CLINICAL OFFICER’S CRASH COURSE

FIRST EDITION, 2021

SURGERY
Notices

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changes in research methods, professional practices, or medical treatment may become necessary.

Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any information,
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dose or formula, the method and duration of administration, and contraindications.

It is the responsibility of practitioners, relying on their own experience and knowledge of their patients, to make diagnoses, to
determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions.

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© 2021 by clinical officer’s crash course series

Published by clinical officer’s crash course series

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All rights reserved. The text of this publication, or any part thereof, may not be reproduced in any

manner whatsoever without written permission from the publisher.

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PREFACE

Author

In recent years there have been an increase of schools providing clinical medicine program. This program is
quite big, the curriculum keeps being updated, many schools do not have materials to help students study
and most of schools do not cover everything the student is supposed to study according to the curriculum
which leaves students in the position to learn many things entirely on their own which is very difficult.

The ever-increasing depth of knowledge has led to even greater exhaustion, and the volume of material is
often daunting.

The Clinical Officer’s Crash Course in Surgery is an invaluable revision aid for clinical officer students
approaching their intermediate and final exams. The rate of change in modern medicine is staggering and to
keep up to date with all aspects of such changes is virtually impossible. This book provides a concise account
of a broad range of general, ear, nose and throat surgery from the salient features of history taking and clinical
examination to investigations and further management.

This book covers everything that is supposed to be taught to clinical officers according to the curriculum.

Crash Course will also be of great help to clinical officers in their time of clinical rotations leading up to
preparation for higher professional exams.

I hope that this book will serve students well as a revision guide from the start of their studies to the end.

Jeremie Bahati

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We want to hear what you think. What do you like or not like about the notes?
Please email us at cocrashcourse@gmail.com

iii
 Contents

PREFACE .................................................................................................................................................................... II
1. HISTORY-TAKING AND PHYSICAL EXAMINATION ............................................................................. 1
HISTORY-TAKING ................................................................................................................................................... 1
PHYSICAL EXAMINATION.................................................................................................................................... 3
2. PRINCIPLES OF INVESTIGATION ................................................................................................................ 4
3. PREPARING A PATIENT FOR SURGERY/MANAGEMENT OF A PATIENT REQUIRING
SURGERY ...................................................................................................................................................................... 5
PREPARATION/MANAGEMENT OF A PATIENT REQUIRING AN ACUTE SURGERY............................ 5
4. ANAESTHESIA USED IN GENERAL SURGERY ......................................................................................... 7
GENERAL ANAESTHESIA ..................................................................................................................................... 7
REGIONAL(LOCAL) ANAESTHESIA ................................................................................................................... 7
6. SURGICAL INCISIONS ..................................................................................................................................... 9
7. SUTURES AND SUTURING TECHNIQUES ............................................................................................... 10
SUTURES .................................................................................................................................................................. 10
SUTURING TECHNIQUES .................................................................................................................................... 11
8. INTRODUCTION TO TRAUMATOLOGY .................................................................................................. 12
INITIAL EVALUATION AND RESUSCITATION OF THE INJURED PATIENT ........................................... 12
INTRAVENOUS FLUIDS, BLOOD AND BLOOD PRODUCTS ........................................................................ 14
9. TOURNIQUETS.................................................................................................................................................. 16
10. DERMATOLOGIC WOUNDS ..................................................................................................................... 17
CLOSED AND OPEN WOUNDS........................................................................................................................... 17
11. WOUND HEALING ....................................................................................................................................... 19
12. AMPUTATION ............................................................................................................................................... 20
13. BURNS AND GRAFTS .................................................................................................................................. 22
BURNS....................................................................................................................................................................... 22
RESURFACING/GRAFTS ...................................................................................................................................... 24
14. HUMAN AND ANIMAL BITES .................................................................................................................. 26
SNAKE BITE ............................................................................................................................................................. 26
DOG BITES ............................................................................................................................................................... 26
BEE STINGS .............................................................................................................................................................. 26
BLACK WIDOW SPIDERS ..................................................................................................................................... 27
BROWN RECLUSE SPIDER BITES ........................................................................................................................ 27
HUMAN BITES ........................................................................................................................................................ 27
15. FRACTURES / DISLOCATIONS ................................................................................................................ 28
HEALING OF FRACTURES ................................................................................................................................... 31
16. DEPRESSED SKULL FRACTURE ............................................................................................................... 35
17. NECK FRACTURE ......................................................................................................................................... 36
18. UPPER LIMBS FRACTURES........................................................................................................................ 37
FRACTURE CLAVICLE .......................................................................................................................................... 37
PROXIMAL HUMERAL FRACTURES ................................................................................................................. 37

iv
 DISLOCATION OF SHOULDER ........................................................................................................................... 38
FRACTURE SHAFT HUMERUS ............................................................................................................................ 38
DISTAL HUMERUS FRACTURES ........................................................................................................................ 39
SUPRACONDYLAR FRACTURE .......................................................................................................................... 39
RADIAL HEAD FRACTURE .................................................................................................................................. 40
FRACTURE BOTH BONES OF THE FOREARM ................................................................................................. 40
ISOLATED DISTAL ULNAR FRACTURE (ALSO CALLED NIGHTSTICK FRACTURE) ............................. 41
MONTEGGIA’S FRACTURE ................................................................................................................................. 41
COLLES’ FRACTURE .............................................................................................................................................. 41
SMITH’S FRACTURE .............................................................................................................................................. 42
19. LOWER LIMBS FRACTURES ...................................................................................................................... 44
FRACTURE FEMUR ................................................................................................................................................ 44
INJURIES OF THE KNEE ........................................................................................................................................ 46
FRACTURE OF TIBIA AND FIBULA .................................................................................................................... 47
INJURIES OF THE ANKLE ..................................................................................................................................... 48
20. PELVIC INJURIES .......................................................................................................................................... 50
FRACTURE PELVIS ................................................................................................................................................ 50
DISLOCATIONS OF THE HIP JOINT ................................................................................................................... 51
21. CHEST/RIB FRACTURES ............................................................................................................................. 53
22. ABDOMINAL AND INTRA-ABDOMINAL INJURIES ......................................................................... 54
PENETRATING TRAUMA..................................................................................................................................... 54
BLUNT TRAUMA .................................................................................................................................................... 54
23. CHEST INJURIES ........................................................................................................................................... 56
HAEMOTHORAX ................................................................................................................................................... 57
SIMPLE PNEUMOTHORAX .................................................................................................................................. 57
TENSION PNEUMOTHORAX .............................................................................................................................. 57
FLAIL CHEST ........................................................................................................................................................... 57
BLUNT CARDIAC INJURY .................................................................................................................................... 58
TRAUMATIC RUPTURE OF THE DIAPHRAGM............................................................................................... 58
RUPTURE OF THE AORTA ................................................................................................................................... 58
RUPTURE OF THE TRACHEA .............................................................................................................................. 58
CARDIAC TAMPONADE ...................................................................................................................................... 58
OESOPHAGEAL DISRUPTION ............................................................................................................................ 59
24. HEAD INJURIES ............................................................................................................................................ 60
HEAD INJURY ......................................................................................................................................................... 60
EXTRADURAL HAEMATOMA ............................................................................................................................ 62
SUBDURAL HAEMATOMA ................................................................................................................................. 62
SUBARACHNOID HAEMORRHAGE (SAH) ..................................................................................................... 63
RAISED INTRACRANIAL PRESSURE ................................................................................................................. 63
25. INJURIES OF THE SPINE............................................................................................................................. 65
INJURIES OF THE CERVICAL SPINE .................................................................................................................. 65
THORACIC AND LUMBOSACRAL SPINE INJURIES ...................................................................................... 65
26. SPINAL CORD INJURY ................................................................................................................................ 67
CAUDA EQUINA SYNDROME ............................................................................................................................ 67
SPINAL SHOCK....................................................................................................................................................... 68
NERVE HEALING ................................................................................................................................................... 68
28. SURGICAL INFECTIONS ............................................................................................................................ 69

v
 CELLULITIS ............................................................................................................................................................. 69
ERYSIPELAS............................................................................................................................................................. 69
ABSCESS ................................................................................................................................................................... 69
CARBUNCLE ........................................................................................................................................................... 70
BOIL ........................................................................................................................................................................... 70
HIDRADENITIS ....................................................................................................................................................... 70
NECROTIZING FASCIITIS .................................................................................................................................... 70
GAS GANGRENE .................................................................................................................................................... 71
SEPTICAEMIA ......................................................................................................................................................... 71
ACUTE PYOMYOSITIS........................................................................................................................................... 71
SURGICAL SITE INFECTION (SSI)....................................................................................................................... 72
29. HAND INFECTIONS ..................................................................................................................................... 72
31. ULCERS ............................................................................................................................................................ 74
TROPHIC ULCER (PRESSURE SORE/DECUBITUS ULCER) .......................................................................... 74
MARJOLIN’S ULCER .............................................................................................................................................. 74
DIABETIC ULCER ................................................................................................................................................... 74
32. MUSCULO-SKELETAL DISORDERS ....................................................................................................... 76
BACKACHE ............................................................................................................................................................. 76
OSTEOPOROSIS ...................................................................................................................................................... 77
OSTEOARTHRITIS .................................................................................................................................................. 78
SEPTIC ARTHRITIS................................................................................................................................................. 78
OSTEOMYELITIS..................................................................................................................................................... 79
SCIATICA ................................................................................................................................................................. 82
PATHOLOGICAL FRACTURES ........................................................................................................................... 82
33. NEOPLASMS OF THE SKIN AND SUBCUTANEOUS TISSUES ....................................................... 83
BASAL CELL CARCINOMA ................................................................................................................................. 83
SQUAMOUS CELL CARCINOMA ....................................................................................................................... 83
MELANOMA ........................................................................................................................................................... 83
34. FOREIGN BODIES IN GIT .......................................................................................................................... 84
FOREIGN BODY OESOPHAGUS .......................................................................................................................... 84
FOREIGN BODIES IN THE STOMACH ............................................................................................................... 84
FOREIGN BODY IN THE RECTUM. ..................................................................................................................... 84
35. CONDITIONS OF THE ABDOMINAL WALL, PERITONUEM .......................................................... 85
APPLIED ANATOMY ............................................................................................................................................. 85
PERITONITIS ........................................................................................................................................................... 85
36. ABDOMINAL HERNIAE .............................................................................................................................. 88
INGUINAL HERNIA .............................................................................................................................................. 89
FEMORAL HERNIA ................................................................................................................................................ 89
UMBILICAL HERNIA............................................................................................................................................. 90
PARAUMBILICAL HERNIA (SUPRA- AND INFRAUMBILICAL HERNIA)............................................................... 90
EPIGASTRIC HERNIA ............................................................................................................................................ 90
INCISIONAL HERNIA ........................................................................................................................................... 90
37. CONDITIONS OF THE BILIARY SYSTEM .............................................................................................. 92
ACUTE PANCREATITIS ........................................................................................................................................ 92
CHOLANGITIS ........................................................................................................................................................ 92
BILIARY COLIC ....................................................................................................................................................... 93
ACUTE CHOLECYSTITIS ...................................................................................................................................... 93
GALLSTONE ILEUS ................................................................................................................................................ 94

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 GALLSTONES .......................................................................................................................................................... 94
CHOLEDOCHOLITHIASIS ................................................................................................................................... 95
SURGICAL JAUNDICE (OBSTRUCTIVE JAUNDICE) ............................................................................................... 96
38. CONDITIONS STOMACH&INTESTINES .............................................................................................. 97
INTESTINAL OBSTRUCTION .............................................................................................................................. 97
PEPTIC ULCER DISEASE ....................................................................................................................................... 98
BOWEL PERFORATION ........................................................................................................................................ 99
ACUTE APPENDICITIS........................................................................................................................................ 100
INTUSSUSCEPTION (ISS) .................................................................................................................................... 100
SIGMOID VOLVULUS (VOLVULUS OF PELVIC COLON) ...................................................................................... 101
PYLORIC STENOSIS DUE TO CHRONIC DUODENAL ULCER ................................................................... 101
ROUNDWORM OBSTRUCTION (ASCARIS LUMBRICOIDES) ............................................................................. 102
39. CONDITIONS OF THE RECTUM, ANUS AND PERI-ANAL AREA ................................................ 103
HAEMORRHOIDS(PILES) ................................................................................................................................... 103
FISTULA IN ANO) ................................................................................................................................................ 103
ANAL FISSURE (FISSURE IN ANO) ................................................................................................................... 104
PERIANAL ABSCESS ............................................................................................................................................ 104
INTESTINAL ATRESIA ........................................................................................................................................ 104
HIRSCHSPRUNG’S DISEASE (AGANGLIONIC MEGACOLON) ............................................................................. 104
IMPERFORATED ANUS ...................................................................................................................................... 105
40. CONDITIONS OF THE KIDNEYS, URETERS AND URINARY BLADDER .................................. 106
HEMATURIA ......................................................................................................................................................... 106
RENAL CALCULI.................................................................................................................................................. 106
HYDRONEPHROSIS (HN) ................................................................................................................................... 107
NEPHROBLASTOMA (WILMS’ TUMOUR) ...................................................................................................... 108
RENAL CELL CARCINOMA ............................................................................................................................... 108
CANCER OF THE BLADDER .............................................................................................................................. 108
SCHISTOSOMA HAEMATOBIUM (ENDEMIC HAEMATURIA, URINARY BILHARZIASIS) ................................. 109
41. CONDITIONS OF THE PROSTATE GLAND ........................................................................................ 110
PROSTATITIS ......................................................................................................................................................... 110
BENIGN PROSTATIC HYPERTROPHY............................................................................................................. 111
CARCINOMA PROSTATE ................................................................................................................................... 111
42. CONDITIONS OF THE URETHRA .......................................................................................................... 113
STRICTURE URETHRA ........................................................................................................................................ 113
HYPOSPADIAS...................................................................................................................................................... 113
EPISPADIAS ........................................................................................................................................................... 113
RETENTION OF URINE ....................................................................................................................................... 114
URINE INCONTINENCE ..................................................................................................................................... 114
43. CONDITIONS OF THE TESTIS, EPIDIDYMIS, AND SCROTUM ................................................... 116
TESTICULAR TORSION....................................................................................................................................... 116
ACUTE EPIDIDYMITIS ........................................................................................................................................ 116
TESTICULAR CANCER........................................................................................................................................ 116
HYDROCELE ......................................................................................................................................................... 116
VARICOCELE ........................................................................................................................................................ 116
UNDESCENDED TESTIS (CRYPTORCHIDISM) .............................................................................................. 117
44. CONDITIONS OF THE PENIS AND PREPUCE .................................................................................... 118
PHIMOSIS ............................................................................................................................................................... 118
PARAPHIMOSIS.................................................................................................................................................... 118

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 BALANOPOSTHITIS ............................................................................................................................................ 118
PRIAPISM ............................................................................................................................................................... 118
CARCINOMA PENIS ............................................................................................................................................ 118
45. CONDITIONS OF THE BREAST .............................................................................................................. 120
MASTITIS................................................................................................................................................................ 120
FIBROADENOMA................................................................................................................................................. 120
BREAST CYSTS ...................................................................................................................................................... 121
BREAST CANCER ................................................................................................................................................. 121
PART II. EAR, NOSE AND THROAT DISORDERS ........................................................................................ 123
THE EAR .................................................................................................................................................................... 123
HISTORY TAKING AND PHYSICAL EXAMINATION OF EAR PATIENT ................................................. 123
PERICHONDRITIS ................................................................................................................................................ 123
FURUNCULOSIS ................................................................................................................................................... 124
OTITIS EXTERNA .................................................................................................................................................. 124
OTOMYCOSIS ........................................................................................................................................................ 124
TRAUMATIC CONDITIONS ............................................................................................................................... 124
PSEUDOCYST PINNA .......................................................................................................................................... 125
WAX IMPACTION ................................................................................................................................................ 125
FOREIGN BODIES OF EAR .................................................................................................................................. 125
ACUTE SUPPURATIVE OTITIS MEDIA ............................................................................................................ 125
CHRONIC SUPPURATIVE OTITIS MEDIA ...................................................................................................... 127
COMPLICATIONS OF SUPPURATIVE OTITIS MEDIA.................................................................................. 127
MASTOIDITIS ........................................................................................................................................................ 128
DEAFNESS ............................................................................................................................................................. 128
HEARING AIDS ..................................................................................................................................................... 129
COCHLEAR IMPLANTS ...................................................................................................................................... 129
CONDITIONS OF THE NOSE AND SINUSES ................................................................................................. 130
TRAUMATIC CONDITIONS ............................................................................................................................... 130
FOREIGN BODIES IN THE NOSE ....................................................................................................................... 130
ACUTE RHINITIS OR CORYZA.......................................................................................................................... 130
ALLERGIC RHINITIS ........................................................................................................................................... 131
NASAL POLYPI ..................................................................................................................................................... 131
EPISTAXIS .............................................................................................................................................................. 132
SINUSITIS ............................................................................................................................................................... 133
FRACTURES OF THE MAXILLA ........................................................................................................................ 134
FRACTURES OF LOWER THIRD OF FACE ...................................................................................................... 134
CONDITIONS OF THE THROAT ........................................................................................................................ 135
LUDWIG’S ANGINA ............................................................................................................................................ 135
ACUTE PHARYNGITIS ........................................................................................................................................ 135
ACUTE TONSILLITIS ........................................................................................................................................... 135
CHRONIC RECURRENT TONSILLITIS............................................................................................................. 136
TONSILLECTOMY ................................................................................................................................................ 136
PERITONSILLAR ABSCESS OR QUINSY .......................................................................................................... 137
ACUTE RETROPHARYNGEAL ABSCESS ........................................................................................................ 137
ACUTE LARYNGITIS ........................................................................................................................................... 137
CHRONIC LARYNGITIS ...................................................................................................................................... 138
ACUTE EPIGLOTTITIS ......................................................................................................................................... 138
ACUTE LARYNGOTRACHEOBRONCHITIS(CROUP) .................................................................................... 138
ACUTE TRACHEITIS ............................................................................................................................................ 139
FOREIGN BODIES IN THE LARYNX ................................................................................................................. 139

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 FOREIGN BODIES IN THE TRACHEA .............................................................................................................. 139
FOREIGN BODIES IN THE BRONCHUS ........................................................................................................... 139
TRACHEOSTOMY ................................................................................................................................................ 139
FURTHER READING .............................................................................................................................................. 141

ix
 1. HISTORY-TAKING AND PHYSICAL EXAMINATION
Introduction
A patient usually comes to see a doctor with a
specific problem (a symptom) and the doctor’s
aim is to make the patient better.
To do this, the doctor tries to work out what is
causing the problem (the diagnosis), determine
its severity (assessment) and then institute
appropriate treatment
The history is the single most important factor in
making a diagnosis. Although this textbook is
primarily concerned with eliciting abnormal
physical signs, these are not always present at the
time a patient presents. The history directs the
clinician to search for the physical abnormalities
and find them at the earliest possible stage of the
disease, thus facilitating further management.
The skilled clinician becomes an expert on the
pattern of diseases, but their greatest skill is to
listen to what the patient volunteers. This is the
key to the diagnosis and the clinician must not
shape, elaborate, flavour or direct a history into a
particular category just so that it fits a classical
package. Such prompting may result in
misdiagnosis.
Sometimes it is not possible to make a diagnosis.
However, the process of assessment serves to
exclude serious abnormalities, allowing the
clinician to reassure the patient and advise
symptomatic treatment. This strategy is based on
the nature and duration of the symptoms. It
allays the patient’s fears and avoids an
overinvestigation of trivial and self-limiting
disease.
A decision must be made, however, on whether
the patient needs to be seen again for further
assessment. Continual explanation to the patient
and good patient rapport are of vital importance
and will translate into a more accurate diagnosis
and increased patient knowledge. Management
occasionally has to be initiated before a definitive
diagnosis has been made, such as in the control
of severe pain or haemorrhage.
The following scheme for history-taking is
intended as an introduction to the subject and
outlines the prime headings that need to be
considered when interviewing each patient.
HISTORY-TAKING
First record the date and time of the
examination. Note the patient’s name, age, sex,
occupation (past and present) and who they live
with at home (including any dependents). The
history emerges from the patient’s description of
the problem, directed by your planned
questioning. It is conveniently recorded under
the following six headings.
1. Present Illness
• Presenting Complaint(s)
• History of Presenting Complaint(s)
• Previous History of Presenting Complaint(s)
2. Past Medical History
3. Drugs and Allergies
4. Social and Personal History
5. Family History
6. Review of Systems
Common important symptoms in general
surgery
Pain
Pain is the most common and important
symptom in surgical practice. (It used to be said
with some truth that pain and blood were the
only two events that brought patients quickly to
the doctor.) Pain is universal and can be caused
by benign or malignant disorders and elective or
acute conditions.
The information required to establish the clinical
significance of pain:
It is worth studying these questions and
reshuffling them into a form that you can easily
remember, perhaps converting them into an
acronym or an anagram.
SOCRATES is a well-known example:
• S: Site;
• O: Onset;
• C: Character;
• R: Radiation;
1
 • A: Associations;
• T: Timing;
• E: Exacerbating/relieving factors;
• S: Severity.
The most reliable way to obtain precise
information on the location of pain is to ask the
patient to point to the exact site of the pain and
where it radiates. Pain may be localized or
diffuse and can be referred. Localized pain is
either musculoskeletal in origin or is indicative of
disease, trauma or inflammation in the affected
region. Pain may be referred to the
corresponding sensory dermatome. This is
exemplified by shoulder tip pain due to a
subphrenic abscess causing irritation of the
ipsilateral phrenic nerve.
Cause of Pain
It is important to ask the patient’s opinion on the
cause of their pain as they may know or think
they know what this is. They may be afraid or
unwilling to tell you the cause as there may be a
guilt complex, such as with current or previous
self-abuse, but there may still be some hints on
the underlying cause of the pain. Such clues must
be carefully noted. The patient may well have
given a lot of thought to the potential causes of
their pain, and it is important to identify areas of
anxiety, which can often be treated by immediate
reassurance.
Different types of pain:
• Colicky pain: obstruction of a hollow organ,
e.g. biliary, intestinal or ureteric colic
• Somatic pain: inflammation of parietal
peritoneum, e.g. peritonitis
• Burning pain: mucosal injury, e.g.
heartburn/reflux oesophagitis
• Intermittent claudication: muscle ischaemia
during exercise, e.g. peripheral vascular
disease
• Rest pain: critical limb ischaemia, e.g.
peripheral vascular disease
• Root pain: irritation of nerve roots, e.g.
prolapsed intervertebral disc.
Indigestion/dyspepsia
Types:
• Peptic ulcer
• Reflux
• Malignancy
• Non-ulcer
• Gallbladder
Dysphagia
• Indicates obstruction or motility disorder of
the oesophagus
• Should always be investigated
• Painful dysphagia is called odynophagia
Anorexia and weight loss
• Often an indication of malignancy
Vomiting
• Frequency: gastroenteritis causes frequent
vomiting
• Does vomit contain bile? No bile in patients
with pyloric stenosis
• Does vomit contain food particles? Old food
present in pyloric stenosis
• Does vomit contain fresh blood? Blood that
appears after the onset of forceful vomiting
indicates an oesophageal tear
• Does vomit contain ‘coffee grounds’ (blood
partially digested by HCl and pepsin in the
stomach)?
• Are there other symptoms/signs (pain,
nausea, constipation, headache, jaundice)?
Altered bowel habit
• Constipation or diarrhoea or both
• Feeling of incomplete evacuation after
defecation (tenesmus)
• Blood per rectum should always be
investigated
• Foul-smelling diarrhoea that floats
(steatorrhoea) indicates malabsorption
• Foul-smelling dark tar-like motion (melaena)
indicates proximal gastrointestinal tract
bleeding
Bleeding per rectum
2
What colour is the blood? Is it pink-red and only sclera. Good lighting is essential, particularly for
on the paper when wiping? Does it splash in the the detection of abnormal discoloration (pallor,
pan? (Both suggest a case from the anal canal.) Is cyanosis, jaundice).
it bright red on the surface of the stool (suggests
a lower rectal cause)? Is the blood darker with Palpation
clots or marbled into the stools (suggests a Palpation relies on the tactile sense organs in the
colonic cause)? Is the blood fully mixed with the fingers to outline surface irregularities, tension of
stool or altered (suggests a proximal colonic the abdominal walls, lumps and enlarged organs.
cause)? The exercise should be carried out by a relaxed
warm hand and should be conducted gently and
PHYSICAL EXAMINATION
in an orderly fashion. In general, the more you
press, the less you feel, and worse still, the
General principles
patient is hurt.
Physical examination must be thorough and
efficient without being overdone and exhausting
Percussion
to the patient. Percussion is very useful for establishing the
consistency of a swelling or organ. Thus a solid
Whichever system or anatomical region is
lump or organ is dull to percussion. A fluid-
examined, the process relies on four skills, i.e.
containing cyst or body cavity (peritoneal,
inspection, palpation, percussion and auscultation,
thoracic) is stony dull to percussion. For the same
and is designed to elicit the appropriate clinical
reason a distended urinary bladder is detected as
signs. Whereas examination of the various
a localized dull swelling in the suprapubic
systems is crucial to the management of patients
region. By contrast, air-containing organs
with medical disorders, in surgical practice
(normal ventilated lung, air-containing hollow
physical examination is more commonly focused
abdominal viscera) are resonant on percussion
on anatomical regions (head and neck, ear, nose
(much like a drum). When using percussion to
and throat, breasts, abdomen and limbs),
outline the size or margins of an organ, one
although assessment of the respiratory,
should percuss from the resonant to the dull
cardiovascular and renal systems is often also
area. The point where the note changes marks the
necessary. Certain vital signs such as
margin of the organ.
temperature, blood pressure, pulse rate, pulse
volume and respiratory rate are performed Auscultation
routinely in all but minor cases.
Auscultation with the stethoscope requires
Inspection considerable experience to recognize the normal
from the abnormal, and is used to examine the
Inspection requires a trained eye actively to
lungs (normal and adventitial breath sounds),
detect abnormalities. Inspection consists of a
heart sounds and murmurs, abdominal bowel
detailed and systematic scrutiny of the
sounds, and bruits over stenotic or dilated
anatomical region and entails close observation
segments (aneurysms) of arteries.
of abnormal movements of the parietes and body
contour, as well as surface abnormalities (scars,
surface lesions, lumps, bulges) and complexion
of the skin, lips, conjunctival membranes and

3
 2. PRINCIPLES OF INVESTIGATION

Introduction outcome, e.g. prostate cancer. The proof that is

necessary can only be provided through
Throughout this book reference is made to
randomized controlled trials of a screening
investigations carried out in patients suspected of
procedure.
having various surgical disorders. Although
specific investigations provide valuable Investigations commonly used in the assessment
information, their indiscriminate use constitutes of patients.
bad practice; not only is it wasteful of resources
but it may also put patients and staff at risk (e.g. 1. Blood investigations
contrast media may induce anaphylaxis). The • Haematology
risk to the patient correlates with the degree of
• Biochemistry
invasiveness of the procedure and a spectrum of
• Blood gas analysis
risk exists.
• Immunology
Screening 2. Microbiology
Investigations may be used for general 3. Imaging
population screening of common conditions or
may be directed towards subpopulations known • X-rays
to be at increased risk of developing a condition. ▪ Barium studies
Before an investigation can be used as a ▪ Water-soluble contrast studies
screening tool, it is desirable that a number of ▪ Cholecystography and cholangiography
criteria should be fulfilled. ▪ Intravenous urography, cystography
1. The disease should be relatively common and ▪ Arteriography
have serious sequelae. ▪ Venography
▪ Myelography
2. The condition should be identifiable at a stage • Computed tomography
where intervention is effective. • Magnetic resonance imaging
3. The investigation should be non-invasive and • Ultrasound
acceptable to patients to ensure good • Nuclear medicine studies
compliance. 4. Endoscopy

4. The investigation used should identify all 5. Function tests

affected individuals (sensitivity) and avoid
mistaken diagnosis in unaffected individuals • Pulmonary function
(specificity). • Oesophageal motility
• Urodynamics
5. The investigation should be relatively • Anorectal manometry
inexpensive.
• Nerve conduction studies
Few screening investigations fulfil all these 6. Vascular
criteria. The limitations of a particular
• ECG
investigation are quoted as the false-positive rate
• Holter monitoring
(mistaken diagnosis in unaffected individuals)
and the false-negative rate (failure to identify all • Echocardiography
affected individuals). In some cases, there is • Duplex scanning
debate as to whether earlier identification of the • Plethysmography
disease process makes any difference to overall • Ankle/brachial pressure index

4
 3. PREPARING A PATIENT FOR SURGERY/
MANAGEMENT OF A PATIENT REQUIRING
SURGERY

There are 2 types of surgeries in terms of timing: • Perianaesthetic

• Postoperative
• Elective surgery: this is the type of surgery System assessment (most commonly used)
that has been scheduled several days before.
E.g. cesarian section. • Cardiac

• Acute/emergency surgery: this is the type of • Respiratory

surgery that was not planned at all. E.g.
• Endocrine
emergence laparotomy.
• Haemostasis
The preparation for these types of surgeries is not
similar. And each surgery may require specific • Gastrointestinal
set of preparations. It is important to understand
different surgeries and how patients for such are • Nutrition
prepared and managed. Principles of system assessment
Assessment of patients for surgery and • A good history and clinical examination will
preoperative medical management. uncover most problems
Definition • Investigations should be used to confirm or
Preoperative assessment: a process that provides quantify clinical findings
information on risk, defines and reduces the • The most useful investigations are those that
extent of known risks, and discovers unknown give functional information
risks in a patient prior to surgery
• Ask the experts (anaesthetist or physician) if a
Goals of preoperative assessment difficult problem is encountered.
• Assess risk of surgery vs. risk of medical or no Management
treatment
• Attention should be given to prophylaxis
• Document extent of known disease
• Nutritional support essential before and
• Discover unknown disease after surgery: alimentary route is preferable.
• Plan prophylactic or definitive treatment of PREPARATION/MANAGEMENT OF A
comorbid conditions that might complicate or
adversely affect surgery PATIENT REQUIRING AN ACUTE

• Patient selection: based on the best available SURGERY.

evidence and the preoperative assessment, the
patient is given the facts about an operation
(success rate and complications) and advised
whether they would or would not be a
suitable candidate for that operation. Only
after this can the patient make an informed
choice
Methods of assessment
Assessment based on patient pathway
While each hospital has its own set of guidelines
regarding surgery below is a general preparation
and management for a patient requiring an acute
surgery.
History
1. Chronic cough, smoking, alcohol, drug intake,
drug allergy.

• Preoperative

5
2. Any previous diseases like hypertension,
diabetes mellitus, epilepsy, bronchial asthma,
tuberculosis, hepatitis, cardiac diseases.
3. Drug therapy: Steroids, antihypertensives,
sedatives, antibiotics, antiepileptics.
Consent
1. Explain the surgical procedure including the
risks and possible complications and address
the patient’s questions and worries.
2. Ensure consent is obtained and consent
forms are signed, for proceeding to surgery
and other procedures if they are anticipated.
That includes blood transfusion.
Preoperative Investigations
Haematocrit, blood sugar, blood urea, serum
creatinine, electrolytes, chest-X ray, ECG, blood
grouping, blood-gas analysis, cardiac assessment.
Preoperative Treatment
1. Control of respiratory and cardiac diseases.
2. Improvement of Hb% status, if anaemia is
present.
3. Preoperative antibiotics are given.
4. Blood should be kept ready for major cases.
5. Starvation for 4 hours for liquids and six hours
for solids.
6. Bladder and bowel should be emptied to
prevent soiling on the operation table.
Urinary catheter may be passed and enema
may be given.
7. Dentures, contact lenses, jewellery must be
removed.
8. Surgical area should be cleaned and properly
prepared.
9. Ensure the IV line is put and functional.
10. Ensure to keep fluids and electrolytes
balanced.
11. Nasogastric Tube. NOT required unless the
patient is vomiting or gastric
distension/surgery is likely.
6
 4. ANAESTHESIA USED IN GENERAL SURGERY
GENERAL ANAESTHESIA
It means abolition of all sensations, i.e. touch,
pain, posture and temperature with a state of
reversible loss of consciousness.
It has got three components:
(1) Analgesia. (2) Hypnosis. (3) Muscle relaxation.
ANAESTHETIC AGENTS
➢ Volatile anaesthetics: They vaporise in room
air.
▪ Agents used are: Ether, trichloroethylene,
halothane, enflurane, isoflurane,
sevoflurane.
▪ Ether which is irritant, unpleasant,
flammable, is commonly used agent in
developing countries.
▪ Enflurane and isoflurane are non-
inflammable, nonexplosive, non-irritant
and stable. Here anaesthesia is rapid with
faster recovery.
➢ Gaseous anaesthetics:
▪ Nitrous oxide: It is non-inflammable, non-
irritant, good analgesic but weak
anaesthetic agent. It is given along with
30-50% oxygen for balanced anaesthesia
▪ Cyclopropane is highly flammable.
➢ Intravenous anaesthetics:
➢ Thiopentone: It is ultrashort acting
barbiturate which causes hypnosis during
induction of anaesthesia. It does not have
analgesic effect. It causes hypotension,
respiratory depression, laryngeal and
bronchospasm. Recovery is rapid.
Extravasation of drug can cause skin
ulceration.
Intra-arterial injection causes vasospasm
and gangrene.
Dose: 4-7 mg/kg.
Methohexitone sodium.
Propanidid. 4-7 mg/kg. It can cause
anaphylaxis.
➢ Ketamine: Dose: 2 mg/kg IV. It is a good
analgesic. It causes dissociative anaesthesia. It
can lead to hypertension, apnoea,
laryngospasm. In children it can be given IM-
5 mg/kg. It does not require intubation for
small procedures.
➢ Propofol: It is widely used induction agent
which has got predictable onset and recovery.
It has got least side effects on CVS and
respiratory system. It is also used for total IV
anaesthesia. Dose: 1-2.5 mg/kg.
➢ Fentanyl is neuroleptanalgesic. It causes
sedation, catatonia, dissociation, hypotension
and preferred in asthmatics.
COMPLICATIONS OF GENERAL
ANAESTHESIA
➢ Intra-arterial injection of the drug.
➢ Myocardial depression and cardiac arrest.
➢ Hypertension.
➢ Laryngeal and bronchial spasm.
➢ Cardiac arrhythmias.
➢ Respiratory failure.
➢ ARDS.
➢ Mendelson’s syndrome: It is due to
regurgitation of the acid from the stomach
causing aspiration of acid leading into
bronchospasm, pulmonary oedema and
circulatory failure. This is treated with
oxygen, suction, hydrocortisone,
aminophylline, antibiotics, Ryle’s tube
aspiration and ventilator support.
➢ Hypoxia.
➢ Pneumothorax.
➢ Anaphylaxis.
➢ Malignant hyperthermia: It is an inherited
myopathic disorder occurs under
anaesthesia due to drugs like halothane,
scoline. There is marked increase in
metabolic rate, with rise of temperature.
There is high levels of CPK enzyme.
Condition will cause metabolic acidosis and
hyperkalaemia. It has got high mortality.
Treatment is IV dantrolene, cooling, oxygen
and cold IV fluids.
➢ Hypothermia.
REGIONAL(LOCAL) ANAESTHESIA
Mode of action: It causes temporary conduction
block of the nerve, thus preventing the
propagation of nerve impulse.
Advantages of local anaesthetic agent:
• Technically simpler.
• General anaesthesia is avoided.
• Consciousness is retained.
• Patient can have food earlier after surgery.
Drugs used:
7
 • Cocaine, procaine, cinchocaine—amino • Topical-4%.
esters. • Infiltration block: 0.25%.
• Field block 0.5%.
• Lignocaine, prilocaine, bupivacaine, • Nerve block 1.0 %.
ropivacaine—amino amides. • Epidural 1.5, 2.0%.
• Spinal 5%.
Lignocaine/lidocaine/xylocaine: It is the It can be used with or without adrenaline.
commonest local anaesthetic agent used. It is Xylocaine with adrenaline has got longer duration
available as 0.25-5% concentrations. of action.
It creates relatively bloodless field.
It is metabolised in the liver and excreted in the
kidney as xylidines. It is also an antiarrhythmic But it should not be used in places where end
drug and so commonly used in cardiology and arteries are present like glans penis, ear lobule,
cardiac surgery. tip of the nose, lip, fingers and toes.
Side effects: Giddiness, headache, postural
hypotension, tinnitus, circumoral anaesthesia. Bupivacaine (Marcaine): It has got prolonged
Dose: 4 mg/kg effect lasts for 90 minutes. action. It is a vasodilator also.
▪ Dose: 3 mg/kg.
Uses ▪ Epidural block: 0.5%
▪ Spinal 0.5% 3 ml.

8
 6. SURGICAL INCISIONS

ABDOMINAL INCISIONS ➢ Thoracoabdominal.

Principles
• Incision should be long enough for a
good exposure.
• Splitting the muscle is better than
cutting, except rectus muscle.
• Avoid cutting nerves and vessels in the
abdominal wall.
• Retract muscle, abdominal organs
towards the neurovascular supply.
• Insert a drainage tube through a
separate incision.
• Transverse incisions are better than
vertical incisions.
• Close the wound layer by layer.
➢ Subumbilical.
➢ Incision for lumbar sympathectomy.
➢ Lower midline.
➢ Lower right or left paramedian.
➢ Incisions for appendicectomy—McBurney’s,
Rutherfold
➢ Morrison’s, Lanz, laparoscopic.
➢ Pfannenstiel incision.
➢ Lower horizontal.
• Upper incisions are always better.
• Horizontal incisions are better.
• Paramedian is better than midline.

Complications of Abdominal Incision

• Wound infection.

• Burst abdomen.

• Fistula formation.

• Wound pain.

• Incisional hernia.

• Adhesion and its complication.

Different abdominal incisions are:

➢ Upper midline.
➢ Upper right paramedian.
➢ Upper left paramedian.
➢ Kocher’s incision (right subcostal).
➢ Left subcostal.
➢ Bucket handle.
➢ Upper horizontal.

9
 7. SUTURES AND SUTURING TECHNIQUES
SUTURES
Features of ideal suture material
• Adequate tensile strength
• Good knot holding property
• Should be least reactive
• Easy handling property
• Should have less memory
• Should be easily available and cost
effective
CLASSIFICATIONS OF SUTURES
Sutures can be classified in categories.
CLASSIFICATION I (ABSORBABLE VS
NONABSORBABLE)
Absorbable Suture Materials
• Plain catgut is derived from submucosa of
jejunum of sheep.
▪ It is yellowish white in colour.
▪ It is absorbed by inflammatory reaction
and phagocytosis— absorption time is 7
days.
▪ It is used for subcutaneous tissue,
muscle, circumcision in children.
• Chromic catgut is catgut with chromic acid
salt.
▪ It is brown in colour.
▪ Its absorption time is 21 days.
▪ It is used for suturing muscle, fascia,
external oblique aponeurosis, ligating
pedicles, etc.
• Vicryl (Polyglactic acid):
▪ It is synthetic absorbable suture material.
▪ It gets absorbed in 90 days.
▪ Absorption is by hydrolysis.
▪ It is violet in colour (braided).
▪ It is multifilament and braided.
▪ It is very good suture material for bowel
anastomosis, suturing muscles, closure of
peritoneum.
• Dexon (Polyglycolic acid) is synthetic
absorbable suture material like vicryl. It is
creamy yellow in colour (braided).
• Maxon (Polyglyconate) monofilament.
• PDS (Poly Dioxanone Suture material) is
absorbable suture material. It is creamy in
colour with properties like vicryl.
It is costly but better suture material than vicryl.
• Monocryl (Polyglecaprone) monofilament.
• Biosyn (Glycomer) monofilament.
Uses of absorbable suture materials
• In bowel anastomosis like
gastrojejunostomy, resection and
anastomosis. Vicryl is used
• In cholecystojejunostomy (CCJ),
choledocho-jejunos tomy (CDJ),
pancreaticojejunostomy. Vicryl is used
• In suturing muscle, fascia, peritoneum,
sub cutaneous tissue, mucosa
• In ligating pedicles. 1-zero chromic
catgut or vicryl are used, e.g. ligation of
pedicles during hysterectomy
• In circumcision, usually 3-zero plain or
chromic catgut are used.
Absorbable suture materials should not be used
for suturing tendon, nerves, vessels (vascular
anastomosis).
Nonabsorbable Suture Materials
• Silk is natural, multifilament, braided, non-
absorbable suture material derived from
cocoon of silkworm larva.
It is black in colour. It is coated suture material to
reduce capillary action.
• Polypropylene (Prolene) is synthetic,
monofilament suture material. It is blue in
colour. It has got high memory. (Memory of
suture material is recoiling tendency after
removal from the packet. Ideally suture
material should have low memory.) (Prolene
mesh used for hernioplasty is white in
colour).
• Polyethylene (Ethylene) is synthetic
monofilament nonabsorbable suture
material. It is black in colour.
• Cotton is twisted multifilament natural
nonabsorbable suture material. It is white in
colour.
• Linen is derived from bark of cotton tree.
• Steel, polyester, polyamide, nylon are other
non absorbable suture materials.
Uses of nonabsorbable suture materials
10
 • In herniorrhaphy for repair CLASSIFICATION IV
• For closure of abdomen after laparotomy
• For vascular anastomosis (6-zero), nerve • Monofilament: Polypropylene, polyethylene,
suturing, tendon suturing PDS, catgut, steel.
• For tension suturing in the abdomen
• Multifi lament: Polyester, polyamide, vicryl,
• For suturing the skin
dexon, silk, cotton.
CLASSIFICATION II (NATURAL VS
CLASSIFICATION V
SYNTHETIC)
Natural • Coated.

• Catgut. • Uncoated.
• Silk.
• Cotton. Numbering of Suture Material
• Linen. 2-Thick. For pedicle ligation.
Synthetic 1-
0-zero.
• Vicryl, dexon, PDS, maxon. 1-zero.
• Polypropylene, polyethylene, polyester, 2-zero. For bowel suturing.
poly amide. 3-zero.
4-zero.
CLASSIFICATION III 5-zero. For vascular anastomosis.
6-zero.
• Braided: Polyester, polyamide, vicryl,
7-zero.
dexon, silk. 8-zero.
9-zero. For ophthalmic surgery. Requires
• Twisted: Cotton, linen.
operating microscope.
Classification of sutures and needles
NATURAL SYNTHETIC
Absorbable Non- Absorbable Non-absorbable
absorbable
Catgut Silk •Polyglycolic acid • Nylon (monofilament)
Chromic (Dexon) • Polypropylene
catgut •(Vicryl) (monofilament)
•Polydiaoxanone (PDS) • Mersilene (braided
polyester)

SUTURING TECHNIQUES

1. Continuous suturing

2. Interrupted simple suturing

3. Interrupted mattress suturing

4. Subcuticular suturing

5. Horizontal tension suturing

6. Vertical tension suturing

Fig. Types of
suturing.

11
 8. INTRODUCTION TO TRAUMATOLOGY
INTRODUCTION
Trauma, or injury, is defined as cellular
disruption caused by an exchange with
environmental energy that is beyond the body’s
resilience which is compounded by cell death
due to ischemia/reperfusion.
INITIAL EVALUATION AND
RESUSCITATION OF THE INJURED
PATIENT
Primary Survey
The Advanced Trauma Life Support (ATLS)
course of the American College of Surgeons
Committee on Trauma was developed in the late
1970s, based on the premise that appropriate and
timely care can significantly improve the
outcome for the injured patient. ATLS provides a
structured approach to the trauma patient with
standard algorithms of care; it emphasizes the “
golden hour” concept that timely, prioritized
interventions are necessary to prevent death and
disability.
The initial management of seriously injured
patients consists of phases that include the
primary survey/ concurrent resuscitation, the
secondary survey/diagnostic evaluation,
definitive care, and the tertiary survey. The first
step in patient management is performing the
primary survey, the goal of which is to identify
and treat conditions that constitute an immediate
threat to life. The ATLS course refers to the
primary survey as assessment of the “ABCs”
(Airway with cervical spine protection, Breathing,
and Circulation). Although the concepts within
the primary survey are presented in a sequential
fashion, in reality they are pursued
simultaneously in coordinated team
resuscitation. Life-threatening injuries must be
identified and treated before being distracted by
the secondary survey.
Airway
The first step in the evaluation of trauma is
airway assessment and protection.
• An airway is considered protected if the
patient is conscious and speaking in a
normal tone of voice.
• An airway is considered unprotected if there
is an expanding hematoma or subcutaneous
emphysema in the neck, noisy or “gurgly”
breathing, or a Glasgow Coma Scale <8.
An airway should be secured before the situation
becomes critical. In the field an airway can be
secured by intubation or cricothyroidotomy. This
is called a “definitive airway.” In the
emergency department, it is best done by rapid
sequence induction and orotracheal intubation,
with monitoring of pulse oximetry. In the
presence of a cervical spine injury, orotracheal
intubation can still be done as long as the head is
secured and in-line stabilization is maintained
during the procedure. Another option in that
setting is nasotracheal intubation over a
fiberoptic bronchoscope. If severe maxillofacial
injuries preclude the use of intubation or
intubation is unsuccessful, cricothyroidotomy
may become necessary.
In the pediatric patient population (age <12),
tracheostomy is preferred over
cricothyroidotomy due to the high risk of airway
stenosis, as the cricoid is much smaller than in
the adult.
Breathing and ventilation
Once a secure airway is obtained, adequate
oxygenation and ventilation must be ensured. All
injured patients should receive supplemental
oxygen and be monitored by pulse oximetry. The
following conditions constitute an immediate
threat to life due to inadequate ventilation and
should be recognized during the primary survey:
tension pneumothorax, open pneumothorax, flail
chest with underlying pulmonary contusion, and
massive air leak. All of these diagnoses should be
made during the initial physical examination.
Breath sounds indicate satisfactory ventilation;
absence or decrease of breath sounds may
indicate a pneumothorax and/or hemothorax
and necessitate chest tube placement. Pulse
oximetry indicates satisfactory oxygenation;
hypoxia may be secondary to airway
compromise, pulmonary contusion, or
neurological injury impairing respiratory drive
and necessitate intubation. Measurement of CO2
(capnography) is also very useful.
Circulation with Hemorrhage Control
12
With a secure airway and adequate ventilation
established, circulatory status is the next priority.
An initial approximation of the patient’s
cardiovascular status can be obtained by
palpating peripheral pulses.
Clinical signs of shock include the following:
• Low BP (<90 mm Hg systolic)
• Tachycardia (heart rate >100 bpm)
• Low urinary output (<0.5 ml/kg/h)
Patients in shock will be pale, cold, shivering,
sweating, thirsty, and apprehensive.
In the trauma setting, shock is either
hypovolemic (secondary to hemorrhage and the
most common scenario) or cardiogenic
(secondary to pericardial tamponade or tension
pneumothorax due to chest trauma).
Hemorrhagic shock tends to cause collapsed neck
veins due to low central venous pressure (CVP),
while cardiogenic shock tends to cause elevated
CVP with jugular venous distention. Both
processes may occur simultaneously.
In pericardial tamponade, there is typically no
respiratory distress, while in tension
pneumothorax there is significant dyspnea, loss
of unilateral breath sounds, and tracheal
deviation.
Treatment of hemorrhagic shock includes
volume resuscitation and control of bleeding, in
the OR or ED depending on the injury and
available resources. Volume resuscitation is
initially with 2L of Lactated Ringer’s solution
unless blood products are immediately available.
In the setting of trauma, transfusion of blood
products should be in a 1:1:1 ratio between
packed RBCs, fresh frozen plasma, and platelets.
Resuscitation should be continued until BP and
heart rate normalize and urine output reaches
0.5–1.0 ml/kg/hr. In the setting of uncontrolled
hemorrhage, permissive hypotension is
recommended to prevent further blood loss
while awaiting definitive surgical repair, but a
mean arterial pressure >60 mm Hg should be
maintained to ensure adequate cerebral
perfusion.
The preferred route of fluid resuscitation in the
trauma setting is 2 large bore peripheral IV lines,
16-gauge or greater. If this cannot be obtained,
percutaneous subclavian or femoral vein
catheters should be inserted; an acceptable
alternative is a saphenous vein cut-down. In
children age <6, intraosseus cannulation of the
proximal tibia or femur is the alternate route.
Pericardial tamponade is generally a clinical
diagnosis and can be confirmed with U/S.
Management requires evacuation of the
pericardial space by pericardiocentesis,
subxiphoid pericardial window, or thoracotomy.
Fluid and blood administration while evacuation
is being set up is helpful to maintain an adequate
cardiac output.
Tension pneumothorax is a clinical diagnosis
based on physical exam. Management requires
immediate decompression of the pleural space,
initially with a large-bore needle which converts
the tension to a simple pneumothorax and
followed by chest tube placement.
In the non-trauma setting, shock can also be
hypovolemic because of massive fluid loss such
as bleeding, burns, peritonitis, pancreatitis, or
massive diarrhea. The clinical picture is similar to
trauma, with hypotension, tachycardia, and
oliguria with a low CVP. Stop the bleeding and
replace the blood volume.
Intrinsic cardiogenic shock is caused by
myocardial damage (e.g. myocardial infarction or
fulminant myocarditis). The clinical picture is
hypotension, tachycardia, and oliguria with a
high CVP (presenting as distended neck veins).
Treat with pharmacologic circulatory support.
Differential diagnosis is essential, because
additional fluid and blood administration in this
setting could be lethal, as the failing heart
becomes easily overloaded.
Vasomotor shock (from anaphylaxis, high spinal
anesthesia, or spinal cord transection) causes
circulatory collapse. Patients are flushed, “pink
and warm” with a low CVP. Treatment with
phenylephrine and fluids is aimed at filling
dilated veins and restoring peripheral resistance.
Disability and Exposure
The Glasgow coma scale (GCS) score should be
determined for all injured patients.
It is calculated by adding the scores of the best
motor response, best verbal response, and the
best eye response. Scores range from 3 (the
lowest) to 15 (normal). Scores of 13 to 15 indicate
13
mild head injury, 9 to 12 moderate injury, and 8
severe injury.
The GCS is a quantifiable determination of
neurologic function that is useful for triage,
treatment, and prognosis.
Neurologic evaluation is critical before
administration of neuromuscular blockade for
intubation. Subtle changes in mental status can
be caused by hypoxia, hypercarbia, or
hypovolemia, or may be an early sign of
increasing intracranial pressure.
An abnormal mental status should prompt an
immediate reevaluation of the ABCs and
consideration of central nervous system injury.
Deterioration in mental status may be subtle and
may not progress in a predictable fashion. For
example, previously calm, cooperative patients
may become anxious and combative as they
become hypoxic. However, a patient who is
agitated and combative from drugs or alcohol
may become somnolent if hypovolemic shock
develops. Patients with neurogenic shock are
typified by hypotension with relative
bradycardia, and are often first recognized due to
paralysis, decreased rectal tone or priapism.
Patients with high spinal cord disruption are at
greatest risk for neurogenic shock due to
physiologic disruption of sympathetic fibers;
treatment consists of volume loading and a
dopamine infusion which is both inotropic and
chronotropic. Seriously injured patients must
have all of their clothing removed to avoid
overlooking limb- or life-threatening injuries.
Summary : Immediately life-threatening
injuries to be identified during the primary
survey
Airway
• Airway obstruction
• Airway injury
Breathing
• Tension pneumothorax
• Open pneumothorax
• Massive air leak
• Flail chest with underlying
pulmonary contusion
Circulation
• Hemorrhagic shock
• Massive hemothorax
• Massive hemoperitoneum
• Mechanically unstable pelvis fracture
with bleeding
• Extremity blood loss
• Cardiogenic shock
• Cardiac tamponade
• Neurogenic shock
Disability
• Intracranial hemorrhage/mass lesion
• Cervical spine injury
Secondary Survey
After the ABC’s have been evaluated and any
immediate life-threatening emergencies
addressed, trauma evaluation continues with the
secondary survey which is composed of a
complete physical exam (head to toe) to evaluate
for occult injuries followed by chest x-ray and
pelvic x-ray. The secondary survey may be
augmented with further imaging studies
depending on the mechanism of injury and
findings on examination. Any change that occurs
requires complete re-evaluation.
INTRAVENOUS FLUIDS, BLOOD AND
BLOOD PRODUCTS
Intravenous fluid therapy
During your time on the wards you will always
see patients on drips; when you are a house
officer, you will be responsible for siting the drip
and managing the fluids from day to day.
Intravenous fluid therapy is used extensively in
surgery; indeed it is of vital importance that
patients are adequately resuscitated prior to
surgery, especially in the emergency situation.
The indications for fluid therapy are as follows.
14
 • Preoperative resuscitation, e.g. before
emergency surgery, elective surgery in a
jaundiced patient.
• Replacement of abnormal losses, e.g.
vomiting, diarrhoea, ileostomy bags.
• Provision of normal daily requirements
if patient is nil by mouth.
• Postoperative resuscitation.
• Electrolyte disorders.
Thus patients not eating or drinking must be
provided with their daily requirements, i.e. 2.5–3
L of water, 100 mmol Na+ and 60 mmol K+.
Types of fluids
On the wards you will mainly use crystalloids to
provide the normal daily requirement and
replace additional losses. Three major types of
fluid are used: 0.9% sodium chloride, dextrose
saline and 5% dextrose. The composition of these
fluids is shown below.
• 1 L 0.9% sodium chloride contains 153
mmol NaCl.
• 1 L dextrose saline contains 31 mmol
NaCl + 40 g dextrose.
• 1 L 5% dextrose contains 50 g dextrose.
Potassium can be added to these solutions in the
form of potassium chloride (KCl).
Other fluids encountered in practice
• Hartmann’s solution is the replacement fluid
favoured by anaesthetists because it is a
physiological mixture of ions and water: 1 L
Hartmann’s solution contains 2 mmol Ca2+, 5
mmol K+, 29 mmol HCO3 –, 110 mmol Cl– and
131 mmol Na+.
• All the solutions described so far have been
crystalloids and are not confined to the
intravascular compartment.
On occasions, for example if a patient is shocked
due to haemorrhage, fluid replacement of the
intravascular compartment is essential. In these
circumstances, gelatin colloid solutions are used.
These are solutions of saline and gelatin: 1 L
synthetic colloid contains 35 g gelatin, 6.25 mmol
Ca2+, 145 mmol Cl– and 145 mmol Na+.
Because gelatin has a high molecular weight, it is
confined to the intravascular compartment and
thus acts as a plasma expander.
Blood & blood products available for therapy.
Definitions
Blood: a complex fluid vital for life that is
circulated around the body in arteries and veins
by the pumping action of the heart.
Plasma: the fluid component of circulating blood
in which the formed elements such as
erythrocytes, leukocytes and platelets are
suspended.
Stored whole blood: blood from which no
constituent has been removed.
Red cell concentrates (packed red cells): solutions
of erythrocytes obtained from blood after the
plasma has been removed. They also contain
some white cells
Platelet concentrates: solutions containing platelets
that are frequently derived from several donors
Fresh frozen plasma: plasma prepared from the
supernatant liquid obtained by centrifugation of
one donation of whole blood.
15
 9. TOURNIQUETS
A tourniquet is used to cut off the blood supply
to a limb temporarily so that a bloodless field is
created while performing the surgery. Limb
should be exsanguinated before
applying/inflating the cuff of the tourniquet. It is
done using a bandage or pressurized Rhys-Davis
exsanguinator.
Uses
• To attain bloodless field in limb surgeries—
upper and lower limbs, orthopaedic
surgeries, soft tissue tumours, amputations.
• It is used (rubber tourniquet) to access veins
for IV injec-tions and IV sampling.
• Tourniquet is used in diagnostic tests for
varicose veins, purpura (ITP), carpal tunnel
syndrome, tetany.
• It is used as a first aid in bleeding conditions
of limbs, snake bite (it is controversial).
• Tourniquets are often used for small
procedures in fingers and toes.
Types
• Rubber tourniquet
• Martin’s tourniquet.
• Pneumatic tourniquet
• Esmarch rubber elastic bandage
tourniquet.
• Conn pneumatic tourniquet
Tourniquet time for upper limb is one hour and
for lower limb is two hours.
Contraindications
• In all peripheral vascular diseases and
atherosclerosis.
• Infection.
• Deep venous thrombosis.
• Crush injuries.
• Sickle cell disease.
Complications
• Crushing effect on muscles in thigh
occurs leading to crush syndrome.
• Tourniquet palsy in upper limb (radial
nerve involvement)—neuropraxia.
• Infection.
• Improper application of tourniquet leads
to more bleeding.
• Forgetting the removal of tourniquet or
taking more time to release may
compromise the blood supply of the
limb leading to severe ischaemia and
gangrene.
• Skin blistering and necrosis.
16
 10.DERMATOLOGIC WOUNDS

CLOSED AND OPEN WOUNDS admitted and evaluated by ultrasound or CT

scan abdomen and observed. Often wound
Wound Definition exploration is needed under general
anaesthesia in operation theatre.
A wound is a break in the integrity of the skin or
tissues often, which may be associated with Classification of Surgical Wounds
disruption of the structure and function.
a. Clean wound
CLASSIFICATION OF WOUNDS
• Herniorrhaphy.
Classification based on Type of Wound.
• Excisions.
(a) Clean incised wound is a clean cut wound
with linear edge. • Surgeries of the brain, joints, heart,
transplant.
(b) Lacerated wounds have ragged edges with
devitalisation of some part of tissues. Wound • Infective rate is less than 2%.
excision and primary suturing is done.
b. Clean contaminated wound
(c) Bruising and contusion: Minor soft tissue
• Appendicectomy.
injury with discoloration and haematoma
formation without skin break. • Bowel surgeries.

(d) Haematoma: this is a collection of blood in a • Gallbladder, biliary and pancreatic

tissue. It may be surgeries.
subcutaneous/intramuscular/subfascial/int
ra-articular. Small haematoma will get • Infective rate is 10%.
absorbed. Large haematoma once get
c. Contaminated wound
infected forms an abscess and so it should be
drained under general/regional anaesthesia • Acute abdominal conditions.
adequately. Often haematoma contains only
reddish plasmatic fluid which can be • Open fresh accidental wounds.
aspirated with wide bore needle.
• Infective rate is 15-30%.
(e) Puncture wounds and bites.
d. Dirty infected wound
(f) Abrasion: It is superficial and is due to
• Abscess drainage.
shearing of skin where the surface is rubbed
off. It heals by epithelialisation. It is only • Pyocele.
epidermal injury exposing dermis and
dermal nerves. • Empyema gallbladder.

(g) Traction and avulsion injury. • Faecal peritonitis.

(h) Crush injury: It is caused by war wounds, • Infective rate is 40-70%.

road traffic accidents, tourniquet. It leads to:
Management of Wounds
Compartment syndrome.
(a) Wound is inspected and classified as per the
(i) Penetrating wounds—commonly due to stab
type of wounds.
injuries. Common example is stab injury
abdomen. Stab wound may be small on body (b) If it is in the vital area, then:
surface but damage to the deeper organs like
liver, spleen, major vessels like inferior vena • The airway should be maintained.
cava/mesenteric vessels or intestines may be • The bleeding, if present, should be
extensive and life-threatening. Patients with
controlled.
stab injury over abdomen should be

17
 • Intravenous fluids are started.
• Oxygen, if required, may be given.
• Deeper communicating injuries and
fractures, etc. should be looked for.
(c) If it is an incised wound then primary
suturing is done after thorough cleaning.
(d) If it is a lacerated wound then the wound is
excised and primary suturing is done.
(e) If it is a crushed or devitalised wound there
will be oedema and tension in the wound. So
after wound debridement or wound excision by
excising all devitalised tissue, the oedema is
allowed to subside for 2-6 days. Then delayed
primary suturing is done.
(f) If it is a deep devitalised wound, after wound
debridement it is allowed to granulate
completely. Later, if the wound is small
secondary suturing is done. If the wound is large
a split skin graft (Thiersch graft) is used to cover
the defect.
(g) In a wound with tension, fasciotomy is done
so as to prevent the development of
compartment syndrome.
(h) Antibiotics, fluid and electrolyte balance,
blood transfusion, tetanus toxoid (0.5 ml
intramuscular to deltoid muscle), or antitetanus
globulin (ATG) injection.
Wound debridement (wound toilet, or wound
excision) is liberal excision of all devitalised
tissue at regular intervals (of 48-72 hours) until
healthy, bleeding, vascular tidy wound is
created.
Primary suturing means suturing the wound
immediately within 6 hours. It is done in clean
incised wounds.
Delayed primary suturing means suturing the
wound in 48 hours to 10 days. It is done in
lacerated wounds. This time is allowed for the
oedema to subside.
Secondary suturing means suturing the wound in
10-14 days or later. It is done in infected wounds.
After the control of infection, once healthy
granulation tissue appears, secondary suturing is
done.
18
 11.WOUND HEALING

Wound healing is complex method to achieve

Phases of wound healing
anatomical and functional integrity of disrupted
tissue by various components like neutrophils, Vascular response → blood
macrophages, lymphocytes, fibroblasts, collagen; coagulation/thrombosis → inflammation → new
in an organised staged pathways. tissue formation → epithelialisation → wound
contraction →remodelling.
Types of Wound Healing
Primary Healing (First Intention) Factors Affecting Wound Healing
Local factors
• It occurs in a clean incised wound or surgical
wound. Wound edges are approximated • Infection
with sutures. There is more epithelial • Presence of necrotic tissue and foreign
regeneration than fi brosis. Wound heals body
rapidly with complete closure. Scar will be • Poor blood supply
linear, smooth, and supple.
• Venous or lymph stasis
Secondary Healing (Second Intention) • Tissue tension
• Haematoma
• It occurs in a wound with extensive soft tissue
• Large defect or poor apposition
loss like in major trauma, burns and wound
• Recurrent trauma
with sepsis. It heals slowly with fibrosis. It
leads into a wide scar, often hypertrophied • X-ray irradiated area
and contracted. It may lead into disability. • Site of wound, e.g. wound over the joints
and back has poor healing
• Re-epithelialisation occurs from remaining • Underlying diseases like osteomyelitis
dermal elements or wound margins. and malignancy
Healing by Third Intention (Tertiary Wound • Mechanism and type of wound—
Healing or Delayed Primary Closure) incised/lacerated/crush/avulsion
• Tissue hypoxia locally reduces
After wound debridement and control of local
macrophage and fibroblast activity
infection, wound is closed with sutures or
covered using skin graft. Primary contaminated General Factors
or mixed tissue wounds heal by tertiary
• Age, obesity, smoking
intention.
• Malnutrition, zinc, copper, manganese
Stages of Wound Healing • Vitamin deficiency (Vit C, Vit A)
• Anaemia
• Stage of inflammation.
• Malignancy
• Stage of granulation tissue formation
and organisation. Here due to • Uraemia
fibroblastic activity synthesisation of • Jaundice
collagen and ground substance occurs. • Diabetes, metabolic diseases
• Stage of epithelialisation. • HIV and immunosuppressive diseases
• Stage of scar formation and resorption. • Steroids and cytotoxic drugs
• Stage of maturation. • Neuropathies of different causes

19
 12.AMPUTATION

Indications
Principles in Amputation
• Gangrene due to atherosclerosis,
• Adequate blood supply of the fl ap
embolism, diabetes, ergots.
should be maintained.
• Trauma: To save life in crush injuries.
• Proper marking of the skin incision is
• Neoplasms: Osteosarcomas, Marjolin’s
essential.
ulcer, melanomas.
• Tourniquet should not be used if
• Gas gangrene.
amputation is done for vascular
• Severe sepsis.
diseases.
• Occasionally severe elephantiasis,
• Proximal part of the flap contains muscle
madura foot, when all other methods
component but distal part should
have failed to help.
contain only skin and deep fascia.
• Dead, dying, devitalised tissues.
• Flap length should be adequate; not
• Severe deformity congenital or acquired. short. It should be ideally semicircular
Types not rectangular to get a conical stump.
It can be: • Nerve should be pulled down and cut
using a sharp knife and allowed to
• Non-end bearing/side bearing—Weight
retract into the soft tissue otherwise
is taken up by the joint.
neuromas may develop.
• End bearing/cone bearing—Weight is
• In crush injury/entrapment
taken up by the body.
injury/sepsis—guillotine amputation is
It can be: done. Later skin is pulled down by using
skin traction, eventually to have better
• Weight bearing.
skin coverage.
• Non-weight bearing.
• Bone should be cut with beveling and all
It can be: sharp margins should be rounded.
• Postoperatively regular dressings are
• Provisional amputation with flap – later
done
final formal amputation may be
• Stumps can be side bearing (sutures are
required.
on the side); end bearing/conical
• Guillotine amputation which always
(sutures are on the end) or cylindrical.
requires revision formal amputation.
• Postoperatively active exercise should be
• Formal amputation – is definitive one.
given to the proximal joint so that
Types of Flaps prosthesis can be fi t to it properly.
• Long posterior flap in below-knee • If there is sepsis especially in gangrene
amputation. limb, flaps should be left open or loosely
sutured otherwise fl ap necrosis occurs.
• Equal flaps in above-knee amputation.
• Proper anatomy of muscles and
Evaluation of the Patients who need Amputation neurovascular bundle around should be
• Haematocrit, control of anaemia by known in all amputations.
transfusing blood/packed cells. Different Amputations
• Control of infection using antibiotics.
• Ray amputation
• Decision of level of amputation by skin
• Transmetatarsal amputation (Gillies’)
temperature, arterial Doppler.
• Lisfranc‘s amputation (Tarsometatarsal
• Informed consent should be taken.
amputation)
• Plan for prosthesis and rehabilitation by
• Chopart‘s amputation (Midtarsal
physiotherapist and rehabilitation team.
amputation)

20
 • Syme’s amputation Late
• Modifi ed Syme‘s amputation
• Pain,
• Pirogoff‘s amputation
• ulceration of stump,
• Below-knee amputation
• Ring sequestrum formation,
• ‘Peg-leg’ amputation
• Fap necrosis,
• Transcondylar-Gritti-Stokes amputation
• Painful scar,
• Above-knee amputation
• Phantom limb
• Hip disarticulation
• Hind quarter amputation Other Complications
• Krukenberg’s amputation • Scar hypertrophy,
• Interscapulothoracic amputation • Skin thickening,
Postoperative Period • Hyperkeratosis,
• Papilloma,
• Physiotherapy is advised.
• Eczema,
• Regular dressings are done.
• Lymphoedema,
• Crutch is used initially, after 3 months
• Boils,
prosthesis is placed (where possible).
• Bursae over bony point can occur which
• Rehabilitation is important.
are treated accordingly.
COMPLICATIONS OF AMPUTATIONS • Spur,
Early • Osteophyte formation,
• Causalgia,
• Haemorrhage,
• Jactitation of the stump,
• Haematoma,
• Stump aneurysm,
• Infection.
• Stump fracture.

21
 13.BURNS AND GRAFTS
BURNS
Types of burns
• Thermal injury
o Scald—spillage of hot liquids
o Flame burns
o Flash burns due to exposure of natural
gas, alcohol, combustible liquids
o Contact burns—contact with hot
metals/objects/mate-rials
• Electrical injury
• Chemical burns—acid/alkali
• Cold injury—frost bite
• Ionising radiation
• Sun burns
Pathophysiology
Local response
• Zone of coagulation: coagulation
necrosis, irreversible tissue loss
• Zone of stasis: decreased tissue
perfusion, potentially salvageable
• Zone of hyperaemia: increased tissue
perfusion, invariably recovers
Systemic response
Mediated by cytokines and inflammatory
mediators, present in burns of > 30%
• Cardiovascular: increased capillary
permeability, vasoconstriction,
decreased myocardial contractility
• Respiratory: bronchoconstriction, ARDS
• Metabolic: threefold increase in basal
metabolic rate, splanchnic
hypoperfusion
• Immunological: downregulation of both
cell-mediated and humoral immune
response
Classification of Burns
I. Depending on the Percentage of Burns
Mild (Minor):
• Partial thickness burns < 15% in adult or
<10% in children.
• Full thickness burns less than 2%.
• Can be treated on outpatient basis.
Moderate:
• Second degree of 15-25% burns (10-20%
in children).
• Third degree between 2-10% burns.
• Burns which are not involving eyes, ears,
face, hand, feet, perineum.
Major (severe):
• Second degree burns more than 25% in
adults, in children more than 20%.
• All third degree burns of 10% or more.
• Burns involving eyes, ears, feet, hands,
perineum.
• All inhalation and electrical burns.
• Burns with fractures or major mechanical
trauma.
II. Depending on thickness of skin involved
A. First degree: Here the epidermis looks red and
painful, no blisters, heals rapidly in 5-7 days by
epithelialization without scarring.
C. Second degree: The affected area is mottled,
red, painful, with blisters, heals by
epithelialisation in 14-21 days.
• Superficial second degree burn heals,
causing pigmentation.
• Deep second degree burn heals, causing
scarring, and pigmentation.
C. Third degree: The affected area is charred,
parchment like, painless and insensitive, with
thrombosis of superficial vessels. It requires
grafting. Charred, denatured, insensitive,
contracted full thickness burn is called as eschar.
These wound must heal by re-epithelialisation
from wound edge.
D. Fourth degree: Involves the underlying
tissues—muscles, bones.
III. Depending on thickness of skin involved
22
A. Partial thickness burns: It is either first or
second degree burn which is red and painful,
often with blisters.
B. Full thickness burns: It is third degree burns
which is charred, insensitive, deep involving all
layers of the skin.
Assessment of Burns
• Wallace’s rule of nine is used for early
assessment.
Rule of Nine
(Wallace’s rule of “9”), Percentage of burns in (A) Adults;
(B) Children
• Using the Lund and Browder chart is better
method for assessing the burns wound. Here
each part of the body is individually assessed
for involvement of burns.
• Patient’s entire hand area is 1%. Clean piece
of paper is cut to the size of hand and
through that percentage of burns is assessed.
Clinical Features
• History of burn.
• Pain, burning, anxious status, tachycardia,
tachypnoea, fluid loss.
• In severe degrees features of shock.
Tolerable temperature to human skin is 40°C for
brief period.
Investigations
The number of investigations will vary with the
type of burn but most patients require:
• Full blood count, haematocrit, urea and
electrolytes;
• Group and save/cross-match;
• Microbiology swabs of burn wounds.
Electrical injuries also require:
• 12-lead ECG;
• Cardiac enzymes (high-tension injury).
Inhalational injuries require:
• Chest X-ray;
• Arterial blood gases (can be useful in any
burn because base excess is predictive of
amount of resuscitation required).
Effects of Burn Injury
• Shock due to hypovolaemia.
• Renal failure.
• Pulmonary oedema, respiratory
infection, adult respiratory distress
syndrome (ARDS), respiratory failure.
• Infections
• GIT: Hypovolaemia, ischaemia of
mucosa, erosive gastritis—Curling’s
ulcer (seen in burns > 35%).
• Fluid and electrolyte imbalance.
• Postburn immunosuppression
predisposes to severe opportunistic
infection.
• Eschar formation and its problems like
defective circulation, ischaemia when it
is circumferential.
• Electrical injuries often cause fractures,
major internal organ injury, convulsions.
• Development of contracture is a late
problem. It leads to ectropion,
microstomia, disability of different
joints, defective hand functions, growth
retardation causing shortening.
• Inhalation burn causes pulmonary
oedema, respiratory arrest, ARDS.
• Chemical injury causes severe GIT
disturbances like erosions, perforation,
stricture oesophagus (alkali), pyloric
stenosis (acid), mediastinal injury.
• Other problems commonly seen are
DVT, pulmonary embolism, urinary
infection, bed-sores, severe malnutrition
with catabolic status, respiratory
infection.
• Complications of burns contracture itself
like hypertrophic scar, keloid formation.
• Toxic shock syndrome: It is a life-
threatening exotoxin mediated disease
caused by Staphylococcus aureus. It is
common in children, presents with
23
 rashes, myalgia, diarrhoea, vomiting,
and multi organ failure with high
mortality.
Causes of death in burns
• Hypovolaemia (refractory and
uncontrolled) and shock
• Renal failure
• Pulmonary oedema and ARDS
• Septicaemia
• Multiorgan failure
• Acute airway block in head and neck
burns
MANAGEMENT OF BURNS
Initial management
• Stop the burning process and keep the
patient away from the burning area.
• Clothing should be removed
• Cooling of the part by running water for
20 minutes
• Cleaning the part to remove dust, mud,
etc
• Chemoprophylaxis—tetanus toxoid;
antibiotics; local antiseptics
• Covering with dressings by different
methods
• Comforting with sedation and pain killer
Definitive Treatment
• Admit the patient.
• Maintain airway, breathing, circulation.
• Assess the percentage, degree, and type
of burn.
• Keep the patient in a clean environment.
• Sedation and proper analgesia.
• Patient should be in burns unit (ideally
air-conditioned) with barrier nursing,
sterile clothes, bed sheets with all aseptic
methods.
• Fluid Resuscitation
Formulas to calculate the fluid replacement:
1. Parkland regimen: Commonly used: 4
ml/% burn/kg body weight/24 hours.
✓ Maximum percentage considered is
50%.
✓ Half the volume is given in first 8
hours, rest given in 16 hours.
NOTE: Fluids used are normal saline, ringer
lactate, Hartmann fluid, plasma. Ringer lactate is
the fluid of choice. Blood is transfused in later
period (after 48 hours).
• Urinary catheterization to monitor output;
30-50 ml/hour should be the urine output.
• Tetanus toxoid.
• Monitoring the patient: Hourly pulse, BP,
PO2, PCO2, electrolyte analysis, blood urea,
nasal oxygen, often intubation is required.
• Ryle’s tube insertion initially for aspiration
purpose later for feeding (Enteral feeding).
• Antibiotics : Penicillins, aminoglycosides,
cephalosporins, metronidazole.
• Culture of the discharge; total white cell
count and platelet count at regular intervals
are essential to identify the sepsis along with
fever, tachycardia and tachypnoea.
• In burns of oral cavity tracheostomy may be
required to maintain the airway.
• Total parenteral nutrition (TPN) is required
for faster recovery, using carbohydrates,
lipids, vitamins.
• Intensive nursing care.
Local Management
Dressing at regular intervals
✓ Open method with application of silver
sulfadiazine without any dressings, used
commonly in burns of face, head and
neck.
✓ Closed method is with dressings done to
soothen and to protect the wound, to
reduce the pain, as an absorbent.
✓ In burns of head and neck region,
exposure treatment is advised.
✓ Slough excision is done regularly.
✓ After cleaning with povidone iodine
solution silver sulfadiazine ointment is
used. It is an antiseptic and soothening
agent. It causes neutropenia.
Surgery
RESURFACING/GRAFTS
Excising the burn wound is only part of the
battle. The main challenge is to resurface the
excised wound. There are various approaches to
this:
Skin autografts
24
If the burn wound is less than 50% of total body
surface area, then it can be covered with the
patient’s own skin (autograft).
Skin allografts
Cadaveric skin can be used as a temporary
biological dressing. The storage solution
decreases the antigenicity of the skin and the
burn patient is relatively immuno-suppressed, so
the graft is not rejected for a few weeks.
Skin xenografts
Porcine skin can also be used as a temporary
biological dressing.
Synthetic skin
There is much research being directed at creating
artificial skin. Integra is the most commonly used
variety and consists of an artificial neodermis
and a silicone top layer.
Cultured skin
An alternative approach is to grow the patient’s
own skin in culture. A small skin biopsy is taken
on the day of admission and within 2–3 weeks
sheets or suspensions of keratinocytes are
available.
25
 14.HUMAN AND ANIMAL BITES
Tetanus prophylaxis and wound care are
required for all bites
SNAKE BITE
Snake bites do not necessarily result in
envenomation, even if the snake is poisonous (up
to 30% of bitten patients are not envenomated).
The most reliable signs of envenomation are
severe local pain, swelling, and discoloration
developing within 30 minutes of the bite.
If present, draw blood for grouping and
crossmatch (they cannot be done later if needed),
coagulation studies, and liver and renal function.
Management
First Aid
The initial management includes dealing with
airway, breathing and treatment of shock.
The only valid first aid is reassurance and to
splint the extremity during transportation. Do
not make cruciate cuts, suck out venom, wrap
with ice, or apply a tourniquet.
Hospital care
✓ The bite wound is identified and assessed.
✓ It is thoroughly cleaned with debridement.
✓ Polyvalent anti snake venom (against cobra,
krait, vipers) should be given. It should be
given earliest within 4-24 hours.
✓ Tetanus toxoid.
✓ IV fluids, blood transfusion and plasma.
✓ Antibiotics.
✓ Urine output measurement.
✓ Monitoring by regular checking of blood
urea, serum creatinine and bleeding and
clotting time.
✓ In cobra bite, there is neuromuscular
blockade and paralysis occurs. So
neostigmine should be given 0.5 mg IV every
half hourly and later repeated as required. It
is given along with 0.6 mg of atropine.
✓ In viper bite DIC is common. So heparin is
given as 10,000 to 15,000 units loading dose
and later 5,000 units as maintenance dose 8th
hourly.
Complications of Snake Bite
✓ Cellulitis and gangrene of the part.
✓ Deep venous thrombosis [DVT].
✓ Pancytopenia.
✓ DIC and haemorrhage.
✓ Neurological complications.
✓ Septicaemia.
✓ Renal failure.
✓ Marjolin’s ulcer.
DOG BITES
Dog bites are considered provoked if the dog was
petted while eating or otherwise teased. No
rabies prophylaxis is required, other than
observation of the dog for developing signs of
rabies. Because bites to the face are very close to
the brain, it might be prudent to start
immunization and then discontinue it if
observation of the dog is reassuring.
Unprovoked dog bites or bites from wild
animals raise the issue of potential rabies. If the
animal is available, it can be euthanized and the
brain examined for signs of rabies.
Otherwise, rabies prophylaxis with
immunoglobulin plus vaccine is mandatory.
BEE STINGS
Bee stings kill many more people than snakebites
because of an anaphylactic reaction. Wheezing
and rash may occur, and hypotension when
present is caused by vasomotor shock (“pink and
warm” shock). Epinephrine is the drug of choice
(0.3–0.5 ml of 1:1,000 solution). The stingers
should be removed without squeezing them.
Other clinical Features and Management
✓ Pain in the local region, oedema, pruritus,
flushing.
✓ Laryngeal oedema, bronchospasm.
✓ Muscle spasm, convulsions.
26
 ✓ Renal failure in severe cases.
✓ Soda bicarbonate is used to neutralise the
bee venom.
✓ Antibiotics and antihistamines.
BLACK WIDOW SPIDERS
Black widow spiders are black, with a red
hourglass on their belly. Bitten patients get
nausea, vomiting, and severe generalized muscle
cramps. The antidote is IV calcium gluconate.
Muscle relaxants also help.
BROWN RECLUSE SPIDER BITES
Brown recluse spider bites are often not
recognized at the time. In the next several days, a
skin ulcer develops, with necrotic center and a
surrounding halo of erythema. Dapsone is
helpful. Surgical debridement of all necrotic
tissue is needed. Skin grafting may be needed
subsequently.
HUMAN BITES
Human bites are bacteriologically the dirtiest bite
one can get. A classic human bite is the sharp cut
over the knuckles on someone who punched
someone else in the mouth and was cut by the
teeth of the victim. They often show up in the
emergence department with a cover story, but
should be recognized because they need
specialized orthopedic care.
Management
✓ Proper wound toileting is very important.
✓ Within 12 hours, incised wound is closed
primarily.
✓ All lacerated wounds and wound which is
seen after 12 hours is left open. Wound is
closed secondarily.
✓ Antibiotics are must in all mammalian bites.
✓ Human bite is very dangerous bite.
27
 15.FRACTURES / DISLOCATIONS
Introduction
Fractures are a common medical problem: most
people have broken a bone or know someone
who has. Bones are familiarly regarded as inert
things that are important for body structure.
Definitions
Fracture is a break in the surface of a bone, either
across its cortex or through its articular surface.
Dislocation is a complete and persistent
displacement of a joint.
Subluxation is partial dislocation of a joint.
Sprain is a temporary subluxation of a joint due
to ligament injury and the articular surfaces
return to normal alignment.
Strain is a tear in the muscle.
The bone can break within its soft tissue
envelope and may not communicate to the
exterior (simple or closed fractures) or it may rip
through its soft tissues or the soft tissue itself
may be damaged by the external forces, exposing
the bone to the external atmosphere (compound or
open fractures). If the former event is bad, the
latter event is catastrophic. In both the situations
depending on whether the force is direct (as in
direct impact in RTA) or indirect (e.g. through the
muscle action), and depending on the amount of
force applied, the direction of force, age and
other factors, different fracture patterns are
produced and each one poses a problem peculiar
to its own.
TYPES OF FRACTURES
• Simple or compound (Figs, A and B).
• Based on the extent of fracture line:
– Incomplete fractures—it involves only one
surface or cortex of the bone.
– Complete fracture—here the fracture involves
both the cortices and the entire bone.
A complete fracture could be undisplaced or
displaced.
• Based on fracture patterns (orthopedic trauma
association classification—Figs A to E)
– Linear fractures: These could be transverse,
oblique or spiral. Any fracture that forms an
angle less than 30° with the horizontal line is
called transverse. Angle equal to or more than
30° is termed oblique.
– Comminuted fractures: Here the fracture
fragments are more than two in number. They
are further sub-classified into ≥ 50 percent
comminution or more than 50 percent
comminution. Butterfly-shaped fractures are also
included in this group and could be less than 50
percent or equal to or more than 50 percent.
– Segmental fractures: A fracture can break into
segments and the segment could be two-level,
three-level, and a longitudinal split or
comminuted.
– Bone loss: This could be a < 50 percent bone loss,
more than 50 percent bone loss, or a complete
bone loss.
28
 (f) Torus fracture: This is just a buckling of the
outer cortex.

Atypical fractures: (A) Compression, (B)

Pathological, (C) Greenstick, and (D) Torus
fractures

Remember

• Greenstick fracture—occurs in children.

• Stress fracture—common in athletes.

Fig. Types of fractures based on fracture patterns:
• Fatigue fractures—in occupations like police,
(A) Transverse, (B) Spiral, (C) Oblique, (D)
nurse, etc.
Comminuted, and (E) Segmental fractures.
• Pathological fractures—usually seen in
elderly people.

• Hairline or crack fracture—is a special

Atypical Fractures (Figs, A to D) variety of incomplete fracture.

(a) Greenstick fractures: It is seen exclusively in DISPLACEMENT OF FRACTURES

children. Here the bone is elastic and usually
A complete fracture usually gets displaced due to
bends due to buckling or breaking of one
various factors already mentioned. Depending
cortex when a force is applied. This is called a
on the direction of force, mode of injury, pull of
greenstick fracture.
the muscles, a fracture can show any one of the
(b) Impacted fractures: Here the fracture fragments following displacements or angulation (Figs A to
are impacted into each other and are not D):
separated and displaced.

(c) Stress or fatigue fractures: It is usually an

incomplete fracture commonly seen in
athletes and in bones subjected to chronic and
repetitive stress (e.g. third metatarsal fracture,
fracture tibia, etc.).

(d) Pathological fractures: It occurs in a diseased

bone and is usually spontaneous. The force
required to bring about a pathological fracture
is trivial. Types of angulations in fractures: (A) Medial, (B)
Lateral, (C) Anterior, and (D) Posterior
(e) Hairline or crack fracture: It is a very fine break
in the bone that is difficult to diagnose Clinical Features
clinically. Radiology usually helps or still
better is CT scan.

29
The signs of fracture are: A patient with limb
injuries may present with the following
complaints.
• Deformity;
• Tenderness;
• Swelling;
• Abnormal mobility;
• Discoloration or bruising;
• Loss of transmitted movements;
• Shortening; and
• Crepitus.
Crepitus is perceived as a grating or grinding of
the broken bone ends, although this sign should
not be purposefully elicited as it will cause
intense pain to the patient.
Some important deformities in orthopedics: (A)
Dinner fork deformity, (B) Swan neck deformity,
(C) Anterior dislocation of hip, and (D) Posterior
dislocation of hip.
Clinical manifestations due to neurovascular
injuries:
Certain fractures are known to cause
neurovascular damage quite frequently, e.g.
supracondylar fracture of humerus in children.
The familiar five Ps detects impending vascular
damage and nerve injuries are detected by the
classical deformities and screening tests.
About Five Ps
• Pain
• Pallor
• Paresthesia
• Pulselessness
• Paralysis
Investigation of fractures
Radiography
It is an important diagnostic tool for fractures.
Minimum two views, anteroposterior and lateral
are required as bone is a cylinder. Sometimes, an
oblique view and other special views are
required depending upon the clinical situations
and bone under study.
Vital facts: About plain X-ray
Radiological clues one should look for on plain
X-rays for diagnosis of fractures:
• Where is the fracture?
• Situations: Whether it is in the diaphysis,
metaphysis, epiphysis and the articular
surface.
• Anatomy: Look for the fracture line, whether
it is transverse, oblique, spiral, segmental,
comminuted, etc.
• Also look for the alignment, angulation,
displacement, rotation, etc.
• Number: How many fragments are seen?
• Bone condition: Identify whether the bone is
normal or pathological.
• Joint involvement: Look for the extension of
the fracture line into the joint, joint swelling
and for evidence of dislocation.
• Soft tissue swelling: The extent of the soft
tissue swelling indicates the severity of the
injury.
Pitfalls of X-ray
• Presence of a fracture line on an X-ray helps
confirm the diagnosis but its absence does not
rule out a fracture.
• Hairline fractures tend to be missed (e.g.
scaphoid).
• Some dislocations, if associated with fractures
could be missed (e.g. Monteggia fracture).
• In comminuted fractures the number of
fragments could be misleading.
• Beware of artifacts they could mislead you.
30
• Be careful in interpreting fracture-like
appearances, e.g. apophysis.
• Avoid interpreting a low quality X-ray.
Role of X-ray
• Helps confirm the clinical diagnosis.
• Helps study the fracture anatomy.
• Helps study the fracture displacement.
• Helps to detect crack and stress fractures.
• Helps to plan the treatment.
• Helps to detect fracture dislocation
combinations, e.g. Monteggia.
• Helps to ascertain post-reduction status of
fractures.
• Helps in medicolegal study.
Remember the rules in X-rays
• Better no X-ray than one view X-ray.
• X-ray is a shadow. It conceals and distorts.
Hence, interpret X-rays with caution.
• A joint above and joint below should be
included with the fracture under study.
• The fracture should be in the middle of the
film.
• Exposure should be adequate and the soft
tissue shadow should be delineated
properly.
• X-rays should be read by holding the film in
an anatomical position.
• Proper protective measures against radiation
should be adopted.
• Avoid unnecessary X-rays.
• Check X-rays are to be taken without
disturbing the plaster cast.
CT Scan and MRI
These are the most sophisticated investigative
methods available now in orthopedics. Both are
noninvasive and are extremely useful in
detecting both soft tissue and bony injuries.
Note:
CT scan: This is helpful in detecting fracture of
skull, pelvis, spine and identifying loose bodies
in the joint.
MRI: This is useful to diagnose any fracture. In
addition, it helps to identify soft tissue and
ligament injuries. It is certainly the ‘Gold
Standard’ but has its Achilles heel in being
expensive.
HEALING OF FRACTURES
Bone has a natural tendency to heal and, unlike
any other connective tissue, has a remarkable
repair mechanism that ultimately results in bone
regeneration and structural integrity; it is literally
‘as good as new’. The pathophysiology of
fracture healing is summarized in the Figure
below.
This remarkable process and its mechanism
remain poorly understood but there are a
number of points worth noting.
• Bones heal in the presence of some movement.
This is clear from the example of broken ribs,
which unite efficiently (albeit painfully) with
prodigious external callus formation. It appears
that movement stimulates union but the
movement must be small and must not be in
certain directions. Essentially, bones are
stimulated by micromovement directed along
their axis and heal least efficiently if subject to
shearing forces or large movements.
• The converse also holds true: although bones
will heal if there is no movement, they do so
very slowly and by an entirely different process
that does not utilize natural external callus
formation. This alternative method of fracture
healing appears to be similar to the normal
remodelling processes of bone, which are slow
but sure.
Figure. The pathophysiology of fracture healing.
31
MANAGEMENT OF FRACTURES
The goal of fracture management is to restore the
anatomy back to its normal or as near to normal
as possible.
Conservative Methods
Management of Simple Fractures
Simple fractures are managed by conservative
and operative methods.
1. For undisplaced fractures, incomplete
fractures, impacted fractures:
a. Cuff and collar sling: For upper limb fractures.
b. Strapping: For fracture clavicle, fracture ribs,
finger or toe fractures, etc.
c. Plaster slabs: Plaster of Paris slabs can be used
to support the injured limb usually as a first
aid measure.
d. Rest and nonsteroidal anti-inflammatory drugs
(NSAIDs): For pain relief and to reduce the
inflammation.
e. Masterly inactivity in certain cases like
impacted fracture neck of femur, etc.
Management of Open fractures
Open (or, less meaningfully, compound) fractures
are serious Injuries. Considerable violence is
required to cause this type of injury and because
there is a break in the skin, bacterial
contamination of the bone occurs. The strategy of
treatment is to clean the wounds as soon as
possible and remove all dead tissue
(débridement), thus preventing the development
of infection. Open fractures are surgical
emergencies and, provided the patient’s general
condition permits, formal surgical wound
débridement should be performed as soon as
possible and preferably within 6 h of injury.
Wounds must be left open, and closed either as a
secondary procedure after a few days or left to
heal spontaneously. Such patients all need
supplementary broad-spectrum antibiotics and
some form of tetanus prophylaxis, i.e. tetanus
toxoid booster to those with a previous
immunization record or human anti-tetanus
globulin for those with no previous active
immunity.
Definitive management
The essential strategy of long-term fracture
management must be to return patients to their
preinjury level of function by the safest means.
The basic goals of management are resuscitation,
reduction, retention and rehabilitation (4Rs).
1. Resuscitation:
Resuscitation is the topmost priority if the patient
is in shock following a fracture.
A to F management proposed is to be followed in
all situations of emergencies.
2. Reduction:
Reduction of the fracture fragments if it is
displaced. Usually it is done under general
anesthesia after adequate radiographic study.
Reduction methods are:
a. Closed reduction:
It is adopted usually for simple fractures. The
technique followed is traction and counter
traction method. It is a blind technique and needs
considerable skill and expertise. It commonly
results in malunion.
b. Continuous traction:
Certain examples where continuous traction can
be used for reduction of tractions are Gallows
traction for fracture shaft femur in children,
balanced skeletal traction for adult shaft femur
fractures, etc.
c. Open reduction:
Open reduction may be required, whereby the
fracture site is opened surgically and the
fragments are relocated directly under vision
(e.g. unstable fracture of both forearm bones).
Open method is indicated once, the conservative,
fixed reduction methods fail and when there are
specific indications.
Indications
Absolute
• Failed closed reduction
• Displaced intra-articular fractures
• Type III and IV epiphyseal injuries
• Major avulsion fractures
• Nonunion
• Replantation of extremities
32
Relative • Apposition: Apposition can be achieved
simply by using semiflexible wires known as
• Multiple fractures
‘K’ (for Kirschner) wires
• Delayed union
• Interfragmentary compression is usually
• Loss of reduction
achieved by screws or occasionally by
• Pathological fractures
tension band wires.
• For better nursing care
• Onlay devices are metal plates that are used to
• To avoid prolonged bed rest
buttress weak structures around joints and to
• Closed methods ineffective in Galeazzi
fix long bones in the upper limb.
fracture, Monteggia fracture, femoral neck
• Intramedullary or inlay devices are the most
fracture, etc.
satisfactory method of fixation. They achieve
Questionable alignment without unduly disturbing natural
bone healing.
• Neurovascular injury
e. External fixation: When fractures are open
• Open fractures and associated with extensive soft-tissue damage
• Cosmetic reasons and contamination, neither plaster casting nor
• Economic consideration internal fixation is appropriate. Plaster splints are
unsuitable because the wounds become
Contraindications for open reduction inaccessible for inspection and dressing, while
• Infection internal fixation is hazardous because of the very
high risk of wound infection.
• Small fragments
A compromise solution is to apply an external
• Weak and porotic bone fixation device.
• Soft tissue damage
• Undisplaced or impacted fractures A disadvantage of external fixators is the risk of
• Poor general and medical condition infection at the pin sites.

3. Retention 4. Rehabilitation
This is by way of physiotherapy and exercises
Once the fracture fragments are reduced, it has to
be retained in that position till the fracture unites, (both active and passive).
otherwise it tends to get displaced due to the Complications of fractures
action of muscles, gravity and inherent factors.
These can be early or late and a direct
Retention methods are: consequence of the injury or associated with the
a. By plaster of Paris splints: this is the most treatment applied
common splint employed. It could be a slab Early direct complications
(encircles half the limb) or a cast (encircles the
whole limb) or a functional brace (which permits Specific to the fracture
mobility while the fracture is still under the cast).
• Infection in open fractures
b. By continuous traction to overcome the
• Associated stretching or crushing of nerves
muscle forces after closed reduction. The traction
could be skin or skeletal traction and is employed • Very rarely, damage to a blood vessel or its
as fixed, balanced or combined types of tractions. lining causes thrombosis

c. Use of functional braces: this can be used after • Compartment syndrome caused by localized
three weeks, once the fracture becomes sticky. swelling

d. Internal fixation: Where accurate reduction General

and holding of fractures are required, internal
fixation is performed. However, internal fixation All these general complications should be
is technically very demanding, has many anticipated and are very rare
complications and, most important of all, • Fat embolism
prevents natural healing. If fixation is to be used
• Renal failure
it can be achieved in a number of ways.

33
 • Unrecognized hypovolaemic shock
• Muscle wasting due to immobility
Complications associated with treatment
• Infection of internally fixed fractures
• Surgical damage to vital structures such as
nerves or blood vessels
• Compartment syndrome
• Pressure damage to skin or nerves from
excessively tight bandages and splints
Late bone complications
• Malunion due to poor supervision of healing
• Non-union usually associated with:
(a) Excess movement
(b) Insufficient movement
(c) Poor local blood supply due to either
anatomy (e.g. tibia) or a lot of trauma
damage
• Growth arrest in children due to epiphyseal
damage
34
 16.DEPRESSED SKULL FRACTURE

• It is a common neurosurgical problem • Convulsions

among the head injuries. • Meningitis
• It means fracture depression is more than the
Investigations
depth of inner table of the skull.
• CT scan.
Problems in depressed fracture
Treatment
• Tear in the dura beneath
• Haematoma in the deeper plane • Antibiotics, anticonvulsants.
• Injury to the cerebrum • Elevation of the depressed fracture: Burr holes
• Injury to the venous sinuses—may cause life- are made in the adjacent normal skull.
threatening haemorrhage. Fracture should not Fracture is elevated. Bony fragments and
be elevated in such occasion, as it itself can necrotic materials are removed. Dural tear is
precipitate bleeding closed with interrupted sutures.

35
 17.NECK FRACTURE
Fig. Neck trauma zones.
Neck is divided into zones for managing neck
injuries
• Zone I: From clavicle to cricoid cartilage
• Zone II: From cricoid cartilage to angle of the
mandible
• Zone III: Above the angle of the mandible
Indications for Neck Exploration in Injuries
• Expanding haematoma.
• Uncontrolled external haemorrhage.
• Decreased carotid pulse.
• Stridor, hoarseness, dysphonia, haemoptysis.
• Severe dysphagia, odynophagia.
• Blood in oropharynx.
Management
In all patients with severe blunt trauma to the
neck, the integrity of the cervical spine has to be
ascertained. Unconscious patients and conscious
patients with midline tenderness to palpation
should be evaluated initially with CT scan, and
potentially followed with MRI depending on
findings. Conscious patients with no symptoms
(are not intoxicated, have not used drugs, or have
no ‘distracting’ injury) can be clinically evaluated
for a cervical spinal injury; however, if CT scan of
the head is being obtained, it is generally
accepted to extend the study to include the
cervical spine.
Treatment
• The neck is explored with adequate incision
under general anaesthesia.
• The injured structure like vessels,
oesophagus, trachea, muscles are sutured.
• Antibiotics.
• Blood transfusion is given as required.
• Ryle’s tube for 5-7 days.
36
 18.UPPER LIMBS FRACTURES

FRACTURE CLAVICLE • Malunion

Mechanism of Injury PROXIMAL HUMERAL FRACTURES

Direct
Due to fall on the point of the shoulder. This is
the most common mode of injury accounting for
91 percent of the cases.
This is common in elderly patients and it
accounts for 4 to 5 percent of all fractures. It is
more common in elderly females due to
osteoporosis.

Direct trauma over the clavicle due to RTA, Mechanism

direct injury, etc. accounts for 8 percent of the
cases
Indirect fall on the outstretched hands accounts
for 1 percent of the cases.
Classification of Fracture Clavicle (Allman’s)
Group I is fractures involving middle one-third
of the shaft.
Group II is fractures involving the lateral third
distal to the attachment of the coracoclavicular
ligament.
Group III are medial third fractures
Clinical Features
The patient presents with pain, swelling,
deformity and inability to raise the shoulder.
Radiographs
• Fall on the outstretched hands is the classical
history.
• Blow on the lateral side of the arm is the other
mode of injury.
Clinical Features
The patient complains of pain, swelling and other
features of fractures. Movements of the shoulder
joint are grossly restricted.
Investigations
• Plain X-rays of the shoulder: Trauma series
consists of AP, lateral, and axillary view of
shoulder joint in scapular plane
• Laminagrams to judge the articular defects.
• CT scan helps to study the fracture lines with
greater accuracy.

• Routine AP view of the clavicle Management

Treatment Nonoperative Treatment

Conservative Methods Indications
This is the treatment of choice in fracture clavicle
• Undisplaced fractures
and consists of the following methods:
• Surgical neck fractures
• Cuff and collar sling for undisplaced
fractures • Poor health
• Strapping of the fracture site after reduction • Poor surgical risks
of the fracture.
• Billington Yoke method uses a plaster of • Very old patients.
Paris over a well-padded figure of ‘8’ Conservative treatment
dressing.
• Figure of ‘8’ • Rest,
• NSAIDs,
Surgery is rarely indicated and consists of open • sling,
reduction and rigid internal fixation. • ice and
• heat therapy in the initial stages.
Complications of Fracture Clavicle
• U–slab
• Neurovascular injury Treatment facts

37
About 80 to 85 percent of proximal humeral
fracture can be treated by conservative methods.
Operative Treatment
Open reduction internal fixation (ORIF)
Complications
• Joint stiffness is due to periarticular fibrosis.
• Malunion is due to the varying muscle forces.
• Avascular necrosis is seen in fracture of the
anatomical neck.
TREATMENT
Pain relief & reduction
Anterior dislocation of the shoulder is an
emergency and has to be immediately reduced.
Closed reduction:
Kocher’s method Most effective and commonly
followed method.
After the reduction, the arm should be fastened
to the chest with a body bandage for a minimum
period of three weeks

• Nonunion of surgical neck.

Complications

• Recurrent dislocation
• Myositis ossificans due to vigorous massage
• Unreduced dislocation
and treatment.
• Traumatic osteoarthritis
DISLOCATION OF SHOULDER • The risk of developing secondary
osteoarthritis following anterior dislocation
Shoulder joint is vulnerable for dislocation more of shoulder is 10 to 20 times greater than
often than any other joint in the body. The normal people
extreme mobility it enjoys jeopardizes its
• Axillary nerve damage
stability. The shoulder has an “Achilles point” at
the inferior part of the capsule providing the joint FRACTURE SHAFT HUMERUS
with a potential weak spot, so much so that 99
percent of the anterior shoulder dislocation Fracture shaft humerus is more common in
occurs here. adults than in children.

ANTERIOR DISLOCATION OF SHOULDER Mechanism of Injury

As mentioned earlier, this is the most common • Direct force: This may produce a transverse or
type of shoulder dislocation. comminuted fracture.
• Indirect force: It is due to fall on an
Mechanism of Injury
outstretched hand and this will produce an
It could be due to either direct or indirect forces. oblique or spiral fracture.
The latter is more common. • Birth injuries: This is the second most
Clinical Features common birth fracture after clavicle.

• Severe pain Clinical Features

• Inability to use the shoulder joint. Clinical features show all the signs and
symptoms of a fracture. A careful neurological
• Arm held in a position of abduction and and vascular assessment is important. Injury to
external rotation. radial nerve is common in fractures at the spiral
groove or lower one-third of humerus.
• Loss of sensation on the outer aspect, of the
upper arm and is called the ‘Regiment Radiographs
Badge’ sign.
Radiography of the entire upper arm including
RADIOGRAPHS both the shoulder joint above and the elbow joint
below should be taken.
• AP X-Ray
• Transthoracic lateral x-ray Treatment Methods
• CT Scan Conservative Methods
• MRI

38
This consists of splinting the fracture if it is • Frail and debilitated patients.
undisplaced. In displaced fractures, splinting is
• Extreme osteoporosis.
done after closed reduction preferably under GA.
• Local conditions of the skin not conducive
Operative Treatment
for surgery.
Internal fixation
• Open degloved or crushed elbow.
Indications

• Failed conservative treatment. Methods

• Multiple fractures and unstable fractures. • Overhead skeletal traction through the
• Multisystem injuries. olecranon
• Radial nerve palsy after closed reduction.
• Initial traction converted to cast, cast brace or
• Pathological fractures.
hinged brace.
• Compound fractures with vascular injuries.
• Segmental fractures. Operative Treatment
• Intra-articular extension into shoulder and Open reduction with rigid internal fixation.
elbow joints.
• Bilateral humeral fractures. SUPRACONDYLAR FRACTURE
• Brachial plexus injuries.
Supracondylar fractures of the humerus is very
• Ipsilateral shoulder or forearm fractures.
common in children.
Complications
Mechanism of Injury
• Radial nerve injury
Fall on an outstretched hand with
• Vascular injury
hyperextension at the elbow with abduction or
• Malunion
adduction, with hand dorsiflexed.
• Nonunion
Classification
DISTAL HUMERUS FRACTURES
Supracondylar fracture is broadly classified into
Rare fractures. extension type and flexion type. In extension type,
the fracture line runs upwards and backwards; and
Mechanism of Injury
in flexion type, it runs downwards and forwards.
These injuries are mainly due to longitudinal
force through the elbow that is flexed beyond Extension type of supracondylar fracture is
90°. further classified into the following subtypes.

Clinical Features Gartland’s Classification (In Children)

The patient presents with pain around the elbow, • Type I: Undisplaced
gross swelling, deformity, severe loss of elbow • Type II: Displaced, but posterior cortex is
movements, crepitus and neurovascular intact.
impairment may be present in the forearm or • Type III: Displaced, but no intact posterior
hand. cortex and the distal fragment could be
either displaced:
Radiographs
a) Posteromedial or
Good quality AP and lateral views of the plain X- b) Posterolateral.
ray are enough to make an accurate diagnosis.
Clinical Features
Treatment
• Gross pain and swelling,
Goal of treatment is to restore the anatomical • S-shaped deformity of the upper arm
configuration of the joint surface. • Loss/reduced of both active and passive
Nonoperative Treatment movements of the elbow.
• Arm is short, forearm is normal in length.
Indications

39
Radiographs Type IV: Radial head fracture with posterior
dislocation of elbow.
X-ray of the elbow
Clinical Features
Management
• Pain on the lateral side of the elbow,
Conservative management: Initially, closed
reduction is tried under general anesthesia by • Minimal swelling and restriction of elbow
traction and counter traction methods. movements and supination,

Surgery. • Pronation of the forearm.

Closed reduction and percutaneous fixation • Tenderness over the radial head
(PCIF):
• Crepitus can be elicited.
Complications
Investigation
These are broadly divided into two categories:
Plain X-ray of the elbow
1. Those that cause functional impairment of
the extremity and is more serious. Treatment

2. Those that produce only cosmetic sequelae. This varies according to the type of fractures.

Complications Causing Functional Impairment Type I

• Neurological involvement Non operative means

• Vascular injury • Aspiration of elbow within first 24 hours
• Ulnar nerve injury decreases pain
• Anterior interosseous nerve injury • Early mobilization within 24 hours
• Median nerve injury
Type II
• Radial nerve injury
• Loss of mobility • Excision head of radius
• Myositis ossificans
Type III
Complications that produce cosmetic
• Radial head excision is indicated within first
abnormalities
24 hours.
• Cubitus varus (Gunstock elbow) • Excised head is replaced with prosthesis
• Cubitus valgus Type IV

RADIAL HEAD FRACTURE • Prompt reduction of the dislocation

• Assess status of the head
Radial head fracture is a common injury in adults
and is rare in children. Complications

• Injury to the posterior interosseous nerve,

Mechanism of Injury
• osteoarthritis and
• Indirect trauma due to fall on an outstretched • elbow stiffness
hand.
FRACTURE BOTH BONES OF THE
• Direct trauma due to RTA, assault, etc. in
adults. FOREARM

Mason’s Classification Mechanism of Injury

Type I: Undisplaced fracture.
Type II: Marginal fracture with displacement.
Type III: Comminuted fractures.
Fracture both bones of forearm in adults are
frequently due to RTA, falls, assault, etc.
Clinical Features

40
 • Severe pain,
• swelling and deformity of the forearm.
• Restricted movement of the forearm
• Other features of fractures
Radiographs
The AP X-ray, lateral and oblique views of the
forearm help to make an accurate diagnosis.
Treatment
Conservative treatment: Undisplaced, incomplete
fractures are treated by immobilization with an
above elbow plaster slab or cast.
Surgery
• ORIF
• Intramedullary fixation: IM nail fixation of
both bones fractures with K-wires, Rush
nails, etc.
Complications of Fracture Both Bones of Forearm
• Volkmann’s ischemia
• Delayed union and nonunion
Conservative methods: The type I fractures are
treated by immobilization with an above elbow
plaster slab or cast for a period of 3-4 weeks.
Surgery: Type II and III varieties are treated by
open reduction and rigid internal fixation with
plate and screws.
MONTEGGIA’S FRACTURE
It is a fracture upper third of ulna with
dislocation head of the radius.
Mechanism of Injury
Monteggia’s fractures are more common in
children and are due to fall on the outstretched
hands either in hyperpronation or in
hyperextension.
Clinical Features
Pain, swelling, deformity and severe loss of
forearm movements.
Radiographs
• Plain X-ray of the forearm

• Malunion
Treatment
Monteggia’s fracture can be managed
• Cross union
successfully in children by conservative methods
ISOLATED DISTAL ULNAR and by operative methods in adults.

FRACTURE (ALSO CALLED Complications

NIGHTSTICK FRACTURE) • Unreduced dislocation head of radius.

This is relatively rare when compared to fracture
both bones of the forearm.
It is usually due to direct blow on the
subcutaneous border of the ulna.
Clinical Features
• Pain, swelling and deformity along the
subcutaneous border of the forearm.
• Rotational movements of the forearm are
restricted.
Radiograph
The AP, lateral views of the forearm helps to
make a diagnosis.
• Posterior interosseous nerve palsy.
• Malunion of fracture ulna.
• Nonunion of fracture ulna.
• Myositis ossificans.
• Synostosis between radial head and
proximal ulna.
• Tardy posterior interosseous nerve palsy.
• Proximal migration of radius.
• Dislocation of inferior radioulnar joint.
• Cubitus valgus deformity.
COLLES’ FRACTURE
This is also called as Poutteau’s fracture in many
parts of the world. Abraham Colles first
described it in the year 1814.

Treatment Definition
It is not just fracture lower end of radius but a
fracture dislocation of the inferior radioulnar.

41
The fracture occurs about 1½” (about 2.5 cm)
above the carpal extremity of the radius.
Following this fracture, some deformity will
remain throughout the life but pain decreases
and movements increase gradually.
Mechanism of Injury
The common mode of injury is fall on an
outstretched hand with dorsiflexion ranging
from 40-90° (average 60°).
Here fracture reduction is carried out by closed
methods under general anesthesia (GA) or local
anesthesia (LA).
Operative methods: Operative treatment is rarely
required for Colles’ fracture and may be required
in the following situations:
Indications: Extensive comminution, impaction,
median nerve entrapment and associated injuries
in adults.

The force required to cause this fracture is 192 kg Complications

in women and 282 kg in men. Early complications
1. Unstable reduction
Fracture pattern It is usually sharp on the palmar
aspect and comminution on the dorsal surface of 2. Median or ulnar nerve stretched
the lower end of radius.
3. Compartmental syndrome
Clinical Features
4. Post reduction-swelling
Usually, the patient is an elderly female in her
60s and the history given is a trivial fall on an 5. Anesthesia problems
outstretched hand.
6. Injury to proximal segment of the bone
The patient complains of pain, swelling, during reduction.
deformity and other usual features of fracture at
Late complications
the lower end of radius. Though dinner fork
deformity is a classical deformity in a Colles’ 1. Malunion
fracture, however, it is not found in all cases but
2. Rupture of extensor pollicis tendon
seen only if there is a dorsal tilt or rotation of the
distal fragment. However, the styloid process test 3. Sudeck’s osteodystrophy
is more reliable. There are six classical
displacements in a Colles’ fracture: 4. Frozen shoulder

1. Dorsal displacement 5. Carpal tunnel syndrome

2. Dorsal rotation
6. Nonunion
3. Lateral displacement
4. Lateral rotation SMITH’S FRACTURE
5. Impaction
6. Supination It is a fracture of distal one-third of radius with
palmar displacement.

Radiology Hence, it is called as reverse Colles’ fracture.

Radiographs of the wrist and both AP and lateral
views of the affected wrist and lower end of the
radius are taken
Treatment Methods
Aim
The aim of treatment is to restore fully functional
hand with no residual deformity. The treatment
methods include conservative methods,
operative methods and external fixators.
Conservative
However, it is less common than Colles’ it is
readily confused with Colles’ fracture.
Mechanism of Injury
There are three modes of injury like fall on the
back of the dorsum of the hand, fall on the
forearm in supination and a direct blow to the
flexed hand.
Clinical Features
Pain, swelling, deformity and loss of wrist
functions.

42
The deformity is opposite to that of Colles’
fracture and is called the ‘garden spade’
deformity.
Radiograph
Anteroposterior view of the wrist shows the
carpus proximally displaced. There will be
anterior displacement of the fragment with
palmar angulation of distal radial articular
surface. The ulnar styloid process is frequently
fractured.
Treatment
The treatment of choice is closed reduction and
immobilization in a long arm cast with forearm
in supination and wrist in extension. For unstable
fractures, fixation with percutaneous K-wire or
open reduction and plate fixation may be
required.
Complications
• Misinterpretation of radiographs for Colles’.
• Other complication of Colles’.
43
 19.LOWER LIMBS FRACTURES
FRACTURE FEMUR
FRACTURE NECK OF FEMUR
Fracture neck femur could be intracapsular or
extracapsular. Intracapsular fracture neck femur
is notoriously known as an orthopedic enigma,
since a permanent solution for its treatment still
eludes the orthopedic surgeon.
Etiology
• It is common in older patients with
osteoporosis or osteomalacia (12%) and in
them; usually it is fracture through a
pathological bone.
• It is common in elderly women secondary to
senile osteoporosis. It also causes marked
comminution of the posterior cortex and thus
decreases the quality of reduction.
Mechanism of Injury
• Majority are due to trivial fall, because of
direct blow over the greater trochanter.
• Second mechanism is mainly due to lateral
rotation of the extremity, which causes
marked posterior comminution of the neck.
• Recent suggested mechanism is cyclical
loading due to muscle force and torsion.
• Major trauma in young adults like road
traffic accident (RTA), fall, etc.
Classification
Many classifications are proposed for fracture
neck femur. Few important ones are mentioned
here.
Broad Classification
• Intracapsular—from subcapital area to the
middle of the neck.
• Extracapsular—from base of the neck to the
pertrochanteric region.
Causatively
• Stress fractures (seen in soldiers, athletes,
etc.)
• Pathologic fractures (seen in osteoporosis,
etc.)
• Postirradiation fractures.
Garden's classification
This is the most accepted classification and is
based on the pattern of fracture line and the
displacement of the fracture:
• Garden I: Incomplete fracture
• Garden II: Complete fracture but undisplaced
• Garden III: Complete fracture with partial
displacement
• Garden IV: Complete fracture with total
displacement.
Clinical Features
Usually, the patient is an elderly female and
gives history of trivial trauma like slip and fall in
the bathroom. The patient complains of pain and
restriction of movements of the affected hip.
Investigations
Radiography
Consists of routine AP and lateral views of the
hip joint.
Other Investigations
• Oxygen tension measurement
• Venography
• Intraosseous pressure recording
• Isotope scanning
• Bone scan with technetium-99m, sulphur
colloid, etc.
Treatment
Fracture neck femur is an orthopedic emergency,
which needs to be reduced and fixed within 24
hours to get an optimum result.
Aims of Treatment
• Early anatomical reduction, which helps and
prevents further vascular damage.
• Impaction of the fracture fragments.
• Rigid internal fixation: Enables
revascularization from the surrounding soft
tissues and uninjured bones, which helps in
early callus formation.
Treatment Plans as per Garden's Classification
44
Garden I:
• Conservative Hip spica is applied if fracture
is several weeks old and if the patient is unfit
for surgery.
• Surgical multiple pins by Moore, Knowles
cannulated screws, etc.
Garden II: Here the fracture is complete and may
be displaced. Hence, it is fixed with either DHS
or multiple cannulated AO screws.
Garden III/IV: Conservative treatment is rarely
indicated except in severely ill patients and
mentally ill patients, e.g. hip spica and well leg
traction.
Surgery is the treatment of choice.
Surgery: Goal of surgery is anatomical reduction,
impaction and stable internal fixation.
• OR+IF
Complications of femoral neck fracture
• Thromboembolism
• Nonunion
• Avascular necrosis
PROXIMAL FEMUR FRACTURES
SUBTROCHANTERIC FRACTURE
Mechanism of Injury It is usually due to direct
trauma due to RTA or fall and is common in
young individuals.
It can be broadly considered under two headings:
Stable fracture: Intact or possible to re-establish
boneto-bone contact of the medial and posterior
femoral cortex anatomically.
Unstable fracture: Posteromedial cortex apposition
is not obtainable.
Clinical Features
The patient presents with pain, swelling,
shortening, complete external rotation deformity
and other usual features of fractures
Radiographs
Radiograph helps to study the level and pattern
of fracture and thereby plan the treatment.
Treatment
Conservative: Methods are advocated if the
patient is young. In severely comminuted
fractures, modified cast brace with pelvic band is
used.
Surgery: This is the preferred method of
treatment in adults and ORIF is chosen for those
fractures, which can be made stable by closed or
open reduction.
Complications
• Malunion: This is a possibility with
conservative treatment.
• Shortening.
• Nonunion due to soft tissue interposition
and is relatively rare.
• Secondary osteoarthritis of the hip.
• Contralateral hip and knee pain due to limp
and altered weight bearing mechanism.
FRACTURE SHAFT FEMUR
Fracture shaft femur is a serious injury and is
usually due to severe violence. It may be
associated with severe blood loss (up to 1,500
ml), multiple fractures and multisystem injuries,
but heavy musculature, however, provides
unlimited blood supply and thus the fracture
heals well.
Mechanism of Injury
Usually, it is due to major violence, and is
common in young adults because the strong
metaphyseal areas transmit the forces to the shaft
causing fracture. In old age, the metaphyseal
areas are brittle and hence the shaft fracture is
rare, but fracture of metaphyseal region is
common.
Clinical Features
Apart from all the features of fractures, there
could be:
• shortening of the lower limb
• complete external rotation deformity
• Features of shock, like unconsciousness,
pallor, cold nose, tachycardia, cold and
clammy skin, hypotension, etc.
Radiographs
Routine anteroposterior and lateral views.
Management
45
Conservative
• Traction: This could be:
▪ Skin traction: It is useful only during
transportation as a first aid measure.
▪ Skeletal traction: It is useful only in early
stages and hence its role is limited.
However, the patient treated in traction
shows 100 percent union, but it causes
shortening, and hence is not acceptable.
The average time of traction required is
12 weeks and this gives rise to
recumbency complications like bedsores,
pneumonia, renal calculus, etc.
Surgery
The best method of managing a fracture shaft
femur in adults is by ORIF. The choice of the
implants could be from a standard
intramedullary nail (K-nail), interlocking nail or
plating.
Complications
Immediate complications:
These are life threatening and include:
▪ Shock,
▪ fat embolism
▪ neurovascular injury to the femoral
artery, sciatic nerve, etc.
Delayed complications
▪ Refracture
▪ Complications of fixation devices
▪ Nerve injury
▪ Malunion
▪ Nonunion
▪ Joint stiffness
INJURIES OF THE KNEE
FRACTURE OF PATELLA
Patella is the largest sesamoid bone in the body.
Incidence is around 1 percent of all skeletal
fractures.
Mechanism of Injury
Direct trauma: This is due to dashboard injuries
and due to direct fall over the patella. They
usually cause comminuted fractures, and are the
common causes.
Indirect trauma (Quadriceps contraction): Sudden
forceful contraction of the quadriceps as in sports
person and athletes can cause patellar fractures.
Here the fracture is usually transverse and
sometimes avulsion fractures of the proximal or
distal poles may be seen.
Age: Common in 20-50 years age group.
Male: Female = 2: 1.
Classification
• Undisplaced:
▪ Transverse fracture—these account for
nearly 50-80 percent of cases. About 80
percent occur in the middle-third.
▪ Stellate fracture.
▪ Vertical fracture.
• Displaced: If displacement is > 3 mm and if
articular incongruity > 2 mm:
▪ Transverse—involving upper or lower
poles (50-85%).
▪ Oblique fracture.
▪ Vertical fracture (12-27%).
▪ Comminuted fracture (30-35%).
▪ Polar—could be proximal or distal.
▪ Osteochondral fractures.
Clinical Features
• The patient gives history of trauma following
which there is pain and swelling at the knee
joint.
• The patient is unable to extend the knee and
both the active and passive movements are
restricted.
• On examination, there could be a palpable
gap, tenderness, signs of effusion and a
positive patellar tap
Investigations
• X-Ray
• CT scan, bone scan and tomography are
other useful investigations.
Management
Undisplaced Fracture
46
 • Compression bandage, ice applications,
aspiration of hemarthrosis, cylindrical cast in
extension, or long leg cast for 4-6 weeks.
• Functional cast brace is also effective.
• The patient is advised early weight bearing
and quadriceps exercises.
Displaced Fracture
In this variety, surgery is the treatment of choice.
Surgery is performed as early as possible
preferably within 7 days.
Surgical Methods
• Open reduction and internal fixation
• Patellectomy (for communited fracture)
Complications
Postoperative complications:
• Early fracture dehiscence,
• postoperative infection,
• refracture (1-5%),
• avascular necrosis (25% incidence in
proximal pole).
Delayed complications:
• Knee stiffness,
• Osteoarthritis of the patellofemoral
• Knee joint extensor lag.
• Delayed union,
• Nonunion,
• Loss of knee motion.
Disadvantages of Patellectomy
• Strength of quadriceps returns slowly
although knee motion is regained quite fast.
• Obvious atrophy of the quadriceps muscle
persists for months and often permanently.
• Protection of the knee by the patella is lost.
• Pathological ossification may develop where
the patella is excised.
ACUTE DISLOCATION OF PATELLA
Lateral dislocations of patella are very common
and are due to lateral force acting on a semi-
flexed knee.
Patient complains of severe pain, swelling and
inability to bend the knee. Patella is seen and felt
on the lateral side.
Treatment
Closed reduction and above knee POP casting is
done under GA. Immobilization in a long leg cast
may be required for a period of 4 weeks.
FRACTURE OF TIBIA AND FIBULA
PROXIMAL TIBIAL FRACTURES
Incidence
One percent of all fractures and 8 percent of
fractures in elderly people.
Mechanism of Injury
It is due to valgus or varus force with axial
loading.
Causes
• Fifty-two percent—due to auto-pedestrian
• injuries (Bumper injuries).
• Seventeen percent—due to fall from heights.
• Thirty-one percent—miscellaneous causes
(football or soccer injuries).
Types
• Articular variety
• Nonarticular variety.
Clinical Features
• Pain,
• Swelling,
• Deformity,
• Haemarthrosis,
• Decreased movements of the knee
• Instability in valgus or varus.
• There could be features of compartment
syndrome of the leg, disturbed peripheral
vascular and nerve functions of the leg.
Investigations
The routine AP and lateral radiographs of the
knee help to demonstrate majority of tibial
condyle fractures.
Management
Aim
• To produce a knee that extends fully and
flexes to at least 120°.
• Restoration of normal articular surface and
ligament repair are both important in
preventing late instability.
47
Conservative treatment is indicated for plateau III Major • Complete
fractures with < 4 mm depression or displacement
displacement. • Major comminution
• Major open fracture
Undisplaced fracture: Above knee, POP cast with
5° flexion or cast bracing is used. Clinical Features
In these fractures, the common symptom is pain
Displaced fracture: Closed reduction, with or
and the obvious sign is the deformity, apart from
without skeletal traction and a long leg cast is
other features of fractures.
used.
Radiographs
In depressed fractures: For less than 8 mm
depression, above knee cast. For depression of Radiograph for acute cases require AP and lateral
more than 8 mm with a large split fragment, views.
skeletal traction is applied. For more than 8 mm
with smaller split fragment, ORIF is done with Methods of Treatment
bone grafting after elevation of the depression. Conservative management is done in majority of
Surgery cases and consists of the following options:

• ORIF • Long Leg Plaster Casts

• Sarmiento's Total Contact below Knee Cast
Complications • Functional Braces
These include: • Pins above and below the Fracture

• DVT, Surgical Treatment

• Compartment syndrome,
• Peroneal nerve palsy,
• Popliteal artery laceration,
• Nonunion (rare),
• Malunion
• Degenerative arthritis.
Only 5 percent of the cases require operative
treatment in tibial fractures. The options include:
• Internal Fixation
• External fixation
Complications of Tibial Fractures

FRACTURES OF TIBIA AND FIBULA • Delayed union

• Nonunion
Tibial shaft fractures are the most common long • Infected nonunion
bone fractures and they are famous for high • Malunion
incidence of open fractures.
• Shortening
Mechanism of Injury • Infection
• Compartmental syndromes
• RTA—37.5 percent
• Joint stiffness
• Sports—24.7 percent
• Refracture
• Assaults—4.5 percent
• Fat embolism
• Falls—rest.
• Claw toes—due to tethering of long
Classification extensors over callus.

Ellis classification INJURIES OF THE ANKLE

Grades of severity Features
I Minor • Undisplaced Mechanism of Injury
• Not angulated
• Minor comminution Ankles are usually injured due to low injury
• Minor open fracture rotational forces due to:
II Moderate • Total displacement
• Twisting injury while walking, running,
• Small degree of
sports, athletes, etc. are the most common
comminution
• Minor open wound mode of ankle injuries.

48
• Fall from a height: Ankle injuries are indirect
injuries here brought about by the displacing
talus.
Clinical Features
• History of inversion injury,
• Pain,
• Swelling,
• Deformity of the ankle.
• Movements are decreased,
• Drawer's test, inversion and eversion stress
tests may be positive.
Note the color and condition of the skin. Examine
the entire leg.
Investigations
• Anteroposterior, lateral and mortise non-
weight bearing views of the ankle are
recommended in the radiographs.
• CT scan, MRI and arthroscopy evaluation is
extremely helpful.
Treatment
Goals
• Anatomical positioning of the talus beneath
the tibia.
• To obtain a joint line that is parallel to the
ground.
• Smooth articular surface.
If these three things are not achieved,
posttraumatic osteoarthritis results.
Stable injuries: No reduction is required,
immobilization with only plaster splints till the
swelling decreases and then a below knee plaster
cast is applied with foot in neutral position.
Unstable injuries: Require reduction and
immobilization in plaster casts.
Complications of Ankle Fracture
• Posttraumatic arthritis,
• Reflex sympathetic dystrophy,
• Neurovascular injury (injury to posterior
tibial vessels and nerve),
• Nonunion (due to soft tissue interposition),
• Malunion.
49
 20.PELVIC INJURIES

FRACTURE PELVIS Clinical points: Milch signs

Destot’s sign: Large hematoma above inguinal

Stable Pelvic Fracture
These fractures do not involve the pelvic ring
and they are minimally displaced.
Unstable Pelvic Fracture
They involve the pelvic ring and are widely
displaced.
History
Pelvic fractures usually occur due to high-
velocity trauma following a road traffic accident
(RTA) or due to fall from a height.
The relative incidences are as follows:
• RTA—80.7 percent.
• Fall—16.1 percent.
• Compression fracture—rest.
Mechanism of Injury
ligament or scrotum.
Roux’s sign: Distance from greater trochanter to
pubic spine is increased on affected side.
Earle’s sign: On per rectal examination, the bony
prominence or a large hematoma can be palpated
Investigations
Radiography
Different radiographic views are recommended
to study the fracture configuration,
displacements, etc.
• Plain AP view.
• Oblique view—45° oblique projections.
• Internal and external rotation view.
• Inlet view—40° caudad view.
• Outlet view—40° cephalad view.

There are four mechanisms by which pelvic ring CT Scan

fractures are produced: Further radiographic studies include CT scans
and 3-dimensional imaging. This is the gold
• Lateral compression.
standard in the evaluation of pelvic fractures.
• Anteroposterior compression.
• Vertical shears forces. Management
• Inferior forces (e.g. fall on buttocks).
One should remember that pelvic fractures are
Classification usually due to high-velocity trauma and is
associated with multiple fractures and multiple
Broadly speaking, the pelvic fractures can be system injuries.
placed under two categories.
Resuscitation and correction of hypovolemic
• Fractures not Affecting the Integrity of the shock takes precedence over the management of
Pelvic Ring fracture per se. nevertheless, once the general
• Fractures Affecting the Integrity of the Pelvic condition is stabilized attention should be given
Ring to treat the fracture, which will prevent further
blood loss and damage to visceral organs.
Clinical Features
Symptoms Treatment Methods
The patient most often gives a history of high Initial treatment is carried out as follows:
velocity trauma and usually presents in a state of
hypovolaemic shock. Features of intra-abdominal • Resuscitation and other general measures, to
injuries and genitourinary injuries are frequently improve the general condition of the patient.
present. • Blood transfusion and other medical and
surgical emergency measures are carried out.
Clinical Tests
Avulsion fractures:
• Compression test
• Distraction test • Bed rest,
• Direct pressure test • Traction,

50
 • Physiotherapy Mechanism of Injury

Undisplaced fractures: The notorious incriminating forces that knock the

• Bed rest,
• Traction,
• Pelvic slings ,
• Nonsteroidal anti-inflammatory drugs
(NSAIDs).
Displaced fractures:
• Reduction by lateral compression methods
• Spica cast,
• Canvas sling or external fixators.
• Open reduction and external fixation (ORIF).
Complications
• Intra-abdominal haemorrhage
• Injuries of Lower Urinary Tract (All pelvic
fractures must be assumed to have urinary tract
injuries until proved otherwise.)
▪ Rupture of urethra and rupture of
urinary bladder.
Other Injuries
Testicular injuries and vaginal lacerations, bowel
and rectal injuries and urethral injuries are all
common and require immediate surgical
intervention.
hips out of its safe confines could arise from three
sources:
• The front part of the flexed knee striking
against an object (dash board events).
• From the sole of feet with the ipsilateral knee
extended.
• From the greater trochanter.
• Rarely it could be from the posterior pelvis.
• Left hip may develop a pure dislocation of
the hip since the left foot is on the clutch
with the hip and knee flexed at 90o.
• Right hip may develop a fracture dislocation,
because the right foot is either on the brake
or accelerator pedal with the hip in 60-70o of
flexion and slight abduction.
Classification
Depending upon the position of the head with
respect to the acetabulum, hip dislocations are
classified as:
• Posterior dislocations: Commonest and is seen
in 80-90 percent of the cases.
• Anterior dislocations: Seen in 10-15 percent.
• Central dislocations: Relatively rare.

Other Complications POSTERIOR HIP DISLOCATIONS

• Loss of reduction, Clinical Features

• Sepsis,
• Thrombophlebitis,
• Delayed union,
• Nonunion,
• Post-traumatic arthritis,
• Fat embolism,
• Major arterial injuries,
• abdominal wall injury,
• Neurological injuries.
DISLOCATIONS OF THE HIP JOINT
Causes
• High speed RTA’s.
• Violent falls from heights.
• Sports related injuries.
• Industrial accidents.
• Natural calamities, etc.
Note: Nearly 70-100 percent of the hip
dislocations are due to RTA.
• History of trauma
• Flexion, adduction and medial rotation
deformity of the affected limb.
• Marked shortening and gross restriction of
all hip movements.
• Head of the femur is felt as a hard mass in
the gluteal region and it moves along with
the femur.
• There could be features of sciatic nerve
palsy.
• It may be difficult to feel the femoral pulse
(Vascular sign of Narath is negative).
Investigations
Before Reduction
• Laboratory tests: Hb percent, BT, CT, Blood
group, RBS, etc. needs to be done as for any
other major surgery.
• Plain X-ray of the hip

51
 • What to look for in the initial X-ray:
• Are the femoral heads symmetric in size?
• Is the joint space symmetric throughout?
• Is the head large (anterior dislocation) or
small (posterior dislocation)?
• Is the Shenton’ line maintained or broken?
• Is the greater trochanter prominent
(posterior) or inconspicuous (anterior)
reverse with lesser trochanter?
• Is the femoral neck normal?
After Reduction
Plain X-ray of the hip
What to look for?
• Is there any incarcerated osteochondral
fragment within the joint?
• Is the joint space asymmetric?
• Look for the anterior and posterior ace
tabular wall.
• Look for any indentation on the femoral
head.
CT scan
CT Scan should be routinely done after a
successful or failed closed reduction. The
importance of CT lies in:
• Assessing the femoral head.
• To demonstrate the presence of small
intraarticular fragments.
• To assess the congruence of the femoral head
and acetabulum.
• Osteochondral fractures, occult impactions,
• indentations and other fractures are easily
seen on a CT.
MRI
As an adjunct to CT it helps to evaluate the
integrity of the labrum and assess the vascularity
of the femoral head.
Management
All hip dislocations are emergencies and need to
be reduced within 6-12 hours following injury to
prevent troublesome late complications like AVN
and traumatic degenerative hip. Once reduction
is done urgency is reduced and now the
diagnostic workup, CT scan and surgical
intervention if necessary can all be done once the
general condition of the patient is stabilized.
Goal of Treatment
Prompt reduction of the femoral head.
Types of reduction: This is either closed or open.
Postoperative Treatment
• Skeletal traction (10-15 lbs) with the hip in
slight abduction and extension.
• Within 3-5 days, gentle active and passive
exercises in traction are begun.
• Traction to be maintained for 6-8 weeks.
• Later protected weight bearing is allowed.
Complications
• Myositis ossificans (2%)
• Sciatic nerve injury
• Traumatic osteoarthritis due to avascular
necrosis (35%)
• Recurrent dislocation
• Unreduced dislocation
• Irreducible dislocation (31%)
52
 21.CHEST/RIB FRACTURES
These are relatively rare injuries and are usually
due to direct trauma. The rib usually breaks at
the angle, which is a point of maximum
convexity.
Clinical features
The patient complains of pain in the affected
region and has difficulty in breathing. He also
complain inability to sleep on the affected side or
lift weights and has difficulty in traveling or
carrying out his day-to-day activities.
Radiology
Plain X-ray of the chest helps to detect the rib
fractures with reasonable accuracy.
Principles of Treatment
It is essentially conservative. Intercostal muscles
provide natural immobilization to the fractured
ribs and hence no aggressive management is
required.
Conservative Measures
Strapping, ultrasound or TENS, etc. are effective
in reducing the pain. Occasionally, a local
infiltration of hydrocortisone helps. Very rarely,
the fracture fragments may pierce the pleura
causing pneumothorax, hemothorax, etc. These
are dangerous injuries and needs to be managed
aggressively.
Chest physiotherapy: This essentially consists of
deep breathing exercises, which are progressively
made more vigorous to improve the mobility of
the thorax.
53
 22.ABDOMINAL AND INTRA-ABDOMINAL INJURIES
General Clinical Features
✓ Features of shock—pallor, tachycardia,
hypo tension, cold periphery, sweating,
oliguria.
✓ Abdominal distension.
✓ Pain, tenderness, rebound tenderness,
guarding and rigidity, dullness in the
flank on percussion.
✓ Respiratory distress, cyanosis depending
on the amount of blood loss.
✓ Bruising over the skin of the abdominal
wall (London’s sign).
✓ Features specific of individual organ
injuries.
Investigations
1. Ultrasound abdomen. FAST is Focused
Abdominal Sonar Trauma. It is not reliable for
bowel or penetrating injuries. It often needs to be
repeated.
2. Diagnostic peritoneal lavage (DPL)
It has got 98% accuracy rate.
It is the procedure of choice in physiologically
unstable patient with blunt abdominal injury
(like with spinal injury, unconscious patient).
3. CT scan is indicated in assessing
retroperitoneum, solid organ injuries. It is
noninvasive and highly specific.
4. Diagnostic laparoscopy (DL) is valuable
method in stable abdominal trauma patient.
Classification of abdominal trauma
For the sake of evaluation and management,
abdominal trauma is divided into penetrating
and blunt trauma based on the mechanism of
injury.
PENETRATING TRAUMA
Penetrating trauma is further differentiated into
gunshot wounds and stab wounds as the pattern
of injury based on mechanism is quite different.
• Gunshot wounds to the abdomen require
exploratory laparotomy for evaluation and
possible repair of intra-abdominal injuries, not to
“remove the bullet.” Any entrance or exit wound
below the level of the nipple line is considered to
involve the abdomen.
• Stab wounds allow a more individualized
approach. If it is clear that penetration has
occurred, e.g. protruding viscera, exploratory
laparotomy is mandatory.
• The same is true if hemodynamic instability or
signs of peritoneal irritation develop.
In the absence of the above, local wound
exploration may be performed in the emergence
department to assess whether or not the anterior
rectus fascia has been penetrated.
• If the fascia is not violated, the intra-abdominal
cavity likely has not been penetrated and no
further intervention is necessary.
• If the fascia has been violated, surgical
exploration is indicated to evaluate for bowel or
vascular injury, even in the setting of
hemodynamic stability and lack of peritoneal
findings on physical examination. If there is any
question, perform CT.
BLUNT TRAUMA
Blunt trauma to the abdomen with obvious signs
of internal injury requires emergent surgical
evaluation via exploratory laparotomy.
The occurrence of blunt trauma even without
obvious signs of internal injury requires further
evaluation because internal hemorrhage or bowel
injury can be slow and therefore present in a
delayed fashion.
Signs of internal bleeding include:
• A drop in BP,
• A fast and/or thready pulse,
• A low CVP, and
• Low urinary output.
Patients tend to be cold, pale, anxious, shivering,
thirsty, and perspiring profusely. These signs of
shock occur when 25–30% of blood volume is
acutely lost, ~1,500 ml in the average-size adult.
There are few places in the body that this volume
of blood can be lost without being obvious on
physical or radiographic exam.
That leaves the abdomen, retroperitoneum,
thighs (secondary to a femur fracture), and pelvis
as the only places where a volume of blood
significant enough to cause shock could “hide” in
54
a blunt trauma patient that has become unstable.
The femurs and pelvis are always checked for
fractures in the initial survey of the trauma
patient by physical exam and pelvic x-ray.
So a patient who has experienced blunt trauma
who has become hemodynamically unstable with
normal chest and pelvic x-rays likely has intra-
abdominal bleeding.
Diagnosis can be quickly utilizing the “FAST”
exam: Focused Abdominal Sonography for
Trauma.
Bedside U/S evaluates the perihepatic space,
perisplenic space, pelvis, and pericardium for
free fluid.
• A stable patient in whom the diagnosis is less
definite should be taken for a more definitive
study, i.e., CT scan.
The abdominal compartment syndrome
The abdominal compartment syndrome is when
the pressure in the peritoneal cavity is elevated
and leads to end-organ injury. This occurs when
a significant amount of fluid is administered in
an effort to resuscitate a patient in hypovolemic
shock. Bowel edema develops, increasing intra-
abdominal pressure, which is detrimental for
several reasons.
• First, the elevated pressure leads to
decreased perfusion pressure to the viscera,
contributing to acute kidney injury and
possibly bowel and hepatic ischemia.
• Second, the upward pressure of the viscera
on the diaphragm prevents adequate
expansion of the lungs and ventilation,
contributing to respiratory failure.
• Therefore, if bowel edema is observed or
intra-abdominal pressure is elevated
following surgical exploration, the abdomen
is not closed, rather left open.
• Similarly, if a patient is not surgically
explored but undergoes a significant volume
resuscitation and abdominal compartment
syndrome develops, a decompressive
laparotomy may be indicated. Incidentally,
this can occur in non-trauma scenarios
requiring massive fluid resuscitation, most
notable severe pancreatitis.
A ruptured spleen
A ruptured spleen is the most common source of
significant intra-abdominal bleeding in blunt
abdominal trauma. Given the limited function of
the spleen in the adult, a splenic injury resulting
in hemodynamic instability or requiring
significant blood product transfusion is an
indication for splenectomy. Post-operative
immunization against encapsulated bacteria is
mandatory (Pneumococcus, Haemophilus
influenza B, and meningococcus).
Management Concepts in Abdominal Trauma
1. Resuscitate patient and perform primary
and secondary surveys
2. Deal with abdominal injury:
✓ Unstable patient: surgery
✓ Stable patient: ultrasound, CT, peritoneal
lavage, diagnostic laparoscopy, then
surgery if indicated
3. Antibiotics: give aerobic and anaerobic
cover.
55
 23. CHEST INJURIES

Chest injuries are common in civilian life, ✓ U/S abdomen to look for associated
although the overall mortality is usually less than abdominal injuries. FAST (Focused
10%. Many of the patients who die following abdominal sonar trauma).
thoracic trauma do so after reaching hospital, in ✓ CT chest and CT abdomen.
the so-called ‘golden hour, indicating that the
majority of chest problems are under the Treatment
treatable umbrella of most doctors. Initial First Aid

Causes a) Airway: Prevention of aspiration, plastic

airway, intubation, tracheostomy.
• Road traffic accidents. b) Breathing: ICT placement, supportive
• Industrial accidents. measures.
• Blast injuries. c) Circulation: Fluid therapy, CVP line, blood
• Crush injuries. transfusion.
• Stab injuries. d) Look for disability.
• In children, ribs are malleable and so fracture e) Expose the patient properly for proper
breathing and assisting.
ribs are rare.
f) Assess the patient properly.
• In elderly because of rigid ribs fracture is
g) Examine the patient thoroughly.
common.
h) Evaluate the patient for associated injuries
• First and second ribs are protected by like of head, abdomen, fracture limbs, spine.
clavicle and so their fracture is uncommon.
• 11th and 12th ribs are floating ribs and so Further Treatment
their fracture is rare. • Fracture rib without complication is treated
Clinical Features of Chest Injuries with analgesics and rest.
• Haemothorax, pneumothorax should be
• History of trauma, painful breathing, cough,
treated with inter-costal tube drainage (ICT)
haemoptysis, pain in the chest wall,
with underwater seal.
sometimes external wound may be present
• Flail segment should be treated accordingly.
(in communicating wounds).
• Blood transfusion is done whenever
• Features of shock when major vessels are
required.
involved, i.e. tachycardia, hypotension, cold
• Antibiotics like penicillin, cefotaxime, etc. to
periphery.
prevent infection.
• Respiratory distress—tachypnoea, cyanosis,
• Nasal oxygen, throat suction.
respiratory difficulties.
• Ventilator support with IPPV (Intermittent
• Tenderness over the fracture site.
positive pressure ventilation), with regular
• Dullness on percussion with decreased
monitoring of blood gas.
breath sounds signifies haemothorax.
• Tracheostomy/endotracheal intubation is
Resonant with decreased breath sound
done whenever required.
confirms pneumothorax.
• Antibiotics, bronchodilators, often steroids
• Surgical emphysema with palpable crepitus
are other supportive measures required.
may be present.
Principles of Management of Chest Injuries
Investigations
• Pulmonary physiotherapy.
✓ Chest X-ray shows haemothorax,
• Aspiration of secretions—trachea,
pneumothorax, fracture ribs.
nasotracheal, oral, pharyngeal.
✓ Hb%, PCV to assess blood loss.
• Pain relief—oral narcotics, intercostal nerve
✓ Blood grouping and cross matching.
block, epidural anaesthesia.
✓ Blood gas analysis, i.e. PO2 and PCO2.

56
 • Respiratory supports—encourage coughing,
chest percussion, deep inspiration efforts,
humidification, mobilisation.
• ICT placement for haemo/pneumothorax.
• Management of shock.
• Focused abdominal sonography on trauma
(FAST).
• Surgery when indicated—thoracotomy and
proceed.
• Management of complications—DVT and
embolism, tracheostomy problems, ICT
problems, sepsis, ARDS, empyema
treatment, bronchopleural fistula, bronchial
stenosis, chylothorax, clotted haemothorax,
atelectasis.
Complications
✓ Infections—empyema, lung abscess,
pneumonia, septicaemia.
✓ Respiratory failure.
✓ Traumatic asphyxia.
✓ Traumatic shock lung.
✓ Disseminated intravascular coagulation (DIC).
✓ ARDS (Adult respiratory distress syndrome).
HAEMOTHORAX
It is blood in pleural cavity. It causes pain, shock,
as it is very irritant to pleural cavity.
It is a good culture media for bacteria and so
infection is quite common.
Causes
• Trauma.
• Postoperative: pulmonary, cardiac,
oesophageal surgeries, cervical
sympathectomy, leak from CVP monitor
line.
• Tumours of lung, mediastinum, pleura.
• Leaking aneurysms.
• Spontaneous.
There may be rib fractures in traumatic haemo
thorax.
Investigations
• Chest X-ray.
• Aspiration (pleural tap).
• Chest CT scan.
Treatment
1. ICT placement in the mid-axillary line in
the 6th intercostal space.
2. Antibiotics, bronchodilators.
3. Thoracotomy
SIMPLE PNEUMOTHORAX
Simple pneumothorax results from penetrating
trauma such as a weapon or the jagged edge of a
fractured rib.
There is typically moderate shortness of breath
with absence of unilateral breath sounds and
hyperresonance to percussion.
Diagnosis is confirmed with chest x-ray and
management consists of chest tube placement.
TENSION PNEUMOTHORAX
✓ During inspiration, air is pumped into the
pleural cavity through a valvular opening in
the visceral pleura and underlying injured
lung.
✓ Lung collapses first, and as air continuously
collects in the pleural cavity, mediastinum
shifts towards the opposite side, further
decreasing the volume of the functioning
lung.
✓ Further increase in the pleural pressure,
reduces the venous return, atrial filling, and
ventricular filling and so cardiac output and
cardiac function.
Management
✓ Once clinically diagnosed, a wide bore
needle is immediately placed in the second
intercostal space in midclavicular line, and a
sterile glove is kept on the hub (blunt) end of
the needle to create a valve so as to prevent
inward sucking of air from outside.
✓ Nasal oxygen is used.
✓ Once patient is better, chest X-ray is done.
✓ Later an intercostal tube is passed.
✓ Antibiotic, analgesics are given.
✓ In severe cases ventilator support with IPPV
is required.
FLAIL CHEST
Flail chest occurs with multiple rib fractures that
allow a segment of the chest wall to cave in
57
during inspiration and bulge out during
expiration (paradoxical breathing). The real
problem is the underlying pulmonary contusion.
Contused lung is very sensitive to fluid overload.
Pulmonary dysfunction may develop, thus serial
chest x-rays and arterial blood gases have to be
monitored.
Treatment includes:
➢ Fluid restriction,
➢ Strapping of flail segment,
➢ Positive pressure ventilation and
➢ Pain management.
BLUNT CARDIAC INJURY
Blunt cardiac injury should be suspected with the
presence of sternal fractures. ECG monitoring
will detect any abnormalities. Although serum
troponin level was historically obtained,
elevations do not generally change management
and are therefore not indicated, as treatment is
focused on the complications of the injury such
as arrhythmias.
TRAUMATIC RUPTURE OF THE
DIAPHRAGM
Traumatic rupture of the diaphragm shows up
with bowel in the chest (by physical exam and x-
rays), almost always on the left side (the liver
protects the right hemidiaphragm). All
suspicious cases should be evaluated with
laparoscopy. Surgical repair is typically done
from the abdomen.
RUPTURE OF THE AORTA
Traumatic rupture of the aorta is the ultimate
“hidden injury.” It most commonly occurs at the
junction of the arch and the descending aorta
where the relatively mobile aorta is tethered by
the ligamentum arteriosum. Such an injury
requires a significant deceleration injury and is
totally asymptomatic until the hematoma
contained by the adventitia ruptures resulting in
rapid death. Suspicion should be triggered by
one of the following:
✓ Mechanism of injury
✓ Widened mediastinum on chest x-ray
✓ Presence of atypical fractures such as the
first rib, scapula, or sternum, which
requires great force to fracture
Diagnosis is made with CT angiogram. Surgical
repair is indicated once the patient has been
stabilized and more immediate live-threatening
injuries have been managed.
RUPTURE OF THE TRACHEA
Traumatic rupture of the trachea or major
bronchus is suggested by developing
subcutaneous emphysema in the upper chest and
lower neck, or by a large “air leak” from a chest
tube.
Chest x-ray and CT scan confirm the presence of
air outside the bronchopulmonary tree, and
fiberoptic bronchoscopy is necessary to identify
the injury and allow intubation past the injury to
secure an airway. Surgical repair is indicated
Differential diagnosis
✓ Subcutaneous emphysema
✓ Rupture of the esophagus and
✓ Tension pneumothorax.
CARDIAC TAMPONADE
Cardiac tamponade is the accumulation of fluid
in the pericardial sac, which restricts the filling
and contraction of the heart and leads to shock. If
this fluid is blood, it can come from disruption of
the great vessels or the heart itself, most
commonly as a result of penetrating injuries,
although severe blunt trauma can also be a cause.
As little as 20 mL of blood can cause symptoms.
Clinical features
The three classic diagnostic features of cardiac
tamponade namely elevation of jugular venous
pressure (JVP), decline in blood pressure and
muffled heart sounds (known as Beck’s triad).
Additionally, the patient may demonstrate
pulsus paradoxus and a rise in venous pressure
with inspiration (also known as Kussmaul’s
sign).
Investigation
Chest X-ray and U/S confirms the diagnosis.
Treatment
58
 ➢ Pericardial tap, as early as possible to allow
heart to expand adequately.
➢ Occasionally, open pericardiotomy is
required.
OESOPHAGEAL DISRUPTION
The oesophagus is most commonly traumatized
by penetrating trauma. However, the oesophagus
can tear due to forceful expulsion of contents
from the stomach during huge impacts. This
causes gastric contents and air to leak into the
mediastinum, resulting in mediastinitis and air in
the subcutaneous tissues of the neck, recognized
as surgical emphysema. Patients may also
develop a pneumothorax, usually more common
on the left than the right.
The diagnosis is confirmed when particulate
gastric matter is recovered from the chest tube.
Prompt diagnosis and repair produce the best
results in these patients.
59
 24.HEAD INJURIES
HEAD INJURY
The causes of head injury are many and varied,
although it is common to see ‘head injury’ as the
only description of the incident in hospital notes.
Every effort must be made to discover its
underlying cause, paying particular attention to:
• the likely speed of impact;
• any events that may have led to the injury
(e.g. epilepsy, subarachnoid haemorrhage,
alcohol consumption);
• any events after its occurrence (e.g.
vomiting, epilepsy, talking).
Pathophysiology
The brain within the skull is liable to injury when
deceleration occurs, i.e. when the neck flexes,
extends or rotates.
As the brain moves within the cranial cavity, it
may strike sharp objects such as the sphenoid
wing and the frontal and occipital poles. In
addition, points where the brain is tethered, such
as the foramen magnum and the cranial nerves,
are also potential sites of injury. Shaking of the
brain when the skull moves at high speed
therefore results in haemorrhage in the
subarachnoid space and at the frontal, temporal
and occipital poles and in tearing of nerves and
vessels. This damage can occur without the head
being struck, for example in a high-speed car
crash or in a fall from a height in which the body
decelerates rapidly. It may also be associated
with direct damage from a blow or a penetrating
wound.
Primary damage
Damage that occurs to the brain immediately as
the result of the trauma
• Diffuse neuronal damage
• Shearing lesions
• Contusions
• Lacerations
Damage from Cerebral concussion
• Temporary physiological paralysis of
nervous system
• Loss of consciousness
• Post-traumatic amnesia
• Full recovery is expected
• Residual complications may develop
Secondary damage
Primary damage can be exacerbated by
secondary damage (i.e. further insults to the
damaged brain).
The main secondary effects are:
• Respiratory complications,
• Perfusion failure,
• Intracranial haematoma,
• Cerebral swelling,
• Epilepsy,
• Infection
• Hydrocephalus.
• CSF rhinorrhoea or CSF otorrhoea.
• Brain herniation
Cause of death in head injury
• Brain hypoxia
• Coning
• Diffuse severe irreversible neuronal injury
• Death may be due to other injuries like
abdominal/thoracic
• Metabolic changes
• Aspiration in unconscious patient.
Clinical features
• Temporary physiological paralysis of
nervous system, Loss of consciousness, Post-
traumatic amnesia indicate concussion.
• Headache, nausea, vomiting, a falling pulse
rate and rising blood pressure indicate
cerebral oedema
• Pupillary inequalities or abnormal light
reflex indicate intracranial haemorrhage
Other features
• CSF leak or bleeding from nose
• Blood collection in the orbit
• Black eye
• Battle’s sign—ecchymosis over the mastoid
• Haematoma of scalp
• Panda sign—bilateral black eye
Clinical Approach of a Patient with Head Injury
1. Detail history of injury has to be taken and also
the process of deterioration—rapid or gradual.
60
2. History of alcohol intake: Alcohol intake
mimics head injury and alcoholism itself may
mask the features of head injury.
3. Neurological assessment: By
• Level of consciousness
• Glasgow coma scale
• Pupillary reaction to light and size
• Pulse
• Temperature
• Blood pressure
• Respiratory rate
• Reflexes
• Limb movements—normal/mild weakness/
severe weakness/spastic
flexion/extension/no response
4. Status and protection of airway.
5. General assessment and other injuries like
fractures, abdominal organ injuries, thoracic
injuries are looked for.
6. Presence of any scalp haematoma, fractures of
skull bone which may be depressed has to be
looked for.
7. Any blood from nose or ear, CSF rhinorrhoea
or CSF otorrhoea has to be looked for.
Investigations
• X-ray skull: To look for fracture, relative
position of the calcified pineal gland,
presence of intra cranial air.
• Serum electrolyte measurement.
• Blood grouping and cross matching.
• CT scan: Plain (not contrast) to look for
cerebral oedema, haematomas, midline shift,
fractures, ventricles, brainstem injury.
• Carotid arteriography.
• Investigations for other injuries like
ultrasound of abdomen.
• Monitoring of intracranial pressure.
Treatment
General
• Protection of airway using mouth gag, endo
tracheal intubation or tracheostomy,
whenever required.
• Throat suction, bladder and bowel care and
good nursing are very essential.
• Nasal oxygen, or often ventilator support.
• IV fluids initially, later Ryle’s tube feeding
has to be done.
• Electrolyte maintenance.

Glasgow Coma Scale/Adelaide Coma Scale Drugs

(children)
Adults Infants/childre • Sedation is avoided.
n • Analgesics and anticonvulsants like
Eye 4 Spontaneous Spontaneous phenytoin or phenobarbitone is started.
openi 3 To voice To voice
ng • Diuretics are given to reduce cerebral
2 To pain To pain
1 None None oedema—either mannitol 20%, 200 ml IV 8th
Verbal 5 Oriented Alert, normal hourly or frusemide 40 mg IV 8th hourly. It
vocalization should not be given in case of intracranial
4 Confused Cries, but
haematoma.
consolable
3 Inappropriate Persistently • Antibiotics like penicillins, ampicillins are
words irritable given to prevent the onset of meningitis.
2 Incomprehensib Restless, • Corticosteroids, either dexamethasone or
le words agitated,
moaning betamethasone is used commonly, but its
1 None None beneficial effect is not confirmed.
Motor 6 Obeys Spontaneous,
respo commands purposeful Indications for surgery
nse 5 Localizes pain Localizes pain
• Acute extradural haematoma.
4 Withdraws Withdraws
3 Abnormal Abnormal • Acute subdural haematoma.
flexion flexion • Depressed skull fracture.
2 Abnormal Abnormal
extension extension Complications of Head Injuries
1 None None
Total score-15 • Brainstem injury—due to coning.
Mild head injury: score 13-15 • Compression over cerebellum and medulla.
Moderate head injury: 9-12
Severe head injury: less than 8 (3-8)

61
 • CSF rhinorrhoea: Due to communication
between intracranial cavity and the nose.
Meningitis is the common complication of CSF
rhinorrhoea.
EXTRADURAL HAEMATOMA
• It is collection of blood in the extradural
space between the dura and skull.
• Most common site is temporoparietal region. It
can be unilateral or bilateral.
Usually, it is associated with fracture of
temporoparietal region.
Pathology
Immediately after injury, there is transient loss of
conscious-ness and the patient soon becomes
normal. Later after 6-12 hours, he again falls ill
and the condition deteriorates.
This is the time taken to develop raised
intracranial pressure, coning and its effects. This
crucial time gap which is unnoticed and often
missed is called as “ lucid interval”.
Clinical Features
• History of transient loss of consciousness
following a H/o blow or fall.
• Patient soon regains consciousness and again
after 6-12 hr starts deteriorating (Lucid
interval).
• Later the patient presents with confusion,
irritability, drowsiness, hemiparesis on same
side of the injury. Initially pupillary
constriction and later pupillary dilatation
occurs on the same side, finally becomes
totally unconscious – Hutchinsonian pupils.
• Death can occur if immediate surgical
intervention is not done.
• Features of raised intracranial pressure like
high blood pressure, bradycardia, vomiting
is also seen. Occasionally convulsions may
be present.
• Wound and haematoma in the temporal
region of scalp may be seen.
Investigations
• X-ray skull may show fracture of temporal
bone.
• Electrolyte estimation.
• CT scan head is diagnostic. Extradural
haematoma shows biconvex lesion.
Treatment
• Immediate surgical intervention is a must to
save the life of the patient.
• Craniotomy is done and cranial flaps are
raised. The dura is opened and the clot is
evacuated.
• Antibiotics and anticonvulsants are given
postoperatively.
• Analgesics
• General measures—catheter; fluid therapy
• Prevention post-traumatic complications
Complications
• Post-traumatic epilepsy
• Meningitis
• Post-traumatic amnesia
SUBDURAL HAEMATOMA
Types
• Acute
• Chronic
Acute Subdural Haematoma
• It is a collection of blood between the brain
and dura. It is due to injury to the cortical
veins and often due to laceration of cortex of
brain which bleeds and blood gets collected
in the subdural space forming a haematoma.
• Here haematoma is extensive and diffuse.
There is no lucid interval. There is severe
primary brain damage.
• Haematoma may be of coup and contre-coup
type.
• Loss of consciousness occurs immediately
after trauma and is progressive.
• Convulsion is common.
• Features of raised intracranial pressure is
obviously seen—high BP, bradycardia,
vomiting.
• Focal neurological deficits or hemiparesis
can occur.
• CT scan shows concavo-convex lesion.
Treatment
• Antibiotics, anticonvulsants.
• Surgical decompression is done by
craniotomy.
Chronic Subdural Haematoma
62
It is due to the rupture of veins between dura
and brain (cerebral hemispheres), causing
gradual collection of blood in subdural space.
Clinical Features
• Common in old age, with history of minor
trauma.
• Patient presents with confusion,
disorientation, gradually with altered level
of consciousness and drowsiness.
• Later convulsions, features of intracranial
hyper tension, features of coning develops.
• Extensor plantar response and pupillary
changes develop eventually.
Investigations
• CT scan (shows concavo-convex lesion).
• Serum electrolytes.
• Blood grouping and cross matching.
Differential Diagnosis
• Electrolyte imbalance.
• Intracranial space occupying lesion.
Treatment
• Craniotomy and evacuation of clot is done
when required on both sides.
• Antibiotics.
• Anticonvulsants for 3 years.
Complications
• Epilepsy
• Meningitis
• Coning
• Neurological deficits
SUBARACHNOID HAEMORRHAGE
(SAH)
It is a type of intracranial haemorrhage into the
subarachnoid space usually from basal cisterns.
It may be spontaneous or following trauma.
Causes
• Intracranial aneurysms—commonest cause
(50%)
• Hypertension
• A-V malformations
• Blood dyscrasias
• Anticoagulant drugs
• Brain tumours (malignant)
Clinical Features
• Sudden onset of severe headache with
vomiting.
• Features of raised intracranial pressure.
• Photophobia.
• Neck stiffness.
• Focal neurological deficits: hemiplegia,
dysphasia.
• Eye changes: ptosis, dilated pupil, changes in
the eyeball movements.
• Sudden loss of consciousness.
• Features of brain oedema and cerebral
ischaemia. In 40% of recovered patients,
rebleeding occurs in 6-8 weeks which is
commonly fatal.
Differential Diagnosis
• Meningitis.
• Coning due to any cause.
Investigations
• Lumbar puncture should be done to
differentiate from meningitis.
✓ It has to be done carefully as it may
precipitate coning.
✓ In subarachnoid haemorrhage, blood-
stained CSF is collected.
• CT scan.
• Carotid and vertebral angiogram.
RAISED INTRACRANIAL PRESSURE
ICP normally varies between 4 and 14 mmHg.
Sustained ICP levels above 20 mmHg can injure
the brain.
Increased ICP can injure the brain in several
ways.
Clinical features
• Headache,
• Nausea,
• Vomiting,
• Progressive mental status decline.
• Cushing’s triad is the classic presentation of
intracranial hypertension, bradycardia, and
irregular respirations.
63
 • Focal neurologic deficits such as 1. Airway protection and adequate ventilation
hemiparesis may be present if there is a
2. A bolus of mannitol up to 1 g/kg causes
focal mass lesion causing the problem.
free water diuresis, increased serum
Investigations osmolality, and extraction of water from the
brain
Head CT and rapid neurosurgical evaluation.

Management

64
 25.INJURIES OF THE SPINE

Incidence of Spine Injuries • Prevent further neurological damage.

• Aid neurological recovery.
• Male: Female = 4: 1
• Obtain and maintain spinal stability.
• Injury is common at the cervicothoracic and
• Aim at early functional recovery.
thoracolumbar regions
• Modes of injury: Treatment methods
–RTA—45 percent. At the Accident Site
–Falls—20 percent.
Resuscitation and transport is important. All
–Sports injuries (diving)—15 percent.
unnecessary neck movements should be totally
–Acts of violence—15 percent
avoided. If the patient needs resuscitation, it has
INJURIES OF THE CERVICAL SPINE to be carried out with a lot of care.

At the Hospital
Causes
Nonoperative treatment: Most cases can be
• Fall from height
treated nonoperatively by halo vest, four post-
• Diving injuries cervical collars, Minerva jacket, cervical collars,
• Road traffic accidents (RTAs etc.
• Gunshot injuries, etc
Surgical Treatment
Mechanism of Injury
Indications: Unstable injuries with or without
• Pure flexion force neurological damage require surgery.
• Flexion rotation force
• Axial compression • OR+IF
• Extension force THORACIC AND LUMBOSACRAL
• Lateral flexion
• Direct injuries SPINE INJURIES

Clinical Features Mechanism of Injury

Symptoms
• Fall from a height.
• Upper neck pain that becomes worse with • RTA: Seat belt injury (chance fracture).
movement. • Other causes like gunshot injuries, assault,
• Occipital headache. etc.
• Neck stiffness.
Clinical Features
• Rarely vertigo, auditory or visual
disturbances, etc. • History of trauma due to RTA or fall from a
height
Signs
• Pain;
• Decreased range of neck movements. • Posterior swelling,
• Neck muscle spasm is seen. • Tenderness,
• Palpable interspinous gap
Investigations
• Neurological involvement: paraplegia or
• Radiography signs of individual nerve root involvement.
• Myelography • Spinal shock is present for 24 hours during
• CT Scan which all the reflexes are lost.
• MRI • Cauda equina paralysis is present if the
Treatment lesion is below L1.
Goals of treatment of cervical spine injury • Exaggerated lumbar lordosis in old cases.

• Realign the spine.

65
Investigations
• Radiography of the affected spine this is the
preliminary investigation and all three views
(AP, lateral and oblique) are taken.
• MRI
• CT scan.
Management
This is discussed under two heads.
1. Management at the site of accident
Consider all patients with spine injury to have
neurological damage, shift them to the hospital
with utmost care, and caution avoiding all
unnecessary movements.
2. Definitive treatment at the hospital
• Practice: Caution in handling the neck.
• Examination: The general condition and
other systems like CNS/CVS/RS/PA/GI
tract, etc. Also, examine from head to toe, the
presence of other fractures, head, chest
injuries, blunt injury abdomen and pelvic
fractures.
• Evaluate: The spine injury by gentle careful
clinical examination. This has to be
supplemented by proper investigations like
X-ray, CT-scan, MRI, etc.
• Assess: Carefully assess the level and extent
of neurological damage by examining the
dermatome, myotome and reflexes.
For stable fracture without neurological deficit:
Treatment:
• Bed rest,
• NSAIDs and
• External spine supports like brace, corsets,
etc
For stable fracture with neural deficit
If neurological damage is incomplete,
• IV steroids are given for 4 days.
• Anterior decompression and anterior
interbody fusion is done in the first stage,
followed by posterior segmental spinal
stabilization.
Unstable fracture without neurological deficit
• This is best treated by early open reduction,
internal fixation and fusion is done
preferably within 12-24 hours. It is done with
spinal cord monitoring.
Unstable fracture with neurological deficit
• Decadron 4-6 mg/every 6 hours IV for 3
days
• Early open reduction and internal fixation
and fusion
66
 26.SPINAL CORD INJURY

Spinal cord could be damaged due to injuries of 3. Bowel program.

spine extending from cervical vertebrae to the
thoraco-lumbar junction. Below this, the cord • Reflex emptying of the bowel with
ends and the cauda equina begin. suppository stimulation is the goal of bowel
training.
Pathology • Family education
The pathology may vary from extradural • Physical therapy
hemorrhage to cord concussion, laceration to • Occupational therapy
cord crushing. • Social therapy.

Clinical Classification of Neurological Damage CAUDA EQUINA SYNDROME

• Complete paralysis. Cauda equina syndrome is seen in injuries below
the level of first lumbar vertebra.
• Sensory paralysis.
It is essentially injury to the nerve roots below L1.
• Motor paralysis useless.
Causes
• Motor paralysis useful.
• Tumors of the spine.
• Recovery.
• Pott’s disease.
Clinical Assessment
• Protrusion of disk—large midline disk
General examination: This consists of
prolapse at 4-5.
examination of the head, chest, pelvis and other
systems for incidence of injuries and recording • Fracture dislocation of the thoracolumbar
the vital statistics. spine.
Neurological examination: Examine the level of Clinical Features
the vertebral injury and find out the level of the Symptoms
corresponding cord injury.
• Back pain,
Investigations • Perineal pain,
• This consists of plain radiograph of the • Difficulty in micturition,
affected part. • Impotence in male, etc.
Sensory signs: area of saddle-shaped
• MRI and CT scan
hyperesthesia and later anesthesia (involving
Treatment buttocks, anus and perineum).

•First aid as already discussed. Motor signs: Flaccid paralysis below the knee.

•Management of vertebral fracture and
dislocations.
•Rehabilitation programs in neurological injury
following spinal fracture are as follows:
1. Paralyzed Bladder
• Urinary retention catheter is placed in the
bladder for 24-48 hours.
• After 48 hours, intermittent catheterization is
started, to develop the automatic reflex
emptying of the bladder.
2. Bedsore management
Reflexes: Ankle jerk is lost and the knee jerk is
increased due to the weakness of the opposing
hamstrings.
Bladder symptoms: retention of urine with
overflow.
Anal sphincter relaxation: leading to
incontinence of the bowels.
Investigations
Plain X-ray, CT scan, MRI of the affected part.
Treatment

67
Prompt surgical intervention is the treatment of
choice. This consists of operative stabilization of
the fractures, bowel, back and bladder care and
other rehabilitating measures.
SPINAL SHOCK
A state of “spinal shock”, i.e. temporary electrical
dysfunction.
Features
• Sensory loss.
• Flaccid paralysis.
• Visceral paralysis.
• Reflexes are in abeyance.
• Anal reflex lost (anal wink lost).
Usually
• Eight hours later concussion regresses.
• Seven to ten days later complete recovery. If
the reflexes, do not return within 24 hours
to 10 days a diagnosis of complete cord
transection is made.
NERVE HEALING
Nerve injuries are very common Peripheral
nerves are a complex arrangement of axons,
nonneuronal cells, and extracellular elements.
There are three types of nerve injuries:
• Neurapraxia (focal demyelination),
• Axonotmesis (interruption of axonal
continuity but preservation of schwann cell
basal lamina), and
• Neurotmesis (complete transection).
Nerve healing stages:
(a) Survival of axonal cell bodies;
(b) Regeneration of axons that grow across the
transected nerve to reach the distal stump;
and
(c) Migration and connection of the
regenerating nerve ends to the appropriate
nerve ends or organ targets.
Several factors play a role in nerve healing, such
as growth factors, cell adhesion molecules, and
nonneuronal cells and receptors. Growth factors
include nerve growth factor, brain-derived
neurotrophic factor, basic and acidic fibroblastic
growth factors, and neuroleukin.
68
 28.SURGICAL INFECTIONS
CELLULITIS
Cellulitis is defined as an infection of the
subcutaneous tissues. Two distinct types are
recognized.
Acute pyogenic cellulitis
Acute pyogenic cellulitis is the common type of
cellulitis and is caused by Streptococcus
pyogenes.
It is characterized by a dark-red skin
discoloration, heat and oedema and is often
associated with lymphangitis and
lymphadenopathy (see earlier).
The most virulent form of this streptococcal
infection is called erysipelas, which most
frequently affects the face, producing a
characteristic butterfly erythema. Erysipelas is a
rarely seen condition today.
Treatment
• Immobilization,
• Elevation of the affected part
• Intravenous antibiotics (penicillin or
erythromycin).
Anaerobic cellulitis
This type of cellulitis is much more sinister and
fortunately rare. It is known as the ‘flesh-eating’
infection (Meleney’s gangrene) and is caused not
by a single organism but by a combination of
aerobes (Streptococcus pyogenes, Staphylococcus
aureus, Escherichia coli, Proteus, Klebsiella,
Pseudomonas aeruginosa) and anaerobes
(Bacteroides, anaerobic cocci, Clostridium). These
act synergistically to cause extensive tissue
destruction and death.
Two clinical syndromes are recognized in this
type of infection.
• Progressive bacterial synergistic gangrene.
• Necrotizing fasciitis
Treatment
• Surgery to remove the necrotic tissue,
• Appropriate antibiotics depending on
sensitivity.
• Systemic support in an intensive care unit
The mortality from anaerobic cellulitis is high.
ERYSIPELAS
It is a spreading inflammation of the skin and
subcutaneous tissues due to infection caused by
Streptococcus pyogenes.
Sites
• Orbit, face and ear lobule—most common.
• Hands and scrotum.
• Umbilicus in infants.
• Decubitus ulcer of lower limb occasionally.
Clinical Features
• Toxaemia is always a feature.
• Rash is fast spreading and blanches on
pressure.
• Rash is raised with sharp margin.
• Redness becomes brown and later yellow
with vesicles.
• Discharge is serous (In cellulitis discharge is
purulent).
• In the face and orbit it causes severe oedema.
• Milian’s ear sign is a clinical sign used to
differentiate erysipelas from cellulitis
wherein ear lobule is spared. Skin of ear
lobule is adherent to the subcutaneus tissue
and so cellulitis cannot occur. Erysipelas
being a cutaneous condition can spread into
the ear lobule
• Disease is common in poorly hygienic
debilitated individuals.
• Septicaemia, localised cutaneous and
subcutaneous gangrene are the dangerous
problems.
• Lymphoedema of face and eyelids can occur
later due to lymphatic fibrosis.
Treatment is with penicillins.
ABSCESS
Pyogenic Abscess
It is a localised collection of pus in a cavity lined
by granulation tissue, covered by pyogenic
membrane. It contains pus in loculi. Pus contains
dead WBC’s, multiplying bacteria, toxins and
necrotic material.
Mode of Infection
• Direct
69
 • Haematogenous
• Lymphatics
• Extension from adjacent tissues
Bacteria Causing Abscess
• Staphylococcus aureus.
• Streptococcus pyogenes.
• Gram-negative bacteria (E. coli,
Pseudomonas, Klebsiella).
• Anaerobes.
Clinical Features
• Fever often with chills and rigors.
• Localised swelling which is smooth, soft and
fluctuant.
• Visible (pointing) pus.
• Throbbing pain and pointing tenderness.
• Brawny induration around.
• Redness and warmth with restricted
movement around a joint.
• Rubor (redness); dolor (pain); calor
(warmness); tumour (swelling) and
functiolaesa (loss of localised and adjacent
tissue/joint function) are quite obvious.
(Commonly cellulitis occurs first which
eventually gets localised to form an abscess.)
Investigations
• Total count is increased.
• Urine sugar and blood sugar is done to rule
out diabetes.
• USG of the part or abdomen or other region
is done when required.
• Chest X-ray in case of lung abscess.
• Gallium isotope scan is very useful.
• CT scan or MRI is done in cases of brain and
thoracic abscess.
Complications of an Abscess
• Bacteraemia, septicaemia, and pyaemia.
• Multiple abscess formation.
• Metastatic abscess.
• Destruction of tissues.
• Antibioma formation (common in breast
abscess).
• Sinus and fistula formation.
• Large abscess may erode into adjacent
vessels and can cause life-threatening
torrential haemorrhage, e.g. as in pancreatic
abscess.
• Abscess in head and neck region can cause
laryngeal oedema, stridor and dysphagia.
• Specific complications of internal abscess
depend on the affected organ.
Management
• Analgesia
• Broadspectrum antibiotics are started
(depending on severity, extent and site of the
abscess).
• Drain the abscess (open or closed).
• Wound is not closed. Wound is allowed to
granulate and heal. Sometimes secondary
suturing or skin grafting is required.
• Pus is sent for culture and sensitivity.
CARBUNCLE
A carbuncle is a serious infection by
staphylococcus aureus characterized by an area
of subcutaneous necrosis with a honeycomb of
small abscesses. It is particularly common in
diabetics and can cause considerable disability.
Treatment is with anti-biotics and, rarely,
surgery.
BOIL
A boil (furuncle) is a skin abscess that involves a
hair follicle and its associated gland. Caused by
S. Aureus. Boils are found commonly on the face,
neck and axilla. Treatment is by incision and
drainage and better hygiene. Systemic antibiotics
are not indicated.
HIDRADENITIS
Hidradenitis suppurativa is an infection of the
apocrine glands in the skin. It is common in the
axilla and the groin.
Irritation by deodorants and excessive sweating
have been implicated as precipitating factors. The
patient presents with multiple tender swellings
under the arm or in the groin; these enlarge and
discharge pus. Unless the area is kept very clean,
recurrence is common and often surgery is
required to excise the involved skin.
NECROTIZING FASCIITIS
Necrotizing fasciitis is a deep cellulitis affecting
the fascial planes. Initially the overlying skin is
relatively normal while the necrotic process
proceeds underneath. The patient becomes
extremely toxic and later the skin becomes
70
painful, red and necrotic as it is deprived of its
blood supply.
Management
• IV fluids, fresh blood transfusion.
• Antibiotics depend on C/S or broad-
spectrum antibiotics.
• High dose penicillins are very effective.
Clindamycin, third generation
cephalosporins, aminoglycosides are also
often needed.
• Catheterisation and monitoring of hourly
urine output.
• Haematocrit, serum creatinine assessment.
• Pus culture, blood culture.
• Electrolyte management and monitoring.
• Control of diabetes, if patient is diabetic.
• Oxygen, ventilator support, dopamine,
dobutamine supplements whenever
required.
• Radical wound excision of gangrenous skin
and necrosed tissues at repeated intervals.
GAS GANGRENE
Gas gangrene, the scourge of all wounded
soldiers since men began to assault each other, is
rare in civilian practice.
Occasionally gas gangrene follows operations
such as amputation for lower limb ischaemia.
Cause: clostridial species (Clostridium
perfringens, 65% of cases; C. novyi, 30%; C.
septicum, 15%)
Clinical features
• Spreading gangrene of the muscles
accompanied by oedema,
• Blackening of the tissues,
• Crepitus (from gas production),
• Foul-smelling discharge.
• Profound toxaemia and
• Shock.
Treatment
• Wide excision or amputation of all necrotic
and ischaemic tissue with free drainage and
• high-dose antibiotic therapy, including
penicillin and metronidazole.
• Hyperbaric oxygen may be helpful in some
cases and should be administered if
available.
The outlook for patients with this condition is
still grim.
SEPTICAEMIA
Presence of overwhelming and multiplying
bacteria in blood with toxins causing SIRS
(Systemic inflammatory response syndrome) or
MODS (Multiorgan dysfunction syndrome).
Types
a. Gram +ve septicaemia is due to
staphylococci, strepto-cocci,
pneumococci, etc. It is common in
children, old
b. age, diabetics and after splenectomy
c. Gram –ve septicaemia is common in acute
abdomen like peritonitis, abscess,
urinary infections, biliary infections,
postoperative sepsis.
Investigations
• Urine/pus/discharge culture.
• Blood culture.
• Haematocrit.
• Electrolyte assessment.
• PO2 and PCO2 analysis.
• Blood urea, serum creatinine, liver function
tests.
Treatment
• Antibiotics like cefoperazone, ceftazidime,
cefotaxime, amikacin, tobramycin,
metronidazole.
• Fresh blood transfusion.
• Adequate hydration.
• Oxygen supplementation.
• Ventilatory support.
• Electrolyte management.
• Parenteral nutrition (TPN).
• CVP line for monitoring and perfusion.
• FFP or platelets in case of DIC.
ACUTE PYOMYOSITIS
• It is infection and suppuration with
destruction of the skeletal muscle, commonly
due to Staphylococcus aureus (90%) and
Streptococcus pyogenes, occasionally due to
Gram-negative organisms.
• It is common in muscles of thigh, gluteal
region, shoulder and arm.
71
• Precipitating factors are:—trauma,
malnutrition, anaemia, and
immunosuppression.
• Pain, oedema, tenderness over the site with
apparently normal overlying skin.
• Induration and muscle spasm is typical.
• Fever, jaundice, uraemia (acute renal failure)
are common.
Management
• Creatine phosphokinase will be very high.
• MRI is useful. US guided pus aspiration is
also done.
Treatment is antibiotics, radical wound excision
with removal of pus and all necrosed muscle and
compartment release.
Haemodialysis is needed until recovery if there is
renal failure. Later secondary suturing or skin
grafting is needed.
SURGICAL SITE INFECTION (SSI)
Surgical site infection is the second most
common complication following surgical
procedures (first being postoperative
pneumonia) due to virulent bacterial entry,
altered wound microenvironment, and changed
host defense. Prevention of SSI can be achieved
by better preoperative preparation; proper
infection control during surgery; adherence to
principles of preventive antibiotic therapy; better
surgical techniques to reduce hematoma, tissue
injury and foreign bodies within the surgical site;
29.HAND INFECTIONS
Most suppurative hand infections follow
penetrating trauma and the causative organism is
usually Staphylococcus aureus. Human bites are
commonly the result of punching someone in the
mouth.
Specific sites of infection
• Paronychia: this refers to infection of the soft
tissue adjacent to the nail. It is probably the
most common site of infection in the hand
and is usually caused by Staph. aureus.
Treatment is surgical incision and drainage.
• Pulp space infections are also known as
felons. Again, they require surgical drainage
by opening the pulp.
prevention of tissue hypoxia with enhanced
oxygen support.
Common Sources of Infection
• Surgical wards, wounds, ulcers, catheters,
drains, sputum, urine, faeces, open wounds.
• Operation room without proper ventilation,
nurses, surgeons.
• Operation methods, sterilisation of
instruments.
Organisms Causing SSI
• Commonly Staphylococcus aureus. Any
organisms like clostridia, Gram-negative
bacteria can cause SSI.
• Bacteria present in a wound with no signs or
symptoms of
Management of SSI
• SSI is managed depending on the type of
SSI—superficial, deep or organ space.
• debridement.
• Sutures are removed to allow free drainage
of infected material.
• Infected fluid is sent for culture and
sensitivity and suitable antibiotics are
started.
• Once wound shows signs of healing by
healthy granulation tissue, secondary
suturing is done. Often it is allowed to heal
by scarring.
• Tendon sheath infections are rare but
serious. Pus tracks along the flexor sheath and
if untreated the tendons can rupture. The
finger involved becomes swollen and assumes
a flexed position. There is exquisite pain on
passive extension of the finger. The treatment
involves opening the flexor sheath and
irrigation with a feeding catheter.
• Palmar bursae infections can also occur.
Treatment involves surgical incision and
evacuation of the pus.
• Thenar space infections arise in the space
under the thenar muscles and above the
adductor pollicis muscle. These infections are
commonly drained through an incision on the
dorsum of the hand.
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• Midpalmar space infections occur deep to débridment + penicillinase-resistant penicillin
the flexor tendons of the ulnar three fingers. + metronidazole
Purulent infections in this space points in the
• Animal bites: local infection. Organism
third and fourth web spaces where incisions
involved is Pasteurella multocida. Treatment
for drainage can be made.
is débridment + appropriate antibiotic
• Human bites: infection over metacarpal heads
where tooth laceration occurs. Organism
involved is Eikenella corrodens. Treatment is

73
 31.ULCERS
Definition
An ulcer is a break in the continuity of the
covering epithelium, either skin or mucous
membrane due to molecular death.
TROPHIC ULCER (PRESSURE
SORE/DECUBITUS ULCER)
Pressure sore is tissue necrosis and ulceration
due to prolonged pressure. Blood flow to the skin
stops once external pressure becomes more than
30 mmHg (more than capillary occlusive
pressure) and this causes tissue hypoxia, necrosis
and ulceration. It is more prominent between
bony prominence and an external surface.
Factors causing pressure sore
❖ Normal stimulus to relieve the pressure is
absent in anaesthetised patient
❖ Nutritional deficiencies worsens the necrosis
❖ Inadequate padding over the bony
prominences in malnourished patients
❖ Urinary incontinence in paraplegia patient
causes skin soiling-maceration-infection-
necrosis.
Sites
❖ Over the ischial tuberosity.
❖ Sacrum.
❖ In the heel.
❖ In relation to heads of metatarsals.
❖ Buttocks.
❖ Over the shoulder.
❖ Occiput
Clinical Features
❖ Occurs in 5% of all hospitalised patients.
❖ Painless ulcer which is punched out.
❖ Ulcer is nonmobile with base formed by
bone.
Staging of pressure sore
It is graded according to depth as follows:
❖ Erythema;
❖ Blister;
❖ Full-thickness skin loss into
subcutaneous tissue;
❖ Muscle breakdown;
❖ Bone/joint involvement.
Treatment
❖ Cause should be treated.
❖ Nutritional supplementation.
❖ Rest, antibiotics, slough excision, regular
dressings.
❖ Vacuum assisted closure (VAC)
❖ Surgical intervention
❖ Psychological counselling.
MARJOLIN’S ULCER
❖ It is slow growing locally malignant lesion—a
very well differentiated squamous cell
carcinoma occurring in an unstable scar of
long duration.
❖ It is commonly seen in chronic venous ulcer
scar. Often it is observed in burns scar and
scar of previous snake bite.
❖ Lesion is ulcerative/proliferative.
❖ Edge may be everted or may not be. It is
painless as scar does not contain nerve fibrils.
It does not spread into lymphatics as scar is
devoid of lymphatics. Induration is felt at the
edge and base. There is marked fibrosis also.
❖ Once lesion spreads into adjacent normal
skin, it can spread into regional lymph nodes
behaving like squamous cell carcinoma.
❖ Managed by edge biopsy and wide local
excision and grafting.
DIABETIC ULCER
Causes
❖ Increased glucose in the tissue precipitates
infection.
❖ Diabetic microangiopathy which affects
microcirculation.
❖ Increased glycosylated haemoglobin
decreases the oxygen dissociation.
❖ Increased glycosylated tissue protein
decreases the oxygen utilization.
❖ Diabetic neuropathy involving all sensory,
motor and autonomous components.
❖ Associated atherosclerosis.
74
Sites Multiple deeper abscesses; osteomyelitis of
deeper bones are common
❖ Foot-plantar aspect—is the most common
site. Reduced leukocyte function; resistant
infection; spreading cellulitis
❖ Leg.
Arterial insufficiency
❖ Upper limb, back, scrotum, perineum.
Septicaemia; diabetic ketoacidosis
❖ Diabetic ulcer may be associated with
ischaemia. Associated cardiac diseases like ischaemic
heart disease
❖ Ulcer is usually spreading and deep.
Treatment
Investigations
❖ Control of diabetes using insulin.
❖ Blood sugar both random and fasting.
❖ Antibiotics.
❖ Urine ketone bodies.
❖ Nutritional supplements.
❖ Discharge for culture and sensitivity.
❖ Regular cleaning, debridement, dressing.
❖ X-ray of the part to see osteomyelitis.
❖ Once granulates, the ulcer is covered with
❖ Arterial Doppler of the limb; glycosylated
skin graft or flap.
haemoglobin estimation.
❖ Microcellular rubber (MCR) shoes to
Problems with diabetic ulcer
prevent injuries; care of foot.
Neuropathy, in foot—clawing of toes,
hammer toe (due to intrinsic muscle
paralysis)

75
 32.MUSCULO-SKELETAL DISORDERS

BACKACHE Metabolic causes

❖ Osteoporosis
CAUSES OF BACKACHE
❖ Osteomalacia
Common causes
Degenerative conditions
❖ Back muscle sprain
❖ Osteoarthritis
❖ Prolapsed lumbar intervertebral disk
❖ Lumbar spondylosis
❖ Obesity
Referred pain from
❖ Poor posture
❖ Gynecological diseases
❖ Facet joint arthritis
❖ Genitourinary diseases
❖ Unaccustomed activities
❖ Gastrointestinal conditions, etc.
❖ Occupational causes
Presenting Complaints
Uncommon causes
❖ Pain
Congenital causes (4 ‘S’)

❖ Scoliosis ❖ Neurogenic Claudication

❖ Spondylolisthesis ❖ Other Complaints

There may be history of stiffness, pain in other

❖ Spina bifida
joints (e.g. rheumatoid arthritis), constitutional
❖ Spondylolysis symptoms (e.g. tuberculosis, malignancy, etc.),
genitourinary complaints, etc.
Infective conditions
Physical examination
❖ Osteomyelitis
a. Physical signs
❖ Tuberculosis
❖ Stance and gait
❖ Brucellosis, etc.
❖ Spasms
Traumatic causes
❖ Movements
❖ Vertebral body injuries, posterior arch
fractures ❖ Swelling

❖ Muscle sprain/strain ❖ Tenderness

❖ Prolapsed disk b. Neurological Examination

Inflammatory causes c. Other Examinations

❖ Rheumatoid arthritis Other examinations include examinations of the

adjacent joints, peripheral pulses, abdominal,
❖ Ankylosing spondylitis and other SSAs
rectal or paravaginal examinations.
Neoplasm
Investigations
❖ Benign—osteoid osteoma
❖ Blood tests
❖ Malignant—secondary, multiple myeloma,
❖ X-ray
etc.
❖ Myelography

76
 ❖ CT scan Clinical Features

❖ MRI Scan Early symptoms:

Treatment Pain

Detect and treat the underlying cause ❖ Acute pain in middle or low thoracic or high
lumbar region
The treatment for backache:
❖ Sudden movement, sitting, sneezing, cough,
❖ NSAIDs, etc. increases pain.
❖ Muscle relaxants,
❖ Rest relieves it.
❖ Physiotherapy, Most common symptom of osteoporosis is back
❖ Traction, pain secondary to vertebral compression.

❖ Use of belts and corsets Investigation

Proper postural habits, back exercises and back ❖ Radiographs

education go a long way in preventing the
❖ Densitometry
backache. Surgery is done for specific indications
❖ Transiliac bone biopsy
OSTEOPOROSIS
❖ Blood chemistry
Definition
Management of Osteoporosis
It is a generic term referring to a state of
Preventing osteoporosis is lot easier than treating
decreased mass per unit volume of a normally
it.
mineralized bone due to loss of bone proteins.

Causes The treatment plan consists of general measures

exercises and drug therapy.
1. Disuse
General measures
❖ Prolonged bed rest or inactivity.
❖ High protein and calcium rich diet.
❖ Prolonged casting or splinting.
❖ Rest that is adequate.
❖ Paralysis, space travel, etc.
❖ Muscle relaxants and supports like belt,
2. Diet collar, etc. for symptomatic relief of pain.

❖ Calcium, protein, vitamin C low in the ❖ Spinal orthosis when patient is erect and
diet. mobile.

❖ Chronic alcoholism. Exercises

❖ Anorexia nervosa. ❖ Exercises like walking and light aerobics are

beneficial .
3. Drugs: Whose prolonged use causes
osteoporosis are heparin, methotrexate, ❖ Posture exercise
ethanol, glucocorticoids, etc.
❖ Fall prevention is
4. Idiopathic
❖ of utmost importance.
5. Genetic
Drug Therapy in Osteoporosis
6. Chronic illness
Drugs form the mainstay of treatment of
7. Neoplasm osteoporosis.

8. Endocrine abnormalities Drugs preferences in osteoporosis in order of

importance

77
 ❖ In all age groups: Calcium and vitamin D. • Physical examination

❖ Perimenopausal and early menopause: • Symptomatology

Hormonal replacement therapy.
• Radiography
❖ Next 10 years after first perimenopausal
treatment: SERMS (e.g. Raloxofene). • Blood tests

❖ After 65 years preferably: Alendronate. • CT scan and MRI.

❖ For severe pain due to vertebral fractures: Management

Calcitonin. Non-surgical options
❖ Combination of the above drugs. • Weight loss,

OSTEOARTHRITIS • Use of a stick,

Osteoarthritis is a syndrome of pain and • Rest

limitation of movement associated with a
• Physio-therapy.
breakdown of the balance between the wear and
repair processes in the joint. • Analgesia may be used subsequently or in
parallel with these measures.
Aetiology
Surgical options
❖ Age more than 40 years
For most forms of arthritis there remain four
❖ Female
options:
❖ Hereditary conditions
• Nothing,
❖ Previous joint injuries
• Arthroplasty (joint replacement),
❖ Obesity
• Arthrodesis and
❖ Diseases of the joints
• Osteotomy.
❖ Poor posture
SEPTIC ARTHRITIS
❖ Occupational stress
Acute septic arthritis
❖ A combination of the above factors.
Aetiology
Clinical presentation
❖ Blood-borne in origin, from a distal site of
Typical symptoms of osteoarthritis: trivial infection.
• Pain ❖ From an adjacent infected bone
• Early morning stiffness ❖ Direct penetration of the joint (rare).
• Restricted range of joint movements Three groups are at risk:
• Swelling of the joints. • Children;
Joints usually affected • Immunosuppressed adults;
• Weight bearing joints like hip, knee, ankle, • Anyone with chronic degenerative joint
etc. disorders
• Spine Causative Organisms
• Fingers. • Staphylococcus aureus (50%),
Diagnosis • Streptococcus (20%),

78
 • Pneumococcus (10%), Chronic septic arthritis

• Gonococcus, Aetiology

• E. coli, etc. Tuberculosis is still an important cause.

• H. influenzae is very common in children Clinical presentation

less than 2 years.
• Chronic malaise,
Clinical presentation
• Weight loss
In children,
• Marked muscle wasting around the affected
• Nasty acute illness joint.

• The child is unwell with a high fever. • The radiographs show highly characteristic
loss of bone density.
• The affected joint is held stiff and is hot and
tender. Management

The other patient groups often present with a
much less florid picture. The immunosuppressed
or the chronically abnormal joint may give a false
impression of a minor upset. The patient remains
unwell for many days before presenting with a
septicaemia, which is often difficult to ascribe to
any source.
Investigations
• Joint Aspirate and Synovial Fluid Analysis
• Laboratory Investigations
➢ WBCs (polymorphs) are raised to 50,000-
1,00,000 (80% of cases),
➢ ESR increased more than 20 mm/hr (in
50% of cases),
➢ Hb percentage decreases.
➢ Blood culture is positive in 35-50 percent
of the cases.
➢ CRP should be done within 24 hours of
presentation.
Treatment is by chemotherapy and only rarely is
surgery necessary. Combinations of drugs such
as ethambutol and rifampicin are given for many
months.
Complications of septic arthritis
• Joint destruction.
• Pathological dislocation.
• Osteoarthritis in later years.
• Ankylosis—fibrous or bony.
• Acute osteomyelitis.
• Amyloidosis very rarely develops.
• Septicemia, pyemia, etc.
OSTEOMYELITIS
Osteomyelitis is defined as a suppurative process
of the bone caused by pyogenic organisms or
simply a pyogenic infection of the cancellous
portion of the bone.

Management Classification

Treatment consists of surgery and intravenous The three types based on:
antibiotics.
• Duration of symptoms,
Antibiotics should be given according to culture.
o Acute (<2 weeks)
In children, the first-guess antibiotic should be an
o Subacute (2-3weeks)
antistaphylococcal agent as this is still the most
likely infecting organism. o Chronic (>3 weeks)
In adults, penicillin should be given o Residual
intravenously to cover the risk of gonococcal
infection. • Route of spread of infection.

79
 o Hematogenous (most common) General Features

o Direct • Fever (95%)

• Sweating
o Contiguity
• Chills and rigors
• Host response. • Patient is usuallyin shock
• Increased temperature
o Pyogenic
• Increased pulse rate
o Non pyogenic • Anemia (?)
• Signs of dehydration and Shock
ACUTE OSTEOMYELITIS
Local Features
Etiology • Local swelling (80%)
General factors • Limitation of movement (50%)
• Tenderness (80%)
(a) Infections • Local erythema (50%)
• Staphylococcus aureus (60-85%): This is the • Raised temperature (50%)
most common organism causing acute • Fluctuation present (20%)
osteomyelitis. • Effusion (10%)
• Streptococcus hemolyticus (8-10%) • Decreased movements (50%)
• Salmonella is relatively rare and presents an Investigations
interesting picture as most of its features Acute osteomyelitis
start with “S”
✓ Symmetrical involvement of bones • Laboratory investigations
• Bone scan
✓ Severe osteomyelitis
Chronic osteomyelitis
✓ Spine may be involved
• Radiology
✓ Sickle cell anemia present Management
✓ Stool culture may be positive. Acute osteomyelitis is an orthopedic emergency,
(b) Anemia which needs in patient admission.

(c) Debility General Management (RESTS)

(d) Poor nutrition
(e) Poor immune status
Local factors
Responsible for localization of infection at
metaphysis, especially in children.
• Hairpin bend vessels
• Metaphyseal hemorrhage
• Defective phagocytosis
• Rapid growth at metaphysis
• Necrotic tissue acts as a culture media
• Anoxia
• Vasospasm
Clinical Features
This consists of general and local signs
• Rest in bed; protect affected part with splints
to alleviate pain and spasm.
• Elevation of the part, warm and moist packs
to reduce the swelling.
• Systemic treatment—blood transfusions,
intravenous fluids to correct shock and
hypovolemia.
• Treatment—with antibiotics helps to reduce
toxicity.
• Surgery—properly indicated and timed to
prevent complications.
Local Management
The focus here is on well-timed surgery.
Nade’s indications for surgery
• Abscess formation.
• Severely ill and moribund child.

80
 • Failure to respond to intravenous antibiotics Clinical Features
for more than 48 hours.
Symptoms
Differential Diagnosis
• Fever,
• Acute Septic Arthritis
• pain,
• Scurvy
• swelling
• Acute Anterior Poliomyelitis
Signs
• Cellulitis
• Erysipelas, • Irregular thickening of bone
• Erythema nodosum, • Sinuses
• Ewing’s sarcoma, • Scars and muscle contractures
• Sickle cell anemia. • Shortening or lengthening of the bones
Complications (seen in 5% of the cases) • Deformities and decreased movements
• Pathological fractures
• Septicemia and pyemia.
Note: Sequestra: It is a dead bone within a living
• Septic arthritis bone and is defined as an infected granulation
• Chronic osteomyelitis tissue. The inflammatory foci are surrounded by
• Pathological fractures and growth sclerotic bone supplied with blood and covered
disturbances are relatively rare. by periosteum, scarred muscle and subcutaneous
• Recurrence. tissues.

SUBACUTE OSTEOMYELITIS Investigations

Subacute osteomyelitis is caused by • X-ray,

Staphylococcus aureus.
The patient complains of pain without
constitutional symptoms. Temperature may be
increased or normal.
Blood culture is positive in only 60 percent of the
cases, and WBC and ESR are raised in only 50
percent of the cases.
• Sinogram,
• CT scan,
Management
Goal: Eradication of the infection by achieving a
viable and vascular environment.
• Sequestrectomy and resection of scarred
and infected bone and soft tissue.

Subacute osteomyelitis is due to: • Appropriate antibiotics.

• Increased host resistance. • Reconstruction of both the bone and soft

• Lowered bacterial resistance. tissue defects.
• If antibiotics are administered before
Complications
symptoms appear.
Pathological fracture is by far the most common
CHRONIC OSTEOMYELITIS complication.

Osteomyelitis lasting for more than three weeks. Common Complications

Chronic osteomyelitis can arise from any one of
• Acute exacerbation of existing chronic
the following ways:
disease
• Sequelae of acute osteomyelitis (5-10%) • Growth disturbances
• Following compound fractures • Deformities
• Following surgery on bones and joints
RESIDUAL OSTEOMYELITIS
• Chronic from the beginning (e.g.
tuberculosis, syphilis, Brodie’s abscess)
In residual osteomyelitis, there is complete
• Anaerobic organisms (sclerosing absence of signs and symptoms. There are no
osteomyelitis of Garre) draining sinuses. There is soft tissue scarring,
• Fungal osteomyelitis.

81
skin is fixed to the bone and the underlying bone
is sclerotic.
SCIATICA
Sciatica is defined as a radiating pain along the
course of the sciatic nerve and is felt in the back,
buttocks, posterior of the thigh, legs and the foot.
It is commonly due to disk prolapse.
The other causes are:
• Spondylolisthesis.
• Sacroiliac joint arthritis.
• Affliction of the nerve root by herpes
simplex virus can cause radicular pain.
• Tuberculoma causing cord compression.
• Lymphomas and pelvic malignancy.
• Incurled thickened ligamentum flavum.
• Cysts of the sacral nerve root.
• Intraspinal neurofibromas and other tumors.
• Hemorrhage in the ependymoma can cause
sudden and gross neurological deficit,
mimicking acute disk prolapse.
• Diabetic neuropathy, etc.
Progressive signs and unremitting symptoms
should alert the clinician to a neoplastic
pathology.
Management
• Analgesia
• Refer to a surgeon
PATHOLOGICAL FRACTURES
When a fracture occurs through a bone, which
has already been weakened by a generalized or
localized skeletal disorder, it is called a
pathological fracture.
Unlike traumatic fractures, these fractures take
place either spontaneously or due to trivial
trauma.
Common causes for pathological fractures
Local disorders
a. Metastatic carcinoma: The primary could be
in the lungs, breast, prostate, thyroid or
kidney.
b. Bone cyst of a long bone.
Generalized disorders
(a) Senile osteoporosis
(b) Paget’s disease of bone
Clinical Features
The patient usually complains of fracture
following a trivial trauma. He or she complains
of having suffered pain or discomfort in the
region of the affected bone some time before the
fracture.
Investigations
• Laboratory investigation: Hb, TG, DG, ESR,
serum Ca, P, alkaline and acid phosphatase.
• Plain X-ray of the affected bones including
the joint above and below.
• CT scan and MRI are of extreme importance
to determine the extent of pathological
involvement.
• Bone scan is helpful in determining the
spread of disease.
Treatment
Conservative treatment has little role in the
treatment of pathological fractures. The
treatment recommended is open reduction, rigid
internal fixation.
The aim is to obtain quick union and mobilize the
patient early.
Do you know the most common causes of
pathologic fractures?
1. Osteoporosis first
2. Metastasis into the bones next
82
 33. NEOPLASMS OF THE SKIN AND SUBCUTANEOUS
Cancer of the skin is typically seen in people who
live where the sun is fierce, and who by virtue of
occupation or hobby are out in the sun all day.
Types:
• Basal cell carcinoma: 50% of cases
• Squamous cell carcinoma: 25% of cases
• Melanoma: ≥ 15% of cases (incidence is
rising)
Diagnosis is done by obtaining tissue from a
biopsy of the lesion (shave, punch or excisional
biopsy). Excisional biopsy is the most accurate in
diagnosis, especially when melanoma is
suspected.
BASAL CELL CARCINOMA
Clinical features
May show up as a raised waxy lesion or as a
nonhealing ulcer.
It has a preference for the upper part of the face
(above a line drawn across the lips). It does not
metastasize, but can kill by relentless local
invasion (“rodent ulcer”).
Treatment
Local excision with negative margins (1 mm is
enough) is curative, but other lesions may
develop later.
SQUAMOUS CELL CARCINOMA
Squamous cell carcinoma of the skin shows up as
a nonhealing ulcer, has a preference for the lower
lip (and territories below a line drawn across the
lips), and can metastasize to lymph nodes.
Excision with wider margins is needed (0.5–2
cm), and node dissection is done if they are
involved. Radiation treatment is another option.
MELANOMA
Melanoma usually originates in a pigmented
lesion. A mnemonic to identify them is ABCD.
TISSUES
• Asymmetric (A)
• Irregular borders (B)
• Different colors (C) within the lesion
• Diameter (D) >0.5 cm
Melanoma should also be suspected in any
pigmented lesion that changes in any way
(grows, ulcerates, changes color and/or shape,
bleeds, etc.).
The prognosis of melanoma is directly related to
the thickness or depth of invasion (Breslow
measurement); the deeper the thickness/depth of
invasion, the worse the prognosis.
Treatment
Melanoma-in-situ (non-invasive melanoma)
carries an excellent prognosis and can be
effectively treated with local excision (5 mm
margins).
Metastatic malignant melanoma
Metastatic malignant melanoma (from a deep,
invasive primary) is a bizarre, unpredictable, and
fascinating disease. Melanoma metastasizes to all
the usual places (lymph nodes, liver, lung, brain,
and bone), but it also metastasizes to remote and
bizarre locations (e.g. the muscle of the left
ventricle, the wall of the
duodenum…anywhere!).
Prognosis
It has no predictable timetable. Some patients are
full of metastases and dead within a few months
of diagnosis, while others go 20 years between
resection of their primary tumor and the sudden
explosion of metastases.
Interferon is the current adjuvant systemic
therapy for high-risk melanoma. Newer drugs
such as ipilimumab and vemurafenib are being
explored for treatment.
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 34.FOREIGN BODIES IN GIT
FOREIGN BODY OESOPHAGUS
Common Foreign Bodies
❖ Coins, metals, plastics.
❖ Dentures.
❖ Pins, toothpicks, batteries.
❖ Fish or meat bones—dangerous—40%.
❖ Food (meat—common/vegetables)
impaction—45%.
Sites of Impaction in Oesophagus
❖ Cervical constriction—C6.
❖ Broncho-aortic constriction—T4.
❖ Diaphragmatic constriction—T10.
❖ Pre-existing malignancy or inflammatory
stricture site.
Features
❖ Sudden dysphagia with chest pain and
breathlessness.
❖ Later features of shock, sepsis, mediastinitis,
empyema.
Management
❖ X-ray shows site and level of the F/B.
❖ Endoscopic removal can be tried.
❖ Impacted large F/B should be removed by
thoracotomy.
❖ Antibiotics, jejunostomy, TPN, ICT are also
required.
FOREIGN BODIES IN THE STOMACH
Ingested foreign bodies are usually
asymptomatic. Removal of sharp or large objects
should be considered. This can usually be done
endoscopically, with an overtube technique.
Recognized dangers include aspiration of the
foreign body during removal, and rupture of
drug-containing bags in “body packers.” Both
complications can be fatal. Surgical removal is
recommended in body packers, and in patients
with large jagged objects. Corrosive objects (e.g.,
watch batteries) should be removed promptly.
FOREIGN BODY IN THE RECTUM.
Foreign body entrapment in the rectum is not
uncommon.
Depending on the level of entrapment, a foreign
body may cause damage to the rectum,
rectosigmoid, or descending colon. Generalized
abdominal pain suggests intraperitoneal
perforation.
Evaluation of the patient includes inspection of
the perineum and a careful abdominal
examination to detect any evidence of
perforation. Plain films of the abdomen are
mandatory to detect free intra-abdominal air.
Management
Foreign bodies lodged low in the rectum may
often be removed under conscious sedation with
or without a local anesthetic block. Objects
impacted higher in the rectum may require
regional or general anesthesia for removal. Only
rarely will a laparotomy be required to remove
the object.
84
 35.CONDITIONS OF THE ABDOMINAL WALL,
PERITONUEM
APPLIED ANATOMY
Peritoneum
It is a serous membrane lining the abdominal
cavity. It is composed of outer fibrous tissue layer
(which gives strength) and inner mesothelial cell
layer (secretes fluid giving lubricating function to
the peritoneum).
Parts of Peritoneum
1. Parietal peritoneum: It lines the inner surface
of the abdominal wall, under surface of
diaphragm and pelvic wall. It is loosely attached
to the overlying walls and can be easily stripped
off. It is innervated by the somatic nerves, so pain
sensitive. Anterior peritoneum is most sensitive
when compared to pelvic peritoneum.
2. Visceral peritoneum: It lines the outer surface
of the abdominal viscera, firmly adherent, cannot
be stripped off. It is innervated by autonomic
nervous system; hence not pain sensitive.
Peritoneal cavity
It is the potential space between the parietal and
visceral peritoneum. Normally it contains 100 ml
of clear, straw coloured fluid secreted by the
mesothelial cells. The peritoneal fluid represents
a plasma ultrafiltrate, with electrolyte and solute
concentrations similar to that of neighboring
interstitial spaces and a protein content of less
than 30 g/L, mainly albumin. Its quantity and
quality varies in pathological conditions. It has
got lubricating function, allowing frictionless
movements of adjacent peritoneal surfaces.
Spaces in peritoneal cavity
Peritoneal cavity being largest cavity in the body
is divided into different spaces by ligaments and
mesenteries. Eleven ligaments are—coronary,
gastrohe-patic, hepatoduodenal, falciform,
phrenicocolic, splenorenal, gastrosplenic,
duodenocolic, gastrocolic; mesenteries are—
transverse mesocolon and bowel mesentery.
Intra-abdominal spaces are nine in number; they
are—right and left subphrenic, subhepatic, lesser
sac, supramesenteric, inframesenteric, right and
left paracolic gutters, and pelvic.
Peritoneal cavity is surgically divided basically
into supracolic and infracolic compartments.
Vascular Supply and Lymphatic Drainage of
the Peritoneum
• Parietal peritoneum:
✓ Somatic blood vessels of abdominal and
pelvic walls
✓ Its lymphatics join those in the body wall
and drain to parietal lymph nodes
• Visceral peritoneum
✓ Visceral peritoneum is best considered as an
integral part of the viscera which it overlies
✓ It thus derives its blood supply from the
viscera
✓ Its lymphatics join the visceral vessels to
drain to the regional lymph nodes.
Innervation of the Peritoneum.
• Parietal peritoneum:
✓ Branches from somatic efferent and afferent
nerves
✓ These also supply segmental muscles and
skin respectively of the overlying body wall
✓ Parietal diaphragmatic peritoneum is
supplied with afferent fibres from the
phrenic nerves (centrally) and by the lower
six intercostal nerves and subcostal nerves
(peripherally)
• Visceral peritoneum:
✓ Branches of visceral afferent nerves which
travel with the autonomic supply to the
underlying viscera
PERITONITIS
Peritonitis – inflammation of the serosal
membrane that lines the abdominal cavity and
the organs contained therein.
Aetiology
The peritonitis can be bacterial or chemical.
85
BACTERIAL PERITONITIS
Bacterial peritonitis is divided into four types.
1. Primary bacterial peritonitis (Rare): It is
commonly due to pneumococci, and can
occasionally be due to streptococci, haemophilus,
gonococcus (rare now) and other gram-negative
(Escherichia coli) organisms. It can also be due to
Chlamydial, fungal or mycobacterial infection.
**Mortality is high
2. Secondary bacterial peritonitis
It is secondary to any bowel or other visceral
pathology, e.g. perforation, appendicitis.
Escherichia coli (70%) is the most common
organism involved. Other bacteria are—aerobic
and anaerobic streptococci, Clostridium welchii,
bacteroides, staphylococci, Klebsiella, Salmonella
typhi.
3. Tertiary peritonitis: occurs in intensive care
patients and is defined as persistent or recurrent
intra-abdominal infection after an adequate
treatment for primary or secondary peritonitis
usually after 48 hours.
It is common in immunosuppressed individual
with ineffective peritoneal host defenses against
microbes. Infection due to E. faecalis, E. faecium, S.
epidermidis, P. aeruginosa, C. albicans are common
in such patients. Virulence and resistance to
drugs are other factors.
Mortality rate is > 50%. Problems are—DIC,
septicaemia, uraemia (haemodialysis may be
needed), haemorrhage, pneumonia, ARDS.
4. SPONTANEOUS BACTERIAL
PERITONITIS (SBP)
SBP is defined as bacterial infection of ascitic
fluid in the absence of an intra-abdominal
surgically treatable source of infection.
It is seen in:
• Infants and children commonly.
• In nephritic syndrome.
• In adults, with cirrhosis, most common
cause.
• In patients who has undergone
splenectomy.
• Patients with ascites due to any cause.
• Malnutrition and malignancy.
CHEMICAL PERITONITIS
In this instance the peritoneal inflammation is
initially chemical in nature, e.g. early stages of
perforated duodenal ulcer, extravasation of
uninfected urine (bladder injuries) or bile (after
biliary operations). However, if treatment is
delayed, secondary infection supervenes within a
few hours.
Peritonitis can be:
✓ Localized or
✓ Generalized (diffused)
Clinical features of peritonitis
• Sudden onset of pain which is severe.
• Fever, vomiting.
• Tenderness—initially localised later becomes
diffused.
• Rebound tenderness—Blumberg sign.
• Guarding and rigidity, dull flanks on
percussion.
• Tachycardia, tachypnoea.
• Distension with silent abdomen.
• Eventually leading to Hippocrates facies,
septicaemic shock and loss of consciousness.
• Bowel sounds are absent due to paralytic
ileus.
• Fever may be absent in severe peritonitis due
to loss of pyrogenic reaction. Total count also
may be very low in severe peritonitis.
INVESTIGATIONS
Lab investigations
• Total count is increased.
• Electrolyte study.
• Blood urea and serum creatinine.
• Serum amylase if four times the normal
value, it is significant. LFTs also should be
done.
• Platelet count, bleeding time, clotting time,
prothrombin time are to be assessed in
severe peritonitis.
• Four quadrant abdominal tap—reveals pus
or infected fluid. In suspected pancreatitis
fluid should be analysed for amylase level
(which will be high). Often US guided
aspiration is better and more accurate.
• Pus M/C/S
86
 • Plain X-ray abdomen (in erect posture)—will
show ground-glass appearance along with
gas under diaphragm in the presence of
perforation.
• U/S abdomen—shows fluid in the
abdominal cavity.
• Also clinches the other causes like
haemoperitoneum, pancreatitis.
• Diagnostic laparoscopy. It can also be used
as therapeutic for duodenal ulcer perforation
or primary peritonitis to give peritoneal
wash.
• CT scan is often useful to confirm the cause
or to rule out conditions like pancreatitis. CT
scan detects bowel ischaemia, gangrene,
perforation, internal hernias and quantity of
pus/fluid in the peritoneal cavity.
Differential diagnosis
❖ Pancreatitis
❖ Intestinal obstruction
❖ Ruptured ectopic pregnancy
❖ Acute pyelonephritis
❖ Acute mesenteric ischaemia
❖ Diabetic acute abdomen
TREATMENT
1. Patient should always be admitted
2. Analgesia (parenteral)
3. Ventilate the patient
4. Intravenous fluids: Normal saline, Ringer’s
lactate are usually used.
5. Catheterisation
6. Nasogastric tube aspiration—to decompress
bowel; to reduce toxic fluid; to prevent
aspiration.
7. Total parenteral nutrition.
8. Blood samples are taken for blood grouping
if the patient is to undergo surgical
treatment following resuscitation.
9. Antibiotics (empirically until the actual
bacterium is isolated): combination of
aminoglycosides (eg: gentamicin )
cephalosporins and metronidazole
10. Blood transfusion, FFP, platelet transfusions
if indicated.
11. Sitting propped up position, early
mobilisation, exercise, respiratory
physiotherapy, prevention of DVT using
heparin/low molecular heparin are
essential.
12. Surgical correction of underlying cause
(laparotomy).
13. Monitoring the patient using PO2, PCO2,
electrolytes, and pulse oximeter.
Complications
❖ Septicaemia.
❖ Paralytic ileus, adhesions, intestinal
obstruction.
❖ Respiratory infection.
❖ ARDS,
❖ bronchopneumonia.
❖ Electrolyte imbalance,
❖ DVT.
❖ Renal failure.
❖ MODS.
❖ DIC.
❖ Formation of subphrenic abscess, pelvic
abscess and other intraperitoneal abscess.
❖ Burst abdomen;
biliary/gastric/enteric/faecal fistula
formation; later incisional hernia.
87
 36.ABDOMINAL HERNIAE

Hernia is defined as an abnormal protrusion of a
viscous or a part of a viscous through an
opening, artificial or natural with a sac, covering
it.
Types
Common
• Umbilical (8.5%) /paraumbilical
• Inguinal ((73%)(direct and indirect)
• Femoral (17%)
• Incisional
Uncommon
• Epigastric
• Gluteal, lumbar, obturator
AETIOLOGY
• Straining.
• Lifting of heavy weight.
• Chronic cough (tuberculosis, chronic
bronchitis, bronchial asthma, emphysema).
• Chronic constipation (habitual, rectal
stricture).
• Urinary causes
• Old age—BPH, carcinoma prostate.
• Young age—stricture urethra.
• Very young age—phimosis, meatal stenosis.
• Obesity.
• Pregnancy and pelvic anatomy (especially in
femoral hernia in females).
• Smoking.
• Ascites.
• Appendicectomy through McBurney’s
incision may injure the ilioinguinal nerve
causing right sided direct inguinal hernia.
Hernia gets reduced on its own or by the patient
or by the surgeon. Expansile impulse on
coughing present.
2. Irreducible Hernia
Here contents cannot be returned to the abdomen
due to narrow neck, adhesions, over crowding.
Irreducibility predisposes to strangulation.
3. Obstructed Hernia
It is an irreducible hernia with obstruction, but
blood supply to the bowel is not interfered. It
eventually leads to strangulation.
4. Inflamed Hernia
It is due to inflammation of the contents of the
sac, e.g. appendicitis, salpingitis. Here hernia is
tender but not tense; overlying skin is red and
oedematous.
5. Strangulated Hernia
It is an irreversible hernia with obstruction to
blood flow.
Classification II
1. Congenital—Common
It occurs in a preformed sac/defect. Clinically
may present at a later period due to any of the
precipitating causes like in indirect inguinal
hernia.
2. Acquired
It is secondary to any causes which raise the
intra-abdominal pressure leading into weakening
of the area like in direct inguinal hernia.

PARTS OF HERNIA Classification III: According to the Contents

Hernia comprises of: • Omentocele—omentum.

• Enterocele—intestine.
• Covering. • Cystocele—urinary bladder.
• Sac. • Littre’s hernia—Meckel’s diverticulum.
• Content. • Maydl’s hernia.
CLASSIFICATION OF HERNIA • Sliding hernia.
• Richter’s hernia—part of the bowel wall.
Classification I (Clinical)
Classification IV: Based on Sites
1. Reducible Hernia
• Inguinal hernia—occurring in inguinal canal.
• Femoral hernia—occurring in femoral canal.
• Obturator hernia.

88
 • Diaphragmatic hernia.
• Lumbar hernia.
• Spigelian hernia.
• Umbilical hernia.
• Epigastric hernia.
INGUINAL HERNIA
Indirect hernia
It comes out through internal ring along with the
cord. It is lateral to the inferior epigastric artery.
Direct hernia
It occurs through the posterior wall of the
inguinal canal through ‘Hesselbach’s triangle’.
Clinical Features
• Prevalence of inguinal hernia is 25% in
males; 2% in females.
• It is more common in males (20 : 1 :: Male :
Female).
• Patient presents with dragging pain and
swelling in the groin which is better seen
while coughing and stan ding; and felt
together with an expansile impulse.
• In infants, swelling appears when the child
cries and is often translucent.
• Inguinal hernia in females: Increased
thickness of labium majus on palpation,
when compared to contralateral side.
Investigations
• Chest X-ray to rule out chronic bronchitis.
• Ultrasound of abdomen.
• Tests relevant for precipitating causes.
Management
• Herniotomy (excision of the hernial sac) +
herniorrhaphy (repair or buttressing of the
weakness in the posterior inguinal canal).
• In infants (always indirect hernia), only
herniotomy is required for effective
treatment.
Complications of hernia repair
• Haemorrhage
• Haematoma, seroma
• Infection—1-5%
• Haematocele
• Post-herniorrhaphy hydrocele, lymphocele
• Hyperaesthesia over the medial side of
inguinal canal due to injury to
iliohypogastric nerve—neuralgia (15%)
• Recurrence—10-15%
• Osteitis pubis
• Injury to urinary bladder/bowel
• Testicular atrophy, penile oedema rarely can
occur
FEMORAL HERNIA
A femoral hernia emerges through the femoral
canal and may be felt as a soft swelling below
and lateral to the pubic tubercle. It is a protrusion
of peritoneum through the femoral canal, below
which it emerges subcutaneously.
Aetiology
• Wide femoral canal.
• Multiple pregnancies.
Clinical Features
• Common in females (2:1 ratio), common in
multi para.
• Rare before puberty. 20% occurs bilateral,
however, more common on right side.
• Presents as a swelling in the groin below and
lateral to the pubic tubercle (Inguinal hernia
is above and medial to the pubic tubercle).
• Swelling, impulse on coughing, reducibility,
gurgling sound during reduction, dragging
pain, are the usual features.
• When obstruction and strangulation occurs
which is more common, presents with
features of intestinal obstruction—painful,
tender, inflamed, irreducible swelling
without any impulse. They also present with
abdominal distension, vomiting and features
of toxicity.
• Gaur’s sign: In femoral hernia, distension of
superficial epigastric and/or circumflex iliac
veins occurs due to the pressure by the
hernial sac.
Often on medial side, a portion of bladder forms
the wall of the femoral hernial sac—sliding—
femoral hernia
Treatment
• Surgical repair
89
UMBILICAL HERNIA
• It is herniation through a weak umbilical scar
(cicatrix).
• It is common in infants and children, occurs
commonly due to neonatal sepsis.
• Male : female :: 2:1.
• It is seen in 20% of newborn infants.
• Umbilical hernia is common in Down’s
syndrome, Beck-with-Weidman syndrome.
Clinical Features
• Presents with a swelling in the umbilical
region within first few months after birth, the
size increases during crying. It is
hemispherical in shape.
• Defect can be felt with finger during crying.
• Occasionally it can go for irreducibility and
obstruction which presents with pain,
distension, vomiting.
Treatment
Initially conservative. In 93 to 95% of cases, it
disappear spontaneously in few months after
birth (masterly inactivity).
It can be hastened by adhesive strapping across
the abdomen.
Indications for Surgery
• If persists even after the age of two years.
• If the defect is more than 2 cm in size.
• Acquired/adult umbilical hernia.
PARAUMBILICAL HERNIA (Supra- and
Infraumbilical Hernia)
These herniae occur in obese adult women and
are prone to strangulate. The defect occurs
through the midline just above the umbilicus.
The sac may contain omentum or small intestine
or both and, because of the narrow neck,
strangulation is relatively common. With long-
standing herniae, adhesions occur between the
con-tents and the wall of the sac so that the
hernia becomes irreducible.
Predisposing factors
• Obesity
• Multiple pregnancies
• Flabby abdominal wall
Clinical Features
• Common in females (5:1 ratio).
• It presents as a swelling which has smooth
surface, distinct edges, soft, resonant with
dragging pain and impulse on coughing.
Large hernias can present with intestinal
colic due to subacute intestinal obstruction.
Eventually strangulation can occur.
Treatment
Is always surgery
EPIGASTRIC HERNIA
These usually small but often quite painful
swellings occur in the midline between
xiphisternum and umbilicus. The swelling most
frequently consists of herniation of
extraperitoneal fat through a small defect in the
linea alba.
Pain is localized to the site with tenderness on
pressure, but it may also simulate the symptoms
of peptic ulcer.
Clinical examination reveals a tender swelling in
the midline. Sometimes incarcerated fat becomes
devascularized and necrotic.
Treatment is surgical and may be carried out
under local anaesthesia
INCISIONAL HERNIA
• This is a hernia that protrudes through a
defect in an old abdominal wound. Wound
infection predisposes to incisional hernia.
• It is common in old age and obese
individuals.
• It occurs in 10% of abdominal surgeries; 70%
occurs in first 5 years; 30% occurs in 5-10
years.
Clinical Features
• Swelling in the scar region.
• Pain.
• Impulse on coughing.
• Gurgling sound.
• Often bowel peristalsis may be visible under
the skin.
• Eventually features of irreducibility,
obstruction, strangulation is seen.
• Hernia is common in lower abdomen.
Investigations
90
Always the precipitating factors must be looked Treatment for Incisional Hernia
for:
Mesh repair of the incisional hernia defect is
• Chest X-ray. always better and ideal with less chances of
recurrence.
• U/S abdomen.

• Tests relevant for causes.

Summary of Common abdominal herniae and their management.

Site of defect Treatment

Umbilical Umbilicus Observe
Paraumbilical Just above umbilicus Surgical repair
Epigastric Midline between umbilicus and Surgical repair
xiphisternum
Inguinal:
Indirect Deep inguinal ring Infant: herniotomy only
Adult: herniotomy/herniorrhaphy.
Direct Posterior wall Herniorrhaphy
Femoral Femoral canal Surgical repair
Incisional Previous abdominal wound Surgical repair

91
 37.CONDITIONS OF THE BILIARY SYSTEM
ACUTE PANCREATITIS
Acute pancreatitis is seen as a complication of
gallstones, or in alcoholics.
Clinical Features
• Sudden onset of upper abdominal pain
which is referred to back. Pain is severe,
agonizing and refractory. Pain may be
relieved or reduced by leaning forward.
• Vomiting and high fever, tachypnoea with
cyanosis.
• Tenderness, rebound tenderness, guarding,
rigidity and abdominal distension, severe
illness.
• Features of shock and dehydration.
• Grey-Turner’s sign, Cullen’s sign, Fox sign.
Investigations
• Serum amylase is very high (>1000 Somogyi
units) or shows rising titre.
• Amylase creatinine clearance ratio is
increased. It is - urine amylase/serum
amylase X serum creatinine/ urinary
creatinine X 100. Normal value is 1-4%.
• Serum lipase more specific than amylase.
Serum lipase level after rise persists for
longer period than amylase. Pancreas is the
only source unlike amylase, hence more
specific.
• Plain X-ray shows
❖ ‘Sentinel loop’ of dilated proximal small
bowel.
❖ Distension of transverse colon with
collapse of descending colon (colon cut
off sign).
❖ Air-fluid level in the duodenum.
❖ Renal halo sign.
❖ Obliteration of psoas shadow.
❖ Localized ground glass appearance.
• U/S abdomen.
• Spiral CT is better—gold standard.
Treatment
Conservative Treatment
• Commonly opted.
• Rehydration using ringer lactate, normal
saline, dextrose saline, plasma and fresh
blood transfusion/packed cells.
• Pain relief by pethidine
• In severe haemorrhagic episodes, fresh
frozen plasma and platelet concentrate may
be required in anticipation of DIC and
haemorrhage.
• Nasogastric aspiration, urinary
catheterisation to maintain and monitor
urine output 50 ml hourly.
• Antibiotics like third generation
cephalosporins, imipenem, meropenem,
cefuroxime are used
• Calcium gluconate 10 ml 10% IV 8th hourly
is given as patient will be hypocalcaemic.
• Total Parenteral Nutrition (TPN) using
carbohydrate, amino acids, vitamins,
essential elements.
• Proper electrolyte management with
monitoring is needed.
Surgery
• Laparotomy
COMPLICATIONS OF ACUTE PANCREATITIS
• Shock—Hypovolemic and septic
• Respiratory failure and ARDS—Common in
7 days
• Septicaemia—Common after 7 days
• Hypocalcaemia
• Disseminated intravascular coagulation
(DIC)
• Acute renal failure
• Pancreatic pleural effusion (left sided 20%)
• Pancreatic pseudo aneurysm
• Pancreatic ascites
• Colonic stricture
• Pseudocyst of pancreas
• Chronic pancreatitis
• Splenic vein thrombosis
• Pancreatic abscess
CHOLANGITIS
Acute bacterial cholangitis is a serious life-
threatening emergency caused by infection of an
obstructed biliary tract.
92
Clinical features
• Patients are often older and much sicker.
• Temperature spikes to 104–105°F, with chills,
and very high white blood cell count
indicating sepsis.
• There is some hyperbilirubinemia but the
key finding is extremely high levels of
alkaline phosphatase.
• Charcot’s triad is the presence of fever,
jaundice, and right upper quadrant pain and
is suggestive of ascending cholangitis;
Reynolds pentad is those 3 symptoms plus
altered mental status and evidence of sepsis
(most commonly, hypotension), which
further suggests the diagnosis.
Treatment
• IV antibiotics
• Emergency decompression of the common
duct is lifesaving;
• Eventually cholecystectomy has to be
performed.
BILIARY COLIC
This occurs when a stone temporarily occludes
the cystic duct. This causes colicky pain in the
right upper quadrant radiating to the right
shoulder and back, often triggered by ingestion
of fatty food, accompanied by nausea and
vomiting, but without signs of peritoneal
irritation or systemic signs of inflammatory
process.
Diagnosis & Treatment
• The episode is self-limited (10, 20, maybe 30
minutes), or easily aborted by
anticholinergics.
• U/S establishes diagnosis of gallstones and
elective laparoscopic cholecystectomy is
indicated.
ACUTE CHOLECYSTITIS
• Commonly it occurs in a patient with pre-
existing chronic cholecystitis but often also
can occur as a first presentation.
• Usual cause is impacted gallstone in the
Hartmann’s pouch, obstructing cystic duct.
Causative bacteria are:
• E. coli—most common
• Klebsiella, pseudomonas, proteus
• Strep. faecalis
• Salmonella
• Clostridium welchii
Classification
• Acute calculous cholecystitis.
• Acute acalculous cholecystitis.
Mode of Infection
• Haematogenous through hepatic artery—
cystic artery.
• Portal vein.
• Through bile after filtering in the liver via
portal circulation.
Complications of Acute Cholecystitis
1. Perforation, which usually occurs in the
fundus or in the neck (Hartmann’s). It can
cause cholecystoduodenal,
cholecystointestinal or cholecystobiliary
fistula.
2. Peritonitis.
3. Pericholecystitic abscess, empyema GB.
4. Cholangitis and septicaemia.
5. Empyema gallbladder, gangrenous
gallbladder
Clinical Features
• Sudden onset of pain in the right
hypochondrium, with tenderness, guarding,
and rigidity.
• Palpable, tender, smooth, soft gallbladder.
• Area of hyperaesthesia between 9th and 11th
ribs posteriorly on the right side (Boas’s
sign).
• Jaundice may be present.
• Fever, nausea, palpable tender mass in GB
region (25%).
• Tachycardia and toxic features.
Investigations
• Ultrasound abdomen—very useful, reveals
presence or absence of gallstones; and
thickening of gall bladder wall.
• Plain X-ray abdomen
• LFT. Increased serum bilirubin often signifies
cholangitis or stone in the CBD.
Treatment
1. Hospitalisation.
93
 2. Initially (nonoperative) conservative
treatment (95%):
3. Nasogastric aspiration.
4. IV fluids.
5. Analgesics and antispasmodics.
6. Broad spectrum antibiotics (cefoperazone,
ceftazidime, ceftriaxone, cefotaxime +
amikacin, tobramycin + metronidazole
{antimicrobial}).
7. Observation.
8. Follow-up U/S scan.
9. Later after 3-6 weeks, elective
cholecystectomy
GALLSTONE ILEUS
This condition, which characteristically affects
the elderly, is due to intraluminal intestinal
obstruction by a large gallstone that enters the
intestinal tract through a fistula, usually between
the gallbladder and the duodenum.
Clinical features
The patient presents with acute intestinal
obstruction, which in the vast majority affects the
small bowel. Characteristically, the level of the
obstruction is changing until the stone becomes
firmly impacted, usually in the terminal ileum.
Diagnosis
The condition is diagnosed preoperatively if gas
is demonstrated in the biliary tract or the
gallstone is visualized, usually in the right iliac
fossa.
Treatment
The treatment requires emergency surgical
intervention in all patients. The operation
consists of removal of the impacted calculus
through a small enterotomy and the
cholecystoduodenal fistula is dealt with at a
subsequent operation.
GALLSTONES
Based on chemical composition, gallstones are
classified into cholesterol, black pigment and
brown pigment stones.
Cholesterol stones. These are preceded by the
formation of biliary sludge They have a protein
matrix but are composed predominantly of
cholesterol, with varying amounts of bile
pigments and calcium salts deposited on the
periphery. Cholesterol gallstones do not
commonly harbour bacteria and are not usually
associated with infected bile.
Black pigment stones. They are composed of
bilirubin polymers without calcium palmitate,
small amounts of cholesterol and a matrix of
organic material. Associated infection is present
in less than 20% of patients. Although haemolytic
states predispose to the formation of black
pigment stones, most occur in patients without
detectable chronic haemolysis.
Brown pigment stones. In contradistinction to the
above types, brown pigment stones form in the
bile ducts (primary ductal calculi) and are
associated with infection of the biliary tract.
Brown pigment stones contain calcium
bilirubinate, calcium palmitate and only small
amounts of cholesterol bound in a matrix of
organic material.
Risk factors for gallstone prevalence and
symptomatic gallstone disease.
• Increased prevalence
• Female sex*
• Obesity*
• Age*
• Genetic and ethnic factors*
• Diet depleted in fibre and high in animal
fats*
• Diabetes mellitus*
• Ileal disease and resection
• Haemolytic states†
• Infections of the biliary tract†
• Parasitic infestations†
• Cirrhosis†
• Cystic fibrosis
Precipitation of symptomatic disease
• Pregnancy
• Clofibrate
• Thiazide diuretics
• ?Oral contraception
* Increased prevalence of cholesterol stones.
† Increased prevalence of pigment stones.
Clinical features
90% of gallstones are (probably) asymptomatic.
94
 The symptoms may be acute, chronic or absent
when gallstones are diagnosed as an incidental
finding during the investigation of patients for
unrelated disorders. In patients with chronic
symptoms, it is important to exclude other
disorders that might be responsible.
Spectrum of symptomatic gallstone disease.
• Chronic cholecystitis
• Acute biliary colic/acute cholecystitis
• Jaundice due to large bile duct obstruction
• Cholangitis/septicaemia
• Acute gallstone pancreatitis
• Biliary fistulous disease
• Gallstone ileus
Diagnosis
• Abdominal ultrasound
Treatment
• Asymptomatic gallstones are left alone.
• Symptomatic gallstones are treated based on
the cause.
CHOLEDOCHOLITHIASIS
It is stones in the CBD and biliary tree.
Classification
i. Primary—Rare—brown pigment stones.
ii. Secondary—Common—black pigment
stones/cholesterol stones. It is seen in 15% of
gallstone disease; 75% are cholesterol stones,
15% are pigment stones.
Primary stones
They are formed in CBD and biliary tree itself,
and are multiple, often sludge like, commonly
pigment or mixed type, extends into hepatic
ducts (Brown pigment stones).
Causes:
1) Defective pathophysiology of biliary tree
causing stasis, biliary dyskinesia
2) Congenital conditions like Caroli’s disease,
choledochal cyst.
3) Infections and infestations like clonorchiasis,
ascariasis.
4) Others: Low protein diet, malnutrition,
obesity, females, old age.
Secondary biliary stones
• They are from gallbladder (gallstones)
• Secondary stones are better and easier to
manage than primary stones.
Clinical Features
✓ Incidental CBD stones along with
jaundice/without jaundice.
✓ Pain: It may be biliary colic; nonspecific
abdominal pain; pain of ascending
cholangitis, pain of pancreatitis.
✓ Jaundice—most common clinical
manifestation.
✓ Fever with chills and rigors.
✓ Charcot’s triad of ascending cholangitis
❖ Intermittent pain (may be colicky)
❖ Intermittent fever
❖ Intermittent jaundice
Complications
• Liver dysfunction and biliary cirrhosis.
• White bile formation and liver failure.
• Suppurative cholangitis.
• Liver abscess.
• Septicaemia.
• Pancreatitis
Investigations
• U/S abdomen; CBD diameter > 1 cm
indicates biliary obstruction.
• ERCP, gold standard for diagnosis.
• Liver function tests.
• Endoultrasonography is useful (EUS). It is
more accurate.
Treatment
• Injection Vit. K 10 mg IM once a day for 5
days or FFP infusion to correct the
prothrombin time.
• IV antibiotics (cefoperazone, cefotaxime).
• Correction of dehydration.
• IV Mannitol daily 200 ml BD to prevent
hepatorenal syndrome.
• ERCP—Therapeutic,
• Open cholecystectomy
95
SURGICAL JAUNDICE (Obstructive 3. Obstructive: CBD stones, biliary stricture,
parasitic infestation.
Jaundice)
4. Neoplastic: Carcinoma of head or
Definition periampullary region of pancreas,
cholangiocarcinomas, Klatskin tumour.
It is the jaundice that develops due to biliary
obstruction, partial or complete or intermittent. It 5. Extrinsic compression of CBD by lymph
causes conjugated hyperbilirubinaemia. Normal nodes or tumours.
serum bilirubin level is 0.2-0.8 mg/dl. Scleral
icterus is visible when serum bilirubin level Investigations for Obstructive Jaundice
exceeds 2.5 mg/dl. 1. LFTs
Causes Elevations of both fractions of bilirubin, modest
1. Biliary atresia. elevation of transaminases, and very high levels
of alkaline phosphatase.
2. Choledochal cyst.
2. Ultrasound
3. CBD stones.
Management
4. Ascending cholangitis.
Surgery to treat the underlying cause
5. Biliary strictures.
Adequate preparation of the patient for surgery
6. Sclerosing cholangitis.
• Proper diagnosis and assessment
7. Carcinoma of head and periampullary • Correction of metabolic abnormalities,
region of the pancreas. • improvement of the general condition,
8. Cholangiocarcinoma. • Prophylactic antibiotics like third generation
cephalosporins.
9. Extrinsic compression of CBD by lymph • Injection vitamin K IM 10 mg for 5 days
nodes or tumours. • Repeated monitoring by doing prothrombin
10. Parasitic infestations. time, electrolytes
• Fresh Frozen plasma
Clinical Features • Adequate hydration is most important
• Severe jaundice. 5/10% dextrose
• Pruritus, more on the back and forearms. • Blood transfusion in case of anaemia
• Fever, may or may not be present. • Mannitol 100-200 ml BD IV to prevent
• Loss of weight. hepatorenal syndrome
• Loss of appetite. • Catheterize and monitor urine output
• Pain in right hypochondrium, palpable hourly.
gallbladder, hydrohepatotic palpable, • Management of pruritus: cholestyramine.
smooth, soft, nontender liver are other Complications
features. • Infections (cholangitis, septicaemia, wound
• Steatorrhoea (more fatty stool) due to infections);
improper absorption of fat soluble vitamins. • Disorders of the clotting mechanism;
Classification of Causes of Obstructive • Renal failure;
Jaundice
• Liver failure;
1. Congenital: Biliary atresia, choledochal cyst. • Fluid and electrolyte abnormalities.

2. Inflammatory: Ascending cholangitis,

sclerosing cholangitis.

96
 38.CONDITIONS STOMACH&INTESTINES
INTESTINAL OBSTRUCTION
Definition:
Failure of the intestines to propel its contents.
Complete intestinal obstruction: total blockage
of the intestinal lumen, whereas incomplete
obstruction denotes only a partial blockage.
Obstruction may be acute (hours) or chronic
(weeks), simple (mechanical), i.e. blood supply is
not compromised, or strangulated, i.e. blood
supply is compromised.
Common causes
• Extramural: adhesions, bands, volvulus,
herniae (internal and external), compression
by tumour (e.g. frozen pelvis)
• Intramural: inflammatory bowel disease
(Crohn’s disease), tumours, carcinomas,
lymphomas, strictures, paralytic (adynamic)
ileus, intussusception
• Intraluminal: faecal impaction, foreign
bodies, bezoars, gallstone ileus
• Small-bowel obstruction is often rapid in
onset and commonly due to adhesions or
hernia
Pathophysiology
1. Bowel distal to obstruction collapses
2. Bowel proximal to obstruction distends and
becomes hyperactive. Distension is due to
swallowed air and accumulating intestinal
secretions
3. Bowel wall becomes oedematous. Fluid and
electrolytes accumulate in the wall and
lumen (third-space loss)
4. Bacteria proliferate in the obstructed bowel
5. As the bowel distends, intramural vessels
become stretched and the blood supply is
compromised leading to ischaemia and
necrosis.
Clinical features
• Classical Features: Vomiting, colicky
abdominal pain, abdominal distension,
absolute constipation (i.e. neither faeces nor
flatus)
• Dehydration and loss of skin turgor
• Hypotension, tachycardia
• Abdominal distension and increased bowel
sounds (after a few days there is silence)
• Empty rectum on digital examination
• Tenderness or rebound indicates peritonitis
Investigations
• X-rays
✓ Chest X-ray: elevated diaphragm due to
abdominal distension
✓ Abdominal X-rays: show distended
loops of small bowel, with multiple air-
fluid levels.
• Haemoglobin, packed cell volume: elevated
due to dehydration
• White cell count (WCC): normal or slightly
elevated
• Urea and electrolytes: urea elevated, Na+ and
Cl– low
Treatment
1. Nill Per Os,
2. Decompress the obstructed gut: pass
nasogastric tube
3. Replace fluid and electrolyte losses: give
Ringer’s lactate or saline with K+
supplementation
4. Monitor the patient: fluid balance, urinary
catheter, temperature, pulse, respiration,
blood tests
5. Request investigations appropriate to likely
cause
6. Surgery if:
(b) Underlying cause needs surgical
treatment (e.g. hernia, colonic
carcinoma)
97
 (c) Patient does not improve with • The primary cause is treated.
conservative treatment (e.g. adhesion • IV fluids.
obstruction) • Electrolyte management.
(d) Signs of strangulation or peritonitis are • Catheterisation and urine output
present measurement.
• Decompression of the large bowel
7. Tachycardia, pyrexia and abdominal
tenderness indicate the need to operate STRANGULATED OBSTRUCTION
whatever the cause Strangulated obstruction occurs due to
PARALYTIC ILEUS (Adynamic Intestinal compromised blood supply leading to bowel
ischemia. It starts as described above, but
Obstruction)
eventually the patient develops fever,
It is a state in which intestines fail to transmit leukocytosis, constant pain, signs of peritoneal
peristalsis due to failure of neuromuscular irritation, and ultimately full-blown peritonitis
mechanism, i.e. Auerbach’s and Meissner’s and sepsis.
plexus.
Emergency surgery is required.
• It may be localised or generalised.
Complications of intestinal obstruction
Causes
• Peritonitis
• Postoperative • Hypovolaemic and septic shock
• Infective—pus, blood, bile, toxins, enteritis • Renal failure
• Uraemia • ARDS
• Hypokalaemia • Intra-abdominal abscess formation
• Spinal injury • Moribund status
• Retroperitoneal haemorrhage Postsurgery Complications
• Spinal surgery
• Pelvic abscess.
• Plaster jacket
• Subphrenic abscess.
Clinical Features
• Biliary or faecal fistulas.
• No passage of flatus. • Burst abdomen.
• No bowel sounds. • Bands and adhesions.
• Marked abdominal distension. • Incisional hernias.
• Vomiting of large volume of fluid.
• Tachycardia.
PEPTIC ULCER DISEASE
• Respiratory distress due to pressure over the
Peptic ulcers are focal defects in the gastric or
diaphragm. duodenal mucosa that extend into the submucosa
• High pitched tinkling note ‘like bells at or deeper. They may be acute or chronic and,
evening pealing’. ultimately, are caused by an imbalance between
• Dull abdominal pain (not colicky). mucosal defenses and acid/peptic injury.
• Features of fluid/protein/electrolyte
Etiology
imbalance.
Investigations • H. pylori infection
• NSAID use,
• Serum electrolyte estimation: Especially
• Acid-peptic injury of the gastroduodenal
serum potassium.
mucosal barrier.
• ECG.
• Stress
• X-ray abdomen.
• Acid hypersecretion.
• Ultrasound abdomen to find out the possible
cause of ileus, e.g. sepsis. Clinical Manifestations.
Treatment
Abdominal pain.
• Nasogastric aspiration.

98
The pain is typically non radiating, burning in
quality, and located in the epigastrium.
Patients with duodenal ulcer often experience
pain 2 to 3 hours after a meal and at night. Two
thirds of patients with duodenal ulcers will
complain of pain that awakens them from sleep.
The pain of gastric ulcer more commonly occurs
with eating and is less likely to awaken the
patient at night.
Other signs and symptoms:
• Nausea,
• Bloating,
• Weight loss,
• Stool positive for occult blood, and
• Anemia.
Investigations
• Full blood count: to check for anaemia
• Urea and electrolytes
• Faecal occult blood
• Barium meal
• Urease breath test: non-invasive method of
assessing presence of H. pylori infection.
Used to direct therapy or confirm eradication
Management
Medical
General management
• Avoid smoking and foods that cause pain
• Antacids for symptomatic relief
• H2 blockers (cimetidine)
Specific management: eradication of H. pylori
infection
• Dual therapy: antibiotic + PPI (e.g.
omeprazole)
• Triple therapy (used most often): acid
inhibition (one of omeprazole, lansoprazole,
pantoprazole, ranitidine bismuth citrate) +
antibacterial treatment (two of
clarithromycin, amoxicillin, metronidazole)
for 1 week is highly effective in eradicating
H. pylori
• Quadruple therapy: PPI, bismuth,
metronidazole and tetracycline
• Re-endoscope patients with gastric ulcer
after 6 weeks because of risk of malignancy
Surgical
• Only indicated for failure of medical
treatment and complications
Complications
The three most common complications of PUD,
in decreasing order of frequency are:
• Bleeding,
• Perforation, and
• Obstruction.
BOWEL PERFORATION
Clinical Features
• Severe persistent pain in the epigastrium
initially, later in the right side abdomen and
finally becomes generalised.
• Pain is of sudden in onset,
• Pain often radiates to right scapular region.
• Pain becomes more on movements.
• Tenderness and rebound tenderness is seen
(Blumberg sign) all over the abdomen.
• Fever, vomiting, dehydration, oliguria
occurs.
• Patient is toxic, with tachycardia,
hypotension, tachypnoea.
• Abdominal distension occurs.
• Guarding and rigidity,
• Dullness over the flank
• Obliteration of liver dullness
• Silent abdomen with absence of bowel
sounds.
• Tenderness felt on per rectal examination.
• Often slow, small perforation presents with
subacute features, but diffuse peritonitis
eventually sets in 24-48 hours.
Investigations
• Plain X-ray abdomen (erect posture): Shows
gas under diaphragm in 70% of cases. In 30%
of cases, there is no gas under diaphragm
• U/S abdomen shows free fluid and often
gas.
• CT scan abdomen is very sensitive
investigation whenever there is absence of
gas under diaphragm. It rules out other
conditions like pancreatitis. Gastrograffin
upper GI study also confirms the perforation.
Treatment
• Patient is advised admission.
99
 • IV fluids—Ringer lactate, normal saline,
dextrose saline.
• Antibiotics—Cefotaxime, metronidazole,
amikacin.
• Catheterisation.
• Ryle’s tube aspiration.
• Surgery: Emergency laparotomy.
ACUTE APPENDICITIS
Organisms: E. coli (85%), enterococci, (30%),
streptococci, Anaerobic streptococci, Cl. welchii,
bacteroides.
Clinical features
The classic picture of acute appendicitis begins
with anorexia, followed by:
• Vague periumbilical pain that several hours
later becomes sharp, severe, constant, and
localized to the right lower quadrant of the
abdomen (McBurney’s point)
• Leiomyoma of intestine
• Meckel’s diverticulum
• Carcinoma
• Purpuric submucosal haemorrhages
Clinical Features
• Common in males (3:2).
• Common in 6-9 months. But can also occur at
later age grouped children.
• Commonest cause of intestinal obstruction in
infancy.
• Initial colicky abdominal pain (75%) which
eventually becomes severe and persistent.
• Sudden onset of pain in a male child, with
progressive distension of the abdomen,
vomiting, with passage of “red-currant-jelly”
stool. It is usually not found in adult ISS.
• Often ISS is recurrent, when it gets reduced,
child automatically becomes asymptomatic.
Abdominal palpatory findings in ISS

• Tenderness, guarding, and rebound found to • Palpable mass (85%)

the right and below the umbilicus (not ❖ Sausage shaped smooth, firm mass
elsewhere in the belly)
❖ Mass does not move with respiration
Diagnosis
❖ Mobile in all directions
Modest fever and leukocytosis in the 10,000–
15,000 range, with neutrophilia and immature ❖ Resonant
forms ❖ Mass contracts under the palpating
Treatment fingers

Emergency appendectomy. ❖ Mass appears and disappears

• Empty right iliac fossa

INTUSSUSCEPTION (ISS)
• Features of intestinal
Definition obstruction/peritonitis—later

It is telescoping or invagination of one portion Investigations

(segment) of bowel into the adjacent segment. • Barium enema shows typical claw sign or
Types coiled spring sign (Pincer end).
• Ultrasound shows target sign or
1. Antegrade: Most common. pseudokidney sign or bull’s eye sign, which
2. Retrograde: Rare (jejunogastric in is diagnostic.
gastrojejunostomy stoma). • Doppler may show mass with doughnut sign
and is useful to check blood supply of bowel.
It can be single or multiple (rare).
• Plain X-ray abdomen shows multiple air
Causes fluid levels.

• Change in diet during weaning Treatment

• Upper respiratory tract viral infection • Ryle’s tube aspiration.
• Intestinal polyps • IV fluids.
• Submucous lipoma • Antibiotics.

100
 • Catheterisation. PYLORIC STENOSIS DUE TO
• Surgery
CHRONIC DUODENAL ULCER
VOLVULUS

Definition Pathology

It is the twist (rotation) in the axis of the loop of
the bowel either clockwise or anticlockwise.
SIGMOID VOLVULUS (Volvulus of
Pelvic Colon)
Chronic DU after many years undergoes scarring
and cicatrisation causing total obstruction of the
pylorus, leading to enormous dilatation of
stomach.
Clinical Features

Volvulus of the sigmoid colon tends to occur in • Pain is severe, persistent, in epigastric
elderly, constipated, institutionalized patients region, and also with feeling of fullness.
who are mentally defective. • Vomiting—large quantity, foul smelling and
frothy, vomitus contains food consumed on
Types
previous day (partially digested or
1. Acute. undigested food).
• Loss of periodicity.
2. Recurrent.
• Loss of appetite and weight.
Clinical Features • Visible gastric peristalsis (VGP)—may be
elicited by asking the patient to drink a cup
• Pain in the abdomen
of water.
• Absolute constipation
• Confused status because of alkalosis and
• Enormous distension of abdomen,
electrolyte changes.
• Late vomiting and eventually dehydration.
• Electrolyte changes: Because of vomiting,
• Features of peritonitis.
hypochloraemic, hyponatraemic,
• Hiccough and retching can occur.
hypokalaemic, hypocalcaemic,
Investigations hypomagnesaemic alkalosis occurs. It causes
paradoxical aciduria.
1. Plain X-ray:(diagnostic in 70-80%)
• Mass is never palpable.
• Ω sign (omega sign)—single, grossly
Investigations
distended loop of colon arising out of the
pelvis and extending towards the 1. Barium meal study:
diaphragm.
• Absence of duodenal cap.
• Coffee-bean sign or Bent-inner tube sign.
• Dilated stomach where greater curvature is
2. Contrast enema
below the level of iliac crest.
Birds beak sign (ace of spades appearance) • Mottled stomach.
• Barium will not pass into duodenum.
Treatment
2. Gastroscopy to rule out carcinoma stomach
• RT aspiration. and to visualise the stenosed area.
• IV fluids.
3. Electrolyte study for correction of electrolyte
• Catheterisation. imbalance.
• Antibiotics.
Surgery 4. ECG to check for hypokalaemia.

Decompression of the loop may be possible in Differential Diagnosis

subacute obstruction. More often, laparotomy is Carcinoma pylorus—here mass may be palpable
required.
Treatment

• Correction of dehydration and electrolytes

by IV fluids—normal saline or double

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 strength saline, calcium, potassium, Investigations
magnesium.
• Small bowel enema/barium meal follow
• Blood transfusion is given if there is
through may show roundworms in the
anaemia.
ileum.
• TPN support.
• US can demonstrate the worms
• Stomach wash to clean the stomach contents
• Blood may show eosinophilia, anaemia,
(using normal saline) is given using stomach
hypoalbuminaemia.
tube like Eswald’s
• Stool examination may show ova.
• Surgery
Treatment of roundworm obstruction
ROUNDWORM OBSTRUCTION
• Drugs—piperazine citrate, mebendazole,
(Ascaris Lumbricoides)
albendazole
Features • Most often by conservative treatment,
worms get dispersed and passed per anally.
• Worm colic. But patient requires nasogastric aspiration,
• Toxicity—fever, tachycardia. IV fluids, antibiotics, and observation
• Subacute intestinal obstruction. • If patient is not responding then laparotomy
• Acute intestinal obstruction with palpable is done.
roundworm bolus per abdomen. • Perforation due to worm requires immediate
• Perforation laparotomy, removal of worms and closure
• Dyspepsia, malabsorption, iron deficiency of perforation.
anaemia.

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 39.CONDITIONS OF THE RECTUM, ANUS AND PERI-
ANAL AREA

HAEMORRHOIDS(PILES) • Third degree: prolapses and requires manual

reduction
Definition • Fourth degree: prolapses but cannot be
reduced manually, often requires urgent
A submucosal swelling in the anal canal arising
from the anal cushions and consisting of a dilated surgery
venous plexus, a small artery and areolar tissue. Treatment
Internal haemorrhoids only involve tissues of • Conservative: sitz bath, bulk laxatives, fluids
upper anal canal; external haemorrhoids involve
and high fibre diet, drugs—(analgesics and
tissues of lower anal canal
for reducing the itching)
Aetiology • Bleeding internal piles; injection
sclerotherapy, Barron’s bands, cryosurgery
• Hereditary.
• Prolapsing external: haemorrhoidectomy
• Straining,
• Diarrhoea, Complications
• Constipation, • Profuse haemorrhage
• Hard stool, • Strangulation
• Low fibre diet, • Thrombosis
• Overpurgation, • Ulceration.
• Carcinoma rectum, • Gangrene.
• Pregnancy, • Fibrosis.
• Portal hypertension (rare cause) • Stenosis.
• Idiopathic cause • Suppuration, leads to perianal or
Found at the 3, 7 and 11 o’clock positions in the submucosal abscess.
anal canal.
FISTULA IN ANO)
Classification
Definition/aetiology
First degree haemorrhoids
• Abnormal communication between perianal
• Piles within that may bleed but does not
skin and anal canal established that persists
come out
following drainage of a perianal abscess
Second degree haemorrhoids • May be associated with Crohn’s disease
(multiple fistulae), ulcerative colitis or
• Piles that prolapse during defecation, but
returns back spontaneously tuberculosis
• Low: below 50% of the external anal
Third degree haemorrhoids sphincter
• Piles prolapsed during defecation, can be • High: crossing 50% or more of the external
replaced back only by manual help anal sphincter
Clinical features
Fourth degree haemorrhoids
• Chronic perianal discharge
• Piles that are permanently prolapsed • External orifice of track with granulation
Clinical features tissue seen perianally
Treatment
• First degree: bleeding/itching only
• Second degree: prolapse during defecation, • Low: probing and laying open the track
spontaneous reduction. (fistulotomy)

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 • High: seton insertion, core removal of the
fistula.
ANAL FISSURE (FISSURE IN ANO)
Definition
Longitudinal tear in the mucosa of the anal canal,
in the midline posteriorly (90%) or anteriorly
(10%)
Aetiology
• 90% caused by local trauma during passage of
constipated stool and potentiated by spasm of
internal analsphincter
• Other causes: pregnancy/delivery, Crohn’s
disease, sexually transmitted infections (often
lateral position)
Clinical features
• Exquisitely painful on passing bowel motion
• Small amount of bright-red blood on toilet
tissue
• Severe sphincter spasm
• Skin tag at distal end of tear (‘sentinel pile’)
Treatment
• First line: stool softeners/bulking agents,
local anaesthetic gels, 0.2% GTN ointment
• Second line: botulinum toxin injection,
lateral internal sphincterotomy
PERIANAL ABSCESS
Aetiology
Focus of infection starts in anal glands
(‘cryptoglandular sepsis’) and spreads into
perianal tissues to cause:
• Perianal abscess: adjacent to anal margin
• Ischiorectal abscess: in ischiorectal fossa
• Pararectal abscess: above levator ani
Clinical features
• Painful, red, tender, swollen mass
• Fever, rigors, sweating, tachycardia
Treatment
• Incision and drainage
• Antibiotics
INTESTINAL ATRESIA
Intestinal atresia presents early in the newborn
period.
The atretic segment(s) can affect any part of the
gastrointestinal tract; the proximal small bowel is
more commonly affected than distal small bowel
and the colon is the least commonly affected.
Usually caused by impairment of the blood
supply to the affected segment of intestine, can
occur relatively late in fetal life, after meconium
has passed into the distal bowel.
CLINICAL FEATURES
• Signs and symptoms of intestinal obstruction:
❖ vomiting (usually bilious),
❖ abdominal distension,
❖ constipation and
❖ colicky abdominal pain.
The level of the atresia will determine which
symptoms and signs predominate; a high small
bowel atresia will present early with vomiting
but abdominal distension, colicky pain and
constipation may not be prominent features.
Diagnosis
Abdominal films aid the diagnosis.
Fluid-filled loops of distended obstructed
intestine with or without fluid levels are usually
diagnostic in a proximal atresia.
Management
Surgical treatment involves resection of the ends
of the atretic segments and anastomosis of the
ends.
Complication of surgery
❖ Short-gut syndrome.
HIRSCHSPRUNG’S DISEASE
(aganglionic megacolon)
It is a congenital, familial condition, occurring in
newborn due to the absence of ganglion cells—
Auerbach’s and Meissner’s plexus in anorectum,
which may extend proximally either a part or full
length of the colon.
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The newborn affected by Hirschsprung’s disease Management
is usually large and postdates at birth. There is a
Surgical correction
strong association with Down’s syndrome.

Clinical features IMPERFORATED ANUS

❖ The cardinal symptom is chronic Imperforated anus may be the clinical

constipation. presentation noted on detailed examination of
the newborn. If so, the others have to be ruled
❖ The baby usually presents in the first few
out as detailed above.
days of life having failed to pass meconium.
For the imperforated anus itself, look for a fistula
❖ The baby stops feeding, develops abdominal
nearby (to vagina or perineum).
distension and vomits, often bilious fluid.
• If present, repair can be delayed until further
❖ Plain abdominal X-ray will reveal gas down
growth (but before toilet training time).
to the distal colon but no gas in the rectum.
Treatment
Diagnosis
Surgical repair
Diagnosis is made with full-thickness biopsy of
rectal mucosa.

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 40.CONDITIONS OF THE KIDNEYS, URETERS AND
URINARY BLADDER

HEMATURIA RENAL CALCULI

Hematuria is the most common presentation for Renal stones: concretions formed by precipitation
cancers of the kidney, ureter, or bladder. of various urinary solutes in the urinary tract.
They contain calcium oxalate (60%), a mixture of
Types
calcium, ammonium and magnesium phosphate
(a) Gross (visible to unaided eye). (triple-phosphate stones are infective in origin;
30%), uric acid (5%) and cystine (1%).
(b) Microscopic (> 5 RBC’s/HPF).
Aetiology
❖ Early (initial) haematuria: Urethral origin,
distal to external sphincter ❖ Diet- vit A deficiency
❖ Climate- hot climate
❖ Terminal haematuria: Bladder neck or ❖ Infection in kidney
prostate origin ❖ Prolonged immobilisation
❖ Diffuse (total) haematuria: Source is in the ❖ Hyperparathyroidism
bladder or upper urinary tract ❖ Hyperoxaluria
❖ Cystinuria (Autosomal recessive).
Causes ❖ Stasis due to obstruction to urine flow.
❖ Renal injury ❖ Medullary sponge kidney.
❖ Urinary stones ❖ Others: Sarcoidosis, myelomatosis, gout,
❖ Wilm’s tumour idiopathic hypercalciuria, hypervitaminosis
❖ Tuberculosis D, neoplasms on treatment,
❖ Renal cell carcinoma hypomagnesuria (Mg++ in urine acts as a
❖ Cystitis complexing agent and prevents nucleation
❖ Bladder tumour normally).
❖ Urinary bilharziasis ❖ Renal tubular acidosis
❖ BPH, carcinoma prostate Clinical features
❖ Renal infarct
❖ Glomerulonephritis • Calyceal stones may be asymptomatic
❖ Blood dyscrasias • Ureteric colic: severe colicky pain radiating
Investigations from the loin to the groin and into the testes
or labia associated with gross or microscopic
❖ Urine culture and sensitivity haematuria
❖ Ultrasound • Bladder calculi present with sudden
❖ Cystourethroscopy interruption of urinary stream, perineal pain
❖ IVU look for function of the kidneys. and pain at the tip of the penis.
❖ Urinary cytology
❖ Bleeding time; clotting time; Investigations
prothrombin time; platelet count. • Full blood count, urea and electrolytes,
❖ CT abdomen. serum creatine, calcium, phosphate, urate,
❖ Renal function tests proteins and alkaline phosphatase
Management • Urine microscopy & culture
Cause should be identified and treated. • Plain abdominal X-ray (90% of renal calculi
are radiopaque)
• IVU confirms the presence and identifies the
position of the stone in the genitourinary
tract

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• A renogram C. Intraluminal:
• 24-h urine collection
1. Stone in the renal pelvis or ureter.
• Stone analysis
Management 2. Sloughed papilla in papillary necrosis.

• Pain relief for ureteric colic: pethidine Bilateral

• High fluid intake
A. Congenital:
• 80% of ureteric stones pass spontaneously:
stones < 4 mm in diameter almost always ❖ Congenital stricture of external urethral
pass; stones > 6mm almost never meatus, pinhole meatus.

Indications for surgical/and intervention ❖ Congenital posterior urethral valve.

• Kidney stones: symptomatic, obstruction, B. Acquired:

staghorn
❖ BPH.
▪ PCNL (Percutaneous Nephrolithotomy).
❖ Carcinoma prostate.
• Ureteric stones: failure to pass, large stone,
obstruction, infection ❖ Postoperative bladder neck scarring.

▪ Ureterolithotomy ❖ Inflammatory/traumatic urethral stricture.

• Bladder: all stones ❖ Phimosis.

▪ Mechanical lithotripsy or open surgery ❖ Carcinoma cervix.

HYDRONEPHROSIS (HN) ❖ Bladder carcinoma.

❖ Congenital PUJ is the most common cause

It is an aseptic dilatation of pelvicalyceal system of HN.
due to partial or intermittent obstruction to the
outflow of urine. Clinical Features

Aetiology A. In unilateral cases:

It can be unilateral or bilateral. ❖ Dull aching loin pain with dragging

sensation or heaviness.
Unilateral
❖ Mass in the loin which is smooth, mobile,
A. Extramural:
ballotable, moves with respiration with
1. Aberrant renal vessels (vein or artery). dullness in renal angle and a band of colonic
resonance in front.
2. Compression by growth (carcinoma cervix,
carcinoma rectum). ❖ Attacks of acute renal colic.

3. Retroperitoneal fibrosis. ❖ Often patient may be having Dietl’s crisis—

after an acute attack of renal colic, swelling
4. Retrocaval ureter. in the loin is seen which disappears after
sometime following passage of large volume
B. Intramural:
of urine.
1. Congenital PUJ (pelviureteric junction)
❖ Dysuria, haematuria, if infected fever and
obstruction.
tenderness in renal angle.
2. Ureterocele.
B. In bilateral cases:
3. Neoplasm of ureter.
From lower urinary tract obstruction.
4. Narrow ureteric orifice.
❖ Loin pain
5. Stricture ureter following removal of stone,
pelvic surgeries or tuberculosis of ureter.

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 ❖ Features of bladder outlet obstruction— A combination of surgery, radiotherapy and
frequency, hesitancy, poor stream chemotherapy.

❖ Kidneys are often not palpable if renal RENAL CELL CARCINOMA

failure develops early.
Definition
From bilateral upper urinary tract obstruction.
Renal cell carcinoma (also known as
❖ Loin pain, mass in the loin, attacks of renal
hypernephroma and Grawitz tumour): malignant
colic
lesion (adenocarcinoma) of thekidney
❖ In bilateral cases, when it is severe, features Epidemiology
of renal failure like oliguria, oedema,
hiccough may be present. • M/F ratio 2 : 1
• Uncommon before age 40 years
Complications
• Accounts for 2–3% of all tumours in adults
1. Pyonephrosis. and 85% of all renal tumours (the other renal
tumours are urothelial tumour, Wilms’ tumour
2. Perinephric abscess.
and sarcoma)
3. Renal failure in bilateral cases. Aetiology

Investigations • Diet: high intake of fat, oil and milk

❖ Blood urea and serum creatinine.
❖ Urine for microscopy.
❖ U/S abdomen: Investigation of choice.
❖ CT scan is diagnostic.
• Toxic agents: lead, cadmium, asbestos,
petroleum byproducts
• Smoking
• Genetic factors
• Other diseases: von Hippel–Lindau
syndrome, adult polycystic disease

Treatment Clinical features

Always conservative surgeries which are aimed Full-blown picture produces:

at conserving the kidneys are done.
▪ Hematuria,
1. The cause is treated
▪ Flank pain, and
NEPHROBLASTOMA (WILMS’ ▪ A flank mass.
TUMOUR) It can also produce hypercalcemia,
erythrocytosis, and elevated liver enzymes.
Nephroblastoma is a malignant mixed renal
tumour that occurs predominantly in children Diagnosis
and usually appears at about 3 years of age.
CT gives the best detail, showing the mass to be
Approximately one-third are hereditary. heterogenic solid tumour.

Clinical features Treatment

The tumour may present with pain but many are Surgery is the only effective therapy.
detected serendipitously during a well-baby
examination. CANCER OF THE BLADDER

Diagnosis Cancer of the bladder (transitional cell cancer in

An abdominal mass is the usual physical finding.
Ultra-sonography and enhanced CT scanning
support the diagnosis
Treatment
most cases) has a very close correlation with
smoking (even more so than cancer of the lung).
Clinical features
• The most common symptom is painless
intermittent haematuria

108
 • Sometimes there are irritative voiding Complications
symptoms (dysuria and frequency).
• Ureteral and urethral stricture, recurrent
Diagnosis UTI, bladder calculi, urinary fistula.
• Squamous cell carcinoma of the bladder
Cystoscopy preceded by CT scan.
Investigations
Management
• Cystoscopy and biopsy.
Surgery and intravesical BCG
• IVU.
SCHISTOSOMA HAEMATOBIUM • Cystography.
• Urine microscopy
(Endemic Haematuria, Urinary
Treatment
Bilharziasis)
• Long-term Praziquantel or metrifonate.
Clinical Features • Surgery for thimble bladder—ileo-or
• Initially cutaneous lesions like utricaria caecocystoplasty.
develops lasting for few days. • Cystoscopic diathermy fulgaration of
• Then after a period of 4-8 weeks, fever, along papillomas.
with features of eosinophilia develops. • Radical cystectomy, if it is squamous cell
• Eventually, after many months it causes carcinoma of the bladder.
intermittent, pain-less, terminal haematuria.

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 41. CONDITIONS OF THE PROSTATE GLAND
PROSTATITIS
Acute bacterial prostatitis
The major cause is aerobic Gram-negative bacilli,
of which E. coli is seen in 80% of patients.
Pseudomonas and enterococcus are also
commonly found.
Possible routes of infection
• Ascending organisms from the urethra,
• Reflux of infected urine into prostatic ducts,
• Lymphatic spread from the rectum or
haematogenous spread.
Clinical features
• Pyrexia,
• Rigors,
• Low back pain,
• Dysuria,
• Urinary frequency and
• Urgency.
• Perineal heaviness, pain on defaecation.
Rectal examination reveals an extremely tender
prostate that is swollen, warm and firm.
Investigations
• Urine culture
• Prostatic massage will express pus and
bacteria; however, this is generally avoided
in the acute setting because of pain and risk
of bacteraemia.
Treatment
Antimicrobial agents directed at the specific
organism.
Initial therapy usually includes intravenous
antibiotics for acute pyrexic episodes, changing
to oral agents after about 1 week. Subsequent
oral therapy should continue for 1 month to
prevent progression to chronic bacterial
prostatitis or prostatic abscess formation.
Chronic bacterial prostatitis
Chronic bacterial prostatitis is an indolent non-
acute infection of the prostatic ducts and glands.
It is the most common cause of relapsing urinary
tract infection in men.
The causative agents are similar to those of acute
bacterial prostatitis.
Clinical features
Some patients are completely asymptomatic and
are diagnosed only on the basis of bacteriuria
found incidentally on urinalysis.
Symptoms
• Dysuria,
• Frequency
• Urgency,
• Perineal discomfort
• Low back
Examination of the prostate may range from
normal to boggy or at times indurated.
Investigations
Urine culture
If urine is sterile, sequential collections of
specimens from the urethra, midstream urine
and prostatic secretions should be performed.
Differential diagnosis
• Cystitis,
• Haemorrhoids and
• Anal fissures.
Treatment
• Treatment of chronic bacterial prostatitis is
directed at eradicating the prostatic focus of
infection.
• Trimethoprim is recommended for patients
with normal renal function.
• Combination of trimethoprim and
sulfamethoxazole for 12 weeks have the best
success rates.
Non-bacterial prostatitis
Non-bacterial prostatitis often presents with
dysuria, perineal discomfort or low back pain,
although repeated cultures fail to reveal an
infectious agent.
Treatment usually starts with antibiotics, but if
unsuccessful symptomatic treatment can be tried
with antiinflammatory and anticholinergic agents
and α-adrenergic antagonists.
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BENIGN PROSTATIC HYPERTROPHY • Cystoscopy

Definition
Benign prostatic hypertrophy: a condition of
unknown aetiology characterized by an increase
in size of the inner zone of the prostate gland.
Epidemiology
• Benign prostatic hypertrophy is present in
50% of 60–90-year-old men.
Pathophysiology
• Microscopic stromal nodules develop around
the periurethral glands.
• Glandular hyperplasia originates around
these nodules
• As the gland increases in size it compresses
the urethra, leading to urinary tract
obstruction.
Clinical features
• Weak stream
• Frequency, Hesitancy, Urgency,
Intermittency
• Nocturia
• Dribbling
• Dysuria, Straining to void
• Urge incontinence
• Acute urinary retention
• Overflow incontinence
• Palpable (or percussable) bladder
• Enlarged smooth prostate on digital rectal
examination.
Prostatism is a combination of symptoms like
frequency both at day and night, poor stream,
delay in starting and difficulty in micturition.
Management
Medical
• α-Adrenergic blockers (e.g.
phenoxybenzamine, prazosin)
• Antiandrogens acting selectively at prostatic
cellular level (e.g. finasteride)
• Intermittent self-catheterization
• Balloon dilatation and stenting of prostate
Surgical
• Majority of patients are treated surgically
• Surgical removal of the adenomatous portion
of the prostate
• Transurethral resection of the prostate
(TURP)
• Open prostatectomy, which may be
transvesical or retropubic.
Prognosis
• Majority of patients have very good quality
of life after prostatectomy.
CARCINOMA PROSTATE
• It is the most common malignant tumour in
men over 65 years.
• Carcinoma prostate occurs in peripheral
zone in prostatic gland proper, i.e.
commonly in posterior lobe. So
prostatectomy for BPH does not confer
protection against development of carcinoma
prostate.
• Incidence of prostate cancer in men over 80
years is 70%.

Investigations Histology
Staging of carcinoma prostate
• Urinalysis for evidence of infection or
haematuria Occult—Diagnosed after investigation due to
suspicion
• Urine culture
• Full blood count, urea and electrolytes, Stage I—Tumour confined to prostate/local
serum creatinine nodule
• Uroflowmetry
Stage II—Tumour involving capsule or diffuse
• Pressure–flow studies type
• Residual volume measurement (normal <
Stage III—Tumour involving seminal vesicle
100 mL)
• Ultrasonography of kidneys and bladder Stage IV—Extension into adjacent tissue
• Transrectal US
• Prostate specific antigen (PSA)
• IVU

111
TNM staging of carcinoma prostate
T1 – Incidentally confirmed carcinoma after
prostatectomy
• T1a – Tumour occupying less than 5% of
specimen
• T1b – Tumour occupying more than 5% of
specimen
• T1c – Tumour impalpable but suspected by
high PSA
T2 – Tumour nodule palpable on rectal
examination.
❖ On per rectal examination, prostate feels
hard, nodular, irregular often with loss of
median groove
❖ Incidental carcinoma after TURP or after
PSA analysis
❖ Features of renal failure
❖ Anaemia secondary to extensive bone
marrow invasion and also due to renal
failure
Investigations

• T2a – Single nodule palpable on digital • Prostate specific antigen (PSA): More than 10
examination within prostate capsule nmol/ml is suggestive.
• T2b – Nodule involving both lobes • Transrectal ultrasound (TRUS) is very useful.
T3 – Tumour extends through the capsule • U/S, abdomen,
• T3a – Extension through capsule one or both • MRI to evaluate local invasion and regional
• T3b – Extension to seminal vesicles lymphadenopathy
T4 – Tumour which is fixed or spread to adjacent • Tests to rule out secondaries
structures like pelvic wall and rectum other than ❖ Full Blood Count
seminal vesicles
❖ Comprehensive metabolic panel
Spread
❖ X-ray
• Local spread
❖ Bone scan
• Blood spread
• Lymphatic spread ❖ LFTs

Clinical features Treatment

❖ Commonly asymptomatic • Radical prostatectomy

• Radical radiotherapy.
❖ Bladder outlet obstruction and so retention
• TURP + Bilateral orchidectomy + External
of urine
radio therapy for bone secondaries +
❖ Haematuria, frequency Flutamide or Honvan
• Drugs (hormones antagonists)
❖ Pelvic pain, back pain, arthritic pain in
sacroiliac joint.

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 42. CONDITIONS OF THE URETHRA

STRICTURE URETHRA 2. Visual internal cystoscopic urethrotomy

or stricturotomy
Classification: Aetiologically.
3. External urethrotomy by open method.
1. Congenital.
4. Urethroplasty.
2. Inflammatory:
Complications of stricture urethra
a. Post-gonococcal is most common (70%).
• Retention of urine
b. Tuberculous. • Urethral fistula
• Infection—urethritis, cystitis, pyelonephritis
c. Other infection (urethritis).
• Urethral diverticula
3. Traumatic: Bulbous, membranous. • Periurethral abscess
• Bilateral hydronephrosis
4. Postinstrumentation: Catheter, dilator,
cystoscope. • Stone formation
• Renal failure
5. Postoperative: Prostate surgery (4%), • Due to straining—hernia, haemorrhoids,
urethrostomy. rectal prolapse
Clinical features HYPOSPADIAS
• Poor urinary stream
It is the most common congenital malformation
• Forking and spraying of the stream
of urethra wherein external meatus is situated
• Incomplete emptying
proximal than normal, over the ventral (under)
• Frequency, dysuria aspect of the penis.
• Retention and often with overflow
• Pain, burning micturition, suprapubic Features
tenderness • Absence of urethra and corpus spongiosum
• Thickening and button-like feeling in bulbar distal to abnormal urethral orifice.
urethra (Bulbous urethra is felt clinically by • Bowing or bending of penis distal to
lifting the scrotum in midline in the abnormal urethral opening (chordee), with
perineum) poorly developed prepuce over inferior
Investigations aspect.
• Urine soakage over the scrotum with
• Urine microscopy and culture. dermatitis and infection.
• Blood urea and serum creatinine. • Associated congenital anomalies are known
• IVU to see hydronephrosis and function of to exist.
kidney.
• U/S abdomen. Treatment
• X-ray of pelvis to see old fracture with • Surgical correction/reconstruction
history of trauma.
In hypospadias, circumcision is contraindicated
• Ascending urethrogram is an essential
as prepucial skin is required for future
investigation to see the site, type, extent and
urethroplasty.
false passage.
• Urodynamic studies. EPISPADIAS
• Urethroscopy
• Here the urethra opens on the dorsum of the
Treatment penis, proximal to the glans.
1. Intermittent dilatation

113
 • It is associated with a dorsal chordee, ectopia
vesicae, urinary incontinence, separated
pubic bones.
• It is uncommon in females.
Treatment
• Correction of incontinence of urethra.
• Urinary diversion.
RETENTION OF URINE
❖ It is accumulation of urine in the urinary
bladder.
❖ It is very common in men who already have
significant symptoms from benign prostatic
hypertrophy.
❖ It is often precipitated during a cold, by the
use of antihistamines and nasal drops, and
abundant fluid intake.
Types
❖ Acute
❖ Chronic
❖ Retention with overflow
Causes
In males
❖ BPH in old.
❖ Stricture urethra in young.
❖ Trauma—urethral/pelvic.
❖ Postsurgical—perineal surgeries like
haemorrhoidectomy; fistulectomy; fi
ssurectomy; pelvic surgeries; surgeries for
fracture hip/fracture pelvic bone.
❖ Bladder outlet obstruction.
❖ Carcinoma of prostate.
In females
❖ Uterine prolapse.
❖ Urethral stricture.
❖ Uterine/Ovarian surgeries.
In infants and children
❖ Posterior urethral valve.
❖ Meatal stenosis.
Clinical Features
The patient wants to void but cannot, and the
huge distended bladder is palpable.
Investigations
❖ U/S abdomen.
❖ Blood urea, serum creatinine.
❖ Urine microscopy.
Treatment
❖ Urinary catheterisation using Foley’s
catheter.
❖ If it fails then suprapubic cystostomy (SPC)
using Malecot’s catheter is done.
❖ The cause is treated.
❖ Intermittent catheterisation in case of
neurogenic bladder.
URINE INCONTINENCE
Incontinence is the involuntary loss of urine.
Urine loss may occur through the urethra or, less
commonly, from an abnormal extraurethral route
such as a vesicovaginalfistula or ectopic ureter.
Classification according to anatomical
abnormality
I. Urethral incontinence
This is the most common form of incontinence in
which there is involuntary loss of urine through
the urethra. This form of incontinence may be
due to urethral, bladder or non-urinary causes.
II. Non-urethral incontinence
Loss of urine from an abnormal extraurethral
orifice may indicate fistula or ectopic ureter.
Classification according to clinical presentation
1. Stress incontinence
Very common in middle-age women who have
had many pregnancies and vaginal deliveries.
They leak small amounts of urine whenever
intra-abdominal pressure suddenly increases.
This includes sneezing, laughing, getting out of a
chair, or lifting a heavy object.
2. Urge incontinence
Unstable detrusor contractions produce
frequency, urgency and urge incontinence. This
114
may be due to neuropathic bladder injury
(detrusor hyperreflexia) or idiopathic unstable
detrusor contractions. Increased sensory
stimulation by stones, tumours or infection may
also cause similar symptoms.
3. Nocturnal enuresis
Bed-wetting in older children is abnormal and
may be associated with daytime voiding
abnormalities such as frequency and urgency,
consistent with unstable detrusor activity. In
older men, bed-wetting may represent an over-
distended bladder due to bladder outflow
obstruction.
4. Constant urinary wetness
This may be due to urinary fistula or ectopic
ureter.
Assessment
❖ A detailed history to assess the pattern of
voiding and incontinence will help in
diagnosis.
❖ Physical examination including neurological
examination.
Investigations
❖ Urine microscopy & culture
❖ IVU
❖ Cystoscopy
❖ Cystogram
Treatment
A. URGE INCONTINENCE
If urge incontinence is due to infection, stone or
tumour, these causes must be treated
appropriately.
Pharmacological therapy
Drugs with an anticholinergic and/or smooth-
muscle relaxant effect may be used (e.g.
oxybutynin, emepronium carageenate, flavoxate
hydrochloride).
Surgery
Surgery is occasionally necessary.
B. STRESS INCONTINENCE
• For early cases, pelvic floor exercises may be
sufficient.
• For advanced cases with large cystoceles,
surgical repair of the pelvic floor is indicated.
• For extreme cases, surgical reconstruction of
the pelvic floor may be needed.
C. OVERFLOW INCONTINENCE
Overflow incontinence due to outflow
obstruction as a result of BPH or urethral
stricture is treated by TURP or urethrotomy
respectively.
D. NOCTURNAL ENURESIS
• As children grow older an increasing number
achieve continence.
• Management consists of bladder training
during the day, gradually increasing the
interval between voiding, combined with
voiding last thing at night.
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 43. CONDITIONS OF THE TESTIS, EPIDIDYMIS, AND
TESTICULAR TORSION
Testicular torsion is seen in young adolescents.
There is severe testicular pain of sudden onset,
but no fever, pyuria, or history of recent mumps.
The testis is swollen, exquisitely tender, “high
riding,” and with a “horizontal lie.” The cord is
not tender.
This is one of the few urologic emergencies, and
time wasted doing any tests is tantamount to
malpractice.
Immediate surgical intervention is indicated.
After the testis is untwisted, an orchiopexy is
done to prevent recurrence.
ACUTE EPIDIDYMITIS
Acute epididymitis can be confused with
testicular torsion. It is seen in young men old
enough to be sexually active, and it also starts
with severe testicular pain of sudden onset.
There is fever and pyuria, and although the testis
is swollen and very tender, is in the normal
position. The cord is also very tender. Acute
epididymitis is treated with antibiotics, but the
possibility of missing a diagnosis of testicular
torsion is so dreadful that sonogram is done to
rule it out.
TESTICULAR CANCER
Testicular cancer affects young men, in whom it
presents as a painless testicular mass.
DIAGNOSIS
Blood samples are taken pre-op for serum
markers (α-fetoprotein [AFP] and β-human
chorionic gonadotropin [β-HCG]).
TREATMENT
Radical orchiectomy is performed by the inguinal
route.
Further surgery for lymph node dissection may
be done in some cases. Most testicular cancers are
exquisitely radiosensitive and chemosensitive
(platinum-based chemo-therapy), offering many
SCROTUM
options for successful treatment in advanced,
metastatic disease.
HYDROCELE
A hydrocele is a collection of fluid within the
tunica vaginalis and may be congenital (infantile
hydrocele) or acquired.
Infantile hydrocele is due to a patent processus
vaginalis, which allows fluid from the abdominal
cavity to collect in the scrotum. If the
communication is wider, a hernia results. Most of
these hydroceles will close spontaneously by the
end of the first year of life. Persistent hydroceles
require ligation of the patent processus vaginalis
at the deep inguinal ring.
Adult hydroceles are non-communicating, i.e.
there is no patent processus vaginalis. These
hydroceles may be idiopathic or secondary to
intrascrotal pathology such as tumour, torsion,
trauma or infection. Hydroceles secondary to
underlying disease tend to be acute, while those
that are idiopathic in nature are chronic.
Hydroceles are fluctuant, unless very tense, and
they transilluminate.
The swelling lies anterior to the testis. However,
the testes may be impalpable within a tense
hydrocele. Hydroceles should not be tapped
because of the risk of introducing infection or
causing haemorrhage into the hydrocele by
inadvertently stabbing a vein.
Hydroceles are dealt with by excision of the
hydrocele sac or plication of the sac (Lord’s
procedure).
VARICOCELE
A varicocele is a scrotal mass due to varicosities
of the pampiniform plexus of veins above the
testis.
The majority of varicoceles (95%) are left-sided
and are due to incompetence, or absence, of the
valve at the termination of the left testicular vein
before its insertion into the renal vein.
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Clinical features reside in the retroperineum, in the internal
inguinal ring, in the inguinal canal, or even at the
• Swelling in the root of the scrotum
external ring.
• Dragging pain in the groin and scrotum
• “Bag of worms” feeling Clinical Presentation.
• Impulse on coughing The incidence of undescended testes is
• On lying down it gets reduced (except in approximately 30% in preterm infants and 1% to
renal cell carcinoma) 3% in term infants.
Differential Diagnosis For diagnosis, the child should be examined in
the supine position, where visual inspection may
• Hydrocele.
reveal a hypoplastic or poorly rugated scrotum.
• Inguinal hernia.
Usually a unilateral undescended testicle can be
• Lymph varix.
palpated in the inguinal canal or in the upper
• Lipoma of the cord. scrotum. Occasionally, the testicle will be
Investigations difficult or impossible to palpate, indicating
either an abdominal testicle or congenital absence
• Venous Doppler of the scrotum and groin.
of the gonad.
• U/S abdomen to look for kidney tumour.
• Semen analysis. Treatment
Treatment The risk of malignant change in an undescended
testis is probably 30 times greater than in a
Indications for surgery
normally descended testis.
• Pain
Males with bilateral undescended testicles are
• Oligospermia—usually in 6-12 weeks
often infertile.
oligospermia improves
The gonadal veins may be ligated within the Orchidopexy before the age of 8 years.
inguinal canal (low tie) or in the retroperitoneum
If a patient is aged 10 years or greater,
above the deep ring (high tie).
orchidectomy is preferred to orchidopexy
UNDESCENDED TESTIS
Complications
(CRYPTORCHIDISM) Despite early orchidopexy, as many as 20% of
patients with unilateral undescent will be
The term undescended testicle (cryptorchidism)
infertile, while the remainder will produce sperm
refers to the interruption of the normal descent of
of poor quality.
the testis into the scrotum. The testicle may

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 44.CONDITIONS OF THE PENIS AND PREPUCE
PHIMOSIS
It is inability to retract the prepuce over the
glans.
Causes
1. Congenital—in which case the child has
pinhole meatus and ballooning of prepuce
occurs when the child urinates.
2. Balanitis (inflammation of glans) and balano-
posthitis (inflammation of glans, prepuce
and sac). Common in diabetics.
Treatment
Circumcision.
PARAPHIMOSIS
❖ Inability to place back (cover) the retracted
prepuceal skin over the glans.
❖ It causes ring like constriction proximal to the
corona and prepuceal skin.
❖ As a result the glans will be swollen,
oedematous with severe pain and tenderness.
❖ Often glans will undergo necrosis or becomes
gangrenous.
❖ Paraphimosis is precipitated after sexual
intercourse or iatrogenically after urethral
catheterisation.
Treatment
• Manual reduction of prepuceal skin.
• If not possible, initial dorsal slit is made to
relieve the oedema and compression.
antibiotics and analgesics are given.
• Circumcision is done as a part of emergency
treatment if the tissues are not too
oedematous or after 3 weeks.
BALANOPOSTHITIS
It is inflammation of glans and prepuce—
(Inflammation of prepuce is posthitis; of the
glans is balanitis).
Causes
• Diabetes mellitus.
• Candidiasis.
• Venereal diseases like syphilis, herpes.
It can cause phimosis, carcinoma penis.
Clinical Features
Pain, swelling, discharge.
Treatment
• Antibiotics.
• Circumcision.
• The diabetes is controlled.
PRIAPISM
❖ It is persistent, painful erection of penis.
❖ Corpora cavernosa are filled with blood due
to defective venous drainage. Glans and
corpus spongiosum are not involved.
Causes
• Idiopathic thrombosis of corpora cavernosa
• Idiopathic thrombosis of prostatic venous
plexus
• Sickle cell disease
• Leukaemia
• Secondary deposits in corpora cavernosa
• Spinal injury or diseases
Investigations
Relevant for specific causes.
Treatment
• Anastomosis between corpora cavernosa and
saphenous vein.
• Anastomosis between corpora cavernosa and
corpus spongiosum.
CARCINOMA PENIS
It is commonly squamous cell carcinoma, but
melanoma, adenocarcinoma from Tyson’s gland,
basal cell carcinoma and secondaries may also
occur.
Aetiology
❖ Chronic balanoposthitis, phimosis.
❖ Sexually transmitted diseases.
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 ❖ Leukoplakia of glans.
❖ Long-standing genital warts.
❖ Paget’s disease of penis (Erythroplasia of
Querat is persistent rawness of glans penis).
❖ Condyloma acuminata (by human papilloma
virus), balanitis xerotica obliterans.
❖ HIV infection—HPV-16.
❖ Circumcision during infancy confers total
immunity against carcinoma penis.
❖ It is common in Asia and Africa.
Clinical Features
❖ In an adult, recent onset of phimosis should
raise the suspicion of carcinoma penis.
❖ Lesion is painless initially but later becomes
painful due to secondary infection, often
accompanied by discharge which is foul
smelling, purulent and irritating.
❖ Altered urinary stream.
❖ Fungation and induration, everted edge,
often extending into the body of penis.
❖ Palpable hard, nodular inguinal lymph
nodes on both sides may be present. External
iliac lymph nodes may be palpable.
❖ Pain, oedema, tenderness, redness develops
once infection occurs.
Investigations
1. Edge biopsy from the lesion shows
squamous cell carcinoma with epithelial
pearls.
2. FNAC of lymph nodes
3. U/S abdomen, to look for involvement of
external iliac lymph nodes.
TNM staging
T0 – No primary tumour
Tis – Carcinoma in situ
T1 – Tumour < 2 cm without deep invasion
T2 – Tumour between 2-5 cm with minimal deep
invasion
T3 – Tumour > 5 cm with deep
invasion/urethral spread
T4 – Tumour spread to adjacent tissues
N0 – No nodal spread
N1 – Mobile regional nodes—unilateral
N2 – Mobile regional nodes—bilateral
N3 – Fixed regional nodes
M0 – No distant spread
M1 – Distant spread present
Treatment
• If growth involves the glans without
extending into the proximal part of shaft of
the penis, then partial amputation of the
penis is done.
• In case of carcinoma in situ, T1 lesion of
glans penis or well differentiated tumour in
young individual: circumcision and curative
radiotherapy to the penis
• Total scrotectomy with orchidectomy.
• Role of radiotherapy in carcinoma penis
❖ Carcinoma in situ
❖ Small lesion less than 2 cm
❖ Lesion confined to glans
❖ Small lesion in young individual
❖ Advanced inoperable disease
❖ Palliation to inoperable inguinal
nodes in groin
❖ Postoperative radiotherapy
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 45.CONDITIONS OF THE BREAST
MASTITIS
Types
1. Subareolar.
2. Intramammary.
3. Retromammary (submammary).
Subareolar Mastitis
❖ It is the infection under the areola due to
cracks in the nipple or areola. It results from
an infected gland of Montgomery or a
furuncle of the areola.
❖ Often it is associated with duct ectasia—
causing formation of abscess, sinus and
fistula.
❖ It is common in nonlactating women.
Clinical features
❖ Red, inflamed, edematous areola with a
tender swelling underneath.
❖ Nipple retraction may develop.
Treatment
❖ Incision and drainage
❖ Cover with broad spectrum antibiotics.
Intramammary Mastitis (Breast Abscess)
a. Lactational abscess of the breast:
Usually infection of the pregnant or lactating
breast with Staphylococcus aureus.
Clinical features
Patient presents with redness, swelling, heat,
throbing pain in the breast and purulent
discharge from the nipple.
Treatment
❖ Antibiotics (flucloxacillin) initially
❖ If an abscess develops, incision and drainage
will be required.
Lactation/breast-feeding does not need to be
suppressed while the abscess is being treated
b. Nonlactational abscess of the breast:
It commonly occurs in duct ectasia and
periareolar infections.
Common organisms are bacteroides, anaerobic
streptococci, enterococci and gram negative
organisms. It is commonly recur-rent with tender
swelling under the areola.
Treatment:
❖ Antibiotics.
❖ Repeated aspirations.
❖ Drainage and later cone excision of the
duct is done.
Retromammary Mastitis
It is due to tuberculosis of the intercostal lymph
nodes or ribs beneath or suppuration of the
intercostal lymph nodes.
Breast is normal.
Investigations:
❖ Chest X-ray, FNAC, ESR.
❖ Peripheral smear.
❖ U/S of breast and chest wall.
❖ Often CT scan chest may be needed.
Treatment:
❖ Cause has to be treated.
❖ Drainage through
submammary/retromammary incision.
FIBROADENOMA
Fibroadenoma is seen in young women (late
teens, early twenties) as a firm, rubbery mass that
moves easily with palpation. Fine-needle aspirate
(FNA) or core biopsy is sufficient to establish
diagnosis. Removal is optional but generally
recommended (most women want them out).
Giant juvenile fibroadenoma (>5cm) is seen in
very young adolescents, where it has very rapid
growth. Removal is needed to avoid deformity
and distortion of the breast.
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BREAST CYSTS
The development of breast cysts is so common as
to be part of the normal process of involution of
the breast in women in the premenopausal years.
Cyst size varies with menstruation due to
influence of ovarian hormones.
Cysts can be multiple (50%). Often bilateral.
Cysts can be recurrent (50%).
Risk of breast cancer in breast cyst is very less
(0.1%). But incidental associated carcinoma may
be present in 3% of breast cysts.
Clinically features
Smooth, soft, fluctuant often transilluminating
well-localised swelling may be felt.
Differential diagnoses
❖ Bloodgood cyst,
❖ Haematoma,
❖ Cystic necrosis in a carcinoma,
❖ Brodie’s disease,
❖ Galactocele,
❖ Lymph cyst,
❖ Hydatid cyst.
Investigations
❖ US of breast;
❖ FNAC.
❖ Mammography to rule out associated
carcinoma.
Treatment
Cysts require no treatment unless they are
associated with a persistent lump, recur
repeatedly in the same area or the cyst fluid is
blood-stained then surgical excision is indicated.
BREAST CANCER
Breast cancer predisposing factors.
• Genetic
• Hormonal
❖ Early mearche
❖ Late menopause
❖ Hormone replacement therapy (> 10
years)
❖ Nulliparity
❖ Late first birth
• Family history
Clinical features
Breast cancer should be suspected in any woman
with a palpable breast mass, and the index of
suspicion increases with the patient’s age, breast
lump (in postmenopausal women almost all new
lumps represent breast cancer).
Other strong indicators of cancer include:
❖ Ill-defined fixed mass
❖ Retraction of overlying skin.
❖ Recent retraction of the nipple
❖ Eczematoid lesions of the areola
❖ Reddish orange peel skin over the mass
(peau d’orange)
❖ Palpable axillary nodes
❖ bloody nipple discharge;
❖ mammographic screening abnormalities.
If neglected breast cancer may ulcerate through
the skin of the breast.
Investigations
All patients presenting with a breast lump
should have a clinical, radiological and
pathological assessment (known as triple
assessment) carried out during their first visit to
the clinic.
Triple assessment.
1. Physical examination
2. Radiological assessment
❖ Ultrasound in patients under 35 years
old
❖ Mammography in patients over 35 years
old
3. Pathological assessment
❖ Fine-needle aspiration cytology
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 ❖ Trucut biopsy Ca15.3 (a relatively specific breast cancer
tumour marker).
In more advanced cases, the following
investigations should be performed: Staging

❖ liver ultrasound; Breast cancer is staged according to the TNM

classification (T, tumour size; N, nodes; M,
❖ bone scan; metastases).
❖ blood tests, e.g. full blood count, liver
function tests, carcinoembryonic antigen,
TNM classification.
T0 Carcinoma in situ or microinvasion
T1 Tumour < 2cm
T2 Tumour 2–5 cm
T3 Tumour > 5cm
T4 Overlying skin or underlying muscle attachment

N0 No axillary nodal involvement

N1 Free axillary nodes (histologically less than three involved nodes)
N2 More than three involved nodes or fixed axillary nodes
N3 Supraclavicular nodes involved

M0 No metastases
M1 Metastatic disease present

Management/treatment oestrogen or progesterone receptor-positive

tumours)
❖ Lumpectomy or Mastectomy + Radiotherapy
❖ Chemotherapy
❖ Hormonal therapy (Tamoxifen (or some
other antioestrogen, e.g. aromatose inhibitor)
should be given to all patients with

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 PART II. EAR, NOSE AND THROAT DISORDERS
THE EAR
HISTORY TAKING AND PHYSICAL
EXAMINATION OF EAR PATIENT
HISTORY TAKING
1. History taking of an ear patient is like history
taking in any other discipline of medicine.
The scheme is similar and includes the
following points such as
• Chief complaints with duration
• History of present illness
• Past history
• Personal history
• Family history.
2. General physical examination includes lymph
nodes of neck.
• Cardiovascular system (CVS)
• Central nervous system (CNS) with
cranial nerves (VIIth and VIIIth)
• Examination of respiratory system.
3. Local examination of ear, nose and throat.
Chief Complaints
Always begin by asking the patient—what has
brought you here?
All complaints should be mentioned in
chronological order, i.e. the older complaint, first.
Main chief complaints of ear disease are as
follows:
• Discharge from Ear
• Discharge from middle ear
• Hearing Loss
• Vertigo
• Noises in the Ear
• Earache
• Otalgia
• Other Symptoms of Complications
Head ache, fever, facial deformity or swelling
behind the ear or aphasia.
EXAMINATION OF EAR
• Pinna: On inspection and palpation, the
pinna is examined for any deformity, scar
mark (of any previous surgery for
preauricular sinus, Lemperts endaural
incision), sinus opening, swelling, tender
ness, painful movement, tragus sign and
circumduction sign.
• Preauricular and postauricular region:
Look for any swelling, sinus, fistula, scar
mark (postaural Wilde’s incision), tender
ness or edema.
• External auditory meatus: It is examined
for any wax, fungus, foreign body, debris,
discharge, polyp and swelling and most
importantly for sagging of posterosuperior
wall of meatus.
• Tympanic membrane: It is pearly gray in
color and all the standard landmarks on it
have to be identified such as Handle of
malleus (HOM), short process of malleus,
anterior and posterior malleolar folds,
umbo and cone of light
• Examination of ear can also be done with
the help of otoendoscopes with the
advantage of being quick and the findings
can be recorded.
• Tuning fork tests: Rinne’s test, Weber’s test
and absolute bone conduction (ABC) test
must be done.
• Examination of eustachian tube patency:
Besides a bedside test of putting some dye
or ear drops, such as Chloromycetin in the
ear and feeling its bitter taste in the mouth
in case of a perforation.
PERICHONDRITIS
Perichondritis is inflammation of the
perichondrium covering the cartilage of the
pinna and may follow trauma leading to
hematoma and infection or may also follow otitis
externa or a furuncle of the pinna or follow
operations such as cutting the cartilage in the
presence of infection.
Signs/symptoms
There is uniform enlargement of pinna, surface is
red and shiny. There is severe pain along with
constitutional disturbances such as fever, malaise
and body aches. Recurrent infection may result in
cauliflower ear or Boxer ear.
Treatment
1. Broad spectrum antibiotics such as
amoxicillin, ciprofloxacin with or without
tinidazole or injection gentamicin 80 mg
IM two times a day.
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 2. Anti-inflammatory drugs such as
ibuprofen or paracetamol.
3. Local application of magnesium sulfate
dressing or ichthyol in glycerin.
4. Once abscess is formed I and D has to be
done.
FURUNCULOSIS
Furunculosis is a staphylococcal infection of hair
follicles, which are present in cartilaginous part
of the external auditory meatus.
Clinical features
1. Severe pain spreading to jaw or head, but
hearing is almost normal.
2. Swelling of canal and Tragus sign
positive, i.e. tenderness on pressing the
tragus.
3. Examination shows swelling with a
bursting point in the canal, tympanic
membrane is normal.
4. Postauricular sulcus is obliterated if
infection spreads posteriorly. Regional
lymph nodes are tender and enlarged.
Treatment
1. In recurrent cases diabetes should be
ruled out.
2. Antibiotics (broad spectrum) and anti-
inflammatory drugs.
3. Meatus is packed with a wick soaked in
antibiotic steroid cream, which acts as a
splint and prevents movements of
cartilaginous part and also helps in
relieving tension by counter pressure.
4. Hot fomentation locally is soothing and
incision is usually not required.
OTITIS EXTERNA
Otitis externa is a generalized infection of skin of
the external auditory canal and may be acute or
chronic. It is also called Swimmer ear.
Etiology
1. Predisposing factors are hot and humid
climate (Singapore ear).
2. Scratching with dirty nails or objects.
3. Bathing and swimming in dirty pools.
4. Allergic diathesis.
5. Excessive sweating changes pH of the canal
from acid to alkaline, which favors growth of
organisms.
Bacteriology
Staphylococci, Streptococcus haemolyticus,
Pseudomonas pyocyanea (Ps. pyocyanea), B.
proteus and Escherichia coli (E. coli).
Clinical features
1. Pain or discomfort, tenderness, discharge,
which is serous with debris filled in canal.
2. No hearing loss.
3. Edema, redness and tenderness on
circumduction sign, i.e. pinna when moved
in all directions causes pain.
Treatment
Systemic antibiotics (cloxacillin 500mg qid for
7days), anti-inflammatory drugs, local treatment
such as removal of debris and wick soaked in
antibiotic steroid cream, avoidance of any
predisposing factors.
OTOMYCOSIS
Otomycosis is a fungal infection of external
auditory canal usually caused by Aspergillus
fumigatus, Aspergillus niger or Candida albicans.
Clinical Features
1. Seen during hot and humid atmosphere.
2. Irritation, itching, dull pain and
discharge.
3. Sense of blockade with mild conductive
loss.
4. Wet blotting paper like debris in canal,
upon which mycelia can be seen is the
characteristics of otomycosis.
Diagnosis
It is confirmed by microscopic examination.
Treatment
• Keeping the ears dry
• Removal of fungal mass from canal
• Spirit cleaning 2 to 3 times
• Antifungal drops such as clotrimazole or 2
percent salicylic acid in alcohol
• Local application of gentian violet
• Use of amphotericin B is sometimes done in
resistant cases.
TRAUMATIC CONDITIONS
HEMATOMA OF PINNA
Hematoma of pinna is usually seen in fights
where due to trauma a fluctuant swelling
appears under the skin. Usually, there are no
constitutional symptoms unless an infection
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supervenes. Its persistence deprives blood
supply to perichondrium, leading to infection
and necrosis. If not treated may lead to
cauliflower ear also called Boxer’s ear.
Treatment
• Incision and drainage and proper
compression of the wound to prevent
accumulation of blood or fluid.
• Antibiotics to prevent secondary infection
• Anti-inflammatory are also given.
FROSTBITE
Frostbite is commonly seen in extremely cold
weather and as the skin lining the lateral surface
of pinna is firmly adhered to the cartilage with
minimal subcutaneous tissue making it more
prone to frostbite.
Best treatment is prevention besides the role of
vasodilators, rewarming at 38° to 42°C, the
application of 0.5 percent silver nitrate and
systemic antibiotics.
PSEUDOCYST PINNA
A soft cystic swelling appears on the pinna
beneath the skin and is usually because of
trauma.
Treatment
Treatment is aspiration or incision and drainage
under aseptic conditions.
WAX IMPACTION
The wax is excreted out due to movements of
jaw, while eating or talking. It collects in
excessive amount in dry hot humid or dusty
occupation or if there is excessive desquamation
from canal. Wax performs antibacterial function
and it is a nature’s way for removal of dust and
foreign material.
Clinical features
Sense of blockage, itchiness, hearing is
diminished, earache, tinnitus and vertigo.
Treatment
If hard, it should be softened by wax solvents, i.e.
soda glycerin, etc. and then removed by
syringing with sterile normal saline water at
body temperature or may be with wax hook.
FOREIGN BODIES OF EAR
Foreign bodies may be animate, such as insects,
flies, maggots or cockroaches or may be
inanimate, such as organic, i.e. seeds, peas or
beans and inorganic, i.e. beads, buttons, rubber,
etc.
Clinical features
Intense irritation, earache and diminished
hearing.
Treatment
Usually removed under local or general
anesthesia. Animate foreign body, if living is first
killed by putting some oily drops and removed
by forceps or syringing.
Inanimate foreign bodies are removed under
general anesthesia by ring curette or syringing. If
foreign body is impacted, it is removed under
general anesthesia by endaural or postaural
route.
Complications
• Injury to tympanic membrane, ossicles and
labyrinth.
• Otitis externa/otitis media.
• Foreign body granuloma.
• Tetanus may occur from sharp
infected foreign bodies.
ACUTE SUPPURATIVE OTITIS MEDIA
Acute suppurative otitis media is a pyogenic
bacterial infection of the middle ear. It is a
common disorder occurring at all ages and
particularly in children.
Aetiology
The predisposing factors include the following:
• Nasopharyngeal or nasal packs
• Adenoids
• High deviated nasal septum
• Nasal polypi
• Rhinitis and sinusitis
• Tumours of the nose and nasopharynx
• Anatomical factor: Short, straight and wide
eustachian tube in young children
• Babies fed in supine position, particularly
bottle-fed babies, become more prone to
ASOM.
Causes of Acute Otitis Media
• Acute tonsillitis/adenoiditis, cleft palate.
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 • Influenza/common cold.
• Coryza of measles, scarlet fever, whooping
cough.
• Sinusitis, DNS and polypi.
• Hemotympanum/trauma to the tympanic
membrane (TM).
• Barotrauma/diving.
• Temporal bone fracture.
Routes of Infection
• Through eustachian tube opening
• Ruptured TM
• Hematogenous (sometimes only).
Organisms
• Streptococcus pneumoniae (most common)
• Haemophilus influenzae (Pfeiffer’s bacillus)
• Moraxella catarrhalis
• Staphylococcus pyogenes
• Streptococcus pyogenes
• Branhamella catarrhalis.
Pathology and Clinical Presentation
Various stages which occur during this disease
process are the following:
Stage of tympanic congestion or Tubal Catarrh
The mucoperiosteum of middle ear reacts to the
invading organism by hyperaemia. During this
stage, the patient complains of pain and
sensation of fullness in the ear. The tympanic
membrane looks congested. There occurs no
significant hearing loss at this stage.
Stage of exudation
As the inflammatory process progresses, an
exudate collects in the tympanic cavity. The
patient complains of marked pain in the ear with
deafness. The tympanic membrane shows
bulging and looks more congested.
Constitutional symptoms like fever and malaise
occur.
Stage of Suppuration
In this suppuration stage, there is formation of
pus in the middle ear.
Clinical feature
• Pain in the ear becomes severe and
throbbing
• Temperature is 102 to 103°F
• Conductive deafness.
On examination, the TM is red and bulging and
may show a yellow spot of future perforation
(nipple-like protrusion).
Mastoid tenderness may be present in the
suprameatal triangle.
Stage of Resolution
• In this stage, the TM ruptures with release
of pus, with or without a little blood and
the symptoms subside.
• Fever comes down and the earache is
relieved.
• On examination, discharge is seen coming
through the perforation of the TM which is
usually in its anteroinferior part. In due
course of time, perforation may heal up or
may persist.
Stage of Complications
• These may occur, if treatment is inadequate
or due to high virulence of organisms or if
the patient has poor resistance.
• The disease may spread beyond the middle
ear cleft leading to acute mastoiditis, facial
nerve palsy, abscess formation,
labyrinthitis, petrositis, meningitis, lateral
sinus thrombosis or brain abscess.
Diagnosis
Diagnosis of AOSM is based on:
• History of the upper respiratory catarrh or
trauma to the ear of the patients.
• Examination of tympanic membrane.
• Tuning fork (TF) tests and pure tone
audiometry (PTA).
Differential Diagnosis
• Referred otalgia
• Furunculosis
• TM joint arthritis
• Acute parotitis.
Management
• Antibiotics for 5 days (ampicillin 50 mg/kg
in 6th hourly doses or amoxicillin 25 mg/kg
in 8th hourly doses).
• Nasal and systemic decongestants in the
form of nasal drops such as xylometazoline
or oxymetazoline every 4 to 6 hours. These
help in natural drainage of discharge.
• Analgesics and anti-inflammatory drugs as
such or in combination with decongestants
have to be given to relieve the pain.
• Myringotomy is the treatment of choice if
the patient presents with a red bulging
drum.
Complications of Acute Otitis Media
• Mastoiditis
• Facial nerve palsy
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• Petrositis • Discharge is mucopurulent, not foul smelling
• Lateral sinus thrombosis and is aggravated with upper respiratory
• Intracranial complications. catarrh (URC)
• Hearing loss is usually conductive type and
CHRONIC SUPPURATIVE OTITIS of moderate intensity (35-40 dB). Hearing is
better when ear is discharging due to
MEDIA shielding effect of round window or
discharge covering the perforation
DEFINITION • Pain is not present unless CSOM is
Chronic suppurative otitis media (CSOM) means associated with acute otitis externa or
chronic or long-standing infection of the complications.
• Examination of ear shows a perforation of
mucoperiosteal lining of the middle ear cleft,
tympanic membrane, which is central with
which is characterized by:
variable shape and size.
• Discharge Investigations
• Deafness
• Perforation of the tympanic membrane • Blood for hemoglobin (Hb), total leukocyte
(TM) count (TLC), differential leukocyte count
(DLC), bleeding time (BT), clotting time
Types (CT)
• Urine for routine examination
1. Tubotympanic or safe type
• Culture and sensitivity of ear discharge to
2. Atticoantral or unsafe type.
select proper antibiotics
Etiology • X-ray paranasal sinuses (PNS) (to rule out
sinusitis)
• Always a sequelae of acute suppurative • X-ray both mastoids lateral oblique view
otitis media (ASOM) which has not been (Schuller’s view) shows clouding of cells,
treated adequately but no cavitation
• Once the permanent perforation takes place, • PTA to see the amount and type of hearing
entry of infection takes place through loss.
external auditory meatus or eustachian tube • Examination under microscope is very
• Occasionally, a traumatic perforation may helpful particularly in doubtful cases of
get infected and CSOM ensues. type of CSOM.
Common Causes of Chronic Otitis Media Management
• Inadequate/poorly selected antibiotic 1. Aural toilet
therapy in ASOM 2. Antibiotics are given depending upon culture
• Late treatment of acute otitis media (AOM) and sensitivity report of discharge. Usually, a
• Upper airway sepsis like allergy, adenoid combination of Amoxy-clox (1 TDS) or
and tonsil disease ciprotinidazole (1 BD)
• Lowered resistance, e.g. malnutrition, 3. Role of decongestants and antiallergics:
anemia pseudoephedrine, cetrizine or oxymetazoline
• Particularly virulent infection, e.g. measles. or saline nasal drops in infants.
Predisposing Factors 4. After care to prevent recurrence, it is advised
to keep ears dry, avoid swimming and
These may be: avoiding URC.
5. Treatment of any predisposing factors such
• Infection from tonsils, adenoids and sinuses as deviated nasal septum (DNS), sinusitis,
• Allergy polypi, allergy or adenotonsillar infection is
• Eustachian tube dysfunction very important to complete the cure and
• Malnutrition prevent recurrence.
• Hypogammaglobulinemia 6. If the perforation is larger: myringoplasty or
• Bathing and swimming in dirty water. tympanoplasty.
Bacteriology COMPLICATIONS OF SUPPURATIVE
Pseudomonas, Proteus, Escherichia coli and anaerobes
OTITIS MEDIA
(Bacteroides fragilis and Peptostreptococcus).
Clinical Features
CLASSIFICATION OF COMPLICATIONS

127
1. Extracranial (Intratemporal): • Discharge persisting beyond 3 weeks after
ASOM points towards acute mastoiditis
1. Acute mastoiditis • Positive reservoir sign which means meatus
2. Subperiosteal abscesses. fills up immediately after cleaning.
3. Petrositis and Gradenigo’s syndrome • Patient looks ill, toxic and pulse rate is
4. Labyrinthitis increased.
5. Facial nerve palsy • Ear discharge is of pulsatile in nature
6. Osteomyelitis of temporal bone • Swelling on the mastoid with tenderness
7. Septicemia or pyemia and accentuation of postaurical sulcus
8. Otogenic tetanus. • A small perforation of TM is seen usually
2. Intracranial: along with conductive deafness.
1. Extradural abscess Management
2. Subdural abscess
3. Otogenic meningitis • Antibiotics—penicillin 5 to 10 lac 6th hourly
4. Otogenic brain abscess or cephalosporins, i.e. Cefotaxime 1 gm IV
5. Lateral sinus thrombosis or IM twice daily for 7 to 10 days.
6. Otitic hydrocephalus. • Anti-inflammatory drugs.
• Myringotomy for drainage of pus from the
MASTOIDITIS middle ear.
• Cortical mastoidectomy or Schwartz
Masked or Latent Mastoiditis operation, if conservative treatment fails in
48 hours.
• Masked mastoiditis results from
inadequately treated cases of ASOM or Complications of Acute Mastoiditis
those cases that were resistant to drugs;
• Subperiosteal abscess
therefore it is a good practice to do culture
• Facial nerve palsy
sensitivity of the ear or nasal discharge.
• Labyrinthitis
• It is a slow process of destruction of
• Petrositis
mastoid air cells without acute features.
• Intracranial abscess.
There exists unextinguished infection in the
• Meningitis
mastoid.
• Lateral sinus thrombosis.
• Clinical features are no pain, no fever; there
is persistent discharge of mucus and DEAFNESS
deafness in a treated case of ASOM, feeling
of being unwell, malaise, headache and Deafness denotes loss of auditory function and
mastoid tenderness with mild conductive depending upon the severity of hypoacusis,
hearing loss.
deafness may be mild, moderate, severe or total.
• X-ray both mastoids shows coalescence of
air cells and cloudiness. Classification
• Treatment is cortical mastoidectomy with
full doses of antibiotics depending upon Deafness is classified into three groups.
culture report to avoid intracranial
complications. 1. Conductive deafness: This occurs when the
sound conducting mechanism of the ear is
ACUTE MASTOIDITIS defective. The lesion could be anywhere
from the external auditory canal to the
• Acute mastoiditis occurs when the infection footplate of stapes.
from mucosa of middle ear cleft spreads to 2. Sensorineural deafness: This type of
bony walls of mastoid antrum. deafness is due to abnormality in the
• Usually, it occurs in a well-pneumatized cochlea, auditory nerve, neural pathway or
mastoid bone. their central connections with the auditory
• Beta-hemolytic streptococci are the usual cortex.
organisms. 3. Mixed deafness: It denotes that both
conductive and sensorineural abnormality
Clinical Features is present in the deaf person.
• Recurrence of pain after ASOM, is WORK OUT OF A CASE OF DEAFNESS
important
• Fever is of low grade and of intermittent 1. Tests of hearing and equilibrium
type

128
 2. Venereal disease research laboratory (VDRL)
test
3. X-ray and computed tomography (CT) scan
4. Cardiovascular system (CVS) examination
5. Central nervous system (CNS) examination.
MANAGEMENT OF DEAFNESS
Management of Conductive Deafness
It depends upon the cause of hearing loss such
as:
• Removal of any cause in the external
auditory meatus which may be wax, mass
or stenosis
• If there is perforation, treatment will be
myringo or ossiculoplasty, tympanoplasty
• In case of otospongiosis, stapedectomy is
done
• Lastly, hearing aids will be useful in those
cases where surgery is not possible.
Management of Sensorineural Deafness
• Counselling
• Hearing aids
HEARING AIDS
Hearing aid is a device used to amplify the
sounds for pronounced irreversible hearing loss
and helps in clarity of hearing. All hearing aids
have three parts.
a. Microphone collects the sound and transforms
acoustic signals into electrical signals into
electrical energy. It has a diaphragm with an
electromagnet behind it.
b. Amplifier magnifies electrical
signals/impulses by use of transistors and
the usual range of amplification of hearing
aids is 250 to 400 Hz.
c. Receiver transforms this electrical energy
back into sound waves, which have much
greater amplitude than the one received at
microphone.
Types of Hearing Aids
Depending upon placement of hearing aid
Wearable hearing aids
• Body worn aids
• Post aural aids/Behind the ear (BTE)
• Spectacle aids
• In the ear (ITE) aids
• Canal type aids (In the canal [ITC]),
completely in canal [CTC]
• Contralateral routing of signals (CROS)
hearing aid for severe unilateral SNHL
Nonwearable aids
• Portable aids
• Group hearing aids
• Inductance loop systems
• Radio transmission aids.
COCHLEAR IMPLANTS
• It is an electronic device, detects mechanical
sound energy and converts it to electrical
signals, stimulates the cochlear nerve
directly and therefore replaces the function
of cochlea
• It differs from hearing aid, which amplifies
the sound only and stimulates the cochlear
hair cells, while cochlear implant by passes
the cochlea
Bilateral deafness with inability to benefit from
conventional hearing aid is an indication for
cochlear implant.
Benefits of Cochlear Implants
• Implant will not produce normal hearing,
but enables the person to hear environmental
sounds and speech at comfortable loudness
level
• It enhances lip reading and helps speech
production in prelinguals
• It helps in building self-confidence of patient
and is more helpful in patients who could
hear earlier and than lost their hearing.
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 CONDITIONS OF THE NOSE AND SINUSES

TRAUMATIC CONDITIONS Treatment

FRACTURE NOSE
It may be simple with or without displacement.
Aetiology and assessment
• Roadside accidents or fights and boxing.
• Patients’ nose should be examined along
with gentle palpation of dorsum for
crepitus or sensation of springing opposite
the depressed fracture.
Investigations
• X-rays confirm the diagnosis.
Treatment
Reduction under local anesthesia (LA)/general
anesthesia (GA) with plaster of Paris (POP) or
any other synthetic fixture for 2 to 3 weeks to
stabilize the fracture.
1. No treatment, if it is asymptomatic.
2. Silastic button may be used to close the
perforation and lessen the symptoms.
3. Excessive crusting can be removed by
alkaline nasal douches.
4. Small to medium size perforation can be
closed by raising flaps and stitching on the
perforation.
5. Cause of perforation must be looked into.
FOREIGN BODIES IN THE NOSE
Foreign bodies may be organic such as wood,
paper, cotton foam or rubber and inorganic such
as metal, button, beads, plastic. Unilateral foul-
smelling discharge in a child is pathognomonic
of a foreign body.
Treatment is removal under LA/GA.
ACUTE RHINITIS OR CORYZA

SEPTAL PERFORATION 1. Frequently referred as common cold, it is seen

in adults or children during their early stage.
Important Causes
2. Incubation period varies from 1 to 3 days and
1. Traumatic—which may be surgical or usually transmission occurs by droplet infection
accidental such as sneezing, coughing, talking or schooling
2. Ornamental
years due to lack of resistance to infection.
3. Nose picking
4. Chemical sniffing such as chromium/nickel 3. It may also follow exposure to cold and wet
5. Cocaine sniffing season.
6. Granulomatous disorders such as syphilis,
leprosy or lupus or midline granulomas 4. Predisposing factors may be change of climate,
7. May follow repeated cauterization of septum temperature, humidity, poor nutrition, chronic
8. Complication of septal abscess, if drainage is sinusitis, fatigue, diabetes, tuberculosis and
delayed dysfunction of thyroid.
9. Maggots in the nose
10. Foreign bodies of longstanding duration 5. Causative agents are the viruses such as
causing rhinovirus, influenza and parinfluenza virus,
1. pressure necrosis syncytial virus, enteric cytopathogenic human
11. Malignancy of nose orphan (ECHO) virus, coxsackie, adeno and
12. Idiopathic. reoviruses. Secondary invading agents are:
Symptoms Streptococcus, Moraxella catarrhalis, Haemophilus
influenzae, Staphylococcus and pneumococci.
• May be asymptomatic
• Excessive crusting causing mild nose bleed 6. It spreads by kissing and through food, finger
• Whistling if perforation is small and and fomites.
anterior.
Clinical Features
Signs
1. Firstly, there is dryness and ticklish spot in
On anterior rhinoscopy, perforation is seen and the throat or nasopharynx, followed by
structures on the other side of nasal cavity are soreness on swallowing.
visible.

130
 2. Then there is sneezing, discharge from the
nose and nasal obstruction.
3. Mucous membrane of nose and throat is
swollen and congested.
4. Fever appears due to toxemia.
5. On 2nd or 3rd day, there is thick discharge,
which is mucopurulent, nasal obstruction
increases and on 5th day onwards,
symptoms start decreasing and recovery
occurs.
6. Complications of coryza may be
nasopharyngitis, sinusitis, eustachian tube
(ET) catarrh, otitis media, lymphadenitis,
respiratory tract infection, tonsillitis,
nephritis and rheumatism.
Treatment
• Complete bed rest
• Hot water bath is quite helpful
• Vitamin C, 500 mg bid for 10 days
• Antibiotics to prevent complications and
secondary infection
• Antihistaminics and anti-inflammatory
drugs are given symptomatically 2 to 3
times a day
• Smoking and hard drinks are avoided.
Remember, the dictum—if you do not treat
cold, it takes 7 days; and if you treat it, it takes
one week only. Choice is yours.
ALLERGIC RHINITIS
• X-ray paranasal sinus (PNS)
• Special tests for allergy
Treatment
• Avoiding the Possibly known Factor of
Allergy
• Drugs
1. Antihistamines
2. Sympathomimetic drugs
3. Role of steroids
4. topical nasal sprays
5. Sodium chromoglycate nasal spray
• Hyposensitization or Immunotherapy.
NASAL POLYPI
Polyp formation in nose is quite common. A
polyp is pedunculated hypertrophied
oedematous mucosa.
Polypi commonly arise from the ethmoid
labyrinth and sometimes may arise from the
maxillary antrum. When this projects posteriorly
in the nasopharynx it is called an antrochoanal
polyp.
Aetiology
Aetiology of polyposis is uncertain. Various
views have been put forward to explain the
causation.

1. Bernoulli phenomenon
Seasonal Allergic Rhinitis (Hay Fever) 2. Polysaccharide changes
3. Vasomotor Imbalance
Hay fever is season specific because of
4. Role of allergy
prevalence of pollens of grasses, flowers, trees or
5. Infection
shrubs. It may affect the nasal, pharyngeal or 6. Mixed aetiology
bronchial mucous membrane.
Clinical Features
Perennial Allergic Rhinitis
The main symptoms are nasal obstruction,
Perennial allergic rhinitis is due to exogenous hyposmia and postnasal drip. Associated with
allergens such as inhalants, i.e. house dust, these are symptoms of rhinorrhea, sneezing and
mattress, furniture, soaps, creams, perfumes, sometimes headache.
odors of fish, egg and coffee. This type of allergic
rhinitis is present throughout the year. Investigations
• X-ray examination of the paranasal sinuses
Clinical Features
helps in diagnosis.
Symptoms • CT scan clinches the diagnosis and shows
• Irritation and itching of eyes and palate the exact extent of the polyp.
• Sneezing, 10 to 15 at a time Treatment of Nasal Polyp
• Nasal obstruction
• Rhinorrhea A. Medical Treatment:
• Increased lacrimation
• Decreased or loss of sense of smell. • Local and systemic corticosteroids,
• Antihistamines,
Investigations • Decongestants and/or antibiotics.
B. Surgical Treatment:
• Blood for total leukocyte count (TLC)

131
 1. Functional endoscopic sinus surgery (FESS) Aetiology
is the surgical treatment of choice.
2. Nasal Polypectomy The main causes of epistaxis are grouped as
Differences between Antrochoanal polypi and under:
Ethmoidal polypi
1. Local
Antrochoanal Ethmoidal a. Trauma: External trauma to the nose
Polypi Polypi (accidental), repeated nose picking
Aetiology Unknown Bernoulli (intentional), surgical trauma (iatro-genic),
Accessory phenomenon, foreign body in the nose (ani-mate or
Ostium polysaccharide inanimate).
changes, b. Infection
Vasomotor c. Physiological epistaxis
imbalance, d. Congenital
allergy, e. Tumours
infection, mixed 2. Systemic diseases
Age Children and Adults a. Hypertension
adolescent b. Bleeding diathesis
c. Leukaemia
Origin Maxillary Ethmoids
d. Anaemia
Antrum
e. Uraemia
Appearan Unilateral, Usually
f. Exanthematous fevers like measles,
ce Single bilateral and
mumps, typhoid
multiple
g. Hodgkin’s disease
Site Posteriorly Anteriorly
h. Cirrhosis of liver
(choana)
i. Acute nephritis
EPISTAXIS j. Vitamin K deficiency
k. Mitral stenosis
Epistaxis or nose bleeding is a very common 3. Hormonal factors
condition. The bleeding can be unilateral or a. Puberty
b. Pregnancy
bilateral.
c. Granuloma gravidarum
Little’s Area d. Vicarious menstruation
4. Idiopathic.
The anteroinferior part of the septum is the most
common site of bleeding in majority of the cases. Investigations
This is a highly vascular area marking the 1. Hematological investigations:
anastomosis between the branches of various ✓ Hemoglobin (Hb), total leukocyte count
blood vessels supplying the nose. Branches from (TLC),
✓ differential leukocyte count (DLC),
• The anterior ethmoid, bleeding time (BT), clotting time (CT), and
• Sphenopalatine, PBF.
• Greater palatine and ✓ Prothrombin time.
• Superior labial arteries take part in this ✓ Thromboplastin generation test.
anastomosis (Kiesselbach’s plexus) 2. Biochemical:
There is a venous plexus near the posterior end ✓ Blood sugar
of the inferior turbinate called Woodruff’s area, ✓ Blood urea
which is another common site of bleeding in the ✓ Liver function tests.
nose. 3. Complete urine examination
4. Radiological investigations:
Hypertension is a very common disease and ✓ X-ray nose, PNS and nasopharynx
causes epistaxis frequently in elderly patients. ✓ Computed tomography (CT) scan nose,
The site of bleeding is usually high up posteriorly PNS and nasopharynx.
in the nose. Some well-defined cause may be 5. Other investigations: Depend upon the possible
evident on examination. cause.

Factors like coughing, sneezing, straining and Management

blowing play a contributory role by causing rise Aims of Treatment
in the vascular pressure. 1. To assess general condition of patient.

132
 2. To control hemorrhage. Local Symptoms
3. To treat underlying cause.
1. First aid measures 1. Feeling of discomfort in postnasal space.
2. Nasal obstruction.
In majority of the cases of epistaxis, the bleeding 3. Loss of vocal resonance (dead voice).
is minor and stops spontaneously. When a 4. Loss of sense of smell.
patient is seen during a bleed, he is asked to 5. Nasal or postnasal discharge or drip.
clean the nose which is then pinched for about 10 6. Cough
minutes. 7. Pain in the sinuses.
Signs
This stops the bleeding by pressure. Once the
bleeding is controlled, the nose is examined and Usually, no external signs are present except in
the site located. fulminating cases where, there may be redness
and oedema of the soft tissues of the face over the
1. Cauterisation
sinus involved.
2. Nasal packing (anterior or posterior)
3. Adjuvant therapy Investigations
• Bed rest and sedation are important.
• Antibiotics are prescribed if the nose is • The X-ray examination of paranasal
packed, sinuses, occipitomental view (Water’s
• Various haemostatic preparations like view),
adenochrome, vitamin C and K, and • CT sinuses is diagnostic.
calcium preparations play only an adjuvant
Treatment
role in stopping the bleeding.
• Bedrest is important in the acute stages.
SINUSITIS
• Antibiotics: Amoxicillin 500 mg three-times
daily (TDS) or any other broad spectrum
The mucosal inflammation of the paranasal
antibiotic (BSA) for 10 to 14 days and not one
sinuses may be acute or chronic process.
week to avoid recurrence. If there is no
response in 3 to 5 days, change over to
ACUTE SINUSITIS
clarithromycin/azithromycin/ cefixime.
• Nasal decongestants
Aetiology
• Medicated steam inhalations
1. Infections • Analgesic and antipyretic drugs
• Nasal infections • Surgery: if the symptoms do not subside
• Tooth infections Complications of acute sinusitis
2. Swimming and bathing in infected ponds or • Osteomyelitis of maxilla and frontal bone.
pools • Orbital cellulitis.
3. Trauma to the Sinuses • Orbital abscess formation.
4. Mechanical Obstruction • Intracranial complications like cavernous
5. General Diseases : Influenza, measles, sinus thrombosis, meningitis and
whooping cough and pneumonia may lead to intracranial abscess.
sinusitis. • Chronic sinusitis.
• Middle ear infection.
Bacteriology • Pharyngitis.
Commonly a mixed group of organisms are • Laryngitis/tracheobronchitis.
isolated which include: • Mucocele/pyocele.
• Oroantral fistula
❖ Pneumococcus,
CHRONIC SINUSITIS
❖ Streptococcus,
❖ Staphylococcus,
Chronic sinusitis is usually the result of
❖ Haemophilus influenzae and
❖ Moxeralla catarrhalis incompletely resolved acute sinusitis. It may
follow insidiously after repeated attacks of
Clinical Features common cold or tooth infection which induce
General Symptoms chronic changes in the sinus mucosa.

Malaise, headache, fever (not very high), sore The bacteriological and aetiological factors are
throat, facial pain and periorbital edema. usually the same as for acute sinusitis.

133
Occasionally chronic sinusitis may be due to both middle also involving the posterior wall of
aerobic and anaerobic organisms or may even be antrum on each side.
fungal in origin.
Le-Fort III fracture: This injury causes a
Clinical Features craniofacial dissociation and the fracture line
separates the bones of the middle portion of the
The main symptoms are as follows:
face from the cranium. The fracture line passes
1. Nasal obstruction through the zygomatic arches, zygomatic process
2. Nasal discharge of frontal bones, back of orbit, ethmoids, lacrimal
3. Abnormalities of smell bone, frontal process of maxillae and nasal bones.
4. Headache Posteriorly the fracture line passes through the
5. Epistaxis pterygoid plates. In this way the maxilla, the
The general symptoms of chronic sinusitis nasomaxillary and malar-zygomatic complex on
include a sense of tiredness, low grade fever and both sides are separated from the cranium.
a feeling of being unwell. Depending upon the severity of trauma, the
patient’s complaints can be epistaxis, nasal
Investigation
obstruction, deformity of face, improper bite and
• Plain X-ray examination of the paranasal diplopia.
sinuses.
• CT sinuses remains the radiographic Treatment
investigation of choice.
Proper reduction of displaced fragments
• Proof puncture
maintaining the useful bite of teeth. The
Treatment of Chronic Sinusitis fragments are kept in position by interdental
wiring, plaster of paris head cap or crossbars
• Antibiotics: preferably after the culture
passed through the mandible or cranium till
sensitivity test
• Local and systemic decongestants, and union occurs.
• Analgesics
FRACTURES OF LOWER THIRD OF
• Surgical procedures like antrum washout
for maxillary sinusitis FACE
Complications of chronic Sinusitis
These include fractures of mandible. Subcondylar
1. Osteomyelitis region fractures are the most common (35%)
2. Mucocele of the Paranasal Sinus followed by those of angle, body and symphysis.
3. Intracranial Complications Most fractures are caused by indirect trauma to
• Meningitis
chin.
• Cerebral Abscess
• Cavernous Sinus Thrombosis Clinical Features
• Mucocele
• Oroantral fistula • If undisplaced fracture, pain and trismus are
mainly observed and there is tenderness at
FRACTURES OF THE MAXILLA the site of fracture.
• Displaced fragments of mandible result in
Le-Fort of Paris, in 1901 classified maxillary malocclusion of teeth and deviation of jaw to
fractures into three types: opposite side

Le-Fort I fracture (Guerin’s fracture): It is a Diagnosis

lower maxillary fracture where the fracture line
• X-ray skull (posteroanterior [PA] view) and X-
passes through the alveolar process, palate and
ray right and left oblique view of mandible.
pterygoid process. It is a fracture of the tooth
bearing segment of the maxilla. Management

Le-Fort II fracture: It involves both sides of the Management is by interdental wiring,

face. The fracture line passes through nasal intermaxillary fixation, trans-osseous wiring and
bones, frontal process of maxilla, lacrimal bones, bone plates by both open or closed reduction
orbital plate, infraorbital mar-gin, anterior wall of techniques.
the maxilla and pterygoid processes in the

134
 CONDITIONS OF THE THROAT
LUDWIG’S ANGINA
This is an acute inflammatory condition
producing cellulitis of the floor of the mouth,
often caused by sepsis in the mouth.
Clinical features
The patient is toxic and presents with swelling
and oedema of the floor of the mouth and
brawny induration of the submandibular and
submental region. There occurs difficulty in
swallowing and breathing as the tongue is
pushed up by the oedematous tissues of the
floor. The oedema may spread to the larynx.
Treatment
Heavy doses of antibiotics, clindamycin with
metronidazole are given. If the infection does not
subside, it may require incision and drainage.
Respiratory obstruction may need a
tracheostomy.
ACUTE PHARYNGITIS
Acute pharyngitis is the most common type of
sore throat seen in viral conditions such as in
common cold, measles, influenza and typhoid. It
may be seen after certain drugs such as arsenic,
mercury or dental sepsis. Although usually viral,
bacteria such as Streptococcus, Pneumococcus or
Haemophilus influenzae may also be the causative
agents.
Clinical Features
1. Feeling of rawness of throat
2. Fever, body aches, pain on swallowing
3. Dry cough
4. Examination shows congested mucosa of
pharynx, uvula, tonsils and pillars. Edema
with some discharge over these
ACUTE TONSILLITIS
Acute tonsillitis is an acute inflammation of
faucial tonsil, which is most commonly seen in
children or adolescents.
Types
1. Acute catarrhal—in which mucosa over
the tonsils is congested
2. Acute follicular—a severe form in which
pus points are seen at the mouth of crypts.
3. Parenchymatous—the tonsils are
congested and enlarged
4. Membranous type—exudates on the
medial surface coalesce to form a
membrane.
Causative Organism
• Streptococcus pneumoniae (β-hemolytic
streptococci) [90%]
• Staphylococcus
• Pneumococcus
• Haemophilus influenzae
• Diphtheroids
• Viral infections.
Predisposing Factors
• Upper respiratory tract infections
• Chronic sinusitis, chronic tonsillitis
• Lower body resistance
• Blood dyscrasias
• Exposure to contagious infection
• Excessive use of cold drinks.
• Excessive pollution
• Foreign body impaction.
Clinical Features
Symptoms
• Sudden onset with fever of more than 40°C;
• Bodyaches
• Throat pain or raw feeling in throat
• Painful swallowing
• Thick and muffled voice
• Trismus and pain referred to ear
• Foul breath.
Signs
• Markedly congested pillars
• Enlarged and red tonsils
• Crypts filled with purulent material
resembling yellow beads of pus
• Jugulodigastric nodes are enlarged and
tender
• Tongue may be coated.
Diagnosis
• Blood for hemoglobin (Hb), total leukocyte
count (TLC), and differential leukocyte
count (DLC) shows increased polymorph
count
• Throat swab for culture and sensitivity
Treatment
• Complete bed rest
• Soft, warm and simple diet
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 • Antibiotics such as amoxicillin, cefadroxil in
appropriate doses for 5 to 7 days
• Anti-inflammatory drugs
• KMnO4 gargles (1: 4000)
• Vitamins such as vitamins C, D, B complex
• Lozenges with local, anesthetic action.
Complications
• Peritonsillitis and quinsy
• Parapharyngeal and retropharyngeal
abscesses in the throat
• Laryngeal edema
• Otitis media
• Septicemia
• Septic foci leading to subacute bacterial
endocarditis (SABE), nephritis or rheumatic
fever, brain abscess, mediastinitis aspiration
pneumonia.
CHRONIC RECURRENT TONSILLITIS
Chronic recurrent tonsillitis is a chronic recurrent
infection of the faucial tonsils with at least 4 to 6
attacks of acute tonsillitis in a year.
Types
Types of chronic recurrent tonsillitis may be of:
• Chronic parenchymatous type as seen in
children
• Chronic fibrotic
• Septic type of tonsillitis seen in adults
following recurrent attacks.
Aetiology
Etiology of chronic recurrent tonsillitis usually
follows recurrent attacks of acute tonsillitis;
hence, causative agents and predisposing factors
remain the same.
Clinical Features
• History of recurrent sore throat and
difficulty in
• swallowing
• History of rise of temperature and
bodyaches
• Halitosis
• Hawking sensation and unpleasant taste
• Dry cough and failure to grow.
On Examination
Tonsils may be enlarged as in parenchymatous
type or may be embedded due to fibrosis, may
show important cardinal signs such as:
1. Pus coming out from crypts on pressing
through anterior pillar
2. Anterior pillars are flushed
3. Jugulodigastric glands are enlarged, but not
tender.
4. Tonsillar cyst may be seen on the surface in
case the mouth of crypt is blocked.
Diagnosis
Diagnosis of chronic tonsillitis is made by typical
history of the case and presence of three cardinal
signs of chronic septic tonsillitis.
Management
1. Improve the nutrition and dietary habits of
the patient.
2. Remove any predisposing factors.
3. If in spite of all precautions, the patient
continues to have frequent attacks, treatment
is tonsillectomy operation
4. If the operation is contraindicated due to
some reasons, long-acting penicillin, gargles
with an astringent solution and Mandle’s
throat paint may be advised.
Complications
• Pharyngitis, laryngitis, quinsy
• Ear infections or effusion in middle ear
• Sleep apnea syndrome
• Rheumatic fever
• Cardiac complications endocarditis
• Glomerulonephritis.
TONSILLECTOMY
Absolute Indications:
1. Hypertrophied tonsils causing obstructive
symptoms like obstructive sleep apnoea.
2. Suspicion of malignancy
3. More than one attack of peritonsillar abscess
4. Tonsillitis resulting in febrile convulsions
5. Persistent or recurrent tonsillar hemorrhage.
Relative Indications:
1. Recurrent acute tonsillar infections either
more than six per year or more than five per
year for two consecutive years.
2. Cases with chronic enlargement of regio-nal
lymph nodes in association with sore throat.
3. Tonsillectomy is indicated when it is thought
that tonsillar infection is producing
secondary effects in other organs.
4. Carriers of diphtheria and Streptococcus
haemolyticus as proved by repeated throat
swabs, who are a potential source of
infection.
5. Eating or swallowing difficulties
6. Failure to thrive
7. Halitosis
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PERITONSILLAR ABSCESS OR
QUINSY
1. Peritonsillar abscess is a collection of pus in
the peritonsillar space which lies between
the superior constrictor laterally and capsule
of the tonsil medially.
2. It is usually unilateral and affects adult
males mostly.
3. Infection usually starts in intratonsillar cleft
due to blockage of mouth of crypts following
an attack of acute tonsillitis, from where it
spreads beyond the capsule causing
peritonsillitis, which may then lead to
peritonsillar abscess.
Etiology
1. Recurrent attacks of acute tonsillitis cause
obstruction and obliteration of intratonsillar
clefts and the infection spreads to
peritonsillar area causing suppuration.
2. Foreign bodies in tonsil may also lead to
quinsy.
Causative organisms are the same as in acute
tonsillitis.
Clinical Features
• The patient looks ill and febrile (40°C)
• Odynophagia
• Dribbling saliva
• Inability to open mouth (trismus is less
marked as compared to parapharyngeal
infection)
• Muffled voice.
On Examination
• The affected side is congested and bulging.
• Tonsil is pushed downwards and medially
• Edema of uvula and it is pushed to the
opposite side
• Pillars are congested
• Halitosis
• Trismus
• Jugulodigastric glands tender and enlarged.
Differential Diagnosis
• Acute tonsillitis
• Malignancy of tonsils
• Parapharyngeal abscess.
Treatment of Quinsy
1. Medical management
i. Broadspectrum antibiotics, such as
ampicillin/ amoxicillin or 3rd generation
cephalosporins, in sufficient doses.
ii. Anti-inflammatory drugs and analgesics
such as ibuprofen or nimesulide.
iii. Condy’s gargles.
iv. Soft, bland and warm diet.
2. Surgical management:
Incision and drainage of abscess must be done as
early as possible which will relieve the symptoms
immediately.
ACUTE RETROPHARYNGEAL
ABSCESS
Aetiology
It is an uncommon condition, usually affecting
children. It results from suppuration of the
retropharyngeal lymph nodes secondary to
infection in adenoids, sinuses or tonsils.
The abscess may occur in adults after trauma by
a foreign body or on endoscopy.
Clinical Features
• The patient complains of fever, malaise and
difficulty in swallowing. The abscess in the
late stages may present with respiratory
difficulty.
• The patient is ill, febrile and looks toxic.
• The posterior pharyngeal wall may appear
bulging.
Treatment
• Systemic antibiotics (depending on the
culture) are given.
• Analgesics
• Incision and drainage of abscess..
CHRONIC RETROPHARYNGEAL ABSCESS
• This occurs due to tuberculosis of the
cervical spine.
• Lateral X-ray of the neck showing widening
of the prevertebral space in retropharyngeal
abscess shows destruction of the vertebra.
Treatment
• Fluid replacement
• Antibiotic coverage for aerobic and
anaerobic organisms.
• Incision and drainage of the abscess
• Antitubercular treatment
ACUTE LARYNGITIS
Acute laryngitis is a viral or bacterial
inflammation of the larynx.
Causes
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 • It may just be a part of upper and lower • Steroids are quite helpful
respiratory tract infections as seen in • Avoid smoking
influenza or common cold • Speech therapy
• Sudden exposures, smoking and working in • Endoscopic stripping of vocal cords may be
polluted environments are additional risk done.
factors
• Overuse of voice during cold, inhalation of ACUTE EPIGLOTTITIS
irritant fumes or trauma may also lead to
acute laryngitis Acute inflammation of epiglottis is more
• Interarytenoid area is mostly affected commonly seen in children. It is usually caused
• Adenoviruses are usually the causative by Haemophilum influenzae type-B and causes are
organisms predisposing to secondary same as that leading to acute laryngitis.
bacterial infection.
Clinical Features
Clinical Features
• Hot potato voice
• Hoarse voice, dysphonia or aphonia • Respiratory obstruction causing dyspnea
• Fever, pain and malaise especially in children and may be the cause
• Cough, dyspnea and stridor in children of death
• Movements of vocal cords may be slightly • Fever and severe pain in the throat
restricted. • Difficulty in swallowing
Treatment • Tripod sign. Child uses his arms to fix the
chest and leans forward to breathe
• Complete bed rest and vocal rest • Indirect laryngoscopy examination shows
• Antibiotics bright red edematous epiglottis obstructing
• Anti-inflammatory drugs including steroids the airways
• Soft-bland diet • X-ray lateral view shows swollen and
• Avoid irritants, e.g. smoking, tobacco, rounded epiglottis called thumb sign.
alcohol
Treatment
• Cough linctus
• Hot fomentation of neck. • Complete bed rest
• Voice rest
CHRONIC LARYNGITIS
• Systemic antibiotics amoxicillin or a
combination with clavulanic acid. Or third
Chronic inflammation of the larynx may present
generation cephalosporin or chloromycetin
as a diffuse lesion or produce localised effects in
are the drugs of choice
the larynx. A variety of factors are responsible. • Corticoids (100 mg IV 4–6 hourly) and anti-
inflammatory drugs
1. Chronic infection
• Tracheostomy in case respiratory distress
2. Vocal abuse
occurs.
3. Smoking
4. Alcohol ACUTE
5. Irritant fumes
LARYNGOTRACHEOBRONCHITIS(Cr
Clinical Features
oup)
• Hoarseness of voice.
• Tiredness of voice.
Acute laryngotracheobronchitis is a dangerous
• Foreign body sensation in the throat
infection seen mostly in children, which involves
• Frequently cough to clear his throat.
tracheobronchial tree.
Physical examination
Causative agents
Examination reveals a red, hyperaemic, and
irregular laryngeal mucosa. It appears swollen • Viruses: myxovirus, parainfluenza virus
and thickened. The mucosa is diffusely involved. type I and II
The cords may appear granular and thickened. • Streptococcus, Staphylococcus and H.
Influenzae.
Treatment Clinical Features
• Remove the cause whatsoever • Sudden onset of fever
• Voice rest

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 • Painful croupy cough with hoarseness
• Respiratory distress with inspiratory stridor
• Toxemia, cyanosis and circulatory failure
• Examination shows crepts and ronchi due
to sticky secretions
• Steeple sign on X-ray showing a narrow
subglottis is typical of this disease.
Treatment
• Admission to hospital is mandatory
• Intravenous antibiotics
• Anti-inflammatory drugs
• Oxygen inhalation
• Intravenous hydrocortisone injection
• Steam inhalation
• Toilet of tracheobronchial tree
• Tracheostomy for respiratory distress if
required.
ACUTE TRACHEITIS
1. Acute tracheitis is an inflammation of the
lining membrane of trachea, which may
follow laryngitis and bronchitis. It may be
caused by bacteria or viruses.
2. The patient presents with cough and
retrosternal pain or discomfort along with
difficulty in respiration and croupy noise.
Mild constitutional symptoms may be
present such as body aches and fever.
3. It is treated by antibiotics and anti-
inflammatory drugs along with antitussive
agents and steam inhalation.
FOREIGN BODIES IN THE LARYNX
A foreign body lodged in the larynx obstructs
inspiration as well as expiration and produces
change in the voice. There may occur complete
asphyxia which is further aggravated by the
glottic oedema.
FOREIGN BODIES IN THE TRACHEA
The main symptom is dyspnoea with stridor.
The changing position of the foreign body in the
trachea may give rise to signs like an audible slap
and a palpatory thud. Depending upon the
obstruction one can hear an asthamatic type of
wheeze in such cases.
FOREIGN BODIES IN THE
BRONCHUS
Foreign bodies usually get arrested in the right
main bronchus because it is wide and is more
line with the trachea than the left main bronchus.
The immediate effect of the foreign body in the
bronchus is respiratory obstruction which could
be partial or complete.
Clinical Features
A sudden episode of choking, coughing,
dyspnoea and wheezing.
Investigations
• X-rays of the chest
• Bronchoscopy
Treatment
• Foreign bodies in the larynx and the
subglottic region are removed by direct
laryngoscopy.
• Tracheostomy may be required initially to
overcome the respiratory obstruction.
• Foreign bodies in the trachea and bronchi
are removed by bronchoscopy.
• Impacted foreign bodies in the bronchus
may require thoracotomy.
TRACHEOSTOMY
This is a procedure wherein an opening is made
in the anterior tracheal wall which is brought to
skin by inserting a tube.
Indications for Tracheostomy
1. Tracheostomy may be needed to relieve
respiratory obstruction which may be due the
following:
a. Inflammatory diseases of the upper
respiratory tract like acute laryngo-
tracheobronchitis, laryngeal diphtheria and
acute epiglottitis.
b. Impacted foreign bodies in the larynx or
trachea.
c. Trauma such as laryngeal injury, maxillary
and mandibular fractures, inhalation of
irritant fumes or corrosive poisoning
causing laryngeal oedema.
d. Angioneurotic oedema.
e. Tumours and cysts of the larynx and
laryngopharynx.
f. Bilateral vocal cord paralysis.
2. Tracheostomy may be needed to prevent
aspiration of fluids, pus or blood from the
trachea. Diseases like bulbar paralysis leads to
pharyngeal paralysis and incompetence of the
laryngeal sphincteric mechanism which leads to
overspill of oral secretions into the larynx. Hence
tracheostomy is required to separate the lower
respiratory tract from the pharynx.
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3. Tracheostomy is indicated in certain diseases
which lead to retention of secretions in the lower
respiratory tract.
These conditions include bronchiectasis, lung
abscess, chronic bronchitis, etc. Tracheostomy
may be needed in various conditions like head
injury and diabetic coma for proper suction of
secretions in the lower respiratory tract.
4. Tracheostomy is indicated in certain conditions
leading to respiratory insufficiency.
Contraindications of tracheostomy
• Children younger than 12 years
• Anatomic abnormality of trachea
• Pulsating blood vessels over the site of
tracheostomy
• Active neck infection
• Occluding thyroid mass in the neck
• Short or obese neck
• Bleeding disorder
• History of difficult intubation
Types of Tracheostomy

• Poliomyelitis, The urgency with which a tracheostomy may be

• Polyneuritis, done is used to classify this operation.
• Chest injuries (flail chest), etc.
1. Emergency tracheostomy
5. Muscular spasms and recurrent laryngeal
2. Elective tracheostomy
nerve spasm as in tetanus necessitate a 3. Permanent tracheostomy
tracheostomy.

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 FURTHER READING
1. Alfred Cuschieri (2003), clinical surgery, 2nd
Ed, Massachusetts, Blackwell Science
2. Bhat SR (2019) SRB’s Manual of Surgery 4th
Ed. New Delhi: Jaypee Brothers.
3. F. Charles Brunicardi (2015),Schwartz’s
Principles of Surgery, 10th Ed, New York,
McGraw-Hill
4. John Ebnezar (2010), Textbook of orthopedics,
4th Ed. New Delhi: Jaypee Brothers.
5. Margaret Farquharson, James Hollingshead
and Brendan Moran (2015), Farquharson’s
Textbook of operative General surgery, 10th Ed,
London, CRC Press
6. Rains H, Richie D (2003) Bailey, Hamilton,
Bailey & Love's Short Practice of Surgery 26th
ed. London: H. K. Lewis.
7. USMLE Step 2 CK I (2017), Lecture Notes
2017 Surgery, New York, Kaplan Medical
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