of much value.
(b) Excretory urogram is very much diagnostic. Persistent filling defect or space occupying lesion
may be seen in the pelvis or ureter.
(c) Retrograde urography is usually not required, but if the dye excretion is not enough in excretory
urography, this examination should reveal the filling defect.
(d) Chest X-ray should be taken routinely although metastasis to the lung is uncommon.
(e) Selective renal angiography is not as helpful as in renal cell carcinoma. It may reveal an enlarged
pelviureteric artery or even a tumour blush.
4. CYSTOSCOPY.— This is essential in all haematuria cases. Blood may be seen coming from one
ureteral orifice. Ureteral catheter should be passed through it for retrograde urography to see any filling
defect. During cystoscopy search should be made for ‘satellite’ tumours in the urinary bladder.
5. TUMOUR MARKERS.— This hardly has become a diagnostic procedure in these tumours. An elevated
level of urinary carcinoembryonic antigen (CEA) has been noticed in 2/3rd of these cases.
Treatment.—
In this condition radical nephrectomy is insufficient, as this tumour shows a tendency to produce seedl
in the lower urinary tract. So the treatment is radical nephroureterectomy. This includes excision of the
kidney and all perinephric tissue including regional lymph nodes, the ureter and the periureteral portion of
the bladder en bloc. So it must be remembered that the intramural portion of the ureter alongwith the
ureteric orifice must be excised.
It goes without saying that it must be confirmed that the other kidney is normally functioning.
Any associated bladder tumour should be dealt with simultaneously.
Radiotherapy.— As this tumour is radioresistant, radiotherapy has got no role to play in this condition.
It should be remembered that 5 years survival rate after operation is 52% for so-called benign papillary
tumours, 17% for papillary tumours with infiltration and 7% for sessile carcinoma.
SQUAMOUS CELL CARCINOMA OF THE RENAL PELVIS
Aetiology.— Such tumour only develops after metaplasia of the normal transitional epithelium of the
renal pelvis. Such metaplasia is usually associated with longstanding chronic inflammation or presence of
calculus. Vitamin A deficiency has also been incriminated. Metaplasia may occur at scattered areas or may
replace the entire pelvic mucosa.
Pathology.— These tumours are sessile infiltrating tumours and carry worse prognosis. First there may
be leukoplakia formation. These are usually associated with chronic infection or lithiasis.
Microscopic picture shows typical squamous cell carcinoma as elsewhere in the body.
Spread is mainly by lymphatics to the regional lymph nodes.
Treatment.— This is almost similar to the papillary carcinoma, except for the fact that retroperitoneal
lymph node dissection may be required.
Epidermoid carcinoma is almost always fatal within 1 year.
ADENOCARCINOMA OF THE RENAL PELVIS
These are usually mucin secreting tumours and arise only after metaplastic changes of the transitional
epithelium. Such changes usually occur after chronic inflammation and these changes are called ‘pyelitis
cystica ’ and ‘pyelitis glandularis Only after these changes that gradually adenocarcinoma starts developing.
TUMOURS OF THE URETER
These tumours are basically a type of transitional cell carcinoma. The range varies from a low to high
grade malignancy. These tumours may be primary or secondary to the similar tumours in the renal pelvis or
bladder.
Tumours of the ureter are rare. Majority (about 2/3rds) occur in men. Most of these tumours are seen
in lower ureter. Almost all are transitional cell carcinomas. Squamous cell carcinoma is rare.
Clinical features.— Haematuria is again the most common symptom, but it is usually intermittent and
quite profuse. There may be dull pain over the kidney due to ureteral obstruction. There may be clot colic.
Treatment.— Nephroureterectomy as mentioned for papillary carcinoma of renal pelvis is the treatment
of choice.
LAPAROSCOPIC NEPHRECTOMY
This operation was first carried out by Clayman et al in 1991. The procedure is a complicated one and
should not be undertaken by the inexperienced laparoscopist.
Indications.— (i) This technique is probably most useful for the removal of bumt-out glomerulonephritic
or pyelonephritic kidney.
(ii) The bumt-out stone kidney where there has been perinephric inflammation. But the dissection is
difficult one.
(iii) The value of this procedure for the malignant kidney is in dispute. It is not suitable for large
adenocarcinomas. It may be suitable for small peripheral tumours.
Transperitoneal approach.— The patient is placed on the operating table as for open renal surgery.
Endoscopic access is obtained by a 10 mm umbilical port or a port placed about 5 cm lateral to the midline
in the plane of the umbilicus towards the side of the affected kidney. A 5 and 12 mm ports are placed in the
mid clavicular line and two further 5 mm ports are placed in the midaxillary line under direct vision.
The dissection is commenced incising the posterior peritoneum along the line of Todt lateral to the
colon from the hepatic or splenic flexure, depending on the side, down to the iliac fossa. The colon is
displaced medially and the ureter is visualised in the retroperitoneum. The ureter is dissected and divided
at the level near the iliac vessels and is followed upwards till the renal
pelvis is exposed. Dissection is now carried out in the peripelvic fat to
reveal the renal vessels entering the hilum anterior to the pelvis. 1 cm length
of each vessel is dissected free. The vessels are now transected and divided
with the Endo-GIA clamp passed through the 12 mm port. This instrument
places two rows of staples across each vessel and divides the vessel
automatically between the staples. The kidney is now gradually dissected
from the surrounding perinephric fat and fascia. The kidney is thus mobilise
Through the 12 mm port a specially made impermeable sac is introduced
into the peritoneal cavity. The margins of the neck of the sac are opened
with graspers passed through any of the 3 lateral ports. The kidney is
manipulated into the sac. A drawstring at the neck of the sac is pulled and
the neck of the sac is withdrawn through either 10 mm or 12 mm port.On
the surface the neck is grasped by 2 or 3 artery forceps. The kidney within
the abdomen is fragmented with commercial disintegraters or chopped up
with a pair of surgical scissors passed through the neck of the sac. The
fragmented kidney is then aspirated and the sac withdrawn from the abdom
cavity.
10 mm and 12 mm ports are sutured, while 5 mm ports require simple
butterfly dressing.
Retroperitoneal approach.— The patient is again placed in the lateral
Fig.57.19.— Shows sizes (in position. Access to the retroperitoneum is achieved by primary insufflation
millimetres) and positions of ports with the Veress needle passed through a small puncture in the lumbar fascia
used for laparoscopic nephrectomy below the 12th rib and 2.5 cm lateral to the erector spinae muscle. About
and nephroureterectomy.
1-2 L of carbondioxide is insufflated. A 10 mm port is made followed by
insertion of the laparoscope. A second 5 mm port is then made under direct vision in the midaxillary line.
Perinephric and periureteric fat are dissected to expose the posterior surface of the kidney, which is eleva
and pushed forward to expose the renal artery and vein entering the hilum. Through a 12 mm port inserte
in the midaxillary line, the Endo-GIA clamp is passed, the vessels are stapled and transected. The ureter is
traced downwards and divided. The kidney is either bagged and macerated or a small 3 cm incision is ma
in the lumbar fascia and the mobilised kidney is removed intact. It must be remembered in the retroperito
approach that there should not be any breach in the peritoneum, otherwise the gas will escape into the
peritoneal cavity and it will obscure the view to work on. One may then have to revert to the transperiton
approach. More recently a technique has been developed of inserting a balloon into the retroperitoneum t
develop a space. The balloon is then removed and a laparoscope is passed into the developed space.
NEPHROURETERECTOMY.— This operation is carried out for transitional cell carcinoma. Preliminar
circumcision of the ureteric orifice is carried out in the bladder with cystoscopic diathermy. The intramura
ureter is sealed. The laparoscopic approach through the retroperitoneum is carried out which has been
described above. After kidney mobilisation, the ureter is traced down into the retroperitoneum across the
iliac vessels towards the bladder. By simple traction with forceps the ureter is everted from the bladder w
and then cross-stapled with the endostapler. The intramural portion of the ureter is divided and the urete
and kidney are removed by bagging manoeuvre. The macerating procedure must be carefully observed
laparoscopically to ensure that there is no spillage of malignant material into the peritoneal cavity.
1105
CHAPTER- 50
THE URINARY BLADDER

Development.— The urinary bladder is developed from two sources — 1. The trigone is developed from the ends of the
mesonephric ducts (mesodermal origin) and 2. The rest of the bladder is developed from entodermal cloaca.
1. The entodermal cloaca is divided into two portions, the dorsal portion forms the rectum, whereas the ventral portion becomes
subdivided into three portions — (a) the cephalic vesico-urethral portion into which the allantoic canal opens and the mesonephric
ducts open, (b) the middle narrow channel, the pelvic portion and (c) a caudal phallic portion is closed externally by the urogenital
membrane. The 2nd and the 3rd parts constitute the urogenital sinus. The cephalic vesico-urethral portion forms the major part of the
urinary bladder except the trigone.
The portion of the urogenital sinus which forms the bladder is prolonged above to the umbilicus in the form of a narrow canal,
which is termed urachus.
2. With the gradual descent of the openings of the mesonephric ducts and with the absorption of the mesonephric ducts
alongwith caudal portion of the ureteric buds, the trigone is formed. That is why the two ureteric orifices become separated. The
trigone starting from the ureteric ridge above and the urethral opening below is developed from absorption of mesonephric duct and
caudal portion of the ureteric buds. It also forms the upper part of the posterior wall of the prostatic urethra upto the opening of the
prostatic utricle.
After birth, the urinary bladder descends so that urachus becomes prolonged. Its lumen gradually obliterates, but persists as a
fibrous cord, which is called median umbilical ligament.
SURGICAL ANATOMY —
The urinary bladder is a reservoir for the urine. Its size varies with the amount of urine it contains. When empty it is placed
entirely within the lesser pelvis, but as it becomes distended it expands upwards and forwards into the abdominal cavity. At this time it
comes in direct contact with the lower abdominal wall without intervention of the greater sac of the peritoneum. That is why it is better
to distend the bladder before abdominal incision for suprapubic
cystostomy to get into the bladder without opening the peritoneal
cavity so there is no chance of infecting the peritoneal cavity.
It has the BASE at the posterior surface which is directed back
wards and downwards. In the male it is related to the rectum, but its
upper part is separated from the rectum by the rectovesical pouch of
peritoneum. In the female it is closely related to the anterior wall of
the vagina. The bladder has a NECK which is the lowest and most
fixed part of the bladder. It lies 3 to 4 cm behind the lower part of the
symphysis pubis. Within it lies the internal urethral orifice. In the
male the neck rests on the base of the prostate and in the female it is
related to the pelvic fascia. The bladder has an APEX, which is di
rected upwards and forwards towards the umbilicus, to which is at
tached the remnant of the urachus which forms the median umbilical
ligament. The SUPERIOR SURFACE is triangular in shape In the
male it is completely covered with peritoneum and it is in contact
with the sigmoid colon and the terminal coils of small intestine. In the
female it is almost entirely covered with peritoneum except near its
posterior border where the peritoneum is reflected from it to the uterus
at the level of the internal os (i.e. the junction between the body and
cervix of the uterus) forming the vesico-uterine pouch. In front the
Fig. 58.1.— Diagrammatic view of interior of blad
superior surface is continuous with the apex of the bladder. The blad
der. 1.—Anteriorwall. 2.— Internal urinary meatus.
der has got INFEROLATERAL SURFACE on each side.
3.—Trigone. 4.— Inter-ureteric bar. 5. Retrotrigonal
As the bladder fills with urine, the borders of the empty blad
area. 6.— Fundus. 7.— Lateral wall. 8.— Right uret
der become rounded off and it assumes an ovoid form. It gradually
eric orifice. 9.— Lateral recess.
pushes off the parietal peritoneum from the lower part of the anterior
abdominal wall so that the inferolateral surfaces rest against the anterior abdominal wall without intervention of peritoneum for some
distance above the symphysis pubis.
At birth, the bladder lies at a higher level than in the adult. The neck is at the level of the upper border of the symphysis pubis
and the bladder is an entirely abdominal organ extending about V3rds of the distance up to the umbilicus. As the child grows, it
progressively descends until it reaches its adult position (an entirely pelvic organ) shortly after puberty.
LIGAMENTS.-(i) True lateral ligament is condensation of fibroareolar tissue on each side of the bladder connected to the
tendinous arch of the pelvic fascia.
(ii) Lateral puboprostatic ligament is also a condensation of fibro-areolar tissue which extends from the neck of the bladder
to the anterior end of the tendinous arch of the pelvic fascia.
(iii) Medial puboprostatic ligament is also a condensation of fibro-areolar tissue which passes from the anterior aspect ofthe
prostate to the pubic bone near the middle of the symphysis. In the female this ligament is called pubovesical ligament.
70
(iv) The median umbilical ligament, which has been mentioned above, is the remains of urachus and joins the apex of the
bladder to the umbilicus.
(v) Posterior ligament is also a condensation of fibroareolar tissue which envelops on each side the vesical venous plexus and
starts from the lateral border of the base of the bladder to end in the internal
iliac vein.
Interior of the bladder.— Except the trigone of the bladder, the
mucous membrane of the bladder is loosely attached to the muscular coat,
that is why it appears folded when the bladder is contracted. Only in the
trigone, which is a triangular area, the mucous membrane is firmly bound to
the muscular coat and that is why it always looks smooth. Its base is formed
by the intemreteric ridge which connects the two ureteric orifices and is
formed by the longitudinal muscle coats of the ureter; and the apex is formed
by the internal orifice of the urethra. The mean capacity of the bladder in the
adult is 220 cc. Individuals normally feel to micturate when the bladder
contains about 300 cc. of urine.
Structure.— The bladder has 3 coats :—
(i) The serous or peritoneal coat is not present all over. It mainly
covers the superior surface.
(ii) The muscular coat contains layers of unstriped muscular fibres.
The muscles of the bladder are known as ‘detrusor muscle’. There are an
external and an internal layers of longitudinal muscles and a middle layer of
circular muscles. The middle circular layer is very thin and irregularly scat
tered except at the lower part of the bladder where it gradually becomes
Fig 58.2.— Cystoscopic view of normal left thickened and forms sphincter vesicae. which surrounds the internal urethral
ureteric orifice orifice.
(iii) The mucous coat is pale rose in colour. The epithelium is of
transitional variety. Over the trigone the mucous coat is closely attached to the muscular coat and looks smooth. In other part of the
bladder the mucous coat is loosely attached to the muscle coat so thrown into folds or rugae when the bladder is empty. There are no
true glands in the mucous membrane, though there are true mucous glands near the internal urethral orifice. Transitional epithelium of
the ureter and bladder contains alkaline phosphatase, though its significance is not clear. There is no muscular mucosae.
Vessels and nerves.— ARTERIES.— The principal arteries are the superior and inferior vesical arteries, branches of the
anterior trunk of the internal iliac artery. The obturator and inferior gluteal arteries also send small branches to the bladder. In the
female uterine and vaginal arteries also send small branches to it.
VEINS.— Veins of the bladder form a plexus on the inferolateral surfaces just above the prostate. From this, plexus of veins
passes backwards in the posterior ligament of the bladder to end in the internal iliac vein.
NERVES.— The efferent parasympathetic fibres for supply of the bladder arise from the 2nd to 4th sacral segments of the spinal
cord (S2-S4) (nervi erigentes). These fibres convey motor fibres to the detrusor muscles and inhibitory fibres to the sphincter vesicae
The sympathetic efferent fibres arise from the lower two thoracic and upper two lumbar segments of the spinal cord (Tn and L, and
2). These fibres supply inhibitory fibres to the detrusor muscles and motor fibres to the sphincter vesicae. That means when there is
stimulation of parasympathetic nerves, there is contraction of the detrusor muscle and relaxation of the sphincter vesicae. When there
is stimulation of sympathetic fibres, there is relaxation of the detrusor muscles and contraction of the sphincter vesicae. The pain fibres
from the bladder, which are concerned with over-distension of the bladder or presence of stone or inflammatioa are carried by both
sympathetic and parasympathetic nerves, that is why simple division of sympathetic nerves does not relieve bladder pain. In the spinal
cord the pain fibres lie in the lateral spinothalamic tracts. Sense of overdistension is conveyed by afferent sympathetic nerves to the
brain. Though the process of micturition is a stretch reflex whose centre lies in S2, 3 and 4 segments of the spinal cord and contraction
of the detrusor muscle is caused by the efferent fibres ofthe parasympathetic system coming from those segments, yet if the place is not
suitable for micturition, the process can be inhibited by cerebral control (the cortical impulses may be transmitted via sympathetic
system and somatic system by pudendal nerves to the sphincter urethrae).
CONGENITAL ANOMALIES OF THE BLADDER
EXSTROPHY (ECTOPIA VESICAE)

This is due to complete ventral defect of the urogenital sinus and the overlying skeletal system. The
of the bladder which develops from the ventral wall of the urogenital sinus and the infraumbilical part of
abdominal wall fail to develop. So not only the anterior or ventral aspect of the urogenital sinus fails to fo
overlying muscles and bones fail to develop.
In this case there is a big spherical or oval defect in the anterior abdominal wall below the umbilicus
occupied by the inner surface of the posterior wall of the bladder. The mucosal edges fuse with the skin. U
THE URINARY BLADDER 1107
to the abdominal wall from the ureteric orifices. The rami of the pubic bones are widely separated. The pelvic
loses its rigidity. The recti muscles which inert on to the pubic rami become widely separated from each othe
part of the abdomen. Epispadias is almost always accompanied with it.
Incidence.— Ectopic vesicae is a rare occurrence and its incidence is once in 50,000 births.
Types.— Two types are commonly encountered with — complete and incomplete varieties. The complete
is more common and is just described. In incomplete variety the pubic bones are united and the external genita
normal or there is epispadias.
1. Males are more often affected than females. The ratio is 4 : 1.
2. Due to pressure of the viscera behind it, the posterior wall of the bladder protrudes through the defect
deep red in colour. Frequently the everted mucous membrane becomes ulcerated and painful. It may underg
changes and may form adenocarcinoma.
3. It bleeds readily.
4. When this mucous membrane is gently pulled upwards, more pale wet trigone becomes visible. Efflux
of urine can be seen from the ureteric orifices.
5. A line of demarcation becomes obvious between the protruding mucous membrane and the adjacent s
6. When the exposed bladder wall is pushed behind with the fingers the firm edge beneath the mucocuta
ous junction can be felt as the defect in the abdominal wall.
Associated abnormalities — Other congenital anomalies are frequently associated with it. These are :
1. The rami of pubic bones are widely separated. The symphysis pubis is absent and in its place there is a
thick fibrous band. This makes the pelvic ring less rigid. The femurs are rotated externally and the child wad
like a duck (waddling gait).
2. The umbilicus is absent. There may be umbilical hemia.
3. Genitalia.—
(a) In the males :
(i) Epispadias is almost always present.
(ii) The penis is broader and shorter than normal. It is drawn up and fixed to the abdominal wall.
(iii) The scrotum may be ill-developed.
(iv) The testes may be normal or ectopic or maldescended.
(v) The prostate and seminal vesicles are often rudimentary or absent.
(b) In the females :
(i) The clitoris is usually cleft.
(ii) The labia minora are separated.
(iii) There may be anomalies in the development of uterus and vagina.
4. Anal sphincter is often lax.
5. Hemiae :
(a) Umbilical hemia may be present.
(b) There may be inguinal hemia of one or both sides. Bilateral hemiae may be associated with
undescended testes when sex differentiation becomes difficult.
Complications.—
1. The exposed vesical mucous membrane is usually ulcerated with haemorrhage. It may become painfu
2. Recurrent ascending infection is common. It may make the patient’s life miserable and it is difficult to
control such infection.
3. Hydronephrosis may be caused by ureterovesical obstruction.
4. Continuous bad odour of urine accompanies the patient.
5. Metaplastic change may take place at the exposed mucous membrane of the urinary bladder and this
initiate formation of adenocarcinoma.
6. Half of the patients die of renal failure.
Treatment.—
1. Obviously the treatment is operation. First of all diversion of urine has to be performed. Later on, afte
some months the urinary bladder is excised and closure is done. The operation is performed between 4 and 6
years of age. In this case diversion of urine is done into the sigmoid colon. But problem of infection has not m
this operation very successful. Stricture at the site of anastomosis (uretero-sigmoidal), recurrent pyelonephrit
hyperchloraemic acidosis are the reasons of ultimate death of patients.
2. Diversion of urine into an ileal conduit with excision of the bladder can be performed at 5 years of age
As problem of infection is less, renal function is better maintained and this is a better operation.
3. Recently attempts are being made to reconstruct the bladder and sphincter within first year of
osteotomy of both iliac bones are made just lateral to the sacroiliac joints, the bladder is closed. The urethr
reconstructed behind the pubis. The pubic bones are now brought in the midline and fixed together. The p
of incontinence is difficult to tackle. Similarly urinary infection and stone formation and ultimately renal f
are also difficult to control. Various operations have been suggested for incontinence at bladder neck regio
overall success rate is limited.
PERSISTENT URACHUS
Embryologically the allantois which connects the urogenital sinus with the umbilicus ultimately becom
urachus. Normally the urachus is obliterated and is represented by a fibrous cord which is called median
umbilical ligament and extends from the apex of the bladder to the umbilicus.
Anomalies of the urachus —
1 Patent urachus.— Occasionally the urachus may remain patent, so that a fistula exists between the ap
of the urinary bladder and the umbilicus. This is the urinary fistula of the umbilicus. In this case urine drains
constantly from the umbilicus. Though this is congenital, yet this is only manifested in the adult or even ol
The reason is that contraction of the bladder starts at the apex of the organ and passes towards the base an
ultimately to the neck As the urachus opens at the apex of the bladder, it is closed during contractions of t
bladder and urine does not come out through the patent urachus. Urinary leakage through the umbilicus
reveals urinary fistula, becomes only evident when there is some urinary obstruction at the lower urinary
enlarged prostate, stricture urethra etc.
TREATMENT — Since urinary leakage due to patent urachus is not possible without an obstruction
lower urinary tract, the treatment is directed to get rid of such obstruction. If still the leak continues, the
treatment is excision of the umbilicus with excision of the urachus down to the apex ofthe bladder with cl
of the urinary bladder.
2 Incomplete obliteration.— This is in fact more common than the previous condition. The umbilical en
ofthe urachus fails to obliterate giving rise to urachal sinus of the umbilicus. Such sinus discharges small a
of mucus from the umbilicus. It becomes often infected, when pus drains out from the umbilicus.
Sometimes the vesical end fails to obliterate, whereas the umbilical end obliterates normally. This do
produce any symptom and remains unknown to the patient.
TREATMENT.— Urachal sinus with persistent discharge and dermatitis require excision of the urach
remnant
3. Urachal cyst.— If the ends of the urachus obliterate leaving the middle portion of the urachus p
cyst may form by secrction of the patent portion of the duct. Such cyst may become quite large. It represen
immobile swelling in the midline in the hypogastrium deep to the umbilicus.
If the cyst becomes infected, it becomes painful and tender.
Sometimes adenocarcinoma may occur in a urachal cyst or in the patent vesical end of the urachus.
Stones may develop in urachal cyst which is easily identified by straight X-ray.
TREATMENT — Whenever diagnosis is confirmed, treatment is excision of the urachal cyst alongwi
remains of the urachus. It may require closure of the apex of the urinary bladder. If adenocarcinoma has
developed in the cyst, radical resection is required.
INJURIES TO THE BLADDER

Major portion of the urinary bladder is extraperitoneal, whereas a minor portion particularly the
superior surface of the bladder is intraperitoneal. So injuries to the bladder may be either extraperitoneal,
which constitute 80% of bladder injuries or intraperitoneal which constitute 20% of all bladder injuries.
Aetiology.— Extraperitoneal injuries are mainly caused by fracture of the pelvis, which is com
monly seen in road traffic accidents. About 15% of all pelvic fractures are associated with concomitant
bladder or urethral injuries
Intraperitoneal injuries are usually caused by a blow or kick or fall on to a fully distended bladder.
It often occurs in drunk individuals.
There are other causes of injury to the bladder which include stab wounds and gun shot wounds.
In this group iatrogenic causes are also included which are passage of cystoscope, endoscopic resection
or diathermic coagulation of bladder tumours and extensive pelvic operations.

Pathology.— When the pelvis is fractured, fragments from the fracture may perforate the blad
der. This perforations usually result in extraperitoneal rupture. This causes extravasation of urine
which has been discussed in detail in chapter 59 of The Prostate & Urethra’. Gradually infection may
develop to cause deep pelvic abscess and severe pelvic inflammation from extravasation.
When the bladder is full to its capacity, a direct blow to the lower abdomen may cause bladder
disruption. This type of rupture is an intraperitoneal rupture of the bladder. Usually a linear laceration
occurs at the dome of the bladder which will allow the urine to flow into the peritoneal cavity. If the
urine is sterile, patient may not complain of any symptom for several days and diagnosis remains
obscure If the urine is infected, immediate peritonitis and acute abdomen will develop.
Extraperitoneal rupture — As mentioned earlier extraperitoneal injury of the bladder is mainly
caused by pelvic fracture. The diagnosis of pelvic fracture is easily made by lateral compression on the
bony pelvis, which will evoke pain and crepitus at the fractured site. When this is associated with
lower abdominal and suprapubic tenderness one may suspect extraperitoneal rupture of the bladder.
This may be associated with dullness to percussion in the suprapubic region. The patient often tries to
pass urine, when blood and even clots in the urine will come out.
SPECIAL INVESTIGATIONS.— Catheterisation is usually required in patients with pelvic trauma,
which reveals haematuria. But catheterisation will be difficult or impossible in case of urethral injury
with bloody discharge
A plain X-ray demonstrates pelvic fracture. There may be haziness over the lower abdomen due
to blood and urine extravasation.
An excretory urography should always be performed to exclude kidney and ureteral injuries.
Diagnosis is confirmed by pushing contrast medium into the bladder. About 120 ml of sterile
isotonic saline is mixed with 60 ml of 35% Hypaque or Conray and this solution is introduced into the
bladder and an X-ray is taken. The patient is asked to pass urine and again an X-ray is taken. This will
demonstrate areas of extraperitoneal extravasation With intraperitoneal rupture, this examination will
show free contrast medium within the abdomen.
Cystoscopy is not very helpful as bleeding and clot obscure visualisation and prevent accurate
diagnosis
Intraperitoneal rupture — The peculiarity of this condition is that after the rupture, the patient
often neither has any complaint, nor he feels the desire to pass urine. Sometimes patient complains of
sudden, agonising pain in the hypogastrium with severe shock. Such injury to the bladder often occurs
by direct blow to the full bladder in a drunk patient.
On examination the abdomen is distended. After a few hours there may be abdominal rigidity
which indicates peritonitis. Though the patient has not passed urine, yet the bladder is not distended as
evident by percussion This is an important sign and should be remembered by the students. If there is
considerable amount of urine in the peritoneal cavity, shifting dullness may be elicited
Rectal examination should be performed as this may reveal bulging of the rectovesical pouch
SPECIAL INVESTIGATIONS.— Catheterisation reveals empty bladder.
A plain X-ray in the erect position may show ground-glass appearance of the lower abdomen due
to presence of urine in the peritoneal cavity.
A peritoneal tap' may reveal urine in the peritoneal cavity.
Instillation of radio-opaque solution into the bladder as mentioned in the extraperitoneal rupture
often confirms the diagnosis.
TREATMENT —
A. Emergency conservative measures.— Shock and haemorrhage should be treated by proper
resuscitation.
B. Surgical treatment.— When rupture of the bladder has been diagnosed, operation should be
performed without delay.

A lower midline abdominal incision is made. Before reaching the bladder, one may see pelvic
haematoma and extravasation of urine. The haematoma and urine are cleaned and the bladder is
opened in the midline.
EXTRAPERITONEAL RUPTURE.— After opening the bladder, the inside is carefully inspected
to the detect rupture or laceration. It is better to repair extraperitoneal rupture intravesically. The
rupture is closed from within with Dexon or chromic catgut in two layers. Sometimes lacerations may
extend into the bladder neck which should be repaired meticulously. After repair of the rupture, an
indwelling urethral catheter is introduced and the midline bladder wound is closed around a suprapubic
drainage. Another suprapubic corrugated rubber sheet drain is given to the retropubic space.
INTRAPERITONEAL RUPTURE.— This should be repaired through transperitoneal approach
The rupture is closed with Dexon or chromic catgut in two layers. The peritoneal cavity is cleared of
urine and blood. An indwelling urethral catheter is passed. The wound of the bladder is then closed in
separate layers leaving a suprapubic drain.
CYSTITIS
AETIOLOGY.— Cystitis is much more common in women than in men probably due to short
urelhra through which the bacteria ascend.
Cystitis also accompanies haematogenous renal infection in rare cases.
Lymphatic spread from infected cervix is also a probable cause of cystitis though rare.
Bowel infections e.g. appendicular abscess, diverticulitis etc. may cause cystitis by involving
bladder by contiguity.
In men, cystitis is almost always secondary to some other causes e.g. infection of the prostate,
enlarged prostate associated with residual urine, presence of vesical calculus or an ulcerated vesical
neoplasm.
PREDISPOSING CAUSES.— The various predisposing causes which may indulge to cause cysti
tis are being mentioned here — 1. Presence of a calculus, foreign body or neoplasm in the bladder
2. Obstruction in the urethra due to urethral stricture or enlargement of prostate or prostatic
carcinoma or stenosis of the external urinary meatus may lead to stasis and formation of residual urine
in the urinary bladder which initiate cystitis.
3. Presence of diverticulum in the bladder may cause cystitis due to residual urine inside the
diverticulum.
4 Injuries or diseases of the spinal cord which hinders proper evacuation of the bladder may lea
to cystitis.
5. Presence of vesicoureteral reflux may incite cystitis.
6. Malnutrition with lowered general resistance and particularly avitaminosis may lead to cystitis.
Routes of infection —
1. Ascending infection from the urethra is the commonest. That is why cystitis is very common in
females who possess short urethra. E. coli which originate in the bowel, contaminate the vulva and
perineal region. From these regions they get easy access to the bladder in case of females. Passage of
urethral instruments may cause cystitis in either sex.
2. Haematogenous infection from kidney may cause cystitis, but rare.
3. Lymphatic spread from neighbouring viscera has also been noticed. These viscera are mostly
infected cervix, fallopian tube, vagina, sigmoid colon etc. This is also comparatively rare.
CAUSATIVE ORGANISMS.- The most common infecting agent is E. coli. This is followed by
Proteus mirabilis, particularly in young women, Staphylococcus aureus. Staphylococcus albus. various
Streptococci, Pseudomonas and Klebsiella. Schistosoma haematobium produces cystitis which may be
complicated by stone formation and high incidence of cancer. Mycotic infection ofthe bladder is rare.
Monilial vaginitis may secondarily infect bladder. Veiy rarely actinomycosis may involve the bladder
by direct extension from lesions in the bowel.

Tuberculous cystitis is a specific form of cystitis which has been discussed later in this section.
The students must remember that in this condition there will be plenty of pus cells without any
organisms found with ordinary staining (abacterial pyuria). But besides tuberculous cystitis, abacterial
pyuria is also seen in abacterial cystitis (See page 1159) or in an ulcerative bladder carcinoma.
PATHOLOGY —
MACROSCOPIC FEATURES.— In acute cystitis, the mucous membrane of the bladder is swol
len, intensely red and congested. The normal glistening appearance of the mucous membrane is lost.
Multiple foci of submucosal haemorrhage are noticed. The mucosa is oedematous and its surface is
covered with purulent membrane. Superficial ulcers are occasionally seen. In the trigone there may be
tiny clear cyst, known as ‘bullous oedema’. The muscularis is usually not involved.
In chronic cystitis, the bladder may show thickening of its wall with corresponding reduction in
the size of the cavity. There may be hypertrophy of the muscular tissue. The mucous membrane is dull,
rough and mottled with the brown remains of old haemorrhages. In places it may be ulcerated. The
mucous membrane is firmly attached to the muscle coat owing to fibrosis of the submucosa.
MICROSCOPIC FEATURES.— In acute cystitis, it is the submucous coat which shows major
changes. There is much congestion and dilatation of capillaries. There is infiltration with the cells of
acute inflammation. The superficial layers of the epithelium may be desquamated, but the deeper layer
remains intact. Leucocytic infiltration may extend into the muscle, but otherwise the muscle layer
remains unaltered.
In chronic cystitis, all coats are involved. There is diffuse fibrosis which is most evident in the
submucosa. The mucosa is ulcerated in places. There may be abundant formation of granulation tissue
covered by epithelium giving rise to polypoid excrescences.
SYMPTOMS.— Severity of the symptoms depends on severity of the disease.
(i) Increased frequency of urine both in day and at night is the most important symptom. This
may disturb sleep of the patient at night which may make the patient drawn and tired.
(ii) Urgency is also a very characteristic symptom of this condition. At times the desire to
micturate becomes so urgent that incontinence may result.
(iii) Pain, though often associated with, is not a major symptom. Pain varies from mild to agonising
in severe cystitis. When the superior surface of the bladder is involved pain is referred to the suprapubic
region. When the trigone is involved pain is referred to the
tip of the penis or the labia majora.
(iv) Haematuria.— It should be remembered that cys
titis is the commonest cause of haematuria. Such haematuria
is usually terminal that means at the end of micturition
Later on as severity increases, the whole urine may be blood
stained, but it will be more so at the end of micturition.
(v) Pyuria.— This is often seen in cases of cystitis.
PHYSICAL SIGNS.— Examination of the abdomen
is usually normal. Tenderness may be elicited at the
suprapubic region.
Rectal examination should always be performed It
may reveal an enlarged prostate (benign enlargement of
prostate) which is the cause of cystitis. It may reveal an
enlarged firm and tender prostate (acute prostatitis as the
cause of cystitis). It may reveal presence of residual urine.
In female, pelvic examination is highly important to
exclude any pathology in the genital system as the cause
of cystitis.
1. Blood examination.— White blood count is usually elevated. E.S.R. is also increased.
2. Urine examination usually shows pus cells, bacteria and red blood cells. In case of presence of
associated prostatitis threads may be seen in the initial specimen, so midstream urine specimen should
be taken for culture and sensitivity test.
3. X-rays are not indicated unless stasis or renal infection is suspected. X-ray is also required if
the patient fails to respond to adequate antibiotic treatment for cystitis or the infection is recurrent and
there is presence of obstruction, vesicoureteral reflux, tuberculosis or calculus.
4. Cystoscopy is contraindicated in acute phase. But it should be done 10 days later when
haematuria is continuing to exclude presence of vesical neoplasm or stone or foreign body.
TREATMENT.—
A. GENERAL MEASURES—
1. The patient is urged to drink plenty.
2. Alkalinisation of the urine should be achieved. This provides symptomatic relief. By raising
the pH of the urine, it counteracts the burning sensation of acidic urine which normally accompanies
infection. 60 to 20 g of sodium bicarbonate may be given for this.
3. Antispasmodics.— Various antispasmodics e.g. baralgan, buscopan, atropine with phen-
obarbital or tincture of belladonna may be used. This relieves muscular spasm and provides consider
able relief to the patient.
4. Urinary tract analgesic.— Phenazopyridine is an urinary tract analgesic. 100 mg tablets of
phcnazopyridine (pyridium) may be used in the dosage of 2 tablets thrice daily after meals provides
considerable relief.
5. Local heat.— Hot sitz baths may ease severe pain and spasm.
B. SPECIFIC TREATMENT — Antibiotics are prescribed according to the sensitivity test report.
A few antibiotics are particularly effective in cystitis. These are nalidixic acid 500 mg, nitrofurantoin
100 mg tablets, amoxycillin, trimethoprin and sulphamethoxazole, chloramphenicol, ampicillin etc.
TUBERCULOUS CYSTITIS
Tuberculous cystitis is
never a primary disease and it
is usually secondary to tubercu
lous kidney in majority of cases.
Rarely it may be secondary to
tuberculosis of the prostate,
seminal vesicles and epididy
mis. Occasionally it may be sec
ondary to tuberculosis of the ad
jacent organs e.g. the fallopian
tubes.
Pathology.— As mentioned
above tuberculous cystitis is
usually secondary to tuberculo
sis of the kidney. In this case
the disease starts at the ureteric
opening. When the condition is
secondary to tuberculosis of the
Fig. 58.4.— Cystoscopic view of tuberculous cystitis, with retracted prostate, the neck of the blad
right ureteric orifice surrounded by tubercles. der is involved first. The earli
est change is pallor of the mucosa due to submucous oedema. Later on tiny white translucent tubercle
covered by epithelium develops. Gradually tubercles enlarge in size and coalesce. The overlying
epithelium shreds off and characteristic tuberculous ulcer forms. This ulcer is round with ragged and
overhanging edges and covered with grey shaggy floor. Though it covers a considerable area, it is
seldom deep and perforation of the bladder is almost unknown. There is considerable submucous
fibrosis which also prevents penetration of such ulcer. Fibrosis causes reduction in the capacity of the
bladder which becomes smaller in size and is often called ‘thimble’ bladder.
Treatment.— 1. MEDICAL TREATMENT.— This includes antitubercular drugs alongwith nutri
tive diet and sanitorium regime. In majority of cases this treatment is enough to cure not only
tuberculosis of the bladder but also tuberculosis of the kidney.
In some intractable cases instillation of antitubercular agent into the bladder has been effective. B53 is
a soap derived from a branched fatty acid which possesses a good antitubercular power. 0.5% of such
solution with local anaesthetic should be instilled into the bladder and retained for 1 hour daily. This is
continued for 14 days which comprises a course. Such a course may be repeated after an interval of 1 week.
2. SURGICAL TREATMENT.— When renal damage has been excessive so that the condition
fails to respond to medical treatment, removal of the kidney alongwith the ureter (nephroureterectomy)
should be considered. With removal of the offending kidney the bladder lesion starts recovering soon
When the bladder has been considerably contracted with reduction of its capacity to a great extent,
some sort of operation should be performed to increase the capacity of the contracted bladder The
bladder should be first made free from ulcerations by medical treatment and even by nephroureterectomy.
Once the bladder is free from ulceration, ileocystoplasty should be performed in which a portion of
small intestine (ileum) is sutured to the dome of the contracted bladder. If the ureter is seen to be
involved evidenced by dilatation on excretory urography, it should be implanted into the newly con
structed pouch of intestine.
ABACTERIAL CYSTITIS
It is a rare and abrupt condition with marked local vesical reaction. The condition is characterised by
presence of pus in the urine, but without any accompanying bacteria.
Aetiology.— It is mainly seen in young men and women and occasionally in children particularly the boy
Usually a history of recent exposure can be elicited. Mycoplasma and chlamydia organisms have been isolat
from these cases. Similarly an adenovirus has also been isolated from the urine of children suffering from th
disease. Sometimes pleuropneumonia-like organisms (PPLO) are detected by special cultural methods from
of these cases.
Pathology.— The main pathology is acute inflammation of the bladder. The mucosa is red and oedemato
with superficial ulceration. A thin membrane of fibrin often lies on the wall. Some dilatation of the lower ur
is usually noticed. This may be due to an inflammatory reaction around the ureteral orifices.
Microscopically, the mucosa and submucosa are infiltrated with neutrophils, plasma cells and eosinophil
Submucosal haemorrhages are common, similarly there are superficial ulceration of the mucosa.
Clinical features.— As mentioned earlier young individuals are mostly affected of which males dominate.
There is urethral discharge which at times clear and mucoid, but in majority of cases it is purulent. Symptom
acute cystitis appear abruptly. Patient complains of frequency, urgency and burning sensation. Terminal ha
is quite common. Suprapubic discomfort or pain is quite often complained of particularly when the bladder
These symptoms are relieved after micturition. There is no fever or malaise in contradistinction to acute cyst
Special investigations.— All investigations should be performed to exclude tuberculous cystitis.
Excretory urography is usually not diagnostic, but it may show dilatation of lower ureters and presence
vesicoureteral reflux.
Cystoscopy is contraindicated. If it is performed due to inability to diagnose or in the suspicion of tuber
one can see redness and oedema of the mucosa with superficial ulceration. Bladder capacity is markedly red
Treatment.—
Peculiarly enough this disease often cures spontaneously particularly in children. But to shorten the per
discomfort the following treatment may be adopted :—
A. General measuresBladder sedatives, analgesics and antispasmodic may be used with hot sitz baths.
B. Specific treatment.— Tetracycline or chloramphenicol 1 g daily in divided doses for 3 to 4 days usually
cures this condition in 75% of cases. Streptomycin 1 to 2 g daily intramuscularly for 3 to 4 days is also effectiv
Neoarsphenamine is the drug of choice. It is introduced in the dose of 0.3 g intravenously and 0.45 g i.v.
subsequently every 3 to 5 days for a total of 3 to 4 injections.
INTERSTITIAL CYSTITIS (HUNNER’S ULCER)
This condition has variety of names. The main feature is a localised inflammatory thickening in the centre of
which there is a minute exquisitely tender ulcer which comes
and goes. That is why this condition is also called ‘elusive
ulcer’.
Aetiology.— This is still obscure. The possibility is that an
infective process starts in the paravesical tissues secondary to
infection somewhere in the body. This may be from a nearby
viscus or from a distant focus.
Pathology.— The main pathology is an interstitial cystitis
leading to localised submucous fibrosis. The affected area shows
inflammatory thickening. There is also fibrosis. This leads to
avascular atrophy of the mucous membrane and ultimately ulcer
formation. The bladder capacity is reduced often to even 60 ml.
Microscopically, there is oedema, congestion and round cell
infiltration affecting all the coats of the bladder, particularly the
submucosa. There is granulation tissue in the submucosa just
below the ulcer. The muscular layer is hypertrophied.
It is a condition which is peculiarly seen mainly in women.
The disease is of long duration marked by periodic attacks of
severe pain on distension of the bladder, frequency of micturition
and great decrease of bladder capacity. Increased frequency seems to be the leading symptom Which is comp
of in both day and night almost every hour. Pain is the next common complaint which is aggravated by diste
of the bladder and is relieved to certain extent by voiding. In early cases the urine is clear and sterile, but in l
cases it contains pyogenic bacteria in half the cases. Haematuria is the third symptom which is detected in no
more than 70% of cases.
Special Investigations.— Cystoscopy — reveals the lesion which is mostly seen in the dome of the bladder.
There is an intense congested area, in the centre of which there is an ulcer, which bleeds easily.
Treatment.—
As the aetiology is not known, treatment is difficult. Local hydrocortisone irrigation of the bladder, thou
effective in few cases, is not a proven treatment. Light diathermy coagulation of the ulcer helps for sometime
Intravesical instillation of dimethylsulphoxide has been proved to be effective in majority of cases.
The best and only curative treatment is operation. Urine diversion is the most successful operation.
Ileocystoplasty after excision of the affected bladder wall (mostly dome of the bladder) is the second operatio
which has attained some success, though has failed to relieve permanently.
VESICAL CALCULUS
Incidence.— Vesical calculus was quite common previously in the 19th century. Gradually its
incidence has come down particularly in children and adolescents. This seems to be due to improved
diet rich in protein and abolition of malnutrition.
Types.— Two types of vesical calculi are found —
1. Primary vesical calculus, which develops in the sterile urine and mostly originates in the
kidney which passes through the ureter into the bladder. Here it becomes enlarged.
2. Secondary vesical calculus, is the one which occurs in presence of infection. This type of
calculus mostly originates in the bladder. In this group may be included another type of vesical
calculus which occurs by deposition of urinary salts upon a foreign body in the bladder.
Composition of the vesical calculus.— Chemically the PRIMARY STONES may be either of
oxalate type (calcium oxalate) or uric acid and urate type or cystine type.
1. The Oxalate calculus is of moderate size and is usually solitary. It is known for its uneven
surface which is covered with bristles and spines. Though calcium oxalate is white, yet this stone often
looks dark brown or black due to incorporation of blood pigment on it. This stone is particularly prone
to cause haematuria due to its spiky surface.
2. Uric acid and urate calculus is smooth, round or oval. This type of calculus may be solitary or
multiple. The colour varies from pale yellow to light brown. Pure uric acid stone is not radio-opaque.
3. Cystine calculus is usually associated with cystinuria. It is also mostly solitary but may be
multiple. It is often radio-opaque due to its high sulphur content.
SECONDARY vesical calculus is mostly made up of triple phosphate (ammonium, magnesium and
calcium phosphate). This is seen in alkaline infected urine when there are urea splitting organisms which
split urea into ammonium compounds. The stone which grows by depositing urinary salts around foreign
body is also made up of triple phosphate. Even desquamated epithelium and bacteria may form nidus for
deposition of triple phosphate and formation of phosphate calculus. It is dirty white in colour.
CLINICAL FEATURES.— Males are more often affected in the ratio of 8:1. Clinically three
types of bladder stones are noticed — 1. Usual type, which gives rise to symptoms, 2. Silent type,
which is asymptomatic and 3. Masked type.
A vesical calculus usually remains free in the bladder and moves about according to the position of
the patient. It gravitates to the most dependent part which is the neck of the bladder in erect posture
and behind the interureteric ridge in recumbent posture.
1. USUAL TYPE.— The symptoms which are usually complained by patients with vesical calculus
are as follows :
(i) Frequency.— Increased frequency is the earliest and commonest symptom of vesical calculus.
Frequency is mostly noticed by day. The most characteristic feature is that the patient does not feel
satisfied after complete voiding and he feels to come back again for urination.
(ii) Pain.— Pain and discomfort is particularly complained of at the end of micturition. Such pain
is referred to the tip of the penis or to the labia majora at the end of micturition. This seems to be an
extremely important symptom and almost diagnostic of vesical calculus. Such pain is due to the
presence of vesical calculus on the trigone of the bladder. Pain or discomfort is also complained of in
the suprapubic region and this is aggravated by running and jolting. This pain passes off as the patient
lies down. This is due to the fact that the stone moves away from the sensitive trigone area and falls
into the pouch behind the interureteric ridge. So the patient sleeps peacefully throughout the night
even without frequency. Pain is mostly complained of when the stone is of oxalate type.
(iii) Haematuria.— Terminal haematuria is a quite frequent symptom of vesical calculus. This is
also mostly seen when the stone is of oxalate variety due to its spiky surface which abrades the
sensitive mucus membrane of the trigone and causes bleeding. This also gives rise to pain. Students
should keep in mind that terminal haematuria is usually due to bladder pathology may it be due to
calculus or due to cystitis.
(iv) Dysuria. — Sudden interruption in the flow of urine by the vesical calculus blocking the
internal urethral meatus is sometimes complained of. The patient may restart the flow of urine by
change of posture.
(v) Acute retention of urine is extremely rare from vesical calculus, though have been complained
by a few adults.
2. SILENT TYPE.— When the vesical calculus lies in a diverticulum of the bladder or in the post
prostatic pouch, it remains symptomless for quite a long time. These stones are usually discovered
either by straight X-ray of the abdomen or by cystoscopy which is performed for some other purpose.
3. MASKED TYPE.— In a few cases of vesical calculus the symptoms of cystitis dominate, so that
the patients are treated in that line and the stone is masked. It should be remembered that a patient
who frequently comes with the complaint of cystitis should be investigated thoroughly to exclude
presence of vesical calculus.
PHYSICAL SIGNS.— Abdominal examination is usually negative except in some cases where
tenderness in the suprapubic region may

be elicited.
Rectal or vaginal examination should
be performed in all cases of vesical cal
culus. One may be able to palpate the
vesical calculus by this examination if
the stone is of moderate size. Bimanual
examination i.e. abdominorectal or
abdominovaginal examination may en
able the clinician to palpate vesical cal
culus of moderate size
1. Urine examination may reveal
R.B.C., pus cells and/or crystals of stone.
2. Straight X-ray usually reveals
vesical calculus in about 95% of cases.
X-ray of KUB region (Kidney, Ureters
and Bladder) should be done to exclude
any associated calculus in the kidney or
in ureter.
3. Excretory urography should al
ways be performed to know the func
tional status of the kidneys. It will also
reveal a filling defect in cystography
when the stone is not opaque.
4. Cystoscopy. This is essential to
Fig 58 6 — Straight X-ray showing vesical calculi (up know the type of stone and to exclude
per group of shadows) and also prostatic calculi (lower any other pathology e.g. diverticulum,
group of shadows).
tumours of the bladder, enlarged pros
tate etc. associated with the calculus. This ex
amination also detects stones which are non
opaque to X-ray.
TREATMENT.—
In majority of cases surgery is required to
remove the stone unless the stone is very small
which may pass out spontaneously with the
urine or may be removed by means of an
evacuator after passing the largest size cannula
through the urethra. The vesical calculus is
removed by either of the two methods —
suprapubic lithotomy or litholapaxy.
1.
ticularly performed when the case is
contraindicated for litholapaxy. The method
of suprapubic cystostomy is described below:
A vertical midline suprapubic incision is made
The skin and the subcutaneous tissue are divided
Fig. 58 7.—Straight X-ray showing calculus in the bladder
along the line of the incision. The linea-alba is
divided The rectus muscle and the pyramidalis are retracted. By means of gauze, the peritoneum is stripped
upwards and the anterior wall of the urinary bladder will be exposed This is recognised by its longitudinal
muscle fibres and large veins coursing over its surface longitudinally. Two stay sutures are inserted through the relatively
avascular part of the bladder wall. Two pairs of tissue forceps can be used for the same purpose. The stay s attires are lifted
upwards and a stab-incision is made between the two stay sutures on the bladder wall till the urine comes out. As soon as
the urine starts coming out, it is sucked out by a sucker machine and the incision is elongated with a pair of scissors as
necessity demands.
If the operation is being performed for removal of a calculus, a finger is introduced into the bladder to determine
whether the stone is lying free in the bladder or is impacted in a diverticulum. Free stones are easily removed by means of
lithotomy forceps or scoops. Impacted calculi should be dislodged first and then removed. In most ofthe cases, if the urine
is not infected and if intra-vesical bleeding has been well controlled, the cystostomy wound is closed and the bladder is
drained by urethral catheter. In suturing the bladder, it is advised not to penetrate the mucous membrane, lest it forms a
nidus for stone formation. But practically, even if this rule is not rigidly followed, nothing happens. The abdominal wound
is closed with a drain in the retropubic space of Retzius.
Postoperatively, the catheter is joined with a disposable polythene bag for close drainage of urine to prevent infection
of the urinary tract. The drain is removed from the retropubic space after 48 hours, if no extra-leakage occurs. The catheter
is left in situ for about a fortnight for proper healing of the bladder wall.
2. Litholapaxy.— This method consists of crushing the stone by means of a lithotrite and subsequent
evacuation of the fragments with a special evacuator. Not all cases of vesical calculi are suitable for this meth
There are numerous contraindications. These are :
(i) Due to stone — (a) When the stone is too big i.e. more than 2 inches in diameter, (b) when the stone
small, (c) when the stone is too hard or too soft (cystine stone) or (d) when the stone is impacted in a divertic
(ii) Due to bladder — presence of (a) enlarged prostate or (b) stricture which cannot suitably be dilated.
OPERATION.— Urethral catheter is first introduced and
the bladder is washed. The bladder is now distended. The catheter
is withdrawn. The lithotrite is now introduced. The method of
introduction is more or less same as passing a metal bougie. As
soon as the instrument is introduced into the bladder, the jaws
should be pointed upwards. The stone gravitates down and is
grasped by opening the jaws of the instrument (Fig 58.8). After
grasping the stone, the instrument is brought to the centre of the
bladder to avoid injury to the bladder mucosa which may be
entrapped within the jaws of the instrument. The screw on the
handle of the instrument is used to crush the stone. This
procedure is repeated till the largest remaining fragment is small
enough to pass through the evacuating cannula.
The lithotrite is withdrawn with closed jaws. A large
evacuating cannula (Bigelow’s) is passed into the bladder and
the fragments of crushed stones are aspirated by repeated
Fig.58.8.— Litholapaxy. The bladder stone is grasped compressing and releasing the attached rubber bulb,
between the two jaws of the lithotrite before crushing. 3 Modern lithotripsy.— This technique is used
nowadays in many specialised units. Energy is generated by mechanical means using a steel ball which is fir
in a closed chamber at the proximal end of the endoscopic probe. This helps in breaking the stones into smal
pieces. The endoscopic probe comes in 3 different sizes. Usually the largest size (9F) is used for bladder calcu
After the patient is cystoscoped, the probe is placed close to the stone and fired. One must be very careful no
to damage the bladder wall.
DIVERTICULUM OF THE BLADDER
Definition.— It is a pouch-like opening which communicates with the bladder through a narrow mouth.
Types.— Usually two types are detected — congenital diverticulum and acquired diverticulum. There is
a third type which is known as traction diverticulum.
I. CONGENITAL DIVERTICULUM.—
It is an extremely rare incidence and is usually seen in infants and young children. Congenital diverticul
is situated in the midline near the apex and represents the unobliterated vesical end of the urachus. Such
congenital diverticulum may also occur on the posterior surface ofthe bladder and causes chronic infection
a place for stone formation. So the latter type always requires excision.
II. ACQUIRED DIVERTICULUM.—
This is usually noticed in men over 50 years of age. It is uncommon in women. It is usually associated w
some form of urethral obstruction e.g. contracture of the bladder neck, benign enlargement of prostate, fibr
prostate, urethral stricture or congenital valves of posterior urethra.
Such diverticulum usually occurs on the lateral wall of the bladder above and to the outer side of one
ureteric orifice. Very occasionally it may occur in the midline just above the interureteric ridge. The size of
diverticulum varies from a very small size to a very large size which may be even larger than the bladder i
Diverticulum may be solitary or multiple.
The basic cause of such acquired diverticulum is the rise of intravesical pressure due to obstruction in t
urethra. Normally the intravesical pressure is about 35 cm of
water at the commencement of micturition. With increase in
®
intravesical pressure the mucous lining between the muscle
bundles protrude out to form small saccule. In the beginning
the wall of this saccule is formed by all the coats of the
bladder, but as the sac enlarges, the muscle becomes thinned
out over the fundus and may eventually disappear.
Complications.—
1. INFECTION.— Due to disappearance of the muscle in the

wall of the sac, the diverticulum is unable to empty itself. So the
urine becomes stagnant and infection starts. Such infection usually
persists and even if it is cured by suitable antibiotics, there is every
chance for reinfection to occur. When diverticulum is present for a
long time, peridiverticulitis may occur and lead to adhesions
between the diverticulum and the surrounding structures.
2. FORMATION OF CALCULUS.— Due to stagnation and
Fig.58.9. Stone in a vesical diverticulum. infection, the condition is ideal for formation of phosphate calculus
(triple phosphate) in the bladder or in the diverticulum. About l/5th of all cases of diverticulum, a calculus may be seen. In
majority of cases the calculus lies within the bladder, though in a few cases calculus is seen within the diverticulum (Fig.58.9)
Occasionally a dumb-bell shaped calculus may be seen which fills the diverticulum and protrudes into the bladder.
3. OBSTRUCTION.— As this type of diverticulum is more common near the ureteric orifice, it may so happen that
the opening of the ureter may be dragged or
cause obstn^m flwv
are of acquired variety, the clinical features of this condition only will be discussed. About 95% of
cases are males above 50 years of age.
SYMPTOMS.— There is no typical symptom of a vesical diverticulum. Symptoms due to cystitis
dominate. Increased frequency, haematuria, urgency are symptoms of this group. In some cases mic
turition may occur twice one after the other. The first one is from the urinary bladder and the second
from the diverticulum — first specimen is clear, whereas the second specimen is cloudy due to
presence of infection. This is the only pathognomonic symptom of a vesical diverticulum. Symptoms of
complications such as those of presence of a vesical calculus or those of hydronephrosis and infections
of the kidney may be noticed in a few cases.
PHYSICAL SIGNS.— Examinations usually do not reveal any abnormality. Even rectal or vaginal
examination may not reveal presence of a diverticulum.
1. EXCRETORY UROGRAPHY should be performed in all cases to exclude any obstructive feature of th
diverticulum and to know of the condition of the kidney of the affected side. Cystography may detect the pr
of diverticulum by showing a project on outside the bladder. It also indicates the size of the diverticulum
2. RETROGRADE CYSTOGRAPHY may be required when excretory cystography fails to produce enoug
concentration of dye in the bladder to delineate the diverticulum. First the bladder is emptied of unne and th
a radio-opaque dye is introduced through the catheter. Radiographs are taken before and after micturition to
the position of the diverticulum and its capacity.
3. CYSTOSCOPY.— This is a very useful mean to diagnose a diverticulum. The clear cut hole of the
diverticulum which is usually of a diamater of a Lead Pencil is very clearly seen through cystoscopy. If the
bladder is not distended enough, the opening of the diverticulum may be closed. In this case the radiating pl
of the mucous membrane is seen from a point which is the orifice of the diverticulum. In these cases one may
detect the opening of the diverticulum. So it is the rule to get the bladder fully distended before cystoscopy i
performed for search of diverticulum. The bladder should be well irrigated before cystoscopy is performed s
the infected cloudy urine is cleared off to get a clear view of the inside of the bladder. Sometimes an expert c
pass a cystoscopy into the diverticulum and examine the interior of the diverticulum to exclude any neoplas
there.
4. ULTRASONOGRAPHY.— This is a non-invasive useful method to diagnose bladder diverticulum wh
other methods have been failed or contraindicated.
T reatment.—
Unless the diverticulum is quite small and uninfected and there is no evidence of urethral obstruc
tion, operation is justified.
OPERATION.— Before the operation it is the usual practice to give bladder washes with an indwelling
urethral catheter. Proper antibiotic should be started before the operation is contemplated.
First cystoscopy is performed and a large ureteric catheter is passed through the ureteric orifice on the
affected side and left in situ. The bladder is distended and the patient is placed in Trendelenburg position.
A midline suprapubic incision is made and is deepened till the anterior wall of the bladder is reached. B
incising the bladder, the peritoneum is dissected upwards from the superior surface of the bladder till the
diverticulum is reached. Now the diverticulum is cleared from the surrounding structures by sharp and blun
dissection. The whole of the diverticulum is now freed till the neck is reached. Now the bladder is incised in
midline anteriorly. The fluid inside the bladder is sucked out. The interior of the bladder is thoroughly inspe
A strip of gauze is packed inside the diverticulum. Once the whole of the inside of the diverticulum is packe
with the strip of gauze, it is now easy to complete the freeing process of the diverticulum from surrounding
structures from the outside of the bladder. Once the whole of the diverticulum has been freed and the neck i
clearly felt to be free from surrounding structures particularly the ureter, the neck of the diverticulum is cut
its attachment to the bladder from outside with a diathermy knife. After the diverticulum has been separated
strip of gauze is removed and the resulting opening of the diverticulum is closed by two layers. The cystosto
incision is sutured around a Malecot catheter and the abdominal wall is closed leaving a corrugated drain in
retropubic space.
Sometimes the diverticulum is densely adherent to the surrounding structures so that it cannot be freed
dissection. In this case the neck of the diverticulum is cleared and the ureter is kept safe out of the diverticul
The neck is now cut with diathermy knife so that the diverticulum now becomes separated from the bladder
1120
opening is closed by two layers. The diverticulum is left in situ. The bladder incision and abdominal incision are
closed as above. A separate corrugated drain is placed close to the diverticulum and left there for 2 or 3 days.
If there is any enlarged prostate or bladder neck contracture as the cause of urethral obstruction to cause such
diverticulum, prostatectomy or operation for bladder neck contracture is performed at the same time as diverticulum.
III. TRACTION DIVERTICULUM OF THE BLADDER —
When a portion of the bladder becomes a part of the contents of the inguinal or femoral hernia, it
is called a traction diverticulum. About 1 to 2% of inguinal or femoral hemiae contain such diverticu
lum of the bladder. This condition is relatively more frequently seen in femoral hemia and in direct
inguinal hemia.
Clinical features.— The only characteristic history a patient may give is that he remains unsatis
fied after micturition until or unless he exerts pressure on the hernia to push more urine out.
NEOPLASMS OF THE BLADDER

Classification.—
A. PRIMARY NEOPLASMS.—
L Epithelial tumours which constitute more than 95% of cases.
1. Benign tumours.—
Papilloma — either solitary or multiple.
2. Malignant tumours —
(i) Transitional cell carcinoma — either de novo or secondary to papilloma.
(ii) Squamous cell carcinoma.
(iii) Adenocarcinoma.
II. Connective tissue tumours.— Angioma, endometrioma, myoma, fibroma, pheochromocytoma
(arising from accessory adrenal tissue in the bladder wall) and malignant sarcoma.
B. SECONDARY TUMOURS.—
(i) Extension of malignant neoplasm from a neighbouring organ particularly sigmoid colon,
rectum, uterus or ovary.
Sometimes carcinoma of the pelvic colon or rectum first presents with symptoms of cystitis and
cystoscopy reveals an area intense inflammation which is the first site involved by the carcinomatous
lesion. Later on even a vesico-rectal or vesico-intestinal fistula may develop.
(ii) Papilloma or papillary carcinoma of the pelvis of the kidney may spread to the bladder by
seedlings implantation.
(iii) Prostatic carcinoma may involve bladder by direct spread, but this is a rare occurrence.
EPITHELIAL TUMOURS
AETIOLOGY.—
1. It is an established fact that prolonged exposure to certain carcinogens is associated with a high incidence
of vesical neoplasm. Recent work suggests that the multiple transitional cell tumours involving the urinary tract
e.g. renal pelvis, ureter and bladder are probably caused by carcinogens. Whatever may be the chemical nature of
these carcinogens, a few industries have been incriminated to cause bladder tumours and that bladder tumours are
now considered as occupational hazards. The industries responsible are dyeing industry, rubber and cable
industries, certain types of plastic industry, printing industry, leather industry etc. Gas workers and sewage
workers are also involved. Bladder tumour has become a prescribed industrial disease. Tumours occurring in
these industries are accepted for compensation.
It has been seen that aromatic amines (e.g. benzidine, 2-naphthylamine, 4 aminodiphenyl) are responsible
carcinogens. These amines are metabolised to orthoaminophenols by the liver and conjugated there with sulphate
or glucuronic acid and then excreted through the kidneys. These materials are attacked in the urine by Beta-
glucuronidase, which hydrolyses to form orthophenols which are liberated. These orthophenols are found in
increased concentration in the urine of patients who are having vesical tumours. There is evidence that the
activity of urinary Beta-glucuronidase is increased by the presence of vesical infection, in presence of other
cancers, renal infection, urolithiasis, renal cyst and benign enlargement of the prostate.
2. Smoking has been incriminated as a cause of vesical

neoplasm. It has been recently shown that in smokers there is
increase in carcinogenic metabolites of tryptophan excreted in
the urine. There is also increased urinary excretion of products
with the orthoaminophenol structure in persons who are chain
smokers. It has been suggested that cigarette smoking contrib
utes directly to the origin of bladder cancer. On cessation of
smokings the levels of carcinogens excreted in the urine return
to normal.
3. A number of other physical agents e.g. phenacetin, artifi
cial sweeteners (saccharin), excessive caffeine intake and cyclo
phosphamide have been implicated as to be associated with
increase of urothelial tumours.
4. There is a geographical distribution of bladder cancer. In
Africa and Egypt the incidence is more. This probably relates to
the high frequency of bilharzial infestation. There is evidence
that the activity of urinary Beta-glucuronidase is also increased
in schistosomiasis infestation. In areas where schistosoma
haematobium is endemic, bladder cancer is more common. An
Fig. 58.11— Cystoscopic view of papilloma
other interesting feature is that high incidence of squamous type
of bladder showing early signs of malignant
change. of bladder cancer is noticed in these areas and in patients suffer
ing from severe vesical schistosomiasis.
Benign papillary tumours.— A papilloma of the bladder is a soft, shaggy, villous tumour
consisting of a number of finger like processes covered by many layers of epithelial cells (3 or 4 layers
of transitional epithelium). The villi may spring directly from a small circumscribed area of the
mucosa or may arise from a well defined pedicle. In case of the former the villi are longer, fragile and
delicate and looks like sea-anemone with delicate tentacles moving with the flow of urine. In case of
the latter the villi are shorter and look like raspberry.
In these villi there are connective tissue stroma which are exceedingly delicate and vascular
consisting largely of capillary loops. The epithelial cells are arranged at right angles to the stroma
being separated from it by a basement membrane. As mentioned earlier there are 3 or 4 layers of cells
and these are of regular size and shape
The usual SITES of benign papillary tumours are — (i) just outside to the ureteric openings, (ii) at
the neck of the bladder and (iii) rarely in the vault of the bladder.
It is not uncommon to find multiple growths.
It must be remembered that inspite of having all the characteristics of a benign tumour, papilloma
of bladder may yet recur after removal, infiltrate the deeper tissues and set up secondary growths So
this benign tumour has a strong tendency to become malignant or it is the beginning of a malignant
tumour. It cannot be denied that when the pathologist labels a tumour as a benign papilloma, he is in
danger of conveying to the surgeon a false sense of security, although not if the surgeon fully realises
the usual natural history of these tumours. The disease apparently originates in multiple foci in the
bladder mucosa, appears first as one benign tumour and may continue to appear, so repeated biopsy for
years are required. For this reason many surgical pathologists no longer call such a tumour as a
papilloma, but as a grade I carcinoma.
CARCINOMA OF THE BLADDER
There are three types of carcinoma of the bladder — 1. Transitional, 2. Squamous and 3
Adenocarcinoma. By far the majority (about 95%) is transitional in origin.
TRANSITIONAL CELL CARCINOMA.— Two types are usually seen — (a) the papillary type,
which is less malignant and (b) nodular type, which is also known as invasive type and carries bad
71
prognosis.
(a) Papillary type.— These are papillary tumours which grow from the bladder mucous mem
brane. These may be single or multiple at the time of presentation. The differentiating feature from a
benign papilloma is that malignant tumour has a wider base and the area around the tumour looks
oedematous with dilated blood vessels.
The most common sites are (i) on the base of the bladder (about 80%) just outside the ureteral
orifices, (ii) in and around the trigone area. Generally speaking the larger the tumour and broader the
base, the more malignant it is. Nodular tumour is more malignant than the papillary type.
(b) Nodular type.— This is usually soiid in consistency which invades muscle quickly. There may
be tufted appearance from outside. These tumours are large and broad based. Sometimes these may be
ulcerated. The incidence of metastasis is more.
The grade and the stage of the tumours.—
Grade.— According to the degree of cell differentiation carcinoma of the bladder has been
classified into various grades —
Grade I.— The cells are well differentiated. The lamina propia is usually not involved. It is
papillary in type. It usually has a narrow base. These are usually curable by transurethral means and
are radioresistant.
Grade II.— Here the cells show less differentiation and show a tendency to invade the lamina
propia. but not the detrusor muscle. The tumours are larger than grade I tumours and have a wider
base. These are also curable by
transurethral resection and these
are also radioresistant.
Grade III and IV.— These
neoplasms are poorly differenti
ated or anaplastic. These tend
to be nodular rather than papil
lary. These are quite invasive.
These tumours are not good for
transurethral resection, but are
sensitive to radiotherapy.
Stage.—
Clinical staging depends on
the degree of invasion. Two types
of staging are used — 1 The inter
national system, which is mostly
used in U.S.A., uses letters O, A,
Bl. B2, C and D to indicate vari
ous stages. 2. The other type is the
TNM classification, which is most
ly used in U.K. and the letter T’ is
used to indicate the various stages
of tumour invasion e.g. T1.T2. T3
andT4;N is used toindicate lymph
node involvement e.g. NO, Nl; M
is used to indicate distant meta
stasis e.g. M1. NO means no lymph
node involvement and MO means
Fig.58.12— Schematic diagram to show the clinical staging of no distant metastasis. The various
bladder carcinoma. See the text. stages according to international
system and TNM classification are mentioned below :—

State 0(TIS).- This is carcinoma in situ ora papillary tumour which has not invaded the lamina propria
Stage A(T1).- The tumour has invaded the lamina propria but not the muscle of the bladder
Stage B1(T2).— The tumour has extended into the superficial half of the detrusor muscle.
Stage B2 and C(T3).— Tumour has invaded the full thickness of the muscle and is mobile
Stage D (T4).— The tumour has invaded the adjoining tissues and organs or has involved prostate. The
tumour has become fixed.
Stage D1(N1).~ The tumour has involved lymph nodes but not above bilurcation of the aorta.
Stage D2(M1).— The tumour has metastasised to the periaortic lymph nodes and to the distant organs
Even after successful treatment of grade I and grade 11 types or stage O and A types, there is a definite
tendency of new tumours to develop elsewhere in the bladder. This suggests that the appearance of these
tumours is related to increased susceptibility of the urothelial mucosa to neoplastic proliferation, perhaps in
response to carcinogens.
Spread.—
1. Direct spread. It is the commonest type of spread which gradually involves the neighbouring viscera.
2. Lymphatic spread. This occurs only when the tumour has invaded the perivesical tissue Most
commonly vesical neoplasms metastasise to the superior vesical and inferior vesical lymph nodes, internal ilia
and common iliac group of Ivmph nodes and subsequently to the lymph nodes at the bifurcation of the aorta
3. Haematogenous spread. - This is not very common in case of vesical neoplasms. But once the tumour
has spread to the perivesical tissue or peritoneum, there is a chance of vascular spread. The bones, the liver
and the lungs are at times affected. In fact such spread is the cause of death of 30% of patients
4. Spread by implantation or seedlings. Such spread is a feature of urothelial neoplasia. By this spread
multiple tumours may be seen in the bladder When the bladder is empty a new tumour may develop in the
place of the mucosa which kisses' or comes in contact with the bladder tumour.
5. Allantoic spread. Through the remnant of allantois growth may spread to the peritoneum where it
may form malignant deposits.
SQUAMOUS CELL CARCINOMA.— About 5% of vesical neoplasms are of squamous cell variety.
Squamous cell tumours are usually solid in consistency and often invade the detrusor muscle. Such carcinoma
is seen when squamous metaplasia or keratinisation has occurred. This is often secondary to chronic irritation
or stone disease. These tumours are highly malignant (anaplastic), deeply invasive and metastasise easily. Thi
tumour shows high incidence in patients with vesical bilhar/.iasis.
ADENOCARCINOMA.— This constitutes about 1% of vesical neoplasm. It often arises in urachal
remnant. Occasionally adenocarcinoma may develop in other sites This carcinoma may derive from epithelial
nests of Brunn Evidence of cystitis cystitica and cystitis glandularis is often present in the neighbourhood of
the tumour. This tumour is also seen as a complication of exstrophy of the bladder. The tumour is usually sess
and mucous producing. It usually occurs at an earlier age than transitional cell carcinoma of the bladder
Symptoms.— (i) Painless haematuria is the earliest and most common symptom Haematuria is usually
intermittent as with all tumours of the urinary tract. Bleeding may be mild or severe, transient or prolonged
Bleeding may occur once or twice and then it may stop to start again after many months to cause concern
Bleeding may be so profuse as to cause clot retention. Occasionally it may require emergency admission and
blood transfusion immediately.
(ii) Sometimes infection may supervene to cause cystitis and the patient presents with symptoms of
cystitis e.g. increased frequency, urgency, burning sensation on micturition etc. Recurrent cystitis should aro
use suspicion of presence of bladder tumour.
(iii) Occasionally a pedunculated tumour may occlude the bladder neck to cause sudden stoppage of flo
of urine (acute retention of urine), which may restart with change of posture.
(iv) Pain in the pelvis indicates extravesical spread. This is more common in case of solid nodular
tumours. It is usually associated with frequency and discomfort or pain during micturition. Pain in the loin
may be noted if the growth has obstructed ureteral orifice producing hydronephrosis. This may be compli
by ascending infection to cause pyelonephritis.
In late cases pain may be referred to the suprapubic region, the groin, the perineum and to the medial
of the thigh when the tumour has gone extravesically and has involved nerves.
Physical signs.— In majority of cases no abnormality can be detected on physical examination Only at
the time of ureteral obstruction, renal tenderness or enlargement may be detected in the loin.
Occasionally a suprapubic swelling may be detected which is either a large cancer or due to urinary
retention caused by invasion of the bladder neck by the tumour.
BIMANUAL EXAMINATION (abdominorectal in case of male or abdominovaginal in case of female)
is of greatest importance in estimating the clinical staging of the bladder tumour. The bladder must be empty
and this examination should be done under general anaesthesia with the patient fully relaxed. This should
be performed before and after endoscopic surgical treatment of the tumour. The right index finger is intro
i nto the rectum in case of male or into the vaginum in case of female. The four fingers of the left ha
in the suprapubic region and are pushed down.
In T1 cases, the tumour is usually not palpable bimanually. Only very large frondy tumour may be fel
soft and mobile thickening.
In T2 cases, bimanual examination reveals no more than smooth induration of bladder wall. There ma
be rubbery thickening of the bladder wall.
In T3 cases, a hard mobile lump is felt on bimanual examination.
In T4 cases, the tumour is not only very easily palpable bimanually, but the tumour remains fixed and
not mobile.
1. Blood examination - Anaemia is not uncommon due to loss of blood, infection or uraemia.
2. URINALYSIS.— The urine may be very' bloody, but between the bouts of bleeding few or no red ce
may be found. Pus and bacteria may be detected in the urine. Urine should be examined for culture and
sensitivity test. It should be examined for papanicolaou staining to detect malignant cells. Well differentia
tumours shed round cells of rather uniform size with large nuclei, whereas anaplastic tumours shed large
epithelial cells often in clumps with very large dark staining nuclei. A simple technique for urine cytologic
study is to put 1 drop of 1% solution of toluidine blue into the urinary sediment.
3. CYSTOSCOPY.— This is the main investigation in a case of haematuria. This examination almost
always reveals the tumour. Biopsy of the lesion should be performed routinely. A few very small tumours
be missed by cystoscopy. These can be visualised if the patient is given tetracycline for a few days before
cystoscopy This usually gives ultraviolet illumination to the tumour.
Carcinoma in situ is often difficult to diagnose When an area shows erythema with velvet appearance
this should be suspected and biopsy should be taken.
4. EXCRETORY UROGRAPHY
is essential, not only to know about the
function of the kidneys, but also
cystography may reveal the tumour it
self with filling defect. There may be
distortion of the uniform outline of the
bladder. Irregularity of the bladder wall
also indicates invasive tumour. This
examination may reveal obstructive fea
tures, if present, due to involvement of
Fig 58.13.— Ultrasonography to show three types of tumours of ureteric orifice. This may lead to
bladder B indicates urinary bladder, a.— Shows polypoid tumour
without evidence of infiltration, b.— Broad based sessile tomourwith
hy dronephrosis and may affect the func
flattening of the bladder wall, indicative of infiltration c.— Tumour tion of the kidney which may be indi
with infiltration into the surrounding tissues of pelvis. cated by excretory urography.
THE URINARY BLADDER J125
5. Retrograde cystogram may be required if excretory cystogram is not good enough.

6. VESICAL ANGIOGRAPHY may yield information about the depth of infiltration of the tumour.
7. CT SCAN may also give satisfactory information regarding the depth of the tumour and it also reveals
presence of any enlarged metastatic lymph nodes. The rate of accuracy is approximately 80%. This study may
be further enhanced by filling the bladder with air.
8. ULTRASONOGRAPHY is of some value though not consistent in estimating stage of the tumour.
9. MAGNETIC RESONANCE IMAGING (MRI).— Although CT has made a tremendous contribution to
the staging of invasive bladder tumour, the technique has well known disadvantages. The most significant of
these is its inability to stage early tumours confined to the bladder wall and difficulty in diagnosing early org
invasion. MRI demonstrates extra vesicle spread slightly better than CT, which is best appreciated on a Tl-
weighted sequence. However T2-weighted images are valuable for assessing adjacent organ invasion into the
prostate or seminal vesicles in the male or into the vagina and cervix in the female. The overall accuracy of M
compared with CT is not significantly different since the accuracies of MRI range from 70% to 96%, whereas
those of CT from 60% to 92%. However in staging of the disease MRI provides additional informations.
10. Lymphangiography may be performed to exclude lymphatic metastasis. Accuracy rate is only 50%.
11. TUMOUR MARKERS.— An increased level of urinary or plasma carcinoembiyonic antigen is
found in 60 to 70% of cases. Following definitive treatment, this level usually goes down, but rises again whe
recurrence or metastasis develops. Urinary immunoglobulins (IgG and IgA) are also elevated in patients with
bladder carcinoma.
TREATMENT.— There is considerable disagreement about the proper treatment of vesical neoplasms.
The straightforward approach is — transurethral resection should be performed for low grade superficial
tumours, whereas for more malignant and invasive tumours the surgeons must choose between radiotherapy
radical surgery for a combination thereof.
The treatment is being discussed according to the stage of the tumour for proper understanding.
I. TIS, NO, M0 — CARCINOMA IN SITU.— These are usually flat, non-invasive carcinoma in situ, which
often presents with symptoms resembling interstitial cystitis in men of middle age. Provided there is no evide
of invasion, this lesion should be managed conservatively by repeated cystoscopy and excision biopsy of
unstable areas. About 60% of these patients can be expected to show progression to infiltrating carcinoma, bu
it should be remembered that the remainder may live for many years without progression.
II. Tl, NO, M0 TUMOURS.— This category now includes all papillary tumours, both non-infiltrating
and infiltrating (not beyond submucosa) in which biopsy shows no evidence of invasion of muscle. This
comprises majority of the bladder neoplasms (approximately 80%). Cystodiathermy or transurethral resection
is the main treatment. If the tumour is too large, the bladder may be opened and the tumour is removed
transvesically. Care being taken to saucerize deeply into the wall of the bladder in order to remove the base o
the tumour completely. This procedure will cure many of the papillary carcinomas of this stage. All patients w
Tl tumours should be followed up with regular check cystoscopies until the bladder has been clear for at leas
5 years. Ideally all check cystoscopies should be performed under general anaesthesia. Recurrences are
expected in about 50% of patients, which are also controlled by cystoscopic diathermy.
An alternative approach to the treatment of large superficial tumours has been introduced. Under epidur
anaesthesia a large balloon or condom tied on to a catheter is introduced into the bladder and inflated to at le
10 mm Hg above diastolic blood pressure for 6 hours. This causes ischaemic necrosis ofthe tumour, which is
subsequently passed away through urethra. After 4 to 6 weeks a review cystoscopy is performed and any sm
residual tumour is then dealt with endoscopic resection.
Interstitial irradiation with radon seeds, radio-gold or radio-tantalum does not increase the expected 80%
5 years survival rate for papillary well differentiated (Tl) tumours compared with cystodiathermy, but may
reduce recurrence.
Intravesical chemotherapy is attractive as an adjuvant measure or alternative treatment for the bladder
which has multiple recurrences at each check cystoscopy. Thiotepa was first used intravesically and about 40
of cases of multiple superficial tumours were cleared but the drug was easily absorbed and fatal bone marrow
depression was recorded. Intravesical Epodyl has the advantage that it is not absorbed and free from syste
side effects. 100 ml of 1 % solution of Epodyl in sterile water should be introduced for 1 hour once weekly
12 weeks, then monthly for a year, then three monthly for at least 7 years. Intravesical chemotherapy is in
in patients with widespread multiple superficial lesions.
III. T2, N0/N1, MO TUMOURS.— When infiltration is confined to the superficial muscles (T2 tumour
endoscopic diathermy alone is inadequate. When the T2 tumour is solitary with a base not exceeding 4 to
in diameter, transvesical excision combined with interstitial irradiation is effective. If the tumour is situate
towards the vault of the bladder, partial cystectomy is justified. Approximately 50% of patients treated by
of these two methods will be alive for 5 years. Limited preoperative external beam irradiation in associatio
with interstitial therapy appears to reduce the incidence of local wound recurrence and increase the 5 yea
survival rate.
If the tumour is multiple or too extensive for local treatment, choice lies between external beam irradi
total cystectomy or preoperative irradiation and cystectomy. In general, the more undifferentiated the tum
the more radiosensitive it is.
IV. T3, N0/N1, MO TUMOURS.— The prognosis of this group of tumour is extremely grave. The cho
lies between (i) radical cystectomy and (ii) radical radiotherapy with or without salvage cystectomy. A
combination of preoperative radiotherapy and radical cystectomy has produced improved result with 5 y
survival rate upto 50%. Whereas preoperative radiotherapy and radical cystectomy should be restricted to
patients under 65 yrs, radical radiotherapy with salvage cystectomy is good for patients above 65 yrs. In c
of radical radiotherapy optimal dose is 6,000 rads given over a period of 6 weeks or more. If after irradiati
viable tumour is still demonstrable, cystectomy, can be considered. In case of preoperative irradiation a d
of 2,000 to 4,000 rads are given followed by radical cystectomy and pelvic node dissection.
CHEMOTHERAPY.— Palliation of advanced high grade vesical neoplasms with parenteral chemothe
has been reported. The drugs used are 5- fluorouracil, methotrexate, adriamycin, cyclophosphamide, cis-
platinum. Promising results have been achieved with parenteral cyclophosphamide, cis-platinum and
doxorubicin. Doxorubicin is injected 10 to 20 mg into the tumour 1 to 2 times per week. About 80% succes
has been claimed. There has been several attempts to improve on the result of single agent chemotherapy
2 or 3 drugs combination. But so far none of the combinations has produced a significantly better respons
PARTIAL CYSTECTOMY.— This means that the tumour along with the surrounding 1 inch of health
margin of the bladder wall is resected in its entire thickness. Not many malignant tumours yield themselv
this operation, since many of them are situated near the trigone.
The bladder is exposed by the usual suprapubic route. The bladder is incised well away from the tumour. If the tumour
is situated on the superior surface, the peritoneum has to be opened. The surface of the tumour is first lightly coagulated
to prevent possible implantation of tumour cells. The incision in the bladder wall is now extended with a diathermy to
remove the tumour together with 1 cm of healthy bladder wall. As soon as the excision is carried out, tissue forceps are
applied to the margins of the cut bladder, so that they are not retracted. The bladder wound is closed around a cystostomy
tube. If the surgeon is very confident that the haemorrhage has been well controlled, he can rely on simple transurethral
drainage. This will definitely shorten the convalescent period.
If the ureteric orifice has been implicated by the tumour, the ureter should be divided at a safe distance from the growth
before the excision of the actual tumour is carried out. After the excision has been completed and the defect in the bladder
wall has been closed, the ureter is reimplanted into the bladder.
This operation is probably most suitable for lesion involving muscles in the vault of the bladder.
TOTAL CYSTECTOMY.— This operation implies removal of the entire bladder, together with the
seminal vesicles and the prostate. This operation is indicated in case of (i) infiltrative growths involving th
internal meatus and (ii) both ureteric orifices, (iii) profuse papillomatosis, (iv) recurrence after adequate
radiotherapy, (v) recurrence after partial cystectomy.
OPERATION.— A lower left paramedian incision is made. The peritoneal cavity is opened. First of all the spread of
the growth is assessed by inspecting the growth, surrounding tissue, the meatus, the kidneys, the iliac and para-aortic lymph
nodes, the liver and for peritoneal metastasis. When it has been decided that total cystectomy will be carried out, the ureters
are isolated and divided as low as possible. A suitable catheter is passed along the lumen of each ureter and the urine is
allowed to drip into the bottle placed away from the operation area. The anterior division of the internal iliac arteries are
ligated to reduce haemorrhage.

The bladder, the overlying peritoneum, the seminal vesicles, the prostate and all the fasciae and surrounding areolar
tissues are removed en bloc. The vas deferens are identified at the base of the bladder and severed between ligatures. This
vas deferens will lead to the correct plane between the prostate and the rectum which is followed till it leads to the superior
and inferior vesical vessels, which are ligated and divided. The lymph nodes in the pelvis along the anterior trunk of the
internal iliac artery and its branches should be removed.
The ureters are now used for urinary diversion, the best of which is the ileal conduit.
HAEMATURIA
Haematuria is a common symptom of the urinary disease. The most common cause of haematuria is cyst
As haematuria is often the only symptom of various tumours affecting the urinary system, a thorough
investigation should always be performed in a case of haematuria to find out its cause. Enquiiy must be mad
about its quantity and its relation to micturition. Haematuria may be microscopic in a few conditions particu
ureteric stone. Haematuria may be profuse as may be seen in enlarged prostate, (a) When blood appears at th
beginning of micturition the cause is often in the urethra, (b) When haematuria occurs mostly towards the en
of micturition, the cause is mainly in the urinary bladder, (c) When haematuria is intimately mixed througho
the process of urination, the cause is mainly in the kidney or ureter. A list of various causes of haematuria is
given below
Causes.— The various causes can be conveniently described under four headings — A. Lesions of the
urinary tract; B. Diseases of the adjacent viscera involving the urinary tract; C. General disorders; D. After
ingestion of certain drugs.
A. Lesions of the urinary tract:—
I. KIDNEY.—
Congenital — Polycystic kidney.
Traumatic — Ruptured kidney (important cause).
Inflammatory — Tuberculosis (important cause) and acute pyelonephritis (rare).
Neoplastic — Adenocarcinoma of the kidney (important cause), nephroblastoma of the kidney,
papilloma of the renal pelvis and angioma.
Others — Stone, infarction and essential haematuria.
II. URETER.—
Papilloma (important cause) and stone.
III. BLADDER.—
Traumatic — Rupture.
Inflammatory— Cystitis (very common cause). Tuberculosis and Bilharziasis.
Neoplastic — Papilloma and carcinoma (very common cause).
Others — Stone.
IV. PROSTATE.—
Benign hypertrophy of prostate (very common cause) and carcinoma of prostate.
V. URETHRA.—
Traumatic — Rupture.
Inflammatory — Acute urethritis.
Neoplastic — Transitional cell carcinoma.
Others — Stone.
B. Diseases of the adjacent viscera :—
Acute appendicitis, salpingitis and pelvic abscess. The inflammatory process may spread to the ureter and
bladder. Carcinoma of the rectum and cervix uteri may infiltrate the bladder to cause haematuria.
C. General disorders :—
I. BLOOD DISORDERS.— Purpura, sickle cell anaemia, haemophilia, scurvy and malaria.
II. INFARCTION.— Arterial emboli from myocardial infarct and subacute bacterial endocarditis.
III. CONGESTION.— Right heart failure and Renal vein thrombosis.

IV. COLLAGEN DISEASES.
D. Drugs:— Anticoagulant drugs, hexamine, sulphonamides and salicylates — when given in larg
doses.
ANURIA
ANURIA means absence of excretion of urine from the kidneys for minimum 12 hours. There is another term called
OLIGURIA, which means excretion of less than 300 ml of urine in 24 hours (a day).
Anuria may occur due to various causes which can be conveniently described under three headings — I. Pre-renal
causes, II. Renal causes and III. Post-renal causes.
I. Pre-renal anuria.— Normally the systolic blood pressure in the glomeruli is about 90 to 100 mm Hg. When this
blood pressure falls below 70 mm, filtration from glomeruli ceases. So any cause which lowers the blood pressure may
cause anuria. These causes are severe haemorrhage, shock, extensive bums, dehydration from vomiting or diarrhoea or
excessive sweating, spinal anaesthesia (which lowers blood pressures) and cardiac failure.
TREATMENT.— Treatment is directed to raise the blood pressure by administering intravenous dextrose-saline
solution. In case of haemorrhage blood transfusion is required. It will be seen that when the blood pressure is raised to
normal level urine excretion is also started. It must be remembered that treatment should be immediate, as hypotension for
a longer period may cause damage of renal epithelium, glomerular damage and even tubular necrosis to pass the condition
to one of renal anuria.
II. Renal anuria.— This is mostly due to damage or ischaemia of the glomeruli and of the renal tubular epithelium.
The main causes are:
(i) Incompatible blood transfusion; (ii) Crush syndrome; (iii) Severe shock for long period (more than 2 hours); (iv)
Bilateral pyelonephritis; (v) Concealed accidental haemorrhage and abortion; (vi) Acute pancreatitis; (vii) Bacteraemic
shock; (viii) Operation on jaundiced patient; (ix) Certain drugs e.g. cephalosporins, aminoglycosides; (x) Certain poisons
e.g. toxin of eclampsia, contrast media for aortography, chemicals — mercury salts, carbon tetrachloride etc.
Renal anuria can be reversible and then it goes through three phases — 1. Phase of oliguria, 2. Phase ofdiuresis and
3. Phase of recovery.
CLINICAL FEATURES.— Patient passes dark urine of a constant specific gravity of 1.010 or is found on
catheterisation. The patient becomes anorexia with hiccough. Gradually the patient starts vomiting which becomes copious
and effortless. Abdominal distension is quite common. Systolic blood pressure may be elevated after 2 or 3 days to even
upto 200 mm Hg. If the patient is still untreated, he complains of thirst and gradually becomes drowsy. On examination,
one can find dry skin and dry brown tongue. The pulse rate becomes slower and irregular. Respiration also becomes slower
and gradually passes into Cheyne-Stokes respirations. Ultimately the patient passes into delirium and coma.
TREATMENT.— Diagnosis must be established first and postrenal or obstructive anuria must be eliminated by
radiography and ultrasound.
In case of incompatable blood transfusion, the blood transfusion should be immediately stopped and diuresis is
provoked with mannitol or 500 ml Rheomacrodex given intravenously. The next part of treatment is as follows.
The most important fact in the management of renal anuria is to restrict introduction of fluid. Most of the deaths in this
condition have been caused not by urea or end products of nitrogen metabolism, but due to excess of water and electrolytes
particularly potassium. The treatment is conveniently described according to the phase of renal anuria —
1. PHASE OF OLIGURIA.—
(a) Intake of water.— Water should be given considering the loss of water which has occurred in the last 24 hours.
Considering the losses by lungs, skin and faeces in anuric stage, the fluid intake should be restricted to 500 ml + the volume
vomited or lost by gastric aspiration in 24 hours. If the patient is pyrexic, an extra 400 ml is allowed for each degree rise
of the patient’s temperature above 37° C. When the weather is hot, extra fluid may be given considering chance of excess
sweat, but under no circumstance the intake should exceed 1000 ml per day. Proper hydration can be assessed by moisture
of the tongue and wet skin.
(b) Electrolyte balance.— It must be remembered that sodium chloride or bicarbonate or lactate should never be
infused in this condition. Similarly fluid containing potassium should be prohibited, as rise in serum potassium is the
greatest threat to the patient’s life in this condition. If serum potassium is seen to be above normal level, calcium resonium
enema is a simple method to exclude potassium. This ion exchange resin may be used orally. Whenever intravenous fluid
is required it should be given by 5% dextrose solution. A little amount of insulin may be added to this solution to lower
serum potassium level. This method may be applied primarily in case of raised serum potassium level.
(c) Diet.—The diet should be free of protein and rich in carbohydrate. Approximately 2000 calories are required per
day. When there is excessive vomiting, intravenous feeding is required and a nasogastric tube should be inserted.
(d) Antibiotics.— These patients are prone to be involved by various infections. Swabs should be taken from sputum,
nose and throat and urine and are sent for culture. If any infection is detected, it should be treated with proper antibiotic.
Care must be taken not to use excessive dosage as urinary excretion is less in these patients, and not to use nephrotoxic
antibiotics.
(e) Proper nursing care.— Proper intake and output chart should be maintained. Blood pressure, pulse rate and
respiratory rate should be noted every 4 hours. E.C.G. monitoring is highly important to avoid potassium excess. Frequent
serum sodium and potassium estimations should be recorded in the chart.
(f) Dialysis.— When the urea and potassium levels rise dangerously in the blood and is associated with significant
uraemic symptoms e.g. vomiting, muscular twitching and altered states of consciousness, there is no way out but to
perform dialysis to remove the waste products. One of the two methods is usually adopted — (i) peritoneal dialysis
and (ii) haemodialysis.
(i) Peritoneal dialysis.— Peritoneal dialysis can be performed under local anaesthesia by insertion of a
fenestrated catheter into the peritoneal cavity. The catheter is introduced just inferior to the umbilicus in the midline.
Sterile dialysis fluid is injected into the peritoneal cavity through the catheter. After a variable time the fluid is drained
into a close drainage system. The process is repeated in cycles. The main disadvantage of this peritoneal dialysis is
potentiality of introducing infection into the peritoneum. It is rather slow in correcting metabolic imbalance. Recent
abdominal surgery is a contraindication to the peritoneal dialysis.
(ii) Haemodialysis.— A double-lumen catheter is introduced over a guide-wire into one of the great veins e.g.
jugular, subclavian or femoral. Dialysis fluid is introduced through the catheter. A few sessions of haemolysis is an
effective life saving measure. Between sessions of dialysis, heparin solution is used to keep the lines patent. The main
advantage of haemodialysis is that the metabolic abnormalities are corrected rapidly. The disadvantage is that heparinisation
is necessary.
Haemofdtration.— This is particularly required for actually ill patients. It is almost like haemodialysis which is
performed outside the body with the help of an extracorporeal machine. The advantage is that appropriate concentration
of various ingredients e.g. glucose, sodium, calcium, magnesium, chloride and lactate can be added in the plasma as
may be required.
2. PHASE OF DIURESIS.— When diuresis starts the input should be equal to the output of urine in the previous
24 hours + daily invisible losses. Usually this phase does not begin before 7 days of oliguric phase. This is the time
taken for the epithelium of the lower nephrons to regenerate sufficiently to prevent resorption of glomerular filtrate,
so urine starts passing. In this stage there is often greater loss of sodium and potassium, so these should be replaced.
When the amount of urine reaches one litre per day, then only blood urea starts falling. Diet is similar to that described
in the phase of oliguria.
III. Post-renal anuria.— This is usually due to obstruction to the flow of urine through the lower urinary tract.
This is mostly due to renal stone obstructing the urinary tract and hence it is often called calculus or obstructive anuria.
Other causes of post-renal anuria are malignancy — advanced pelvic cancer causing bilateral ureteric obstruction,
iatrogenic — when the ureters are accidentally tied off during any pelvic surgery, retroperitoneal fibrosis, biharziasis
and very rarely crystaluria. According to Swift Jolly s classification calculus anuria may occur due to —
(i) A stone obstructing the ureter of the only functioning kidney, the other kidney being — (a) congenitally
absent or (b) destroyed by disease or (c) surgically removed.
(ii) Both ureters are obstructed by stones.
(iii) Stones obstructing one ureter, while the other kidney, being healthy, ceases to function. The reason of
cessation of the function of the other kidney is not fully known though it is believed that it may be due to reno-renal
reflex. Urinary excretion of the other kidney will start as soon as the calculus obstruction of the other side is removed.
CLINICAL FEATURES.— Usually males are affected between the ages of 40 and 60 years.
Symptoms.— Often the patient gives a long past history of urinary calculus. In about l/5th of cases no previous
history is received.
Onset is usually sudden with an attack of ureteric colic. The colic may disappear, but is replaced by a constant
severe pain in the loin. In a few rare cases there may not be any ureteric colic, but there is a history of increasing
oliguria for several days followed by anuria. After about 3 to 6 days, during which the patient may continue his usual
work, he gradually complains of headache, sleeplessness and lassitude as the blood urea gradually rises. Later on
uraemia develops.
On examination there may be tenderness and muscle guard on the obstructed kidney. Sometimes a lump may be
detected in the loin which is a large palpable kidney. It must be remembered that this kidney is usually functionless
due to hydronephrosis or pyonephrosis. A functioning kidney which has recently been obstructed by calculus anuria
is usually not palpable.
MANAGEMENT.— 1. First a catheter has to be passed to exclude retention. That means no urine will come out
through the catheter except a very small amount of blood stained urine.
2. A straight X-ray of the KUB region is taken to detect the obstructing stone. Sometimes the stone may not be
visible due to superimposed bone and/or intestinal gas shadows. This investigation may show an enlarged pathological
kidney on the other side.
Ultrasound is not helpful to detect the stone, but may demonstrate dilated pelvis and calyces.
3. Next a cystoscopy is done and catheterisation of both the ureters is performed. If the catheter can be passed
above the stone, it is left in situ for 48 to 72 hours to overcome the danger and to bring back the patient’s general
condition to satisfactory level. 1 ml of liquid paraffin is injected through the catheter and then the catheter is
removed in an attempt to expel the stone spontaneously. If catheterisation does not help to remove the stone,
ureterolithotomy should be performed, or if the stone is impacted at the ureteric orifice, meatotomy may be performed
to extract the stone. If the stone is impacted in the lower l/3rd of the ureter, a Dormia basket may be used to extract
the stone.
4. Percutaneous nephrostomy.— The collecting system of the obstructed kidney is punctured under ultrasound
control. A guide wire is passed down the needle. A few small dilators are then passed till a special nephrostomy tube
can be inserted. This provides drainage of urine or pus without removing the definite stone.
5. When no stone is detected in X-ray and catheterising cystoscope or percutaneous nephrostomy could not relieve
the obstruction, the kidney should be explored. Pyelostomy or nephrostomy may be necessary.
In this connection Cabot’s method of nephrostomy is quite helpful. In this technique both pyelostomy and
nephrostomy is performed with a single tube (a malecot catheter may be used). First a pyelostomy is made then
nephrostomy is performed. With the help of a guide wire the end of the malecot catheter is drawn through the
pyelostomy and through the nephrostomy and ultimately the end is taken out of the body and is anchored to the surface.
The draining tip of the malecot catheter remains within the pelvis of the kidney. The pyelostomy incision is closed.
The advantage of this technique are — (i) that it provides double drainage both nephrostomy and pyelostomy; (ii)
Inadvertent removal of the tube is not possible, as a self-retaining catheter is used and (iii) there is a scope to change
the tube by rail-road method if longer drainage becomes necessary.
6. Insertion of a stent.— Nowadays open J-stent is inserted to drain the ureter into bladder. A retrograde
ureterogram under fluoroscopic control is made to know the cause of obstruction. A guide-wire is introduced through
the ureteric orifice and guided up the ureter into the renal pelvis. The J-stent is then carefully passed over the guide
wire and pushed up the ureter until the top of the stent is curling in the renal pelvis leaving a satisfactory length of
stent within the bladder. Now the guide-wire is removed and the end of the stent curl to form a J-shape to secure the
stent in position. This stent is a foreign body and is prone to infection and encrustation if neglected. This J-stent can
also be introduced through a nephrostomy. Stent can be replaced with topical urethral anaesthesia using flexible
cystoscope.
7. General treatment is almost same as renal anuria before relieving the obstruction.
Other causes of post renal anuria are treated as follows :—
(a) Malignancy.— When advanced pelvic cancer causes bilateral ureteric obstruction, the cancer is in late stage
and most of the cases are ‘inoperable’. For prostatic carcinoma, hormone manipulation should be tried. In case of
carcinoma of the cervix, radiotherapy often offers good result. In case of advanced carcinoma of the ovary or primary
bladder or rectal carcinoma, the prognosis is grave. The only way to relieve obstruction is by placing a nephrostomy
tube, but the quality of life of these patients still remains poor and only death is delayed to some extent.
(b) Iatrogenic.— If the condition is recognised during operation, the sutures should be released. Only in very
late cases it may be required to reimplant the ureters into the bladder with Boari flap or some method of urinary
diversion may be adopted.
(c) Retroperitoneal fibrosis.— In the beginning a J-stent is inserted up the ureter through the constricted portion
to relieve the obstruction. The cause should be found out. Steroids may be used to achieve regression of the fibrotic
process. If this fails, ureterolysis and wrapping the ureters in omentum may be required. One should exclude malignancy
or lymphoma as the cause of such fibrosis.
(d) Bilharziasis.— Systemic treatment is performed by praziquantel or metriphonate for quite a few months for
dead ova to be expelled.
(e) Crystaluria.— In these cases the patients should be advised to stop taking sulphonamides. High fluid intake
is required. Those patients who are at risk to develop uric acid crystals, allopurinol should be given orally.
RETENTION OF URINE
Retention of urine means accumulation of urine in the urinary bladder. The patient is unable to pass
urine or passes small quantity of urine. It must be remembered that there is a difference between anuria,
in which the kidneys fail to excrete urine and there is no urine in the urinary bladder; and retention of urine
in which the kidneys excrete urine normally and the urinary bladder contains urine but the patient is unabl
to pass urine. There is one similarity in anuria and retention of urine that the patients fail to pass urine in
both these conditions. Retention of urine can be of three types — (i) Acute retention, (ii) Chronic retention
and (iii) Acute on chronic retention.
(i) Acute retention is sudden inability to pass urine and it is a painful condition.
(ii) Chronic retention is gradual accumulation of urine in the bladder due to inability of the patient
to empty the bladder completely. The result is an enlarged painless bladder, which may reach upto umbilic
without even knowledge of the patient.
(iii) Acute on chronic retention is a condition in which acute retention superimposes on chronic retention.
That means a patient who is already suffering from chronic retention and the bladder is already half full,
suddenly the patient becomes unable to pass urine at all and the bladder becomes completely full with a
terrific pain. This usually occurs due to cold weather, drinking of alcohol or idiopathic suppression of act
of micturition.
Causes of retention of urine.—
A. Mechanical :
(a) Urinary bladder.— Stones, tumour, blood clot and contracture of the bladder neck.
(b) Prostate.— Prostatic abscess, benign and malignant prostatic enlargements.
(c) Urethra.— Urethral stricture, rupture, congenital valves, foreign body, acute urethritis, stone,
growth, pin-hole meatus, meatal ulcer with scarring.
(d) Prepuce.— Phimosis.
From outside —
Pregnancy (retroverted gravid uterus), fibroid, ovarian cyst, carcinoma of the cervix uteri and rectum
and any pelvic growth.
B. Neurogenic :
(a) Spinal cord diseases e.g. disseminated sclerosis, tabes dorsalis, transverse myelitis etc.
(b) Injuries and diseases of the spine e.g. fracture-dislocation, Pott’s disease etc.
(c) Miscellaneous e.g. post-operative retention, hysteria, tetanus, drugs such as anticholinergics, smooth
muscle relaxants, tranquillizers etc.
CLINICAL FEATURES.— Typical symptom is that the patient has not passed urine for several hours.
He is unable to do so at the present moment also. In acute retention the patient is in extreme pain and he
wants to be relieved immediately. In chronic retention there is almost no pain.
On examination, a full bladder can be diagnosed by palpation in case of thin person otherwise dullness
on percussion above the symphysis pubis indicates presence of distended bladder. Extent of dullness
indicates extent of distended bladder.
An attempt should always be made to know the cause of retention of urine. In males the common
causes are benign hypertrophy of prostate and malignant prostate in old individuals and urethral stricture
in young individuals. In the female this condition is much less common, though it is occasionally seen in
pregnancy (retroverted gravid uterus), in fibroid, in case of rectal or pelvic growth, in multiple sclerosis
and hysteria.
MANAGEMENT.— After a careful examination to detect the cause of retention of urine, a dose of
Omnopon is administered to relieve anxiety and the patient should take a hot bath to diminish internal cong
Hot and cold application may be given to the suprapubic region. This sometimes helps the patient to pass u
by diminishing congestion at the bladder neck. If this fails, a catheter should be passed, preferably
in the operation theatre using full aseptic care. The external genitalia are cleansed using an antiseptic soapy
solution (Savlon). Local anaesthetic ointment may be introduced down the urethra. After waiting for a few
minutes for full effect of this ointment, a self-retaining Foley catheter of reasonable size should be introduced
through the penis down the urethra into the bladder. In case of females after proper cleaning, the labia shou
be held apart using the index and middle fingers of the left hand to push the catheter through the urethral
opening. If the cause is urethral stricture, simple rubber catheter may not be passed. In this case a gum elasti
catheter (Gibbon’s) may be tried and if this fails a metal catheter should be tried. It must be remembered tha
force should never be employed while passing a catheter, lest a false passage should form with bleeding per
urethra. In case of enlarged prostate, metal prostatic catheter may be used which has a long curve to fit in th
long curved urethra pathologically formed by the enlarged lobes of the prostate. Once the catheter has been
introduced into the bladder, urine should not be allowed to come out in force and intermittent closure shoul
be made to prevent evacuation suddenly. Sudden evacuation may cause bladder shock and even haematuria
Closed drainage system should be adopted to prevent introduction of infection into the bladder.
If after considerable attempts with various catheters, catheterisation into the bladder has not been possib
one of the following four methods may be adopted —
1.Suprapubic puncture.— A lumbar puncture needle is introduced through the suprapubic region into th
bladder to relieve acute retention.
2. Suprapubic cystostomy— Under local anaesthesia a small (approximately 'A an inch) vertical incision
is made in the suprapubic region in the midline. The incision is deepened. The linea alba is divided and the
two recti are separated with retractors. The anterior wall of the bladder can be seen. A trocar and cannula is
pushed into the bladder with a sharp thurst. The trocar is removed and a self-retaining catheter is introduce
through the cannula with an introducer. The cannula is taken out. The abdominal incision is closed with a st
to secure the catheter to the skin.
3. Immediate prostatectomy.— In case of benign enlargement of prostate with retention of urine many
urosurgeons follow this technique as it introduces least infection. But it has the disadvantage of doing the
operation on a patient with high urea level. So those patients are only chosen who are otherwise fit and the
urea level is not that high. Transurethral prostatectomy is often performed in these cases.
4. Urethral instrumentation — which has been dicussed in detail in the section of ‘dilatation’
in treatment of urethral stricture’ in page 1 2 1 1
Retention with overflow.— In this condition the patient fails to control, so that small amounts of urine
come out involuntarily from time to time from a completely filled bladder. It usually follows a neglected chr
retention case, though it may occur rarely in acute retention also. Retention with overflow has also been refe
under incontinence and prostatic enlargement.
The treatment is decompression of the bladder, which must be carried out slowly.
NEUROGENIC BLADDER DYSFUNCTION

Physiology of micturition.— When urine accumulates inside the bladder, the detrusor muscle stretches to
accommodate the increasing volume of urine. When the volume of urine is sufficient, the pressure increases until it
stimulates the spinal cord reflex which is under the control of cortical centres and leads to the contraction of the detrusor
muscles. This muscular contraction increases intravesical vesical pressure to 15 to 30 cm of water. It also opens the bladder
neck (internal sphincter) and shortens the urethra. Voiding is resisted by the contraction of the striated muscles ofthe
perineum and external sphincter. When these relax, urination starts.
Uninhibitated neurogenic bladder.— Dysfunction of this type of bladder is similar to that of infant in whom the
cortical integration is lacking. Aetiology includes cerebral vascular accidents and multiple sclerosis. The symptom is urgent
voiding without voluntary control. Cystometrogram reveals abrupt increase in pressure during filling, even at low volumes
Treatment is parasympatholytic drugs such as banthine (methantheline) 50 mg 4 times daily.
Reflex (automatic) neurogenic bladder.—This type of dysfunction occurs due to traumatic transection of the spinal
cord above the level of supply to the urinary bladder (i.e. T9). This typically occurs when the lesion in the spinal cord is
between C7 and T9. When the lesion is above C7, extensive atrophy of the cord takes place below the site of transection
and usually prevents the development of a reflex arc. As the upper motor neurone is interrupted, increased sensitivity of
THE URINARY BLADDER J133
the neuromuscular junction and ganglionic synapses result in increase in pressure within the urinary bladder which
exceeds 15 cm of water, which is greater than control. So even if the bladder is not totally full, urination occurs, which
cannot be controlled.
Treatment.— See next page.
Centrally denervated neurogenic bladder.— Dysfunction is the result of denervation of the segments of spinal
cord which are concerned with innervation of the bladder. Such dysfunction may occur in meningomyelocele or occult spina
bifida (most common cause). Such dysfunction may also occur from traumatic, neoplastic or congenital lesions ofthe sacral
segments or cauda equina.
The symptoms are overflow incontinence and recurring infections. The bladder becomes large and smooth walled
with large amount of residual urine. Cystometry reveals large capacity associated with low pressures.
Management.— Conservative managements include encouragement of the patient to strain and empty the bladder
at frequent intervals and administration of antibiotics to prevent concurrent infection.
Surgical treatment is directed at reducing the resistance of the urethra by transurethral resection of the bladder neck
or sphincterotomy and balancing the detrusor function. This results in improved emptying of the bladder. Long term
antibiotics are however required. Intermittent self-catheterisation may be required to maintain satisfactory emptying of
bladder at periodic intervals. A few drugs may be used to increase detrusor tone (cholinergic) and to decrease bladder neck
tone (sympatholytic).
Nerve supply to the bladder.— Urinary bladder receives both sympathetic and parasympathetic supply.
The sympathetic fibres come from spinal cord segments eleventh thoracic to second lumbar (Til to L2). These fibres
pass via pre-sacral hypogastric nerves and the sympathetic chains to the inferior hypogastric plexus and thence to the bladder.
The parasympathetic innervation is derived from the anterior primary divisions of the 2nd, 3rd and 4th sacral
segments (S2, 3 and 4), of which S3 is the main segment. These fibres pass through the pelvic splanchnic nerves to the
inferior hypogastric plexus, from which these fibres reach the bladder.
It should be remembered that the spinal cord at its lower end (at vertebral levels Tl 2 to L1) is to certain extent dilated
before it ends by tappering This region correlates with the cord segments S2 to S4 which is the micturition centre.
MOTOR INNERVATION.— Motor nerves to the detrusor muscle mainly come from the parasympathetic system.
Only the trigonal portion of the bladder receives innervation from the sympathetic outflow of the spinal cord alongwith
the bladder neck, seminal vesicles and vas deferens. So damage to the sympathetic nerves will disturb function of the
trigone, bladder neck and seminal vesicles. As a result seminal emission and bladder neck closure do not occur with
ejaculation
The external sphincter, which is striated muscle, with the other striated musculatures of the perineum is supplied
by the 2nd, 3rd and 4th sacral segments through pudendal nerve. The external urethral sphincter innervation arises
principally from the S2 and to a lesser degree from S3 nerves.
SENSORY INNERVATION can be divided into exteroceptive (pain, temperature and touch) and proprioceptive
(response to stretch). AfTerents usually pass through sympathetic nerves to the spinal cord segments Tl 1 to L2. Painful
stimuli of overdistension also travel through sympathetic nerves and through the spinal cord to the brain. Stretching of
the muscle fibres (detrusor) through proprioceptive sensation initiates a reflex which is mediated through the
parasympathetic nerves and causes the detrusor muscle to contract. This also causes relaxation of the bladder neck and
relaxation ofthe external sphincter. This causes micturition to take place. So it is clear that the act of micturition is a stretch
reflex which can be inhibited by the cerebral control if the time or place is not suitable.
Management of the bladder in spinal injuries.— Immediately after spinal cord injury spinal shock occurs, which
may last for a few days, weeks or even months.
SPINAL SHOCK.— In spinal shock the bladder becomes atonic. It will gradually recover its contractile ability. Injury
to the sacral cord, if complete enough, may leave the bladder permanently flaccid, which is known as autonomous bladder.
Moreoflen however these lesions are partial and a mixed degree of detrusor weakness is noticed. In case of lesions of the
spinal cord above the centre of micturition, the bladder becomes hypertonic and this hypertonicity is more in cervical cord
injury and decreases in injuries of the thoracic cord. This is called automatic bladder.
During the spinal shock stage, some type of bladder drainage must be instituted immediately. Chronic over
distension can damage the detrusor muscle and limit functional recovery of the bladder. Intermittent catheterisation using
strict aseptic technique has proved to be the best form of management. On one hand it avoids urinary tract infection, on
the other hand it avoids complication due to prolonged indwelling catheterisation. Irrigation of the bladder with antibiotic
solutions and use of systemic antibiotics do not significantly lower the long-term risk of bladder infection. The meatus
should be lubricated to avoid meatal ulceration and stricturing.
When peripheral reflex excitability gradually returns, urodyanamic evaluation should be performed. A cystogram
should be performed to rule out reflux.
High fluid intake is always advised. This reduces stasis and decreases concentration of calcium in the unne.
Ambulation of the patient even in a wheel chair is helpful and should be done as soon as possible. These measures improve
urethral transport of urine, reduce stasis and lower the risk of infection.
AUTOMATIC BLADDER.— When the lesion in the spinal cord is above the level of centre of micturition (S2, 3
and 4) a reflex or automatic bladder will result. In this condition when the bladder fills to certain limit, the detrusor muscle
contracts reflexly and the bladder empties without any cerebral control and hence it is also known as reflex bladder. Such
reflex contractions usually occur at the intervals of 1 to 4 hours, however this period will be shortened if there be infection.
It must be remembered that emptying is never complete and some residual urine exists. After spinal shock, that the bladder
is becoming automatic is indicated by (i) erection of penis (return of bulbo-cavemosus reflex), (ii) return of anal reflexes
and (iii) return of perineal sensation.
Return of the following reflexes indicate that automatic bladder is in the offing.—
(i) Bulbo-cavemosus reflex — This reflex is initiated by putting one finger behind the patient’s scrotum and the
bulb of penis is gently pressed. With the other fingers the glans penis may be pinched. The contraction can be felt in the
bulbo-cavemosus muscle. If erection of penis is maintained alongwith this test, it signifies that the sacral centre is intact.
(ii) Superficial anal reflex.—If the skin ofthe perineum ispricked, it produces a visible contraction ofthe external
anal sphincter.
(iii) Internal anal reflex.— If a finger is inserted into the anal canal in a normal individual, it is grasped by the
smooth fibres of internal sphincter. This reflex is mediated by the sacral parasympathetic reflex pathways. If the sacral
centre is destroyed, the internal sphincter no longer grasps the finger.
(iv) Return of perineal sensation.
If the lesion in the spinal cord is above the level of the sympathetic supply of the bladder (Tl 1), the sympathetic
innervation remains intact and the patient can appreciate the filling of the bladder. So he can understand the warning of
automatic voiding and can prepare himself without wetting the bed.
Management at this stage is to rehabilitate the bladder to a functional state. The patient should be able to have 2 to
3 hours between voidings. Voiding is initiated using trigger techniques — tapping the abdomen suprapubically, scratching
the skin of the lower abdomen, squeezing the penis etc.
These patients may be helped by low dose anticholinergic medication or by placing an electrode on the pudendal nerve
to effect chronic stimulation of the urethral sphincter. Parasympatholytic drug particularly oxybutynin chloride (Ditropan)
5 mg two or three times daily or dicyclomine hypochloride (Bentyl) 80 mg in four divided doses daily have been used with
some success. Propantheline bromide (Probanthine) 15 mg 30 minutes before meals and 30 mg at bed time may be used.
These drugs may not be effective if incontinence is present.
Patients may be evaluated for a bladder pacemaker primarily by urodynamic monitoring of the bladder. Electrodes
are implanted on the motor nerve roots of the sacral nerves (mainly S3, occasionally S4) to produce detrusor contraction
on stimulation. Steps are then taken to reduce sphincter hypersensitivity by selectively dividing selective branches of the
pudendal nerves. The electrodes are connected to a subcutaneous receiver (pacemaker) that can be controlled from outside
the body.
Urinary diversion for irreversible and progressive deteriorated cases should be considered. A variety of procedures
are available including the ileal conduit, cutaneous ureterostomies, ureterosigmoidostomy etc.
AUTONOMOUS BLADDER.— When the lesion in the spinal cord completely destroys the micturition centre (S2
to 4 and cauda equina), volitional voiding cannot be accomplished. The internal sphincter becomes also atonic allowing
incontinence. The result is therefore constant dribbling. There is accumulation of huge residual urine. It causes back
pressure on the kidneys producing hydronephrosis or even pyonephrosis.
Management is mainly bladder training and care. With manual expression of the bladder the patient can evacuate.
Intermittent catheterisation every 3 to 6 hours will eliminate residual urine, help to prevent infection, avoid incontinence
and protect against damage to the upper urinary tract. It can be learned by the patients. Parasympathomimetic drugs are
at times of value in assisting evacuation of bladder. These may be helpful in symptomatic treatment of milder types of
flaccid neuropathic bladder. The usefulness is best judged during urodynamic evaluation. Bethanechol chloride
(Urecholine) is the drug of choice and is given orally 25 to 50 mg every 6 to 8 hours.
Surgery in the form of transurethral resection is indicated for hypertrophy of the bladder neck or an enlarged prostate
which may cause obstruction of the bladder outlet and retention of huge residual urine. It also helps in all patients by
weakening the outlet resistance so that better voiding is possible by abdominal straining. But one must weigh its efficacy
against its disadvantage of giving rise to incontinence.
THE URINARY BLADDER -1135
URINARY DIVERSION
‘Urinary diversion’ means diversion of urinary pathway from its natural path. Urinary diversion may be temporary
procedure to relieve distal obstruction e.g. tubed nephrostomy.
It may be performed as a permanent procedure and this reconstructive surgery is gradually acquiring a common place.
The indications for permanent urinary diversion are — (a) when the bladder has to be removed, (b) when the sphincters
of the bladder and the detrusor muscle have been damaged or have lost their normal neurological control, (c) when there
is irremovable obstruction in the bladder and distal to that, (d) in cases of ectopic vesicae and (e) when there is incurable
vesico-vaginal fistula.
Methods of urinary diversion.—There are various methods of urinary diversion which include both temporary and
permanent procedures. The type of operation to be used in a particular case should be judged according to its merit. The
methods are —
(i) Pyelostomy or nephrostomy or urethrostomy (with indwelling catheters) — temporary procedures.
(ii) Suprapubic cystostomy — temporary procedure.
(iii) Bladder diversion.
(iv) Rectal bladder.
(v) Cutaneous ureterostomy.
(vi) IJretero-sigmoidostorny.
(vii) Ureteric transplantation into isolated ileal or colonic conduit.
The commonly used methods are discussed below :—
Uretero-sigmoidostomy.— The advantage of diverting urine into the colon is that no collection apparatus is
necessary. However anal sphincter must be competent. Before performing this operation, the patient must prove that he
can control at least 200 ml of fluid in the rectum. This operation is in fact the first widely employed and successful form
of intestinal urinary diversion. With the advent of ilial conduit many urological surgeons have abandoned this operation
due to its complication of hyperchloraemic acidosis.
Technique.—The colon is prepared as before colonic surgery. The abdomen is opened by right lower paramedian incision.The patient is
placed in the T rendelenburg position. The right ureter is first found out as it crosses the bifurcation ofthe right common iliac artery. An incision
is made on the peritoneum on the medial side of the ureter thus avoiding damage to the ureteric vessel. The ureter is dissected out from its bed
and cleared till its entry into the bladder. The ureter is then divided and the distal stump is ligated. The proximal end is trimmed obliquely and
slit anteriorly for 1 cm. The sigmoid colon is now taken out. An incision is made on the anterior wall of the colon by which the peritoneal and
muscular coats are divided but not the mucous membrane. The incision is about 4 cm in length. At the lowermost part ofthis incision the mucous
membrane is incised. The ureter is now anastomosed to the incised mucous membrane with interrupted 4/0 chromic catgut. The upper part of
the incision is now closed by interrupted sutures over the ureter. Thus the ureter is laid on a tunnel within the muscular coat of the sigmoid colon
(Leadbetter anastomosis). The peritoneal incision is now sutured around a ureteric implant to make the site of anastomosis extraperitoneal.
The left ureter is now found out and is implanted into the sigmoid colon a tittle above the right ureter in a similar manner. A Foley's catheter
is introduced through the anus into the rectal ampulla and the balloon is inflated. The urine excreted through the catheter is measured. If
satisfactory urinary excretion is noticed with a full fluid intake, the catheter is removed on the 3rd day.
Various modifications have been made on this operation with variable success by urosurgeons e.g. Nesbit, Cordonnier etc.
COMPLICATIONS —
(i) Reflux of urine.— Pressure within the colon may cause reflux of urine upwards to the kidney. That is why Leadbetter made the
anastomosis through amuscular and submucosal tunnel to prevent this. Sigmoid myotomy has been performed to decrease intracolonic pressure
to overcome this problem.
(ii) Biochemical changes.— Sigmoid colon absorbs chloride and urea and this causes hyperchloraemic acidosis in these cases
following operation. There is also potassium depletion. When severe, the patients complain of loss of appetite, weakness, thirst and diarrhoea.
Gradually the respiration becomes rapid and deep. Ultimately the patient may be comatosed. Mild acidosis may remain unrecognised for quite
a long time. These cases may produce osteomalacia from calcium excretion. Bone pain and even pathological fracture may occur.
These complications can be prevented to certain extent by emptying the rectum very frequently (about 2 hourly). This minimises acidosis
to a great extent. The patient should avoid added salt in the diet, on the contrary he should take a mixture of potassium citrate and sodium
bicarbonate thrice daily. Calcium should also be added in the diet. Regular biochemical analysis should be performed. In an established case
the patient should be given a suitable dose of sodium bicarbonate intravenously to combat acidosis and an amount of potassium also
intravenously.
(iii) Renal infection.— Organisms from the sigmoid colon may find easy access through the ureters into the kidney and cause
infections like pyelonephritis, which becomes difficult to control. Almost always an appropriate antibiotic should be given e.g. iuradantin or
ampicillin to prevent pyelonephritis.
(iv) Stricture formation.—There isapossibilityofstricture formation attheanastomosingsite.ForthatNesbit,Cordonnier,Maiberger
and Mathisen have introduced various modifications to avoid stricture formation including Leadbetter.
Ileal conduit— This is the most frequently employed form of permanent urinary diversion.
Technique.— A segment of terminal ileum of about 6 to 8 inches in length, approximately 12 inches proximal to the ileocaecal junction
is selected for ileal conduit. Its blood supply is kept intact. It is desirable to keep a shorter segment of ileum to avoid resorptive complications.
The left ureter is first isolated and divided near its opening into the bladder. The distal segment is ligated and the proximal segment is brought
through the pelvic mesocolon and its end is cut obliquely to perform end-to-side anastomosis with the isolated segment of ileum. The right ureter
is also cut obliquely and is also anastomosed to an elliptical opening made in the side ofthe ileal segment. The method of anastomosis is ofNesbit
type i.e. without any tunnel. The proximal end ofthe conduit is closed. The distal end ofthe ileal segment is brought out through a stab incision
in the right lower abdomen and the ileostomy care is almost similar to that of permanent ileostomy discussed in the chapter of ‘The Colon’.
Ureteric anastomosis may be made creating a non-refluxing submucosal tunnel (Cordonnier).
RESULTS and COMPLICATIONS —
(i) Infection.— Incidence of pyelonephritis is considerably reduced in this technique.
(ii) Urinary leakage at uretero-ileal anastomosis is a complication which can be avoided by meticulous anastomosis.
(iii) Viability of the terminal portion of the conduit at the stoma has become a problem in a few cases.
(iv) Stenosis at the ureteroileal junction and stenosis ofthe stoma have been noticed in a few cases. Very occasionally stenosis ofthe
entire conduit has occurred due to chronic inflammatory reaction with progressive fibrosis in the mucosa and submucosa of the isolated ileal
segment.
(v) Stricture of the ileal loop is probably much more common than previously reported and is probably inflammatory rather than
ischaemic.
(vi) Resorptive problems.— Resorption of chloride, excretion of potassium and recirculation ofurea are less noticed in this operation
particularly when shorter segment of the ileum is used. This can be corrected by hydration and administration of sodium potassium citrate
mixture.
Colon conduit— Increasing recognition of ileal conduit diversion has prompted reconsideration oftechniques and renewed enthusiasm
for the use of colon as urinary conduit. A very short segment of colon may be employed (rarely more than 8 to 10 cm) to minimise the possibility
of stagnation and resorption. In addition, the colon conduit is more appropriate for reattaching the conduit to the infarct bowel or to the bladder
itself. It also offers the opportunity for non-refluxing uretero-enteric anastomosis utilising the tunnel principle of Leadbetter. But gradually it
is appreciated that this procedure may exhibit coloureteral reflux at sometime, as also ureterocolonic stenosis and obstruction.
However the incidence of complications after ileal conduit colon conduit, or even ureterosigmoidostomy notes no great difference in the
rate of complications among these three major urinary diversion procedures.
Ileocaecal segment— Use of the caecum and terminal ileum as a bladder substitute has been used with some success. The ureters have
been implanted into the caecum and the ileum intussuscepted into the caecum and the proximal open end is brought out to the skin for subsequent
intermittent catheterisation. In another technique ureters have been implanted into the terminal ileal segment, urinary drainage into the caecal
reservoir and the interposition of a partially inverted segment of ileum connecting the caecum to the skin.
Lowsley’s operation.— The rectosigmoid junction is divided completely and its lower end is closed. The ureters are implanted into the
excluded lower segment, so that the rectum now functions as a bladder. The proximal cut end of the sigmoid colon is now mobilised sufficiently
to draw through the perineum anterior to the anus within the external sphincter. So that both the original canal and the new canal are surrounded
by external sphincter. It is also called rectal bladder.
Fig.58.14.— Shows different methods of ureterocolic or uretero-ileal anastomosis. A — Leadbetter type.

B.— Nesbit type and C.— Cordonnier type.
1137
CHAPTER-51
THE PROSTATE AND URETHRA
Development.—
In the male, the prostatic part of the urethra above the orifice of the prostatic utricle is derived from vesicourethral
portion of the cloaca which forms the anterior and the lateral walls except the posterior wall which is formed by
incorporation of the caudal ends of the mesonephric ducts. The remainder of the prostatic part, the membranous part and
probably the part within the bulb of the penis are all derived from the urogenital sinus. The succeeding portion as far as
the glans is formed by the fusion of the genital folds. So upto this part is derived from the endoderm. At the tip of the glans
an ingrowth of surface epithelium occurs to meet the anterior extremity of the endodermal urethra (urethral plate). So this
part develops from the surface ectoderm and its lymphatics drain into the superficial inguinal lymph nodes.
In the female, the whole of the urethra is derived from the vesico-urethral portion of the cloaca. It is homologous to
that part of the prostatic urethra in the male which lies above the orifices of the prostatic utricle and the ejaculatory ducts.
The prostate starts developing during the 3rd month with a number of outgrowths from the proximal part of the
urethra. At first 14 to 20 such outgrowths develop from the endoderm around the whole circumference of the urethra, but
mainly from the lateral aspect and not from the dorsal wall of the urethra. These outgrowths give rise to glands ofthe outer
zone of the prostate. Later on outgrowths arise from the dorsal wall of the urethra above the opening of the mesonephric
ducts and possibly these are of mesonephric and paramesonephric origin covering the cephalic end of the Mullerian
tubercle. These constitute the glands of the inner zone. These outgrowths are solid at first and branch at their tips. Gradually
these become tubular and invade the surrounding masenchyme which gradually differentiate to form prostate.
In the female similar outgrowths do appear, but remain rudimentary.
ANATOMY
THE PROSTATE.—The prostate is composed of glandular tissue in a fibromuscular stroma. It surrounds the first
part of the urethra (prostatic urethra). It measures about 3 cm in vertical diameter, 4 cm transversally at the base and about
2 cm anteroposteriorly. It is somewhat conical in shape with the base upwards and the apex downwards. It has a posterior,
an anterior and two inferolateral surfaces.
The BASE is directed upwards and is directly continuous with the neck of the urinary bladder. The urethra enters
the base nearer its anterior border. The APEX is directed downwards and is in contact with the fascia on the deep surfaces
of the Sphincter urethrae and the Transversus perinei profundus. The POSTERIOR SURFACE is flattened from side-to-
side and slightly convex from above downwards. It is related to the anterior surface of the rectum from which it is separated
by the capsule and some loose connective tissue.There is a depression in this surface near its upper border, through which
the two ejaculatory ducts enter the prostate. This depression serves to divide the posterior surface into upper and smaller
part which is called the median lobe and lower and larger portion which is called the posterior lobe. This posterior lobe
presents as a shallow median furrow and two lateral lobes (right and left ) lie in front of this. These lateral lobes form
the main mass of the gland and adenomata often occur here. These two lateral lobes are continuous in front with a small
lobe (anterior lobe) or isthmus. This anterior lobe or isthmus consists of mainly fibromuscular tissue and is devoid of
glandular substance. So adenoma never occurs here.
The ANTERIOR SURFACE lies about 2 cm behind the pubic symphysis from which it is separated by a plexus of
veins and some loose fatty tissue. By puboprostatic ligaments it is connected near its upper end to the pubic bones. The
INFEROLATERAL SURFACES are related to and supported by the anterior parts of the levator ani, which is called the
levator prostatae, from which it is separated by a plexus of veins embedded in the fibrous tissue.
Lobes.— From the description above it is clear that there are 5 lobes in the prostate — 1 anterior lobe, 1 posterior
lobe, 2 lateral lobes and 1 median lobe. Adenomata usually occur in the lateral lobes and in the median lobe. The median
lobe, when it is enlarged, projects into the bladder through the internal urethral sphincter. It pushes the mucous membrane
of the urethra before it and extends into the bladder and may block the internal meatus to cause retention of urine. Straining
to micturate will push this median lobe into the internal urethral meatus which is thus entirely blocked so straining at
urination will further stop the flow instead of increasing it.
Adenoma never occurs in the posterior lobe, but this lobe is often the site of primary carcinoma.
Fascial relations.—
1. CAPSULES.— There are two capsules of the prostate — true and false.
(i) The true capsule is formed by a condensation at the periphery of the prostate.
(ii) The false capsule is formed by the visceral layer of the pelvic fascia. The prostatic venous plexus which lies
around the sides and base of the gland, lies between the two capsules. This plexus receives in front the deep dorsal vein
72
of the penis and ends in the interal iliac veins.

Ther6 is also a capsule known as surgical capsule which only develops in case ofbenign hypertrophy ofthe prostate
and is formed by the non-adenomatous tissue of the prostate which is pushed to the periphery of the gland (prostate) by
the adenoma of the prostate.
2. FASCIAE BEHIND THE PROSTATE : Rectovesical fascia or thefascia ofDenonvilliers or prostato-peritoneal
fascia.— In early foetus at about 4th month the rectovesical peritoneal pouch extends downwards to the pelvic floor and
separates the prostate from the rectum. Gradually the lower part of this pouch becomes obliterated and the fused peritoneal
layers form a fascia behind the prostate which extends from the urogenital diaphragm below to the peritoneum
(rectovesical pouch) above. This is called the fascia of Denonvilliers, within which there is a potential space which is
known as the space ofDenonvilliers or the retroprostatic space of Proust.
Structure.— As mentioned above the prostate is covered by a thin but firm capsule (true capsule) which is firmly
adherent to the prostate and is structurally same as the stroma of the gland.
The prostate consists of glandular substance and muscular tissue. The glandular substance is composed of numerous
follicles. The follicles open into elongated canals whichjoin to form 12 to 20 small excretory ducts. The epithelium which
lines the canals and follicles is of columnar variety. The prostatic secretion and the secretion of the seminal vesicles
together form the bulk of the seminal fluid. The prostatic secretion is slightly acidic and contains acid phosphatase and
fibrinolysin. The prostatic ducts open mainly into the prostatic sinus in the floor of the prostatic urethra.
The muscular tissue forms the main portion of the stroma, the connective tissue being very scanty. Immediately
beneath the capsule there is a dense layer of muscle, which forms an investing sheath for the gland. Around the prostatic
urethra there is a dense layer of circular fibres which are continuous above with the inner layer of the muscular coat of
the bladder.
Histological sections of the prostate in fact do not show Lobar pattern of the organ, but it shows two well defined
concentric zones of glandular tissue. The larger outer zone is composed of long branched glands, the ducts of which curve
backwards to open mainly into the floor of the prostatic sinuses, though some may open into the lateral walls of the urethra.
The inner zone consists of a set of submucosal glands, the ducts of which open into the floor of prostatic sinuses.
Carcinoma affects almost exclusively the outer zone, while benign hypertrophy particularly affects the inner zone of
glands.
MALE URETHRA.— It is about 18 to 20 cm in length and extends from the internal urethral orifice in the urinary
bladder to the external urethral orifice at the tip of thepenis. It is divided into 3 portions viz. (i) prostatic urethra, the portion
lies within the prostate, (ii) membranous urethra, the portion between the prostate and the bulb ofthe penis and (iii) spongy
urethra, the portion which is contained in the corpus spongiosum penis.
Prostatic u reth ra.— It is the widest and most dilatable part of the urethra. Prostatic urethra lies nearer the anterior
than the posterior surface of the prostate. On the posterior wall there is a median longitudinal ridge which is termed the
urethral crest. On each side of the crest there is a shallow depression, termed the prostatic sinus. Floor of this sinus is
perforated by the orifices of the prostatic ducts. At the middle of the urethral crest lies the verumontanum or colliculus
seminalis. There is a slit like orifice at the tip of this elevation which is the orifice of the prostatic utricle. On each side
of this slit like orifice, there is the small opening of the ejaculatory duct. The prostatic utricle is a blind tube which is about
6 mm in length and runs upwards and backwards within the substance of the prostate behind the median lobe. Its walls
are composed of fibrous tissue, muscular fibres and mucous membrane. It is developed from the paramesonephric duct
and is thought to be homologous with the vagina of the female.
The membranous urethra.— It is the shortest (approximately 2 cm in length) and least dilatable portion ofthe
urethra. It runs a slightly curved course downwards and forwards from the prostate to the bulb of the penis. It perforates
the perineal membrane, after which it becomes spongy urethra about 2.5 cm (1 inch) below and behind the symphysis
pubis. The membranous urethra is surrounded by the fibres ofthe sphincter urethrae. The bulbo-urethral glands are placed
one on each side of this portion of the urethra.
The spongy u rethra.—* It is about 15 cm in length. It commences below the perineal membrane and passes forwards
to the front of the lower part of the symphysis pubis and then, in the flaccid condition of the penis, it bends downwards
and forwards. This portion of the urethra is narrow with a uniform diameter of 6 mm inside the body of the penis. Inside
the bulb of the penis it is dilated to form the intrabulbar fossa. Within the glans penis it is again dilated and forms the
navicular fossa. The bulbo-urethral glands, though lie by the sides of the membranous portion of the urethra, open into
the spongy portion about 2.5 cm (1 inch) below the perineal membrane.
The external urethral orifice is the narrowest portion ofthe urethra and it is a saggital slit of about 6 mm long, bounded
on each side by a small labium. The urethral glands open into small orifices into the lining membrane of the urethra These
are mucous glands. There are a few small pit-like recesses or lacuni of various sizes, which may intercept the point ofthe
catheter during its passage through the urethra. One lacuna is the largest and is situated on the roof of the navicular fossa
THE PROSTATE AND URETHRA 1139
and this is called lacuna magna.
Fig. 59.1.— Diagrammatic view of inside of prostatic Fig. 59.2.— Urethroscopic view of verumontanum.
urethra. U.C.— Urethral crest. P.S.— Prostatic sinus.
V.— Verumontanum. P.U.— Opening of prostatic utricle.
E D.— Ejaculatory duct.
Sphincters.— There are two sphincters of the urethra — (i) internal sphincter or sphincter vesicae at the neck of the
bladder and (ii) an external sphincter or sphincter urethrae which surrounds the membranous urethra. The former sphinc
ter is involuntary and is supplied by the sympathetic nerves (Til, 12 and LI and 2). The latter consists of striped muscle
and is supplied by the perineal branch of the pudendal nerve (S-2,3 and 4). It is under voluntary control after early infancy.
The female urethra.— It is about 4 cm in length and 6 mm in diameter. It begins at the internal urethral orifice of the
bladder and then runs downwards and forwards being embedded in the anterior wall of the vagina and ends at the external
urethral orifice, which is an anteroposterior slit. It is situated in front of the opening of the vagina just behind the glans
clitoridis. Except during the passage of urine the walls of the urethra remain in apposition. It perforates through the
perineal membrane. Many small mucous urethral glands open into the urethra. There are also a few lacuni open into the
urethra. Near the lower end of the urethra a number of urethral glands are grouped together and open into a duct named the
paraurethral duct which runs down in the submucous tissue to end in a small aperture on the lateral margin of the external
urethral orifice. The urethral glands are considered to be homologue of male prostate. Developmentally the female urethra
corresponds to that part of the prostatic urethra which lies above the opening of the prostatic utricle.
BENIGN ENLARGEMENT OF THE PROSTATE
A few other names have been given to this condition. These are : senile enlargement of the prostate, ad
enoma, adenomyoma, benign prostatic hyperplasia or hypertrophy and nodular hyperplasia. The last name w
suggested by Moore and this seems to be the most accurate nomenclature so far as its pathology is concerned
Before considering aetiology of benign hypertrophy of prostate, hormonal influence on the prostate
should be considered. The principal hormone, which acts on prostate, is testosterone secreted by the Leydig
cells of the testis under the control of luteinizing hormone (LH) of anterior pituitary, which is again under
control of luteinizing hormone-releasing hormone (LHRH) of hypothalamus. An enzyme called 5 a-reduc-
tase, which is present in high concentration in prostate, converts testosterone to 5-dihydrotestosterone (DHT)
In old age serum oestrogen is increased which acts on the hypothalamus decreasing the secretion of LHRH an
hence LH, causing ultimately decrease in serum testosterone level. Moreover oestrogenic steroids secreted
the adrenal cortex in aging male play a part in disrupting the balance between DHT and local peptide grow
factors thus increasing the risk of benign prostatic hyperplasia.
Aetiology.—
Though the pathology has been well established that it is a nodular hyperplasia, but its cause is not kn
definitely. It is a disease process with a well-defined age incidence. It is essentially a disease of old age, after
50 years. Only under the rarest circumstances it may occur in early life. Sir Benjamin Bordie’s adage is ver
appropriate in this respect. He said, ‘when the hair becomes grey and thin, when there forms a white zone
around the comea, at the same time ordinarily, I dare say invariably, the prostate increases in volume’. Th
condition is also known in animals particularly in dogs.
Two theories have been put forward to indicate the cause of such hypertrophy of the prostate, of whic
first is more accepted than the second one.
(i) THE HORMONE THEORY.— There is a relationship to hormonal activity with much experimenta
and clinical evidence. Orchidectomy causes atrophy of the gland and terminates the elaboration of prostat
fluid. Dogs with sertoli cell tumours (oestrogen producing) of the testis do not develop prostatic hyperpla
In men previous castration seems to prevent prostatic hypertrophy. However, administration of oestrogen
little if any effect upon the size of the gland, although some atrophy of the epithelial structure may be noti
microscopically. Certainly androgens cannot be blamed for this hyperplasia, as the disease occurs at a tim
when the androgenic activity of the individual is decreasing. Therefore an imbalance between androgen a
oestrogen may be the causative factor. It may be that the androgen diminishes as the age advances, while
quality of the oestrogen is not decreased equally. So the prostate may have enlarged due to relative predo
nance of oestrogenic hormone. In this respect this condition is almost similar to fibroadenosis of the breas
It is well established now that Dihydrotestosterone (DHT) influences growth of prostate. 5 a-Reductas
turns testosterone to DHT. So any drug which inhibits this enzyme may reduce the growth of benign hyp
phy of prostate. Such drug (Finasteride) has been used and under trial for this disease.
(ii) THE NEOPLASTIC THERAPY.— As mentioned earlier proponents of this theory are reducing ver
fast. According to this theory benign enlargement of the prostate is considered to be a benign neoplasm i.e
adenoma or adenomyoma of the gland. As there may be considerable fibrous tissue involved in such neop
it may be also fibromyoadenoma.
PATHOLOGY.—
The changes are of two main types — overgrowth of the glandular elements and overgrowth of conne
tissue elements. Depending upon which element predominates, the consistency of the enlarged prostate w
vary. In case of overgrowth of glandular elements consistency is softer in comparison to overgrowth of co
tive tissue element, in which the consistency will be firmer.
Enlargement of the gland is due to formation of one or more nodules. These nodules may fuse togethe
form one mass which can be readily shelled out. Glandular hyperplasia affects the inner submucous grou
glands which enlarges at the expense of the rest of the organ. It compresses the rest of the gland to such an
extent that it forms a ‘false capsule’ (or surgical capsule) consisting of outer part of the gland which structu
ally consists of fibrous tissue with a little muscular tissue and very little glands. A line of cleavage is readi
up between the nodular mass and the surgical capsule.
The enlargement may involve any part of the gland except the posterior lobe and anterior lobe. The tw
lateral lobes and the median lobe are frequently involved. When the subcervical glands are mainly involv
hyperplasia, the median lobe enlarges. It gradually projects upwards into the bladder through the interna
sphincter. Sometimes both lateral lobes may also project into the bladder, so that when viewed from with
sides and back of the internal urethral meatus are surrounded by intravesical projection of prostatic tissue
which looks like a collar.
The fibrous median bar should not be confused with prostatic hypertrophy. This causes urinary obstr
tion without prostatic hypertrophy. It represents the end results of an inflammatory fibrosis due to under
chronic prostatitis.
Microscopic appearance — This is one of glandular hyperplasia combined with fibrous and muscular
overgrowth. There is first hyperplasia of the stroma around the ducts, acini and urethra. The stroma is richer
smooth muscle than normal. There may be masses of lymphoid tissue in the stroma which may be mistaken fo
evidence of inflammation. There is a great proliferation and budding of ducts and acini. The epithelium
becomes cylindrical with papillary projections, which may be so abundant as to almost fill the glandular
spaces. So the nodules are due to hyperplasia of both stroma and the glands. When the fibrous and muscle
tissue of the stroma undergo more hyperplasia than the glands, the nodules will be firm. Corpora amylacea m
be present but not as much as in normal prostate.
Secondary effects due to prostatic enlargement.—
1. CHANGES IN THE URETHRA.—
(i) The prostatic urethra elongates. This elongation is more pronounced in the portion above the verumontanum
which becomes about twice its normal length. This is due to enlargement of the prostate upwards and as majority of the
glands of the prostate lie above the level of the verumontanum.
(ii) The normal posterior curve of the prostatic urethra becomes exaggerated, so much so that it requires a specially
angled metal catheter for using in these cases (known as prostatic metal catheter).
(iii) The urethra becomes compressed laterally so that it takes a shape of an anteroposterior slit due to enlargement
of two lateral lobes.
(iv) In rare cases one lateral lobe may be enlarged predominantly to cause lateral distortion of prostatic urethra. This
causes difficulty to introduction of catheters.
2. CHANGES IN THE BLADDER.—
(i) As the degree of obstruction increases the vesical detrusor muscle undergoes compensatory hypertrophy to
overcome the increasing urethral resistance. The muscle may become more than 2 cm thick. It should be remembered that
there is little relationship between the size of the gland and the severity of the symptoms. Due to urethral obstruction
alongwith compensatory hypertrophy of the detrusor muscle there will be (a) trabeculation of the bladder wall, (b) hyper
trophy of the trigone and interureteric ridge and (c) formation of diverticula.
When compensatory hypertrophy fails, and the vesical muscle becomes exhausted, urine is then retained in the
bladder in increasing amounts to cause chronic urinary retention and the thickened bladder wall may gradually become
attenuated and atonic. Ultimately a stage of overflow incontinence may set in, in which the urine may pass out from
overdistended bladder without the knowledge of the patient.
(ii) When the median lobe enlarges and projects into the bladder through the internal sphincter, a pouch develops
posterior to this projection, which is called the post-prostatic pouch, into which urine becomes stagnant and the patient
cannot evacuate the bladder completely.
(iii) This stagnant pool of urine, which is called the residual urine, may cause infection within the bladder or cystitis
and calculus formation.
Cystitis in this condition is not uncommon and usually occurs from (a) residual urine in the post-prostatic pouch, (b)
stagnant urine in the diverticula, (c) stagnant urine in chronic retention of urine and (d) may be precipitated by catheterisation.
Calculi often develop in this condition and these calculi are usually phosphate calculi (mostly triple phosphate). Such
calculi are (a) commonly seen in the post-prostatic pouch or (b) secondary to cystitis.
(iv) Enlarged prostate may compress on the prostatic venous plexus which lies between the true and false capsule of
the prostate and this may cause congested veins or ‘vesical piles’ at the base of the bladder. This may cause haematuria
from rupture of these congested veins as oesophageal pile rupture causes haematemesis.
3. CHANGES IN THE URETERS AND KIDNEYS.—
(i) Due to hypertrophy of the trigone and interureteric ridge, there is downward traction on the intramural segment
of the ureter. This causes obstruction to the flow of urine and causes hydroureter and hydronephrosis. Increasing intravesi
cal pressure also causes the same pathology.
(ii) Significant residual urine may lead to chronic retention of urine and vesical distension. This may damage the
sphincter mechanism around the ureteric orifices permitting reflux of urine from the bladder into the dilated ureters
(vesicoureteral reflux). This may also be due to incompetence of uretero-vesical ‘valves’.
(iii) Due to reflux of urine into the ureters, ascending infection reaches the kidneys to cause acute or chronic pyelo
nephritis. Such infection may also rarely come from the blood stream or lymphatics.
(iv) Following infection of the kidney, the renal function may be lowered leading to uraemia. This may also be due
to increased back pressure or development of chronic interstitial nephritis.
4. CHANGES IN SEXUAL URGE.— In early stage of prostatic enlargement there is increased libido. Later on the
patient may become impotent.
As mentioned earlier benign enlargement of prostate seldom causes symptoms before the age of 50 yea
It should be remembered that there is no direct relation between the degree of enlargement and the severit
symptoms.
SYMPTOMS.—
(i) Hesitancy.— The patient notices that he must wait for urination to start. If he strains, he has to wait
more as the median lobe bends down on straining to obstruct the internal urethral orifice (Figs. 37.3 & 37.4
page no. 409 of ‘A Manual on Clinical Surgery’ by Dr. S. Das).
(ii) Dysuria.— The stream is often weak and tends to dribble towards the end of micturition. Because o
increased urethral resistance and derangement of the internal urethral opening, more force is required for
urination.
(iii) Frequency.— This seems to be the earliest symptom in majority of the cases. In the beginning fre
quency is mostly nocturnal. The patient gets up twice or more during night. Such frequency is mainly due
vesical introversion of the sensitive prostatic mucous membrane due to its enlargement upwards. Gradual
frequency is experienced in both by day and night. This is due to irritability of the bladder and the amoun
residual urine. The more is the amount of residual urine, more is the frequency. Such residual urine also ca
infection and cystitis develops, which further causes increased frequency.
(iv) Urgency is also a characteristic symptom of this condition. As the internal sphincter mechanism is
deranged due to invasion of the prostate into the bladder, a little urine escapes into the prostatic urethra, w
is highly sensitive and causes an intense desire to urination.
(v) Haematuria.— This is quite common in this condition. It is due to rupture of dilated veins at the ba
of the bladder which are apt to rupture during straining. Occasionally gross haematuria may occur. Other
causes of haematuria in this condition are (a) cystitis, (b) calculi and (c) erosion of a portion of intravesical
of enlarged prostate.
(vi) Pain.— There are various causes of pain in this condition, though benign enlargement of prostate
itself is a painless condition. The causes of pain are due to secondary changes caused by prostatic enlargem
These are (a) cystitis, which causes variable suprapubic pain, (b) acute retention, (c) hydronephrosis, which
causes dull ache in the loin and (d) due to greatly enlarged prostate giving rise to a feeling of weight in the
perineum or fullness in the rectum.
(vii) Retention of urine.— (a) Acute retention may cause intense pain due to sudden blockage of urin
caused by enlarged median lobe obstructing the internal urethral orifice or enlarged lateral lobes blocking
urethral opening due to oedema. This often occurs after a heavy drink of alcoholic liquors or when the pat
goes out in cold night. Postponement of micturition for sometime may also precipitate acute retention. Thi
an extreme painful condition and compels the patient to go to nearby hospital to be relieved.
(b) Chronic retention, the causes of which are discussed above, is a relatively painless condition and i
may lead to overflow incontinence.
(c) Acute on chronic retention is also seen in this condition.
(viii) Renal failure.— Sometimes the patient with benign enlargement of prostate presents with signs of
renal failure.
(ix) Prostatism.— It is a group of symptoms of disturbed voiding in aging individuals. There may be
various reasons of prostatism which include impairment of sphincter mechanism of the bladder and neuro
cular co-ordination, benign prostatic hyperplasia etc. The basic problem is bladder outflow obstruction (BO
The symptoms of‘Prostatism’ can be classified into 2 groups —
Obstructive Irritative
Poor flow, which does not improve, Increased frequency;
rather worsens by straining;
Dribbling; Urgency;
Hesitancy. Nocturnal incontinence (enuresis).
PHYSICAL SIGNS.—
General examination.— This should be performed carefully to exclude renal insufficiency. Blood pres
sure and heart should be examined by a cardiologist to make the patient risk-free for operation.
Examination of the nervous system is important to eliminate neurological lesions e.g. tabes dorsalis,
disseminated sclerosis, diabetes mellitus, Parkinson’s disease etc. which may give rise to bladder outflow
obstruction almost similar to that produced by benign hyperplasia of prostate. A pressure-flow urodyanamic
study should be carried out to diagnose bladder outflow obstruction. Examination of perianal sensation and
tone is useful in detection of S2 to S4 lesion which also causes bladder sphincter problem.
Local examination.— Abdominal examination may only reveal a full bladder at times. The loins should
be carefully examined to exclude renal enlargement due to hydronephrosis.
Rectal examination should be carried out carefully after evacuating the bladder. Ordinarily left lateral
position is quite good for such examination. When the lateral lobes are enlarged, rectal examination detects
such enlargement. The surface of the enlarged prostate is usually smooth and convex. It is usually firm in
consistency. A sulcus should be felt in the midline between the two lobes. The rectal mucosa can be easily
moved over the enlarged prostate. It is difficult to palpate the median lobe enlargement, which is often intra
vesical. So if on rectal examination the prostate does not appear to be enlarged, it cannot be considered that t
patient is not suffering from enlarged prostate. Residual urine may be felt as a fluctuating swelling just above
and behind the prostate. Bimanual examination, after evacuating the bladder is a good method to feel the
intravesical median lobe enlargement.
If possible, the patient should be watched at the time of micturition. The loss of projectile stream and
dribbling are good findings in favour of this diagnosis. A graphic record of patient’s stream and the degree o
outflow obstruction may be determined by micturograph.
1. Examination of the urine.— The urine should be examined for evidence of infection, blood and for
presence of sugar (to exclude diabetes). The urine should be cultured and tested for sensitivity to different
antibiotics.
2. Examination of the blood.— Serum urea, N.P.N. and creatinine should be performed to assess renal func
tion besides the usual blood count, haemoglobin estimation and E.S.R.
Estimation of prostate-specific antigen (PSA).— PSA is a glycoprotein, whose function is to facilitate
liquifaction of semen. It is now being used as a marker for prostatic disease. It is measured by immunoassay
technique and the normal upper limit is about 4nmol/ml. It is more important in the diagnosis of carcinoma
prostate, in which case the level goes upto 15nmol/ml in localised cancer to 30nmol/ml in case of metastatic
cancer. However in benign hyperplasia of prostate the level goes upto 4-10nmol/ml.
3. STRAIGHT X-RAY.— (i) This may show presence of calculus either in the bladder (in the postprostatic
pouch or in the diverticulum) or in the kidney.
(ii) It may show degenerative disease of the lumbar spine and may show sclerotic bone metastasis from
carcinoma of the prostate.
(iii) It may show shadows of enlarged kidneys due to hydronephrosis.
(iv) It may also show the shadow of enlarged bladder due to chronic retention.
4. EXCRETORY UROGRAPHY is highly important and should be performed in all cases except where
there are signs of renal failure and where the blood urea is above 60 mg percent.
(i) It will indicate the function of each kidney.
(ii) Evidence of obstruction leading to hydroureter and hydronephrosis may also be evident by this investi
(iii) Intravesical encroachment of the prostate may be revealed by a smooth filling defect at the bladder nec
(iv) Diverticula may be detected, if present.
(v) Voiding cystourethrography may show ureteral reflux.
(vi) Post-voiding film is mandatory to reveal the amount of urinaiy retention (residual urine).
(vii) Urodyanamics.— If the diagnosis has not been made, this investigation may establish whether bladder
outflow obstruction is present or not. The intravesical pressure, the bladder capacity and recordings of residu
urine may be obtained easily. Voiding

pressure and flow rate may be measured.
Bladder outlet may be visualised if a video
unit is attached to it.
5. CYSTOSCOPY.— This inves
tigation is also of great value. This with
panendoscopy the urethra is inspected and
enlargement of the prostatic lobes can be
assessed. It can also exclude presence of
a urethral stricture. Cystoscopy should
always be performed particularly when
prostatectomy is performed through ret
ropubic route.
(i) Bladder changes like trabe-
culation, presence of diverticulum or sto
nes may be detected. It also excludes pres
ence of any growth in the bladder.
(ii) The residual urine may be mea
sured.
(iii) Marion’s sign is often positive.
In normal individual, the internal urethral
meatus and ureteric orifices are not vis
ible in the same cystoscopic field. But in
case of prostatic enlargement, this is possible, as the urethral opening is pushed up into the bladder.
(iv) Even an intravesical enlargement may hide one or both ureteric orifices from the cystoscopic view.
6 . ULTRASONOGRAPHY.— This can detect the size of prostate most accurately. This can also indicate
if there is hydronephrosis or hydroureter. In fact due to the progress made in the quality of ultrasound exa
nation over the last few years, the need for excretory urography has been diminished.
7. TRANSRECTAL ULTRASOUND SCANNING.— This imaging technique offers accurate estimation
of prostatic size. It is probably more effective in detection of associated early prostatic cancer. If such suspi
cion is not there, it is not required to use routinely. It is used when the level of PSA is high or the surface of
prostate is hard and irregular.
TREATMENT.—
Since benign prostatic hyperplasia is not a progressive disease, there is a good place for conservative
therapy. THE MAIN INDICATIONS FOR OPERATION ARE —
1. Acute retention.— Patients with benign enlargement of prostate often present with acute retention of
urine which compels the patients to seek relief. Postponement of micturition for a considerable time, cold
weather, indulgence to alcoholic liquor etc. precipitate acute retention of urine.
2. Chronic retention.— A residual urine of 200 cc. or more is an indication for operation. Sometimes the
patient remains unaware of the retention, when the bladder has distended upto umbilicus with associated
hydroureter and/or hydronephrosis and a raised blood urea.
3. Prostatism.— Considerable frequency of micturition in day and night, dysuria, delay in starting and
poor stream — all indicate for prostatectomy. It must be understood that frequency alone should not be the
indication for prostatectomy. Nobody knows the natural progression of symptoms in benign enlargement
prostate. But it is certain that it rarely gets worse after 10 years. So a patient who is suffering from this dise
with minor complaints for more than 1 0 years and who have become otherwise very elderly, can be exemp
from operative treatment.
4. Haemorrhage.— Bleeding from engorged venous plexus is not unusual in benign enlargement of pros
tate. Operation is indicated in these cases. Clot retention due to severe bleeding, which cannot be drained
properly by a catheter should undergo immediate prostatectomy.

5. Complications.— When benign enlargement of prostate is associated with other complications, such
diverticulum or stone formation, it should be subjected to prostatectomy.
Among the indications mentioned above, the only vague indication is prostatism. In this, degree of symp
toms should be such that the patient himself requests for relief by operation. This will vary, since one man m
be distressed at micturition three times during the night, whereas another may not be particularly inconve
nienced by nocturia of six times.
A. CONSERVATIVE MEASURES.—
(i) Regular prostatic massages may combat prostatic congestion.
(ii) To protect vesfcal tone the patient should be cautioned against excessive intake of fluid in a short
period of time. Similarly alcohol should be forbidden due to its diuretic effect. Rapid distension of the bladde
may cause the hypertrophic muscles to lose tone and may lead to exacerbation of symptoms or even acute
retention. The patient should void as soon as he feels the urge to do so, thus preventing the bladder from bein
overdistended. Fluid intake should be limited in the evening. Propantheline may be used to get rid of irritativ
symptoms.
(iii) Use of antiandrogen therapy — oestrogens or orchidectomy may have beneficial effect, but the cost
to the patient is too much in the form of impotence.
(iv) Testosterone, if given to these cases, has produced improvement in the obstructive symptoms by
increasing vesical tone. Carcinoma of the prostate must be excluded as androgen therapy will hasten its grow
(v) The pharmacological management of benign prostatic hyperplasia is now very much discussed. The
drugs, which have got the beneficial effect on this condition, are mentioned below.
Since two major tissue components of the prostate — stroma and epithelium — have potentially differen
susceptibility to drug therapies (antiandrogens and 5-alpha-reductase inhibitors act mainly on epithelium;
whereas alpha-blockers, aromatase inhibitors and antioestrogens affect largely the stomal component of be
nign hypertrophy of the prostate) there is a good theoretical basis for testing combination therapies in this
disease. Cyproterone acetate is a synthetic antiandrogen with additional progestational activity, which has
been shown to inhibit prostatic growth in experimental animals. In benign hypertrophy this drug has shown
improve urinary flow and to alleviate the symptoms of bladder outflow obstruction. Flutamide is a non-stero
dal antiandrogen which is effective orally and is metabolished in the body to hydroxylated derivative that
competes directly with both testosterone and DHT (Dihydrotestosterone) for androgen binding sites. In a
study where flutamide is used in patients with benign hypertrophy, after 3 months there was 25% reduction
prostate volumes as measured by transrectal ultrasonography. LHRH analogues are now available, which act
by transiently stimulating and then blocking pituitary receptors controlling the secretion of LH, thereby redu
ing testicular androgen secretion to castrate levels. It has shown that 30% prostatic volume reduction in pa
tients with benign hypertrophy has been reported after treating with either LHRH analogue or cyproterone
acetate. Very recently the 5-alpha-reductase inhibitors which inhibit the conversion of testosterone to DHT
which is considered to be causing hyperplasia of prostate alongwith the local peptide growth factors are intro
duced in this disease. These drugs are taken for a year. One can expect a shrinkage of 25% of the prostate
gland. Both these groups of drugs have almost similar effect in improvement of symptoms, though the forme
group is quicker in action, though have more side effects. Only one drug in this group — Proscar (Finasteride
has been extensively tried in clinical evaluation in benign hypertrophy cases. This drug has been used at a
dosage of 5 mg/day. Suppression of DHT was well maintained and prostatic shrinkage was evident in the ra
of 20%. A number of studies have confirmed that phenoxybenzamin, a combined alpha-1 and alpha-2-
adrenoreceptor blocker, reduces prostatic urethral pressure profile and significantly improves both symptom
of prostatism and urinary flow rates. However side effects e.g. orthostatic hypotension, dizziness, tiredness h
led to discontinuation of therapy. Another alpha-1 selective adrenoreceptor blocker prazosin, has been used i
hypertrophic prostate in the dose of 2 mg/bd for 4 weeks. Both improvement of symptoms and enhanced
uroflow have been noticed. Another second generation alpha-blocker, doxazosin in a dose of 1 mg/day in
creasing to 4 mg/day, has shown improvement of symptoms and uroflow. Aromatase inhibitors and antioes
have also been used in this condition. The best known and widely used aromatase inhibitors are
aminoglutethimide and ketoconazole. However use of these drugs have led to certain bad side effects like
lassitude, depression and gynaecomastia. Perhaps a more logical approach is to block the effect of oestroge
the level of the prostate by means of antioestrogen therapy (an oestrogen receptor antagonist). Tamoxifen i
the best in this group, though its use in the dose of 80 mg/day for 4 weeks demonstrated no useful effect. M
be that this treatment is too short a period to detect an effect on the prostate. Recently a new antioestrogen
183720, which is a more potent antioestrogen than tamoxifen has been used, but it seems that it becomes m
useful if used in combination with a 5-alpha-reductase inhibitor e.g. finasteride.
(vi) In aetiology it has been discussed that Finasteride, a 5 a-Reductase inhibitor is on trial for this
disease. The dose recommended is 5 mg per day for 6 months.
(vii) A neurotransmitter drug has been used which blocks a adrenergic receptor — a adrenergic blocker
This is also under trial. Probably it relaxes the internal sphincter for better drainage of the bladder.
(viii) The drug Speman has also been used with some success.
B. SURGERY—
The indications for surgery have already been narrated. The operation which is performed to cure this
condition is prostatectomy. The term ‘prostatectomy’ is a misnomer, as it is not excision of whole of prostate
but enucleation of the nodular hyperplastic prostatic tissue, keeping intact the surrounding surgical capsul
the prostate, which is nothing but the compressed peripheral glandular tissue of the prostate.
A word of caution is probably of great importance at this stage before advising surgery to a patient. He
must be made aware of the facts that a few complications may occur later after operation —
1. The success rate is more in case of patients with acute or chronic retention. Patients with mild symp
toms only be benefited in 65% of cases in comparison to more than 90% of cases of the previous group. So
case selection is important and the symptoms should be severe enough to ask for surgery.
2. Patients may suffer from erectile impotence in 5% of cases.
3. Retrograde ejaculation occurs in about 50% of cases following prostatectomy.
4. Incontinence is often complained of following prostatectomy, as the internal urethral sphincter is oft
damaged. This incontinence is usually temporary. Care must be taken to avoid incontinence which is descr
later in this section under the heading of ‘Postoperative Complications’.
5. The risk of reoperation after transurethral resection is about 10% to 15% within 10 years following
prostatectomy.
6 . Severe sepsis is found in about 5% of cases and severe haematuria in about 3% of cases.
7. Death after transurethral prostatectomy is almost nil (less than 0.5%).
Four main types of prostatectomy are commonly practised. These are : I. Suprapubic prostatectomy, II.
Retropubic prostatectomy, III. Transurethral prostatectomy and IV. Perineal prostatectomy.
I. Suprapubic prostatectomy.—
The scientific basis of this operation is that there is a plane of cleavage between the adenomatous part o
the gland and the false capsule composed of compressed normal prostate. It is through this plane of cleava
that the gland is enucleated leaving behind false capsule, which contracts and forms a scaffold on which th
new prostatic urethra is regenerated, the epithelial lining originates from the mucosa above and below. In
operation, the prostate is approached through the bladder by a suprapubic incision.
Preliminary vasectomy.— Previously this was done as a routine before prostatectomy to prevent spread of infection
from the prostatic bed to the epididymis. With the advent of various spectrum antibiotics and with the improvement in
aseptic procedure, this operation is rarely required nowadays. A small incision is made over each superficial inguinal ring.
The vas deferens is isolated from the spermatic cord, a loop of vas is brought out, a pair of artery forceps is applied to each
end of the loop of vas. The portion of the loop between the two pairs of the artery forceps is resected and the ends are
ligated with silk or catgut.
POSITION.— The patient is placed in Trendelenburg position and the surgeon stands on the left side of the patient.
The towels are so placed that the penis is available and the surgeon will also get an access to the rectum.
INCISION.— Pfannenstiel incision is made, which is nothing but a curved incision just above the pubic crest start
ing from the lateral margin of one rectus to the lateral margin of the other rectus muscle.
TECHNIQUE OF OPERATION.— The incision is gradually deepened through the skin and the two layers of subcu
taneous tissue. While doing that, one will come across the superficial epigastric vessels which are divided between liga
tures. The anterior rectus sheath is incised transversely along the length of the incision and the margins are gradually
retracted upwards and downwards as far as possible by blunt and sharp dissections. The two recti muscles and the pyrami-
dalis are retracted apart from each other. Fascia transversalis is incised. The extraperitoneal fatty tissue is exposed. This fat
is gradually wiped upwards with a piece of gauze till the anterior surface of the distended bladder will be under view. Care
must be taken not to open the peritoneum during this process. The anterior wall of the bladder is identified by the presence
of longitudinal muscles and veins running along its surface. The bladder is opened in a similar manner as has been
described under the heading of suprapubic cystostomy. The opening in the bladder is made in the upper part. The size and
consistency of the prostatic gland are determined. Presence of calculi and diverticulum are excluded. A self-retaining
retractor is applied to widely expose the interior of the bladder.
Enucleation — The surgeon introduces his index finger for a short distance into the cleft of the urethra and then the
anterior commissure (through which the two lateral lobes are joined) is split by forward pressure ofthe finger to reach the
plane of cleavage between the glandular enlargement and the false capsule. The finger is now swept round the prostate till
the intra-vesical part of the gland has been freed round its circumference. The gland is now taken out by tearing across the
urethra from before backwards. According to the disposition of this plane, the tear takes place in an oblique direction
upwards and backwards to a point on the posterior wall above the verumontanum, so that the posterior lobe and the
ejaculatory ducts are left undisturbed. If the enucleation is not done through the plane of cleavage, considerable venous
haemorrhage may be encountered and seminal vesicles or the ejaculatory ducts may run the risk of being damaged.
Sometimes it may not be possible to enucleate the gland completely particularly on the posterior aspect of the gland
due to localised fibrosis, hi such cases, the enucleation is completed by diathermy dissection under direct vision.
Sometimes, particularly in obese patients, it may be difficult to push the index finger round the circumference to
enucleate the enlarged prostate. In that case, the index finger of the left hand may be introduced into the rectum and is used
to push the gland forward to facilitate enucleation by the right hand.
Arrest of haemorrhage.— After enucleation of the prostate has been performed, the prostatic bed is packed tightly
with a roller gauze and left in situ for about 5 minutes. Self-retaining retractors are reinserted and the bladder is dried out
by suction. The pack in the prostatic bed is now slowly withdrawn. The cavity is inspected for spurting vessels. They are
secured by long artery forceps and electro-coagulated. This is continued till all major vessels have been secured and the
haemorrhage is reduced to slight oozing. Any tags of mucosa or remnant of the prostatic tissue within the cavity are
removed. A Foley’s catheter is passed through the urethra and its balloon is inflated and inserted comfortably within the
prostatic bed. This will exert pressure upon the prostatic bed and thus will control haemorrhage.
Harris' technique is to introduce lateral stitches inserted with his boomerang needle to control the prostatic branches
of the inferior vesical artery. He also closed the raw areas by stitching the mucosa of the posterior lip of the internal meatus
to the urethral mucosa. He also narrowed the cavity in front of the urethral catheter to control haemorrhage. Now-a-days
the use of boomerang needle is becoming obsolete. But it is a good practice to insert stitches at the free lateral angles of the
prostatic bed to control the prostatic arteries.
Trigonectomy.— After enucleation of the prostate, it is frequently found that the mucosa of the bladder neck together
with submusculature forms a prominent shelf overhanging the prostatic cavity. This shelf will share in the subsequent
contraction of the prostatic bed and will cause obstruction. To avoid such a complication, a wedge of tissue would be cut
with diathermy electrode from the posterior aspect of the bladder neck, which forms the shelf. The apex of the wedge
extends upto a point between the two ureteric orifices. While performing trigonectomy, care must be taken to save the two
ureters which should be catheterised. It is better to do this wedge resection before attempting to arrest haemorrhage from
the prostatic bed as it will facilitate proper inspection of the bed and identification of the bleeding points. Trigonectomy
itself may cause a little bleeding but one or two such bleeding vessels will require ligation or diathermy coagulation.
Suprapubic drainage.— If haemorrhage has been adequately controlled and infection is absent, the bladder may
safely be closed. The Foley’s indwelling urethral catheter acts as drainage of the bladder. The closure of the bladder
definitely shortens the convalescent period but the surgeon must have adequate experience to be satisfied with the effec
tive arrest of haemorrhage. Otherwise clot retention will give tremendous trouble in the early postoperative period. If in
doubt, the bladder is closed around a suprapubic drainage, at the same time there will be Foley’s indwelling urethral
catheter inside the prostatic bed. 100 ml of 5% citrate solution is pushed into the bladder through the urethral catheter and
left inside by spigotting the two catheters. The abdominal wound is closed with a drainage in the retropubic space.
POSTOPERATIVE TREATMENT.— After suprapubic drainage, the urethral catheter is connected with a drip of
sterile water and the suprapubic catheter is connected to a bottle hanging outside the bed. By this, the bladder is washed
out and hardly gives any chance for clot retention to occur. This also minimises sepsis. The retropubic drainage is removed
after 48 hours. When the fluid coming out is absolutely free from blood-stain, the cystostomy tube can be removed after 4
days. The urethral catheter is kept for about 10 days. For the last 6 days, suprapubic wound should be free from urine
leakage. If at all urine comes out, one can use surface suction provided with a tube which is pushed through the suprapubic
opening upto the surface of the bladder. Just after removal of the urethral catheter, partial lack of control is expected for a
week or so. Gradually this goes off and normal micturition starts.
When there is no suprapubic drainage, the Foley’s catheter should have three ends — one end to inflate the balloon,
the second one for drainage and the third one to introduce sterile water through drip system for continuous bladder wash.
In this case the convalescent period is less and when the fluid coming out is absolutely free from blood, the catheter can be
removed from 5th to 8th day.
An intravenous drip, which was introduced preoperatively for transfusion of blood, is still continued with 5% Dex
trose solution for 1 day or so. The patient will start taking fluid by mouth in the evening. It is of no use increasing the load
to the heart of an old man by increasing infusion of fluid. The patient is allowed to drink freely, so that there will be more
urine and less chance of postoperative infection. It is a good practice to do a routine haematological examination to see
that the patient’s Hb is upto the standard. Urine examination should be carried out for culture and sensitivity test and he is
given the right antibiotic.
II. Retropubic prostatectomy.— Millin described this operation in 1945.
Position of the patient and the incision are same as those of the suprapubic prostatectomy.
TECHNIQUE OF OPERATION.— In this operation the prostate is approached through the retropubic space in front
of the bladder, instead of going through the bladder as done in suprapubic prostatectomy.
After the anterior wall of the bladder has been exposed, the bladder is emptied. A self-retaining retractor is placed in
position, the lateral blades of which retract the two recti muscles and the middle blade depresses the bladder which is
protected by a wet mop. This retractor is named after Millin who first performed this operation. With small piece of gauze,
the anterior surface ofthe prostate in the retropubic space is cleared. The veins will be seen running in front of the capsule
of the prostate. The large veins are first sutured between the proposed line of incision. With a cutting diathermy, a trans
verse incision is made through the fascial sheath, the fibrous capsule and the surgical capsule of the prostate about 2 cm
below its junction with the bladder. As soon as the adenoma is reached, it will be visualised by its rather whitish colour.
The two margins of the incision are now slightly undermined upwards and downwards. A finger is introduced through this
incision to enucleate the adenomatous mass. The urethra and the mucosal cuff connecting it with the bladder are divided
to bring the adenomatous mass out.
Arrest of haemorrhage.— A roller gauze is packed in the prostatic bed and left there for about 5 minutes. The packing
is now gently withdrawn and the bleeding points are electrocoagulated. It is a good practice to insert two stitches one on
each angle of the prostatic bed to control the prostatic branches of the inferior vesical artery. Remaining nodules of the
prostatic tissue or loose tags of the capsule or the mucosa are removed. A Foley’s catheter is now introduced per urethra
to the prostatic bed. The bulb of the catheter is inflated. A final inspection is made to be sure that the haemorrhage has been
controlled properly.
The incision in the false capsule is now closed with a continuous catgut suture. This suture must be placed closely, so
that it will not only arrest haemorrhage but also will prevent leakage of urine.
Closure of wounds.— A corrugated rubber sheet drain is placed near the suture line. The abdominal wound is closed
round this drainage. The bladder is irrigated a few times with sterile water and then 100 cc of 5% citrate solution is pushed
through the urethral catheter and the catheter is spigotted.
POSTOPERATIVE TREATMENT.— The drain at the retropubic space is removed after 48 hours. It is a good
practice to use Foley’s catheter with 3 ends. One end is used to inflate the bulb of the catheter. The 2nd end is used to
irrigate the bladder, while the 3rd end is used for drainage. The 2nd end is joined to a drip set containing sterile water and
the 3rd end is joined to a polythene bag to collect urine outside the bed. This continuous bladder wash is continued till the
urine collected in the bag becomes clear. At this time the continuous bladder wash is stopped and the catheter is kept for
4 to 5 days after operation, after which it is removed. Millin advised that the catheter could be removed on the 3rd
postoperative day unless there was any contraindication. The suprapubic wound generally heals in 10 to 15 days time.
THE ADVANTAGES OF RETROPUBIC PROSTATECTOMY.— (i) The main advantage, claimed by Millin, was
that it provides a direct access to the prostatic cavity to enable the surgeon to deal with haemorrhage effectively, (ii)
Postoperative bleeding, if at all takes place, will not be inside the bladder but will be in the retropubic space. Blood can
easily come out from this space through the drainage opening, (iii) Probably the most important advantage is its relatively
short convalescent period. So the patient becomes ambulant quickly.
The only disadvantage of this operation is that the interior of the bladder is not exposed, so presence of stone,
diverticulum or neoplasm may be missed. It is always advisable to perform cystoscopy just before retropubic prostatec
tomy.
III. Transurethral prostatectomy.—

INDICATIONS.— (i) Prostatectomy through this route is indicated when the patient presents with urinary obstruc
tion, but there is no gross enlargement of the gland, particularly the lateral lobes, (ii) This method is ideal for small fibrous
prostate, (iii) middle lobe enlargement, (iv) small adenomatous prostate and (v) carcinoma.
The resection is carried out under direct vision either by means of a wire loop diathermy or by a circular punch. The
instrument is of large calibre and meatotomy or urethral dilatation may be required before introduction. It goes without
saying that it is the operation for specialists and the general surgeons hardly venture to perform this operation.
PUNCH PROSTATECTOMY.— A ‘cold punch’, which is a direct vision lenseless cystoscope, is used to resect
obstructing prostatic tissue in punches. The instrument has a sheath, which has a curved beak bearing a lamp to illuminate
the urethra and the bladder. On the opposite side of the sheath, there is a large gap just close to the bend of the sheath.
Within the sheath, there is a tubular knife, which moves to and fro, instead of a telescope.
The sheath has an obturator to facilitate its introduction into the bladder. After introduction, the obturator is taken out.
Now under direct vision, the sheath is gradually withdrawn till an adenomatous mass of the prostate protrudes through the
gap of the sheath. At this time, the tubular knife is inserted and pressed home with a punching movement to shear off the
projecting tissue. The knife is partially withdrawn and the sheath is moved slightly, so that another mass of glandular
tissue projects through the gap, which is again sheared off by the tubular knife.
This process continues till the whole of the adenomatous prostate or fibrous prostate, which is causing obstruction, is
removed. The cuts are made in an upward direction, away from the verumontanum, so external sphincter is not damaged.
The irrigation is arranged to remove the tissues by presence of fluid. The sheath has a separate channel to pass a
diathermy electrode to arrest bleeding. This ‘cold punch’ technique, according to its advocates, has the advantage that the
cutting is made with a sharp knife, instead of the diathermy current, so the questions of devitalisation of the prostatic tissue
and sepsis do not arise.
DIATHERMY LOOP RESECTION.— The instrument used in this technique was first designed by McCarthy, which
was of course subsequently slightly modified by different urologists. The instrument is called ‘prostatic electrotome’ of
McCarthy. Like the previous instrument, it has got a sheath but unlike the previous one, the sheath is straight. The sheath
has got a telescope within which it supports a diathermy electrode, consisting of a loop of tungsten wire. A ball electrode
can be substituted for the wire loop to coagulate bleeding vessels.
The earlier instrument designed by McCarthy has been replaced by single-hand-operated instrument used under video
control. Further advancement has been made by the development of rigid lens system by Prof. Harold Hopkins. It must be
remembered that all patients undergoing this treatment should receive broad-spectrum prophylactic antibiotics with
amoxicillin plus cefuroxime intravenously from the time of start of anaesthesia.
Like the previous operation, the sheath with the obturator in position, is introduced into the bladder. After this, the
obturator is taken out and the telescope with the electrode wire loop fully retracted, is introduced into the sheath.
The loop electrode is first pushed inside the bladder and then retracted till it engages the upper limit of the obstructing prosta
tissue. The current is then switched on and the loop is slowly retracted to shear off a strip of the gland. Strips of tissue are cut fro
the bladder neck down to the level of verumontenum. Cutting is performed by a high frequency diathermy current which is applie
to the loop of the resectoscope. The bleeding points are coagulated. If the verumontenum is kept as a guide to the most distal p
of the resection, there is no chance of damage to the external sphincter. The ‘chips’ of prostate are removed from the bladder by
evacuator. At the end of the procedure careful haemostasis should be maintained. In case of small prostate or bladder neck sten
it is better to divide the bladder neck and prostatic urethra with a diathermy electrode. The cutting is usually commenced anterio
in the midline and then a succession of cuts are continued round the circumference of the prostatic urethra till its starting point is
reached. It cannot be over emphasised that the resection should be confined to the part of the gland above the level of the verum
tanum. So long as the resection continues, continuous irrigation is maintained to keep the field of vision clear and not obscured
haemorrhage. Now-a-days often 1.5% isotonic glycine is used for irrigation to prevent hyponatraemia, which may be caused by
continuous irrigation with sterile water. Recent introduction of continuous flow resectoscopes makes evacuation of the prostatic
‘chips’ easy and swift particularly in experienced hands. The bleeding points are dealt with button electrode.
After the operation is over, the bladder is drained with a three way self-retaining catheter. The bladder is also irrigated
by this catheter with isotonic saline. Irrigation is continued till the outflow is pale pink or almost clear. The catheter is kept
for continuous drainage for at least 2 days. The catheter is usually removed on the third postoperative day.
Postoperatively, care should be taken against clot retention. Continuous bladder wash may be instilled or repeated irriga
tion of the bladder can be carried out. The catheter is withdrawn after 2 days. The patient becomes ambulant since then.
IV. Perineal Prostatectomy.—
This operation has never attained any popularity in Great Britain or in India. The operation was first advocated by
Young and is followed in certain institutions in USA.
A metal bougie is passed through the urethra. An inverted U-shaped incision is made with its centre 4 cm in front of the
anus and extending to a point 2.5 cm in front of the ischial tuberosities. The incision is deepened through the skin and
subcutaneous tissue till the anterior margin of the anal sphincter is exposed. The incision is further deepened in front of the
anal sphincter and behind the transverse perineal muscles and the bulb of the urethra. The rectourethralis muscle is divided an
the rectum is pushed backwards to expose the membranous part of the urethra and the apex of the prostate. The dissection is
further continued through the layers of the fascia of denonvilliers. This exposes the fascial sheath covering the posterior
surface of the prostate. A transverse incision is made through the true and the false capsules of the prostate 2 cm above its ap
The capsular flaps are separated. The bougie is now removed and a Young’s retractor is introduced to retract the margins of th
capsule. The adenomatous part of the prostate is now enucleated and the mucosal connections with the bladder and with the
urethra are divided. The capsular flaps are sutured together and the perineal wound is closed around drainage.
Postoperative complications.—
1. HAEMORRHAGE.— This is most important and most serious immediate complication after prostatectomy. Reaction
ary haemorrhage is quite troublesome after any type of prostatectomy. If the blood has not been adequately washed out from
the bladder there is ‘chance of clot retention’ which may result from blockage of the catheter or the drainage tube by blood clot.
Instillation of citrate solution and continuous bladder wash have gone a long distance to prevent this complication. Sometimes
injection of glycerin or pepsin to dissolve the blood clot may be indicated. If this bleeding appears to be excessive, traction to
the Foley catheter to hold the balloon tightly against the prostatic bed may be recommended. Only rarely it may be necessary
to return the patient to the operation theatre for evacuation of blood clots and to resuture the prostatic bed to stop haemorrhage
Secondary haemorrhage may occur around the 10th postoperative day. The cause is usually urinary infection or over
exertion of the patient. The patient should immediately go for bed rest, he is encouraged high fluid intake and a suitable broad
spectrum antibiotic is started. If clot retention occurs, a catheter will have to be passed and the bladder wash is started.
2. INFECTION.— Slight infection after this type of operation is unavoidable owing to the presence of large raw
surface in the prostatic bed. But serious degree of sepsis is uncommon unless the bladder was previously infected. Urine
should always be sent for culture and sensitivity test to find out the proper antibiotic to be administered. Continuous
bladder wash does prevent sepsis but one must be sure that he is using a real sterile water. The urine should be made a bit
acidic, so that the organisms find difficult to survive in this medium.
3. EPIDIDYMITIS.— Not infrequently this complication was met with previously and so some surgeons prefer to
perform bilateral division of the vas deferens as a routine procedure before prostatectomy.
4. RENAL FAILURE.— One must ascertain the renal function status before doing prostatectomy. It is fairly a major
operation and if the kidneys are already not functioning properly due to back pressure, they are liable to fail after opera
tion. Infusion of fluid should be given very cautiously, since in renal failure excessive fluid intake will simply aggravate
the condition.
5. CARDIAC AND RESPIRATORY COMPLICATIONS.— As the patients are fairly old. these complications are liable
to occur in early postoperative days. Preoperatively, the condition of the heart and the lungs should be assessed properly to
prevent this complication. Once this complication occurs, it has to be treated accordingly, preferably by the physicians.
6. STRICTURE OF THE BLADDER NECK.— After the removal of the prostatic adenoma, there always remains a
shelf of tissue at the bladder neck. This takes part in the generalised contraction of the prostatic bed and produces late
stricture. This complication is prevented by doing trigonectomy.
7. RETROGRADE EJACULATION AND IMPOTENCE.— All patients having prostatectomy may suffer from this
complication in various degrees. This occurs when the bladder neck is made incompetent. In a few patients this may
disturb their normal lives.
8. STRICTURE OF THE URETHRA.— This may occur secondary to clumsy instrumentation, after use of a large
catheter or using resectoscope for too long a period. These strictures usually occur either in the bulb of the urethra or just
inside the external meatus. In early cases simple bouginage may cure the condition. In late cases it may be necessary to cut
the dense fibrotic stricture with optical urethrotome.
9. OSTEITIS PUBIS.— This is another late complication of the operation and this is due to the spread of infection
from the retropubic space. When the bony changes have already taken place, the posterior surface of the symphysis pubis
is incised and the necrotic cartilage and bone are curetted out. Penicillin and Streptomycin are instilled into the bone. The
wound is closed with a corrugated drain.
The particular complications which may occur after transurethral resection of prostate are :—
1. PERFORATION.— Perforation of the bladder or the prostatic capsule may occur at the time of TUR (transurethral
resection of prostate). This usually occurs when the field of vision has been obscured by heavy haemorrhage. This is particu
larly come across in cases of large juicy prostate. An attempt should be made to achieve haemostasis and to abandon the
operation. A second attempt should be made when bleeding has completely subsided and the patient is fit for operation.
2. INCONTINENCE.— Continence is maintained by two sphincters — internal urethral sphincter and external ure
thral sphincter. As the internal urethral sphincter has been damaged by the pathological process of the benign hypertro
phy ofthe prostate or by the operation either open prostatectomy or transurethral prostatectomy, all efforts should be made
to preserve the external sphincter. During transurethral surgery, if resection is limited to above the verumontanum, injury
to external sphincter is impossible. If transurethral resection is extended downwards beyond the verumontanum, there is
a chance of injuring the external sphincter. The outcome is disastrous. The use of powerful anticholinergic agents or
imipramine may be helpful. Sometimes urodynamic investigations have shown that not all of these patients have sphinc
ters damaged.
Newer techniques.— Two techniques have been used recently for prostatectomy which deserve mention,
though these are still in experimental stage.
1. LASER TREATMENT.— Two methods have been used in this treatment — (i) a noncontact probe
method and (ii) contact side-firing laser.
In the first method the probe is used to vaporize the prostatic tissue under direct vision. The advantage
this technique is that the bleeding is minimal and bladder neck incision can be carried out. For small prostat
gland this technique can be used as a day-case.
In the second method lower energy is used in laser with greater penetration. This causes necrosis of the
prostate gland to a varying thickness. Such energy can be applied transurethrally under direct vision or
transurethrally with the help of ultrasound. The necrotic tissues slough out and a suprapubic catheter is kep
several weeks for this purpose. This treatment can also be performed as a day-case or a short-stay procedure
However general anaesthesia is necessary.
2. MICROWAVE TREATMENT.— Microwave is focused within the prostate to destroy prostatic tissue.
Such destruction depends on the heat produced with the microwave. In the first generation machines the he
produced was between 40° C and 45° C. But newer machines can provide temperature more than 50° C and
destroy more areas of prostate to improve the obstructive symptoms. The microwave source may be within
rectum or within the urethra. Recent machines use the intraurethral route.
Laser treatment is however better than microwave treatment in improving the symptoms of the patients
Intraurethral stents — are now being used in the management of retention who are grossly unfit for
surgery.
Management of retention of urine with enlarged prostate.— Some 30% of patients, who come for
prostatectomy, do so because of acute or chronic retention of urine. The treatment for these cases, which is
recommended nowadays, is immediate one-stage prostatectomy for patients with good general condition
without clinical signs of infection or renal insufficiency. Those patients, in whom immediate prostatectomy
cannot be performed, should have preliminary drainage with indwelling urethral catheter followed within 7
10 days by prostatectomy (semiurgent prostatectomy). Suprapubic cystostomy only is reserved for very poo
risk patients.
Preliminary suprapubic cystostomy, which was often practised previously, not only introduces infection
into the bladder but makes the prostatectomy more difficult.
Of the two types of treatment, which are advocated nowadays, preliminary drainage by indwelling ure
thral catheter finds greater acceptance. It allows congestion of the prostate and bladder to subside. During th
7 days period, the surgeon will do all necessary investigations and at the same time will improve the patient
general conditions. He should also lower the patient’s blood urea level. With antibiotic cover, the danger of
infection is seldom serious.
CARCINOMA OF THE PROSTATE

Carcinoma of the prostate is the 4th most common cause of death from malignant disease in men. It is th
commonest malignant condition in men over the age of 60 years. It increases in frequency there after and
probably afflicting 25% of men in the 8 th decade. In a series of autopsies in men over 80 years of age 2/3rds
had prostatic cancer.
Aetiology.—
The disease is rare in Orientals, but more common in blacks. It is also common among the whites in New
Zealand and Scandinavian countries. It is rare in Japan, though it is quite common in American Negroes in
whom it is more aggressive.

The true cause of prostatic carcinoma is not definitely known, but its growth is strikingly influenced b
sex hormones. Administration of androgens usually increases the rate of growth of this tumour and increa
the acid phosphatase level of the serum. Oestrogen therapy or orchidectomy slows down the growth of th
tumours and maintains the amount of acid phosphatase in the blood at a normal level. Determination of th
amount of acid phosphatase in the serum is therefore an index of the presence and aggressiveness of the
tumour.
PATHOLOGY.—
SITE.— Carcinoma commences in that portion of the gland, which is free from the ordinary benign
hyperplasia, namely the posterior lobe. Carcinoma arises in atrophic, not hypertrophic areas and in particu
in posterior lobe compressed by nodular hyperplasia. It is obvious that a prostatectomy, which leaves mos
the posterior lobe, is no guarranty against subsequent development of carcinoma in that lobe. It must be
remembered that a few carcinomas may be found within the hyperplastic benign prostatic lobes. These tum
are usually very small and are called ‘occult’ or ‘academic’ cancers. These are often completely removed b
intracapsular enucleation of the enlarged gland.
MACROSCOPIC FEATURES.— The chief characteristic feature of this growth is its consistency,
which is hard and dense comparable to that of a scirrhous carcinoma of the breast. When the tumour is cu
imparts the same gritty sensation to the knife as is felt in scirrhous carcinoma. The surface is irregular, wit
lobulation. So the hard consistency, irregular surface and lack of lobulation are the characteristic features o
carcinoma of the prostate.
MICROSCOPIC FEATURES.— As the prostate is mainly a glandular structure consisting of ducts
and acini, so the microscopic pattern of the carcinoma of the prostate is an adenocarcinoma. It shows varyin
degrees of differentiation. When the tumour is anaplastic, the diagnosis is easy, but when it is differentiate
is difficult to distinguish this lesion from benign hyperplasia. The prostatic glands are surrounded by a lay
myoepithelial cells. The first carcinomatous change is the loss of this layer, so that the glands seem to lie
adjacent to each other with no stroma separating them. Mitoses are infrequent, and their absence is no evi
of the benign nature of the lesion. Invasion of the perineural sheaths may be seen even in a fully differenti
tumour. So loss of normal configuration is more important than the appearance of individual cells. Conflu
of acini, infiltration ofthe stroma, the perineural lymphatics and the capsules are the characteristic features
this condition.
A few transitional cell carcinomas may arise from the epithelium of the ducts. These are highly malignan
and usually cause osteolytic bone metastases which are usually hormonal independent. These tumours re
poorly to radical surgery, so radiation therapy is indicated.
Squamous cell carcinoma is extremely rare.
HISTOPATHOLOGICAL GRADING.—
GX — grade cannot be assessed.
GO — no evidence of anaplasia.
G1 — low grade malignancy.
G2 — medium grade malignancy.
G3 — high grade malignancy.
Spread.—
1. Local spread.— The growth commences as a rule in the posterior lobe. By direct spread it gradua
involves the lateral lobes. It cannot extend backwards due to the presence of the strong fascia ofDenonvill
So the lesion tends to grow upwards along the line of the ejaculatory ducts and emerge at the upper borde
the prostate to involve the seminal vesicles. By careful rectal examination one may readily feel such extens
Later on the neck of the bladder and gradually the base is involved. Invasion of the trigone with ulceration
usually a later occurrence. Further upwards extension may obstruct the lower end of one or both ureters.
the former will cause hydronephrosis and hydroureter, the .latter may give rise to anuria. In very late case
rectum may become stenosed by infiltrating growth around it. But the mucosa of the rectum remains
unaffected.
2. Lymphatic spread.— Lymphatic spread occurs by either permeation or embolism. Either of the two
groups of lymphatics may be involved — (i) growth may involve lymphatics which pass along the sides of the
rectum to reach the lymph nodes along the internal iliac vein, (ii) Growth may involve the lymphatics which
pass over the seminal vesicles and follow the vas deferens to drain into the external iliac lymph nodes. From
both internal iliac group and external iliac group of lymph nodes, the growth reaches the retroperitoneal lymp
nodes, later on the mediastinal lymph nodes and occasionally the left supraclavicular lymph nodes (Virchow’s
nodes) may become involved.
There is an abundant nerve supply in and around the prostate and these nerves are accompanied by
lymphatics. Lymphatic permeation and lymphatic embolism are common by this route. When perineural
lymphatics are involved, patient complains of pain.
3. Blood spread.— Spread to distant parts may occur through the blood stream. Cancer prostate is the
most common site of primary neoplasm for skeletal metastasis, which is followed by the cancers of the breasts
the kidney, the bronchial tree and the thyroid gland in that order of frequency. The tumour embolus penetrate
into the periprostatic venous plexus from where the tumour cells pass along the vertebral system of veins
during coughing or sneezing. Through these veins the tumour cells easily reach the pelvis and vertebral bodie
of the lower lumbar vertebrae. This has been demonstrated by Batson. The bones which are usually involved
according to frequency are the pelvis, lower lumbar vertebrae, thoracic vertebrae, heads of the femur, the ribs,
the humerus, the skull and the clavicle. It should be remembered that bone metastasis in case of prostatic
carcinoma is usually osteosclerotic in nature in contradistinction to the carcinomas in other parts of the body
which cause osteolytic bone metastasis. Only occasionally the transitional cell carcinoma of the prostate may
produce osteolytic bone metastasis.
Lungs and liver metastases are rare in prostatic cancer due to spread by blood stream.
The single main presenting symptom peculiar to cancer of the prostate is obstruction to flow of urine
causing acute or chronic retention of the urine. A cancer prostate may present in various types.
TYPE I.— Occult type, which means that at the time of routine histological examination of the tissue
removed by prostatectomy shows presence of carcinoma.
TYPE II.— The patient presents with symptoms of prostatism, similar to those described in benign
prostatic enlargement. The only difference is the short history (upto 6 months) in case of carcinoma of the
prostate.
TYPE III.— Patients present with acute or chronic retention, on rectal examination hard consistency
and irregular surface in prostate are felt.
TYPE IV.— Symptoms due to metastasis.— One out of 20 patients may have their first symptoms from
metastasis. Pain in the lumbosacral region which may radiate to the hips or down the legs should arouse
suspicion of malignancy of the prostate. Spontaneous fracture of femur or humerus may occur from carcinoma
of the prostate. Patient may simply present with loss of weight and anaemia. Latter may be due to destruction
of bone marrow by bone metastases. Haematuria may occur late in the course of disease if the bladder or
urethra is invaded. Symptoms of renal insufficiency may be the first symptoms due to obstruction of the ureter
by the primary tumour or compression of the ureters by masses of iliac lymph nodes secondarily involved.
PHYSICAL SIGNS.— Abdominal examination usually reveals no abnormality, except when the patient
presents with retention of urine, when distended bladder can be detected. Similarly ureteral obstruction may
cause hydronephrosis which will be revealed by bimanual palpation of the loin. Careful examination may
reveal nodular liver.
General examination should be performed carefully to exclude anaemia, tenderness in the spine, enlarged
lymph nodes in the abdomen or in the supraclavicular fossa.
Rectal examination is by far the most important examination for the diagnosis of cancer prostate. Cancerous
hard nodules, irregular induration, obliteration of the median sulcus, and non-mobility of the rectal mucosa
over the enlarged prostate suggest carcinoma of the prostate. The differentiating points between benign
73
enlargement of prostate and carcinoma of the prostate as revealed by rectal examination are as follows :—
Benign hyperplasia of prostate Carcinoma prostate

1. Size.— The size may be quite big. i. xhe size is usually not very big.
2. Consistency.— It is firm and elastic. 2. Hard.
3. Surface.— Smooth. 3 Irregular and nodular.
4. The midline sulcus between the two lateral 4 . The sulcus is usually obliterated,
lobes is well felt.
5. The seminal vesicles — feel normal. 5. These may be invaded by the tumour and feel
hard and irregular.
6 . The gap between the enlarged prostate and the 6 . This gap is obliterated by invasion of the
lateral pelvic wall is clear on both sides. cancer.
7. The rectal mucous membrane moves free over 7. The rectal mucous membrane is adherent and
the enlarged prostate. cannot be moved over the prostate.
Clinical staging.—
By bimanual examination under anaesthesia one can clinically assess the extent of the tumour.
TNM system of classification as revised in 1974 :—
The various clinical examinations and special investigations which are performed to clinically stage
tumour and its metastases are as follows :—
T categories.— Clinical examination, urography, endoscopy and biopsy.
N categories.— Clinical examination, lymphography and/or urography.
M categories.— Clinical examination, chest X-ray, bone scan and determination of the acid phosphata
level.
T (PRIMARY TUMOUR) — '
TO — no tumour palpable. This category includes those cases of the incidental finding of cancer in
operative or biopsy specimen.
Tl — tumour is intracapsular surrounded by palpably normal gland.
T2 — tumour is confined to the gland. Smooth nodule may deform the contour but the lateral sulc
the seminal vesicles are not involved.
T3 — the tumour has extended beyond the capsule with or without involvement of the lateral sulc
and/or seminal vesicles.
T4 — the tumour is fixed and had invaded the neighbouring structures.
N — REGIONAL LYMPH NODES —
NO — no evidence of involvement of regional lymph nodes.
N1 — involvement of a single regional lymph node.
N2 — involvement of multiple regional lymph nodes.
N3 — fixed mass of regional lymph nodes.
N4 — involvement of juxta-regional lymph nodes, which are common iliac or para-aortic nodes.
M — DISTANT METASTASIS —
MO — no evidence cf distant metastasis.
Ml — distant metastases present.
Mia — evidence of occult metastases, detected by biochemical and/or other tests.
Mlb — evidence of single metastasis in a single organ.
Mlc — multiple metastases in a single organ.
Mid — multiple metastases in multiple organs.
1. Blood examination— Anaemia is often detected through this examination. This may be secondary to extensive marro
invasion or secondary to renal failure or due to haemorrhage or infection. Blood urea, NPN, serum creatinine should be pe
formed to detect renal function. The PSP may be depressed due to back pressure and renal impairment.
T2 T3 T4
Fig. 59.4.— Shows the clinical stages of prostatic carcinoma. TO — no evidence of a primary cancer.
Tl — tumour nodule in palpably normal gland. T2 — smooth nodule which deforms the contour of the
gland. T3 — the tumour has extended beyond the capsule or has invaded seminal vesicles. T4 — the
tumour is fixed or has invaded the neighbouring structures.
2. Urinalysis.— This should be performed to exclude any infection or haemorrhage.
3. Liver function tests should be performed to exclude any metastasis in the liver.
4. STRAIGHT X-RAY of the abdomen may not give any definite information of the disease itself, but it gives valuable
information as to whether bone metastasis is present or not. The commonest primary malignant lesion which causes osseous
metastasis is carcinoma of prostate. Sclerotic metastasis in the pelvic bones and lumbar vertebrae are quite common in this con
dition. The finding should be differentiated from Paget’s disease of bone. Osteolytic metastases may also be seen in cancer of the
prostate and may coexist with sclerotic ones.
5. EXCRETORY UROGRAPHY is necessary to know (i) whether there is ureteric obstruction due to invasion of the
tumour, (ii) whether there is ureteral obstruction due to metastasis in the lymph nodes or (iii) there is urinary retention.
6. CHEST FILM is necessary to exclude metastasis in the lungs, involvement of hilar lymph nodes and osseous metastasis
in the ribs.
7. ULTRASONOGRAPHY may give information of ureteral obstruction which may cause hydronephrosis or hydroureter.
Transrectal ultrasonography is now often used particularly in screening to detect early carcinoma of the prostate. This can
be compared with screening mammography for breast cancer. This technique is considered to be the best method for staging of
cancer prostate. But it must be confessed that its efficacy is less than mammography in detecting prostatic cancer.
8. MAGNETIC RESONANCE IMAGING (MRI).— This investigation is being used mainly in specialised centres for
staging of prostatic cancer. CT is almost incapable in staging prostatic tumours unless the disease is grossly advanced. On T2-
weighted MRI, tumours of the prostate appear as areas of comparatively low signal in comparison to the high signal normal
prostate. Small tumours arising in the central zone can be difficult to identify, as tumour signal in this area is often close 'O that
ofthe normal tissues. However advanced spread beyond the gland is often best identified on a Tl-weighted image, where tumour
fat contrast is accentuated. Following injection of intravenous contrast medium prostatic tumours enhance and this may be
valuable for defining both the intraprostatic extent of the tumour and spread beyond die gland. Spread of tumour into the seminal
vesicle is also clearly demonstrated. Accuracy of MRI for staging prostate cancer is about 80% to 90%. It is only rivalled by
transrectal ultrasound in this examination.
Another important application of MRI in prostatic cancer is the diagnosis of spinal cord compression due to metastatic bone
involvement. MRI avoids the need for myelography and provides better information. It also indicates the small extradural lesions,
which may be treated before neurological damage has occurred.
9. BONE SCAN.— This is much more effective than simple

straight X-ray. This is performed by injection of "Tc (techne
tium) and the isotope is then monitored using a gamma camera.
The isotopes will conglomerate in an area of increased blood
flow producing ‘hot’ areas. Such hot areas may be found in os
teomyelitis, healing fracture, arthropathies (particularly osteoar
thritis) and Paget’s disease. These conditions should be excluded.
However bone scan should not be used routinely. This investiga
tion should be restricted to cases where PSA level is more than
20nmol/ml.
10. LYMPHANGIOGRAPHY.— This procedure is increas
ingly used to seek evidence of metastasis to the pelvic nodes.
Positive nodes preclude radical prostatectomy. This is also im
portant for staging the tumour. As lymphangiography is associ
ated with both false positive and false negatives, lymph node
biopsy is more important for accurate staging.
11. BIOPSY.— Prostatic biopsy — A needle biopsy speci
men taken from the posterior aspect of the gland through the
perineum is more reliable than obtained transurethrally. Various
needles have been used and the accuracy has been claimed in the
range of more than 80%. Such biopsy may be performed without
general anaesthesia as an outpatient procedure. Besides positive
proof of the diagnosis, biopsy also indicates the grade of malig
nancy of the tumour With a very small nodule, such biopsy may
be negative. In a few cases implantation of the tumour in the
needle track have been recorded, but this is very much theoretiFig. 59 5.— Transrectal ultrasound showing an
cal. Considering these facts, there may be a good place of pros echopoor lesion (cancer) at the apex of the prostate
tatic biopsy. gland (shown by arrow).
Presently transrectal biopsy using an automated gun with
appropriate antibiotic cover is used. Several cores are re
quired to make a definite diagnosis.
12. ASPIRATION OF BONE MARROW — from the
posterior iliac crest may show malignant cells. This also
helps for clinical staging of the tumour.
13. TUMOUR MARKERS.— Serum acid phos
phatase is normal with cancer strictly localised to the pros
tate, though this determination has been considered impor
tant in diagnosis and staging of prostatic cancer. When the
cancer has extended outside the prostatic capsule and me
tastases are present about 70% of patients have elevated lev
els of this enzyme. This is considered to be pathognomonic
of advanced disease whether or not metastasis is detected.
The serum alkaline phosphatase is also elevated in
patients with metastases in bone. It is therefore worth doing
both acid and alkaline phosphatase estimation as part of the
search for distant metastasis. Urinary cholesterol is also el
evated in many patients.
Hydroxyproline urinary excretion may deserve more
attention. It has been used as an index of bone destruction in
metastatic cancer, but it needs a low gelatine diet for 24
hours before urine collection. This lias restricted its popu
larity.
Prostate-specific antigen (PSA).— This is the most Fig. 59.6.— On T2-weighted MRI, tumours of the prostate
important tumour marker now available. It has been de appear as areas of comparatively low signal. In this figure
scribed earlier in the section of‘benign enlargement of pros one can see a tumour (t) replacing the left side of the gland.
tate’. Here it will suffice to say that if PSA is more than The normal right side of the gland (g) emits high signal. Note
lOnmol/ml, it is suggestive of a case of prostatic cancer. Ifthe high signal of urine in the transurethral resection of the
the PSA is more than 35nmol/ml, it is a case of advanced prostatic defect centrally (shown by arrow).
prostatic cancer. A decrease in the level of PSA indicates a

good prognostic sign.
TREATMENT.—
Patients with carcinoma of the prostate may
present with acute retention of urine. Relatively
sudden attack of dysuria with very short history of
other urinary troubles should give rise to suspicion
of this diagnosis. Rectal examination will confirm
the diagnosis. Acute retention should be relieved
immediately. Firstly a simple rubber catheter should
be tried to introduce. If it fails, gum-elastic cath
eter should be tried. If catheterisation becomes very
difficult even after bouginage, transurethral resec
tion should be performed to relieve the retention.
As soon as the retention is relieved, by whatever
method applied, stilboestrol should be started 5 mg
daily.
Carcinoma of the prostate should be treated
according to the stage of the disease or the patho
logical type of the tumour:
LATENT CARCINOMA (TO, NO, MO; Stage
I).— In this group there is no evidence of tumour
on clinical examination, but carcinoma is detected
histologically usually in tissue removed by pros
tatectomy. Investigations show no evidence of me
tastasis. When the pathologist has found that the
focus of carcinoma was entirely confined within the
gland, the surgeon may be happy that he had re
moved the tumour completely. It seems reasonable
to conclude that no active treatment is indicated for
well differentiated focal carcinoma detected in pro
static specimens removed at operations. But follow-
up should be continued till progression of the pro
static cancer becomes evident.
However the more diffuse or less differenti
ated tumours may need immediate radiotherapy in
a recommended dose of 5,000 rads over 4 weeks.
CARCINOMA CONFINED TO THE PROS
TATE (T1-T2, NO-NI. MO; Stage II).— This group
includes small nodule (Tl) and large tumour de
forming the contour of the prostate but are still con
fined within the capsule (T2). In fact these tumours
are uncommon and probably represent less than 5%
of cases. There are various options to treat these
cases — (i) radical prostatectomy or (ii) radical ra
Fig. 59.7.— Bone scan using Sr.87. Metastatic deposits are seen
with concentration of the isotope. A — shows the lumbosacral diotherapy or (iii) endocrine therapy.
region with deposits at lower end of lumbar spine, right ilium (i) Radical excision.— Radical perineal pros
and left ischium. B — shows upper part of chest with deposits at
tatectomy is often used in U.S.A. particularly in
inner end of right clavicle and upper part of sternum. clinics like the Mayo clinic. The 15 years survival
rate for patients with tumours confined to 1 lobe is 33%. This is the group which do good with radical pro
ctomy particularly when the patient is below the age of 70 years, free from serious unrelated disease, no
evidence of metastasis and prostatic induration does not exceed 1.5 cm in diameter. Adjuvant radiotherap
offers nothing to the patient undergoing radical prostatectomy. Early androgen ablation seems to offer ex
lent chances for 5-year progression-free survival to most men with stage T1-T2 prostate cancer. In this resp
early hormonal therapy seerns to be even better than early androgen ablation.
(ii) Radical radiotherapy.— External beam megavoltage methods have been claimed successful. 7,000
rads of irradiation was given to the prostate and 5,000 rads to the pelvis using a sandwich technique. Rece
iodine125 seeds have been implanted into the prostate gland alongwith lymph node dissection for staging.
lymph node negative cases 5 years survival rates have been quoted as 100%.
(iii) Endocrine therapy is discussed below.
LOCALLY ADVANCED DISEASE (T3-T4, N0-N1, M0; Stage III).— Between l/3rd and 1/2 ofthe
patients, presenting with prostatic cancer, have locally extensive disease with no evidence of distant meta
sis. 50% of these patients are expected to have lymph node metastasis. The results of radical prostatectom
poor in this group of patients. The capsule appears to provide an effective barrier against the spread of tu
and once this is breached, dissemination of the disease is likely to occur. So under these circumstances, loc
treatment to the prostate alone is unlikely to eradicate the disease. The results of radical prostatectomy are
poor in this group of patients. Various adjuvants have been used in an attempt to improve the result of ra
prostatectomy in locally advanced disease. Infiltration of the prostatic bed with radio-active colloidal gold
(l98Au) has been supplemented with radical prostatectomy. Direct retropubic implantation of the prostatic
tumour with 125I seeds has been tried. This will provide low energy irradiation (half life 60 days), in the tu
no less than 8,000 rads in two months. External beam radiation therapy should ensure a more satisfactory
dose distribution and the field can be extended to include para-aortic and pelvic lymph nodes. This group
should be treated by endocrine therapy. Preliminary endocrine treatment has been tried.
Extended surgical excision, in this patient, should be reserved for the rare cases, who have failed with
hormonal and other methods of treatment and yet continue to exhibit local growths, which are incapacita
but without evidence of metastasis.
DISSEMINATED DISEASE (T3-T4, N0-NI, MI; Stage IV).— Between l/3rd and 1/2 of all patients with
prostatic cancer have metastases at the time of presentation. Hormonal therapy is the best in these cases.
These are treated with Stilboestrol 5 mg/day. The main problem of this therapy is the increased incidence
cardiovascular deaths. The question still exists whether these cardiovascular problems, caused by stilboes
are dose dependent or not. In stage III until it is needed, oestrogen therapy should be withheld. If needed,
dose of 1 mg/day should be given. In stage IVpatients, there seems to be no justification for withholding th
treatment and it seems clear that it should be given in adequate doses. The minimum is 5 mg stilboestrol/
Honvan 100 mg tds. or Premarin (conjugated natural oestrogen) 2.5 mg tds., which may have lower incide
of cardiovascular side effects, should be tried. Oestrogen therapy will effect a great improvement in abou
of cases. The effect starts as early as 48 hours of commencing the treatment and symptomatic changes occ
even within 2 weeks. The prostate becomes smaller and softer. But stilboestrol is notorious to produce car
vascular calamities which may lead to even death of the patient. To minimise the side effects of stilboestro
Honvan (Phosphorylated diethylstilboestrol) may be administered orally or intravenously. At first 100 mg
injected thrice a day for 10 days. The dose is increased to 200 mg and eventually to 500 and to 1,000 mg on
21 st day. The dosage is then gradually decreased until one 200 mg injection given weekly or even month
may be replaced by oral therapy of 100 mg daily.
Orchidectomy.— Charles Huggins in 1941 showed that bilateral orchidectomy can be performed for
androgen ablation in prostatic cancer. He received Nobel Prize for this. Nowadays subcctpsular bilateral
orchidectomy is performed as an alternative or an adjuvant to the stilboestrol therapy.
Those patients who may eventually relapse and may present problems, should be treated with bilatera
adrenalectomy or medical suppression of the adrenals with cortisone 50 to 75 mg daily or pituitary ablation
by surgical hypophysectomy or cryosurgery or by needle implantation with radio-active yttrium needles.
fill metastasis may be treated with local external beam irradiation. For extensive skeletal metastasis, intrave
nous radio-active phosphorus (32P) should be given.
Other drugs.— Because of concern over the potential cardiovascular hazards of oestrogen, alternatives have been
sought, but none has been shown to have any significant advantages over stilboestrol. Progestogens have the attraction
that they inhibit androgen production and do not produce feminisation. Recent clinical trials have evaluated more prom
ising result from these drugs. Medroxyprogesterone (Provera) was shown to have lot of advantages over 1 mg stilboestrol
daily. Cyproterone acetate, which blocks adrenal and testicular androgens, is undoubtedly effective but it is an expensive
drug and does not have much advantage over stilboestrol. Other drugs which are available to reduce testosterone level are
LHRH agonists. These drugs initially stimulate the hypothalamic LHRH receptor and then down-regulate it resulting in
cessation of pituitary LH production, so that testosterone production is decreased. In the first few days (10 days or so)
serum testosterone level may increase and during this period it is better to give cyproterone acetate. These LHRH agonists
are now available as monthly depot injection. This peptide is rapidly degraded in the gastrointestinal tract, thus requiring
a parenteral mode of delivery. Two daily parenteral formations leuprolide (Lupron) and goserelin (Zoladex) have gained
widespread support. Leuprolide is given by daily subcutaneous injections or a depot preparation of Zoladex is given 3.6
mg subcutaneously daily. The safety and efficacy of LHRH analogues are readily apparent. Another drug, flutamide,
which is a pure antiandrogen is being currently used in this condition. Aminoglutethamide which is also an androgen
inhibitor, is being currently used.
Chemotherapy.— A few cytotoxic drugs have been identified which show some activity against prostatic cancer.
These are adriamycin, cis-platinum, cyclophosphamide and 5-fluorouracil. An interesting approach to chemotherapy has
been to combine the drug with the hormone. For example oestrogen in combination with the alkylating agent nitrogen
mustard (Estracyt) was designed to be transported to the site of tumour and there causes release of cytotoxic drugs in high
concentration. Responses at the rate of 20 to 30% have been noticed.
Radical perineal prostatectomy.— The initial steps of this operation upto the exposure of the prostate are more or less
similar to those of perineal prostatectomy as has been described under ‘Benign hypertrophy of prostate’. The membranous
urethra is divided below the apex of the prostate. The prostate is displaced backwards, so that its anterior surface is
cleaned. A transverse incision is made on the anterior surface of the bladder just above the base of the prostate. The
ureteric orifices are identified and the bladder neck is divided. The vas deferens are divided between ligatures. The vessels
supplying the prostate are secured and divided. The entire prostate with its fascial sheath and the seminal vesicles is
removed in one piece. The nearby lymph nodes should be dissected and included in the removal of the prostate. The
vesical outlet is now united to the membranous urethra over an indwelling catheter. The perineal wound is closed around
free drainage.
PROSTATITIS
Infection usually involves 3 structures simultaneously — the prostatic urethra, the prostate and the
seminal vesicles which lead to posterior urethritis, prostatitis and seminal vesiculitis. Symptoms of one of
these may dominate.
ACUTE PROSTATITIS AND PROSTATIC ABSCESS

Aetiology.— Usually the infecting organisms reach the prostate through blood from distant foci e.g. infected tonsils,
furuncles, carious teeth or even diverticulitis. So in majority of cases infection is haematogenous, but in a few cases
infecting organisms ascend through the urethra to involve the prostate. This is called ascending infection.
The organisms which are mostly responsible are E.Coli, Staphylococcus aureus and albus and Streptococcus faecalis.
Gonococcus when involves the prostatic urethra may also involve the prostate.
Pathology.— The prostate becomes oedematous and angry looking. When the abscess has formed, the consistency
becomes soft. Similar changes may be found in the seminal vesicles.
Macroscopic examination, reveals pockets of pus here and there. Granulomatous prostatitis is a type of acute pros
tatitis. It is also a febrile disease at the onset and is usually associated with pyuria. The prostate becomes firm and may be
stony hard to mimic carcinoma.
Microscopically, the acini and ducts are destroyed and replaced by abundant exudate. The stroma is infiltrated with
polymorphonuclear leucocytes, lymphocytes, plasma cells and multinucleated giant-cells. In some cases there may be
great collection of eosinophils. Foreign body giant-cell may be numerous. The stroma shows increased fibrosis to give
! 160 A CONCISE TEXTBOOK OF SURGERY
characteristic consistency which is very firm or even hard.

It is thought that this condition is caused by severe inflammatory reaction. The microscopic feature ver
resembles plasma cell mastitis or chronic thyroiditis. A history of allergy is often detected.
SYMPTOMS.— The patient feels ill and feverish. When the temperature becomes high there may be rig
aches all over particularly in the back. Vesical irritability i.e. burning sensation during micturition, increase
and urgency may be noticed. Purulent urethral discharge may be noted which is described as urine contain
Haematuria may be present. There may be perineal heaviness, rectal irritation and pain on defaecation. Sw
gland causes urinary retention.
When the prostatic abscess develops, the temperature rises sharply and the patient often feels rigor. Th
perineal and rectal pain often with tenesmus to be confused with anorectal abscess. But rectal examination
enlarged and extremely tender prostate which is softened in one place. Retention of urine is likely to occur
PHYSICAL SIGNS.— As mentioned above the patient is usually prostrated with high fever.
RECTAL EXAMINATION reveals an exquisitely tender and enlarged prostate. It may fluctuate which
formation inside the prostate. One lobe may be more swollen than the other. Seminal vesicles may also be
enlarged.
In granulomatous form, the prostate is enlarged and indurated, thus simulating carcinoma. It may requi
months for resolution.
Special Investigations.— 1. Blood examination.— The white blood count is very much elevated.
2. Urinalysis may show pus and bacteria on stain and culture. Sensitivity test should be done.
3. Examination ofprostatic secretion.— Examination of specimen of expressed prostatic secretion (EPS) is
after the first voided and mixed stream urines is of conclusive importance in the final localisation of the in
prostate. The full evaluation of a specimen of EPS includes its microscopic examination, culture by conven
and definition of certain chemical characteristic of which the pH is most easily accomplished in routine pra
prostatitis the EPS is purulent on microscopy and produces growth of micro-organism on culture.
4. Instrumental examination e.g. cystoscopy and urethroscopy.— This is contraindicated in the acute stag
exception to this rule is to relieve acute urinary retention due to prostatic oedema or abscess.
Complications.—
1. Acute urinary retention.
2. Acute cystitis and even pyelonephritis—due to ascending infection or spread of infection by haemat
This is particularly apt to happen if the prostate is massaged or if instrumentation is performed during acu
3. Acute epididymitis may also occur due to prostatic massage or instrumentation in acute stage.
4. Prostatic abscess, if forms and remains untreated, may rupture spontaneously into the urethra or re
perineum.
TREATMENT —
A. General treatment.— As soon as the diagnosis is suspected, the patient is put to bed and is advised to
excessive fluids. Analgesics may be required during excessive pain. Sitz baths will afford some relief and m
resolution of inflammation. Antispasmodics may be prescribed to relieve vesical irritability.
B. Specific treatment.— According to the type of organisms, 4 antimicrobials are very active in prostatic
These are erythromycin, trimethoprin, cefazolin and cephalexin. When the infecting organism is E. Coli or
negative rod, a combination of sulphamethoxazole 800 mg and trimethoprin 160 mg should be administer
daily orally for 10 to 40 days. In case of gram positive organisms e.g. Staphylococcus albus, the best antibio
erythromycin which has the property to achieve effective concentration within the prostatic acini and duct
should be continued for at least 2 weeks till there are signs of resolution.
After subsidence of acute symptoms and the development of sterile urine, the prostate should be mass
material should be sent for culture and sensitivity test. On completion of the initial antibiotic treatment, co
should be given to follow-up treatment with a sulphonamide preparation which may be of the long-acting
is continued for several months. Nitrofurantoin in a dose of 400 mg daily is as good. The rationale for this
not much to yield effective antibiotic concentration in the prostate itself, but to maintain the lower urinary
pathogens.
When the prostatic abscess has developed, if a catheter is passed to relieve acute retention of urine, som
abscess is ruptured into the prostatic urethra. However such drainage is insufficient and thus the conditio
chronic prostatitis. So the pus should be drained out completely and the perineal route is the best. So surg
drainage seems to be the best, though many urosurgeons prefer drainage of the abscess by unroofing of th
transurethral resection.
Granulomatous prostatitis may respond well to corticosteroids.
CHRONIC PROSTATITIS
Aetiology.— There are various causes of chronic prostatitis.
(i) Inadequate treatment of acute prostatitis.
(ii) It may develop secondary to cystitis or pyelonephritis.
(iii) Chlamydial infection has now been incriminated as causing chronic prostatitis. The chlamydial cu
difficult to obtain except in specialised laboratories.
(iv) Trichomonas has been found to be a cause of chronic prostatitis and such infection may be commo
husband and wife.
(v) Infections may reach the prostate via two routes — ascending through the urethra or haematogenous.
Pathology.— In chronic prostatitis the gland becomes firmer than normal as a result of fibrosis.
Microscopically, the ducts contain pus and their lining cells degenerate. The lumen of the ducts may beco
with epithelial debris and/or pus. Later on firbosis occurs in the stroma so that the gland becomes smaller a
Similar changes are also found in seminal vesicles which are usually involved alongwith prostate.
Clinical features.— SYMPTOMS.—
(i) Many patients are asymptomatic.
(ii) Symptoms accompanying a mild exacerbation may include urethral discharge and symptoms of c
(iii) Fullness in the perineum or low back pain is often complained with.
(iv) Urethral discomfort during ejaculation may be felt.
(v) Unexpected low grade fever is sometimes noted.
(vi) Phsychosomatic complaints e.g. insomnia, emotional tension and nervousness may be associated w
or impotence.
PHYSICAL SIGNS.— Rectal examination may reveal a normal or boggy, indurated prostate. There may
fibrosis. Crepitation may be felt if stones are present. Massage of the prostate produces a secretion which co
At times the prostate may be slightly tender.
Special Investigations.— 1. Urinalysis may reveal pus and bacteria in the urine. Three glass urine test may re
prostatic thread in the first glass.
2. Examination ofprostatic fluid should be examined both unstained and stained. Unstained specimen may
trichomonas or lecithin bodies. A stained specimen shows many pus cells and sometimes bacteria.
3. Plain X-ray or excretory urograms will be normal unless the condition is complicated with prostatic enla
urethral stricture or chronic pyelonephritis.
4. Instrumental examination, particularly urethroscopy may reveal inflammation of the prostatic urethra a
verumontanum is enlarged and oedematous. Pus may be seen coming out from the prostatic ducts.
TREATMENT.— A. General measures.— Daily sitz baths may hasten resolution of infection.
B. Specific treatment.— Combination of trimethoprin and sulphamethoxazole (septran) is the most
antibiotic. This should be administered for a long time followed by a urinary antiseptic as already described
prostatitis. Septran should be continued for about 28 days. Prostatic massage should be given every 2 weeks
drainage. Intercourse should therefore be encouraged.
When trichomonas is the responsible agent, Flagyl (metronidazole) 400 mg thrice daily orally after meal
prescribed for 10 days to both the partners.
If chlamydial infection is suspected, treatment should be with erythromycin 500 mg 4 times daily for 3 t
In intractable cases, which are not responding favourably to medicinal treatment and when there is palp
abnormality such as nodularity and fluctuation in the prostate, transurethral prostatic resection is indicated pa
to open up locules for better drainage.
TUBERCULOSIS OF THE PROSTATE AND SEMINAL VESICLES
Aetiology.—This is usually secondary to renal tuberculosis (60% of cases) or pulmonary tuberculosis (30%
Pathology.— Tuberculosis of 1 or both seminal vesicles is more common than the tuberculosis of the pros
these areas tuberculosis may spread to the epididymis.
Clinical features.— (i) Urethral discharge is often the first symptom, even when the prostate is normal to f
rectal examination.
(ii) Mild ache in the perineum is quite common.
(iii) Infertility.— With tuberculosis of the prostate and both seminal vesicles, fertility of the patient is m
reduced. About 80% of these cases become sterile.
(iv) Frequent micturition and terminal haematuria are often complained of when the posterior urethra is involved.
(v) Painful blood stained ejaculation is almost pathognomonic of this condition.
PHYSICAL SIGNS.— Rectal examination may reveal nodules in the prostate.These nodules are not stony hard as
one may experience in carcinoma. Often a large solitary mass is felt in the midline. The seminal vesicles are felt enlarged
and nodular due to tuberculosis. Cold abscess may form in the prostate, when it will be felt soft with fluctuation. Such
cold abscess usually ruptures into the urethra and extremely rarely into the rectum or through the perineum.
Special Investigations.— 1. Bacteriological examination of the seminal fluid yields positive cultures for tubercle
bacilli in majority of cases of tuberculous prostatitis.
2. Straight X-ray may show calcification of the prostate. Large scattered areas of calcification in the prostate suggests
tuberculosis than anything else.
3. Urethroscopy will show dilated prostatic ducts. This with finding of tubercle bacilli in the ejaculate confirm the
diagnosis.
Treatment.—
General treatment of tuberculosis should be given. No prostatic massage should be encouraged. Urethral instrumen
tation should be avoided.
If cold abscess is formed, it should be drained through perineum and should not be allowed to rupture spontaneously.
URETHRA
INJURIES TO THE URETHRA
Urethral injuries are uncommon and usually occur in men. Such injuries usually affect two parts of the
urethra — 1. Rupture of the bulbous part of the urethra and 2 Rupture of the membranous part of the urethr
1 RUPTURE OF THE BULBOUS PART OF THE URETHRA (ANTERIOR URETHRA).—
Aetiology.— It is usually caused by straddle-type fall, that means fall astride a projecting object. Nowada
such injury is seen in cycle accidents, in gymnastic accidents (fall astride the beam) and while walking over
a loose manhole cover. In fact this is a direct injury to the perineal region between the scrotum anteriorly and
anus posteriorly
SYMPTOMS.— Patients usually present with a history of fall on the perineum. The typical three
complaints are usually noted — local pain in the perineum, bleeding per urethra and inability to pass urine.
SIGNS.— Almost always there is a tender swelling in the perineum. Rectal examination reveals a
normally situated prostate (this differentiates this condition from rupture of membranous urethra).
When such case presents late, there is massive urinary extravasation and infection in the perineum and
scrotum. The lower abdominal wall may also be involved. The skin is usually swollen and discoloured.
Management.— Two types of rupture are usually noticed — complete or mcomplete(whcn some part of
the circumference of the urethral wall remains intact). The patient should be instructed not to pass urine to
prevent extravasation. The patient should not be catheterised in the ward. He should be properly prepared a
taken to the operation theatre. Chemotherapy is started immediately.
If the patient has given a history that he had already passed urine after the injury and there is no sign of
extravasation, it is obvious that the rupture is incomplete.
If the patient had not passed urine since the accident, and there is obvious perineal haematoma. an attem
should be made to pass a soft catheter through the urethra. If this is successftil. the catheter is kept in situ, an
expectant treatment should be given. Perineal haematoma may be drained, if required.
If the catheter cannot be passed the patient is kept in the lithotomy position and a midline perineal incis
is made to expose the ruptured urethra. An attempt is made to suture end-to-end the whole circumference o
the urethra with fine catgut, the knots of which are left outside of the wall. It is usually done by interrupted
suturing. If the proximal end of the urethra cannot be found out. a suprapubic cystotomy is performed and
curved sound is passed through the internal urethral meatus to the bulbous urethra.This will reveal the prox
end and the similar end-to-end suturing is performed as mentioned above. If the bladder is opened, it is dra
by a suprapubic catheter. If the repair of the urethra has been accomplished without opening the bladder, a
retaining catheter is passed through the ruptured urethra into the bladder. Sometimes the whole circumfere
of the urethra is not sutured, but a few stitches are applied at the roof of the urethra as well as at the lateral w
keeping open the floor. The perineal wound is not stitched, but it is packed.
Chemotherapy is continued till the perineal wound is healed completely. To select the proper drug, urin
should be cultured. The perineal wound is dressed regularly with weak Eusol solution till it heals completel
The self-retaining catheter, which acts as a splint, rather than for drainage purposes, is removed after two
weeks. A perineal leak may be present for a few days. Bougies are started passing. At first the dilatation is
carried out every two or three days. When the urethra can accommodate a normal size bougie, the suprapub
drainage is removed. The dilatation is continued and generally the result is satisfactory.
If the patient comes too late to the hospital, after complete rupture of the anterior urethra suprapubic
cystostomy is performed and an incision is made at the perineum to expose the ruptured urethra. It is of no
to apply stitches to the urethra, since these will not hold and the friable tissues will give way. An indwelling
catheter is pushed through the urethra into the bladder and this acts as a splint for healing of the urethra. Th
perineal incision is left open for drainage.
Complications.—
(i) SUBCUTANEOUS EXTRAVASATION OF URINE.— This is discussed later in this chapter.
(ii) STRICTURE — is a common complication. This complication may be treated by regular dilatation
or internal urethrotomy. Only occasionally surgical reconstruction may be required when the stricture has
significantly reduced the urinary flow.
2. RUPTURE OF THE MEMBRANOUS URETHRA (POSTERIOR URETHRA) —
Aetiology.—This usually occurs as a result offracture ofthe pelvis. It is said that about lOto 15%of cases
of fractured pelvis sustain either rupture of membranous urethra or extraperitoneal rupture of bladder or bo
The urogenital diaphragm is attached to the lower part of the pubic rami. When pelvic fractures occur from
blunt trauma, the membranous urethra is sheared from the apex of the prostate at the prostatomembranous
junction. Most common causes of pelvic fracture are road traffic accident, severe crush injuries and falls from
buildings.
Pathology.— The urethra usually is sheared off just proximal to the urogenital diaphragm, so that the
prostate is displaced superiorly by the developing haematoma in the periprostatic and perivesical spaces and
posteriorly with the urinary bladder due to disruption of the puboprostatic ligaments.
Clinical features.— It must be emphasised in the beginning that every care should be taken to find out
injury to the head, thorax or abdo
men or fracture of the long bones
and not to concentrate wholly to the
pelvic fracture and rupture of mem
branous urethra The above-men
tioned injuries are more dangerous
and require early attention than rup
ture of membranous urethra.
SYMPTOMS.— Two main
complaints of the patient with only
rupture of membranous urethra are
blood at the external urinary me
atus and inability to micturate.
SIGNS.—- Blood at the ure
thral meatus is the single most im
portant sign of urethral injury The
importance of this finding cannot
Fig. 59 .6.— Rupture of membranous urethra with extravasation of be over emphasised and this should
urine within the pelvis. Note that the prostate is displaced upwards immediately indicate not to pass a
and posteriorly with rupture of puboprostatic ligaments. urethral catheter. There may be
suprapubic tenderness and a large develop

ing pelvic haematoma.
Rectal examination may reveal a large
pelvic haematoma with the prostate dis
placed superiorly, so that it may not be
palpable, or if palpable with the tip of the
finger. Even a tense pelvic haematoma may
resemble prostate on palpation. It must be
remembered that the prostate cannot float or
be displaced superiorly if the puboprostatic
ligaments remain intact. Partial disruption
of membranous urethra is not accompanied
by prostatic displacement.
X- ray may indicate fracture of the bony
Fig. 59.7.— Shows management of membranous urethral rup pelvis.
ture. Foley catheter is within bladder with a silk thread tied to the Management.— This is mostly a com
eye of the catheter. Suprapubic bladder drain and retropubic dr plete rupture and diagnosis between this
ain are seen. condition and extraperitoneal rupture of the
bladder is rather difficult.
A vertical incision is made just above the symphysis pubis to expose the extra-peritoneal tissues in which
bladder urine will be seen. This is cleared and the anterior wall of the bladder will be exposed. If the bladder
is empty, the injury is vesical and if it contains some urine, a ruptured urethra is the probable diagnosis. In th
latter case, it is rather impossible to repair by suture and the surgeon should be content with splinting the
ruptured urethra with a self-retaining catheter. The bladder is opened and a bougie is passed in retrograde
manner along the urethra to the site of the rupture. A second bougie is passed through the external meatus a
the two bougies are made to contact each other. The first bougie is now slowly withdrawn, which is followed
by the second bougie, till the second bougie enters the bladder. A rubber tube is now fitted over the tip of thi
2nd bougie and is secured by a ligature. The bougie is now withdrawn through the external meatus. Therefor
the tip of a Foley catheter is attached to the rubber tube, which has come out through the external meatus Thi
is known as Rail-road’ technique The rubber tube is now withdrawn from the bladder to draw the Foley
catheter into the bladder. The bulb of the catheter is now inflated and a length of a silk is tied to the eye of the
catheter in order to facilitate subsequent changing of this Foley catheter. A Malecot catheter is now pushed
through the cystostomy wound and this cystostomy is closed around the catheter. The retropubic space is
drained. The silk, which is fixed to the tip of the Foley catheter, is brought outside the abdomen and wound
round a gauze piece, which is strapped to the anterior abdominal wall.
Postoperatively. a traction is applied to the catheter by a weight, which is about 1 Kg. for the first 4 days
followed by Vi Kg. for the next 10 days. The Foley catheter is used for traction for a fortnight and the catheter
should be changed biweekly with the help of the silk strand. The drain at the retropubic space is removed aft
48 hours. After the Foley’s catheter has been removed, the silk thread is used for the passage ofbougies to dil
the urethra. When a normal bougie can be passed through the urethra, the suprapubic drainage is closed
intermittently to see that the patient is micturating properly. After that the suprapubic drainage is removed
Complications.—
1. URETHRAL STRICTURE.— This is the most important complication of this condition. Stricture is
usually very short and direct vision urethrotomy with an optical urethrotome which is passed endoscopicall
offers easy and rapid cure. Should this measure fail, a complex urethroplasty may be necessary. A transpubi
approach has been advocated by a few surgeons which allows a satisfactory end-to-end anastomosis to be
performed.
2. UR1NAR YINCONTINENCE.— This complication usually occurs due to severe damage to the externa
sphincter mechanism. The difficult surgical manoeuvres at the bladder neck may also damage the internal
hral sphincter. It is noted in about ‘/3rd of patients. Incontinence seldom requires transpubic reconstruction.
3. IMPOTENCE.—This is also a common sequel of this injury. It seems to be due to disruption of th
supply at the time of the fracture. The incidence may vary from 30% to 80%. The incidence may be reduced
to 10% by suprapubic drainage with delayed urethral reconstruction. Impotence is permanent in about 10%
of cases. If impotence is still present 2 years after reconstruction, implantation of penile prosthesis should be
considered.
EXTRAVASATION OF URINE
When urine comes out through rupture in the urethra, it is called extravasation of urine’. The spread of
the extravasated urine depends on the part of the urethra through which urine has come out.
Superficial extravasation due to rupture of the bulbous urethra.—
Bulb of the urethra often ruptures from injury to the perineum or when a periurethral abscess bursts. Th
urine first collects in the superficial perineal pouch, which is bounded below by the fascia of Colles and abo
by the inferior fascia of the urogenital diaphragm. The space is closed posteriorly by the fusion of the two fa
and laterally by their attachment to the ischio-pubic rami. In front, this space is open and urine passes throu
this open space into the scrotum, penis and the anterior abdominal wall, deep to the fascia of Scarpa. The
extravasated urine cannot spread downwards into the thigh due to the attachment of the fascia of Scarpa to
fascia lata of the thigh.
TREATMENT.— Urgent operation should be accomplished. Multiple incisions are made in the
extravasated tissues. These incisions should be deep enough to penetrate the limiting fascia. When a case
presents with extravasation of urine, it is already a late case and direct end-to-end suturing of the urethra is
almost impossible as the sutures will cut through the oedematous inflamed tissues of the urethra. That is wh
suprapubic cystostomy is performed with the patient in the lithotomy position, a metal bougie is passed thr
the bladder and through the internal urethral meatus to the perineum and another metal bougie is passed fr
the external urinary meatusto the perineum. A midline incision is madeon the perineum. By rail-road’ meth
a sialastic tube with multiple holes (or Foley’s catheter of average size) is introduced into the urinary bladde
The bladder is closed around a malecot catheter. The perineal wound is left widely open with packs.
A course of antibiotics is continued till healing is complete. The urine should be sent for culture
immediately and for reculture after a week. The perineal wound is dressed daily with a weak Eusol solution
The catheter is removed after 10 to 14 days. A voiding study (urethrography) is performed after 2 to 3 week
through the suprapubic catheter. Removal of suprapubic cystostomy catheter may be done if no extravasati
is documented. Healing at the site of injury may result in stricture formation. These should be treated by int
urethrotome through endoscopy. Only rarely surgical reconstruction may be required.
Deep extravasation due to rupture of the posterior urethra.—
This rupture is commonly due to fractured pelvis and occurs mostly at the junction between the prostat
and the membranous urethra just above the urogenital diaphragm. If the puboprostatic ligaments are torn,
prostate together with the neck of the bladder is displaced upwards and posteriorly causing wide separation
between the severed ends of the urethra. The extravasated urine collects in the cave of Retzius and ascends i
the extraperitoneal space behind the fascia transversalis.
Such deep extravasation may also occur in case of extraperitoneal rupture of bladder. In this condition
urine extravasates in the layers of the pelvic fascia and in the retroperitoneal tissue.
TREATMENT.— It is necessary to drain the retropubic space (cave of Retzius). Simultaneously one
should perform suprapubic cystostomy. Rest of the treatment is according to rupture of posterior urethra or
extraperitoneal rupture of the bladder.
URETHRITIS
There are various types of inflammation which may affect urethra.
Ulcccation of the urethral meatus.—
In male children ulceration ofthe urethral meatus is particularly seen after circumcision. It takes place about 6 months
to 18 months after the operation. Lack of protection of the urethral meatus by prepuce seems to be the main cause This
leads to friction of the urethral meatus against the clothings.

First an ulcer develops at the urethral meatus which is covered by a scab. This scab usually closes the meatus and
the child micturates by bursting this scab. So micturition is often accompanied with pain and a few drops of blood may
be passed. When the scab is thus shade off, raw ulcer becomes visible, which is again covered by a new scab and this process
continues. In late untreated cases cicatricial contracture of the meatus may result to cause a pin-hole meatus (acquired).
MANAGEMENT.-— This condition is often associated with alkaline urine. The glans and external urethral meatus
are washed with a solution of boric acid, which is prepared by boiling boric acid crystals in water. 5% boracic ointment
should also be applied on the ulcer. These agents neutralise the alkaline urine for cure of the condition.
When cicatricial contracture has already developed, medicinal treatment does not help and operative meatotomy
remains the only answer.
Acute non-gonococcal urethritis.—
AETIOLOGY.— Acute urethritis is usually an ascending infection, but it may be caused by descending infection
from infected prostate. Such urethritis may also follow catheterisation, accidents or trauma or deliberate insertion of
foreign bodies. Oxaluria, urinary calculi or even gout has secondarily caused this type of urethritis.
No specific organism has been incriminated. Both gram-negative rods and gram-positive cocci are occasionally found.
About 27% of normal young men harbour ureaplasma urealytica (Mycoplasma T). This may cause non-specific urethritis
in 75% of cases. Mycoplasma hominis has also been incriminated to cause such condition. These mycoplasmas are normal
inhabitants of both the vagina and the urethra in both sexes. Whether these are truely the aetiological agents is a subject
of controversy. Chlamydia A (types D-K) has also been suspected as this is an important source of pelvic inflammatory
disease. Trichomonas vaginalis may cause male urethritis.
PATHOLOGY.— If urethritis is severe enough, a periurethral abscess may form. Rarely urethral stricture may
develop. In the acute stage, the mucosa is red, oedematous and covered with a purulent exudate. It may be ulcerated in
a few places.
Microscopic examination shows marked oedema and infiltration with leucocytes, plasma cells and lymphocytes.
Capillaries are markedly dilated. The glands of Littre are engorged and full of pus cells.
Symptoms.— Urethral discharge is the main symptom. It may be as profuse as in gonorrhoea or it may be less. Dysuria
is often associated with. Urethral discharge is scanty and often thin mucoid, though it may be profuse and purulent. Urine
is usually clear unless the discharge is excessive. Reinfection is common in about 20% of cases either due to reinfection
or due to infection coming from prostatitis. Epididymitis is often seen. But urethral stricture rarely results.
Signs.— On examination, the lips ofthe meatus are often red, oedematous and everted. The discharge is usually scanty
and thin mucoid, but it may be profuse, thick and purulent. The discharge should be examined unstained and in stained
specimens. This may reveal the organisms mentioned above.
COMPLICATIONS.— (i) Prostatitis; (ii) Cystitis; (iii) Periurethral abscess; (iv) Urinary fistula from periurethral
abscess and (v) Urethral stricture.
TREATMENT.— The combination of sulphonamide and either tetracycline or erythromycin gives the best result.
These drugs are effective against both chlamydia and U.urealytica. These drugs should be given for 14 days. Contacts must
be investigated and the individual of other sex should be similarly treated.
In case of females, acute urethritis is seldom seen except in association with gonorrhoea. Such non-gonorrhoeal
infection, if occurs, involves the cervix rather than the urethra. In rare cases of urethritis, the patient presents with pain
during micturition, urgency and even terminal haematuria. Urethral tenderness is an important sign. Treatment is similar
to that of the male.
Chronic urethritis.—
AETIOLOGY.— This is rarely seen and may be the sequel of incompletely healed acute urethritis or such infection
may have come from chronic prostatitis.
PATHOLOGY.— The urethral mucosa becomes granular and appears dull red. Microscopically one will see
lymphocytes, plasma cells, a few leucocytes and fibroblasts.
CLINICAL FEATURES.— Urethral discharge is again the main symptom but it may only be noticed before the first
urination after waking up. Prostatitis or cystitis is often present.
LABORATORY FINDINGS.— Quite often no bacteria may be present at all. This may suggest infection with
chlamydia or U.urealytica. Occasionally rods and cocci may be seen. Culture should be done if trichomoniasis is suspected.
TREATMENT.— The treatment is almost same as nonspecific acute urethritis, except there may be some psychic
problem which should be tackled by a psychiatrist.
Reiter’s disease.—
It is a syndrome which consists of subacute urethritis, conjunctivitis, and arthritis. There may be sometimes
keratoderma blennorrhagicum which is characterised by nodules, vesicles and pustules affecting an area ar
or the sole.
Urethritis is usually seen 4 to 6 weeks after contact (incubation period is 4 to 6 weeks). Conjunctivitis is
unilateral but it may become bilateral in 50% of cases. Iritis may gradually follow. Arthritis is usually comp
2 weeks after urethritis.
TREATMENT.— Ophthalmic complications should be treated by ophthalmic surgeons. Various antibio
be tried. Graduated dose of triple typhoid vaccine (TAG), though tried earlier for arthritis, is now obsolete.
Gonococcal urethritis.—
Gonorrhoea is primarily a urethral infection. It is a self-limiting disease and the bacteria die out within
Infection does not confer immunity against reinfection.
Neisseria gonorrhoeae (gonococcus) is almost without exception transmitted through sexual contact. T
organisms are kidney-shaped diplococci with their relatively flat surfaces apposed to each other. These are
organisms and are typically found within the neutrophils, though they are frequently found extracellularly
organisms affect primarily.
In the male — the urethra In the female — urethra, cervix
rectum and anal canal and rectum and anal canal and
oropharynx. oropharynx.
Gonorrhoea in the male.—
Incubation period is 2 to 10 days, that means first symptom develops after 2 to 10 days of sexual exposu
A. Symptoms.— The first symptom is urethral discharge which is seropurulent at first and becomes puru
on. Burning pain during micturition and urethral itching are not uncommon. Frequency, urgency and noct
when the posterior urethra and the prostate become involved.
B. Signs.—There may not be any definite physical sign. The meatus may be red and oedematous with it
The mucosa and the submucosa are inflamed and thickened and the urethra becomes tender.
SPECIAL INVESTIGATIONS.— The urethral discharge should be examined as unstained and stained
Unstained specimen is particularly required to exclude trichomonas. Grams stained urethral discharge will
numerous pus cells and both intra- and extracellular gram negative diplococci (gonococci). Two glass urine t
the first glass to be hazy, whereas the second glass is clear. The second glass also becomes hazy or cloudy w
urethra is also involved. Gonococci may be cultured in a special medium as they die rapidly on drying.
COMPLICATIONS —
Local Complications.—(i) Posterior urethritis, (ii) prostatitis, (iii) acute epididymoorchitis, (iv) periurethri
abscess formation and (v) urethral stricture.
General Complications or Metastatic Complications.— (i) Gonococcal arthritis (acute polyarthritis) may dev
or monoarticular disease with effusion may be seen. These usually respond to definitive antibiotic therapy,
iridocyclitis, (iii) septicaemia, (iv) meningitis, (v) endocarditis.
TREATMENT.— The gonococcus is very sensitive to most antibiotics. Previously penicillin was an effe
against this organism. But gradually it is becoming increasingly resistant to penicillin producing penicillina
3 gram stat with probenecid 1 gram to delay excretion is an effective antibiotic. Procaine penicillin 1.5 to4 m
with probenecid is also effective except for resistant cases. Co-Trimoxazole (Septran) 4 tablets b.d. for 5 day
effective. Kenamycin 2 gram stat is very effective though it is ototoxic. Tetracyclines also cure 90% of cases.
The discharge usually disappears in 12 hours. In 10% of cases a scanty thin discharge will remain follow
which will disappear within a few days.
It must be noted that serologic tests for syphilis must be done in 3 weeks and then after 3,6 and 12 mon
sex partner should always attend investigation and treatment, if necessary.
Gonorrhoea in the female.—
The importance of this condition in females is that it often remains symptomless and majority of the ca
out when their male partners have been affected.
The condition primarily affects the urethra and the cervix in female. There will be reddening or erosion
A mucopurulent discharge is seen on the cervix. There may be slight vaginal discharge (copious vaginal di
commonly due to concomitant trichomonal vaginitis). There may be slight dysuria due to involvement of t
careful examination one may find bead of pus at the meatal orifice after emptying Skene’s tubules by milki
down against the posterior ramus of the pubis.
COMPLICATIONS —
Local complications.—
(i) Salpingitis occurs in about 10% of cases and the patient presents with lower abdominal pain and tenderness
due to involvement of one or both tubes. Infertility may occur due to involvement of both tubes.
(ii) Proctitis is seen in more than 50% of cases.
(iii) Bartholinitis leading to bartholin’s abscess may occur in a few cases.
General complications.— Same as those in males.
TREATMENT is same as that of the males.
URETHRAL STRICTURE
Aetiology.— Nowadays acquired urethral stricture is rare. There are various causes of stricture of the
urethra. The commonest is the traumatic particularly rupture of the membranous urethra following fracture
of the pelvis. It sometimes follows endoscopy. The various causes of urethral stricture are :—
I. Congenital.
II. Traumatic.— It may follow rupture of bulbous or membranous urethra.
III. Inflammatory.— Gonorrhoea is the commonest in this group, followed by non-gonorrhoeal acute
urethritis, followed by tuberculosis.
IV. Instrumental.— Introduction of indwelling catheter in inexperienced hands. Introduction of
endoscopy.
V. Postoperative — following prostatectomy or amputation of penis.
CONGENITAL STRICTURE has been considered later in this chapter.
TRAUMATIC STRICTURE.— This often follows delayed treatment of rupture urethra. Such rupture is
commonly seen either in the bulbous part of the urethra or membranous part of the urethra.
INFLAMMATORY. — In this group post-gonorrhoeal stricture is by far the most common, though its
incidence is coming down rapidly due to availability of suitable antibiotics against gonorrhoea. Sites.— Post
gonorrhoea! stricture is commonest (i) in the bulb, which constitutes about 70% to 80% of cases. Next in
frequency is (ii) at the penoscrotal junction. The least common site is (iii) in the distal part of the spongy urethra.
Often one can see multiple strictures in this condition. When there are two strictures the deeper stricture is
narrower and when there are three stricture the deepest is the narrowest
It must be remembered thatpost-gonorrhoealstricture is never seen in the membranous or in prostatic parts
of the urethra. Usually post-gonorrhoeal stricture develops during the first year after gonorrhoeal infection
though difficulty of micturition may not be experienced before 10 years.
INSTRUMENTAL STRICTURE.— This usually occurs from trauma due to passage of too large an
endoscope. If indwelling catheter has been introduced roughly such stricture may occur following injury to the
urethral mucous membrane. If indwelling catheter is kept for a long time, urethritis may ensue, which may
cause stricture.
POSTOPERATIVE STRICTURE.— Whatever method is applied, about 3% to 4% of cases following
prostatectomy, urethral stricture occurs. Such stricture is usually situated at the proximal end of the prostatic
urethra. The stricture may take a form of a shelf at the junction of the bladder with the prostatic bed. It may
be opened perurethrally and its edges are resected with a urethrotome. While doing suprapubic or retropubic
prostatectomy, such shelf may be resected with a pair of scissors and then the margins are carefully sutured.
Postoperative stricture may also follow partial or complete amputation of the penis. How to avoid this
complication has been discussed with the respective operations.
Pathology.— Whatever may be the cause of stricture, it is usually caused by infiltration of round cells and
fibroblasts into the periurethral tissue. This usually follows injury or inflammation to the urethral mucosa
Gradually there is scar formation in the periurethral tissue. This gradually encroaches the mucous membrane
and narrows the lumen of the urethra. The peculiarity is that in the bulbous urethra the fibrosis is most evident
in the roof, whereas in the penile urethra it is more seen in the floor.
COMPLICATIONS —
1. The major complication of stricture of urethra is obstruction to the outflow of urine. This gradually
causes dilatation of the urethra proximal to the stricture, compensatory hypertrophy of the bladder musculature
with formation of diverticuli. Back pressure may culminate in hydronephrosis or hydroureter.
2. Because of stasis infection occurs which causes prostatitis, cystitis and pyelonephritis.
3. Due to stasis of urine and infection, calculi formation is quite likely e.g. bladder calculus, renal calculus
in the pelvis of the ureter.
4. Due to infection of the stagnant urine just proximal to the stricture periurethral abscess may develop.
It may rupture through the skin causing urinary fistula. This condition is often caused by streptococci and
anaerobic organisms. Patient complains of pain in the perineum with high temperature and rigor and rapid
pulse rate. On examination, a tender swelling may be felt in the perineum in case of bulbar periurethral abscess
and on the undersurface of the penis in case of penile periurethral abscess. Later on such abscess may burst
into the exterior to cause urinary fistula. When periurethral abscess occurs just proximal to a tight urethral
stricture, the patient passes most of his urine through many such urinary fistulae. The condition is called
watering-can perineum.
Urethral diverticulum may develop due to increased intraurethral pressure proximal to the stricture. Such
diverticulum may also develop due to long standing presence of a urethral calculus or it may be congenital
5. Retention of urine is due to obstruction to the flow of urine by the urethral stricture.
6. Hernia, haemorrhoides or rectal prolapse may occur due to straining to overcome obstruction to the flow
of urine by the urethral stricture.
Clinical features.— SYMPTOMS.— Gradual diminution of the force and calibre of the urinary stream
is the most common initial symptom. Sudden urinary retention may occur if an infection or oedema occurs at
the site of stricture. Careful history taking may suggest previous urethral injury or severe untreated gonorrhoea
Symptoms of cystitis e.g. increased frequency, urgency or nocturia are late to appear. In contradistinction to
obstruction due to an enlarged prostate, the patient is considerably younger.
SIGNS.— In long standing cases it is often possible to palpate the stricture. A tender mass may be present
if periurethral abscess has developed. In late untreated cases one may find urinary fistulas. Prostatic massage
and culture of secretion may reveal evidence of prostatitis.
X-RAY FINDINGS.— Urethrogram and voiding cystourethrogram will reveal the site, length of the
stricture or presence of a diverticulum proximal to the stricture. Excretory urograms may reveal urinary calculi
or calculi within the diverticulum of the bladder or changes compatible with pyelonephritis.
Urethroscopy confirms the diagnosis of urethral stricture very precisely. The stricture is seen as white
fibrous tissue around a small hole. The urethra may be centrally situated or towards the roof or the floor The
stricture may take the form of a crescent.
T reatment.—
DILATATION.— For dilatation of the stricture the patient has to be taken to the theatre and it is done
under strict aseptic technique. Before dilatation is performed, the patient should pass urine The glans penis
and urinary meatus are cleansed with antiseptic solution. The urethra is filled with mild antiseptic solution
and local anaesthetic. Dilatation is now carried out gently with bougies of increasing size.
There are three types of instrumental dilatation — intermittent, continuous and rapid dilatation.
Intermittent dilatation.— This is by far the most popular method of the 3 types of instrumental dilatation
A stricture is not cured by single dilatation. It requires repeated dilatations at regular intervals. At the
commencement, a medium size bougie is taken to dilate the stricture. Subsequently, bigger size bougies are
introduced to dilate the stricture. This dilatation, at first, is done biweekly and every time the largest bougie
is inserted. After this, dilatation is done weekly for a month Then dilatation is done fortnightly for 3 months
Then once a month for 6 months. Then quarterly for a year, then 'A yearly for 2 years and lastly once a year
(preferably on the birthday to remember).
Continuous dilatation.— In this technique, under urethroscopy, gum-elastic bougies in the name of
Filiform bougies, varying in size from 1 to 3 cm, are passed through the stricture. What is done is that two or
three Filiform bougies are passed through the urethra and by to and fro movement, one will pass through the
stricture. Very few urethral strictures are impassable to these Filiform bougies.
When such a bougie is passed, it is left in position for 12 hours for sufficient dilatation to facilitate
subsequent intermittent dilatation to be continued. Otherwise followers’ made up of gum-elastic material, can
74
be screwed to the filiform bougie, whose calibre is gradually becoming larger for immediate dilatation of the
stricture.
Rapid dilatation.— That means full dilatation in one sitting can be performed by the Kohlmann dilator.
It inflicts much trauma and is not used nowadays.
SURGERY —
1. EXTERNAL URETHROTOMY.— This operation is performed in case of impassable stricture. The
patient is placed in the lithotomy position. Wheelhouse’s staff is passed into the urethra down to the stricture,
its grooved surface should face the surgeon. An incision is made at the midline of the perineum and the urethra
is opened on the groove of the staff for about an inch. About a quarter of an inch of the urethra just distal to
the stricture is left uncut. The staff is now rotated and withdrawn till the terminal hook is made to retract the
upper angle of the opened urethra. The margins of the split urethra are retracted by tissue forceps or stay sutures.
Through the lower angle of the opened urethra, a fine probe-pointed director is inserted through the stricture.
The floor of the stricture is cut by running a knife along the groove of the director. Being guided by the groove
of the director, a Teale’s gorget is passed towards the bladder until a flow of urine comes out. The director is
taken out. The Wheelhouse’s staff is removed and a large polythene catheter is passed through the penile
urethra till its tip appears through the opened urethra. The tip of the catheter is then pushed towards the bladder
being guided by the trough of the Teale’s gorget. The gorget is taken out only after interrupted stitches are
passed through the normal urethra distal to the stricture. The perineal wound is left unsutured.
Postoperatively the bladder should be washed daily to control sepsis. The floor of the urethra is formed
by granulation tissue after which the usual intermittent dilatation regime is started throughout the patient’s
life.
2. INTERNAL URETHROTOMY.— This operation is particularly indicated when it seems impossible
to get a bougie passed through the stricture. Under direct vision down the panendoscope the filiform guide is
introduced through the stricture. The obturator of the urethrotome is now removed and the stricture is then
cut under vision with a sharp knife blade that can be projected from the tip of the instrument. By a sharp thrust
of the knife the roof (12 o’clock position) of the stricture is divided. If this gives unsatisfactory opening of the
stricture a second cut is performed at the floor (6 o’clock position). Now a gum elastic catheter can be passed
after removing the urethrotome. The catheter is retained for 3 days, after which intermittent dilatation should
be continued. The advantages of this method are that the cutting of stricture is done under direct vision
minimising the chance of false passage formation and the stricture is cut in one position without causing
generalised trauma to it. The procedure can be repeated if necessary after 3 months when urethroscopy should
be performed to know the condition of the stricture. The results are quite satisfactory (70% to 80%).
3. URETHROPLASTY OR SURGICAL RECONSTRUCTION — If the above methods fail, open
surgical methods in the form of urethroplasty should be resorted to.
If there is a short stricture in the bulbous urethra, it may be excised and end-to-end anastomosis is
performed.
Long strictures particularly in the anterior urethra are best treated by splitting the urethra and suturing
the edges of the open urethra to the adjacent skin. A Denis-Browne type of repair is then performed (Johanson’s
urethroplasty).
When the stricture is in the membranous urethra, it presents difficult problem. A perineal skin flap may
be constructed (technique devised by Blandy) or a scrotal tunnel is taken up to be sutured to open edges of the
urethral defect (Turner-Warwick technique). Tubed scrotal flap pull-through urethroplasty devised by Mr
Innes Williams has also been satisfactory as reported by a few centres. The end of the scrotal flap is fastened
to a catheter, which is pulled up in the Badenoch-fashion into the bladder. The tube is sewn into the form of
a skin lined tube. After 3 weeks the catheter is withdrawn and the scrotal tube is found to have healed. There
are various other methods of urethroplasty which are described in the various text books of Urosurgery, but
beyond the scope of this book.
CONGENITAL ANOMALIES OF THE URETHRA

There are a few anomalies of the urethra which are too rare to require any mention e.g. duplication of the urethra,
congenital absence of the penis (apenia), megalopenis or micropenis. A few congenital anomalies, though rare, sometimes
seen in surgical practise and are mentioned below :—
Congenital urethral stricture.—
The two common sites are — the membranous urethra and in the region of the corona. The effects of such urethral
stricture are mainly obstruction to the flow of urine and back pressure from obstruction leading to hypertrophy of detrusor
muscle, ureterovesical reflux, hydronephrosis and hydroureter. Secondary infection is also common.
MANAGEMENT.— When a baby presents with the symptoms mentioned above, excretory urograms should be
performed alongwith post-voiding film. Urethrogram may be necessary to delineate the site, degree and length of the
stricture.
Cystoscopic examination should be performed but the passage of the instrument may be arrested by the stricture.
Urethral dilatations with sounds or filiform bougies with followers are main treatment. Such strictures do respond well
to dilatation, but if fails internal urethrotomy or surgical repair of the stricture (urethroplasty) is performed.
Congenital valves of the posterior urethra.—
Congenital posterior urethral valves are usually seen on the floor of the prostatic urethra just below the
verumontanum. Occasionally one may see these valves above the verumontanum. The peculiarity of these valves is that
these allow the catheter to be passed easily, but obstruct the outflow of urine. Three types of clinical presentations are seen
— (a) when the valves are incomplete, the patient may reach adolescence or adult life without symptoms, but hypertrophy
of the detrusor muscle, vesical diverticula, dilatation of the prostatic urethra and hypertrophy of the trigonal muscles are
often noticed, (b) Patients with moderate obstruction and abnormal urograms usually present earlier and (c) severe
obstruction with uraemia.
The most reliable method to confirm the diagnosis is voiding cystourethrography, that means radiographs are taken
during the act of micturition after the bladder has been fdled with contrast medium. This will indicate the presence of
valves and obstruction to the flow of urine. Cysto-urethroscopy fails to identify the valves as the irrigating fluid flows into
the bladder with fully opening of the valves.
TREATMENT.— Suprapubic cystostomy is performed as an emergency life saving procedure. Once the urea and
NPN levels in the blood have come down to normal level, transurethral resection of the valves should be performed. After
treatment, the hypertrophy of the trigone muscles and detrusor muscles subside. Sometimes removal of the valves may
not be sufficient as hydroureter has become atonic and the condition does not resolve. In these cases loop cutaneous
ureterostomies may have to be performed to preserve renal function. Proper antibiotics should always be given for a long
course as infection is difficult to control in these cases.
Anterior urethral valves.—
In a few rare instances anterior urethral valves have been reported. A voiding cystourethrogram is again the best
investigation for diagnosis. The valves are destroyed by transurethral route by fulguration through panendoscopy or by
fragmentation by the passage of sounds.
Congenital obstruction of the neck of the bladder (Marion’s disease).—
The symptoms are almost identical with those of the congenital valves ofthe posterior urethra. Diagnosis can be made
by cystoscopy through which hypertrophied interureteric ridge can be seen. Voiding cystourethrography will show non
filling of the posterior urethra.
TREATMENT is Y-V plasty.
CONTRACTURE OF THE BLADDER NECK
AETIOLOGY.— It is usually due to congenital muscular hypertrophy at the neck of the bladder or fibrosis
at the same place as a sequel to chronic prostatitis in men or urethro-trigonitis in females.
CLINICAL FEATURES.— Patient may present at any age starting from young children to above 50 years.
When the aetiology is congenital muscular hypertrophy, patients are usually young children. Dysuria is the
main symptom with ultimate development of hydroureter and hydronephrosis. Recurrent urinary infections
are also common presentation. A distended bladder is easy to feel. Similarly hydronephrosis is also detected
by swelling in the loin. Secondary infection may lead the condition to severe pyelonephritis.
When the condition presents after the age of 50 years, it is difficult to differentiate from benign enlargement
of the prostate from symptoms point of view. That straining helps to increase the flow of urine and that there
is no prostatic enlargement are the findings in favour of this condition.
TREATMENT-
MEDICAL TREATMENT.— Alpha blocking agents e.g. phenoxybenzamine have been used to relax the
bladder neck. There is an important side effect of this drug, that is postural hypotension.
SURGICAL TREATMENT.— This is often required as the medical treatment is mostly a failure.
(i) Transurethral resection of the bladder neck has been performed with some success. The condition
may recur in a few cases due to inadequate division of the fibres at the bladder neck.
(ii) Bonnin ’v operation.— Though transurethral resection is gaining popularity, yet this open operation
is suitable for failure cases. An Y-shaped incision is made on the anterior wall of the bladder near its neck.
The apex between two limbs of the Y is brought down to the end of the vertical limb of the Y to make the incision
a V-shaped one. This will increase the circumference of the neck of the bladder. The V-shaped incision is now
sutured.
URETHRAL CALCULUS
Calculi may occur in the urethra, though rarely, than in other parts of the urinary tract. Such calculus may be formed
behind a urethral stricture or in an urethral diverticulum. These calculi are usually composed of phosphates. Calculus may
secondarily come to the urethra from above and become arrested in the prostatic (rarest), bulbous or in penile part of the
urethra. Such migratory calculi are usually seen in children due to the comparatively large neck of the bladder which allows
these calculi to pass through.
NEOPLASMS OF THE URETHRA

These are extremely uncommon. The varieties of neoplasms which can be seen in the urethra are—polyp,
papilloma, angioma and carcinoma
Polyp.— These are usually seen around verumontanum. A few cases of congenital urethral polyp have
been noticed. Otherwise these are usually associated with chronic urethritis. So urethritis should be treated
alongwith destruction of the polyp.
Papilloma.— These are usually seen in the fossa navicularis just inside the external urinary meatus.
Occasionally multiple papillomas of the posterior urethra have been detected which are usually associated with
papilloma of the bladder. Slight haematuria with the onset of micturition is the main symptom.
Angioma.— Haematuria is the main complaint, which is often profuse and may occur independent of
micturition.
Treatment of all benign neoplasms is diathermy coagulation through a urethroscope.
Carcinoma.— This is extremely rare Profuse urethral discharge is the main symptom. It is often
associated with or cause of urethritis. Later on the discharge becomes blood-stained. A tendency to bleed easily
during instrumentation is very much suspicious. Biopsy establishes the diagnosis.
Treatment.— When the carcinoma is in the anterior urethra, either partial or total amputation of penis is
required according to the site of carcinoma.
When carcinoma is situated in the posterior urethra, more extensive operation in the form of radical
prostatectomy should be considered.
1173
CHAPTER- 52
TESTIS, EPIDIDYMIS AND SCROTUM
DEVELOPMENT OF THE TESTIS
EMBRYOLOGY —
Testis develops in the lumbar region from the thickened epithelium on the medial side of the mesonephric ridge in
the 5th week. This thickened epithelium continues to proliferate displacing the mesonephros in a dorsilateral direction
and forming a projection into the coelomic cavity, which is termed the genital ridge. Upto the 7th week the genital gland
possesses no differentiating feature. The proliferating epithelium on the surface sends a number of cellular cords inwards
which are known as testis cords. At the 7th week a mesenchyme cuts off the testis cords from the surface and forms the
tunica albuginea. At this stage one can differentiate between testis (where tunica albuginea is prominently present) and
ovary (where tunica albuginea is absent). The testis cords encroach on the medulla where they unite with the network
derived from the mesenchyme and become rete testis. The premordial germ cells are incorporated in the cords (testis
cords), which later become enlarged and canalised to form the seminiferous tubules. The cells derived from the surface
of the gonad form the supporting cells of Sertoli. The interstitial cells of the testis are derived from the mesenchyme which
do not become incorporated into the tubules. The cords of the rete testis canalise at a later stage and become connected
to the mesonephric duct by 5 to 12 most cephalic of the persisting tubules and these become exceedingly convoluted and
form the lobules of the head ofthe epididymis. The mesonephric duct becomes the canal of the epididymis and the ductus
deferens of the testis.
DESCENT OF THE TESTIS.—At first, the testis lies on the dorsum ofthe abdominal wall. Mesenchymal cells form
a cord which extends from that part of the skin which later forms the scrotum, through the inguinal fold to the lower pole
of the testis. This cord later becomes a fibromuscular bundle and is termed the gubemaculum testis. It traverses the site
of the future inguinal canal, which is formed around it by the muscles of the abdominal wall as they become differentiated
The testis descends along the path of the gubemaculum whether or not due to pull of it. A fold peritoneum protrudes down
the inguinal canal along with the testis forming the processus vaginalis. The lower pole ofthe testis is kept in apposition
with the deep inguinal ring by the
gubemaculum until the 7th month
Suddenly the testis passes through the
inguinal canal and gains the scrotum
As it descends, it is necessarily accom
panied by its peritoneal covering and
by a fold of peritoneum from the adj oin-
ing peritoneum from the iliac fossa
which is drawn down as the processus
vaginalis as also its blood vessels and
nerve supply. The peritoneal covering
of the testis which represents the distal
end of the processus vaginalis and into
which the testis projects, is termed the
tunica vaginalis testis. The part of the
processus vaginalis which is associated
with the spermatic cord in the scrotum
and in the inguinal canal normally be
Fig.60.1.— Diagram showing human gubemacular apparatus and
testicular descent. comes obliterated. The fascial covering
of the testis and spermatic cord includ
ing the Cremaster are developed from the surrounding structures as the testis descends.
Time-table of testicular descent.—
In the lumbar region in the 2nd month of foetal life.
In the iliac fossa — 3rd month of foetal life.
At the deep inguinal ring — till the 7th month.
Travels the inguinal canal — in the 7th month.
At the superficial inguinal ring — at the later part of the 7th month or 8th month.
Scrotum (its final position) — testis enters the scrotum in the 9th month.
Factors which cause descent of testis.—
(i) Shortening and active contraction of the gubemaculum.

(ii) Increased intra-abdominal pressure.
(iii) Active contraction of the lower fibres of the internal oblique muscle which squeezes the testis through the
canal.
(iv) Higher temperature of the abdominal cavity, which is detrimental to spermatogenesis.
(v) Hormone, specially Chorionic gonadotrophin from the maternal circulation helps descent of the testis.
Causes of undescended testis.—
(i) Abnormality of the gubemaculum testis.— Gubemaculum plays a major role in descent of testis
and abnormality of this structure may result in undescended testis.
(ii) Intrinsic testicular defectThe testis may be insensitive to gonadotrophins and may not act to it
This may lead to undescended testis.
(iii) Deficient gonadotrophic hormonal stimulation.—Lack of adequate maternal gonadotrophins may
be a cause of incomplete descent.
(iv) Obstruction due to adhesions of the testis.
(v) Short vas deferens.
(vi) Short testicular vessels or pampiniform plexus.
(vii) Imperfectly developed testis interferes with its own descent.
UNDESCENDED TESTIS
Definition.— An undescended testis is one which has failed to descend to the scrotum and is retained at
any point along the normal path of its descent.
Undescended testis is more common on the right side (50%). It is less common on the left side (30%). About
20% cases are bilateral. When both the testes are absent in the scrotum, the condition is called cryptorchidism
(Hidden testes). As the right testis descends later than the left testis, undescended testis is more common on
the right side
Pathology of undescended testis.—
(i) Growth of the testis.— It is clear now that scrotal temperature is at least 1°C cooler than the
abdominal temperature. Proper development of spermatogenic tubules cannot take place in abdominal cavity
As a result the spermatogenic tubules are of diminished size and fewer spermatogonia have been detected in
undescended testis in boys at about 6 years of age. After 6 years of age, changes become more obvious. The
diameter of the tubules is smaller than normal. The number of spermatogonia decreases. Fibrosis is noticed
between the tubules.
After puberty, the difference is obvious and the undescended testis is much smaller and flabby than the
normal intrascrotal testis. The undescended testis is hardly more than 'A the size of its intrascrotal counterpart
(ii) Internal secretoryfunction.—Fortunately the Leydig cells are not affected by body temperature and
are therefore usually found in normal numbers in undescended testis. So secondary sex characters appear and
endocrinologic cause of impotence is rare in this group. However in bilateral cryptorchidism, androgen level
is diminished to certain extent.
(iii) Epididymis remains separated from the testis by a long mesorchium, which is the primitive
mesogenitale which connects the genital fold to the mesonephros. So torsion of testis is more common.
(iv) Sometimes an undescended testis is associated with a hernial sac. In a series, about 90% of cases
of undescended testis were associated with patent processus vaginalis.
(v) Undescended testis may be associated with other urinary tract abnormalities.
(vi) Chance of malignancy is more in undescended testis. The chance is more if the undescended testis
remains in a patient of 10 years of age or older and many surgeons recommended orchidectomy for unilateral
undescended testis at this age group rather than orchidopexy.
Types of undescended testis.—
(a) Lumbar testis.— Complete failure of descent and the testis remains whence it was developed.
(b) Iliac testis.— Testis remains just deep to the deep inguinal ring.
TESTIS, EPIDIDYMIS AND SCROTUM 1175
(c) Inguinal.— The testis is in the inguinal canal.

(d) At the superficial inguinal ring.—The testis frequently comes to rest just outside the external inguinal
ring.
(e) Scrotal testis.— The testis lies in the upper part of the scrotum. It is often a retractile testis due to
contraction of overactive cremaster muscle. In this case the scrotal sac is of normal size. The testis is also of
normal size. The testis can also be brought down to the scrotum.
HISTORY.— Age.—Undescended testes are usually noticed in children, but are occasionally not noticcd
until adolescents or even adult life.
SYMPTOMS —
(i) Obviously absence of one or both testes from the scrotum is the commonest presenting symptom. In
fact the child or the parents first notice that the scrotum is not developed, rather than absence of testis within it.
(ii) Occasionally patients present in adult life with infertility, though secondary sex characteristics are
usually normal.
(iii) In a small proportion of cases patients present with indirect inguinal hernia i.e. a swelling in the
groin, along with undescended testis.
PHYSICAL EXAMINATIONS—
(i) The first thing which should attract clinician’s eye is absence of a testis or both the testes from the
scrotum. An incompletely descended testis should lie anywhere on the line of normal descent i.e. at the neck
of the scrotum, just outside the superficial inguinal ring, in the inguinal canal or deep to the deep inguinal ring
(ii) The testis is only palpable when it is at or outside the superficial inguinal ring.
(iii) When the testis is within the inguinal canal, it is hardly palpable as the soft testis of the early life
is submerged in the nonresisting floor of the inguinal canal and covered by tendinous aponeurosis of external
oblique. It must be remembered that when a testis is palpable in front of the inguinal canal it is an ectopic testis
lying in the superficial inguinal pouch, a space lined by loose areolar tissue superficial to the external oblique
aponeurosis and it is not an undescended testis. Such testis is often retractile testis and attains that position
by the strong contraction of the cremaster muscle which is very well developed in childhood. This condition
is often confused with incomplete descended testis. But two points should be borne in mind to differentiate this
condition from incomplete descended testis — (a) In this case the scrotum is normally developed, whereas
scrotum is under-developed in case of incompletely descended testis, (b) Such testis can be milked into the
scrotum. Any testis that can be manipulated into the scrotum is a retractile and not undescended testis.
(iv) If the testis is not palpable, one can press firmly along the line of the inguinal canal to see if there
is tender area or a point where testicular sensation is evoked.
(v) It must be remembered that undescended testis is often associated with indirect inguinal hernia and
one should always examine for presence of such hemia.
(vi) Occasionally one may feel a lump in the line of the testicular descent and there is an empty scrotum
particularly in adults. Such swelling should arouse suspicion of malignancy in case of adults. The risk of
malignancy in an incompletely descended testis is about 50 times more than in a descended testis.
Complications of incomplete descent.—
1. Torsion of the testis.
2. Epididymo-orchitis in an incompletely descended testis often gives rise to difficulty in diagnosis, but
absence of testis in the scrotum of the corresponding side should arouse suspicion.
3. An associated indirect hemia or interstitial hernia is frequent with incompletely descended testis and
it is quoted as high as 80% of cases.
4. AtrophyAn incompletely descended testis is smaller than the normally descended testis and it may
undergo more atrophy particularly when it is situated in the inguinal canal due to recurrent trauma.
5. Pain.—A testis situated in the inguinal canal is often liable to trauma and gives rise to pain in the groin.
6. Sterility.— In bilateral cases this may be seen.
7. MalignancyAn incompletely descended testis runs the risk of being malignant 50 times more than
that of normally descended testis. Such malignancy is more common in abdominal testis rather than inguinal
testis. Seminoma is more common in such malignancy.
TREATMENT.—
A. Hormone therapy.—
This should not be used as a routine treatment for incompletely descended testis. The only indications for
hormone treatment are —
(i) When the surgeon is not sure whether the case is one of retractile testis or not.
(ii) In case of bilateral incomplete descended testis associated with hypogenitalism and obesity this is
the treatment of choice. It is said that hormone works better in bilateral cryptorchidism, but one cannot waste
valuable time by giving hormone, when there is more chance of getting an almost normal testis if orchidopexy
is performed before 6 years of age. In bilateral cryptorchidism some physicians have claimed success upto 10%.
If the hormone treatment becomes successful, the testis would have descended by puberty without any
treatment. Many of the undescended testes are in fact retractile testes.
The hormone mostly used is the Chorionic gonadotrophin in doses of 5000 i.u. intramuscularly daily for
3 to 5 days. It may be given in another dose of pregnyl (Chorionic gonadotrophin extracted from the placenta)
which is given 1000 i.u. (international units) twice a week until the testis descends. The course should not be
exceeded for more than 10 weeks and it should never be repeated. If the child refuses to accept injections.
Methyltestosterone 5 mg/d may be given by mouth for 1 month.
B Surgical treatment.—
1. Orchidopexy is the treatment of choice. Since definite histologic change can be demonstrated in an
incompletely descended testis by 6 years of age, placement of the testis in the scrotum (orchidopexy) should
be accomplished by the age of 5 years. Now with the aid of modem anaesthetics orchidopexy can be performed
even earlier. It is unnecessary to do this operation before completion of second birthday of the child. After 6
years the percentage of successful operation falls considerably.
In case of cryptorchidism (bilateral incompletely descended testis) one side should be operated on 6 months
earlier than the other side.
Operative procedures.— An incision is made over the inguinal canal (as for the operation for inguinal
hernia). The inguinal canal is opened, (i) LENGTHENING OF THE SPERMATIC CORD.—
(a) Generally the ductus deferens is amply long enough to bring the testis to the scrotum. It is the
mesoblastic elements of the cord which are shortened i .e. coverings of the cord and vessels of the testis. The
cord and testis are freed from the surrounding structures. A search should be made to find out an inguinal
hernial sac.
(b) The hernial sac is dissected free from the surrounding structures and a herniotomy is performed.
(c) All fibrous and fascial bands that fix the cord in the inguinal canal are divided. This is particularly done
near the internal inguinal ring where all the coverings of the ring are divided. Fibrous bands are severed Only
the vas and its blood vessels and the testicular blood vessels and nerves are preserved.
(d) The testicular vessels are dissected from the peritoneum to which these are usually adherent. By this
whole procedure the wide outward curve of the vessels is abolished and the spermatic cord gains about 1 inch
in length.
(e) If this is not sufficient the fascia transversalis medial to the deep inguinal ring is incised upwards and
medially parallel to the inferior epigastric vessels (sometimes this vessel may have to be sacrificed between
ligatures). By this procedure the course of the spermatic cord becomes more direct.
(f) If still the testis cannot be brought down to the scrotum, one may have to divide major part of the
pampiniform plexus between ligatures. Only 2 veins are kept intact. This will also lengthen the spermatic cord.
(ii) RETAINING THE TESTIS IN THE SCROTUM — Testis shows a tendency to retract even if it has
been brought down to the scrotum. A few operations are suggested to fix the testis in position. These are:—
(a) External anchorage.— The simplest method of fixing the testis in its scrotal bed is to pass a stitch
through the tunica albuginea at the lowerpole of the testis and to bring this out through the bottom of the scrotum
to anchor it to the skin of the inner side of the thigh by tying it over a piece of gauze. The stitch is kept in position
for no less than 3 weeks. After that the stitch is removed. In most cases, the testis remains in the scrotum.
, (b) Keetlev-
Torek opera
t i o n - The testis
L is brought out
through the bot
tom of the scro
Anterior superior
tum and is placed
in the subcutane
Inguinal ligament
ous tissue of the
Testis in superficial
inguinal pouch inner side of the
thigh, where it is
secured by stitc
(a)
hes to the fascia
lata of the thigh.
The wound in the
thigh is closed.
A second
operation is per
formed at about
4 months later
than the first one.
The testis is sepa
rated from the th
igh and is placed
in the scrotum.
The wounds of
the thigh and the
scrotum are su
tured. Sometim
es the testis is
kept in a pocket
(</> between the scro
tal skin and the
Fig. 60.2.— Shows the technique of elongation of the spermatic cord in case of undescended testis, dartos muscle by
a.—Shows the most common position of undescended testis, b. & c.—Show dissection of the testismaking a small
alongwith its spermatic cord. d.— Shows the technique of adoption of shorter straight path of theopening through
testicular vessels and the spermatic cord to bring down the testis to scrotum. the dartos mus-
cle. This will give a better anchorage to the testis.
(c) Ombredanne ’s operation.— In this operation, the undescended testis is brought out through a small
opening in the median septum of the scrotum to lie with its fellow in the opposite compartment. This operation
has come into disrepute as not only it is difficult to make an opening on the median septum of the scrotum,
but also the testis shows a tendency towards retracting as it is not properly anchored.
(d) Denis Browne's operation. — In this operation the neck of the scrotum is narrowed with a purse-string
catgut suture and the testis is anchored with an absorbable suture which passes through the scrotal skin to be
anchored to the skin on the medial aspect of the thigh. The suture is kept in position for 2 to 3 weeks.
(e) Dartos pouch.— A pouch is made between the Dartos muscle and the scrotal skin. The incompletely
descended testis is brought down to the corresponding compartment of the scrotum and is pushed through an
opening in the Dartos muscle into the Dartos pouch. The opening in the Dartos muscle is closed by catgut sutures.
TWO STAGE OPERATION.— Sometimes the spermatic cord cannot be sufficiently lengthened to bring
the testis into the scrotum. In this case, after first stage of mobilisation, the testis is anchored with a non
absorbable suture. 6 months later fur
ther mobilisation is attempted and in
this case it may be possible to
lengthen the cord further and the tes
tis may be brought down to the scro
tum. The testis is retained in the scro
tum by one of the above methods.
2. Orchidectomy.— It is only
advocated when the opposite testis is
normal. The indications are :—
(i) After puberty.
(ii) When the incompletely de
scended testis cannot be brought
down to the scrotum.
3. Orchidocelioplasty.— This
means abdominal replacement of the
testis. This is only indicated when the
other testis has been removed previ
ously and this testis cannot be brought
down to the scrotum. This operation
is justified on 2 grounds —
(i) It preserves internal secre
tion of the testis and
(ii) The testis is protected from
trauma.
LAPAROSCOPY IN UNDE
Fig. 60.3. — Methods of orchidopexy. a.— External anchorage, b.-
Ombredanne’s operation, c.— Dartos pouch. SCENDED TESTIS.—
In case of non-palpable unde
scended testis, the surgeon is often posed with difficulty of locating the testis. HCH stimulation by injection
may raise serum testosterone level and thus the position of the testis may be
detected. But this test is not helpful in unilateral impalpable undescended
testis. Moreover HCH stimulation may help therapeutically in that the testis
may descend and may become palpable.
The methods, now at hand, to locate non-palpable undescended testes
are — ultrasound scan of abdomen including pelvis and CT Scan of the abdo
men. But these non-invasive techniques can detect only in 40 to 50% of cases.
Aortography with selective gonadal angiography may locate the testis but not
without complications. Magnetic Resonance Imaging has an accuracy of 50%
in locating undescended abdominal testis.
Laparoscopy through a small hold is definitely quite helpful to detect
undescended testis. Access is made into the abdominal cavity. The retroperi
toneal area and the area of the inguinal ligament are inspected. If a reasonable
sized testicle is identified and it is decided to proceed to orchidopexy in due
course, the spermatic vessels are divided between ligatures and 6 months
later orchidopexy may be performed when collateral vessels along vas
Fig. 60.4.— Shows the port sizes
deferens have developed sufficiently to keep the testicle viable. If there is a in millimetres and positions of
small insignificant testicular remnant, simple dissection and removal may be ports used for the treatment of
carried out. cryptorchid testis.
TESTIS. EPIDIDYMIS AND SCROTUM 1179
ECTOPIC TESTIS
An ectopic testis is one in which the testis fails to descend into the scrotum and is deviated from its normal
path of descent.
It is by far much less common than undescended testis. An ectopic testis is an otherwise a normal testis,
but an undescended testis is often underdeveloped.
According to Lockwood the gubemaculum testis has five tails :
1. The scrotal tail — which is the main one.
2. Pubic tail — attached to the pubic tubercle.
3. Perineal tail — attached to the perineum.
4. Inguinal tail — attached to the front of the inguinal canal.
5. Femoral tail — attached to the saphenous opening.
The scrotal tail is the strongest and the other tails normally disappear and that is why the testis normally
descends to the scrotum. In case one of the four accessory tails becomes stronger, the testis is drawn towards
the attachment of that tail and then the testis is called an ‘ectopic testis'.
Positions of the ectopic testis.—
(a) Superficial inguinal pouch.— This is the commonest type. The testis lies lateral to the superficial
inguinal ring, in the plane between the aponeurosis of the external oblique and the membranous layer of the
superficial fascia (fascia of Scarpa). This is due to the pull of the inguinal tail.
(b) Pubopenile ectopia.— This is extremely rare. The testis lies in front of the pubis at the root of the
penis. It is due to pull of the pubic tail.
(c) Perineal ectopia.— The testis lies in the superficial perineal pouch i.e. under the fascia of Colies and
between it and the superficial perineal muscles. A swelling is seen in front of the anus on one side of the
midline. It is due to pull ofthe perineal tail.
(d) Crural or femoral ectopia.— The testis lies at the roof of the thigh near the fossa ovalis (saphenous
opening). It is due to pull of the femoral tail.
COMPARISON BETWEEN UNDESCENDED TESTIS AND ECTOPIC TESTIS
Undescended testis Ectopic testis
1. The testis is arrested in its normal path of 1. The testis deviates from its normal path of
descent. descent.
2. Undescended testis is usually undeveloped. 2. The testis is fully developed.
3. Scrotum is not developed on that side and 3. Though empty, the scrotum is usually fully
empty. developed.
4. The length of the spermatic cord may be 4. The length of the spermatic cord is usually
short. longer.
5. Spermatogenesis is poor after 6 years of age. 5. Spermatogenesis is perfect.
6. Undescended testis may be associated with 6. This is never associated with indirect inguinal
indirect inguinal hemia. hemia.
7. Treatment — mainly operation, though hor 7. Treatment is operation and is usually success
mone therapy may be tried in selected cases. ful.
Operation is not at all successful after pu
berty.
8. Complications.— List of complications has 8. Complications.— The main complication is
already been mentioned. liability to injury.
TORSION OF THE TESTIS OR TORSION OF THE SPERMATIC CORD

Torsion of the spermatic cord or torsion of the testicle is an uncommon condition which is limited to
peripubertal males. The importance of this condition lies in the fact that it causes strangulation of the blood
supply to the testis and unless it is treated within 3 to 4 hours, testicular atrophy is inevitable.
(i) Inversion of the testis.
(ii) Long mesorchium — in this case the body of the testis only rotates without involving the spermatic
cord, that means torsion of the testis occurs without torsion of the spermatic cord.
(iii) Undescended or ectopic testis.
(iv) High investment of tunical vaginalis — it causes the testis to hang within the tunica vaginalis which
may initiate rotation.
(v) A voluminous tunica vaginalis — this also gives adequate space to the testis to rotate.
It should be borne in mind that the abnormality which causes torsion is usually bilateral.
Initiating factors.— Spasm of the cremaster muscle which inserts onto the cord obliquely seems to be the
main initiating factor. During contraction of the abdominal muscles the cremaster muscle also contracts. Con
traction of this muscle causes the left testis to rotate anti-clockwise and the right testis clockwise. Contraction
of cremaster occurs at the time of straining at stool, lifting heavy weight and coitus. It must be remembered that
torsion also occurs during sleep and in most instances there is congenital abnormality either in the descent of
the testis or in the tunica vaginalis or in the spermatic cord.
Pathology.— Torsion usually occurs from within outwards that means the left testis rotates anti-clock
wise and the right testis rotates clockwise. With the vascular occlusion which occurs in torsion, there is oedema
of the testis and the cord upto the point of occlusion. Gradually it leads to gangrene of the testis and epididy
mis.
HISTORY.— Age.— Torsion is most commonly seen between 10 and 25 years of age. As the cause is
congenital, the second most common incidence is seen during infancy.
SYMPTOMS.— Patient suddenly complains of severe pain in one testicle or in the groin. The pain is
sudden and agonizing. Pain is often referred to the lower abdomen and in right side, appendicitis has been
wrongly diagnosed in such cases. Nausea and vomiting are very common.
In completely descended testis diagnosis is rather easier, but in incompletely descended testis it is difficult
to differentiate it from a strangulated inguinal hemia.
LOCAL EXAMINATION.— The scrotum is swollen and tender. The scrotum may also be normal or red
and oedematous. Sometimes it is difficult to differentiate it from acute epididymo-orchitis. Elevation of the
scrotum usually relieves pain in epididymo-orchitis, but increases the pain in torsion of the spermatic cord.
In torsion testis, if the testis can be carefully palpated, it is often lying in the horizontal position.
Gradually within a few hours after onset the patient becomes pyrexic with slight leucocytosis.
Torsion can be differentiated from epididymitis by using Doppler stethoscope in conjunction with
ultrasound. The testis which has been made ischaemic with torsion will not echo sound; hypervascularity of
epididymis will increase sound. Differentiation can also be done by a rectilinear scan following intravenous
injection of "mTc. The Doppler stethoscope in conjunction with ultrasound is very simple test which
quickly diagnoses this condition.
Magnetic Resonance Imaging (MRI).— The twisted stalk of the testis and the thickened proximal
spermatic cord of testicular tortion are well revealed by MRI. In tortion, epididymitis and orchitis MRI is used
in preference to ultrasonography, as the latter requires manipulation of the scrotum, which is extremely
painful.
The two most important differential diagnoses are —
(i) Acute epididymo-orchitis — in case of torsion of completely descended testis. Epididymitis is un
usual before the age of 25 years.
(ii) Strangulated inguinal hemia — in case of torsion of incompletely descended testis.
Other important conditions are —
(iii) Mumps orchitis.
(iv) Trauma.
When in doubt, it is better to consider the diagnosis as torsion of the testis and the testis should be
explored immediately. Even in wrong diagnosis surgical exploration will not do any harm but waiting for
making correct diagnosis may lead to death of the testis.
Treatment.—
(i) If the patient comes to the surgeon early, manual detorsion may be tried. It should be remembered that
in torsion the left testis rotates anticlockwise and the right testis rotates clockwise. Therefore for detorsion the
concerned testis should be rotated in the opposite direction that means the left testis should be ‘screwed’,
whereas the right testis should be ‘unscrewed’. Detorsion will relieve pain immediately, so, this is a good index
to know that the manoeuvre has been correctly performed otherwise pain will increase.
Even if detorsion is successful surgical fixation of both testes should be done within the next few days.
(ii) If manual detorsion fails, immediate surgical exploration should be performed. If the testis is viable,
it must be fixed so that torsion does not recur. Even though the viability of the testis is questioned the seminif
erous tubules may be necrotic, yet the most hardy interstitial cells may become viable. Excision of the parietal
tunica vaginalis will cause the testis to stick to the scrotal wall.
Immediate operation should be performed on suspicion alone. Every minute counts and testis cannot
survive more than 6 hours of ischaemia.
Scrotal incision is usually preferred. Transverse incision is often applied. The incision is made deep, till
the testicle and the cord are dissected out. The direction of torsion should be noted. It is generally anticlockwise
on the left side and clockwise on the right side. The testicle is untwisted and it is wrapped in a warm pack. A
similar incision is made on the other side of the scrotum and the non-twisted testicle is delivered, noting any
abnormal anatomy that may be present. If the affected testis seems viable, it is returned to the scrotum and is
anchored to the side wall of the scrotum taking firm bite of the tunica with a fine nylon stitch. 2 or 3 such
stitches should be applied. Such fixation should be made on both sides. Excision of the parietal tunica vaginalis
may be performed to cause the testis to stick to the scrotal wall.
If the testis is obviously dead and black, it must be removed. A strong artery forceps is placed across the
cord and the cord is divided distal to the artery forceps to remove the testis. The cord is now tied with strong
catgut. If there is any hope of viability, the testicle should always be returned to the scrotum.
As the predisposing factors which cause torsion are bilaterally present, it is always advisable to fix the
opposite testis in the same fashion at the same sitting.
(iii) When the patient comes too late after days or weeks the torsion has occurred, one cannot achieve
much by exploring the affected side; but the opposite testis must be fixed as early as possible. Orchidectomy
of the affected testis is justified.
Prognosis.— If detorsion is done within 12 hours of onset — the result is good with 100% success.
If detorsion is done from 12 to 24 hours after torsion has occurred — recovery is possible in majority of
cases. Detorsion can be advised even from 24 to 36 hours, but preservation is doubtful.
If the case is delayed by more than 48 hours — orchidectomy is more advisable than detorsion operation.
VARICOCELE
Varicocele means varicosity of the veins of the spermatic cord. The veins become dilated, elongated and
tortuous. The veins of the spermatic cord include the pampiniform plexus i.e. testicular veins and the cremas
teric veins. Occasionally testicular veins may be normal, but the cremasteric veins become varicosed.
Surgical anatomy.— Veins of the spermatic cord include 3 groups of veins —
(i) Veins draining the testis and epididymis.
(ii) Veins accompanying the vas deferens.
(iii) Veins of the cremasteric muscle.
Veins of the testis and epididymis which form the pampiniform plexus is the most bulky constituent of the
spermatic cord. As the veins pass up from the testis and epididymis they are about 15 to 20 in numbers. As the
veins pass through the inguinal canal upwards they become reduced in number to 4 to 8. Just deep to the deep
inguinal ring these veins further coalesce to form two veins. When these two veins enter the abdomen they
unite to form a single vein, called the testicular vein and moves upwards by the side of the testicular artery in
the posterior abdominal wall behind the peritoneum. The right testicular vein drains into the inferior vena
cava, whereas the left testicular vein drains into the left renal vein at right angle. These testicular veins are
mostly devoid of valves except near their terminations where they are provided with valves.
The cremasteric veins anastomose freely with the testicular veins and these veins drain into the inferior
epigastric vein.
Causes.— (i) Majority of the cases are idiopathic and no definite cause can be detected, though valvular
incompetence has been incriminated (Fig.60.5).
(ii) Tall, thin, visceroptotic men are prone to develop this condition.
(iii) As the left testicular vein drains into the left renal vein at right angle, some obstruction at the place of
drainage is expected.
(iv) Sometimes the left testicular artery arches the left renal vein and may obstruct it, this will lead to
obstruction in drainage of the left testicular vein and varicocele may occur.
(v) Sometimes cremasteric veins become dilated which freely communicate with the pampiniform plexus
and drain into the inferior epigastric veins.
(vi) Varicocele may be secondary to renal cell carcinoma of the left kidney. The growth from the renal
cell carcinoma blocks the renal vein by venous permeation and prevents drainage of the testicular vein as the
left testicular vein drains into the left renal vein. So sudden onset of varicocele in middle aged man should
arouse suspicion of a renal cell carcinoma of the left kidney.
Predilection for the left side.— In more than 90% of cases the varicocele is seen on the left side. The
possible causes are:
(a) The left testicular vein drains into the left renal vein at right angle so there is chance of blockage of
drainage from the left testicular vein. But the right testicular vein opens obliquely into the inferior vena cava
and this drainage occurs freely.
(b) The total length of the testicular vein is more on the left side than on the right side — as the left
testicular vein drains at a higher level and the left testis hangs at a lower level.
(c) In about 15% of cases left testicular artery arches over the left renal vein and thus obstructs it and
hence to drainage of the left testicular vein.
(d) The loaded sigmoid colon may press upon the testicular vein and cause varicocele due to obstruction
in drainage.
(e) The left suprarenal vein also drains into the left renal vein and circulating adrenalin may cause con
striction of the testicular vein at the site of drainage.
(f) Occasionally the left renal vein may pass between abdominal aorta behind and the superior mesenteric
artery in front and may be pressurised by these two arteries which may lead to obstruction in its drainage and
hence the testicular vein to cause varicocele of the left side.
(g) Incompetent valves are more common in the left testicular vein.
Varicocele and spermatogenesis.— Varicocele increases temperature in the scrotum and this seriously
depresses spermatogenesis. To react to the rise of temperature on the left side of the scrotum, the dartos relaxes
and the left side scrotum elongates in a natural attempt to overcome the rise of temperature. So left side of the
scrotum hangs down. It must be confessed at present that there is no definite evidence that varicocele
depresses spermatogenesis and that varicocelectomy improves semen quality, spermatogenesis and rate of
conception.
HISTORY.— (i) Age.— It is more commonly seen in young adults.
(ii) Climate.— It is more frequent and more troublesome in hot climates.
(iii) Type of individual.— Tall, thin visceroptotic men are more often affected than short and fat indi
viduals.
SYMPTOMS.— (i) Small and symptomless varicocele occur in l/4th of normal men.
(ii) When the vein becomes large, they may cause a vague, dragging sensation and aching pain in the
scrotum or groin. Pain is due to the fact that the elon

gated scrotum can no longer support the testis and
its full weight is borne by the cord. The pain be
comes worse on prolonged standing or exertion.
(iii) A few patients may present with subfertility.
Bilateral varicoceles particularly can cause oligosper
mia and subfertility.
This condition should always be examined in
the standing posture, as the varicocele disappears
as the patient lies down.
On inspection one can see the dilated veins as
also impulse on coughing. The scrotum on the
affected side hands lower than normal.
On palpation the dilated veins typically feel like
a ‘bag of worms'. Impulse on coughing can be felt
distinctly. But this is thrill-like and not expansile in
nature as in case of congenital hemia. After occlud
ing the superficial inguinal ring with a thumb if the
patient is asked to stand up the varicocele fills from
below. After lightly holding the varicocele between
the thumb and the fingers, the patient is instructed
to bow down — this will minimise tension within
the veins.
In long standing cases the concerned testis
becomes smaller and softer than its fellow of the
opposite side.
Treatment.—
1. Conservative treatment.— No treatment is
required unless the varicocele is thought to contrib
ute to infertility or is painful or so large as to disturb
the patient. Scrotal support and reassurance often
relieve discomfort.
2. Operative treatment.— Indications for
operation are :—
(i) Varicocele is painful and is worrying the
patient inspite of conservative treatment.
(ii) The varicocele is so big as to disturb the
patient.
(iii) When varicocele contributes to infertility.
(iv) When the testis hangs at an abnormally low
level.
(v) When this condition makes one medically
unfit for any job.
CLASSICAL OPERATION.— Incision is made
as performed for inguinal hemia. The spermatic cord
is dissected out. All the coverings of the cord are Fig. 60.5.— Retrograde cremasteric venogram showing valvu
lar competence in the upper figure without varicocele; whereas
carefully split. The vas deferens with its artery and
there is distinct valvular incompetence and free flow into the
two veins of the pampiniform plexus with nerve fibres scrotum in the lower figure with presence of varicocele.
are separated from the main mass of the varicocele. Two clamps are applied to the main mass of varicocele
above and below with a gap of about 2 inches in between. The affected veins are ligated and divided so that the
intervening 2 inches of the main mass of the pampiniform plexus is removed. The clamps are then approximated,
the main mass of pampiniform plexus are tied proximal and distal to the division and the ends of the ligature
are tied together. So that the upper end of the pampiniform plexus lies in close proximity to the distal end of the
pampiniform plexus and the testis is lifted up.
SCROTAL APPROACH.— This operation is less preferred to the previous one. Through scrotal incision
the varicose veins are exposed. After separating two veins for maintenance of venous return the main mass of
the tortuous pampiniform plexus is ligated and divided.
The disadvantages of this technique are —
(i) It is difficult to dissect the veins separately just above the testis.
(ii) Free anastomosis exists in this area, so the operation is hardly successful.
(iii) Bleeding is more troublesome.
(iv) Scrotal haematoma may complicate the convalescent period and infection following operation may
mar the effectivity of the operation.
(v) There is chance of damage to the testicular artery.
PALOMO OPERATION.— In this operation the testicular veins are ligated just above the deep inguinal
ring. An incision is made 1 inch above the level of the deep inguinal ring. The parietal muscles are separated
as performed in gridiron incision. The extraperitoneal fat and the peritoneum are retracted medially. The
testicular veins are exposed, which lie on the posterior abdominal wall lateral to the external iliac artery. The
testicular veins are ligated.
This operation is simple and can be performed under local anaesthesia. There is less chance of jeopardising
the blood supply to the testis as even if the testicular artery is ligated, the testis will get adequate blood supply
from the anastomosis between the cremasteric artery and artery to the vas.
Its main disadvantage is that it aggravates the varicocele in 10% of cases.
Laparoscopic varicocele ligation.— This is an ideal procedure for gaining familiarity with laparoscopic
surgeiy. The object of the operation is to clip and divide the dilated testicular vein or veins at the internal
inguinal ring. Through the 5 mm lateral port, simple grasping forceps are passed and through the midline
subumbilical port a pair of endoscissors is inserted. The vessels at the inguinal ring are usually clearly visible
behind the peritoneum covering which is picked up with forceps and incised with the scissors. The vein or the
veins are dissected free from the vas and the testicular artery over a length of about 2 cm. Through the lower
midline 10 mm port an endoscopic liga-clip applicator is passed and the veins are clipped and divided with
endoscissors.
This operation can be performed as a day case and it takes about 30 minutes to complete.
CYSTS CONNECTED WITH THE EPIDIDYMIS
Cysts which may occur in connection with the epididymis can be divided into two broad groups —
1. CYSTS OF THE EPIDIDYMIS, which are congenital and usually derive from an embryonic remnant
around the epididymis and is filled with crystal clear fluid. These are usually multilocular cysts.
Aetiology.— These cysts are due to cystic degeneration of—
(a) Remnants of the paramesonephric or Mullerian duct — the appendix of the testis (sessile hydatid of
Morgagni).
(b) Remnants of the mesonephric duct or Wolffian duct system —
(i) The paradidymis or organ of Giraldes — this is the most common cause.
(ii) Appendix ofthe epididymis or pedunculated hydatid of Morgagni.
(c) The vas aberrans of Haller.
2. SPERMATOCELE — which is an acquired condition and a unilocular retention cyst derived from
some portion of sperm-conducting system of the epididymis.
CYSTS OF THE EPIDIDYMIS

(i) Though congenital, these cysts are usually found during middle life.
(ii) The condition is often bilateral.
(iii) These cysts are situated behind the body of the testis.
(iv) These are tense cysts. These consist of aggregation of a number of small cysts which feel like bunch
of tiny grapes.
(v) Fluctuation is difficult to elicit.
(vi) Transillumination test — these are brilliantly translucent, but are finely tessellated due to presence of
numerous septa giving an appearance of Chinese lantern.
(vii) The content of the cyst is crystal clear fluid (cf. spermatocele — which contains barley-water like
fluid), which will be evident on aspiration.
Cysts of the epididymis should be differentiated from —
Cyst of appendage of the testis.— This cyst is a small globular swelling at the superior pole of the
testis. It is unilateral (cf. cyst of the epididymis — which is often bilateral). When pedunculated this may
undergo axial rotation. The treatment of such cyst is removal of the cyst after ligation and division of the
pedicle.
Treatment.—
(i) If the cyst is small no treatment is required.
(ii) If the cyst is large and causing discomfort, some surgical treatment has to be contemplated —
(a) Aspiration is useless, as these cysts are usually multilocular.
(b) Excision of the cyst is all that is required. Such excision should be performed through scrotal incision.
Excision must be complete. The main disadvantage of such excision is that infertility may result from blockage.
The patient should be informed about this before operation.
SPERMATOCELE
This is an acquired condition. It is a unilocular retention cyst formed in the epididymis, derived from
retention of a portion of sperm-conducting duct of the epididymis. Obviously such cyst contains fluid
resembling barley-water containing spermatozoa.
(i) Patient presents with a scrotal swelling, which is usually small. Occasionally the swelling may be big
enough to make the feel that he possesses three testicles.
(ii) The swelling is situated in the head of the epididymis, above and behind the body of the testis. The
testis can be felt separate from the swelling.
(iii) The cyst is soft (cf. cyst of the epididymis — which is tense).
(iv) Fluctuation test is difficult to elicit, but is usually positive.
(v) Transillumination test — is negative (cf. cyst of the epididymis).
(vi) The fluid within the cyst resembles barley-water, which is revealed on aspiration.
Treatment.—
(i) Small spermatocele — does not require any treatment.
(ii) Big spermatocele causing discomfort and anxiety to the patient — always requires treatment.
Treatment includes —
(a) Aspiration — may be useful as it is a unilocular cyst.
(b) Excision of the cyst — is performed through a scrotal incision. Excision must be complete. The thin
coverings of the cyst are carefully peeled off layer by layer. Any residual attachment to the epididymis should
be ligated and divided.
75
EPIDIDYMO-ORCHITIS
This can be divided into acute epididymo-orchitis and chronic epididymo-orchitis.

ACUTE EPIDIDYMO-ORCHITIS.— In fact epididymis is first inflamed, which is known as
epididymitis and later on infection spreads to the testis and then the condition is called epididymo-
orchitis.
Aetiology.— At first infection reaches the globus minus of the epididymis via vas deferens and the
infection usually comes from either urethra, prostate or seminal vesicles. Such infection may be of two
types — (1) Sexually transmitted group from urethritis. This occurs in young patients and causative
organism is mostly Chlamydia or N.Gonorrhoea.
(2) The other type is associated with hydrostatic pressure associated with voiding or physical strain
which force infected urine from urinary tract infection or prostatitis or following prostatectomy or following
prolonged catheterisation through urethra or prostate via ejaculatory ducts and the vas deferens to the
epididymis. The causative organism is mostly Escherichia coli, Streptococcus, Staphylococcus or Proteus
or pseudomonas. Infection may reach epididymis through perivasical lymphatics.
Pathology.— At first there is cellulitis of the lower pole of the epididymis. Infection spreads from
the lower pole to the upper pole. The whole epididymis becomes swollen and indurated. Small abscesses
may be seen. Tunica vaginalis secretes serous fluid which becomes purulent. Gradually the testis
becomes swollen due to congestion and later on involved by infectious process. The tubular epithelium
may show necrosis. Infection may resolve completely without residual injury, but peritubular fibrosis
may result and occlude the ducts. So bilateral epididymitis may lead to low level of fertility or even
sterility.
Clinical features.— The initial symptom is pain and swelling of the epididymis alongwith fever,
malaise and chills. Urinary tract infection is often present with symptoms of frequency, urgency and
dysuria. The epididymis and testis both start swelling and become quite painful. The scrotal wall
becomes red, oedematous and glossy. Epididymis may become adherent to the scrotal wall. Occasionally
the infection may go up to abscess formation and discharge of pus may occur through the scrotal
skin.
It must be remembered that acute epididymo-orchitis often follows prostatectomy and urethral
instrumentation. It is particularly common when there is an indwelling catheter with associated infection
of the prostate. In case of indwelling catheter, closed drainage often reduce the incidence of epididymo-
orchitis alongwith early use of antibiotics.
SIGNS.— The scrotum is usually enlarged with overlying skin oedematous and reddened. In early
stage swollen and tender epididymis can be separated from the testis, but later on both testis and epididymis
become one mass with great tenderness. There may be secondary hydrocele which is lax. There may be
urethral discharge.
Palpation of prostate may indicate acute or chronic prostatitis.
Two conditions should be kept in mind when one comes across a case of acute epididymo-orchitis.
Firstly it may develop from mumps in about 18% of males suffering from mumps when the partial
swelling of parotids is getting reduced. The main problem in this condition is that it may cause testicular
atrophy, which if occurs on both sides may even lead to infertility. It must be remembered that epididymitis
may even occur in mumps in absence of parotitis particularly in infanis.
Another condition — acute tuberculous epididymitis may occur in rare cases when it does not respond
to antibiotics and the vas becomes thickened.
Finally epididymo-orchitis may be involved by infections with other enteroviruses, brucellosis and
lymphogranuloma venereum.
Special Investigations.— Haemogram shows marked elevation of white cell count with shift to left.
Culture for urinary infection, scan and ultrasound of the scrotum may help in the diagnosis. A previous
history of prostatectomy and long term urethral catheterisation give hint to the diagnosis.
Treatment.— So long acute symptoms are present the patient should rest in bed with elevation of the
scrotum with a scrotal suspensory bandage and cotton wool. Doxycycline 100 mg daily is particularly
effective in young individuals with Chlamydial infection. If any organism can be isolated from urine, it
should be cultured and tested for sensitivity to chose the right antibiotic. Otherwise broad spectrum
antibiotics with ampicillin, tetracycline or aminoglycocides may be tried. The patient must drink plenty
of water. Antibiotic treatment should be continued until inflammation has totally subsided. Only if abscess
has been formed, surgical intervention is required in the form of drainage. There is always a chance of
some atrophy of the testis.
Vasectomy may be considered if acute epididymis is of retrograde type following prostatectomy or
prolonged use of intraurethral catheter.
CHRONIC EPIDIDYMO-ORCHITIS.—
Aetiology.— Tuberculosis is the main cause of chronic epididymo-orchitis and the infection is
retrograde from a tuberculous focus in the seminal vesicles.
Clinical features.— It is mainly the cragging swelling of the epididymis which is firm and aches a
little. Gradually the whole epididymis is involved but the testis remains almost unaffected. Secondary
hydrocele is present in 30% of cases which is lax. If one tries to feel the seminal vesicles, it will be swollen
and indurated. Gradually cold abscess develops in the epididymis and may burst in the posterior aspect of the
scrotum to cause sinuses in the scrotum. In many cases this condition is associated with renal tuberculosis.
Special Investigations.— Urine and semen should be examined for tubercle bacilla. Chest radiography
and intravenous urogram may indicate tuberculosis of the lungs and renal tuberculosis respectively.
Treatment.— Primary tuberculous focus must be treated with antitubercular drugs. It must be remembered
that antitubercular drugs are less effective in genital tuberculosis. So if resolution does not occur after a full
course of antitubercular chemotherapy, epididymectomy and even orchidectomy should be advised.
Chronic non-tuberculous epididymitis does occur following failure to resolve the acute epididymo-
orchitis. The diagnosis is difficult, but in this case the swelling is larger and smoother and the testis is
also very much involved. It is always essential in this case to exclude urethral stricture causing reflux
of urine along the vas deferens to involve the epididymis. Chronic non-tuberculous epididymitis does also
occur in sarcoidosis.
Treatment is vigorous antibiotics. If there is no resolution after 6 weeks one may consider
epididymectomy or orchidectomy.
ORCHITIS.— Only infection of the body of the testis occurs in case of syphilitic orchitis. Three
varieties can be recognized —
• Interstitial fibrosis causing painless destruction of the testis.
• Congenital syphilis may cause bilateral orchitis.
• In 3rd stage of syphilis there may be gumma of the testis causing unilateral painless swelling
of the testis which grows slowly. The testis feels harder and heavy and becomes difficult to differentiate
from tumour of the testis. ,
Another condition causes only orchitis and that is leprous orchitis. This causes testicular atrophy.
1. Torsion of testis.— In acute epididymo-orchitis this condition has to be differentiated. Prehn’s
sign is important in this respect — the scrotum is gently lifted up towards symphysis pubis. This will
relieve pain in acute epididymo-orchitis and increase pain in torsion of testis.
2. Torsion of appendages of testis.— In early stage palpation of tender appendage may differentiate,
but in later stage testis becomes swollen causing difficulty in diagnosis.
In both these conditions early exposure is required if any doubt exists about diagnosis.
3. Testicular tumour is difficult to differentiate in chronic epididymo-orchitis. Careful palpation
may differentiate testicular tumour from normal epididymis. Scrotal ultrasonography is often helpful. If
still in doubt one should explore the testis.
HYDROCELE
A hydrocele is an abnormal collection of serous fluid in the tunica vaginalis of the testis or within some
part of the processus vaginalis.
According to aetiology hydrocele can be divided into two categories —
1. Primary or idiopathic hydrocele — the cause of which is unknown i.e. there is no associated disease
in the testis or the epididymis.
2. Secondary hydrocele — when hydrocele is secondary to a disease in the testis and/or in the epididymis.
A secondary hydrocele is usually small and lax.
PRIMARY OR IDIOPATHIC HYDROCELE

Five varieties of such hydrocele can be seen —
(i) Vaginal hydrocele — the commonest.
(ii) Encysted hydrocele of the cord.
(iii) Infantile hydrocele. -»
(iv) Congenital hydrocele, s Unusual.
(v) Funicular hydrocele.J
Three very rare varieties are —
(vi) Hydrocele of the canal of Nuck.
(vii) Hydrocele of the hemial sac.
(viii) Hydrocele en bisac.
VAGINAL HYDROCELE.—
This is by far the commonest variety of hydrocele. In this condition there is abnormal accumulation of
serous fluid within the tunica vaginalis.
Aetiology.—
Though there is no associated disease of the testis or the epididymis, yet there must be some reason
why abnormal accumulation of serous fluid takes place in some individuals and not in all. The possible reasons
are:
(a) Defective absorption of hydrocele fluid by the tunica vaginalis — this is said to be the most common
cause though the reason is still obscure. Damage to the endothelial wall by low grade infection is the most
probable explanation.
(b) Excessive production of fluid within tunica vaginalis.
(c) Interference with drainage of fluid by the lymphatic vessels of the cord.
(d) There may be some connection with the peritoneal cavity as in the congenital variety.
Composition of the hydrocele fluid.— The hydrocele fluid is amber coloured. Its specific gravity varies
between 1.022 to 1.024. It contains water, inorganic salts, 6% of albumin and some fibrinogen and in old-
standing cases variable amount of cholesterol and tyrosine crystals. Due to the presence of fibrinogen, the
hydrocele fluid, when comes in contact with blood, clots firmly. When it does not come in contact with blood,
the hydrocele fluid does not clot.
HISTORY.—
Age.— Primaiy hydrocele is common in middle-aged people. It is not uncommon in children.
Geographical distribution.— Hydrocele is more common in tropical countries.
SYMPTOMS.— In majority of cases the only complaint is — swelling of the scrotum. Occasionally
patient does not seek advise till the sac has attained enormous size.
Slight amount of discomfort or pain may be associated with.
LOCAL EXAMINATIONS.— (i) Position.— Though hydrocele is often unilateral, it may be bilateral as
well.
(ii) On inspection one side or both the sides of the scrotum are enlarged with a notch at the middle of the
affected side of the scrotum. This is quite characteristic.

(iii) It is a purely scrotal swelling and one can get above the swelling (cf. inguinal hemia).
(iv) Fluctuation test — is positive, as it is a cystic swelling. The cyst is often tense in primary hydrocele
(cf. secondary hydrocele when — the swelling is lax).
(v) Transillumination test — is always positive as the hydrocele fluid is clear (except probably some
cases of secondary hydrocele when it is secondary to epididymo-orchitis and the fluid becomes turbid or in
some cases of filarial hydrocele when the skin and the tunica are thick).
(vi) On percussion it is always dull (cf. inguinal hemia).
(vii) Reducibility.— Vaginal hydrocele cannot be reduced.
(viii) Palpation of the testis.— Though occasionally testis may be palpable posterior to the vaginal hydrocele,
but as a rule the testis cannot be felt separately as the fluid of hydrocele surrounds the body of the testis. In
case of secondary hydrocele when it is lax the testis may be palpable through the fluid.
Scrotal ultrasound may be performed to know if the testis is normal or not. Acute hydrocele may occur in
young men due to testicular neoplasm.
1. Inguinal hemia.
2. Haematocele.
3. Pyocele.
4. Chylocele.
5. Filariasis of the scrotum.
6. Cysts in relation to the epididymis.
7. Encysted hydrocele of the cord.
8. Tumours of the testis.
Complications of a hydrocele.—
(i) Infection.
(ii) Atrophy of the testis.
(iii) Rupture — may be traumatic or occasionally spontaneous.
(iv) Haematocele — may result from trauma, but occasionally may occur spontaneously.
(v) Hernia of the hydrocele sac — occurs in only long standing cases. The sac herniates through the
dartos muscle due to tension of the fluid.
(vi) Calcification of the sac — sometimes occurs in longstanding cases.
Treatment.— Operation is definitely the treatment of choice.
INCISION.— (a) For small hydrocele incision is made vertically on the affected side of the scrotum
lateral to the median raphe.
(b) The incision, even in small hydroceles, may be placed on the median raphe to facilitate operation on
both sides. It is better to perform operation on both the sides even for unilateral cases, as there is predilection
for hydrocele to develop on both sides one after the other. In this case incision is deepened till the tunica
vaginalis of one side is approached. The operation is performed. The testis is put back into its own chamber.
Now the other side is approached through the same incision and the incision is deepened till the tunica vaginalis
of the other side is reached.
(c) In case of big hydrocele, excision of distal part of the scrotal skin is required to reduce the size of the
scrotum. For this purpose a transverse elliptical incision is made round the lower part of the scrotum. The
incision is deepened till the tunica vaginalis is reached. This incision exposes both the sides of scrotum. The
skin and dartos muscle distal to the incision are removed and after the operation the proximal margin of the
incision is closed by interrupted sutures.
(d) When small hydrocele is associated with an inguinal hernia, the incision is made as performed in case
of inguinal hemia. When the spermatic cord is reached the testis with the tunicavaginalis is pulled up through
the inguinal incision. Eversion of the sac is performed. The testis is sent back into the scrotum and the inguinal
operation is completed.
Types of operations.—
1. Jaboulay’s method of eversion of sac.— This radical method of operation is mostly practised now-a-
days for small and medium size hydroceles. An incision is made on the scrotal wall on the side of the hydrocele.
The incision is gradually deepened till the tunica vaginalis is reached. In this process one will come across a
few vessels which have to be ligated. As soon as the tunica vaginalis is reached, the vaginal sac is separated
from the rest of the scrotal wall by a finger. The sac is held in one hand and with another hand the tunica
vaginalis is incised. As soon as the incision is made, fluid will come out of the sac. The two margins of the
incision are held with two pairs of artery forceps and held upwards. The incision is extended upwards and
downwards to allow the testis to come out through this opening. The testis is brought out through the opening
and the two margins of the tunica vaginalis are sutured behind the testis, so that the secreting surface of the
tunica vaginalis will be lying outside. Care must be taken not to strangle the testicular vessels. The scrotal
wound is now sutured.
After dressing the wound, the patient should be instructed to wear suspensory bandage. Proper antibiotics
should be administered. The stitches are removed from the scrotal wall after 7 days.
2. Lord’s procedure of excision of sac.— This operation is mainly indicated for big size hydrocele. The
steps of operation upto opening of the tunica vaginalis are same as those ofthe previous operation. The tunica
vaginalis is now sutured with 10 to 12 catgut or Dexon sutures from the outedge of the tunica to the reflection
of the tunica from the testis and the epididymis. When these sutures are tied, the whole tunica is bunched at the
edge of the testis.
3. Excision of the sac.— The tunica vaginalis is separated from the dartos muscle. By incising the tunica
vaginalis, the fluid inside is drained. The whole of the sac of the tunica vaginalis is excised leaving a margin of
Vz inch by the side of the testis and epididymis. Bleeding from the cut margin is always considerable and is
controlled either by continuous mattress suture or with diathermy. This operation is particularly indicated in
case of:
(i) Haematocele;
(ii) Infected sac.
4. Subtotal excision is indicated in bigger hydroceles, where the incision is made in a circular fashion
at the middle of the scrotum. The incision is deepened till the sac of tunica vaginalis is reached. The skin
below the incision is excised and thrown away. The tunica vaginalis is now separated from the remaining
scrotal wall and subtotal excision of the tunica vaginalis is made. The tunica vaginalis is now sutured behind
the testis as Jaboulay’s method and the scrotal wound is closed as usual. Drainage may be required if there is
excessive oozing, otherwise it should better be avoided. This operation is aimed at reduction of the size of the
scrotum.
Drainage.— Unnecessary drainage is not at all advised. Drainage is only indicated —
(i) When the hydrocele is a big one.
(ii) When the surgeon is not sure about haemostasis.
(iii) In case of haematocele.
(iv) In case of filariasis.
(v) In case of infected sac.
Drainage is provided with a corrugated rubber sheet which is fixed to the skin with nylon or silk. The
drainage must be removed within 48 hours or earlier if the soakage is much less.
Tapping.— This operation, though not a radical treatment, is often indicated in case of old patients.
While tapping, the position of the testis is ascertained by fingers and pushed posteriorly. A wheal of local
anaesthetic solution is raised in an area of the scrotal skin that is free of visible vessels and rather dependent.
Incision is made on this place of the scrotal wall till the tunica vaginalis is reached. A fine trocar and a cannula
are then thrust into the sac through the scrotal incision. The fluid is evacuated slowly to avoid shock. Once all
the fluid has been evacuated, the cannula is withdrawn and the wound in the scrotal wall is sealed with tine, iodine.
Deposits of blood on the walls of the sac increase its thickness. After tapping, always examine the testis to
exclude neoplasm.
CONGENITAL HYDROCELE.—
In this condition the processus vaginalis remains patent so there is direct communication of the tunica
vaginalis with the peritoneal cavity. The communicating orifice at the deep inguinal ring is too small for the
development of a hemia.
DIAGNOSTIC FEATURES.— (i) Congenital hydrocele is present since birth.
(ii) When the patient lies horizontal, the hydrocele disappears as the fluid in the tunica vaginalis drains
into the abdominal cavity. In the erect posture hydrocele appears again.
(iii) In contradistinction to assumption, congenital hydrocele is not easily reducible due to narrowness of
the deep inguinal ring.
(iv) This condition may be associated with tuberculous peritonitis in children.
FUNICULAR HYDROCELE.—
In this condition the processus vaginalis remains patent upto the top of the testis where it is shut off from
the tunica vaginalis.
DIAGNOSTIC FEATURES.— (i) The swelling is inguinal rather than scrotal.
(ii) The testis can be felt separately.
(iii) Other features are similar to those of congenital hydrocele.
INFANTILE HYDROCELE.—
This condition is just opposite to the funicular hydrocele that means the tunica vaginalis is continuous
with the processus vaginalis which is shut off from the peritoneal cavity at the deep inguinal ring.
DIAGNOSTIC FEATURES.— (i) Not necessarily it is seen in infants, it is often seen in adults.
(ii) It gives rise to an inguinoscrotal swelling, very much similar to the inguinal hemia. It is not reducible
and there is no impulse on coughing.
(iii) It is a cystic swelling.
(iv) Fluctuation test is positive.
(v) Transillumination test is positive.
(vi) It does not disappear when the patient lies down.
ENCYSTED HYDROCELE OF THE CORD.—
When the central portion of the processus vaginalis remains patent, but its upper and lower parts are
obliterated, such condition is developed. Fluid accumulates in the patent portion of the processus vaginalis and
presents a swelling in relation to the spermatic cord hence it is called encysted hydrocele of the cord. Such
swelling is a localised oval cystic swelling situated in the scrotal region, inguinoscrotal region or in the inguinal
region.
DIAGNOSTIC FEATURES.— (i) Oval cystic swelling in relation to the spermatic cord.
(ii) Such cystic swelling is seen in the inguinal, inguino-scrotal or scrotal region depending on which part
of the processus vaginalis is patent.
(iii) The testis can be felt separate from the swelling.
(iv) In the swelling fluctuation test and transillumination test are positive.
(v) As the upper part of the processus vaginalis is obliterated — the swelling is not reducible and cough
impulse is absent.
(vi) Traction test.— This important test is pathognomonic of this condition. When gentle traction is exerted
on the testis the swelling moves downwards and becomes less mobile.
HYDROCELE EN BISAC OR BILOCULAR HYDROCELE —
In this rare condition the hydrocele has two intercommunicating sacs — one above and one below the
neck ofthe scrotum. The upper sac has no connection with the processus vaginalis and it is in fact the herniated
tunica vaginalis. The upper sac lies superficial to or partly within the inguinal canal or it may be situated in
between the muscle layers.
Cross fluctuation between the two sacs of the hydrocele is the most pathognomonic sign of this condition.
HYDROCELE OF THE HERNIAL SAC.— Sometimes hydrocele may associate with the hernial sac the
reason is that some fluid gets stagnated within the hernial sac when a tag of omentum blocks the opening of the
sac at the deep inguinal ring.

HYDROCELE OF THE CANAL OF NUCK.— This condition is the female counterpart of the previous
condition. It is seen in females in relation to the round ligament. Both the above conditions are true inguinal
swellings.
Treatment of other types of hydrocele.—
Hydroceles in infants should be left alone as they may disappear spontaneously.
If they persist, operation is the treatment of choice.
The steps of operation are — (a) The sac is dissected off the spermatic cord, (b) The sac is opened and the
fluid is drained, (c) The inside of the sac is inspected, (d) The sac is ligated at the deep inguinal ring and
divided, (e) The distal part of the sac is pulled out through the inguinal incision, (f) The testis is inspected, (g)
The tunica vaginalis is everted, (h) The testis is pushed into the scrotum, (i) The sac i.e. the patent processus
vaginalis is excised.
Treatment of encysted hydrocele of cord.—
Excision of the cyst.
SECONDARY HYDROCELE
Secondary hydrocele is an abnormal collection of fluid into the tunica vaginalis which accompanies disease
of the testis and/or the epididymis. The usual causes according to frequency are :
(i) Acute epididymo-orchitis.
(ii) Chronic epididymo-orchitis.
(iii) Syphilitic affection of the testis.
(iv) Malignant disease of the testis.
(v) Trauma.
(vi) Lymphatic obstruction. J.Rare
(vii) Post-herniorrhaphy hydrocele. J
In the last condition secondary hydrocele is due to damage of the lymphatic vessels of the tunica vaginalis,
which pass with those of the testis along the spermatic cord.
A secondary hydrocele hardly becomes big enough. It is lax, so palpation of the testis and epididymis is
not difficult. If the testis and the epididymis are not palpable due to excess collection of fluid, diagnosis of
secondaiy hydrocele is only possible after the fluid of the hydrocele has been aspirated out.
HAEMATOCELE
Haematocele can be divided into two categories — 1. Recent haematocele and 2. Old haematocele.
Recent haematocele. — The causes are —
(i) Trauma.
(ii) Tapping or aspiration of a hydrocele.
(iii) Neoplasm of the testis (rare).
Recent haematocele is almost always ushered with recent trauma followed by pain and swelling. In case of
tapping, immediate refdling is complained with.
Whether it is from trauma or from tapping of a hydrocele, a recent haematocele should always be treated
with urgent operation and exploration. The blood clots are evacuated. The tunica vaginalis if damaged, should
be excised. Otherwise eversion of the sac is performed. If rupture of the testis has occurred, a linear rupture
should be carefully sutured. When a segment of the testis has been damaged, that segment is wedge resected
and the tunica albuginea at the margins of the wedge are sutured carefully.
Old haematocele.— Slow haemorrhage into the tunica vaginalis gives rise to such condition. The patient
remains completely ignorant about the condition. Gradually he notices swelling ofthe one side ofthe scrotum.
Histoiy of trauma cannot be elicited. It is sometimes difficult to differentiate this condition from neoplasm of
the testis unless exposed.
In hydroceles and varicoceles MRI is quite diagnostic.
Treatment — Surgical exposure is the treatment of choice to detect the innocent nature of the swelling.
The testis is often disorganised and damaged and orchidectomy should be called for in these cases. Often the
testis becomes small and atrophic due to pressure of the haematoma.
TUMOURS OF THE TESTIS

Tumours of the testis are uncommon and few clinicians outside special centres will encounter, with any
frequency, the problems they pose in management. The importance of testicular tumour are :—
1. These tumours occur predominantly in young population.
2. About 99% of these tumours are malignant.
3. These tumours comprise slightly more than 1 % of all malignant tumours in the male. But these tumours
are the commonest form of malignancy encountered in males between 25 and 35 years of age.
Predisposing factors.— As with majority of neoplasms little is known about the cause of such tumours.
However several predisposing influences have been noticed.
1. UNDESCENDED TESTIS.— Although germ cell tumours can occur in infancy, yet these are uncommon
until puberty. The incidence of teratomas peak between 20 and 30 years of age and seminoma occurs mostly
between 30 and 40 years. Mixed germ cell tumours (GCT) peaks in the 3rd decade. Many risk factors promoting
the development of GCT have been identified, but perhaps the best known and most consistent being a histoiy
of cryptorchidism, which is itself increasing in incidence. Cryptorchidism-associated tumours are much higher
amongst black (40%), although overall testicular cancer is rare in blacks. Approximately 10% of tumours
occur in testes that are or have been maldescended, indicating that males with cryptorchidism have a chance of
developing testicular malignancy which is increased about 35 times compared with normal population. The
risk is 6 times greater for intra-abdominal testes than for lower-lying testes. Another peculiar feature which has
been noticed is that a person with cryptorchidism testis is more liable to have a tumour in the opposite normal
testis than is a person without cryptorchidism. Approximately one in five tumours occurring in patients with
unilateral maldescence appear in a normally descended testis.
Orchidopexy if performed after 6 years of age has no influence in minimising development of tumours in
testis. If orchidopexy is done before the age of 6 years, opinions vary. According to some chance of malignancy
is less. According to the others the risk remains the same and that age of orchidopexy has no effect on the risk
of cancer. A further surgical debate for the benefit of orchidopexy to prevent the development of GCT at
present is as follows. It must be remembered that adverse histological changes start to appear in the maldescended
testis at the age of 2 years, so it might be that only orchidopexy done at a very young age before 2 years can
reduce the risk of development of GCT.
Bilateral cryptorchidism is associated with the secretion of excessive quantities of gonadotrophins and
that the undescended testis functions abnormally and reacts in a peculiar fashion to androgens and
gonadotrophins. This may give some clue as to the cause of more chance of testicular tumours in maldescended
testis.
2. TRAUMA is often suggested as a causative factor though there are no grounds for support of this view.
Trauma merely draws the patient’s attention to the lesion. It may be possible that in some cases it may hasten
the growth of pre-existing tumour.
3. Hormonal factors are thought to contribute in the development of GCT. The peak incidence seen after
puberty suggests a link with testosterone or pituitary hormones. Exposure to maternal oestrogen occurs in
utero, in which dizygous twin pregnancies, known to have higher maternal oestrogen levels than monozygous
twins, are associated with a higher incidence of testicular cancer.
4. Exposure to environmental oestrogens may promote GCT. Synthetic oestrogens are found in many
modem substances e.g. detergents and plastics, but unlike naturally occurring oestrogens they do not bind to
sex hormone binding globulin (SHBG). The main sites of oestrogen action in males occur in the testis, prostate
and associated organs, though oestrogen receptors areâlso widespread in the gut, brain, heart etc. The enzyme
aromatase is found in the former sites and is responsible for catalysing the final step in the conversion of
androgens to oestradiol. There is no definite evidence yet that oestrogen exposure is harmful and may lead to
the evolution of GCT.

5. Another potential hormonal factor in the rising incidence of GCT relates to the population exposure to
DDT. The main metabolite of DDT is a potent androgen receptor antagonist. Although DDT has been banned
or severely restricted for the past 20 years, it has a half-life of 60 to 100 years and it has accumulated in the
food chain and is still detectable in human beings.
6. Genetic predisposition is another contributor to the aetiology of GCT as in many other malignancies.
About 1% to 2% of patients with GCT will also have an affected 1st degree relative. Conversely having a
brother or father affected constitutes 3 to 4 fold increased relative risk. The commonest chromosomal abnormality
is presence of an isochrome of the short arm of chromosome 12, which is seen in 90% of cases.
Contralateral testicular biopsy.— Approximately 2% of those who have GCT will develop a second
primary in the other testicle. A large study of contralateral testicular biopsies showed evidence of intra-epithelial
neoplasia (TIN) in 5%. Contralateral biopsy for all those presenting with GCT between 15 and 50 years is
often recommended. However contralateral biopsy is not a routine practise currently in U.K.
Classification of testicular tumours.—
There are numerous classifications, but the most accepted one is that described by the Testicular Tumour
Panel of Great Britain —
A. Germ cell tumours (GCT).—
(a) Seminoma — 45%.
(b) Teratoma — 38%.
(i) Teratoma differentiated (TD).
(ii) Malignant teratoma, intennediate (MTI) (Teratocarcinoma).
(iii) Malignant teratoma, undifferentiated (MTU) (Embryonal carcinoma).
(iv) Malignant teratoma, trophoblastic (MTT) (Choriocarcinoma).
(c) Combined tumour consisting of seminoma and teratoma — 14%.
B. Non-germ cel! tumours.—
(a) Interstitial tumours— 1.5%.
(b) Lymphoma.
(c) Other tumours.
The pick incidence of teratoma is between 25 and 30 years of age and that for seminoma is between 35
and 45 years of age and combined tumours occupy an intermediate age distribution.
Testicular tumours can be broadly classified into 2 main divisions :
1. Germinal tumours, constituting nearly 98% of the total and are presumed to arise from primordial sex
or germ cells.
2. Non-germinal tumours, constituting the remaining less than 2% of cases which take origin from the
non-germinal elements of testis. The non-germinal testicular tumours are almost always benign.
PATHOLOGY
Seminoma.— This is the most common form of testicular tumour in the adult. They almost never occur in
infancy.
For obscure reasons, the typical seminoma is somewhat more frequent in the right testis than in the left.
Seminoma starts in the mediastinum of the testis and as it grows it compresses the surrounding testicular tissue.
Macroscopically, it has a homogeneous grey-white or pink coloured lobulated cut surface, usually devoid
of haemorrhages or necroses. In over half the cases the entire testis is replaced. The spermatocytic pattern is
more likely to be slightly mucoid and may exhibit small areas of cystic necrosis and sometimes focal
haemorrhages. The tunica albuginea is a surprisingly effective barrier which is not penetrated. Occasionally
the tumour may extend to the epididymis or spermatic cord.
Microscopically, there are three types of seminoma — (i) typical seminoma, (ii) anaplastic seminoma and
(iii) spermatocytic seminoma. .
(i) The typical seminoma presumably derives from the proliferation of primary germ cells and presents
sheets of uniform so called ‘seminoma cells’ divided into poorly demarcated lobules by delicate septa of
fibrous tissue. The classic ‘seminoma cell’ is large and round to polyhedral, has a distinct cell membrane, a
clear cytoplasm and a large central hyperchromatic nucleus with one or two prominent nucleoli. Mitoses are
infrequent. Tumour giant cells may be present. The amount of stroma varies greatly — sometimes it is scanty
and other times it is abundant. The septa which form lobules, are infiltrated with lymphocyte in 80% of cases.
These lymphocytes are believed to reflect an autoimmune response and there is evidence that more lymphocytes
mean better prognosis.
(ii) Anaplastic seminoma — presents greater cellular and nuclear irregularity with more frequent tumour
giant cells. These giant cells are much bigger than the seminoma cells and mitoses are always present.
Lymphocytes and granulomatous reactions are infrequent.
(iii) Spermatocytic seminomas contain three varieties of cells — (a) small cells with narrow rim of
eosinophilic cytoplasm resembling secondary spermatocytes, (b) medium sized cells with eosinophilic cytoplasm
and (c) scattered giant cells either uni- or multinucleated.
A seminoma metastasises almost exclusively by the lymph vessels. It occasionally disseminates through
blood stream.
Teratoma.— Teratoma derives from totipotential cells having the capacity to differentiate into any of the
three germ layers — ectoderm, mesoderm and entoderm. This tumour may occur at any age from infancy to
adult life, though the highest incidence is between 25 and 35 years of age. Often the mesodermal element
predominates.
Macroscopic appearance.— Teratoma is devoid of the homogeneous appearance of the seminoma. Its cut
surface shows multiple cysts, haemorrhages and varying consistency in different parts. It is yellowish in colour.
Cartilaginous nodules are also seen.
Microscopic features.— Microscopically testicular tumour can be divided into four varieties, mentioned
in the classification.
(i) TERATOMA DIFFERENTIATED (TD).— Teratoma differentiated shows two variants — (a) cystic
teratomas (dermoid) and (b) mature solid teratomas. Cystic teratomas are relatively infrequent in the testis but
are the most common form of teratoma in the ovary. Cystic teratomas have better prognosis. Mature solid
teratomas are composed of heterogeneous collection of differentiated cells e.g. muscle bundles, islands of
cartilage, clusters of squamous epithelium, neural tissue and bits of intestinal wall all embedded in a fibrous or
mixed stroma. In more benign form all elements are differentiated and present no elements of potentially
malignant embryonic cells. The solid variants occur with greater frequency in infancy and childhood. Solid
teratomas in the adults contain element of immature tissue.
(ii) MALIGNANT TERATOMA, INTER MEDIATE (MTI).— This variety contains elements of immature
tissue e.g. primitive neuroectoderm, entoderm etc. Often the cancerous foci are intermixed. Sometimes these
malignant foci reproduce the pattern of embryonal carcinoma or choriocarcinoma.
(iii) MALIGNANT TERATOMA ANAPLASTIC (UNDIFFERENTIATED) (MTA), EMBRYONAL
CARCINOMA.— Since embryonal carcinomas are derived from embryonic cells, the tumours can exhibit all
the varied cell populations. Thus embryonal carcinoma may present a bewildering array of histologic patterns
recapitulating all of the embryonic or differentiated cell types derived from ectoderm, mesoderm and entoderm.
Embryonal carcinomas are seen in two forms — adult form and infantile form. In the adult form there is a
small tumour that does not replace the entire testis, but bulky tumours may be found. On cut surface the tumour
is basically grey-white, poorly demarcated with foci of haemorrhages and necroses. Histologically the cells
grow in alveolar, glandular, tubular or papillary patterns. More undifferentiated lesions present sheets of cells.
The neoplastic cells have epithelial appearance and are anaplastic with hyperchromatic nuclei having prominent
nucleoli. Mitotic figures are frequent, so are the tumour giant cells.
The infantile form is the most common testicular tumour in infants and children. On cross section it
presents a homogeneous yellow-white mucinous appearance. Microscopically there are varying spaces lined
by flattened embryonal epithelial cells. The individual tumour cells are quite anaplastic and contain vacuoles
and granules of alpha-fetoprotein. The vacuoles may coalesce to produce large clear area. This tumour is often
called ‘yolk sac tumour’.

Invasion and metastases occur earlier in the course of the disease. Due to relatively rapid growth of the
tumour, haemorrhage and necrosis are common. Spread is more through blood vessels and lungs are affected
earlier. Lymphatic metastasis to abdominal lymph nodes are also seen.
(iv) MALIGNANT TERATOMA TROPHOBLASTIC (MTT), CHORIOCARCINOMA.— This highly
malignant form of testicular tumour is composed of both cytotrophoblast and (plasmodial) syncytiotrophoblast,
both cell types must be present to make the diagnosis.
It is a rare testicular tumour. The lesion is usually very small and often they cause no testicular enlargement,
only small palpable nodule may be detected. The primary lesion may be a haemorrhagic or a clotted mass in
which bits of grey tumour can tr seen. This is the most characteristic feature of this neoplasm. Microscopically
the syncytiotrophoblastic cell is large with many irregular hyperchromatic nuclei and an abundant eosinophilic
vacuolated cytoplasm. The cytotrophoblastic cells are more regular, polygonal with distinct cell border with a
single fairly uniform nucleus. These grow in cords or masses usually the syncytial cells form a cap around a
cluster of cytotrophoblastic cells.
This neoplasm of the testis liberates chorionic gonadotrophins (CG) which can be detected in the urine or
serum. It is said that a diagnosis of choriocarcinoma should not be made in the absence of elevated levels of
CG. This occasionally can cause gynaecomazia. Majority of these cancers metastasise widely by haematogenous
route virtually to any organ in the body. The primary testicular focus may be difficult to detect and disseminated
metastases steal the show. Spread also occurs by lymphatics. This tumour is highly lethal and almost all patients
are dead within 1 year. Despite all combinations of surgery, radiation and chemotherapeutic efforts, 5-year
survival rate is less than 5%.
SPREAD
Like other malignant tumours, the germinal tumours of the testis spread by 1. Direct spread, 2. Lymphatic
spread and 3. Blood spread.
1. DIRECT SPREAD.— This spread ^ v,
occurs by invasion and infiltration. The
or b>^ trocar and cannula to draâ small ^^

hydrocele, spread involves the scrotal wall 0 j|
and ultimately fungates through the skin on hs
the anterior aspect of the scrotum as the ^ 'B
testis is anteriorly located in comparison to jj
Direct spread gradually involves the ... . V .

epididymis and the spermatic cord. This - i
finding is of sinister prognostic importance ..^y-' jflP st
since involvement of the upper part of the a
cord is associated with a reduced chance of .,
cure.
2. LYMPHATIC SPREAD.— Before
discussing the lymphatic spread, it is worth
while to recapitulate the lymphatic drainage
of the testis.
Lymphatic drainage of the testis.— Four to eight lymphatic vessels pass from the mediastinum testis along
the spermatic cord to the deep inguinal ring. The lymphatics of the testis usually follow the venous drainage of
the testis. The lymphatics from the testis run upwards in the spermatic cord and pass through the deep inguinal
ring. They then divide into a few branches and course upwards alongwith the testicular vessels in the posterior
abdominal wall, being adherent to the posterior peritoneum. These lymphatics drain into the para-aortic group
of lymph nodes in the region of the origin of the testicular arteries from the aorta. The efferent lymphatics from
these lymph nodes drain into the thoracic duct to the left supraclavicular fossa which drains into the left
brachiocephalic vein. So in advanced cases of testicular tumours the left supraclavicular lymph nodes (Virchow’s
nodes) may be involved.
Some lymphatics from the medial side of the testis run along the artery to the vas and drain into a lymph
node lying at the bifurcation of the common iliac artery.
It must be remembered that contralateral lymph nodes may be affected by lymphatic spread.
Until and unless the scrotum is involved, inguinal lymph nodes are not affected.
Seminomas metastasise almost exclusively through the lymph vessels. Teratomas also spread by this
route but it has got a predilection towards blood borne metastasis.
3. BLOOD SPREAD.— Whereas seminoma only occasionally metastasises through blood stream,
teratoma almost always spreads by this route. Choriocarcinoma is particularly notorious to spread very early
through this route and patients often present with metastatic features when the growth is insignificantly
small. Lungs, liver, bones, brain are the usual sites involved through this spread.
CLINICAL FEATURES
HISTORY.— Age.— Teratoma commonly occurs between the ages of 20 and 30 years and seminoma
between the ages of 30 and 50 years.
The presenting features vary in each case and can be broadly classified into 3 groups — 1. The typical
group, 2. The metastatic group and 3. The atypical group.
1. Typical Group.—
(i) Painless swelling of the testis is the commonest presentation (80% of cases). The earliest symptom of
testicular tumour is a mass in the testis. A sense of heaviness is complained of. This usually occurs when the
testis has reached twice or thrice its normal size. Though the testis is easily palpable, yet the patient usually
does not report to the clinician before 4 months of onset of symptoms. It usually takes about 20 days to double
the size of the testis in a malignant teratoma.
(ii) Pain is occasionally complained of. Such pain is dull aching or dragging in character. Pain may be felt
in the scrotum or in the groin. Pain is complained of in only l/3rd of cases.
(iii) A history of trauma may be received in about 10% of cases. Though some surgeons tried a lot to find
out trauma as an aetiological factor yet it seems trauma merely calls attention to the testicular enlargement and
it does not initiate the neoplasm.
2. Metastatic Group.—
Sometimes patient may present with symptoms due to metastasis rather than testicular swelling. Sometimes
patients ignore the testicular swelling considering it to be hydrocele and gives more importance to the other
symptoms which are due to metastasis. These symptoms are :
(i) Patient may present with abdominal or lumbar pain and/or an abdominal swelling. This is more
common in seminoma, as lymph spread is early. The abdominal mass is the enlarged para-aortic group of
lymph nodes. This also causes abdominal or lumbar pain.
(ii) Patient may present with chest pain, cough, haemoptysis and/or dyspnoea. These are due to pulmonary
metastasis from teratoma of testis.
(iii) Jaundice and palpable liver may be the only presenting feature of a case of teratoma.
(iv) Patient may present with swelling in the supraclavicular region which are enlarged supraclavicular
lymph nodes (Troisier’s sign).
3. Atypical Group.—
A few cases of testicular tumour present atypically, so much so that the diagnosis of testicular tumour
becomes difficult. Such cases are :
(i) Slow growing tumour.— Patient notices swelling of the scrotum for 2 to 3 years, which he ignores as
a hydrocele.
(ii) Fast growing tumour.— Some tumours are so highly malignant particularly choriocarcinomas, that
the patient dies of metastasis before he realises that testis is the root of all troubles.
(iii) Some cases present as epididymo-orchitis or mumps orchitis. Clinicians start giving antibiotics without
any material relief. One must remember that these cases should be suspected as malignancy.
(iv) A few cases may present only with gynaecomastia, as may happen in interstitial cell tumours or even
choriocarcinoma.
(i) The body of the testis is enlarged. The swelling is usually smooth (as in seminoma) or may be lobulated
(as in teratoma). It is usually firm in consistency, but may be hard. Consistency is usually equal all over in
seminoma, but consistency may vary in teratoma with one or more softer bosses.
(ii) Loss of testicular sensation is a very pathognomonic feature of seminoma and teratoma of testis. Such
loss of testicular sensation is quite early and complete. One must be gentle in palpating the testis lest dissemination
should take place.
(iii) Secondary hydrocele may be present in only 1/1 Oth of cases. It is usually tax and does not come in the
way of palpation of the testis.
(iv) The epididymis is normal in the beginning, but it may be involved later in the disease so that it
becomes flattened and incorporated in the growth.
(v) The spermatic cord remains normal for quite a long time. As the testicular tumour gradually enlarges,
the spermatic cord may be thickened due to cremasteric hypertrophy to pull up the heavy testis and engorgement
of testicular vessels. But it must be remembered that the vas deferens is never involved.
(vi) Rectal examination should always be performed. In a typical case of testicular tumour no abnormality
of the prostate or seminal vesicle may be detected through this examination.
GENERAL EXAMINATION.— The possible sites of metastasis should now be examined.
(a) The other testis should be carefully examined, as bilateral tumours are not unknown.
(b) Abdomen is carefully palpated particularly above the umbilicus for palpation of para-aortic lymph
nodes or below in the iliac regions for common iliac lymph nodes.
(c) One must exclude liver enlargement.
(d) The cervical region is examined, particularly the left supraclavicular fossa to exclude any lymph node
enlargement there.
(e) Ankle oedema should be excluded. Massive lymph node involvement may cause inferior vena cava.
obstruction and ankle oedema.
(f) Para-aortic lymph node enlargement may cause ureteric obstruction with hydronephrosis, so kidneys
must be palpated carefully.
(g) One should also examine to exclude gynaecomazia.
Clinical staging.— A simple staging system may be adopted —
Stage I — tumour is confined to the testis (lymphogram negative).
Stage II — lymphogram positive or other evidence of retroperitoneal nodes involvement. Nodes involved
must be all below the diaphragm.
Stage III — supradiaphragmatic lymphatic spread (mediastinal and/or cervical lymph nodes).
Stage IV — extra-lymphatic spread to lung, liver etc.
1. Chest radiography and whole lung tomography — are essential in teratoma. This is done to detect
pulmonary metastasis or detection of enlargement of pulmonary and mediastinal lymph nodes. Para-vertebral
nodal masses and enlargement of paratracheal nodes may also be detected by this investigation.
2. Lymphography.— This is performed to detect involvement of para-aortic lymph nodes. Being in the
abdomen it is difficult to palpate slight enlargement of these lymph nodes. Nodal metastasis is indicated by
filling defect or nodal enlargement with pseudolymphomatous lacy appearance. In case of massively enlarged
nodes there may be virtually no entry of contrast medium into the lymph node mass.
3.1. VP.— This is performed — (i) To detect displacement of ureter and obstructive features in the kidney
due to enlargement of para-aortic nodes.
(ii) To locate the exact position of the kidneys, so that they may be properly shielded while radiating the
abdominal nodes to prevent damage to the kidney by radiation.
4. Hormone studies.— (i) Human chorionic gonadotrophin (Beta human chorionic gonadotrophin) (Beta
HCG) should be assayed in 12 hour collection of urine by radio-immune assay technique.
(ii) Alpha fetoprotein (AFP) is a valuable marker not only to detect metastatic teratomas (three quarters
of teratomas produce either AFP or Beta HCG).
(iii) Lactic dehydrogenase (LDH) — is also
raised in a few teratomas.
5. Renal function test.— EDTA or creatinine
clearance will indicate effect of obstruction on
kidney due to ureteric obstruction.
6. CT Scan of the upper abdomen to detect
enlarged retroperitoneal lymph nodes of the pre-
and para-aortic group.
7. Ultrasound.— Ultrasound is now the
investigation of choice in testicular neoplasm. It is
often used as it is less expensive and less time
consuming. However infiltration of the testis by
leukaemia or lymphoma is difficult to diagnose by
this technique.
8. Magnetic Resonance Imaging (MRI).—MRI
is capable of producing images of scrotal contents
with exquisite anatomical detail and is sensitive
technique for detecting focal lesion of the testis.
However, ultrasound remains the investigation of
choice as it is less expensive and time-consuming. 03.60.7.- Tl-weighted MRI image in coronal section showing
. i i • i i • 1 - 1 r e s i d u a l retroperitoneal nodal masses tor metastatic testicular
Neither technique con elates well with histological tumour. Nodal masses are shown by arrows, renal artery by r'
findings and local staging of primary testicular inferior vena cava by V and aorta by a’,
neoplasms. .
MRI is now quite helpful in detecting intra-abdominal and intrathoracic secondaries. Subsequent MRIs
may also detect the response of therapy.
9. Gallium scan.— Recently 67Ga has been found to be valuable for locating seminoma deposits. This is in
contrast to teratoma where isotopic tumour localisation has proved disappointing.
10. Isotopic liver scan and ultrasonic scan of the upper abdomen.— This is to detect liver involvement.
11. Inferior venacavogram — may be performed to detect pressure on inferior vena cava by the involved
lymph nodes particularly in case of right sided tumours.
TREATMENT.—
A. As soon as the diagnosis is confirmed inguinal orchidectomy with high cord ligation at the deep
inguinal ring is mandatory.
B. Then the treatment defers according to the histopathological report of the testis whether it is seminoma
or teratoma.
A. Orchidectomy.— The main objects of the operation are :—
(a) Removal of the primaiy tumour.
(b) To obtain the biopsy specimen for histopathological report, which helps further treatment of the
secondaries. This is the best form of getting the biopsy specimen without disturbing the tunica albuginea,
which acts as a barrier for direct spread of the tumour mass.
Technique.— Through an inguinal incision the inguinal canal is opened. The spermatic cord is dissected
out. It is ligated at the level of the deep inguinal ring and then divided just distal to the ligature. The incision is
extended downwards to the scrotum. The spermatic cord is gradually dissected from the surrounding tissues
downwards and ultimately the spermatic cord alongwith the testis is removed.
After orchidectomy, there may be recurrence in the scrotal skin. Some surgeons advise haemiscrotectomy
i.e. excision of that half of the scrotum together with orchidectomy.
When the diagnosis is in doubt, it is better to explore the affected testis.
Exploration.— A soft clamp is applied at the spermatic cord to prevent dissemination of the malignant
cells. The testis is opened up by making a small incision on the tunica albuginea. The suspected part is excised
and then sent for frozen section biopsy. The tunica albuginea is closed carefully. If the histopathological report
goes in favour of malignancy, orchidectomy is performed through inguinal incision with division of the cord at
the deep inguinal ring.
B. Subsequent treatment for seminoma and teratoma differs. The treatments are as follows :
SUBSEQUENT TREATMENT OF SEMINOMA.— Testicular seminoma is a remarkably radiosensitive
tumour and vigorous attempt should be made to irradiate the tumour even in patients with advanced disease.
Stage /.— Radiation therapy is given to the para-aortic and ipsilateral pelvic lymph nodes, the field extending
from D10-11 interspace to the lower border of the obturator foramen. Anterior and posterior fields are treated
alternatively. The fields extend laterally to the hila of the kidneys. The contralateral testis is protected from
scattered radiation by means of thick lead cup. It is preferable to use high energy X-rays — either 6 MeV or
8 MeV linear accelator is employed. The penetrating beam of this apparatus facilitates irradiation of deeply
seated structures such as the retroperitoneal lymph nodes with high doses resulting in short treatment exposures,
and the sharply defined beam edges which minimize irradiation to critical adjacent structures such as kidney
and testis. A mid-point dose of 3000 rads is derived in VA to 4 weeks time. In case scrotal sac is involved —
the scrotal sac is irradiated and the inguinal nodes are included in the fields. The scrotal sac is treated with
orthovoltage X-rays (250 K.V.) and the groin nodes by extending the megavoltage field. A lead shield is
always prepared which protects the contralateral testis.
Stage II.— If the lymphogram is positive, a similar field is used and in this case the dose to the involved
nodes is increased to 3500 rads. Following completion of the abdominal radiation and after a period of 4
weeks the mediastinal and supraclavicular nodes are irradiated.
Stage III.— The approach is identical to that mentioned in stage II.
Stage IV.— 67Ga scan is a useful method of detecting the sites affected by seminoma. A few organs may be
irradiated, as seminoma is basically a radiosensitive tumour. Thus for example, pulmonary and hepatic irradiation
may be carried out with some prospect of success. Irradiation may be preceded or followed by chemotherapy.
In presence of widespread disease the best plan is to attempt to irradiate all identifiable disease and then to
follow this with chemotherapy. A combination chemotherapy containing cis-platinum has been very effective
in treating testicular tumour. With this treatment 40% survival has been achieved at the end of 36 months.
SUBSEQUENT TREATMENT OF TERATOMA —
Stage I.— The treatment policy is almost similar to that described for seminoma, however the radiation
dose to the nodes is increased to 4,000 to 4,500 rads in 4 to 5'A weeks.
Stage II.— In this particular group controversies still exist between radical node dissection and radiotherapy.
To chalk out best plan of treatment, stage II teratoma can be divided into two groups :— Ha (small volume
lymph node metastasis) and lib (bulky lymph node metastasis). The cure rate in these two groups is strikingly
different with 80% cure rate in stage Ha, whereas 35% in stage lib.
In this group a higher risk of relapse (40%) has been noted. It has recently been shown that adjuvant
therapy of 2 cycles of bleomycin, etoposide and cisplatin (BEP) is an acceptable and justifiable way of virtually
eliminating the risk of relapse in this group.
Excision of the residual lumps requires careful preoperative localisation by CT scanning, so that optimum
surgical approach can be planned. The relation of the mass to the renal vessels is of paramount importance.
Stage I and Ha patients are followed closely after radiation therapy with chest X-rays and CT scan at
monthly intervals for the first 6 months and at 2-monthly intervals for 1 year. Whole lung tomography may be
performed at intervals during this follow-up period. Early detection of lung metastasis should be followed by
chemotherapy and lung irradiation.
Retroperitoneal lymph node dissection or radical excision of the retroperitoneal lymph nodes.— This
operation is more popular in United States. Whether this operation is always justified or not is a controversial
issue. In many series published in U.S.A. the survival of patients with positive nodes was 48.6%, which is
almost similar to studies from Great Britain for lymphographic stage II patients who were treated by irradiation.
Irradiation also minimises unnecessary radical retroperitoneal node dissection for histologically-negative lymph
nodes. There is no evidence at present to suggest superiority of either irradiation or lymphadenectomy in the
management of retroperitoneal node metastasis from testicular teratoma.
CT scan should be performed to detect the exact position of the mass and its relation. A long midline
incision provides excellent access for the mass situated below the renal vessels. If the mass extends above the
renal vessels, a thoracoabdominal incision is required. One can make a separate staged approach that means
separate incisions for dissection of wide-spread retroperitoneal lymph node metastasis.
It must be remembered that more than 20% of cases who underwent para-aortic lymphadenectomy
reported permanent impotence or retrograde ejaculation following this procedure. This has made it unpopular
in U.K. and in other European countries. Whereas chemotherapy or radiotherapy will not have such adverse
effect.
Stage III.— Treatment is almost identical to that mentioned for stage II.
Stage IV.— In this stage a combined chemotherapy-radiotherapy approach is employed. Where there is
more widespread dissemination chemotherapy alone is indicated.
Chemotherapy has revolutionised the treatment of teratoma testis. The development of effective
chemotherapy with cis-platinum, vinblastine and bleomycin (PVB) for testicular cancer has been the most
dramatic advance in oncology during the past decade. Sometimes etoposide may be substituted for vinblastine
and a combination of bleomycin, etoposide and cis-platinum (BEP) was evaluated and shown to be as effective
as PVB, but less toxic. However it must be concluded that ideally all residual masses should be removed after
completion of chemotherapy, first to define whether or not there is active malignancy in the lump and secondly
because complete surgical removal and follow-up chemotherapy appear to offer best chance of cure.
Patients with liver metastasis carry a particularly bad prognosis and the median survival for this group has
been less than 4 months.
Combined chemotherapy has often been used with success in stage IV patients particularly where extra
lymphatic spread is confined to the lungs. Chemotherapy is used to secure maximal tumour regression and
radiation is then directed to the sites of initially detected disease. After chemotherapy the lymph nodes (iliac,
para-aortic, mediastinal and cervical) and both lungs are irradiated. The use of chemotherapy increases the
sensitivity of the lung to irradiation and profound changes in pulmonary function can occur.
LONG TERM TOXICITY.— Unlike many other solid tumours, patients can expect an additional life span
of approximately 50 years after treatment, thus long term and late effects assume great importance. Alterations
of gonadotrophin levels and Leydig cell insufficiency are particularly common, which cause fertility adversely,
but it usually returns to normal in those who had normal spermatogenesis prior to diagnosis.
Other long term sequelae include renal impairment, arterial hypertension and elevation of serum cholesterol.
There is an increased incidence of Raynaud’s phenomenon in 30% of cases, thought to be related to bleomycin
exposure. Cumulative dose of platinum may cause ototoxicity in 20% of cases and peripheral neuropathy in
15% of cases.
Concern has also been raised about the possible carinogenic effects of chemotherapy in the long term.
Etoposide is known to be leukaemogenic and secondaiy tumours have been reported following etoposide
containing therapy. Overall, it has been shown that among long-term survivors with testicular tumour, there is
76
an elevated risk of developing certain types of acute leukaemia, non-Hodgkin’s lymphoma, melanoma and
cancers of the connective tissue, thyroid, pancreas, bladder, kidney, prostate and G.I. tract.
In nutshell four courses of cis-platin-based combined chemotherapy (BEP) given at 3 weekly intervals is
the standard treatment for good prognosis metastatic GCT. Intermediate/poor risk prognostic categories may
be treated by BEP, alternating cyclical regimens or the early introduction of high dose therapy.
After chemotherapy for GCT, current standard practice includes resection of all masses greater than 1 cm
in diameter as approximately 50% of these will contain either undifferentiated or mature teratoma.
Management of residual masses.— In most patients, these are located in the retroperitoneal space, but
residual pulmonary metastases also occurred and should be managed similarly. In pure seminoma, residual
masses can be safely observed on serial scans and most will shrink and calcify over time. A growing mass
however would indicate recurrent disease requiring further treatment. In nonseminomatous GCT, residual
masses may contain necrotic or fibrotic tissue, differentiated teratoma or a mixture of all these elements. These
must be surgically removed before it enlarges locally and becomes inoperable. Current policies should include
resection of all masses greater than 1 cm in diameter.
Conclusion.— Recent interest in the aetiology has highlighted a number of common and widespread
environmental features that may prove to increase the risk of GCT in men. However further investigation is
required in this area.
The treatment of GCT has not changed a great deal in the last 5 years, although there is a trend toward
more S equent use of chemotherapy in the earlier stages. The long-term risk and toxicities of such treatment
will require careful prospective evaluation. As outlined above, a major surgical controversies still exist. First,
the benefits and risks of contralateral testicular biopsy and second the correct identification of residual masses
containing undifferentiated or mature teratoma which require surgical removal.
A further surgical debate is the benefit of orchidopexy to prevent the development of GCT. It must be
remembered that adverse histological changes start to appear in the maldescended testis at the age of 2 years,
so it might be that only orchidopexy done at a very young age before 2 years can reduce the risk of development
of GCT.
Prognosis.— The ultimate prognosis in testicular malignant disease depends upon the stage of the disease
at diagnosis, the histologic character of tumour and the vigor with which therapeutic measures were pursued.
With the advent of radiation and chemotherapeutic regimens the outlook for patients with testicular carcinoma
is becoming increasingly better.
Seminoma.— With no metastasis the survival rate is about 95% after 5 years. If there are metastasis the
survival rate drops considerably according to the stage of metastasis. Even in stage IV cases 40% survival may
be achieved after 5 years with irradiation and chemotherapy.
Teratoma.— Without metastasis 5 year survival rate may be even 85%. In stages III and IV the survival
rate considerably declines and even with chemotherapy one cannot except more than 50% survival rate.
INTERSTITIAL CELL TUMOURS

These tumours are usually benign. These tumours occur early in life and arise either in cells of Leydig or
those of Sertoli.
Leydig cell tumour.— Tumours of the Leydig cells are musculinising and they elaborate androgens.
These tumours are often called pre-pubertal tumours, as they occur before puberty. These tumours secrete
androgen. In children this tumour induces sexual precocity and extreme muscular development.
These neoplasms cause small nodules ranging from 1 cm to 10 cm in diameter. Bilateral neoplasms are
encountered in 10% of patients. On cut section this tumour looks uniform yellow-brown colour.
Histologically the Leydig cells can be seen. These Leydig cells are large, round or polygonal with abundant
granular eosinophilic cytoplasm and round central nucleus. The cytoplasm frequently contains lipid granules
and rod-shaped crystalloids of Reinke. The cells are seen in diffuse sheets or masses separated by a fibrous or
a hyaline stroma.
Sertoli cell tumours.— This tumour is rarer than Leydig cell tumour. Since this tumour arises in the cells
of Sertoli, there is excessive output of feminising hormone. This results in loss of libido, aspermia and
gynaecomazia. Aschheim-Zondek test becomes positive.

This neoplasm appears as small firm nodule or rarely as bulky tumour. On cross section it looks
homogeneous, greyish-white to yellow in colour.
Histologically the cells are quite distinct and are either tall, columnar or polyhedral with abundant vacuolated
cytoplasm. Uniformity of cell size and shape is the rule and mitoses are rare.
Sertoli cell tumour is also benign.
Treatment of interstitial cell tumour is orchidectomy. As these are usually benign tumours orchidectomy
is curative.
IDIOPATHIC GANGRENE OF THE SCROTUM

Aetiology.— This is exactly not known. It is characterised by sudden appearance of scrotal inflammation
in an apparently healthy individual. Some minor injuries or scratch in the perineum may precede. Some operative
procedures e.g. dilatation of stricture or opening of a periurethral abscess or injection of anal fissure may be
followed by such condition.
Obliterative arteritis of the arterioles due to infection seems to be the basic pathology of this condition.
The infecting agents are the haemolytic streptococcus associated with other organisms e.g. staphylococci,
E.Coli, Cl. Welchii etc. which set up a fulminating inflammation in the scrotal subcutaneous tissue.
Clinical features.— Sudden appearance of pain and inflammation in the scrotum is the first symptom and
sign. This is often associated with fever, anaemia and prostration. In the beginning the scrotum is only involved.
Gradually cellulitis spreads to the perineum, penis, lower abdominal wall and upper part of the thigh same as
the superficial extravasation of urine. If untreated, the scrotal skin sloughs out and the testis covered with
tunica remains free from gangrene.
Treatment.— The discharge is sent immediately for culture and sensitivity test. Before the report comes
in one should start an antibiotic immediately — either chloramphenicol or gentamycin or cephalosporin. The
local area is covered with antiseptic dressing. Between the dressings acriflavine bath to the scrotum should be
given. If the response is not that prompt, the gangrenous skin is excised for better drainage and stoppage of
spread of gangrene.
When the inflammation has subsided, the tunica vaginalis should be covered with either by the remaining
scrotal skin or after eversion of sac the testes are implanted to the medial sides of the thighs.
CARCINOMA OF THE SCROTUM

Aetiology.— It is often an occupational hazard. It is sometimes seen in chimney-sweepers and those
working in cotton industry — mule spinners (The lubricating oil from the spinning genny is carcinogenic). It is
also seen in tar and shale oil workers.
In majority of cases no definite aetiology could be found out. It is a rare condition in India and Asiatic
countries.
Pathology.— It is usually a squamous cell carcinoma.
Clinical features.— The growth usually takes the form of an ulcer. It may start in a wart. In untreated
cases it involves the underlying testis.
Treatment.— Surgeiy is the most suitable treatment. The growth is excised with a considerable margin of
healthy tissue by diathermy.
Postoperatively antibiotics are given to the patient. If inguinal lymph nodes are enlarged and do not
subside with antibiotic treatment and feels hard, a block dissection of the inguinal nodes and external iliac
nodes should be carried out on both sides.
SEBACEOUS CYSTS OF THE SCROTUM

This is a very common condition. Multiple sebaceous cysts cover the whole of the scrotum. No definite
aetiology is known. If the sebaceous cysts are localised to one area, that area of the skin should be excised
followed by primary suturing. When the whole scrotum is involved, the big cysts localised to one area should
be excised.
1204
CHAPTER - 53
ItftEMKlS'•-W-: • V - . . . j
DEVELOPMENT OF PENIS
The penis is developed from a surface elevation, termed the genital tubercle, appears at the cranial end of the cloaca] mem
and lengthen to form the phallus. An entodermal plate, the urethral plate grows forwards from the walls of the cloaca and urog
sinus towards the tip of the organ. The raised margins from both sides of the urethral plate form the genital folds. The phallus e
to form the penis and its apex constitutes the glans. The genital folds fuse with each other from behind forwards enclosing t
portion of the urogenital sinus behind to form the bulb of the urethra and the greater part of the spongy urethra. So that th
urethra is mainly, if not wholly, entodermal in origin. In this way as the phallus lengthens, the urogenital orifice is carried o
it reaches the glans.
While these changes are in progress, two genital swellings (labioscrotal folds) have appeared on each side of the base of the
phallus and extend caudally, separated from the genital folds by distinct grooves. The genital swellings meet each other ven
anus and unite to form the scrotum.
At the tip of the glans an ingrowth of surface epithelium occurs to meet the anterior end of the urethral plate. The disi
the cells of this ingrowth results in the formation of the terminal part of the urethra within the glans. This part is ectodermal in origin
and is drained by the lymphatics draining into the inguinal group of lymph nodes.
The prepuce begins to develop in the 3rd month at a time when the urethra still exhibits its primary orifice at the base of
A ridge consisting of a mesodermal core covered by epithelium appears proximal to the neck of the penis and extends forwa
glans. Deep to this ridge, there is solid lamella of epithelium which extends backwards to the base of the glans. As the ureth
to form the terminal part of the urethra, the ventral horns of this ridge fuse to form the frenulum. Over the dorsum and sid
the epithelial lamina breaks down to form the prepucial sac and thus the prepuce becomes free from the surface of the glans. The
the prepuce grows forward as a free fold of skin over the terminal part of the glans. The prepucial sac may not be complete
month or more after birth. Presence of some connecting strands may still interfere with the retraction of the prepuce after
HYPOSPADIAS
This is a condition in which the external meatus of the urethra is situated at some point on the undersurface
of the penis or perineum. This is the commonest congenital malformation of the urethra.
Incidence.— It occurs once in every 350 males.
Types.— According to the position of the abnormal external meatus, hypospadias has been classified into
5 varieties. See Fig.20.3 in page 336 ofthe author’s ‘A TEXTBOOK ON SURGICAL SHORT CASES’
1. GLANDULAR VARIETY.— In this case the ectopic external meatus is situated on the under surface of
the glans. There is often a blind depression at the normal site of the external meatus. Occasionally a channel
may exist between the normal site and ectopic opening. The part of the urethra which is not formed is ectodermal
and developed by the ingrowth of the surface epithelium to join the tip of the urethral plate. In this congenital
variety the ingrowth does not occur or it fails to canalise. This is the commonest variety of hypospadias.
2. CORONAL VARIETY.— Here the external meatus is situated at the corona glandis i.e. at the junction
of the undersurface of the glans with the body of the penis.
3. PENILE VARIETY.— Here the external meatus is situated at any part of the undersurface of the body
of the penis. The chordee is a prominent feature and in extreme cases the penis may become curved ventrally.
4. PENOSCROTAL.— The ectopic urethral opening is situated at the junction of the penis and the scrotum.
5. PERINEAL VARIETY.— In this case the scrotum is split and the urethra opens between its two halves.
This variety is often associated with bilateral undescended testis. In this case the sex determination of the child
becomes difficult.
Except the glandular variety the other varieties are due to failure of fusion of the genital folds in varying
degrees.
Pathology.— Besides the abnormal position of the external urethral meatus, the other associated
abnormalities are as follows :
(a) In the penile variety the urethra and the corpus spongiosum distal to the ectopic opening are absent.
These structures are represented by a fibrous cord. Due to contracture of this fibrous cord, the penis is curved
ventrally, which is known as chordee. The further away the opening from the normal position, i.e. the further
proximally the ectopic opening is placed, the more pronounced is the bowing or the chordee.
THE PENIS 1205
(b) In all types, the ectopic meatus is narrow, so that it may cause varying obstruction to the urinary flow.
(c) Hypospadias is almost always associated with a small penis, as development of phallus and genital
folds are affected.
(d) In all cases the inferior aspect of the prepuce is poorly developed. As the superior aspect of the
prepuce is almost normally developed whereas the inferior aspect is poorly developed, the prepuce takes the
form of a hood and is called ‘hooded prepuce’.
(e) Hypospadias is usually not associated with urinary incontinence.
(f) Perineal hypospadias is often associated with bilateral undescended testes. Sex differentiation of the
child becomes difficult in these cases — male child is mistaken for a female. In difficult case sex may be
determined by genetic sex through karyotyping and adrenal function test by determining 17-oxysteroids and
17-ketosteroids.
Complications of hypospadias.—
(i) There may be some obstruction of urinary outflow.
(ii) The stream of urine may be deflected downwards thus spoiling the underwears.
(iii) Due to presence of chordee, in the penile variety, erection is difficult and painful.
(iv) Due to chordee, intercourse may be difficult or impossible.
(v) Infertility is usually associated with penoscrotal and perineal variety.
(vi) Sex determination may be difficult in case of perineal variety.
Treatment.—
In case of glandular hypospadias, no treatment is required, except meatotomy and dilatation of the external
urethral meatus, when it is too small.
In case of other varieties, a plastic operation is performed to bring the external urethral meatus to its
normal position as far as practicable. There are many operations advocated by various surgeons all over the
world. This indicates that no operation has been very satisfactory. Denis-Browne’s operation is still the simple
and most accepted operation.
Operation of hypospadias is performed in two stages :
Stage I— consists of straightening of the penis, which is performed preferably between 1 Zz to 2 years and
Stage II— consists of reconstruction of the urethra which is preferably done between 5 to 7 years of age.
STRAIGHTENING OF THE PENIS.— A transverse incision is made on the ventral aspect of the penis
distal to the external meatus. This incision extends laterally upto the prepuce on each side. The skin flaps are
undermined. The fibrous cord is exposed. This cord is dissected free and removed. After this, the external
meatus will recede towards the perineum. Any additional fibrous bands, which will prevent straightening out
of the penis, will be similarly divided. The skin wound is now repaired longitudinally. If there is any tension in
the suture line, a release incision is made at the midline on the dorsum of the penis.
RECONSTRUCTION OF THE URETHRA.— The one, which will be described here, was advocated by
Denis-Browne and this operation can be attempted by the general surgeons and the result is also satisfactory.
Firstly the urinaiy bladder should be drained by perineal urethrostomy. A Malecot catheter is introduced into
the bladder through a small incision at the bulbous pail of the urethra. A U-shaped incision is made, starting
from the glans, the two limbs of the incision join just proximal to the external meatus. The lateral flaps are
undermined, not only on each side, but also backwards towards the perineum. When this undermining has
reached the scrotum, a small drainage wound is made on each side to avoid haematoma formation. The lateral
flaps are now sutured together in the midline over the isolated strip of skin left between the limbs of the
U-shaped incision. To relieve tension in the suture line, a release incision may be required at the midline along
the dorsum of the penis. The suturing at the midline on ventral aspect is important and should be done in the
fashion of tension sutures applied for the abdominal wall.
Postoperative treatment.— At the dorsum of penis, where release incision has been made, the wound
should be dressed with penicillin tulle or with sofra-tulle. The patient should be given proper antibiotics, the
sutures are removed after a week. The urethrostomy tube is withdrawn after a fortnight and the fistula closes by
itself within a week.
Presently a neourethra is created that runs from the ectopic meatus to the end of the glans and this
neourethra is covered with skin taken elsewhere from the penis.
For the more severe deformity with a proximal meatus and chordee, one of the 4 techniques is usually
performed. These are :—
(i) Divine-Horton s filp-flap technique was often used previously in which glans is undermined and a
V-shaped flap is formed. The proximal urethra is circumcised with long proximal flap to form ventral neourethra.
The urethra is pulled up and sutured on the V-flap. The V-flap is anchored to the corporal tissue. The lateral
glandular wings are approximated with completion of glans closure.
(ii) The Hodgson III technique with a vertical pedicle graft from the dorsal skin is used.
(iii) Currently the more popular one-stage procedure is to use an island flap of ventral preputial skin in a
transverse manner with separate blood supplies to the dorsal skin which is used as urethral island flap rnd
neourethra. In this technique the ventral preputial shiny skin is fanned out. A rectangle of skin is measured
from it with its blood supplies and rolled into the neourethra. This neourethra is anastomosed with the proximal
urethra and delivered to the tip of the glans where a channel is priorly developed with plastic scissors. This is
ultimately covered with Byars’ flap from the dorsal penile skin which is brought around laterally to the midline
ventrally.
(iv) Van der Meulen's operation is suitable when the meatus lies in the distal half of the penis. A
circumferential skin incision is made starting proximal to the external meatus running distally on either side of
the midline towards the corona so as to leave 1 cm wide strip of skin. The incision is then extended along the
free margin of the prepuce. The skin incision is undermined along the length of the shaft of the penis. The
chordee is resected and the skin left distal to the external meatus is sutured with fine needle in the midline to
form the neourethra. Now the skin from the dorsal aspect of the prepuce is rotated to cover the ventral aspect
of the neourethra. An oblique incision on the dorsum of the penis allows the flap to be rotated more freely.
Suture material used in hypospadias repair is mostly 6/0 coloured ophthalmic chromic with a cutting needle.
Vertical mattress suture is probably the best and overlapping of skin edges should be avoided.
ONE-STAGE HYPOSPADIAS SURGERY.— In late 1950s one-stage hypospadias surgery became popular
when surgeons became confident with their ability to remove chordee tissue in its entirety. Now that the
artificial erection technique has been introduced, more and more surgeons prefer to adopt this one-stage
procedure. The Devine-Horton’s procedure (flip-flap technique) included a free full-thickness graft of preputial
skin which is anastomosed proximaliy to the urethra and distally through the glans penis. An island flap of the
dorsal preputial skin is made in a transverse manner having separate blood supplies. This is now rotated
ventrally to make the proximal anastomosis to the urethral meatus, while the distal portion is tunnelled through
the glans to form the new meatus. The dorsal skin with its blood supply from its base is used for cover (Byars’
flaps) of this neourethra.
Certain UNIVERSAL PRINCIPLES to be adopted in hypospadias surgery.—
(a) Urinary diversion.— Urinary diversion is almost always employed before reconstruction operation.
Simple suprapubic drainage through a small transverse incision in the lower abdomen over a filled bladder is
probably the best. No. 14 or No. 16 Malecot catheter can be easily placed under direct vision and fixed to
the skin with nylon. The main advantages of suprapubic drainage are that the tube obstruction can be easily
taken care of; The child can be easily handled at home and the hospital stay can be shortened. The disadvantages
are that it leaves a scar in the abdomen and there is a chance of small leak of urine through the repair. There are
other suprapubic drainage catheters newly introduced in the market, which may be tried.
Perineal urethrostomy is a popular mode of drainage among many surgeons. But there is the problem of
frequent tube obstruction which require continued hospitalisation. Small silicon Foley catheter (8,10,12F) are
available with larger internal diameters.
(b) Haemostasis.— It is a good technique to use epinephrine injection in the concentration of 1/1,00,000
or 1/2,00,000 in 1% or Vi% xylocaine to attain haemostasis and avoid unnecessary oozing during surgeiy for
hypospadias. A time is required after injection to have maximum effect. In no instance the use of epinephrine
has caused tissue ischaemia. After operation adequate pressure dressings are needed for control of haemostasis.
THE PENIS . 1207
(c) Urethral stent.— No. 8F polyurethral feeding tube is left through the neourethra till the first dressing
change. A suture in the glans is used to fix the stent in place.
(d) Suture material.— Vertical mattress sutures are most helpful for proper approximation of the skin
edges. 6/0 coloured ophthalmic chromic catgut with cutting needle is the best for this operation. Nylon sutures
may only be used as pull-out sutures.
(e) Meatal stenosis.— While tunnelling the pedicle graft of neourethra through the glans, a generous
incision of glandular tissue is required to avoid meatal stenosis. The channel should allow No. 12 to No. 14
French sound to pass with ease. The meatus should be kept patent with sound dilatation daily with lubricant
jelly.
(f) Inadequate chordee resection.— This is probably the most common fault in the part of the inexperienced
surgeons. The chordee should be completely resected with the use of artificial erection technique now available.
Dissection around the lateral aspects of the glans is very important. Dorsal tunica plication may be helpful for
minor residual chordee.
(g) Fistula formation.— Small fistulas after this operation are not unusual. Very small fistulas can be
repaired as a day case without use of diversion. However larger fistulas may require extensive mobilisation
with urinary diversion for proper closure.
(h) Hypospadias cripples.— Failed hypospadias repair is the most uncalled for challenge to the surgeons.
Excessive scarring of the penile repair may cause contraction and stenosis to lead to failure of the procedure.
In these cases Cecil-Culp manoeuvre using scrotal skin for coverage is most useful. One must wait till the
previous operation scar matures to undertake this operation.
CONCLUSION.— Success in hypospadias surgery depends only on surgical experience and not on the
technique. It is probably the operation for specialist. The surgeon who wishes to do an occasional hypospadias
repair should be encouraged to work along with someone with experience. One-stage technique is probably
more popular nowadays with fresh tissue planes and development of axial flaps for urethroplasty without using
scarred tissue are probably the main reasons in favour of this method. A secondary surgery rate for fistulas and
strictures of 25% is acceptable, but with experience one must try to lessen this percentage.
EPISPADIAS
In this congenital anomaly the external urethral opening is situated on the dorsum of the penis.
Incidence.— In contrast to hypospadias, epispadias is extremely rare. It is seen once in 30,000 males.
Types.— Three varieties are usually come across :
1. Glandular.
2. Penile.
3. Total, which is associated with ectopia vesicae.
Like hypospadias, in the penile variety of epispadias, the penis is curved upwards.
Treatment.—
Glandular variety may not require any operation.
For the other two varieties urethroplasty or reconstruction of the urethra has to be performed.
In the penile variety the operation is performed almost in the fashion of Denis-Browne. The operation is
usually performed at the age of 3 years. The margins of the groove distal to the external opening are made raw
and undermined and are sutured in the midline over a catheter. This is known as Duplay’s Operation.
ECTOPIA VESICAE (SYN. EXSTROPHY OF THE BLADDER)

This is a congenital abnormality in which there is incomplete development or absence of the infraumbilical
part of the anterior abdominal wall, associated with incomplete development of the anterior wall of the bladder.
Incidence.— Obviously ectopia vesicae is rare and its incidence is once in 50,000 births.
Types.— Two types are commonly encountered with — complete and incomplete varieties. The complete
variety is more common. In incomplete variety the pubic bones are united and the external genitalia are almost
normal.
Clinical feature.—
1. Males are more often affected than females. The ratio is 4:1.
2. Due to pressure of the viscera behind it, the posterior wall of the bladder protrudes through the defect. This is deep
red in colour. Frequently the everted mucous membrane becomes ulcerated and painful. It may undergo metaplastic
changes and form adenocarcinoma.
3. It bleeds readily.
4. When this mucous membrane is gently pulled upwards, more pale, wet trigone becomes visible. Effluxes of urine
can be seen from the ureteric orifices.
5. A line of demarcation becomes obvious between the protruding mucous membrane and the adjacent skin.
6. When the exposed bladder wall is pushed behind with the fingers the firm edge beneath the mucocutaneous junction
can be felt as the defect in the abdominal wall.
7. Associated abnormalities are :
(i) Usually the umbilicus is absent, (ii) There may be umbilical hernia, (iii) There may be inguinal hemia of one side
or both sides. Bilateral hemia may be associated with undescended testes when sex differentiation becomes difficult, (iv)
Rectal sphincter is often lax. (v) The penis is broader and shorter than normal, (vi) The prostate and seminal vesicles are
often rudimentary or absent, (vii) The testes are normal and are normally descended in majority of cases, (viii) In females
the clitoris is cleft and the labia minora are separated, (ix) The pubic bones are separated, but are connected with strong
ligament, (x) The linea alba is wide in the same proportion as the separation of the pubic bones, (xi) Recurrent attacks of
ascending infection make the patient’s life miserable. About half the patients die of renal failure before 30 years of age.
COMPLICATIONS.—
(a) The exposed vesical mucous membrane is usually ulcerated and becomes painful.
(b) Continuous bad odour of urine accompanies the patient.
(c) Recurrent ascending infection makes the patient’s life miserable and it is difficult to control such infection.
(d) Metaplastic change may take place at the exposed mucous membrane of the urinary bladder and it may be the
ultimate site of an adenocarcinoma.
(e) Half of the patients die of renal failure.
Treatment.—
1. Obviously the treatment is operation. First of all diversion of urine has to be performed. Later on, after some months
the urinary bladder is excised and closure is done. The operation is performed between 4 and 6 years of age. In this case
diversion of urine is done into the sigmoid colon. But problem of infection has not made this operation very successful.
Stricture at the site of anastomosis (uretero-sigmoidal), recurrent pyelonephritis and hyperchloraemic acidosis are the
reasons of ultimate death of patients.
2. Diversion of urine into an ileal conduit with excision of the bladder can be performed at 5 years of age. As problem
of infection is less, renal function is better maintained and this is a better operation.
3. Recently attempts are being made to reconstruct the bladder and sphincters within first year of life. At first os
teotomy of both iliac bones are made just lateral to the sacroiliac joints, the bladder is closed. The urethra is reconstructed
behind the pubis. The pubic bones are now brought in the midline and fixed together. The problem of incontinence is
difficult to tackle. Similarly urinary infection and stone formation and ultimately renal failure are also difficult to control.
Various operations have been suggested for incontinence at bladder neck region, but overall success rate is limited.
BALANOPOSTHITIS
Inflammation of the glans is called balanitis, and inflammation of the prepuce is called posthitis. As the
preputial sac is in contact with the glans, the opposing surfaces are involved almost simultaneously, hence the
term ‘balanoposthitis’ is used.
A few predisposing factors are often incriminated —
(i) Candida albicans is often the causative factor, particularly in sexually active persons. The glans
penis will show red patches which may be itchy. The prepuce looks white with longitudinal Assuring particu
larly at the tip.
(ii) Monilial infection is quite common under the prepuce.
(iii) Herpes genitalis, is often a recurrent infection. It starts as itchy vesicles which are soon replaced by
shallow and painful erosions. This condition is mainly caused by herpes virus hominis HPV type 2 (occasion
ally type 1). This virus is transmitted sexually. There may be painful inguinal lymphadenopathy. Sometimes
pain along the distribution of the sensory nerves, usually genitofemoral, precedes the vesicles. The urethra
THE PENIS 1209
may be involved and may cause retention of urine if the S2 and S3 nerves are involved. Acyclovir is quite
effective in treating herpes genitalis, but it may recur.
(iv) Primary chancre (syphilis).
(v) Drug hypersensitivity — in these cases the glans penis becomes discoloured painlessly.
(vi) Poor maintenance of hygiene of the glans and prepuce — often encourages accumulation of debris in
the preputial sac resulting irritation and non-specific inflammation.
(vii) Diabetes — definitely makes the patients more susceptible to such infection encouraging both candidal
balanoposthitis, herpes genitalis and even non-specific inflammation.
Symptoms of balanoposthitis is mainly itching and/or discharge from the preputial sac. In case of more severe
inflammation the glans and the foreskin look red and pus exudes. There is always difficulty in retracting the foreskin.
Clinical examinations to be made as follows. First the foreskin is palpated. Next the foreskin should be re
tracted and the inside of the prepuce as also the glans are examined properly. It must be remembered that balano-
posthius is often associated with penile cancer, warts and syphilitic chancre. If the foreskin cannot be retracted, in
case of severe inflammation, it may be necessary to perform a dorsal slit. Inguinal lymph nodes must be examined.
Treatment— Broad spectrum antibiotics should be started orally as soon as the diagnosis is made. Local
hygiene is extremely important. The part should be remained clean and some local antibiotic drug may be
used. In case of severe inflammation dorsal slit of the prepuce must be made for quick healing. After 2 months
of complete healing it is better to perform circumcision.
BALANITIS XEROTICA OBLITERANCE
The aetiology is still unknown, though there is a higher incidence of associated autoimmune disorders. Men between 20 to
of age are mostly affected. The patient presents with urinary symptoms with meatal stenosis or phimosis. The lesions appear a
plates on the surface of the glans. The prepuce becomes thickened, fibrous and is difficult to retract.
SYPHILITIC CHANCRE
It was previously called Hunterian chancre. Nowadays it is extremely rare. The primary sore (chancre) is usually an ulcer o
prepuce (more often in the fraenum) or on the glans (more often in the coronal sinus). It occurs in primary stage of syphilis an
incubation period is 3 to 4 weeks from the exposure.
It is a painless superficial ulcer with a well defined margin raised above the surface. Beneath the ulcer there is an indistinc
indurated lump of about 5 to 10 mm in diameter which is called the base (indurated base) of the ulcer. The edge is slopping an
So the whole thing feels like a button. It must be remembered here that the chancre on genitalia is painless but on other sites
and lips they tend to be painful. The ulcer is usually covered with a slough of serous discharge which demonstrates spirochaeta
in dark-ground illumination. It is not fixed to deeper structures.
The inguinal lymph nodes are invariably enlarged, mainly on the affected side. They feel rubbery, discrete, freely mobile a
PHIMOSIS
When the orifice of the prepuce (foreskin) is too small to permit its normal retraction over the glans penis,
the condition is called phimosis. In children upto 3 years the prepuce is normally adherent to the glans penis,
so that retraction of the prepuce may be difficult. The external meatus however is clearly seen and when the
prepuce is separated from the glans by dividing the adhesions by means of a probe, the prepuce can be retracted
over the glans upto the corona glandis. These cases are not typical phimosis.
Aetiology.— 1. CONGENITAL.— In these cases the prepucial orifice is narrow since birth. In extreme
cases the prepucial sac balloons out when the patient micturates and a weak thin stream of urine flows.
2. ACQUIRED.—
(a) Inflammatory.— Phimosis may result from scarring following long standing inflammation of the glans
(balanitis) or of the prepuce (posthitis) or a combination of both (balanoposthitis).
(b) Traumatic.— Occasionally a vigorous trauma to the prepuce may cause prepucial fibrosis resulting in
narrowing of the opening of the prepuce. This may result also from forceful stretching.
(c) Neoplastic.— Underlying carcinoma may lead to narrowing of the prepucial orifice. This must be
suspected in an old subject who is recently complaining of phimosis.
HISTORY.— Age.— Congenital phimosis presents in the first few years of life. Acquired phimosis may
present later in life according to the cause of phimosis.
SYMPTOMS.— Difficulty in micturition is the main symptom. In a case of typical congenital phimosis, the
mother complains that when the child micturates the prepuce balloons out and the urine comes out in thin stream.
In an old case of phimosis, patient may present with recurrent balanitis causing pain and purulent dis
charge coming out through the prepucial orifice. The condition is also seen in acquired phimosis following
recurrent balanoposthitis.
Occasionally, patient may present with paraphimosis if the tight foreskin gets retracted and stuck behind the
glans penis. Patient comes with swollen glans penis as the retracted foreskin is causing obstruction to the venous
outflow leading to oedema and congestion of the glans which in turn make reduction of the prepuce more difficult.
LOCAL EXAMINATION.— Diagnosis is easy. When the opening of the prepuce is so small that it cannot
be retracted over the glans penis, it is a case of phimosis.
In case of adult, one should carefully examine for the infection of the prepuce or glans penis. One must
remember of the presence of carcinoma beneath the prepuce which may result in phimosis.
Complications.—
(i) Balanoposthitis — which may be recurrent.
(ii) Prepucial stone or calculus.— This may occur when the smegma does not get access and is retained
for years to cause such calculus. Smegma alongwith urinary salts make such calculus.
(iii) Paraphimosis.
(iv) Obstruction to the flow of urine may result in residual urine, hydroureter and hydronephrosis. In these
cases one must exclude pin-hole meatus or atresia meati which may lie hidden by the phimosis.
(v) Carcinoma.— Phimosis itself is an aetiological factor in the development of carcinoma of the penis.
Muslims and Jews who practise religious circumcision are almost immune to the development of carcinoma of
the penis. If an old man presents with phimosis, a careful examination must be made to exclude a hidden
carcinoma of the prepuce or the glans penis beneath the prepucial sac.
Treatment.— The treatment is circumcision.
When phimosis is associated with considerable inflammation of the prepuce, a dorsal slit of the prepuce is
performed, which is followed by circumcision at a later date when infection has subsided.
CIRCUMCISION.— The operation is usually performed under general anaesthesia in case of children, however
local anaesthesia may be employed in case of adult. First of all sub-prepucial adhesions are severed by blunt dissection
with a probe. This should be done all throughout the circumference. Two pairs of artery forceps are applied to the
prepuce and a dorsal slit is made with scissors upto 1 cm of the corona. Then the prepuce with the mucous membrane
layer is divided parallel to the corona glandis 1 cm distal to it till the frenum is reached. Here artery forceps is applied
to secure the artery of the frenum and then division of the foreskin is completed. All the bleeding vessels are ligatured
with particular care to secure the artery of the frenum. One may use catgut suture for artery of the frenum. Now the skin
of the prepuce is sutured to the mucous membrane with fine interrupted catgut sutures.
The wound is dressed with sofratulle or penicillin-tulle dressing. The patient is discharged in the afternoon.
PARAPHIMOSIS
When a phimotic prepuce is forcibly retracted over the glans penis and it is stuck behind the glans penis, a condition
is created which is known as paraphimosis. This constricting band of phimotic prepuce behind the corona glandis causes
obstruction to the venous outflow, which leads to oedema and congestion of the glans. The glans swells leading to more
difficulty in retracting back the prepuce. The prepucial constricting band also gets oedematous and swollen. In neglected
cases gangrene may result, unless the constricting band is released.
It is an emergency condition and patients present with severe pain and swelling of the glans penis.
It is uncommon for the urethra to be compressed, so that micturition is normally not affected.
Treatment.—
(i) 1 ml of isotonic saline and 150 units of hyaluronidase is injected into each lateral aspect of the swollen ring of
the prepuce. The swelling is gradually reduced due to absorption of the oedema fluid and after 15 minutes reduction may
be performed with ease. Multiple punctures may be made in the oedematous prepuce in the idea to drain the fluid out, so
that reduction may be performed.
(ii) If above method becomes unsuccessful, the patient has to be general anaesthetised and the constricting band is
dorsally slit. Thereafter the narrow cuff of skin which forms the constricting band is excised. Reduction is now easy.
THE PENIS 1211
Circumcision may be performed immediately or later according to the circumstances.

LYMPHOGRANULOMA VENEREUM (SYN. LYMPHOGRANULOMA INGUINALE)
It is an acute as well as chronic venereal disease caused by a virus Chlamydial trachomatis (chlamydia A). It is transmitted
exclusively by sexual intercourse. It involves the skin of the penis and regional lymph nodes. In the female however the perir
nodes are also involved.
Clinical features.— The primary lesion at the site of introduction of the agent is in fact insignificant. This lesion is a fleeting,
painless, genital papule or ulcer which is often unnoticed by the patient and is reported in only \ / i o f the cases.
This is soon followed by (about 2 weeks later) progressive swelling and enlargement of the inguinal lymph nodes. The ove
becomes red and fluctuation develops. These swelling of the nodes create large and painful bubos. In the beginning the nodes
As the inflammatory process extends into the perinodal tissues, the nodes become matted together. Gradually suppurative ne
and fluctuant sacs are formed. These bubos may rupture through the skin to produce draining sinus. Sinus formation is almost ine
untreated cases. In the male the adenopathy is almost invariably localised to the inguinal region and is usually bilateral. Howe
female, the adenopathy may or may not affect the inguinal nodes depending on the location of the primary lesion. If the vagina or the
posterior fomix is the site of primary lesion, the pelvis and perirectal nodes are involved which may cause vaginal or rectal st
In later stage, in a small percentage of cases there is lymphatic obstruction leading to oedema and elephantiasis of the ex
In the female vaginal stricture or rectal stricture is not uncommon. Even this condition may cause elephantiasis of the leg (ve
(i) The Frei skin test is of value in ruling out this disease. The suppurative exudate from bubo of a known case is diluted a
heat-treated to make the antigen for the skin test. When this antigen is injected into the skin of the suspected patient, redne
induration after 48 hours of injection indicates positive test.
(ii) A complement-fixation test is more specific — particularly when progressively rising titres can be demonstrated during the
disease process.
(iii) Isolation of the causative agent is even more definite test. Indirect immuno-fluorescence test for specific antibodies
lymphogranuloma venereum antigens if present is almost diagnostic.
Treatment.— A few antibiotics have been found successful in this disease. Oxytetracycline 500 mg 4 times daily or erythrom
in the same dose or sulphonamide 1 g 4 times a day for 14 days is curative. The fluctuant bubos should not be incised, as this will
invariably lead to sinus formation. Aspiration in such cases is indicated.
GRANULOMA INGUINALE
It is a chronic granulomatous condition, usually of the genital region, caused by Calymmatobacterium granulomatis. better know
as Donovania Granulomatis. This causative agent is seen within the phagocytic mononuclear cells as encapsulated gram-negative
cocco-bacilli or rod like forms, referred to as Donovan bodies. This condition should not be confused with lymphogranuloma ingu
which is of viral aetiology, whereas this condition is a bacterial disease.
This condition is uncommon and is occasionally seen in Europe and in the United States. It is included in the group of vene
diseases, though the evidence that the disease is spread by sexual contact is somewhat equivocal.
The incubation period varies from 7 days to 1 month, but may be much longer.
Clinical features.— The initial lesion is an inflammatory papule at the site of inoculation, on the perineum, vagina, cervix or
Extragenital lesions are encountered in lips, oral cavity, oesophagus and larynx. The original papule enlarges, ulcerates and be
chronic spreading lesion having a necrotic centre and raised inflammatory border. Characteristically this border is rounded an
accumulation of granulation tissue. More chronic lesion may assume greyish colour especially at the edges. This is due to exce
which may cause large and irregular scars resembling keloid. Malignant change may occasionally develop after months or years. E
inflammatory scarring may cause lymphatic obstruction and elephantiasis of the external genitalia resembling that described in lym
phogranuloma inguinale. The ulcerated area rarely bleeds if touched due to presence of immense granulation tissue, but it is
Drainage occurs along the lymphatics to the regional lymph nodes and leads to suppurative necrosis and fluctuant enlargem
resembling bubos.
Special Investigations.— Confirmatory test is finding of Donovan bodies in silver stains of smears of the exudate or biopsy s
Treatment.— Oxytetracycline seems to be the best drug at the dose of 500 mg 4 times daily for 20 days. Streptomycin in the
divided doses for 5 days or Cotrimoxazole (not ordinary sulphonamide) 2 tablets twice daily for 10 days is also effective to cur
PEYRONIE’S DISEASE
This condition is fibrosis in one corpus cavemosum leading to formation of an indurated plaque. Rarely there may be calcif
or ossification.
Aetiology is unknown. Trauma has been incriminated as initiating this condition. It is sometimes associated with Dupuytren’
contracture.
Clinical features.— The patients are usually over 40 years of age. Their main complaint is pain and curving of the penis on
erection. After a few weeks the pain disappears.
Examination reveals an indurated mass felt on the dorsal surface of one corpus cavemosum.
Treatment.— There is hardly any treatment of this condition. Some cases show spontaneous disappearance of the indurated
in over 5 years. Injection of hydrocortisone into the indurated plaque may be tried with some success. Total result,is unsatisfa
TUMOURS
BENIGN TUMOURS
Except condyloma other benign tumours e.g. lipomas, neuromas, fibromas etc. are extremely rare in the
penis so much so that they need not require mention even.
CONDYLOMA
Three types of condyloma occur in the penis.—
(i) Condyloma acuminatum of viral origin is relatively frequent in the penis and require wide description.
(ii) Giant condyloma, which is rare.
(iii) Syphilitic condyloma lata is same as condyloma lata occurring in the mucocutaneous junction anywhere
in the body particularly at the anal region.
CONDYLOMA ACUMINATUM.—
Such lesion may grow in moist mucocutaneous surface including the vaginal, anal or urethral mucosa. In
the penis these lesions are mostly seen near the coronal sulcus and inner surface of the prepuce. These are
usually sessile or pedunculated, red papillary excrescences that vary from minute lesions of 1 to several
millimetres in diameter upto large Raspberry-like masses several centimetres in diameter.
PATHOLOGY.— Histologically these consist of branching papillary villus, with connective tissue
stroma covered by a thickened hyperplastic epithelium with considerable hyperkeratosis and thickening of the
underlying epidermis. Clear vacuolisation ofthe prickle cells may appear and is said to be the characteristic of
these lesions. Normal orderly maturation of the epithelial cells is preserved but may be slightly modified by
increased mitotic activity in the basal layers. The basement membrane is usually intact and there is no evidence
of invasion of underlying stroma.
Such lesions are caused by the human papilloma virus (HPV) and are sexually transmitted.
Treatment.— Either of the two methods may be employed — (i) chemical or (ii) surgery.
(i) Chemical.— Podophyllin 25% in spirit may be locally applied to the wart with a stick and the
surrounding area is powdered for protection. It is washed after 6 hours.
Trichloroacetic acid is more satisfactory for hard warts and for intrameatal warts. Both the acid and
podophyllin together may be applied with better efficacy. Always adequate care should be taken for
application of these chemicals. Patients should not be allowed to use the chemical themselves lest severe bum
should result.
(ii) Surgery.— Cryosurgery is successful in the treatment of these warts.
Particularly in case of parianal warts surgery should be advised under general anaesthesia. The whole
lesion is excised after infiltration to the subcutaneous tissue with diluted adrenalin solution. After operation
patients should be followed up to detect possible recurrence.
GIANT CONDYLOMA.—
This rare lesion is not of viral origin. It is of larger size than condyloma acuminatum. This lesion
displays somewhat greater cellular pleomorphism but it usually does not present atypia and anaplasia, which
are typical of carcinoma.
MALIGNANT TUMOURS
Malignant tumour in the penis means squamous cell carcinoma. Only in extremely rare cases one may find
malignant melanoma, haemangiosarcoma or fibrosarcoma.
CARCINOMA OF THE PENIS
Squamous cell carcinoma of penis represents about 1% cancer in the male.

Aetiology.—
1. Phimosis.— Circumcision performed in the first few days of life confers protection against
THE PENIS 1213
malignancy. This is an accepted fact and it is for this reason that carcinoma of the penis is virtually unknown
among Jews (in whom ritual circumcision is performed very early) and it is extremely rare among muslims (in
whom circumcision is performed between 4 and 10 years). Obviously carcinoma is more common in men who
have not been circumcised in early infancy. Presumably, circumcision protects against tumourogenesis by
preventing accumulation of smegma and minimising the tendency to irritation and infection.
2. Balanoposthitis.— Chronic balanoposthitis or recurrent attacks of balanoposthitis predispose to
carcinoma.
3. Condyloma acuminata or penile warts are often considered to be a premalignant condition.
4. Leukoplakia of the glans penis is also considered to be a premalignant condition. In this condition areas
of white, boggy epithelium are seen. The leukoplakia resembles patches of greyish-white paint. It is a painless
condition. There is evidence of hyperkeratosis and acanthosis (thickening of the underlying epidermis).
5. Paget’s disease.— This is an area of chronic, red eczema of the glans penis or inside of the prepuce.
The lesion oozes and forms crust. Paget’s disease is the intraepithelial stage of squamous cell carcinoma,
histologically almost similar to that occurs in the nipple of the breast. This disease often escapes detection until
carcinoma develops. Treatment is diathermy excision.
6. Erythroplasia of Queyrat.— It causes a dark red, flat but slightly indurated patch on the glans penis or
inner side of prepuce. It may be slightly raised or nodular. This condition occurs most often in the penis. But it
may occur on the vulva or in the mouth.
7. Bowen's disease — is a curious form of carcinoma in situ. It is only seen in patients over 35 years of age.
It is prone to involve the shaft of the penis. It appears as a thickened, opaque plaque with shallow ulceration
and crusting. Over the span of years these lesions may become invasive and are transformed into characteristic
squamous cell carcinoma.
Pathology.— The lesion usually begins on the glans or inner surface of the prepuce near the coronal
sulcus. The first change is a small area of epithelial thickening accompanied by grey and Assuring of the
mucosal surface. Gradually an elevated leukoplakic patch is produced which usually ulcerates when a diameter
of approximately 1 cm is reached.
Macroscopically two varieties are usually seen — (i) Ulcerative variety, which is commoner and (ii)
papilliferous variety.
(i) In ulcerative variety the lesion presents as a large characteristic malignant ulcer having necrotic
secondarily infected bases with ragged, irregular and heaped-up margins. In advanced cases the ulcero-invasive
disease is seen which has almost destroyed the entire tip of the penis and a portion of the shaft.
(ii) The papilliferous variety simulates the condyloma and gradually progresses to form a cauliflower
like, fungating mass. As this tumour enlarges, it undergoes central ulceration and may be transformed into
ulcerative lesion.
Microscopically both the ulcerative and papilliferous lesions are squamous cell carcinomas exactly
resembling those that occur elsewhere on the skin surface.
Spread.— (a) Direct spread.— For quite a long time the growth is limited to the glans and inner surface
of the prepuce. Gradually the foreskin is infiltrated, similarly more and more areas of glans will be involved.
Direct spread to the body of the penis does not take place before 6 months to 1 year, as the fascial sheath
of the corpora cavernosa acts as a barrier. Once this barrier is broken, the growth rapidly spreads along the
shaft of the penis. Peculiarly enough the urethra is not infiltrated by carcinoma.
(b) Lymphatic spread.— As squamous cell carcinoma anywhere in the body, lymphatic spread is early.
Lymphatics from the prepuce and glans penis drain into the superficial inguinal lymph nodes of both sides.
Some of the lymphatics from the glans drain into the deep inguinal lymph nodes. So enlargement of the
inguinal lymph nodes is often seen quite early in carcinoma of the penis. But such enlargement may be simply
inflammatory and not metastatic.
Once the shaft of the penis is involved, the iliac group of lymph nodes may be involved. Moreover the
efferents from the inguinal nodes drain into the external iliac nodes, which are also involved eventually.
(c) Blood spread.— This spread occurs late and rarely. Such spread occurs when the growth is anaplastic
and is more virulent. Distant organs such as lungs, liver, brain and bones may be affected. Prognosis is extremely
poor.
HISTORY.— Age.— Though carcinoma of penis commonly affects individuals of the middle or old age,
yet it can occur in the young. About 40% of the sufferers are under 40 years of age.
SYMPTOMS.— Patients often present with a lump or an ulcer representing the papilliferous or ulcerative
variety of the carcinoma of penis respectively. Sometimes patients present with mild irritation and purulent
discharge from the prepuce. Such cases require dorsal slit to detect the growth. If the patient ignores the
previous symptoms, they may present afterwards with blood stained foul discharge from the prepuce or the
growth is seen which has eroded the prepuce. Carcinoma as such is a painless condition. But if there is too
much of associated infection, the lesion may be painful.
In more than half the cases the inguinal lymph nodes are enlarged. In half of these cases it is due to
inflammation and not metastasis.
LOCAL EXAMINATION reveals the carcinomatous lesion which may be papilliferous or ulcerative.
The gross features have been described in the section of pathology.
By nature carcinoma of the penis is a slow growing and locally metastasising lesion.
Only in very late and untreated cases inguinal lymph nodes may fungate through the skin of the groin and
may erode the underlying femoral vein or the artery to cause torrential haemorrhage and even death.
TREATMENT.—
The first step in treating penile cancer is to obtain adequate biopsies to establish a positive diagnosis. This
is best performed in the operation theatre with the patient under either regional or general anaesthesia. At
times, it is difficult for the pathologists to differentiate between condyloma acuminatum and squamous cell
carcinoma or verrucous carcinoma and well differentiated squamous cell carcinoma. Verrucous carcinoma is
particularly slowly growing but relentlessly expanding variant of squamous cell carcinoma and accounts for
approximately 5% to 10% of squamous cell carcinoma. It presents as a warty, densely keratinized surfaced
with a sharp and definite margin with an inflammatory infiltrate in the adjacent stroma. The treatment of this
condition is wide surgical excision i.e. partial amputation of penis when glans or distal shaft is involved. When
the lesion occurs on the proximal shaft, total amputation of penis is required. Very recently Laser treatment
with neodymium : YAG Laser is gradually replacing surgery.
A. TREATMENT OF THE PRIMARY.— There are two methods of treatment for primary growth —
1. Radiotherapy and 2. Surgery.
h RADIOTHERAPY.— This is indicated for small and well differentiated growths limited to the glans
penis.
Its advantages are — (i) that the result is same or even better than surgery and (ii) it avoids mutilating
operation.
Its disadvantages are — (i) it may cause bad scarring which result in painful erection and (ii) it may cause
postoperative sterility.
It is contraindicated in (i) big growth, (ii) growth involving the shaft and (iii) anaplastic tumour.
If not already performed a dorsal slit should be made to provide proper exposure of the growth to the
radiotherapy. Methods of radiotherapy are :—
(a) Implantation of flexible radioactive tantalum wires — which offer a total dose of6000 rads in 5 to 7
days, (b) Medium or high voltage X-rays, known as teleradiation, which offers 5000 to 6000 rads in divided
doses in 5 weeks, (c) Surface radiations may be given by radium mould applicator worn intermittently or
continuously, so that it can offer 5000 to 6000 rads in 7 to 10 days.
2. SURGERY.— This is indicated —
(i) In anaplastic growth, (ii) In case of a big growth, (iii) When there is infiltration to the shaft of the
penis, (iv) When radiotherapy has failed.
Methods of surgery are :—
(a) Partial amputation — used for distal growth limited to glans penis.
THE PENIS 1215
(b) Total amputation of penis — performed in (i) advanced case involving the shaft of the penis and (ii) in
case of anaplastic lesion.
Partial amputation of the penis.— This operation is indicated when the growth is confined to the glans
and prepuce only and has not spread to the body of the penis.
A fine catheter is applied round the base of the penis as a tourniquet. A long ventral flap is made whose
breadth is equal to the half of the circumference of the penis and the length is equal to the diameter of the penis.
A short flap !4 inch long is made on the dorsal aspect. The flaps are dissected back to their bases. The coipus
spongiosum is isolated from the corpora cavernosa by inserting a fine scalpel on either side of the corpus
spongiosum and divide Vi inch distal to the proposed level of section of the corpora cavernosa. The corpora
cavernosa are now divided at the level of the base of the flaps. The tourniquet is removed and the bleeding
points are now secured by ligatures. A small opening is made in the ventral flap and the corpus spongiosum is
brought out through the opening. The two flaps are now sutured together at the dorsum of the penis. The
sutures should be well spaced for adequate drainage of the haematoma, which may be formed beneath the flap.
The end of the emerging urethra is split for a distance of 1 cm and each half is sutured to the skin of the flap.
This is done to prevent subsequent stricture formation. A self-retaining catheter is then introduced.
On first three postoperative days, dressing should be done daily. The catheter is removed on the 5th day.
Total amputation of the penis.— This operation is indicated when the malignant tumour has involved
the body of the penis.
The patient is placed in lithotomy-Trendelenburg position. A metal bougie is passed per urethra. A racket
shaped incision is made encircling the base of the penis and is carried vertically downwards in the midline of
the scrotum to the perineum upto a point 1 inch in front of the anus. By dissection exactly in the midline the
scrotum is split into two halves. The penis is then mobilised by dividing the suspensory ligament and the dorsal
vessels are secured. The perineal part of the incision is more deepened and the margins are retracted to expose
the bulbous part of the urethra and the two crura. The crura are detached from the ischio-pubic rami with the
help of a raspatory. The bougie is removed and the bulb of the urethra is divided about 2 inches distal to the
perineal membrane. The urethra is dissected out of the muscular tissues of the bulb.
The wound is repaired by suturing the two flaps in the midline. A small drain is left at this part. The
posterior part of the incision is closed round the stump of the urethra. The urethral stump is split into 2 halves
which are sutured above to overlap the skin margins. A self-retaining catheter is pushed through the urethra
into the bladder and left in situ for a few days until the wound heals, after which the catheter is taken out.
B. TREATMENT OF THE SECONDARY.—
Until recently it was believed that penile carcinoma can at times bypass the inguinal lymph nodes and
drain directly into the pelvic lymph nodes. But recent anatomic and clinical studies convincingly demonstrated
that the lymphatic channels do not lead to the pelvic nodes directly from the penis and that the patients never
may have iliac lymph node metastasis without inguinal lymph node involvement.
(i) No enlarged lymph nodes.— After the treatment of the primary growth the patient is carefully followed
up. To be on the safe side one may perform a sentinel lymph node biopsy after the primary tumour has been
excised. A 5 cm incision is made parallel to the inguinal ligament 2 finger breadths lateral and 2 finger breadths
distal to the pubic tubercle. The incision lies over the saphenofemoral junction. The sentinel lymph nodes can
be palpated under the flap towards the pubic tubercle. It lies near the superficial epigastric vein. The surgeon
must take the correct lymph node. The pathologist should examine multiple histologic sections to reduce the
possibility of over looking micrometastasis.
(ii) There are enlarged lymph nodes, which are not fixed.— (a) It is advisable to wait for at least 3 weeks
after the primary growth has been treated. Antibiotic should be given continuously for 1 week or 10 days. If the
enlarged lymph nodes are due to inflammation, the lymph nodes will decrease in size or disappear. In these
cases no other treatment is required except careful follow-up. One can perform lymph node sampling or sentinel
lymph node biopsy to detect quickly whether the enlargement is due to metastasis or not.
When the lymph nodes do not decrease in size, on the contrary if they are more enlarged after 3 weeks,
bilateral block dissection of the inguinal lymph nodes should be performed.
Block dissection for both the sides may be performed in one sitting or preferably the contralateral side
block dissection is carried out at a later date.
(b) When the surgeon is definite that the enlarged lymph nodes are due to metastasis, surgery of the
primary growth may be accompanied by block dissection of the inguinal nodes of the side which is more
affected. The contralateral side block dissection is performed at a later date.
Only occasionally bilateral block dissection can be performed with the surgery for the primary growth in
the same operation if the surgeon is confident about the condition of the patient.
(iii) When the enlarged inguinal lymph nodes are massive, fixed and inoperable — surgery is difficult in
these cases and deep X-ray therapy should be tried. Radiotherapy causes some temporary improvement. These
cases may be treated with chemotherapy, if possible.
SYSTEMIC DISEASE WITH MULTIPLE METASTASIS.—
Chemotherapy is probably the best treatment in these cases. 4 chemotherapeutic agents have shown activity
against penile carcinoma. These are methotrexate, cis-platin, bleomycin and 5-fluorouracil.
Prognosis.— 5-year survival rate when tumours are localised to the penis (stages I & II) is 65% to 90%.
When inguinal lymph nodes are involved, but not with involvement of iliac lymph nodes, the 5-year survival
rate ranges from 30% to 50%. Presence of iliac node involvement significantly decreases the 5-year survival
rate to 20%. In systemic disease with distant metastases the survival rate is 0.
BUSCHKE-LOEWENSTEIN TUMOUR
This is a rare tumour which affects the penis. It is a locally invasive tumour. It does not spread to lymph
node or metastasise.
Treatment is surgical excision, as radiotherapy is ineffective.
1217
Index
A clinical features of, 800 Alveolar abscess, 457 treatment of, 915
complications of, 801 Ameloblastoma, 451 Appendicular tumours, 916
pathogenesis of, 798 Amoebiasis, 929 Apudomas, 560
Abacterial cystitis, 1113 pathology of, 799 pathology of, 930 Arterial by-pass grafting, 198
Abdominal aortic aneurysm, treatment of, 801 treatment of, 931 Arterial embolectomy, 229
248 Acute dilatation of the Amoebic abscess of liver, 766Arterial ulcer, 158
ruptured, 251 stomach, 755 clinical features of, 767 Arteriography, 194
treatment of, 249 Acute intramammary mastitis treatment of, 768 Arteriovenous aneurysm, 245
Abdominal dehiscence, 1023 of breast, 577 Ampullary dilatations, 854 causes of, 245
Abdomino-perineal resection,Acute intussusception, 887 Amputation of penis, 1215 clinical features of, 247
974 clinical features of, 888 partial, 1215 manifestations of, 246
Abducent nerve, 323 pathology of, 887 total, 1215 treatment of, 247
Aberrant renal vessels, 1032 treatment of, 889 Anaplasia, 102 Assessment of thyroid
Aberrations of normal deve Acute lymphangitis, 286 Anaplastic carcinoma of the function, 528
lopment & involution Acute pancreatitis, 839 thyroid, 548 Astrocytoma, 442
(ANDI), 581 (See pancreatitis) Anderson-Hynes pyeloplasty, Atrial septal defect, 666
Abscess, 78 complications of, 851 1058 Auriculotemporal syndrome,
of the axilla, 80 Acute paronychia, 349 ANDI, 581 497
gluteal, 81 Acute pericarditis, 674 Aneurysm, 239 Autoimmune thyroiditis, 551
of the groin, 80 Acute pyelonephritis, 1059 clinical features of, 241 Automatic bladder, 1134
popliteal, 80 clinical features of, 1060 complications of, 243 Autonomic nervous system,
Abscess of the spleen, 829 pathology of, 1060 effects of, 242 331
Accessory nerve, 323 treatment of, 1061 treatment of, 244 Autonomous bladder, 1134
Achalasia of the oesophagus, Acute tetanus, 171 types of, 241 Axillary nerve, 324
691 Adamantinoma, 451 Aneurysmorrhaphy (Matas’), Axillo-femoral graft, 199
clinical features of, 691 Addison’s disease, 567 245 Axonotmesis, 312
diagnosis of, 692 Adenocarcinoma, 133 Angiodysplasia of colon, 987
treatment of, 692 Adenocarcinoma (Renal cell Angionephrotomogram, 1044
Acid base balance, 38 carcinoma) of kidney, 1092Ankylosing spondylitis, 410 B
Acidosis, 38 clinical features of, 1094 Annular pancreas, 837
metabolic, 38 pathology of, 1092 Anomalies of development of Balanitis xerotica obliterance,
respiratory, 39 special investigations of, umbilicus, 988 1209
Acinic cell adenocarcinoma, 1095 of urachus, 988, 991 Balanoposthitis, 1208
493 spread of, 1093 of vitello-intestinal duct, Balloon transluminal
Acoustic neurofibroma, 443 treatment of, 1097 988, 991 angioplasty, 198
Acquired Autoimmune Adenocarcinoma of renal Anorectal abscesses, 955 Barium meal X-ray, 718
Haemolytic Anaemia pelvis, 1103 Antegrade urogram, 1043 Barrett’s oesophagus, 689
(AIHA), 825 Adenoid cystic carcinoma, 493 Anterior compartment Basal cell carcinoma, 126
Acquired cysts, 95 Adenolymphoma, 492 syndrome, 209 aetiology of, 126
Acquired heart diseases, 669Adenoma, 112 Anterior Resection of Rectum, clinical features of, 127
Acrocyanosis, 215 Adenoma of the thyroid, 544 954 pathology of, 127
Actinomycosis, 90, 459 papillary, 545 Antibioma, 578 treatment of, 128
of breast, 579 Adenomatous polyp, 969 Anuria, 1128 Basal cell carcinoma of anal
facio-cervical, 460 Adjuvant therapy of breast Aortic arch occlusive disease, canal, 985
Actinomycosis of colon, 931 cancer, 613 207 Basal secretion of stomach,
Active immunization, 171 Adrenal medulla, 568 Aortic insufficiency, 672 718
Acute acalculous cholecystitis,
Adrenalectomy, 197,565,571Aortic stenosis, 672 Baso-squamous carcinoma,
810 Adrenocortical insufficiency, Aorto-iliac occlusion, 199 129
Acute appendicitis, 905 567 aetiology of, 199 Bassini's operation, 1010
complications of, 911 Adrenogenital syndrome, 566 clinical features of, 199 Bazin’s ulcer, 161
differential diagnosis of, 913
Adson’s test, 525 treatment of, 200 Bedsores, 237
treatment of, 913 AIDS, 93 Ape-like’ hand, 329 Belsey Mark IV operation, 687
Acute arterial occlusion, 226 Ainhum, 239 Apical infection, 350 Benign breast disease, 580
aetiology of, 226 Aldosteronism, 565 Appendicitis, 905 Benign enlargement of the
clinical features of, 227 Alkalosis, 39 Appendicular abscess, 911 prostate, 1139
treatment of, 229 metabolic, 39 treatment of, 911 clinical features of, 1142
Acute cholecystitis, 798 respiratory, 40 Appendicular mass, 911 pathology of, 1140
77
special investigations of, Buerger’s position, 195 clinical features of, 644 treatment of, 658
1143 Buerger’s test, 189 pathology of, 642 Cardiac catheterization, 665
treatment of, 1144 Bulbar tetanus, 171 secondary, 650 Cardiac massage, 659
Benign lymphoma of rectum, Burgess amputation, 345 special investigations of, external, 659
969 Burkitt’s lymphoma, 301 647 open, 659
Benign neoplasms of the Burkitt’s tumour, 456 spread of, 644 Cardiac tamponade, 673
breast, 590 Burst abdomen, 1023 staging of, 646 Cardiogenic shock, 19
Benign tumours, 103, 111 Burst finger, 370 treatment of, 648 Caroli’s disease, 790
Bilateral breast cancer, 615 Buschke-Loewenstein Carcinoma of the maxillary Carotid angiography, 438,445
Bilateral calculi, 1085 tumour, 1216 antrum, 455 Carotid body tumour, 514
Bile duct carcinoma, 819 Carcinoma of the oesophagus,Carotid occlusive disease, 206
Bile duct stricture, 815 698 Carpal-Tunnel syndrome, 365
Billroth I gastrectomy, 730 c aetiology of, 698 Cat-scratch disease, 298
Billroth II gastrectomy, 729 clinical features of, 700 Cattell’s operation, 1027
Biochemical studies for BreastCalcaneum spur, 375 diagnosis of, 700 Causalgia, 331
Ca, 607 Calcium, 35 pathology of, 699 Causes of dysphagia, 707
Biopsy of the breast, 606 deficiency of, 35 treatment of, 701 Cellular space infection of
Blind loop syndrome, 877 excess of, 35 Carcinoma of the pancreas, hand, 357
Block dissection of neck, 309Calcium stone disease, 1078 859 Cellulitis, 84
Blood group, 49 Cancer en cuirasse, 604 Carcinoma of the parotid Cephalic tetanus, 171
Blood loss, measurement of, Cancrum
43 oris, 462 gland, 494 Cerebral compression, 437
Blood storage, 48 Capillary filling time, 189 Carcinoma of penis, 1212 Cerebral concussion, 427
Blood substitutes, 54 Carbuncle, 83 pathology of, 1213 Cerebral contusion, 427
Blood supply of stomach, 709Carbuncle of kidney, 1065 clinical features of, 1214 Cerebral irritation, 427
Blood transfusion, 47 Carcinoembryonic antigen treatment of, 1214 Cerebral laceration, 427
complications of, 51 (CEA), 608 Carcinoma of the prostate, Cerebral puncture, 446
Body water, total (TBW), 24 Carcinoid of appendix, 916 1151 Cervical disc protrusion, 393
Boerema-Crile operation, 782Carcinoid of small intestine, clinical features of, 1153 Cervical lymph node
Boil, 77 879 pathology of, 1152 enlargement, 525
Bone scan for Breast Ca, 607 Carcinoid tumour of rectum, special investigations of, Cervical rib, 222, 523
Bone X-ray for Breast Ca, 607 978 1154 clinical features of, 223
Bonnin’s operation, 1172 Carcinoma of bile duct, 819 treatment of, 1157 pathology of, 223
Bowen’s disease, 154 Carcinoma of the bladder, Carcinoma of the rectum, 969 treatment of, 224
Brachial plexus, 323 1121 clinical features of, 971 types of, 223
lower lesion (Klumpke), 324 clinical features of, 1123 special investigations of, 972
Cervical rib excision, 225
upper lesion (Erb-Duche- spread of, 1123 spread of, 970 Cervical spondylosis, 399
nne), 324 squamous cell, 1123 staging of, 971 Cervico-thoracic
Brain abscess, 441 staging, 1122 treatment of, 973 sympathectomy, 213, 333
Brain oedema, 428 transitional cell, 1121 Carcinoma of scrotum, 1203 Chancre of the lip, 463
Brain scan, 446 treatment of, 1125 Carcinoma simplex, 133 Chancroid (Ducrey's), 163
Branchial arches, 503 Carcinoma of breast, 594 Carcinoma of the stomach, Charles’ operation, 292
Branchial cyst, 504 aetiology of, 594 745 Chest X-ray for Breast Ca, 606
Branchial fistula, 506 clinical features of, 601 clinical features of, 749 Chemotherapy for Breast Ca,
Branchiogenic carcinoma, clinical staging of, 602 pathology of, 747 613, 616
507 pathology of, 595 special investigations of, 751
Chemotherapy in rectal Ca,
Breast abscess, 579 spread of, 599 treatment of, 752 977
Breast cancer in pregnancy, treatment of, 608 Carcinoma of the thyroid, 545Chilblains, 160
615 Carcinoma of the cheek, 466 anaplastic, 548 Cholangiocarcinoma, 775
Breast carcinoma, 594 Carcinoma of colon, 941 follicular, 547 Cholangiography, 791
Breast reconstruction, 618 aetiology of, 942 medullary, 548 operative, 791, 805
Brodie-trendelenburgtest, 262 clinical features of, 943 papillary, 546 percutaneous
Bronchiectasis, 638 pathology of, 942 Carcinoma of the tongue, 470 transhepatic (PTC), 793
Brucellosis, 299 special investigations of, 944 clinical features of, 471 postoperative, 792
Bubonocele, 1000 treatment of, 946 spread of, 471 Cholecystectomy, 804
Buerger’s disease, 219 Carcinoma of the gallbladder, treatment of, 472 mini cholecystectomy, 807
aetiology of, 219 817 Card test, 329 Cholecystitis, 798
clinical features of, 220 Carcinoma of the lip, 475 Cardiac arrest, 657 acute, 798
pathology of, 220 clinical features of, 476 diagnosis of, 658 acute acalculous, 810
treatment of, 222 treatment of, 477 pathogenesis of, 657 chronic, 811
Buerger’s exercise, 195 Carcinoma of the lung, 641 pathology of, 658 chronic acalculous, 811
INDEX 1219
Cholecystography, 790 Complications after gastric Corrosive oesophagitis, 696 Denis Browne’s operation for
intravenous, 791 operations, 730 Countrecoup injury, 427 undescended testis, 1177
oral, 790 Complications of acute Cracked nipple, 590 Dental cyst, 450
Cholecystostomy, 803 pancreatitis, 849 Cranial nerves, 322 Dentigerous cyst, 451
Choledochal cyst, 788 Compound palmar ganglion, Craniopharyngioma, 444 De Quervain’s disease, 362
Choledocholithiasis, 811 368 Crohn’s disease of colon, 927Dermoid cyst, 96
Choledochoscopy, 793 Computed Tomography treatment of, 928 ofthe head, 421
Choledochotomy, 814 (CT scan) of brain, 438 Crohn's disease of intestine, implantation, 98
retroduodenal, 814 Computed Tomography 871 sequestration, 97
supraduodenal, 814 (CT scan) of kidney, 1045 clinical features of, 872 sublingual, 465
transduodenal, 814 Condyloma acuminatum, treatment of, 873 teratomatous, 99
Cholelithiasis, 795 984, 1212 Crossed renal ectopia, 1032 tubulo-dermoid, 99
effects & complications of,Condyloma, giant, 1212 Crush syndrome, 23 Dermolipomatous grafts, 186
797 Condyloma lata, 163 Crushing injuries of thorax, 631
Desmoid tumour, 150, 993
Cholesterosis, 811 Congenital abnormalities of Crushed wounds, 1 Devine operation, 754
Chopart’s amputation, 344 anal-canal, 978 Cryopathic ulcer, 160 Dextran, 55
Christmas disease, 47 Congenital abnormalities of CT scanning of brain, 446 Diabetic gangrene, 235
Chronic arterial occlusion, 187 pancreas, 837 CT scan for breast Ca, 607 Diabetic ulcer, 161
Chronic cholecystitis, 803 Congenital abnormalities of CT scan in urosurgery, 1045 Diaphragm, 655
clinical features of, 803 spleen, 822 Culp pyeloplasty, 1058 Diaphragmatic hemia, 655
pathology of, 803 Congenital anomalies of the Curly toes, 375 Diffuse lipoma of the cord, 1005
treatment of, 804 bladder, 1106 Cushing's syndrome, 563 Digital Subtraction Arterio
Chronic constrictive Congenital anomalies of the Cyclical nodularity of breast, graphy (DSA), 1044
pericarditis, 674 breast, 575 586 Direct inguinal hemia, 1001
Chronic intramammary Congenital anomalies of the Cylindroma, 493 Disappearing pulse, 190
mastitis of breast, 578 gallbladder, 787 Cyst of the breast, 584 Discharge from nipple, 588
Chronic lymphocytic of cystic artery, 787 Cyst of the epididymis, Discharge from umbilicus, 992
leukaemia, 831 of cystic duct, 788 1184, 1185 Discography, 327
Chronic myeloid leukaemia, of hepatic ducts, 787 Cysts ofthe liver, 769 Discolouration of umbilicus,
832 Congenital anomalies of the non-parasitic cysts, 769 993
Chronic pancreatitis, 852 kidney, 1032 hydatid cyst, 769 Diseases of the umbilicus, 989
Chronic prostatitis, 1161 Congenital anomalies of the Cysts in the mouth, 463 Dissecting aneurysm, 253
Chronic pyelonephritis, 1062 ureter, 1033 mucous retention, 464 aetiology of, 253
treatment of, 1063 Congenital anomalies of the Cysts of the pancreas, 855 clinical features of, 254
Chronic stenosis, 742 urethra, 1170 pseudocyst, 855 pathology of, 253
Chronic subareolar mastitis, Congenital biliary atresia, 789 true cyst, 856 treatment of, 254
579 Congenital cysts, 94 Cysts ofthe spleen, 829 Diverication of recti, 1028
Congenital heart diseases, 663
Chronic relapsing pancreatitis, Cystectomy, 1126 Diverticula of small intestine,
852 acyanotic, 664 partial, 1126 875
clinical features of, 852 cyanotic, 667 total, 1126 Diverticulitis, 932
pathogenesis of, 852 Congenital hydrocele, 1191 Cystic disorders of the kidney, complications of, 934
pathology of, 852 Congenital megaureter, 1033 1032 treatment of, 933
treatment of, 853 Congenital oesophageal Cystic hygroma, 287, 507 Diverticulosis, 931
Chronic tetanus, 171 atresia, 678 Cystine calculi, 1079 Diverticulum of the bladder,
Chronic venous insufficiency,Congenital obstruction of Cystitis, 1110 1117
284 neck of bladder, 1171 abacterial, 1027 acquired, 1118
Claw hand, 329 Congenital pyloric stenosis, 711aetiology of, 1110 clinical features of, 1118
Cleft lip, 479 Congenital torticollis, 390,513 clinical features of, 1111 congenital, 1117
Cleft palate, 482 Congenital urethral stricture, pathology of, 1111 traction, 1120
Coarctation of aorta, 665 1171 treatment of, 1112 treatment of, 1119
Cockett & Dodd operation, Congenital valve of posterior tuberculous, 1112 Diverticulum of the pharynx,
270, 285 urethra, 1171 Cystosarcoma phyllodes, 592 520
Cold abscess, 82 Contracture of bladder neck,Cystogram, 1043 Divine-Horton s flip-flap
Cold abscess in the neck, 517 1171 Cystoscopy, 1046 technique, 1206
Collar-stud abscess, 519 Contusion of lung, 628 Doppler ultrasound, 191, 277
Colloid carcinoma, 133 Cooley’s anaemia, 826 D Dragstedt’s test, 718
Colloid goitre, 532 Corkscrew oesophagus, 693 Drainage procedures of
Colonoscopy, 945 Com, 151 Defibrillation, 660 pancreatic duct, 854
Common peroneal nerve, 329Coronary by-pass operation, Denis Browne’s operation forDuctal carcinoma of the
Complete scrotal hemia, 1000 673 hypospadias, 1205 breast, 595
Duct papilloma, 593 Ependymoma, 443 intracanalicular (soft), 591 diabetic, 235
Duct of Santorini, 836 Epidermoid carcinoma, 129 pericanalicular (hard), 591 dry, 233
Duct of Wirsung, 836 Epidurography, 397 Fibrocystic disease of pancreas,moist, 233
Duhamel’s operation, 919 Epigastric hernia, 1022 838 treatment of, 236
Dumb-Bell parotid tumour, Epispadias, 1207 Fibroma, 113 Gardner’s syndrome, 941
494 Epithelioma, 129 Fibrosarcoma, 149 Gastric carcinoma, 755
Duodenal atresia, 890 Epulis, 448 Filarial lymphadenitis, 297 (see carcinoma of stomach)
Duodenal ulcer, 715 carcinomatous, 450 Fine Needle Aspiration Gastric function tests, 717
clinical features of, 716 fibrous, 448 Cytology (FNAC), 606 Gastric neoplasms, 744
pathology of, 715 giant-cell, 449 Fissure-in-ano, 966 Gastric polyps, 744
special investigations of, 717granulomatous, 449 aetiology of, 966 Gastric secretion, regulation
treatment of, 720 myeloid, 449 clinical features of, 967 of, 710
Duplication of ureter, 1033 Erb-Duchenne palsy, 324 pathology of, 966 Gastric ulcer, 715
Dupuytren's contracture, 360Erysipelas, 85 treatment of, 967 clinical features of, 716
Duval’s pancreatojejuno- Escharotomy, 69 Fistula, 165 pathology of, 715
stomy, 854 Estimation of prostatic specific
Fistula-in-ano, 956 treatment of, 720
Dysphagia, 707 antigen, 1143 clinical features of, 957 Gastrinoma, 866
Dystrophy, 102 ESWL, 1081 high level fistula, 957 Gastrojejunostomy, 725
Exchange of fluid and electro low level fistula, 957 anterior, 727
lytes (normal), 25 treatment of, 958 Gaucher’s disease, 838
E Excretory urogram, 1042 Flail chest, 625 Giant cell lymphoma, 300
Exocrine secretion of Flatulent dyspepsia, 798 Giant-celled reparative
Echocardiography, 662 pancreas, 836 FNAC of breast, 606 granuloma, 453
Echoencephalography, 437, Exomphalos, 1021 Foetal lobulation of kidney, Giant condyloma, 1212
446 Exploratory burr-hole, 434 1032 Giant fibroadenoma, 592
Ectopia vesicae, 1106, 1207 Exposure of kidney, 1086 Foley pyeloplasty, 1058 G.I. tract bleeding, 755
Ectopic testis, 1006, 1179 Exstrophy, 1106 Follicular carcinoma of the lower, 985
Ectopic thyroid tissue, 553 Exstrophy of bladder, 1207 thyroid, 547 upper, 755
Ectopic ureteric orifice, 1033, Extracellular fluid, 25 Follicular odontome, 451 Glandular carcinoma, 133
1039 Extracorporeal Shock Wave Fore-quarter amputation, 343Glandular fever, 298
Electroencephalography, 445 Lithotripsy, 1081 Fracture and dislocations of Glioblastoma multiforme, 442
Electrolyte balance, 28 Extracorporeal Shock Wave spine, 411 . Gliomas, 442
Electromagnetic flow meter, Lithotripsy (ESWL) of Fracture of pelvis, 416 Glisson’s capsule, 758
193 gallstones, 808 Fracture of the ribs, 621 Glomus tumour, 119
Embolectomy, 229 Extradural abscess, 440 complications of, 622 Glucagon, 837
Emboli, 226 Extradural haemorrhage, 431Fracture of the skull, 422 Gluteal hemia, 1030
Empyema thoracic, 633 Free thyroxin index, 529 Goitre, 530
Encephalography, 445 Freiberg’s disease, 384 colloid, 532
Encephaloid carcinoma, 134 F Frei’s test, 298 diffuse hyperplastic, 531
Encysted hydrocele of the Frey's syndrome, 497 nodular, 532
cord, 1005, 1191 Fallot’s tetralogy, 667 Froment’s sign, 329 retrosternal, 533
Endocrine secretion of Familial polyposis coli, 940 Frostbite, 238 simple, 530
pancreas, 837 Fasciocutaneous flap, 185 Funicular hemia, 1000 toxic, 535
Endocrine therapy in Breast Fat embolism, 439 Furring of the tongue, 474 Gonococcal urethritis, 1167
Ca, 616 Fat necrosis of breast, 577 Gonorrhoea in female, 1167
Endometrioma of rectum, 969 Fegan’s treatment, 267 Gonorrhoea in male, 1167
Endometrioma of umbilicus, Felon, 351 G Goodsall’s rule, 957
992 Felty’s syndrome, 828 Granulation tissue formation,
Endorectal ultrasonography Femoral canal, 1016 Gaillard Thomas' incision, 579 4
(ERUS), 972 Femoral hernia, 1016 Galactocele, 586 Granuloma inguinale, 1211
Endoscopic pyelolysis, 1058 clinical features of, 1017 Gallbladder carcinoma, 817 Graves’ disease, 535
Endoscopic Retrograde coverings of, 1017 Gallstone, 795 Gritti-Stokes’ amputation, 346
Cholangiopancreato treatment of, 1018 effects & complications of,Gynaecomastia, 576
graphy (ERCP), 795 Femoro-femoral cross over 797 Gynaecomazia, 576
Endoscopic sclerotherapy, 783 graft, 199 Gallstone colic, 798
Endoscopy, 719 Femoropopliteal occlusion, 203Gallstone dissolution, 806,808
Endoscopy of urinary tract, clinical features of, 203 Gang':on, 366 H
1046 treatment of, 203 Ganglioneuroma, 571
Enterocele, 1003 Femoral ring, 1016 Gangrene, 232 Hadfield’s operation, 589
Enteroteratoma, 991 Fibroadenoma of breast, 590 causes of, 234 Haemangioma, 116
INDEX 1221
arterial, 119 Horse-shoe kidney, 1034 care of, 926 Intracranial tumours, 442
capillary, 117 Hour-glass stomach, 743 continent (Koch), 926 Intramammary mastitis, 577
cavernous, 118 Hunner’s ulcer, 1114 Immunotherapy in rectal Ca, acute, 577
plexiform, 119 Hunterian chancre, 162 977 chronic, 578
Haematocele, 1192 Hutchinson’s freckle, 137 Imperforate anus, 978 chronic subareolar, 579
Haematoma, 577 Hutchinson’s pupil, 428 Implantation dermoid, 366 subareolar, 578
Haematuria, 1127 Hydatid cyst of liver, 769 Impulse on coughing, 1003 Intraurethral stents, 1151
Haemophilia, 47 clinical features of, 770 Incarcerated hemia, 996 Invagination test, 1003
Haemorrhage, 42 pathology of, 769 Incised wounds, 1 Irreducible hemia, 996
primary, 42 treatment of, 771 Incisional hemia, 1025 Ischaemic colitis, 929
reactionary, 42 Hydrocele, 1188 aetiology of, 1025 Ischaemic heart disease, 672
secondary, 43 bilocular, 1191 clinical features of, 1026 Ischiorectal abscess, 956
treatment of, 44 congenital, 1191 treatment of, 1027 Ischiorectal space, 951
Haemorrhoids, 959 funicular, 1191 Indirect inguinal hemia, 1000
clinical features of, 960 infantile, 1191 Infections of breast, 577 J
complications of, 961 primary, 1188 Infections of cellular spaces of
secondary, 960 secondary, 1192 the hand, 357 Jaboulay’s operation, 1190
Haemorrhoidectomy, 964 vaginal, 1188 Infection of foot, 378 Jodbasedow syndrome, 544
closed, 965 Hydrocele en bisac, 1191 Infection stone disease, 1151Juvenile polyp, 968
submucous, 965 Hydronephrosis, 1052 Infectious mononucleosis, 298
Haemostasis, 46 bilateral, 1053 Infective ulcer, 159
congenital anomalies of, 47 clinical features of, 1056 Inflamed hemia, 998
K
Hairy tongue, 474 primary, 1054 Inflammatory carcinoma of
Kaposi’s sarcoma, 151, 153
Hallux rigidus, 383 treatment of, 1057 breast, 599
Kay’s histamin test, 718
Hallux valgus, 381 Hydrops gallbladder, 798 Ingrowing toe nail, 376
Keel operation, 1027
Hamartoma, 121 Hypercalcaemia, 35 Inguinal hemia, 998
Keetley Torek operation, 1177
Hammer toe, 385 Hyperhidrosis, 331 contents of, 999
Keller’s operation, 382
Hartmann’s operation, 977 Hyperkalaemia, 32 Injuries of the bladder, 1108
Keloid, 152
Harvey’s sign, 190 Hypematraemia, 29 Injury to the brain, 426
Keratoacanthoma, 154, 478
Hashimoto’s disease, 551 Hyperparathyroid crisis, 559 Injuries of the hand & fingers,
Keratosis, 478
Head injury, 422 Hyperparathyroidism, 555 368
Klumpke palsy, 324
management of, 435 primary, 555 Injury to the heart &
Kohler’s disease, 375
Hepatic abscesses, 764 secondary, 559 pericardium, 630
Krukenberg’s tumour, 601
Hepatic artery & veins, 759 tertiary, 559 Injuries ofthe kidney, 1048
Kveim test, 299
Hepatic cysts, 768 Hypersplenism, 829 clinical features of, 1049
Kyphosis, 409
Hereditary spherocytosis, 824Hypertrophic scar, 152 pathology of, 1048
Hemia-en-glissade, 1004 Hypocalcaemia, 35 treatment of, 1050
Hemioplasty, 1008, 1012 Hypocorticism, 567 Injuries of liver, 762 L
Herniorrhaphy, 1007, 1009 Hypoglossal nerve, 323 clinical features of, 763
Herniotomy, 1007,1008 Hypokalaemia, 31 treatment of, 763 Lacerated wounds, 1
Hesselbach’s triangle, 999 Hyponatraemia, 29 Injuries of the rectum & Laceration of lung, 628
Hiatus hemia, 689 Hypoparathyroidism, 559 anal canal, 983 Lactational carcinoma of
paraoesophageal or Hypospadias, 1204 Injuries of the ureter, 1051 breast, 599
rolling, 690 operations of, 1205 Injuries to the urethra, 1162 Langenbeck’s operation, 483
sliding or axial, 689 Hypothyroidism, 552 of anterior urethra, 1162 Laparoscopic abdomino
HIDAscan, 793 Hypovolaemic shock, 13 of bulbous urethra, 1162 perineal excision, 976
Hill operation, 687 clinical features of, 14 of membranous urethra, Laparoscopic anterior
Hirschsprung’s disease, 917 clinical monitoring of, 14 1163 resection, 977
treatment of, 918 pathophysiology of, 13 of posterior urethra, 1163 Laparoscopic appendi
Histiocytic lymphoma, 302 treatment of, 16 Instrumental examination of cectomy, 916
Hodgkin’s disease, 303 the urinary tract, 1046 Laparoscopic nephrectomy of
clinical features of, 303 Insulin, 837 kidney, 1103
clinical staging of, 304 I Insulinoma, 865 Laparoscopic repair of hemia,
laparotomy for, 307 Intermittent claudication, 188 1012, 1020
pathology of, 305 Idiopathic gangrene of Interstitial cell tumours of Laparoscopic varicocele
treatment of, 306 scrotum, 1203 testis, 1202 ligation, 1184
Hollander's insulin test, 718 Idiopathic thrombocytopenic Interstitial cystitis, 1124 Laparoscopy in undescended
Homan’s sign, 274 purpura (ITP), 826 Interstitial hemia, 1114 testis, 1178
Homer's syndrome, 324 Ileal conduit, 1135 Intracellular fluid, 24 Laryngocele, 522
Horse-shoe fistula, 959 Ileostomy, 926 Intracranial infections, 440 Lasegue’s sign, 404
Laser treatment in prostate, Lymphoedema, 288 Mastectomy, 609 Milnes-Walker operation, 782
1151 primary, 288 extended radical, 611 Minor salivary gland tumours,
Latent tetanus, 171 secondary, 289 modified radical, 611 495
Lateral popliteal nerve, 329 Lymphogranuloma inguinale, radical, 610 Mirault-Blair operation, 480
Leprosy, 91 297, 1211 super-radical, 611 Mitral insufficiency, 671
Leukoplakia, 467 Lymphogranulom a venereum, total, 610 Mitral stenosis, 669
Lewis-Tanner operation, 702 297, 1211 Maydl’s hemia, 998, 1004 Mitral valvotomy, 671
Leydig cell tumour, 1202 Lymphosarcoma, 300 Mayo’s operation, 382, 1022 Mixed lymphoma, 302
Lieno-renal shunt, 784 Lymphovenous shunt, 293 McBride operation, 382 Mixed tumour of parotid, 489
Lingual thyroid, 475, 553 McEvedy operation, 1019 Modified Whipple operation,
Lipoma, 114 Meckel’s diverticulum, 875 855
Lisfranc’s amputation, 344 M Meconium ileus, 892 Molluscum fibrosum, 125
Litholapaxy, 1117 Median nerve, 327 Molluscum sebaceum, 154
Lithotomy, suprapubic, 1116Macrocheilia, 475 Median rhomboid glossitis, Mondor's disease, 579
Lithotripsy, 1117 Macroglossia, 473 474 Morrissey’s test, 263
Littre's hemia, 1004 Madelung's deformity, 360 Mediastinal cyst, 654 Moses’ sign, 275
Liver abscesses, 764 Madura foot, 373 Mediastinal emphysema, MRI in breast, 605
amoebic abscess, 766 Magenstrasse, 710 629, 651 MRI in cardiac surgery, 662
pyogenic abscess, 764 Magnesium, 33 Mediastinal tumours, 652 MRI in urosurgery, 1046
Liver angiography, 779 deficiency of, 33 Mediastinum, 651 Mucoepidermoid carcinoma,
Liver scan for Breast Ca, 607 excess of, 34 Medullary carcinoma, 134 492
Liver, surgical lobes of, 758 Magnetic Resonance Imaging Medullary carcinoma of Muscle pedicle flap, 1028
functions of, 760 (MRI) of spine, 398 breast, 596 Myelocele, 390
injuries of, 760 of brain, 446 Medullary carcinoma of the Myelography, 397
lymphatics of, 760 of breast, 605 thyroid, 549 Myeloid metaplasia, 829
nerves of, 760 of kidney, 1046 Medullary sponge kidney, 1039Myocutaneous flaps, 185
Lobular carcinoma of breast, Main en griffe, 329 Medulloblastoma, 442 Myoma, 113
597 Malignant melanoma, 137 Megacolon, 917
Lockhart-Mummery aetiology of, 137 acquired, 919
operation, 954 clinical features of, 142 primary, 917 N
Lockwood operation, 1020 pathology of, 138 secondary, 919
Long thoracic nerve, 325 spread of, 141 Meig’s syndrome, 633 Naevus, 136
Lord’s operation for treatment of, 146 Melanomas, 135 blue, 136
hydrocele, 1190 Malignant melanoma of benign, 136 compound, 136
Lord’s procedure, 963 anal canal, 985 juvenile, 137 junctional, 136
Lotheissen’s operation, 1019Malignant neoplasms of the malignant, 137 Nagamatsu incision, 1087
Low back pain, 402 breast, 594 Meleney’s ulcer, 164 Necrosing pyelitis, 1064
LowerG.I. tract bleeding, 1185Malignant schwannoma, 335 Meningioma, 443 Needle biopsy in breast, 606
Lumbago, 404 Malignant tumours, 103, 126 Meningocele, 388 Needlescopic
Lumbar disc prolapse, 394 aetiology of, 106 Meningomyelocele, 389 cholecystectomy, 808
Lumbar hemia, 1029 spread of, 108 Mesenteric arteries occlusion,Neoplasms of the anal canal,
Lumbar spondylosis, 400 Mallet finger, 364 207 984
Lumbar sympathectomy, 334Mallet thumb, 364 Mesenteric cysts, 903 Neoplasms of appendix, 916
Lumbosacral strain, 404 Mallory-Weiss syndrome, 695Mesenterico-caval shunt, 785 Neoplasms ofthebladder, 1120
Lung abscess, 638 Malnutrition, 56 Mesentery, 901 Neoplasms of the cheek, 466
Lung cyst, 640 Mammary duct ectasia, 586 Mesh closure, 1028 Neoplasms of kidney, 1091
Lung tumours, 640 Mammography, 603 Metaplasia, 102 Neoplasms of the lip, 475
benign, 640 Management of advanced Metastatic tumours of brain,Neoplasms of the liver, 772
malignant, 641 cases of breast cancer, 615 443 .benign neoplasms, 772
Lupus vulgaris, 162 Management of chest injuries, .malignant neoplasms, 773
Metastatic tumours of liver, 775
Lymphangiography, 289 630 clinical features of, 776 .metastatic tumours, 775
Lymphangiography in Management of open wounds pathology of, 775 Neoplasms of the oesophagus,
urosurgery, 1044 of thorax, 630 treatment of, 776 697
Lymphangioma, 120, 287 Management of retention of Metatarsalgia, 384 benign, 697
Lymphangiosarcoma, 287 urine with enlarged Metyrapone test, 564 malignant, 698
Lymphangitis of the hand, 359 prostate, 1151 Microdochectomy, 589 Neoplasms of the pancreas,
Lymphatic drainage of breast,March fracture, 376 Microwave treatment in 859
574 Marion’s disease, 1171 prostate, 1151 endocrine neoplasms, 865
Lymphatics of stomach, 709 Marjolin’s ulcer, 134 Midgut volvulus, 891 Neoplasms of the rectum &
Lymphocytic lymphoma, 302 Martorell’s ulcer, 160 Mikulicz disease, 496 anal canal, 968
INDEX 1223
Neoplasms of renal pelvis & Ochsner’s clasping test, 327 lymphomatosum, 492 complications of, 735
ureter, 1101 Oculomotor nerve, 322 Papilloma, 111 pathology of, 715
Neoplasms of the salivary Odontomes, 450 Papilloma & papillary carci Peptic ulcer haemorrhage, 739
gland, 489 follicular, 451 noma of renal pelvis, 1101 management of, 740
Neoplasms of small intestine,Oesophageal diverticulum, 694 Papilloma of urethra, 1172 Percutaneous nephrolithotomy
878 Oesophageal perforation, 679Parabronchial diverticulum, (PCNL), 1080
Neoplasms of the stomach, 744 clinical features of, 680 695 Percutaneous transhepatic
.malignant neoplasms, 745 instrumental, 680 Paradoxical respiration, 626 Cholangiography (PTC),
Neoplasms of the thyroid, 544 spontaneous, 680 Paralytic ileus, 880 793
benign, 544 traumatic, 680 treatment of, 886 Perforated peptic ulcer, 735
malignant, 545 treatment of, 681 Paraphimosis, 1210 Perianal abscess, 955
Neoplasms of the umbilicus, Oesophageal transection for Parathyroid, 554 Periarterial sympathectomy,
991 portal hypertension, 783 Paraumbilical hernia, 1021 334
Neoplasms ofthe urethra, 1172 Oesophagocardiomyotomy, Parenteral fluid therapy, 36 Pericarditis, 674
Nephrectomy, 1085 693 ' Parenteral nutrition, 58 acute, 674
Nephroblastoma, 1098 Olfactory nerve, 322 Park’s operation, 965 chronic constrictive, 674
Nephrolithotomy, 1084 Oligodendroglioma, 442 Parana’s space, 357 Perineal hernia, 1030
Nephrostomy, 1085 Ombredanne’s operation, infection of, 359 Perineal prostatectomy, 1149
Nephrotomography, 1042 1177 Paronychia of hand, 349 Perinephric abscess, 1066
Nephroureterectomy, 1070, Omentocele, 1003 acute, 349 Peritonitis, 893
1104 Omentum, greater, 901 chronic, 350 diffuse, 894
Nerve of Bell, 325 Omphalitis, 989 of foot, 377 management of, 895
Nerve suture, 318 Onychogryphosis, 377 Parotid calculi, 500 Persistent urachus, 1108
results of, 320 Opisthotonus, 170 Parotid fistula, 496 Perthes' test, 263
Neurapraxia, 312 Optic nerve, 322 Parotid gland, 487 Peustow’s longitudinal
Neurilemmoma, 122, 335 Orchidectomy, 1199 Parotitis, 487 pancreatojejunostomy, 854
Neuroblastoma, 570 Orchidopexy, 1176 acute suppurative, 487 Peutz-Jegher’s syndrome,
Neurofibroma, 122 Oscillometer, 190 recurrent subacute & 878, 937
cutaneous, 125 Osteoclastoma of jaw, 453,454 chronic, 488 Peyronie’s disease, 1211
dumb-bell shaped, 126 Osteomyelitis of the jaw, 458Partial cystectomy, 1126 Pharyngeal pouch, 520
elephantiasis, 125 Osteomyelitis of skull, 440 Partial gastrectomy, 728 Pharyngoesophageal
generalized, 123 Osteosarcoma of jaw, 455 Billroth I gastrectomy, 730 diverticulum, 694
plexiform, 125 Oxalate stone, 1079 Partial nephrectomy, 1085 Pheochromocytoma, 568
solitary, 122 Oxyphil adenoma, 492 Partial thickness skin graft, 179
Phimosis, 1209
Neurogenic bladder Passive immunization, 172 Phlebography, 275
dysfunction, 1132 Patch grafting, 180 ascending functional, 275
Neurogenic shock, 20 P Patent ductus arteriosus, 664 radionuclide, 276
Neurogenic ulcer, 159 Patent urachus, 991, 1108 Phlebothrombosis (DVT), 274
Neuroma, 121 Pachydermatocele, 125 Patent vitello-intestinal duct,Phonangiography, 192
Neurotmesis, 314 Paget’s disease of breast, 598 990 Phyllodes tumour, 592
Nipple discharge, 587 Paget’s disease of the jaw, 453
PB.I., 528 Physiology of pancreas, 836
Nipple inversion, 589 Pain in the foot, 375 Peau d’ orange, 599 Pick’s disease, 674
Nipple ^retraction, 589 Painful heel, 379 Pedicle graft, 182 Piles (See haemorrhoids), 959.
Nissen fundoplication, 686 Palma operation, 271 bridge, 182 Pilonidal sinus, 981
Nodular goitre, 532 Palpation of peripheral pulses, direct, 182 of umbilicus, 990
solitary nodule, 533 190 tube, 183 Pinch grafts, 182
Non-Hodgkin’s Lymphomas Pancreaticoduodenectomy, Pelvic abscess, 899 Pirogoff’s amputation, 345
(NHL), 303, 831 862 Pelvic kidney, 1032 Pituitary adenoma, 443
Non-specific infections of thePancreatitis, 839 Pelvirectal abscess, 956 Pituitary irradiation, 565
kidney, 1058 acute, 839 Pelvirectal space, 951 Plantar fasciitis, 380
Non-specific mesenteric chronic, 851 Penetrating wounds, 1 Plasma, 54
lymphadenitis, 902 clinical features of, 841 Penetration into neighbouringPlatelet rich plasma, 54
Nuclear medicine breast pathogenesis of, 839 viscera, 743 Pleomorphic adenoma, 489
imaging technique, 606 pathology of, 840 Pentagastrin test, 718 Plethysmography, 192, 277
special investigations of, 841
Pen test, 327 Pleural effusion, 618, 632
treatment of, 844 Peptic ulcer, 712 Plummer Vinson syndrome,
o Pancreatojejunostomy, 854 acute peptic ulcer, 712 695
Papillary carcinoma of the aetiology & Plunging ranula, 512
Obstructed hemia, 996 thyroid, 546 pathogenesis of, 712 Pneumothorax, 623
Obturator hemia, 1030 Papillary cystadenoma chronic peptic ulcer, 712 Polya gastrectomy, 729
Polycystic kidney, 1035 tuberculous, 1161 Raspberry tumour, 991 Roentgenographic examina
clinical features of, 1036 Pruritus ani, 984 Raynaud’s disease, 210 tions in urology, 1041
complications of, 1037 Pseudocyst of the pancreas, clinical features of, 211 Rule of ‘9’, 64
treatment of, 1037 855 pathophysiology of, 210 Ruptured abdominal
Polyps of colon, 936 Pseudopancreatic cyst, 855 treatment of, 212 aneurysm, 251
hyperplastic, 938 Psoas abscess, 1106 Raynaud’s syndrome, 209 Rupture of anterior urethra,
juvenile, 937 Pulmonary arteriography, 282 aetiology of, 209 1162
neoplastic, 938 Pulmonary embolectomy, 283Reconstruction of breast, 618Rupture of bulbous urethra,
Polyps, gastric, 744 Pulmonary embolism, 281 Rectal sling operation, 954 1162
Polyposis coli, familial, 940 clinical features of, 281 Rectopexy, 954 Rupture of intestine, 874
Polyp of urethra, 1172 pathophysiology of, 281 Rectosigmoidectomy, 954 Rupture of membranous
Popliteal aneurysm, 252 treatment of, 282 Recurrent inguinal hemia, urethra, 1163
Popliteal artery entrapment Pulmonary radioisotope 1014 Rupture of posterior urethra,
syndrome, 208 scanning, 282 Recurrent tetanus, 171 1163
Pbrtacaval shunt, 784 Pulmonary tuberculosis, Recurrent thyrotoxicosis, 542
Rupture of the spleen, 822
Portal hypertension, 777 surgical treatment of, 636 Reducible hemia, 996 clinical features of, 823
aetiology of, 777 Pulp space infection, 351 Reflux oesophagitis, 682 pathology of, 822
clinical features of, 778 Pyaemic abscess, 81 complications of, 685 treatment of, 824
emergency operations of, Pyelolithotomy, 1083 with stricture, 687 Ruptured Tendo-Achilles, 386
782 Pyelonephritis, 1059 treatment of, 685 Rupture of urethra, 1162
management of, 780 acute, 1059 Reiter’s disease, 1166
shunt operations of, 783 chronic, 1062 Renal abscess, 1065
Portal vein, 759 Pyloric stenosis, 742 Renal angiography, 1043 s
Post anal dermoid, 980 Pyloroplasty, 727 Renal calculus, 1071
Postcholecystectomy Finney, 727 aetiology of, 1071 Sacrococcygeal teratoma, 980
symptoms, 809 Heinke-Mikulicz, 727 clinical features of, 1074 Saint’s triad, 797
Post traumatic amnesia (PTA), Pyogenic arthritis of finger, 356primary, 1073 Salt intake & output, 26
427 Pyogenic granuloma, 154,478 secondary, 1074 Saphena varix, 1006
Post traumatic pulmonary Pyonephrosis, 1064 special investigations of, Saphenous opening, 1017
insufficiency, 628 1076 Sarcoidosis, 299, 828
Potassium, 30 treatment of, 1078 Sarcoma, 148
deficiency of, 31
Q types of, 1073 Kaposi’s, 151, 153
excess of, 32 Renal cell carcinoma, 1092 Sarcoma of breast, 620
Quart, 609 Sarcoma of the stomach, 754
Potato tumour, 514 Renal cysts, 1032
Pratt’s test, 262 solitary, 1038 Scalenotomy, 226
Primary hyperparathyroidism, R Renal function tests, 1040 Scalenus anticus syndrome,
555 Renal pedicle 222
Primary toxic goitre, 535 Radial bursa infection, 355 sympathectomy, 1058 Schatzki ring, 696
aetiology of, 535 Radial nerve, 325 Renal scintiscan, 1046 Scheuermann’s disease, 410
clinical features of, 536 Radical gastrectomy, 752 Resection of rectum, anterior,Schistosomiasis, 832
treatment of, 538 lower radical, 753 954 Schwannoma, 122
Proctitis, 983 total radical, 752 Rest pain, 151 Schwartz’s test, 263
Prolapse of intervertebral disc, upper radical, 753 Retention of urine, 1131 Sciatica, 404
392 Radical mastectomy, 610 Reticulum cell sarcoma, 301 Sciatic hemia, 1030
Prolapse of rectum, 952 extended, 611 Retraction of nipple, 589 Sciatic nerve, 329
complete, 953 modified, 611 Retractile testis, 1005 Scirrhous carcinoma, 134
partial, 952 super-, 611 Retrograde traumatic amnesiaScirrhous carcinoma of breast,
Prostatectomy, 1146 Radical nephrectomy for (RTA), 427 596
complications of, 1150 renal cell carcinoma, 1097Retrograde urogram, 1042 Scleroderma, 693
perineal, 1149 Radicular cyst, 450 Retromammary abscess, 579 Sclerosing adenosis, 582, 586
radical perineal, 1159 Radioactive fibrinogen test, Retroperitoneal lymph node Scoliosis, 407
retropubic, 1148 276 dissection, 1201 Sebaceous cyst, 99
suprapubic, 1146 Radioisotope renography, Retropubic prostatectomy, of the head, 421
transurethral, 1149 1046 1148 Sebaceous cyst of scrotum,
Prostatic abscess, 1159 Radiotherapy for Breast Ca, Retrosternal goitre, 533 1203
Prostatic specific antigen 617, 619 Richter’s hemia, 1004 Sebaceous horn, 101
(PSA), 1156 Radiotherapy in rectum, 977 Riedel's thyroiditis, 552 Secondary carcinoma of lung,
Prostatitis, 1159 Ramstedt’s operation, 711 Risus sardonicus, 170 650
acute, 1159 Ranula, 464 Rodent ulcer, 126 Secondary carcinoma of
chronic, 1161 deep or plunging, 512 (see basal cell carcinoma) lymph nodes, 307
INDEX 1225
Secondary carcinoma of predisposing factors of, 130Sympathectomy, 196,332 Torsion of the spermatic cord,
umbilicus, 992 sites of, 130 cervico-thoracic, 333 1179
Seminoma of testis, 1193 spread of, 131 indications of, 332 Torsion of the testis, 1005,
treatment of, 1199 Squamous cell carcinoma of lumbar, 334 1179
SEMS, 706, 978 renal pelvis, 1103 peri-arterial, 334 Torticollis, 390
Senile keratosis, 153 Stapled anastomosis, 977 Synovial sarcoma, 151 congenital, 390
Sentinel Node biopsy, 612 Stenosing tenovaginitis, 362 Syphilis, 88 secondary, 392
Septic shock, 20 Stemomastoid tumour, 513 of the mouth, 463 Total cystectomy, 1126
Serocystic disease of Brodie, Stomatitis, 461 Syphilis of breast, 579 Tourniquet test, 262
592 angular, 462 Syphilitic chancre, 1209 Toxic goitres, 535
Sertoli cell tumour, 1202 aphthous, 461 Syphilitic lymphadenitis, 297 multinodular, 543
Serum PBI, 528 gangrenous, 462 Syphilitic ulcer, 162 primary, 535
Serum-P&T4,528 monilial, 461 Syringomyelocele, 390 secondary, 543
Serum TSH, 529 traumatic, 461 toxic nodule, 543
Sever’s disease, 379 ulcerative, 462 Toxoplasmosis, 299
Shouldice repair, 1011 Stove-in-chest, 625 T Transitional cell carcinoma,
Shunt operations for portal Straight leg-raising test, 396 134
hypertension, 783 Strangulated femoral hemia, Takayasu’s arteritis, 207 Transposition of great vessels,
complications of, 785 treatment of, 1020 Tanner’s operation, 782 668
lieno-renal shunt, 784 Strangulated hemia, 997 Tapping of hydrocele, 1190 Transrectal ultrasonography,
mesenterico-caval shunt, Strangulated inguinal hemia, Tea-pot stomach, 743 1045
785 treatment of, 1014 Tension pneumothorax, 623 Transsphenoidal hypophy
porta-caval shunt, 784 Strangulated omentocele, 997Teratoma of testis, 1195 sectomy, 565
Sialolithiasis, 498 Strangulated Richter’s hemia, treatment of, 1199 Transurethral prostatectomy,
Sickle cell anaemia, 827 997 Tetany, 542 1149
Sigmoid volvulus, 934 Strawberry gallbladder, 811 Thalassaemia, 826 Traumatic asphyxia, 629
Simmond’s operation, 381 Stress fracture, 384 Thecal whitlow, 353 Traumatic chylothorax, 630
Sinus, 165 Stricture of bile duct, 815 Thermography in breast, 604 Traumatic fat necrosis of
examination of, 165 Stricture of oesophagus Thiersch’s operation, 959 breast, 577
Sister Mary Joseph’s nodule, (benign), 696 Thompson operation, 292 Traumatic haemothorax, 624
992 Struma ovarii, 533, 544 Thoracic outlet syndrome, Traumatic pneumothorax, 623
Sjogren’s syndrome, 496 Subareolar mastitis, 578 215 Traumatic rupture of
Sliding hemia, 1004 Subclavian steal syndrome, 206 aetiology of, 216 diaphragm, 627
Soave’s operation, 919 Subclavian vertebral disease, anatomy of, 215 Traumatic shock, 19
Sodium, 28 206 clinical features of, 217 Traumatic ulcer, 158
Soft chancre, 163 Subdural abscess, 441 pathology of, 216 T3 resin uptake, 529
Solar keratosis, 153 Subdural haemorrhage, 429 treatment of, 218 Trigeminal nerve, 322
Solitary renal cyst, 1038 Subhyoid bursal cyst, 516 Thoracoabdominal injuries, Trigeminal neuralgia, 322
Spermatocele, 1185 Sublingual dermoid cyst, 465, 631 Trigger finger, 363
Spigelian hemia, 1030 511 Thromboangiitis obliterans, Trochlear nerve, 322
Spina bifida, 387 Submammary incision, 579 219 Tropical splenomegaly, 832
occulta, 387 Submandibular calculi, 498 (See Buerger’s disease) Tropical ulcer, 159
Spironolactone test, 566 Submandibular gland Thromboendarterectomy, 197Truss, 1007
Splenectomy, 832 tumours, 495 Thrombophlebitis, 273 TSH stimulation test, 530
indications of, 832 Subphrenic abscess, 897 Thrush, 461 T3 suppression test, 529
postoperative complica Subtotal thyroidectomy, 540 Thyroglossal cyst, 508, 553 Tuberculosis, 86
tions of, 834 complications of, 541 Thyroglossal fistula, 510 pathology of, 87
preoperative management,Sucking wounds, 630 Thyroglossal tract, 553 Tuberculosis of breast, 579
833 Suppurative tenosynovitis, Thyroid crisis, 542 Tuberculosis of the intestine,
technique of, 833 353 Thyroid insufficiency, 542 869
Splenic vein thrombosis, 833 Suprapubic lithotomy, 1116 Thyroiditis, 551 hyperplastic, 869
Splenomegaly, 830 Suprapubic prostatectomy, acute suppurative, 551 ulcerative, 870
Spondylolisthesis, 400 1146 autoimmune, 551 Tuberculosis of kidney, 1067
traumatic, 402 Surgical emphysema, 622 Riedel’s, 552 clinical features of, 1068
Spongioblastoma polare, 442 Surgical lobes of liver, 758 subacute, 551 pathology of, 1067
Spread of breast carcinoma, Surgical treatment of pulmo Thyroid scan, 530 treatment of, 1070
599 nary tuberculosis, 636 Thyroid storm, 542 Tuberculosis of the prostate &
Squamous cell carcinoma, 129 Swellings of the neck, 501 Thyroid uptake test, 529 seminal vesicles, 1161
clinical features of, 131 Swenson's operation, 918 Thyrotoxicosis, 535, 536 Tuberculous arthritis of foot,
pathology of, 130 Syme’s amputation, 344 Tinel’s sign, 313 379
Tuberculous cystitis, 1112 actinomycotic, 163 Undulent fever, 299 Ventriculography, 445
Tuberculous lymphadenitis, arterial, 158 Upper G.I. tract bleeding, 755Vesical angiography, 1044
296 base of, 157 Urachal cyst, 991, 1108 Vesical calculus, 1114
Tuberculous peritonitis, 899 Bazin’s, 161 Urachus, patent, 991 clinical features of, 1115
Tuberculous ulcer, 162 classification of, 157 Ureteral stone, 1087 composition of, 1114
Tubular adenoma of colon, 938 cryopathic, 160 clinical features of, 1088 treatment of, 1116
Tularaemia, 299 diabetic, 161 treatment of, 1089 Villous adenoma of colon, 939
Tumours of the anal caned, 984edge of, 156 Ureterocele, 1034 Villous adenoma of rectum,
Tumours of the bladder, 1120 examination of, 156 Ureterolithotomy, 1091 969
benign papillary, 1121 floor of, 157 Ureteroscopy (URS) of Vincent’s angina, 462
epithelial, 1120 infective, 159 kidney, 1082 Volar space infection, 352
Tumours of bronchi & lung, 640Martorell’s, 160 Ureterosigmoidostomy, 1135 middle, 352
benign, 640 Meleney’s, 164 Urethral calculus, 1172 proximal, 352
malignant, 641 neurogenic, 159 Urethral stricture, 1168 Volkmann’s ischaemic
Tumours of the cheek, 466 syphilitic, 162 treatment of, 1169 contracture, 366
Tumours of the colon, 936 traumatic, 158 Urethritis, 1165 Volvulus, 934
Tumours of the head, 421 tropical, 159 acute non-gonococcal, 1166 of caecum, 936
Tumours of kidney, 1091 tuberculous, 162 chronic, 1166 of sigmoid, 934
Tumours of the liver, 772 venous, 159 gonococcal, 1167 Von Recklinghausen’s
.benign tumour, 772 Ulcerative colitis, 920 Urethroplasty, 1170 disease, 555
.malignant tumours, 773 aetiology of, 920 Urethroscopy, 1147
.metastatic tumours, 775 clinical features of, 921 Urethrotomy, 1170
Tumours of the oesophagus, complications of, 923 external, 1170 w
697 « pathology of, 920 interned, 1170
benign, 697 special investigations of, 922
Uric acid calculi, 1079 Wallerian degeneration, 246
malignant, 698 treatment of, 924 Urinary diversion, 1135 Wardill’s operation, 484
Tumours of the pancreas, 859Ulcerative stomatitis, 462 Urograms, 1042 Warthin’s tumour, 491
Tumours of the peripheral Ulcers of the tongue, 468 excretory, 1042 Warts, 151
nerve, 335 aphthous, 468 retrograde, 1042 Water deficit, 27
Tumours of rectum & anal carcinomatous, 469 Water excess, 27
caned, 968 chronic non-specific, 469 V Waterhouse-Friderichsen
Tumours of renal pelvis & dental, 468 syndrome, 568
ureter, 1101 herpetic, 469 Vagotomy, 723 Water intake, 25
Tumours of salivary gland, 489 syphilitic, 468 highly selective, 725 Water output, 25
Tumours of small intestine, 869tuberculous, 468 selective, 725 WDHA syndrome, 867
Tumours of spinal canal, 407 Ullman’s sign, 402 truncal, 724 Web space infection, 353
Tumours of the spleen, 829 Ulnar bursa, infection, 354 Valvular repair, 272 Wells operation, 953
Tumours of the stomach, 744Ulnar nerve, 328 Van der Meulen’s operation, Whipple’s operation, 862
malignant tumours, 745 Ultrasonography of 1206 White line of Hilton, 951
Tumours of the testis, 1193 gallbladder, 792 Varicocele, 1005, 1181 Whole thickness skin graft, 180
clinical features of, 1197 Ultrasound in breast, 604 clinical features of, 1182 Wdms’ tumour, 1098
pathology of, 1194 Ultrasound in kidney, 1044 treatment of, 1183 Wolfe’s skin graft, 180
spread of, 1196 Umbilical adenoma, 991 Varicose veins, 256 Wound contraction, 3
treatment of, 1199 Umbilical calculus, 992 clinical features of, 261 causes of, 3
Tumours of the thyroid, 544 Umbilical dermatitis, 990 complications of, 264 factors inhibiting, 4
benign, 544 Umbilical discharge, 992 surgical anatomy of, 256
malignant, 545 Umbilical fistula, 990, 993 surgical pathology of, 259
Tumours of the tongue, 469 Umbilical granuloma, 990 treatment of, 265
Tumours of ureter, 1103 Umbdical hemia, 1021 Vascular anomalies of colon,
Tumours of vertebral column,Undescended testis, 1006, Xeroradiography of breast,
987
405 1174 604
Venous thrombosis, 272
Typhoid enteritis, 877 causes of, 1174 deep (DVT), 274
clinical features of, 1175 superficial, 273
u complications of, 1175 Venous ulcer, 159,268
treatment of, 1176 Ventral hemia, 1025 Zollinger-Ellison syndrome,
Ulcer, 156 types of, 1174 Ventricular septal defect, 666 866

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!'■!■■' ' . • ' , ■ ■.

Senior Consnltant Surgeon

Copyright © DR. S. DAS.

First Edition ......................................... June, 1994

Second Edition ............................ September, 1999

Third Edition ........................................ June, 2001

Fourth Edition ................................February, 2006

Fifth Edition .......................................March, 2008

Sixth Edition .......................................... July, 2010

US $ 27.00 Rs. 778.00

June, 1994. S. DAS.

13, Old Mayors’Court, S. DAS.

38. THE BILIARY SYSTEM 786

CHRONIC ARTERIAL OCCLUSION

6. Pre-gangrenous state.— The combination of rest pain, colour changes, hyperaesthesia

performed to exclude presence of abdominal aortic

used to get a direct arterial visualization.

Rise of skin temp. - Rise of mouth temp.

MANAGEMENT. — Management of cases of chronic

2. ADRENALECTOMY.— This operation is only used in cases of Buerger's disease with

VARIOUS SITES OF CHRONIC ARTERIAL OCCLUSIONS

Occasionally an acute episode of

FEMORO POPLITEAL OCCLUSION

mr\ Another peculiar

and there is no obstruction of

CAROTID OCCLUSIVE DISEASE—

Superior mesenteric artery embolization.— This is a common example of acute occlusion.

2. It may be a secondary manifestation of some other probably more serious disease. A

downwards and laterally to

THORACIC OUTLET SYNDROME

may be obstructed where it

On auscultation one may get supraclavicular bruit.

OPERATIVE MANAGEMENT.— This is indicated to those, who do not respond to four or

BUERGER’S DISEASE (THROMBOANGIITIS OBLITERANS)

CERVICAL RIB AND SCALENUS ANTICUS SYNDROME

(a) When conservative treatment fails.

ACUTE ARTERIAL OCCLUSION

Ischaemia in these peripheral nerves lead to

• Clear line of demarcation is present. • Line of demarcation is vague.

• There may be loss of sensation.

• Osteomyelitis affecting different bones e.g. calcaneum, cuneiforms, metatarsals.

ABDOMINAL AORTIC ANEURYSMS

PHYSICAL EXAMINATION.— For abdominal aneurysm, the abdomen is palpated with

PREOPEFtATIVE EVALUATIONS include special investigations mentioned above, an

(iii) When immediate rupture seems likely, operation should be performed.

VARICOSE VEINS OF THE LOWER LIMBS

LONG (GREAT) SAPHENOUS VEIN.—

SHORT (SMALL) SAPHENOUS VEIN.—

Fig. 16.1 .— Direction of blood flow in the

till the deep fascia is reached. The

Fig. 16.8.— Ascending phlebography showing normal filling

The test is positive only during the

TREATMENT OF ESTABLISHED CASES.—

CHRONIC VENOUS INSUFFICIENCY

The ulcers may appear spontaneously or follow trivial trauma.

DISEASES OF THE LYMPHATICS

(a) SIMPLE AND CAPILLARY LYMPHANGIOMA.— This type presents as circumscribed

COMPUTERISED TOMOGRAPHY.— Though a single axial CT slice through the midcalf

DISEASES OF LYMPH NODES

(iv) Malignant lymphoma, lymphocytic type (well-differentiated);

detect pulmonary tuberculosis or bronchogenic carcinoma as the cause of enlargement of cervical

VARIOUS TYPES OF LYMPH NODE INVOLVEMENT ARE

(i) Lymphocytosis in the blood is a very characteristic feature of this disease.