University of Medicine and Pharmacy

Targu-Mures, Romania
General Medicine Faculty
The Third Discipline of Surgery

SURGICAL PATHOLOGY

Author
Assoc. Prof. Marius Coroş, MD, PhD
The Head of The Third Discipline of
Surgery
 About the course of surgical pathology
Author’s notes
 The surgical pathology course is meant especially for the fourth
year students of general medicine, but the information
contained in it can also be useful to residents and young
doctors who wish to refresh their theoretical knowledge about
surgical diseases.
 The main goals of the course are to provide fundamental
knowledge about the specialty of general surgery and surgical
pathology, to make students to understand the
pathophysiological bases of potential surgical diseases, to
provide information required to diagnose diseases that require
surgical treatment and also to make students to understand
the main methods of surgical treatment and their physiological
bases.
 The course covers the entire topics necessary to students, being
based on academic curricula.
 Given the large amount of information, I tried to edit the
course in a more easily “digestible” form, with many pictures
and graphics which are more suggestive as thousand of words.
 Without claiming the originality of data, I tried that
information contained in course to be updated with the latest
diagnosis and treatment methods. Sources of inspiration were
very varied, based mainly on data found freely on the Internet.
So, the curse is a compilation of data from many sources
(books are written from books) but also based on my personal
surgical experience. Many pictures are from the casuistic of the
surgical clinic where I’m working, but also pictures were
taken from the Internet.
 Because I found gaps in students' knowledge of anatomy,
generally each issue begins with a refresher on the anatomy of
that region. Surgery without anatomy is unthinkable! Each
surgical procedure is based on solid knowledge of anatomy. I
emphasized the aspects of surgical anatomy, which differs
somewhat from conventional descriptive anatomy, with
reference to practical aspects.
 The course represents the basic information necessary for
students, but I strongly encourage students to read from
other sources too, especially from bibliography required for
the license and residency exams.
 Many of these information will be completed and detailed
during the internship when students will make surgical cases
presentations.
 I will be very grateful if my students will give a feedback if
they find errors or inadvertences in the course and I am also
open to any proposals to improve the course.

Assoc. Prof. Marius Coroş, MD, PhD

University of Medicine and Pharmacy Targu-Mures, Romania
Email: corosmarius@yahoo.com
 SURGICAL
PATHOLOGY
Introductory course
 General surgery
 Just like others say about their specialty that is the most
important, so I say that surgery is probably the most
important medical specialty in saving as many lives and
cure many diseases.
 General surgery is a very vast medical specialty and
specialists in this field should acquire multiple skills to
treat an enormous variety of diseases. For better
treatment, from this specialty have emerged a number of
other surgical specialties focused on certain areas dealing
with a well defined group of diseases belonging to
different systems or organs.
 Almost all organs, systems or tissues, have a pathology
that requires surgical solution as the only method or in
combination with other methods.
 Surgery – Why is important

 SURGICAL PATHOLOGY - EVERYWHERE

 Brain – neurosurgery
 Eyes – ophthalmology
 Face – esthetic surgery
 Nose, Ears, Neck – ORL
 Thyroid – endocrine surgery
 Breast – surgery S
 Thorax, lungs– thoracic surgery
 Digestive tract – general or digestive surgery
U
 Kidney, bladder, prostate – urology R
 Uterus, annexes – gynecology
G
E
 Bones, joints – orthopedics R
 Skin – dermatologic surgery
 Reconstructive and plastic surgery Y
 Trauma – emergency surgery
 Oncologic surgery
 Vascular and heart surgery
 Metabolic surgery
 The basic skills of general surgery are absolutely
necessary to any doctor or nurse regardless their
specialty. Most such skills are acquired by the 3rd year
college students in the classes of semiology and surgical
practice. Starting with rules of asepsis and antisepsis,
any doctor should know the basic methods of rescue
and life support, which are learned for the first time, in
classes of surgery. Maneuvers as injections, hemostasis,
airway release, cardiopulmonary resuscitation,
thoracocentesis should be known by any doctor.
 These are just a few aspects that make the surgery the
most important medical specialty.
 Just think how many young patients would die because
of acute appendicitis in the absence of surgical
treatment !
 Common features of surgery
1. Invasive method - the main feature is the
invasiveness which often involves incisions in the skin
and / or mucous membranes, total or partial removal of
tissues, organs or pathologic processes or implantation
of different kind of devices or prosthesis. That is the
main reason why many patients are afraid to seek
medical attention postponing the consultation as much
as possible, situation that leads to late presentation in
advanced stages of disease. Patients are afraid about
pain, scars, mutilation.
 In now days surgery became less and less invasive, less
mutilant with the condition of an early detection of the
disease. Minimal invasive procedures (eg. laparoscopy,
surgical endoscopy) have been developed followed by a
very rapid healing and less postoperative complications.
2. Surgery has a vital risk – surgery is an extreme
solution of treatment applied in certain cases when
other methods fail.
 Surgery represents a trauma for the body and the body
reacts to this trauma in different ways maintaining the
homeostasis.
 The vital risk represented by operative and
postoperative mortality rate markedly depends on
preoperative health status of the patient. In young
patients without other co-morbidities this risk is very low
(about 0%-1%) but unfortunately in elderly the risk is
higher depending on the associated illnesses
(cardiovascular, pulmonary, diabetes, etc.).
 To reduce this risk patients must be thoroughly assessed
before operation and other co-morbidities must be
adequately treated.
 In many cases the risk is not due to the surgery itself but
to the underlying disease. The vital risk depends mostly
on patient’s general condition but also on possible
surgical complications.
 Surgery is applied just in those cases where there are no
other solutions and the patient would die in the absence
of surgical therapy. That is a reason why the patient,
relatives and the surgeon should assume this vital risk.
 Do not promise and never give to the patient or relatives
the feeling that the operation has no risks. The patient
must be correctly informed about all risks.
3. Anesthetic risk – Surgery is performed under
anesthesia which may be local, regional, spinal or
general anesthesia. Anesthesia has its own risks which
are cumulated to those of surgical procedure.
 The type of anesthesia applied depends on
anesthesiologist considering the patient’s biological
status, but minimal surgical interventions are performed
under local anesthesia performed by surgeon itself.
Even the local anesthesia is burdened by vital risk
considering the possible anaphylactic reaction to
anesthetic solution. Patients must be carefully tested
for allergic reactions before applying the anesthesia.
 Despite of all precautions there are cases of sudden
death during maneuvers of anesthesia.
4. Septic risk – Surgery means incisions, incisions mean
solution of continuity in skin or mucosa representing a
gate of entrance for germs with the consequence of
local or general (spread) infections. This is the reason
why surgeons especially and all the staff working in
surgery must comply with all rules of asepsis.
 There are operations with a higher risk of infection
represented especially by those performed on the
digestive tract which is populated by many germs
especially anaerobic. Development of new generations
of antibiotics is of real help but these must be used
with discernment not to select resistant strains.
 Wound suppuration results in prolonged hospitalization
increased costs and not rarely vicious scars and
incisional hernias.
5. Risk of contamination – this risk endangers both
the patients and the surgeon.
 Surgical team has the risk of contamination by
various mechanisms (accidental wounds, splash in
the eye) with the patient's biological products which
may contain pathological germs such as HIV,
hepatitis viruses, bacteria, TB, Echinococcus, other
microorganisms.
 On the other hand the patients have also the risk to
be contaminated with germs from surgical team or
more frequently from other patients in so called
nosocomial infections.
6. Produces irreversible effects – In most cases surgery
produces irreversible effects on body’s anatomy and
physiology. Removal of organs, part of them or tissues is
not desired by surgeon and is performed just in certain
cases because every organ has its well defined role in
the organism. There are rare cases when normal
considered organs are removed just to prevent
development of serious illnesses (eg. bilateral
mastectomy in patients with positive BRCA, or
oophrectomy in advanced breast cancer treatment).
 Most of these changes do not impair the patient’s quality
of life (cholecystectomy, appendectomy, etc) or their
function may be compensated by drugs (eg. drugs
containing thyroid hormones after total thyroidectomy).
 Some anatomical changes are intentionally produced to
improve the patient’s condition (eg. gastric sleeve or
gastric by-pass for morbid obesity).
 Surgery may produce changes in patient’s psychological
status and fortunately in most cases changes are good.
Some irreversible changes are very apparent especially in
plastic surgery influencing deeply the patient’s psyche.
When changes are made especially on the patient’s
demand for esthetic purposes all precaution must be
taken and all the possible complications should be
explained to the patient prior to operation.
 Other permanent changes will affect negatively the
patient’s psyche and quality of life (eg. total mastectomy,
rectal amputation, etc) but these are performed just
when absolutely necessary.
7. Produces immediate results - Unlike other
specialties, surgery produces immediate results being
very efficient in life saving and healing.
8. Surgery is spectacular – based on the above
statement, yes surgery is spectacular and represents a
source of inspiration for many pictures or movies.
Almost every artistic movie concerning the medical
activity is based on surgery and in very rare cases or
never on other non-spectacular specialties
(endocrinology, dermatology, etc).
9. Surgery is stressful – Surgery presumes in many
cases emergency and emergency is stressful.
 Surgery is not for everyone ! Surgery is a specialty for
those physicians who are mentally balanced and stable,
with a good health condition being able to resist for long
periods of time standing, for those able to work in team,
for those who can afford to miss more time from home
and family, for those able to perform duties at any hour
of day or night, for those who like the challenge, for
those who do not like monotony, for those willing to
constantly improve and be open minded and up-to-date
with medical knowledge and surgical procedures. If all
these conditions are met, then surgery is not stressful
for surgeon.
 The most stressful is decision making – the surgeon
must choose the right moment and the right attitude to
save the patient. For optimum results vast knowledge
is necessary but doubled by experience. In surgery
better to learn from other’s mistakes than from yours.
 Not always the surgeon can guide his actions based on
protocols. There are many cases when improvisations
are necessary, making surgery an art.
 In surgery, from ecstasy to agony is just a step. Even if
the surgery went perfectly, unexpected complications
may occur. Stress does not end with operation, it
becomes even more intense in postoperative period, but
stress is counterbalanced by satisfaction of life saving.
10. Surgery presumes work in team – for best result
well trained teams are necessary. Depending on
operation type the team is formed by two or three
surgeons, a scrub nurse, anesthesiologist, and auxiliary
staff (totally about 7-8 persons in an operating room).
Every component of the team should know its
responsibilities.
11. Legal (judicial) risk - Surgery is one of the specialties
with the highest legal risk because it is an invasive
method burdened by risks including that vital and
produces irreversible effects o patients.
 Surgeons are increasingly facing multiple civil liability
claims from their patients.
 Malpractice insurance in Romania unfortunately does
not cover compensations for moral damages.
 Most often patients sue doctors for the inconvenience
caused by surgery due to lack of communication between
doctor and patient. Surgeons have to take every
precaution to prevent such situations. It must be
allocated enough time for discussion with the patient and
relatives to explain in detail the benefits of surgery but
also its limitations and possible complications.
 Patients must sign informed consent before surgery
although this document is not a legal guarantee that the
doctor will not be sued.
 Another very important precaution is that the patient's
medical records should be very well documented even
with intraoperative films or pictures. Surgeons must be
increasingly aware of the importance of maintaining
patient medical histories. These are the most important
legal documents that can help the doctor in the conflict
with the patient.
12. Surgery is a costly specialty – to perform
operations of performance, minimal invasive with
minimum damages to the patient, special and very
costly devices instruments and are necessary. In
addition, the consumption of sanitary materials during
operation and after is high because all these materials
are disposable.
 There are cases when minimally invasive surgery
allows the patient to be discharged the same day or
the day following surgery, with low costs, but there are
serious cases that require prolonged hospitalization
with very high costs.
 Hippocratic oath
(fragment from original version)
 “All that may come to my knowledge in the
exercise of my profession or in daily commerce
with men, which ought not to be spread
abroad, I will keep secret and will never reveal.
 To consider dear to me, as my parents, him who
taught me this art; to live in common with him
and, if necessary, to share my goods with him;
To look upon his children as my own brothers,
to teach them this art. “
 Surgical diseases
Important aspects !
THE PATIENT IS THE MOST
IMPORTANT FOR US !
1. There are no illnesses outside the patients !
2. Do not forget the patient ! We will treat the patient
not the disease !
3. We do not operate for the sake of work or for science !
We don’t make experiences on patients !
4. The treatment must be adapted to each patient !
Patients are different and may have more or less
associated diseases which must be considered.
5. There are no pure surgical illnesses ! In most cases we
combine surgical treatment with other kind of
treatments (medical , oncological, etc.) Those illnesses
for which the principal solution is surgery take part
from the family of SURGICAL PATHOLOGY.
6. The basic principle in surgery is: “PRIMUM NIL
NOCERE !” a Latin phrase that means "First, do
no harm“.
7. The surgeon is ethically obliged to maintain the
confidentiality of the clinical record and, in principle,
access to the record by third parties should be
restricted.
 General aspects concerning surgical
diseases

 Regardless the organ affected the pathology

may be represented by:
1. Malformations
2. Injuries (trauma)
3. Infections – Inflammations
4. Degenerative illnesses
5. Tumors
1. Benign
2. Malign
Phases of surgical management

 The diagnosis which is based on:

1. History
2. General and local examination
3. Laboratory and paraclinical examinations
 Preoperative preparation
 Surgical treatment
 Postoperative care
 Evaluation of late results (outcome)
SURGICAL PATHOLOGY OF
THE ABDOMINAL WALL
Anatomy of the abdominal wall
1. Hernias
2. Incisional hernias
3. Eviscerations
4. Diaphragmatic hernias, ruptures and
relaxations
DEFINITIONS
Hernia – represents the protrusion of an organ or a part
of it, outside the abdominal cavity (under the skin or in the
thoracic cavity) through a congenital or acquired route,
located in a naturally weaker zone of the abdominal wall
(hernial region), so that the structural integrity of the
abdominal wall is not destroyed.
Incisional hernia – represents also the protrusion of an
organ or a part of it, under the skin, but usually through a
breach located in any region of the abdominal wall most
often following the destruction of the integrity of the
abdominal wall.
Evisceration – represents the protrusion of an organ or a
part of it outside the abdominal cavity in direct contact
with the atmosphere as a consequence of a breach
through the entire abdominal wall thickness.
 Anatomy of the abdominal wall – surgical
aspects
The role of the abdominal wall
Contention - keeps the viscera in a closed cavity.
Protection - provides protection from outside
aggressions, maintaining local constant conditions.
Participation in physiological processes (by increasing
intra-abdominal pressure - coughing, phonation,
defecation, urination, etc.) and also to the kinetic of the
trunk and of the whole body in general.
The shape of the abdominal cavity
Egg-shape - but to describe the anatomic elements is
compared with a parallelepiped with six walls which are:
– Anterior or ventral
– Posterior
– Lateral – 2 2 postero-lateral walls
– Superior – the diaphragm
– Inferior – the pelvic floor

Ventral wall – ventral hernia

Postero- Postero-lateral wall

lateral wall
Intra-abdominal pressure
Forces acting against the abdominal wall

Egg shape
Features of the abdominal wall
1. It is an active structure, mobile (not as a rigid tube) able to
change its shape and size, thus changing the intra-abdominal
pressure.
2. It is a musculo-fibrous structure (muscles, fascia, ligaments) and
bones on which the soft parts are inserted (column, ribs, pelvis).
3. Its structure is diverse being different from one region to another
depending on the function played by that region.
4. Normal abdominal wall structure is symmetrical.
The layers of the abdominal wall
1. Skin (epidermis, derma)
2. Fatty tissue with fibrous condensation (fascia Scarpa, Fascia
Camper, fascia cribriformis, etc)
3. Muscles and fascias
4. Fascia transversalis
5. Preperitoneal space (Bogros, preperitoneal fat)
6. Peritoneum
Abdominal wall layers
 Division in quadrants and regions of the abdominal wall

9- quadrants scheme 4 - quadrants scheme

R hypo- L hypoc- Upper Upper

Epigastric right left
chondrium hondrium

R flank Umbilical L flank

Lower Lower
right left
Hypogastric L iliac
R iliac
 „The weak regions of the abdominal wall – or the
hernial regions” :
1. The inguinal canal;
2. The vascular-nervous region at the root of leg (vascular
gap, muscular gap);
3. The umbilicus;
4. The Linea alba;
5. The semilunar line of Spiegel and especially Spiegel
points (intersection with the Douglas arch, right and
left);
6. The lumbar triangle (Jean Louis Petit) → posterior;
7. The lumbocostal quadrangle (Grynfelt) → posterior;
8. The pelvic floor – obturator canal, sciatic foramen
9. The diaphragm – esophageal hiatus
Epigastric hernia
Spigelian hernia
Umbilical hernia

Subumbilical Inguinal hernia

hernia Femoral hernia
 Posterior abdominal
wall hernias

External Postero-
oblique Latissimus
dorsi inferior
muscle The last serratus
muscle rib muscle
Iliac crest Olique-internal
muscle
Spinal muscles

triangle Petit quadrangle Grynfeld

 HERNIA – generalities
Exceptions from the definition of hernia (“protrusion of an
organ outside the abdominal cavity”) : INTERNAL
HERNIAS which represent the penetration of intestines
through holes (breaches) or intrusion in cavities
preformed or acquired within the peritoneal cavity.
Preformed:
– Through the foramen of Winslow – TREITZ hernia
– Inside the small pouches formed by the peritoneal folds
(periduodenal, periappendicular, retrocecal or intersigmoidian) –
RIEUX hernia
Acquired - various postoperative breaches in the
mesentery or mesocolon : – PETERSEN hernia
Various types of internal hernias:
– A = foramen of Winslow
– B = transmesocolic
– C = intersigmoid
– D = pericecal
– E = transmesenteric
– F = paraduodenal
 Etiopathogenesis
Physical effort!
Chronic cough
Chronic constipation
Difficult urination
Tumors, ascites Lowering the
strength of the
abdominal wall

Rising
intraabdominal Congenital deficiencies
pressure Subnutrition
Wasting disease
Obesity
Repeated pregnancies
Abdominal wall strength and structural integrity
depend on factors :
Constitutional (genetic) - congenital hernias
Nutritional - obesity, vitamin deficiencies, etc
Educational – sports
Pathological - trauma, subnutrition, paralysis, etc.

Forces that act against the abdominal wall depend

on factors :
Voluntary factors - physical effort
Involuntarily factors
Physiological – pregnancy
Pathological
– Intra-abdominal - ascites, tumors, etc.
– Extra-abdominal - trauma
 Classification
1. Depending on the way of development and the
structure of the abdominal wall hernias may be:
Congenital
– Embryonic - the parietal defect appears before the 4th
intrauterine months (the peritoneum is not yet developed)
– Fetal - the parietal defect appears after the 4th intrauterine
months (the peritoneum is developed and the hernial sac is
present)
– Of the small child
– Of the adult
Acquired
– Of weakness (usually bilateral direct inguinal hernias)
– Of force
2. Depeneding on the anatomical region:
– Ventral hernias
Inguinal
By frequency:
Femoral
- Inguinal hernia → 75%,
Umbilical
- Femoral hernia → 5 %;
Periumbilical
- Umbilical hernia → 5 %;
Epigastric
- Epigastric hernia → 5 %;
Spiegel hernia
– Posterior hernias
Lumbar (Petit, Grinfeld)
– Of the pelvic floor
Sciatic hernia
Obturator hernia - through the obturator foramen
Perineal hernia
– Of the superior wall (diaphragmatic)
Ventral hernias
 SPIGEL HERNIA
Rectus abdominis

Semilunar line of
Area of most
Spiegel
frequent Spigelian
hernias

Hesselbach triangle
Arcuate line of Douglas
 Aponeurosis

Rectus abdominis
sheath

Skin
Fatty tissue
Oblique external muscle
Oblique internal muscle
Transverese muscle
Peritoneum

SPIGEL HERNIA

Spiegel hernia
Lumbar hernias (posterior)
1. Jean Louis Petit lumbar triangle,
delimited between the iliac crest (caudal), the rear edge of the
external oblique muscle (above) and latissimus dorsi muscle edge
(rear).
through this area are passing:
– The subcostal nerve
– The iliohipogastric nerve
– The ilioinghinal nerve
– The last two lumbar veins
Hernia is relatively easily visible
2. Grynfeltt quadrangle
delimited between:
– postero-inferior serratus muscle (supero-medial),
– the last rib (supero-lateral),
– olique-intern muscle (infero-lateral) and
– spinal muscles (infero-medial)
 Pelvic floor hernias – most of them are congenital
hernias
1. Through the perineal holes
– Lateral hernias - between levator ani muscle fibers and
sacrococgigian muscle
– Medial anterior - Elytrocele [Gr. elytron = sheath, kele =
hernia] is a vaginal hernia. The sac is represnted by an
extension of the peritoneal cavity (pouch of Douglas ) between
the rectum and the posterior wall of the vagina.
– Medial posterior - Hedrocele [Gr. hedra = anus] is a rectal
hernia. The extension of pouch of Douglas protrudes through
the posterior wall of the rectum.
Perineal hernias contain fluid, fat, any part of the
intestine, the rectum, or the bladder.
 Normal

Hedrocele Elytrocele
2. Through the obturator canal – a passageway that
contains the obturator artery, obturator vein, and
obturator nerve – obturator hernia.
3. Through the sciatic foramen - a passage from the
pelvis to the gluteal and peroneal regions formed by
the hip bone, the sacrospinous ligament, and the
sacrotuberous ligament – sciatic hernias (rare)
 Diaphragmatic hernias
Diaphragmatic hernia is a defect or hole in the
diaphragm that allows the abdominal contents to move
into the chest cavity.
The following types of diaphragmatic hernia may
exist:
Congenital diaphragmatic hernia
– Morgagni's hernia - anterior
– Bochdalek hernia - posterior
Hiatal hernia
Iatrogenic diaphragmatic hernia
Traumatic diaphragmatic hernia
 Morphopathology
Hernia has three anatomical components:
1. The hernial canal
2. The hernial sac
3. The content of the sac
The canal – in most cases there is a real canal which
has an internal and an external ring but there are
cases when the canal is absent being represented only
by a hole in the abdominal wall (eg. Umbilical hernia).
The trajectory of the canal may be perpendicular to the
abdominal wall and that determines the direct hernias,
or oblique that determines the indirect hernias (oblique
hernias)
 Skin Peritoneum

Hernial sac

Small
intestine

Umbilical
ring

Rectus abdominis
muscle
 Depending on the position of the sac in the canal
(degree of protrusion) hernias can be :
1. Hernial point – the sac protrudes into the canal being
located at the internal ring
2. Interstitial hernia – the sac is contained inside the
canal between the two rings: internal and external
3. Complete hernia – the sac protrudes under the skin.
It has exceeded the external ring.
The sac has 3 portions:
– Neck
– Body
– Fundus
Depending on its shape it can be: - globular, pear-
shaped, conical, cylindrical, spherical.
The sac can be free or adherent to surrounding tissues.
Hernias could have: a single sac or multiple sacs.

Neck
Body

Fundus
The sac may be partially or totally absent
– Totally absent – in embryonic hernias when the peritoneum is
not yet developed.
– Partially – in sliding hernias which occur when an organ drags
along a part of the peritoneum or in other words, the organ is
part of the hernia sac. The colon and the urinary bladder are
often involved.

Fascia
transversalis
Muscle Peritoneum Hernial sac
Skin
Peritoneal
Peritoneal cavity
cavity Colon

Hernia
ring eum
n
ito
er
tr op
Re

Pubis
Peritoneal cavity

Anterior wall of the sac

= parietal peritoneum

Posterior wall of the sac

= visceral peritoneum
(can not be separated from
the bowel)

SLIDING HERNIA
 The content of the sac
It can be any intra-abdominal organ except the
pancreas
Depending on what the sac contains hernia may be:
– Enterocele - intestines
– Epiplocele – great omentum
– Littre hernia - diverticulum Meckel
– Garengoff hernia - vermiform appendix

Depending on evolution, hernias can be classified as:

1. Uncomplicated hernias (simple, reducible hernia)
2. Complicated hernias (irreducible, incarcerated,
strangulated, etc)
Clinical picture of uncomplicated hernia
(simple, reducible)

Clinical picture is represented by symptoms and signs.

Physical signs are dominant.
Symptoms:
The onset: is insidious with mild pain in a hernial region
during an effort but the pain gradually disappears.
The patient observes the appearance of a bulge that
gradually increases in volume, especially in standing
position and on physical efforts, which is spontaneously
reducible in supine position or after manual maneuvers.
There may be present other symptoms too, depending
on which organ is herniated.
Physical examination
Inspection
– In standing position: the presence of a tumor in a hernial zone
which is bulging under the unmodified skin of the region.
– At coughing effort the tumor is increasing in volume.
– In supine position the bulge reduces its volume or disappears.
Palpation
– Bulge of soft elastic consistency, painless, which can be reduced
by taxis into the abdominal cavity on a trajectory through a gap
or hole.
– To the effort of cough the impulsion sign (the hernial sac
pushes the fingers) can be felt when the finger(s) are still in the
hernial canal and then after removing the finger the expansion
sign can be observed (the hernial sac bulges under the skin).
On auscultation:
– Nothing or intestinal sounds can be heard.
bulge
Palpation
Umbilical

Inguinal
Umbilical hernias
Symptomatic hernias - are those cases when the
hernia is a symptom of another disease usually more
serious, which produces an increase of intra-abdominal
pressure. (cirrhosis, intra-abdominal mass, tumors of the
colon, prostate adenoma, chronic cough, etc)

Ascites
Intraabdominal tumoral mass of 5 Kg
Symptomatic umbilical hernia
Varicose veins
Ascites
Coercible hernia = the hernia which remains in the
abdomen after the taxis maneuvers.
Incoercible hernia = the hernia which immediately
restores (usually hernias with large ring).
The positive diagnosis – is easy, based on history
and physical examination
A tumor which bulge under the skin, since more time,
usually appeared after a physical effort, which gradually
increases in volume especially on physical effort, but
reduces itself or disappears in the supine position or by
taxis, tumor which appears in a region of low resistance
of the abdominal wall, which can be reduced by digital
taxis showing the sign of impulsion and expansion at the
effort of cough.
Differential diagnosis – sometimes diagnosis may
be difficult especially in femoral hernias, perineal
hernias, obturator hernias and posterior hernias.
Differential diagnosis must be done with other tumors of
the respective anatomical region.
Sometimes other complementary investigations are
necessary: ultrasound, CT-scan, barium swallow or
enema, cystoscopy, phlebography, etc).
Treatment
Only surgical ! Patel said: “the surgery is the rule in
hernia treatment and the contraindication is the
exception."
Contraindications
1. Very bad general condition of the patient who can
not withstand the operation or the anesthesia. In
this cases orthopedic methods with content devices
(harness) can be indicated.
2. Relative contraindications
1. Neighborhood tissue suppurations - to be resolved before
surgery.
2. Coagulation disorders
3. Symptomatic hernias in which case the main disease must
be treated at first.
Inguinal Hernia Belts - for Men
Surgery
The aim of surgical treatment is to repair the parietal
defect and reinforce the abdominal wall to prevent the
relapse of the hernia.
There are 3 operative steps:
1. Finding and dissecting the sac
2. Treating the content and resection of the sac
3. Closing the parietal defect and/or reinforce the abdominal wall
It is considered an aseptic operation, suppuration being an
indicator of compliance with aseptic intra and postoperative
procedures.
The prognosis is favorable, the hernia being compatible
with life as long as incarceration or strangulation does not
occurs.
Postoperative prognosis is also good, being very low
relapse rates according to compliance with postoperative
physical efforts avoidance, the state of the abdominal wall
and surgical technique used.
Complicated hernias
The most frequent complications are:
Incarceration = the intestinal loops are unable to return
into the abdominal cavity (are trapped into the sac) due
to a compression at level of internal or external ring, but
the blood circulation is not particularly affected. However
a bowel obstruction will develop and eventually will lead,
through distension, to ischemic lesions of the bowel wall
(similarity to: jailed but not convicted to death).
Strangulation = besides the bowel can not return into
the abdominal cavity, the compression at the
strangulation ring is so great that it affects the
vascularization and the intestinal loop "dies" (similarity
with a jailed one convicted to death by strangulation –
hanging).
Frequency of incarceration: 3-15%
Incarceration usually after an intense physical effort or
after a rich meal.
Complication appears more frequently in hernias with
narrow ring (parietal defect).
The femoral hernias are more frequent incarcerated due
to the rigid, inextensible hernial canal.
The inguinal and femoral hernia incarcerate more
frequently on the right side due to longer dimension of
the mesentery on this side.
 Morphopathology – 3 stages of evolution:
1. Venous stasis stage – the intestinal loop is distended
with edematous and thickened walls - the color is violet,
cyanotic - there is a lymphatic and venous stasis, but
the peristaltic movements are present. On the
peritoneal surface there are petechiae. In the sac there
is a serocitrin and then haemorrhagic exudate. The is a
mesenteric edema with blood suffusions. The lesions in
this stage are reversible.
2. Stage of ischemia and thrombosis – the intestinal loop
becomes darker without peristaltic movements, the fluid
in the sac is bloody, and there is a mesenteric edema
with blood suffusions. The content of the intestine is
bloody due to ischemic lesions of the mucosa. In most
cases lesions are irreversible requiring resection of the
affected intestinal loop.
3. Stage of necrosis (gangrene and perforation) –
intestinal loop is soft, greenish-black with necrotic
spots, progressing toward perforation and the fluid in
the sac is fecaliod. This is an irreversible stage. Bowel
lesions are most serious at the side of strangulation
ring. Lesions progress to a pyo-stercoral phlegmon
with acute inflammatory signs and then fistulization.

Strangulated intestinal loop is

distended with edematous and
thickened walls - the color is
violet, cyanotic.
Incarcerated left inguinal hernia
pyo-stercoral phlegmon
The length of strangled loop can be variable - 10-20
cm reaching even to 1 m in large umbilical hernias.
 Particular forms of incarcerated hernias:
1. Richter hernia is represented by a lateral pinch of the intestine.
2. Maydl hernia is a represented by a retrograde strangulation of
intestine in "W“. Ussualy the intra-abdominal intestinal loop is
more affected by ischemic lesions than those in the sac.
Intestines must be carefully inspected during operation.
Richter hernia

The ring of strangulation

Necrotic intestinal wall

 Clinical picture of incarcerated hernia
Symptoms
Sudden onset usually after a physical effort or a rich meal.
Intense pain in a hernial region.
The tumor grows in volume, becomes increasingly painful
and is not reducible.
Intestinal occlusion phenomena occur when intestinal
loops are in the sac (the transit for gases and faces
stopps, bloating an vomiting appear).
When only the omentum is present in the sac, the oclusion
symptoms usually are absent.
In Richter hernia (lateral pinch) symptoms may be
confusing because there is no intestinal occlusion and
even diarrhea may be present yet the intestinal wall
necrosis is progressing.
Signs
On inspection a tumor can be observed in a hernial
region which does not reduce in supine nor increases in
volume at the effort of coughing.
On palpation the bulge is very painful, of hard
consistency, can not be reduced by taxis and the sign of
expansion at coughing is absent.
On percussion – painful dull sound.
Later in evolution the signs of intestinal obstruction with
distended meteoristic abdomen appear.
In advanced stages signs of pyo-strercoral phlegmon are
found.

Evolution – to death if the patient is not operated.

Incarcerated umbilical hernia
The diagnosis – usually is easy when a history of hernia
is present. Sometimes is very difficult (obturator hernia,
some femoral hernias, etc) – In such cases the patient is
operated for intestinal obstruction and the hernia diagnosis
is an intraoperative surprise.
Differential diagnosis – must be made with other
painful tumors in that zone.
Treatment – the absolute indication is the surgical
treatment.
Taxis = manual reduction maneuvers (manipulation) are
contraindicated. EXECPTION – newborns and small
children (immersion in warm bath and administration of
sedatives and musculo-relaxant drugs may lead to
resolution of incarceration).
Taxis can lead to severe complications which endanger the
patient’s life.
 Complications of taxis:
1. False reduction of the sac content. The intestinal loop
remains still incarcerated intra-abdominal.
2. Intra-abdominal reduction of an unviable intestin will lead to
peritonitis.
3. Perforation of the intestinal loop.
Surgical treatment – has 4 stages:
1. Discovering the sac and the strangulation site
2. Sectioning the strangulation ring (Kelotomy – introduced by
Ambroise Pare)
3. Treatment of intestinal lesions
4. Reinforcement of the abdominal wall
Options for treatment of intestinal lesions:
1. Lidocaine infiltration of the mesentery to relief the angiospasm
in cases when the intestine are at limit of viability.
2. Clogging the intestinal ring of strangulation
3. Loop resection with TT or LL anastomosis
4. Resection of the omentum

Strangulation ring
The most intense
lesions are at this site
Other
complications:
Hernias with
adhesions
Voluminous
hernias with loss of
domain ("lost their
right of domicile“)
Tumors in the
hernial sac
Peritonitis in the
hernial sac
Voluminous hernias with loss of domain ("lost their
right of domicile“)
Because the abdominal cavity shrunk the content of the
sac (intestines, epiploon) cannot be introduced back into
the abdominal cavity. A portion of epiploon or intestines
has to be removed (undesirable).
Forced reduction will produce serious cardio respiratory
disorders with possible exitus due to lift of diaphragm.
Progressive preoperative pneumoperitoneum (PPP) is
used to prepare hernias with loss of domain operations.
Goni Moreno, distinguished surgeon from Argentina, 50
years ago developed a method in which a progressive
amount of room air was injected preoperatively into the
peritoneal cavity over a period of weeks. In this manner,
the patient becomes adjusted to an increased
intraabdominal pressure and tolerates the sudden
reduction of the viscera during the repair, free of
respiratory distress as it occurs with the standard
technique.
INGUINAL HERNIA
 History
Hammurabi of Babylon Described hernia reduction and application of bandages to
(1700 BC) prevent protrusion
Hippocrates (400 BC) Described hernia as "a tear in the abdomen."
Galen (200 BC) Described the anatomy of the abdominal wall
Heliodorus (200 BC) Described his original method for hernia repair.
Celsus (100 AD) Introduced translumination; described clinical signs that
differentiate a hernia from a hydrocele
Paulus Aegina Divided hernia into enterocele (abdominal viscera descend into
scrotum), and bubonocele (swelling remains in the groin and
does not descend into the scrotum)

Maupassius (1559) First operation to relieve a strangulated hernia

Caspar Stromayr (16th Wrote Practaica Coposa; defined direct and indirect hernias;
century) stressed importance of high dissection of the indirect sac;
sanctioned removal of testicle and spermatic cord for indirect
hernia
Littre Reported a Meckel's diverticulum in a hernia sac
DeGarengeot Described the appendix in a hernia sac
Vesalius (Flemish) and
allopius (Italy) Poupart Described the inguinal ligament.
(France)
Heister First to describe direct hernias. (1724)
Pott (England) Anatomy of congenital hernias; methods of incarceration
Camper (Holland) Described the superficial subcutaneous fascia
Scarpa (Italy) Described deep subcutaneous fascia; anatomic and surgical
importance of sliding hernias (en glissade) (1814)
Sir Ashley Cooper (England) Described anatomy and surgical treatment of crural and
umbilical hernias; anatomy of the groin including the
superior pubic (Cooper) ligament; cremasteric fascia and the
transversalis fascia
Hunter Emphasized the role of the processus vaginalis
Morton Described the conjoined tendon.
Cloquet Noted postnatal closure of the processus vaginalis; made
observations of the iliopubic tract
Hesselbach (Germany) Defined iliopubic tract; described importance of the medial
triangle of the groin (included the femoral canal). ; described the [1]

"corona mortis" (arterial circle formed by the deep epigastric and obturator arteries).

De Gimbernat Described medial ligament of the femoral canal (lacunar

ligament), and division of that ligament in the treatment of
strangulated femoral hernias.
Richter (Germany) Described partial obstruction and incarceration of a wall of the
bowel in a hernia defect. [2,3]
 Anatomy

ab do minus
s
Rectu
Antero-superior
Iliac spine

In
Inguinal region
gu
Malgaigne line in
al
l ig
. Po Tuberculum
u pa
rt pubicum
 Layers of the anterior abdominal wall:
1. Skin
2. Camper’s fascia (fatty)
3. Scarpa’s fascia (membranous)
4. Deep fascia
5. External oblique muscle
6. Internal oblique muscle
7. Transverse abdominis muscle
8. Transversalis fascia
9. Preperitoneal fat Bogros
10. Parietal peritoneum
The inguinal canal

It is 4 cm long
It is located just above the inguinal ligament and
carries the spermatic cord (male) or the round ligament
of the uterus (female), and the ilioinguinal nerve.
Its boundaries are:
1) Anterior wall – aponeurosis of external oblique muscle
2) Posterior wall – transversalis fascia and the conjoint tendon
3) Roof – internal oblique and transverse abdominus
4) Floor – inguinal ligament (superior surface)
The two openings of the canal are the deep inguinal
ring (the entrance) and the superficial inguinal ring
(the exit).
Lateral view
 Hesselbach’s Triangle
Hesselbach’s (Inguinal) triangle is an important structure
of weakness as it is the site for direct hernias. The
triangle has the following borders:

1. Medial – the
border of rectus
abdominus
2. Inferior - the
inguinal ligament
3. Lateral – the
inferior epigastric
vessels
Internal aspect
1
2
3
The spermatic Cord
The spermatic cord begins at the deep inguinal ring
(inferior to the epigastric vessels) and passes into the
inguinal canal, exiting at the superficial inguinal ring and
ends in the scrotum at testes.
The spermatic cord is covered by:
– Internal spermatic fascia (derived from transversalis fascia)
– Cremasteric fascia (derived from internal oblique)
– External spermatic fascia (derived from external oblique)
The spermatic cord contains:
– Ductus deferens (and its artery)
– Testicular artery
– Cremasteric artery
– Panpiniform plexus
– Genital branch of the genitofemoral nerve
– Sympathetic nerve fibers
– Lymphatic vessels
Spermatic cord
Inside view of the abdominal wall in hypogastric region:
There are 3 umbilical folds : median (urachus), medial
(umbilical artery) and lateral (inferior epigastric artery)
which delimit 3 fossas (lateral, medial, supravesical).
Intra-abdominal aspect
Urachus

Umbilical artery (lig)

I. Epigastric artery

Deep inguinal ring

Lateral fossa
Medial fossa

Supravesical fossa

Vas deferens

Urinary bladder
 Inguinal hernia classification
Depending on the degree of progression of the sac
into the inguinal canal:
1. Hernial point
2. Interstitial hernia
3. Inguino-pubian (bubonocele)
4. Inguino-funicular
5. Inguino-scrotal (labial)
Inguino-pubian hernia
Inguino-scrotal
Inguino-scrotal
Other classification:
a) Indirect external (oblique-external) hernia
b) Direct hernia
c) Indirect internal (oblique-internal) hernia
Pantaloon hernia/ Saddle Bag hernia: a combined direct
and indirect hernia, when the hernial sac protrudes on
either side of the inferior epigastric vessels.
 Urachus

Umbilical artery
Oblique external
Direct hernia hernia Epigastric artery

Deep inguinal ring

Oblique internal Lateral fossa
hernia Medial fossa

Supravesical fossa

Vas deferens

Urinary bladder
Indirect Hernias (congenital)
These are the most common inguinal hernias, and are
outpouchings lateral to the inferior epigastric vessels.
Abdominal contents enter the deep inguinal ring via a
hernial sac (a congenital abnormality – a persistent
processus vaginalis). The hernia then passes the full
length of the inguinal canal to exit through the superficial
ring and enters the scrotum.

Direct Hernias (acquired)

Direct hernias occurs MEDIAL to the epigastric vessels.
They do not protrude through any ring, but through an
area of weakness in the posterior wall of the inguinal
canal; this area is likely to be Hesselbach’s triangle. The
hernia is often parallel to the spermatic cord, but almost
never enters the scrotum. Is the result of repetitive
pressure, strain or injury, further weakening the
structural integrity and function of the abdominal wall in
the inguinal area.
Features of inguinal hernias:
Indirect hernia - frequent
– Congenital or hernia of force
– Through the internal inguinal ring
– The sac has a long neck, pear shaped
– It can be reduced by a trajectory from down to up and from medial
to lateral
Direct hernia - frequent
– Hernia of weakness
– Frequently bilateral – in elderly
– Through the Hesselbach’s triangle
– Globular shape sac
– The sac is reducible by a trajectory perpendicular on the
abdominal wall
Oblique intern hernia - rare
– Hernia of weakness
– Frequently the sac contains the bladder
 Differences between
congenital and acquired hernia

Congenital hernia
Through the peritoneo-vaginalis canal (processus
vaginalis) in men and Nuck canal in women, canals
which remain persistent.
The sac is located inside the spermatic cord and
sometimes intestines are in direct contact with testis
(tunica albuginea) in men.

Acquired hernia
The peritoneo-vaginalis and Nuck canals are closed.
The organs in the sac never come in direct contact
with testes (they are separated by tunica vaginalis).
Acquired Congenital
 There are 4 types of
congenital
inguinal hernia
1. Inguino-testicular

2. Funicular
1 2

3. Funicular with cyst

of the spermatic
cord

4. Associated with
hydrocele
4

3
 Congenital inguinal hernia associated with ectopic
testes may be:
1. Inguino-preperitoneal – the testicle is located at
internal ring and the sac is under the peritoneum
2. Inguino-intestitial - the testicle is located inside the
inguinal canal and the sac is between muscular layers
3. Inguino-superficial - the testicle is located at external
ring and the sac is under the skin

Testicle at internal Testicle inside the Testis is blocking the

Inguinal ring inguinal canal external inguinal ring
Other classifications
The most commonly used classification by members of
the American Hernia Society are the classical
Indirect/Direct designation, that of Nyhus, and that of
Gilbert/Rutkow and Robbins.
Nyhus developed a classification designed for the
posterior approach based on the size of the internal ring
and the integrity of the posterior wall. According to this
scheme:
Type 1 is an indirect hernia with a normal internal ring;
Type 2 is an indirect hernia with an enlarged internal ring;
Type 3a is a direct inguinal hernia;
Type 3b is an indirect hernia causing posterior wall
weakness;
Type 3c is a femoral hernia; (???? – confusion with inguinal)
Type 4 represents all recurrent hernias.
Gilbert classification
Five types of primary and recurrent inguinal hernias.
Types 1, 2 and 3 are indirect hernias; types 4 and 5 are
direct.
Type 1 hernias have a peritoneal sac passing through an intact internal ring
that will not admit 1 fingerbreadth (ie,<1 cm.); the posterior wall is intact.
Type 2 hernias (the most common indirect hernia) have a peritoneal sac
coming through a 1-fingerbreadth internal ring (ie, ≤2 cm.); the posterior wall is
intact.
Type 3 hernias have a peritoneal sac coming through a 2-fingerbreadth or
wider internal ring (ie, >2 cm.).
Type 3 hernias frequently are complete and often have a sliding component.
They begin to break down a portion of the posterior wall just medial to the
internal ring.
Type 4 hernias have a full floor posterior wall breakdown or multiple defects in
the posterior wall. The internal ring is intact, and there is no peritoneal sac.
Type 5 hernias are pubic tubercle recurrence or primary diverticular hernias.
There is no peritoneal sac and the internal ring remains intact. In cases where
double hernias exist, both types are designated (eg, Types 2/4).
In 1993, Rutkow and Robbins added a type 6 to the Gilbert classification to
designate double inguinal hernias and a type 7 to designate a femoral hernia.
 Laparoscopic classification
Closely related to Hyhus’s – based on transabdominal
aspect
– Type 1 – Congenital with narrow internal ring
– Type 2 – External with dilated internal ring
– Type 3 – Posterior wall with defect
Type 3 A – Direct hernia
Type 3 B – Oblique hernia with a large Internal ring – the
inguinal canal is shortened
Type 3 C – Femoral hernia
– Type 4 – Recurrent hernia
Bilateral inguinal hernia – laparoscopic aspect
Clinical picture
The patients complaints about the occurrence of a bulge
in the inguinal region which progressively enlarges
especially on physical efforts but it reduces its volume in
supine position or it can be reduced by taxis. The main
complains is the unaesthetic aspect of the region and the
mild local pain.
On inspection, in standing position, a bulge can be
observed in the inguinal region deforming the region.
The bulge may be small limited only to the inguinal
region (inguino-interstitial and inguino-pubian) or it may
distend the scrotum in men or labia in women (inguino-
funicular or inguino-scrotal or labial). During the effort of
cough the bulge enlarges. In supine position the bulge
reduces its volume or completely disappears.
On palpation the bulge has a soft consistency and it can
be reduced into the abdominal cavity by a trajectory
which depends on the type of hernia. In oblique-external
hernias the trajectory is from down to up and from medial
to lateral through the external inguinal ring above the
inguinal ligament. In direct hernias the trajectory is
perpendicular to the abdominal wall above the inguinal
ligament.
On auscultation intestinal sounds may be heard when
there are intestines in the sac.
Both inguinal regions must be inspected and also both
testicles and inguinal lymph nodes must be palpated.
Diagnosis is simple based on clinical aspects. In rare
cases ultrasound examination is necessary.
Clinical examination
Observation
Palpation
Auscultation
Standing, coughing
Supine position
DO NOT FORGET TO
EXAMINE THE TESTICLES !
Testicular tumor
Differential diagnosis: – Cysts of the spermatic cord
– Femoral hernia – Lipoma
– Between different types of – Tumors of the testis
inguinal hernia – Lymphadenopathy
– Hydrocele – Ectopic testes
– Varicocele
Hydrocele Varicocele Normal
 Lipoma

Very confusing. Inguino-scrotal hernia

Looks like femoral hernia
A hydrocele testis is the accumulation of fluids around
a testicle being caused by fluid secreted by the tunica
vaginalis. It can be the result of cancer, trauma (such as
a hernia), or orchitis. It may be treated surgically. A
common way of diagnosing a hydrocele is by attempting
to shine a strong light through the enlarged scrotum. A
hydrocele will usually pass light, while a tumor will not.
TRANSLLUMINATION
By holding a light behind the scrotum
one can easily determine whether the
mass is cystic (light shines through) or
solid (light blocked by the mass).
Let you diagnose if is either a
hydrocele or a hernia and not a tumor
Varicocele is an abnormal enlargement of the veins
draining the testicles (of the pampiniform plexus). The
right testicular vein drains into the inferior vena cava,
while the left testicular vein drains into the left renal vein
at a right angle. This anatomical difference favors the
appearance of the varicocele almost in all cases on the
left side of the scrotum.
Upward flow of blood in the veins is ensured by small
one-way valves that prevent backflow. Defective valves,
or compression of the vein by a nearby structure, can
cause dilatation of the veins near the testis, leading to
the formation of a varicocele.
Varicocele pathogenesis
The final diagnosis should be a complete
one and should mention the followings:

Morphological type: direct or indirect

Anatomoclinic type of hernia:
– Inguino-interstitial, or
– Inguino-pubian, or
– Inguino-funicular, or
– Inguino-scrotal (labial)
Evolutive type:
– Uncomplicated (reducible)
– Complicated (what complication)
Treatment
The rule is: surgical treatment
Exception is: wearing content devices (belts)
Surgical treatment

In open surgery there are 3 steps:

1. Finding and dissecting the sac
2. Treating the content of the sac
3. Reinforcing the inguinal wall using one of the multiple possible
procedures
Procedures (some of them are just of historical
interest)
1. Anatomic procedures (respect or reconstruct the
inguinal canal)
2. Non-anatomic procedures (abolishes the inguinal
canal)
1. Retrofunicular – all layers are sewn behind the spermatic cord
2. Prefunicular – all layers are sewn in front of the spermatic cord
3. Procedures with transposition of the spermatic cord
4. Plastic procedures
5. Laparoscopic procedures
Anesthesia – any type (local, epidural, rahidian,
general). The patient must be tested for allergy to the
anesthetic agent.
Incisions – the most often used is Bassini incision.
Annandale – Lawson Tait access (through the peritoneal
cavity) is used to close the internal inguinal ring when
laparotomy is indicated for other intra- abdominal
pathology.
Anatomic procedures
Bassini 1890 - Edoardo Bassini is considered the
father of the modern era of the inguinal hernia surgery.
The principle: reinforce the posterior wall of the inguinal
canal suturing under tension (it is not a tension free
procedure) the Henle’s ligament to the inguinal
ligament (Poupart). Also the transversalis fascia is
reinforced and the internal inguinal ring reshaped. The
inguinal canal is restored suturing the edges of external
oblique aponeurosis in front of the spermatic cord.
Tension in the suture line probably accounts for many
recurrences after the Bassini repair.
Bassini procedure
Technique:
The skin and then the external oblique fascia is incised
opening the inguinal canal. The spermatic cord is
isolated. Spermatic fascia and cremaster muscle are
incised and the hernial sac is discovered. If the sac
cannot be found inside the spermatic cord, an incision
through the abdominal wall above the internal ring may
be performed (LaRoque incision) and by digital
exploration through the peritoneal cavity the opening of
the sac is found (Reymond maneuver).
The sac is isolated and then opened. The content of the
sac is inspected and treated if necessary. The sac is
ligated at level of its neck under direct visualization. The
excess of sac is then resected (Socin).
The conjoint tendon of Henle is sewn to the inguinal
ligament reinforcing the posterior wall of the inguinal
canal and recalibrating the internal inguinal ring. Then
the edges of the oblique external aponeurosis are sewn
in front of the spermatic cord restoring the inguinal canal.
Bassini procedure
 ANDREWS / HACKENBRUCH procedure –restores the
inguinal canal
The cranial edge of the oblique extern muscle aponeurosis is used to
reinforce the posterior wall of the inguinal canal, being sewn together
with the Henle’s ligament to the inguinal ligament.
The inguinal canal is restored using the caudal portion of the OE
aponeurosis.
Other procedures also restore the inguinal canal but they
are using the ligament of Cooper for reinforcement
(prevents femoral hernia).
– Lotheisen (1942) –was the first who proposed the
use of ligament of Cooper (other procedures are :
Hashimoto and McVay ).
McVay – Hashimotto procedure
The conjoined tendon of Henle and the transversalis
fascia are anchored to the Cooper's ligament with 2 or 3
sutures being careful not to narrow excessively the
femoral canal. The repair is then continued laterally with
sutures between the conjoined tendon and Poupart’s
ligament until the internal ring reapproximation admits
only a fingertip alongside the spermatic cord. The
spermatic cord is replaced in the normal anatomical
position within the inguinal canal and the external
oblique aponeurosis is closed over the cord.
The procedure creates a high tension between
anatomical structures and sometimes relaxing incisions
in rectus abdominis sheath are necessary.
The Cooper’s ligament is the strongest anatomical
element of the region. This procedure is used especially
in large and difficult hernia repairs, including incisional
hernias.
 Shouldice procedure
(1945)
Transversalis fascia is divided from
the internal inguinal ring to the
pubic tubercle and then reinforced
using a continuous suture using a
lapel procedure. The medial edge
of the fascia transversalis is sewn
to the inguinal ligament.
Then a third suture line brings the
conjoined tendon to the inguinal
ligament. At the level of the pubic
bone, this suture doubles back,
attaching the same structures in a
more superficial plane and the
suture is tied to itself at the internal
ring.
 Milestones in Hernia Repair: The Listerian Era
http://www.medscape.org/viewarticle/420354_3

Marcy (1871) Publication of original paper on antiseptic

herniorrhaphy ("A New Use of Carbolized
Catgut Ligature")

Czerny (1876) Described ligating and excising the indirect

peritoneal sac through the external ring
Kocher Twisted and suture-transfixed the peritoneal
sac in the lateral muscles. through the
external ring

MacEwen (1886) Reefed the peritoneal sac into a plug to block

the internal ring.
Lucas-Championniere Opened the external oblique aponeurosis to
expose the entire inguinal canal.
Nonanatomic procedures
Retrofunicular procedures – the external Everything is sewn behind the
oblique aponeurosis is sewn to the spermatic cord. The superficial
inguinal ligament behind the spermatic
cord. inguinal ring is translocated in
– POSTEMPSKI front of the internal inguinal
– WISSE ring.
Everything is sewn anterior to
Prefunicular procedures – the external the spermatic cord. The
oblique aponeurosis is sewn tot the internal ring is translocated
inguinal ligament in front of the
spermatic cord. behind the superficial inguinal
– FORGUE ring
– GIRARD
– FERRARIS
– PASOKUKOTHI Martinov principle
– VILANDRE
– TH. IONESCU White to white
– BINET (aponeurosis to
– WOFLER
– MUGNAI aponeurosis)
– HALSTEDT Red to red (muscle to
– MARTINOV
– KIMBAROVSKI
muscle)
Retrofunicular Prefunicular
Procedures with transposition of the
spermatic cord
In cases of recurrent indirect hernias with incompetent
internal ring, another internal ring is performed, the old one
being closed.
– Schmieden - dislocates the testes from the scrotum
– Marin Popescu-Urlueni – does not dislocate the testicle

Popescu
Plastic procedures
With autologus material – (patient’s own biologic material)
– Skin - Loeve Rehn
– Fascia transversalis - Ziemann
– Hernial sac– Lischied
– Cremaster Muscle– Brenner
– Aponeurosis – Adler
– Sheath of the rectus abdominis – Halsted , Vreden
– Fascia lata – Wangensteen, Binet
With homologus material– (from the same species)
With heterologus material
– Natural– (from another species)

– Synthetic - MESHES - modern era of surgical

treatment
 Replaced rubber, metals and animal products. Initially
used for sutures, later knitted or woven into patches for
Nylon (1944)
hernia repair; disintegrates in tissue and loses most of
its tensile strength within 6 months.
Polyethylene mesh High-density polyethylene mesh (Marlex, 1958) resistant
(1958) to chemicals and sterilizable, but unraveled after being
Polypropylene mesh cut. Modified to polypropylene mesh (1962). Available
(1962) under various trade names (Hertra-2, Marlex,
PROLENE, Surgipro, Tramex, Trelex). Available as a
flat mesh as well as 3-dimensional devices (Altex,
Hermesh3, PerFix Plug, PROLENE Hernia System). [23]

Polyester mesh Composed of polyester fiber with the characteristics of

(MERSILENE) (1984) filigree; can be inserted into narrow spaces without
distortion. [16]

Expanded Teflon product; produces minimal adhesions when

polytetrafluoroethylene placed intraperitoneally. Does not allow significant fibroblastic or
[22,24]

angiogenic ingrowth; must be removed if infection occurs.

Polyglycolic acid mesh Absorbable mesh; loses strength after 8 -12 weeks;
(Dexon) should not be used as a sole prosthesis for the repair of
Polyglactin 910 mesh abdominal or groin hernias
(Vicryl)

http://www medscape org/viewarticle/420354 3

Texture of meshes
Tension free procedures
The most important progress in hernia surgery has been
the development of tension-free repairs.
The important fundamental principle of this technique is to
avoid tension on tissues and to neither cut nor sew muscle
together in an unnatural high-tension fashion.
In 1958, Usher described a hernia repair using Marlex
mesh. The benefit of that repair he described as being
"tension-eliminating" or what we now call "tension-free".
He opened the posterior wall of the inguinal canal and
sutured a Marlex mesh between the conjoined tendon and
to the shelving edge of the inguinal ligament.
 Stoppa (1967) used a large
mesh places in the preperitoneal
space to repair bilateral inguinal
hernia demonstrating that hernias
does not require closure of the
abdominal wall defect per se. The
mesh is held in place by intra-
abdominal pressure, an
application of Pascal's principle.
Wantz furthered Stoppa's work by
Mesh
using it for unilateral hernia repair.

Essential to these and all subsequent tension-free repairs

is the application of a barrier prosthesis, usually a
permanent mesh.
1993 RUTKOW – ROBINS procedure
A flower-shaped polypropylene mesh is us as a stopper
(plug) which is introduced into the internal ring to
occlude it and to prevent hernia relapse. Above it, an
onlay graft with slit (to accommodate the spermatic cord)
is fixed.
Rutkow-Robins
1997 - PROLENE Hernia System (PHS) is a bilayer
patch repair using a three-in-one device (“H” form) with a
round disc for properitoneal repair, a plug effect of
connector, and an oblong shaped onlay component.
PROLENE Hernia System - 1997
LICHTENSTEIN – 1984 - Lichtenstein described the
technique of tension-free mesh reinforcement of the
posterior wall of the inguinal canal. This type of hernioplasty
has become the most widely used technique around the
world and represents a milestone in the history of inguinal
hernia surgery.
ProGrip Mesh is a self-fixating mesh which has small,
absorbable, polylactic acid grips on one side to secure
immediate fixation to the abdominal wall, eliminating the
need to suture the mesh into place. It is used with
Lichtenstein’s technique.
 Skin incision

Incision of the oblique

external aponeurosis opening
the inguinal canal
Isolation of the spermatic cord

The hernial sac is opened

Isolating the sac from the The sac completely isolated
elements of the spermatic cord

Ligation of sac at the level of The sac is resected

its neck
 Parietex mesh The mesh is applied

Closing the aponeurosis Suturing the wound

 Laparoscopic approach
As in other cases, the main benefit of laparoscopic approach is the
minimal invasive procedure with a faster recovery of the patient.
However, there are still controversies over the cost-efficiency in
laparoscopic approach. It is a more difficult approach for hernias,
being necessary special equipment, general anesthesia and a
skilled surgeon.
Many techniques were used to repair hernia like:
1. Simple closure of the internal rings procedure reported first in
1982 by Ger R. was associated with a high early recurrence
rate.
2. Plug and patch repair
3. Intraperitoneal onlay mesh repair (uses a siliconed mesh)
4. Transabdominal preperitoneal mesh repair (TAPP)
5. Total extraperitoneal repair (TEP)

Ger R. The management of certain abdominal herniae by intra-abdominal closure of the neck of the sac.
Preliminary communication. Ann R Coll Surg Engl 1982; 64: 342-4
Bilateral inguinal hernias and recurrent inguinal hernias
are the main indications for laparoscopic approach with
definite benefit over conventional surgery to the patients.
Contraindications are represented by: incarcerated or
irreducible hernias, giant hernias, recurrent hernia after
laparoscopic approach, prior groin irradiation.

LAPAROSCOPIC TOTAL EXTRAPERITONEAL

APPROACH (TEP) - was first described by Arregui in
1991
The principle is the same as in Stoppa’s procedure: a
mesh is applied in the preperitoneal space as a barrier
that reinforces the weak zones of the inguinal region.
The dissection of extraperitoneal space by the
laparoscopic extraperitoneal approach is technically
more demanding because of the limited working space
and a different perspective of anatomy but It is now the
preferred laparoscopic technique for the repair of
inguinal hernia.
An inflatable balloon is used to dissect the
extraperitoneal space and create working room. The
hernial sac is reduced and a mesh is applied over the
whole inguiono-femoral region (prevents indirect an
direct inguinal hernia and femoral hernia). The mesh is
held in place using staples, or by the pressure of the
peritoneum alone (Pascal’s principle).
LAPAROSCOPIC TRANSPERITONEAL APPROACH
(TAPP) – was described by GILBERT in 1985
For this approach the pneumoperitoneum is induced and
trocars are placed into the peritoneal cavity in appropriate
position for the inguinal region.
The hernial sac is reduced and the peritoneum is
sectioned to access the properitoneal space where the
mesh is applied over the weak zones of the region and
held in place by stitches or staples. The peritoneum is
sewn to its anatomical position over the mesh.
POSTOPERATIVE COMPLICATIONS
Local complication after hernioplasty are rare being
represented by:
– Hematomas
– Seromas
– Hemorrhages from the wound
– Wound infections – generally will lead to hernia recurrence
– Scrotal edema
– Testes necrosis – when spermatic artery is injured
– Hernia recurrence - there are many causes but recurrence appear
mostly after classic procedures when tissues are sewn under
tension. Wound suppuration, obesity and physical efforts are
favosing factors.
– Inguinal neuralgia – when the ilioinguinal or iliohypogastric nerve is
entrapped in scar tissue, mesh or sutures.
FEMORAL HERNIA
Femoral hernias occur just
below the inguinal ligament,
through a naturally weakness
called the femoral canal.
Femoral hernias are a
relatively uncommon type,
accounting for only 3% of all
hernias.
While femoral hernias can
occur in both males and
females, almost all of them
develop in women because
of the wider bone structure of
the female pelvis.
Anatomy
The femoral canal is a short (2 cm long) conical shape
canal bordered by:
1. anterosuperiorly by the inguinal ligament
2. posteriorly by the pectineal ligament lying anterior to the
superior pubic ramus
3. medially by the lacunar ligament of Gimbernard
4. laterally by the femoral vein
It contains fatty tissue and the lymph nodes of Cloquet.
Because of its narrow lumen and rigid walls femoral
hernia are more likely to strangle than inguinal hernia.
It appears more frequently in women because their
basin have a more horizontal position than in men.
The hernial sac is elongated with a long neck and there
are many layers in front of it which makes it more
difficult to dissect.
Clinical picture
Symptoms and signs are almost similar to any other
abdominal wall hernias.
It appears as a bulge in the groin.
The bulge is typically smaller or may not be visible in a
prone position.
Cough impulse is often absent and should not be relied
on solely when making a diagnosis of femoral hernia.
The sac of a femoral hernia lies below an imaginary line
drawn between the anterior superior iliac spine and the
pubic tubercle (Malgaigne line), whereas an inguinal
hernia starts above this line.
Femoral hernias strangles more often than the inguinal
hernia due to the rigid walls of the femoral canal.
 Anatomoclinical types
of femoral hernias:
1. Laugier hernia – through
the Gimbernart’s lacunar
ligament
2. Cloquet hernia – under the
pectineal fascia
3. Retrovascular Serafini
hernia – posterior to the
femoral vessels
4. Prevascular Moskovitz
(Velpeau) hernia – in front
of the femoral vessels
5. Laterovascular
6. Miolacunar Hesselbach
hernia – through the
lacuna muscularis (psoas
muscle)
Diagnosis
The diagnosis is largely based on clinical signs and
symptoms. However, in obese patients, imaging
(especially ultrasonography, but also CT or MRI) may be
helpful.
The uncomplicated hernia is reducible by taxis from
downwards to upwards through a canal that passes
under the inguinal ligament, while the inguinal hernia can
be reduced through a canal that passes over the same
ligament.
Note! Femoral hernia sac can be located as well in the
inguinal region (above the inguinal ligament),
eventhough its origin is under the inguinal ligament,
leading to confusion with inguinal hernia.
 Differential diagnosis

In uncomplicated cases In incarcerated cases

Tuberculosis cold Lymphadenitis of the
abscess Cloquet nodule
Femoral artery aneurysm Phlebitis of the great
Ectasia of the saphena saphenous vein
magna vein
Lipomas
Inguino-femoral
lymphadenopathy
Treatment
The same goals as in inguinal hernia repair: finding and dissecting
the sac, treating the content, resecting the sac and reinforce the
anatomical region to prevent relapse.
Approaches – incisions:
1. Femoral
2. Extended femoral
3. Inguinal
4. Laparotomy - Lawson Tait procedure
5. Laparoscopy

3 4

2
1
Procedures (Many of them just of historical interest)
By femoral approach
1. Forced descent of the femoral arch
BERGER – the femoral arch is sewn to the pectineal fascia
TRICOMINI – makes a purse string
ZATEPIN – descends the femoral arch using a wire passed
under the pubic arch
RANY – fixes with nails the arch to the pubis
2. Relaxed descent of the femoral arch
FABRICIUS – the Gimbernard ligament is cut and the femoral
arch is sewn to the pectineal fascia
DELAGENIER – uses the Cooper’s ligament for reinforcement
By extended femoral approach
– Double curtains procedure CADENAT
– KEYNE – uses the rectus abdominis sheath
 Femoral approach

Femoral arch

Sac

Pectineus m. suture threads

FABRICIUS – BERGER
(femoral approach)
 Double curtain procedure CADENAT
(extended femoral approach)
1. Henles’s ligament is sewn to Cooper’s ligament
2. Inguinal ligament is sewn to fascia pectinealis
 By inguinal approach
The skin incision is the same as for inguinal hernia. The sac is
found in the groin region, dissected and then passed underneath
the inguinal ligament and ascended into the inguinal region. This
approach offers a better access to the neck of the sac. The sac is
resected and then the femoral opening is narrowed suturing the
Henle’s ligament and inguinal ligament to the Cooper’s ligament.
– RUGGI – PARLAVECHIO – is the procedure most often used
– CODIVILA
– ROBINEAU
Plastic procedures
1. Procedures that use autologous tissues
– STRECHI – round ligament
– POLYA – saeratius muscle
– WATSON – pectineus muscle
– HOFFNER – saphenous magna vein
– GOROSLOVSKI – pectineal aponeurosis
– TURNER - pectineal aponeurosis and psoas fascia
2. Procedures that use meshes
 RUGGI – PARLAVECHIO procedure
(by inguinal approach)
Henle’s ligament + inguinal ligament to Cooper’s ligament
UMBILICAL HERNIA
At the umbilicus, the peritoneum makes a condensed fold,
so called Richet’s fascia, which determines two types of
umbilical hernia → direct hernia (in the absence of
Richet’s fascia) and indirect umbilical hernia (oblique
inferiour or superior).
General data
The typical patient with an umbilical hernia is an overweight
multiparous woman, aged between 35 and 50. Women are
affected 3-5 times more frequently than men.
Ascites (cirrhosis, carcinomatosis, etc) is a major factor that
contributes to the developing of hernia and makes it more
difficult to treat. In this case we are talking about a
symptomatic hernia.
The etiology is multi-factorial, but chronic intra-abdominal high
pressure and weakness of the abdominal wall structures are
of most importance.
Some hernias can be big enough, some of them with loss of
domain, with a parietal defect of about 10-15 cm in diameter,
but most of them are small (about 5 cm). The content of the
sac is represented by epiploon, small and large bowel.
Classification

Congenital
– Embryonic – the defect appears before the 3rd i.u.
month when the peritoneum is not yet developed.
– Fetal – the defect appears after the 4th i.u. month. The
sac is present because the peritoneum is developed in
this stage.
Accuired
– Of the small child
– Of the adult
Of weakness
Of pressure
Combined
Symptomatic

– Oblique hernia
– Direct hernia
 Symptomatic umbilical hernia

20% of patients with

ascites develop umbilical
hernia.
In 10% of cases an
ulceration of the skin will
develop which causes the
opening of the hernial sac
and umbilical fistula.
Postoperative mortality
rate is about 2% if the Male, 35 years old, alcoholic, chronic
pancreatitis, thrombosis of the portal
hernia is repaired without vein, portal hypertension, ascites. Two
treating the ascites. types of hernia: umbilical + right
inguinal
Treatment

Omphalectomy (removal of the umbilicus) in advanced

forms, followed by abdominal wall repair.
Procedures
– Ed. Quenu – the edges of the parietal defect are
sewn together.
– Sapiejko-Picoli – the margins are sewn one over the
other “in lapel” to a better reinforcement of the
abdominal wall.
– Mayo-Menge – is a complex procedure consisting in
omphalectomy, closure of the peritoneum,
approximation of the two rectus abdominis muscles
on median line, suture of the rectus abdominis sheath
in a duplicate way (“in lapel”) in cranio-caudal
direction.
Eduard Quenu and Sapjeiko procedures
Plastic procedures, using:
Skin (after removing the fatty tissue and epidermis
– of historical interest)
MESHES
– By open, classic, approach
– By laparoscopic approach
For young children, under 5 years old, conservative
methods (corset wearing that opposes bulging the
hernia) could be worn, because the umbilical defect may
heal after some years due to the development of the
abdominal wall structures.

Postoperative relapse rate = 10-30%, grater after

procedures that do not use meshes.
1. The mesh is sutured on the fascial plane after rectus abdominis
muscles approximation. (Onlay)
2. 2. The mesh is fixed under the rectus abdominis sheath in front of
the peritoneum (in the preperitoneal space) and then the two edges
of the rectus abdominis are approximated.
3. When the parietal defect is large and gap’s edges cannot be
approximated the mesh can be positioned inside the peritoneal
cavity. In this case a special siliconated mesh is used to prevent
adhesion to intestines.
 Laparoscopic approach
Trocars placement

Working
trocar

Optic trocar

Working
trocar
The mesh overlaps the ombilical ring and is fixed in place
using 2-4 threads and takcs which may be non-
absorbable or absorbable applied using a special device
called Protack or Absorbatack.
EPIGASTRIC HERNIA
It appears in the epigastric region in the midline through
the intricated fibers of the linea alba.
The first to protrude is the properitoneal fatty tissue – the
so called preherniar lipoma – which produces a cone of
the peritoneum (the sac).
Usually hernias are of small dimension – 1-2 cm diameter,
and difficult to diagnose in obese patients. On palpation a
small, painful bulge can be felt under the midline skin of
the epigastric region.
There are two clinical forms:
– Painful
– Painless
Frequently they are associated with other pathology of the
supramesocolic organs (peptic ulcer, gastric cancer, gall
stones, etc.) This is the reason why pre- and intra-
operative investigation of these organs is recommended.
Treatment consists in removing the prehernial lipoma
and reinforcement of the linea alba with sutures, with or
without using a mesh.
SPIGELIAN HERNIA
Spigelian hernia appears under the aponeurotic layer
between the rectus abdominis muscle medially, and the
semilunar line laterally, at or below the linea arcuata.
The bulge is not very evident because the sac does not
lie below the subcutaneous layer but under the
aponeurosis.
It can be highlighted by ultrasound examination.
The treatment is surgical consisting in abdominal wall
repair through classical open approach or by
laparoscopic approach. In open approach the incision is
placed on the hernial area, the muscular layer dissected,
the sac is found and reduced into the abdominal cavity
or resected, and then the posterior rectal sheath is
reinforced and the other layers re-approximated. Another
possible reinforcement of the abdominal wall through this
procedure is using a mesh.
By laparoscopic
approach (which is most
frequently used in now
days) the parietal defect
is covered by a silicone-
coated mesh kept in
place using tacks and
threads. The procedure
is similar to that applied
in umbilical hernia.
Laparoscopic approach
ensure a very fast
recovery of the patient
who in most cases is
discharged in the next
day after the operation.
OBTURATOR HERNIA
 The obturator canal lies between the obturator
membranes. It contains the the obturator nerve and
vessels. The canal has rigid walls which determines the
frequently incarceration of these hernias.
Usually the patient is operated for intestinal occlusion (as a
result of incarceration), the hernia being an intraoperative
surprise.
The Romberg’s sign can be observed in this type of
hernias due to the compression on the obturator nerve - the
thigh is flected in abduction position with external rotation of
the knee (antalgic position). The pain is felt in a region just
up and medial to the knee which is the area of skin
innervation of the obturator nerve.
Treatment – surgical by open or laparoscopic approach.
The herniated intestinal loop is treated, if necessary
resected and the internal obturator ring is closed in different
ways (sutured, plugged or with meshes).
 ISCHIADIC HERNIA
The greater sciatic notch – divided into 2 holes by the
pririformis muscle
1. Suprapiriform foramen – crossed by the superior
gluteal vessels and nerves.
2. Infrapiriform foramen – crossed by the sciatic nerve,
femurocutanate nerve and inferior gluteal vessels
and nerves.
These types of hernia are very rare and the diagnosis
is difficult because the sac is located under the gluteal
muscles.
It must be differentiated from a gluteal abscess and
other tumors in that region.
INCISIONAL HERNIAS
Incisional hernias (eventration) represent the total or
partial protrusion of abdominal viscera, under the skin,
through a defect in the abdominal wall…. – (almost the
same definition as in hernia…. but) …..the integrity of the
anatomical structures of the abdominal wall being
affected (in most cases by surgery) and incisional
hernias may appear in other zones not just in hernial
zones as in case of common hernias (where the
abdominal wall is naturally weaker).
They are called “incisional” because they appear most
often after surgeries which require laparotomy.
Classification
Traumatic
– Postoperative – “incisional hernias”
– Non surgical – accidentally ( as a consequence of blunt or
penetrating trauma of the abdomen)
Non traumatic
– Various deficiencies (protein, vitamins, etc) and other
pathologies – in fact there is a relaxation of the abdominal wall
structures. It is asymptomatic and will not lead to incarceration.
– Obstetrical - diastasis of the rectus abdominus muscles –
weakening of the fascial membrane (linea alba) connecting the
rectus muscles. It is asymptomatic and will not lead to
incarceration.
Risk factors
A. Local factors and surgical technique
After laparotomies the integrity of the abdominal wall is
affected. The resulting scar is not as strong as normal
tissues and can break on intense efforts. On the other
hand there are a lot of other factors that could lead to the
impairment of the healing process resulting a breach of the
abdominal wall under the skin.
1. Wound suppuration - is the most important and
frequent cause of incisional hernias.
2. Abdominal cavity drainage – The drainage promotes
local suppurative process.
3. Incision type - vertical laparotomies predispose more
frequently to incisional hernias but on the other hand
oblique incisions, perpendicular on the nerves
direction, lead to a relaxation of the abdominal wall
beneath the incision because they cut the nerve
supply of the muscles.
B. General factors
1. Obesity – It is associated more frequently with
diabetes, wound suppuration and an increased intra-
abdominal pressure.
2. Age – healing process is affected at advanced ages.
3. Debilitating factors - catabolic conditions,
malnourishment, hypoproteinemia, anemia, cancer,
which disturb the healing process.
4. Postoperative broncho-pulmonar complications –
coughing effort increases the intra-abdominal pressure.
5. Other factors - treatment with steroids, chemotherapy
radiation, etc. - they interfere with the healing process.
6. Intense physical efforts after surgery.
More than 50% of incisional hernias develop within the first 2
years after the primary operation.
The frequency rate is approximately 2-11%.
The onset is as an asymptomatic bulge noticed by the
patient. Over the time, incisional hernia enlarges and
becomes more evident and painful.
Symptoms like vomiting, constipation, or severe pain can be
associated with incarceration or strangulation.
The evident appearance of the hernia makes it easily to
diagnose, often requiring no testing outside of a physical
examination.
The parietal breach may be of different sizes from small to
very large with fibrous inexetensible margins.
The sac may be unique or multiple (multilocular).
The content of the sac is represented by abdominal viscera
(intestines, great omentum) which are adherent to each other
and to the sac.
 Superjacent skin is thin with scars, sometimes presenting
with trophic disorders.
The clinical evolution and complications are similar to
those encountered in other types of hernias.
(incarceration, irreducibility, etc)
Treatment
The treatment has the same targets and steps as in other
abdominal wall hernias – dissection of the sac, treatment
of the content (adesiolisis, partial resection of the great
omentum or bowel resection in incarcerated hernias) and
reinforced closure of the parietal defect to prevent
relapses.
There are many surgical procedures. The approach may
be by classical laparotomy or by laparoscopy.
 6 rules to be respected for surgery:

1. Skin infectious lesions must be treated prior to surgical

treatment
2. Rigorous compliance with intra- and postoperative
asepsia
3. Perfect hemostasis
4. Use slow absorbable sutures
5. Use of antibiotics
6. Hernia repair will be performed only after 6 to 9 month
from the last operation
Contraindications
Major loss of abdominal domain
Severe debilitation
Fewer than 5 years life expectancy
Respiratory distress
Pregnancy
Portal hypertension
Renal failure with presence of peritoneal dialysis
catheter
There are many procedures that do not use prosthetic
materials. They can be used in small or medium size
hernias. The tension in the suturing line in this kind of
repairs is the reason why the relapse rate reaches 50%.
– Eduard Quenu – approximates the margins of the
parietal defect with interrupted sutures.
– D’Alain Cotiades – used especially in diastasis recti,
reinforces the abdominal wall on median line without
opening the peritoneal cavity, approximates the
median margins of the rectus abdominus muscles.
– Sapjeiko-Picoli – reinforces the abdominal wall using
a double layer technique.
– Maydl -restores abdominal wall suturing each
anatomical plan separately. It is used for incisional
hernias after appendectomy.
 Plastic procedures use prosthetic materials (meshes) to
reinforce the abdominal wall. There are different types
and sizes of meshes, usually of polypropylene, which
are more and more better adapted and accepted by
human tissues.
1. Onlay procedure. The mesh is sutured to anterior
rectus sheath after fascial defect has been closed
primarily.
2. Inlay procedures– after resection of the sac the
mesh is sutured to the defect margins. Special
meshes must be used (see below) which do not
adhere to the viscera. It is a tension free procedure.
3. Rectorectus procedure. The mesh is placed
between peritoneum and rectus muscles (Rives-
Stoppa technique).
4. Underlay procedure. The mesh is placed on the
inner surface of the abdominal wall on the
peritoneum. Special meshes must be used. One
surface of these meshes, that is in direct contact
with intra-abdominal organs, is siliconed so that
tissues can not adhere to it. This kind of meshes are
used when the parietal defect is large and cannot
be entirely closed and also in laparoscopic
approach. The technique of the laparoscopic
approach is similar to that described at umbilical
hernia.
Onlay mesh
Laparoscopic approach
Postoperative complications
Intestinal lesions
Wound Infection
Mesh infection – aprox 7%
Persistent seroma
Prolonged pain
Ileus
Bleeding/Hematoma
Recurrence after mesh repair aprox-10%
Respiratory distress
Abdominal compartment syndrome
Skin necrosis
EVISCERATION
 Evisceration represents the protrusion (extrusion) of the
viscera outside the peritoneal cavity, in direct contact with
atmosphere, through a solution of continuity in the
abdominal wall (wound dehiscence).
There is no sac like in hernia and the skin is opened.
Causes
– Postoperative disruption of the wound
– Posttraumatic – penetrating wounds (accidental or by
aggression)
Risk factors
A. Determinant factors:
– Intra-abdominal high pressure
– deficiencies in healing process
B. Contributing factor leading to poor healing:
– Advanced age
– Hypoproteinemia, hypovitaminosis, - anemia, cancers
– Obesity
– Diabetes
C. Factors contributing to increased intra-abdominal
pressure :
– Chronic bronchopneumopathy
– Prostate adenoma, postoperative ileus
D. Local factors – wound infection
E. Deficiencies of surgical technique:
– Incorrect approximation of wound margins, ischemic
sutures
– Inadequate suture materials
– Drainage through the wound
Postoperative evisceration usually occurs between day 5
and 10 and it is announced by a small hemorrhage
through the wound. After that, during an episode of high
intra-abdominal pressure (coughing, effort) the intestines
protrude outside the abdominal cavity on the skin.
This is an emergency situation and the patient must be
operated as soon as possible.
There are situations when the eviscerated organs remain
enclosed under the skin – is the so called blocked
evisceration. In this case if digestive transit is
maintained, operation can be postponed. The
evisceration will develop an incisional hernia which will
be operated later in better conditions.
Treatment
Evisceration is an emergency condition and treatment
measures must be taken as soon as possible.
Evisceration means peritonitis.
General measures: hydro-volemic, electrolytic, and
acido-basic rebalancing, hypoproteimenia will be
corrected, antibiotherapy and other specific measures
will be taken.
Eviscerated organs will be copiously washed and
replaced into the abdominal cavity. The contaminated
edges of the wound including a combination of the
peritoneum and rectus fascia are excised. The
abdominal wall will be sutured in a single layer with
interrupted or running sutures.
DIAPHRAGMATIC
HERNIAS
Development of the diaphragm
The diaphragm develops from 3 anatomical structures
which merge to form the diaphragm.
– The septum transversarium, and
– 2 Ustkov’s folds – muscular part of the diaphragm
Deficiencies of diaphragm development, will lead to
congenital diaphragmatic hernia.
Weak zones of the diaphragm
The diaphragm is a fibro-muscular structure that
separates the thoracic cavity from the abdomen.
Weak zones are all diaphragmatic holes through which
diverse anatomical structures are passing from
abdominal and thoracic cavity (aortic hiatus, esophageal
hiatus, VCI, ductus thoracicus, splanchnic nerves,
azygos veins, etc.).
 Diaphragmatic hernias
Diaphragmatic hernia is a defect or hole in the
diaphragm that allows the abdominal contents to move
into the chest cavity.
The following types of diaphragmatic hernia may exist:
Congenital diaphragmatic hernia
– Morgagni's hernia - anterior
– Bochdalek hernia - posterior
Hiatal hernia
Iatrogenic diaphragmatic hernia
Traumatic diaphragmatic hernia
Classification
1. Congenital
– Embryonic – maldevelopment appears in the first 3 month of
intrauterine life
– Fetal - the defect appears after the third intrauterine life
Agenesia of one or both diaphragm in most cases is
incompatible with life. Over 80% are located on the left
side.
Partial defects - can be operated with better prognosis
2. Acquired
– Traumatic - diaphragmatic ruptures
Blunt trauma
Penetrating trauma – stab wound (thoracic or abdominal)
– Nontraumatic
Hiatal hernia
 Congenital hernias
There are two more frequent congenital diaphragmatic
defects where abdominal viscera can herniate into the
thoracic cavity:
– anterior - through the Morgagni-Larrey’s orifice
– posterior - through the Bochdalek’s costo-vertebral
foramen
Large congenital hernia are manifested shortly after
birth. Symptoms are: respiratory distress, apparent
dextrocardia, a scaphoid abdomen and radiological
appearances of bowel in the hemithorax.
Treatment involves urgent nasogastric suction, to
prevent distension of the bowel and further compression
of the lung and general resuscitation before surgical
repair.
Bochdalek hernia
This is s the most common diaphragmatic hernia in
children.
The principal symptom is severe respiratory distress.
Frequency: approximately one of every 2,500 live
births. They are twice as common in male as in female
neonates. Mortality ranges from 45% to 50%.
There is a classic triad:
1. respiratory distress
2. apparent dextrocardia
3. scaphoid abdomen
Treatment
Immediately after birth, neonates with Bochdalek hernia
are taken to the operating room.
For hernia on the left side, the transabdominal subcostal
approach is generally preferred, whereas for hernia on
the right side, a transthoracic approach is preferred.
The herniated organs are restored in the abdominal
cavity and the defect is closed with interrupted
nonabsorbable sutures. Large defects may be closed
with a patch of mesh. The pleural cavity is drained with a
tube placed on water seal.
Morgagni hernia

The cause of Morgagni hernia (Giovanni Battista Morgagni)

is the to maldevelopment of the septum transversum which
failed to merge to the sternal and costal elements.
The hernia is located anterior between the sternal and
costal attachments of the diaphragm.
They are most commonly seen on the right side.
These hernias are generally asymptomatic and are usually
detected as incidental findings on radiographs.
The most commonly involved abdominal organ is the
transverse colon and the great omentum.
De defect is sutured with nonabsorbable sutures.
Morgagni hernia
 Hiatal hernia
The stomach protrudes into the thoracic cavity through
the enlarged esophageal hiatus.
Anatomy
The length of the esophageal hiatus is approximately 2 cm.
The size of the hiatus narrows whenever intra-abdominal
pressure rises.
The lower esophageal sphincter (LES) is an area of
smooth muscle approximately 2.5-4.5 cm in length. The
upper part of the sphincter normally lies within the
diaphragmatic hiatus, while the lower section normally is
intra-abdominal.
The visceral peritoneum and the phrenoesophageal
membrane cover the abdominal esophagus. The
phrenoesophageal ligament is a fibrous layer of connective
tissue arising from the crura, and it maintains the LES
within the abdominal cavity.
Intrathoracic protrusion on the cardia is favored by the
laxity of the diaphragmatic fixating structures (Laimer-
Bertelli membrane, gastro-phrenic ligament, etc.).
Obesity, pregnancy, physical efforts and age, are
contributing factors.
The gastroesophageal
junction acts as a
barrier to prevent reflux
of contents from the
stomach into the
esophagus and the
consequent esophagitis
(GERD –gastro
esophageal reflux
disease). The
components of this
barrier include the
diaphragmatic crura, the
LES, and the angle of
Hiss.
Types of hiatal hernia
1. Short esophagus (brachiesophagus)
– the esophagus is shortened, the cardia is
intrathoracic
2. Sliding hernia - is the most common - 95% of cases
– The length of the esophagus is normal but the
cardia slips intrathoracic.
3. Rolling hernia (paraesophageal hernia)
– The length of the esophagus is normal, the cardia is
intra-abdominal but the stomach is protruded intra-
thoracic.
– The widened hiatus permits the fundus of the
stomach to protrude into the thorax besides the
esophagus.
Sex: more common in females than in males probably
due to the intra-abdominal high pressure during
pregnancies.
Age: Incidence of hiatal hernias increases with age;
approximately 60% of individuals aged 50 or older have
hiatal hernia - especially due to the loss of muscular
tonicity and elasticity of the fixing elements of the
esophagus.
Para-esophageal hernias tend to become more
voluminous over time.
Symptoms: By far, most hiatal hernias are
asymptomatic and are discovered incidentally.
There is no direct correlation between hernia size and
intensity of symptoms.
In 5% of cases hernia evolves to complication such as:
gastric volvulus, perforation, strangulation, all of them
threatening the life of the patient.
The most common complication is reflux esophagitis
The symptoms associated with hiatal hernia are variable
but generally include:
– Heartburn - 30 - 60 minutes after eating
– Regurgitation - worsened with lying flat
– Excessive belching
– Aspiration - stomach contents refluxed into the airway
– Asthma - chronic result of aspiration
– Chest pain - burning mid-chest pain
– Difficulty swallowing
– Pain with swallowing
– Bleeding
– Stomach twisting and perforation
– Obstruction
Investigations
Barium swallow in Trendelemburg position will highlight
the reflux of contrast into the esophagus and the position
of cardia or stomach above the diaphragm.
CT scan
The stomach in the thoracic cavity - paraesophageal hernia
 Esophago-gastroscopy – advantages: can evaluate the
esophageal mucosa status – esophagitis ? Biopsy

Intragastric view of the herniated portion of the stomach

endoscope
Treatment
Asymptomatic hernias are not treated as long as they
remain undiagnosed.
The diagnosed hernias, if manifested by various
digestive and /or thoracic symptoms could benefit from
medication and/or surgery.
If there is a reflux esophagitis, treatment will target the
following aspects:
1. Lifestyle changes
2. Antacid medications
3. Stimulation of gastric motility and evacuation
4. Surgical methods that oppose to gastroesophageal reflux
 SURGICAL TREATMENT
– Surgery is necessary only in the minority of patients
with complications of GERD despite aggressive
treatment with proton pump inhibitors (PPIs).
– It is recommended especially for paraesophageal
hernias.
– Goals of treatment are:
1. Repositioning the stomach and the cardia intra-abdominal
2. Recalibrating the esophageal hiatus
3. Making an antireflux valve
Possibilities
Abdominal or transthoracic approach
Classic or laparoscopic
Pure endoscopic approach NOTES (Natural orifice
translumenal endoscopic surgery)
Procedure: The eso-gastric junction is exposed. The
hiatal hernia is easily observed in rolling hernias.
The lesser omentum is sectioned preserving the hepatic
branches of vagus nerves and vascular branches. The
right diaphragmatic crus is exposed and the dissection
continues in the fatty tissue between the esophagus and
crus. The peritoneum above the esophagus is cut and
dissection goes on toward the left crus. The aim is to
free up the esophagus and to replace the cardia into the
abdomen.
Then, the gastro-splenic and gastrophrenic ligaments
are divided to free up the fundus of the stomach.
There are more types of procedures to perform an
antireflux valve.
Procedures - antireflux valve:
The gastric fundus is twisted around the abdominal
esophagus (Nissen, Belsey, Toupet procedures) or used
as an anterior flap (Dor procedure).
Hill's procedure fixes the cardia posterior to the
diaphragmatic crus and increases the angulation of the
Hiss angle.
Laparoscopic approach - Nissen procedure

Working
trocars

Retractor
trocar

Optic trocar
 Liver

Hernia

Eso

Stomach
Hernia
Posterior
mediastinum
Esophagus

Right crus

Stomach
Recalibrated
hiatus
Esophagus

Posterior
Left Vagus nerve
crus
Right
crus
 Esophagus

Stomach

Fundus

“shoe shine maneuver”

Nissen completed
Thoracic approach – Collis Belsey procedure – uses part
of the stomach to add length to the esophagus by cutting
the stomach at level of Hiss angle. The crura are re-
approximated and esophageal hiatus is narrowed.
TIF (transoral incisionless fundoplication) procedure
The TIF procedure treats GERD and is performed
endoscopically through the mouth. No incisions are required.
It uses a special endoscope (EsophyX) which reinforces the
gastroesophageal junction by folding (plicating) the upper
portion of the stomach around the gastroesophageal junction
for about 270 degrees and securing it in place by special
fasteners.
EsophyX device
DIAPHRAGMATIC RUPTURE
 Mechanism:
– Closed trauma – blunt abdominal trauma which rises
the intra-abdominal pressure
– Open or penetrating trauma (wounds) – stab,
gunshot, etc
Transabdominal
Transthoracic
Due to the gradient of pressure
between the abdominal (high)
and pleural cavity (low), intra-
abdominal organs (colon,
stomach, spleen, small bowel,
omentum) protrude into the
thorax, where they become
adherent to the intrathoracic
organs (lung, pericardium, etc).
In cases of penetrating trauma, both intra-abdominal
and intra-thoracic organs may have serious lesions, not
just the diaphragm. In these cases surgeons must
carefully inspect all organs inside the both abdomen and
thorax.
All these cases are emergencies and must be operated
in as soon as possible but after a good evaluation and
investigation of the patient (ultrasound, chest
radiography, CT-scan, etc).
As a rule, for live saving, solving the intrathoracic lesions
has priority against the abdominal lesions.
In case of transthoracic penetrating wound the surgical
approach will be through a thoracotomy. When intra-
abdominal organs are also affected, a laparotomy can be
performed if lesions can not be managed through the
diaphragm. For example a splenectomy can be
performed through the diaphragmatic breach.
When the entrance of the traumatic agent is the
abdomen, a laparotomy will be performed and if on
exploration diaphragmatic lesions are found, if necessary
(when other intrathoracic lesions are present), the
laparotomy can be associated with thoracotomy or
transformed in thoraco-phreno-laparotomy.
The diaphragm is sutured with interrupted non
absorbable sutures.
The diaphragm rupture after blunt abdominal trauma is
much more frequent on the left hemidiaphragm (the right
is protected by the liver), at the level of centrum
tendinosum (central tendon).
Most often the patients have politrauma and are
unconscious.
The first measures are those for life support, but
concomitant good clinical and paraclinical evaluation
must be carried out.
Bowel sounds may be heard in the chest and the chest
radiograph may reveal bowel gas in the lung fields. A
contrast study (when possible) will confirm the diagnosis.
A CT-scan must be performed.
Thoracotomy will be the first choice of exploration and
then if necessary a laparotomy.
Thoracic radiogram CT scan

Stomach ascended into thorax left diaphragmatic rupture

Occasionally, the injury is overlooked and the patient
presents some time later with a diaphragmatic hernia.
In these cases the diaphragmatic lesion will be solved
through a thoracotomy approach as the test of time
proved that intra-abdominal lesions are not present.
(peritonitis, hemoperitoneum)
There are cases in which diaphragmatic hernia are
incarcerated with damage of the intra-abdominal organs,
especially colon or small intestine. It happens especially
when the diaphragmatic defect is small. The diagnosis is
usually difficult and represents an intraoperative
surprise. A more detailed history on these patients
reveals a history of abdominal trauma or other
mechanisms of sudden increase of intra-abdominal
pressure.
There are 3 clinical phases of diaphragmatic injuries
(described by Grimes).
– 1. Acute phase - in the same day with the trauma.
– 2. The second or latent phase - if the injury is not
recognised in the early phase. It is an asymptomatic
phase but intra-abdominal viscera evolve into
gradual herniation.
– 3. The third phase is that of complications
(obstruction, incarceration, strangulation, perforation,
peritonitis, pleural effusions, etc).
 EVENTRATIONS
(RELAXATION) OF THE
DIAPHRAGM
Diaphragmatic relaxation represents the total or partial
relaxation of the diaphragmatic muscles due to primary
or acquired, traumatic or non traumatic, phrenic nerves
palsy or diaphragmatic muscle lesions or degeneration.
The diaphragm is the major respiratory muscle.
When it contracts it lowers and the intrathoracic pressure
lowers too, so inspiration takes place. When it relaxes, the
intra-abdominal pressure pushes the diaphragm upward,
the intrathoracic pressure rises and expiration takes
place.
An important condition for proper ventilatory function is
that both diaphragm (left and right) to run simultaneously.
A large diaphragmatic relaxation produces significant
breathing changes through several mechanisms.
– First – the lung volume on that side is reduced.
– Second – It produces a paradoxical respiration with
pendulating air from one lung into the another one.
The consequence is the hypoventilation, hypoxia,
dyspnea, bronchopneumonia.
The mediastinum is also pendulating with each
respiration.
Atelectais
It is a rare condition in adults.
It is asymptomatic when relaxation is minor and diagnosis
is made incidentally on a chest radiography.
In complete relaxation (more frequently on the left side)
symptoms may be represented by:
– respiratory distress with dyspnea, tachypnea, cyanosis
– tracheal and cardiac shift
– decreased breath sounds over the affected area
– asynchronous chest wall movement

And may evolve to:

– chronic pulmonary suppuration
– diaphragmatic rupture
– ulcer and volvulus of the stomach
– death
Eventration of the left diaphragm
Treatment
Surgery is indicated only in symptomatic relaxations.
The aim of surgery is to fix the diaphragm in
inspiration position so that paradoxical movement and
mediastinal pendulating are minimised.
It can be performed by thoracotomy or by minimal
invasive approach (thoracoscopy).
There are three main procedures of phrenoplaty:
1. Phrenoplication
2. Incision followed by double layers suture
3. Dual-layer sandwich mesh repair

Phrenoplication Dual-layer phrenoplasty

 THYROID SURGICAL
PATHOLOGY
3 reasons to operate thyroid

1. Goiter
2. Hyperthyroidism
3. Thyroid cancer
History
1812, Gay-Lussac discovered iodine as an element in goiter’s
etiopathogeny.
1833, Boussingault prescribes iodized salt in goiter treatment.
1836, T.W. King, English pathologically described thyroid follicles,
thyroid vascularization and issued several theories on the origin of
colloid.
1870, Fagge demonstrated that absence of thyroid function is the
cause of sporadic and congenital cretinism.
William Gull si William Ord clarified the role of thyroid in myxedema
pathogenesis.
The most important contribution: Theodor Kocher, Bern, Switzerland
surgeon who published the thyroidectomy technique. In 1882 had a
postoperative mortality rate of 2.4%. He operated over 5000 cases.
Billroth introduced the subtotal thyroidectomy to prevent the
laryngeal nerve lesions and tetania due to parathyroidectomy.
Thyroid cancer was described by Halsted who named it
sarcomatous degenerescence.
Anatomical aspects
The thyroid is an endocrine gland located in the anterior
region of the neck below the larynx in front of the first 3-4
tracheal rings. Its shape is like the "H" letter consisting
of two lobes connected by an isthmus. It weighs about
25-30 grams. Lobes height and thickness is about 5-6
cm. It has a reddish brown color and soft consistency.
Nearly 50% of thyroid glands exhibit a pyramidal lobe
arising from the centre of the isthmus.
Thyroid gland is wrapped by a sheath. Between the own
thyroid capsule and the sheath there is connective tissue
and blood vessels.
Relationship – relevant surgical aspects:
Anterior – the gland comes in contact with the
pretracheal fascia and subhyoid muscles (sternohyoid,
omohyoid, sternothyroid, thyrohyoid). Sometimes, when
very large goiter need to be operated, resection of these
muscles facilitates the removal of the gland.
Lateral – It has relations with the jugular vein and carotid
artery. These vascular structures are important and must
be protected during operations on thyroid gland. In very
advanced cases of thyroid cancer the jugular vein may
be compressed or invaded and it can be resected during
classical neck dissection operation.
Medial – it has relations with the larynx, trachea,
pharynx, esophagus and recurrent laryngeal nerves.
These relations are also very important. In voluminous
goiters trachea may be compressed with consecutive
respiratory impairment (dyspnea).
After a long period of time of compression on the trachea,
the cartilaginous structure of the tracheal rings becomes
very weakened (tracheomalacia) and after thyroid removal
the trachea collapses leading to asphyxia. In such cases
tracheostomy is the procedure that saves the patient’s life.
Injuries of the larynx or trachea during operations on
thyroid are very rare but possible.
Posterior – the gland comes in relations with the recurrent
laryngeal nerves, esophagus, cervical sympathetic chain
and parathyroids. Compression on laryngeal nerves will
lead to hoarseness, on esophagus to dysphagia and on
sympathetic chain to Claude-Bernard-Horner syndrome.
Lesions of these structures, especially of the recurrent
nerves are possible. Due to the very close relations with
the parathyroid glands, there is the chance to remove
these glands together with the thyroid lobes during
thyroidectomy that will lead to parathyroid insufficiency.
Inferior – the inferior thyroid vascular pedicle and
recurrent laryngeal nerves. At this site most often the
recurrent laryngeal nerves may be damaged due to their
intimate relations with the inferior thyroid vessels which
must be resected during thyroidectomy. Sometimes the
inferior pole of the thyroid lobe may plunge under the
sternum making the operation more difficult.
Superior - the superior thyroid vessels and laryngeal
nerves. At this site there is a risk to damage the superior
laryngeal nerves during vessels resection for
thyroidectomy. Due to the coiled shape of the superior
thyroid artery it may retract under tissues after resection
being difficult to find them and make the hemostasis if
necessary.
Arterial supply
– Superior thyroid artery
From external carotid artery
– Inferior thyroid artery
From thyreo-cervical trunk

Venous drainage
– Superior thyroid vein – to internal jugular v
– Middle thyroid vein - to internal jugular v
– Inferior thyroid vein – to brachio-cephalic venous
trunk
Lymphatic
drainage
The lobes of the gland, as well as the isthmus, contain
many small globular sacs called follicles. The follicles
are lined with follicular cells and are filled with a fluid
known as colloid that contains the prohormone
thyroglobulin. The follicular cells contain the enzymes
needed to synthesize thyroglobulin, as well as the
enzymes needed to release thyroid hormone from
thyroglobulin. When thyroid hormones are needed,
thyroglobulin is reabsorbed from the colloid in the
follicular lumen into the cells, where it is split into its
component parts, including the two thyroid hormones
thyroxine (T4) and triiodothyronine (T3). The hormones
are then released, passing from the cells into the blood
stream.
Histology
 GOITER
Endemic Thyroid Dystrophy
(ETD)
Goiter = Enlargement of the thyroid gland due
to hyperplastic and hypertrophic processes of
dystrophic nature, that affect thyroid follicles,
connective and vascular tissues.
 Why ETD ?
Endemic = constantly is found in certain geographical
areas with iodine deficiency in water and food – (Ex.
Maramures region).
Thyropathic = because in the centre of the disease the
thyroid glad is whose function and structure is altered.
Dystrophic = because the metabolism disorder affects
the whole body.
 It is estimated that goiters affect as many as 200 million
of the 800 million people who have a iodine deficient
diet.
Etiopathogenesis
Determinant conditions
1. Exogenous factors – Iodine deficiency in water and
foods. The amount of iodine required is 100-150
gamma/day. In the absence of iodine, compensatory
thyroid tissue hyperplasia occurs.
2. Goitrogens: cassava, cabbage, cauliflower, Brussels
sprouts and turnips. These interfere with T3/T4
synthesis.
3. Endogenous factors
– Braking intestinal absorption of iodine. Intestinal flora,
excess of calcium, magnesium salts. - Fluoride causes
increased elimination of iodine.
– Substances that inhibit the entry of iodine in the thyroid
(thiocyanate, perchlorate) - cassava contains a
thiocyanate which inhibits iodide transport within the
thyroid.
– Substances that interfere with hormone biosynthesis
(Thyouracil). In excess iodine administration does not
have the opposite effect.
– Drug induced goiter: sulfonamides and
phenylbutazone inhibit organification of iodine; iodine
containing drugs such as amiodarone interfere with
thyroglobulin proteolysis; iodine or lithium interfere
with thyroglobulin breakdown and release of T3/T4
Adjuvant factors - socio-economic (diet)
Predominant biological - age, sex, repeated
pregnancies, breastfeeding
Genetic - unclear
Morphopathology
Goiters with normal location
– Parenchymal goiter (diffuse hyperplasia). Enlarged gland entirely
smooth, regular, uniform appearance on section. Histologically”: "
macro- microfolicular colloid adenoma”
– Nodular goiter - circumscribed nodule separated from the gland by
a fibrous tissue which allows enucleation. When there are more =
multinodular. Nodes may look different on section, some are solid,
cystic others. Histologic appearance of acinar adenoma (vesicles of
different sizes) or trabecular adenoma (cords of epithelial cells
without vesicles with colloid)
– Cystic goiter - enlargement of vesicles of a colloid goiter. Content =
serous or blood. True cysts = lining of secretory epithelium, False
cysts = the epithelium is missing. Colloid goiter: means massive
storage of colloid within follicles often with flattened epithelium.
– Varieties: Nodulocystic, calcified, vascular
Nodulocystic goiter
Multinodular goiter
Goiters with abnormal location
– Plunged goiter – frequently encountered in elderly with
pulmonary emphysema. The goiter is located (plunged)
in the retrosternal space.
– Endothoracic goiter (medial or lateral)
– Ectopic goiters – they do not have any connection with
the thyroid gland. They develop on heterotopic thyroid
tissue islands. The most common sites are the base of
tongue, larynx, trachea and rarely the pericardium.
Struma ovarii is a rare ovarian tumor defined by the
predominant presence of thyroid tissue. Most
commonly, they occur as part of a teratoma, but may
occasionally be encountered with serous or mucinous
cystadenomas. Struma ovarii were first described in
1899 and comprise 1% of all ovarian tumors.
Chest X-ray of a Patient
with large compressive
Substernal goiter showing
tracheal deviation to the
left side
Symptoms
Sex: The female-to-male ratio is 4/1
Age: The frequency of goiters decreases with advancing
age, but on the other hand, the incidence of thyroid
nodules, increases with advancing age.
In the initial phase, without functional disorders, there
are no symptoms. The patient discovers incidentally a
swelling in the neck, or the doctor at a routine examination.
In advanced stages because of the anatomic relationship
of the thyroid gland to trachea, larynx, superior and inferior
laryngeal nerves, and esophagus, abnormal growth may
cause a variety of compressive syndromes.
Signs
Physical examination: is best performed with the
patient upright, sitting or standing.
On inspection: Symmetrical or asymmetrical
deformation of the anterolateral neck region. Skin of
normal appearance, nonadherent to the gland. Dilated
superficial venous network in large goiters.
On palpation: The tumor is mobile to the lateral
mobilization and follows cranio-caudal direction
movements of the larynx during swallowing. They are of
variable consistency. Parenchymatous goiter is elastic.
Vascular goiter is depressible and soft bruit could be
heard. Colloidal goiter is irregular, lobular and soft.
Nodular goiter consistency is high and irregular.
 Cervical lymph nodes must be palpated for signs of
metastatic thyroid cancer.
Classification

I grade (small): can be observed just during deglutition

II grade (medium): do not exceed the lateral margin of
the sternocleidomastoid muscle
III grade (big): exceeds the lateral margin of the
sternocleidomastoid muscle
IV grade (gigant): exceeds the cervical region and is
visible from distance
Compressive syndromes
Laryngeal nerves: - hoarseness, dysphonia, bitonal
voice
Larynx and trachea: - dyspnea of effort, asphyxia
Esophagus: - dysphagia
Large vessels: - cyanosis of the face, headache,
epistaxis, tachycardia
Vagus nerves: - cardiac arrhythmias and respiratory
disorders
Cervical sympathetic chain: - Claude Bernard-Horner
Syndrome (myosis, palpebral ptosis, enophtalmia, facial
redness).
Claude Bernard-Horner Sdr.
Investigations
For the morphology of the thyroid gland:
– Ultrasound examination – uninvazive, very useful, it
guides the fine needle aspiration biopsy (FNAB)
– CT scan or MRI – more details about relationship
with other surrounding tissues
For the endocrine function of the thyroid:
– Thyroid scintigraphy - images of the thyroid
obtained after intravenous injection of Tc-99m or after
the oral ingestion of radioactive iodine (I131). Very
useful also for locating the ectopic thyroid tissue.
– Lab tests (TSH, FT3,T3, FT4, T4,TbG etc)
For histology diagnosis:
– FNAB (fine needle aspiration biopsy)
 scintigraphy

A = normal thyroid,
B = Graves disease: diffuse increased uptake in both thyroid lobes,
C = Plummer's' disease (TMNG, toxic multinodular goiter),
D =Toxic
E = Hypothyroidism
FNAB
Differential diagnosis
1. Congenital disease - Cyst of the thyroglossal duct,
branchial cleft cysts
2. Acute thyroiditis
3. Subacute thyroiditis
4. Chronic thyroiditis
5. Hydatid cyst of the thyroid
6. Thyroid TB
7. Thyroid syphilis
8. Thyroid cancer
9. Cervical lymph nodes
10. Parathyroid tumors
11. Carotid artery aneurysm
12. Cystic hygroma
Thyroglossal duct cyst
Treatment
Prophylactic– iodized salt, and tablets or potassium
iodide solution.
Curative - as in the prophylactic but higher doses and
more prolonged. If after 2-6 months the goiter volume
does not reduce, surgery is indicated.
Other causes of enlarged
thyroid gland
Nodules
Acute thyroiditis
Subacute thyroiditis - de Quervain
Chronic Thyroiditis (Hashimoto, Riedel)
 Solitary thyroid nodule
2-4% of adults, up to 50% of elderly
Usually women are most affected
Up to 10% are malignant
Single and cold (on nuclear scan) nodules are risk
factors for malignancy, but 80-90% will be benign.
Risk factors for cancer are radiation to head and neck,
rapidly enlarging nodule, ipsilateral adenopathy, male
patient, age <20 years or >70 years
Evaluated with ultrasound guided fine needle aspiration
to rule out malignancy
 Acute thyroiditis
Via blood or direct seeding from upper respiratory
infections
Sudden onset of pain and glandular enlargement
Treatment: antibiotics, drainage, fistulectomy
Gross appearance: normal or slightly enlarged thyroid
gland, painful, with Celsian signs present and may have
suppurative areas.
 Subacute thyroiditis
Also called de Quervain’s thyroiditis or granulomatous
thyroiditis
Rare, much less common than Hashimoto’s thyroiditis, but
the most common cause of thyroid pain.
75% in women, usually at age of 30-50 years
Gross appearance - focal to diffuse enlargement of thyroid
gland up to 2x normal size. It may be asymmetric with
nodules of variable size. May be firm, but does not adhere
to surrounding structures.
Etiology may be systemic viral infection, since associated
with epidemics of measles, mumps, Coxsackie,
adenovirus and influenza.
Self limited, usually resolves in 6-8 weeks with only 1%
having permanent hypothyroidism.
Treatment - none or antiinflammatory, propranolol if
thyrotoxicosis.
 Hashimoto’s thyroiditis
(lymphocytic thyroiditis)

Autoimmune disease with goiter. There are elevated

circulating anti-thyroid antibodies.
90-95% in women, age 45-65 years.
Adults present with painless, gradual thyroid failure due
to autoimmune destruction.
Diffuse symmetric enlargement of thyroid gland (25 to
250g) with intact capsule, pyramidal lobe may be
prominent. May have adhesions but thyroid gland is
easily separated from other structures.
 Riedel’s thyroiditis
(fibrous or “woody” thyroiditis)
Densely fibrotic inflammatory process involving thyroid
gland and adjacent neck tissue.
Rare (0.05% of thyroidectomy specimens), slight female
predominance, usually age 40-60 years.
Associated with inflammatory fibrosclerosis / multifocal
systemic fibrosclerosis.
Gross appearance: extensive stony hard fibrosis
involving a goitrous thyroid gland and infiltration into
adjacent muscle and other structures, obliterating tissue
planes at surgery. Binds soft tissues of neck in an “iron
collar” that may compress the trachea.
 HYPERTHYROIDISM

Overactivity of the thyroid gland

which produces excessive thyroid
hormones and accelerates metabolism
in the peripheral tissues.
The thyroid gland produces hormones which regulate
different processes :
Tri-iodothyronine (T3) – (7% of total) - a follicular
hormone
Thyroxin (T4) - (93% of total) - a follicular hormone
Reverse T3, synthesized in the fetal thyroid and in
peripheral tissues from T4. This is the biologically
inactive form of thyroid hormones.
T4 is the major secretory product of the thyroid gland but
T3 is biologically more active than T4.
Calcitonin is secreted from the parafollicular cells and is
a Calcium lowering hormone.
Central regulation of thyroid hormone secretion

The thyroid gland is controlled by the activity of the hypothalamic-

pituitary-thyroid axis
C cells secrete calcitonin, which
lowers serum calcium by promoting
bone absorption of calcium and
inhibiting bone resorption by
osteoclasts; in humans, has only a
minor role in calcium homeostasis
Clinical picture
4 stages :
1. Neurogenic – with nonspecific symptoms,
2. Neurohormonal – with all specific symptoms
due to increased thyroid hormone,
3. Visceral stage - with complications especially
cardio-vascular,
4. Cachectic stage
 GRAVES’ DISEASE
Autoimmune disorder with thyrotoxicosis
The cause is unknown
It affects 2% of women in US and 0.3% of men
85% of patients are women, usually aged between 20-40
years
Classic clinical presentation was described by Graves
Basedow and characterized by the tetrad:
1.goiter
2.exophthalmia
3.tachycardia
4.tremors
Initially the first signs are of neuro-psychological and
are manifested by emotional lability, irritability, psycho-
motor instability, hyperactivity, agitation, loss of
memory.
Cardiovascular symptoms are early and constant.
Palpitations, tachycardia, arrhythmias, heart failure,
toxic myocarditis. Tachycardia> 100 beats / min. is
persistent during sleep and worse at efforts. At
auscultation functional systolic murmur can be heard.
Systolic pressure increases and diastolic pressure
decreases.
Thyroid hypertrophy is almost constant. Elastic
consistency, smooth surface with thyroid thrills and
bruits. In thyroid toxic adenoma (TTA) a solitary nodule
is found.
Changes in skin and appendages. Pink, warm, moist,
smooth skin. Increased sweating. Perithyroidian red spots
(Maranon sign ) presternal red spots (spots of shame).
Pretibial myxedema. Diffuse pigmentation disorders:
Melasma (also known as "Chloasma faciei“), vitiligo,
alopecy, white hairpiece (Sabouraud sign), axillary hair
loss (Williams sign). Brittle nails with longitudinal and
transverse striations.
Weight loss (85% of cases). Increased appetite,
increased bowel movements.
Termofobia, sensitivity to heat, increased tolerance to
cold
Irregular or absent menstrual periods, enlarged
breasts in males
Finger tremor, eyelid tremor, tongue tremor.
Hyperthyroidism may also cause its patients to have an
expression of fright or extreme anxiousness. This may
be related to the peculiar eye signs characteristic of
hyperthyroidism. These eye signs include eyelid
retraction, a prominent staring appearance, infrequent
blinking, light sensitivity and bulging.
CLINICAL FORMS
1. Pure hyperthyroidy (Thyrotoxicosis)
2. Graves-Basedow disease
3. Toxic adenoma (Plummer’s disease)
4. Hyperthyroidized goiter
Evolution
– Acute hyperthyroidism
– Chronic hyperthyroidism
Symptoms
– Forms with predominant central signs (exophtalmia)
– Forms without thyroid hypetrophism
– Cardiothyreosis
– Forms with predominant digestive syndromes
Particular forms
– Hyperthyroidism on a thyroid cancer
– Iatrogenic hyperthyroidism (Jod-Basedow phenomenon) -
Kocher)
– Reactive hyperthyroidism in other diseases or poisonings
Investigations
LABORATORY
Thyroid Stimulating Hormone (TSH) – will be low in hyperthyroidism
Free T4 (free thyroxine) - high
Triiodothyronine (T3) radioimmunoassay (RIA) or free T3 - high
Thyroxine (T4) - high
Thyroid autoantibodies: TSH receptor antibodies (TRAb) or Thyroid-stimulating
immunoglobulins (TSI)
Thyroid Binding Globulin
PBI = protein bound iodine (4-8 gama%) or BEI= butanol extracted iodine
MB (basal metabolism rate) normal –5+15 %
IMAGING
Ultrasound
Iodine Uptake Scan. Normal 0-45% at 10 min, 20+-5% at 2 h, 40+-5% at 24 h
Radioactive iodine thyroid scan-with either I132 or 99mTc.
CT scan
ECG
Thoracic and cervical radiography
INVASIVE
Thyroid Needle Biopsy
Treatment
Anti-thyroid drugs - Two common drugs which actually
interfere with the thyroid gland's ability to produce its
hormones
– Methimazole (Tapazole, Thyrozol)
– Propylthiouracil (PTU)
Other drugs
– Beta blokers – propranolol
– Other medicines depending on associated pathology
Radioactive iodine treatment
– This treatment takes advantage of the fact that thyroid
cells are the only cells in the body which have the
ability to absorb iodine. By giving a radioactive form of
iodine, the thyroid cells which absorb it will be
damaged or killed.
Surgical removal of the gland or nodule
 Hyperthyroidism – Surgical treatment
Indications
ABSOLUTE
1. Hyperthyroidism associated with thyroid cancer
2. Toxic Thyroid Adenoma
3. Severe forms that do not respond to conservative
treatment during the last 3-6 month
4. Visceralized hyperthyroidism
5. Hyperthyroidized goiters
RELATIVE
1. All other forms that do not have absolute indications
2. Hyperthyroidism of the child
3. Hyperthyroidism during pregnancy.
Contraindications
1. Forms without thyroid hypertrophy
2. Multiendocrine forms
3. Forms with predominance of the central component
4. Forms associated with other more severe illnesses
5. Forms associated with psychotic disease
Preoperative preparation
General measures
– Bed rest, isolation, hypocaloric diet, eliminating
stimulants
Specific measures
– Sedative and hypnotic medication (valium,
fenobarbital, etc).
– Lugol – reduces the gland volume and increases it’s
consistency. (3X1 drops/day).
– Administration of anti-thyroid medication will be
discontinued with 10-15 days before surgery.
Associated medication – as needed
– Hydrocortisone 100 mg/day
– Cardiotonics
– Propranolol, etc
When is the right moment to operate ?
Criteria
1. Decreased heart rate below 100/min
2. Rebalancing of metabolism
3. Weight gain
4. Disappearance or improvement of
neuropsychological agitation
5. Decreasing the gland volume with increasing its
consistency
 GOITER
Surgical treatment
Anesthesia
– OTI – orotracheal intubation – there are special canula with
sensors for laryngeal nerves to monitor nerve damage during
operation
– Local - the advantage was the intraoperative recognition of
laryngeal nerve lesion – when talking with the patient voice
changes (hoarseness) indicate that the laryngeal nerve is affected
Approach – Kocher incision
Steps
Subcutaneous hemostasis, cutting the platysma
Preparation of the superior skin flap till the thyroid
cartilage
Cutting the longitudinal anterior rafe of the neck
Entering the thyroid lodge to explore thyroid lobes
Kocher incision
Types of operations

1. Nodule enucleation
2. Unilateral subtotal hemythyroidectomy
3. Bilateral subtotal thyroidectomy
4. Total hemythyroidectomy (unilateral thiroidectomy,
lobectomy)
5. Total thyroidectomy (bilateral total lobectomy)
6. Combinations – associated with sternotomy or
transthoracic approach for intrathoracic or plunged
goiters.
Total thyroidectomy (bilateral)
Complications
Intraoperative
– Hemorrhages
– Gaseous embolia
– Cardiac arrest
– Mechanical respiratory complication
– Laryngeal nerves injury
Early postoperative
– Bleeding, suppurations, seromas
– Disorders of phonation and respiration (tracheal
compression, laryngeal edema, bilateral damage to
the laryngeal nerves, tracheomalacia)
– Spasmophilia crisis and tetany due to the removal of
the parathyroid glands
– Thyroid storm
Tracheomalacia is characterized by flaccidity of the
supporting tracheal cartilage, and reduced anterior-
posterior airway caliber. These factors cause tracheal
collapse, especially during of increased airflow, such as
coughing, crying, or feeding. Tracheostomy is indicated.
Thyroid storm is a rare and potentially fatal
complication of hyperthyroidism. It typically occurs in
patients with untreated or partially treated thyrotoxicosis
who experience a precipitating event such as surgery.
There is an excess TSH release caused by fast
decreasing of blood levels of thyroxin.
Patients typically appear markedly hypermetabolic with
high fevers, tachycardia, nausea and vomiting, tremors,
agitation, and psychosis. Untreated the patients may
become stuporous or comatose with hypotension.
THYROID CANCER
Epidemiology
Thyroid cancer is the most common endocrine
malignancy, accounting for 1.9% of all new malignant
tumors.
Female/male ratio close to 3:1
80-90% appears on a preexisting goiter (nodular goiters)
More frequent at ages between 30 and 60.
Etiology
Causing factors – Radiation ? (Radiation exposure
significantly increases the risk of developing thyroid
malignancies, particularly papillary thyroid carcinoma.
After the nuclear accident at Cernobil the incidence was
higher)
Preneoplastic conditions – Hashimoto’s chronic
thyroiditis
Classification
Histopathology
– Papillary carcinoma – 80%
– Follicular carcinoma – 10% From follicular cells

– Anaplastic carcinoma - most aggressive

– Medullar carcinoma – 5% From neuro-endocine cells
calcitonin producing – C cells

– Lymphoma from intrathyroid lymphoid tissue

– Sarcoma from connective tissue

Stages

1. Cancer localized to the gland

2. Regional cancer, extracapsular
3. Disseminated cancer
Preclinical clandestine life of the tumor may last more
than 20 years and without any treatment the clinical
evolution may last till 12-18 month.
10-15% of patients with papillary and folicullary
cancers, present with lymph node or lung metastases.
Anaplastic cancer has a rapid course and early
dissemination.
Lymphatic spread of cancer cells
Symptoms
Few and unspecific
Sudden growth in volume of the gland
A painless, palpable, solitary thyroid nodule discovered
by patients or physicians on routine palpation of the
neck.
Patient’s age under 30 or over 60
Appearance and accentuation of compressive symptoms
(dysphonia, hoarseness, dysphagia,etc)
Signs

Nothing at all, or…

Increased consistency of the gland
Palpable nodule
Palpable cervical lymph nodes
Palpable metastases
Penetrating in the surrounding tissue
Skin exulceration in very advanced cases
Signs of compression on anatomical structures (Ex:
Claude Bernard H. syndrome)
 Claude Bernard-Horner Sdr.

74 years old, thyroid cancer penetrating the sympathetic

cervical chain and the esophagus. Claude Bernard-Horner
syndrome, dysphagia, dyspnoea
Surgery: gastrostomy for alimentation and tracheostomy
 Carotid artery

71 years old women, advanced thyroid

cancer, exulcerated with central necrosis,
and putrid odor
Right carotid artery and jugular vein
occluded by tumor thrombus
Surgery: cytoreduction
Paraclinical investigations

Imaging
– Ultrasound - cannot distinguish benign from malignant nodules
– CT scam, MRI scan - evaluate soft-tissue and extension of large
or suspicious thyroid masses
– Radioiodine imaging can determine the functional status of a
nodule. Carcinoma cannot be excluded based on radioiodine
scans.
Laboratory
– Serum thyroid-stimulating hormone (TSH) is a highly sensitive
measure for hyperthyroidism or hypothyroidism. However,
neither low nor high TSH can rule out malignant disease.
– Elevated serum calcitonin is highly suggestive of medullary
thyroid carcinoma
Histological diagnosis

Fine needle aspiration biopsy (FNAB)

Frozen sections examination
Histopathological examination of the operatory specimen

RESULTS

Benign - in approx. 70% cases

Malignant - in about 5%.
Suspected malignancy - in about 10%.
Can not be determined - in about 15% of cases.
Treatment – is multimodal & multidisciplinary
SURGICAL
– Total thyroidectomy
– Neck dissection – regional lympadenectomy
– Palliative – Tracheostomy, gastrostomy for
alimentation
ADJUVANT
– Radioiodine therapy in differentiated cancers in which
cells uptake Iodine
– Local radiotherapy in forms without iodine uptake
– Radioimunotherapy
– Cobaltotherapy
– Hormonal therapy, regional intra-arterial
chemotherapy
About 4-6 weeks after
surgical thyroid removal,
radioiodine therapy is
started to detect and
destroy any metastasis and
any residual thyroid tissue.
Therapy will be
administered until no
further radioiodine uptake
is noted.
Patients will take thyroid
replacement therapy (L-
thyroxine) for life,
especially after total
thyroidectomy.
Whole body imaging
Neck dissection
In palpable lymph node metastases, a modified radical
neck dissection is performed.

Lymph node groups

1. Submaxillary
2. Superior jugular
3. Medial jugular
4. Inferior jugular
5. Accessory chain
6. Juxta-thyroid
7. Anterior mediastinal
19 years old female.
Papillary carcinoma
with metastases in
bilateral cervical lymph
nodes
Total thyroidectomy
with modified neck
dissection
2007
One month later
2008 2011
 Prognosis
Thyroid cancer almost always is curable. Tumors are
slow growing and are associated with a very favourable
prognosis (except anaplastic type)

Thyroid 10-year
cancer 5-year survival survival
type

Stage I Stage II Stage III Stage IV Overall Overall

Papillary 100% 100% 93% 51% 96% - 97% 93%
Follicular 100% 100% 71% 50% 91% 85%
Medullary 100% 98% 81% 28% 80% - 86% 75%
Anaplastic (always stage IV) 7% 7% - 14% (no
data)
BREAST SURGICAL
PATHOLOGY
 Content
1. The importance of breast pathology
2. Surgical anatomy
3. Clinical examination of the breast
4. Malformations
5. Inflammations
6. Degenerative diseases
7. Tumors
a) Benign
b) Malignant
8. Particular forms of breast cancer
The importance of breast pathology
 The breast may be affected by a large variety of
pathology. Both benign and malignant type of pathology,
affect with predilection women at any age but may affect
men also.
 Breast cancer, as well as cancer in general, remains a
particular health problem despite of world wide efforts of
researchers and physicians and huge funds allocated for
prevention and treatment of this disease.
FACTS
1. Breast cancer is the most common cancer in women
worldwide.
2. Breast cancer is the third disease among the most
common diseases in the world.
3. One of eight women is likely to develop breast cancer
in their lifetime.
4. In USA 2/3 of operated women for breast cancer do not
have axillary lymph node metastases.
5. In Romania 85% of women operated with breast cancer
are in advanced stages.
 Particular factors to be considered in breast
pathology:

1. The breast, in women, beyond the role of breastfeeding

(which is however limited to a short period of lifetime), has
mainly an erotic and esthetic role, and therefore, the
breast pathology has a strong echo in the mental sphere
of the woman.
2. Surgery, where is indicated, takes into account more and
more the psycho-affective aspect, tending to be less
mutilant possible, but however it must also take into
account the invasive nature of the disease.
3. The breast is an easily accessible organ for examination,
facilitating early detection of pathological changes. The
sooner a breast lesion is discovered, the smaller will be
the unpleasant consequences of the possible surgery.
 BREAST ANATOMY
 Knowing the breast anatomy is of particular importance
for clinician (and not only), especially in cancer cases,
for several reasons:
1. To be able to establish a correct diagnosis,
2. To be able to perform adequate surgery,
3. To perform the radiotherapy in indicated regions,
4. To be able to foresee eventually relapses of breast
cancer.
Embryology
 Mammary glands begin to develop from the 6th week of
intrauterine life from two ectodermal thickening called
mammary crests. These crests are located along the
lines described by Schultze (1892) as "milk lines" which
join the axillary region to homolateral groin.
Along these mammary crests there are
6-7 nodules, which in mammals will
develop more pairs of mammary glands.
In humans, the caudal portion of the
crests will disappear remaining only the
thoracic portion. This will determine, in
normal cases, the development of one
single pair of mammary glands in
pectoral region. There are cases when
supernumerary mammary glands, or
just components of the breast (eg.
Schultze line – nipples) may develop along the “milk
milk line lines”.
 In women, initially under the action of estrogen and
subsequently in combination with progesterone,
mammary glands undergo significant changes till to the
stage of mature breast. This process generally takes 3-4
years and is completed in general at the age of 16.
Subsequent physiological changes occur during
pregnancy and lactation and menopause.
 In men, normally breasts remain almost unchanged, but
size and structure changes may occur under certain
conditions under the influence of various hormonal factors
(gynecomastia).
The breast
Location
 Breasts are located in the antero-superior region of the
chest. In women the classical breast area is extended
cranio-caudal between the second and the sixth rib and
in transverse direction between the margin of the
sternum and the anterior axillary line. In men this area is
limited solely to the breast areola region, being
rudimentary represented.
 The breast is enclosed between two thin sheets of
superficial fascia of the pectorals.
Extension
 The mammary gland area in women is extended in
cranio-caudal direction between the clavicle and the
superior margin of the rectus abdominis and in
transverse direction between the margin at the sternum
and latisimus dorsi muscle.
 Breast limits Extension of mammary gland

Nipple–areola
complex
between the 4th
and the 5th ribs
 The mammary gland has a more extended area than the
breast. This aspect is very important because on this
area pathological processes of the breast tissue may
occur, and also for surgery because these are the limits
within which the surgeon must perform a radical
mastectomy for breast cancer.
 The axillary extension of the mammary gland (axillary
tail) is of special interest because it is often affected by
pathological processes. In some women this extension is
well represented and can be confused with a lipoma, an
axillary adenopathy, or a supernumerary breast. Usually
it becomes more evident during the premenstrual period
and lactation.
 The internal surface of the gland is attached to the
pectoralis fascia by fibrous strips called Cooper’s
ligaments.
External appearance
 Two hemispherical shape masses, whose size and
weight vary from person to person based on race, age,
and the various physiological stages. Generally the left
breast is bigger than the right one.
 In the central zone there is the areola, a hyperpigmented
skin area, whose size also varies from person to person.
 Under the areola’s skin there are many nervous fibers
and smooth muscles arranged in circular and
longitudinal layers, which by contraction decrease and
wrinkle the surface causing elongation and turgor of the
nipples.
 The areola has small prominences: the Montgomery
tubercles, which are large sebaceous glands which
increase in volume during pregnancy and lactation.
 Breast structure
The nipple, is a
cylindrical-conical
prominence, of 10-12
mm length and 8-10
mm in diameter. There
are 15-20
galactophorous pores
of the lactiferous ducts.

Montomery

areola nipple
 For better guidance in locating various pathological
processes, the breast was arbitrary divided into four
quadrants by two lines, one vertical and the other
perpendicular through the centre of the nipple.
1. supero-external (SE) - over 50% of breast cancers are located in
this quadrant.
2. infero- external (IE)
3. supero-internal (SI)
4. infero-internal (II)
PA
SI SE
C
 Two more quadrants are added: II IE
one central (C) corresponding to
retroareolar area and the
another which is the axillary Breast quadrants
extension quadrant (AE) of the
gland.
The structure of the breast
 There are four types of tissues :
1. Milk-producing mammary gland,
2. Milk ducts,
3. Fatty tissue, and
4. Connective and fibrous tissue, and also blood vessels, lymphatics and
nerves.
 The gland is composed of 15-20 lobes. It is entirely
enveloped by fatty tissue with the exception of the
retroareolar region.
 The adipose layer under the skin is organized in lodges
separated by fibrous bands (Cooper’s ligaments), which on
palpation give the feeling of a granular surface. Do not
confuse these fatty lodges with tumors.
 The gland itself is fixed to the internal surface of the derm
by the Duret crests which are of special importance
because via these structures the malignant process can
spread to the skin. When these crests are invaded by the
tumoral process the skin becomes fixed to the gland and it
can be retracted which is a clinical sign for cancer.
Breast structure
 The retromammary layer is a space by which the
mammary gland can slide on the surface of the large
pectoral muscle fascia. Invasion of this layer and
penetration into the pectoral muscle, leads to fixation of
the gland to the underlying muscle highlighted by the
Tillaux maneuver.
 In very rare cases, the glandular tissue may cross the
retrommary fatty layer penetrating into the pectoral
muscle. This was the justification for Halsted radical
mastectomy where pectoral muscles were removed
together with the breast.
Microscopic anatomy
 The glandular parenchyma is divided into lobes (15-20),
lobules and acini. In their delimitation contributes the
stroma represented by interlobular dense connective
tissue and intralobular loose tissue, forming septs along
which blood vessels and lymphatics are passing.
 The functional units of mammary gland are the acini.
 Each lob has a milk duct which opens separatelly at the
surface of the nipple. The lobes are orientated radially
around the areola.
 Radial incisions in case of a mammary gland abscess

That’s why

The lobes are orientated radially around the areola.

 Each lactiferous (milk) ducts has a lactiferous sinus
located at the base of the nipple. The diameter of these
ducts is 2 to 4 mm. Inside there is a double layer
epithelium: cuboid cells at the level of lobules and
cylindrical shape cells in extra-lobular space. The
external layer has myoepithelial cells.
 These ducts are responsible for the majority of breast
pathology. It is considered that neoplastic lesions have
the starting point is these ducts and less in the acini.
 Also the breast fibrocystic disease has the starting point
in these ducts.
Vascularization and innervation
Arteries
 Internal mammary artery (from subclavian artery),
 Lateral thoracic artery ( from axillary artery)
 Intercostal artery branches (from thoracic aorta).
 Other sources: thoracic suprema artery, arteries of
pectoral muscles, thoracoacromial artery, subscapular
artery, thoraco-dorsal artery and superficial thoracic
artery.
Arterial sources of the breast
Veins
 The venous drainage of the breast is organized in two
networks: one superficial and another one deep.
 The superficial network forms around the areola a
venous plexus so called the Haller’s circle.
 Through the venous system cancerous cells are carried
to the first filtrating station: the lungs, and then towards
other organs where metastases are relatively frequent:
liver, bones, brain.
Innervation
 Breast skin innervation is provided by brachial cutaneous
nerve and branches from the intercostal nerves 4, 5, 6.
 Breast parenchyma receives sympathetic branches that
reach the secretory units along the intercostal nerves 2,
3, 4, 5 and 6.
 The lymphatic system is of particular interest in breast
surgery due to tumor extension mainly on this route with
particularly prognostic effect.

 There is a superficial network which collects lymph from

skin and a deep parenchyma network.

 Between those two lymphatic network there are two

areas of connection, one at the areola where there is a
superficial lymphatic plexus and one subaureolar
(Sappey) and the other at the breast periphery.

 Along these lymphatic routes, propagation of the cancer

is possible from depth to surface, which is the base for
indication to remove the areola in mastectomies for
breast cancer.
There are two main lymphatic drainage routes:
 External mammary route (axillary route) - it drains the
lymph to the ipsilateral axillary lymph nodes. 75%-97% of
cancer cells are carried through this route. On the trajectory
of this route there is a lymph node (Sorgius) located at the
edge of the great pectoralis muscle.
 Internal mammary route, which travels along the internal
mammary arteries towards the internal thoracic lymph nodes
(internal mammary lymph nodes), located retrosternal in the
intercostal spaces 1 to 5.
 From here the lymph goes to:
– Supraclavicular lymph nodes
– Cervical lymph nodes
– On the left side to the thoracic duct and left lymphatic duct
– On the right side to the right lymphatic duct
– To the Pirogoff jugulo-subclavian confluence
– To the mediastinal lymph nodes and broncho-aortic nodes
Lymphatic routes
Besides these primary routes, there are other secondary
routes such as:
1. Transpectoral route – starts from the inner surface of
the breast, passes through the pectoralis major to the
Rotter’s interpectoral lymph nodes and then to the
axillary apical lymph nodes.
2. Retropectoral route – starts from the inner part of the
SE quadrant, passes behind the pactoralis major towards
the apical lymph nodes.
3. Intercostal route - along the intercostal vessels direct
to the intercostal lymph nodes and from there to the
internal mammary lymph nodes.
4. Contralateral axillary route - Although rare, it is still
possible that tumoral cells from breast to reach the lymph
nodes from contralateral axila.
5. Inferior route - described by Gerota (Romanian
physician and anatomist) which drains the lymph to the
epigastric region and diaphragmatic nodules.
Lymphatic drainage of the breast
Anatomy of the axilla
 Axilla is a pyramidal shape structure with the tip facing the cervical
region which is the junction between the arm and the chest.
 It has a tip, a base and 4 walls
 The content of the axila is represented by:
– Arteries:
 Axillary artery, Veins:
The veins are omonim
 Lateral thoracic artery,
to the arteries
 Subscapular artery,
 Thoracodorsal artery
– Nerves:
 Brachial plexus,
 Intercostobrachial nerve,
 Thoracicus longus (Charles Bell – respiratory) nerve,
 Subscapular nerve,
 Thoracodorsal nerve,
 Intercostal nerves
– Fatty tissue
– Lymph nodes
Walls of the axilla Berg’s axillary lymph nodes classification
 Anglo-American surgeons use Berg’s axillary lymph
nodes classification that divides in three main categories
based on prognostic and their relationship with pectoralis
minor muscle:
 Level 1 - are lymph nodes located under the lateral edge of the
pectoralis minor (lateral posterior and anterior)
 Level 2 - are lymph nodes lying underneath the muscle between
the medial and lateral edge
 Level 3 - lymph nodes located medial or above the medial edge
of the muscle (apical, subclavian)
 In fact this classification is used in the TNM system for
malignant breast tumors. To this group, called regional lymph
nodes (N), in the TNM classification is added also the
ipsilateral internal mammary lymph group. Intramammary
lymph nodes are encoded as axillary lymph nodes in the
TNM classification.
 Any other metastatic lymph nodes are coded as distant
metastases (M1) including subclavian, or contralateral
cervical lymph nodes.
CLINICAL EXAMINATION
OF THE BREAST
 The diagnosis is based on 3 elements:
1. History
2. Clinical examination
3. Paraclinic investigations
 Clinical examination is the most important phase of the
diagnosis because:
1. In most cases it is the first method of diagnosis,
2. In advanced cases the method is sufficient, the
physical signs of neoplasia being obvious,
3. Local examination performed by woman itself (self
examination) is the most effective method of
screening for early detection of breast cancer if other
better methods are not available through a national
screening program.
 40% of tumors detected at mammography can not be
detected by palpation !
 Clinical examination just of the breast is not enough!
General clinical examination of the patient should be also
performed!
Local examination of the breast
 Not only the breast considered ill will be examined, but
also:
- The contralateral breast,
- The both axillae,
- The supraclavicular and cervical lymph nodes
 The examination can be performed both in orthostatic and
supine position. The standing position is preferred.
1. Inspection
2. Palpation
 A. Inspection.
The patient in front of doctor with arms hanging
The following aspects will be noted:
 The position of the line between the two nipples. This
is supposed to be horizontal in normal cases. If there
are changes in shape and volume of the breast the
line becomes oblique.
 The breast volume. Any expansive process in the
breast will lead to more or less increase of the breast
volume. This aspect is often observed in phyllodes
tumors.
 The shape of the breast. As long as the tumor is small
there won’t be any changes in breast shape. As it
grows, alteration of breast shape will appear as
irregular elevations (bulges) or as depressions (skin
retraction).
 Tu Phyllodes

Tu Phyllodes
 The aspect of the skin.
– The colour can be normal. In some advanced cases
and in acute inflammatory breast cancer, the colour
turns to reddish as in an inflammatory process making
possible confusion with acute mastitis.
– Skin surface may look as an orange peel (peau
d’orange) very suggestive for breast cancer. It is caused
by lymphatic stasis in the derm as the lymph ducts are
blocked by the tumoral process.
– Exulceration of the skin appears in advanced cases.
– Venous network become visible being augmented in
advanced cases, and also in phyllodes tumors.
– Nodules of permeation appear also in advanced
neglected cases.
Venous network more visible
Tumoral nodules of permeation Tumoral nodules of permeation
Ulceration with necrosis
Nipple retraction

Skin of orange peel

 The aspect of areola. The areola may be affected by
tumoral processes like Paget’s disease. The aspect is
similar to an exema.

 The aspect of the nipple. Very suggestive for cancer is

the unilateral retraction of the nipple recently installed.

 Pathological discharge from the nipple. It could be:

serous, brownish, lactescent, purulent, haemorrhagic.
The most suggestive for cancer is the unilateral
spontaneous haemorrhagic discharge which appears
especially in case of intraductal papilloma.
 Breast lump with nipple retraction
Paget’s disease of the breast
The patient raises her upper limbs
above the head.
 By this maneuver, other aspects can
stand out that do not occur in initial
position. This can produce changes in
the shape of the breast, nipple
retraction or modifications become
more visible.
The patient bent forward with hands on
hips.
 In this position breasts are hanging,
pathological changes can be
obeserved in the breast bearing a
malignant process. The breast hangs
less if the tumor is fixed to the pectoral
muscles or chest wall.
 B. Breast palpation
Rules:
1. The optimal period for breast palpation is between the
5th and the 7th day after the onset of menstruation.
2. Always start with the breast considered normal.
3. Palpation is done with
fingertips 2-4 for breast palpation
palmar face of outstretched
fingers 2-5.
4. Palpation must be gentle.
5. Palpation must explore the
entire breast area.
6. Both axillae and cervical
lymph nodes should be
palpated.
There are four stages of palpation
1. Gross palpation described by Velpeau, trying to
capture any tumor formation. It is only an
orientative palpation.
2. Palpation of finesse that must follow a certain
scheme not to omit any breast areas.
3. Tumor palpation.
4. Palpation of the areola and the nipple.

Palpation of finesse
 Circular - concentric
 Spiral
 Radial
 No matter which method is chosen. The breast tissue
should be compressed against the chest wall and all
quadrants should be cheeked.
Palpation will notice the following features of the
tumor:
1. Number - How many tumors are found.
2. Location - Most tumors are located in the SE
quadrant.
3. Dimensions - Generally, breast tumors found
incidentally on palpation are of 2-3 cm in diameter. If
the breast is not too voluminous, tumors can be
detected at a diameter of 1 cm.
4. Form - The form can be spherical or irregular.
5. Consistency - Generally they are of hard consistency.
6. Sensitivity - Malignant tumor is not painful on
palpation (at least in the early stages and if there is no
inflammatory process associated).
7. Tumor surface - The surface is irregular in cancer but
smooth in fribroadenoma.
8. Tumor delimitation - Cancer is poorly demarcated
from the surrounding tissues.
9. Tumor mobility – Breast cancer in first stages is
mobile, without having the mobility of a breast
fibroadenoma. As it developes, it becomes more and
more fixed because of tissue invasion.
10. Adhesion - Adherence to the skin can be appreciated
through two maneuvers:
– Ianisevsky sign. Wrinkling of the skin above the tumor is
impossible because of tumor infiltration and edema.
– Dupuytrain sign. To lateral displacement maneuver of the
tumor, behind it, the skin develops a depression.
– Adherence to the pectoral muscles can be demonstrated with
the Tillaux maneuver.
Dupuytrain sign
Tillaux maneuver – the doctor opposes to the adduction
movement of the patient’s arm (the pactorals muscles will
contract) and with the other hand palpating the breast he
will notice that the tumor becomes fixed as the pectorals
muscles contract.
Palpation of the areola and the nipple.
 The nipple is gently grasped between the index finger
and thumb and compressed.
 In case of a breast cancer or an intracanalicular
papilloma, blood may leak through the nipple.
 In case of an intracanalicular papilloma, beneath the
nipple a tumor of about 1 to 1.5 cm can be felt
 Nipple retraction is caused by neoplastic infiltration
and can not be reduced manually.
 Palpation of lymph nodes

A
B

A: Cervical nodes on the neck

B: Supraclavicular nodes just above the collarbone
C: Infraclavicular nodes just behind the collarbone
D: Axillary nodes in the armpit
BREAST MALFORMATIONS
Classification
Malformations
–Of number
–Of volume
–Of shape
Malformations
–congenital
–acquired
Abnormalities of number
1. Amastia
 Represents the congenital absence of one or
both breasts.
 It is sometimes associated with the absence of
sternal portion of the large pectoralis major
(Poland Syndrome).
 It may be associated with other malformations
such as the absence of internal genital organs,
ribs 3-4 or the upper limb.
 It is more frequent in men.
 Amastia is complete if the areola and the nipple
are absent.
2. Athelia
 Is represented by the absence of the nipple
associated or not with the absence of the
areola.
 It may occur at a normal located breast but are
more frequent at supernumerary breast.
 3. Amazia
 refers to a condition where mammary gland is absent, either congenital
or iatrogenic acquired. The nipple and areola are present.
4. Polymastia
 It is a frequent (1-5%) congenital malformation where more than two
breast are present.
 It can be complete when all the anatomical structures of the breast are
present or incomplete when just the mammary gland is present.
 The favorite locations are along the milk crests of Schultze. The most
frequent location is the axillary region. There can be present up to 8
supernumerary breasts.
 It may have a familial character, being transmitted autosomal dominant
from man to man in the same family, but can be sporadic also.
 Supernumerary breasts may be affected by the same pathologies as
the normal breasts.
 5. Polithelia
 Is the condition represented by multiple nipples associated or not
with areola.
 Frequency: 2%
 Usually they appear symmetrically along the milk crests, but can
occur anywhere. They can be rudimentary or functional.
 Sometimes are associated with congenital urinary malformations.
May serve as cutaneous paraneoplastic markers for urogenital
malignancies.
 Not of particular clinical importance unless they are affected by
morbid processes.
Polithelia
Abnormalities of volume
1.Anisomastia
 Is due to uneven development of breasts and their asymmetrical
location. If the aesthetic defect is important it can be corrected by
various operations of mammoplasty.

2. Atrophy of the breast (micromastia)

 Is characterized by an insufficient development of the breast uni- or
bilaterally.
 Is due to hormonal insufficiency or to general illnesses such as:
tuberculosis, cirrhosis, syphilis, or other factors.
 Treatment consists of treating the endocrine deficiency and also
silicone implant may solve de defect.
 3. Breast hypertrophy (macromastia)

 It is the consequence of hypertrophy based on proliferation of breast

parenchyma (acini, ducts) and the stroma is oedematous infiltrated.
 An obvious cause is unknown, hormonal factors being incriminated
and race (more common in black women). Another cause is the
development of the mammary gland during pregnancy returning to
the normal breast volume being incomplete.
 Breasts gradually increase reaching impressive dimensions and
weight (7-8 kg), most often in addition to a normal silhouette.
Increased breast weight will lead to deformation by stretching and
ptosis. They become painful and exerted traction on the chest. Skin
redness is often with visible superficial venous network and
frequently intertrigo appears in the submammary groove.
 Treatment in less severe forms is represented only by support with
suitable bras and anti-estrogen therapy. In advanced forms the
surgical treatment is recommended represented by mammoplasty
reduction.
 4. Gynecomastia

 It is the development in excess of the breasts in men. It appears

more frequently in teenagers.
 Physiological gynecomastia occurs in new born, prepubertal and in
senescence due to an excess of estrogen.
 The cause is the excess of estrogen or androgen hormone
deficiency.
 Increased estrogen levels may be due either to hyperproduction
(testicular or adrenal tumors) or iatrogenic (administration of
estrogens), or liver failure (cirrhosis) to metabolize the estrogens.
 Testicular endocrine insufficiency may have multiple causes: genetic
(Klinefelter syndrome), hereditary (disturbances in hormones
synthesis), congenital (anorhidia, cryptorchidism), acquired (trauma,
orchitis, hydrocele, varicocele, tumors)
 Initial treatment is conservative trying to resolve deficiencies or by
administration of testosterone hormone or tamoxifen to block the
estrogen receptors. The subcutaneous mastectomy is indicated in
rebel cases.
Gynecomastia
 Abnormalities of shape
1. Inverted nipple
 It is a relatively common abnormality and occurs mainly
during puberty. It has an incidence of 2% in women. It is
bilateral in 25% of cases.
 Nipple retraction may have different degrees of:
flattening, umbillication and invagination. Han and
Hong (Han 1999) classified nipple retraction into 3
grades as follows:
– Grade 1 - retracted nipple returns easily in the normal position
and this position is maintained without the need for traction.
Slight compression or soft pinching of the skin around areola
causes the nipple to return to normal position.
– Grade 2 - nipple can be brought to its normal position only by
traction and tends to retract after traction.
– Grade 3 – the nipple is strongly retracted, and it is difficult to
reverse back into normal position even by forced traction.
Inverted nipple
Inverted nipple
 Breastfeeding is not contraindicated in inverted nipple,
but it can raise problems that can be overcome by
educating mothers on special techniques or by using of
special suction devices.
 Inversion may promote nipple infection.
 Surgical correction is possible, but is not indicated at
young ages because it may harm galactophorous ducts.
 Appeared in mature woman, nipple retraction is an
alarming sign that could mean:
1. most often, a neoplastic process, especially if the
retraction is circumferential,
2. an inflammatory process underlying the nipple,
3. a ductal ectasia associated with periductal fibrosis
 2. Breast ptosis
 Breasts tend to descend over time due to their own weight.
 Breasts only support is the skin and the Cooper’s ligaments.

 Ptosis is mainly due to weakening of supportive fibrous breast

elements (Cooper’s ligament) as a result of deficiencies in the
structure of collagen and elastic tissue, or idiopathic (frequently is
associated with varicose veins, hemorrhoids, hernias, flat feet, stretch
marks, etc.) or due to ovarian hormones and thyroid disorders, either
due to aging processes. Another cause is breast hypertrophy.
 It occurs mainly in postmenopausal multiparous with repeated
lactations.
 It has 4 phases of evolution: mild, marked (the nipple in normal
position, breast lower pole down), complete (nipple is also lowered)
and bulky prolapse (ptosis is associated with marked hypertrophy).
 Treatment is surgical with aesthetic visa in most cases. The aim is to
restore the breast with the nipple in the normal position and to restore
its normal shape and volume. The operation can involve the skin only
in mild forms, but in forms with hypertrophy a glandular reduction is
also necessary.
 Breast ptosis

Level A = Normal breast

Level B = Mild breast ptosis
Level C = Moderate breast ptosis
Level D = Severe breast ptosis
Level E = Glandular or pseudo ptosis
INFLAMATORY AFECTIONS
OF THE BREAST
 Mastitis
 Mastites are inflammatory diseases of the breast due to
infection, usually having the entrance gate the milk
pores of the nipple or the skin pores.
 The infection can affect the mammary gland and other
anatomical structures (skin, subcutaneous tissue,
muscle fascia) – paramastitis.
 Paramastitis can affect the pre(supra)mammary tissues
(suprammamary mastitis) or the retrommamary
tissues (retromammary mastitis or inframastitis).
 When the infectious inflammatory process extends to
the whole breast we talk about panmastitis.
 Most commonly incriminated etiologic agent is
Staphylococcus aureus and Streptococcus. There may
be fungal infections also.
 It can be acute or chronic mastitis. / Specific or
nonspecific.
 Acute mastitis can occur at any age but usually during
lactation (puerperal mastitis).
 Mastitis may be secondary to an infected hematoma or
may be a metastatic abscess during a general infectious
disease.
 Puerperal mastitis: is a nonspecific acute inflammation of
the mammary gland that occurs in the period of pregnancy
and more frequently during lactation.
 The most often involved microorganism is S. Aureus.
through the nipple’s pores or through skin erosions, cracks
or sores on the nipples. The favoring factor is the stasis of
the milk in the breast. Infections play only a minor role in
the pathogenesis of both puerperal and nonpuerperal
mastitis in humans and many cases of mastitis are
completely aseptic under normal hygienic conditions.
 Prophylactic measure are very important: complete
emptying of the breast and rigorous local hygiene.
 There are two phases of evolution:
1. Congestive phase (Acute galactophoritis)
2. Phase of collection (Breast abscesses)
Clinical picture
 In the congestive phase, the patient experiences
intense pain in the breast, which becomes swollen.
Because of the pain the patient does not empty the
breast milk leading to stasis and favor the infection.
Celsian signs appear. The breast is increased in volume,
firm, very painful with local temperature increased and
diffuse skin redness. The nipple can be modified and with
purulent discharge. The patient is feverish and
inflammatory painful axillary adenopathy may be present.
 In the collection phase, the inflammatory processes
usually focus on a particular region, where the touch may
feel fluctuence. In untreated forms infection may extend
to the entire breast (panmastitis) and may spontaneously
fistulize to the skin.
 Acute mastitis

Celsian signs
 Breast abscesses: are localized breast suppurations
probably related to obstruction of lactiferous ducts.
 They can be located:
1. Subcutaneous
2. Sub areolar, - the most frequent
3. Interlobular (periductal inflammation),
4. Retromammary
5. Central (simple or multiple)
 Symptoms and signs: pain, redness, local swelling,
hyperthermia. Drained fluid from the nipple after
compression leaves a yellow stain (Budin sign). There
may be present axillary inflammatory adenopathy.
Different types of breast abscesses
 Acute mastitis should be differentiated from other
diseases with similar symptoms such as :
1. Paramastitis
2. Breast engorgement (due to expansion and
pressure exerted by the synthesis and storage of
breast milk.)
3. Breast sarcoma
4. Inflammatory breast cancer !

Treatment
 Prophilaxy
– Compliance with local hygiene measures
– Complete emptying of breast milk at each feeding
 Curative
– In congestive phase
 Broad-spectrum antibiotics - 96% of cases have favorable
evolution
 Evacuation of breast milk by milking or vacuum aspiration
 Interruption of breast feeding from that breast - even weaning
 Local cold compresses
 Immobilization and breast suspension plus compression
dressing.
– In collection phase (fluctuence)
 In general anestehesia
 Incision, evacuation, debridement, drainage, dressing. In
superficial abscess the skin incision may be arcuated parallel
with Langer lines, for a better aesthetic effect, but in profound
abscesses radial incisions are indicated to avoid sectioning the
milk ducts.
 Perform antibiogram !
 Radial incisions in case of a mammary gland abscess

That’s why

The lobes are orientated radially around the areola.

Debridement Drainage
 Chronic breast abscess
 It is the consequence of an unresolved acute mastitis.
 Signs: a hard lump in the breast, infiltrating the surrounding
tissues, dimpling and puckering of the skin. Painful to touch
and on compression sometimes purulent nipple discharge.
Peu d'orange and retraction of the nipple may be present.
 Axillary lymph nodes are enlarged.
 At incision: thick sterile pus surrounded by fibrous tissue.
 Because of local features it is difficult to make a differential
diagnosis with the breast cancer. A thorough history of the
patient could reveal an acute mastitis treated years ago.
Also the skin scar present on the breast may help to make
the difference.
 The treatment is incision or excision with histopathological
examination
BENIGN TUMORS OF THE
BREAST
Breast fibroadenoma
 Breasts fibroadenoma (or adenofibroma) are benign
fibroepithelial tumors of the mammary gland (contain
epithelial and stromal elements). The predominance of the
epithelial component determines the name of
adenofibroma while the predominance of stromal
component determines the name of fibroadenoma.
 The notion of complex fibroadenoma refers to the
fibroadenomas which have: cysts larger than 3 cm in
diameter, sclerosing lesions, epithelial calcifications and
apocrine papillary modifications.
 The pure adenoma is very rare being a proliferation of
only the epithelial elements. It has 2 forms:
– Acinar form : normal or cystic acinar proliferation
– Tubular form : may appear during lactation (lactation adenoma)
 There are two forms of fibroadenomas:
1. Juvenile fibroadenomas, which appear in young
women and teenagers, and
2. Myxoid fibroadenomas, in Carney’s Syndrome, which
is a dominant autosomal neoplastic syndrome which
includes myxomas of the skin and mucosa and
endocrine dysfunctions.
 Fibroadenoma is the most frequent benign tumor of the
breast. Young females under 40 years age are
predominantly affected. In 10-15% of cases they are
multiple.
 Even they are considered benign, yet they have a
potential of malignant transformation (mostly
sarcomatous) in percentage of 3-4%. Patients with
multiple fibroadenomas or complex types have a higher
risk (twice) of breast cancer.
 Fibroadenomas represent a hyperplasic or proliferative
process started from a terminal milk duct. The cause is
unknown.
 Aproximativelly 10% of them disappear in a year and the
grate majority stop their evolution after they reach 2-3 cm
in diameter. They can regress in postmenopausal period
or they calcify. On the other hand they can rapidly grow
during pregnancy, during treatment with substitutive
feminine hormones or during immunosuppressant
treatment, when they can simulate a breast cancer.
 There is no racial predilection
 Fibroadenomas may be located anywhere in the breast.
Clinical picture
 On inspection nothing can be noticed when they are
small. As they grow a bulge under the skin can be
observed. In giant forms (phyllodes tumors) the breast is
highly modified with distended skin, with marble like
appearance, with visible vascular network.
 On palpation, the fibroadenoma has some characteristic
features that makes it easy to diagnose and differentiate
from other tumors. There is a tumour of about 1-5 cm
diameter, of hard-elastic consistency, with smooth
surface, well delimited from surrounding tissues, painless,
and the most important feature: very mobile.
 In the axilla there are no pathological enlarged lymph
nodes.
 Paraclinical investigations for diagnosis are: ultrasound
examination, mammography, tru-cut biopsy and
excisional biopsy.
 When the diagnosis is very clear, based on clinical
features, a lumpectomy may be performed, followed by
histopahological examination.
 When the diagnosis is not very clear, a biopsy from the
tumor (tru-cut biopsy under ultrasound guidance) is
indicated.
 Clinical features of the fibroadenoma help to differentiate
it from breast cancer which has the following features: it
has a very weak delimitation from surrounding tissues, it
is not so mobile as fibroadenoma or is quite fixed in
advanced stages, its surface is irregular and frequently it
is associated with enlarged axillary lymph nodes.
Other affections for differential diagnosis are:
1. Breast cysts – elastic consistency, also mobile but on ultrasound
examination the content is fluid in contrast with fibroadenoma
which is solid. At fine needle aspiration fluid can be obtained.
2. Sclerocystic mastopathy – feeling like “lead shots" under the
skin on palpation, ultrasound shows multiple small cystic
formations of various sizes, usually symmetrical, often painful,
sometimes with greenish nipple discharge.
3. Breast lipogranulomas – poorly delimitated mass with reduced
mobility due to chronic inflammatory process, possibly
associated with axillary inflammatory adenopathy.
4. Lipomas – have softer consistency and are more superficial
5. Other tumors of the breast
Treatment
 Simple fibroadenomas are tumors well incapsulated which
can be easily enucleated. The operation of election is a
lumpectomy with a margin of security of 1 cm around the
tumor, and in cases of multiple or diffuse fibroadenomas a
quadrantectomy can be performed. In complex cases a
skin sparing mastectomy can be performed.
 The surface section of the fibroadenoma has a pearly
white color which is bulging under the effect of elastic
fibers while in malignant tumor the section area is flat
sometimes with yellow spots and hard calcified areas.
 Prognosis is favorable but keep in mind that the risk of
breast cancer is twice as higher in women with history of
operated fibroadenoma and the risk of sarcomatous
transformation is about 3%.

Cancer

Fibroadenoma
Fibrocystic mastopathy
mastoses
( Reclus disease)
 Proliferative lesion that occurs in women around age 30,
but can be seen at any age.
 Endocrine factors are involved: hyperfoliculinemia,
hyperthyroidism, genital or thyroid dysfunctions.
 Gross appearance: multiple cysts of various sizes, filled
with clear or cloudy yellow-brown liquid, surrounded by
sclerous tissue. Predominant one of the two components.
 Microscopic appearance: microcysts surrounded by fibrotic
walls, with cylindrical secretory epithelium with
mitochondria and multiple granules, hypo or atrophic
breast tissue; epithelial changes may transform into
malignancy.
 Clinical: embarrassment or local pain, spontaneous or
provoked, especially during menstruation. Palpation
reveals tumors (sizes from mm to 2-3 cm) disseminated or
grouped, uni or bilateral (usually), mobile, firm, slightly
painful, increase in menstrual period. Axillary adenopathy
usually is absent.
Fibrocystic mastopathy
Only in 5% of cases, changes can be considered at risk
of developing cancer.
Treatment
1. In early or localized forms in women under 35 years -
conservative treatment – hormones, local applications
(Mastoprofen) - after pregnancy and lactation the
disease may regress.
2. In rapidly growing forms or in case of ineffective
medication treatment - quadrantectomy.
3. For diffuse forms that include all the gland -
subcutaneous mastectomy
Breast cysts
 Cysts are the most common "tumors" of the breast.
 Cysts are rare in women over 50 years and generally do
not have any relationship with breast cancer.
 On palpation they are mobile with smooth surface and of
elastic consistency. Can be or not painful.
 They are related to papillomas tumor type. The histologic
features are of apocrine metaplasia (the inner lining layer
of large cysts is composed of apocrine cells).
 Intraoperative they look dark ("blue dome cysts")
 Can be treated by simple evacuation through fine needle
aspiration or excision. Needle aspiration in most cases is
guided by ultrasound. When extracted fluid does not
contain blood, cytotlogical examination is nod needed
because there is no suspicion of cancer but when blood is
present in fluid it must be examined cytologically.
 In most cases cyst evacuation by aspiration is the
definitive treatment method.
Breast cyst on ultrasound examination
FNA guided by ultrasound
Cyst excision
 Galactocele

 A cystic tumor that contains milky substance

which appears usually during breast feeding
period. Once lactation has ended, the cyst will
disappear on its own without intervention. It is
usually located beneath areola, and due to
abrupt suppression of lactation
Intracanalicular papilloma
 Intracanalicular papillomas are cell proliferation in the
mammary ducts.
 Gross appearance: Intraductal vegetations of a few
mm, red multi ramified, epithelium developed in the
ducts, located in the center of the gland and subareolar
region. The ducts are enlarged but with thin walls and
contain a brownish fluid.
 Microscopic appearance: vascular axis covered by
cylindrical epithelium (papilloma). At the periphery
hyperplastic alterations are present. Focal areas of
hemorrhage and necrosis are also present. Can
accommodate atypical hyperplasia and ductal
carcinoma in situ. If the epithelium is double layer
columnar cell, it becomes noninvasive papillary
carcinoma.
Clinical picture:
 Common in women aged between 30-50 years, with:
1. Serous or sero-sanguinous discharge for long periods of time,
2. Small, round tumor under the nipple, that does not adhere to the
skin,
3. Traction of the nipple mobilizes the tumor (related to milk duct),
4. Serous or sero-sanguinous discharge on nipple compression,
5. No axillary adenopathy.
 Multiple intraductal papillomas occur in approximately
10% of cases, tend to occur in the younger patients and
are less often associated with nipple discharge.
Paraclinical diagnosis:
– Ultrasound examination
– Mamography
– Galactography
– Mammary ductoscopy
– Cytological examination of nipple discharge
Tratament :
 Deciding on the appropriate surgery is problematic due to
the difficulty in discriminating between intraductal
papilloma and breast cancer.
 When the lesion is located to a single duct,
microdochectomy gives satisfactory results in younger
patients with a minimal interference with the breast. In
older patients where breast-feeding is not required, major
duct excision may be preferable.
 When a specific duct cannot be identified then blind
excision of the retro-areolar ductal system is usually
performed (central quadrantectomy) followed by
histological examination.
Prognosis: the incidence of malignancy (invasive or in situ)
associated to papilloma varies between 1 and 23% A
solitary papilloma is not thought to be a pre-malignant
lesion and is considered by some to be an aberration
rather than a true disease process.
 Multiple intraductal papillomas are more susceptible to
develop carcinoma.
 Intracanalicular papilloma - dilated
duct (3 mm ) at a distance of 1.5 cm
intracanalicular papilloma
from the nipple

Ultrasound examination Galactography

Ductoscopy
 NIPPLE DISCHARGE
Nipple discharge is an event that causes discomfort and
anxiety to women.
In this area significant progress have been made in
recent years through the development of diagnostic
procedures.
Physiopathology:
 The causes that lead to discharge from the nipple are not yet
fully elucidated. In most cases it is associated with endocrine
disorders and/or certain drug treatments. They are often
associated to ductal ectasy and/or fibrocystic changes in the
mammary gland. Changes are often bilateral.
 A less common noncancerous etiology is the ductal ectasy
associated with periductal inflammatory process
(galactophoritis)
 The most common cause is the intraductal proliferation of
ductal epithelium as a result of a hyperplastic process,
micropapillar proliferation, papillomas and/or ductal
carcinomas.
 The vast majority of intraductal changes that produce nipple
discharge are located in the first 1-4 cm of the lactiferous
duct from the nipple.
Nipple discharge- causes
 Frequency: - 3-8%.
 Mortality and morbidity: the vast majority of patients heal
after surgery. If the etiology is the cancer, mortality rate is
the same as in case of other breast cancers. Of course, in
case of early diagnosis (occult) the prognosis is even
better.
 Race: there are no differences between races.
 Sex: Nipple discharge can occur in both sexes but is more
common in women. When it occurs in young men is due to
a ductal ectasy similar to that of gynecomastia without
hormone-related disorders. But, breast cancer is more
common in men with nipple discharge.
 Age: disease can occur at any age.
 Subclinical nipple discharge occurs more frequently in
women who use birth control pills and substitutive hormone
therapy.
Clinical picture
 In most cases, nipple discharge are bilateral
 The aspect of the discharge may be:
– Clear (aqueous)
– Serous (yellowish)
– Lactescente (white)
– Sero-sanguinolent
– Sanguinolent
 To be considered nipple discharge, discharges must take
place outside the period of lactation, to be spontaneous and
persistent.
 Suspicion of cancer increases if the discharge is located
only at one breast, from a single pore and is sanguinolent.
Also if a tumor can be felt on palpation and if the patient is
over 50 years old.
 After investigations, when suspected lesions are not
malignant, in 73% of cases, nipple discharge regress
spontaneously within 5 years.
Investigations
1. Mammography – not always relevant
2. Galactography (ductography) is performed by injecting
a contrast iodine solution through a pore and making
mammograms. After nipple disinfection a ductogram
cannula is gently insert in the incriminated pore and
slowly injected approximately 0.2 to 0.8 ml of iodine
solution. Then cranio-caudal and latero-lateral
mammograms are performed.
Galactography is not indicated when:
– Nipple discharge is bilateral
– Secretion is not spontaneous or it cannot be obtained by
compression of the nipple and so neither the pore can be
observed
– Secretion occurs from many pores
3. Other tests:
 Breast ultrasonography

 Cytological examination of nipple discharge -

may reveal neoplastic cells but the rate of false
negative results (17.8%) and false positive (2.6%) is
quite high.
 Hemocult test can be performed to detect minimal
bleeding from the nipple.
 Ductoscopy
Galactorrhea is usually not associated with breast cancer
and the more, when it is bilateral.
 Galactorrhea may occur due to:
1. local stimulation of the nipple
2. chest wall trauma
3. consumption of various drugs (contraceptives
fenotiazide, antihypertensive, etc)
4. hypoparathyroidism
5. pituitary adenomas
6. amenorrhea
Treatment
Surgery is indicated in the following cases:
1. Discharge from a single pore, unilateral. Additional
argument for surgery is palpable tumors, lesions found
after paraclinical investigations, and age over 40
years.
2. Indication of surgical treatment is supported by the
suspicion of an existing cancer.
3. Recommended operation is the quadrantectomy. The
breast sector (quadrant) corresponding to the
incriminated duct and pore is excised followed by
frozen section histopathology examination and
eventually conversion to mastectomy.
 BREAST CANCER
Unfortunately, we not know yet the cause of breast
cancer and yet we can not prevent it, but history
does not stop there.
Features of breast cancer
1. It affects a woman's organ that besides the biological
role of breastfeeding has a very important aesthetic and
erotic role with deep implications on women’s psyche
and personality.
2. It is easy to detect by palpation or minimally invasive
examination at low-costs.
3. Particularly it affects older women (over 50 years). It is
very rare in young.
4. It is one of the forms of cancer, which if early diagnosed
has one of the highest rates of post-therapy survival.
5. Breast cancer is one of the slowest developing tumor.
Since the beginning of the process until a tumor of 1 cm
in diameter could pass even 10 years.
Epidemiology
 Breast cancer is the most common cancer in women
worldwide, comprising 16% of all female cancers. It is
thought to be a disease of the developed world because a
majority (69%) of all breast cancer deaths occurs in
developing countries (WHO Global Burden of Disease,
2004).
 Incidence rates vary greatly worldwide, with age
standardized rates as high as 99.4 per 100 000 in North
America. Eastern Europe, South America, Southern Africa,
and western Asia have moderate incidence rates, but
these are increasing. The lowest incidence rates are found
in most African countries but here breast cancer incidence
rates are also increasing.
Morbidity
• Breast cancer ranks among the most common 3
diseases in the world
• A new case at every 30 seconds
Mortality
• One death every in 1.5 minutes.
• It is the second cause of mortality after lung cancer

Five Year Survival Rate By Age

Younger than 45 81%
Ages 45-64 85%
Ages 65 and older 86%

Source: American Cancer Society

In Romania
 Breast cancer mortality has increased from 15.60/000 as
it was in 1978 to 23.27/ 000 in 1996. WHO estimated for
Romania, after 2000, that breast cancer mortality
increased by 7%. Annual mortality is around 2,500
cases.
 1% of women get breast cancer each year, which is
about 4200 new cases per year.
 Two thirds of patients are first diagnosed in advanced
stages of disease (stages III and IV), in most cases a
total mastectomy being the only surgical alternative.
Etiopathogeny
Risk factors
A. Factors that can not be modified
B. Factors that can be modified (depend on our willing)
 Gender. The most important factor. It is known that in
male breast cancer appears in a very small percentage:
1-5%.
 Race. White women have a slightly increased tendency
to develop breast cancer compared to black women. But
the latter are usually diagnosed in more advanced stages
with lower survival rate. Also Hispanic women and Asian
have a lower risk.
 Age. The breast cancer incidence increases with age
being the highest in the sixth decade.
 Genetic factors. About 5% -10% of cases can be
considered hereditary due to genetic mutations.
 Incidence Rates by Race

Race/Ethnicity Female Source: National Cancer

Institute, SEER Cancer
All Races 127.8 per 100,000 women
Statistics Review, 2007.
White 132.5 per 100,000 women Statistics
Black 118.3 per 100,000 women

Asian/Pacific Islander 89.0 per 100,000 women

American Indian/Alaska Native 69.8 per 100,000 women

Hispanic 89.3 per 100,000 women

Probability of Developing Breast Cancer Within the Source: Among those

Next 10 years
cancer free at age
By age 20 1 out of 1,760 interval. Based on cases
By age 30 1 out of 229 diagnosed 2000-2002. "1
By age 40 1 out of 69 in" are approximates.
By age 50 1 out of 42 Source: American Cancer
By age 60 1 out of 29 Society Breast Cancer
By age 70 1 out of 27 Facts & Figures, 2008-
Lifetime 1 out of 8
2009.
 BRCA1 (breast cancer 1), BRCA2 (breast cancer 2)
 BRCA1 is located on the long arm of chromosome 17
(17q), BRCA2 on chromosome 13q and BRCA3 gene
on chromosome 13q21
 Women who have inherited mutations by deletion in
BRCA1 and BRCA2 have an increased risk of
developing breast cancer by 56-85% rate and also
ovarian.
 BRCA1 is found in 3% of of breast cancer in general
and 70% in women with hereditary of breast cancer.
 BRCA2 mutation is identified in 10-20% of families with
breast and ovarian cancer risk and only in 2.7% of
women with early breast cancer. The risk of breast
cancer for women carrying BRCA2 is 25-30%.
 HER2 (sau HER2/neu) (human epidermal growth factor
receptor 2) is a surface gene that plays a key role in
regulating cell growth. When HER2 is altered more
HER2 receptors will be produced which leads to
increased cell multiplication. HER2 is found in 25-30% of
women with breast cancer. They can be detected in
tissues sample collected by biopsy or surgery.
 Personal history of breast cancer. A woman who was
treated for breast cancer has a 3-4 times higher risk of
developing contralateral breast cancer and on a remnant
mammary gland after surgery, which is different from
tumor recurrence.
 Radiotherapy in breast area in history. If women,
especially in childhood, have received chest radiation
therapy in other diseases such as Hogkin, or other types
of cancers, have an increased risk (after some 12 times
greater) of developing breast cancer
 Personal history of epithelial hyperplasia. In these
cases the risk increase depending on the type of
hyperplasia as follows:
– Typical epithelial hyperplasia - the risk is 1.5-2 times higher
– Atypical epithelial hyperplasia - the risk is 4-5 times higher
– Atypical ductal hyperplasia - risk increases 10 times over the
next 10 years from diagnosis
– Nonproliferative disease of the breast (adenosis, cysts, ductal
ectasy, fibroadenoma, fibrosis, mastitis, apocrine metaplasia
and moderate squamous hyperplasia) are not associated with
risk of breast cancer.
 Early menarche (under 12) and late menopause (over
55 years) are considered factors that may increase
cancer risk.
 Anthropometric factors. Anthropometric studies on
patients with breast cancer revealed an interesting
fact, namely that the rapid growth in childhood and the
adult height higher are associated with an increased
risk of breast cancer.
B. Factors that can be modified and are related to
way of life. It was found that the habits practiced in
adolescence may influence the risk of breast cancer
later in life.
 Substitutive hormonal therapy. It's a proven fact that
using substitutive hormones (estrogen, progesterone)
after menopause increases the risk of breast cancer.
These hormones are usually prescribed by doctors to
prevent undesirable effects of postmenopausal
hormone decline. Estrogens are indicated for
prevention of osteoporosis, but they can cause uterine
cancer also.
 Oral contraceptives. Use of oral contraceptives has a
low risk in determining breast cancer, and this usually
occurs after a usage of over 10 years. But the risk
disappears after discontinuation.
 Pregnancy. Women who gave birth the first time after the
age of 30, just as those who have never given birth,
have a higher risk of developing breast cancer.
 Breastfeeding. Some studies have suggested that
breastfeeding, especially continued for 1.5-2 years would
had a protective role against breast cancer but there is
no unanimity of opinion in this regard.
 Obesity. Is associated with an increased risk of breast
cancer in postmenopausal women. Fat tissue has the
ability to turn other hormones into estrogen. The risk of
breast cancer is higher due to higher amount of
estrogens.
 All these factors listed above, although not have the
same risk weight, have in common an element, namely:
the endogenous or exogenous hormones.
 Diet and vitamins.
– Fats - high-fat diet, unlike in other types of cancer, in
case of breast cancer is not associated with a higher
risk of carcinogenesis.
– Vegetables and fruits also do not seem to influence
the risk of breast cancer.
– Microlelements (trace elements) and vitamins may
have a role but there is no clear data in this regard.
– Alcohol. Women who consume alcohol have a higher
risk of breast cancer but this risk is relatively small for
small amounts of alcohol. This relative risk increased
with 7% for every 10 grams of alcohol consumed.
 Smoking - while smoking does not appear to induce
breast cancer, women who smoke have a mortality rate
higher by 25%.
 Ionizing radiation increases the risk of breast cancer
especially if used at a young age. Radiological chest
exploration should be avoided wherever possible at a
young age.
 Chemicals. Although numerous experimental studies in
animals have found mammary carcinogenic substances,
none with this effect was found in humans.
 Environmental and occupational factors. It seems that the
polluted environment of large urban agglomerations and
the stress are negative risk factors.
 There is an increased incidence of breast cancer among
airplane stewardess, incriminated factor being the more
intense cosmic radiation at higher altitudes.
 Other factors
 Breast implants. - there is no clear evidence that implants
would lead to increased incidence of breast cancer, but
implants make mammography difficult.
Classification of risk factors according to their
importance

 High risk:
1. The existence of genetic markers of susceptibility
(BRCA 1, BRCA 2)
2. Family history of breast cancer unilateral or
bilateral, especially in first degree relatives
3. Personal history of breast cancer
4. History of hyperplastic mastopathies
5. Hormone replacement therapy (to treat
postmenopausal symptoms),
6. History of ovarian or endometrial cancer
 Moderate risk:
1. Age
2. Family history of breast cancer occurred before menopause
3. Radiation of the chest
4. Small and repeated breast trauma

 Low risk:
1. History of breast cancer occurred after menopause
2. Nuliparity
3. First birth at an older age than 30
4. Early menarche before age 12
5. Late menopause, occurring over the age of 55
6. Obesity occurred after menopause (increases risk by 80%)
7. Daily consumption of alcohol
8. Diet rich in fat and carbohydrates
9. Oral contraceptive used more than 10 years
Primary prevention of breast cancer
1. Avoiding exposure to radiation (avoiding unnecessary
radiological examinations, avoid prolonged exposure
to ultraviolet radiation)
2. Physical activity has beneficial effects through several
mechanisms.
3. Limitation or exclusion of alcohol consumption.
4. Maintaining an ideal weight through diet and exercise
especially after menopause.
5. Hypocaloric diet with a low-fat but high in vegetables,
fruits, trace elements and vitamins, especially in
adolescence.
6. Avoid as much as possible hormone replacement
therapy and birth control pills.
7. Giving birth and breastfeeding at a young age would
be beneficial.
American Cancer Society recommends the following
steps to detect early breast tumors:
1. Women aged over 20 years - breasts self-examination
should be performed every month.
2. Women between 20 and 39 years - should be clinically
examined at least once every three years.
3. Women aged over 40 years - should be clinically
examined at least once a year, in addition self-
examination monthly and annual one mammography
exam.
Evolution and symptoms

 An adult body normally produces as many new cells as

are needed to replace those lost, maintaining constant the
cell mass. Tumor cells multiplication instead does not
keep this balance. They are growing at a rate faster than
normal cells causing tumor masses.
 Tumor cells, unlike normal ones, are no longer so strictly
linked together to form tissues. Tumor cells have the
ability to spread in various ways in any region of the body.
The immune system can not cope with this invasion and
tumor cell metastases appear.
 The underground breast cancer life is very long. Tumor
growth is measured in doubling time. A doubling time is
the length of time required for tumor cell mass to double
in volume.
 It takes about 23 doubling times starting from a tumor cell
to reach a tumor mass large enough to be seen at
mammography and approximately 30 times (1 billion
cells) to be palpable.
 Doubling period can be short, sometimes for only 10
days, or longer, for years. An average period is of 4
months.
 For example, if a first tumor cell occurred in the age of 40
and if we believe it is a fast growing tumor with a
doubling period of two months, four years must pass until
the tumor can be detected on mammography, so at the
age of 44 years. As the tumor can be detected by
palpation have to pass about 5 years, so when the
patient will have 49 years, that is after 9 years from first
appearance of tumor cells.
Clinical picture
 There is no unique clinical picture of breast cancer since
there are many clinical forms. Symptoms are closely
related to stage of the tumor.
 Initially, breast cancer does not have any symptoms.
0.5% of breast cancer are asymptomatic. Pain occurs
rarely, in 10% of patients (continuous or intermittent,
localized or irradiated pain).
 The tumor is usually detected by the patient itself during
toilet.
 Local evolution of breast cancer is by direct extension to
the surrounding tissues along the connective tracts, along
ducts and invasion of lymphatic and blood vessels.
Local extension
 Extension in skin surface by invasion of Duret crests
and Cooper ligaments.
 In this stage the skin becomes fixed, infiltrated and can
not be folded (Ianisevski’s sign) and to side
displacement maneuver of the tumor a depression
appears behind it (Dupuytrain’s sign).
In a later stage the tumor infiltrates the deep skin, blocking
the local lymphatic circulation. Skin pores expands and
appears the aspect of orange peel (peau d’orange)
peau d’orange
Then, invading the skin, tumor leads to ulceration which
has irregular borders, purple color, endured margins and
necrotic tissue in the bottom.
Bleeding and infectious complications are common in this
stage.

Ulcerated breast cancer

 Dermal tumor nodules may appear at some distance
from the tumor due to local lymphatic spread.
 If the tumor is located in the central quadrant it may
produce nipple retraction through invasion of milk
ducts and connective tracts ( important diagnostic sign).
 Retraction is fixed, irreducible, unilateral and acquired.
 Ducts invasion also causes nipple discharge (serous,
sanguinolent or lactescent either spontaneously or on
compression)
 Extension in depth to the pectoral muscles. Tillaux
maneuver (during pectoral muscle contraction in forced
adduction the tumor becomes fixed to the chest wall)
 Invasion may progress to the chest wall structures
(muscles, ribs) and then to pleura and lungs.

Tillaux maneuver
 The section surface of tumor has a characteristic
aspect: flat, stellate, with irregular edges, of hard
consistency with yellow spots or areas of calcification or
areas of necrosis.

Skin retraction
Regional extension
 It takes place along the main and secondary lymphatic
routes.
 Along the lymphatic route there is a lymph node which
is most likely to retain first the cancer cells: the
sentinel lymph node.
 This node can be find and removed for examination by
methods using radiotracers and dyes tracers. Biopsy of
this lymph node can be performed to find if it is invaded
or not by the cancerous cells. Histopathological
findings are very important in choosing the type of
surgery which will be applied (with or without axillary
lymphadenectomy).
Lymphatic spread of tumor
Noduli Noduli
Noduli supraclaviculari axilari
axilari
contralaterali

mamari interni
Noduli

Noduli
epigastrici,
diafragmatici
 Axillary lymph nodes affected by metastases gradually
increase in volume so they begin to compress and invade
the axillary vessels and nerves causing pain in upper
limb.
 Lymphatic invasion extends to the subclavian and
supraclavicular lymph nodes group with the consequence
of lymphedema of the upper limb but also open
secondary lymphatic channels to contralateral armpit.
 Lymph node invasion is the most important prognostic
factor, efforts in this area currently being targeted to
detect breast cancer before this stage.
 Tumors located in the internal quadrants spread most
commonly to internal mammary lymph nodes which can
not be detected by clinical examination.
Remote extension
 is achieved by both lymphatic and venous routes.
 Tumoral cells invade the microcirculation and are taken
by venous torrent towards superior vena cava. From here
they follow the natural path to the right heart and then to
the lung which represents the first major systemic filter.
The second filter is represented by liver.
 The vast majority of tumoral cells remain stuck in the first
filter (the lung) filter and start to develop lung metastases.
 Lung metastases are manifested initially by decreasing
exercise capacity, dyspnea at effort, and then even at
rest.
 In advanced forms irritating cough and dyspnea is
increasing more and more going to exitus, both by
reducing the lungs hematosis surface to and
paraneoplastic pleurisy.
 Much of tumor cells can escape this filter and enter the
pulmonary artery bloodstream from where the path is open
to any region of the body.
 Other most common sites of metastases are the liver and
bone.
 Liver metastases determs symptoms like: weight loss, loss
of appetite, digestive problems and eventually jaundice.
There may be a dull pain under right costal margin
produced by Glisson’s capsule distension. Liver
metastases can be detected by ultrasound examination of
the liver or by CT scan.
 Bone metastases appear to be the most common
sites of metastasis in breast cancer. They are present
in approximately 25% of cases. These metastases are
manifested mainly by early pain. Most frequent
complication of bone metastases is pathological
fractures.
 Bone metastasis can be observed on bone radiograms
which reveal bone circumscribed demineralization
and/or at radioscintigraphy or CT scan or PET scan.
 Other regions of metastasis: the brain, spine, spinal
cord, etc. but not Kidneys
 In conclusion, although in early stages the breast
cancer does not cause pain, there are other symptoms
that should be warning signs for women and to
determine them to contact a doctor.

1. The appearance of a breast tumor and/or axillary

enlarged lymph nodes
2. Changes in breast shape and size, and nipple
symmetry
3. Changes of skin surface (orange peel, tumor
nodules, ulceration, increased vascular drawing)
4. Nipple discharge, especially sanguinolent
5. Recent nipple retraction
Paraclinical and laboratory examinations
in breast cancer
 To treat a breast cancer, first the doctor must answer
to 2 questions:
1. Has the woman a breast cancer ?
2. What is the exact location and extension of the tumor ?
Imaging examinations
 Mammography and breast ultrasound are the most
frequent investigations used in this field.
Mammography
 It can find breast tumors in an early stage, about 2
years before they can be detected by palpation.
 Mammography does not prevent breast cancer!
 Mammography uses X rays. Radiation level is very low
(0.1 Gy).
 Each breast is compressed horizontally and then obliquely and x-
rays are taken in each position.

 There are two types of mammograhy:

1. Screening mammography which is performed in
women with no complaints in the breast area.
2. Diagnostic mammography – for women who has
some complaints or modification in breast area
Screening versus Diagnostic Mammography

 Screening mammography
1. It is applied to asymptomatic women
2. Purpose is detection of possible abnormalities
3. Standard two views of each breast (mediolateral oblique and
craniocaudal) are taken
4. Images are read by radiologist
 Diagnostic mammography
1. Applied to symptomatic (palpable finding, pain, spontaneous
nipple discharge, etc)
2. Call back of a patient with an abnormal screening mammogram
3. Views are tailored to the patient's problem (may include spot or
magnification views, additional projections, and ultrasound).
4. Usually performed in the presence of the radiologist and
interpreted at the time of the examination.
 An improvement in this field is the digital mammography
which stores and analyze the information on a computer.
 Detectable tumor size on mammography is an average
of 1 cm. diameter. In the table below are given for
comparison of approximate sizes mammary tumors
detected by mammography and by palpation.

1 cm.

1,5 cm.

2 cm.

3,5 cm.
 Mammographic features of a malignant tumor are:
1. Irregular whitish mass with marginal spicule
2. Clusters of microcalcification
3. Calcification less than 0.5 mm diameter
4. Deformation of local architecture
5. Density asymmetry
6. Skin retraction
7. Peritumoral edema

 Mammographic features of a benign tumor are:

1. Circumscribed mass
2. Fat-containing lesion
3. Macrocalcifications
4. Round, uniform density, large, coarse
5. Widely scattered
Mammograms
Interpretation of mammograms
 Standardization system BI-RADSTM (Breast Imaging
Reporting and Database System) to characterize the
mammographic images:
1. Category 0 - image inconclusive, it is necessary to
carry out other imaging
2. Category 1 - negative
3. Category 2 - benign character changes
4. Category 3 - probably benign but require tracking
changes
5. Category 4 - suspicious for cancer changes -
requires biopsy
6. Category 5 - highly suggestive of cancer changes
Breast ultrasonography

Indications:
1. To investigate tumors detected by mammography or
palpation and for biopsy guidance.
2. To differentiate the cystic from solid tumors.
3. To explore the breast tumors that can not be evaluated
by mammography (or are not visible, either because of
location, either due to dense breast tissue in young
women)
4. To explore the axillary lymph nodes.
5. To explore the breast tissue in mastitis – abscess
formation
6. To guide the biobpsy
7. In pregnant women because there is no radiation
exposure.
 Limits of the method:
– It takes longer time to investigate the patient
– Can not detect microcalcifications
– Isn’t so accurate than biopsy, there are frequently false negative
and false positive conclusions
– Examiner's experience is an important related factor
 Advantages of the method:
– Does not use radiation
– Can differentiate between a solid and a cystic structure
– Offers the possibility to explore in multiple levels
– It is cheap
 Malignant features of the tumor:
– Lesion is taller than it is wide
– Decreased hyperechogenicity
– Marked acoustical shadowing
– Spiculation
 Nuclear magnetic resonance imaging (MRI)
 It provides valuable information about tumor extension.
The main drawback is the price far above the
mammography examination.
 Indications:
1. Preoperative staging in breast cancer for possible or
multi-focal disease,
2. Detection of implant rupture,
3. Patient with metastatic breast cancer,
4. Occult breast cancer,
5. Differentiation between scar and tumor recurrence,
6. Screening of high-risk patients.
 Recommendations for Breast MRI Screening as an Adjunct to
Mammography– “Cancer Screening Guidelines for Breast Screening
with MRI as an Adjunct to Mammography” by ACS
 Recommend Annual MRI Screening (Based on Evidence*)
– BRCA mutation
– First-degree relative of BRCA carrier, but untested
– Lifetime risk 20–25% or greater, as defined by BRCAPRO or other models that
are largely dependent on family history
 Recommend Annual MRI Screening (Based on Expert Consensus Opinion )
– Radiation to chest between age 10 and 30 years
– Li-Fraumeni syndrome and first-degree relatives
– Cowden and Bannayan-Riley-Ruvalcaba syndromes and first-degree relatives
– Insufficient Evidence to Recommend for or Against MRI Screening
– Lifetime risk 15–20%, as defined by BRCAPRO or other models that are largely
dependent on family history
– Lobular carcinoma in situ (LCIS) or atypical lobular hyperplasia (ALH)
– Atypical ductal hyperplasia (ADH)
– Heterogeneously or extremely dense breast on mammography
– Women with a personal history of breast cancer, including ductal carcinoma in
situ (DCIS)
 Recommend Against MRI Screening (Based on Expert Consensus Opinion)
– Women at <15% lifetime risk
 Transverse high-resolution MR
Breast cancer
mammography of breast and
implants.
Note the implant twisting on the
upper (left) image and the implant
valve on the lower (left) image
CT scan
 This method of investigation is not routinely used to
diagnose breast tumors due to exposure to radiation. It
is however very useful in advanced stages of disease
to assess the extension of neoplastic process in the
chest wall structures or distant metastases detection.
CTLM (Computed Tomography Laser
Mammography)
 Uses laser technology to produce three-dimensional
images of the breast. It does not create any discomfort.
CTLM is a method of looking at the blood flow to the
breast and thereby should visualize tumor
angiogenesis. It can images through implants and
dense breast tissue easily, unlike mammography.
Mammogram CTLM
Scintimammography (Sestamibi)

 It is based on the fact that the radiant substance is

captured at a greater extent by tumors than normal
tissue due to their increased metabolism.
It is used in selected cases as:
1. For patients with dense breast tissue difficult to
investigate with other imaging methods.
2. When a breast tumor can be felt but it can not be
detected by mammography or ultrasound.
3. Breast implants
4. When multiple, multifocal tumors are suspected.
5. When after mastectomy tumors appear at the level of
postoperative scar.
6. To explore the axilla in detecting metastatic lymph
nodes or for sentinel node biopsy.
Sestamibi
P.E.T. - Positron Emission Tomography
 The principle is the same as in Sestamibi.
 Post-therapy is particularly useful for detecting any
remaining cancer and active areas and to detect lymph
node or distant metastases.
Other imaging investigations:
 Chest radiograph
 Bone radiography
 Bone scintigraphy
 Thermography -The area around the cancer tissue has a higher
temperature because of rich blood supply and more intense
metabolism
 Electrical impedance scanning (EIS)

Thermography
Investigation methods of milk ducts
1. Ductography (Galactography) - is an x-ray
examination that uses mammography, a low-dose x-ray
system for examining breasts, and a contrast material to
obtain pictures, called galactograms, of the inside of the
breast's milk ducts.
 Indications:
– Unilateral persistent sanguinolent nipple discharge
 Contraindications:
– Allergy to contrast substance
– Difficult to achieve in the following conditions:
 Previous operations on the nipple
 Inverted nipple
2. Ductal lavage - Examines the cells in wash liquid.
3. Ductoscopy - It is capable of detecting smaller abnormalities
than mammograms, MRI or ultrasound tests.
Ductogram. Magnification view demonstrates filling
defects approximately 1.5 cm from the nipple
Normal Papilloma

Ductoscopy
 TUMORAL MARKERS IN BREATS CANCER
 Tumoral markers are substances that can be detected
in small amounts in blood, urine and various tissues.
Measurement of these markers is useful in detection
and diagnosis of various cancers.
 Usefulness:
1. Determination of cancer risk in some people
2. Detect cancer in the body
3. Reflecting the stage of the disease
4. Monitoring the effectiveness of cancer treatment
5. Early tumor recurrence detection
6. Prognosis estimation of the case
 marker
ER/PR Estrogen receptors bind to cancer cells stimulating
(estrogen/ their proliferation and differentiation. Progesterone
progesteron is also a mitogenic factor stimulating the mammary
receptor) epithelium.
Determination of ER and PR receptors by
immunohistochemistry has become an important
standard for clinical labor as the presence of these
receptors influence therapeutic measures and
prognosis of patients.
The patients with breast cancer who have both types of
receptors (70% cases) have the best remission to
treatment with Tamoxifen, while those with only one
type of receptor (30%) have poor results, and those
with low levels of receptors (less than 10%) had
poor results also.
BRCA1 Women who have inherited mutations by deletion in
(breast cancer 1) BRCA1 and BRCA2 have an increased risk of
Chromozom 17q developing breast cancer by 56-85% rate and also
ovarian.
BRCA2
(breast cancer 2) BRCA1 is found in 3% of of breast cancer in general and
Chromozom 13q, 70% in women with hereditary of breast cancer.
BRCA2 mutation is identified in 10-20% of families with
breast and ovarian cancer risk and only in 2.7% of
women with early breast cancer. The risk of breast
cancer for women carrying BRCA2 is 25-30%.

HER-2/neu Is a surface gene that plays a key role in regulating cell

(human epidermal growth. When HER2 is altered more HER2 receptors
growth factor will be produced which leads to increased cell
receptor 2) multiplication. HER2 is found in 25-30% of women with
breast cancer. They can be detected in tissues sample
collected by biopsy or surgery.
Gene ERBB2 localised In women with metastatic HER2 positive is indicated
on chromozom Herceptin (Trastuzumab) - a monoclonal antibody
17q21.1 produced by biotechnology.
CA 15-3 It is a marker used to monitor treatment
(Carbohydrate Antigen effectiveness in advanced breast
15-3) (Cancer Antigen cancer.
15-3) Antigen oncofetal Rarely is increased in the early stages of
(from blood) the disease.
CA-125 also known as mucin 16 For following the response to treatment
and predicting prognosis after
treatment. It is especially useful for
detecting the recurrence of ovarian
cancer.
CA 27-29 It is found in the blood of the vast majority
of the patients with breast cancer.
It is used together with other tests to
monitor the treated of breast cancer in
stage II and III
It is an independent factor for predicting
tumor recurrence
 Invasive methods of diagnosis
Breast biopsy
 The only examination that can make with certainty the
diagnosis of cancer is histopathology which can be
obtained by biopsy.
 Confirmation of breast cancer before surgery is useful
because it influences the magnitude of this act, if it is
necessary and subsequent treatments as well.
 Types of breast biopsies:
1. Percutaneous
– Fine needle aspiration
– Tru Cut biopsy
– Vacuum assisted biopsy
– ABBI (advanced breast biopsy instrumentation)
2. Surgical
– Incisional
– Excisional
1. Fine needle aspiration (FNA)
 Indications:
– Tor tumors of cystic nature
– For solid lesions in stage T3 or T4, or axillary and loca
locall
recurrences
Due to possible false negative results, this type of
investigation is not very suitable for exploring tumors
of less than 1 cm.
 Cytological examination is required in the following
situations:
1. Hemorrhagic fluid is extracted
2. After aspiration the tumor mass does not disappear completely
3. It is a recurrent cyst
4. There is a suspicion for cancer on mammogram
Breast FNA guided by ultrasound
2. Tru cut biopsy
 It is also a percutaneous method. The essential
differences from fine needle aspiration biopsy are:
1. It uses a thick needle, specially fitted with a cutting
mechanism
2. The process of obtaining biopsy material is cutting
not aspiration
3. The material obtained is a cylinder of tissue, enough
to differentiate between invasive and noninvasive
type of cancer
4. Core needle biopsy is not suitable for cystic lesions
The principle of Tru Cut biopsy
Biopsy gun

Tru Cut biopsy

Guided by ultrasound
Advantages:
– Sample tissue with enough cellular material to detect
breast cancer
– Harvested fragments can demonstrate relationship with
the surrounding tissue ad can make the difference
between in situ and invasive cancer.
Disadvantages:
– As a biopsy, it harvests only fragments of tissue, not
the entire tumor. Even if the fragment does not contain
cancer cells is not an absolute guarantee that the
patient is not suffering from breast cancer.
– The method cannot be applied to women with breast
implants as the risk for perforation the implant.
3. Vacuum assisted biopsy

 The novelty of the method is that the biopsy needle is

adapted to a vacuum system. By using vacuum, breast
tissue is absorbed into the needle slot ensuring a better
sampling. 3-6 specimens are extracted.
Stereotactic breast
vacuum assisted biopsy
4. ABBI - Advanced Breast Biopsy
Instrumentation
 This type of biopsy uses a thicker needle of
0.5 to 2 cm in diameter.
 The intention of this type of biopsy is to
extract as much tissue as possible, even
the entire tumor if the size permits.
 Is carried out only with stereotactic
equipment. Rarely used in now days.
SURGICAL BIOPSIES
1. Excisional biopsy
 It is the most commonly used.
 The surgeon will remove the tumor with a safety margin
of normal tissue around it.

2. Incisional biopsy
 This applies when the breast tumor is larger (more than
4 cm diameter) or diffuse, or when chemotherapy and
radiotherapy are the primary treatment.
 Surgeon excises only a portion that is suggestive for
cancer.
Advantages of surgical biopsies:
 Ensures the diagnosis in almost 100% cases being the
"gold standard" in this sense.
 In case of small tumors it can be regarded as definitive
surgical therapy method (lumpectomy) if the tumor was
excised with negative margins.
Summary of breast biopsy methods
STAGING OF BREAST
TUMORS

TNM classification
The T stages (tumor)
 TX means that the tumor size cannot be assessed
 T1 – The tumor is no more than 2 centimeters (cm)
across
T1 is further divided into 4 groups
T1mic – under a microscope the cancer cells can be
seen to spread less than 0.1cm into surrounding tissue
(microinvasion)
T1a – the tumor is more than 0.1 cm but not more
than 0.5 cm
T1b – the tumor is more than 0.5 cm but not more
than 1 cm
T1c – the tumor is more than 1 cm but not more than
2 cm
 T2 – The tumour is more than 2 centimeters, but no
more than 5 centimeters across
 T3 – The tumour is bigger than 5 centimeters across
 T4 is divided into 4 groups
– T4a – The tumor has spread into the chest wall
– T4b – The tumor has spread into the skin
– T4c – The tumor is fixed to both the skin and the
chest wall
– T4d – Inflammatory carcinoma – this is a cancer in
which the overlying skin is red, swollen and painful to
the touch
T stage
The N stages (nodes)
 NX means that the lymph nodes cannot be assessed (for example, if
they were previously removed)
 N0 – No cancer cells found in any nearby nodes
 N1 – Cancer cells are in the upper levels of lymph nodes in the armpit
but the nodes are not stuck to surrounding tissues
 N2 is divided into 2 groups
– N2a – there are cancer cells in the lymph nodes in the armpit, which are
stuck to each other and to other structures
– N2b – there are cancer cells in the lymph nodes behind the breast bone
(the internal mammary nodes, which have either been seen on a scan or
felt by the doctor. There is no evidence of cancer in lymph nodes in the
armpit
 N3 is divided into 3 groups
– N3a – there are cancer cells in lymph nodes below the collarbone
– N3b – there are cancer cells in lymph nodes in the armpit and under the
breast bone
– N3c – there are cancer cells in lymph nodes above the collarbone
The M stages (metastases)
 M0 – No sign of cancer spread
 M1 – Cancer has spread to another part of the body, apart from the
breast and lymph nodes under the arm
AJCC stage grouping (American Joint Committee on
Cancer)
– Stage 0 Tis N0 M0
– Stage I T1* N0 M0 – (*T1 includes T1mic)
– Stage IIA T0 N1 M0 - T1* N1** M0 - T2 N0 M0
(*T1 includes T1mic **The prognosis of patients with pN1a disease is
similar to that of patients with pN0 disease.)
– Stage IIB T2 N1 M0 - T3 N0 M0
– Stage IIIA T0 N2 M0 - T1*N2 M0 - T2 N2 M0 - T3 N1 M0 - T3
N2 M0 ( *T1 includes T1mic)
– Stage IIIB T4 Any N M0 - Any T N3 M0
– Stage IV Any T Any N M1
 Overall survival of breast cancer patients according to American Joint Commission on Cancer
(AJCC) stage. The relative survival rates of 50,834 patients with breast cancer stratified for
stage at presentation between 1983 and 1987. Note that survival rates decrease with increasing
stage at initial presentation. Additionally, patients with invasive cancers continue to die of
disease beyond the 6-year period illustrated
TREATMENT OF BREAST
CANCER
The natural history of breast cancer. This graph
displays the overall survival of patients with
untreated breast cancer.
COMPLEX MULTIMODAL TREATMENT
1. Surgical
2. Adjuvant
– Radiotherapy
– Chemotherapy
– Hormonal therapy
– Immunotherapy
– Others
 Selection of local and systemic treatment modalities and
priorities of application depends on a number of factors
and prognostic predictors including:
1. Tumor histology
2. Clinical and pathological features of tumor
3. Lymph nodes status
4. Tumor hormone receptor
5. HER2 marker level
6. Distant metastases
7. Existing comorbidities
8. Age of patient
9. Menopausal status of the patient
10.Patient preferences
– Breast cancer in men is treated in the same way as in
postmenopausal women
4 groups of breast cancer

1. Non-invasive carcinoma (stage 0)

– ductal carcinoma (DCIS)
– lobular carcinoma (LCIS)
2. Operable invasive carcinomas
– stage I
– stage II
– some of stage IIIA
3. Inoperable invasive cancers
– stage IIIB
– stage IIIC
– some stage IIIA
4. Cancers with distant metastases or recurrent (stage IV).
 1. NON-INVASIVE CARCINOMAS
 The goal of treatment in carcinoma in situ is either to
prevent invasion or to diagnose invasive component as
long as it is still located at the breast.

A. lobular carcinoma (LCIS)

 Treatment is simple surveillance because the risk of
invasive cancer in time is very low (about 21% to 15)
 Bilateral simple mastectomy with or without
reconstruction is another alternative.
 Tamoxifen therapy for 5 years significantly reduces
(56%) the risk of invasive cancer.
B. Ductal carcinoma in situ (DCIS)
 In patinets with extended DCIS, simple mastectomy
is indicated without axillary lymphadenectomy.
 In patients with limited DCIS conservative surgery is
enough if margin resections are tumor free.
(lumpectomy, quadrantectomy)

 Radiotherapy is indicated after excision in all tumors

larger than 5 cm.
 Tamoxifen is indicated to reduce the risk of a primary
tumors in the contralateral breast and local
recurrence in those with conservative surgery
 2. INVASIVE BREAST CANCER
STAGES I, IIA AND IIB
 Surgery is represented by total mastectomy with axillary
lymphadenectomy or conservative surgery with axillary
lymphadenectomy.
 Contraindications for breast-conserving therapy requiring
radiation therapy include:
– Absolute:
 Prior RT to the breast or chest wall
 RT during pregnancy
 Diffuse suspicious or malignant appearing microcalcifications
 MuIticentric disease
– Relative:
 Multifocal disease requiring two or more separate surgical incisions.
 Active connective tissue disease involving the skin (especially
scleroderma and lupus)
 Tumors > 5 cm (category 2B)
 Axillary lymphadenectomy
– level I and II of lymph nodes must be removed.
 Sentinel node biopsy may be considered in the
following cases:
1. Nonpalpable axillary lymph nodes
2. Tumor less than 5 cm diameter
3. Without having had breast surgery on the same
breast
4. Without preoperative treatment with chemotherapy,
radiotherapy or hormone therapy

 If the sentinel node can not be identified or on frozen

sections metastases are found, axillary
lympadenectomy should be performed.
 3. INVASIVE BREAST CANCER – STAGE III
A. Locally advanced cancer but operable - T3N1M0
– Surgical treatment consists of total mastectomy
with axillary lymphadenectomy ± reconstruction
– Treatment is the same as in stage II
B. Locally advanced cancer – inoperable - stages IIIB
and IIIC
– Stage IIIB T4, any N, M0
– Stage IIIC any T, N3, M0
 It begins with preoperative chemotherapy followed
by mastectomy with lymphadenectomy if remission is
obtained.
Time interval between surgery and radiation therapy
Breast irradiation should be started as soon as possible
after surgery and not later than 12 weeks after, except for
patients in whom radiation therapy is preceded by
chemotherapy. However, the optimal interval between
BCS and the start of irradiation has not been defined.
4. ADVANCED STAGE WITH METASTASES OR
LOCAL RECURRENCE
A. Recurrence
 Recurrence after conservative surgery - radical
mastectomy with lymphadenectomy chemo-hormonal
therapy (to keep in mind that the patient have already
received radiation!)
 Relapse occurs after total mastectomy - excision
without "heroic operation" followed by local
radiotherapy (if there was no previous irradiation).
 If relapse cannot be removed the patient will benefit
from local radiotherapy.
B. Metastases
 Palliative treatment in this stage is trying to prolong the
life.
 Surgery comes into discussion in the following
circumstances:
1. Mastectomy or excision of recurrences with the
purpose of "cleaning" the ulcerated lesions which
has become infected.
2. Oophrectomy (ovarectomy) in premenopausal
patients.
3. Bone marrow transplantation (autologous) or stem
cell transplantation combined with high dose radio-
chemotherapy.
Surgical treatment
1. Tumor removal (+ / - Lymphadenectomy)
– Conservative surgery
1. Lumpectomy
2. Quadrantectomy
3. Extended quadrantectomy
– Mastectomy
1. Simple mastectomy
2. Skin sparing mastectomy
3. Mastectomy with axillary lymphadenectomy
– Maden
– Patey
– Halsted - limited indications (tumor infiltration of the pectoral
muscles)
– “Heroic" operations (Ugon, Dubau, etc.) have no indication in
now days
2. Surgery to remove the lymph nodes
 Sentinel node biopsy
 Axillary lymphadenectomy
 Internal mammary lymphadenectomy
3. Breast reconstruction surgery
4. Endocrine surgery (oofrectomy)
 Sentinel lymph node biopsy (SLNB)

 Axillary lymph node metastases remain the most

important prognostic factor in breast cancer and also a
basis that guides the adjuvant therapy.
 Sentinel node is the first node on the lymphatic route
where the probability of metastasis is high and early.
 Only about 30% of women who require axillary node
sampling actually have metastasis to the lymph nodes.
 Lymphatic mapping and sentinel lymph node biopsy can
identify the patients with positive nodes, thus saving the
majority of women from an axillary dissection.
 In most cases the sentinel lymph nodes are located in
the axilla but there are cases when the sentinel lymph
node is located elsewhere, or there are more than a
single sentinel lymph node. This are the reasons why the
lymphatic mapping prior operation is important.

Possible locations of sentinel

III
lymph node
II
I

Axillary level I, II and III

Internal mammary chain
Supraclavicular and cervical
Intramammary
Interpectoral (Rotter)
Other locations
Mapping using Technetium 99 – shows intramammary sentinel lymph node
 Mapping is useful also for guiding the radiation therapy.
 Contraindications of SLNB:
 Contraindications related to tumor:
– Tumors larger than 5 cm diameter or advanced local
stage
– Patients with palpable axillary lymph nodes
– Patients with pure ductal carcinoma in situ
 Contraindications related to the patient:
– Previous breast surgery or armpit surgery
– Preoperative chemo-radiotherapy
– Patients with multicentric tumors in the same breast
that are in different quadrants.
– Pregnancy
– Allergy to technetium 99m sulphur colloid
 There are two methods used for sentinel lymph node
detection: one using radioisotopes (Technetium 99) and
the other which is using a dye (metilen blue or
isosulphan blue). In many cases, for better results the
two methods are combined. The advantage of
radioisotope method is that it allows the preoperative
mapping guiding the surgeon and also the radiotherapy.
The dye method is cheaper.
 The tracer is injected around the tumor or areola. It flows
via the lymphatic network toward the first lymph node of
the lymphatic route that drains also the tumor. This first
node can be detected in two ways depending on the
traces used. If technetium 99 was used a special gamma
detection device and probe is necessary for detection. If
dye was used the lymph node will be detected by its blue
color.
Blue dye is injected around the areola
A local massage is performed for a faster diffusion of the dye
After 10-15 minutes incision in the axilla may be performed for detection of node
Sentinel lymph node
Gamma detection device
 The excised node will be sent to histologic examination.
In the result is negative the axillary lymphadenectomy is
not necessary but if tumoral cells were found the axillary
dissection should be performed. Preventing unnecessary
axillary dissection is important in preventing associated
complications (seroma, shoulder and upper limb pain,
lymphedema, scars, etc)
 Lumpectomy
 It is a surgical method applied for early stages of cancer
which removes the tumor with surrounding healthy
tissue. Almost always is followed by six weeks of
radiotherapy. The specimen is examined by pathologist
and if the tumor is too close to the margin of resection
the surgeon must perform a re-resection at the same
site.
 Quadrantectomy (segmental mastectomy): removal
of a quadrant of mammary gland.
 Partial mastectomy (or extended quadrantectomy):
removal of more than a quadrant of the breast.
 Usually, after these operations external radiation therapy
is given for a period of six weeks.
 Skin-Sparing Mastectomy – removes the entirely
mammary gland and the areola but sparing the skin. A
"keyhole"–like or other types of incision are performed.
This type of operation is used when a breast
reconstruction is intended - an expander in introduced
under the pectoral muscle and after a while it is replaced
by silicone.
 Simple or total mastectomy: removes the entire
breast, but without axillary lymph nodes and underlying
muscles. The skin incision is elliptical including the
areola and nipple. It may be oblique or horizontal
depending on breast volume and shape.
 Modified radical mastectomy – removes the
mammary gland between boundaries: sternum, clavicle,
latisimus dorsi and the origin of rectus abdominis, and
also removes the axillary lymph nodes of level I and II.
Level III lymph nodes are not dissected.
– Madden mastectomy – removes the entire breast +
level I and II axillary lymph nodes.
– Patey mastectomy – the same as in Madden
procedure but the pectoraslis minor insertion is
sectioned for a better access to the axilla.
 Radical mastectomy - amputation of the breast
(Halsted operation) presumes mastectomy plus a wide
excision of the pectoral muscles and axillary lymph
nodes. In now days this type of operation is no longer
performed, just in cases when muscles are invaded by
tumor.
Modified radical mastectomy
Incision Mastectomy

Tumor

Breast

Axilla
Advanced cases of breast cancer
Mastectomy was performed just for cleaning the area not with radical
intention
Recurrence operated – large excision with omentoplasty
(when the wound cannot be closed and the pectoralis
muscle was excised remaining only the chest wall, the great
omentum may be used to cover the rib cage and promote
granulation) – followed by skin grafting.
Postoperative complications

 Post-mastectomy
– Subcutaneous hematoma
– Wound infection
– Skin necrosis
– Chest paresthesia
– Postoperative local pain
– Seroma
– Lymphedema
– Keloid scars
– Granulomas
– Tumor recurrence
 After axillary lymph node dissection:
– Lesions or thrombosis of the axillary vein
– Seroma
– Lymphedema: The reported prevalence rate of lymphedema is
approximately 11%. Extensive surgery, RT, and advanced age are
recognized risk factors for arm edema.
– Impairment of shoulder movements. Symptoms include
decreased range of motion of the shoulder, a problem that may be
improved with early participation in a physical therapy program.
– Damage to the brachial plexus, with chronic pain and varying
degrees of decreased grip strength occurring in up to 15% of
patients and lasting for more than a year after surgery
– Chest wall pain
Lymphedema
Local recurrence
 Post-therapy follow-up program for patients
with breast cancer

Year 1 Year 2 Years 3-5 > 5 Years

Clinical
4 month 4 month 6 month 12 month
examination
If If If
Chest radiography Initial
necessary necessary necessary
Mammography 12 month 12 month 12 month 12 month
If If If
Bone scintigraphy Initial
necessary necessary necessary
INFLAMMATORY BREAST
CANCER
IBC
Klotz-Volkmann’s disease
 Inflammatory breast cancer is particularly serious invasive
form of primary breast cancer, characterized by rapid
evolution and clinical appearance of a breast inflammatory
process.
 The incidence is 1-6% being more common in African-
American population (10.1%) than in Caucasian
population (6.2%). It tends to be diagnosed in younger
women compared to non-IBC breast cancer.
 The characteristic aspect of inflammation is given by the
obstruction of the skin lymphatic vessels due to lymphatic
invasion by tumor cells.
 Like other types of breast cancer, it can occur in men, but
usually at an older age than in women. Some studies have
shown an association between family history of breast
cancer and IBC.
Signs and symptoms
 The onset is often sudden.
 Women have breast pain and nipple discharge may occur.
 On clinical examination the breast is swollen, deformed,
with skin erythema and edema, increased local
temperature. The aspect is that of “peau d’orange” or
"orange peel".
 Axillary lymph nodes are increased in volume and
sensitive.
 In more advanced forms contralateral axillary lymph nodes
are also affected.
 All this aspects are very similar to acute mastitis and
confusion is not rare. In this event, patients are treated for
a long time with antibiotics and antiinflammatory drugs but
as they do not heal, suspicion of a cancer arises.
Diagnosis
 The only investigation that could make the correct
diagnosis is biopsy.
 Usually the first examination is breast ultrasound to
reveal some collections. This is of no use for correct
diagnosis in this case.
 Eventually cytology of nipple discharge could detect
cancerous cells.
 Inflammatory cancer is characterized as a high
histological grade invasive carcinoma, the presence of
molecular markers including high aggressiveness of S
phase, aneuploidy, lack of ER receptors and a large
increase in markers of p53 and epidermal growth factor.
Treatment
 The treatment is complex, aggressive, including
chemotherapy, radiotherapy and mastectomy with axillary
lymphadenectomy if after chemotherapy the response is
favorable, plus hormone therapy if estrogen receptor are
present.

 With aggressive treatment using multimodal approach,

the 5 year survival rate improved significantly from an
average of 18 months to 50% at 5 years.
PAGET’S DISESE OF THE
BREAST
Sir James Paget (1814-1899)
 Paget's disease has an incidence of 1-3% of all breast
cancers in women. It may occur rarely in males also.
 The average age of patients with breast Paget's disease
is 53-59 years, 5-10 years more than for the patients
with breast cancer. Age limits in which the disease was
found is between 24 and 84 years.
 The diagnosis of certainty is established only by
histopathological examination that emphasizes the
unique features of Paget's cells.
Pathophysiology:
 Although the pathophysiology of Paget's disease has
long been controversial, most authors now agree that
the origin of the disease is the neoplastic cells of the
intraductal breast cancer that invade the skin retrograde
through the nipple’s pores.
Signs and symptoms
 An itchy rash on the nipple and areola, which then
ulcerates.
 Ulceration is regularly covered by crusts leaving a false
impression of healing. Small vesicles may appear on the
affected skin area. Lesions do not heal with topical
treatments and tend to extend in surface.
 Symptoms can last for many years until the patient
decides to consult a doctor. The lesion is often
interpreted as a dermatitis, eczema or psoriasis.
 The disease may be associated with nipple discharge of
various types, but the bleeding should be a warning sign
for both patient and physician.
 Nipple retraction is also a sign indicating the presence of
a retroareolar cancer.
 Unlike exema, skin lesions in Paget's disease have
relatively well defined edges and are infiltrated. The
diameter of these lesions can be between 3 and 15 cm.
 In 30-50% of cases is usually associated a palpable
tumor which is located behind the nipple in most cases
(70% at a distance less than 2 cm from the nipple), but it
can be located anywhere in the mammary gland (about
30% are located away from the skin changes)
 Axillary adenopathy in the early stages is present in
approximately 25% of cases. The incidence of axillary
lymph node metastases is 50-60% in all cases, higher
when the tumor is already palpable.
Clinical forms:
 Previously described is the typical form.
 There are approximately 20-30% of cases in which
just a breast tumor is present, without typical skin
manifestations associated.
 When the single manifestation is nipple discharge, the
risk of axillary lymph node metastases is 5%.
 There are also cases (7% -26%) when the typical skin
manifestations of Paget's disease are not accompanied
by an associated breast cancer.
 Pigmented mammary Paget's disease is rare, being
described both in men and women with intraductal
breast cancer spread to the epidermis through a ductal
pore.
Pigmented mammary Paget's disease
Differential diagnosis will be done between other
conditions with similar symptoms located at the areola
and nipple:
1. Bowen's disease - squamous cell carcinoma in situ
2. Contact dermatitis
3. Nodular cutaneous amyloidosis
4. Malignant melanoma
5. Ductal adenoma
6. Adenomatosis
7. Nipple erosions
Diagnosis
 It may be easy, as long the consulting physician has
sufficient knowledge of breast pathology. Otherwise
confusion with exema or other inflammatory skin
disease is possible.
 Investigation which has the highest chance of diagnosis
is biopsy of the skin lesion, followed by histology.
 Mammography is the routine examination which may
reveal, in some cases (50-70%), the presence of
mammary tumor, located behind the nipple either
associated with another region or even the presence of
microcalcifications. A negative result does not exclude
the possibility of cancer.
Treatment
 It is mainly surgical. Extension of breast excision is based on
disease stage and location of the tumor.
1. If there is no palpable tumors and if the mammography is negative,
the operation is excision of areola and nipple followed by
radiotherapy.
2. If there is a retroareolar palpable tumor, and nowhere else, and if
histopathology reveals a carcinoma in situ - lumpectomy with
excision of the nipple and areola will be performed.
3. If tumor is invasive, sentinel node biopsy is recommended followed
by lymphadenectomy if metastases are present, and mastectomy.
4. In advanced cases or if the tumor is located away from the skin
lesions, mastectomy with axillary lymphadenectomy is indicated.
5. Radiotherapy is usually used after mastectomy. Chemotherapy and
hormone therapy depend on tumor histological and
immunohistological features.
Prognosis
 Patients with palpable breast tumors have a lower survival
rate than those with nonpalpable tumors, and also those
with invasive forms and axillary lymph node metastases
(between 100% and 0% survival rate at five years,
depending on evolution stage).
PHYLLODES TUMOR
 Phyllodes tumor is a rare tumor, more often benign than
malignant, that appears exclusively in women.
 It occurs in any human race and any age with a majority in
the 5th decade.
 It occurs more frequently on the left breast. It is a large (5-
30 cm) and mobile tumor. It represents less than 1% of all
breast cancers.
 It is the most common form of cancer derived from non-
epithelial cells, occurring only in the breast.
Symptoms
 The patient notices the occurrence of a firm consistency
tumor, mobile, well circumscribed, in the breast.
 Tumor tends to increase rapidly in volume. Rarely extends
to the areola and nipple and ulcerates.
 The patients with metastases will have the symptoms of
those organs where metastases are.
On clinical examination:
 The presence of a tumor of firm consistency, mobile, well
circumscribed, non-adherent.
 Superjacent skin is stretched, shiny with visible vascular
design (marble like).
 The clinical appearance is very similar to breast
fibroadenoma and so mammographic images.
Paraclinical investigations
 The only way to correctly diagnose is surgical biopsy
because there is no marker for this type of tumor, and
mammographic images can not distinguish between
malignant and benign form.
Phyllodes tumor
Section surface
Mammogram
Phyllodes tumors
The differential diagnosis must be made with:
– Angiosarcoma
– Breast cancer
– Giant fibroadenoma
– Acute inflammatory cancer
– Sclerosing adenosis
– Liponecrosis
– Fibrocystic mastitis
– Breast abscess
– Acute mastitis
Treatment
 It is only surgical: mastectomy without axillary
lymphadenectomy.
 For the benign forms the prognosis is very good.
 In malignant forms recurrences are more
aggressive as the primary tumor. Most frequentlly
the metastases are located in lungs followed by
bone, heart and liver. The vast majority of
patients with metastases die within 3 years of
treatment. Unfortunately there is no cure for
systemic metastases.
OCCULT BREAST CANCER
 Breast cancer is manifested from the beginning only by
axillary lymph node metastases or rarely with distant
metastases without mammary tumors that can be
detected on physical examination or mammography.
 Rare cases <1%
 The most frequent symptoms are: moderate pain in
armpit, more as a local embarrassment and eventually,
found by self examination a tumor at this level without an
obvious cause.
 If breast lesions which could explain the axillary
adenopathy are not found, a careful examination of all
areas that drain to the axilla must be performed. There
are cases when minor skin lesions, sometimes
apparently cured can be easily overlooked. History is
important and may reveal recent injuries in this areas.
The differential diagnosis should be made with other
diseases that can cause unilateral axillary lymph
nodes enlargement such as:
Benign
 Wounds (accidental wounds, scratching cat bites, insect bites, etc.).
 Panaritium
 Folliculitis, and other infectious lesions
 Hidrosdenitis axillaris
 Acute and chronic mastitis
 Phlebitis spontaneous, traumatic or paratherapeutic of the upper
limb.
 Antiperspirants and deodorants
Malignant
 Other skin cancers (melanoma)
 Pleuro-pulmonary tumors
 Cancers of the lymphatic system
Investigations
 Mammography can reveal microcalcifications even before
the tumor becomes palpable and ultrasound can be
helpful in detecting small cystic lesions. All other
necessary investigations will be performed (chest
radiography, CT or better MRI scan, PET scan, tumoral
markers, etc)
 If all the investigation find nothing, usually follows a
therapeutic test period, of about 10 to 15 days with anti-
inflammatory drugs.
 Axillary node biopsy is the next step in establishing the
etiology when inflammatory treatment fails.
Treatment
 Do not forget that the presence of axillary metastases
proven by histopathology, represents at least stage II of
breast cancer.
 Radical mastectomy with axillary lymphadenectomy is
most frequent applied.
 Radiotherapy on the entire breast gland of first intention,
without mastectomy, after axillary lymhadenectomy
could be another choice.
 To these, chemotherapy and hormone therapy are
added depending on the type and stage of breast
cancer.
Prognosis
 Many studies have shown that the prognosis for occult
breast cancer is the same or even better than for
palpable tumors at the same stage (still more than stage
II).
 Most important prognostic factor in these cases is the
number of lymph nodes affected by metastases.
 In one study, survival rate at 5 years was 87% when the
number of lymph nodes was between 1 and 3, and
decreased to half (42%) when their number was 4 or
higher.
BREAST CANCER IN MEN
 They represent only 1% of all breast cancers. In
Western developed countries the incidence of breast
cancer in men is 1/100.000 men but in African countries
the incidence is much higher.
 It can occur at any age but is most commonly
diagnosed after the age of 60 years.
 Determinant causes are not known.
 The following types of breast cancer usually occur in
men:
1. Infiltrating ductal carcinoma. The vast majority of
patients have this type of cancer.
2. Ductal carcinoma in situ (intraductal carcinoma)
3. Inflammatory carcinoma
4. Paget's disease of the breast.
5. Lobular carcinoma in situ has not been found in
breast cancer in men.
Cancer

Breast liposarcoma
 Symptoms and signs are similar to those in women with
breast cancer
Staging of breast cancer in men:
 Stage 1 - tumor diameter is less than 2 cm. Lymph nodes are not
affected and there are no signs of distant metastases.
 Stage 2 - the diameter of the tumor is between 2 and 5 cm. It may
adhere to structures such as skin and pectoral muscle. Usually there
are enlarged axillary lymph nodes but no evidence of distant
metastases.
 Stage 3 - Tumor more than 5 cm in diameter, can adhere to
adjacent structures (skin, muscle). Usually there are enlarged axillary
lymph nodes but no evidence of metastases.
 Stage 4 - any size tumor, with enlarged to lymph nodes and distant
metastases.
Diagnosis is the same as for women.
The treatment is the same as for women.
– Tamoxifen hormone therapy is also indicated in men
especially in forms of cancer with ER / PR positive
receptors.
 The survival rate is the same as for women in the same
stage of evolution, but men breast cancer generally is
discovered in more advanced stages.
 The prognosis depends on:
– Stage of cancer
– Histopathological type
– Some features of tumoral cells
– Bilaterality
– Age and health of the patient
BREAST CANCER AND
PREGNANCY
 Tumors most commonly associated with pregnancy are:
1. Cervical cancer
2. Breast cancer
3. Malignant melanoma
4. Lymphomas
5. Thyroid cancer
 Fortunately the incidence of these cancers is quite low
during pregnancy. For this reason there are no
statistical studies on many cases, sporadic cases being
reported in the literature.
 Cancer during pregnancy raises special ethical and
psychology problems.
 The patient must choose between maintaining the
pregnancy and cancer treatment.
 Breast cancer incidence is about 0.01 to 0.03% of
pregnant women and are most often found in women
who delay pregnancy until the age between 30 and 40
years.
 During pregnancy significant breasts changes occur
which make difficult early detection of small tumors.
 In pregnant women in general tumors are detected with
a delay of five months from the nonpregnant.
 Also pregnant women have a 2.5 times higher chance of
being diagnosed with metastatic breast cancer.
 Mammographic examination is avoided during
pregnancy due to exposure to radiation. Any breast
changes considered abnormal will be examined by
ultrasonography.
 Biopsy is encumbered with the risk of suppurations,
hematoma and bleeding in pregnant women. It is done
under the protection of antibiotics.
Abnormal breast changes during pregnancy
and breastfeeding
 Breast cysts
 Galactocele (cysts filled with milk)
 Breast fibroadenoma

 Nipple discharge
 Breast inflammation
Breast cancer treatment during pregnancy
 Treatment of breast cancer in pregnant women is mainly
surgical: lumpectomy or mastectomy with or without axillary
lymphadenectomy according to the presence of increased
axillary lymph nodes, and tumor stage.
 If the woman is in the last 2-3 weeks of pregnancy, surgery
may be postponed until after birth.
 If the tumor was diagnosed during the first weeks of
pregnancy, abortion and complex treatment of cancer
would be the best choice.
 Radio-chemotherapy and hormono therapy will not be used
during pregnancy.
 If breast cancer was found postpartum, the same principles
of treatment as provided in any woman will be applied, with
breastfeeding discontinuation.
 Prognosis of breast cancer during pregnancy is identical to
that of nonpregnant women in the same stages.
 Pregnancy after breast cancer treated in
history
 Women who have been treated previously for breast
cancer could have a normal pregnancy in future. The
minimum duration of time from diagnosis and treatment
of breast cancer to pregnancy should be at least 2 years.

Breast cancer effects on fetus

 So far, no cases of metastases at the fetus from breast
cancer have been cited, but there were several cases
cited in the literature of metastases in the placenta.
SURGICAL PATHOLOGY OF
THE ESOPHAGUS
 Surgical anatomy
1. Esophageal syndrome
2. Achalasia
3. Esophageal diverticula
4. Cancer of the esophagus
5. Esophageal varices
Surgical anatomy

 Esophagus is a musculomembranuos tubular organ lying

between the pharynx and stomach.
 The average length is 25 cm. and 1.5-2 cm diameter.

esophagus segments
esophagus curves

Cervical

Thoracic

Abdominal
 The esophagus has three physiological straits important
in the development of postcaustic strictures.
1. Cricoidian strait at 15 cm from dental arch
2. Bronchoaortic strait at 25 cm
3. Diaphragmatic strait at 40 cm
Cervical esophagus
 At the level of cricoid cartilage, on the posterior aspect,
there is a weakness in the esophageal wall between the
lower edge of the inferior pharyngeal constrictor
muscle and the upper edge of the crico-pharyngeal
muscle. It is the Leimer’s triangle of weakness (also
known as Killian's triangle ) which is important in the
development of cervical esophageal diverticulum -
Zenker's diverticulum.
Anatomical relations:
 Cervical esophagus.
– Anterior - trachea (membranous part), thyroid gland, parathyroid
gland and recurrent laryngeal nerves.
– Posterior - vertebral column.
– Lateral - common carotid artery and the left thoracic duct.
 Thoracic esophagus
– In the upper mediastinum it lies between the trachea and spine.
Then down and right behind the aortic arch toward the posterior
mediastinum.
– Anterior it has relationships with the trachea, right bronchus
pericardium, left atrium and diaphragm.
– Posterior relations are: aortic arch, intercostal arteries, thoracic
duct and hemiazygos vein and the diaphragmatic portion of the
aorta.
– On the left, bordering the aorta, subclavian artery, left thoracic
duct, recurrent laryngeal nerve and left pleura.
 – On the right side it comes in contact with the pleura and the right
hemiazygos vein. Right vagus nerve has a trajectory behind to the
esophagus while the left is located above. Thoracic duct has an
upward trajectory initially on the right side of the esophagus, then,
from the fourth thoracic vertebra it passes behind to the left side.

 Abdominal esophagus
– Anterior is covered by the parietal peritoneum and comes in
contact with the left liver lobe and left vagus trunk.
– Posterior it has relations with the posterior vagus nerve and aorta
through the left diaphragmatic pillar.
– Lateral has relations with the diaphragm pillars.
– Between the esophagus and the diaphragm there is interposed
connective tissue (membrane of Leimer-Bertelli Treitz) and
muscle fibers that are drawn from the diaphragm and dissolve into
the esophageal wall (Rouget’s muscle).
Vascular supply
 Arteries - Esophagus the weakest
vascularized segment of the digestive
tract.
– Branches of arteries: inferior thyroid,
subclavian, esophago-bronchial artery
(directly from the aorta), intercostal
arteries, the own esophageal arteries,
gastric coronary, diaphragmatic.
 Veins – there are two venous
plexuses:
– submucous and
– periesophageal
– From the upper esophagus the blood is
drained into the azigos veins and from the
inferior portion into the coronary gastric
vein and portal system. (PORTO-CAVAL
SHUNTS)
 Lymphatics – the lymph is collected by two
plexuses: muscular and submucous.
 Lymphatic plexuses being very elongated explains
the spread of tumoral cells in the esophageal wall far
from the primary tumor (6 cm), so giving the
possibility of 2-3 concomitant esophageal tumors.
 Lymphatics drain into the lymph nodes:
1. cervical
2. paratracheal
3. posterior mediastinal
4. gastrohepatic ligament
5. celiac
 Innervation is sympathetic (paravertebral ganglia,
celiac and semilunar) and vagal. There are two
intramural plexuses: of Auerbach and Meissner
important in esophageal contraction for swallowing.
Physiology
 The main function of the
esophagus is in swallowing.
 Factors: gravity and
esophageal peristaltic wave.
 There must be a coordination
between peristaltic waves and
opening of the cardia (It opens
on a pressure of 20 cm water
column). Missing of this
coordination will lead to
esophageal functional
syndromes (Ex. achalasia).
 ESOPHAGEAL SYNDROME
PRODUCED BY ORGANIC OR/AND FUNCTIONAL
DISORDES
1. Dysphagia. Sometimes may have a short onset and
evolution when functional disorders are the cause. If
there are anatomical lesions, dysphagia is usually
progressive manifested initially for solids and and then
for liquids. In cardioaspasm the reverse situation exists
= "paradoxical dysphagia“
2. Pain. Retrosternal and epigastric
3. Regurgitation. Not to be confused with vomiting. The
content is undigested food from esophagus not from
stomach. It may occur early in high stenosis or late in
the lower.
4. Hypersalivation (syalorrhea) due to vagus nerve
irritation by esophageal distension.
ACHALASIA
cardiospasm
 Incomplete lower esophageal sphincter (LES)
relaxation when the alimentary bolus reaches at this
level, increased LES tone, and aperistalsis of the
esophagus.
Causes
1. Idiopathic – not known
2. Trypanosoma Cruzii infection (Chagas disease)
3. Tumors in this area
4. Degeneration of vagus nerves nuclei
5. Pharmacology disorders of chemical mediators from the
neuromuscular plate at lower esophageal sphincter
3 criteria for defining achalasia:
1. Spasm of the lower esophageal sphincter
2. Association with abnormal esophageal peristalsis
3. Esophageal contractions weak or nonexistent,
aperistaltic, biphasic or multiphasic.
Morphopathology
 The abdominal esophagus has normal dimensions.
 The thoracic esophagus is very dilated (dilatation
hasn’t any connection to age disease) The esophageal
wall may be very thin. The mucosa may be bold with
esophagitis or may be thin and atrophic.
 Cardia hasn’t any modification.
 The intramural plexuses of Meissner are altered
especially in the lower part of the esophagus.
History
 Sir Thomas Willis in 1672, was the first who described
the disease.
 In 1881, von Mikulicz described the disease as
cardiospasm to demonstrate that it is due to a
functional disorder not to a mechanical one.
Epidemiology
 Frequency: 1 to 100,000
 Sex: male/female = 1/1
 Age: 25-60 years; < 5% in children

Physiopathology
 Food accumulates in the esophagus leading to its
expansion and dilatation. After a while the food manage
to pass into the stomach according to the Hurst low – the
LES will open only when the intra-esophageal pressure
is high enough to force the opening. (The pressure is
higher then the LES contraction force – 20 cm of water
column). When the intra-esophageal pressure lowers,
the LES will close again and the food can not pass into
the stomach.
Symptoms
 Commonly achalasia appears in patients with
neuropathic disorders, in hypothyroidians, addicts, etc,
usually after strong emotions.
1. The debut is insidious
2. Dysphagia is capricious even paradoxical
3. Regurgitation of undigested foods
4. Retrosternal pains due to esophagus distension
5. Sialorrhea (Hyper salivation)
6. Fetid halitosis
7. Dyspnea, palpitations
Complications
1. Pulmonary complications are the most frequent as a
consequence of regurgitation.
2. Bleedings from ulceration of the esophagus mucosa.
3. Malignization is more frequent then in the absence of this disease
Diagnosis
 The main investigation is esophagography or
continuous fluoroscopy (barium swallow). On
radiograms the excessive dilatation of the esophagus
above the narrowing, with the absence of normal
peristaltic movements can be seen. The appearance is
like “bird’s beak” or similar to “sigmoid” colon. An air-
fluid margin is often seen.
 Esophagoscopy (endoscopic examination) shows the
permeability of the cardia.
 Esophageal manometry (esophageal motility study) –
measures the esophageal muscle’s tonus during
swallowing. Lack of LES relaxation and absence of
peristaltic movement are revealed.
Dilated esophagus

LES
Differential diagnosis
1. Cancer of the lower third of the
esophagus
2. Benign esophageal strictures
(postcaustic)
3. Schatzki ring
4. Esophageal diverticules
5. From outside compression of the
lower part of the esophagus
Treatment
 Nitrites and calcium channel blockers (nifedipine) –
produce a relaxation of LES – success in 10% of cases –
it is applied especially to elderly who do not support other
invasive procedures.
 Botox injections – applied by endoscopy approach –
success rate 30% - can induce inflammatory local
reactions which make more difficult an eventually
subsequent operation – it is also indicated in elderly.
 Pneumatic dilatation of LES –some muscle fibers are
disrupted - success rate 70-80%. More then 50% of
patients require more then one session – perforation rate
is about 5% - subsequent gastro-esophageal reflux rate
is about 25%
Surgical treatment - is indicated when other
conservative methods failed.
 HELLER’s procedure (extramucosal cardiomyotomy) -
it cuts the muscular layer (myotomy)
( of the inferior part
of the esophagus (LES). It can be performed by
laparotomy, laparoscopy or by thoracic approach.
 SAUERBRUCH’s procedure (eso-gastrostomy) - the
risk of gastro esophageal reflux is higher.
 SWEET-KAZANSKI’s procedure (polar superior
gastrectomy) – rarely applied.
Myotomy of the lower
esophagus (5 cm) and
proximal stomach (1.5 -
2.5 cm) followed by a
partial fundoplication to
prevent
gastroesophageal
reflux.
The operation relieves
symptoms in 85-95% of
patients, and the
incidence of
postoperative reflux is
10-15%.
Fundoplication
Sweet’s gastrectomy
Types of esogastrostomy
ESOPHAGEAL DIVERTICULA
1. Diverticula of pulsion (of pressure)
2. Diverticula of traction

 Diverticulus is a sacciforme dilatation of the

esophageal wall with various locations at
different levels which communicates with the
esophagus lumen through an opening of various
caliber.
 ZENKER’s diverticulum (of pressure)

History
 In 1877, Friedrich Albert von Zenker, professor of
pathology at Erlangen – Germany University, described it
first.
 At the beginning of the twenty century Killian
demonstrated that this diverticulum is produced through a
weak zone of the pharyngo-esophageal wall (the triangle
of Leimer or Killian’s dehiscence).
 In 1886 Wheeler is the firs doctor who performed a
resection of this kind of diverticulum.
 The Zenker diverticulum results from the posterior
herniation of the hypopharyngeal mucosa near its
junction with esophagus.
 To its occurrence contribute more factors exerted at the
level of Leimer's triangle:
– The natural weakness of this zone
– The increased pressure on this region during swallowing
process due to a lack of relaxation of the cricopharyngeal
muscle when the alimentary bolus arrives.
 It has a slow progressive evolution and may thus vary
in size from a beam to an apple or even to a head of a
foetus, determining compressions against the
esophagus.
 The clinical symptoms depend on the evolutive stage.
Epidemiology
 Prevalence: 0.01-0.1%
 Adults over 60 years
 Slight predominance in males
Symptoms.
 Deglutition disorders, progressive dysphagia without
pain (90% of patients), regurgitations, sialorrhea fetid
halitosis.
 May appear also cough and hoarnes due to
compression on laryngeal nerves.
 Regurgitations are produced mainly when the patient is
leaning forward – “shoelace sign”
 Sometimes the diverticulum may be observed as a
tumor bulging in the antero-lateral region of the neck.
Complications
 Weight loss
 Pneumonia of aspiration 30%
 Ulceration and perforation
 Eso-tracheal fistula
 Bleeding
 Esophageal stenosis
 Malignant transformation – squamous epithelioma (0.2-
0.4%)

Diagnosis - is based on radiological investigation.

Barium swallow and fluoroscopy. The endoscopic
examination has the risk of perforation.
Zenker’s diverticulum
Differential diagnosis must be done with:
1. Achalasia,
2. Esophagus tumors,
3. Esophageal strictures,
4. Esophagitis,
5. Aorta aneurism,
6. Mediastinal and pulmonary cysts.
Commonly the confusion is made with other fluid-air
formations of intrapulmonary or mediastinal
collections (abscesses, cysts, hydatid cyst).
Treatment
 Conservative in elderly and small size diverticulum
 Surgical
1. By left cervical approach
 Diverticulectomy
 Myotomy
 Myotomy + diveticulopexy
2. By endoscopic approach
 Stapler
 Laser
Resection of diverticulum using a lineal stapler
Myotomy
Myotomy + diverticulopexy
 Endoscopic stapling

A linear Endo-GIA stapler is used transorally to cut and

staple the inferior margin of the diverticulum opening,
enlarging it in a “V” shape.
 Diverticula with thoracic location
 Less frequent than cervical location
 Peribrochial location – when they are located near the
trachea bifurcation.
 Epidiaphragmatic (epiphrenic) location – located near
the diaphragm.
 Commonly they are of small dimension causing few
symptoms. Frequent are associated with other
esophageal affections.
 Surgical indication have only those diverticula with
severe symptoms or complications (esobronchial fistula)
 For peribronchial diverticula the surgical approach is
through a right thoracotomy and for epiphrenic location
the left thoracotomy.
Diverticulum

Hiatal hernia
 Diverticula of traction
 They have thoracic location.
 They are produced by traction exerted on esophagus by
adhesions with surrounding organs as the result of
inflammatory processes. (pleurisy, mediastinal
adenopathy, etc)
 No symptoms.
 They are discovered accidentally.
 Radiologic aspect is characteristic – cones with the tip
oriented upwards.
 Do not need any treatment.
ESOPHAGEAL CANCER
 As frequency it is on the 4th place after gastric, colon
and rectal cancer.
 Esophagus cancer is the most deadly cancer of the
alimentary tract, even more than pancreatic cancer.

Features:
1. Very extended in surface and depth.
2. Difficult to treat.
3. Treatment is followed by modest results.
Epidemiology
 Sex: It is 7 times more frequent in men as in women
 Age: average age is 69-70 years.
 Race: The squamous cancer is 3 times more often seen
in blacks, whereas adenocarcinoma is more frequent in
whites.
 Geographical distribution: It is 20-30 times more
frequent in China and other Asiatic countries than in US.
 Prognosis: Just 2/3 of treated patients survive at 2 years.
Etiology and risk factors
 The presence of risk factors doesn’t necessarily mean
that the cancer will appear, but the probability is much
higher.

1. Age > 55 years,

2. Smoking and alcohol abuse,
3. Hypoproteic, hypocaloric and rich in fats diet,
4. Gastroesophageal reflux and Barrett esophagitis,
5. Achalasia
6. Plummer-Vilson syndrome,
7. Tylosis (palmoplantar keratoderma)
8. Diverticula
9. Benign stenosis
10. Local radiations
Morphopathology
 Based on location it can be:
1. Of the superior 1/3
2. Of the mid 1/3
3. Of the inferior 1/3

 Based on histological aspect:

1. Squamous epithelioma (mostly spinocellular)
2. Glandular epithelioma - mostly in the lower part of
the esophagus (Adenocarcinoma)
3. Other rare forms of cancer: sarcoma (<1%),
lymphoma (1%), carcinoma with small cells (2%),
mucoepidermoid carcinoma(<1%), adenocystic
carcinoma (<1%) and spindle cell carcinoma (5%).
 Adenocarcinoma - its predilection location is the
lower part of the esophagus being encountered mostly in
high developed western countries.
 It represents more than 50% of all esophagus cancers.
 From histological point of view it is very similar to the
gastric cancer and is developed almost every time on a
base of Barrett ulcer.
 Approximately 1% of patients with Barrett ulcer will
develop a cancer during one year without treatment.
 Monitoring the patients with Barrett ulcer is indicated
because:
– 1) there is no evidence that the medical treatment will vanish the
risk of cancer
– 2) diagnosed in early stages it can be cured
The incidence of esophageal
cancer according to
esophagus segments
 Squamos cell epitelioma - is mostly encountered in
the upper part of the esophagus. Microscopic aspect is
initially as a plate and then exophytic and polypoid forms
may appear.

Cancer extension
 Tumoral cells will spread in surface and depth invading
surrounding tissues and organs (trachea, bronchus, aorta,
pleura, etc). An important feature is that local spread of
the tumor may be far from the original site due to enlarged
lymphatic network eyes, so multifocal tumors may be
encountered over a distance of 5-6 cm from the
originating tumor.
Stadialization
 Stadialization is of important value for treatment indications
and from prognosis point of view.
 It is important to be established before the beginning of
treatment. Unfortunately this goal is difficult to achieve
because the esophagus is an organ which is difficult to
explore.
 Many investigations are necessary to evaluate the
penetration of the tumor through the esophageal wall (T
stage) and also for lymph nodes involvement (N stage).
 The most useful investigations are:
– Esophagoscopy with multiple biopsies
– Endoluminal ultrasound examination
– CT scans and MRI scans
– Thoracoscopy and laparoscopy
 Even with all these investigation, many time a correct
stadialization can be done jus during operation. Don’t forget
that this type of cancer may be multifocal.
TNM classification

T stage
T1: Tu located on mucosa
T2: Tu has penetrated the muscularis layer
T3: Tu has penetrated the whole esophageal wall
T4: Tu is invading the surrounding tissues or organs
N stage
NX: nodules involvement can not be established
N0: there are no lymph nodes involved
N1: lymph nodes are affected by metastases
M stage (metastases):
MX: can not be appreciated
M0: there are no metastases
M1: there are metastases at distance
STAGES
STAGE I: T1 N0 M0
STAGE IIA: T2 N0 M0 or T3 N0 M0
STAGE IIB: T1 N1 M0 or T2 N1 M0
SGTAGE III: T3 N1 M0 OR T4 any N M0
STAGE IV: any T any N M1
Skinner’s WNM classification modified by Ellis
 This classification is more adapted to reality and
prognosis

W stage – grade of wall penetration.

N stage
1. N0 - without metastases
2. N1 – less than 5 lymph nodes are involved
3. N2 – more than 5 lymph nodes are involved
 Skinner’s WNM classification
modified by Ellis

Stage W N M
0 W0 N0 M0
W0 N1 M0
I
W1 N1 M0
W1 N1 M0
II
W2 N0 M0
III W2 N1 M0
W0 N2 M0
IV
any W any N M1
Lymphatic spread of tumor
Symptoms
 The onset is insidious and that’s why many patients are
diagnosed in advanced stages of evolution. The main
symptoms are:
1. Dysphagia – initially for solids and then for fluids
2. Important weight loss
3. Pain – retrosternal and epigastric
4. Superior digestive bleedings
5. Other symptoms from invaded or compressed organs
(cough, dispnoea, eso-tracheal fistula, etc)
Investigations
 The most important is endoscopy because of direct
visualization and biopsies can be performed.
 Radiological (barium swallow) investigation is also
very important to establish the precise location and
relations with surrounding organs.
– Axial or marginal stenosis, with rigid wall and lacunar aspects,
are the radiological features.
 Endoluminal ultrasound is important for T or W stage.
 CT and MRI scan for tumoral extension.
 Bronchoscopy is useful to reveal the penetration in
trachea and bronchial tree.
 Differential diagnosis with: benign stenosis, achalasia,
diverticula, reflux esophagitis.
 Esophageal
tumor
Midd third
Inferior third

Barium swallow
Endoscopic aspects
Endoscopic ultrasound examination

TU
Tumor
Treatment
 Treatment is complex and multimodal - mainly
surgical plus radio-chemotherapy (preoperative for
patients over 75 years for tumor conversion and also
postoperative)
 Other modalities of treatment are :
 With laser (tumor vaporization)
 Electrocoagulation
 Stents
Surgical treatment
 More aspects must be considered:
1. Most patients are elderly with associated illnesses
2. They are hypoproteic, cashectic through inanition.
3. With altered respiratory function which
contraindicates the thoracotomy.
 There are two types of operation:
1. CURATIVE, and
2. PALLIATIVE
 In choosing the type of operation that will be applied
some aspects must be considered:
1. Location of the tumor
2. Age of the patient
3. Biologic status
4. Tumor extension
5. Intraoperative staging
Location in the superior third of the esophagus
 Tumors in this location are mostly squamous being
encountered more frequently in women.
 Tumors located at the entrance in the thoracic cavity
are frequent inoperable due to early invasion of the
trachea and great vessels.
Location at the thoracic esophagus
 Those located in the superior part are frequently
inoperable due to rapid invasion of the surrounding
organs. They are operable only if they are not
penetrating the esophageal wall and are not spread in
more than 4 lymph nodes
 In those situations chemotherapy and radiotherapy
would be indicated as a first step for tumor conversion.
Location at abdominal esophagus and cardia
 Majority of them are adenocarcinoma and are suitable
for en-block resection.
1. Radical intention surgery: the goal is tumor ablation
by resection in oncological limits associated with loco-
regional lymph nodes excision and reestablishment of
the digestive tract continuity.
2. Palliative (operation of necessity when tumors are
evidently unresectable or the patients cannot be
operated):
– Palliative resections
– By-passes
– Stent application
– Different kinds of stomas for alimentation
(gastrostomy, jejunostomy)
Criteria for palliation:
1. Age over 75 years
2. Recurrent laryngeal nerve palsy
3. Horner syndrome
4. Spinal cord persistent pain
5. Diaphragmatic relaxation (phrenic nerve palsy)
6. Malign pleural effusion
7. Respiratory obstruction or eso-bronchial fistula
8. Length of the tumor more than 9 cm
9. More than 20% weight loss
10. Multiple lymph node metastases and metastases at
distance
11. Impaired ventilatory function FEV1 <1.25 L (FEV1; the
volume of air exhaled in one second during a forced
maximal exhalation)
12. Other
Preoperative preparation
 Volemic, proteic and hydro-electrolytic rebalancing.
 If there is a marked hypoproteinemia, a feeding
jejunostomy is the first step, and this is also useful in
postoperative period. Jejunostomy is preferable instead
of gastrostomy because the stomach will be probably
used for esophagoplasty.
 The colon must be prepared in the eventuality of an
esophagoplasty using the colon when stomach is not
suitable.
 All other comorbidities will be treated.
Gastrostomy
Extension of the resection
 Due to the extensive local spread, the resection must be
performed at least at 10 cm above the tumor and that
means, in almost all cases, total esophagectomy and
esophagus reconstruction using the stomach, colon or
small intestine.
 Resection and approaches depend very much on tumor
location.
Resection for cervical location
 Three approaches:
1. The first is the cervical approach – the esophagus is
discovered in the cervical portion and resecability is
assessed. If it resectable, the esophagus will be
sectioned above the tumor in oncological limits and
regional lymph nodes will be excised. If necessary
laryngectomy will be performed and also tracheotomy.
2. Right thoracic – Through a right postero-lateral
thoracotomy the thoracic esophagus will be dissected.
3. Abdominal – the stomach (gastric tube) or the colon is
prepared to be ascended in the cervical region to be
anastomosed with the esophagus.
 When the tumor is unresectable:
– Feeding gastrostomy
– Tracheostomy when the larynx is involved in the tumoral process
 1

3
Cervical approach

Thoracic approach
Esophageal resection for thoracic and
abdominal location of tumors
 Possibilities:
1. Resection en-block – with curative intention
2. Palliative resections
3. Other possible palliative operations
 Feeding gastrostomy
 Feeding jejunostomy
 Esophageal by-pass
Curative resection for thoracic location of
tumors
 2 or 3 approaches:
1. Starting with the thoracic approach through a right
postero-lateral thoracotomy and assessment of tumor
resecability. If the tumor is resectable, the esophagus and
lymphatic tissue are prepared and separated from
neighboring structures.
 If an intrathoracic anastomosis is planned in case of a
lower intrathoracic location of tumor (Ivor Lewis operation)
the esophagus is resected above the tumor. In this case
the cervical approach is not necessary.
 If a cervical anastomosis is planned the thoracotomy is
closed and two drainage tubes are placed in pleural
cavity, following the abdominal and cervical approaches.
 If the tumor is not resectable, a palliative operation is
chosen.
2. The next step is the abdominal approach. In this
stage the abdominal metastases are assessed and
also the modality of esophageal reconstruction using
the stomach or the colon. In this phase it is still
possible to abandon the esophagectomy. The stomach
or colon is prepared for esophagoplasty.
3. The cervical approach is used when the entire
esophagus is replaced by a gastric tube or the colon
and the anastomosis is performed in the cervical
region. The esophagus is sectioned in the cervical
region. From this point, there is no possibility to return
– esophagectomy and esophagoplasty must be
performed. The stomach or the colon is ascended in
the cervical region and the anstomosis is performed
reestablishing the continuity of the digestive tract.
Curative resections for the tumors of the
abdominal esophagus
 The operation starts with the abdominal approach. The
resecability is assessed and also if the stomach can be
used for esopahgoplasty.
 There are two main possibilities for continuing the
operation:
1. By transhiatal approach (Orringer Akiyama), or
2. By right thoracotomy (Ivor Lewis operation)
There are other possibilities also.
Operations may be performed :
1. By laparoscopic approach, or
2. By thoracoscopic approach
Transhiatal esophagoplasty (Orringer Akiyama)
 There are two approaches: the first is abdominal and the
second cervical.
 The abdominal esophagus is prepared first and then the
thoracic esophagus by blunt dissection using fingers
closely applied to the esophagus through the
diphragmatic hiatus. The esophagus is separated by
surrounding organs. Bleeding is minimal due to poor
vascularisation.
 Through the left cervical incision the cervical esophagus
is found and separated. Then it is dissected downwards
using the same blunt dissection until both hands meet in
the mediastinum. The esophagus is transected in the
cervical region and then stripped out through the hiatus.
In most cases pleural lesions will not occur.
Transhiatal esophagectomy
 Cervical incision

The cervical
Esophagus prepared

Blunt dissection along the

thoracic esophagus
 The greater curvature of the
stomach is used for the new
esophagus. The lesser
curvature is resected.
Resection can be performed
more easily using staplers.
 As both vagus nerves are also
resected a pylorotomy is
needed (after vagotomy the
pylorus becomes hypetonic).
 The arterial supply of the
gastric tube will be ensured
only by the gastroepiploic
arteries which must be
carefully protected against
damages.
Stripped esophagus Esophagus

Tumor

Stomach
Stomach

Gastric tube made using staplers

Making the gastric tube by hand sewing
 The gastric tube is ascended orthotopic in the cervical
region where the eso-gastric anstomosis is performed.
 When the stomach is not suitable for esophagoplasty
(small stomach, previous operations on stomach, etc),
the most frequent organ used is the colon (ascending or
transverse colon especially). The colon must be
prepared before operation.
 When the right colon is used the ileocolic and right colic
vessels are resected and also appendectomy is
performed. The arterial supply will be ensured by the
middle colic artery or left colic artery. The cecum is
ascended to the cervical region either in orthotopic
position or via retrosternal route. The transverse colon is
sectioned and the proximal end is anastomosed to the
stomach. The distal end is closed and the digestive tract
is reestablished by ileotransversostomy. The ascending
colon will be in isoperistaltic position facilitating the
swallowing.
Cervical region

Cecum

As
ce
nd
ing
co
lon
Transverse colon

Esophagoplasty using the ascending colon

Ivor –Lewis operation
 In this type of operation the inferior portion of the
esophagus and the upper part of the stomach are
resected, and the anstomosis is performed inside the
right thoracic cavity. The operation presumes a double
approach: right thoracotomy and laparotomy.
 Through the thoracic approach the esophagus is
dissected and resected above the tumor. Through the
abdominal approach the upper part of the stomach is
resected also. The stomach is then ascended into the
right hemithorax and the anstomosis between the two
organs is performed. At the end the right pleural cavity is
drained and drains are sealed under water (Bulau).
 Pylorotomy is also needed because the both vagus
nerves are transected.
 The removed esophagus may be replaced by other parts
of the digestive tract such as stomach, colon (right or
transverse most often) or small intestine. Small intestine,
even it has a very good vascular supply, is rarely used
due to short mesentery which does not allow ascending
it till the cervical region.
 In these kinds of operations preserving a good vascular
supply of the digestive segment used for esophagoplasty
is of utmost importance to prevent necrosis or
anstomotic leaks.
Palliative operations
 Palliative resections are indicated just for tumors of the
distal esophagus.
 By-passes (the colon being used mostly) – are rarely
performed due to the bad prognosis
 Feeding stomas are frequently used in preoperative
period and also in unresectable cases
– Gastrostomy
– Jejunostomy
 Endoscopic procedures are less invasive
– Stents – unfortunately expensive
– Laser
– Other
Gastrostomies
 Braun Pezzer tube

Witzel jejunostomy on omega loop with

Braun fistula
Esophageal stent
 Prognosis

Avg. survival Survival rate at 5

years

Radical intention 2 years 25-30%

treatment
Palliative 6-7 month <5%
treatment
ESOPHAGEAL VARICES
 Esophageal varices are dilated veins in the esophageal
wall under the mucosa layer, due to increased pressure
in portal vascular system.
 They have been first described by Wolf în 1928.
 Due to the gravitational forces, varices are located
mainly in the lower third of the esophagus. Varices may
be also found in the upper portion of the stomach.
 Portal vein with a caliber of 6-8 mm is formed by
confluence of superior mesenteric vein with the splenic
vein behind the head of the pancreas.
 The blood flow in the portal vein is about 1.5 l/min
representing ¼ from cardiac output.
 Portal vein supplies 75% of blood volume that passes
through the liver and 60% of its oxygen.
Portal vascular system
 Normal portal vein pressure is 5 mm Hg. Pressure
above this value leads for the first to splenomegaly and
thrombocytopenia.
 The esophageal varices are a later complication which
appears at values above 12 mmHg in portal pressure.
 The rupture risk of varices is 9% at a pressure of 13
mmHg and it rises at 72% at a pressure of 17 mmHg.
 The main complication of varices is BLEEDING
 When bleeding occurs, the patient becomes a major
emergency case.
 Almost 50% of patients will develop bleeding from
varices.
 Even though gastric varices are bleeding less frequently
than esophageal, the hemorrhage is more severe and
associated with a higher mortality rate.
 Mortality rate in ruptured esophageal varices is 40-70%
at the first manifestation.
 Bleeding will stop spontaneously in about 60-70% of
cases. However rebleeding will occur in 40% of cases in
the next 72 hours. Every bleeding episode will shadow
more an more the prognosis.
 The high mortality rate comes from some factors as:
– Liver insufficiency
– Sepsis
– Exsanguination
– Brain edema
– Complications of the anemia
 Superior digestive bleeding is the most difficult to treat
when it is due to cirrhosis and portal hypertension.
 Fast evolution, high frequency of bleeding events,
jaundice, ascites and neuropsychiatric manifestations
are factors of severe prognosis.
 Association between cirrhosis and peptic (gastric,
duodenal) ulcer is well known and rises the risk because
the cirrhotic patient will bleed 2 times more frequently
than the patient without ulcer and 3 times more than
those with ulcer but without cirrhosis.
 Hematemesis in patients with liver cirrhosis may occur
from 3 sources:
– Esophageal varices – 50% of cases
– Gastric varices – 30% of cases
– Gastro-duodenal ulcer – 9% of cases
– Combined sources
Causes of portal hypertension
 Prehepatic (portal vein obstruction)
– Congenital atresia or stenosis
– Portal vein thrombosis
– Splenic vein thrombosis
– Extrinsic compression (tumors)

 Hepatic
– Cirrhosis
– Congenital liver fibrosis
– Idiopatic portal hypertension
– Schistosomiasis

 Posthepatic
– Budd.Chiari syndrome
– Constrictive pericarditits
– Arterio-portal fistula
– Increased splenic flow
Clinical aspects. In cirrhosis the following aspects may
be noticed:
1. Distended abdomen, Ascites, Splenomegaly,
Hepatomegaly
2. Visible venous network even periumbilical “jelly fish
head” aspect (caput medusa)
3. Cruveilhier-Baumgarten murmur (heard in epigastric
region due to collateral connection between portal
system and repermeabilised umbilical vein)
4. Spider angiomata
5. Gynecomastia, testicular atrophy and disappearance
of men pattern hair in men
6. Carmine lips, palmar erythema
7. Hemorrhoids
8. Jaundice
9. Encephalopathy manifestation
10. etc
Laboratory data - reveal the liver impaired function and
immunosuppression:
1. Albumin levels are low
2. Decreased values of coagulation factors (II, V, VII,
IX, and X)
3. Hyperamonemia
4. Thrombocytopenia, Leukopenia, Neutropenia
5. Anaemia
6. Aminotransferases (AST and ALT), bilirubin, are
elevated
7. Others
Child-Pugh classification of cirrhosis

Score 1 Score 2 Score 3

Criteria
Ascites Absent Moderate Severe
Encephalopathy Absent Moderate Severe till coma
Albumin (g/L) > 3,5 2,8 – 3,5 < 2,8
Bilirubin (mg/dL) <2 2–3 >3
Prothrombin time (sec. over 1–4 4–6 >6
normal value)

CIRRHOSIS CLASSES
A = score 5 -6
B = score 7 - 9
C = score 10 and higher
The higher the score the worse prognosis.
Paraclinic diagnosis of varices
 Esophageal varices are diagnosed most frequently by
endoscopic investigation (esophagoscopy) and more
rarely by barium swallow (esophagography).
Endoscopic aspects and classification of esophageal
varices

Grade Endoscopic aspect

I. Dilated veins (< 5mm) limited to the mucosa
II. Straight dilated veins (> 5 mm) bulging in lumen
III. Tortuous large veins which partially obstruct the
lumen
IV. The lumen is completely obstructed by enlarged
veins and there are “cherry red spots and red
sign” with a high risk or rupture
 Abdominal ultrasound investigation is a harmless
investigation but it can not directly observe the varices. On
the other hand it offers many important information such
as:
1. Morphology and dimensions of liver and spleen,
2. Vascular information: portal, mesenteric and splenic
veins diameters, presence of portal cavernoma,
repermeabilization of umbilical vein, etc.
3. Presence of ascites
4. Duplex Doppler Sonography can detect the direction of
blood stream in the portal system.
 CT and MRI scans give extra information about
anatomical structures and the morphology of the portal
system and the aetiology of portal hypertension. It is used
mainly when a porto-systemic shunt is proposed or in case
of liver transplant.
 Angiographic examinations
1. Splenoportography – rarely used in now days
2. Selective arteriography of the superior mesenteric
artery – venous phase
3. Transhepatic portography
4. Hepatic phlebography
Imagistic criteria for portal hypertension
diagnosis are:
1. Portal vein diameter >13mm (57% sensitivity, 100%
specificity)
2. Superior mesenteric and splenic veins diameter >10
mm
3. Gastric vein diameter >4mm
4. Recanalization of umbilical vein >3mm (Cruveilhier-
von Baumgarten syndrome)
5. Lack of respiratory increasing of splanchnic veins
diameter (80% sensitivity, 100% specificity)
6. Esophageal and gastric varices
7. Hepatic centrifugal venous flux (82% sensitivity,
100% specificity)
8. Portal cavernoma
9. Splenomegaly
10. Ascites
Differential diagnosis: with other causes of
upper digestive bleeding
1. Esophagus carcinoma
2. Superior vena cava obstruction
3. Klippel-Trenaunay and Parkes-Weber – syndromes
(rare)
4. Gastro-duodenal ulcer
5. Haemorrhagic gastritis (medication)
6. Gastric cancer
7. Mallory-Weis syndrome
8. Diverse coagulopaties
9. Other causes of haemathemesis
 The diagnosis is quite easy in the presence of other
symptoms and signs of cirrhosis but must be confirmed
by endoscopy.
Treatment
 In emergency
– Haemostasis by compression using the Sengstaken- Blakemore or
Linton-Nachlas tube.
– Surgical haemostasis
– Medical treatment
 Elective
– Surgical decrease of portal pressure (portosystemic shunts, azigo-
portal deconnection)
– TIPS (Transjugular Intrahepatic Portosystemic Shunt)
 Endoscopic treatment
– Rubber band ligation
– Sclerotizing substances (Sodium Tetradecyl Sulfat, Cyanoacrylat)
– Coagulation with Argon plasma
 Maintaining
– Medical – medicines
– Lifestyle changes
– Diet etc,
 Liver transplant
Treatment of superior digestive bleeding in
emergency condition
 The primary goal is to stop the bleeding and rebalance
the patient (these are performed simultaneously).
1. Rapid clinical evaluation of the patient (blood pressure,
heart rate, temperature, blood oxygenation, central
venous pressure, diuresis, etc).
2. Mounting a central venous catheter for fluids
administration and other drugs.
3. Urinary catheter.
4. Orotracheal intubation if the patient is unconscious.
5. Nasogastric tube insertion to evaluate the bleeding and
gastric lavage (not recommended by some authors
because it may produce rupture of the varices)
Resuscitation
 If blood transfusion is not available in the first moment,
intravenous albumin in saline solution or saline will be
administered in patients without ascites or other signs of
hepatic decompensation.
 Once the fluid has been restored, solution with low sodium
(dextrose 5%) is administered.
 Fresh frozen plasma is administered to patients requiring
massive blood transfusions. Hematocrit must be brought
and maintained at the minimum of 30%.
 Calcium is also administered.
 Platelets are given when platelets are < 50.000/mL.
 Gastric emptying, lavage, enemas and administration of
lactulose for decreasing the amonemia.
 Absorbable oral antibiotics should be given for the same
purpose (Neomycin 4x1 gr / day for a week).
 The patient will receive treatment with vitamin K.
Pharmacotherapy
 Octreotide acetate (Sandostatin) - by inhibiting the
release of vasodilators hormones (eg glucagon) indirectly
produce vasoconstriction in splanchnic territory with the
consequent decrease in portal flow. Should be
administered iv. in dose of 50 micrograms for 5-10 min
followed by a maintenance dose of 50 micrograms / hour
for 3-5 days.
 Vasopressin (Pitressin) (posterior pituitary hormone)
produced direct vasoconstriction of vessels on splanschic
territory being able to reduce 60-75% of variceal bleeding
by reducing portal flow. There are several side effects by
vasoconstriction in other areas (heart, intestines, etc.). It
is given iv. dose of 20 units for 20-30 min, and then 0.2 to
0.4 units/min. Along with vasopressin and nitroglycerin is
administered to counteract the vasoconstrictor effects on
the myocardium.
 Ocreotide or vasopressin may be discontinued after 24
hours of cessation of bleeding.
Hemostasis by balloon tamponade
 The most commonly used is the Sengstaken-Blakemore
tube. The method has a success rate of 90% in stopping
bleeding but is very unpleasant for the patient and has
certain risks (pulmonary aspiration, esophageal rupture,
esophageal mucosa injury and ulceration, etc.) with a
mortality rate of 5%.
 The tube can be used for gastric lavage and monitoring
of any bleeding from associated peptic ulcer.
 Linton-Nachlas tube has one pear-shaped balloon and is
indicated for bleeding from gastric varices.
 Balloons must be deflated after 24 hours and if the
bleeding has stopped and there is no possibility of
endoscopic methods, the tube will remain in place since
a few days for a possible recurrence of bleeding when
the balloons can be reinflated.
Sengstaken-Blakemore tube
Linton-Nachlas tube
Hemostasis by balloon tamponade
Endoscopic procdures
 Endoscopic procedures for definitive hemostasis must
be applied as soon as possible if the bleeding can be
controlled by pharmacotherapy methods.
 Sclerotherapy and ligation have a success rate higher
than hemostasis with balloon tamponade.
 Both methods are effective, but ligation is encumbered
by fewer complications as sclerotherapy (bleeding,
perforation, necrosis, stenosis, pleural collections, etc.).
 Concomitant use of Vasopresin and Ocreotide increases
the success rate in these maneuvers.
Hemostatic surgery
 If the bleeding could not be stopped by tamponade
or/and drugs, or the hospital do not have endoscopy
facility, or bleeding could not be solved by repeated
endoscopic maneuvers, hemostatic surgery, is required.
 Minimum possible intervention is exploratory laparotomy
with longitudinal gastrotomy and haemostasis by ligation
of sight bleeding varices usually located in the fornix or
pericardial.
 Other more laborious maneuvers such as porto-
systemic shunts or azigo-portal deconnection are
burdened by high mortality in emergency. But when
there are no other solutions, they may be performed in
emergency condition also.
TIPS (Transjugular Intrahepatic Portosystemic Shunt)
 A better alternative to surgical solution, is TIPS, which can
be a preceding procedure in liver transplantation.
 Under flouroscopic guidance, a catheter is inserted by
transjugular approach through a suprahepatic vein,
transhepatic into an important branch of portal vein.
 The transhepatic path is dilated with a balloon and then a
metal stent is insert which keeps the path open and
connects the portal to systemic circulation. The shunt
reduces pressure in the portal vein and in distended
varices.
 The method is burdened by risks of immediate
complications (hematoma, liver capsule rupture, pulmonary
edema, etc.) and late: portal encephalopathy (20-35%),
shunt stenosis and thrombosis, recurrent bleeding.
 Its mortality risk is only 10% which is a major advantage
over surgery.
 The Sugiura-Futagawa procedure introduced in 1967 is
a non-shunting operation to treat bleeding from
esophageal varices. Esophageal transection is
associated with devascularization of left esophageal and
gastric border starting intra-thoracic from the lower
pulmonary vein and continuing intra-abdominal peri-
gastric plus ligation of short gastric vessels, splenectomy,
vagotomy and pyloroplasty.
 Bataglia and collaborators, performs: a transection of
the eso-gastric junction and reanastomoses it with a
stapler plus devascularization of the top half of gastric
body, devascularization of the last 10 - 12 cm of thoracic
esophagus and performs an antireflux fundoplication, all
made exclusively by laparotomy approach, with
splenectomy only in case of severe hypersplenism.
Azigo-portal deconnection Sugiura-Futagawa
 Elective surgical treatment

Contraindications for surgery:

1. jaundice + ascites + edema + liver atrophy, or
2. jaundice + ascites + increased amonemia

 Since the introduction of porto-caval shunt by Whipple

in 1945, portal hypertension surgery has evolved
steadily.
Vascular surgical procedures to reduce portal
pressure (porto-systemic shunts)
 Such surgery is applied as secondary prevention only
after the failure of other less invasive methods for the
prevention of bleeding from esophageal varices.
 However, in these situations, besides the liver
transplantation, these methods are the only giving the
chance of survival.
 The aim is to decrease the portal pressure by derivation
through the shunt of the portal blood into the systemic
circulation. In most cases there will be also a beneficial
effect on ascites in cirrhosis.
 This shunt, however, may have some negative effects on
the brain (portal encephalopathy) that must be taken into
account.
 Throughout history a high variety of shunts have
developed which proves that none is ideal.
 In principle there are two types of shunts:
A. Troncular shunts:
1. Termino-lateral portacaval shunt (TANSINI)
2. Double portacaval shunt Mc Dermott
3. Latero-lateral portacaval shunt (ECK)
 The disadvantage is the decrease of portal flow in liver
accelerating the development of liver failure.
B. Radicular shunts
1. Termino-lateral mesenteric-caval shunt (BOGORAZ,
DRAPPANAS)
2. Termino-lateral cavo-mesenteric shunt (MARION),
3. Mezenterico-caval in "H" shunt with Dacron graft (DRAPANAS-
BANCU-PAPAI),
4. Spleno-renal shunt (after splenectomy) (BLAKEMORE-LINTON),
5. Distal spleno-renal shunt (WARREN) - most often used
6. Coronaro-caval shunt (INOGUCHI),
7. Spleno-renal shunt with interposition and ligation of splenic vein
before flowing into the portal vein (NAGASUE),
8. Porta-renal shunt (left renal vein is implanted in the portal,
mesenteric or splenic vein)
9. Omfalo-caval shunt,
10. Spleno-caval shunt (ASADA),
11. Spleno-suprarenal shunt
• In Warren procedure:
• The distal end of the splenic vein is connected to the left renal vein
and the left gastric vein is disconnected from the portal vein. The
results are:
1. The blood reflux from porta to the stomach lowers
2. The blood flows from the varices through the splenic vein, to the
left renal vein and empties into the inferior vena cava.
3. Pressure in the varices lowers
4. The blood flow to the liver is maintained through the portal vein.
 Portal hypertension surgery is a palliative surgery.
 Its primary aim is to stop the bleeding.
 It has an increased rate of postoperative morbidity
and mortality.
 Most common postoperative complications are:
1. Portal encephalopathy
2. Rebleeding
3. Shunt thrombosis
 Liver transplant remains the surgical option for cure.
SURGICAL PATHOLOGY OF
THE STOMACH AND
DUODENUM
 Surgical anatomy
1. Peptic ulcer
– Gastric ulcer
– Duodenal ulcer
2. Gastric cancer
3. Gastric volvulus
4. Operated stomach pathology
The stomach
Anatomy
 The stomach is the most dilated portion of the digestive
tract between the esophagus and small intestine. It is an
intraperitoneal organ.
 Gastric capacity = 1000-1500 ml.
 The stomach is held in place by ligaments, anatomical
structures more or less loose which give it a certain
mobility. The most fixed areas are: the cardia -which
continues the esophagus, and pylorus - continuing with
the duodenum. Excessive laxity of the ligaments may
cause gastric volvulus.
 The stomach has two faces, two curves and two
openings (cardia and pylrus).
Ligaments of the stomach
1 gastrocolic
2 gastrosplenic
3 gastrofrenic
4 gastrohepatic – pars flacida
5 gastrohepatic – pars densa
 Behind the stomach there is a virtual cavity named
“bursa omentalis” which communicates with the
peritoneal cavity through the Winslow hiatus (Epiploic
foramen). This aspect is important because the cavity
may become the place of different kind of collections
during pathological processes (retrogastric abscess
during peritonitis, pancreatic pseudocyst in acute
pancreatitis, etc).
 Through the Winslow foramen, incarcerated internal
hernia of Treitz may occur.
 Relations with the surrounding organs are important
especially in case of gastric tumors which can penetrate
these organs (pancreas, colon, mesocolon, spleen,
liver).
Arterial supply
The stomach has a very good vascular supply. It has 4
arterial sources, all from the celiac trunk. These arteries
form two vascular arches along the two curves.
1. Left gastric artery (coronary) - from the celiac trunk
2. Right gastric artery (pyloric) – from the hepatic artery
3. Left gastroepiploic artery – from the splenic artery
4. Right gastroepiploic artery – from the gastroduodenal
artery

Venous drainage
 The veins have the same trajects as the arteries and
they flow into the portal system. Left and right gastric
veins flow directly into the portal vein, the left
gastroepiloic via the splenic vein and right gastroepiploic
vein via the superior mesenteric vein.
Lymphatic drainage
 There are four areas of lymphatic drainage of the
stomach:
– area I- the superior region of the lesser curvature from where the
lymph is drained towards the lymph nodes around the gastric
artery, celiac trunk and right paracardial.
– area II- antral region of the lesser curvature is drained towards
suprapyloric and hepatic pedicle’s nodes.
– area III- the superior region of the greater curvature is drained
towards the lymph nodes of left gastro-epiploic artery, spleen
hilum and left paracardial.
– area IV- antral region of the grater curvature is drained towards
the lymph nodes of the right gastro-epiploic artery and
subpyloric.
 Knowing the lymphatic drainage of the stomach is
important, to be able to perform radical oncological
operations that besides removing the tumoral area
should also perform regional lymphadenectomy
according to the lymphatic drainage map.
 There have been described 16 groups of lymph nodes
draining the stomach, of particular importance in lymphatic
excision in surgical treatment of gastric cancer:
1. Right paracardial 9. At celiac trunk
2. Left paracardial 10. From spleen hilum
3. Along the lesser 11. Along the splenic artery
curvature 12. In the hepato-duodenal
4. Along the grater ligament
curvature 13. Retroduodenopancreatic
5. Right suprapyloric 14. At the origin of the
6. Subpyloric superior mesenteric
7. Along the left gastric artery
artery 15. Along the mid colic artery
8. Along the common 16. Paraaorto-caval
hepatic artery
Innervation
 Knowing it is important to understand various
physiological processes of motility and gastric secretion,
very important in gastric surgery especially in peptic ulcer.
 Sympathetic innervation is derived from spinal segments
T5-T10 through the great splanchnic nerve and celiac
ganglia and also from fibers of perivascular plexuses.
 Parasympathetic innervation is provided by the 2 vagus
nerves (anterior and posterior).
 The two vagus nerves innervate the digestive tract till the
transverse colon. Lesions of these nerves will affect more
or less the function of these organs.
 Vagus nerves ramify into more branches like: direct
branches, hepatobilliary branches and two motor nerves
(Latarjet). Cutting the Latarjet nerves will results in atony
of the antrum ("gastric mill") and spasm of the pylorus.
Vagus nerves
Gastric wall structure
 The stomach has the thickest wall from all segments of
the digestive tract.
 The layers from outside to inside are:
– Serosa (visceral peritoneum)
– Muscular: longitudinal (outer), circular (mid), oblique
(inner).
– Submucosa - composed of loose connective tissue, full
of vascular, lymphatic and nervous (Meissner)
plexuses. Vascular plexuses are particularly well
represented, making a true "sponge filled with blood."
– Mucosa - forms longitudinal and transverse folds
(rugae). Gastric glands, simple or ramified, tubular
type, are named after the region where they are found:
cardial, fundic, pyloric. Antral mucosa cells have
endocrine secretory function, the best represented
being the gastrin-secreting G cells.
Gastric wall layers
 Type of cells:
1. Mucus producing cells
2. Parietal cells – producing HCl
3. Zymogen cells – producing pepsine
4. Endocrine cells
1. G cells producing gastrin
2. ECL (enterochromaffin-like cells) producing histamine
3. Delta cells producing somatostatin
 The gastric juice secreted in amount of 1.2-1.5 liters
per day is a colorless, clear to slightly opalescent fluid,
with a very low pH because HCl content. It contains
99% water and 1% solids: organic and anorganic.
 Gastric mucus - secreted by epithelial and mucous cells
of the fundic and pyloric glands. It provides physical
protection against ingested particles and prevents direct
contact between the HCl and digestive enzymes and the
underlying mucosa.
 HCl roles:
– Activates the pepsinogen to pepsin
– Breaks down food proteins in more digestible forms of
acidoproteins
– Solubilizes the nucleoproteins and collagen
– Converts Fe3 + to absorbable Fe2 +
– Antiseptic role – due to its corrosiveness the HCl kills
any pathogens. HCl is so strong that if it wasn't for the
mucous membrane that protects the stomach lining,
the acid would digest the stomach.
– Stimulates the Delta cells producing somatostatin
 Digestive enzymes:
1. Pepsin -a proteolytic enzyme secreted in the inactive form of
pepsinogen.
2. Labferment (gastric rennin, from the gastric secretion of
newborn babies) is involved in casein coagulation.
3. Gastric lipase acts on short chain fatty acids, being important in
infants.
4. Cathepsin - proteolytic enzyme, plays a role especially in
infants.
5. Gelatinase - degrades the gelatin 400 times more intense than
pepsin.
6. Other enzymes, carbonic anhydrase, lysozyme, gastric urease.
 Intrinsic factor (Castle) - secreted by parietal cells is
involved in the absorption of vitamin B12 (Castle
extrinsic factor).
Physiology
 The stomach has a motor and secretory function,
particularly important in the early stages of digestion.
 Motor function allows the storage of foods, their kneading
and mixing with digestive juices and their progression into
the duodenum. The stomach is normally completely
emptied in 3-4 hours.
 Motor activity of gastric emptying ( "anthro-pyloric pump")
is ensured by gastric antral peristaltic waves with a
regularity of 3/minute. The function is controlled by vagal
and sympathetic autonomic nerves and also by some
hormones.
 Secretory function is exocrine and endocrine.
 Exocrine function = gastric juice, with intense acid pH, in
volume of 1,5-3 l/24 hours. It is composed of
hydrochloric acid, enzymes (pepsinogen) and mucus.
 Endocrine function – the stomach wall secretes several
polypeptides with hormonal role, of which the best
known are gastrin and somatostatin.
– Gastrin is secreted in the antrum. Gastrin acts on
enterochromaffin-like cells in the gastric corpus to
release histamine, which stimulates parietal cells to
produce acid.
– Somatostatin has a role in regulating acid secretion
and gastrin secretion.
 Regulation of gastric secretion– there is a complexe
neuro-endocrine mechanism that regulates the
secretion in three phases:
1. The cephalic phase - as much as 20-50 % of the maximal acid
response to a meal – in this phase the vagal mechanism plays
the principal role.
2. The gastric phase – the endocrine regulation is the most
important but also the vago-vagal reflexes mediate acid
response to distension.
3. The intestinal phase (5 - 10% response) by cholinergic neural
regulation and by endocrine regulation through Gastrin,
Secretine and Cholecystokinin.
 Vagus nerves play an important role on the regulation
of acid secretion, gastrin release, and histamine
production. On this fact is based the vagotomy as a
method of treatment of peptic ulcer which was
introduced in practice by Dragstedt in 1943.
 The cephalic phase of acid secretion occurs even before
food enters the stomach. Secretion is stimulated by the
sight, smell, thought, or taste of food. When appetite is
depressed this part of the cephalic reflex is inhibited.
From the cortex stimuli are transmitted to the amygdala
and hypothalamus and through the dorsal motor nuclei
of the vagi to the vagus nerves.
 Important role in this stimulation have the excitatory
action of thyrotropin-releasing hormone (TRH) as well as
the serotonin containing neurons.
The duodenum
 Duodenum, is the initial portion of the small intestine
being the most fixed part. It extends between pylorus
and duodeno-jejunal flexure (Treitz angle).
 Duodenum is a secondary retroperitoneal organ being
covered by peritoneum (coalescence fascia of Treitz).
Due to its retroperitoneal position it is an organ which is
difficult to approach during operation.
 Duodenum has a horseshoe shape being divided into
four parts:
1. Top (D1) - duodenal bulb
2. Descending (D2)
3. Horizontal (D3)
4. Ascending (D4)
 The duodenum is neighboring with many organs:
– D1 with: the liver, gallbladder and liver pedicle
– D2 with: the liver, gallbladder, right kidney,
transverse mesocolon, right colon and intestinal
loops
– D3 : anterior with the root of mesentery (superior
mesenteric artery and vein) and posterior with the
aorta
– D4 with: gastric antrum, jejunal loops and bursa
omentalis
 Duodenal wall structure: There are 4 layers: serosa,
muscular, submucosa, and mucosa.
 The circular folds (Kerkring) are missing in the upper
portion. Brunner glands, specific to the duodenum, are
more common in D1. Secretion of these glands is clear,
viscous, alkaline (pH 8,2-9,3). In the mucosa there are
also Lieberkuhn intestinal glands.
 Although duodenal vascularization is quite rich, the
retroperitoneal duodenal wall is not a good material to be
sutured and anastomoses are at high risk primarily due
to the lack of visceral peritoneum (except D1), also due
to the poor developed muscular layer and to the bilio-
pancreatic content which is intensive peptic.
Physiology
 In duodenum the food is mixed with the biliary and
pancreatic secretion necessary for digestion. The acid
content of the stomach entering the duodenum is
neutralized by the alkaline secretions of the duodenum.
 Secretin and cholecystokinin hormones are released
from cells of the duodenal epithelium as a response to
acidic and fatty stimuli when gastric chyme reaches into
the duodenum.
– Secretin is a hormone with regulatory effect on the pH of the
duodenal contents via the control of gastric acid secretion and
buffering with bicarbonate from pancreas.
– Cholecystokinin causes the release of digestive enzymes and
bile from the pancreas and gallbladder, respectively. It also acts
as a hunger suppressant.
PEPTIC ULCER
 Peptic ulcer is a local anatomical expression of a
general disease. It is mostly located in the stomach or
duodenum, and less often in another segment of the
digestive tract.
 It is represented by an ulceration located initially on the
mucosa and then penetrating gradually all the other
layers of the wall.
 For many years it was considered that it is the result of
faulty lifestyle, particularly in terms of stress and diet, but
modern theories associate ulcers with bacterial infection
and the use of drugs.
 Gastric ulcer and duodenal ulcer was associated under
the generic name of "ulcer disease" or “gastro-duodenal
ulcer”. As knowledge has progressed it was found that
gastric ulcer und duodenal ulcer are two distinct
diseases which have more differences than similarities.
For this reason the two conditions should be treated
separately.
GASTRIC ULCER
 The incidence increases steadily with age, the tip
being reached in the 6th decade of life.
 The ratio between men and women is 2/1 but in India
is about 18/1.
 Only in Japan the gastric ulcer is more common than
duodenal ulcer (1 case per 1,000).
Etiopathogenesis
 The predominant role in the etiology of gastric ulcer is
the less efficiency of local defense factors as a result
of the imbalance that occurs between aggression and
defense factors of the gastric mucosa.
 Gastric mucosal defense factors are:
1. The viscous alkaline mucus
2. The tight connection between gastric epithelial cells
3. The renewal of epithelium lining every 3 days
 Aggression factors are:
1. Acid-peptic hypersecretion
2. Gastric motility disorders in gastric stasis or delayed emptying
3. Duodenal-gastric reflux which impairs the mucus barrier
4. Helicobacter pylori infection is less important in the genesis of
gastric ulcers than in the duodenal ulcer. It was found only in 20%
of cases, while in the etiology of duodenal ulcer in 90% of cases.
5. Exogenous factors: treatment with nonsteroidal anti-inflammatory
drugs, intra-arterial chemotherapy, cortisone, excessive use of
laxatives.
6. Smoking, stress
7. Zollinger Elisson syndrome
8. Genetic factors (blood group O)
 Depending on their depth ulcers may be acute or
chronic.
 The most frequent location is the lesser curvature. Then
follows, in order: anterior wall, posterior wall, prepyloric
region, grater curvature. Almost half of gastric ulcers are
located in the antral region.

Helicobacter pylori
Johnson’s classification of gastric ulcers
depending on location and secretory status:
 Type I: ulcers located high on upper part of the lesser curvature. Acid
secretion is reduced to normal values. Gastritis and duodenal reflux
occurs. The incidence is 50-60% of patients.
 Type II: located on the lesser gastric curvature, and associated with
pyloric or duodenal ulcer. The level of gastric secretion may be normal
or increased and gastric emptying is delayed. It is considered
secondary to duodenal ulcer and appears in 23-25% of cases.
 Type III: ulcer is located in antrum, prepyloric, which acts as a
symptomatic duodenal ulcer. Is associated with acid hypersecretion.
 To this classification Conter and Kauffman added two new types: type
IV, ulcer on the lesser curvature near the gastroesophageal junction
and type V: ulcer at any location appeared after consumption of
aspirin or NSAIDs.
Gastric ulcers classification
Symptoms
 The evolution is in acute episodes interrupted by
asymptomatic periods.
 The main symptom is pain, usually epigastric, but other
locations are possible depending on the location of the
lesion. It is like burning, cramping, twisting or lancinant,
induced or exacerbated by food ingestion and relieved
by evacuation of the stomach.
 Nausea and vomiting appear inconsistent in disorders
of gastric evacuation. Vomiting often have a calming
effect on pain.
 Retrosternal heartburn occurs mainly in high position
ulcers or in those associated with gastroesophageal
reflux.
 Other symptoms are related to complications.
Diagnosis – Imaging
 X-ray with barium contrast may indicate the diagnosis
in 80% of cases. Direct radiological sign is the niche
(ulcer crater) that appears as a filling defect on gastric
contour of several forms: small, triangular, medium-
sized, pedunculated, large with 3 levels inside : barium,
secretion fluid an air (Haudek), giant.
 After evacuation, the barium remains in the niche as a
"persistent spots." Sometimes ulcerous niche is
surrounded by a halo of edema given, the aspect of
“target /halo sign“ (en cocarde)
 Indirect radiological signs are deformation of the lesser
curvature, spastic contraction ring of the garter curvature
in ulcer region ("finger showing the lesion"), convergence
of mucosal folds toward the ulcer.
Spot
Convergent folds
Gastroscopy is the main investigation for diagnosis. It
directly visualizes the ulcer and also allows lesion biopsy
sampling.
 A single biopsy sampling has an accuracy for a
malignant ulcer in 70% of cases, while 7 biopsies taken
from the ulcer base and margins increase the accuracy
to 99%.
Differential diagnosis
 The main problem of differential diagnosis remains the
gastric cancer. Gastric cancer has radiological and
endoscopic characteristic features that will be described
in other chapter, but the main criteria of differentiation is
the pathological result of endoscopic biopsies.
 Based only on symptoms, differential diagnosis must be
made with a number of other diseases causing upper
abdominal pain (duodenal ulcer, pancreatitis, biliary
colic, hiatal hernia, angina etc.)
Evolution and complications
 Gastric ulcer is a chronic disease developing for years.
Remarkable progress in the last years of medication
treatment made the healing of gastric ulcer to be the
rule.
 Complications of gastric ulcer may be acute or chronic
and can occur at any stage of development.
1. Bleeding - in about 40% of patients, is more serious
and refractory than that of duodenal ulcer. It may take
the form of occult bleeding or hematemesis and/or
melena.
2. Perforation is the most common complication of
gastric ulcer. It appears often as the first manifestation
of disease (onset by complication). Especially ulcers on
the anterior wall of the stomach perforate.
3. Penetration is a particular form of perforation and
appears especially when ulcers are located on the
posterior wall. The most frequent organ involved is the
pancreas but may be also the colon.
4. Stenosis can occur either as a pyloric stenosis when
ulcers are located prepyloric or as a mediogastric
stenosis.
5. Malignization. It is estimated that the percentage of
malignization of gastric ulcers is about 3%, and rarely
a malignant ulcer can be differentiated from a primary
gastric cancer.
Stress ulcer
 It is a special clinical form appeared on a normal mucosa
due to extreme stress situations: multiple trauma, burns,
major insufficiencies (respiratory, liver, kidney), prolonged
surgery, brain damage, etc.
 There is a redistribution of blood circulating mass which
decrease gastric irrigation, inducing an "acute" decrease
of defense capacity of the gastric mucosa.
 Lesions may be single or multiple (erosive gastritis).
Always ulcers are "acute" not surrounded by inflammatory
reaction. Upper gastrointestinal bleeding is the
manifestation. Usually it is slow, intermittent, in rare cases
heavy and fast.
 Stress ulcer treatment is prophylactic, of the causal
disease and also curative that consists of installing a
gastric suction tube, local hemostatics and general
replacement of lost blood, and when these measures
prove ineffective, surgical hemostasis including vagotomy
and in rare cases even total gastrectomy are necessary.
Treatment
 Medical treatment of gastric ulcer uses the same drug
groups as in duodenal ulcer.
 Healing of ulcers should always be confirmed by
endoscopy and always compared with previous
examinations. Any failure or delay in patient’s response
to medical treatment means that the patient is a possible
candidate for surgery.
 Surgery
 The indications of surgical treatment can be classified
into absolute and major.
 1. Absolute indications refer to complicated gastric ulcer,
regardless of what the complication is. Surgery may be
an immediate urgency or elective surgery.
 2. Major indications include:
a) Cases where proper medical treatment for 3-6
weeks did not lead to ulcer healing or at least a 60%
reduction in size,
b) Mild or moderate bleeding ulcer at the 2nd or more
event or accompanied by chronic anemia,
c) Perforated and covered ulcer,
d) Old ulcers, leading to deformation of the stomach or
duodenal bulb,
e) Gastric ulcer in the elderly,
f) Associated with duodenal ulcer,
g) Those patients who do not have access to a proper
health care.
 The objectives of surgical treatment in gastric ulcer are:
– a. Ulcer ablation (gastric resection)
– b. Breaking the pathogenic chain, and
– c. Restoration of physiological digestive circuit
 Location of ulcers is the basic criterion in choosing the
level of gastric resection.
 Types of resection most often used :
– Antrectomy
– Inferior 2/3 of resection the stomach
– Hemigastrectomy
– Resection of the superior pole of the stomach
– Total gastrectomy
 Vagotomy as a procedure used to decrease the acid-
peptic secretion, associated with pyloroplasty or
antrectomy, comes into discussion especially in cases
with acid hyper secretion and stress ulcers.
several variants of resection
 Restoration of digestive tract continuity in case of inferior
gastric pole resection it can be achieved by either
anastomosis of the remaining stomach to the duodenum
(anastomosis Pean-Bilroth I) or to the first jejunal loop
brought to the stomach (Bilroth II) as an "omega" or "Y"
(Roux) loop in front of the transverse colon or through the
mesocolon.
Internal
Hernia !
 Surgical treatment of gastric ulcer
complications is almost similar to
that of duodenal ulcer
complications.
In case of perforated ulcer:
1. Simple suture of the ulcer or suture
with omental pach (Opel, Graham)
2. Ulcer excision and suture
3. Gastric resection including the ulcer
4. Troncular vagotomy plus antrectomy
including the ulcer
 Histology examination of the
resected stomach is mandatory. A
malignant histopathologic finding
requires in most cases
reintervention to perform a more
radical gastric resection.
DUODENAL ULCER
 Duodenal ulcer occurs more frequently in adulthood and
the maximum incidence is between 30 and 50 years, and
the ratio between men and women is 4/1-6/1. It is about
4 times more common than gastric ulcer.
 Duodenal ulcer never turns malignant.
 The incidence of duodenal ulcer decreased in last
decades due to the development of new antisecretory
drugs, but still remains at 1-2%.
 In now days admission in hospital is required only in
complicated cases of duodenal ulcer.
Etiopathogenesis
 Determinant (endogenous) factors:
– Gastric acid hypersecretion
– Decrease of duodenal mucosal defense capacity.
– Helicobacter pylori infection, is now recognized as a major
factor for the development of ulcer disease and an important
risk factor in gastric cancer. The presence of bacteria was
found at 90% of patients with duodenal ulcer.
 Predisposing (exogenous) factors:
– External factors incriminated in duodenal ulcer are: Smoking,
alcohol, poor nutrition, chronic intake of inflammatory drugs,
psychological factors.
– The genetic factors are also important because the disease
occurs in members of the same family and in those with O (I)
blood type.
Morphopathology
 Duodenal ulcer appears as a single or multiple ulceration
located with predilection in the duodenal bulb. (D1)
 The ulcer crater has an inflammatory reaction around it
which over the time turns into fibrosis which is specific
for the callous ulcer.
 In case of healing, the ulcer leaves a white scar, as a
star, visible macroscopically. The process of fibrosis can
lead to duodenal deformation and appearance of
stenosis and pseudodiverticula.
Symptoms
 The main symptom is the epigastric pain manifested as a
burning discomfort, cramping or twisting. Usually it occurs
at 1-2 hours after ingestion of food. It can appear at night
or morning and it gives the feeling of "hunger pain". The
pain relieves after the ingestion of milk and alkali.
 The picture above is so called “the small periodicity” in
duodenal ulcer (pain-ingestion-relief-pain). Symptoms
usually are exacerbated in spring and autumn – “the grate
periodicity” (seasonal).
 As the disease progresses, the character of pain may
change.
 Vomiting is not characteristic for uncomplicated duodenal
ulcer, but when it occurs it has a pain-relieving effect.
 Other possible symptoms are characteristic for
complicated forms.
Signs
 Physical examination is usually negative, but it could
reveal a sensitivity to palpation in the epigastrium and
duodenal point.
 Phenotypic appearance of the patient suffering from
duodenal ulcer is usually of an asthenic, brunette, with a
disorganized diet, smoker and possible alcoholic and
coffee consumer. (“Ulcerous aspect patient")
Paraclinical diagnosis
 The barium swallow may reveal the peptic ulcer by direct
and/or indirect imagistic signs.
 The direct sign is the niche, which appears as a filling
addition or as a suspended spot surrounded by a halo.
 Indirect signs are: the convergence of the mucosa folds,
rapid evacuation of the duodenum, duodenal deformity in
old scar, when it takes the form of "clubs", "hourglass",
"hammer", etc.
 Barium swallow can make the diagnosis in only 50% -
60% of cases, but this percentage may reach up to 95%
for ulcers larger than 1 cm and when dual contrast is
used.
ULCER
 Endoscopy is the standard method of diagnosis of
duodenal ulcer, with a specificity over 90%.
The differential diagnosis must be made with other
conditions associated with epigastric pain.
A. Digestive diseases to be differentiated from a
duodenal ulcer are:
– Gastric ulcer and cancer – the pain does not have the
character of small periodicity and sesonality and it appears
immediately after food ingestion. Gastric biopsy is very
important.
– Acute gastric volvulus - the pain is intense, with abdominal
distension, intense nausea the patient being not able to vomit,
and the nasogastric tube cannot be introduced into the
stomach (triad Borchordt). Chronic volvulus gives more
discrete symptoms, with less pain, associated with the feeling
of early satiety, dysphagia, dyspnea.
– Gastric TB and syphilis – permanent epigastric pain in a patient
with history of tuberculosis or syphilis. Gastroscopy with biopsy
and specific laboratory tests will make the difference.
– Biliary diseases - biliary colic occurs after certain foods, is
located in the right upper quadrant with radiation in the
scapulovertebral space, is not calmed after alkaline and antacid
intake but is calmed after antispastic drugs, is often associated
with nausea and vomiting and sometimes jaundice and fever.
Abdominal ultrasound shows the gallstones. Murphy maneuver
reveals pain in the cystic point.
– Acute pancreatitis – The pain is localized in the epigastrium with
transverse radiation, does not respect the small and grate
periodicity, appears after an excessive consumption of food
and/or alcohol, is accompanied by nausea and vomiting, the
general status is altered going up to state of shock. Ultrasound
and CT scan reveal changes in pancreas, serum and urinary
amylases are generally elevated.
– In chronic pancreatitis the epigastric pain is still present, but
without the small and grate periodicity, does not calm after
alkaline or food intake, in a patient with a history of recurrent
acute pancreatitis, digestive disorders and often diarrhea.
Ultrasound examination and CT can reveal the presence of
Wirsung duct dilation and pancreatic lithiasis.
– Pancreatic cancer - continue lancinant epigastric pain with
radiation to the back, calmed in the "Mohammedan“ position.
The patient presents progressive weight loss. In cephalic
location verdinic jaundice and Courvoisier-Terrier sign are
present. Ultrasound and CT scan reveal the tumor.
– Ascending and transverse colon tumors are manifested by pain
rather colicky accompanied by diarrhea and/or constipation.
Often patients are anemic with progressive weight loss.
Irigography and colonoscopy with biopsy can establish the
diagnosis.
 – Abdominal angina - entero-mesenteric ischemia in patients with
atrial fibrillation, aterosclerosis, and history of previous
thromboembolism. The pain appears postprandial, is
lancinante, located mainly around the umbilicus, with impaired
general condition, flatulence, vomiting and bloody stools, with
the possibility of entero-mesenteric infarction and evolution to
death. The diagnosis is difficult, often established only by
laparotomy. Selective mesenteric angiography can make the
diagnose.
B. Neighbourhood disorders :
– Renal colic - intense pain located in lumbar region radiating into
inghino-scrotal (labial) region, accompanied by nausea,
vomiting, dysuria, polakyuria, hematuria. Giordano sign positive.
Ultrasound may reveal dilation of the upper urinary tract and
stones. Antispastic drugs may calm down the pain.
– Hiatal hernia – the pain is located mainly retrosternal, heartburn
and regurgitation often associated due to esophageal reflux, with
cardiac arrhythmias and dyspnea. Barium swallow in
Trendelemburg position and esophagoscopy will make the
diagnosis.
– Internal hernia - intense colicky abdominal pain followed by
occlusive phenomena with vomiting. Most cases are intraoperative
surprises.
– Postero-inferior myocardial infarction – intense epigastric pains
sometimes difficult to distinguish from an abdominal disease. This
condition must be considered in any intense epigastric pain,
especially in predisposed patients because of the potential to
evolve to exitus. ECG and cardiology specialty examination and
laboratory tests can rule out a heart attack.
– Basal pneumonia and pleurisy - pain is usually located at a
hemithorax or hypochondrium, accompanied by respiratory events
(cough, dyspnea), fever, having no connection with alimentation.
Fluoroscopic examination reveals pleuro-pulmonary changes.
 – Diseases of the spine - can generate pains in epigastric or
hypochondrium region misleading the diagnosis. Postural pain
usually is enhanced by certain movements, and reduced by
antiiflamatory and muscle relaxant drugs.
– Other systemic diseases that can mimic symptoms of a duodenal
ulcer: diabetes, saturnin colic, tabes, porphyria, are rarely
encountered in clinical practice.

Evolution and complications

 Complications can occur at any time and are
represented by:
1. Bleeding,
2. Perforation,
3. Stenosis, and
4. Penetration.
Particular forms of duodenal ulcer
 Postbulbar ulcer is an ulcer located below the D1 or D2
above the Vater’s ampulla. It is difficult to diagnose and
often is diagnosed intraoperatively. Frequently
complicated by bleeding, stenosis and penetration into
the pancreas.
 Double or multiple ulcers, known as "kissing ulcer“ or “in
mirror” is a severe form, frequently complicated by
bleeding and perforation.
 Zollinger-Ellison syndrome is a condition characterized
by the appearance of multiple ulcers in the digestive
tract, due to peptic acid hypersecretion consecutive to
increased gastrin secretion derived from a pancreatic
tumor (gastrinoma).
Treatment of duodenal ulcer
Medical treatment has two goals: pain relief and healing
the lesion.
1. Last generation antacids (proton pump inhibitors) –
(Controloc, Nexium, Omeprazole, etc)
2. Digestive mucosa protective drugs – (contain
Aluminium, Bismuth, etc)
3. Eradication of Helicobacter Pylori (Amoxicilin,
Clindamycin, etc)
4. Diet
Surgical treatment
 It has become increasingly rare, practically addressed
to complicated cases.
 The objectives of surgery are:
1. Decrease the acid secretion
2. Removal of the lesion when possible
3. Ensure gastric drainage as physiological as possible
 Decreased gastric acid secretion can be achieved
through three surgical procedures:
1. Parasympathetic denervation - elimination of vagus nerve
stimulation of acid secretion
2. Gastric resection more or less extensive – decreases the
parietal cell mass
3. Antrectomy – decreases the secretion of gastrin
 Surgical vagotomy cuts off the vagal innervation of
the gastric wall in order to reduce gastric secretion.
There are 4 types of vagotomies:
1. Truncal vagotomy - the two vagus nerve are cut at
trunk level.
2. Selective vagotomy (Jackson-Franksso) - cuts off the
vagus nerves after separation of the hepatobiliary
branches.
3. Supraselective vagotomy (highly selective, parietal cell
vagotomy) (Amdrup) - cuts off the vagal branches
strictly near the gastric wall so that the other branches,
including Latarjet nerves remain integer. No
associated procedure of gastric emptying is necessary.
4. Psterior vagotomy associated with anterior sero-
myotomy (Taylor operation) spares the anterior vagus
and its motor branches.
 Gastric emptying procedures associated to
vagotomy are:
1. Operations that address to the pylorus:
1. Extramucosal pylorotomy (Fredet) - pyloric muscle is sectioned
leaving the mucosa layer integer.
2. Pylorotomy-plasty (pylorus is sectioned including the mucosa
and then sutured in a manner that enlarges the pyloric opening)
(Heineke-Mikulicy, Finney, Mayo, Strauss, Horsley, Chabal,
etc.)
3. Pylorectomy-plasty (a partial excision of the pylorus including
the ulcer is performed) (Wangensteen, Judd-Starr, Mayo, etc.)
2. Antroduodenostomy – an extrapyloric communication
between antrum and duodenum is performed (Villard-
Jaboulay, Pean, Burlui)
3. Gastroenteroanastomosis (GEA)
4. Antrectomy
Antro-duodenostomy
 Vagotomy associated with antrectomy is currently
considered the most appropriate method of surgical
treatment. Restoration of digestive continuity is
performed by a Billroth I or II type anstomosis.
Complications of
duodenal ulcer
 BLEEDING
 This complication appears in 1/3 of cases being the
main cause of mortality from this disease. Modalities of
onset can be dramatic, with haematemesis or melaena
or insidious. It may be the first manifestation of the
disease.
 Most often, the erosion occurs in the posterior wll of the
duodenal bulb where the ulcer erodes the pancreatico-
duodenal artery.
 Symptoms are related to acute anemia: pallor, sweating,
thirst, restlessness, faintness, tachycardia, hypotension.
 Manifestation:
– Haematemesis
– Hematochezia
– Melena
 Bleeding peptic ulcer is a major health problem

Incidence Recurrence

19.4–79.0 cases Till 31%

at 100,000/year in 90% take places in
Europa the first 7 days
Bleeding peptic
ulcer

Mortality Cost

Avg. at 30 days (USA) $5.7 Bilion/year

8.7%

1
Lau JY, et al. - Gastroenterology 2008;134(4 Suppl1):A32;
2
Bini EJ & Cohen - J. Gastrointest Endosc 2003;58:707–1;
3
Chiu PW, et al. - Gut 2003;52:1403–7;
4
Sonnenberg A & Everhart JE. - Am J Gastroenterol 1997;92:614–20
 Diagnosis is based on digestive endoscopy, that may
reveal more than 90% of recent or ongoing bleeding.
 Treatment. Upper gastrointestinal bleeding is a surgical
emergency and the patient will initially admitted to a
department of surgery and depending on the severity of
bleeding in the intensive care unit for better monitoring.
When hemostasis can be achieved by conservative
methods or by endoscopy, the patient may be
transferred to the gastroenterology department.
 The main purpose of treatment is to stop the bleeding,
rebalancing the patient and prevent rebleeding.
 Treatment may be medical, endoscopic or surgical
 General measures: Ensure adequate venous access
(central venous catheter) for administration of fluids and
for measuring the CVP (central venous pressure),
nasogastric tube to monitor bleeding and gastric lavage,
urine probe to monitor urine output, blood pressure
monitoring, pulse oximetry, etc.
 Fluid rebalancing by replacing lost blood, crystalloid and
macromolecular solutions.
 Antacids (80 mg in bolus over 30 minutes, followed by a
continuous infusion of 8 mg esomeprazole/h administered
for 3 days) and hemostatics (Adrenostazin, Vit. K, Ca)
 Gastric aspiration with lavage and medication can stop
the bleeding if it is not from an important vessel
(gastroduodenal artery). It is very important that the
stomach to be emptied. Lavage is performed with cold,
alkaline and hemostatic solutions (adrenostazin) until
clarification of lavage fluid.
 Endoscopic hemostasis is the most effective method of
definitive nonsurgical hemostasis. It can be performed in
various ways: by elctrocoagulation, Argon coagulation,
laser coagulation, sclerotising substances (Polidocanol)
 Embolization is another possibility to obtain hemostasis.
Terminal vascular branches (muscular) are easier to
embolize than gastro-duodenal artery.
Surgical treatment
 Indications:
Absolute
1. Failure of conservative therapy (25%)
2. Haemodynamic instability despite sustained resuscitation (more than
three units of blood transfused);
3. Bleeding relapse after initial stabilization (up to two attempts at
endoscopic hemostasis);
4. Shock associated with recurrent bleeding;
5. Small persistent bleeding, requiring more than three units of blood per
day
6. Association to bleeding of another complication
7. Patient with evident cardiac or cerebral vascular afection
8. Patient older than 60 years
Relative
1. A rare blood group or difficult typing
2. Refusal of transfusion
3. An associated gastrinoma
4. Future need for major surgery (heart transplant, kidney)
5. Patients who can not meet an adequate lifestyle and disease treatment
 Surgical treatment includes the following
possibilities:

1. Antrectomy + troncular vagotomy + Bilroth I or II

anastomosis.
2. Truncal vagotomy+(pylorectomy) pyloroplasty (anterior
ulcer is excised).
3. Truncal vagotomy + pyloroplasty + vascular suture (for
posterior ulcers). Leaving in place the ulcer is
encumbered by the risk of recurrent bleeding.
4. Gastric resection 2/3 + Bilroth I or II anastomosis.
 PERFORATION
 The first cases of ulcer perforation were reported in 1817
by Traves, and in 1884 Mikulicz first described treatment
methods.
 In the past the incidence of perforation was about 10%
but it decreased after modern antacid drugs were
introduced.
 In half of cases the perforation takes palce in the free
peritoneal cavity (the ulcer is located on the anterior
duodenal wall).
 In about 40-50% the perforation is sealed (covered) by
neighboring organs: the liver, gall bladder, ligament, as a
defense reaction of the body that tries to isolate the
pathologic process.
 The clinical picture is dominated by generalized
peritonitis symptoms and signs. First chemical and then
bacterial peritonitis.
 The onset is sudden with intense epigastric pain (“as a
knife stabbing") that can migrate into the right iliac fossa an
then quickly generalized.
 Initially epigastric pain and then located in the right iliac
fossa, lead to confusion with acute appendicitis.
 General signs may be: fever, tachycardia, pallor, superficial
tachypnea and signs of acute dehydration.
 After several hours the symptoms fade away, as
hypovolemic shock sets up. Abdominal wall contraction is
replaced by abdominal distension, nausea and vomiting are
frequent, bowel movements are absent, hypotension and
tachycardia are increasing gradually.
 Without any treatment the death in most cases will appear.
Signs
 The patient is immobilized by pain in fetal position
(mobilization worsens the pain) with “peritonitic face” in
later stages (pallor, cold sweat, sunken eyes).
 The pain may radiate to shoulder (Kehr sign) as a result
of diaphragmatic peritoneum irritation.
 Abdominal muscle contraction is characteristic ("Board-
like rigidity " with visible muscles reliefs) which does not
participate to the respiratory movements.
 Mandel sign is positive (causing pain on abdominal wall
percussion) and on auscultation there is abolition of
bowel movement as ileus is installed.
 Blumberg sign is positive, liver dullness may miss (due
to pneumoperitoneum)
 Douglas sac is very painful at rectal digital examination.
Investigations
 Pathognomonic radiologic sign is pneumoperitoneum
(intraperitoneal free air) visible under the diaphragm in
standing position or periumbilcal (Judin sign) in supine,
for approx 75% of cases. In doubtful cases a water-
soluble gastroduodenogram will show the leak from the
duodenum.
 Ultrasound examination may reveal fluid in the peritoneal
cavity.
Pneumoperitoneum
Differential diagnosis:
– Acute pancreatitis
– Appendicitis
– Acute cholecystitis
– Enteromesenteric infarction
– Myocardial infarction

Treatment of perforated duodenal ulcer is surgical

performed in emergency condition.
 Exception. Conservative treatment is possible for recent
perforated ulcer (less than 4-6 hours) and it was first
described in 1935 by Wangensteen. Observations were
confirmed in 1946 by Taylor. Basically, a nasogastric
tube is placed and a continuous aspiration is performed.
All biological parameters will be corrected and broad
spectrum antibiotics will be administered.
 In the first 6 hours after perforation, laparoscopic approach
may tempted but after this interval the classic approach is
indicated.
 Surgical therapeutic possibilities are:
– Suture of the perforation with or without omental patch and a
thorough abdominal lavage. Patch (seal) can be done with
omentum (technique falsely attributed to Graham, as originally
described by Cellan-Jones) or falciform ligament. Up to 71% come
to require subsequent definitive surgery.
– Vagotomy + pyloroplasty or pylorectomy-pyloroplasty.
– Antrectomy + vagotomy and gastro-duodenal anastomosis (Pean-
Bilroth I)
– Gastric resection 2/3 with anastomosis Bilroth I, II or Roux.
 Risk factors affecting prognosis are: delayed treatment (>
24 hours), preoperative shock (BP < 100 mmHg), and
concurrent serious medical illness. When all three are
present the mortality rises to 100% (Grade C).
 STENOSIS
(Narrowing and obstruction)
 Incidence: 5-10% of untreated patients, affecting gastric
emptying.
 Location may be the pylorus, duodenal bulb or postbulbar
region.
 Two forms which are in fact evolutionary stages:
– functional stenosis - pyloric spasm, acute edema and
inflammation - reversible with medical treatment, and
– Organic stenosis - fibrous scar tissue due to hyperplasia
- irreversible, of surgical indication.
 The stomach changes in an effort to adapt its functions to
the new conditions. In the first stage the stomach has kept
its tone in an attempt to overcome the obstacle.
 As the lesion develops the stomach enters the stage of
compensated stenosis with gastric hypersecretion and
increased movements. The third phase is the gastric
asystole, characterized by a more dilated atonic stomach
which reaches down into the pelvis.
Symptoms are determined by the evolutionary stage.
 Thus, initial clinical stage will be dominated by intermittent
colicky epigastric pains, which ameliorate after vomiting.
 In compensated stage, the pain diminishes but becomes
permanent and is accompanied by a feeling of fullness in
the stomach. Vomiting is more rare but becomes
abundant, effortlessly and contain ingested food but
without bile content. Patients still complain of constipation.
 Decompensated phase is characterized by the
appearance of edema due to severe cachexia and
denutrition.
Clinical examination reveals epigastric bulging, gastric
capotement present in 60% of cases and gastric
peristaltic waves may be observed through the abdominal
wall. (Walton)

Laboratory analysis will show dehydration and electrolyte

imbalance, and in advanced stages increased creatinine
and urea. Frequent vomiting containing HCl with loss of Cl
and K will induce an increase in plasma bicarbonates as a
compensatory phenomenon, leading to the metabolic
hypokalemic and hypochloremic alkalosis plus
hypocalcemia (Darrow syndrome)
Diagnosis is based on:
 Endoscopy - viewing the stenosis that cannot be passed
by the endoscope and a high quantity of gastric fluid of
stasis.
 Radiological examination with contrast, which highlights
significant distension of the stomach, which takes the
form of a "sink“ often under the iliac crests. The contrast
substance "falls" in gastric liquid of stasis as
"snowflakes“.
Stomach
Differential diagnosis must be made with other conditions
that can cause difficulties in gastric emptying, as follows:
1. Antral stenosing cancer- sometimes the tumor is palpable,
suggestive radiographic appearance at barium swallow,
endoscopy with biopsy makes the diagnosis.
2. Pancreatic tumor penetrating the duodenum - usually there is an
associated mechanical jaundice and bilious vomiting. Ultrasound
and CT scan show the tumor.
3. Gastric ptosis - although X-ray shows a big stomach, the
discharge is present especially after right lateral decubitus.
Epigastric pain appears in orthostatic position. Endoscopy does
not find any stenosis.
4. Chronic gastric volvulus - suggestive radiographic appearance at
barium swallow.
5. Gastroduodenal mucosal prolapse - the diagnosis is made by
gastrography with contrast substance.
Treatment
 May be conservative in the functional phase consisting in
continuous gastric aspiration, gastric lavage with
hypertonic solutions, administration of antacid and
atispastic drugs, antiinflammatory (cortisone), fluid,
eletrolytic and protein rebalancing.
 More than 75% of patients are treated in the organic
phase requiring surgery that is identical with the surgical
treatment of duodenal ulcers.
 A good preoperative preparation is needed to correct
imbalances. A nosogastric tube will be inserted and
gastric lavage will be perform for 2-3 days. That will
evacuate the undigested food and will increase the
tonicity of the stomach. Hypoproteinaemia will be
corrected by total parenteral nutrition in the first days.
Surgery should not be postponed too much as the overall
condition of the patient may degrade.
Bilateral truncal vagotomy + antrectomy + Pean
reconstruction
 PENETRATION

 Ulcer penetration is actually a perforation in an area of

the duodenum covered by the surrounding organs.
Penetration occurs most frequently in ulcers located on
the posterior wall toward the pancreas. Penetration may
also occur in hollow organs such as colon, gallbladder
and main bile duct and may form fistulas with these
organs.
 If in his penetrating evolution the ulcer meets blood
vessels these are eroded with the consequent bleeding.
Gastro-duodenal artery is most often interested in this
process.
The clinical picture is characterized by: changes of pain
character with appearance of symptoms from penetrated
organs, increased frequency of upper gastrointestinal
bleeding and ulcer resistance to proper treatment.
Diagnosis is made by radiologic and endoscopic
explorations.
Treatment is only surgical. In most cases the ulcer’s crater
cannot be removed being represented by the penetrated
organ itself.
 Duodenal resection is made under the crater which
remains outside the digestive tract (it is excluded).
 Restoration of digestive continuity is achieved either by
Bilroth I anastomosis or Bilroth II or Roux.
GASTRIC CANCER
 The stomach is one of the most common site of cancer in
the digestive tract, ranking second after the colon and
rectum.
 The first gastric resection was performed by Billroth in
1891, and the first resection for cancer belongs to
Schlatter in 1897. Despite the abundance of articles on
gastric cancer, the only who have made contributions in
terms of improved postoperative outcomes were those
related to early diagnosis of disease (early cancer) by
screening of Japanese researchers.
Epidemiology
 Up 2-3 decades ago the stomach cancer ranks first in the
hierarchy of digestive cancers before colorectal cancer.
As the knowledge about etiopathogenesis and treatment
methods developed, gastric cancer incidence decreased
constantly.
 However, with 930,000 new cases per year and 700,000
deaths, gastric cancer remains a particular problem,
especially in Asian countries (Korea, China, Taiwan and
Japan) where 60% of new cases occur. Areas with the
lowest incidence are African countries.
 Age most affected is 50-60 years. Gastric cancer occurs
rarely under the age of 30 and is 2-3 times more
common in men than in women. After the age of 40 there
is a linear increase of carcinogenic risk.
 Gastric cancer mortality, although decreasing still
remains high. The disease prognosis remains reserved,
5-year survival rate in Europe is 9-22%.
Etiopathogenesis
 Etiology of gastric cancer is obscure. It is recognized that
on a genetic predisposition basis, a number of
predisposing factors may lead to the development of
cancer.
 Predisposing factors that have a certain role in the
genesis of gastric cancer are: certain gastric diseases,
Helicobacter pylori infection, diet and socio-economic
conditions.
1. Atrophic gastritis appears to be the most important in antral cancer
genesis (6 times increased risk)
2. Gastric ulcer has a significant potential for malignancy, especially
in locations of the lesser curvature
3. Gastric adenomatous polyps, and especially those over 2 cm in
diameter
4. Intestinal metaplasia, Menetrier disease, Zollinger-Ellison
syndrome.
5. Previous gastric resection - Balfour is the first surgeon who in 1922
made the correlation between gastric cancer and previous
operations on the stomach for benign disease. Patients with distal
gastric resection in their history (mostly for gastric ulcer) have a 4-7
times greater risk of developing gastric cancer on the remaining
stump, due to duodenal-gastric reflux. The average time between
resection and cancer onset is 25.8 years.
6. Infection with Helicobacter pylori seems to increase the risk of
gastric cancer by 3-6 times in association with gastric mucosal
atrophy.
7. Diet is considered a major factor in gastric cancer. The relationship
does not necessarily refer to some kind of food but to the way of
food preservation and their nitrate content, which the body turns
into nitrites and then into nitrosamines. Smoked conserved food
have a carcinogenic role compared to those preserved by cold.
Anatomopathology
 Location of gastric cancer is compared to the long axis of the
stomach. Approximately 40% of cases develop in the lower (antral)
part of the stomach, 40% in the middle (corpus), 15% in the upper
part (cardia/fundus) and almost 10% comprise more than one
region.
 Macroscopic aspect (Borrmann’s classification):
– Type I: polypoid
– Type II: fungoid
– Type III: ulcerative
– type IV: infiltrative
– Unclassifiable.
 The most common classification is that of Marson and Dawson:
– Vegetative with variable extent, located mostly in the fundus and body
of stomach
– Ulcerative of different sizes, with predominant antral location
– Infiltrative with the disappearance of mucosal folds, which can occur in
any location. (linitis plastica, which gradually infiltrates the entire
stomach)
Morphological and clinical classification of gastric
cancer:
1. "in situ" - limited to the epithelium, without exceeding the basal
membrane
2. "early" (early gastric carcinoma) - limited to the mucosa and
submucosa, regardless of size and presence or absence of
metastasis
3. "invasive" - extended beyond the submucosa
 Superficial or early cancer is an important prognostic factor.
Endoscopic appearance is classified as:
1. Type I, exophitic, corresponds to a malignant polyp.
2. Type II, superficial, can be raised, flat and bumpy.
3. Type III, ulcers.
Each of these types may be microscopic:
1. well differentiated
2. medium or less differentiated
3. undifferentiated (mucus-secreting)
 Histopathological classification (WHO)
Epithelial tumors Non-epithelial tumors
 Leiomyoma
1. intraepithelial neoplasia –
 Schwannom
adenoma
 granular cell tumor
2. carcinoma  Glomic tumor
• Adenocarcinoma (95%)  Leiomyosarcoma
intestinal type  gastrointestinal stromal tumors
diffuse type (plastic linitis) (GIST)
• papillary adenocarcinoma • benign
• tubular adenocarcinoma • uncertain malignant, potential
• malignant
• mucinous adenocarcinoma
 Kaposi's sarcoma
• carcinoma with signet ring cells
 Other
• adenoscoamos carcinoma
• scoamoase cell carcinoma
• small cell carcinoma Malignant lymphomas
• undifferentiated carcinoma  cell lymphoma of MALT type
marginal zone
• Others  mantle cell lymphoma
3. carcinoid (well differentiated  large cell lymphoma Diffuse B
neuroendocrine tumor)  Others
Secondary tumors
Spread of gastric cancer
1. By contiguity, successively in all gastric wall layers,
and neighboring organs: liver, pancreas, colon, kidney,
etc.
2. Through the lymphatic vessels towards the lymph
nodes. There are four areas of lymphatic drainage of
the stomach, described in the chapter on anatomy.
3. Through the blood vessels to the liver, lungs, adrenal
glands, ovary, thyroid, etc., where metastases occur.
4. Intraperitoneal, after penetrating the serosa layer,
inducing ovarian tumors (Kruckenberg) or peritoneal
carcinomatosis and ascites.
Pre-therapeutic staging of gastric cancer, according to
UICC
 T-primary tumor
– TX-Primary tumor can not be assessed
– T0-there is noprimary tumor
– T1-tumor invades lamina propria or submucosa
– T2-tumor invades muscle or subserosa layers, with no extension to surrounding
organs
 T2a tumor invades musculare layer
 T2b tumor invades subserosa
– T3- tumor penetrates the serosa, but without invasion of adjacent organs
– T4 tumor invades adjacent organs
 N, lymph nodes
– NX-regional nodes can not be evaluated
– N0-no lymph node metastases
– N1-node metastasis in 1-6 regional nodes
– N2-metastases in 7-15 regional lymph nodes
– N3-metastases in more than 15 regional nodes
 M-Metastases
– MX-metastases can not be assessed
– M0- no distant metastases
– M1-with distant metastases
Stages based on these parameters:
 Stage 0: Tis, N0, M0
 Stage IA: T1, N0, M0
 Stage IB: T1, N1, M0
 Stage II: T1 N2 M0, T2 N1 M0, T3, N0, M0
 Stage IIIA: T2 N2 M0, T3, N1, M0
 Stage IIIB: T4, N0, M0
 Stage IV: T4, N1, 2,3, M0, T1, 2,3, N3, M0, T1-4, N0-3,
M1
Histopathological grading :
 GX - degree of differentiation can not be assessed
 G1 - well-differentiated tumors
 G2 - moderately differentiated tumors
 G3 - poorly differentiated tumors
 G4 - undifferentiated tumors
Symptoms
 Symptoms of gastric cancer are poor and nonspecific in
early stages, leading to delayed diagnosis. Symptoms
are dependent on age, location, extent and type of
tumor. Symptoms are more intense when tumors are
located at openings: pylorus and cardia.
 The development of gastric cancer is divided into three
clinical stages: the onset, the status period and the
terminal stage.
 The onset is insidious characterized by vague dyspeptic
disorders, nausea, anorexia, stomach fullness, weight
loss.
 Pain is continuous or intermittent, occurring early
postprandial. Vomiting or food ingestion does not calm
the pain as in duodenal ulcer. On contrary, food intake
may exacerbate the pain (as in gastric ulcer).
 Anorexia is a consistent symptom, progressive, often
selective, first to meat and then to fat.
 Vomiting occurs when the tumor is located at openings.
In pyloric location vomiting appears late after food intake
but early, as a regurgitation, in cardial location. With time
it becomes more frequent, and may contain dark
digested blood in small quantities.
 Dysphagia occurs in upper locations.
 Upper GI bleeding is rarely massive and less important
than in peptic ulcer.
 Almost 10% of patients have only signs of neoplastic
impregnation (Savitki) - loss of appetite, pallor, fatigue,
asthenia, weight loss, decreased work capacity.
 Less than 10% of patients will experience a complication
of cancer – cardia or pylorus stenosis, upper
gastrointestinal bleeding or perforation with peritonitis.
Clinical signs of inoperability of gastric cancer (even if
palliative operations are possible) :
1. Epigastric palpable tumor.
2. Positive Virchow sign confirmed by biopsy
(metastasis in the left supraclavicular lymph node).
3. Carcinomatous ascites (shifting dullness on
percussion) - confirmed by cytological examination
of fluid extracted by puncture.
4. Palpable tumors in Douglas sac, by rectal or vaginal
examination - (Blumer sign) or Krukenberg ovarian
tumors.
5. Metastatic skin tumors in the abdominal wall or
around the umbilicus (Sister Mary Joseph's lymph
node).
6. Hepatomegaly due to metastases (confirmed by
ultrasound) often associated with jaundice and
cachexia.
Paraclinical investigations
 Gastroscopy is the most important – it visualizes the lesion
and also can perform multiple biopsies.
 Barium swallow – less used in now days, may reveal extra
information. The pathognomonic signs are the lack of filling
with barium, “the cancerous niche” and rigidity of the gastric
wall.
Other useful investigations are:
 Abdominal ultrasound - especially for liver metastases and
ascites.
 Intragastric ultrasound – to assess the degree of wall
penetration and perigastric lymph node involvement.
 CT and MRI scan – to evaluate the relations with other
surrounding organs and metastases.
 PET scan for metastases.
Malign niche
Malign niche
Laboratory:
1. Anemia
2. Hypoproteinemia
3. High erythrocyte sedimentation rate (ESR)
4. Gastric hypo-anacidity
5. High levels of CEA (carcinoembryonic antigen ), CA-122, etc
Complications
 Possible complications of gastric cancer are occult or
gross bleeding, pyloric stenosis, perforation in the
open peritoneum, tumor necrosis, phlebitis,
metastases.
Prognosis
 While remarkable progress in terms of diagnosis and
treatment of gastric cancer were made, improving
outcome depends only on early detection of the
disease. In early stages, "early cancer“ survival rates
are over 90% at 5 years.
Treatment
 Treatment of gastric cancer is complex, multimodal:
surgical and oncological, but surgery remains the most
important.
 Surgery for gastric cancer can be radical or palliative.
 Operations may be performed in emergency condition
for cancer complications or in elective condition.
 Contraindications for radical surgery are related to the
presence of peritoneal carcinomatosis or distant
metastases including liver, although, if they are limited
excision can be performed.
Surgical treatment
 Before operation a good evaluation and preparation of
the patient is necessary. In certain cases colon
preparation is also indicated because in advanced
gastric tumors, located on corpus and grater curvature
the transverse colon or mesocolon may be penetrated
and associated colon resection may be needed.
 Operations may be performed by classic (open)
approach (laparotomy) in most cases or by laparoscopic
approach.
 There are multiple types of laparotomies. Choosing one
of them depends on tumos location and surgeon’s
preference, but in most cases xipho-subumbilical
laparotomy is used.
Types of laparotomies
 Radical surgery is aimed on a complete removal of the
tumor by partial or total gastrectomy or even extended, if
necessary to neighborhood viscera until no visible
macroscopic tumor left. In addition omentectomy and
regional lymphadenectomy are necessary.
 Gastric resection must respect a distance of 6 cm
upward from the intraluminal macroscopic visible margin
of the tumor and 2 cm below it towards the duodenum.
 Depending on tumor location there are more possibilities
for gastric resection:
– Inferior gastric resection which in most cases represents a
subtotal gastrectomy for tumors located on antrum.
– Superior gastric resection (in cardial location of tumor when a
portion of the abdominal esophagus is also resected)
– Total gastrectomy – most often applied.
Gastric resections in cancer,
1 – inferior pole resection (subtotal gastrectomy), 2 – superior pole gastrectomy
3 – total gastrectomy

Gastric resections may be associated with resection or

removal of other organs such as splenectomy and partial
pancreatectomy when the tumor penetrates the pancreas,
or transverse colon when tumor penetrates the colon or
transverse mesocolon.
 Regional lymphadenctomy based on TNM classification
presumes:
– D1 - Removal of a minimum 15 lymph nodes located at less
than 3 cm from the tumor.
– D2 - removal of at least 25 nodules, located at more than 3 cm
from tumor boundaries and
– D3 – removal of at least 25 nodules.
 An efficient lymphadenectomy requires D1 and D2 lymph
nodes removal.
 The Japanese classification is based on 16 lymph node
stations, grouped into three levels according to tumor
location. A good lymphadenectomy requires removal of
N1 and N2 stations.
Station Location of primary tumor
1/3 sup Middle 1/3 inf.
1 Right paracardial N1 N1 N2
2 Left paracardial N1 N3 M
3 Greater curvature N1 N1 N1
4sa Gerater curvature – short gastric vessels N1 N3 M
4sb Greater curvature – left gastroepiploic N1 N1 N3
4d Greater curvature – right gastroepiploic N2 N1 N1
5 Suprapyloric N3 N1 N1
6 subpyloric N3 N1 N1
7 Left gastric artery N2 N2 N2
8a Anterior to hepatic artery N2 N2 N2
8p Posterior to hepatic artery N3 N3 N3
9 Celiak trunk N2 N2 N2
10 Spleen hylum N2 N3 M
11p Splenic artery proximal to spleen N2 N2 N2
11d Splenic artery distal to spleen N2 N3 M
12a Hepatoduodenal lig. left N3 N2 N2
12b,p Hepatoduodenal lig. posterior N3 N3 N3
13 Retropancreatic M N3 N3
14v Superior mesenteric vein M N3 N2
14a Superior mesenteric artery M M M
15 Middle colic artery M M M
16al Aortic hiatus M M M
16a2,b1 Middle paraaortic N3 N3 N3
16b2 Caudal paraaortic M M M
N1 and N2 lymphadenectomy depending on tumor location
Radical gastrectomy
+lymphadenectomy
+ omentectomy

Dotted line shows the

extension of resection
 Restoration of digestive continuity is achieved by gastro-
jejunal anastomosis for lower pole gastrectomy, or eso-
jejunostomy in total gastrectomy, or eso-gastrostomy in
the upper pole gastrectomy.

Esojejunostomy
1. - eso-jejunostomy TL on Y Roux , 2. - eso-jejunostomy TT on Y Roux, 3. -
eso-jejunostomy „sandvwich” Gaham, 4.- eso-jejnostomy TL on omega loop
 Digestive tract
reconstruction with
duodenum maintained in
circuit
1. – direct eso-duodenostomy
2. – eso-jejuno-duodenostomy
with jejunal interposition
(Juvara), 3. –Tomoda, 4. –
Rosanov

Anastomosis with
stapler
Eso-jejunostomy with reservoir
1 – Hoffman, 2 –Saupault, 3 – Hunt, 4 - Mircioiu
 Palliative surgery has no benefit in terms of prognosis,
but is very important in terms of quality of life and
complications prevention.
 It is indicated in patients who do not meet the criteria
for radical surgery.
 Types of palliative surgery are:
1. Palliative gastric resection,
2. Internal derivations (GEA, bilio-digestive
anastomosis)
3. Stomas (gastrostomy, jejunostomy, colostomy).
 Endoscopic resection of gastric mucosa affected by
neoplastic process is technically feasible, but it is
indicated only in the early stages of gastric cancer when
the tumor does not exceed the mucosa and there aren’t
associated lymph node metastases.

Postoperative complications:
 Local complications occur in about 25% of cases but the
most dangerous is the fistula of anastomosis (5-10%),
especially the eso-jejunal, with a high rate of mortality.
 Eso-gastric anastomotic fistulas, after subtotal
gastrectomy or jejuno-jejunal are very rare. Also fistulas
of the duodenal stump have a low incidence compared
to duodenal ulcer cases.
 Gastric cancer in figures
Ratio men / women: 1.71
Average age: 69 years
Endoscopic diagnosis: 96%
Location: inferior third 40%, superior third 20%, middle third
20%
TNM staging as: I (20%), II (17%), III (40%), IV (23%).
Types of operations: subtotal gastrectomy (4/5): 50%, total
gastrectomy: 35 - 40%
Early postoperative mortality: 10 -15%
Postoperative morbidity: 25% anastomotic fistulas
especially
Overall survival at 5 years: 16%
Overall survival at 5 years postoperatively: 24%.
Overall survival at 5 years after radical surgery: 33%.
Measures for prevention of gastric cancer
1. Eat mostly foods with protective role: fresh vegetables,
fruits, milk, corn, etc..
2. Use correct cooking techniques, food preservation and
storage.
3. Avoiding common fat fried or reheated, smoked, canned.
4. Avoid smoking and passive inhalation of cigarette
smoke.
5. Avoid excessive consumption of alcoholic beverages,
especially concentrated alcohol.
6. Periodically health check by medical specialty
examinations (radiology, endoscopy, biopsy) especially
in people at high risk (gastric ulcer and stomach surgery
in history).
 Gastric lymphoma
 Are tumors of mesenchymal origin that represents about
1-3% of malignant tumors of the stomach with an
increased malignancy.
 Malignant lymphoma may be a primitive or secondary
gastric localization in a systemic disease (Hodgkin's
disease, Brill-Symmers disease) and may be
reticulosarcoamas or lymphosarcomas.
 Macroscopic, tumors are large, developed primary in the
submucous layer having its origin in the lymphoid tissue.
In 1/3 of cases the lesions are larger than 10 cm.
 Usually invasion of serosa precedes the mucosa
invasion and metastases in regional lymph nodes (63%)
precede the visceral invasion.
 In 5-23% of cases it affects the whole body or there is a
multifocal location.
 Symptoms are: epigastric pain, hematemesis and
melena, especially occult bleeding. In most patients,
symptoms are vague and nonspecific, and debute prior
the diagnosis with 4-10 months. Frequently the tumor is
palpable in the epigastrium as a mass area.
 Preoperative diagnosis of lymphoma is important
because it allows an accurate assessment of patients for
staging with a high therapeutic importance.
Staging:
 I limited to the gastrointestinal tract
 II abdominal extension from primary location
– II1 local adenopathy (perigastric / mesenteric)
– II2 remote adenopathy (paraaortic / paracaval)
– IIE serosa penetration and invasion of adjacent structures
 IV dissemination or supradiaphragmatic adenopathy
 There is no stage III
Treatment of malignant lymphomas is complex, surgery
associated with radio and chemotherapy.
 Surgery is indicated in the presence of complications, it
should be as conservative as possible and it is not
indicated in stage IV.
 Surgery: subtotal or total gastrectomy and in certain
cases extensive resection of neighboring organs if they
are invaded by tumor. It requires removal of locally
lymph nodes and splenectomy.
Prognosis
 Survival at 5 years in resectable cases is between 40-
70%, depending on lymph nodes status. However, the
prognosis is better than in other gastric tumors.
 Gastric carcinoid
 The term "carcinoid" was introduced by Oberndorfer first
in 1907.
 Carcinoid tumors are neuroendocrine tumors much less
aggressive than adenocarcinomas.
 It can occur at any age between 20 and 90 years,
 Men/women ratio =1/1
 Incidence is 1.2 - 2/100.000 inhabitants.
 It has a reduced capacity to metastasize.
 The incidence of metastasis depends on tumor size,
being less than 15% in tumors smaller than 1 cm and
can reach over 95% of tumors exceeding 2 cm.
 The incidence of carcinoid tumors depending on
location is:
1. 39% small bowel
2. 26% Appendix
3. 15% rectum
4. 10% bronchial tree
5. 5-7% colon
6. 2-4% stomach
7. 2-3% pancreas
8. > 1% liver
 Gastric location is found in less than 2% of statistics in
our country and 7% of cases in the United States
statistics.
 Classification of gastric carcinoid tumors:
1. Type I (75%) - Associated with chronic atrophic gastritis with or
without pernicious anemia. (In autoimmune gastritis there is a
progressive destruction of parietal cells that leads to atrophy,
intestinal metaplasia, and hypergastrinemia. Hypergastrinemia
plays an important role in gastric carcinoid etiopathogenesis)
2. Type II (5%) - In Zollinger Ellison syndrome especially in patients
with multiple endocrine neoplasia type I (MEN1)
3. Type III (20%) - sporadic tumors, are not associated with
hypergastrinemia, are usually located in gastric antrum and
corpus, reaching large even exulcerated with a more aggressive
evolution (survival at 5 years under 50%).

 Over 85% are asymptomatic, 10% have carcinoid

syndrome, manifested primarily by transient erythema
and diarrhea.
 Macroscopic aspect is of a well circumscribed polypoid
formation covered by mucous membrane, or rather larger
infiltrating the whole gastric wall, which on the section
surface have a yellow-gray appearance.
Histological types are:
 I - tumor cells composed of G cells (gastrinoama) - usually
solitary lesions located in the antrum
 II - tumor composed of enterocromafin-like cells (ECL) -
are the most common, usually multiple, located in the
gastric fundus, small, rarely metastasizing or lethal, do not
cause hypersecretion syndrome, may regress
spontaneously or after antrectomy, are usually treated by
local excision or by endoscopic approach.
 The diagnosis of carcinoid tumor is based on clinical and
biochemical carcinoid syndrome, by dosing 5-HIAA (5-
hydroxyindoleacetic acid) in urine, resulting from
degradation of serum serotonin or CGA (cromogranina a),
which seems to be even more specific.
Treatment of choice is tumors removal, either by endoscopic
approach in small tumors or surgically in large, complex or
multiple tumors.
 Chemotherapy proved to be the most effective although
encouraging results are obtained only 20-30% of cases.
 Somatostatin analogues are used to treat carcinoid
syndrome.
The prognosis is excellent compared to other forms of
malignancy, the average 5-year survival rate is 82%, could
reach 94% in localized forms, 64% when regional lymph
nodes involved and 18% in the presence of metastases.
GASTRIC VOLVULUS
 The gastric volvulus means partial or complete twisting
of the stomach around of its one axis.
 Consequences:
– variable loss of blood supply (ischemia) and possible gastric
tissue death
– obstruction of the flow of material through the stomach
 Determinant factors:
1. Gastric stasis due mainly to excessive laxity of the stomach
fixing ligaments
2. Hiatal hernias
3. Dastric adhesions.
 Contributory factors:
1. Increase intragastric pressure by intrinsic or extrinsic obstacles,
benign or malignant
2. Motility disorders of the stomach
3. Low insertion of eso-gastric junction.
 29% cases

59% cases

2 types of gastric volvulus

Symptoms
 In chronic cases the clinical picture is dominated by
epigastric pain that occurs shortly after meals,
accompanied by early satiety, nausea and vomiting or
simply dyspeptic ulcers symptoms.
 In cases of acute onset symptoms are of an acute
surgical abdomen, with rapid precipitation state of
shock. In these cases the clinical triad is described by
Borchardt:
1. Early vomiting followed by incoercible nausea and
inability to vomit
2. Epigastric pain and distention rapidly progressive
3. Failure to insert a gastric tube
 Diagnosis is based, in addition to clinical signs, on
radiological exploration. In acute forms, abdominal X-ray
reveals 1-2 epigastric fluid-air levels or an epigastric
large gaseous distension. In chronic forms barium
swallow will highlight the shape and position changes of
the stomach. Many times this examination reveals the
cause of the volvulus.

Organoaxial volvulus. Upper

GI image shows an upward
rotation of the stomach along
its long axis, which results in
inversion of the greater
curvature (GC) above the
lesser curvature (LC). Arrow =
pylorus.
Treatment
 Surgery may be performed in emergency in acute cases
or it may be postponed or in elective condition in chronic
or intermittent cases.
 Gastric resection is indicated when gastric wall viability is
affected.
 When gastric walls are viable gastropexy (the stomach
anterior wall is fixed by sutures to the abdominal wall)
the method that prevents recurrence of the volvulus.
 Other pathologies that determined the volvulus should
be treated in the same operation : hiatal hernia, extrinsic
or intrinsic compressions, etc.
Mortality rates reach 80% for untreated and 15-20% with
appropriate treatment in acute cases and 0-13% for
chronic cases.
Intraoperative aspect
1. Torsion of the esophagus
2. Duodenum displaced to the left
3. Clockwise torsion of the stomach
4. The great omentum covers the stomach
5. Hemorrhages on the stomach surface
 Abdominal wall

Stomach

Gastropexy – intraoperative aspect

OPERATED STOMACH
PATHOLOGY
 Under this generic name a number of specific late
complications of the stomach surgery are contained.
 Gastric surgery may result in mechanical and
functional disorders by two mechanisms:
1. Mechanical disorders of digestive transit: stenosis,
efferent or afferent loop syndrome, bilio-gastric or
esophageal reflux which are relatively easy to
correct by a surgical reintervention.
2. Functional disorder, occurring in a number of
patients who have received the correct surgery but
can not adapt to changes in local physiology
(dumping syndrome, postprandial hypoglycemia,
metabolic disturbances, diarrhea), which are more
difficult to treat, surgery in these cases assuming a
secondary role.
 Complications of gastric surgery:
Esophageal Small intestine
1. Gastro-oesophageal reflux 1. Diarrhea
2. Dysphagia 2. Dumping syndrome
Gastric 3. Bacterial contamination
1. Delayed gastric emptying syndrome
2. Bezoars 4. Pancreatic insufficiency, celiac
disease, lactase deficiency
3. Anastomosis stenosis 5. Weight loss and malabsorption
4. Stoma inflammation of:
5. Gastric stump gastritis 1. Metals
6. Peptic ulcer 2. Folic Acid
7. Gastric stump cancer 3. Vitamin B12
8. Afferent loop syndrome 4. Calcium
9. Efferent loop syndrome 5. Fats
6. Anemia
Gall bladder
1. Gallstones
 Early postprandial syndrome called
"dumping syndrome"
 It can occur after any type of intervention. Most frequent
appears after Billroth II type operations and less
frequently after vagotomy with the pyloroplasty or GEA.
 Women are more commonly affected.
 It appears more frequently after surgery for duodenal
ulcer than for gastric ulcer or cancer.
 Symptoms are represented by the feeling of rapid
fullness after meals, nausea, even vomiting, belching,
abdominal cramps, diarrhea.
 General symptoms are: generalized sweating,
weakness, dizziness with, pallor or redness of the face,
palpitations. These phenomena may have varying
intensities.
 Symptoms are closely related to diet and they appear
especially after hypertonic food intake.
 Local hyperosmolarity induces a massive bowel fluid
influx, decreasing the circulating blood volume and its
redistribution. Simultaneously a number of vasoactive
substances (serotonine and kinines) are released being
responsible for general symptoms.

The treatment is prophylactic and curative.

 Dumping syndrome prevention refers mainly to making
an accurate indication as well the best surgical
technique.
 Curative treatment may be medical and surgical.
 Medical treatment is the first choice and it can solve up
to 90% of cases. The base of medical treatment is the
adjustment of diet : small and frequent meals, avoiding
carbohydrates and hypertonic solutions (milk, sweet
solutions), postprandial rest. The patient can itself
remove from diet foods which cause symptoms. The only
drug that has shown consistent efficacy is Sandostatin.
 Surgery is applied only in 10% of cases and is indicated
in case of medical treatment failure in severe forms,
extended over 6-12 months, leading to denutrition.
 There is no standard procedure that improves
symptoms.
 The procedure depends on which type of operation was
previously performed and its goal is to slow down the
gastric emptying.
 The best results were obtained using an anastomosis
with Roux–en-“Y” intestinal loop, but if the initial
operation was a gastric resection with gastrointestinal
anastomosis by Roux, the solution is an interposition of
an anisoperistaltic intestinal loop (Soupault-Bucaille
operation).
OBESITY
SURGERY
 Definition
 Obesity is currently defined as an excess
accumulation of body fat so that it can affect the
health.
 Today is a certain relationship between obesity and
diseases with the highest mortality rate: cardiovascular
diseases, dyslipidemia, diabetes, etc.. Thus 85-95% of
diabetics have been or are obese, and over 60% of
those with dyslipidaemia are obese.
 Obesity is not just an image problem, but rather a
problem of health becoming a major cause of morbidity
and mortality.
 Our times opinion has changed radically, not just from
aesthetic point of view, but also from medical.
Calculation formulas for obesity
Wight (in Kg)
1. Body mass index BMI (IMC) =
Height2 (in sqm.)
Classification
Category BMI Mass (weight)
Severe underweight < 16.5 < 53.5 Kg
Underweight 16.5 to 18.5 53.5 - 60 Kg
Normal 18.5 - 25 60 - 81 Kg
Over weight 25 - 30 81 - 97 Kg
Obese Class I 30 - 35 97 - 113 Kg
Obese Class II 35 - 40 113 - 130 Kg
Severe obesity 40 - 45 130 - 146 Kg
Morbid obesity 45 - 50 146 - 162 Kg
Super-obese 50 - 60 162 - 194 Kg
Hyper-obese > 60 >194 Kg
2. Waist
 Low risk <94 cm for men and <80 women
 Medium risk 94-102 cm
 High risk> 102 cm

"The longer the belt, the shorter the life!"

3. Waist-to-hip ratio
 It is an index which provides information on fat
distribution, and it seems to correlate better than BMI
with cardiovascular risk. It is used mainly to classify
obesity as gynoid (gluteo-femoral type) or android
(abdominal type). The abdominal obesity is the type that
is associated with increased metabolic cardiovascular
risk.
Normal values
Normal values
Women <0,8
Men <1
 4. Body fat percentage
A more precise and individualized way to determine the ideal
weight is a test for assessing body fat percentage.
Formula:
Fat % = 1.2 * BMI + 0.23 * age − 5.4 − 10.8 * sex
( where sex =0 if woman and 1 if man)
 This formula takes into account the fact that body fat
percentage is generally 10% higher in women for the
same BMI and also higher in more advanced age even if
weight remains the same. The accuracy of test is 4%
Risk category Men Women

High < 5% < 10%

Low 5 - 15% 10 - 23%

Normal values < 20% < 26%

Moderate risk 20 - 24% 26 - 31%

High risk 25% or above 32% or above

Dysmetabolic Syndrome
(International Diabetes Federation)
 Abdominal obesity (defined by abdominal
circumference > 94 cm for European men and > 80 cm
for European women) plus at least two of the four
elements below:
1. high triglycerides> 150 mg /dL or specific treatment
for this type of dyslipidemia
2. low HDL-cholesterol <40 mg/dl in men and <50
mg/dL in women or specific treatment for this type of
dyslipidemia
3. high blood pressure: systolic BP. 130 mmHg or
diastolic BP. 85 mmHg, or treatment for previously
diagnosed hypertension
4. elevated fasting glucose level >100 mg/dL or
previously diagnosed hypertension treatment
Anatomy of the body fat
 Body fat is classified into:
 subcutaneous fat, and
 visceral (intra-abdominal)
 In women the amount of fat is higher (about 1/5) but it is
mainly subcutaneous and less visceral than in male.
 Visceral fat has its origins in brown adipose tissue,
incorporating a large amount of blood vessels and a
high density of mitochondria which are very active
metabolically.
 Visceral fat generates heat. It acts as a reservoir of fatty
acids which are rapidly released into circulation for
oxidation processes (combustion).
Hunger feeling
 Regulation of feelings of hunger and satiety, is done by:
 glucose (hunger in hypoglycemia and feeling of
fullness in hyperglycemia );
 digestive factors (glucose entering the duodenum is
followed by decreasing hunger);
 neurological factors, they act on the hypothalamus
and cortex. Endogenous obesity is an expression of
neuroendocrine diseases.
Epidemiology
 Obesity is a problem that currently affects civilized world,
where 25% to 50% of the population suffers from
overweight or obesity.
 It is a medical and social problem, reaching epidemic
proportions worldwide, with over 300 million obese
people, medical costs accounting for 2-7% of total
medical costs in developed countries.
http://tatianamasis.wordpress.com/2008/01/23/the-obesity-epidemic/
news.bbc.co.uk/2/hi/health/7151813.stm
In USA
 108 million people are overweight or obese
 65% of adults are overweight or obese
 30% are obese
 The percentage is higher in minority populations and
those with low incomes
 A second cause of preventable death in USA
Causes-Factors

 Diet
 Lifestyle
 Genetic factors
 Medical and psychiatric diseases
 Socioeconomic factors
 Intestinal flora
Classification
 Hyperplastic Obesity with increased number of
adipocytes, depending on the food received in childhood.
 The number of adipocytes in adults is fixed. It
stabilizes around the age of 20 to 23 years.
 Hypertrophic Obesity that occurs in adults due to
reduced physical activity without a proportional reduction
of nutrition.
 With age, physical activity reduces and the caloric
surplus is turned into triglyceride reserves, increasing
the volume of adipocytes.
 Losing weight means lowering the volume, not the
number of adipocytes, which is a fixed value.
Other factors http://www.nature.com/ijo/journal/v30/n11/full/0803326a.htm l

1. Easy access to palatable foods

2. “Car culture”
3. Mechanized manufacturing
4. Insufficient sleep
5. Endocrine disorders, which interfere with lipid
metabolism
6. Decreased variations in ambient temperature
7. Lowering the percentage of smokers (smoking reduces
appetite)
8. Excess of drugs that can lead to weight gain
9. Pregnancy in advanced ages
10. Positive natural selection of individuals with higher BMI
11. Expanding distribution of ethnic groups and other
population groups that tend to obesity
12. Associative tendency of obese people (marriages, etc.)
Neurobiological mechanisms
 The discovery of leptin in 1994 has elucidated a number
of other hormonal mechanisms involved in hunger,
obesity and peripheral insulin resistance.
 A number of other mediators such as ghrelin, orexin,
PYY 3-36, adiponectin, adipokines, etc. were
discovered.
 It is believed that a deficiency of leptin is associated with
obesity but there was found that many obese have high
levels of this mediator due to resistence development to
this mediator.
 Leptin acts on the arcuate nucleus of the hypothalamus
so that the deficiency or resistance to these mediators
leads to overeating, possible mechanism in some
genetic or acquired forms of obesity.
Clinical forms
Gynoid obesity (Rubens) type. (Pear)
 More frequently in women but can occur in adult men
and children of both sexes.
 Skeletal muscle is poorly developed, and adipose tissue
is located in the lower parts of the body, the lower
abdomen (subombilical) on flanks, hips, thighs, knees,
calves.
 The patient hardly moves, gets tired easily and gain
weight quickly. Respiratory complications, heart disease,
osteo-muscular, etc. are frequent. Some forms retain
more water and salt.
 Does not respond to diet or diuretic treatment, but some
results are obtained by corticosteroids. A special form is
Dercum’s cellulitis, in which fat infiltration is painful. The
disease has a familial character.
Android type (Falstaff).
 More frequent in men.
 Adipose tissue develops in the
upper part of the body (neck,
shoulders, upper abdomen).
 Muscles are strong and develope
less adipose tissue than in the
previous form.
 These people always complain of
hunger and eat more.
Sir John Falstaff is a fictional
 Frequently complications occur: character who appears in three
plays by William Shakespeare as
diabetes, hyperuricemia, a companion to Prince Hal, the
future King Henry V. A fat,
dyslipidemia, atherosclerosis, etc. vainglorious, and cowardly knight.
Consequences of obesity
1. Longevity is reduced by 12-15 years
2. Hypertension
3. Dyslipidemia
4. Diabetes type 2 with all its consequences
5. Atherosclerosis, coronary artery disease
6. Vacular accidents (stroke, heart attack)
7. Gall bladder problems (lithiasis)
8. Osteoarthritis
9. Sleep apnea
10. Cancer (endometrial, breast, prostate, colon)
11. Social discrimination
12. Lack of strength and energy
13. General malaise
14. Immobility
15. Headaches
16. Swelling of the legs
17. Varicose veins
18. Hemorrhoids
19. Chronic gastritis
20. Reflux esophagitis
21. Nervous system disorders: insomnia, increased
appetite for food, increased thirst, vegetative disorders
22. Impaired potency
23. Affecting the menstrual cycle
24. Infertility (female extra pounds, make the pregnancy
difficult and sometimes causes abortions)
25. Hydro-saline metabolism disorders
26. Complications after infectious diseases
27. Susceptibility to pneumonia
Recommendation

 Measures
1. Diet
2. Physical activity
1. Changing lifestyle
2. SPA
3. Alternative medicine (acupuncture)
4. Medication
5. Surgery
6. Etiopathogenetic
7. Aesthetic
8. Treatment of related diseases
Benefits of weight loss
 Decreasing the risk of type 2 diabetes
 Lowering blood pressure
 Improving lipid metabolism
 Reducing the risk of sleep apnea
 Reducing symptoms of osteoarthritis
Treatment
 Scientific studies have shown that conservative treatment,
alone can not provide a significant long-term weight loss in
patients with severe obesity. It has been shown that vast
majority of patients regain lost weight over the next five
years, causing depression, anxiety, irritability.
 Despite the fact that conservative methods are mostly
doomed to failure in obtaining sustainable weight loss, is
still better to give the patient the chance to benefit from
these methods before reaching at surgical therapy
beacuse the diet should still be respected in postoperative
period.
 These patients require multiple investigations,
multidiciplinary checkups, expensive treatments and a
continuous monitoring.
Surgical treatment
 Surgery should be reserved for patients with BMI> 40
or BMI> 35 with associated comorbidities.
 Surgery should be considered after failure of
conventional therapy of obesity: diet and behavior
modification, physical activity and pharmacotherapy.

 BARIATRIC SURGERY = surgical maneuvers that are

applied to obese patients in order to normalize their
weight status, not including removal of fat or other
cosmetic surgery techniques.
Contraindications
1. Psychiatric disorders,
2. Adrenal and thyroid disease,
3. Chronic inflammatory pathology of the digestive
system,
4. Alcoholism and drug addiction.

Bariatric surgery is the only treatment for severe

obesity for which there are scientific evidences
regardig mortality reduction
 METHODS
 RESTRICTIVE (reduces the food intake)
 The role of gastric resection is to induce satiety, to limit
the food intake and so inducing the weight loss.
 MALABSORBTIVE (reduces food absorption surface in
terms of food consumption almost unchanged)
 Weight loss is based on fat and protein malabsorption,
 Improves lipid status and glucose control in patients
with dyslipidemia and diabetes,
 Itmay produce Iron (Fe) deficiency - anemia,
deficiency of fat soluble vitamins (A, D, E, K), bone
demineralization, very smelly flatulence due to
steatorrhea
 MIXED
 Restrictive :
 1. Vertical Banded Gastroplasty
 2. Gastric Banding
 3. Intragastric Balloon
 4. Gastric Sleeve
 Restrictive & Malabsorptive
 1. Gastric Bypass
 2. Bilio – Pancreatic Diversion (Scopinaro)
 3. Duodenal Switch (Marceau)
Vertical Banded Gastroplasty
 For maximum BMI of 50
 The ring is mounted to prevent expansion of the stomach
 50-70% loss of extra pounds in the first year
disadvantages:
 Weight loss is less than in malabsorbtive methods (the
gastric bypass)
 Do not restrict intake of hypercaloric liquids and gastric
pouch can swell after overeating
 20% of patients do not lose weight and only half of them
lose 50% of excess pounds
 Weight regain over the next three years
Gastric Banding
 Indicated for BMI = 40-50
 Weight loss of ≈ 50%
 20% without apparent effect
 Complications in 20% cases:
 - Ring slippage
 - Ulceration, perforation of the stomach
 - Enlargement of the upper portion of the stomach
Gastric Banding
adjustable silicone ring
 Intragastric Balloon

•Gastric Balloon - 1990

•It is applied by endoscopic approach
•Induces satiety sensation
•Reversible procedure

•It is reduced after max. 6

month
•The weight loss is 25%-
40% of extra pounds
Gastric sleeve
 Irreversible but simple and without
implantation of foreign bodies
 Does not affect digestion
 Weight loss in the first year 60% of extra
pounds
 May regain weight ≈ 5 years, due to
enlargement of the remaining stomach.
Roux – En – Y Gastric ByPass (RYGBP)

 For BMI> 50
 Only 15-20 cc gastric reservoir remains
 Long-term weight loss 50%
 Requires food intake surveillance and need more
supply with vitamins and minerals
 No serious late complications
 Improve or resolve co-morbidities (diabetes)
Scopinaro Procedure- Bilio – Pancreatic
Diversion
 It is a mixed restrictive and malabsorption method.
 Stomach volume is reduced by resection
 Digested food absorption surface is reduced by bowel
anastomosis close to the cecum.
 Bile and pancreatic juice will be in contact with food only
in the terminal portion of the intestine (the last 65-75 cm
of ileum - only in this portion the digestion will occur).
 Cholecystectomy is associated in most cases.
 Greater weight loss - 80% of surplus
 Risk of hypoalbuminemia, hypovitaminosis and dumping
syndrome
Duodenal Switch (Marceau Procedure)

 The pylorus is
preserved to prevent
dumping syndrome
 A longer digestive
portion of the intestine
is preserved (75-100
cm) for better digestion
Improving the status of co-morbidities in% after GBP
Equipment and special tools

Laparoscopy tower
Instruments
Laparoscopic approach
Gastric sleeve film - http://chirurgiemures.ro/mov/Gastric_sleeve.wmv
SURGICAL PATHOLOGY OF
THE SMALL BOWEL

 Anatomy
1. Intestinal volvulus
2. Intussusceptions
3. Crohn disease
4. Meckel’s Diverticulum
5. Tumors
Anatomy
The small bowel is the longest segment of the digestive
tract extending between pylorus and ileo-cecal valve,
occupying most of the peritoneal cavity.
The small intestine length is about 4-7 meters, with
variations between 3 and 10 meters, depending on the
tonicity, constitutional type, etc.
Small intestine is composed of three parts: duodenum,
jejunum and ileum.
The jejuno-ileum has a diameter of 2-4 cm and describes
“U” shaped 15 -16 loops of which the first 8 to 10 are in
horizontal position belonging to jejunum and the rest in
vertical position belonging to the ileum.
The small intestine is neighbouring with the majority of
abdominal viscera due to the large space they occupy:
up with the transverse colon and mesocolon, down with
the pelvic organs (bladder, rectum, uterus), to the right
with the ascending colon, to the left with the descending
colon, posterior with the retroperitoneal organs and
anterior with the greater omentum.
Except of duodenum, the small intestine is provided with
mesentery.
Mesentery is a dependence of the posterior peritoneum
through which the intestines are fixed to the rear
abdominal wall. The root of mesentery has a fixed edge
of 15-18 cm long and it extends obliquely from the
duodenojejunal flexure (L2 vertebra) to the cecum. In the
mesentery there are vessels (branches of superior
mesenteric artery and veins), nerves and lymphatics, all
covered by fatty tissue.
The distal portion of the
mesentery is much longer
than the proximal and
forms folds. Its greater
length in the last ileal
loops explains why this
loops are commonly
involved in incarceration
on the right side inguinal
and femoral hernias.
The duodenum, the first and shortest (25 cm) part of the
small intestine, and also the widest and most fixed part.
The duodenum begins at the pylorus on the right side
and ends at the duodenal junction on the left side. The
duodeno-jejunal flexure is supported by the attachment
of the suspensory muscle of duodenum (Treitz)

It has 4 segments. The

second, third and part of the
fourth segment are
retroperitoneal. The pancreatic
duct and common bile duct
empty into the second
duodenal segment at level of
major duodenal papilla
through the sphincter of Oddi.
The jejunum and the ileum. Although these two
segments appear similar, there are a few distinguishing
features: the jejunum is thicker and has plicae circulares,
while the ileum has more Peyer's patches. The small
bowel enters the cecum at the ileocolic junction.
Occasionally a remnant of the vitelline (vitellointestinal)
duct persists in the adult as an ileal (Meckle's)
diverticulum, which is situated near the ileocolic junction.
It may contain gastric or pancreatic tissue, and
inflammation of the diverticulum may simulate acute
appendicitis.
Vascularization
The small bowel is the best vascularized segment of the
digestive tract which is an important aspect of a safe
anastomosis.
The duodenum is primarily supplied by the inferior
pancreaticoduodenal artery and superior
pancreaticoduodenal artery (from celiac trunk through
other arteries)
For jejunum and ileum the source of arterial supply is the
superior mesenteric artery (SMA) emerging from the
abdominal aorta below the celiac trunk.
Each of those 12-16 primary branches emerging from
SMA divides into two branches, which unite with
adjacent branches forming a series of arterial arcades
(arches). It may be up to five arterial arcades (in the
longest portion of the mesentery) diminishing in size the
nearer they approach the intestine. From the last arcade,
vessels enter the intestinal wall as vasa recta.
 Venous drainage originates from mucosa and submucosa
network, from where it forms a subserosal network from
which emerge 7-8 venous trunks that converge in the
superior mesenteric vein, a tributary of the portal vein.
Lymphatic vessels, originate from lacteals, in the intestinal
villi which drain into the lymphatic plexuses in the walls.
The lymphatic plexuses drain into lymphatic vessels
between the layers of the mesentery and then sequentially
through three groups of lymph nodes:
1. Juxta-intestinal lymph nodes (close to the intestinal
wall),
2. Mesenteric lymph nodes (scattered among the arterial
arcades), and
3. Central superior nodes (along the proximal part of the
SMA).
Efferent lymphatic vessels from these nodes drain into the
superior mesenteric lymph nodes.
In the lower part of the ileum there are the Peyer's
patches, aggregated lymphoid nodules.
Carcinoma of the intestine can spread to the liver via the
portal vein as well as via lymphatics.
Intestine innervation originates in celiac plexus and
mesenteric artery plexus, from where fibers are
distributed through the perivascular network to the
myenteric plexus (Auerbach) and submucous
(Meissner).
Inside, the small intestine, contains circular valves
(Kerkring's plicaes) with an initially height of 7-10 mm,
that decrease gradually towards the ileum, covered by
intestinal villi that give the soft appearance of the
mucosa. All these elements significantly increase the
contact surface with intestinal content for a better
absorption of nutrients.
The small intestine presents four layer: serous, muscular,
submucosa and mucosa.
Mucosa is best represented, it occupies 2/3 of wall
thickness. Mucosa epithelium is composed of
enterocytes, Goblet cells, Paneth cells, stem cells
enterochromaffin cells, and undifferentiated cells.
SMALL INTESTINE
VOLVULUS
Intestinal volvulus is a distinct clinical form of intestinal
obstruction characterized by a twisting of the intestine or
intestinal segment entirely around its mesenteric axis at
least 360 °.
The pathological process can involve the entire intestine
- total volvulus, that frequently occurs in children. In
these cases it is often involved the right colon also
(common mesentery).
Segmental volvulus occurs mainly in adults, predilectly
in men.
Primary volvulus is mainly due to congenital anomalies
(common mesentery).
Secondary volvulus occurs due to obstructions or
compressions (straps, tumors, adhesions, etc.).
The aspect of the intestinal segment and its mesentery
interested in the pathological process is much like the
aspect of the entero-mesenteric infarction. In the initial
phase the intestine is enlarged with thickened wall,
edematous and red-purple color. Then the segment
becomes brown, inert, non-peristaltic, looking like a
"dead leaf" and has sometimes sphacelated
(gangrenous) areas or macroscopic perforation.
At the base (root) of the twisted bowel there is the ring of
torsion where the most serious lesions are found due to
ischemia.
Fluid in peritoneal cavity looks bloody with fetid smell.
The clinical picture is dominated by symptoms of
intestinal occlusion installed more or less acutely,
followed by rapid onset of the shock. (violent pain, which
does not respond to treatment, intestinal transit stops
with nausea and vomiting, abdominal distension).
Although there are no pathognomonic signs for intestinal
volvulus, X-ray can be useful in highlighting signs of
occlusion, with multiple fluid-air levels.
The differential diagnosis is made with other causes of
acute surgical abdomen: acute pancreatitis, entero-
mesenteric infraction, perforation peritonitis, etc.
Treatment is exclusively surgical and of extreme urgency.
It will be preceded by a short and energetic rebalancing
continued intra and postoperatively.
Surgery may be conservative or radical.
Conservative treatment is indicated in forms with recent
onset where the twisted intestine is still viable. Sometimes
it is difficult to assess the viability. After detorsion, the
intestine is washed with lukewarm saline solution, and
lidocaine may be infiltrated in the mesentery. A special
attention must be given to the root of twisted intestine
where lesions are more important. To prevent the relapse
of the volvulus, enteropexy may be performed.
Where the intestinal segment is compromised, segmental
resection is the solution.
The total volvulus raises difficult problems for surgical
attitude and unfortunately usually is fatal.
INTUSSUSCEPTION
 Intussusception is produced when a segment of
intestine invaginates into the adjoining intestinal lumen,
causing bowel obstruction.
It occurs more frequently in children but can occur in
adults too.
There are two types of intussusception:
1. Secondary or organic when there is a mechanical
obstacle (polyp, tumor, stenosis, etc.)
2. Primary or functional (idiopathic) it occurs in an
unaffected bowel.
An intestinal intussusception, once started, tends to
progress due to intestinal peristalsis. Invagination
process will stop at some length because of the tension
in the stretched mesentery.
Intussusception may occur in any intestinal segment,
but it mostly appears at ileocecal valve where the
terminal ileum invaginates into the ascending colon
favored by the larger diameter of the colon.
The part that prolapses into the other is called the
intussusceptum, and the part that receives it is called
the intussuscipiens.
There are two types of invaginations:
1. Simple – with 3 cylinders
2. Complex with 5 or 7 cylinders
At the neck of intussusception a venous stasis and
swelling of the invaginated loop occurs, which will result
in vascular elements compression, responsible for the
necrosis.
The classic triad of signs and symptoms is: vomiting,
abdominal pain, and passage of blood per rectum.
On abdominal palpation the intussusception can be felt as
a thickened sausage shaped intestinal loop.
Abdominal plain radiography will show a typical pattern of
intestinal obstruction.
Contrast radiography with swallowed barium and
irigography (barium enema) could identify the problem but
the liquid barium is a problem for surgery if a resection of
the bowel is needed.
Radiological appearance at barium enema is the stop of
the contrast substance, taking the form of dome, cup, or
trident, and form of cockade in ortoroentgenograd aspect.
Ultrasound examination is preferred to barium as intestine
intussusception can be identified in most cases.
US aspect
In infants, symptoms are more intense, and the
suspicion of intussusception is more common.
Digital rectal examination must be performed, and may
reveal the presence of blood in stool.
In most cases in adults the patient is operated with the
diagnosis of bowel obstruction, the intususception
process being an intraoperative surprise.
Treatment may be conservative and surgical.
Conservative treatment is indicated in children in the first
6 hours from the debut of symptoms and consists of an
enema (may be with barium) which increases the
pressure in the intestine and may cause the return of the
intestine in its normal position (reduction).
Ileoileal intussusception
The surgical treatment may be represented by intestinal
reduction and if the affected intestine is viable an
enteropexy is performed to prevent relapse. If the
intestine is not viable, or has a dubious viability,
intestinal resection of the affected segment is performed
followed by restoration of the digestive continuity.
The prognosis is very serious in untreated cases or
excessively delayed, and it is significantly improving, in
direct proportion, to the earliness of the intervention.
 CROHN'S DISEASE
(REGIONAL ENTERITIS)
It is a necrotising granulomatous nonspecific
inflammation. Although originally described only for the
terminal ileum, it was subsequently observed in any
intestinal segment, affecting even the colon.
The etiology is not well defined.
It affects both sexes and the age ranges between 20 and
40 years.
Crohn's disease affects 400,000 - 600,000 people in
North America. Prevalence estimates for Northern
Europe have ranged from 27to 48 per 100,000.
Pathology. The favorite location is the terminal ileum, on
the last 30-40 cm. Jejunal location is a rarity.
Common locations of Crohn’s disease
The appearance of the affected intestinal segment differs
as the disease is caught in the acute or chronic stage.
In acute stage the affected loop is red-purple, swollen, stiff,
covered by fibrin deposits. Intestinal wall is thickened and
brittle. Limit to the normal intestine is more or less clear, but
the real limit of the lesion exceeds the apparent
macroscopic limit. The mesentery has an inflammatory
process, edema and enlarged lymph nodes.
In chronic stage, the affected segment looks like a
cardboard being hypertrophied and rigid with
sclerolipomatosis tissue. Due to the bowel wall thickening,
the lumen is much narrowed.
Associated mesentery is retracted and together with the
affected intestine can adhere the to neighboring organs,
gaining a pseudotumoral appearance. Between these
adhesions chronic abscesses may be present.
The affection has a great tendency to fistulization in
neighboring viscera or to the skin.
Aspect of the mucosa in Crohn’s disease
Symptoms. The clinical picture may vary as the disease
is in acute or chronic stage.
In the acute form, occurring mostly in children, the
clinical picture is of an acute appendicitis associated
with diarrhea.
The chronic form, most common, can evolve from
acute form, or may evolve from the beginning as a
chronic form.
Depending on predominant symptoms there may be
several clinical pictures:
– A form that mimics ulcerative colitis manifested by
right iliac fossa pain occurring at 5-6 hours after
ingestion of food, accompanied by diarrhea, even
bloody.
– Occlusive form evolves as a chronic occlusion with
Konig syndrome in the right iliac fossa, and finally as
a complete occlusion.
 – Pseudotumoral form is characterized by the presence
of a right iliac fossa tumor with inflammatory
phenomena associated to chronic pain and
subocclusive symptoms. This form may develop
external fistulas in the abdominal wall or perineum.
Laboratory shows hyperleukocytosis anemia in severe
forms, rarely eosinophilia.
Irigography shows narrowing of the affected segment and
upstream dilatation.
Endoscopic mucosal appearance is "cobblestone"-like
and is seen in approximately 40% of cases. The
gastroenterologist can also perform biopsies from affected
area.
Clinical diagnosis must be supported by histopathological
diagnosis.
Differential diagnosis must be made in acute forms
mainly with acute appendicitis and in chronic forms with
ulcerative colitis, intestinal tuberculosis and intestinal
tumors.
Evolution. Crohn's disease has a long evolution, with
successive acute and subacute episodes with an
increased tendency to chronicity.
Complications are possible at any stage of evolution and
consist of occlusions, perforations, internal or external
fistulization. Fistulas have a chronic evolution leading to
patient weakening.
Treatment. Although, at present time, there is no cure for
Crohn's disease, if it is diagnosed early, the disease can
be treated obtaining long remissions. Medical or surgical
therapeutic indication is determined by the evolutionary
form.
Certain lifestyle changes, including dietary adjustments
can reduce symptoms.
Medication used to treat symptoms of Crohn's disease
include aminosalicylic acid, prednisone,
immunomodulators such as azathioprine, mercaptopurine,
methotrexate, infliximab, adalimumab, certolizumab and
natalizumab. Hydrocortisone should be used in severe
attacks of Crohn's disease.
Surgery is indicated just for complications such as
obstructions, fistulas and/or abscesses, or if the disease
does not respond to drugs.
Resection of a large portion of the bowel is the only one
that has some chance of cure. Perforation suture and
stomas are prohibited as they won’t heal. After the first
surgery, Crohn's usually shows up at the site of the
resection, or in other locations. (another resection may be
necessary within five years).
Prognosis. Crohn's disease is a chronic condition but the
mortality rate is relatively low. However, Crohn's disease
is associated with an increased risk of small bowel and
colorectal carcinoma.
SURGICAL PATHOLOGY OF
THE MECKEL’S
DIVERTICULUM
Meckel’s diverticulum is a true diverticulum of the intestine
located on the antimesostenic edge of the ileum at 70-100
cm away from the ileo-cecal valve and appears with a
frequency of 1-3%, being more common in men.
It has a conical or cylindrical shape, of 5-10 cm long and
doesn’t have its own mesentery. It may be free in the
peritoneal cavity or may be fixed to the umbilicus.
In the mucosa layer may exist heterotopic areas of
gastric, duodenal, pancreatic and rarely colic cells.
Meckel’s diverticulum may be the site or the cause of
many pathological processes such as: ulceration and
bleeding, torsion with necrosis and perforation
inflammation, obstruction with occlusion, tumors, involved
in incarcerated hernias (Littre), etc.
 Meckel diverticulitis
It is an inflammatory acute or subacute process very
similar to acute appendicitis.
Pathological forms are identical: catarrhal, phlegmonous
and gangrenous, with or without perforation.
From clinical point of view there are 2 aspects that may
draw attention to a diverticulitis: the pain located around
the umbilicus associated with muscle contraction and
occlusive symptoms that appear more frequently than in
appendicitis.
Preoperative diagnosis however is rare, patients being
operated in most cases with diagnosis of acute
appendicitis. Therefore, whenever intraoperative
appearance of the appendix does not explain the clinical
symptoms, is indicated to explore the last meter of ileum
to find a possible Meckel diverticulitis.
In some obese patients exploration through the right iliac
fossa laparotomy (Mc Burney incision) is much difficult
than in a laparoscopic approach.
Treatment consists of diverticulectomy, but, unlike
appendectomy, resection of Meckel’s diverticulum
should be large enough to include the intestinal wall
around the base, or a segmental resection of the
intestine (enterectomy) may be applied.
 Diverticulum ulcer
Symptoms are represented by intermittent pain around
the umbilicus associated with bleeding through the
rectum as melena (black stool) or even fresh blood when
there is an abundant bleeding. Another complication is
perforation with generalized peritonitis.
In most cases diagnosis is made intraoperatively when
laparotomy is performed for serious gastrointestinal
bleeding or a peritonitis.
Diverticular ulcer treatment is exclusively surgical and
consists of diverticulectomy.
 Intestinal obstruction
caused by Meckel’s diverticulum ranks second after
bleeding in terms of diverticular complications and
represents about 5% of all causes of intestinal
occlusion.
Mechanisms:
1. By strangulation, if a very long diverticulum is
wrapped around intestinal loop.
2. By volvulus, which can be only diverticular or
enterodiverticular.
3. By invagination, which is also at the beginning only
diverticular, but as progression goes on, it becomes
ileo-ileal and then ileo-colic.
Treatment is diverticulectomy or enterectomy.
 Diverticular hernias
Meckel’s diverticulum may be contained in an inguinal
hernia, femoral or umbilical sac. Hernias containing
Meckel’s diverticulum are called Littre hernias.
 TUMORS OF SMALL
INTESTINE
Small bowel tumors occur in patients over 40 years
old, the benign forms being 10 times more common
than the malignant ones and their common feature is
that they do not have any specific symptoms, only 1 of
10 patients being symptomatic, aspect that delays
much the diagnosis.
BENIG TUMORS
Adenoma - the most frequently encountered especially in
the proximal portion of the intestine.
Leiomyoma - occurs at ages of 40-70 years, with
dimensions of about 2 cm.
Fibroma
Lipoma - represents 8-20% and are located mainly on the
terminal ileum.
Hamartoma - can occur in Peutz-Touraine-Jeghers
syndrome.
Benign neurogenic tumors represent 1% and can be:
schwannomas, ganglioneurinomas, neurofibromas.
Hemangiomas represent 7% and can be: teleangiectasia,
capillary hemangiomas and cavernous hemangiomas.
Lymphangiomas – represent 2% and can be simple and
cavernous.
MALIGNANT TUMORS
Adenocarcinoma
Sarcomas
Lymphosarcoma
Spindle cell sarcoma
Hodgkin lymphoma
Carcinoid tumors – benign but potentially malignant
Symptoms depend on tumor location, the volume and how
their development involve the intestinal lumen.
Symptoms may be: abdominal colicky pains,
subocclusive phenomena, nausea, vomiting, occlusive
symptoms, digestive bleeding, occult or gross
exteriorized in the stool as melena or fresh blood,
sometimes Konig syndrome.
On palpation in some cases the tumor can be felt.
Paraclinical diagnosis of the small intestine tumors is
difficult. Radiological investigations cannot help much.
Endoscopy performed with a thin (5 mm diameter)
endoscope may reach till the lower ileum. CT and MRI
scans are the most important investigation being able to
diagnose 97% of cases. Other possibilities are: video
capsule endoscopy, laparotomy and laparoscopy.
Treatment is only surgical being represented by more or
less wide segmental resection of the intestine.
Prognosis is strictly related to tumor form, benign or
malignant, and also related to the type of tumoral
complication (bleeding, occlusion, perforation).
 LARGE BOWEL
PATHOLOGY
 Surgical anatomy aspects
1. Megacolon
2. Colon polyposis
3. Colon cancer
Some aspects of surgical
anatomy of the colon
 The colon, or the large bowel, extends from the ileocecal
valve described by Bauhin, till the rectum, and lies
around the small intestines.
 Its length is about 1.6-1.7 m and its capacity of 2-3 L.
 It has a minor role in digestion and absorption but a
more important role in evacuation of waste.
 The wall of the colon is much thinner than of the small
bowel and his arterial supply is also poorer, aspects that
make colon surgery more difficult raising special
problems of surgical tactic and technique. Surgery of the
colon is dependant of its vascularisation. The
anastomotic risk is higher.
 Another important aspect is that the content of the colon
is very septic, a good preoperative preparation being
necessary in most cases. Septic risk is much higher in
colic surgery.
 From anatomical point of view the colon is divided in four
segments:
1. Ascending (cecum, and ascending colon)
2. Transverse (hepatic flexure, transverse colon and
lienal flexure)
3. Descending colon
4. Sigmoid colon
 From surgical point of view there are only two segments:
the right colon and the left colon. This segmentation is
also in accordance with the embryology, physiology,
vascularization and innervation of the colon. These two
segments are separated by a functional sphincter, so
called Cannon Boehm, which may be observed on some
radiographies.
 The right colon extends from ileocecal valve till the 2/3
portion of the transverse colon.
 The transverse and sigmoid colon are intraperitoneal
organs being completely covered by visceral peritoneum.
Both segments have mesocolon called transverse
mesocolon and sigmoid mesocolon (mesosigma) and
also are the best vascularized segments of the colon.
They are very mobile and sometimes with an appreciable
length. These are important aspects from clinical and
surgical points of view.
 Due to excessive mobility, tumors located on this
segments can penetrate other anatomical structures
located far from the normal anatomical position of the
colon. For example, there are cases when tumors of the
transverse colon penetrate the urinary bladder or the
uterus (colon ptosis).
 Excessive mobility may cause pathological processes
such as sigmoidian volvulus.
 The length of this segments allows resection of large
portion of the colon and tension free anastomosis.
 Having a better vascularization and being covered by
peritoneum they offer a good material for anastomosis
with lower risk of fistula occurrence.
 The ascending and descending colon are secondary
retroperitoneal, wrapped by peritoneum only on the
front due to coalescence process leading to formation of
Toldt I and Toldt II fascia, thus explaining the easy
extension of cancer on the posterior wall and rapid
penetration into surrounding tissues.
 In some cases the cecum may have an excessive
mobility that can lead to volvulus.
 Right colon is more superficial located and has a much
larger caliber than the left colon, which allows the
development of larger tumors in the absence of
occlusive symptoms. The left colon’s lumen is not so
large, and tumors can’t grow to big dimensions because
they rapidlly induce stenosis and obstruction.The left
angle of the colon is the highest and deepest located
segment of colon being the most difficult to be explored.
 External appearance of the colon is cacacteristic being
different from that of the small intestine. The haustra of
the colon are the small pouches caused by sacculation,
which give the colon its segmented appearance. The
taenia coli runs the length of the large intestine. Because
the taenia coli is shorter than the intestine, the colon
becomes sacculated between the taenia, forming the
haustra.
 The colic wall structure is composed of the same existing
layers throughout the digestive tract (mucosa,
submucosa, muscular, subserosa and serosa or
adventia) but with different features and organization.
 The outer muscular layer consists of longitudinal fibers
concentrated in 3 bands called taenia coli (mesocolic,
free and omental).
Arterial supply (two main sources)
Superior mesenteric artery (SMA) – for the right
colon
1. Ileo-apendicular artery
2. Right colic artery
3. Middle colic artery (inconstant);
Each of these arteries divides into two branches (ascending and
descending) which join together to form a marginal arch
described by Riolan at a distance of 5-7 cm from the colon edge.
From this arch emerge the vasa recta which also divide into
anterior and posterior branches.
Inferior mesenteric artery (IMA) – for the left colon
1. Left colic artery – which divides into an ascending branch to join
the left branch of the colic middle artery and form the Riolan
arcade, and a descending artery to join the ascending branch of
the first sigmoid artery.
2. 3 sigmoid arteries, which join together to for more consecutive
arches
3. Superior rectal artery
 Venous drainage of the right colon. The venous
blood is collected by homonymous veins along the
arteries and then via the superior mesenteric vein
(SMV) flows into the portal vein towards the liver.
 Venous drainage of the left colon is tributary to the
inferior mesenteric vein (IMV) through the
homonymous veins. The IMV flows into the splenic
vein under the Treitz angle of the duodenum and
behind the pancreas.
 Through the venous system tumoral cells
metastasize (spread) to the liver and that’s why they
are the first vascular anatomical elements ligated
and resected during radical oncological operations.
Lymphatic drainage
For the right colon
 Lymphatic drainage starts from the lymphatic parietal
network and goes through four lymph nodes stations :
epicolic lymph nodes (located on the wall of the colon,
pericolic (along the marginal vascular arch), intermediate
(along the colic arteries and veins), superior mesenteric
(at the origin of SMA).
For the left colon
 Lymphatic drainage follows the same four stations:
epicolic, pericolic, intermediate and central (at the root
of the IMA).
 Lymphatic drainage from the entire colon and proximal
two-thirds of the rectum goes to the paraaortic lymph
nodes that then drain into the cisterna chyli.
Anatomical relations of the colon
Right colon
1. Duodenum, liver, gall bladder, stomach, pancreas, small intestine
2. Right kidney, right ureter
3. Testicular / ovarian vessels
4. Iliohypogastric nerves, ilioinguinal and lateral cutaneous femoral
(lumbar plexus branches)
5. Great omentum and abdominal wall
Left colon
1. Spleen, stomach, pancreatic tail
2. Subcostal vasculonervous elements
3. Left kidney and left ureter
4. Iliohypogastric nerves, ilioinguinal, genitofemoral, lateral femoral
cutaneous and femoral (lumbar plexus branches)
5. Testicular / ovarian vessels
6. Left external iliac artery
7. Uterus and adnexa, urinary bladder, small intestines
8. Great omentum and abdominal wall
Physiology
 The large intestine is mainly responsible for storing
waste, absorbing water, maintaining the water
balance, minerals and vitamins (vitamin K).
 It contains nearly 60 varieties of microflora or
bacteria (predominantly anaerobes) which have a
role in fermentation, some nutrient production, acid-
base balance, and to prevent proliferation of
harmful bacteria.
 The right colon is functionally the colon of
fermentation, with role of water absorption, while
the left colon serves mainly to store and evacuate
the feces.
Investigation methods of the colon

 Most investigating procedures for colon are invasive and

encumbered by certain risks (1.9% complications),
especially colon perforation (1/800 colonoscopies).
 The vast majority of these can be performed in
ambulatory conditions.
 Endoscopic investigation methods have become the main
methods of diagnosis in colic pathology. Unlike X-ray, they
provide direct visualization of lesions and allow the
collection of tissue fragments for diagnostic purposes.
 Endoscopic examination (as well radiological) implies a
completely emptied colon.
 Rectosigmoidoscopy and colonoscopy (pancolonoscopy),
are the main investigations.
 Rectosigmoidoscopy investigates the colon up to about
80 cm from the anus, and can be performed on an
outpatient basis (does not require hospitalization). It
takes about 6-10 minutes. The examination is often
enough for screening, given the fact that the vast
majority of colic pathology is localized to the left colon.
 Colonoscopy is a more laborious (it takes 15-30 minutes)
procedure and the endoscope progresses till the cecum.
It can be performed in hospitalized patients but also on
an outpatient basis. Frequently the examination is
performed in intravenous general anesthesia.
 Barium enema or irigoscopy, is the fundamental
radiological method for investigating colon diseases.
 Double contrast barium enema (air is introduced after
evacuation of barium). It is a fine examination that can
identify changes on the inner surface of the colon.

Barium enema Double contrast barium enema

 Virtual colonoscopy – is a three-dimensional
reconstruction of a computed tomography of the colon
using a special software. The main drawback is that it
cannot perform biopsies.

polip
 Other investigations are performed especially for liver
metastases and tumor relations with the surrounding
organs.
Abdominal ultrasound
CT or MRI scan
Urography and cystoscopy when there is a suspicion
of penetration in the uretres or urinary bladder.

Liver metastase Stenosing colon tumor

MEGA-DOLICO-COLON
Mega = large
Dolicho = long
It can be:
1. Congenital
2. Idiopathic
3. Acquired
4. Toxic
5. Symptomatic
CONGENITAL MEGACOLON
(aganglionic megacolon,
Hirschsprung disease)
 Etiopathogenesis: the absence of intramural
ganglia at birth (Meissner’s submucous plexus having a
sensitive role, and Auerbach’s mioenteric plexus with
motor role) of the terminal sigmoid and rectum walls.
The length of bowel that is aganglionic varies.
 Prevalence = 1: 20,000 children, more frequently in
males, often has a familial character.
 Anatomopathology:
 Macroscopic: narrowing of the affected colon and
distension of the superjacent - giant fecaloma
 Microscopy: the absence of intramural ganglionic
plexus
Symptoms
 Symptoms appear few weeks after birth and go
through several successive periods:
1. Neonatal period: constipation, abdominal distension,
pain, postprandial vomiting (signs of low intestinal
obstruction, incomplete or chronic).
2. Infant: big belly giving the child a grotesque
appearance, the same complaints as above.
3. The period of childhood and adolescence: the
persistence of constipation and abdominal
distension, defecation possible only with enema (1
stool at 5-10 days).
 On rectal digital examination the
ampulla is found empty !
Megacolon in infant
Diagnosis is based on:
1. Clinical examination - the distended abdomen
2. Plain abdominal radiography: important and
permanent pneumatic distension of the entire colon
3. Barium enema: narrowed segment of the colon and
superjacent massive distension
4. Sigmoidoscopy with biopsy: histopathology reveals
the aganglionic tissue

Plain abdominal radiography

Evolution: untreated the mortality rate in the neonatal
period is about 60-70%. Those who survive have a less
serious evolution.
 The general condition is influenced and may take two
clinical forms: of chronic toxemia (toxins from the colon
enter the vascular system) and a permanent restrictive
type of respiratory inssuficiency.
Appearance: underweight child, always tired, pale, inert,
with tachypnea and polypnea, and in advanced stages
even cachectic.
 Rarely acute occlusive episodes appear.

Treatment is purely surgical. If occlusion does not

appear, operation is not indicated under the age of 1 year.
Instead, diet is recommended to ensure the intestinal
transit and also small repeated enemas.
 Surgical treatment consists of resection of the abnormal
segment of the colon and restoration of normal transit.
Usually the firs step is a colostomy above the affected zone
which allows the colon normal emptying. After a period,
when the child is in a better condition, resection with
different types of anastomosis can be performed.
 There are two types of operation:
 Swenson’s operation. Resection of the aganglionic
segment of the colon with a pull-through technique (the
anal sphincter is preserved and the normal colon is
pulled through the anal canal). The anastomosis is a
colo-anal type.
 Duhamel operation does not remove the rectum. After
resection, the normal colon is pulled through the
posterior wall of the rectum (in the presacral space) and
through the anus. It preserves a portion of the rectum
for its normal function in defecation process.
 IDIOPATHIC MEGACOLON
 It appears in children aged between 3 and 7 years.
 Causes are unknown.
 Symptoms: chronic constipation, moderate abdominal
distension. On rectal examination the ampulla is
filled with feces.
 Barium enema shows a distension of the entire colon
without narrowing of any segment. Histology reveals the
presence of normal ganglia cells of myenteric plexus.
 In the absence of occlusion the treatment is strictly
conservative with an adequate diet rich in fibers, small
enemas, laxatives and psychotherapy.
 ACQUIRED MEGACOLON
 In Central and South America infection with
Trypanosoma cruzi (Chagas disease) can lead to the
destruction of ganglia cells producing a clinical picture
of a congenital megacolon installed in adulthood.
 Other conditions may induce megacolon in adults such
as: schizophrenia, cerebral atrophy, spinal injury,
parkinson disease, myxedema, amyloidosis,
scleroderma, some drugs, etc

 Rectal examination reveals the ampulla filled with

feces.
 Treatment addresses the underlying disease, with the
careful use of enemas and laxatives or purgatives.
 TOXIC MEGACOLON
 Toxic dilatation of the colon may occur in Crohn's
disease but is more common in ulcerative colitis. This
condition is considered a severe form of ulcerative
colitis presenting additional colonic distension, due to
severe inflammation.
 Treatment addresses the underlying disease.

SYMPTOMATIC MEGACOLON
 It is secondary to a chronic organic barrier, represented
by some incomplete stenosis of the anal canal or rectum.
 Treatment is purely surgical, consisting of removing the
obstacle.
 DOLICOCOLON
very long colon but not enlarged

 Chiray’s typical triad:

1. constipation,
2. abdominal distension,
3. pain.
 Diagnosis is made on irigography that shows long colic
loop and a delay in evacuation of barium, after 2-5 days
(normal evacuation is in the first day).
 Nonsurgical treatment is common (proper diet, laxatives
/purgatives). In case of occlusion (volvulus) surgery is
required (segmental colectomy).
COLON POLYPS
 The intestinal polyp is defined as a mucosal surface
elevation. [Gr. polypous = morbid excrescence, From
polys = numerous + pous = foot].
 Estimated prevalence of asymptomatic polyps in the
general population ranges from 1.6-12%, while in
population over 70 years, may reach 40%.
 Because they are highly prevalent especially with
increasing age, they confer an important predisposition to
colon cancer.
Classification
 Non-neoplastic polyps
 Hyperplastic – are the most common, without
dysplasia. Located in the recto-sigmoid have less then
0.5 cm diameter.
 Submucosal they may be non-neoplastic or neoplastic
represented by benign lymphoid polyps, lipomas,
leomyomas, hmeangiomas. Smooth overlying
mucosa.
 Inflammatory polyps (pseudopolyps): they are benign
without malignant potential. They occur as a result of
regenerating processes of ulcerated mucosa.
 Hamartomatous polyps, which can be found in the
following diseases: Peutz-Jeghers syndrome, Cronkhite-
Canada syndrome, Cowden disease, juvenile polyps (of
retention). They are made up of a mixture of tissues.
 Neoplastic polyps:
 Adenomatous polyps (tubular, tubulo-villous, villous).
Represent 2/3 of colonic polyps. Neoplastic polyps are
considered a premalignant condition and need an
adequate treatment. Time required for development
of cancer from polyps is about 7-10 years.
Endoscopic classification

1. Sessile – the base is attached to the colon wall

2. Pedunculated – a mucosal stalk is interposed between
the polyp and the wall
3. Flat – polyp’s height is less than one-half the diameter
of the lesion
4. Depressed - lesions appear to be particularly likely to
harbor high-grade dysplasia or be malignant even if
small.
 Inherited polyposis syndromes
1. Familial adenomatous polyposis
2. Peutz-Jeghers syndrome
3. Turcot syndrome
4. Juvenile polyposis syndrome
5. Cowden disease
6. Bannayan-Zonana syndrome
7. Gardner's syndrome
 Non-inherited polyposis syndromes
1. Cronkhite-Canada disease
2. Eversmeyerous Polypius
Clinical picture
 Although most polyps are asymptomatic, they are often
in a continuous growth process (may require 10 years to
double their diameter) so may end up producing
symptoms by inducing intussusception or intestinal
ulceration with bleeding.
 Rarely can reach sufficient size or number to produce
obstruction.
 Less commonly, large polyps may secrete mucus enough
to cause diarrhea or enteropathy with protein depletion.
 Polyps can be:
 Unique (solitary polyp)
 Multiple (200-100)
 In a diffuse polyposis (> 100).
Therapy
 Symptomatic (unique or multiple) polyps are usually
treated by endoscopic removal, local resection or
segmental colectomy.
 Asymptomatic polyps may also require their removal.
 It is mandatory for all polyps to find their histological
type by biopsy, and if they are neoplastic they must be
properly removed, to eliminate the risk of progression to
invasive carcinoma
 Stages of degeneration for an adenomatous polyp are:
1. Carcinoma in situ = does not exceed the basal membrane,
2. Microcancer = does not exceed the muscularis mucosae,
3. Invasive carcinoma = muscularis mucosae is invaded
 ADENOMATOUS POLYPS
 2/3 of colonic polyps are adenomas.
 They can be sporadic (mostly occur over 60 years and
the incidence increases with age) or associated with
inherited polyposis syndromes (occurring in young
patients).
 Histologically they are classified depending on the
glandular pattern in:
 Tubular (80% of adenomas with 5% risk of malignancy)
 Villous (5-15% of adenomas with 40% risk of malignancy)
 Tubulo-villous (risk of 22%).

 Large adenomas (> 9mm) may be more common in

African Americans who have a higher risk of right sided
colonic adenomas and may present with cancer at a
younger age (< 50 years) than Caucasians.
 There is an increased incidence of adenomatous polyps
association with invasive carcinoma (one third of
resected carcinomas and 75% of synchronous
carcinomas, are associated at least with one polyp).
 Adenomatous polyps double the risk of metachronous
carcinomas.
 N.B.! Multiple cancer can be synchronous or metachronous;
 Synchronous cancers are cancers developed simultaneously on
different segments of the colon.
 Metachronous cancers are cancers developed in succession
diagnosed at least six months after diagnosis of previous
adenoma.
 The malignant potential of the adenomatous polyps is
considered to be:
 1% for polyps smaller than 1 cm,
 10% for polyps of 1-2 cm and
 50% for polyps larger than 2 cm.
Adenomatous polyp

Stalk
Tubulo-villous polyp
Pathologic Classification
 Low grade dysplasia: characterized by branching crypts
lined by cells with long, thin nuclei that begin to stratify,
resulting in increased nucleus-to-cytoplasm ratio and a
loss of normal goblet cells.
 High grade dysplasia: There is no invasive malignancy,
that means that the muscularis mucosa is not
penetrated by neoplastic cells. Represents an
intermediate step in the evolution from low grade
adenomatous polyp to cancer. It is not associated with
metastasis since there are no lymphatic vessels in the
lamina propria.
Risk factors for cancer
1. Adenomatous polyps > 1 cm in diameter
2. Villous histology – adenomatous polyps with > 25% of
villous histological component
3. High-grade dysplasia – adenomas with high-grade
dysplasia often coexist with areas of invasive cancer in
the polyp
4. Number of polyps: three or more is a risk factor for
development of metachronous adenomas with
advanced pathologic features
Surgical treatment
 For pedunculated polyps (pedicle <1.5 cm in
diameter), the best treatment is endoscopic
polypectomy, which ensures complete removal of the
polyp (histopathological examination must be
performed);
 Sessile polyps have a base > 1.5 cm in diameter. They
can be removed also by endoscopic approach piece by
piece in one or more sessions;
 Possible complication of the endoscopic polypectomy:
1. Perforation – the consequence is general peritonitis
2. Hemorrhage – early or late after 7-10 days
 Segmental colectomy (by laparotomy or laparoscopic
approach) when polyps are big or have a large base of
implantation, or they turned to malignancy.
 Familial Juvenile Polyposis
(FJP)
 Occurrence of 10 or more juvenile polyps.
 Autosomal dominant pattern of inheritance with germline
mutation in SMAD4 gene chromosome 18q21.1 or in the
gene BMPRA1A.
 Associated with increased risk for the development of
colon cancer, and in some families, gastric cancer,
especially where there are both upper and lower
gastrointestinal polyps.
 It may co-exist with Osler-Weber-Rendu syndrome
 Screening: colonoscopy beginning at age of 15 years
 Treatment: colectomy
 Familial Adenomatous Polyposis
(FAP)
 The first cases were described in the mid-nineteenth
century by Corvisart (1847) and Chargelaique (1859).
 It is an inherited, autosomal dominant disease.
 There are numerous adenomatous polyps in the colon.
 This syndrome should not be confused with other
multiple adenomas. The distinction is based on the
number of polyps present in the large intestine. When
there are more than 100 polyps, we speak about a
familial adenomatous polyposis, but usually thousands of
polyps can be meet.
 The disease appears in childhood, and malignization is
the rule (before 40 years).
FAP
FAP
 The incidence of FAP is 1/10,000 births.
 Polyps vary in number, size (1% of them exceeding 1
cm in diameter) and shape (pedunculated or sessile).
 The predilect location is on the left colon.
 Many patients are asymptomatic, the diagnosis often
arises during screening of high-risk patients.
 Bleeding and diarrhea are the most common
complaints, followed by abdominal pain. Weight loss,
anemia or intestinal obstruction suggest malignant
transformation.
 The average age when symptoms appear is around 20
years and the average age of malignant transformation
is 35 years.
 Diagnosis - is established by colonoscopy and double
contrast irigography.

 At time of diagnosis two thirds of patients

already have colorectal cancer.
 Genetic diagnosis (evidence of FAP gene) is routinely
used in Western countries and is an important element
in counseling protocol on family planning.
 Once the diagnosis was established, the whole
gastrointestinal tract will be explored by endoscopic
examination (stomach) or barium swallow (small
intestine).
Variants of FAP
 Turcot syndrome
 Inherited disorder characterized by the association of
adenomatous polyps with tumors of the central
nervous system (medulloblastomas and gliomas)
 Gardner’s syndrome
 Consists of adenomatous polyps, desmoid tumours,
osteomas, epidermoid cysts, lipomas, dental
abnormalities, periampullary carcinomas and juvenile
nasopharyngeal angiofibromas.
 Attenuated FAP
 Milder phenotypical FAP variant; < 100 adenomas
 Fever extracolonic manifestions
 Delayed onset of colorectal cancer (delayed by 12
years)
 The only way to prevent malignant transformation is to
performed total colectomy before the age of 15-20 years.
 Indicated operation in such cases is total procto-
colectomy followed by ileostomy or ileo-anal anastomosis
with ileal reservoir (pouch).
COLON CANCER
Epidemiology
 In most countries colon cancer is the second cause of
death after lung cancer.
 Age of onset: over 40-45 (60-69 years) years, with a
slight male predominance. However, cancer may be also
found in youngs.
 Geographically, the highest incidence reported in North
America (51/105) and the lowest in Brazil (3/105). In
Romania the incidence is 5/105.
 Table 1. – The main types of cancer and related death in 2008 worldwide

Type of cancer Deaths

Lung 1.37 million
Stomach 736 000
Liver 695 000
Colorectal 608 000
Breast 458 000
Cervical cancer 275 000
Topographic distribution
 Approximately 50% of colon cancers are located on
sigmoid colon, 25% on the right colon (ascending and
cecum) and 25% on transverse colon, splenic flexure,
descending colon and hepatic flexure.

34% 62%

Right colon
Left colon
4%

Synchronous
The incidence of synchronous carcinoma varies between 1.5%
and 8% depending on author.
Etiopathogenesis
 The cause of cancer is not known yet. In recent years
numerous studies have been made for a better
understanding of this mechanism, especially with the
help of molecular biology techniques.
 It is known that colic cancer occurrence should be
considered as a result of interaction between individual
genetic and environment factors.
 Although genetic syndromes are well-defined,
environmental factors seem more important. The most
obvious evidence that supports the previous statement is
an increased incidence of colorectal cancer in the
“sophisticated” societies.
 It has been shown that some components of the diet
correlates with geographical variations of the disease.
Environmental and
nutritional factors
 FATS induce changes in faecal PROPHYLACTIC
INDICATIONS
bile acid concentration, mediated by
alterations in intestinal flora.
 To decrease the dietary fat
 VEGETAL FIBRES . (Burkitt theory) content at less than 30% of
 ROLE OF CALORIC INTAKE AND total caloric value of ingested
PHYSICAL ACTIVITY aliments
 OTHER ALIMENTARY FACTORS
Calcium  To eat a greater quantity of
Vitamin D vegetable, fruits and cereals
Vitamin A
Vitamin C
Vitamin E
Selenium
Diallyl sulfide found naturally in garlic
Allyl Methyl Trisulfide - It is a
metabolite of garlic  To decrease alcohol
 ALCOHOL consumption
 ALIMENTARY CARCINOGENES  To avoid fried and smoked
 SMOKING foods.
 Correlational epidemiological studies clearly
demonstrates the link between increased fat intake and
colorectal cancer incidence. Dietary fat increases bowel
transit time and increases the concentration of fecal bile
acids, such as cholic and deoxycholic acid. These bile
acids act as potential carcinogens on the colonic
mucosa.
 In contrast to fat, fibers decrease bowel transit time and
therefore exposure of the bowel to these carcinogens.
Fiber, particularly wheat fiber, has been reported to have
a protective effect against the development of CRC.
Their influence has been extensively studied since
Burkitt popularized the idea that higher colic cancer
incidence in Western countries, is due to decreased in
fiber content of diet.
 There are several mechanisms by which fibers act:
 Increase fecal volume
 Decrease bowel transit time
 Dilution of colic content
 Facilitate the growth of aerobic bacterial population
 Induce alterations of energy metabolism
 Decrease bile acids hydroxylation
 It is assumed that the following factors may have a
protective effect: calcium, vitamin D, vitamin A and beta
carotene, vitamin C, vitamin E and Selenium.
 Aggressive factors that may induce carcinogenesis
include: alcohol and mutagens multiple factors derived
from food preparation process.
Genetic factors
 In the last decades, a series of sequential genetic
changes (mutations) leading to transformation of polyps
into cancer have been found.
 Unfortunately we can not yet interfere with these
processes.
 On the other hand, several genetic markers were found
that can be determined from blood or tissues which are
useful in early detection of cancer.
 Most colorectal cancers develop from adenomatous
polyps. The disease that has the highest risk of colic
cancer is familial polyposis.
 In 1991 a sequence of
chromosome 5q specific gene,
calledMCC (mutated in
colorectal cancer) was identified
as being responsible for sporadic
cases of cancer
 At 6 months after the discovery
of MCC it was discovered the
gene responsible for
adenomatous familial polyposis
AFP which is located in
chromosome 5q. These patients
represent only 1% of those who
develop colorectal cancer.
Deletion of long arm of
chromosome 18, containing
locus called DCC (deletion
colon cancer) that would
lead to changes in the
surface of cancer cells with
loss of normal adhesion and
contact inhibition, with
reactivation of fetal proteins
such as CEA
(Carcinoembryonic antigen ).
 The most common serological marker is CEA,
discovered in 1965 Freedman Philgold in colon cancers.
But it has a low specificity for colic cancer, and
therefore can not be used as a screening test.
 Its main value is as a marker of tumor recurrence after
curative resection. A sustained increase in CEA after
surgery is associated with cancer recurrence in a
proportion of 80-90% and may require a "second look
operation."
Tumoral angiogenesis
 Angiogenesis is a normal and vital process in growth and
development, as well as in wound healing and in granulation
tissue. However, it is also a fundamental step in the transition of
tumors from a dormant state to a malignant one.
 Angiogenesis, the growth of the new blood vessels, is necessary
for cancerous tumors to keep growing and spreading.
 VEGF (vascular endothelial growth factor) and bFGF (basic
fibroblast growth factor) are synthesized inside tumor cells and
secreted into the surrounding tissue. When they encounter
endothelial cells, they bind to specific proteins, called receptors
and activate a series of relay proteins that transmit a signal into
the nucleus of the endothelial cells. The nuclear signal ultimately
prompts a group of genes to make products needed for new
endothelial cell growth.
 Without angiogenesis, tumor growth stops !
Drugs that inhibit this process of angiogenesis can cause
tumor growth stop and even death of the cancerous
tumor.
 Molecular Basis of Colorectal Cancer
Sanford D. Markowitz, M.D., Ph.D., and Monica M. Bertagnolli, M.D.
N Engl J Med 2009; 361:2449-2460December 17, 2009
RISK FACTORS
 A) Genetic:
 Familial adenomatous polyposis
 Gardner, Turcot, Oldfild syndromes
 Peutz Jeghers syndrome
 B) Family
 Familial colorectal cancer syndrome (Lynch I)
 Hereditary adenomatous syndrome (Lynch II)
 Family history of colorectal cancer
 C) Previous illnesses
 Inflammatory bowel disease
 Colorectal cancer
 Pelvic cancer post-irradiation
 Neoplastic colorectal polyps
 D) GENERAL
 All men and women over 40 years
RISK GROUPS
1. Low-risk group: - all asymptomatic individuals over 45
years;
2. High-risk group:
 Families of patients with colorectal cancer - colonoscopy is
recommended periodically to people over 45 years.
 Patients with a history of polyps - colonoscopy should be made in 1-
3 years depending on the type of polyp.
 Patients with a history of colorectal cancer - colonoscopy is dictated
every year
 Patients with a history of inflammatory bowel disease, (the risk
depends on the extension of the inflammatory process and the age
of onset.) This risk is high after 10-15 years of evolution.
3. Very high-risk group:
 Adenomatous family polyposis. Early diagnosis is based on
detecting genetic changes.
 Familial cancer, or Lynch syndromes.
The only method of treatment is the total colectomy because 8 of 10
patients will present tumor recurrence (metacrone) in the remaining
colon in the first years after partial colectomy.
Macroscopic aspect of the tumor
 Ulcerative form - like an ulceration of the mucosa
surface.
 Vegetative form - looks like a cauliflower. More
frequent on the right colon. Can grow at big
dimension.
 Infiltrating form – cardboard aspect. More frequent
on the left colon. Rapidly induces stenosis and
obstruction.
 Diffuse infiltrative form – infiltration is extended at
a large segment of the colon. Like “linistis plastica” of
the stomach.
 Colloid form - gelatinous appearance due to
excessive production of mucus.
 Infiltrative stenotic tumor
Polyp
Ulcerative form
Vegetative form (associated with ulceration)
Cancer spread (dissemination)
 Direct – in surface and depth
 MAC staging stages A, B. - mucosa, submucosa, muscular and
serous layers and then to neighboring structures and organs
 Consequences: stenosis, perforation, penetration, fistulas
 Lymphatic
 Nodules - epicolic, paracolic, intermediate, central (MAC C stage)
 Venous - metastases (liver, lungs, bones, etc. MAC D stage)
 Intraluminal - metacrone tumors ?
 Perineural - along nerves
 Peritoneal – more frequently in the Douglas pouch (Blumer
neoplastic infiltration) by gravitational migration in the large
omentum (neoplastic epiploitis) and ovaries (Krukenberg tumors).
Staging
 Dukes classification of rectal cancer, in 1939 was adopted
for colon cancer. The original classification has undergone
several changes, finally looking like this modified after
Astler-Coller (MAC ):
1. Stage A: tumor not exceeding muscular mucosa and without
metastases in lymph nodes.
2. Stage B
 B1: tumor invades the muscular layer – no lymph nodes involved;
 B2: tumor excedes the muscular layer – no lymph nodes involved;
3. Stage C
 C1 = B1 + lymph nodes
 C2 = B2 + lymph nodes
4. Stage D: with distant metastases.

To this classification B.C.Wood added another two sub stages:

 Stage B3- tumor exceeds the colonic wall and penetrates the
surrounding structures
 Stage C3= B3+lymph nodes
Primary Tumor (T) TNM classification
 TX Primary tumor cannot be assessed
 T0 No evidence of primary tumor
 Tis Carcinoma in situ: intraepithelial or invasion of lamina propria1
 T1 Tumor invades submucosa
 T2 Tumor invades muscularis propria
 T3 Tumor invades through the muscularis propria into pericolorectal tissues
 T4a Tumor penetrates to the surface of the visceral peritoneum
 T4b Tumor directly invades or is adherent to other organs or structures
Regional Lymph Nodes (N)
 NX Regional lymph nodes cannot be assessed
 N0 No regional lymph node metastasis
 N1 Metastasis in 1–3 regional lymph nodes
 N1a Metastasis in one regional lymph node
 N1b Metastasis in 2–3 regional lymph nodes
 N1c Tumor deposit(s) in the subserosa, mesentery, or nonperitonealized pericolic or
perirectal tissues without regional nodal metastasis
 N2 Metastasis in 4 or more regional lymph nodes
 N2a Metastasis in 4–6 regional lymph nodes
 N2b Metastasis in 7 or more regional lymph nodes
Distant Metastasis (M)
 M0 No distant metastasis
 M1 Distant metastasis
 M1a Metastasis confined to one organ or site (for example, liver, lung, ovary,
nonregional node)
 M1b Metastases in more than one organ/site or the peritoneum
Correspondence between classifications

STAGE T N M DUKES' (MAC)

Table nr. III.

0 Tis N0 M0

I T1 N0 M0 A B1
T2 N0 M0

II T3 N0 M0 B2 B3
T4 N0 M0

III any T N1 M0 C1 C2 C3
N2 M0
N3 M0
IV any T any N M1 D
Histopatological types
 The vast majority (90-95%) of colic cancers are
adenocarcinomas. It is the only histologic type
classified in grades were several types of
adenocarcinomas are identified. World Health
Organization (WHO) classified primary tumors of the
colon as:
1. Epithelial tumors
 Adenocarcinomas (90-95%)
 Mucinous adenocarcinomas (17%)
 Adenocarcinomas with signet ring cells
 Squamous cell carcinomas
 Carcinomas adenoscuamous
 Undifferentiated carcinomas
 Unclassified carcinomas
2. Carcinoid tumors (2-7%)
 Argentaffinomas
 Nonargentaffinomas
 Composite
Carcinoid tumors are very rare (2-7%). They are almost always
located in the right colon, often unique and voluminous. When
detected, 75% of them have already metastatic lymph nodes and
liver and hence their poor prognosis.
3. Nonepithelial tumors
 Leiomyosarcoma (0.1 to 0.3%)
 Other - Sarcomas are exceptionally rare.
4. Hematopoietic and lymphoid neoplasms
Malignant lymphoma represents about 10% of all primitive
lymphoma of the digestive tract. Almost all are located in cecum
being ulcerovegetative, often bulky with extension to the
intestines.
5. Unclassified
Paraclinical investigations
 Laboratory does not provide specific elements for the
diagnosis of colon cancer. We can find: anemia,
hypoproteinemia, leukocytosis, increased ESR, alkaline
phosphatase and glutamic-oxalic transaminase also
increased (possible liver metastases).
 Carcinoembryonic antigen (CEA) dosage. It has no
specificity. Only a very high value is suggestive of an
epithelial cancer, especially colorectal, gastric and
pancreatic. Carcinoembryonic antigen dosage is important
for postoperative monitoring of patients
 Detection of faecal occult bleeding (HEMOTEST -
HEMOQUANT) can not be considered as a method of
diagnosis because cancer does not exclude a negative
result and the positive result can be influenced by
numerous factors of error.
 Irigography (simple or with double contrast) (images
of gap, stenosis or stop)

Stenotic colon cancer Tumor of the cecum

 Colonoscopy – in 95-98% of cases can establish the
diagnosis and also can perform biopsies.
 Abdominal ultrasound can evaluate tumors bigger than 1 cm
diameter, metastases in the liver, ascites, lymph nodes.
 CT scan especially for relations with other organs, liver
metastases, lymph node involvement and other distant
metastases.
 MRI – the same as for CT but a bit more detailed; expensive.
 Other : Chest radiography, bone scintigraphy, PET scan, etc

CT – sigmoid tumor
Incisional hernia

CT
Stenosing
descending colon
tumor

Distended ascending
colon
CLINICAL PICTURE
 Symptoms of colon cancer depend on several factors:
1. Location, size and macroscopic appearance of the tumor
2. Stage of the tumor
3. If a patient is admitted in emergency (perforation, stenosis,
hemorrhage) or elective condition.
 The onset is usually insidious with bowel disorders
(constipation, diarrhea or alternating between the two)
and abdominal colicky pains.
 Patients often overlook these symptoms and are treated
for various diseases such as enterocolitis. But when they
notices the blood in the stool they panic and quickly
seek medical attention.
 The period of time elapsed from the onset of symptoms
to admission is generally 6 months but there are not
rare cases of 1-2 years.
SYMPTOMS
 Colicky pains
 Intestinal transit disorders
 Pathological elements in the stool
 MUCUS
 BLOOD
 PUS
 General symptoms of neopastic impregantion
(weakness, fatigue, decreased physical and intellectual
capacity, loss of appetite, sometimes fever).
 Symptoms from other affected organs
 Paraneoplastic symptoms
 TUMORAL COMPLICATIONS

1. STENOSIS – INTESTINAL OCCLUSION – DIASTATIC

PERFORATION, INTUSSUSCEPTION, VOLVULUS
2. TUMOR PERFORATION
EMERGENCY
 STERCORAL PERITONITIS
 COVERED PERFORATION WITH ABSCESS, LOCALIZED
PERITONITIS
3. ULCERATION WITH INFERIOR DIGESTIVE BLEEDING

4. PENETRATION INTO THE SURROUNDING

STRUCTURES – FISTULA FORMATION

5. METASTASES, PERITONEAL CARCINOMATOSIS,

ASCITES
 TUMORS OF THE RIGHT COLON
features
1. Large vegetative tumors
2. Secondary anemia (occult bleeding)
3. Commonly associated with Bauhin valve incompetence
 diarrhea
4. Often palpable
5. Frequently complicated by:
1. Posterior abdominal wall penetration
2. Right ureter and spermatic / ovarian vessels penetration
3. Penetration into the duodenum, right kidney, gallbladder, liver
4. Penetration in iliac vessels, right adnexa
5. Local perforation with abscess formation
6. Ileo-colic intussusception
 TUMORS OF THE TRANSVERSE COLON
features
1. Mobile segment of colon
2. Most often bulky tumor, ulcero-vegetative, easily
palpable.
3. Symptoms are frequently borrowed from neighborhood
organs due to intimate relations with stomach,
pancreas and gallbladder.
4. Dyspeptic disorders can be considered as an expression
of gastroduodenitis, biliary dyskinesia or colitis, until
complications occur in tumor evolution.
5. Tumors may be occlusive, hemorrhagic (persistent and
occult bleeding) and suppurated. Gastro-colic or
jejuno-colic fistulas may occur, manifested by diarrhea,
faecaloid vomiting with severe alteration of general
condition.
 TUMORS OF THE LEFT COLON
features

1. It is the most common location of colon cancer, 75%

located on the sigmoid.
2. Tumors are usually small in volume, infiltrative,
circumferential and stenosing.
3. Constipation, may be interrupted by intermittent
diarrhea (feces accumulated above the obstacle are
liquefied under the action of bacteria).
4. Often complicated by stenosis or occlusion
5. Lower gastrointestinal bleeding
6. Penetration into adjacent organs (bladder, uterus, left
adnexa, intestines, left ureter, left spermatic/ ovarian
vessels, left kidney, pancreas tail).
Clinical examination

 General examination is mandatory

 Muco-cutanate pallor, weight loss, cachexia, jaundice in liver
metastases.
 Other signs of metastases
 Local examination
 Palpable tumor in 20% of cases (cecum and sigma)
 Carcinomatous ascites, peritoneal carcinomatosis (shifting
dullness on percussion)
 On auscultation - Konig sounds - "steam burst like“
 IN EMERGENCY - occlusion or generalized peritonitis signs
 Rectal examination - blood on the glove, palpable
tumors.
Diagnosis is based on:

 History:
 Abdominal colicky pain with bowel disorders, blood in
stool, weight loss
 Clinical examination:
 Palpable tumors, other tumoral complications
 Paraclinical examinations
 Irigography
 Colonoscopy with biopsy
 Ultrasound – liver metastases
 Laboratory – Anemia
 Other – CT, Thoracic X-ray, bones X-ray
 Differential diagnosis with:

 Cecum + ascending  Splenic flexure

 Apendicular block, acute  Pancreatic tail tu.
appendicitis  Left renal tumors
 Right kidney ptosis, renal  Retroperitoneal tumor
tumors  Gastric tumors
 Regional ileitis
 Right renal colick
 Descending colon
 Retroperitoneal tu.  Left renal tu.
 Left renal colick
 Liver flexure
 Cholecystitis
 Sigma
 Right renal tu.  Tumors of the adnexa
 Liver tumors  Volvulus of the sigma
 Diverticulitis
 Transverse colon  Bladder tumors
 Gastroduodenal ulcer
 Gastric cancer
 Pancreatic tu.
 Retroperitoneal tu.
TREATMENT PRINCIPLES
MULTIMODAL & COMPLEXE

 Surgical - The most important - Surgical Oncology!

"No touch isolation" Turnbull’s principle.
1. tumor removal
2. lymphatic excision
3. removal of metastases
 Adjuvant
1. Chemotherapy
2. Immunotherapy
Surgical treatment
1. Preoperative evaluation of the patient
2. Adequate preoperative preparation
 General
 Local
3. Oncological surgery
 tumor removal
 lymphatic excision
 removal of metastases
4. Postoperative care
 The principle of no touch isolation (to prevent spread
of tumoral cells) requires:
 first vein ligation
 ligation of the colon above and below the tumor
 The tumor will be the last to be touched and removed
Preoperative preparation
 Before surgery the patient must be brought in the best
physical and mental condition. A thorough preoperative
preparation is possible in elective cases.
 General preparation is addressed to concomitant illnesses,
hydro-mineral imbalance, anemia, hypoproteinemia, etc.
 Local preparation (preparation of the colon) – the aim is to
evacuate the colon content (mechanical preparation) and to
decrease the colic sepsis by reducing the number and
virulence of germs (antiseptic preparation).
 Mechanical preparation – is achieved by purgation with
special solutions – so called “Wash out” procedure in the
day prior surgery. Antiseptic preparation is performed by
administration of broad spectrum antibiotics (for Gram+,
Gram- and anaerobes).
 In emergency condition, for patient with bowel
obstruction, mechanical preparation by purgation is not
possible. In such cases naso-gastric tube and aspiration
is very important for emptying the stomach and
prevention of aspiration in lungs. If the operation cannot
be postponed, colon content can be evacuated during
operation (anterograde lavage with saline solution on a
tube placed in cecum, ileum or appendix)
Tumor removal
 Principles
 Local, regional and general exploration
 Nu touch isolation technique
 How much to remove ? 5 cm under the tumor and 15 cm above.
 Restoration of digestive continuity by different types of
anastomoses
 Types of operations
 Curative operations
 Palliative operations
 Palliative resections
 External diversion – colostomies
 Internal diversion – ileo-colic anastomosis
 - colo-colic anastomosis
 Surgery of the colon is a risky surgery
 Infectious risk – septic content
 Anastomotic risk – poor vascularization
 Oncologic risk
Types of radical operations
1. Right hemicolectomy + ileo-transversostomy
2. Left hemicolectomy + colo-colic anastomosis
3. Segmental resection with colo-colic anastomosis (Reybard’s op.)
4. Subtotal colectomy + ileo-sidmoidostomy
5. Total colectomy + ileo-rectostomy
6. Total proctocolectomy + ileo-anal anastomosis (pouch) or
ileostomy
7. Hartman’s operation stage I and stage II
8. Anterior rectosigmoidian resection + colo-rectal anastomosis
(Dixon’s op)
 COMPLEXE operation All operations can be performed
by classic approach or by
 SEQUENTIAL operations laparoscopic approach
 RIGHT HEMICOLECTOMY

 The operation can be performed by classical approach

(laparotomy) or by laparoscopic approach. For
laparotomy the xifo-subumbilical incision is the most
frequently used.
 The Turnbul’s “no touch isolation” technique is used.
That means that the tumor is the last one touch during
colectomy. This technique prevents tumoral cells spread
from the tumor. It is supposed that tumor manipulation
and squeezing promote tumoral cells spread into the
blood stream and into the bowel lumen.
 The first step is local, regional and general inspection for
assessing the resecability of the tumor and to detect
metastases especially liver metastases.
 Checking the liver for metastases

Local, regional and general inspection

 The colon is ligated above and beneath the tumor to
prevent intraluminal spread. The vessels of the right
colon are ligated and cut to prevent the spread of
tumoral cells into the blood stream. The regional
lymphadenectomy goes from the left to the right side
toward the colon. The omentum, gastrocolic ligament,
phrenicocolic ligament and transverse mesocolon are
sectioned. The ileum is resected at 10-20 cm from the
ileocecal valve and then the right colon is separated
from the posterior wall (Told I fascia). The transverse
colon is resected at a distance depending on tumor
location.
 The continuity of the digestive tract is reestablished
performing an anastomosis between the ileum and
transverse colon (ileotrasversostomy).
Direction of the lymph nodes dissection
 There are possible two main intraoperative
complications: duodenum injury and right ureter lesion,
encountered especially in large tumors penetrating the
posterior abdominal wall. Lesions must be recognized
and solved during operation.
 If the tumor penetrates other important organs such as:
kidney, duodenum, stomach, pancreas, complex
operations should be necessary, like right nephrectomy,
gastric resection, cephalic duodenopancreatectomy.
 In case of limited number of liver metastases or
clustered metastases, removal of these is beneficial for
the patient prolonging survival. Possible operations are:
metastasectomy (ablation of metastases) liver
resections, destruction of metastases using chemical
(ethanol) or physical methods (electrocautery,
dyathermy, ultrasound).
 Transverse colon tumor
Penetrating the jejunum

cecum Ileum

Right hemicolectomy+
Segmental enterectomy+
Cystectomy
Ovarian cyst
 Stenosing transverse colon with occlusion

Tumor

cecum
 LEFT HEMICOLECTOMY

 This type of operation is applied when tumors are

located on the left colon. Principles of surgical ocology
are the same as for the right hemicolectomy.
 The IMA is resected at 1 cm from its insertion into the
aorta (to preserve the nerves with function in erection)
and lymphadenectomy is conducted from the right to the
left. The first measures in preventing tumoral cells
spread are: ligation of the colon above and beneath the
tumor and ligation and resection of the inferior
mesenteric vein at the level of Treitz angler of the
duodenum.
 Extension of colic resection depends also on tumor
location and length of the transverse and sigmoid colon.
 Restoration of digestive tract
continuity is performed by colo-
colic anastomosis or by colo-
rectal anastomosis.
 If the transverse colon and the
sigma are long enough there are
no problems in anastomosing
those two segments of the
colon. On the other hand there
are situations when the
transverse colon is short and the
anastomosis should be
performed with the rectum. To
descend the colon on a shorter
route, it can be passed through
the mesentery.
 SEGMENTAL RESECTIONS OF THE
COLON
Reybard’s operation
 When tumors are located on a mobile segment of the
colon (sigma or transverse colon) a limited colic
resection can be performed: segmental resection
(Reybard’s operation). The mobility of the colon
conferred by the length of the mesocolon or mesosigma,
permit to perform an anastomosis without tension
between the two ends of the colon.
 The principles of surgical oncology must be applied in
these operation also, even though they are not so radical
as hemicolectomies.
 These types of operations are applied especially for small
tumors in elderly.
 A part of mesocolon or mesosigma containing the
lymphatic drainage basin of the affected segment is also
removed.
 Given the high mobility of the transverse and sigmoid
colon, tumors located on these segments may penetrate
other organs located far away. Most frequently are
invaded: the small intestine, bladder, uterus, annexes,
stomach.

Sigmoid tumor
Penetrating the
Small intestine
 SUBTOTAL AND TOTAL COLECTOMY
 Subtotal colectomy means the removal of a large portion
of the colon but the sigmoid colon or a part of it
remains. The digestive tract is reestablished by
ileosigmodostomy. This type of operation is applied in
synchronous tumors (eg. tumor of the right colon and
tumor of the descending colon) or in cases of stenosing
left colon tumors with intestinal occlusion and very
distended colon upstream the tumor.
 Toatal colectomy presumes removing the entire colon.
The digestive tract is reestablished by ileorectostomy
with or without an ileal pouch. This type of operation is
reserved for polyposis and some synchronous tumors.
 HARMANN’S OPERATION
• It is a sequential operation. In the first operation the
tumor and part of the colon (and rectum) are removed.
The distal end is closed and the proximal end of the
colon is transformed in terminal colostomy. In the
second stage, after some weeks or month the patient is
reoperated and the two ends of the colon (or colond and
rectum) are connected together (anastomosized) in
order to reestablish the natural way of the intestinal
transit.
• Sometimes, the first stage of the procedure, the
colostomy, may be a definitive operation.
• It is applied especially in emergency cases of obstruction
due to stenosing tumors and when colon cannot be
prepared preoperatively. Anastomosis in a single step
operation would be at risk of fistula.
 IN EMERGECY
Intestinal occlusion due to stenosing tumor
 Tumor on the right colon
 Right hemicolectomy
 Ileotransversostomy (internal derivation) –
 Ileosigmoidostomy unresectable tumors

 Tumor on the left colon

 Left hemicolectomy
 Segmental resection
 Hartmann’s operation stage I
 Upstream (of tumor) Colostomy of diversion
 Ileosigmoidostomy For unresectable tumors
 External derivations
 Colostomies and ileostomies represent external
diversion of the intestinal content.
 They are applied in 3 situations:
1. External diversion as a definitive operation. They are
represented especially by terminal colostomies in case of
Hartmann’s stage I operation or after rectal amputation when
tumor can be removed. Other situations are cases where the
tumor is in a so advanced stage that it cannot be removed and
the only solution is an external diversion upstream the tumor.
2. Temporary external diversion for colon emptying in cases of
stenosing tumors. The colostomy is performed upstream the
tumor as a first stage resolving the occlusion and then, after a
while, the main operation of tumor removal is performed.
3. Colostomies or ileostomies of protection. They are performed
upstream an anastomosis to prevent intestinal content to reach
the anastomosis and thus preventing anastomotic fistula. These
types of external diversions are temporary also.
 Internal derivations

 Internal derivations represent bypasses between

different segments of the digestive tract in order to
bypass an obstacle which cannot be removed. The
obstacle is represented by advanced stage of colon
cancer invading other neighboring organs or anatomical
structures or in case of peritoneal carcinomatosis. These
operations are palliative operations aiming to prevent
intestinal occlusion and thus prolonging life.
 The most frequent internal derivations are ileo-
transversostomy (for tumors located on the right colon)
and ileo-sigmoidostomy (for tumors on transverse an
descending colon)
Postoperative care
 There are no major differences from other surgeries on
the digestive tract.
 Fluid, electrolytic and energetic rebalancing
 Pain relief drugs
 Thromboembolism prophylaxis (early mobilization, anticoagulants)
 Antibiotics with broad spectrum
 Wound treatment

 Enteral nutrition is resumed according to digestive

tolerance.
ERAS (Enhanced recovery after colorectal
surgery) principles
 Naso-gastric tube to be removed in recovery before
patient is sent back to the ward.
 Daily physiotherapy, mobilise on day of surgery.
 Soft diet to be started on same day as operation.
 1 litre free fluid - day of op including high energy/high
protein nutritional supplements.
 Urinary catheter remains no longer than 24 hours
following epidural removal.
 If patient has had epidural this should continue for a
minimum of 48, aiming for removal post-op day 2.
 Discharge planning from day 2 post-op.
 +/- stoma care
Postoperative complications
 In colon cancer surgery, postoperative complications are
more frequent and severe than after other abdominal
operations, due to neoplastic disease, relatively poor
blood supply and increased septic content of the colon.
 There is a high risk of suture dehiscence with severe
peritonitis and respiratory, heart, kidney, complications
 Anastomosis dehiscence
 Wound suppuration
 Hemorrhage
 OTHER
Colostomy prolapse
 PROGNOSIS
DUKE’S Prognosis 5
STAGE TNM GROUP GROUP year
survival
Stage I T1 N0 M0 Duke’s A >90%
T2 N0 M0

Stage II T3 N0 M0 Duke’s B 70-85%

T4 N0 M0 55-65%

Stage III any T N1 M0 Duke’s C 45-55%

any T N2, N3 M0 20-30%

Stage IV any T any N M1 Duke’s D < 5%

RECTAL CANCER
Anatomy
 The rectum is the last portion of the digestive tract.
 Recto-sigmoidian junction, 2-6 cm long, is the crossing
from sigmoid colon to the rectum. Taenias disappear
forming a continuous layer as a true circular sphincter.
 Pelvic rectum, about 13 cm long. The caliber is variable
depending on the fullness. Rectal ampulla.
 Ano-rectal junction is represented by ano-rectal line,
(dentate or pectinate line) characterized by the presence
of Morgagni columns which are located between the anal
valves. Ano-rectal line represents the boundary between
the rectum and anal canal, between visceral and somatic
nervous system, between the portal and caval system,
between visceral and somatic lymphatic system.
 The rectum has three portions:
 The upper portion of the rectum is covered by peritoneum
anterior and lateral. It is the intra-peritoneal portion.
 The middle portion is covered by peritoneum only anterior.
Peritoneum reflects on the uterus, forming the bottom of
the recto-uterine sac of Douglas in women and bottom of
recto-bladder bag in men.
 Distal rectum, the third portion, is entirely sub-peritoneal.
Posterior there is the mesorectum which contains blood
vessels, lymphatic nodules and nerve fibers. (in radical
surgery of the rectum, the mesorectum is also removed
together with the rectum). Between prostate and rectum,
there is the prostato-perineal fascia of Denonvilliers which
facilitates dissection. In women there is a recto-vaginal
fascia ending down by recto-vaginal septum described by
Proust Barbilian.
 Supportive anatomical elements of the
rectum
1. Pelvic floor formed by levator ani muscles.
2. Presacrate fascia of Waldeyer
3. Lateral ligaments of rectum which are formed by the
condensation of pelvic fascia
4. Recto-vesical fascia of Denonvilliers, which extends
from rectum behind to the seminal vesicles and
prostate in front
5. Pelvic peritoneum
Relations
 Anterior
– In man - the prostate, seminal vesicles, ductus deferens and
urinary bladder and through the pelvic peritoneum with small
intestines.
– In woman – vagina, uterus, adnexa and small intestines
 Posterior
– Sacrum, coccyx, sacral vessels, sacral sympathetic chains,
branches of the 3rd and 4th sacral nerves, and the superior
hemorrhoidal vessels.
 Lateral
– The intraperitoneal portion comes in relation with the sigmoid,
small bowel, uterine adnexa and the subperitoneal segment with
hypogastric plexus and branches of internal iliac (hypogastric
vessels).
 ANAL CANAL

Anal canal is the terminal portion of the alimentary tract,

the outlet. It has a length of 2-3 cm. It is a straight,
shortest and most fixed portion of the terminal bowel.
Interior aspect
1. Morgagni columns, varying in number from 6 to 14.
2. Anal valves (semilunar envelopes) - anal papillae
3. Anal sinuses or cripts
4. Pectinate line or dentate line.
5. Linea alba HILTON
Arterial supply of the rectum
1. Superior rectal artery (superior hemorrhoidal), terminal
branch of the inferior mesenteric artery, divides into
two branches.
2. Middle rectal arteries from internal iliac artery.
3. Inferior rectal arteries, below the levator ani muscles
comes from the internal pudendal artery.
4. Middle sacral artery, arising from the back of the aorta
at 1 cm. above the bifurcation and goes in front of the
sacrum and coccyx.
 Rectal arteries anastomosize between them forming
intra-and extraparietal anastomotic systems, sufficient
to restore the blood supply after a rectal resection.
Rectal veins
 Originate from rectal venous plexus located in the
submucosa layer. From this plexus start venules crossing
the muscular layer thus creating the rectal or
hemorrhoidal veins.
 Superior rectal vein, collects the blood from the rectal
ampulla and flows into the inferior mesenteric vein.
(portal system)
 Middle rectal veins, are thin, leaving the lower portion of
the rectal ampulla and flowing into the internal iliac veins.
 Inferior rectal veins collect blood from the lower rectum
and anal canal and flow into the internal pudendal veins
which flow then into the internal iliac vein (caval system).
Thus, a communication, of important clinical value,
between the portal system and caval system is performed
through these rectal veins (see the portal hypertension).
There are 4 portocaval
physiologic
anastomoses:
1. Paraumbilical veins -
superficial and inferior
epigastric veins.
2. Superior rectal veins -
inferior and middle
rectal veins.
3. Colic small branches -
lumbar segmental and
renal venous branches.
4. Esophageal veins of
abdomen - esophageal
veins of azygos system.
Lymphatic drainage
 The lymph is drained from a mucous and a submucous
plexus (parietal plexus) towards three pedicles:
1. Superior lymphatic pedicle has four lymph node
stations:
1. The first station is located on the posterior rectal wall and was
described by Gerota.
2. The second station located at the bifurcation of superior
hemorrhoidal artery, it was described by Mondor and receives
also short lymphatic pathways from the anus.
3. The third station (Bacon) is located in front of rectosigma at the
junction between hemorrhoidal and sigmoidian artery, also
known as the " lymphatic mesenteric hilum "
4. The fourth station, is placed at the origin of left colic artery.
2. Lateral lymphatic pedicle includes all the lymph
nodes of the pelvis, as follows:
– Inferior lymph-node-station, located near the middle and
lateral sacral vessels;
– Lateral lymph-node-station, consisting of nodules along the
middle hemorrhoidal and hypogastric vein;
– Anterior lymph-node-station receiving lymph from recto-
urethral muscle.
3. Inferior lymphatic pedicle consists of lymphatics
that drain into the groin lymph nodes.
Innervation
 Sympathetic fibers of the rectum are derived from the
first three lumbar spinal segments, which pass through
the sympathetic ganglionar chains and leave them as
lumbar sympathetic nerve reaching preaortic plexus. From
here, there is an extension along the inferior mesenteric
artery called the inferior mesenteric plexus which reaches
the lower portion of the rectum.
 Presacrat nerve or hypogastric, comes from the aortic
plexus and lateral lumbar splahnic nerves. The trunk thus
formed is divided into two branches which pass on either
side of the pelvis where branches meet the sacral
parasympathetic nervous to form pelvic plexuses. This
innervates the lower rectum, anal canal, bladder and
sexual organs.
 Parasympathetic innervation comes from erigens nerves,
which originate from sacral nerves 2, 3 and 4
 ANAL CANAL
 Motor innervation
– Internal sphincter is innervated by both sympathetic
and parasympathetic. Sympathetic has a stimulatory
effect and parasympathetic inhibitor of the sphincter.
– External sphincter is innervated by the inferior rectal
branch of the internal pudendal nerve and by the
perineal branch of the 4th sacral nerve.
 Sensory innervation
– The skin of the perianal region and anal canal is
innervated by fibers of the inferior rectal nerves.
Sensory fibers are concerned with the reflex control
of the sphincters and with pain. The anal canal is very
sensitive below the pectinate line, so that external
hemorrhoids may be very painful when complicated.
RECTAL CANCER
 Incidence, epidemiology and etiopathogenesis are the
same as for colon cancer
Macroscopic aspect
1. Ulcerate
2. Infiltrative
3. Vegetative

 Penetration into adjacent organs is rapid and more

frequent due to close relations with these organs

Histopathology
– Adenocarcinomas (98%) Extension
1. On surface
– Carcinoid (0.1%)
2. In depth – T stage
– Lymphoma (1.3%) 3. Lymphatic – N stage
– Sarcomas (0.3%) 4. Venous
– Epitheliomas 5. Perineural
– Melanoma located anorectal
Polyp Infiltrating tumor
Ulcerative form
Vegetative form
TNM classification for cancer of the colon
and rectum (AJCC)
 Primary tumor (T)
– TX - Primary tumor cannot be assessed or depth of
penetration not specified
– T0 - No evidence of primary tumor
– Tis - Carcinoma in situ (mucosal); intraepithelial or invasion of
the lamina propria
– T1 - Tumor invades submucosa
– T2 - Tumor invades muscularis propria
– T3 - Tumor invades through the muscularis propria into the
subserosa or into nonperitonealized pericolic or perirectal
tissue
– T4 - Tumor perforates the visceral peritoneum or directly
invades other organs or structures
– Regional lymph nodes (N)
 NX - Regional lymph nodes cannot be assessed
 N0 - No regional lymph node metastasis
 N1 - Metastasis in 1-3 pericolic or perirectal lymph nodes
 N2 - Metastasis in 4 or more pericolic or perirectal lymph
nodes
 N3 - Metastasis in any lymph node along the course of a
named vascular trunk
– Distant metastasis (M)
 MX - Presence of metastasis cannot be assessed
 M0 - No distant metastasis
 M1 - Distant metastasis
Symptoms depend on stage of tumor development.
 In the initial stage
– Asymptomatic for a long period of time, can be
discovered incidentally on endoscopy or rectal
examination
 In phase of state
1. Bleeding ( pathological discharge = blood, mucus,
pus)
– The most frequent symptom - 60% of cases
– Frequent confusion with bleeding from hemorrhoids
– Rarely, massive bleeding with anemia
– Sometimes with blood clots as a "jelly“
– Bleeding may be associated with passage of mucus
and pus
– Blood is mixed with the stool or fecal bolus is marked
by a trail of blood
2. Pain
– Initially as a local rectal embarrassment or intrarectal
foreign body sensation or incomplete evacuation
– Later rectal tenesmus
– In advanced stages intense rectal pain and hypogastric
or sacral due to penetration of surrounding structures

3. Change in bowel habits

– Present in 43% of patients, this symptom has several
different presentations. Often, it occurs in the form of
diarrhea, particularly if the tumor has a large villous
component.
– Some patients experience a change in caliber of the
stool.
– Large tumors can cause obstructive symptoms.
 In the advanced stages
– Intense pain - due to sacral penetration
– Colicky pain – due tumoral obstruction
– Hypogastric and perineal pain - tumor penetration in
the small pelvis organs
– Anal incontinence
– Recto-vaginal fistula, recto-bladder, recto-uterine
– Jaundice due to liver metastases
– Neoplastic impregnation signs (asthenia, malaise,
anemia, weight loss, etc.)
– Compressive edema of the legs and genital organs
Physiscal examination
 75% of rectal tumors can be detected by digital rectal
examination ! (located < 10-12 cm)

Do not forget to palpate the groin lymph nodes!

Features of the tumor must be described:

1. Location from anal verge
2. Position on the rectal wall (ant. post.
lat.)
3. Dimension (extension)
4. Sensibility
5. Surface (ulcerated ?)
6. Delimitation In women vaginal
7. Mobility !!! examination can help
8. Bleeding ?– Look at the finger glove
Paraclinical examinations
 Rectoscopy with biopsy – the most important (if tumor
has a higher location, rectosigmoidoscopy would be
necessary).
 Transrectal ultrasonography – Assessment of
penetration through the rectal wall, relations with
surrounding organs and lymph nodes metastases; it is
72-94% accurate.
 CT scan or MRI – for the same reasons as above but
more expensive and use X-rays (the CT) – but more
precise.
 Abdominal ultrasound – especially for liver metastases
and ascites.
 Chest radiography for lung metastases.
 Intravenous urography or cystoscopy when there is
suspected a fistula formation with the bladder or there is
a compression on ureteres.
Transrectal ultrasonography
 Carcinoembryonic antigen test: Perform a CEA test in all
patients with rectal cancer. A baseline level is obtained
before surgery and a follow-up level is obtained after
surgery. This may alert to a possible recurrence if a
previously normalized CEA begins to rise in the
postoperative period. A CEA higher than 100 ng/mL
usually indicates metastatic disease and warrants a
thorough investigation.
 Differential diagnosis must be performed with other
ano-rectal diseases:
– Hemorrhoids
– Anal fissure
– Ulcerative recto-colitis
– Rectal syphilis
– Crohn disease
– Genito-urinary diseases
– Other
Treatment
 The treatment is complex (multimodal): surgical and
adjuvant oncotherapeutic.
 Therapeutic priority depends on tumor location and size.
 In cancers located in the lower part of the rectum initially
preoperative radiotherapy is indicated for tumor reduction
and after 4-6 weeks follows the surgery. Some authors
advocate also for neoadjuvant chemotherapy for locally
advanced tumors.
 The operative technique varies depending on many
factors among which tumor location is primary.
 Other factors taken into account in the operation are:
tumor stage, age and other associated illnesses of the
patient and the patient's wishes.
 The most important dilemma of the rectal surgery is of
choosing between a radical operation and anal sphincter
preservation.
Surgical treatment
 Implies:
– the removal (excision) of the tumoral rectum
– lymphadenectomy (total mesorectal esxcision) for - tumors of
stage II-III
 Extension of resection. It was found that the tumor does
not infiltrate more than 2 mm from the macroscopic
edge, but however at least 2 cm below the tumor should
be respected as a distance of security. The lower limit of
the resection is dictated by the position of the rectal
tumor and distance from the anal verge.
 Considering that the anal canal is 2-3 cm long plus 2 cm
of security zone, results a distance of about 5 cm from
the anal verge till the inferior margin of the tumor.
Under this limit in most cases the anal sphincter can’t be
saved and a rectal amputation is the major surgical
indication.
 An important step forward in sphincter preserving
surgery is the use of staplers for colorectal
anastomosis lowering as much as possible this
anastomosis near to the anus.
 In ano-rectal cancers the only operation indicated is
abdominoperineal resection of the rectum
(amputation).
Types of operations
 Radical
– Low anterior resection with colorectal anastomosis (Dixon’s
operation) –with or without temporary colostomy or ileostomy
for anastomosis protection
– Ultralow resection with peranal anastomosis (Parks operation)
or intersphincterian anastomosis
– Abdominoperineal resection – rectal amputation (Mile’s
operation) with definitive left iliac anus (terminal colostomy)
– Pull-through operations (Babckoc, Bacon, Mancache, Chiricuta)
– Hartmann’s operation (sequential operation)
– Endoluminal excizion in early stages
 Palliative
– Colostomy, cecostomy, ileostomy
– Palliative resection (Hartmann I step)
Approaches
– Classic – laparotomy, transsacral
– Laparoscopy
– Endoluminal
Anastomoses
– Hand sewn
– Staplers
 Resection of the rectum and especially the colorectal
anastomosis is more difficult in men because of tight
pelvis. Erector nerves must be spared whenever possible
(impotence). However the whole mesorectum containing
lymph nodes should be excised (total mesorectal
excision TME). This is facilitated by the cleavage plane –
the “holy plane”.
Stapled anastomosis
 The evolution of mechanical suture technology experienced
a continuous improvement over the 40 years of history.
 The use of staplers facilitated anastomosis technique
allowing more low rectal resection and anastomosis,
avoiding rectal amputations in many patients.
 Stapler may be used for any anastomosis but they are the
most useful in rectal tumors.
 For sphincter preserving procedures tumors must be
located above 5-6 cm from the anal verge. The 2 cm below
the tumor resection will leave an anorectal stump of only
3-4 cm, the minimum length necessary for colorectal
anastomosis.
 For tumors located under 6 cm the options would be:
– Abdominoperineal resection
– Colo-anal anastomosis (intersfincteric)
– Pull-through procedures
 Single use reloadable linear stapler

Single use curved circular stapler with Tilt-Top™ anvil

Technical details
 The same principles as in conventional surgery must
be respected (anstomosis without tension and a good
arterial supply of the colon) to prevent anastomotic
leaks.
 It is important to verify the integrity of anastomosis:
– Verify the integrity of the tissue ring of the cut edges
– Direct visualization
– Hydro-pneumo verification – the pelvis is filled with saline
solution and air is insufflated through the anus. If air bubbles
occur in saline it means that the anastomosis is not perfect
sealed.
– Palpation
– Endoscopic visualization
Advantages of mechanical suture
 Mechanic anastomosis gives the possibility to perform
safe anastomosis in anatomical areas difficult to reach
where the anastomosis is either impossible or very
unsafe and burdened by high risks.
 Enormous advantage especially in patients with rectal
tumors, in obese male patients with narrow basin,
where we can save many cases ( 50% in our opinion)
of handicap caused by permanent iliac anus.
 Decrease the operation time
 Improving the suture quality
 Decrease intraoperative blood loss
 Decrease intraoperative contamination
Postoperative complications after Low
Anterior Resection
 Anastomotic fistula is the worst. It is life threatening due
to septic shock after peritonitis. To prevent peritonitis,
temporary colostomy or ileostomy may be performed.
 Wound suppuration, bleedings, etc are not so difficult to
treat
 Intestinal obstruction due to adhesions
 Transient urinary dysfunction secondary to weakening of
the detrusor muscle. This occurs in 3-15% of patients.
 Sexual dysfunction is more prominent and includes
retrograde ejaculation and impotence. In the past, this
has occurred in 5-70% of men, but recent reports indicate
that the current incidence is lower.
 Abdominoperineal resection – Rectal
amputation – Miles operation
 This type of operations presumes the removal of the entire
rectum and anal sphincter plus the mesorectum containing
the lymph nodes. It is a mutilating operation because the
patient will remain with permanent iliac anus.
 The main indication is represented by anorectal cancer or
very low rectal cancer.
 In many cases the patient will undergo radiotherapy for 6
weeks before operation.
 The operations can be performed either by classical or by
laparoscopic approach. There are two approaches of the
operation: the abdominal when the rectum and
mesorectum are prepared till the levator ani muscles and
the perineal approach when the anorectum will be
completely freed up.
 Complex operations
 Unfortunately there are many cases with advanced
cancers when the tumor invades other organs being
necessary (when is possible) to perform complex
operations.
Transanal excision
 It may be performed only if:
1. The tumor is in stage 0 or I (Tis, T1)
2. Does not occupy more than one third of the
circumference of the rectum
3. There are no pathological lymph nodes (endorectal
ultrasound verified)
4. Tumor does not involve the anal sphincter
5. Preferably the tumor to be of polipoid form
6. Rectal wall is excised in its entire thickness at least
at 1 cm away from the lesion. With or without
suture of the subperitoneal rectum.
 ANO-PERINEAL
PATHOLOGY

 Surgical anatomy of the anus

1. Anal fissure
2. Hemorrhoids
3. Anoperineal abscesses
4. Fistula in ano
Aspects of surgical anatomy of the anal canal

Muscles of the anal canal

Internal anal sphincter is a circular muscle layer below
the rectum, with a length of 2.5 cm and a thickness of 2-5
mm. Intraoperative its transverse fibers can be seen easily.
Spasm or contraction of the sphincter plays an important
role in the occurrence of anal fissure.
Longitudinal muscle layer of the anal canal consists of
extension of the homonymous rectal muscle and fibers of
pubo-rectal muscle. Its fibers pass over the lower portion
of the external sphincter and insert on perianal skin. These
fibers creates conditions for spread of perianal infection
and defines restricted areas whose distension is
responsible for the intense pressure and pain in these
infections.
External anal sphincter. Some of its fibers insert
posterior on the coccyx, and anterior to the perineal middle
point in men, or are mixed with vaginal sphincter fibers in
women. The major difference between the two sphincters
is of fiber type components: smooth for the internal and
striated for the external sphincter.
Between the two sphincters there is a virtual space called
inter-sphincteric space. This space is important because it
contains 4-8 apocrine glands that can cause infections and
as a dissection plan in surgical interventions on sphincters.
Anal glands may also be the site of origin of an
adenocarcinoma.
The lowermost portion is traversed by a fan shaped
expansion of the longitudinal muscle which splits it up into
8 to 12 discrete muscle bundles.
Pubo-rectal muscle plays a key role in maintaining the
angle between the anal canal and rectum which is
essential in maintaining continence.
The dentate (pectinate) line is the most important
anatomical landmark, both from morphological and
surgical point of view. It separates:
Upward:
– Columnar epithelium
– Autonomous innervation (no sensitivity)
– Portal venous system
– Internal hemorrhoids (not painful)
Downward:
– Stratified squamous epithelium,
– Spinal innervation (very sensitive)
– Systemic circulation
– External hemorrhoids (painful)
Above the pectinate line the mucosa is thrown into 8 to 14
longitudinal folds known as anal column of Morgagni.
The two adjacent column being connected below at he
pectinate line by anal valves (Ball). Morgagni's crypts (or
anal crypts or sinus or saccules of Harner ) are small
pockets between the lower ends of columns with the
same name. These sinus may be of some surgical
significance as some foreign body may lodge in them with
resulting infection or trauma may be inflicted by hard
stools.
Anal papillae are more often absent than present, but
when present, they do not usually arise from the free
edges of the anal valves or crypts as some suppose.
They correspond usually to the rectal columns of
Morgagni . The tips of the papillae frequently project
above the lower margins of the rectal columns.
The perineopelvic spaces

They are directly concerned in the surgical therapy especially

of perianal abscesses and fistula in ano.
1. The perianal space - surrounds the anus and the lower
third of the anal canal. Laterally it is continuing with the
ischiorectal fossa. Posteriorly, it is designated as the post-
anal space.
2. The submucous space – located above the anorectal line
contains the internal hemorrhoidal plexus of veins. This
space is particularly important in hemorrhoids
development.
3. Ischiorectal space - located on both sides of the anal
canal below the pelvic diaphragm. Its base is directed
downwards to the surface and the apex upwards. It
contains ischiorectal fat, inferior hemorrhoidal veins and
nerves crossing transversely, posteriorly, the perineal
and perforating branches (cutaneous) of the pudendal
plexus, and anteriorly, the posterior scrotal or labial
vessels and nerves.
4. The supralevator spaces (pararectal) - above the
levator muscle and below the peritoneal reflections of the
abdominal cavity. These spaces are protected from
infections by fascia barriers.
5. The retrorectal space (Pre-sacral)
This space lies posterior to the rectum and anterior to
the sacrum and coccyx. It has the potential of large
capacity for suppurative processes.
ANAL FISSURE
The anal fissure is a tear in the mucocutaneous layer of
the anal canal.
It affects men and women equally and both the young and
the elderly.
Due to the extremely sensitive anoderm, fissure causes
severe pain during and after defecation.
Causes
Anal fissures are caused most frequently by trauma to
the anal canal by a hard stool or repeated episodes of
diarrhea.
Other traumas that can cause anal fissures are:
introducing anal thermometer, enema cannula,
ultrasound probe, rectoscopy, digital rectal examination
and anal sex.
Other potential causes of fissures are:
– Anal cancer,
– Crohn's disease (4% of patients will have an anal fissure as the
first manifestation),
– Leukemia,
– Tuberculosis,
– Viral infections: cytomegalovirus or herpes, syphilis, gonorrhea,
chlamydia , chancroid (Hemophilus ducreyi), and human
immunodeficiency virus (HIV).
– Some drugs (Antiparkinson) may induce constipation and
others (Nicorandil - vasodilator) directly anal ulceration.
 Fissures usually occur in stressed people or
psychologically labile and sedentary. Also people who
travel a lot (drivers, salesman, etc.) and do not have a
regular stool, are prone to constipation.
Location
The most common location of the anal fissure is the
posterior region (90%) in both women and men.
Location in the front is also possible but more common
in women (10%) than men (1%). Multiple fissures are
also possible.
Why location is predominant posterior?
– Weaker muscles in this region
– Poorer arterial supply
At the lower end of fissure a tag of skin may form,
called sentinel pile.
 fissure

Anal skin tag

Pathophysiology
Most acute anal fissures heal spontaneously or with
appropriate treatment but there are many other which do
not have any tendency to heal and rather become
chronic. The ulceration penetrates deeper and deeper
the layers of the anal canal and a series of complications
appear such as bleeding and intersphincteric abscess.
The reason why these fissures don’t heal is a vicious
circle: anal fissure induces a continuous spasm of the
internal anal sphincter muscle (smooth muscle) and
spasm in turn maintains the fissure. Because of the
spasm, the muscle does not relax on defecation and
fissure open with each bowel movement.
There are two forms of anal fissure: acute and chronic
Acute anal fissure appears as a tear of the anal skin
continued in the anal canal with slightly inflamed edges.
Bleeding is frequent. It is accompanied by spasm of the
sphincter. In this stage the fissure may be cured with
conservative methods (ointments, medication, etc).
Chronic anal fissure is an ulcer like lesion. It appears as
a deep crater with inflamed and hardened edges and a
base containing scar tissue or fibers of internal sphincter.
Muscle spasm in advanced forms is permanent due to
muscle infiltration with fibrous tissue and scar. Local
inflammatory changes can go up to the formation of
abscesses with further development of a fistula. In most
cases surgery is the only way to cure the fissure.
Acute fissure

Chronic fissure
Symptoms
Pain and bleeding are the basic symptoms of anal fissure.
The onset is sudden, usually after a hard stool when the
patient feels a sharp burning anal pain and observes
several drops of blood on toilet paper.
The initial pain disappears but reappears at the next stool.
After defecation the pain recurs with greater intensity and
can last for several hours.
Anal bleedings are also possible, the patient observing
the presence of bright red blood.
The pain can be so severe that patients are unwilling to
have a bowel movement, resulting in constipation and
even fecal impaction. Moreover, constipation can result
in the passage of a larger, harder stool that causes
further trauma and makes the fissure worse.
The pain also can induce dysuria, frequent urination, or
the inability to urinate. Ability to work is also impaired.
Itching (pruritus ani), and a malodorous discharge may
occur due to the discharge of pus from the fissure.
Complications
Anal bleedings
Intersphincteric and perianal abscess. Anal fissures can
be the starting point of purulent collections in the anus
and perianal region, manifested by increased intensity
constant pain, accompanied by fever and swelling of the
perianal region that becomes sensitive to touch.
Perianal fistulas
Mental and work capacity impairment. Even tendency to
suicide have even reported in some people with labile
psychic.
The diagnosis of anal fissure is not difficult being based
on anal pain features and clinical observations.
The diagnosis must be confirmed by a proctologic
examination that can be performed in ambulatory
conditions. Complex anorectal examination (digital and
rectoscopy) should be performed in all cases, even
under anesthesia if necessary, not to miss other more
serious pathology than fissure (anal cancer, Cronh’s
disease, ulcerative colitis, etc).

Anorectal examination
Treatment
The goal of treatment for anal fissures is to break the
vicious cycle of anal sphincter spasm that supports the
repeated tearing of the anoderm.
General treatment
In acute fissures, medical (nonoperative) therapy is
successful in the majority of patients. About 80-90% of
acute fissures will heal under conservative measures as
compared with chronic (recurrent) fissures, which show
only a 40% rate of healing.
Prevent and treat constipation with proper diet with more
vegetables and fruits, with a minimum of 1.5 L of liquid
intake per day, avoiding spicy foods, and possibly mild
laxative administration. Enemas, glycerine suppositories
and purgatives are prohibited.
 Compliance with a strict local hygiene.
 Sitz baths with warm chamomile tea are encouraged,
particularly after bowel movements, to relax the spasm
and to increase the flow of blood to the anus.
 Local ointments with decontracturant, analgesic and
epithelization effect. Usually these ointments are used 3
times/day. Most often used are ointment containing
nitroglycerin 0,2-0,4%
 Other medicines if necessary (anti-inflammatory,
decontracturant, anxiolytics, laxatives).
 Treatment usually lasts three weeks. Some fissures are
already healed after this time. Sometimes, however,
further treatment is required for another 3-4 weeks.
 The patient should be warned that fissure can anytime
reoccur if conditions that led to it (constipation, diarrhea,
etc.) continue.
Botulinum toxin
Botulinum toxin (Botox) relaxes (actually paralyses)
muscles by preventing the release of acetylcholine from
the nerves that normally causes muscle cells to contract.
It has been used successfully to treat a variety of
disorders in which there is spasm of muscles, including
anal fissures. The toxin is injected into the internal anal
sphincter.
The dose is not standardized and has varied from 2.5 to
20 units of toxin in two locations (usually on either side of
the fissure).
Neither this type of treatment ensures a definitive cure
because fissures may reappear.
Surgical treatment
It aims to stop the vicious circle fissure-contracture-
fissure, by cutting the internal anal sphincter.
The anesthesia may be local, spinal or general
according to the patient and doctor preferences.
Partial lateral internal sphincterotomy is the technique
of choice for the treatment of anal fissures. In this
procedure, the internal anal sphincter is cut starting at
its distal most end at the anal verge and extending into
the anal canal for a distance equal to that of the fissure.
The cut may extend to the dentate line, but not farther.
The sphincter can be divided in a closed
(percutaneous) fashion by tunneling under the anoderm
or in an open fashion by cutting through the anoderm.
Following surgery, 93-97% of fissures heal. Recurrence
rates after this type of surgery are low, 0-3%.
The risk of incontinence of stool following surgery is low.
It is important to distinguish between short-term and
long-term incontinence. In the short-term (under six
weeks), the sphincter is weakened by surgery, so
leakage of stool is not unexpected. Long-term
incontinence should not occur after partial lateral internal
sphincterotomy because the internal sphincter is less
important than the external sphincter (which is not cut) in
controlling the passage of stool.
HEMORRHOIDS
also known as piles
Hemorrhoids are vascular structures composed of
veins, arterioles and connective tissue, located in the
rectal submucosa (venous plexus), which have a
physiological role in anal continence, but become
pathological when they increase in volume and have
various complications.
Anorectal canal is not like a pipe with smooth inner
surface. It has overlapping folds (cushions) created by
physiological hemorrhoids in submucosa and
contributing to the tightness of the canal and so to gas
continence.
In gynecologic position submucosal venous cushions
are located at hours 3, 7 and 11 on dial time, the
favorite places where hemorrhoids usually occur.
Frequency
Ten million people in the United States have
hemorrhoids, which represents a prevalence rate greater
than 4%.
Etiology
Genetic (hereditary)
The main cause is a decreased resistance of the venous
wall which becomes weaker and dilates easily. It is due
to a genetic disorder of collagen and elastic fibers with
decreased vein wall elasticity. Usually it has a familial
character (grandparents, parents had hemorrhoids) and
is frequently associated with other diseases such as
varicose veins and flat feet.
Predisposing factors
– Constipation: by forcing the passage of stool it exerts
compression on the hemorrhoidal veins.
– Diarrhea and laxatives: cause mucosa irritation
– Occupational factors: prolonged standing or sitting
(drivers, pilots)
– Rectal cancer - symptomatic hemorrhoids
– Increased intra-abdominal pressure
Pregnancy
Obesity
Ascites
Tumors
– Increased venous pressure
Portal hypertension (symptomatic hemorrhoids)
Classification
Hemorrhoids are divided into internal (above the
dentate line) and external (distal or below the dentate
line). Usually external hemorrhoids are located under the
perianal skin. Mixed hemorrhoids appear when internal
high grade hemorrhoids merge with external
hemorrhoids.
Internal hemorrhoids are classified into four grades.
1. Grade I: No prolapse.
2. Grade II: Prolapse upon defecation but spontaneously reduce.
3. Grade III: Prolapse upon defecation and must be manually
reduced.
4. Grade IV: Prolapsed and cannot be manually reduced.
Prolapsed hemorrhoids are internal hemorrhoids that are
so distended that they are pushed outside the anus.
External hemorrhoids
Mixed hemorrhoid

Hemorrhoidal prolapse

Skin tag
Internal hemorrhoids
Symptoms
Uncomplicated hemorrhoids are asymptomatic.
Complications
1. Bleeding is the most frequent complication and it is a
manifestation of the internal hemorrhoids. Bleeding is
the most frightening symptoms for the patient and
leads him to the doctor. Blood is usually bright red or
dark red color and the patient notices it on toilet paper,
on stool or dripping in the toilet bowl. It is usually a
terminal bleeding, blood is not mixed with the stool but
covering its surface.
Bleeding features are very important for differential
diagnosis of hemorrhage from other causes, especially
ano-rectal cancer.
Anemia due to bleeding from hemorrhoids is a chronic
type feriprive (Iron deficiency) anemia.
2. Hemorrhoidal prolapse, is the prerogative of internal
hemorrhoids. Occurs in advanced stages of
hemorrhoids (stage four). Prolapsed hemorrhoids may
be complicated due to sphincter spasm which
squeezes them, resulting in edema and venous
thrombosis, with intense inflammatory processes and
pain. Hemorrhoidal prolapse may be partially or
completely circular. Inflammation can progress to
necrosis, ulceration, bleedings and suppuration.
3. Hemorrhoidal thrombosis. It occurs more frequently in the
external hemorrhoids. It is due to blood clotting in the
hemorrhoidal veins (flebothrombosis) and if inflammatory
processes are associated, it is called thrombophlebitis.
The patient notices a swelling on the anal ring that
becomes increasingly painful. Associated pain intensity is
variable depending on the size of the associated
thrombosis and inflammation. In most cases pain is
continuous, lasting several days and affects the working
capacity of the patient.
Thrombosed hemorrhoid may progress to regression and
resorption with reduction in volume and improved
symptoms, or may progress to ulceration, bleeding and
suppuration. With resolution of the thrombosis, the
stretched anoderm persists as excess skin or skin tags.
Internal hemorrhoids generally do not produce anal pains.
External hemorrhoid thrombosis
Ulcerated hemorrhoidal thrombosis
Diagnosis is made by proctologic examination and
rectoscopy.
Examination begins with inspection and examination of the
entire perianal area.
Gentle spreading of the buttocks allows easy visualization
of most of the anoderm; this includes the distal anal canal.
Anal fissures and perianal dermatitis (pruritus ani) are
easily visible without internal probing. Prolapse can be
observed when the patient performs a Valsalva maneuver.
Digital examination of the anal canal can identify any
induration or ulcerated areas and also sensibility and anal
sphincter tonus. Be sure to palpate the prostate in all men.
Because internal hemorrhoids are soft vascular structures,
they are usually not palpable.
Anorectoscopy is mandatory for viewing internal
hemorrhoids or other local lesions.
 Differential diagnosis of hemorrhoids should be made
with other diseases of the anorectal region that may cause
pain, bleeding and itching.
Bleeding: Pruritus
– ulcerative colitis – dry skin
– anorectal cancer – diabetes
– Crohn's disease – intestinal warms
– anal syphilis – excesive washing, inadequate
– anal fissure cleaning
– coagulation disorders – food irritants
Pain – medication
– anal fissure – skin disorders, bacteria,
– proctalgia fugax (or levator fungus, etc
syndrome) is a severe,
episodic, rectal and
sacrococcygeal pain. It can be
caused by cramp of the
pubococcygeus or levator ani
– anorectal tumors
– gynecological pathology
– coccidinia
Treatment
It is preventive and curative
Depending on the stage of hemorrhoids, the choice of the
patient and physician’s experience, treatment can be
surgical or non-surgical.
As with any other disease, if the patient presents to the
doctor in early stages of the disease, treatment will be
much less aggressive, painless and can be performed in
ambulatory conditions. In advanced stages, or in case of
serious complications the only possible treatment is
surgical.
Non-surgical methods of internal hemorrhoids are
recommended especially in less advanced stages (I, II and
III). Among these are:
Rubber band ligation - the most widely used
Sclerotherapy
Laser or infrared photocoagulation
Cryotherapy
Rubber band ligation is performed on an outpatient basis.
It's an absolutely painless maneuver and a session
usually lasts less than 5 minutes. Blaisdell and Baron
described and refined ligation therapy.
The procedure is performed using a tubular instrument
connected to a suction pump. The instrument is loaded
with two rubber rings. Internal hemorrhoid is sucked into
the tubular device and the two rubber rings are
downloaded at the root of the hemorrhoid. Thus
hemorrhoid vascularisation is interrupted inducing its
necrosis and detach within 5-7 days. Remaining scar will
heal completely in about 2-3 weeks. The procedure is
done in several sessions depending on the number and
size of hemorrhoids.
Elastic ligation is applied only to internal hemorrhoids.
Device for hemorrhoidal ligation
Hemorrhoid Ligation Scar
Surgery is indicated in advanced stages and
complications of hemorrhoids. Also in external
hemorrhoids. The goal is to remove hemorrhoidal
packages.
There are several methods of surgical treatment
1. Removal (hemorrhoidectomy)
2. Stapling (hemorrhoidopexy)
3. Blood clot (thrombus) removal. An external hemorrhoid is incised
and the blood clot removed.
4. Transanal hemorrhoidal dearterialization and rectal mucosal pexy.
Operations can be performed under local or general
anesthesia, but in most cases are performed in spinal or
epidural anesthesia.
External hemorrhoidal thrombosis is managed by removing
the blood clots and excision of the underlying veins under
local anaesthesia. Remember, acute thromboses
spontaneously resolve in 10-14 days, thus, a patient who
presents late and has diminishing pain is best left alone.
Operative resection is reserved for patients with hygiene
trouble caused by large skin tags, a history of multiple
external thromboses, or internal hemorrhoid trouble.
Milligan-Morgan Technique
Developed in the United Kingdom by Drs. Milligan and
Morgan, in 1937. The three major hemorrhoidal vessels
are excised. In order to avoid stenosis, three pear-
shaped incisions are left open, separated by bridges of
skin and mucosa. This technique is the most popular
method, and is considered the gold standard by which
most other surgical hemorrhoidectomy techniques are
compared.
Ferguson Technique
Developed in the United States by Dr. Ferguson, in 1952.
This is a modification of the Milligan-Morgan technique
(above), whereby the incisions are totally or partially
closed with absorbable running suture.
Milligan-Morgan procedure
Stapled Hemorrhoidopexy (PPH Procedure)
Also known as Procedure for Prolapse & Hemorrhoids
(PPH), Stapled Hemorrhoidectomy, and
Circumferential Mucosectomy.
PPH is a technique developed in the early 90's that
reduces the prolapse of hemorrhoidal tissue by
excising a band of the prolapsed anal mucosa
membrane with the use of a circular stapling device. In
PPH, the prolapsed tissue is pulled into a device that
allows the excess tissue to be removed while the
remaining hemorrhoidal tissue is stapled. This restores
the hemorrhoidal tissue back to its original anatomical
position.
Whitehead hemorrhoidectomy described in 1882 by the
author, with good results, is responsible for the most
serious complications: anal stenosis, ectropion and ano-
cutaneous sensitivity disappearance.
It excises a circular sleeve of anal mucosa with
hemorrhoidal packages, the skin being sutured to the
rectal mucosa.
In Romania the operation was introduced and developed
by Vercescu.
In 1998, Wolff and Culp bring a change in calibration
technique that prevents stenosis of the anal canal with
flaps sutured to the dentate line. The method is
successfully used for irreducible hemorrhoidal prolapse
and can be achieved with a single circumferential flap or
two flaps, right and left, prepared from anal mucosa after
dissection of the hemorrhoidal packages.
Whitehead hemorrhoidectomy
Witehead operation before and after

Circular suture
Postoperative care
The patient is usually discharged on day 2 or 3 after
surgery, but surgery may be performed in terms of one
day surgery.
Recommendations at discharge are:
– Warm sitz bathes
– Ointments with healing effect
– Avoid constipation and diarrhea
– Avoid spicy food
– Paraffin oil to facilitate stool evacuation
– Dressing is not always necessary and is usually dry in a sterile
compress.
Control at 3-4 weeks after surgery involving a digital
rectal examination to assess anal stenosis occurrence.
Postoperative complications
Early: Pain, acute urinary retention, hemorrhage
Late: secondary hemorrhage, anal stenosis, anal fissure
ANOPERINEAL ABSCESSES
Etiology
Staphylococci, Streptococci, Ecoli or Proteus and
anaerobes such as clostridium welchii and bacteroides
are frequently responsible for these abscesses.
In 20% of cases the site of entry of the infective
organism is obvious. Perianal abscess may develop
after:
1. Dorsal anal fissure
2. Anal hematoma
3. Prolapsed thrombosed internal hemorrhoids
4. Following injection of a anesthetic solution or alcohol
in perianal or ischeorectal space in the treatment of
perianal pain
5. Following injection of internal hemorrhoids
6. Injury to anal or rectal mucosa
7. As a complication of hemorrhoidectomy or
sphincterotomy.
Pathophysiology
Anorectal abscess is a Crypto - Glandular disease
because infection of the anal crypts followed by infection
of the anal glands leads to the abscess formation.
Cryptogandular disease in acute stage presents as
anorectal abscess while in chronic sages it presents
as fistula in ano.
According to this theory the first step is the formation of
an intersphincter abscess , due to infection of anal gland
located between the internal sphincter and the
longitudinal intersphincteric muscle fibres. Subsequently
the pus may force its way downward along the
longitudinal fibres to emerge at the anal orifice as perianal
abscess. Laterally it may pass through the longitudinal
muscles and external sphincter to enter the ischiorectal
fossa to give rise to ischiorectal abscess, or it may track
upwards in the intersphincteric space to produce a high
intermuscular abscess. If the pus tracks still higher in the
intersphincteric space it gives rise to pelvirectal abscess.
According to their location abscesses may be:
1. Intersphincteric
2. Submucous
3. Perianal
4. Ischiorectal
5. High intermuscular
6. Supralevator
Clinical picture
Perianal abscesses manifest with symptoms and signs of
an acute perianal inflammatory process. Celsian signs:
tumor, dolor, calor, rubor and functio laesa.
Patient complains of pain, becoming more intense,
localized anoperineal. The patient cannot sit and in most
cases is feverish.
In most cases the classical signs of a perianal abscess
are:
– on inspection a perianal swelling with stretched, shiny, flushing
skin
– on palpation a painful induration with high local temperature
– In advanced cases fluctuency may be felt and in more advanced
cases the ulcerated skin with fistula and pus discharge is present.
– When the abscess has a deep location local signs are not so
obvious.
– On digital rectal examination a painful tender indurated bulge
into the anal canal on that side is felt. The manuever is painful.
Recurrent perianal abscess
Natural evolution of perianal abscesses:
1. Perianal abscesses progress to skin necrosis and outward
fistulization with incomplete abscess evacuation. As
abscess evacuates, the internal pressure drops and pain
decreases. However, the abscess should be operated for a
complete evacuation.
2. Intersfincterian abscess may spontaneously drain intra-anal,
or may progress to other sites (perianal, submucous,
ischiorectal, etc.)
3. Ischirectal abscess evolves with symptoms of sepsis, or
intrarectal fistulization is possible in advanced stages.
4. Supralevator abscess, being very deep, it is difficult to
diagnose. Also evolves with sepsis, and usually fistulization
takes place into the rectum.
5. In rare cases the abscess can progress to a very serious
form of necrotizing fasciitis that extends to the genitals
(Fournier’s gangrene).
Fournier’s gangrene
Diagnosis
Generally is easy and there is no need for special
investigations.
Clinical examination of the perianal region and rectal
examination are sufficient.
In case of deep abscess (supralevator and ischiorectal)
intrarectal ultrasonography and computed tomography
are useful in diagnosis.
Differential diagnosis should be made to other
diseases that evolve with perianal pain and sepsis :
– Bartholin’s abscess
– Hemorrhoidal thrombophlebitis
– Douglas sac abscess
– Gynecological inflammatory disease
– Rectal tumors
Treatment
Usually patients are hospitalized in emergency condition.
The main treatment is surgery plus medication with broad-
spectrum antibiotics at first and then according to the
antibiogram, inflammatory and pain relievers.
Usually treatment consists of incision, evacuation,
debridement, lavage and drainage or swabbing with
hydrogen peroxide. (In spinal or general anaesthesia)
Perianal and submucous abscesses are easily incised.
Incision is made in the maximum fluctuence.
In case of ischiorectal abscesses, perianal skin incision is
guided by the finger introduced into the rectum to find the
collection.
 In case of intersfincterian abscess, pus is discharged
spontaneously during anal dilatation with the anuscope
or after the internal sphincterotomy.
In case of supralevator abscess, the puss is evacuated
intrarectal through an incision of the rectal wall and then
drained out with a transanal drainage tube.
Postoperative evolution
Dressings are applied each day.
Wound will heal gradually by granulation but often (7-
40%) a perianal fistula will remain which should be
operated over a period of 6 weeks. If the wound is
closed completely or the patient does not return for
treatment of perianal fistula, perianal abscess will recur
with high probability over a variable time.
 Incision site Sampling for antibiogram

Puss evacuation Debridement

Lavage with H2O2 Packing the cavity

Retroanal abscess started from a posterior anal fissure
Particular forms of perianal abscesses
Ischiorectal abscess
The only sign of inflammation may be an induration of the
perianal region. The patient presents with pyrexia of
obscure origin without pain of any kind.
Horse shoe abscess
The ischiorectal fossa communicates with that of the
opposite side via the retroanal space and if an ischiorectal
abscess is not evacuated early, involvement of the
contralateral fossa is not uncommon (10-11%) thus giving
rise to a bilateral ischiorectal abscess, the so called “horse
shoe” abscess . In most cases the infection starts from a
posterior anal crypt.
Fournier's Gangrene is a specific form of necrotizing fasciitis. Classically, it
involves the penis and scrotum. Often the underlying cause is related to a
perianal/ischiorectal abscess. The tissue planes in the perineum and groin are all
connected and the aggressive agents of destruction in necrotizing infections
tend to spread along these planes.
Pathonogmonic findings include a wide area of bruising and ecchymosis
involving most of the gluteal skin, crepitus, and skin changes over the base of
the scrotum.
Comorbid diseases that compromise the
immune system have been implicated as
necessary predisposing factors for the
development of Fournier gangrene. The
following are common predisposing
comorbidities:
•Diabetes mellitus (cited most often)
•Morbid obesity
•Cirrhosis
•Vascular disease of the pelvis
•Malignancies
•High-risk behaviors (eg, alcoholism,
intravenous drug abuse)
Fournier's Gangrene •Immune suppression due to systemic
disease or steroid administration
Supralevator abscess is a rare condition and the most
difficult to diagnose.
The patient presents with a septic status with high fever
even pyrexia, with mild continuous pelvic pains.
On rectal examination a bulge of the rectal wall may be
felt with the finger tip.
When the abscess fistulizes into the rectum and stools
contain a large quantity of pus, the diagnose becomes
easier.
CT reveals the collection in the supralevator space.
Surgical treatment consists of a transanal incision of the
rectal wall in the maximum fluctuence. A drainage tube is
placed in the abscess cavity and exteriorized through the
anal orifice.
 PERIANAL FISTULA
Fistula-in-ano

A perianal fistula is an abnormal connection (channel)

between the anal canal and the skin.
History (http://emedicine.medscape.com/article/190234-overview)
References to fistula-in-ano date to antiquity.
Hippocrates made reference to surgical therapy for fistulous disease.
The English surgeon John Arderne (1307-1390) wrote Treatises of
Fistula in Ano; Haemmorhoids, and Clysters in 1376, which described
fistulotomy and seton use.
Historical references indicate that Louis XIV was treated for an anal
fistula in the 18th century. In the late 19th and early 20th centuries,
prominent physician/surgeons, such as Goodsall and Miles, Milligan and
Morgan, Thompson, and Lockhart-Mummery, made substantial
contributions to the treatment of anal fistula.
In 1976, Parks refined the classification system that is still in widespread
use.
Over the last 30 years, many authors have presented new techniques in
an effort to minimize recurrence rates and incontinence complications.
Despite 2500 years of experience, fistula-in-ano remains a perplexing
surgical disease.
Frequency
The prevalence rate is 8.6 cases per 100,000
population.
The male-to-female ratio is 1.8:1.
The mean age of patients is 38.3 years.
Causes:
Primary
– Obstruction of anal gland which leads to stasis and infection
with perianal abscess formation which was previously operated
or with spontaneous fistulization to the skin surface. (the most
common cause)
Secondary
– Iatrogenic (hemorrhoidal surgery)
– Inflammatory bowel diseases (Crohn's disease more common
than ulcerative colitis)
– Infections (viral, fungal or TB)
– Malignancy
– Radiation
Signs and symptoms
Patients often provide a reliable history of previous
pain, swelling, and spontaneous or planned surgical
drainage of an anorectal abscess.
1. Perianal discharge
2. Pain
3. Swelling
4. Bleeding
5. Diarrhea
6. Skin excoriation
7. External opening
Physical examination
An external opening that appears as an open sinus or
elevation of granulation tissue.
Spontaneous discharge via the external opening may be
apparent or expressible upon digital rectal examination.
Digital rectal examination may reveal a fibrous tract
beneath the skin. It also helps delineate any further acute
inflammation that is not yet drained. Lateral or posterior
induration suggests deep postanal or ischiorectal
extension. The sphincter tone and voluntary squeeze
pressures should be assessed before any surgical
intervention to delineate whether preoperative manometry
is indicated.
Anuscopy is usually required to identify the internal
opening.
Ultrasound, fistulography, MRI is not performed routinely but
are helpful in highlighting an occult cause of fistula
recurrence.
 When describing a fistula, it is important to mention the
following aspects:
1. Position of the skin opening on axial images (using
the anal clock).
2. Distance of the opening to the anal verge.
3. Secondary fistulas or abscesses.
Fistula after perianal operated abscess
Several techniques have been described to help locate the
trajectory of the fistula and, more important: to identify
the internal opening.
Instrumental exploration of fistula tract. Care should be
taken to not use excessive force and create false
passages.
If internal orifice can not be detected, blue dye or
hydrogen peroxide may be injected through the external
orifice of the fistula under direct visualization of the
interior aspect of the anal canal.

Metal wire (button probe)

blunt-tipped crypt probe
Differential diagnosis:
Sinus pilonidalis
Other causes of fistula in ano
• Inflammatory bowel diseases (Crohn's disease more common
than ulcerative colitis)
• Infections (viral, fungal or TB)
• Malignancy

Anus

Sacral region

Sinus abscess fistulized in perianal region

Classification
The most widely used classification is the Parks
classification which distinguishes four kinds of fistula:
1. Intersphincteric (70%)
2. Transsphincteric (25%)
3. Suprasphincteric (5%)
4. Extrasphincteric - rare
The most common fistulas are the intersphincteric
and the transsphincteric.
The extrasphincteric fistula is uncommon and only
seen in patients who had multiple operations. In these
cases the connection with the original fistula tract to
the bowel is lost.
Other possible fistulas:
1. No perianal opening (external blind)
2. No internal opening (internal blind)
3. Complex fistulas – multiple, ramified tracts with,
or without multiple external orifices.
A superficial fistula is a fistula that has no relation to
the sphincter or the perianal glands and is not part
of the Parks classification.
These are more often due to Crohns disease or
anorectal procedures such as haemorrhoidectomy
or sphincterotomy.
Superficial fistula
Goodsall’s rule
It relates the external opening of an anal fistula to its
internal opening.
It states that the external opening situated behind the
transverse anal line will open into the anal canal in the
midline posteriorly. An anterior opening is usually
associated with a radial tract.
Anterior fistulas will have a direct track into the anal
canal. Posterior fistulas will have a curved track with
their internal opening lying in the posterior midline of
the anal canal.
An exception to the rule are anterior fistulas lying
more than 3 cm. from the anus, which may have a
curved track (similar to posterior fistulas) that opens
into the posterior midline of the anal canal.
3 cm
Principles of treatment
Anal fistulas never heal spontaneously. The inner wall
of the fistula develops fibers and piogenic membrane
that does not allow spontaneous healing.
Only surgical treatment can heal the fistula.
There are three main procedures:
– Fistulotomy (cutting/opening the fistula tract)
– Fistulectomy (excision the whole fistula tract)
– Seton placement
There are many other surgical techniques including
laser coagulation of the fistula tract and sealing with
fibrin glue.
In simple cases fistulotomy is preferred and in most
cases fistulotomy is preferred to fistulectomy because it
does not involve excision of a portion of the sphincteric
muscle. Seton placement is rarely used due to the fact
that it is a very painful procedure.
Fistulotomy
A probe is passed into the fistula through the external
opening.
The overlying skin, subcutaneous tissue, and internal
sphincter muscle are divided with a scalpel or
electrocautery, thereby opening the entire fibrous tract,
like a book.
Curettage is performed to remove granulation tissue in
the tract base.
Wound is dressed daily to close from depth toward
the surface.
Fistulotomy
 Complete fistulectomy creates
larger wounds that take longer to
heal. The entire fistula tract is
excised with a perianal skin of 1-
2 cm adjacent to the external
orifice. Daily dressing promotes
internal healing before external
closure.
Seton placement (slow
fistulotomy) – An elastic seton
is applied through the entire
fistula and tied outside the anus.
The seton will slowly cut the anal
sphincter from inside out with
consecutive healing.
Postoperative care
– Sitz baths, analgesics, and stool bulking agents
– Importantly, ensure that the internal wound does not
close prematurely, causing a recurrent fistula.
– Wound healing usually occurs within 6 weeks.
Complications
Early postoperative
– Urinary retention
– Bleeding
– Faecal impaction
– Haemorrhoidal thrombosis
Delayed postoperative
– Recurrence
– Anal incontinence
– Anal stenosis
– Delayed wound healing
Outcome and Prognosis
Following standard fistulotomy, the reported rate of
recurrence is 0-18% and the rate of any stool
incontinence is 3-7%.
There are cases with multiple recurrences or complex
fistulas that sometimes require making a temporary
loop colostomy, to devert the faeces from anorectum
and to allow healing after fistulectomy or fistulotomy.
To prevent recurrences several conditions are
necessary:
1. Fistula tract must be removed entirely (fistulectomy) - more
difficult in complex fistulas - fistula track can be marked with
methylene blue dye
2. Internal oriffice should be discovered
3. Wound healing must happen from the depth toward the surface
SURGICAL PATHOLOGY OF
THE APPENDIX

• Anatomy
1. Acute appendicitis
2. Chronic appendicitis
3. Tumors of the appendix
Anatomical aspects
• The appendix is a hollow cylindrical organ like a worm
(hence the Latin name "Appendix vermicularis").
• The length is ranging between 2 and 30 cm., and 0.5 to
0.8 cm in diameter.
• It is located at the base of cecum, at the place of union
of the three teniae coli. This last aspect is particularly
important helping the surgeon to detect the base of
appendix when it is difficult to find it through a small
laparotomy. Another landmark is the constant
implantation of the appendix in cecum at about 2.5 cm
postero-medial to the ileo-cecal valve.
• Histologically the appendicular wall is composed of the
same layers as the intestine. Submucous layer contains
a wide selection (about 200) of lymph follicles hence
the name "abdominal tonsil". Maximum development of
these follicles occurs until the age of 18-25 years, after
that their involution occurs. Inside the appendix there
is a mucus-secreting epithelium.
• Appendix abdominal topography varies depending on
the position of the cecum. In most cases it is located in
right iliac fossa, but in case of a short ascending colon
it can be located under the liver, which raises problems
of differential diagnosis of acute appendicitis with acute
cholecystitis, perforated duodenal ulcer, renal colic,
colon tumor, etc.
• Frequently, the appendix is located behind the
cecum (retrocecal - 65% of cases) or in the pelvic
region (30%).
• In most cases the appendix is located in the right
iliac fossa. There are two notable exceptions
regarding the appendix position:
1. The first is bowel malrotation when cecum and
appendix are located in the left upper quadrant,
and also during pregnancy when the gravid uterus
rises the cecum and appendix in the upper right
quadrant.
2. In situs inversus the appendix is located in the left
iliac fossa, symptoms of the acute appendicitis
being almost similar to that of colic diverticulitis.
• Arterial vascularization of the appendix is provided by
appendicular artery, usually single, derived from the
ileocolic artery or branches. Appendicular vein drains
into the ileocolic vein and then into the superior
mesenteric vein. Lymphatic drainage is towards
lymph nodes along the appendicular artery, then
ileocolic and superior mesenteric artery.
ACUTE APPENDICITIS
• Despite progresses in antibiotic therapy and surgery,
acute appendicitis remains a surgical emergency
being the main cause of admission for acute surgical
abdomen.
• Untreated, it causes serious complications that can
lead to death (perforation, generalized peritonitis).
Therefore early diagnosis and treatment are of
utmost importance.
• Acute appendicitis can create special problems of
diagnosis and treatment in atypical forms. Generally,
one of five appendicitis is misdiagnosed and the
incidence of normal appendix during appendectomy
is estimated at 15-40% of all cases.
History
• Up to 1850 there have been many interpretations of causes that
lead to the right iliac fossa inflammation.
• In 1827, Melier described several cases of appendicitis at autopsy
and formulated the idea that the appendix could be the cause of
death.
• In 1880, both Matterstock in Germany and and With in Norway
published works indicating the appendix as an significant cause of
inflammation of the right iliac fossa.
• In 1886, Reginald Fitz, introduction the term of appendicitis and
recommended the early surgical treatment of disease.
• In 1889, Chester McBurney described the migratory pain and sign,
which bears his name.
• In 1905, Murphy described the symptoms of appendicitis consisting
of pain followed by nausea, vomiting and right iliac fossa muscular
contracture.
• When Fitz described the acute appendicitis, perforated appendicitis
mortality rate was about 30%.
Incidence
• The incidence is 7% - 10% in U.S. and Europe. In
Asian and African countries is lower probably due to
dietary habits.
• Acute appendicitis occurs most commonly in the
second and third decade of life, but can affect any
age. The highest incidence is seen in 10-19 years age
group, where it reaches a frequency of 233 cases per
100,000, with a prevalence for males (male / female
ratio is of 1.4 – 1.7/1).
Etiology
• Determining cause of acute appendicitis is bacterial
infection (infectious theory of Aschoff).
• The main germs involved in acute appendicitis are:

AEROBES
Escherichia coli
Streptococcus viridans spp.
Pseudomonas aeruginosa
Streptococcus Grup D
Enterococcus spp.
ANAEROBES
Bacteroides fragilis
Bacteroides spp.
Peptostreptococcus
Bilophila spp.
Lactobacillus spp.
Fusobacterium spp.
Pathophysiology
• There are two theories:
1. Enterogenic theory : the obstruction of the appendix
lumen is the determining factor.
2. Haematogenic theory justifies appendicitis by blood
dissemination of bacteria usually during a
respiratory infection.
• Complete obstruction of the appendicular lumen by
lymph follicles hyperplasia is the most common cause
of appendicitis.
• In elderly, obstruction is usually a consequence of
fibrosis, coprolites (4%) or malignancies (1%)
(carcinoid, adenocarcinoma or mucocele). In endemic
areas, intestinal parasites can also cause obstruction.
Morphopathology
• In the first 24 hours of onset symptoms, 90% of
patients experience only inflammation or necrosis
of the appendicular wall, but without perforations.
• The are three pathological stages of evolution:
1. catarrhal appendicitis
2. phlegmonous appendicitis
3. gangrenous appendicitis
• Catarrhal appendicitis (congestive): the appendix is
turgid, congested, red-purple, with evident vascular
draw. The mucosa surface is hyperemic, thickened,
with superficial ulcerations. Spontaneous regression
is possible in this stage or it may progress to the
next stage.
• Phlegmonous appendicitis (purulent): enlarged
appendix, in tension and very brittle (must be handled
carefully because it may break). Size is often uneven,
with serosa shine disappeared. Appendix tip is thicker.
In the periappendicular area, frequently there is a
turbid peritoneal reactive fluid. The mesoappendix is
infiltrated and friable. Appendix may adhere to nearby
organs. The content is purulent (appendicular
empyema). Microscopically destruction of lymph
follicles are observed, and their transformation into
small abscesses. Spontaneous regression is rarely
present in this stage.
Phlegmonous appendicitis
• Gangrenous appendicitis (necrotic-haemorrhagic) -
appendicular wall with devitalized areas looking soft and
brown ("withered leaves") with intense edema and
hyperemia of the mesoappendix, often with thrombosed
vessels. The presence of hyperseptic and fetid peritoneal
fluid; Anaerobic microorganisms are present (Clostridium
perfringens, Bacilus funduliformis) with colibacilus and
streptococcus. Spontaneous regression never appears.
Peritonitis is always present. (fist stage of peritonitis)
• In slow-evolving forms, there is a localized peritonitis and
the intestinal loops, omentum and other nearby organs
are trying to isolate and block the expansion of the
inflammatory process, thus developing a periappendicular
block. Antibiotics and local cold applications in this stage
can lead to regression of inflammatory process. Appendix
usually heals with fibrosis process and it may be removed
after a few weeks.
Gangrenous appendicitis
• Evolution of the block, in the absence of appropriate
treatment is usually toward perforation and
periappendicular abscess formation and local peritonitis
(second stage peritonitis). At this stage it is
recommended only abscess incision and evacuation
without appendectomy (oncotomy).
• Unrecognized periapendicular abscess will progress
with increasing pressure of the pus inside the cavity
and fistulization into the peritoneal cavity leding to
generalized peritonitis as a third stroke.
Symptoms
• In classic forms, the onset is acute, the main complaints
being epigastric pain and anorexia.
• Symptoms depend on patient age (infant, adult, elderly),
the anatomical position of appendix (retrocecal,
subhepatic, mezoceliac, pelvic) and on morphopathology
(appendicular block, abscess, diffuse purulent peritonitis
or pseudotumoral appendicitis).
• Pain is the major symptom. It is initially, located within
the epigastrium or peri-umbilical. After a period of time,
ranging between 1-12 hours, it descends in the right iliac
fossa being exacerbated by effort, coughing or sudden
movements. It is not a colicky pain !
• Anatomical variations of the appendix influence the
location of pain (a retrocecal appendix produces a rear
flank pain, a pelvic appendix will induce suprapubic pain
and a retro-ileal appendix will produce pain by irritating
the testicular artery and ureter).
• Anorexia nearly always accompanies acute appendicitis
and it is an early symptom. In over 95% of cases
anorexia is the first symptom, followed by abdominal
pain. If vomiting appears before the pain then the
diagnosis of acute appendicitis is uncertain.
• Nausea and vomiting occur in 75% of patients, but
they are not heavy or lasting, most patients presenting
only one or two vomiting.
• Bowel disorders. Most patients have constipation
before the onset of pain. In elderly pseudo-occlusive
appendicitis may occur with stop of the bowel passage
and abundant vomiting.
Clinical signs
• General clinical signs are not significantly altered in
uncomplicated acute appendicitis.
• The temperature is rarely higher than normal with a
degree, and the pulse is normal or slightly increased .
• Besides the classic appendicitis, when the diagnosis
is easily made, there are many cases, especially in
old age, when symptoms and signs are not at all
characteristic to an acute appendicitis. It is therefore
appropriate a careful examination to be performed.
• The patient will be examined in the supine position
with knees slightly bent.
• The examination begins with inspection of the abdomen
with particular attention to respiratory movements. The
existence of a right iliac fossa scar not always rule out an
acute appendicitis. There are cases of acute appendicitis
on an appendicular stump after an incomplete
appendectomy.
• Then comes the superficial and deep palpation starting
from the left iliac fossa going counterclockwise to the
right iliac fossa.
• Abdominal percussion is very important, often the
diagnosis of peritoneal irritation relies on this maneuver.
• Auscultation has a limited value.
• Digital rectal examination (and vaginal in women) will not
be neglected.
Palpation of the abdomen
Local physical signs in acute appendicitis
• On inspection:
• A slight "delay" in right iliac fossa region of
abdominal wall respiratory movements. In more
advanced stages with peritoneal irritation immobility
of this region can be noticed as a reflex against pain.
In perforated appendicitis with generalized peritonitis
abdominal wall movements are abolished.
• Cough sign (Kusnirenko). Asking the patient to cough
it will have a defense reflex placing hands in painful
region.
• On superficial palpation:
• In typical cases of appendicitis, cutaneous hyperesthesia
is obvious (known as Dieulafoy sign).
• Voskresenski maneuver is: slipping fingers over the right
iliac fossa covered by the patient's shirt causes pain.
• Lanz sign: gliding a sensitivity test needle on the right
iliac fossa and flank skin surface, no longer produces
reflex muscle contraction while in unaffected areas this
reflex occurs.
• On deep palpation
– The pain is the most intense in McBurney's point or
Iacobovici triangle bordered by spino-umbilical line, bi-
spinal line and the lateral edge of the right abdominal
muscle.
• Rovsing's sign is inconsistent, but very specific for acute
appendicitis - Applying a pressure on the left iliac fossa
will push the gas in the colon towards the cecum and will
induce its distension that will produce a pain in the right
iliac fossa.
– Blumberg sign (right iliac fossa pain caused by sudden
decompression of the abdomen after manual
compression in another area - usually the left flank).
– Defense of the abdominal wall muscles is proportional
to the intensity of the inflammatory process in
appendicitis. At the onset of disease, muscular
defense, if present, is usually voluntary. As the
inflammatory process evolves, it intesiffies and
becomes involuntary, muscle spasm turning into a
localized muscle contraction.
– In later stages, an intensely painful tumor, poorly
defined, in right iliac fossa may be palpated: the
periapendicular block.
– In generalized peritonitis, due to perforation of the
appendix, signs of generalized peritoneal irritation are
present.
• Only 50% of patients have typical signs of an acute
appendicitis. Variations of appendix position produce
variations in physical signs.
• Psoas sign (Iavorski-Lapinski) indicates an irritative
process in contact or near this muscle (retrocecal or
retroperitoneal appendicitis). Pain is produced by
iliopsoas muscle contraction during elevating in
extension of the right leg with the patient supine.
• Obturator sign (Romberg) is the occurrence of
hypogastric pain to internal obturator muscle
extension. The sign is put out by the internal rotation
of flexed right thigh with the patient supine.
• On percussion
– Percussion above the iliac fossa is a maneuver
that causes pain in classical acute appendicitis and
it is one of the most accurate signs of peritoneal
irritation ("bell sign " - Mandel)
– Binet sign – Hyper sonority over the cecum area
on percussion due to air content through bowel
paresis and distension. (Stokes's law - "any of
smooth muscle beneath an inflamed serosa layer
enter into paresis")
• Digital rectal examination may reveal tenderness
of the Douglas bag (“the Duglas scream" - Proust
sign) especially in cases of fluid collections at this
level.
• Right iliac fossa classic signs in acute
appendicitis (Dieulafoy triad):
1. Spontaneous and provoked pain
2. Cutaneous hyperesthesia
3. Muscle contracture
Investigations
• Laboratory
• Usual investigations for suspected acute appendicitis are
leukocytosis and urinalysis. In classic cases of acute
appendicitis rarely other laboratory investigations are
needed.
• Leukocytosis value is between 10.000-15.000/mm3.
Leukocytosis in pregnant women is not helpful because it
is high physiologically. White blood cell counts above
these values advocate for a complicated form of acute
appendicitis (perforation). A normal WBC does not
exclude an acute appendicitis.
• Urinalysis examination is mandatory to rule out a possible
urinary infection or reno-ureteral colic. Sometimes,
however, white or red blood cells may be present in
urinary sediment as a result of irritation of the bladder in
an acute appendicitis with pelvic location or of the ureter
in a retroperitoneal location of the appendicitis.
• Ultrasound is considered suggestive if the appendix
is incompressible and has a diameter of 6 mm or
larger, and conclusive in the presence of a shadow
cone generated by a coprolite while an appendix
compressible, of 5 mm or less, excludes an acute
appendicitis .

Other radiological
explorations include
computer tomography,
and scintigraphy with
radiolabeled
leukocytes.
Evolution and complications
• Favorable outcome (rare): remission with
association of symptomatic and antibiotic
medication.
• Unfavorable evolution (common):
Result in severe complications: sepsis (frequently
with bacillus funduliformis) pilephlebitis (with the
consequence of multiple liver abscesses) or local
complications, making different types of peritonitis:
– Localized peritonitis
– Periappendicular abscess
– Generalized peritonitis
Differential diagnosis
• Positive diagnosis of acute appendicitis is based on
clinical and laboratory signs and confirmed
intraoperatively in 85% of cases.
• The differential diagnosis of acute appendicitis
largely overlaps the differential diagnosis of acute
surgical abdomen.
• The most frequent causes of incorrect preoperative
diagnosis (75% of all errors) are in inverse order of
frequency:
1. Acute mesenteric lymphadenitis,
2. No pathological changes,
3. PID (pelvic inflammatory disease),
4. Torsion of ovarian cyst or ovarian follicle rupture and
5. Acute gastroenteritis.
• Acute mesenteric lymphadenitis
Most commonly confused with acute appendicitis in children, is
almost constantly associated with upper respiratory tract infection.
In lymphadenitis, abdominal pain is more diffuse and muscular
defense is not strictly localized as in appendicitis, it is usually
voluntary and rarely reaches to contracture. The presence of
generalized enlarged lymph nodes may settle the diagnosis. Few
hours of observation, since lymphadenitis is a self-limited disease, is
the standard procedure but, if the diagnosis remains uncertain,
surgery is indicated if just to specify the diagnosis.
• Acute gastroenteritis
It is a common childhood disease that can be easily distinguished
from an acute appendicitis. Viral gastroenteritis, is an acute self-
limited infection of diverse etiologies and is characterized by profuse
watery diarrhea, nausea and vomiting. Pains are colicky preceding
diarrheal stools, abdomen is relaxed without local signs.
• Acute cholecystitis
Confusion is possible for a subhepatic located appendix. Ultrasound
can sometimes settle the diagnosis. The treatment is still surgical.

• Perforated peptic ulcer

Perforated ulcer can mimic an acute appendicitis if the stomach
content flows via the right latero-colic space into the iliac fossa and
if perforation is rapidly blocked by neighboring organs. History and
pneumoperitoneum observed on abdominal radiography can rule
out the acute appendicitis.

• Meckel diverticulitis
Meckel diverticulum inflammation produces the same clinical picture
as acute appendicitis. Preoperative differential diagnosis is not
necessary, just for academic purposes, since diverticulitis is
associated with the same complications as appendicitis and
requiring emergency surgery (resection of diverticulum, a procedure
that can be performed by typical incision for appendectomy).
• Ileo-cecal intussusception
Unlike diverticulitis, preoperative differential diagnosis is very
important due to different treatment. Patient age is important:
appendicitis is extremely rare under 2 years while almost all
idiopathic intussusception occur in this age. Ileo-cecal
intussusception typically occurs by an apparent crisis of abdominal
colic. After several hours of onset blood can be noticed in the
stool. Sometimes, in right iliac fossa, a sausage-shaped tumor
mass may be felt. Later, as the intussusception progresses, the
right iliac fossa seems abnormally free. Ileo-cecal intussusception
in infants is treated by barium enema reduction (when no signs of
perforation), so differential diagnosis of acute appendicitis should
be clearly established as barium enemas application in acute
appendicitis in an infant may have catastrophic consequences.
• Regional enteritis
Regional enteritis symptoms (fever, pain and muscular defense in the
right iliac fossa and leukocytosis) are also found in acute appendicitis.
Diarrhea and absence of anorexia, nausea and vomiting favors
differential diagnosis but are not sufficient to exclude an acute
appendicitis, so in many cases of regional enteritis diagnosis is made
intraoperatively.
• Ureteral stones
A stone in the ureter near the appendix can simulate a retro-cecal
appendicitis. Radiation of pain to the labia, scrotum or penis, the
positive sign of Giordano, hematuria and/or absence of fever or
leukocytosis suggest renal colic. Ultrasound or pyelogram usually
confirms stones.
• Gynecological pathology
Acute appendicitis diagnosis errors are most common in young
women. Appendectomy with normal appendix rate, in women aged
between 15 and 45 years, varies between 32-45%. The most common
gynecological diseases which are labeled as acute appendicitis are:
pelvic inflammatory disease, ovarian follicle rupture, torsion of ovarian
cyst or tumor, endometriosis and ruptured ectopic pregnancy. In all
these cases, diagnostic laparoscopy plays an important role.
CLINICAL FORMS BY AGE
• Appendicitis in young children (up to 3 years) represents only 2%.
Diagnosis is difficult due to lack of information about history and
difficult physical examination. Combination of C-reactive protein
(CRP) with leukocytosis and elevated ESR allows the diagnosis of
appendicitis in 96% of cases in children. Attitude of choice is surgery
in doubtful situations.
• Appendicitis in the elderly: due to weaker reactivity, the onset is
attenuated. The disease remains unidentified until its complicated
forms (pseudo-occlusive or pseudo-tumoral) resulting in increased
postoperative mortality. Often, the muscular defense is absent even
in the presence of a perforation with local peritonitis. Differential
diagnosis should be made with cancer of the cecum (in appendicular
block), other types of colon cancer or diastatic perforation due to a
descending colon cancer. Ultrasound, CT scan and colonoscopy are
very useful in these cases. If intestinal occlusion is manifest, surgery
should be performed anyway.
CLINICAL FORMS DEPENDING ON severity
• Toxic form with peritonitis. It occurs more frequently in
children. General signs of intoxication are dominant
whereas abdominal signs are modest. The onset is
sudden with rapid alteration of general condition. The
patient is shocked, pale, with tachycardia and pulse-
temperature dissociation.
• Subacute form with attenuated symptoms, with periods
of remission, with sensitivity of appendicular points but
without muscular defense.
• Diffuse purulent peritonitis: it is the result of an attack of
acute appendicitis interrupted by a brief period of quiet.
It is manifested with symptoms and signs of general
peritonitis. Differential diagnosis is difficult especially with
peptic ulcer perforation. Laparoscopic approach,
whenever possible, is the best solution for diagnosis.
CLINICAL FORMS BY TOPOGRAPHY
• Retrocecal appendicitis - digestive symptoms and signs
are poor, lacking muscle contracture as appendix is not
in direct contact with the parietal peritoneum.
Microscopic hematuria may be present, contributing to
confusion with a urinary disorders.
• Subhepatic appendicitis may cause confusion with acute
cholecystitis. Ultrasound examination may settle the
diagnosis.
• Mesoceliac appendicitis (20% of cases) - evolves as an
occlusive syndrome with fever from the beginning.
Appendix can be located pre-or retro-ileal. The pain is
mostly located around the umbilicus.
• Pelvic appendicitis (10% of cases). It is often interpreted
as salpingitis, acute sigmoid diverticulitis or urinary
problems. Rectal digital examination is painful sometimes
inflamed appendix being felt in the Douglas sac. It can
evolve to pelvic abscess that can open spontaneously
into the rectum, or more rarely in the vagina or bladder.
• Appendicitis on the left side is rare (0.1%) and is due to
situs inversus. The most common confusion is with
diverticulitis, a left ureteral colic or left metroanexitis. In
case of total situs inversus abdominal and chest
radiography (heart and stomach air bubble at right) can
guide the surgeon to this diagnosis.
• Appendicitis in the hernial sac may raise confusion with
incarcerated hernia.
Treatment
• The first report of an appendectomy was made by
Amyan an English army surgeon who performed an
appendectomy in 1735, without anesthesia to a soldier
with perforated appendicitis.
• In England, in the late nineteenth century, surgeon H.
Hancock successfully performed the first appendectomy.
Later, American surgeon C. McBurney published a series
of articles on the diagnosis and treatment of acute
appendicitis.
Indications
• Appendectomy by laparoscopic or classical approach is
still the main method of treatment in appendicitis.
Surgical treatment of uncomplicated acute appendicitis
is an absolute indication.
• Antibiotics in acute appendicitis is associated with
surgical treatment as prophylaxis of septic
complications. The use of antibiotics and ice bag applied
to the iliac fossa in acute appendicitis can not stop
progression to serious complications.
• Contraindications for surgical treatment
There are no contraindications for appendectomy in
acute appendicitis. There is however an exception in
case of periapendicular block, where many surgeons
prefer to perform appendectomy at a later stage after
the remission of inflammatory phenomena.
• In situations of doubt diagnosis, purgatives, enemas
and any painkillers are prohibited, until the acute
appendicular pathology is excluded.
• Surgical techniques
• Appendectomy may be performed in any kind of
anesthesia. Laparoscopic approach need general
anesthesia by orotracheal intubation.
• CLASSICAL APPROACH BY LAPAROTOMY
• Skin incisions:
• After skin incision follows the incision of the aponeurosis of the
external oblique muscle. Then the oblique internal and
transverse muscle fibers are dissociated to reach at fascia
transversalis. The fascia is incised and the properitoneal space is
opened. The peritoneum is found and incised opening thus the
peritoneal cavity which is isolated. Sometimes the appendix may
be found very easily but there are situations of malposition
when appendix is very difficult to be found. Finding the
appendix is facilitated by tracking the tenia of ascending colon
and cecum. At the union of the three tenia, the base of the
appendix should be found.
• Appendectomy can be performed in anterograde (from the tip
to the base) or retrograde fashion (starting from the base). The
mesoappendix cut and vessels are ligated. The appendix is
ligated at the insertion level into the cecum and then cut and
removed. The appendicular stump may be plugged into the
cecum using a purse string.
• Verifying hemostasis and restoration of abdominal wall integrity,
finish the operation.
• LAPAROSCOPIC APPENDECTOMY
• Laparoscopic approach in appendectomy came in use
since 1987, but still exist controversies on the
advantages compared to classical approach.
– It has several advantages:
4. Possibility of visual exploration of the entire abdominal cavity
5. Good postoperative evolution
6. Fast socio-professional reintegration
7. Prevents postoperative adhesions
– But it has disadvantages also:
1. Requires general anesthesia
2. Requires well-trained team
3. Requires expensive equipment
4. Increased time of the intervention
5. Increased risk of dissemination of infection (intraperitoneal
abscesses)
• Contraindications to laparoscopic approach are:
1. Apendicular mucocele
2. Expansive adhesions
3. Abdominal radiotherapy
4. Immunosuppressive therapy
5. Portal hypertension
6. Coagulopathy
7. First trimester of pregnancy
Postoperative care
• Depending on the severity of appendicitis and
postoperative complications, hospitalization varies
between one day and several weeks.
• Postoperative, patients will receive painkillers,
antiinflmmatory, antiemetics and antibiotics
depending on the severity of appendicitis and
complaints.
• Drainage tubes (if there are) will be suppressed
depending on how much they drain.
• Usually patients are discharged on the third
postoperative day with the recommendation to avoid
intense physical activity for 2-4 months, and stitches
are removed on day 7-8 after surgery.
Postoperative complications
• Complications occur in 1-3% of cases after
appendectomies without significant differences regarding
the type of approach (open or laparoscopic).
• Infection remains the most common postoperative
complication being manifested by wound infection or
intra-abdominal abscesses. The occurrence of infection
depends on the severity of appendicitis, the patient's
age, its comorbidities and the type of closure of the
abdominal wall.
• Generally, wound infection rates are accepted up to 5%
and less than 1% for intra-abdominal abscesses.
• Treatment of wound suppuration is wide opening and
lavage with antiseptic solutions, while for intra-abdominal
abscesses percutaneous drainage and antibiotics are
preferred.
• Stercoral fistula is mainly due to a technical fault in
performing the purse string on cecum, when the
needle is inserted through the full thickness of the
cecal wall. It occurs mainly in young inexperienced
operators. Another possible cause is the decubitus
produced by the drainage tube. The wound should be
widelly opened and if there are signs of generalized
peritonitis laparotomy is required with suture of the
cecal lesion. In certain cases even right hemicolectomy
is needed. When the lesion is isolated and fistula
discharge is minimal, conservative treatment of fistula
is tempted, given the chance of spontaneous closure.
• Intraperitoneal bleeding - usually due to skidding
ligation of the appendicular artery. It requires
reintervention for hemostasis.
• Early intestinal obstruction usually occurs as a result
of intra-abdominal adhesions or by a bowel volvulus
around the drain tubes maintained for a long period
of time. It is manifested by bloating, transit stop for
fecals and gas, vomiting. It requires laparotomy with
resolution of the cause that led to occlusion.
Late postoperative complications:
• Appendicitis on appendicular stump is possible in
case of incomplete appendectomy.
• Incisional hernia
PROGNOSIS
• Although postoperative morbidity is around 10%, the
mortality rate is very low being less than 1%. (5%
for patients with associated comorbidities).
CHRONIC APPENDICITIS
• Chronic appendicitis is a set of micro-and macroscopic
lesions resulting from an inflammatory process of
moderate acute appendicitis that, without surgery, has
evolved towards resolution.
• Macroscopic appearance of appendix may be variable:
1. Without obvious changes
2. Sclero-hypertrophic. A thickened, vascularized
appendix with infiltrated mesoappendix and with
enlarged lymph nodes.
3. Sclero-atrophic. A small or thin appendix with areas of
stenosis or uniform caliber.
Symptoms and signs
• There are no specific symptoms for chronic appendicitis.
The clinical picture is very varied and can mimic almost
all abdominal diseases.
• The main complaints of patients are :
– Abdominal pain located mainly in right iliac fossa, flank and
right upper quadrant. The pain has nothing specific.
– Dyspeptic phenomena manifested by bloating, nausea, belching
frequently constipation, etc.
– Neuropsychological complaints represented by fatigue,
insomnia, headache.
• The clinical examination usually reveals a diffuse
abdominal tenderness with moderate pain intensity
within the right iliac fossa. Otherwise there is no other
pathological changes unless there is an associated
pathology.
Diagnosis and treatment
• Except for histopathological examination, no other
paraclinical examination can specify with certainty
the diagnosis of chronic appendicitis.
• The diagnosis of chronic appendicitis is actually made
by exclusion of other conditions that can cause the
patient’s symptoms.
• Treatment is represented by appendectomy
preferable by laparoscopic approach which offers the
possibility of general visual exploration of the
abdominal cavity.
TUMORS OF THE APPNEDIX
• Neoplastic lesions of the appendix are present in
about 5% of the cases examined histologically after
appendectomy performed for acute appendicitis.
Most of these lesions are benign. Malignant tumors
represents only 0.4% of malignant tumors of the
digestive tract.
Classification
• A. Benign tumors:
– Inflammatory pseudotumor (fibroblastic appendicitis).
– Appendicular endometriosis
– Other (mucous hyperplasia or metaplasia, leiomyoma,
neurinoma, lipomas, angioma, etc.).
• B. Benign tumors with malignant potential:
– Appendicular carcinoid.
– Villous appendicular tumor (papillary or adenomatous).
– Benign appendicular mucocele
• C. Malignant:
– Appendicular adenocarcinoma
– Endocrine - malignant carcinoid
– Appendiculare sarcomas (fibroblastoma, lymphocytoma,
lymphoblastoma)
– Lymphoma
– Malignant appendicular mucocele (pseudomyxoma).
Appendicular adenocarcinoma
• It is a rare condition, being found in approximatively
0.2% of all cases of appendectomy.
• The maximum incidence is at age 40-69 years (as in
colic cancer).
• 75% of cases are symptomatic patients being
operated for an acute appendicitis, an abdominal
tumor or intestinal obstruction. It is usually
diagnosed intraoperatively evolving for a long period
of time asymptomatic. Sometimes it can be found on
irrigography.
• Treatment consists of right hemicolectomy
• Prognosis is similar to colon cancer.
Appendicular carcinoid
• Approximately 80% of appendicular tumors are
carcinoid tumors. Appendix is the most frequent
location of carcinoid in the digestive tract (20%).
• The tumor is more common in women, the maximum
incidence being on the 4th and 5th decades of life.
• Tumor cells has argentaffine granules
(argentaffinoma). There are two well-differentiated
carcinoid cell types: EC cells - serotonin-secreting
(more common) and L cells - secrete enteroglucagon
or peptide YY (rare). The origin of cells may be
neural or may be developed from Kulchitsky-Masson
cells from the bottom of Lieberkűhn mucosal glands.
• Another form of carcinoid is the "cup" cells, called
mucinous carcinoid or adenocarcinoid or carcinoma
with "Goblet" cells. It represents only 6% of all
carcinoids appearing especially in the elderly and is
more aggressive than classical carcinoid. Frequently
metastasizes to the ovary and on peritoneal surface.
• In 70% of cases carcinoid tumors are located at the
tip of the appendix giving the appearance of "drum
stick". Tumor growth is slow and spread is late even
when the tumor penetrates the appendicular wall.
Treatment
• Therapeutic attitude depends on the location of the
tumor, its size, presence of metastases plus
histopathological and immunohistochemical
characteristics.
1. If the tumor is located on the body or tip of the
appendix, is less than 2 cm in diameter and is not
associated with metastases, appendectomy is
sufficient.
2. If the tumor is located in the base of the appendix, is
larger than 2 cm and/or is associated with metastasis,
right hemicolectomy is the operation of choice.
• Right hemicolectomy is also indicated when
histopathological examination shows the following
characters:
– tumor is invasive,
– mucin-producing tumor,
– tumor originates in mucous cells
• Prognosis is generally good. Overall survival at 5 years
is 85% and cases with metastases have a better
prognosis than those with metastases from other types
of cancers. The most frequent metastases are in liver,
with a good indication of their removal.
Appendicular mucocele
• Is a unique or multiple cystic dilatation of the appendix,
with a mucoid content.
• There are two histopathological types:
1. Benign mucocele: is an accumulation of mucus
produced by goblet cells into the appendicular lumen,
due to its obstruction. As volume increases, the tumor
may become palpable and complication such as rupture
or twisting may appear.
• It is easy highlighted by ultrasound examination.
• Treatment consists of classical appendectomy with
caution so as not to disseminate the content of tumor
by breaking it.
• As long as there is no preoperative certainty that there
is not a malignant variant, most authors contraindicate
laparoscopic appendectomy in these cases because of
the risk to break the appendix and intraperitoneal
dissemination of cancer.
2. Malignant mucocele (1 case of 9): actually it is a first
degree of mucous papillary adenocarcinoma.
• The mucus contains muciparous cells that can
disseminate after spontaneous or therapeutic
manipulation in the peritoneal cavity, causing peritoneal
pseudomyxoma ("gelatinous disease of the
peritoneum").
• Treatment consists in classic appendectomy, sufficient as
long there are not signs of extravazation in the peritoneal
cavity.
• If there is a broken malignant mucocele, appendectomy
is recommended plus intraperitoneal hyperthermic
chemotherapy (60 minutes at 42.50 C).
• Where the peritoneal pseudomyxoma is present at
operation, appendectomy is recommended associated to
tumoral citorediction and intraperitoneal chemotherapy.
• When there are concomitant mucinous tumors of the
ovary, adnexectomy and even hysterectomy are
recommended.
SURGICAL PATOLOGY OF
THE PANCREAS
 Surgical anatomy of the pancreas
1. Acute pancreatitis
2. Cancer of the pancreas
Aspects of surgical anatomy
 Pancreas = mixed gland
1. exocrine component (glandular acini + ducts of
pancreatic juice excretion)
2. endocrine component (pancreatic islands of
Langerhans, which produce insulin and other
pancreatic hormones, which are released directly
into the blood stream).
 Length: 15-18 cm; Weight: 70-90 g.
 It has 5 segments:
1. Head
2. Uncinate process
3. Neck (isthmus)
4. Body
5. Tail
 The pancreas is located deep in a retroperitoneal region,
represented mainly by the Luschka-Grégoire celiac region,
bounded by the diaphragm, the transverse mesocolon
with its root, T10-L1 vertebrae posterior and anterior by
the lesser gastric curvature and the upper portion of the
duodenum.
 Pancreas and duodenum are secondary retroperitoneal
organs. Due to the presence of the duodeno-pancreatic
fascia of coalescence (Treitz) formed between the parietal
peritoneum and visceral peritoneum, the incision of this
fascia allows duodeno-pancreatic posterior mobilization
(Kocher maneuver) during surgery in this region.
 The pancreas is located across, from duodenal horseshoe
(to the right) and the spleen hilum (to the left), being a
fixed organ.
Anatomical relations
 On front of the pancreas the root of the transverse
mesocolon is fixed dividing the pancreas in two regions:
one inframesocolic and the other supramesocolic.
The head and the neck of the pancreas
 The head is attached to the 2nd and 3rd portions of
duodenum on the right (the duodenal “horse shoe”)
being fixed to the duodenum by the bilio-pancreatic
confluence which flows into the duodenum through the
Vater’s ampulla - papilla major, and papilla minor (for
the Santorini duct).
 The common bile duct (choledocus) passes through the
posterior face of the pancreas and that’s why any
expansive processes of the head of the pancreas will
compress or invade the CBP resulting in mechanical
jaundice.
 Due to intimate relation with the duodenum and CBD,
cancer of the head of the pancreas rapidly invades these
structures inducing jaundice and duodenal obstruction.
Removing the tumors in this case presumes also
removing the whole duodenum and a portion of the
CBD.
 Another important relation of the pancreas in this region
is that with the portal vein which passes on the posterior
aspect of the pancreas between the neck and uncinate
process. Cancer can also rapidly invade this vein
inducing prehepatic portal hypertension and determining
the inoperability of the case. Inoperability is also
determined by invasion of the superior mesenteric artery
(SMA) which passes behind the pancreas to join the
superior mesenteric vein in the root of mesentery.
 Back, the head of the pancreas is also bordered by the
inferior vena cava.
 Due to proximity to the celiac trunk, on top, expansive
process localized in the neck and body of the pancreas
may compress or invade the celiac plexus causing intense
pain radiating to the dorsal region. “Mohammedan”
position of the patient reduces the compression on the
plexus and thus the pain.
The body of the pancreas
 The anterior surface is covered by the parietal peritoneum
derived from the peritoneal sheath of the transverse
mesocolon. It comes in contact with gastric antrum and
corpus through the bursa omentalis. This retrogastric
space communicates with the peritoneal cavity through
the Winslow foramen. This is the site where collections
and effusions may accumulate in acute pancreatitis
leading to development of pancreatic pseudocyst. Incision
of the peritoneal sheath and capsule of the pancreas will
free up the parenchyma allowing its distension in
edematous pancreatitis to prevent ischemia and necrosis.
 Tumors of the body of the pancreas may grow up to
high dimensions as they are asymptomatic for a long
period of time. They may invade the stomach but the
opposite situation is more frequent when gastric tumors
or ulcers invade the pancreas.
 Due to proximity of mesocolon and transverse colon in
pancreatic cancer of the body these structures may be
invaded also.
 Duodenum D3 and D4 can be invaded by pancreatic
tumors located at this site leading to high intestinal
occlusion.
 The left lobe of the liver may be also invaded by tumors
located in the upper part of the body of the pancreas.
The tail of the pancreas
 This segment is located in the left upper quadrant being
bordered anterior by the stomach, posterior by the left
kidney, inferior by the transverse colon and on the left
by the spleen and splenic flexure of the colon.
 Due to very intimate relations with the splenic hilum, the
tail of the pancreas may be injured during splenectomy
leading to pancreatitis of the tail.
 Pancreatic tumors at this site may also grow to high
dimension without symptoms invading surrounding
structures. Unfortunately in most cases, even though the
tumor is resectable, at time of operation the tumor is
spread with liver metastases. Invasion of the splenic vein
leads to segmental portal hypertension.
The exocrine pancreas
 It is a ramified tubulo-acinous gland, structured in lobules
separated by interlobular connective tissue.
 Exocrine pancreatic secretion consists of:
 Trypsin,
 Chymotrypsin, These enzymes
 Carboxipeptidase, contribute to food
 Amylase, digestion:
 Lipase, carbohydrates, proteins,
 Cholesterol-esterase, and fats.
 Phospholipase
 500 to 800 ml pancreatic fluid secreted per day.
 Alkaline pH results from secreted bicarbonate which serves
to neutralize gastric acid and regulates the pH of the
intestine.
 Ductular system is represented by a network of ducts that
carry the exocrine secretions into the duodenum.
– Centroacinar ducts (duct cells actively secret important
quantities of sodium bicarbonate )
– Intra and interlobular ducts
– The main pancreatic duct (Wirsung) located in the
parenchyma close to the posterior aspect of the
pancreas, which open into the duodenum through the
major duodenal papilla (the hepato-pancreatic Vater’s
ampulla)
– Lesser duct (Santorini), accessory duct, drains the
superior portion of head and empties separately into
2nd portion of duodenum at papilla minor.
 Ductal pressure is 15 – 30 mm Hg (vs. 7 – 17 in CBD)
thus preventing biliary reflux and damage to the
pancreatic duct.
The endocrine pancreas
 Consists of 200.000-1.800.000 pancreatic islands (1-2 %
of pancreatic volume), each containing about 200
endocrine cells. Density of the pancreatic islands is
maximum in the tail region of the pancreas.
 Islet cells are of several types :
– Cells A or α (20%, produce glucagon),
– Cells B or β (75%, produce insulin),
– Cells D or δ (produce somatostatin),
– Cells non-β (PP cells, produce pancreatic polypeptid ),
– Cells „D1” (produce vasoactiv intestinal polypeptid VIP),
– Cells G (produce gastrin),
– Cells „C” (clear cells without secretory granules) etc..
 Insulin secretion start from the 5th intrauterine month.
In 30 % of cases Santorini duct is blind, and in 10 % it bears the whole
pancreatic secretion.
Arterial supply of the pancreas - 3 sources:
1. Common hepatic artery
2. Splenic artery (from celiac trunk)
3. Superior mesenteric artery
 There are cases with multiple hepatic arteries (2-3)
when the right hepatic artery is usually a branch of
superior mesenteric artery (SMA), having an initially
retropancreatic route. This requires making a careful
retropancreatic dissection in pancreas excision surgery
to avoid extensive hepatic necrosis, leading to death by
sectioning this artery.
 Preoperative bi-selective arteriography of celiac trunk
and SMA would be very helpful.
 The three biggest pancreatic arterial branches are:
1. Dorsal pancreatic artery
2. Pancreatica Magna (mid portion of body)
3. Caudal pancreatic artery (tail)
The venous drainage follows the arterial supply.
 Anterior and posterior arcades drain the head and the
body.
 Splenic vein drains the body and tail.
 Major drainage areas are:
1. Suprapancreatic vein
2. Retropancreatic vein
3. Splenic vein
4. Infrapancreatic which drains into superior
mesenteric vein
 Ultimately all pancreatic veins drain into the portal
system.
Lymphatic drainage
 The rich periacinar network drains into 5 nodal groups:
1. Celiac
2. Hepatic pedicle
3. Retroduodenopancreatic
4. Superior mesenteric
5. Splenic
Innervation
 Sympathetic fibers come from the splanchnic nerves
 Parasympathetic fibers come from the vagus
 Both give rise to intrapancreatic periacinar plexuses
 Parasympathetic fibers stimulate both exocrine and
endocrine secretion
 Sympathetic fibers have a predominantly inhibitory effect

 Nerves form a rich afferent sensory fiber network around

the pancreas explaining the intense pain in expansive
processes of pancreas and chronic pancreatitis.
Ganglionectomy or celiac ganglion blockade interrupt
these somatic fibers with benefic effect on pancreatic
pain.
 ACUTE
PANCREATITIS
DEFINITION
 Acute pancreatitis represents the anotmo-clinical
expression of the acute syndrome of pancreatic and
peripancreatic autodigestion.
 Acute pancreatitis = acute pancreatic inflammation
usually with rapid onset of pain, accompanied by
vomiting and systemic inflammatory response
syndrome with high levels of pancreatic enzymes in
blood and urine (in urine not always present).
EPIDEMIOLOGY
 Annual incidence is ranging from 9 to 18 per 100,000
population.
 In Europe and other developed nations, more patients
tend to have gallstone pancreatitis, whereas in the
United States, alcoholic pancreatitis is the most common.
MORTALITY/MORBIDITY
 The overall mortality rate of patients with acute pancreatitis
is 10-15%. Patients with biliary pancreatitis tend to have a
higher mortality rate than those with alcoholic pancreatitis.
 In patients with severe disease (organ failure), the mortality
rate is approximately 30%. This rate in mortality has not
dropped in the last 10 years.
 In the first week of illness, most deaths result from
multiorgan system failure (MSOF). In the following weeks,
infection plays a more significant role, but organ failure still
represents a major cause of mortality.
Race
 3 times higher for blacks than whites. These racial
differences are more visible for males than females.
Sex
 In general, acute pancreatitis affects males more often
than females. The etiology in males is more often related
to alcohol; in females, to biliary tract disease.
Age
 The median age at onset depends on the etiology.
 The following are median ages of onset for various
etiologies:
– Alcohol-related - 39 years
– Biliary tract–related - 69 years
– Trauma-related - 66 years
– Drug-induced etiology - 42 years
– Endoscopic retrograde cholangiopancreatography (ERCP)–related -
58 years
– AIDS-related - 31 years
– Vasculitis-related - 36 years
 Hospitalization rates increase with age. For people aged
35-75 years, the rate doubles for males and quadruples
for females.
CLSSIFICATION

1. Histopathologic classification:
 - Edematous acute pancreatitis
 - Necrotic acute pancreatitis
 - Suppurated acute pancreatitis

2. Clinical classification:
 Mild acute pancreatitis (80 %): systemic dysfunctions are
minor and complete reversible. Histopathology reveals
interstitial edema and possible adipose necrosis zones.
 Severe acute pancreatitis: life threatening complications
are present (pancreatic effusions and systemic
complications also).
ETIOPATHOGENESIS
 Causes of acute pancreatitis are various, pancreatic or
extrapancreatic, but the most common (80%) are
represented by alcohol and gallstones:
1. Alcoholic etiology (30%) - more common in young,
urban population, mostly males. It occurs when
regular large amounts of alcohol, over long periods,
are consumed.
2. Lithiasis etiology (50%) - predominantly in the
elderly, rural communities and in females. When gall
stones are not removed, 36-63% of cases are
complicated with recurrent acute pancreatitis due to
migration of stones.
1. METABOLIC FACTORS:
– alcohol
– hyperlipoproteinaemia
– hyperparathyroidism
– hypercalcemia
– drugs (immunosuppressants: azathioprine, 6-
mercaptopurine, corticosteroids, estrogens,
sulfonamides, metronidazole, tetracycline, thiazide
diuretics, furosemide)
– genetic (family)
– toxic (organophosphates, scorpion venom)
– final stage of CRI (involved dyslipidemia,
hemodialysis, peritoneal dialysis)
2. MECHANICAL FACTORS:
– Cholelithiasis,
– Postoperative,
– Posttraumatic (external or surgical injury, ERCP),
– Pancreatic duct obstruction (tumors, ampulla
stenosis, ascaris lumbricoides infestation or
opistorchis sinensis),
– Pancreatic duct bleeding,
– Pancreatic duct stones,
– Chronic pancreatitis (acute spurt),
– Duodenal obstruction,
– Penetrating peptic ulcer,
– Crohn's disease,
– Anatomical abnormalities (pancreas divisum,
annular pancreas, heterotopic pancreas, duodenal
parietal cyst, duodenal duplication, duodenal
diverticula, choledochocele, etc)
3. VASCULAR FACTORS (ischemia):
– after surgery (intraoperative hypotension, cardiopulmonary
bypass)
– organ transplant surgery (kidney, liver, heart)
– hypotension
– Vasculitis (periarteritis nodosa, LES)
– ateroembolism
4. INFECTIOUS FACTORS:
– viruses (mumps, Coxsackie B v., cytomegalovirus, Epstein-Barr
v.)
– bacteria (BK Leptospire, Mycoplasma pneumoniae, Cryptococ),
– yeasts (Aspergillus)
5. VARIOUS CAUSES: cystic fibrosis (mucoviscidosis),
food allergy, pregnancy, end-stage renal failure
associated loop obstruction after GJA, etc.
6. IDIOPATHIC MECHANISM
 Acute pancreatitis was compared by Lucien Leger with "an
explosion in a weapons factory", underlying the fact that
every moment of the pathophysiological chain causes and
aggravates the next moments.
 The cascade of events begins with the intraglandular
activation of digestive hydrolases (proteolytic and lipolytic
enzymes ) and pancreatic lysosomal hydrolases, causing
swelling, hemorrhage and tissue necrosis in the gland and
its adjacent tissues. Exposure of trypsinogen to lysosomal
enzymes is the mechanism for early trypsin activation.
Digestive enzyme release is amplified as acinar cells are
destroyed, leading to a vicious cycle of inflammation and
necrosis.
 In addition to autodigestion (responsible for the
cytosteatonecrosis), vascular lesions are an aggravating
factor. Digestion of vascular walls results in thrombosis and
hemorrhage.
 Al these will lead to = acute hemorrhagic pancreatic
necrosis.
Lipase is involved in saponification process of the
peripancreatic fat ,thus consuming calcium from blood
leading to hypocalcemia and formation of
cytosteatonecrosis spots in the peritoneal cavity.

Cytosteatonecrosis
Cytosteatonecrosis
 The pancreatic fluid rich in enzymes spreads into the
retroperitoneal space (retrocolic, perirenal, the root of
mesentery, mesocolon, celiac region, even in
mediastinum) and can reach down into the scrotum in
severe cases. These effusions consist of necrotic
retroperitoneal tissues worsening the prognosis.
 The fluid may remain stuck around the pancreas forming
pseudocysts. Acute fluid collections occur early in AP in
the peripancreatic areas and are not encapsulated by a
fibrous wall. Pseudocysts are well-developed collections
of pancreatic juice encapsulated by a wall of granulation
tissue (without epithelium). Pseudocysts typically occur
at 4 to 6 weeks after an episode of AP. A pseudocyst that
has become infected transforms into a pancreatic
abscess.
 Peripancreatic fluid may leak into the peritoneal cavity
(through Winslow foramen ) giving rise to ascites.
Systemic response
 Activated pancreatic enzymes and other mediators
entering the systemic circulation via portal and lymphatic
system will lead to installation of the so-called
enzymatic toxemia with its suite of adverse events
leading to the installation MSOF.
 The systemic inflammatory response syndrome
(SIRS) can also develop, leading to the development of
systemic shock. The mediators of inflammation can
become so overwhelming that will lead to hemodynamic
instability and death.
Physiopathological events
 Electrolyte changes: loss of water, hypocalcemia and
hypomagnesemia.
 Cardiovascular failure: hypovolemia leads to
hypotension, associated with toxic or septic myocarditis,
serous or serohemorrhagic pericardial exudate.
 Respiratory complications: hypoxemia with pulmonary
congestion, pulmonary infarction, microatelectasis and in
severe cases pulmonary failure with acute respiratory
distress syndrome and pleural effusions.
 Renal impairment: due to hypovolemia, deposits of
fibrin and fibrinogen, toxic and/or septic glomerular
nephropathy. Patients with acute renal failure have a
significantly higher rate of pancreatic infection and
mortality.
Other systemic disorders
 Liver function impairment (manifested by elevated
serum levels of bilirubin, alkaline phosphatase and
transaminases, due to obstruction of common bile duct,
hepatic parenchymal necrosis and pericholangitis).
 Early intravascular thrombosis (produced by
proteolytic enzymes, documented by decreasing platelet
and fibrinogen) followed by marked thrombocytosis and
hyperfibrinogenemia.
 Enzymatic encephalopathy
 Severe pain (strong nociceptive stimulation of the
aorticomesenteric, aorticorenal and celiac plexuses).
 Bacteremia due to bacterial translocation
LOCAL COMPLICATIONS
 Paralytic ileus (paralysis of the first jejunal loop
determines the classical image of "sentinel loop" on plain
abdominal radiography)
 Duodenal compression due to enlarged head of the
pancreas (vomiting) or bile duct compression
(jaundice)
 Necrotic lesions can extend to the wall of the
stomach, duodenum, transverse colon or common bile
duct resulting in ulceration, bleeding, fistulas, peritonitis,
etc
 Pseudocyst
 Suppurative complications (effusions, abscesses)
MORPHOPATHOLOGY
 Pathological changes of acute pancreatitis are caused by
interstitial inflammation, bleeding, infection and necrosis.
Depending on the extent and intensity of lesions there are
three forms of acute pancreatitis:
 Oedematous (interstitial) form = enlarged pancreas with
a gelatinous edema, sometimes accompanied by lesions of
cytosteatonecrosis
 Necrotic-Hemorrhagic form - (severe form) =
increased pancreas with hemorrhagic and necrotic areas,
of soft and friable consistency. In the further development
necrosis areas will separate forming sequestres.
 Suppurated form - with effusions (considered a
complication of progressive necrotic hemorrhagic form) =
infected pancreatic necrosis and peripancreatic areas,
forming abscesses.
CLINICAL PICTURE

 Although initial symptoms and signs are varied and can

mimic other intra- or extra-abdominal diseases,
diagnosis in most patients, can be established by a
thorough clinical evaluation.
 Typical symptoms are:
1. Upper abdominal pain
2. Nausea
3. Vomiting
4. Low fever
 Pain is a cardinal symptom present in 85-100% of
cases. It has a sudden onset (but not as in peptic ulcer
perforation) preceded by a meal with fat and alcohol,
reaching a maximum of intensity at several hours later
and lasting at least 36-48 hours. Pain gradually
intensifies until reaching a constant ache.
 Location of pain is usually epigastric, radiating in
transverse direction (to the left and right upper
quadrant) and often to the lower back region.
 Severity of pain makes the patient restless, constantly
changing position in order to reduce the pain.
 If etiology is biliary, pain may be similar to biliary colic,
but the persistence of pain after treatment suggests an
acute pancreatitis.
 Nausea and vomiting (70-90%) install early and are
persistent, rarely in large quantities (the vomit fluid is
primarily gastric and duodenal content, not fecaloid).
 Losses by vomiting and impossibility of ingestion are a
major cause of body electrolyte and volume depletion.
 Ileus is initially located in the upper abdomen (stomach,
duodenum, proximal jejunum) and leads to discontinuation
of transit (diarrhea, as well as digestive bleeding, are signs
of severity).
 Fever (usually around 38 °C), present in most cases in the
first few days, usually accompanied by tachycardia. Higher
values announce the presence of necrosis and infection.
 Respiratory disorders (difficult breathing, persistent
hiccups) are due to limitation of left diaphragm movements
(by neighborhood irritation) and left pleural effusion. In
severe cases, signs of acute respiratory failure may
appear.
CLINICAL EXAMINATION
 Clinical signs depend largely on the severity of
pancreatitis.
 Generally the patient is restless because of abdominal
pain.
 Redish face with congested conjunctivae.
 Epigastric tenderness and/or muscular defense (rarely
contracture)
 Sometimes distended abdomen (initially supraumbilical
subsequently diffuse). Bowel sounds are often
hypoactive due to gastric and transverse colonic ileus.
 Often, there is ascites (abdominal shifting dullness on
percussion).
 Jaundice is rarely present and has significance for
severity (due to: common bile duct stones, extrinsic
compression, toxico-septic hepatitis).
Other clinical signs of severity:
 The Cullen sign = discoloration around the umbilicus
resulting from hemoperitoneum.
 The Grey-Turner sign is a reddish-brown discoloration
along the flanks resulting from retroperitoneal blood
dissecting along tissue planes. More commonly, patients
may have a ruddy erythema in the flanks secondary to
extravasated pancreatic exudate.
 Grünwald sign = ecchymosis, large bruise, around the
umbilicus due to local toxic lesion of the vessels.
 Mayo-Robson's sign = pain while pressing at left
costovertebral angle.
 Pleural effusion in the left hemithorax.
 Shock signs: initially the patient is confused, agitated, with
polypnea, tachycardia, cold sweats with vasomotor crises
(red face), possible mild transient hypertension, and
thereafter becomes pale, cyanotic, hypotensive, weak and
rapid pulse, entering into collapse.
 Oliguria and rapidly evolving to oligoanuria.
Cullen sign

Grey-Turner sign
LABORATORY
 Amylasemia (normal 8-32 Wolgemuth U, <150.
Somogy u, <300 Phadebas u.) Hyperamylasemia is
positive at 2-12 hours after onset, reaches a maximum
at 24 hours and returns to normal after 4-7 days (mild
pancreatitis). The diagnosis of acute pancreatitis is
considered when abdominal pain is associated with an
amylasemia 3 times higher than normal. Dosage of
amylase in effusions from peritoneum, pleura and
pericardium has a significant diagnostic value.
 N.B.! In alcoholic pancreatitis with fibrosis and in
necrotic pancreatitis with high volume of destroyed
pancreatic tissue - paradoxically at first sight - normal or
even low serum amylase can be recorded.
 Amylasuria (normal 32-64 W.u., <300 Somogy u.,
<2000 Phadebas u.) is significant at over 10 times
normal values. It occurs later than amylasemia and
persists for a longer time.
 Lypasemia (normal <200 IU) is more frequent and
longer lasting (15 days) than hyperamylasemia. Elevated
lipase levels are more specific to the pancreas than
amylase levels.
 None of these tests is specific for pancreatitis. Elevations
can occur in anyone with small intestinal obstruction,
mesenteric ischemia, tubo-ovarian disease, renal
insufficiency. Rarely, elevations may reflect parotitis.
 NB ! The level of serum amylase or lipase does not
indicate whether the disease is mild, moderate, or severe,
and monitoring levels serially during the course of
hospitalization does not reflect the evolution and
prognosis.
 Hypocalcemia - appears on day 3-5 after onset, due to
cytosteatonecrosis and calcium fixation during this process.
It requires compensation only in case of tetanus.
 Hyperglycemia - due to destruction of a large proportion
of the endocrine pancreas) with glycosuria (both are
criteria of severity.
 Increased blood urea - intense protein catabolism, plus
the functional and then organic ARF.
 Leukocytosis may represent inflammation or infection.
 A CRP (C-reactive protein) value in double figures (ie, ≥
10 mg/dL) strongly indicates severe pancreatitis. CRP is an
acute-phase reactant that is not specific for pancreatitis.
IMAGING STUDIES
 Abdominal plain radiography : In some cases, the
inflammatory process may damage peripancreatic
structures, resulting in a colon cut-off sign, a sentinel
loop, or an ileus.
 Chest X-ray: basal pulmonary atelectasis left
hydrothorax (relatively common), increased
bronchovascular drawing (at the onset of shock lung).
 Gastrointestinal radiography (scopy) with water
soluble contrast agent (after exclusion of a perforated
ulcer) may show antropyloric stenosis, enlarged
duodenal frame, descent of Treitz angle.
sentinel loop
 Abdominal ultrasonography. This is the most useful
initial test in determining the etiology of pancreatitis and is
the technique of choice for detecting gallstones.
Ultrasonography cannot measure the severity of the disease.
 Abdominal contrast-enhanced computed tomography
(CT) scanning. This is generally not indicated for patients
with mild pancreatitis unless a pancreatic tumor is suspected
(usually in elderly patients).
 CT scanning is always indicated in patients with severe acute
pancreatitis and is the imaging study of choice for assessing
complications.
 CT-scan is performed within 72 hours after the onset and
then every 7-10 days (if necessary). It is used as a
prognostic scoring system, having an important impact in
assessing acute pancreatitis severity, and setting correct
therapeutic attitude.
 CT is the preferred test for evaluating severe
pancreatitis and detecting complications, and it
can show:
1. Pancreas increased in volume with more or less
alteration of its structure depending on severity
(edematous poorly defined areas of low density,
necrosis, hemorrhagic lesions, pancreatic abscess with
air pockets and sequesters, etc), irregular glandular
contour and thickened fascia of Gerota.
2. Peripancreatic edema, effusions, peripancreatic
phlegmon, pseudocyst.
3. Retroperitoneal effusions in prerenal spaces, retrocolic,
root of the mesentery, etc
4. Intraperitoneal fluid collections
5. Distended intestines, thickened posterior gastric wall
6. Pleural effusions, basal pulmonary atelectasis
Normal pancreas Acute pancreatitis

Pseudocyst
 Abdominal CT scan grading scale developed by
Balthazar:
A - Normal
B - Enlargement
C - Peripancreatic inflammation
D - Single fluid collection
E - Multiple fluid collections
 Magnetic resonance cholangiopancreatography
(MRCP) has an emerging role in the diagnosis of
suspected biliary and pancreatic duct obstruction in the
setting of pancreatitis. Although not as sensitive as
ERCP, MRCP is safer, noninvasive, and fast, it provides
images useful in guiding clinical care decisions. This
modality should be used if choledocholithiasis is
suspected, but there is concern of worsening
pancreatitis if ERCP is performed.
 Endoscopic ultrasonography (EUS) is an endoscopic
procedure. A high-frequency ultrasound transducer is
inserted into the gastrointestinal tract to visualize the
pancreas and the biliary tract. EUS is helpful in
evaluating microlithiasis and biliary sludge, and can help
identify periampullary lesions better than other imaging
modalities.
 ERCP (Endoscopic retrograde
cholangiopancreatography): can help to determine
the etiology of biliary acute pancreatitis. Performed at
48-72 hours after the onset of AP, it may be
supplemented, if lithiasis etiology is confirmed, with
endoscopic papillosphincterotomy which removes stones
from CBD and allows drainage of CBD if pancreatitis is
associated with cholangitis.
 It is not performed routinely but only in case of
worsening condition (jaundice ) in a patient with
pancreatitis and choledocolithiasis certified by ultrasound
(in case of failure of ERCP, surgery is the solution).
 Paracentesis - is valuable for:
– determining amylase concentrations in peritoneal fluid
– physical assessment of fluid (a severe pancreatitis is characterized
by the presence of dark peritoneal fluid)
 Ultrasound or computer tomography guided aspirative
biopsy may be indicated in necrotic forms to determine the
nature of peripancreatic collection (infection, etc.).
 Diagnostic laparoscopy: is recommended by some in
emergency conditions to confirm the diagnosis and
visualization of lesions, to assess disease severity, but it
cannot provide complete information (does not allow
exploration of the posterior face of the pancreas).
 5% of patients require early laparotomy to exclude or
treat a possible mesenteric infarction, gangrenous
cholecystitis or other conditions requiring urgent surgical
treatment.
 DIFFERENTIAL DIAGNOSIS
Surgical conditions: Medical conditions:
 Perforated ulcer
 Inferior myocardial
 Ulcer penetrating the pancreas infarction
 Biliary colic  Pulmonary embolism
 Intestinal mechanical occlusion,  Reno ureteral colic
enteromezenteric infarction
 Saturnine colic
 Peritonitis,
 Pleuro-pulmonary
 Ruptured aortic aneurysm diseases located at the
 Splenic infarction bottom left thorax
 Acute appendicitis (especially in  Delirium tremens
case of subhepatic retrocecal
appendix)
PROGNOSIS EVALUATION
 Prognosis evaluation uses some prognosis scoring
systems, which in addition to imaging methods, use
several biological parameters and has the advantage
that can be applied routinely allowing continuous
monitoring of patients.
 Due to unpredictable of natural evolution of the
disease, the prognosis evaluation is aimed to early
identification of patients who will develop severe
disease with increased risk of life-threatening
complications, for a rational treatment approach.
 CRITERIA Ranson alcoholic score Ranson biliary
score
1. age > 55 years > 70 years
2. leucocytes > 16.000/mm3 > 18.000/mm3
3. glucose > 200 mg/dl (>11 mmol/l) >12 mmol/l
At admission
4. LDH > 350 u.i./l (> 1,5 x N) > 1,7 x N
5. ASAT (GOT) > 250 u.i./l (> 6 x N) >9xN
6. ureea
7. arterial PO2
8. calcemia
9. albumine

In the first 1. Htc lowering > 10% > 10%

48 hours 2. Ureea rising > 8 mg/dl (> 1,8 mmol/l) > 0,7 mmol/l
(BUN=azot ureic sangvin)
3. calcemia < 8 mg/dl (< 2 mmol/l) < 2 mmol/l
4. Po2 < 60 mmHg < 60 mmHg
5. Bicarbonates lowering > 4 mEg/l > 5 mEg/l
(base deficit )
6. fluid sequestration >6L >4L
 Each positive Ranson parameter is noted with 1 point, so
the score can vary between 0-11 points, a score higher
than 3 already announces the possibility of evolving to a
severe pancreatitis.
 The risk of complications and mortality are proportional to
the score value:
– 0-2p = 2%, mortality
– 3-4p = 15%,
– 5-6p = 40% ,
– 7-11p = 100%

 Currently, the best prognostic score used is

tomodensitometric Balthazar score, based on information
provided by computer tomography.
COMPLICATIONS
 Pancreatic sequestra: delimitation of pancreatic and
peripancreatic necrosis appears in about the second week
(≈ 50% of sterile necrosis will evolve to resorption)
 Effusions - pancreatic necrosis has the tendency to
expand into the retroperitoneum as fat necrosis along
peritoneal insertion reaching up to the mediastinum and
down till the scrotum.
 Infected pancreatic necrosis (pancreatic abscess)
usually occurs in week 2 and is manifested by fever,
abdominal distension, palpable abdominal masses,
pulmonary, renal, and liver complications and positive
blood cultures (50% of cases), most often with Gram-
negative germs. (E. coli, Pseudomonas, Klebsiella, Proteus)
 Infection is the most frightening complication of necrotizing
pancreatitis, and is responsible for 80% of deaths.
Abscess in the tail of the pancreas
 Pancreatic pseudocyst is a collection of fluid located
extra- or intrapancreatic, predominantly in the body
and tail, which occurs in 1% of cases.
 Initially it hasn’t well defined walls, being bounded by
nearby organs and adhesions.
 It contains pancreatic fluid and sometimes necrotic
debris or blood.
 It appears at 2-3 weeks after the onset of necrotic
pancreatitis (persistent pain, upper abdominal tumor
fixed, weight loss). Ultrasound and CT will show the
collection.
 Pseudocyst can evolve to spontaneous remission within
4-6 weeks or to complications (suppuration, intracystic
hemorrhage, intraperitoneal or intradigestive rupture,
compression on the stomach, duodenum and biliary
tract, with stenosis, or on splenic vein with
splenomegaly).
 Intraperitoneal or upper gastrointestinal bleedings caused
by erosion of an artery: pancreatic, left gastric, lienal
artery.
 Internal fistulas
 Biliary or digestive fistulas
 Vascular thrombosis (splenic, portal, mesenteric)

pseudocyst
TREATMENT
 Acute pancreatitis is one of the major therapeutic
emergencies.
 The treatment is complex and can not be standardized,
requiring strict individualization and adaptation to the
clinical, physiological and evolutive stage.
 Patients with known or presumptive diagnosis of severe
acute pancreatitis should be hospitalized in an intensive
care unit for monitoring the vital function of organs and
versatile support.
 Treatment will be conducted by a multidisciplinary team
consisting of intensive care doctor, surgeon,
gastroenterologist and imagistic doctor.
 Goals of treatment in acute pancreatitis are:
1. Limitation of pancreatic inflammation,
2. Breaking the pathophysiological chain that leads to
complications,
3. General support and treating complications.
MEDICAL TREATMENT
Aggressive treatment of hypovolemia and shock
 Fighting respiratory failure: patients with acute
pancreatitis should be closely monitored by pulse
oximetry and blood gas analysis, in order to intervene
immediately in case of respiratory failure. Arterial pO2
below 70 mmHg requires nasal oxygen, while
decreasing pO2 below 60 mmHg is an indication for
tracheal intubation with assisted mechanical
ventilation.
 Putting at rest the pancreas: The aim is to suppress
exo- and endogenous stimuli of pancreatic secretion.
Absolute food abstention and establishing a continuous
nasogastric aspiration.
 Nutritional support: It is important to achieve a high
protein intake (1.5 g/kg/day) and caloric also (25-30
cal/kg/day). Classical parenteral nutrition is
supplemented with modern enteral nutrition achieved
through a jejunal tube placed endoscopically or by
minilaparotomiy in order to avoid the occurrence of
intestinal mucosal atrophy accompanied by bacterial
translocation.
 Restoring electrolyte and acido-basic balance by
adding sodium, potassium, magnesium, calcium.
 Analgesia is a primary objective, given the severity of
pain.
 Stress ulcer prophylaxis is indicated in severe forms
and is performed by parenteral administration of
antisecretory (proton pump inhibitors) antacids
(sucralfate) and gastric aspiration.
 Prophylaxis and treatment of ARF (acute renal
failure) is achieved through: adequate volume
replacement, addition of dopamine infusion (if diuresis
falls below 30 ml/h and creatinine rises above 1.4 mg/dl),
diuretics (dopamine is associated if BUN increases over 20
mg/dl);
 Antibiotics in acute pancreatitis can be for cure (if
infection is set, being conducted on the basis of
antibiogram) or prophylactic.
 Corticosteroid therapy is beneficial in the initial phase
of the disease, both by protecting cell membranes and
due to its antishock, antiinflammatory, antitoxic and
antiallergic effects.
 Inhibition of exocrine pancreatic secretion:
Somatostatin and Octreotide.
 Prostaglandins (PG E1 and PG I2) and vasopressin
appear to improve pancreatic blood flow.
 Anticoagulant therapy prevents thrombosis (involved in
pancreatic necrosis with vascular injury mediated by
trypsin) and severe acute pancreatitis during IDC
(intravascular disseminated coagulation) - anticoagulant
treatment is recommended after 7-14 days of evolution
when there is an increasing hypercoagulability and
increased risk of pulmonary embolism.
SURGICAL TREATMENT
 Most patients with acute pancreatitis will respond
favorably to conservative treatment with complete
remission.
 In necrotic-hemorrhagic pancreatitis surgical treatment
may be classified according to the optimal operative
moment as follows:
1. Immediate emergency interventions (within 8
hours in patients with frank and persistent symptoms
of acute abdomen, peritonitis type, occlusive or
hemorrhagic) after excluding other causes of acute
surgical abdomen. Surgical gestures maximum allowed
are:
 Hematoma evacuation and collections in pancreatic lodge
 Duodeno-pancreatic mobilization
 Longitudinal capsulotomy – sectioning the pancreatic
capsule allowing its distension and preventing ischemic
lesions due to oedema compression
 Pancreatic drainage,
 Peritoneal lavage and drainage
 Associated biliary operations have exceptional
indications (severe acute cholecystitis, with obstructive
jaundice and angiocolitis) and consists of:
– Cholecystectomy,
– Cholecistostomy,
– External biliary drainage - transcystic biliary
decompression or by choledocotomy with Kehr tube
drainage.
2. Early interventions at 8 hours - 7 days, in patients
with confirmed acute pancreatitis who develop early
form of acute surgical abdomen (microbial or chemical
peritonitis, mechanical bowel obstruction, bleeding
intra- and/or retroperitoneal, enteromesenteric
infraction).
 In case of persistent papillary obstruction, endoscopic
approach (ERCP and sphincterotomy) is preferred.
3. Delayed interventions at 8-21 days for removal of
pancreatic (sequestrectomy) and extrapancreatic
necrosis.
4. Scheduled interventions - "late" at 3-6 weeks, for
treatment of pancreatic pseudocysts and abscesses.
Removing pancreas sequestra
 PANCREATIC TUMORS
CANCER OF THE EXOCRINE
PANCREAS
 Exocrine pancreas cancer is the fifth cause of
death from cancer (after lung cancer, colorectal,
breast and prostate).

 Malignant tumors of the exocrine pancreas are

particularly aggressive, with one of the lowest
survival rates at 5 years (3%).
Incidence and etiopathogeny
 The incidence of pancreatic cancer in the U.S. lies about
10/100,000. Estimated new cases and deaths from
pancreatic cancer in the United States in 2011: 44,030
new cases and 37,660 deaths.
 Average age of diagnosis is around 65 years (it is rare
before 40 years, the incidence increasing rapidly in the
elderly).
 Sex ratio shows a slight male predominance (♂: ♀ = 1.5
to 2/1).
 There is a higher incidence in African-American
population and in Hebrew of the USA, and in Polynesian
(lowest incidence appears to be the Indians and people
of the Middle East).
 The exact causes of cancer are not known, but
statistical studies and clinical observations incriminate
some exogenous or endogenous risk factors:
a) exogenous factors:
- Smoking (mainly cigarette, but also cigar or pipe)
are incriminated, inhaled nitrosamines reaching in the
pancreas through blood or bile;
- Diet: increased consumption of unsaturated fats and
animal protein while an increased consumption of
fruits and vegetables, and a diet rich in fibers plays a
protective role. The possible role of drinking coffee,
tea or alcohol is under debate (opinions are divided);
- Other factors involved: professional chemical
agents (naphthylamine, benzidine, oil, etc..),
oncogenic viruses, unfavorable socio-economic
status, etc.
b) predisposing medical conditions:
 calcified chronic pancreatitis
 diabetes mellitus: incompletely elucidated
mechanisms; 15% of pancreatic cancers are associated
with diabetes;
 previous surgery on the digestive tract: gastric
resections (decrease of gastric acidity that cannot
detoxify nitrosamines produced by bacterial metabolism
and as well digestive hormone changes),
cholecystectomy (elevated levels cholecistokinine) etc.
On the other hand, it was found that previous
tonsillectomy, as well as some allergic diseases, are
protective factors (immunological factors involved in
pancreatic carcinogenesis);
 pernicious anemia: is a condition of increased risk
for pancreatic cancer and gastric cancer (possible
trophic effect of chronic hypergastrinemia).
c) genetic factors: their involvement in the etiology is
supported by the existence of family clusters of the
disease, the possible association of the disease in the
context of known genetic syndromes (familial
polyposis, Gardner syndrome, Lynch syndrome,
Hippel-Lindau syndrome, etc.), as well the higher
incidence in certain populations (black, Hebrew,
Polynesian, etc.).
Morphopathology
 Malignant tumors of the pancreas are mostly derived
from exocrine parenchyma, but may develop from
endocrine cells also (Langerhans islets cells
proliferation).
 Ductal adenocarcinoma is the most common
malignant pancreatic tumor (80%) in two thirds of
cases being located in the head, neck or uncinate
process.
 Over 85% of cases, when diagnosed, are already
extended beyond the organ by direct invasion,
perineural and via the lymphatic system.
 Remote metastases occur most commonly in the liver
and peritoneum, the lungs being the extra-abdominal
organ most likely to receive metastases.
 Giant cell carcinoma, squamous cell carcinoma
and acinar cell carcinoma are rare forms and
accompanied by a worse prognosis than ductal
adenocarcinoma.
 Cystic neoplasms (cystadenocarcinoma, papillary
cystic carcinoma, etc.) are rare, found mostly in
women, without preferential topography, reaching
relatively large dimensions at diagnosis (average
diameter of 6 cm). Complete resection is
accompanied by a very good prognosis (survival at 5
years is 50% in cases of incomplete resection and
75% in cases of complete resection), much better
than in ductal adenocarcinoma.
 Histologically, ductal neoplasms are characterized by
the presence of mucin, while acinar neoplasms are
characterized by the presence zymogen granules.
 Endocrine tumors can be benign or malignant,
functional (with excessive hormone production) or
non-functional.
 Pancreatic lymphoma appears as a large tumor
with imprecise limits but with a relatively favorable
prognosis, showing a good response to chemotherapy
and radiotherapy.
 Metastatic pancreatic tumors, although rare
clinically, at necropsy are found in number of 4 times
higher than primitive malignant tumors of the
pancreas. In descending order of frequency they are
found in cases of breast cancer, lung cancer,
malignant melanoma, gastric cancer and colon
cancer.
 ORIGIN TUMOR TYPE
Ductal epithelium Adenocarcinoma (75%)
Carcinoma with giant cells
Squamous carcinoma
Mucinous carcinoma
Microadenocarcinoma
Cystadenocarcinoma
Cystic papillary carcinoma
Unclassified carcinoma

Acinary cells Carcinoma of the acinary cells

Islet cells Malignant insulinoma
Gastrinoma
VIP-oma
Glocagonoma
Nonepithelial tissue Fbrosarcoma
Leomyosarcoma
Hemangiopericytoma
Histiocytoma
Lymphoma
Clinical picture
 Evolution of pancreatic cancer is divided in four stages:
1. Asymtomatic period: there are no specific
symptoms. The disease is discovered incidentally during
investigations for other complaints. The onset of
symptoms is more than 4 month earlier to the moment
of diagnosis.
2. Period of onset: there are insignificant symptoms:
physical and mental fatigue, depression, tendency to
weight loss, possible migratory superficial
thrombophlebitis (Trousseau sign), loss of appetite,
epigastric discomfort discrete dyspepsia. On clinical
examination there are no significant changes. Diagnosis
is possible only by paraclinical investigations. This is the
stage when, if diagnosis is made, surgical treatment
may be curable in oncological terms.
3. Symptomatic stage. Symptoms and clinical signs
depend on where the tumor is located and they are
produced by invasion of the tumoral process into the
neighborhood organs. Clinical and paraclinical diagnosis
is relatively easy but unfortunately surgical treatment, in
most cases won’t have a radical or curable visa.
4. Advanced stage: tumor may be palpable, there are
liver and other systemic metastases, ascites,
supraclavicular lymphadenotaphy (Virchow-Troisier
sign), umbilical metastasis (sister Mary Joseph sign),
signs of portal hypertension, superior digestive bleeding,
and other symptoms and signs of terminal state. Only
symptomatic treatment may be applied.
Clinical picture depending on tumor location
1. Cancer of the head: evolves with specific clinical triad:
1. mild epigastric pains,
2. severe weight loss
3. progressive jaundice (compression of the common bile duct)
 Tumors are earlier diagnosed than in other locations due
to rapid onset of jaundice. Incidence: 66% of all
pancreatic tumors.
2. Cancer located at body of pancreas: evolves with
unspecific clinical picture, so tumor can grow to large
dimensions compressing the retroperitoneal structures,
especially celiac nervous plexus which will induce intense
permanent dorsal pain. Tumor is diagnosed in late stages.
3. Location at the tail of the pancreas: tumors can also
grow to high dimensions being diagnosed in late stages.
They do not produce any specific symptoms till in
advanced stage. May be accompanied by segmental portal
hypertension (on the spelnic vein). Incidence:10%.
Large tumors of

h
ac
the body of the

om
pancreas

st
 Pain features :
– in most cases it is the principal symptom
– localized in epigastric region and irradiates to dorsal, lumbar
or interscapular region
– It is a continuous pain, intense in advanced cases
ameliorated by genupectoral position "Mohammedan prayer
sign" (anterior flexed body – reduces the compression on the
retroperitoneal nervous plexuses)
 Management of pain for patients with pancreatic cancer is one
of the most important aspects of their care.
 Jaundice features:
– It is present in 50% of cases at admission
– Jaundice is not accompanied by pain and fever (like in
lithiasis)
– Color is verdinic (skin has an intense yellow to green color )
– The jaundice is progressive
– It is accompanied by pruritus (itching )
– It does not react to medication (antispastic drugs)
Other possible symptoms:
 Weight loss - by poor appetite, malabsorption, duodenal
stenosis,
 Depressive syndrome (75% of cases),
 Onset of diabetes (50% of cases),
 Gastrointestinal bleeding - secondary to tumoral
invasion of the stomach or duodenum, or due to
esophageal varices appeared consecutive to splenic and
portal vein compression,
 Migratory thrombophlebitis,
 Subcutaneous metastatic nodules,
 Arthritis
PHYSICAL EXAMINATION

1. Jaundice – verdinic
2. Palpable gall bladder (Courvoisier-Térrier sign)
3. Liver globally enlargement (or nodular when
metastases are present)
4. In advanced stage, palpable tumor and ascites
PARACLINICAL INVESTIGATIONS
Laboratory
 Anemia
 Increased ESR
 Increased bilirubin, liver transaminases (ALT - alanine
aminotransferase and AST – aspartate aminotransferase)
 Increased alkaline phosphatase
 Hyperglycemia
 In advanced cases impaired renal function
 Tumoral markers: CA 494, CA 19-9 , α-feto-protein, CEA.
- without absolute specificity
Imaging (confirm or rule out clinical suspicion of
pancreatic cancer):
1. Ultrasound – confirms the presence of pancreatic
structure modification, the tumor, its location and also
the presence of liver metastases, ascites and portal
hypertension. Confusions may appear with chronic
pseudotumoral pancreatitis. It is highly related to
examiner’s experience and ultrasound device
performance.
2. Computer tomography (CT-scan), performed with
oral and intravenous contrast: it has a higher sensitivity
and therefore is used in all cases with suspected
pancreatic cancer, but it can not identify tumors with a
diameter less than 2 cm. As well as ultrasound, it can
also be used to guide further diagnostic maneuvers
(percutaneous biopsy)
3. MRI: no additional advantages.
4. Cholangio CT - provides noninvasive information about
the morphology of the biliary tract.
CT scan
Cholangio-CT
 CT scan

Cancer of the tail of the pancreas Cancer of the body & tail of the pancreas
5. Endoscopic retrograde
cholangiopancreatography (ERCP) can differentiate
cephalic pancreatic tumor from other periampullar
tumors producing obstructive jaundice. It ofers the
posibilty to perform biopsies and also to introduce
stents into the common bile duct in cases of inoperable
patients.
6.Endoscopic ultrasound: especially useful for
evaluating tumors in the head of the pancreas (assess
the actual size and local invasion, and guides the
transduodenal biopsies)
7. Vascular explorations (angiographies)
 - splenoportography: to evaluate the segmental portal
hypertension on the splenic vein.
 - selective angiography of the celiac trunk and SMA.
8. Laparoscopic investigation: assessing the
macroscopic aspect of the pancreatic region,
establishing the resecability and the extension of the
tumor to other organs under direct visualization.
Ultrasonography of the pancreas and liver may be
performed through this procedure using a special probe.
It can guide the pancreatic biopsy.
9. Other investigations
 The only investigation that can make the diagnosis with
certainty is histopathology. There are cases of chronic
pancreatitis mimicking pancreatic cancer very well and
only histopathology can make the difference.
 Histopathological examination can be done by several
methods:
 Cytological examination can be performed from:
– samples obtained by fine needle aspiration (guided imagery)
– cells of duodenal content
– product obtained by endoscopic brushing of the tumor or
laparoscopic exploration
– peritoneal fluid
 Histological examination can be made from:
– cylinder of tissue harvested by tru cut biopsy;
– tissue fragments removed surgically or endoscopically
DIFFERENTIAL DIAGNOSIS
 Other periampullar tumors:
– Ampulla Vater’s tumor,
– Tumors of the common bile duct,
 Duodenal tumors
 Chronic pancreatitis: clinical picture may be very
similar to that of a cancer. In cancer, calcifications are
not so frequent as in chronic pancreatitis.
 Tumors from neighborhood organs penetrating the
pancreas (stomach, colon)
 Tuberculosis or sarcoidosis – biopsy can make the
difference
GRADING
T categories
 TX: The main tumor cannot be assessed.
 T0: No evidence of a primary tumor.
 Tis: Carcinoma in situ (very few tumors are found in this stage)
 T1: The cancer has not spread beyond the pancreas and is smaller than 2
cm (about ¾ inch) across.
 T2: The cancer has not spread beyond the pancreas but is larger than 2 cm
across.
 T3: The cancer has spread from the pancreas to surrounding tissues near
the pancreas but not to major blood vessels or nerves.
 T4: The cancer has extended further beyond the pancreas into nearby large
blood vessels or nerves.
N categories
 NX: Regional lymph nodes cannot be assessed.
 N0: Regional lymph nodes (lymph nodes near the pancreas) are not
involved.
 N1: Cancer has spread to regional lymph nodes.
M categories
 M0: The cancer has not spread to distant lymph nodes (other than those
near the pancreas) or to distant organs such as the liver, lungs, brain, etc.
 M1: Distant metastasis is present.
Cancer stage grouping
 Stage 0: Refers to cancer in situ, in which the cancer has not yet
invaded outside the duct in which it originated (Tis, N0, M0).
 Stage IA: The tumor is 2 cm or smaller in the pancreas. It has not
spread to lymph nodes or other parts of the body (T1, N0, M0).
 Stage IB: A tumor larger than 2 cm is in the pancreas. It has not
spread to lymph nodes or other parts of the body (T2, N0, M0).
 Stage IIA: A tumor extends beyond the pancreas, but the tumor
has not spread to nearby arteries or veins. It has not spread to any
lymph nodes or other parts of the body (T3, N0, M0).
 Stage IIB: A tumor of any size has not spread to nearby arteries or
veins. It has spread to lymph nodes but not to other parts of the
body (T1, T2, or T3; N1; M0).
 Stage III: A tumor has spread to nearby arteries, veins, and/or
lymph nodes but has not spread to other parts of the body (T4, N1,
M0).
 Stage IV: Any tumor that has spread to other parts of the body
(any T, any N, M1).
TREATMENT
 Treatment of pancreatic cancer is complex, multimodal
(surgery, oncology, pain therapy, etc.).
 Tumors located in the head of the pancreas may have the
chance to benefit from radical surgery because, as a result
of mechanical jaundice they produce, they can be found in
less advanced stages than those located in the body of the
pancreas.
 However, only 10-20% of pancreatic cancers benefit from
radical surgery. In most cases, tumor can not be removed
because it penetrates the major vascular structures (portal
vein, superior mesenteric artery) or other organs. In these
cases, only palliative surgery is performed.
 Patients with unresectable cancer have a median survival
of 6 months. Satisfactory solution in these situations is the
endoscopic placement of stents for biliary obstruction
(effectively equal to that of surgical bypass). Only patients
with duodenal obstruction invariably require bypass
surgery.
SURGICAL TREATMENT
 Surgical treatment of pancreatic cancer is dependent
on tumor topography and stage.
 Two types of surgery:
1. Operations with radical intention – they intend
to remove the tumor in oncological safety margins
and the afferent lymph nodes, followed by
restoration of digestive continuity.
2. Palliative operations - do not remove the tumor,
but through different procedures they are trying to
prolong life and improve quality of life in these
patients.
 Radical surgery:
1. Cephalic duodenopancreatectomy
(pancreatoduodenectomy) - for (tumor located at
the head of the pancreas
2. Splenopancreatectomy (corporeo-caudal)
3. Subtotal pancreatectomy
4. Total pancreatectomy
 Palliative surgery
1. For jaundice:
 Open surgery biliary diversion
– External
– Internal
 Percutaneous biliary diversion
 Endoscopic stenting of the common bile duct
2. For duodenal compression
 GEA operation
3. For pain
 Cephalic duodenopancreatectomy - Whipple proc.
(1935)
1. Cephalic pancreatectomy
1. Hepatico-jejunostomy
2. Duodenectomy
2. Pancreato-jejunostomy TL
3. Antrectomy
3. Gastro-jejunostomy TL
4. Choledoco-Cholecistectomy
Pylorus preserving pancreatico-duodenectomy
Traverso-Longmire procedure (1978)

For a better physiological function

Cephalic duodenopancreatectomy with
pancreaticogastrostomy.
Distal Pancreatectomy and Splenectomy
 A distal pancreatectomy is the removal of the tail and
part of the body of the pancreas.
 Tumors of the tail of the pancreas are removed by a
distal pancreatectomy. In cases of cancer, the tumor
often invades the splenic artery or vein. In addition,
cancers in this location can spread to the lymph nodes in
the hilum of the spleen. For these reasons, it is
frequently best to remove the spleen along with the tail
of the pancreas.
 A distal pancreatectomy is performed in much less time
and requires a shorter recovery period. The procedure
can also be performed using laparoscopic instruments.
 In almost all cases of pancreatic cancers when the
tumor is located at the body of the pancreas, the cases
are unresectable due to the high dimension of the
tumor which rapidly invades the nearby anatomical
structures.
 In rare cases when tumors are diagnosed in early
stages two types of operation may be performed:
1. Total pancreatectomy with regional
lymphadenectomy: en block excision of the entire
pancreas together with duodenum, spleen, great
omentum, (antrectomy) and the corresponding
lympatic nodules;
2. Subtotal pancreatectomy : the spleen and almost
the whole pancreas are excised remaining a small part
of the head of the pancreas close to the duodenum.
Intraoperative possible complications
 The most common and unpleasant complications are
intraoperative vascular lesions especially of the portal
vein that cause significant bleeding. They are solved by
suture or vascular reconstruction.
Postoperative complications
 During the 1960s and 1970s, the morbidity and mortality
for pancreaticoduodenectomy were so high that many
thought the operative procedure ought to be abandoned.
During the 1980s, however, many centers reported
mortality rates around 5% and a morbidity of 25% to
35%. Others still reported a mortality of more than 10%
and a morbidity of up to 65%.
Early local complications: (more than 45 types)
 Anastomosis fistulas or leaks (pancreaticojejunostomy,
hepaticojejunostomy and gastrojejunostomy) – are the
most important complications with a high rate of
mortality. The most frequent anastomotic leak is that of
the pancreas with the jejunum. When the defect is minor
conservative treatment may lead to healing but when the
dehiscence is important, surgical repair (reanastomosis or
other procedures) become necessary due to general
peritonitis.
 Peritonitis and intraperitoneal abscesses – as a
consequence of anastomotic leak.
 Intraperitoneal bleeding with hemoperitoneum.
 Wound suppuration.
Palliative surgery
 Unfortunately, almost 90% of pancreatic cancers are
unresectable at time of surgery. To prolong the patient’s
life and relieve symptoms, is necessary to treat the
complications of pancreatic cancer :
– Common bile duct stenosis - with jaundice
– Duodenal stenosis – with vomiting and inanition
– Transverse colon stenosis –with intestinal occlusion
– Pancreatic duct stenosis – with pain
– Pain
Solutions for jaundice
1. External biliary diversion
– Cholecystostomy
– Kehr drainage
2. Internal biliary diversion
– Cholecysto-gastrostomy
– Choledoco-duodenostomy
– Cholecysto-jejunostomy
– Choledoco-jejunostomy
3. Endoscopic biliary stenting
 Cholecystostomy – is an external biliary diversion
rarely used. It is applied just incases where endoscopic
stenting or internal diversion are impossible (lack of
endowment, very ill patients who cannot undergo other
type of operation)
 T-tube drainage (Kehr) of the common bile duct –
the drainage tube is introduced into the CBD during
surgery when the pancreatic tumor is considered
unresectable. The procedure presumes cholecystectomy.
 These types of external drainage unfortunately will lead
to fluid and electrolytes (especially K+) loss being rarely
applied.
 Internal biliary diversion using the gallbladder
could be represented by: cholecystoduodenostomy,
cholecystoantrostomy and cholecystojejunostomy.
Choosing the procedure depends on local anatomical
condition and surgeon’s option.
 Internal biliary diversion using the common bile
duct is performed when the gallbladder cannot be used
either because of an acute cholecystitis or due to the
absence of the gallbladder after cholecystectomy.
 Choledoco-duodenostomy can be performed in many
ways. The most common used is the side-to-side
anastomosis between the CBD and duodenum in
Florken’s fashion.
 The diversion can be performed between the CBD and a
jejunal loop ascended as an “omega loop” or as “Roux-
en-Y” loop. The same jejunal loop can be used for
gastric diversion in case of duodenal compression.
 Nonsurgical biliary diversion.
 There are minimal invasive procedures that can divert
the bile outside or into the duodenum. These are better
supported by patients in advanced stages.
 The most common procedure used today is the
endoscopic transduodenal stenting of the CBD. This
procedure can be also the first step before the radical
surgery, releasing the patient from jaundice.
 In patients who do not support any surgery or stenting
cannot be performed, the percutaneous drainage of the
biliary tract may be a solution. It is performed under
ultrasound and ecodoppler guidance. A catheter is
placed into a biliary duct and bile is diverted outside.
Resolving the duodenal stenosis
 10-30% of patients requiring biliary bypass, develop
later, duodenal obstruction requiring surgical
reintervention. The solution is a gastro-jejunal
anastomosis which can be performed in many ways
using an “omega” loop or a “roux-en-Y” loop.

 Other solution may be represented by placing a

duodenal stent through endoscopic approach.
Duodenal stent - CT aspects

Stent
Fighting pain
 Chemoneurolysis by infiltration with 50% phenol or
alcohol of the celiac plexus during palliative surgery (with
net improvement in pain for several months), either
before or after surgery by percutaneous approach under
radiological or ultrasound guidance.
 This nerve block may last for up to 3 to 4 months as the
nerves were "numbed" and the block tends to wear off
over time.
 Thoracoscopic splanchnicectomy is a minimally
invasive procedure that cuts specific nerve branches.
 Another modality to assist with pain management is
external beam radiation therapy. The radiation beam
is directed at the tumor and may provide fast onset of
pain relief.
SURGICAL PATHOLOGY OF
THE BILIARY TREE
• Anatomical aspects
1. Pathology of the gallbladder –lithiasis
2. Common bile duct lithiasis
3. Non tumoral stenosis of the bile ducts
4. Tumors of the bile ducts
Anatomy
Bile ducts is a system of canals that drain bile from the
liver secreting cells toward the duodenum. Biliary tree
is divided into two regions:
1. Intrahepatic bile ducts – inside the liver
2. Extrahepatic bile ducts - outside the liver
Extrahepatic bile ducts are formed by:
1. Right and left hepatic ducts
2. Common hepatic duct – ductus hepaticus
3. Gallbladder
4. Cystic duct
5. Common bile duct (CBD) – (choledocus) which joins
with pancreatic duct → forming the ampulla of Vater
→ enters duodenum – papilla major.
 The anatomically normal length of the common bile
duct (CBD) is 10-12 cm. and thickness of 6 mm.
The common hepatic duct has rear relations with
portal vein and the right branch of the hepatic artery.
Hepatic artery is located at the left side of the duct.
Hepatic pedicle variants
There are many anatomical variations which need to
be known when operating in this region. These
variations refer especially to the hepatic artery but also
to the biliary tree. Ignoring these variations can be
very dangerous, sometimes life threatening for the
patient.
The common bile duct (choledocus) has 4 portions:
1. Supraduodenal: bordered rear by the portal vein and
to the left by the own hepatic artery.
2. Retroduodenal portion which has relations in front with
the duodenum. It is crossed by gastroduodenal artery.
Posterior is bordered by portal vein and to the left by
the own hepatic artery.
3. Retropancreatic portion has in front the pancreas and
posterior the vena cava and right renal vein.
4. Intraparietal (transduodenal) portion crosses the
duodenal wall thickness together with the pancreatic
duct forming the Vater’s ampulla.
 Gallbladder is a pear-shaped reservoir of 5-12 cm
length located on the visceral surface of the liver, in the
boundary between the two lobes. Gallbladder has three
anatomical segments:
1. Fundus: usually reaches the free edge of the liver being
in contact with the abdominal wall.
2. Body: comes in contact with the liver and inferior with
the transverse colon and D2 duodenum.
3. Cervix (neck) is the terminal portion continuing with the
cystic duct. Here is located the Mascagni’s lymph node
which may become hypertrophic in acute inflammation
of the gallbladder. The terminal portion of the
gallbladder may be dilated by a voluminous biliary
stone, forming the Hartmann’s pouch.
Cystic duct connects the gallbladder to the common
bile duct and has a variable-length.
The coiled fibers of the duct’s wall form the Lutkens
sphincter and the inside lining mucosa disposition
forms the Heister's spiral valves.
From anatomical point of view, the cystic duct forms a
triangle important for surgery:
– Bilio-vascular triangle of Calot: The region bounded
by the cystic duct laterally, the common hepatic
duct medially, and the inferior edge of the liver
superiorly. The cystic artery can be found in Calot's
triangle in about 80% of patients and a careful
dissection of Calot's triangle is important for safe
cholecystectomy.
Vascularization
Intrahepatic bile ducts are perfused by adjacent
vessels.
Common bile duct is irrigated by gastroduodenal,
hepatic and cystic arteries.
Gallbladder’s blood supply comes from the cystic
artery and small vessels from liver. The cystic artery
derives from hepatic artery and usually is located
above the cystic duct. There are a lot of anatomical
variations, and the surgeon must be aware of this and
be very careful not to confuse hepatic artery with the
cystic artery. The cystic artery is solitary in
approximately 75% of cases.
Lymphatic drainage of the gallbladder is carried to the
liver, the most important anatomical structure being the
lymph node of Mascagni.
 GALLBLADDER LITHIASIS
(cholecystolithiasis)

Gallstones is a widespread disease, with a relatively

easy therapeutic solution in uncomplicated forms, but
due to its complications may have an unfavorable
evolution putting patient’s life in danger.
The incidence of gallstones increased in recent decades
from 4% in the 30ies to 27% in year 70. The actual
average incidence is about 20% of the adult population
and it has a higher incidence in blacks.
Etiopathogenesis
Gallstones etiopathogenesis is different depending on
the composition of stones. There are 3 types of stones:
1. Cholesterol stones - vary in color from light-yellow to
dark-green or brown, with oval shape, 2 to 3 cm in
length, often having a tiny dark central spot. To be
classified as such, they must have at least 80%
cholesterol in composition.
2. Pigment stones - are small, dark stones made of
bilirubin and calcium salts that are found in bile. They
contain less than 20% of cholesterol.
3. Mixed stones - other common constituents are
calcium carbonate, palmitate phosphate, bilirubin, and
other bile pigments. Because of their calcium content,
they are often radiographically visible.
 Types of gallstones

Pigmented
Cholesterol

Mixed
Cholesterol gallstone formation has three causes:
1. metabolic
2. mechanical
3. mixed
1. Metabolic causes: stone formation occurs mainly by
breaking the balance between lecithin and bile acids on one
hand (to keep cholesterol in soluble form) and cholesterol
on the other. The cholesterol saturated bile is not sufficient
to explain the occurrence of stones, it requires the
presence of a nucleus of precipitation called nidus,
represented by muco-glycoproteins in the gallbladder wall
or crystals of bilirubin.
2. Mechanical causes are represented by the failure of the
gallbladder to adequately evacuate its contents. Obstacles
can be represented by:
– Sclero-inflammatory stenosis of the cystic duct
– Dystrophic modifications (Cholesterolosis)
– Biliary dyskinesia caused by a lack of synergy between gallbladder
contraction and cystic sphincter relaxation
– Congenital malformation of the gallbladder (Heister valves
hyperplasia)
Brown (bilirubin) pigment stones are formed within the
intraheptic and extrahepatic bile ducts as well as in the
gall bladder. They form as a result of stasis and infection,
usually in the presence of Escherichia coli and Klebsiella
spp.
Pigmented stones occur more frequently in patients with
haemolytic diseases (sickle cell anaemia, hereditary
spherocytosis, thalassaemia) and cirrhosis. Bile in these
patients contains a high concentration of unconjugated
bilirubin and also presents an increased activity of beta
glucuronidase which is an enzyme produced by E. Colli.
Perhaps the enzyme converts the conjugated bilirubin to
unconjugated form which then precipitates to form
stones.
Risk factors for gallstones - four of them have a
greater significance: 4F
1. Female
2. Fourty
3. Fatty
4. Fertile
Sex. Women are twice as likely as men to develop
gallstones. Excess estrogen from pregnancy, hormone
replacement therapy, and birth control pills appear to
increase cholesterol levels in bile and decrease
gallbladder movement, which can lead to gallstones.
Age. People older than age 60 are more likely to
develop gallstones than younger people. As people age,
the body tends to secrete more cholesterol into bile.
Weight. Obesity is a major risk factor for gallstones,
especially in women. The most likely reason is that the
amount of bile salts in bile is reduced, resulting in more
cholesterol.
Rapid weight loss. As the body metabolizes fat during
prolonged fasting and rapid weight loss (such as after
bariatric surgery) the liver secretes extra cholesterol into
bile, which can cause gallstones. In addition, the
gallbladder does not empty properly.
Diet. Diets high in fat and cholesterol and low in fiber
increase the risk of gallstones due to increased
cholesterol in the bile and reduced gallbladder emptying.
Family history. Gallstones are common in relatives,
suggesting a genetic factor.
Cholesterol-lowering drugs. Drugs that lower
cholesterol levels in the blood actually increase the
amount of cholesterol secreted into bile. In turn, the risk
of gallstones increases.
Diabetes. People with diabetes generally have high
levels of fatty acids called triglycerides. These fatty acids
may increase the risk of gallstones.
Symptoms
The disease may progress through three phases of
evolution but not necessarily in that order of succession.
The patient may remain asymptomatic until complications
phase:
1. Dyspeptic phase: digestive discomfort, bloating, nausea,
abnormal intestinal transit, migraines.
2. Pain phase: biliary colic: violent colicky pain usually
located in right upper quadrant or epigastrium, occurring
after meals, with irradiation in the right interscapulo-
vertebral space or shoulder. In most cases the pain is
reduced by treatment with antispastic medication. When
pain doesn’t react to medication it means that there are
some complications such as infection or migration. Pain is
frequently associated with nausea and vomiting.
3. Stage of complications: symptoms are different
depending on the type of complication, but generally
require emergency treatment even surgery.
Physical examination
Outside the biliary colic only a deep tenderness of the
right upper quadrant with positive Murphy maneuver
may be noticed (the patient inspires deeply palpating
right upper quadrant).
There are several clinical forms :
1. Asymptomatic form: the disease is discovered during
an ultrasound or CT examination for another illness.
2. Painful form (with biliary colic)
3. Dyspeptic form (nausea, vomiting, bloating)
4. Tumoral like form (pain associated with intestinal
transit disorders, tumoral mass palpable in the right
hypocondrium)
Positive diagnosis
Is based on history and imaging explorations, less on
physical examination. The most common and useful is
the ultrasound examination which can reveal the
gallstones, their dimension, position and also gives many
important information about the gall bladder, biliary tree
and the surrounding organs.
ERCP and MRCP (magnetic resonance cholagio-
pancreatography) are used only in special cases when
common bile duct lithiasis is suspected.

Gallbladder
Stone

Shadow

Ultrasound examination
Differential diagnosis should be made with other
diseases manifested by pain in the upper abdomen:
Renal colic – the pain usually is located in the lumbar
region irradiating toward the inguinal region and external
genitalia. Giordano sign is positive. Urinalysis is modified.
Ultrasound will reveal the urinary stones or dilated urinary
tract.
Peptic ulcer pain – is locate in the epigastric region, is not
colicky, has the lesser periodicity (pain – food ingestion –
relief – pain), is not calmed by antispastics and gastro-
duoduodenoscopy shows the ulcer.
Acute pancreatitis – the pain is in the epigastrium with
transverse irradiation, associated with vomiting and
altered general condition. High levels of amylases. CT
investigation is very useful.
Transverse colon tumor – the pain is associated with
digestive transit modification, anemia, palpable tumor.
Colonoscopy will highlight the tumor.
Complications
Mechanic
– Hydrops of the gallbladder
– Passage of the stones into the common bile duct with jaundice and
possible pancreatitits
– Biliary-digestive fistulas (cholecisto-duodenal, cholecisto-gastric,
cholecisto-colic) – biliary ileus
– Bilio-Biliary fistulas (cholecisto-choledocian)
Inflammatory
– Acute cholecistitis (edematous, phlegmonous, gangrenous)
– Perforation
Of the posterior wall – intrahepatic abscess
Pericholecistic abscess
Biliary general peritonitis
– Chronic cholecistitis
– Acute pancreatitis
– Cholangitis
Degenerative
– Cancer of the gallbladder
– Cholesterolosis
– Calcium impregnation of the gallbladder
Mechanic complications
Vesicular hydrops – it happens when the stone blocks
the cystic duct. There are intense prolonged colicky
pains. The gallbladder may be palpable. It produces bile
stasis with superinfection and evolution is toward a
possible acute cholecystitis with perforation. The bile in
the gallbladder is discolored.
Migration into the common bile duct. Small stones are
more dangerous as they could migrate through the cystic
duct into the common duct.
The stones smaller than 3 mm in diameter can pass
through the papilla major into the duodenum. If they are
larger, they will remain in the common bile duct. They
may be asymptomatic but periodically will produce
intense prolonged colicky pain accompanied by jaundice
and sometimes fever (acute cholangitis). They also may
induce an acute pancreatitis (as a result of bile reflux
into the Wirsung duct).
Cholecysto-choledocus fistula – appears as a result of
a large biliary stone which develops the Hartmann’s
pouch. Due to compression on common bile duct and
associated inflammatory processes, the wall of the
choledocus will be eroded and the fistula will appear.
Due to compression the most frequent clinical
manifestation is the jaundice. Smaller stones can also
migrate through the fistula into the common bile duct.
Cholecisto-digestive fistulas. The most frequent is the
fistula with the duodenum but the stomach or colon may
be envolved. The pathogenesis is the same as in the
above type of fistula. There are unspecific symptoms. In
some cases when the migrated stone is large it can
produce intestinal obstruction – biliary ileus. On
abdominal radiography air can be observed in the
gallbladder (pneumobilia) and on barium swallow the
barium passes into the gallbladder.
 Hydrops
Migration

Fistulas
Hydrops
Inflammatory complications
Acute cholecystitis – appears as a result of stasis and
infection of the bile inside the gallbladder most often due
to obstruction of the cystic duct. There are also cases of
acute cholecystitis without biliary stones.
Symptoms debut with a biliary colic. The pain becomes
permanent located in the right hypocondrium and
frequently associated with fever, nausea and vomiting.
When chills are present are signs of cholangitis or
abscess formation.
On palpation an intense pain is found in the right
hypocondrium (painful Murphy maneuver), with
muscular defense, even contraction and sometimes the
gallbladder can be palpated. In a next stage, when
surrounding organs come to isolate the inflammatory
process, a subhepatic block will develop containing in
the middle the gallbladder which may perforate and
produce a pericholecystic abscess.
In advanced cases, general signs of infection are present.
If the gallbladder perforates into the peritoneal cavity, the
signs of septic general peritonitis will appear.
Morphological aspects of the acute cholecystitis may be:
edematous, flegnomous ad gangrenous.
Emhysematous acute cholecystitis is a rare but serious
condition caused by anaerobes, which is highlighted at
ultrasound and radiologically examination by the presence
of air in the gallbladder wall.
Germs most often involved are: E. Colli, Klebsiella,
enterococcus, staphylococcus and anaerobes.
Laboratory will show leukocytosis, high ESR and
sometimes higher values of bilirubin.
Ultrasound examination is the most useful – it will show
the presence of stones and also an enlarged gallbladder
with thickened (>3 mm) walls.
CT and MRI scans are indicated in difficult diagnosis
cases.
Chronic cholecystitis is a condition due to repeated
infections of the gallbladder with a good passage of the
bile through the cystic duct. It appears in two
morphological types: hypertrophic and atrophic.
– In hypertrophic type the gallbladder is enlarged with
thick and hard walls of whitish color (sclerosis).
Chronic inflammation may be accompanied by
calcium deposits in the wall. When the whole
gallbladder is calcified is called porcelain
gallbladder. It can be easilly observed on plain
abdominal radiography.
– In atrophyc type the gallbladder is samll molded on
biliary stones.
Acute cholangitis can be life-threatening. Characteristic
symptoms include jaundice, fever, chills, abdominal pain,
and in severe cases, low blood pressure and confusion.
Chronic hypertrophic gallbladder
Porcelain gallbladder Degenerative complications
Gallbladder cancer – even if there
is no demonstrated a direct
correlation between cancer and
stones, the gallbladder cancer is
more often seen in patients with
gallbladder stones.
Cholesterolosis - change in the
gallbladder wall due to excess
cholesterol. The name strawberry
gallbladder comes from the
typically stippled appearance of
the mucosal surface on gross
examination, which resembles
strawberry gallbladder the appearance of a strawberry.
Treatment
Multimodal treatment, but surgery is the most important
due to possible complications. The operation is
cholecystectomy.
Indications:
– Absolute: all acute complications of gallstones
(perforation with peritonitis, biliary ileus, abscesses,
etc.) In most cases surgery will be performed in
emergency condition.
– Definite indications: frequent colicky pains, other
complications such as: biliary fistulas, acute
pancreatitis, jaundice, cholangitis, cancer, etc
– Relative indications: asymptomatic gallbladder
stones (few and not small stones).
 Cholecystectomy can be performed by laparoscopic or
classical (laparotomy) approach.
Classical approach: there are various types of incisions
but the most frequent are the subcostal Kocher’s incision
or median laparotomy. After sectioning the abdominal
wall structures, the peritoneal cavity is exposed and
isolated. A general, regional and local inspection is
performed. Cholecistectomy may be performed starting
from the fundus – so called anterograde
cholecystectomy, from cystic duct – the retrograde
cholecystectomy or from both sides – the bipolar
cholecystectomy. Generally the retrograde procedure is
preferred because:
1. Ligation and resection of the cystic duct as a first step prevents
further migration of stones into the common bile duct during
gallbladder manipulation
2. Ligation of cystic artery prevents further bleeding during
cholecistectomy
The common bile duct is observed and its diameter is
assessed. Palpation between two fingers (to assess the
presence of stones) is possible through the Winslow
foramen.
The cystic duct is discovered, ligated and sectioned.
Then the cystic artery is found in the Callot’s triangle –
sectioned and ligated. From this point the operation may
go on in retrograde way or bipolar. The gallbladder is
divided from its hepatic bed and careful hemostasis is
performed. Lavage and drainage of the subhepatic
space and then suturing the abdominal wall finishes the
operation.
Laparoscopic
cholecystectomy is the
most used procedure in
now days. It is a minimal
invasive procedure which
allows rapid healing and
recovery of the patient.
In the laparoscopic
approach a laparoscopic
tower (CO2 insufflator,
video camera, light source,
electrocautery and monitor)
and special instruments are
needed.
Contraindications for laparoscopic approach are:
Absolute:
1. major coagulation disorders (hemostasis in laparoscopic
approach is more difficult)
2. contraindications for general anesthesia with tracheal
intubation
Relative:
1. Previous supramesocolic surgery (due to adhesions).
Hasson’s technique is used for introduction of the first
trocar (a small incision at umbilicus is performed and
under direct visual control and finger palpation the trocar
is introduced into the peritoneal cavity avoiding intestinal
lesions).
2. Stones in the CBD is a contraindication just for those
centers which are not endowed with special instruments
and surgeons do not have enough experience in this
field.
3. Some patients with pacemaker.
 The patient is positioned in supine, left rotated and in
anti-Trendelemburg position (for a better access to the
gallbladder). The CO2 is introduced through a special
needle (Veres needle) – The intra-abdominal pressure
must reach 12 mm Hg.
There are used 4 ports.
1. The first trocar (10 mm) – at umbilicus (supra or sub) for
laparoscope
2. The second trocar (10 mm) – in the epigastrium for working
instruments (hook, scissors, suction, etc)
3. The third trocar (5 mm)– under the right costal margins for
handling the gallbladder or elevate the liver
4. The fourth trocar (5 mm) in the lower part of the right
hypocondrium for gallbladder manipulation and drainage
Triangulation is very important !
In laparoscopy tension and contra-tension is very
important for exposing tissues which have to be divided.
Principles and technique are almost the same as in
classical cholecystectomy, but using other kind of
instruments.
The cystic duct and artery are sealed by titanium clips
applied with a clip applicator.
The gallbladder is extracted through one of the 10 mm
trocar.
If there is a suspicion of migrated stones into the
common bile duct (enlarged CBD, associated
jaundice), an intraoperative cholangiography through the
cystic duct may be performed. If migration is confirmed,
gallstones can be removed in the same operative time,
endoscopicaly through the papilla major with a
duodenoscope (ERCP). The procedure may be
performed in a later session, but in this case a
transcystic drainage will be installed for CBD
decompression.
Transcystic cholangiography
Endoscope

Stones in the CBD

ERCP
Other possibilities :
In patients with severe comorbidities that contraindicate the
surgery and the gallbladder is under tension (hydrops) or
with empyema (pus) the simplest procedure is the
percutaneous drainage of the gallbladder.
Cholecystostomy is sometimes used in cases of
cholecystitis when the patient is ill, and there is a need to
delay or defer cholecystectomy.
Intraoperative possible incidents:
Break of the gallbladder – not serious incident. Leaked
bile is aspired and stones are collected from peritoneal
cavity (more difficult in laparoscopic approach).
Hemorrhage from cystic artery – the artery is ligated or
clipped.
Lesion of the right hepatic duct or common hepatic duct
– it must be recognized during operation and resolved.
Otherwise, in the postoperative period, biliary fistula
(exteriorized through the drainage tube) and peritonitis
will appear. When the common bile duct was ligated, as
a confusion with cystic duct, jaundice will appear in the
next days. Reintervention and bile duct repair is
mandatory. There are several options to repair the CBD
depending on lesion type.
 Lesions of the hepatic artery – severe complication.
Damage should be solved by suturing or arterial
reconstruction.
Lesions of the liver – bleeding will be stopped by
electrocautery or suturing.
Lesions of the duodenum or colon – should be
recognized and solved by suture during operation.
Otherwise severe peritonitis will develop threatening the
patient’s life.
POSTOPERATIVE COMPLICATIONS
Immediate local complications:
Intraperitoneal bleeding exteriorized through the drain
tubes – hemostasis should be performed.
Bile leakage on drain tubes – aberrant bile ducts
(Luska), cystic duct clip slippage, lesions of the common
or right bile duct, etc.
 General peritonitis
Acute pancreatitis
Jaundice – remnant gallstones into the common bile
duct, lesions of the common bile duct.
Wound suppuration
Late postoperative complications
1. Incisional hernia
2. Remnant gallstones in the common bile duct – stones
can be removed by ERCP
3. Stenosis of the common bile duct
4. Postcholecystectomy syndrome - A wide range of
symptoms occurs that sometimes are considered to be
associated with the gallbladder.
CHOLEDOCOLITHIASIS
(CBD lithiasis)
Choledocolithiasis may be primary or secondary.
Primary: it occurs rarely. Stones are composed of
calcium bilirubinate, often multiple, brownish and of soft
consistency. Favorable conditions for their appearance
are biliary stasis, infection and foreign bodies in the
common bile duct. In Asia stones are frequently
associated with parasitic infections. Gallstones may
come from intrahepatic ducts where are formed as a
result of congenital or acquired stenosis of the main
biliary pathway.
Secondary: the most common, is due to stones
migration from the gallbladder. Migration usually requires
small stones, less than 0.5 mm or a large cystic duct.
Rarely migration can be produced through a cholecysto-
choledocus fistula. Gallstones are usually of cholesterol
with structure and macroscopic properties like
gallbladder stones.
Morphopathology
Number, location and size of stones are important factors.
1. Number: single or multiple stones (sometimes
“steinstrasse” - stone street – the CBD is filled with
many stones)
2. Location:
– Retroduodenal (most common),
– In the terminal portion of the choledocus and may be impacted
into the ampulla of Vater.
– Rare locations: in the intrahepatic biliary tree or in the bile duct
diverticula.
3. Size:
– Under 2 mm, which can cross the papilla
– 3-5 mm stones that can pass through the papilla giving rise to
episodes of jaundice or pancreatic reactions.
– Larger than 5 mm stones that can become impacted into the
papilla.
 CBD lithiasis

Duodenum

Transcystic catheter
 The presence of stones in CBD leads to changes in its
appearance, so in recent cases CBD keeps its normal
venous appearance, but in the long evolving cases,
with repeated episodes of angiocolitis, the wall of the
CBD becomes thickened, whitish with a typical arterial
aspect.
Symptoms
CBD stones can remain asymptomatic for a long period
of time, but may give rise to serious complications:
1. obstructive jaundice
2. cholangitis
3. acute pancreatitis
Charcot-Villard classic triad: pain, fever and
jaundice is characteristic for forms associated with
angiocolitis.
PAIN is intense, continuous, located in the right
hypochondrium. It appears suddenly after meal and may
last several hours. Characteristic is the poor response to
treatment with antispastic drugs which distinguishes it from
simple biliary colic.
FEVER is of septic type being accompanied by chills and
has sudden exacerbations and higher values then in acute
cholecystitis.
JAUNDICE appears at 24 hours after the onset of pain and
is of mechanical type: it is associated with acholic stools
(discolored stools), dark urine and pruritus (because of
the deposition of bile salts).
1. In forms with mobile stones the jaundice is wavy (appears and
disappears as pain comes and goes) and it is due to passenger
cholangitis.
2. Impacted stones cause a progressive jaundice, but not a melas
(verdinic) jaundice (greyish-green to greenish- black) which is
characteristic for malignant stenosis.
 The most serious complications are acute cholangitis
and acute pancreatitis.
1. Acute cholangitis. We can distinguish two forms
depending on the severity:
1. Catarrhal cholangitis : characterized by common Charcot-Villard
classic triad.
2. Suppurated acute cholangitis: extremely serious requiring
antibiotics and emergency biliary drainage.
The classical clinical triad of Charcot is associated with
hemodynamic instability (hypotension leading to shock),
and impaired consciousness from dizziness to coma.
This association is called Reynolds’ pentad.
Bbiliary obstruction is associated with systemic infection
when pressure in the biliary tree exceeds a critical point
and bilio-venous reflux becomes possible with the
consequence of bacteremia and septicemia.
 The most common local septic complications are liver
abscesses, commonly multiple.
Metastatic abscesses can also develop (brain, lungs,
etc) and also endocarditis.
The kidney is affected by a complex mechanism:
prerenal by hypotension and renal impairment by the
action of endotoxins causing tubular necrosis. Clinically
is manifested by renal failure with oligo-anuria. This is
the hepato-renal syndrome or so called cholangitis
icterus uremigene of Caroli.
Bacteria involved are: E. Coli, Klebsiella, Enterobacter
and Enterococci.

2. Acute pancreatitis: is due to the obstruction of

Wirsung duct and bilio-pancreatic reflux in cases when
stones are impacted or pass the papilla.
Laboratory findings emphasize the cholestasis
syndrome:
1. Total bilirubin is increased above 1 mg%, with
predominance of direct fraction over 0.2 mg%. At
level more than 3 mg% jaundice becomes clinically
evident.
2. AP (alkaline phosphatase) increases over 80 ui.
3. Amylasemia is increased in case of associated
acute pancreatitis.
4. Leukocytosis especially over 15000/cm3.
5. Aminotransferases may increase but not at such
levels as in acute viral hepatitis.
Paraclinical investigations:
Abdominal ultrasound: is the exploration of choice. It
can highlight the biliary obstruction in up to 90% of cases
(CBD dilated over 9 mm). Stones can be visualized in
only 30% of cases and 20% of gallstones do not cause
CBD dilatation.
Computed tomography: It has a higher index of
diagnostic than ultrasound. It is indicated especially in
obese patients. It is also useful in the differential
diagnosis of mechanical jaundice (highlights tumors of the
head of the pancreas).
Nuclear magnetic resonance (NMR) and especially
cholangiopancreatography MRI (MRCP): exploration
which has the possibility to highlight the slow flows in the
abdomen such as bile and pancreatic juice. It may reveal
stones in up to 95% of cases. It is indicated especially in
cases when CBD dilatation is not confirmed by
ultrasonography.
 Ultrasound investigation

CBD

Stone
Endoscopic retrograde cholangiopancreatography
(ERCP) is the exploration of choice for diagnosis of CBD
lithiasis and can be also a treatment option.
ERCP is performed through an endoscope with side view.
The papilla is found and a catheter is inserted through it
and the radiopaque dye will highlight the stones. It has
also the possibility to perform papilosphincterotomy and
extract stones from CBD and pancreatic duct.
ERCP is encumbered by some complications of which the
most important are acute pancreatitis and reflux
cholangitis with liver abscesses.
Endoscopic ultrasound examination with transducers
of high resolution (12-15 MHz ), which are inserted in the
duodenum allows the exploration of the CBD with an
index of diagnosis approximately equal to ERCP but
without its possible complications.
Differential diagnosis should be done with other
causes of jaundice:

NON OBSTRUCTIVE JAUNDICE

1. Pre-hepatic jaundice is caused by an increased rate of

hemolysis (malaria, sickle cell anemia, spherocytosis,
thalassemia and glucose 6-phosphate dehydrogenase
deficiency)
The increased production of bilirubin, leads to the
increased production of urobilinogen. Bilirubin is not
usually found in the urine because unconjugated bilirubin
is not water-soluble, so the combination of increased
urine-urobilinogen with no bilirubin in urine is suggestive
for hemolytic jaundice.
Laboratory findings include:
– Urine: no bilirubin present, urobilinogen > 2 units
– Serum: increased unconjugated bilirubin.
 Genetic disorders - present from birth (Crigler-Najjar
syndrome is caused by a defect in the conjugation of
bilirubin, Dubin-Johnson and Rotor's syndromes are
caused by abnormal secretion of bilirubin into bile,
Gilbert's syndrome is caused by a mild reduction in the
activity of the enzyme responsible for conjugating the
glucuronic acid to bilirubin.)
2. Hepatocellular jaundice
– Acute inflammation of the liver (viral hepatitis, toxic hepatitis,
leptospirosis, etc)
– Chronic inflammation of the liver (cirrhosis – viral, alcoholic,
autoimmune, etc)
– Infiltrative diseases of the liver (liver cancer or metastases,
Wilson's disease, etc)
– Inflammation of the bile ducts (primary biliary cirrhosis or
sclerosing cholangitis)
– Drugs (many drugs can cause jaundice and/or cholestasis)
Laboratory: conjugated bilirubin present, urobilirubin > 2 units but
variable, high levels of aminotransferases.
 OBSTRUCTIVE JAUNDICE (Post-hepatic)
1. Tumors of the head of the pancreas
2. Ductal carcinoma
3. Vater’s ampulloma
4. Biliary ducts stenosis
5. Pancreatitis and pancreatic pseudocysts
6. Parasites
In complete obstruction of the bile duct, no urobilinogen
is found in the urine, since bilirubin has no access to the
intestine. In this case, presence of bilirubin (conjugated)
in the urine without urine-urobilinogen suggests
obstructive jaundice.
No single test can differentiate between various
classifications of jaundice. A combination of liver function
tests and other investigations are essential to arrive at a
diagnosis.
TREATMNENT: surgical + medication. Aims:
1. Removing stones from CBD
2. Achieving an efficient drainage of bile into the
digestive tract
3. Removing the gallbladder as a source of gallstones
 Classical surgical treatment by open surgery
Steps:
1. Laparotomy – preferably through a right subcostal
incision because it offers a better access to the
hepatic pedicle.
2. Cholecystectomy (preferably retrograde)
3. Assessing the common bile duct
1. Inspection – diameter, aspect (venous, arterial )
2. Palpation – stones can be felt
3. Radiologic or fluoroscopic – transcystic cholangiography
4. Endoscopic - choledocoscopy
5. Instrumental – Fogarty catheter, Dormia basket
4. Choledocotomy – usually longitudinal
5. Lithotomy – removing the stones from CBD using
the Dejardin forceps or Fogarty catheter or Dormia
basket.
6. Drainage of the CBD
1. External drainage using a Kehr (T) tube – the
choledocus is sutured on a Kehr tube which
serves for calibration and also for securing the
suture by lowering the pressure into the CBD.
This option is used when the CBD is not very
enlarged (<1.5 cm diameter) and the Oddi
sphincter is fully functional, in young patients.
The tube is removed after 3-6 weeks.
Cholangiography
Performed through
The T-tube drain
2. Internal drainage (diversion into the digestive tract)
1. Choledoco-duodenostomy – in most cases a latero-lateral
anastomosis is performed (Florken, Finsterer or other type).
This procedure is used in larger CBD (between 1.5 and 2.5
cm diameter). This situation is encountered in CBD stones
evolving for a longer period of time with repeated
inflammatory processes and primary etiology of the stones.
The communication between CBD and duodenum ensures
further intra duodenal passage of the eventually newly
formed stones. It predisposes to reflux cholangitis
(duodenal content may enter into the CBD). It is performed
in elderly.
2. Choledoco-jejunostomy – is performed in complex forms
when the CBD is very large (>2.5 cm diameter) with multiple
primary stones (steinstrasse) with intrahepatic lithiasis, with
chronic sclerosing papillitis. The best montage is the Roux
type with a long intestinal loop which prevents the intestinal-
biliary reflux.
Pneumobilia after choledoco-duodenostomy (presence
of gas in the biliary system generally after biliary-enteric
anastomosis)

Air in the biliary tree

 Minimal invasive procedures

Laparoscopic approach follows the same purposes as

the classic one, but is more difficult to perform and
requires special instruments. Choledocotomy and
removal of stones followed by T tube drainage is
possible by laparoscopic approach. The vacuity of the
CBD must be checked through choledocoscopy or
fluoroscopy.
If the laparoscopic cholecystectomy was performed and
calculi was found in the CBD on transcystic
cholangiography, they can be removed by endoscopic
approach – ERCP and papilosphincterotomy in the same
operative time or later. The best approach for remnant
CBD stones is the endoscopic one if stones are not very
large and not impacted.
BENIGN STENOSIS OF BILIARY
DUCTS
A rare pathological conditions most commonly
iatrogenic, due to surgical trauma of the bile ducts,
which may remain asymptomatic for a long time but
can cause very serious complications such as: acute
suppurated cholangitis, liver abscesses or secondary
biliary cirrhosis.
Etiopathogeny
1. Classical or laparoscopic surgical procedures with biliary
tract lesions, which may occur by pinching, clipping
suturing or electrocoagulation. Injuries occur during
laparoscopic interventions, hepatic duct being involved
more often, while in classical surgery the CBD is most
often injured. The main causes of injuries are inability to
recognize local anatomy and inexperienced surgical
team.
2. Abdominal trauma
3. Stones with repeated episodes of cholangitis, Mirizzi
syndrome (obstructive jaundice due to a bulky stone in
the Hartmann’s pouch which compresses the CBD)
4. Repeated episodes of acute pancreatitis
5. Chronic pancreatitis
6. Sclerosing cholangitis: stenosis of intra and extrahepatic
bile ducts.
7. Chgolangiopathy during HIV infection
Clinical picture
Lesion usually remains undetectable until the stenosis is
sufficient to produce mechanical jaundice. Rarely other
symptoms such as right upper quadrant pain occur
before jaundice, or illness may begin directly with signs
of suppurated acute cholangitis.
The onset may be sudden or insidious. In insidious forms
of chronic cholestasis, xantelasma appear around the
eyes and dorsal thoracic region. Weight loss raises
problems of differential diagnosis with malignant
stenosis.
Patient’s history is very important and can give details
about the etiology of stenosis: biliary or endoscopic
interventions in the past, recurrent pancreatitis or
cholangitis, etc..
Paraclinical investigations are the same as for CBD
lithiasis.

Benign stenosis of CBD

Xantelasma
Bismuth's classification (1982)
Type 1 - Low CHD stricture, with a length of the
common hepatic duct stump of >2 cm
Type 2 - Proximal CHD stricture-hepatic duct stump <2
cm
Type 3 - Hilar stricture, no residual CHD, but the hepatic
ductal confluence is preserved
Type 4 - Hilar stricture, with involvement of confluence
and loss of communication between right and left hepatic
duct
Type 5 - Involvement of aberrant right sectorial hepatic
duct alone or with concomitant stricture of the CHD
The classification is based on the lowest level at which
healthy biliary mucosa is available for anastomosis and
is intended to help the surgeon choose the appropriate
technique for the repair.
Treatment
Medication is often associated to fight cholangitis in
these patients, and to restore imbalances caused by
prolonged cholestasis.
Antibiotics are mandatory and should include antibiotics
with biliary excretion and to cover the broad spectrum of
gram negative, gram positive and anaerobic germs.
K vitamin for coagulation disorders.
Patients not responsive to conservative treatment (20%)
require emergency biliary decompression.
Decompression can be done surgically or by minimal
invasive approach (percutaneous transhepatic or
endoscopic).
1. Endoscopic decompression is preferable because is
accompanied by morbidity and mortality rates lower
than surgery.
Endoscopic treatment performs a papilosphincterotomy
and then inserts a prosthesis (stent) into the bile duct.
However, plastic stents should be replaced every 4-6
months to prevent cholangitis by their clogging.
The endoscopic treatment of sclerosing cholangitis is
used to prepare the patient for liver transplantation.

2. Percutaneous treatment is more useful in proximal

malignant stenosis or when endoscopic procedure fails.
3. Surgery: is used when endoscopic treatment fails and
in young patients in good biological condition with long
life expectancy to avoid the inconveniences of
endoscopic replacement of the stent.
Surgical treatment varies depending on the site of the
stenosis but in principle is represented by a bilio-
digestive anastomosis between the suprastenotic
segment of bile duct(s) and usually the jejunum
(excluded from digestive circuit in a Roux-en-Y variant)
Surgical treatment has good results but is encumbered
by a higher rate of perioperative mortality and morbidity.
Prognosis
Treated before the onset of chronic complications
(biliary cirrhosis) it have a favorable prognosis, but
depending on the underlying disease. Patients with
stenosis or sclerosing cholangitis occurring in HIV
infection have a poor outcome.
 TUMORS OF THE
EXTRAHEPATIC BILE DUCTS
 TUMORS OF THE GALLBLADDER

1. Benign tumors
Are rare, more frequently in forms of polyps.
Histopathology: papillomas and vesicular adenoma.
Are usually clinically asymptomatic, being discovered
incidentally at ultrasound examination for other
pathology.
Surgery is indicated only in symptomatic forms, but
patients require ultrasound follow-up at 6 months
because of the risk of malignant transformation of
vesicular adenoma. Tumors exceeding 1 cm, or
associated with calculi, or in patients over 50 years,
require cholecystectomy.
Gallbladder polyp
2. Malignant tumors
Incidence: the 5th place among digestive tract
malignancies, and is found in 1% of
cholecystectomies.
Etiopathogenesis. Risk factors:
1. Gallstones: 75-80% of malignancies are associated with
vesicular lithiasis. Stones-cancer relationship is related to the
evolution of the disease (over 15-20 years), and the size of
stones (over 3 cm).
2. Porcelain gallbladder: association of 25%.
3. Benign tumors: adenomas mostly over 1 cm in diameter
appear to be a risk for malignant degeneration.
4. Genetic abnormalities: mutations in the p53 suppressor gene
on chromosome 17 is associated more frequently with
gallbladder cancer.
5. Malformations of bilio-pancreatic tree.
6. Carcinogenic agents: nitrosamines, metilcolantren.
Morphoathology
Macroscopic: more frequently infiltrative forms
Histological classification: adenocarcinomas 80%,
undifferentiated carcinomas 7%, squamous 3% and
mixed 1%.
Evolution and spread: high aggressiveness with frequent
metastases and inoperable forms.
– Local Invasion: The first organ usually invaded is the
liver but spread can be done over the bile ducts.
Cancer can extended through hepato-duodenal
ligament to the duodenum, colon, stomach, pancreas.
– Spread through the lymphatic system to the Mirizzi
lymph node, around the choledocus, pancreatico-
duodenal lymph nodes.
– Venous spread: invasion of the liver at distance from
the gallbladder.
– Peritoneal spread : peritoneal carcinomatosis.
Gallbladder
Mirizzi
Lymph node
TNM classification
T groups
TX: No description of the tumor's extent is possible because of
incomplete information.
T0: No evidence of primary tumor.
Tis: Cancer cells are only found in the epithelium. This is also known
as carcinoma in situ.
T1: The tumor has grown into the lamina propria or the muscle layer
T1a: Tumor has grown into lamina propria.
T1b: Tumor has grown into the muscularis.
T2: The tumor has grown into perimuscular fibrous tissue.
T3: The tumor has grown through the serosa and/or it has grown from
the gallbladder directly into the liver and/or one nearby structure or bile
ducts outside the liver.
T4: The tumor has grown into one of the main blood vessels leading
into the liver (portal vein or hepatic artery) or it has grown into 2 or
more organs outside of the liver.
N groups
NX: Regional (nearby) lymph nodes cannot be assessed.
N0: The cancer has not spread to regional lymph nodes.
N1: The cancer has spread to lymph nodes near the gallbladder,
such as those along the cystic duct, common bile duct, hepatic
artery, and portal vein.
N2: The cancer has spread lymph nodes in the abdomen that are
further away from the gallbladder, such as the lymph nodes lying
along the aorta (periaortic), the vena cava (pericaval), the superior
mesenteric artery, and the celiac artery.
M groups
M0: The cancer has not spread to tissues or organs far away from
the gallbladder.
M1: The cancer has spread to tissues or organs far away from the
gallbladder.
TNM groupings by stage
Stage 0- Tis N0 M0
Stage IA - T1 N0 M0
Stage IB - T2 N0 M0
Stage IIA - T3 N0 M0
Stage IIB - T1-3 N1 M0
Stage III - T4 any N M0
Stage IV - Any T any N M1
Clinical picture
Symptoms of gallbladder cancer overlap with symptoms
of gallstones and biliary colic. Abdominal pain may be of
a more diffuse and persistent nature than the classic
right upper quadrant pain of gallstone disease. Jaundice,
anorexia, and weight loss often indicate more advanced
disease.
Signs
– Jaundice
– Palpable mass in the right upper quadrant
(Courvoisier sign, if this is due to a palpable
gallbladder)
– Periumbilical lymphadenopathy (Sister Mary Joseph
nodes)
– Left supraclavicular adenopathy (Virchow’s node)
– Pelvic seeding: masses palpated on digital rectal
examination (Blumer’s shelf).

Differentials
Acalculous Cholecystitis
Acalculous Cholecystopathy
Ampullary Carcinoma
Bile Duct Strictures
Bile Duct Tumors
Biliary Colic
Biliary Disease
Biliary Obstruction
Carcinoma of the Ampulla of
Vater
Cholangiocarcinoma
Cholangitis
Cholecystitis
Choledochal Cysts
Choledocholithiasis
Cholelithiasis
Clostridial Cholecystitis
Gallbladder Mucocele
Gallbladder Volvulus
Hepatic Carcinoma, Primary
Liver Abscess
Neoplasms of the Endocrine
Pancreas
Pancreatic Cancer
Pericholangitis
Primary Biliary Cirrhosis
Primary Sclerosing Cholangitis
Laboratory
Tumor markers - CA 19-9 may be significantly elevated
in both cholangiocarcinoma and gallbladder cancer.
Liver function tests: Elevated alkaline phosphatase and
bilirubin levels are often found with more advanced
disease.
Ureea, creatinine, urinalysis: assess renal function prior
to performing an enhanced CT scan.
CBC (Complete Blood Count): Anemia may be an
indicator of more advanced disease.

Imaging Studies
Ultrasonography A mass can be identified in 50-75% of
patients with gallbladder cancer. It also can delineate
metastatic lesions in the liver.
Computed tomography can demonstrate tumor invasion
outside of the gallbladder and identify metastatic disease
elsewhere in the abdomen or pelvis. Liver invasion
occurs in 60% of cases, and the combination of CT scan
and US provides accurate details of disease extension.
Magnetic resonance imaging (MRI). It can provide
details of the vasculature for preoperative planning via
magnetic resonance angiogram (MRA) and bile duct
passages via magnetic resonance cholangiogram
(MRCP).
Cholangiography, via a percutaneous route, or
endoscopic retrograde cholangiography (ERCP) may
establish the diagnosis of gallbladder cancer by bile
cytology.
Endoscopic ultrasonography can be useful to assess
regional lymphadenopathy and depth of tumor invasion
into the wall of the gallbladder.
Angiography may be used to confirm encasement of the
portal vein or hepatic artery and may assist in
preoperative planning for definitive resection.
A routine chest radiograph should also be obtained.
Treatment
The only therapy to afford a chance of cure is en bloc
surgical resection of the gallbladder and
surrounding liver tissue (Mirizzi‘s operation).
Adequate surgical margins may be difficult to achieve.
Unfortunately, very few cases are resectable most cases
being in advanced stage of evolution, with bile ducts
invaded, with jaundice, and liver metastases.
The surgical role in treatment of unresectable disease is
usually limited to biopsy of the tumor for diagnosis and
possible biliary decompression procedures.
Adjuvant therapy consists of chemotherapy and
radiotherapy.
Prognosis
Survival at 5 years is correlated with stage of disease at
presentation. Only 10-20% of patients present with
localized disease. The remainder present with regional
or distant spread.
The 5-year survival rates for localized, regional, and
distant disease are approximately 40%, 15%, and less
than 10%, respectively. The median survival for
advanced disease is short (2-4 months).
 TUMORS OF THE BILE DUCTS
Benign tumors are very rare (papillomas, adenomas or
myoblastoamas) the clinical manifestation being the obstructive
jaundice.
Malignant tumors are also rare – compared to gallbladder in
proportion of 1/3.
Etiopathogenesis - risk factors:
1. Parasitic diseases: clonorchis sinensis (especially in Asia - the
parasite lives in the liver of humans, and is found mainly in the common
bile duct and gall bladder, feeding on bile.) or Ascaris lumbricoides are
incriminated in the etiology of biliary neoplasia.
2. Congenital anomalies of the biliary tract, and congenital cysts of
choledocus
3. Benign tumors of the biliary tract
4. Ulcerative colitis is an important risk factor, cancer appearing 10 times
more frequently in these patients than the general population.
5. Sclerosing cholangitis increases the risk 30 times
Histopathology: Cholangiocarcinoma 90%, very rarely
squamous carcinoma, mucoepidermoid or sarcomas.
Macroscopic appearance:
1. The most common infiltrative form (differential to sclerosing
cholangitis very difficult)
2. nodular intramural
3. polypoid (the rarest)
Location
1. Proximal - convergence of bile ducts is involved (Klatskin
tumor).
2. Medium – of the liver pedicle.
3. Distal - retroduodeno-pancreatic choledocus.
Clinical picture: There are 2 phases of evolution:
1. Pre-jaundice phase when diagnosis is difficult with
symptoms of dyspepsia, right upper quadrant pain,
weight loss.
2. Jaundice manifested phase with obstructive
jaundice, acholic stools, dark urine, itching, continue
pain (typically for cancer), rarely phenomena of
cholangitis.
On clinical examination: often hepatomegaly, which
may be associated with palpable gallbladder
(Courvoisier Terrier sign) when tumor is located below
the junction between cystic duct and choledocus.
Paraclinical investigations
Imaging tests:
1. Abdominal ultrasound - shows dilation of CBD or
intrahepatic bile ducts. Retro-duodenal region tumors
are more difficult to reveal due to gases in the
duodenum.
2. CT scan - adds information on local invasion and
distant metastases.
3. MRI and MRCP - have a higher resolution and can
detect small formations with incomplete obstruction.
4. ERCP - highlights precisely the location of the
obstruction, allows a temporary or palliative biliary
stenting; in association with endoscopy offers a better
staging of the tumor in terms of local invasion.
5. Percutaneous transhepatic cholangiography is
especially useful in proximal tumors (Katskin) and also
allows for temporary or permanent biliary
decompression.

CT – tumor in the liver hilum ERCP – Klatskin tumor

Serology tests
The most commonly used marker is the serum CA19-9,
which tends to be elevated in patients with bile duct
cancer. However, this marker is not specific to bile duct
cancer.

Pathology tests
FNA - this involves guiding a thin needle into the lesion,
and gently sucking out cells for microscopic examination.
These procedures have the benefit of not requiring an
operation or general anesthesia.
Bile duct brushings can be performed through an
endoscope to detect malignant cells.
Biopsy of the biliary tract can be performed through the
endoscope or through an exploratory laparotomy.
Treatment
In most cases, the type of treatment (curative or
palliative) which will be applied can be established just
during operation. Decision making is facilitated by
intraoperative ultrasound and cholangiography
exploration.
Curative resections
1. Tumors of the distal 1/3 benefit from cephalic duodeno-
pancreatectomy (the same operation performed for
cancers of the head of the pancreas)
2. Tumors of the middle 1/3 require partial resection
followed by anastomosis of the upper bile duct to a
jejunal loop (Roux-en-Y procedure).
3. Proximal tumors (Klatskin) raises special problems
requiring resection of the junction and anastomosis of
the right and left bile ducts to an intestinal loop. Klatskin
tumors with invasion of the liver requires combining
different types of hepatic resection.
If the tumor cannot be removed surgically, bypass
procedures may be performed to prevent obstruction of
the gastrointestinal and biliary tract, and to relieve the
patient's symptoms.
Tumors that have a free supratumoral segment can
benefit from different types of bilio-digestive diversions:
– Cholecysto-gastro, or duodeno, or jejunostomy
– Choledoco-duodenostomy or choledoco-jejunostomy
– Hepatico-jejunostomy
In Klatskin’s tumors
– Transtumoral forage and drainage could be a solution,
or
– Transparietohepatic biliary drainage, or
– Intrahepatic cholangiojejunostomy, or
– Hepato-jejunostomy, or
– Hapato-gastrostomy
Patients with associated comorbidities where surgery is
contraindicated can benefit from endoscopic techniques
of CBD stenting.
Prognosis: poor, <5% at 5 years
 VATER’S AMPULLOMA
(tumors of the ampulla Vater)
Carcinoma of the ampulla of Vater is a rare malignant
tumor arising within 2 cm of the distal end of the
common bile duct, where it passes through the wall of
the duodenum and ampullary papilla.

Ampulloma

10% are histologically benign

and 90% malignant
Clinical picture
Patients with carcinoma of the ampulla of Vater often
complain of anorexia, nausea, vomiting, jaundice,
pruritus, or weight loss.
Jaundice is intermittent due to partial necrosis of the
tumor which causes a partial dezobstruction. Tumor
necrosis may be associated with an episode of upper
gastrointestinal bleeding with melena (black, tarry, and
foul-smelling stools)
Differentials
1. Bile Duct Strictures
2. Bile Duct Tumors
3. Cholangiocarcinoma
4. Gallbladder Cancer
5. Lymphoma, Non-Hodgkin
6. Pancreatic Cancer
The diagnosis is endoscopic which allows direct
visualization of the tumor and biopsy harvesting and
disposal of biliary prostheses in cases of jaundice.
Association with endoscopic ultrasound, highlights local
invasion.
Evolution and the local extension of tumors is slower
than in case of cholangiocarcinoma.
Radical treatment is cephalic duodenopancreatectomy.
Due to slower development of tumor postoperative
results are more favorable than after resection for
pancreatic or distal CBD cancer.
Transduodenal ampullectomy is an alternative reserved
to patients who do not support the extent of PCD
intervention.
 Ampulloma – CT scan

Dilated CBD and gallbladder gallbladder

SURGICAL PATHOLOGY
OF THE LIVER
 Liver anatomy
1. Liver abscesses
2. Hydatid cyst
3. Liver tumors
 ANATOMY
Liver lies below the right diaphragm in the upper right
quadrant of the abdomen.
It has four lobes of unequal size and shape:
1. Right
2. Left
3. Caudate
4. Quadrate
The weight of the adult liver varies from 1200 to 1800 g.
Functionally, the right and left lobes are of about equal
size and are divided by a line extending from the inferior
vena cava superiorly to the middle of the gallbladder
fossa inferiorly.
The Couinaud classification of liver anatomy divides the
liver into eight functionally independent segments. Each
segment has its own vascular inflow, outflow and biliary
drainage.
There are eight liver segments. Segment 4 is sometimes
divided into segment 4a and 4b according to Bismuth.
The numbering of the segments is in a clockwise
manner.
The liver has three surfaces: superior, inferior and
posterior.
1) The superior (diaphragmatic) surface is convex and
comes up against the diaphragm and the anterior wall of
the abdomen. Right and left lobes are defined by the
falciform ligament. On the right lobe costal arch
impression can be observed and on the left the heart
impression. The diaphragm separates the liver from the
lower part of the lungs and pleura, the heart and
pericardium and the right costal arches from the seventh
to the eleventh inclusive. It is completely covered by
peritoneum except along the line of attachment of the
falciform ligament.
Pathological processes located here (especially hydatid
cyst and abscesses) may affect the pleural cavity
(pleurisy, empyema) and even the lung (bilio-bronchial
fistula).
2) The inferior surface is divided into four lobes by five
fossa, which are arranged in the form of the letter “H”.
The left limb of the H marks the division of the liver into
right and left lobes. It is known as the left sagital fossa,
and consists of two parts: the fossa for the umbilical vein
in front and the fossa for the ductus venosus behind.
The right limb of the H is formed in front by the fossa for
the gall-bladder, and behind by the fossa for the inferior
vena cava. These two fossae are separated from one
another by a band of liver substance, termed the
caudate process.
The bar connecting the two limbs of the H is the porta
(transverse fissure). In front of it is the quadrate lobe
and behind it the caudate lobe.
The inferior surface is in relation with the stomach and
duodenum, the right colic flexure, and the right kidney
and suprarenal gland. Impression of these organs can
be seen on the surface. The surface is almost
completely covered by peritoneum.
The transverse fissure contains the liver hilum formed by
hepatic pedicle consisting of elements: hepatic artery,
portal vein, hepatic duct, lymphatics and nerves. The
hepatic duct lies in front and to the right, the hepatic
artery to the left, and the portal vein behind and between
the duct and artery.
3) The posterior surface is broad behind the right lobe,
but narrows on the left. Over a large part of its extent it is
not covered by peritoneum (pars affixa) and is in direct
contact with the diaphragm.
Fastening elements of the liver are represented by
ligaments, inferior vena cava and hepatic pedicle.
Ligaments. The liver is connected to the diaphragm and
to the anterior wall of the abdomen by five ligaments: the
falciform, the coronary, the two triangular ligaments and
the round ligament which is a fibrous cord representing
the obliterated umbilical vein. The liver is also attached
to the lesser curvature of the stomach by the
hepatogastric and to the duodenum by the
hepatoduodenal ligament (the lesser omentum).
Vascular supply
Common hepatic artery arises from the celiac trunk. It
branches into: hepatic artery and gastroduodenal artery.
Hepatic artery divides in the hilum into right and left
branch. It gives a series of collateral branches: pyloric
artery, cystic artery, terminal branches.
Portal vein is the venous trunk collector of blood from
the digestive tract. The inferior mesenteric vein joins the
splenic vein and is continued by the portal vein. Portal
vein forms behind the pancreas, and also collects: the
gastric vein, left pyloric vein and right superior
pancreaticoduodenal vein. Portal vein has a length of 8-
10 cm and a caliber of 10-11 mm. In the hilum it divides
into two branches (right and left).
Oxygen is provided from both sources; approximately
half of the liver's oxygen demand is met by the portal
vein, and half is met by the hepatic arteries.
Hepatic veins drain the blood from the
liver into the inferior vena cava. They can
be differentiated into two groups, the
upper group, and lower group.
The upper group typically arises from the
posterior aspect of the liver, are three in
number.
The lower group arises from the right lobe
and caudate lobe; veins are variable in
number, and typically smaller than those in
the upper group are
Liver structure
The liver is covered by Glisson capsule which enters the
liver through the hilum following the blood vessels and
together with vascular network divides the liver
parenchyma into lobules.
The liver lobule is the anatomical and functional unit of the
liver. It has the shape of pyramids the base being placed
to the surface of the liver and the tip inward. In cross
section it looks like a polygon with 5-6 sides.
In the center there is a central vein and by joining of at
least three lobules, portal spaces (Kiernan) are formed
between them. These areas include: connective tissue, a
branch of the portal vein, hepatic artery branch, one or
two bile canaliculi (portal triad) lymph and nerves. Blood
flows from the portal space toward the central vein and
the bile in reverse, from the center toward the periphery of
the lobule.
Liver cells are placed in Remark cords arranged radially.
Between liver cells and capillary wall there are Disse’s
spaces. Between vascular endothelial cells, Kupffer cells
are located, phagocytes participating in hemoglobin
degradation. Between the cords narrow spaces are
formed, called bile canaliculi.
LIVER ABSCESSES
 Liver abscess are represented by purulent collections
developed in the liver parenchyma surrounded by a liver
tissue transformed fibrously.
Liver abscesses can be classified according to four
criteria:
Etiology:
1. Pyogenic abscess (produced by microbial pathogens)
2. Parasitic abscess (amebic abscess)
3. Fungal abscess, most often due to Candida species, accounts
for less than 10% of cases.
According to the modality of appearance:
1. Primitive, whose cause is usually unknown
2. Secondary to general, regional or hepatobiliary infection
According to location: in the right lobe, left lobe, deep,
superficial, on the hepatic dome
According to evolution: acute, chronic
 Pyogenic liver abscesses
Etiopathogenesis
It represents approximately 0.10% to 0.27% from the
total number of liver surgery for various affections. It
affects both sexes equally and can occur at any age,
with a maximum around the age of 50.
In most cases the causes of liver abscesses are
unknown or obscure, yet among them are the
followings:
1. Biliary obstruction with cholangitis
2. Septic metastasis from extrahepatic intra-abdominal processes
(appendicitis, acute enterocolitis, acute pancreatitis)
3. Liver injury
4. Supramesocolic surgery
 The most incriminated pathogens are: E. coli,
streptococcus, staphylococcus, and the anaerobic
Bacteroides fragilis.
These germs can reach into the liver through varied
pathways depending on the primary focus. These ways
may be via the bile tree in case of cholangitis, via the
portal vein commonly in enterocolitis, via hepatic artery
in septicemia, via lymphatic vessels from neighboring
septic processes or directly as in surgery and accidents.
Germs can reach into the liver as germs or septic
emboli.
Pathology
The liver abscesses are located more frequent in the
right liver lobe, because the higher blood flux through the
right branch of the portal vein.
Abscess wall consists of liver tissue rich in fibrous tissue.
The content is puss of various aspects depending on the
causing agent.

Abscess
Right lobe
Clinical picture
The most frequent symptoms of hepatic abscess
include the followings:
1. Fever (either continuous or spiking)
2. Chills
3. Right upper quadrant pain
4. Anorexia
5. Malaise
6. Cough or hiccoughs due to diaphragmatic irritation
may be reported.
7. Referred pain to the right shoulder may be present.
 On physical examination:
1. Fever and tender hepatomegaly are the most
common signs.
2. Jaundice may be present in as many as 25% of
cases and usually is associated with biliary tract
disease or the presence of multiple abscesses.
 Topography of liver abscess influences symptoms,
being almost asymptomatic in deep and posterior
abscesses. In the dome surface location,
pleuropulmonary symptoms are associated (pleurisy,
cough, chest pain). The left hepatic lobe abscess can
be confused with subphrenic abscess or perforated
peptic ulcer.
Untreated liver abscess evolve to serious life
threatening complications The most common are:
1. Breaking in the peritoneal cavity with peritonitis
2. Fistulization into the bile ducts with cholangitis
3. Rupture into the pleural cavity with pleural effusion
4. Fistulization into the pericardium with pericarditis or cardiac
tamponade
5. Fistulization into a hollow organ (digestive system), when
symptoms may improve.
Laboratory : an increase in leukocytes, transaminases,
bilirubin, ESR and alkaline phosphatase. Of high
importance in establishing microbiologic diagnosis is the
blood culture drawn during chills.
Imaging studies
Ultrasonography (sensitivity 80-90%) reveals hypoechoic
masses with irregularly shaped borders. Internal
septations or cavity debris may be detected. It may also
evaluate the biliary tree and guide the aspiration of the
cavity. Operator dependence affects its overall
sensitivity.
Computed tomography (CT) scan with contrast
(sensitivity 95-100%) and ultrasonography are the
modalities of choice and also can be used as techniques
for guiding percutaneous aspiration and drainage.
Liver abscess appears as a well-demarcated hypodense
area. Peripheral enhancement is seen when IV contrast
is administered. Gas can be seen in as many as 20% of
lesions. CT scan is superior in its ability to detect lesions
less than 1 cm. This technique also enables the
evaluation for an underlying concurrent pathology
throughout the abdomen and pelvis.

Liver abscess
 Chest radiography may reveal basal atelectasis, right
hemidiaphragm elevation, and right pleural effusion
which are present in approximately 50% of cases;

Positive diagnosis is
based on the triad AP chest X-ray
described by Fontan:
1. pain,
2. fever,
3. hepatomegaly,
plus the rest of the Right diaphragm
symptoms and elevated
paraclinical
examinations
mentioned.
Differential diagnosis should be made with other
processes associated with fever, chills and sepsis.
Often the diagnosis is not easy, patient being treated
with antibiotics without knowing the exact cause.
In the search for the cause of fever, most often a
modification of the liver is found on ultrasonography and
than follows the CT scan.
Even if the abscess is found, it is sometimes difficult to
differentiate it from a tumor with central necrosis or an
infected hepatic cyst. Most time FNA guided by
ultrasonography is the next step in evaluation.
– Hepatocellular carcinoma
– Biliary disease, Cholecystitis
– Pleuropulmonary empyema
– Hydatid cysts
Treatment
Once the diagnosis has been established, the aim of the
treatment is abscess evacuation and antibiotherapy
based on antibiogram.
Abscess evacuation can be achieved by two methods:
percutaneous aspiration and drainage or by laparotomy.
The percutaneous procedure is guided by ultrasound.
The needle penetrates the liver into the abscess cavity.
The pus is aspired to be sent to laboratory for
antibiogram. Then a pigtail (or other) catheter is inserted
into the cavity. The design of this particular style (pigtail)
of catheter includes small holes that allow for drainage
and a coiled end. The coiled end acts to hold the pigtail
catheter in place.
LADS - Liver Abscess Drainage Set

Pigtail set
Surgical treatment consists of laparotomy, identifying the
abscess (in deep location intraoperative ultrasound
guide is very helpful), opening the abscess cavity,
debridement and puss evacuation, lavage and drainage.
 Amebic abscess
This infection is caused by the protozoa Entamoeba
histolytica.
E. histolytica exists in 2 forms: the cyst stage is the
infective form, and the trophozoite stage which causes the
invasive disease. People who chronically carry E.
histolytica shed cysts in their feces. These cysts are
transmitted primarily by food and water contamination.
Cysts are resistant to gastric acid, but the wall is broken
down by trypsin in the small intestine. Trophozoites are
released and colonize the cecum. Trophozoites penetrate
the mucosal layer. Amebae then enter the portal
circulation and travel to the liver where they typically form
large abscesses.
Epidemiology. Worldwide, approximately 40-50 million
people are infected annually. The majority of infections
occur in developing countries: Mexico, India, Central and
South America, and tropical areas of Asia and Africa.
Mortality/Morbidity. Infection with E. histolytica ranks
second worldwide among parasitic causes of death,
following malaria.
Annually, 40,000-100,000 deaths are caused by infection
with E. histolytica.
Per year, a 10% risk of developing symptomatic invasive
amebiasis exist after the acquisition of a pathogenic
strain.
 Sex. Amebic liver abscess has an incidence 7-12 times
higher in males than in females.
Age. The peak incidence occurs in people in their third,
fourth, and fifth decades, although it can occur in any
age group.
Morphopathology. In contrast with pyogenic
abscesses, the wall of this type of abscess is much
thinner, slightly infiltrated fibrously, with eosinophilic
infiltration and the content is viscous, dark-chocolate
brown.
Clinical picture is similar to that of pyogenic abscesses,
but in patient’s history an episode of dysentery that may
be present even with 5-10 months ago.
Recent travel to endemic areas - in 95% of cases the
onset occurs within 5 months of returning from travel to
an endemic area.
 Abdominal pain located in the upper right quadrant is the
most common element in the history and is present in
90-93% of patients.
Diarrhea is present in less than one third of patients at
the time of diagnosis.
The most frequent pulmonary symptoms are cough and
chest pain, which may represent a sign of secondary
pulmonary involvement by abscess rupture in the pleural
cavity.
Physical examination. Hepatomegaly and abdominal
tenderness are present in more than 50% of cases.
There may be present signs of complications (pleural
effusions, pericardium effusions, peritonitis, etc)
Diagnosis is based on history data (traveling in endemic
zones, dysentery diarrhea), symptoms (Fontan triad) and
paraclinical investigations.
Investigations. Imagery is the same as in pyogenic
abscess.
Etiologic agent detection.
Serologic testing is the most widely used method of
diagnosis for amebic liver abscess.
The EIA (enzyme immunoassay) test detects antibodies
specific for E histolytica in approximately 95% of patients
with extraintestinal amebiasis, in 70% of patients with
active intestinal infection, and in 10% of persons who are
asymptomatic cyst passers. The EIA serology findings
revert to negative in 6-12 months following eradication of
infection.
Serum antigen detection - enzyme-linked
immunosorbent assay (ELISA) – 96% positive.
The role of microscopic stool examination is limited. Less
than 30-40% of patients with amebic liver abscess have
concomitant intestinal amebiasis, and 10% of the
population is infected with the nonpathogenic strain of E
dispar.
Stool antigen detection facilitates early diagnosis before
an antibody response occurs (< 7 d) and differentiates
pathogenic from nonpathogenic Entamoeba infection.
Stool antigen detection based on enzyme immunoassay
(EIA) are most common and still quite sensitive.
Polymerase chain reaction (PCR) has high sensitivity for
detecting E histolytica and for distinguishing
nonpathogenic amoebas.
Stool culture for amoeba is sensitive but has limited
availability.
Aspiration of the abscess content is indicated only if
rupture of the abscess is thought to be imminent,
differentiation between amebic abscess and pyogenic
abscess is critical, or no response to antiprotozoal
therapy occurs in 5-7 days.
Amebas rarely are recovered from the aspirate (15%),
and often they are present only in the peripheral parts
of the abscess, invading and destroying adjacent
tissue.
Many possible complications are associated with
aspiration of the abscess. The most common
complications are infection and bleeding. Other
complications include amebic peritonitis or inadvertent
puncture of an echinococcal cyst.
Differential diagnosis should be made with:
1. Pyogenic hepatic abscesses
2. Hydatid cysts
3. Malaria
4. Typhoid fever
5. Cholecystitis
6. Hemangiomas
7. Hepatic carcinoma
8. Hepatic cysts
9. Hepatocellular adenoma
10.Peritonitis and abdominal sepsis
Treatment. Medication treatment is quite more important
than surgery. There are cases of uncomplicated abscesses
which can be treated successfully solely with medication.
Once the diagnosis was established, medication should
start immediately.
Tissue amebicides (Metronidazole, tinidazole, emetine,
and dehydroemetine chloroquine ) will be used and then
luminal treatment (tetracycline diloxanide furoate,
paromomycin, and iodoquinol) will be continued for
eradication of the asymptomatic colonization state.
The goals of pharmacotherapy are to eradicate the
infection, to reduce morbidity, and to prevent complications.
Luminal amebicides fail to eradicate the luminal forms of E.
histolytica in approximately 10-15% of patients therefore, a
follow-up stool examination is recommended after
completion of therapy. A second course of a luminal
amebicide is required in a few weeks if the first course fails
to eradicate the intestinal carriage.
Surgical treatment.
Percutaneous aspiration and/or drainage of the abscess
is indicated in the following situations:
1. high risk of abscess rupture, as defined by cavity size
greater than 5 cm;
2. left lobe liver abscess, which is associated with
higher mortality and frequency of peritoneal leak or
rupture into the pericardium;
3. failure to observe a clinical medical response to
therapy within 5-7 days; and
4. cannot differentiate from a pyogenic liver abscess.
If good results are obtained after medication surgery
should be avoided. Needle aspiration is preferred
instead of drainage due to lower complication rate and
shorter hospitalization.
Prevention
No prophylactic vaccine is available.
Travelers to endemic areas should eat only cooked
foods or fruits peeled by themselves and should avoid
drinking local water, including ice cubes frequently used
for cocktails.
Boiling is the only effective means of eradicating the
cysts in water. Pay attention ! many types of bottled
water in these countries are not properly disinfected.
Vegetables must be cleaned with a strong detergent
soap and soaked in acetic acid or vinegar for
approximately 15 minutes to eradicate the cyst forms.
Change in sexual practices to avoid fecal-oral
contamination.
Prognosis
In most cases, rapid clinical
improvement is observed in
less than 1 week with
antiamebic drug therapy
alone. The average time to
radiological resolution is
approximately 12 months, with
a range of 3 months to more
than 10 years.
Death occurs in approximately
5% of persons having
extraintestinal infection,
including liver abscess.
Rupture into the peritoneal
cavity and the pericardium are
responsible for most deaths.
 HYDATID CYST OF THE
LIVER
Hydatid disease involves the liver in
approximately 75% of cases, the lung in 15%,
and other anatomic locations in 10%.
Hystory
Liver hydatid disease was described even by
Hippocrates (460 BC), but not knowing the parasitic
etiology of the disease.
After more than 2,000 years, Pallas (1781) and Goeze
(1782) made the first scientific descriptions of hydatid
disease of the liver, discovering the parasitic origin of the
disease.
Leuckart and Heupner described the great cycle of
parasite development and transmission opportunities of
larval form in humans. Alexiinski, in 1897, described the
little cycle of parasite development.
The most important concepts about liver hydatid cyst
were provided by J. Deve, in the beginning of the last
century (possibility of secondary echinococcosis, allergy
and anaphylaxis, the parasiticide effect of formalin).
Tomasso Casson, Weinberg and Pârvu later,
established the intradermoreaction and complement
fixation reaction.
By the late nineteenth century just needle evacuation
were performed. Only in 1871 were published, by
Lintemann - Landau and Rivas, the first marsupialization
techniques with catastrophic results. Later authors such
as Thorton, Ossadas or Llobert - Aquarius published
reduction surgical methods for solving the cyst.
Surgical techniques appeared after the development of
asepsis and antisepsis and modernization of intensive
care methods, in the second half of the twentieth
century, had the first encouraging results.
Etiopathogenesis
Hepatic hydatid cyst is due to the development of the
larval vesicular form of the hexacant embryo of Taenia
Echinococcus Granulosus, a tiny tapeworms, less than
1cm long.
Anatomically this helminth (Tape-worm) is composed of
a scolex or head, with hooks and 4 suction cups
(suckers), with which it binds to the gut, a thin and small
neck, which links to the strobila, which is composed of 3-
4 proglottids, the last of which contains 400-800 eggs
(hexacant embryos).
 Strobila

Head
Neck (scolex)

Echinococcus Granulosus
The rear egg-brooding segment merely releases the
eggs into the definitive host animals (usually a wild or
domesticated carnivore, generally of the canine variety)
feces, allowing the transfer of these ova into the outside
world.
The intermediate host animal - usually a livestock animal
species (e.g. sheep, cow, goat, horse, donkey, pig,
camel) or an omnivorous or herbivorous wild animal
species (e.g. marsupial, wild cattle, wild sheep, wild
goat, deer, moose, caribou) consumes grass infested by
parasitic eggs. The larva hatches out of the egg and
migrates through the portal vein into liver and then to
other organs where it will remain as a large larval
tapeworm cyst (hydatid cyst).
Carnivores can eat infested organs with cysts and the
tapeworm will become mature producing eggs.
 The human is a "paratenic host“ - essentially an “accidental'
host - not a normal part of the parasite's usual life cycle.
Pathogenesis
Finally, the occurrence of hepatic hydatid cyst is the result
of four main processes: development of cuticle, cyst
growth, germination and hydatid fluid secretion.
The liver hydatid cyst components:
1. The cyst wall
2. Content
3. Pericyst
The cyst wall is composed of the outer membrane called the
cuticle of yellowish white, gelatinous aspect, about 1 mm
thick and the inner membrane (germinal lining or
membrane - endocyst) which produces the hydatid fluid,
and actively buds off small mini-cysts inside. These inner-
cysts, called "brood capsules" are miniature replicas of
the main hydatid cyst. They may float about freely inside
of the main cyst cavity or they may remain attached to the
inner germinal lining. The brood capsules sometimes
burst, releasing the tiny larval tapeworm protoscolices
into the main cyst - these sediment out with gravity,
settling into the lower regions of the main cyst as a
grainy, tapeworm sediment termed as 'hydatid sand'.
Germinal membrane
The content of the hydatid cyst is a fluid, which in the early
stages is clear and transparent, with a pH of 7.2 to 7.4,
density of 1007 to 1015 and has toxic and anaphylactic
properties. Within the cyst fluid can be seen the so-
called endogenous daughter vesicles, which are
structurally identical to the primary cyst. If the budding
arise outside the primary cyst wall, daughter vesicles are
called exogenous.
The pericyst belongs to the liver being produced as an
outcome of allergic processes and mechanical action
exerted by the cyst on the liver tissue. It consists of three
layers: external, atelectasic, middle, composed of
connective tissue, rich in eosinophils and internal,
fibrohyaline in contact with the parasite.
Once in the human liver, cysts grow to 1 cm during the first
6 months and 2–3 cm annually thereafter, depending on
host tissue resistance.
Daughter vesicles (brood capsules) are small spheres that
contain the protoscolices and are formed from rests of the
germinal layer. Before becoming daughter cysts, these
daughter vesicles are attached by a pedicle to the germinal
layer of the mother cyst. At gross examination, the vesicles
resemble a bunch of grapes.

Daughter vesicles
Pathophysiology
Hydatid disease is not just a local disease of the infested
organ but it has a general character with repercussions
on the whole body,
Over two thirds of hydatid cyst locations are in the liver,
because liver is the first blood filter for the larva
absorbed from the digestive tract. The second filter is the
lung.
The cyst in the liver destroys the hepatic tissue with
compensatory hypertrophy of the adjacent parenchyma.
Cell destruction in this case is secondary to the vascular
thrombosis, and leads ultimately to the phenomena of
cellular degeneration and sclerogenic atrophy, changes
that result in two phenomena: the marginalization of the
cyst and liver cirrhosis, at first localized and then
generalized.
As the cyst grows it compresses the surrounding
anatomical structures (blood vessels, bile ducts, viscera)
leading to local ischemia with the consequence of fistula
formation. The most common the biliary fistulas occur.
Bile enters the cyst and also fluid and daughter vesicles
from the cyst can enter into the common bile duct
causing obstructive jaundice, cholangitis and allergic
symptoms. Permanent passage through the papilla
major of larvae produces local sclerotic inflammatory
phenomena with the result of sclerotic papillitis with the
narrowing of the outlet.
The occurrence of other types of fistula depends on cyst
location. The other most frequent fistula is formed
between the cyst and pleural cavity or lung through the
diaphragm (especially on the right side) in posterior-
superior location, leading to pleural effusions, pleural
hydatidosis and pleuropulmonary fistula (the content of
the cyst flows into the bronchial tree – hydatid vomica).
Once the biliary fistula is formed and the bile flows into
the cyst it becomes infected and the larvae will die. The
cyst may transform into an abscess.
Other fistula may occur between the cyst and: the
stomach, colon, kidney, pericardium, aorta, etc,
depending on cyst location. Most of them are severe life
threatening complications.
If the cyst ruptures into the peritoneal cavity the patient
may die suddenly due to anaphylactic shock. Other
possibilities are: general peritonitis (hydatid peritonitis) or
secondary peritoneal hydatidosis.
During the natural evolution toward healing, dense
calcification of all components of the cyst may occur.
Although the death of the parasite is not necessarily
indicated by calcification of the pericyst, it is implied by
complete calcification
Topographic incidence
Topographic incidence is important for the evolution of the
cyst, complications, diagnosis and surgical tactics.
1. Median or central liver cysts corresponding to the segments I, IV,
V and VIII. They may be superior compressing the cava and
hepatic veins or inferior in front or behind the liver pedicle.
2. Lateral cysts or lobar cysts (20%) corresponding to segments II,
III, VI and VII, may be marginal or inferior being available for
palpation and easier to access surgically.
3. Paramedian cysts on the left or right side, they increase
significantly in volume, and are difficult to diagnose. Frequently
intercept biliary branches being complicated with biliary fistula and
abscess formation.
4. Cysts on the liver’s dome. May be anterior, of large volume being
easily diagnosed and accessible for palpation, or posterior
(segments II, VII and VIII) being more difficult to diagnose and
evolving with compression on diaphragm, cava and hepatic veins.
5. Multiple cysts (10-15%) can be localized in one lobe, or in all liver
parenchyma.
6. Cysts may be unilocular or multilocular.
CT scans – Hydatid cysts of the liver
Epidemiology
Echinococcosis is a very rare condition in the continental
United States (< 1 case per 100,000 inhabitants). It is
also unusual in northern Europe. The endemic areas are
the Mediterranean countries, the Middle East, the
southern part of South America, Iceland, Australia, New
Zealand, and southern parts of Africa. The incidence in
endemic areas ranges from 1-220 cases per 100,000
inhabitants.
Profession. It is more common in those who work with
animals, animal products and those who have pets,
especially dogs.
Geographical distribution
Symptoms
A long time cysts are asymptomatic, even in advanced
stages, or with minor nonspecific signs (allergic
manifestations and transient dyspeptic phenomena),
diagnosis being impossible based on them. In this faze
diagnosis is made accidentally based on abdominal
ultrasound examination performed for other reasons.
Symptoms are caused by cyst complications which may
include:
– Pain – continuous intensified by breath or physical efforts,
located in the upper abdominal quadrants, due to high
dimensions of cyst.
– Compression on other organs – cysts of high volume can
compress other organs causing symptoms like superior intestinal
obstruction (rare) when the duodenum or the stomach is
compressed.
– Jaundice – due to compression on the liver pedicle or by
perforation into the biliary tree with cholangitis.
– Pleuropulmonary manifestation (chest pain,
dyspnoea, cough, expectorations, etc) when the cyst
is located under the diaphragm and induces pleural
effusion or fistula formation into the bronchial tree.
– Symptoms due to perforation in nearby hollow
organs: stomach, duodenum (vomiting hydatid
membranes) - ureter (hydaturia).
– Fever – when the cyst is infected transformed into an
abscess, or due to cholangitis.
– Signs of cirrhosis
– Signs of peritonitis – when the cyst ruptures into the
peritoneal cavity.
– Sudden death – due to anaphylactic shock (rupture
into the peritoneal or pleural cavity) or massive
internal hemorrhage due to perforation of great
vessels (cava, aorta).
Clinical examination
When the cyst is small, or with a deep location, or
uncomplicated, no signs can be observed. In
voluminous cysts with anterior location, the liver is
enlarged (hepatomegaly on percussion) and the cyst
may be palpated.
In the presence of complications various signs appear
depending on complication (jaundice, pleural effusion,
peritonitis, etc)
Diagnosis – is based on the triad:
1. History – patients from endemic zones or professions that
imply animal or animal products handling
2. Symptoms and physical signs – generally lack of information
3. Paraclinical investigations – the most important
Investigations
The most important are the imaging investigations
which easily detect the cyst(s) in the liver, and also can
highlight its features (location, dimension, form,
complications, etc)
Abdominal ultrasonography is usually the first
investigation that diagnoses the cyst (it is the most
harmless investigation). Accuracy depends on
investigator. Some features suggest the echinococcous
etiology: the fine debris (hydatid "sand“), septae and
daughter cysts, floating germinal membrane (endocyst).
Ultrasound classification (WHO)
– a) Cystic lesion- here there is a simple cyst in the affected organ
– not suggestive for echinococcous.
– b) Active cysts- multiple cysts or septae are present in the parent
cyst.
– c) Transitional stage -Daughter cysts may be present in the
parent cyst with hydatid sand or debris within the cyst.
– d) The inactive stage- here the cyst is echogenic and may be
partially or completely collapsed on itself.
 Ultrasound investigation – Hydatic cyst of the liver

Daughter vesicles wavy band of delaminated

membrane within the cyst
Plain abdominal radiography may reveal calcifications
in the pericyst or total calcified cyst. Calcification is seen
on radiography in 20%–30% of hydatid cysts and usually
manifests with a curvilinear or ringlike pattern
representing calcification of the pericyst.

Plain radiography

Calcified hydatid cyst

CT scan with contrast substance offers the best image
about the cyst and many of its features. CT is indicated
in cases in which US fails due to patient-related
difficulties (obesity, excessive intestinal gas, abdominal
wall deformities, previous surgery) or disease
complications. CT has a high sensitivity and specificity
for hepatic hydatid disease. Intravenous administration
of contrast material is not necessary unless
complications are suspected, especially infection and
communication with the biliary tree.
Calcification of the cyst wall or internal septa is easily
detected at CT. Detachment of the laminated membrane
from the pericyst can be visualized as linear areas of
increased attenuation within the cyst. Daughter vesicles
manifest as round structures located peripherally within
the mother cyst.
CT scan

Calcified hydatid cyst

 Hydatid cyst with Hydatid cyst with multiple daughter
collapsed parasitic cysts inside
membranes.
MRI: Images show the cysts adequately, but MRI offers
no real advantage over CT scan.
Laboratory
Routine laboratory blood tests results are nonspecific.
Liver involvement may be reflected in an elevated
bilirubin or alkaline phosphatase level. Leukocytosis may
suggest infection of the cyst. Eosinophilia is present in
25% of all persons who are infected, while
hypogammaglobinemia is present in 30%.
The indirect hemagglutination test and the enzyme-
linked immunosorbent assay (ELISA) have a sensitivity
of 80% overall (90% in hepatic echinococcosis, 40% in
pulmonary echinococcosis) and are the initial screening
tests of choice. The ELISA test is useful in follow-up to
detect recurrence.
Immunodiffusion and immunoelectrophoresis
demonstrate antibodies to antigen 5 and provide specific
confirmation of reactivity.
Differential diagnosis
1. Hepatic cysts
2. Hepatic carcinoma
3. Liver abscess
4. Abdominal abscess
5. Acute liver failure
6. Biliary colic and biliary obstruction
7. Budd-Chiari syndrome
8. Inferior vena cava thrombosis
9. Intra-abdominal sepsis
10. Portal hypertension
11. Tuberculosis
Treatment – is multimodal, medical and surgical
depending on stage of evolution and complications, but
surgery is the only hope for complete cure.
The aim of the medical treatment is to destroy or
inactivate the parasite and of surgical treatment is to
evacuate the cyst, treat the complications and prevent
relapses or secondary infestation.
Medication: two benzimidazoles are used, albendazole
and mebendazole. The optimal period of treatment with
Albendazole ranges from 3-6 months. It is started
preoperatively and continued postoperatively.
Contraindications: Early pregnancy, bone marrow
suppression, chronic hepatic disease, large cysts with
the risk of rupture, and inactive or calcified cysts.
Surgical methods can be performed by:
1. Laparotomy
2. Laparoscopy
3. Punction Aspiration Instilation Reaspiration and
Drainage (PAIRD) method
1. Laparoscopic approach can be performed in rare
cases when the cyst is located in a favorable position
that afford a good access (marginal cysts on the
anterior edge), of small dimensions, calcified, inactive
and not complicated with fistula. The steps are the
same as in other laparoscopic approach and treatment
may be similar to classical surgical methods. Risks are
represented by an impaired access and visibility, intra-
abdominal spread of the infection, bleeding and other
possible complications.
2. PAIRD technique is performed under ultrasound or CT
guidance. The patient is under IOT anesthesia. A
small skin incision is performed and the needle (18–22
gauge) is guided into the cyst’s cavity (punction). The
content is aspired (and sent to cytological examination)
followed by injection of a scolicidal agent (20%
hypertonic saline and 95% ethanol solution
approximately equivalent to one third of the amount
aspirated) for at least 15 minutes, and then
reaspiration of the cystic contents. This is repeated
until the return is clear. The cyst is then filled with
isotonic sodium chloride solution or drained with a
pigtail catheter. Perioperative treatment with
Albendazole is mandatory (4 days prior to the
procedure and 1-3 month after).
3. Open surgery
The most frequent approach used is by a subcostal or
median laparotomy (a good access to the cyst and
liver pedicle is mandatory).
Over the time many surgical techniques have been
developed and the surgeon have to choose which is
the best for the specific case.
Principles of the surgical therapy are:
1. Cyst emptying
2. Cyst Inactivation
3. Treating the residual cavity
Some precautions must be taken during operation:
1. A good isolation of the peritoneal cavity around the
cyst, with gauzes impregnated in alcohol, to prevent
the spread of cyst content.
2. Avoiding electrocautery in cases when alcohol is used
for inactivation.
Cyst inactivation an emptying. Finding the cyst is
generally easy. Difficulties may be encountered in small
cyst and deep location. Intraoperative ultrasound is very
helpful in these cases.
After peritoneal cavity isolation the cyst is punctured and
a quantity of fluid is extracted and examined. If it is
transparent, clear, probably the cyst is active. If the fluid
is yellowish probably there is a biliary fistula and the cyst
may be inactive. If the fluid is transformed in puss there
is a high chance that the cyst is being inactive.
On the same needle alcohol is introduced into the cyst
cavity in order to inactivate the parasite. Scolicidal
agents include: formalin, hydrogen peroxide, hypertonic
saline, chlorhexidine, absolute alcohol, and cetrimide.
The cyst is opened and content is aspirated. All daughter
cysts are removed and also the germinal membrane.
The cavity is copiously washed with alcohol or hydrogen
peroxide and thoroughly inspected for remnant cysts and
biliary fistulas.
 Treating the residual cavity. This step is a challenge for
the surgeon, depending on where the cyst is located.
There have been imagined many techniques in order to
avoid collection into the residual cavity and abscess
formation.
Types of procedures can be classified as:
1. Conservative procedures that leave in place the pericyst
1. External drainage
1. Wide (marsupialization) - Lindemann Landau (1871)
2. Narrow – Rivas
2. Internal drainage (stomach, duodenum, jejunum) – Goinard,
Pelissier (1959)
3. Filling and sealing the cavity with epiploon –Mauclaire (1900)
2. Procedures that remove totally or partially the pericyst
1. Partial pericystectomy – Mabitt Lagrot (1896)
2. Total pericystectomy with opened cyst – Constantini
3. Total pericystectomy with closed cyst – Pozzi (1887), Napalkoff
(1904)
3. Radical procedures that remove the whole cyst and a portion
of the liver
1. Atypical liver resection – Imperatti
2. Major anatomical liver resection
If biliary fistula is observed in
residual cavity, it should be
closed by sutures.
CBD also should be inspected.
Enlarged CBD and jaundice in
history could represent the
presence of daughter cysts in
CBD, in which case the CBD
should be opened, explored
and cysts removed. A “T”-tube Drainage of the
drainage (Kehr) is placed into residual cavity from its
the CBD. It will help to find the lowest part into a
biliary fistulas in the residual
receptacle positioned
cavity and also will prevent
residual chronic biliary fistula at a lower level.
formation by decreasing the
pressure in the CBD.
Intraoperative complications:
1. Difficult access to the cyst – when cyst is located in the
posterior surface of the right lobe of the liver or when
cyst is small with deep location.
2. Anaphylactic shock during puncture of the cyst.
3. Rupture of the cyst during manipulation and spread of
the content into the peritoneal cavity – risk of
secondary peritoneal hydatidosis.
4. Diaphragmatic rupture and opening the pleural cavity
when cysts are located on the postero-superior surface.
5. Bleeding from liver parenchyma.
6. Lesions of surrounding organs (gallbladder, duodenum,
colon, stomach, etc).
7. Other incidents (intra abdominal blast or fire when
electrocautery is used in the presence of alcohol used
for cyst inactivation).
Postoperative care and complications
Usually the postoperative evolution is long and
encumbered with possible complications depending on
many factors such as: cyst location, dimensions,
numbers, presence of biliary fistula, etc.
Drainage tubes are removed depending on quantity
and quality of the drained fluid.
Patient is advised to take parasiticide drugs
(Albendazole)
The most frequent postoperative complications are:
1. Wound infection
2. External biliary fistula
3. Residual cavity abscess
4. Bleeding from residual cavity
5. Relapse of the hydatid cyst
LIVER TUMORS
 Benign tumors
Benign tumors can develop from liver parenchyma cells
(adenoma, cholangioma) or mesenchymal tissue
(hemangioma, lymphangioama, fibroma)
The most common type of benign liver tumor is
mesenchymal hamartoma.
Tumors may be unique or multiple, in one or both lobes,
cystic or solid. Some of them can turn malignant.
They do not have specific symptoms. Clinical picture is
poor. Mild pain in the upper right abdominal quadrant
may appear especially when tumors are large.
Surgical treatment is not needed in most cases.
 Indications for surgical removal of benign tumors are:
1. If it has a high volume with persistent symptoms
2. If the tumor compresses surrounding anatomical structures
(vessels, bile ducts, etc)
3. If there is no possibility to differentiate from a malignant tumor
Classification of benign liver tumors is based on
several criteria, the most complete being the histologic
criteria (Edmonson, Malta and Robbins).
1. Epithelial tumors: adenoma, cystadenoma, papilloma
2. Mesenchymal tumors: cavernous hemangioma, capillary
angioma
3. Mixed tumors: teratoama
4. Tumor-like lesions: focal nodular hyperplasia, anoxic necrosis,
hamartoma
5. Glissonian tumors and of the liver ligaments
LIVER ADENOMA
It occurs more frequently in women and appears to have
hormonal causes (frequently found in women who
consumed oral contraceptives) but may occur in men who
are treated with anabolic steroids.
Tumors are well defined, with or without a capsule. They
are composed of hepatocytes arranged in cords, without
biliary structures and normal liver tissue. Adenomas blood
supply is exclusively arterial. Rarely turn malignant.
There are several types of adenomas:
1. Solitary adenoma is the most common. It may be of
variable size and has a tendency to marginalization. The
tumor adheres or not to parenchyma according to the
presence or absence of the fibrous capsule. Only tumors
> 10 cm diameter are of therapeutic interest due to
possible compression on liver pedicle.
2. Lecene solitary adenoma (liver simple dysembryonic
tumor). The tumoral epithelial cells are similar to
hepatocytes and group in the form of lobules. They are
well encapsulated that allows an easy surgical
approach.
3. Trabecular adenoma: tumoral cells are arranged in
trabeculae, without any lobular organization and
without any capsule; of all adenomas they have the
greatest tendency to turn malignant.
4. Forms less frequent: cholangiomas - benign tumors,
usually of 1-2cm diameter, multiple, grouped or
disseminated in one or both lobes, discovered
incidentally, difficult to differentiate from secondary
liver metastases.
Clinical symptoms are poor, the diagnostic is usually
based on investigations: ultrasound, CT, MRI.
Surgical excision is indicated in large tumors or small
and spread tumors (liver adenomatosis) with clinical
symptoms and when there is no certainty of benignity.
Hemangioma
The most common liver tumor after liver metastases. It
can be seen both in adults and children, which is of
particular importance due to arteriovenous shunts that
may develop.
There are two forms:
1. Diffuse form mostly involving the whole liver, looking
like disseminated telengiectasia .
2. Solitary form may be present in several pathological
types:
– cavernous hemangioma with large vascular spaces
– capillary hemangioma, with more abundant stroma
– schirous hemangioma, vascular spaces collapsed and
abundant stroma,
– hemangioendothelioma.
Symptoms are very poor. However, the following signs
and symptoms may be attributed to hepatic hemangioma:
right upper quadrant pain with palpable tumor, fever,
anemia and biological inflammatory signs (leukocytosis,
elevated ESR, etc.)
Diagnosis of hemangiomas is most often incidental at
ultrasound examination or CT scan where hypodense
areas filling from the periphery to the center after the
administrations of contrast agent may be observed.
The small hemangiomas or located near the bilio-vascular
tree may be diagnosed by scintigraphy with marked red
blood cells and nuclear magnetic resonance.
The indication of surgical treatment is still under debate.
Widely accepted indications are:
1. intense symptoms,
2. changes in shape and volume of the tumor,
3. repeated intratumoral hemorrhage or subcapsular rupture,
4. central necrosis,
5. benign-malignant uncertainty.
Focal nodular hyperplasia (FNH)
Also called solitary hyperplastic nodule, focal cirrhosis,
pseudocirrhosis, mixed adenoma, in our classification is
part of the tumor-like.
FNH occurs in two forms: solid type as a stellar scar
consisting of convergence liver nodules and the
teleangiectatic form with dilated spaces filled with blood
between nodules.
It is usually asymptomatic. In rare cases growing in
volume, rupture or cirrhosis with portal hypertension can
be found. Malignant transformation was not recorded.
As in most liver tumors diagnosis is made by means of
imaging: ultrasound, CT, MRI.
Diagnostic uncertainty dictates surgery and the most
commonly performed surgery is limited to resection, with
good results.
Hepatic cystadenoma (Liver cysts)
Comes in two morphological aspects: solitary or multiple.
They are usually located in the right lobe. Tumor size is
variable containing liquid. Fluid may have different
aspects: serous, sero-hematic. Cystadenoma wall is thin,
transparent, consisting of two layers: one inner epithelial,
and the another fibrous connective outside, always with
a cleavage space between the cyst and the liver
parenchyma.
Symptoms are poor but some may be associated with
digestive disorders: right upper quadrant pain, nausea,
vomiting, flatulence.
Cysts can become complicated by rupture and
hemorrhage or superinfection.
Surgery is required in cases with obvious symptoms and
consist of enucleation, liver resection and rarely
marsupialization.
 Malignant tumors
Like benign tumors, malignant tumors may have:
1. mesenchymal origin (sarcomas, angiosarcomas)
and
2. parenchymal origin –most frequent
(hepatocarcinoma, cholangiocarcinoma)
Liver malignant tumors may be primary or secondary
(metastases), particularly from gastrointestinal
carcinomas.
HEPATOCELLULAR CARCINOMA (HCC)
Most cases of HCC are secondary to either a viral
hepatic infection (hepatitis B or C) or cirrhosis
(alcoholism being the most common cause of hepatic
cirrhosis).
Incidence
Occurs with predilection in males in a ratio of 5:1, with
a maximum incidence and endemic in Asia, Africa,
South America and with low incidence in North
America and Europe.
Risk factors. The main risk factors for hepatocellular
carcinoma are:
1. Alcoholism
2. Hepatitis B
3. Hepatitis C
4. Aflatoxin
5. Cirrhosis of the liver
6. Hemochromatosis
7. Type 2 Diabetes (probably aided by obesity)
8. Toxic substances (vinyl chloride)
Viral infections with hepatitis B, C and D - 60% of
patients with liver cancer are positive for antigen HBs
and HBc and patients with hepatitis C with virus
antibodies antiHBc positive have a risk of cancer 4 times
higher.
Hepatitis B virus is incriminated in the etiology of HCC by
itself, not by induced cirrhosis. As evidenced is the
presence of HB antigen in individuals with HCC who did
not develop cirrhosis. The risk of patients infected with
hepatitis B and C viruses to develop HCC is 7 times
higher.
A particular pathogenetic importance is given to aflatoxin
B1 produced by Aspergillus flavus, whose presence may
cause an 8 times higher incidence of the HCC.
Signs and symptoms
HCC may present with jaundice, bloating from ascites,
easy bruising from blood clotting abnormalities or as
loss of appetite, unintentional weight loss, abdominal
pain, especially in the upper-right part, nausea, emesis,
or fatigue.
Morphopathology
HCC is a tumor of soft consistency of gray-brown
aspect that distinguishes it from cholangiocarcinoma
and liver metastases. It appears either as a single
massive tumor or as disseminated tumor.
Microscopically tumoral cells are like hepatocytes but
multinucleated and giant. Overall tumor is well-
vascularized mainly arterially.
 HCC extension uses the following routes:
1. Nearby extension
2. Through sinusoidal spaces
3. Anterograde extension through venous
hepatic veins and retrograde through portal
veins
4. Lymphatic extension
5. Transdiaphragmatic
Staging
AJCC/UICC Classification System
Diagnosis
The main biological data on a possible HCC are:
accelerated ESR, increased serum bilirubin, increased
LDH, decreased albumin (they announced a poor
prognosis)
Also alpha fetoprotein and GTP may be increased.
Imaging studies are of particular importance. Ultrasound
CT, MRI, scintigraphy (with technetium, colloidal gold or
Galium) for differential diagnosis from liver metastases,
selective angiography.
On CT, HCC can have three distinct patterns of growth:
1. A single large tumor
2. Multiple tumors
3. Poorly defined tumor with an infiltrative growth pattern
The key characteristics on CT are hypervascularity in the
arterial phase scans, washout or de-enhancement in the
portal and delayed phase studies, a pseudocapsule and a
mosaic pattern. Both calcifications and intralesional fat
may be appreciated.
Tumor of the right hepatic lobe
A biopsy is not needed to confirm the diagnosis of HCC
if certain imaging criteria are met but is the single
method of certain histological diagnosis.

CHOLANGIOCARCINOMA
The tumor originates from the intrahepatic bile ducts
epithelium. In terms of etiology, in addition to the factors
referred to CHC, sclerogenic cholangitis lesions have an
important role.
In terms of morphologic characteristics
cholangiocarcinoma usually appears as a single large
tumor with relatively uniform in structure of yellow-gray
color, and cells are small, with voluminous nucleus with
secretion of mucus.
Due to the above characters, cholangiocarcinoma is
sometimes difficult to distinguish from HCC, this being
done by immunohistochemical profile, by highlighting
specific epithelial membrane antigen, cytokeratin and
impregnation of biliary canaliculi with polyclonal
antibody for carcinoembryonic antigen.
The differential diagnosis with liver metastases from
gastrointestinal carcinomas is sometimes impossible,
even after immunohistochemistry tests and laparotomy,
in this case the differential diagnosis is made by
exclusion of primary tumors.
Symptoms have nothing particularly being almost the
same as in CHC, hepatomegaly and jaundice being
frequently met.
 Liver sarcomas
The main types of liver sarcomas: angiosarcoma,
mesenchymoma, hemangioendothelioma. These tumors
are very rare, with non-specific symptoms and have a
very rapid evolution with unfavorable prognosis.
Surgical treatment is indicated only when these tumors
can be found in resectable stages.

Liver metastases
Are by far the most common malignant liver tumors. The
liver is an important blood filter especially for
gastrointestinal tract.
Three major types of secondary liver releases are more
often met:
1. colorectal cancer metastases
2. liver metastases from endocrine cancers, and
3. metastases from other cancers
 Liver metastases of colorectal cancers occur via the
portal system. Usually the evolution of these
metastases is slow depending on primary tumor
characteristics, and they can be treated.
Colorectal cancer metastases are of two kinds:
1. synchronous, when they occur simultaneously with
the primary tumor or shortly after primary tumor
removal, and
2. metachronous, they occur at a distance greater than
five years after primary tumor removal.
In synchronous metastases, symptoms overlaps the
primary tumor and in the metachronous, symptoms are
similar to any other forms of malignant liver tumors.
Diagnosis relies on history, imaging (ultrasound, CT)
biopsy and elevated levels of CEA (carcinoembryonic
antigen).
Liver metastases
 PRINCIPLES OF TREATMENT OF
HEPATIC MALIGNANCY
1. The first line of treatment for the most common type
of primary liver cancer is a transplant. However,
transplants are only feasible when the cancer is caught
early;
The Milan criteria state that a patient is selected for
transplantation when he or she has:
1. one lesion smaller than 5 cm.
2. up to 3 lesions smaller than 3 cm.
3. no extrahepatic manifestations
4. no vascular invasion
Important features that guide treatment
include:
1. size
2. spread
3. involvement of liver vessels
4. presence of a tumoral capsule
5. presence of extrahepatic metastases
6. presence of daughter nodules
7. vascularity of the tumor
2. The second line of treatment for primary liver
cancer is surgical removal (resection) of the
cancerous part of the organ. However, if the cancer is
not caught early, there may not be enough non-
cancerous tissue left to maintain liver function after a
resection. Only one in four liver cancers is caught early
enough for surgery to be effective.
The decision and the extent of surgical resection for
liver metastases are based upon the patient's
condition, extent of the disease, and liver function.
Liver resection, is limited to patients with one or two
small (3 cm or less) tumors and confined to the liver
with no invasion of the blood vessels.
In case of metastases from colorectal cancer, only 10–
20% of patients are candidates for surgery.
The hepatic functional reserve should be sufficient to allow
adequate postoperative liver function. If remnant liver
parenchyma is normal, up to 6 of the 8 anatomical
segments (75% of the volume of the liver) can be resected
without inducing postoperative liver failure. Such major
resections cannot be performed safely if remnant liver
parenchyma is abnormal.
Therefore, before resection for HCC, the non-tumoral
portion of the liver should be biopsied to determine
whether there is associated cirrhosis.
When a portion of a normal liver is removed, the remaining
liver can grow back (regenerate) to the original size within
one to two weeks. A cirrhotic liver, however, cannot grow
back.
The liver failure can occur if the remaining portion of the
liver is inadequate (for example, because of associated
cirrhosis) to provide the necessary support for life. Even in
carefully selected patients, about 10% of them are
expected to die shortly after surgery, usually as a result of
liver failure.
Liver resections can be divided into two groups:
1. anatomical resections removing one or several
segments, and
2. atypical or wedge resections removing a portion of
liver parenchyma surrounding a hepatic lesion.
Resections removing 2 or more continuous segments are
defined as major hepatic resections.
Tumor size is not relevant to resectability; patients who
have circumscribed single tumors are potentially
resectable regardless of tumor size in HCC.
 Four types of major liver resections are commonly
performed:
1. left lateral lobectomy (segments II, III),
2. right hepatectomy (segments V, VI, VII, VIII),
3. left hepatectomy (segments II, III, IV) and
4. extended right hepatectomy also called right
lobectomy (segments IV, V, VI, VII, VIII).
Other types of anatomical resections can be
performed:
1. extended left hepatectomy (left trisegmentectomy)
2. extending a left hepatectomy to segments V and VIII,
3. central hepatectomy (segments IV, V, VIII)
4. bi-segmentectomies (V–VI, VII–VIII, VI–VII
Liver metastases in colon cancer
Atypical resection
Pleomorphic poorly differentiated hepatocellular carcinoma which
reaches the liver capsule (2009)
Postoperative possible complications:
Local
1. Perihepatic fluid collection or abscesses
2. Bile leak
3. Liver failure
4. Bleedings
5. Wound infection
6. Intra-abdominal sepsis
General
1. Pleural effusion
2. Pneumonia
3. Deep vein thrombosis/pulmonary embolism
4. Cardiac failure, myocardial infarction
Prognosis
Liver resection of colorectal metastases is associated
with 3- and 5-year survival rates close to 40% and 25%,
respectively. After resection, recurrences are observed
in two-thirds of the patients and involve the liver in 50%
of the cases.
Postoperative survival rates in HCC are in the range 80-
92% at 1 year, 61-86% at 3 years, and 41-74% at 5
years. During the first 2 years after resection, the
predominant issue is the appearance of intrahepatic
metastases from the resected primary site.
When transplant or resection are not possible,
chemoembolization and radio-frequency ablation are the
treatments of choice. These therapies can be applied
alone or in association.
3. Chemoembolization
It is based on the rich arterial supply of tumors. It
combats cancer in two ways. First, it gives a high dose of
chemotherapy directly to the tumor. Second, it cuts off
the tumor’s blood supply, a process known as
“embolization.” The physician (interventional radiologist)
inserts a catheter into femoral artery and using X- ray
imaging, guides the catheter into the hepatic artery,
which supplies the tumor with blood. Because these
agents are applied only at the tumor site, and because
non-cancerous liver tissue does not rely on the hepatic
artery as its main source of oxygenated blood, healthy
tissue remains unaffected by this treatment.
An alternative to embolization is intraoperative ligation of
the hepatic artery or its branches.
Chemoembolization
may also be used to
shrink liver tumors
while the patient
awaits a donor
organ.
Transarterial
chemoembolization
is the treatment of
choice when the
tumor is greater
than 4 cm in
diameter, or when
there are multiple
lesions within the
liver.
4. Radio-frequency ablation (RFA) is a minimally
invasive treatment for focal cancers. During the
procedure the tumor is destroyed with localized heat
from electrical energy. A special needle is inserted into
the liver tumor, through the skin (or directly in open
surgery) by ultrasound guidance and at its tip intense
heat is generated. Because the heat is generated
within the tumor, surrounding healthy tissue is mostly
spared. This procedure can be performed under local
anesthesia but is usually performed under general
anesthesia. Patients generally stay in the hospital
overnight, but many go home the same day.
The technique has outcomes similar to those of
surgical resection for appropriately selected tumors.
 Radiofrequency ablation can be used alone or in
conjunction with liver resection. Sometimes when
patients have multiple tumors, some of them may be
surgically removed while the remaining disease is
treated with radiofrequency.
Radiofrequency ablation can be performed either
during open surgery, laparoscopy, or percutaneously.
5. Percutaneous ethanol injection (PEI) is very
effective in destroying small HCC tumors. Performed
under percutaneous ultrasound guidance, a needle is
placed into the tumor and absolute alcohol is injected.
For HCC tumors that are ≤2 cm in diameter, PEI
seems to have efficacy similar to that of RFA
6. Systemic chemotherapy
It is based on tumor response to chemotherapy.
Unfortunately it does not exceed an average of 20%.
Survival is short and is measured in months.
For monochemotherapy are used: adriamycin, 5
fluorouracil, nitomicina C. Polichemotherapy does not
provide additional benefits.
 PERITONITIS

Peritonitis is an inflammation of peritoneal

serosa, generalized or localized, of bacterial
or chemical etiology.
ANATOMY
The peritoneum is the serosa membrane that forms
the lining of the abdominal cavity and covers the most
of the intra-abdominal organs. It is the largest serosa
in the body (1.7 to 2 sqm)
The intraperitoneal space is the space located within
the abdominal cavity and wrapped in peritoneum. It is
divided arbitrary and by anatomical structures in some
compartments and recesses creating an
interconnecting network that allows the spread and
sequestration of acute intraperitoneal effusions.
The peritoneal cavity is divided by the transverse
mesocolon in:
1. Supramesocolic space
2. Inframesocolic space
 The small bowel mesentery divides the inframesocolic
space into two comparments:
1. The right infracolic space
2. The left infracolic space
The right and left paracolic gutters are lateral to the
attachments of the peritoneal reflections of the
ascending and descending colon. The right and left
paracolic gutters represent communications between
the supramesocolic and pelvic area.
The falciform ligament separates the right from the left
subphrenic space

Normally, the amount of peritoneal fluid present is less

than 50-100 mL.
CLASSIFICATION
Classification by origin of germs:
1. Primary
 The source of contamination is extraperitoneal,
 Infection is produced via the blood or lymphatic circulatory
system.
 Very rare (5%)
 Monobacterial
2. Secondary
 The most frequent – 95%
 Plurimibrobial
 There is an intraperitoneal source of contamination, such
as:
1. Perforation of intra-abdominal hallow organs
2. Inflammation of abdominal organs
3. Postoperative
 Classification by evolution:
1. Acute – most frequent
2. Chronic – such as:
1. Recurrent inflammatory disease of the intraperitoneal organs
(pelvic)
2. Intraperitoneal presence of foreign substances (talcum, barium)
3. Tuberculosis

Classification by extension:
1. Generalized (diffuse) – extended in the whole peritoneal
cavity
2. Localized – in some peritoneal regions or compartments

Classification by the presence of germs:

1. Bacterial peritonitis (septic) – the vast majority
2. Chemical peritonitis – such as: gastric juice from a perforated
peptic ulcer, bile, pancreatic enzymes (pancreatitis) etc.
 The most common bacteria identified in peritonitis are:
1. Gram-positive (E. coli, Enterobacter, Klebsiela)
2. Gram negative (Enterococci)
3. Anaerobic (Bacteroides, Clostridium)
4. Fungi (Candida)

PATHOPHYSILOGY
Intra-abdominal sepsis from a perforated viscus
results from direct spillage of luminal content into the
peritoneum (eg, perforated peptic ulcer, diverticulitis,
appendicitis, iatrogenic perforation).
With the spillage of the content, gram-negative and
anaerobic bacteria, including common gut flora, such
as Escherichia coli and Klebsiella pneumoniae, enter
the peritoneal cavity.
Endotoxins produced by gram-negative bacteria lead to
the release of cytokines that induce cellular and humoral
cascades, resulting in cellular damage, septic shock, and
multiple organ dysfunction syndrome (MODS).
This evolution depends on two factors:
– 1. number and virulence of germs;
– 2. particular reactivity of the patient;
Chemical (sterile) peritonitis may be caused by
irritants such as gastric juice, bile, blood, or other
substances without bacterial inoculation of the peritoneal
cavity. The most intense pain is caused by gastro-
duodenal juice. Although initially there was no bacterial
contamination, in evolution, the chemical peritonitis will
turn into a septic peritonitis.
Intraperitoneal abscesses occur as a result of the
defense of the host, trying to isolate the infection by
compartmentalization, but fails to completely eliminate
the infection.
The production of fibrin exudates is an important part of
the host defense, but large numbers of bacteria may be
sequestered within the fibrin matrix. It is also an
important factor in development of residual infection and
abscess formation.
In primary peritonitis contamination of the peritoneal
cavity may be due to translocation of bacteria across the
gut wall or mesenteric lymphatics and, less frequently,
via hematogenous seeding in the presence of
bacteremia. More than 90% of cases are caused by a
monomicrobial infection ( gram-negative or gram-
positive). Most cases occur in cirrhotic patients with
ascitis.
The most common cause of postoperative peritonitis
is the anastomotic leak, with symptoms generally
appearing around postoperative days 5-7. Peritonitis
leads to increased hospitalization and mortality rates.
SYMPTOMS
1. Abdominal pain
2. Vomiting
3. Stop of bowel movements
4. Hiccups
Pain – the onset may be sudden, violent, when a hollow
organ is perforated (such as the stomach or duodenum –
like a “knife stab”, or colon) or the onset may be gradual
when infection spreads from an inflamed organ
(appendicitis, pancreatitis, diverticulitis, etc). The initial
location of the pain (localized peritonitis) depends on the
main organ involved, but in few hours it becomes
generalized:
– Stomach and duodenum - in the epigastrium
– Appendicitis - in the right iliac fossa
– Colic diverticulitis – in the left iliac fossa
– Genitalia inflammation – in the hypogastrium
The pain is very intense with maximum of intensity in the
region of causing organ and the patient has an antalgic
position, any movement exacerbating the pain.
Vomiting – initially is reflex (sometimes may be absent
as in perforated peptic ulcer) but as peritonitis
progresses to paralytic ileus it becomes more frequent
with fecaloid content.
Paralytic ileus – bowel movements stop and also the
transit for feces and gases. The abdomen becomes
distended.
Hiccups – as a result of diaphragmatic irritation.
GENERAL AND LOCAL SIGNS

Patient’s position – is generally on lateral decubitus

with legs folded as an antalgic position.
The patient's facial appearance has some features
(peritonitic or Hippocratic face – from Hippocrates who
described it first): “the nose sharp, the eyes sunken, the
temples fallen in, the ears cold and drawn in and their
lobes distorted, the skin of the face hard, stretched and
dry, and the color of the face pale or dusky.… and if
there is no improvement within [a prescribed period of
time], it must be realized that this sign portends death”
Fever: 38-39 gr. Celsius but may be absent at the debut,
in elderly, children and immunosuppressed patients.
Pulse is accelerated in concordance with fever.
 Blood pressure at the beginning is normal but as the
process evolves toward hypovolemic shock, it lowers.
Dyspnea is due to abdominal wall muscle contraction,
diaphragmatic irritation and abdominal distension.
Signs of hypovolemic and/or septic shock: pale skin,
cold and sweaty, hypotension, tachycardia, oligo-
anuria.
LOCAL SIGNS
Inspection: the abdominal wall is immobile, it does not
participate to the respiratory movements ( muscular
contracture) and in non obese patients even the relief
of abdominal muscles is visible.
Palpation:
1. Induced pain – at profound palpation the maximum intensity of
pain is located in the region of causing organ.
2. Muscular defense – the reflex contraction of the
abdominal wall muscles at palpation that resumes after
palpation is finished but reappears in a new attempt. It is
present in the early phases of the peritonitis.
3. Muscular contracture – it is not induced by palpation, the
abdominal wall muscles being contracted permanently.
It is a painful contraction, initial localized and then
generalized. The aspect of “abdomen of board” is most
often seen in chemical peritoneal irritation during peptic
ulcer perforation. Abdominal contracture disappears in
advanced stage of peritonitis being replaced by
abdominal distension.
4. Cutaneous hyperesthesia - increased sensitivity to
sensory stimuli, such as pinch or touch. (Voskresenski
maneuver in appendicitis, Dieulafoy sign)
5. Abolition of cutaneous reflexes – abdominal muscles
won’t contract on skin stimuli.
Percussion - even gentle percussion of the abdominal
wall is very painful (Bell sign). In case of perforated
peptic ulcer the prehepatic dullness disappears due to
the intraperitoneal gas (from stomach). Shifting dullness
is present in intraperitoneal effusions.
Auscultation – in initial phases intestinal movements can
be heard but later these disappear (abdominal
silentium).
Rectal and/or vaginal tact – “The Douglas’s pouch
screaming” = the pain induced by finger palpation of the
Douglas’s pouch.
DIAGNOSIS
In more than 80% of cases the diagnosis relies on
anamnesis and physical examination. Lab and other
investigations serve to determine which is the cause of
the peritonitis and what is the patient’s status.
Lab test will show hyperleukocytosis and other test are
modified depending on current status of the patient.
Radiological examination of the abdomen will show
pneumoperitoneum in case of hollow (stomach,
duodenum, colon) viscus perforation, and hydroaeric
(air-fluid) levels when paralytic ileus is installed.
Ultrasound exam can reveal the intraperitoneal collection
(effusion) and also other pathological changes
suggestive for underlying disease.
Paracenthesis is sometime performed to extract
peritoneal fluid for assessing its macroscopic aspect and
for bacteriological examination and antibiogram for the
sensitivity of an isolated bacterial strain to different
antibiotics. Diagnostic peritoneal lavage may be helpful
in patients who do not have conclusive signs on physical
examination or who cannot provide an adequate history.
Laparoscopy may be performed in uncertain cases,
which may be a way of approach for surgical treatment.
CT scan is performed also in uncertain cases or
uncertain underlying disease. It is very useful to
determine the presence of isolated intraperitoneal
effusions (intraperitoneal abscesses).
Differential diagnosis have to be made with other
conditions manifested by intense abdominal pain.
“Acute medical abdomen” :
– Biliary colic
– Renal colic
– Saturnine colic
– Tabetic colic
– Acute porphyria (rare autosomal dominant metabolic disorder affecting the
production of heme, the oxygen-binding prosthetic group of hemoglobin. It is
characterized by a deficiency of the enzyme porphobilinogen deaminase)

“False acute abdomen” :

– Myocardial infarction
– Basal pneumonia or pleural effusions
– Zona zoster
– Mesenteric lymphadenitis
 Acute surgical abdomen:
– Acute mesenteric ischemia
– Intestinal obstruction
– Acute pancreatitis
– Haemoperitoneum
– Intraabdominal organs torsion (volvulus)
TREATMENT
Peritonitis prognosis depends on: etiology, time elapsed
between onset and treatment and patient’s status and
comorbidity.
Mortality rate ranges between 10-20% and increases to
80% for neglected peritonitis.
Treatment is aimed at three main objectives:
resuscitation, antibiotics and surgery.
1. Resuscitation
– Must be rapid and sustained
– The following objectives:
a) gastric decompression (nasogastric tube, prohibition of
oral nutrition)
b) rebalancing fluid, electrolyte and energy (glucose, saline,
Ringer, blood plasma amino acid solutions)
c) prevention and control of acute respiratory failure (oxygen,
naso-tracheal suctioning secretions, tracheostomy if
necessary)
2. Antibiotics
– Broad spectrum antibiotics, both for aerobic bacteria,
anaerobes and fungi as well.
3. Surgical treatment
– Timing: Patients will be operated as soon as possible,
but their overall condition and associated illnesses will
be considered (preoperative preparations and
vigorous resuscitation are important even if the
operation will be delayed for several hours).
– Choosing the type of operation:
If the diagnosis is known, the incision will be targeted
directly to the septic focus - if the diagnosis is not
known, we perform a median laparotomy (extended if
necessary).
Treatment of lesions will be made in three ways:
– a) Direct closure of perforation (excision - suture);
– b) External drainage of the perforated organ;
– c) Partial resection or removal of the perforated organ;
The peritoneal cavity, will be to wash thoroughly with
warm saline.
Peritoneal cavity drainage will prevent intraabdominal
fluid sequestration and abscesses formation and
provides clues on the integrity of anastomoses (drains
shall be placed in the vicinity of lesion and in declive
areas: Douglas, paracolic subphrenic);
 Possible postoperative complications:
1. Death in the first 2-5 days in toxic-septic shock
2. Intraperitoneal abscesses formation
3. Intestinal occlusion due to intraperitoneal adhesions
4. Wound infection and evisceration or later incisional
hernias
PROGNOSIS
Uncomplicated peritonitis and simple abscesses carry a
mortality rate of less than 5%, but this rate may increase
to greater than 30-50% in severe infections.
Factors that independently predict worse outcomes
include:
– advanced age,
– malnutrition,
– presence of cancer,
– preoperative organ dysfunction.
The concurrent development of sepsis, SIRS (Systemic
inflammatory response syndrome), and MOF (Multiple
organ failure) can increase the mortality rate to greater
than 70%, and, in these patients, more than 80% of
deaths occur with an active infection present.
ETIOLOGIC FORMS OF PRIMARY PERITONITIS
Streptococcus peritonitis
Is produced by beta hemolytic streptococcus in patients bearers of
infectious foci: (angina, erysipelas, otitis, puerperal infections, scarlet
fever).
Intraoperative aspect is: a large quantity of pus of matted, yellow gray
color, without false membranes, without tendency to seclusion.
Peritoneum is intensely congested, and bowels are distended.
Pneumococcal peritonitis
It was the main cause of peritonitis in preantibiotic era.
The frequency in now days is low (occurs in children between 5 and
10 years old).
Caused by encapsulated pneumococcus.
Infectious foci may be: lungs and oropharyngeal infections in patients
with impaired immunity.
Intraoperative aspect is: greenish-white, creamy, odorless pus, with
false membranes, mesenteric lymph nodes swelling and intestines are
congested.
Gonococcal peritonitis
Occurs in girls and young women with poor hygiene.
The propagation is ascending from the external genitalia.
It can occur in men exceptionally (from epididymitis
gonorrhea), in which case, the route of inoculation is
hematogenous.
After a sudden onset with violent pain, symptoms vanish in
4-5 days, which is why the disease was characterized by
MONDOR as a “lightning”.
The peritoneal fluid is gelatinous, greenish, rich in fibrin.
A particular form is represented by of the adherent
perihepatitis in the CURTIS-FITZ-HUGH syndrome, due to
Chlamydia Trachomatis infection: from the salpinx the
infection goes to the perihepatic area, mimicking an acute
cholecystitis. In this case the ultrasound is normal, and
Pap smears confirm infection with Chlamydia.
Tuberculous peritonitis
Peritoneal tuberculosis is an uncommon site of
extrapulmonary infection caused by Mycobacterium
tuberculosis.
Appears more frequently in young people (up to 40
years).
It occurs via hematogenous spread from active
pulmonary or miliary TB. Much less frequently, the
organisms enter the peritoneal cavity transmurally from
an infected small intestine or contiguously from
tuberculous salpingitis
Approximately 70% of patients have symptoms for more
than four months before the diagnosis is established.
This is due in part to the insidious onset of the disease
and because the diagnosis is frequently unsuspected.
Risk factors are: cirrhosis, diabetes mellitus, underlying
malignancy, use of systemic corticosteroids, and AIDS.
However, 20 percent of patients had no risk factor.
 Intraoperative aspects:
1. Wet peritonitis (ascitic form)
– Peritoneal fluid is transparent, yellowish, with a
tendency to coagulation.
– On the serosa there are numerous specific miliary
granules (whitish nodules, small as needle pins with
discontinuous distribution).
2. Dry peritonitis (fibrocaseous, adhesives, plastic
form)
– Fluid volume is reduced, serosa is bold, there are
plurivisceral conglomerates with median location.

3. Purulent form
– There is mass of adherent intestine and omentum
surrounded by tuberculous pus to form a cold
abscess. This may point to the surface, commonly
near umbilicus, or burst into bowel.
Surgical treatment
In cases of fluid collection laparotomy is performed, fluid
is evacuated and abdomen is closed without drainage.
In fibrous form bands of adhesion are divided. If
adhesions are accompanied by fibrous strictures of
ileum, then the affected bowel is excised, if adhesions
only are present, a plication may be performed.
In purulent form cold abscess are evacuated, fecal fistula
is closed, and anastomosis between the segment of
intestine above the fistula and an unobstructed area
below is performed.
 ACUTE LOCALIZED PERITONITIS
Are represented by purulent collections in a limited area
of the peritoneal cavity.
They occur thanks to the defense role of the peritoneum,
which seeks to limit the infection, but can not totally
defeat it.
They are less serious than acute diffuse peritonitis, but
may cause severe complications (rupture in the large
peritoneal cavity, sepsis).
Topographically may be located anywhere but the most
common are those located under the diaphragm and in
the Douglas pouch.
Initially, collection walls are formed by surrounding
anatomic structures but thereafter they become fibrous
hard and thick.
Symptoms varies by location of collection, but general
signs are those that attract attention to the existence of a
septic process.
1. Interhepatophrenic abscess
– Pain in the right upper quadrant and hemithorax;
– Tachypnea with polypnoea;
– Phrenic irritation syndrome (hiccups, pain on the
phrenic nerve route);
2. Left subphrenic abscess
– A collection of pus located between the left
diaphragm and sustentaculum lienalis;
– Spontaneous pain in the left upper quadrant and
hemithorax, pain on palpation of intercostal space,
parietal edema;
3. Subhepatic abscess
– Diffuse abdominal pain or fixed (CARNOT);
– Painful muscular defense, no true contracture;
– Painful dullness in the right upper quadrant;
4. Abscess in the bursa omentalis
– Nonspecific, misleading symptoms
5. Inframesocolic abscesses
– Local pain
– Muscular defense
– Bowel disorder (especially constipation)
– Clinical picture of an intestinal febrile occlusion
6. Pelvic abscesses
– Deep suppuration syndrome
– Signs of pelvic location (rectal and bladder
tenesmus, polyuria, dysuria, diarrhea)
– Digital rectal or vaginal examination is relevant:
Douglas pouch is bulging and very painful (“Douglas
scream").
Investigations
Standard X-ray offers limited information - the only
positive sign is the presence of extralumenal hydroaeric
level.
Ultrasound - describes the wall and the contents of
collection, allowing guided puncture.
Computer tomography - confirms the diagnosis and also
can guide the puncture.
Treatment
Percutaneous drainage, guided by ultrasound or
tomography is the treatment of choice. Effectiveness of
the method is 85%. Complications varies between 0-
15% ( gastrointestinal, pleural, vascular perforation).
Surgical approach - in case of percutaneous drainage
failure, or when additional surgical gestures are required.
The parietal approach should be as direct as possible to
avoid contamination of the pleura or peritoneum. Deep
or multiple collections, require exploratory laparotomy.
INTESTINAL OCCLUSION
 It represents the complete stop of the intestinal transit,
being one
o of the most common abdominal surgical
emergencies.
CLASSIFICATION
The following criteria of classification are used with
immediate practical application:
Etiopathogenic
1. Mechanical - by obstruction, by strangulation;
2. Dynamic - paralytic, spastic;
3. Vascular - embolic, thrombotic.
Topographic
1. High - pylorus, duodenum, jejunum;
2. Intermediate - ileum, transverse and right colon;
3. Low - left colon, sigmoid, rectum.
 DYNAMIC (FUNCTIONAL)
OCCLUSIONS
The function of the autonomic nervous system of the
intestines is disturbed by pathological processes.
There is no intestinal obstacle, the lumen being free.
Diverse etiology:
Abdominal infections (peritonitis)
Injuries (cranio-cerebral, abdominal)
Lung infection (pneumonia)
Systemic infections (septicemia)
Vascular (portal vein thrombosis, myocardial
infarction, entero-mesenteric thrombosis)
Abdominal colic (kidney, biliary)
Metabolic changes in (hypokalemia, hyponatremia,
uremia)
 Dynamic occlusions have the following
characteristics:
General condition declines slowly
Vomiting are abundant
Abdominal distension is great
Intestinal transit stops completely
Untreated, functional occlusions can turn into mechanical
occlusions
Pathologically there are two types of dynamic
occlusions with obvious differences between them:
1. Paralytic occlusions – which occur as a result of
inhibition of intestinal smooth muscles contraction.
Intestines are distended containing gas and liquid.
Intestinal wall is very thin with well visible vascular
drawing.
2. Spastic occlusions - characterized by segments of
intestines with spastic contraction, alternating with
segments of dilated intestines. Intestinal loops are
contracted without evident lumen, with pale serosa and
unapparent vascular drawing.

MECHANICAL (ORGANIC)
OCCLUSIONS
Considering the evolution and physiological
implications, there are essential differences between
the two types of mechanical occlusions: by
obstruction and by strangulation.
1. Occlusions by obstruction (endogenous, exogenous
- inflammatory stenosis, tumor, foreign body, external
compression, adhesions) - are considered occlusions
with "open loop" – the obstructed loop may be
evacuated through its proximal extremity. The intestinal
loop vascularization remains functional and necrosis
and perforation occur later.
2. Occlusions by strangulation (volvulus,
intussusception, incarceration) are considered
occlusions with "closed loop" – the occluded loop can
not be evacuated. The vascularization of the intestine
suffers from the beginning leading to early necrosis and
perforation.
Occlusions by obstruction
Intestinal lumen obstruction is not accompanied by major
circulatory disorders.
Frequently occlusion is preceded by chronic colicky pain
(often due to tumors).
At onset the pain intensity is low, then gradually
increases.
There is a slow progression of symptoms with relatively
good general condition.
Vomiting and abdominal distension appear later.
The abdomen is usually painless and there is no
muscular defense.
Occlusion due to colon cancer is more common when
tumor is located on the left than the right colon.
Occlusion due to a tumor of the right colon progresses
slowly and the tumor may be palpable.
Causes:
Defects of the intestinal wall (inside the wall)
Congenital or acquired defects: stenosis, Meckel diverticulum
Inflammatory: tuberculosis, Crohn's disease, ulcerative colitis
Tumor: benign or malignant
Trauma
Irradiation
Intralumenal obstruction (inside the bowel)
Gallstones
Parasites
Phytobezoar: a concretion formed in the stomach or intestine and
composed chiefly of undigested compacted vegetable fiber
Foreign bodies
Fecaloma
Extrinsic compression (from outside the bowel)
Adhesions
Abdominal tumors
Retroperitoneal tumors
Surgery (foreign bodies forgot in the abdomen)
Occlusions by strangulation (closed loop)
There is an association of intestinal obstruction with
disturbances of vascular supply
The onset is sudden
Pain is violent
Vomiting is early
General condition rapidly declines, the patient is
shocked
Abdominal distension is achieved from the beginning
The abdomen is sensitive to touch, presenting a
defense even located
Bowel movements are interrupted from early moments
Mechanism

1. Volvulus
Torsion of the bowel around an axis
2. Intussusception
Is the telescoping of a bowel segment into another
3. Clamping by peritoneal straps - adhesions
4. Strangulated internal hernias
Are produced by the intrusion of an intestinal loop into
an opening of the peritoneal cavity or a breach of the
mesentery or mesocolon (paraduodenal fossa,
Winslow foramen, parasigmiodian and retrocecal
fossas, postoperative mesenteric defect ).
5. Strangulated external hernias
 TOPOGRAPHYC CLASSIFICATION
1. HIGH LEVEL OCCLUSIONS

The obstacle is located up to the angle of Treitz or up

to the first jejunal loop.
The onset is sudden and with rapid development.
Early and frequent vomiting are reduced in quantity
and lead fast to general status impairment.
Abdominal distension is absent and the intestinal
transit can be maintained (in segments below the
obstructed area).
There is a discordance between the serious general
status and the poor abdominal symptoms.
Are more frequently produced by strangulation
(volvulus).
2. LOW LEVEL OCCLUSIONS

Are located mainly on the large intestine.

The onset is insidious, with mild pain.
Vomiting are missing, or appear late becoming
abundant and fecaloid.
There is an intense abdominal distension.
General condition remains good for a long period of
time.
Are more common produced by obstruction (tumors).
 CLASSIFICATION BY EVOLUTION

1. Acute
The onset is sudden
They generally belong to high occlusion or strangulation
They evolve quickly to hydromineral imbalances
(through early and massive vomiting)
There are early lesions on bowel loops

2. Subacute forms (subocclusion)

Installation is less rapid
Have a slower evolution
Are characterized by mild colicky pains, rare vomiting,
abdominal distension and incomplete abolition of bowel
movements
PATHOPHYSIOLOGY
Obstruction produces superjacent digestive segment
distension.
Distension is produced by:
1. accumulation of air, which comes from
– swallowed air
– bacterial fermentation processes
– diffusion from blood
2. accumulation of fluid into the intestines from
– digestive secretions
– oral food intake
Increasing small-bowel distention leads to increased
intraluminal pressures. This can cause compression of
mucosal lymphatics, leading to bowel wall lymphedema.
With even higher intraluminal hydrostatic pressures,
increased hydrostatic pressure in the capillary beds
results in massive third spacing of fluid, electrolytes, and
proteins into the intestinal lumen.
Ascites
 Accumulation of water and electrolytes in the "third
space " or ghost Randal space leads to:
1. hypovolemia, in addition to the extravascular space
dehydration (interstitial or even intracellular) and
consecutively tissue hypoxia, metabolic acidosis and
functional renal insufficiency.
2. electrolyte disturbances - especially hypokalemia
which lead to heart rhythm disorders.
Abdominal distension induces:
1. Intestinal capillary stasis followed by hypoxia.
2. Intestinal hypersecretion and decreasing intestinal absorption
3. Compression on the inferior vena cava and decrease of
venous return to heart and hypovolemia.
4. Compression on the diaphragm, which reduces expansion of
chest in inspiration, leading to hypoxia and respiratory
acidosis.
Proliferation of bacterial flora in the intestines is followed
by resorption of endotoxins and microbial toxic-septic
shock.
Haemodynamic, metabolic, respiratory, and renal
disorders produced by intestinal transit stop represent
the occlusion shock which in the absence of any
treatment determines the patient's death.
CLINICAL PICTURE
Functional signs:
1. The pain
Is the most constant sign.
Violent, sudden, accompanied by pallor and sweating,
immobilizing the patient to bed, in occlusions by
strangulation.
Less violent crises occurring intermittent with
paroxysmal periods followed by quiet period. In
occlusions by obstruction, the free of pain interval for
jejunum is 2-5 minutes, 5-20 minutes for ileum and over
20 minutes for colon.
Diffuse, continue, unwell defined, accompanied by an
important abdominal distension is present in paralytic
occlusions.
The original location of spontaneous pain, can indicate
where the obstacle is: “where peristalsis dies and starts
the pain, there is the location of obstruction”
2. Vomiting
Less stable than pain.
Important in terms of frequency, quantity and content.
A characteristic of patients suffering from intestinal
obstruction, is the intolerance to any food or fluid intake.
Always are accompanied by nausea, hiccups and
eructation (gastric stasis signs).
In high occlusions, vomiting are early, less abundant,
but common, the content is food or bile and occur by
reflex mechanism.
In low occlusions vomiting are abundant and repeated
at some intervals of time. They are due to stasis and
retrograde peristaltic waves.
Fecaloid vomiting have a serious prognosis.
Bloody vomiting are a sign of extreme gravity (parietal
necrosis).
3. Intestinal transit arrest for gas and faeces, (define
the occlusion)
There are situations in which transit is not completely
abolished, gases and faeces may pas sometimes with
false diarrhea.

Intestinal occlusion
PHYSICAL SIGNS
INSPECTION
1. Distension of the abdomen
It is a constant sign, but not always present.
Its absence may cause errors of diagnosis.
In small bowel occlusions, distension is located particularly around
the umbilicus, but not on flanks.
In large bowel occlusions, abdominal distension is located
predominantly in epigastric region and flanks.
In strangulation the distension occurs suddenly, is asymmetrical,
immobile, elastic on touch and tympanic on percussion (VON WAHL
sign).
In the sigmoid volvulus, bloating is ovoid, located from left iliac fossa
toward the right upper quadrant (BAYER sign).
Peristaltic movements
Peristaltic waves are the manifestation of superjacent loop
contraction.
In thin patients, the peristaltic wave can be seen through the
abdominal wall progressing toward a fixed point (where the obstacle
is located) = KÖNIG sign.
PALPATION
Usually the abdomen is supple, elastic, without
contracture or signs of peritonitis.
The occurrence of contracture, announces the intestinal
loop necrosis with consecutive peritoneal reaction.
A thorough palpation, can detect:
The tumor
“The sausage” of intussusception (BOUDIN sign)
Successive contraction and relaxation of the underlying loop
(BESGES sign)
Points of painful hernia (umbilical, inguinal, femoral). Hernias
often are omitted at examination, especially small strangled
Sensitivity located at 2 cm above his navel (in the small
bowel occlusions) = THEVENARD sign
PERCUSSION
Excessive sonority
Shifting dullness in flanks (GANGOLPHE sign) – sign of ascites
AUSCULTATION
“Steam spout sound” caused by crossing the intestine
content through the narrowed zone (KÖNIG syndrome).
Rapid succession of KÖNIG syndrome, characteristic in
multilevel stenosis (KEBERLE syndrome).
Due to hyperperistalsis, bowel sounds are strong, metallic,
interrupted by crackling that mimics the release of an
intestinal loop from a stenosis (SCHLANGE sign).
In most cases auscultation reveals total silence "silent
abdomen" described by MONDOR.

DIGITAL RECTAL EXAM

May highlight the stenosing tumor
May highlight a distended intestinal loop in the Douglas
pouch (GOLD sign)
May highlight an empty rectal ampulla (HOCHENEG sign)
GENERAL SIGNS
In high level occlusion, the general condition declines
faster and more intensively.
In severe forms, skin and mucous membranes are dry,
the eyes are sunken, and the general condition is
gradually impaired going to exitus.

Distended abdomen – intestinal occlusion

PARACLINICAL INVESTIGATIONS
1. X-ray (plain abdominal radiography, fluoroscopic,
irigography) in supine or better in upright position.
The characteristic picture is that of air-fluid level
(horizontal fluid level and air bubble above).
Gaseous distension of an intestinal loop, appears in the
first 3-6 hours after the clinical onset.
If there are no air-fluid levels at 24 h after the onset of
clinical symptoms, the occlusion is ruled out.
In case of small bowel occlusion, air-fluid images are
numerous, relatively small, are arranged centrally in the
vertical axis and appear as "organ pipes", "swallow
nests" or "stairs“.
In case of large bowel occlusions, air-fluid images are
reduced in number, large in the transverse axis,
arranged peripherally on the colic frame.
In volvulus of sigmoid colon the appearance is typical of
"sand clock".
Small intestine occlusion Large intestine occlusion
Small intestine occlusion Large intestine occlusion
Coffee bean sign

Volvulus of sigmoid colon

 Distended loops and fluid levels may be absent with an
obstruction of the upper jejunum or with closed-loop
strangulating obstructions (as may occur with volvulus).
2. Abdominal ultrasound is less useful because it can
not specify the diagnosis with certainty.
3. Abdominal CT with contrast is useful in some cases
when it can specify the location and cause of intestinal
obstructions especially of tumoral etiology.
4. Colonoscopy – is useful in diagnosis of obstructing
colon tumors.
5. Barium enema – may be also helpful in some cases
(intussusception, volvulus).
6. Laparoscopy and laparotomy are also methods of
diagnosis as in majority of cases the main treatment is
surgical.
CT - Low intestinal
occlusion produced by a
rectal tumor
Enteroclysis is a fluoroscopic X-ray of the small
intestine. Radiocontrast is infused through a tube
inserted through the nose to the duodenum, and images
are taken in real time as the contrast moves through,
aided by administration of methyl cellulose.

Enteroclysis distinguishes
adhesions from metastases,
tumor recurrence, and radiation
damage. It offers a high negative
predictive value and can be
performed with 2 types of
contrast. Barium is safe and
useful when there is no evidence
of bowel ischemia or perforation.
Barium has been associated with
peritonitis and should be avoided
if perforation is suspected.
Laboratory investigations are useful for evaluating the
general condition of the patient, the metabolic changes,
establishing the therapeutic guides and also have some
prognostic significance.
Usually performed: CBC, proteinemia, electrolytes,
serum urea and creatinine, blood pH and acid-base
balance parameters, alkaline reserve.
Note that haemoconcentration may mask some
electrolyte disorders.
POSITIVE DIAGNOSIS of intestinal occlusion is
based on:
1. abdominal pain
2. intestinal transit stop
3. vomiting
4. abdominal distension
5. fluid-air levels on abdominal Rx
Preoperative diagnosis must also specify:
1. obstacle location (high or low occlusion)
2. existence or absence of strangulation (vascular
impairment)
3. occlusion etiology (can not be determined
preoperatively in all cases)
4. metabolic complications
DIFFERENTIAL DIAGNOSIS
Criteria High level occlusion Low level occlusion

Vomiting Occur rapidly after pain Occur late after pain or

even are absent

Intestinal transit Occurs late (gas and stool Rapid onset (rectal ampulla
stop emission is still possible is empty)
from lower intestinal
segments)
Dehydration Rapid Late

General condition Rapid altered Remains relatively good for

a long time (1-2 days)
Abdominal Absent or not very evident Important
distension and with central location
Colicky abdominal Intermittent at 3-5 minutes Intermittent at 5-10 minutes
pains features interval interval
 Criteria High level occlusion Low level occlusion

Rx images aspect Small, numerous, centro- Large, rare and with

abdominal fluid-air levels peripheral location fluid-air
levels
Age Frequent in young patients Frequent in elderly due to
tumors of the colon
History Crohn disease, TB, Colon cancer
laprotomies

Criteria By strangulation By obstruction

Pain Sudden onset Insidious onset

Continuous Colicky
General condition Rapidly altered Slow alteration
Peritonitis Relatively frequent and Is possible but in advanced
rapid due to intestinal and complicated cases
necrosis and perforation especially due to diastatic
perforations
Other differential diagnosis:
1. Pseudo-occlusive appendicitis in elderly
– Signs of paralytic ileus are predominant
– Right iliac fossa pain with muscular defense and
hyperleukocytosis
2. Acute cholecystitis (with or without perforation)
– History
– Right upper quadrant pain, muscular defense in right
hypochondrium
– Ultrasound reveals biliary stones
3. Acute pancreatitis
– Location of pain is usually epigastric, radiating in transverse
direction (to the left and right upper quadrant) and often to the
lower back region
– The presence of “red” shock
– Increased amylasemia and amylasuria
– CT examination reveals the pancreas alterations
4. Entero-mesenteric infarction
– Elderly patients, cardiac rhythm disorders
– Sudden onset, deep presacral pain, pseudo-occlusive
syndrome, false syndrome of internal bleeding
5. Perforated peptic ulcer
– Patient history
– Pneumoperitoneum
– Fever, hyperleukocytosis
6. Renal colic
– When it is violent it is accompanied by reflex ileus
– Location of pain (lumbar), radiation to the external genitalia,
accompanying urinary signs (hematuria, dysuria), suggest the
diagnosis
– Abdominal radiography, urography and ultrasound specify the
diagnosis
7. Acute retention of urine
– Elastic tumor in the hypogastrium
– Ultrasound examination
– Urinary catheterization solves the problem
8. Acute stomach dilatation
– Distension located in the epigastrium
– Pain is continuous
– Hiccups, vomiting
– Splashing sound of the stomach (clapotage)
– X-ray: unique bulky fluid-air level in left upper quadrant
9. Ascites
– Hepatic decompensation, acute renal failure
– Abdominal pain, abdominal distension, vomiting
– History and ultrasound help the diagnosis
10. Hysterical and psychogenic symptoms
– May be accompanied by abdominal distension
– Disappears when patient’s attention is distracted during
examination
TREATMENT
All the patients with bowel obstruction should be admitted
to the surgical service, preferably in the intensive care unit.
Three catheters are applied:
1. Central venous catheter – as a route for fluids and drugs
administration and also for central venous pressure monitoring
2. Naso-gastric – for emptying the stomach and preventing aspiration.
Also for monitoring the quantity and quality of lost fluids.
3. Urinary - to monitor the urine output.
Preoperative preparations:
1. Fluid rebalancing
Loss of fluids must be taken in account, assessed objectively
(gastric aspirate, diuresis, vomiting)
Fluids (5% dextrose and saline) will be administered until the
resumption of normal diuresis (1 ml / minute)
If the patient is shocked, blood or plasma should be
administered
High quantities of fluids will be administered with caution in
elderly (risk of cardiac insufficiency and acute pulmonary
edema)
2. Electrolyte rebalancing
Is based on administration of electrolyte solutions (NaCl, KCl,
Ringer, Saline, etc)
In case of acidosis, serum bicarbonate should be administered
If there is alkalosis with hypochloremia (due to vomiting) 5%
arginine hydrochloride will be used
3. Nutrients rebalancing :
10% glucose (dextrose) solution (buffered with insulin: a unit / 2 g
glucose);
Amino acid solutions
Solution of soluble lipids
Combined solutions
4. Oxygen
5. Antibiotics
6. Associated diseases will be treated (heart, lung, liver)
Rebalancing will continue until the return of pulse rate
and blood pressure as close to normal values, the
resumption of diuresis and improvement of biological
constants. It is required and will be continued also
postoperatively.
 Objectives:
1. Removing or bypassing the obstacle
2. Evacuation of intestinal content and peritoneal
effusions
3. Relapse prevention
4. Treating injuries:
a) Small bowel occlusions
Adhesiolysis
Devolvulation
Reduction of internal strangulated hernias
Removal by enterotomy of biliary stone or foreign body
Bowel resection (when the loop is not viable)
Ileostomy or intestinal bypass (when lesions can not be
removed)
Enteroplication (in patients with intense adhesive syndrome or
recurrent occlusions)
b) Large bowel occlusions
There are two most common situations:
1. The sigma volvulus
Devolvulation and enteropexy (suturing the loop to the abdominal wall to
prevent recurrence)
Resection (followed by end-to-end anastomosis -or, Hartmann’s I operation,
followed by restoration of digestive continuity (Hartmann’s II) after 2-3 weeks);
2. Colon cancer
If the tumor can not be removed:
External diversion – colostomy or ileostomy
Internal diversion (by-pass): ileo-colic bypass
If the tumor can be removed:
Right hemicolectomy
Segmental colon resection
Left hemicolectomy
Subtotal colectomy
Hartmann’s I operation
If patient's general condition is very impaired, we can perform seriated
operations - the first step is represented by a simple colostomy of
diversion which resolves the occlusion. The second step, after
patient’s recovery, is represented by radical surgery.
PROGNOSIS
Negative prognostic factors in the evolution of
intestinal occlusion:
1. The high level of obstruction
2. Occlusion by strangulation
3. Patient’s history (associated illnesses)
4. Elapsed time between onset of occlusion and
surgery
 Particular forms of intestinal
occlusion
INTESTINAL INTUSSUSCEPTION AND SMALL
INTESTINE VOLVUSUS – are described in chapter
of small intestine pathology
COLONIC VOLVULUS
Represents approximately 5% of all cases of intestinal
obstruction and 10-15% of all large bowel obstructions.
The most common site of large bowel torsion is the
sigmoid colon (80%), followed by the cecum (15%),
transverse colon (3%), and splenic flexure (2%).

VOLVULUS OF THE SIGMOID COLON

It is produced by twisting around its axis
Patients with a long and mobile sigmoidian loop are
prone
The cause of torsion may be a congenital peritoneal or
acquired postoperative adhesion band (strap) or the
Meckel’s diverticulum. The presence of a pelvic mass
also increases the risk of developing sigmoid volvulus.
The mass displaces the sigmoid colon sufficiently to
result in torsion of the mesentery and a resultant
volvulus. The association of pregnancy and large ovarian
tumors with sigmoid volvulus is well known.
Is more common in men aged over 50. A higher
incidence of the condition is observed in patients with
Parkinson disease, multiple sclerosis, or spinal cord
injury.
Torsion can be partial or complete (360 °)
A complete volvulus leads to the development of a
closed loop obstruction of the affected colonic segment.
Torsion of the mesosigmoid quickly leads to ischemic
changes of the bowel wall, followed by rapid necrosis
and perforation.
The onset is sudden with violent pain located mainly in
left iliac fossa. On inspection asymmetric abdominal
distension can be observed. The VON WAHL triad is
represented by:
1. Tumor that mimics a balloon
2. Hyper-sonority on percussion
3. Elastic resistance on palpation
Depending on the extent of bowel ischemia or fecal
peritonitis, signs of systemic toxicity may be apparent.
Because of the massive abdominal distension, the patient
may have respiratory and cardiovascular function
compromised.
On plain abdominal Rx
images the twisted loop forms
two large compartments with
a central double wall ending
at the point of the twist --
"coffee bean" sign.
CT scanning is not often
needed, since the plain
radiographic findings are
typical for sigmoid volvulus.
Treatment
Sigmoidoscopy may be used to successfully detorse
and decompress sigmoid colon volvulus in as many as
90% of patients.
The sigmoidoscope or colonoscope is advanced into the
rectum under direct vision. The rectum is insufflated to
allow good visibility and identification of the apex of the
volvulus. Occasionally, the pressure of the air causes
detorsion, reducing the volvulus.
If detorsion does not occur, the spiraling rectal mucosa is
followed upward to the apex, and a soft rectal tube is
passed up through this under direct vision. The tip of the
endoscope can also be used to apply constant pressure
at the apex, which can lead to detorsion and
decompression.
 Surgical treatment
Is indicated in the following situations:
1. In emergency when there are signs and symptoms of intestinal
loop necrosis and / or peritonitis
2. When detorsion failed by endoscopic approach
3. When ischemic lesions are found at endoscopy
Procedures
1. Detorsion and colopexy when the sigmoid loop is viable
2. Hartmann’s I procedure when there are ischemic lesions and
anastomosis is dangerous due to peritonitis
3. Resection followed by colo-rectal anastomosis (hand sewn or
stapled)
VOLVULUS OF THE CECUM
It is much less common than sigmoid volvulus,
predominately affecting women in the sixth decade of
life.
It is due to congenital incomplete posterior fixation of the
cecum or ascending colon associated with an
abnormally mobility.
Adhesions and appendicitis are favoring factors.
Gaseous dilation of sigmoid colon and cecum following
colonoscopy has also been described as a cause of
volvulus.
Cecal volvulus may be organoaxial (cecal or cecocolic
volvulus) or mesentericoaxial (cecal bascule).
In organoaxial volvulus vascular integrity is commonly
affected because of mesenteric torsion. In contrast, in
cecal bascule which occurs when the malfixed cecum
folds anteriorly over the ascending colon the
vascularization is rarely affected, only when the cecum is
very distended.
Clinical picture
The patient may describe previous episodes of
abdominal pain, distension, and obstipation suggestive
of repeated, subclinical episodes of volvulus. After that, a
violent pain installs brutally, located on the right side of
the abdomen. Intestinal transit stops and asymmetrical
abdominal distension appears. (Von WAHL triad). The
right iliac fossa is depressed due to the absence of the
cecum.
Imaging
Cecal volvulus produces large and small bowel
obstruction. Radiographic findings reveal a markedly
distended loop of bowel extending from the right lower
quadrant upward to the left upper quadrant. The small
bowel is distended, whereas the distal colon is
decompressed.
A foldlike termination may be observed at the point of
obstruction in the ascending colon in patients with cecal
volvulus at barium enema examination.
Treatment
1. Endoscopic decompression is successful in only 15-20% of
patients
2. Right hemicolectomy – the most recommended procedure
3. Other procedures: cecostomy, cecopexy
Mesenterico axial volvulus of the cecum
Plain abdominal radiogram

Ce
cu
m

Empty zone
BILIARY ILEUS
Is an obstructive occlusion.
Is produced by the passage of a biliary calculus in the
digestive tract (through a choledocus-duodenal fistula
or cholecysto-gastric or cholecysto-duodenal fistula).
Big calculus stops more frequently in the duodenum
(Bouveret syndrome), in the Treitz angle, the terminal
ileum or more rarely in the jejunum.
Symptoms have three distinct phases:
1. biliary colic, fever and jaundice characteristic for bilio-
digestive fistula
2. free interval
3. occurrence of occlusive syndrome with violent abdominal
colicky pain
Radiology, highlights fluid-air levels, and sometimes
pneumobilia.
 pneumobilia

Calculus
Fluid-air levels

Plain abdominal Rx CT scan

In most cases this is an
intraoperative surprise
Enterotomy – removal of the
stone – enteroraphy.
Hepatobiliary region must be
explored and lesions treated as
necessary.
POSTOPERATIVE OCCLUSIONS
Immediate occlusions
Almost exclusively mechanical
Are produced by gaps or breaches remaining after surgery in
transverse mesocolon, mesentery, omentum – internal hernias
Rises delicate differential diagnosis problems with acute dilation of the
stomach
Early occlusions
Occur within the first 4-7 days postoperatively (adhesions, internal
hernias, etc)
Have an increased rate of mortality
Symptoms are diminished especially by pain medication
Late occlusions
Always mechanical
Causes:
– Adhesion bands
– Extensive adhesions
– Local tumor recurrence
– Metastases
– Radiotherapy (enteritis radica)
MESENTERIC VASCULAR
DISEASE

Acute Mesenteric Ischemia

 ANATOMY
Arterial supply of intestine
Venous drainage of the Lymphatic drainage of the small
small intestine intestine
 Mesenteric vascular disease
This condition includes:
1. Mesenteric artery stenosis or complete obliteration by
emboli, thrombi or other causes
2. Mesenteric vein thrombosis
3. Extralumenal mesenteric artery obstruction due to
aortic aneurysm, dissecting aneurysm, tumors or
compressive adhesion
4. Splachnic artery aneurysms
5. Mesenteric vascular trauma
Mesenteric artery obliteration may be:
– acute or complete (thrombi and emboli),
– gradual or partial (obliterans arterial disease)
The presence of collateral arteries permit a well tolerated
asymptomatic gradual obliteration of the celiac trunk or
superior mesenteric artery and an acute inferior
mesenteric artery obliteration, while an untreated acute
superior mesenteric artery obliteration, leads to intestinal
infarction and death.
Obliteration of venous circulation is usually sudden and
complete, and invariably the result is a thrombosis.
Partial obliteration of mesenteric venous circulation is
usually the result of extrinsic compression and is
asymptomatic.
Obliteration of one of the circulatory system (arterial or
venous) induces the formation of clots (thrombus) in the
other.
Clinical differentiation between arterial and venous
thrombosis is very difficult.
It is estimated that 15-20% of all mesenteric vascular
accidents are due to mesenteric venous thrombosis and
about 50% to arterial thrombosis. The remaining 30-35%
of cases, intestinal infarction occur in the absence of
clear evidence of arterial or venous thrombosis.
Acute mesenteric ischemia
The four major causes of acute mesenteric ischemia
and their incidence are:
1. Superior mesenteric artery embolism (50%)
2. Thrombosis of superior mesenteric artery (15-25%)
3. Mesenteric venous thrombosis (5%)
4. Ischemia without vascular occlusion (20-30%)
Due to local anatomical conditions, typically, the
embolus fixes at the origin of the artery or in one of its
main branches.
Superior mesenteric artery thrombosis typically occurs
at its origin as a consequence of the atheromatous
plaques progression toward complete obliteration.
 Specific risk factors in producing a superior mesenteric
artery stroke are:
1. Old age
2. Atherosclerosis
3. Pathologic conditions with low cardiac output
4. Cardiac arrhythmias
5. Severe cardiac valvulopathy
6. Recent myocardial infarction
7. Abdominal malignancies
PATHOPHYSIOLOGY
Complete or almost complete obstruction of the superior
mesenteric artery causes a spasm in the entire
mesenteric vascular system.
Complete obstruction of the artery will produce
ischemia of intestinal territory from Treitz ligament to the
third left transverse colon. The first 10-12 cm of jejunum
remain, even in these conditions, viable due to vascular
arcades between the superior (from the celiac trunk) and
inferior pancreatico-duodenal arteries (first branch of the
superior mesenteric artery).
Complete occlusion of distal branches (middle colic,
right or ileo-colic) produces segmental ischemia and can
lead to infarction or not, depending on the collateral
arteries status.
Since the mucosa is the layer most sensitive to
ischemia, ulceration and erosion, often manifested
clinically by gastrointestinal bleeding, are the first
manifestations of ischemia and can be identified
endoscopically.
Peristalsis may remain unaltered hours after the onset of
ischemia.
As the process progresses, about 6 hours after the
onset, intestinal wall darkens, becomes cyanotic and
then ultimately gangrenous with multiple perforations.
Bowel ischemia and infarction by mesenteric venous
obstruction can easily be distinguished during operation
from those due to arterial obstruction as the bowel wall is
extensively hemorrhagic and oedematous and
mesentery is more thickened. The mesenteric venous
thrombosis is more virulent in evolution and more difficult
to treat than arterial thrombosis.

mesenteric venous obstruction

 Septic shock and multiple organ failure may occur in
intestinal ischemia in the absence of complete necrosis
or perforation of the intestinal wall due to bacterial
translocation and through the phenomenon of auto-
immune aggression.

CLINICAL MANIFESTATIONS
Regardless of etiology, acute mesenteric ischemia is
characterized by constant abdominal pain in
discordance with other local signs. The pain starts
suddenly, is intense and diffuse, may be accompanied
by vomiting and does not reduce at antialgic
medication. The presence of occult bleeding in the
stool or bloody diarrhea is a late manifestation
indicating the presence of mucosal necrosis and signs
of peritoneal irritation mark the presence of complete
infarction of the bowel wall.
 Patient’s history (atrial fibrillation, atherosclerosis, heart
infarction, strokes etc.) is very important in presuming
the diagnosis.
INVESTIGATIONS
There are no specific laboratory examinations for
intestinal ischemia, so the diagnosis is more one of
presumption based on clinical criteria.
– leukocytosis
– haemoconcentration
– metabolic acidosis with increased serum lactate
– increase in serum amylase and creatine kinase shows wall
necrosis and is usually a late sign
– alpha glutathione s-transferase (alpha-GST) and intestinal fatty
acid-binding protein (I-FABP) are grown in over 70% of cases
Plain abdominal radiography usually does not reveal
anything pathological in 25% of cases.
Suggestive signs could be: distended intestinal loops,
absence of colon haustres due to submucous edema,
bowel wall thickening (in venous thrombosis) and / or the
presence of air in the intestine (in advanced stages of
disease). Making a barium-passage is contraindicated
because it provides little information and interferes with the
angiographic images.
Selective arteriography, with contrast of superior
mesenteric artery and targeted exploration remains the
only conclusive exploration in patients suspected of
mesenteric ischemia.
Making emergency selective mesenteric artery
arteriography and medication administration by direct
infusion therapy is the basis for aggressive acute
mesenteric ischemia diagnosis and treatment, made by
Boley and colleagues since the early '80s.
Abdominal plain radiograph – distended intestinal loops,
bowel wall thickening (arrow) and separation of loops,
characteristic aspects of intraluminal bleeding.
Arteriography almost
always is able to
distinguish between
embolism or thrombosis,
which is of paramount
importance in choosing
the type of surgery. Also,
it can diagnose
mesenteric ischemia
without vascular
occlusion, which is
suitable for medical
treatment.
Selective arteriography of SMA. Selective arteriography of SMA.
Arrow shows the obstruction under Arrow shows the obstruction of
the emergence of the right colic SMA
artery
DIFFERENTIAL DIAGNOSIS
Acute pancreatitis and intestinal obstruction by
strangulation can pose differential diagnosis with acute
mesenteric ischemia. Increased levels of amylasemia on
the onset of disease and increased pancreatic volume at
CT can make the diagnosis of acute pancreatitis.
Differential diagnosis with occlusion by strangulation is
less important, because both conditions require surgery.
In more than 50% of cases, even experienced surgeons
can not make an early diagnosis of intestinal ischemia.
TREATMENT
The main goal of acute mesenteric ischemia treatment is
to restore the discontinued blood flow as quickly as
possible.
The first therapeutic measures are aggressive
hemodynamic monitoring, correction of acidosis, broad-
spectrum antibiotics and bowel decompression by
gastric aspiration.
Anticoagulants should be given to prevent the formation
or extension of thrombosis in all patients without active
bleeding and postoperative.
Emergency surgery is indicated in patients with
suspected clinical or paraclinical intestinal perforation or
gangrene.
 If at intra-operative exploration, intestinal necrosis is
generalized than nothing can be done.
Intestinal resections
To allow survival, at least 50 cm of viable intestine
(preferably 100) are needed. Assessing the viability is
made by palpation of mesenteric pulse and in case of its
absence, mesenteric revascularization will be tried
before resection.
In limited bowel necrosis, intestinal resections are more
or less extensive (segmental enterectomy associated
with right hemicolectomy - if right colon is also affected-
and jejuno-transversostomy).
Angiography (stenting, embolectomy)
In patients whose diagnosis is unclear, making
angiography is imperative to specify the diagnosis and
for possible therapeutic intervention.
Angiography allows the initiation of treatment by direct
intra-arterial infusion of vasodilators and thrombolytic
agents, but also performing endoscopic maneuvers such
as angioplasty, stenting or embolectomy.
As a general rule, intra-arterial papaverine administration
is indicated in all forms of mesenteric ischemia because
vasoconstriction accompanies all forms of ischemia and
persists several hours after resumption of blood flow.
Papaverine may be administered intra-arterial 5 days.
Treatment of mesenteric arterial embolism
The classic treatment of superior mesenteric artery
embolism is laparotomy and embolectomy.
Making an embolectomy involves performing a distal
arteriotomy, retrograde introduction of the catheter
(Fogarty catheter) above the embolus, inflation of the
balloon and carefully extracting the emboli by catheter
retraction.
Then intestines are examined to assess viability and areas
of necrosis are removed.
Intraoperative Doppler ultrasound can be performed to
identify persistent ischemia.
Postoperative administration of papaverine can reduce
vascular spasm.
Sometimes it is required reintervention after 24-48 hours
for resection of ischemic segments of the bowel.
Prevention of new embolic episode is performed by early
mobilization, treating the condition generating the emboli
and administration of anticoagulants.
Treatment of mesenteric arterial thrombosis
Treatment is mainly surgical.
Thrombectomy alone is not effective for long term
because of the existence of atherosclerosis process
responsible for producing thrombosis, thus
thrombectomy is accompanied by mesenteric
revascularization procedures (bypass grafting, superior
mesenteric artery reimplantation into aorta, etc.) and
resection of necrotic bowel segments.
Superior mesenteric artery reconstruction is a procedure
with success rates of 77-79% for long term, despite the
immediate post-operative mortality of 52%.
Conservative treatment in such cases is to keep the
patient under observation and under the protection of
anticoagulants.
Treatment of mesenteric venous thrombosis
Standard treatment in these cases is the administration of
heparin and resection of necrotic bowel segments. Heparin is
administered even in patients with gastrointestinal bleeding if
intestinal infarction risk is higher than that of bleeding.
As with arterial thrombosis in patients with sufficient collateral
mesenteric flow, angiographically proven, treatment may be
conservative (heparinization and monitoring).
Administration of papaverine is indicated in cases of
subsequent venous thrombosis due to coexisting arterial
spasm.
Laparotomy for bowel viability assessment is also
recommended.
Venous thrombosis prophylaxis with anticoagulants (wafarin) is
indicated for at least 6 months.
Thrombolysis with streptokinase or urokinase administration
through the catheter was successfully applied in a small number
of cases.
Treatment of mesenteric ischemia without
vascular obstruction
Initial treatment consists in administration of papaverine
through the angiography catheter left in place and
treatment of the causes that produced vasoconstriction.
In patients without peritoneal signs, repeat angiography
after 24 hours to assess vasoconstriction. Some authors
indicate also administration of heparin to prevent
catheter endovascular thrombosis.
Laparotomy is indicated only in patients with peritoneal
signs, but papaverine is continued postoperatively.
Prophylaxis in such cases is aspirin.
PROGNOSIS
Mesenteric vascular obstruction is often fatal because of
delays in diagnosis and treatment, rapidly extension of
infarction to large territories and difficulty of intestinal
revascularization.
The average mortality ranges from 24-45%, and for
infarctions affecting over half of the length of the
intestine, it increases to 45-85%.
Arterial reconstruction is often technically impossible and
when is performed, is not feasible for long term.
Mesenteric venous thrombosis has a mortality rate of
30% and in the absence of long term therapy with
anticoagulants, about 25% of those who survive develop
a recurrent thrombotic episode.
ABDOMINAL TRAUMA
Background
Trauma is the third cause of death after cardiovascular
diseases and cancers, and up to the 4th decade of life is
the first cause.
The abdomen is one of the most involved part of the
body in trauma, requiring surgical exploration in up to
20% of cases.
Globally, injuries account for 10% of all deaths.
In 1990, approximately 5 million people died worldwide
as a result of injury. Estimations indicate that by 2020,
8.4 million people will die yearly from injury, and injuries
from traffic collisions will be the third most common
cause of disability worldwide and the second most
common cause in the developing world.
Data from the World Health Organization (WHO) indicate
that falls from heights of less than 5 meters are the
leading cause of injury, and car crashes are the next
most frequent cause.
According to national and international data, blunt
abdominal trauma is more common in men. The male-to-
female ratio is 6:4.
Penetrating abdominal trauma involves the penetration
of abdominal wall and violation of the abdominal cavity
by a gunshot or stab wound. The management of
penetrating abdominal trauma has evolved greatly over
the last century. Laparotomy has become the treatment
of choice during World War I, but mortality remained
high. By World War II, early laparotomy resulted in a
survival rate close to 50%.
In recent decades great progresses have been made in
many areas, progresses that increased the rates of
survival after penetrating abdominal trauma:
development of antibiotics, anesthesia methods of
investigation, resuscitation, transportation, surgical
treatment and so on.
The frequency of penetrating abdominal injury across the
globe relates to the industrialization of developing
nations, weapons available, and, significantly, to the
presence of military conflicts. Therefore, frequency
varies. From 1990 to 1995, firearm mortality rates across
the world vary widely, from 0.05 in Japan to 14.24 in the
United States.
Males constitute the great majority of patients with
penetrating trauma.
Injuries are the leading cause of death in patients aged
1-44 years.
 CLASSIFICATION
Abdominal trauma may be classified as BLUNT (closed)
and PENETRATING (open) (wounds).

1. Blunt trauma (Contusion):

– Traffic accidents (most common 50-75%)
– Falls
– Aggressions
– Accidents
– Sport (recreational) and domestic accidents
– Iatrogenic (resuscitation, Heimlich maneuver)
2. Penetrating trauma (Wounds):
– Stab wounds
– Gunshot wounds
 BLUNT TRAUMA
Abdominal cavity can be arbitrarily divided into four areas
where organs are more or less protected by anatomical
structures from external injuries.
1. The upper abdomen (“intrathoracic”) beneath and protected by
ribs cage containing the liver, gallbladder esophagus, stomach,
duodenum, spleen.
2. The lower abdomen or pelvic, protected by pelvic bones
containing the: bladder, uterus with annexes, rectum, some small
intestines
3. The retroperitoneal area containing the kidneys, ureters and
suprarenal glands, pancreas, duodenum, aorta and cava vein.
4. Anterior middle part of the abdomen, the most exposed to trauma
containing small and large intestine, omentum, part of the
stomach.
Pathophysiology
Blunt trauma is produced by collision between the
organism and external agent. There are 3 mechanism
acting during collision:
1. Deceleration – induces high tensions in the fixing
points of intra-abdominal organs resulting in breaking of
fixing anatomical structures of these organs or of the
organ itself. Classic deceleration injuries include hepatic
tear along the coronary ligament, injuries to the renal
pedicles, and mesenteric tears, with resultant of
splanchnic vessels injuries.
2. Crushing - intra-abdominal organs are crushed
directly between the anterior abdominal wall and the
vertebral column or posterior thoracic cage, or as a
result of deceleration. This affects especially solid
viscera such as spleen, pancreas, liver, kidneys.
3. External compression – produces injuries directly to
the abdominal wall and solid intra-abdominal organs or
by rising the intracavitary pressure in hollow viscus may
produce their explosion (blow up).
The liver and spleen and then the small and large
intestines are the most frequently injured organs.
Contusions limited to the abdominal wall
Over 50% are associated with visceral lesions, and may
manifest as:
Sero-hematic Morel-Lavallee effusion: is the result of
tangentially abdominal wall trauma, with accumulation of
sero-hematic fluid under the skin and above the fascial
plane. It appears as a local swelling, bruising and
associated with fluctuence. Treatment includes
percutaneous drainage or in case of massive
accumulation, incision and drainage under antibiotic
protection.

Ultrasound examination
Sub-aponeurotic hematoma: is due to the rupture of
muscles and is frequently located in the sheath of the
rectus abdominis. Symptoms consist of pain
exacerbated by physical activity. Local signs are:
swelling, bruising and sometimes in the extensive forms
transit disorders and pseudo-occlusive syndrome.
Diagnosis is confirmed by ultrasound examination.
Treatment can be conservative (ultrasound guided
puncture, local ice bag application) when intra-abdominal
organs injuries are excluded, or incision and drainage in
case of massive accumulation. When the hematoma is
associated with intra-abdominal injury, laparatomy is
required.

Ultrasound examination
Properitoneal hematoma: appears after important
anterior contusion being associated with muscle
ruptures, subaponeurotic hematoma and intra-
abdominal organs injuries. It induces a peritoneal
irritation syndrome and paralytic ileus. Usually is
treated surgically by laparotomy and thorough
exploration of intra-abdominal organs.
Posttraumatic hernias: appear after abdominal
trauma associated with rupture of the muscular layer.
The clinical aspect is of a reducible swelling usually
associated with local bruising. The diagnosis is
facilitated by ultrasound examination which reveals the
parietal defect. The treatment is strictly surgical as in
incisional hernias.
Posttraumatic eviscerations: appear as a result of a
complete rupture of the abdominal wall interesting the
peritoneum and the skin. It is an emergency because is
always associated with general peritonitis as intra-
abdominal organs are exposed to air. The treatment
consists of wall reconstruction but also thorough
inspection of the abdominal cavity and abdominal
organs.
Evisceration
Contusions (blunt trauma) with visceral
lesions

Usually lesions of the internal organs are produced

by complex mechanisms (presented above:
deceleration, external compression, crushing)
Lesions will be presented later, separately for each
organ.
From pathophysiological point of view, 3 types of
abdominal syndromes may occur:
1. Intraperitoneal hemorrhagic syndrome
General signs: tachycardia, hypotension, dizziness
followed by tendency to collapse, pale skin, and
oliguria.
Local signs: distended abdomen, mild diffuse pain,
mild muscular defense, abolition of bowel movements.
2. Peritoneal irritation syndrome (post-traumatic
peritonitis)
The classic signs are those of a generalized peritonitis.
These two syndromes may develop simultaneously while
the predominant usually is the hemorrhagic syndrome.
3. Late clinical syndromes in which the lesions are
clinically manifested after a more or less asymptomatic
period.
A. The “two-stage hemoperitoneum” – the first stage is
represented by the subcapsular rupture of a
parenchymatous organ, followed by capsule rupture,
after a while, with the appearance of intraperitoneal
bleeding.
B. The “two-stage peritonitis” – the first stage is
represented by the organ trauma and then, the
peritonitis, as the second stage, may occur as a result
of:
– a parietal eschar (decubitus sores) due to necrosis or
compressive hematoma.
– bacterial translocation: appears in traumatic shock when oral
feeding is resumed after a long time.
– necrosis of the intestine due to ischemia as a result of vascular
injuries (ruptures, compressive hematoma of mesenteric
desinsertion with a segmental bowel ischemia).
C. Localized peritonitis: intraperitoneal abscess.
D. Intestinal obstruction by internal hernia (for example a breach
in the mesentery as a result of the abdominal trauma – see at
hernia chapter)
 Penetrating abdominal trauma -
abdominal wounds
Abdominal wounds represent a solution of continuity of the
abdominal skin.
There are two types : penetrating abdominal wounds
when the entire abdominal wall thickness is penetrated and
there is a communication between the peritoneal cavity and
the atmospheric air, and non-penetrating wounds when
only some layers of the abdominal wall are injured but not
the peritoneum.
Non-penetrating wounds may be:
– Simple without association with contusion of the intraabdominal
organs
– Associated with visceral lesions
Penetrating wounds may be:
– Simple without visceral injuries
– With a visceral involvement
– Complex within a polytrauma
Etiopathogenesis:
Wounds caused by firearms (gun shot wounds) Are
characterized by an important transfer of energy and the
impossibility to appreciate the exact extent of intra-
abdominal lesions. The amount of energy transferred
depends on:
1. missile speed
2. missile shape (irregularly shaped splinters cause more serious
injuries)
3. occurrence of secondary missiles (the missile fragments or
fragments of tissue displaced by it)
4. shooting distance
In penetrating abdominal trauma due to gunshot, the
most commonly injured organs are as follows:
1. Small bowel (50%)
2. Colon (40%)
3. Liver (30%)
4. Abdominal vascular structures (25%)
Wounds caused by weapons (stab wounds): they are
more common, and generally, intra-abdominal organ
injuries are more predictable. Usually a single organ is
affected but however, occult injuries can be overlooked,
resulting in devastating complications.
In penetrating abdominal trauma due to stab wounds,
the most commonly injured organs are as follows:
1. Liver (40%)
2. Small bowel (30%)
3. Diaphragm (20%)
4. Colon (15%)

In abdominal trauma the prognosis is correlated with the

number of injured organs, the speed of diagnosis and of
establishing the therapeutic measures.
Diagnosis of abdominal trauma is associated with first
aid measures, measures to maintain vital functions and
to combat the shock.
Priorities in diagnosis and treatment of abdominal
trauma can be grouped in this order:
1. Recognition of the presence of shock or intra-peritoneal
hemorrhage
2. Starting resuscitation measures
3. Assess the cause of shock or hemorrhage (abdominal / extra-
abdominal)
4. Asses the need for emergency laparatomy
5. Completion of secondary examination (laboratory tests) to
detect occult lesions
6. Frequent reassessment: to follow the evolution of the patient
and the possibility of undetected lesions or to detect late lesions
(2 or 3 stages lesions).
History
Sometime impossible or difficult to obtain in dizziness
or unconscious patients.
Obtain information about:
1. The nature and circumstances of injury
2. The time when it occurred
3. The status of the patient at the time of trauma:
physiological (food, stool, urination, pregnancy)
pathological (associated diseases, allergies, previous
interventions, ingestion of medicines or drugs)
4. Pain: timing, location and radiation, the evolution in time.
5. Other symptoms or signs: hematemesis, melaena, rectal
bleeding, hematuria.
Physical examination
Primary survey
Evaluate the mnemonic ABCDE: Airway, Breathing,
Circulation, Disability, and Exposure/Environment. Much of
this evaluation may be performed simultaneously and
problems identified are managed immediately.
The airway is the first to be evaluated for patency, protective
reflexes, foreign body, secretions, and injury.
Breathing is assessed by determining the patient's
respiratory rate, the depth and effort of inspiration.
The circulation assessment begins with an evaluation of the
patient's mental status, skin color, and skin temperature.
Patients in significant hemorrhagic shock will progress from
anxiety to agitation and finally coma if their blood loss
continues unabated. The traditional vital signs of heart rate,
blood pressure, and respiratory rate are not sensitive or
specific for hemorrhagic shock.
Patients without recordable cardiac activity upon
presentation should not be further resuscitated.
Disability is assessed for neurologic deficits before giving
sedation or paralytics. The Glasgow Coma Score and
the gross motor and sensory status of all 4 extremities
should be determined and recorded.
Exposure is very important especially in the patient with
polytrauma. Complete exposure and head-to-toe
visualization is mandatory to discover other potentially
life-threatening injuries.
Once the primary survey is complete, a complete head-
to-toe physical examination is performed as an integral
part of the secondary survey. This detailed examination
may need to be delayed until after operative therapy has
corrected obvious life-threatening injuries.
Secondary survey and injury assessment
Inspection may reveal:
1. Skin lesions (please note the number, location,
dimensions, shape), which can help us to predict the
injured intra-abdominal organ. Multiple wounds may
represent either entrance or exit wounds and must not
be labeled as such, since multiple missiles or foreign
objects may be retained within the body.
2. Abdominal distention, which may mean a bowel
obstruction or hemoperitoneum.
3. A visible mass: which may represent a massive
abdominal hematoma, a traumatic hernia or intra-
parietal collection.
4. A leak through the wound of pathological fluid: blood,
intestinal content, urine.
Palpation:
Parietal injury: a reducible swelling confirms the
traumatic hernia, the presence of fluctuence confirms a
parietal collection
The most important signs are: localized pain, muscle
tension or defense which reveal the peritoneal irritation.
Blumberg maneuver: pain on sudden decompression of
the abdomen as a sign of peritonitis
There are circumstances in which signs of peritoneal
irritation may be misleading or missing:
– False acute abdomen - injuries of the spinal cord, of the base of
thorax, properitoneal hematoma - to be distinguished from true
peritoneal irritation.
– Lack of signs of irritation in patients with severe shock, coma,
poisoning by drugs or alcohol.
Percussion:
– Shifting dullness in lateral quadrants is a sign of intraperitoneal
fluid collection, most often blood.
– Tympanic sound: possible bowel obstruction.
– Induced pain on percussion (Mandel positive maneuver), means
peritoneal irritation.
Auscultation:
– Absence of bowel sounds: peritonitis
– Exacerbation of bowel sounds: mechanical obstruction
– Arterial murmurs: large vessel lesions
– Bowel sounds in the thorax: diaphragmatic rupture
Rectal and vaginal finger examination is mandatory and
can detect:
– Pain induced by palpation of the Douglas pouch: confirms
peritoneal fluid collection and may be associated with
transvaginal or transrectal puncture.
– Local deformation: fractures of the pelvic bones
– Changes of the anal sphincter tone
 Wounds located on the anterior abdomen can be
explored locally to determine whether they penetrate the
peritoneum. On the flank area and back area,
exploration is more difficult and less reliable. Therefore,
flank and back wounds are not explored and are
considered penetrating unless obviously superficial.
Paraclinical investigations
The most important, which in conjunction with clinical
examination may recommend surgical exploration are:
peritoneal lavage and CT scan. In Europe in the first
preferred examination is abdominal ultrasound.
Laboratory tests:
Blood count and blood group (required even if in the first
stage there is no obvious important bleeding).
Leukocytosis, even in the presence of a normal
hemoglobin and hematocrit may reveal haemorrhage.
Coagulation tests and platelets count are important for
further therapeutic decisions.
Amylasemia may be increased in posttraumatic
pancreatitis without a direct correlation with the severity of
injuries.
Transaminases, LDH, gamma GT, can increase in liver
damage.
Urinalysis to detect a hematuria.
Blood glucose, urea and creatinine, electrolytes and
routine tests are to be interpreted in evolution.
Detection of medicines and drugs levels in biological
fluids.
Abdominal ultrasound
It is important because it can be done at bedside in
unstable patients.
The main disadvantage is the lack of sensitivity especially
in penetrating trauma. Some deep lesions could go
unnoticed especially in uncooperative patients with
significant gaseous abdominal distension.
FAST (focused assessment with sonography for trauma)
uses 4 views - of the chest and abdomen (ie, pericardial,
right upper quadrant, left upper quadrant, pelvis)
Ultrasound signs of lesions are:
– The presence of free liquid in the Douglas pouch or
Morrison space
– The presence of fluid in the pleural sinuses or
pericardium
– Parenchymal lesions: spleen or liver rupture with
hematoma
Radiological explorations
Abdominal X-ray highlights the pneumoperitoneum
(hallow organ perforation), fluid-air levels (occlusions),
foreign bodies (bullets) or disappearance of psoas
muscles shadow (in retroperitoneal effusions)
X-ray of pelvis and lumbar spine - fractures
For patients with a good status and clinical course, more
complex investigations can be performed: examination of
the digestive tract with hydrophilic contrast, urography,
angiography.
A chest radiogram is obtained in all patients because
penetration of the chest cavity cannot be ruled out, even
with abdominal stab wounds.
CT scan
It can provide important data regarding the presence of intra-
peritoneal fluid and about its source.
It is the standard examination for the detection of
parenchymatous organ damage.
The indications for performing CT after Peitzman are:
1. Patients hemodynamically stable, but with equivocal clinical
examination
2. Spinal cord injuries (back and flank trauma)
3. Hematuria in stable patients
4. Head trauma
5. Pelvic fractures
CT requires a hemodynamically stable patient. In modern
services spiral CT is performed in all cases of severe
injuries.
The diagnosis of significant penetrating injury should not be
delayed by routinely obtaining CT scans of the abdomen and
pelvis.
Diagnostic peritoneal lavage (DPL) shall be performed
only after inserting a naso-gastric tube and a bladder
catheter for decompression. It is indicated in:
Blunt trauma :
– Unstable patient
– Stable patients with inconclusive clinical examination
Penetrating trauma:
– Stabbed abdominal wound with no signs of peritoneal irritation
– Chest wound under the nipples level (possible diaphragmatic
injury)
– Stabbed wound in the flanks.
Contraindications are:
– Cases where laparotomy is indicated based on clinical
examination
– Open abdominal surgeries in patient’s history (risk to damage
the bowel loops adherent to the abdominal wall)
– Advanced pregnancy
DPL can be performed via open (the catheter is
introduced under direct vision through a small
infraumbilical incision) or closed (blind insertion of the
catheter over a guidewire through a trocar) method.
Aspiration of gross blood or food particles is positive for
peritoneal penetration and organ injury.
If aspiration is negative, 1 liter of warm normal saline is
infused rapidly and allowed to return by placing the bag
on the floor. The fluid is then sent for analysis.
Indications for laparotomy are:
1. More than 100,000 red blood cells/ml, (30 ml of blood in the
peritoneum is enough to return a positive lavage)
2. More than 500 leukocytes/ml
3. The presence of bile, amylase, intestinal or fecal content,
bacteria, fiber, or urine.
4. Failure to recover the fluid is considered positive point
DPL - Aspiration of gross blood
Treatment principles
The management of abdominal trauma varies according
to the following factors:
Mechanism and location of injury
Hemodynamic and neurologic status of the patient
Associated injuries
Institutional resources
Abdominal trauma, either penetrating or blunt, is
considered an emergency, so the patient will be
monitored and resuscitated if necessary in the
emergency room.
After primary evaluation, priority will be given to support
vital functions (ABC): airways will be released and if
necessary the patient should be intubated to ensure
appropriate oxygenation or ventilation. If there are
intrathoracic lesions (ie pneumothorax) these will be
treated with priority to ensure respiratory function.
Airway protection and ventilatory support are followed by
circulatory resuscitation with fluid infusion.
Surgical treatment of abdominal trauma in hospital
setting is adapted to specific lesions but there are some
general principles:
1. Diagnostic maneuvers and then surgery is associated
with concomitant re-balancing maneuvers.
2. The patient should be placed on a cardiac monitor,
pulse oximeter, and 100% nonrebreather oxygen
mask.
3. Antibiotic therapy is mandatory in any penetrating
trauma and in any possible damage to the digestive
tube, covering the whole spectrum ( aerobic and
anaerobic germs ).
4. Tetanus prophylaxis (Tetanus Toxoid), if five years
have passed since the last immunization.
5. Major pain killers to combat pain are used only in
stable patients with complete diagnostic (to avoid
masking symptoms of an acute abdomen).
Abdominal trauma often is a part of polytrauma. For a
good monitoring and resuscitation, in most cases it is
necessary to apply the rule of the four catheters: central
venous catheter, naso-gastric tube, bladder catheter and
tracheal intubation (if necessary).
Nasogastric aspiration is useful because or for :
– Stomach decompression
– Reduces the risk for aspiration into the lungs
– Removes toxins and waste from the stomach
– Highlights the occurrence of upper gastrointestinal bleeding
– It is mandatory prior to DPL
– It is contraindicated in nasal and face bones fractures
Bladder catheterization is useful because:
– Establishes the permeability of urethra
– Solves the acute urinary retention
– Allows tracking the diuresis for assessment of necessary volume
of rebalancing fluids
Central venous catheter is useful for:
– Administration of medication or fluids
– Measurement of CVP (central venous pressure) to assess the
volemic load of the patient
– Collection of blood samples for analysis
 Stomach trauma
The most cases appear in penetrating abdominal wound
and the anterior wall of the stomach is the most affected.
Stomach wounds are usually followed by a generalized
peritonitis, with specific symptoms requiring laparotomy.
Rarely, small lesions may be followed by covered
perforation and peritoneal abscess.
For a positive diagnosis plain abdominal radiography is
helpful in highlighting the pneumoperitoneum.
Contusions are usually followed by a gastric wall
hematoma, clinically manifested by abdominal pain
associated with superior digestive hemorrhage, or if
there is a rupture of the gastric wall, with signs of
peritonitis.
Gastric injuries are classified by AAST (American Society
of Trauma Surgery) in:

1. Gr. I: intramural hematoma less than 3 cm,

incomplete lesion of the wall.
2. Gr. II: intramural hematoma over 3 cm, wall lesion
less than 3 cm.
3. Gr. III: wall lesion grater than 3 cm.
4. Gr. IV: important lesion with damage of the vessels
of the great or lesser curvature.
5. Gr. V: Rupture extended over 50%,
devascularization of the stomach.
 Treatment of gastric lesions:
Contusions without ruptures of the gastric wall can be
treated conservatively with nasal-gastric aspiration,
symptomatic treatment and frequent reassessment. If
laparotomy is necessary, surgery can be grouped as
follows:
1. For Gr. I and II: - evacuation, haemostasis and suture.
2. For Gr. III: - lesion excision and suture, or lesion
excision and gastro-entero anastomosis. (GEA)
3. For Gr. IV - proximal or distal gastrectomy adapted to
concomitant injuries of other organs.
4. For Gr. V: - requires total gastrectomy with eso-jejunal
anastomosis with Roux-en-Y loop or omega loop.
 Duodenal trauma
Represents 1-2% of abdominal trauma and is usually
discovered during laparatomy for hypotension or peritoneal
irritation.
The mechanism depends on the anatomical region involved:
– D3: crushing against the spine.
– Rupture in extremities by traction.
– The explosion of a full duodenum by compression.
Pathological classification of duodenal lesions after AAST:
1. Gr. I: hematoma at the level of a single segment, incomplete parietal
lesion.
2. Gr. II: hematomas in several segments, wall rupture of 50% of the
circumference of a segment.
3. Gr. III: rupture of 50-70% of D2 or 50-100% of D1, D3, D4.
4. Gr. IV: massive laceration of D2, Vater’s ampulla rupture or rupture
of the distal segment of choledocus.
5. Gr. V: massive duodeno-pancreatic damage or devascularization.
Clinical picture:
Is nonspecific, usually manifested by peritoneal irritation
(intraperitoneal rupture) syndrome or internal bleeding.
Postponing the diagnosis and the surgical treatment
over 24 hours leads to 40% mortality.
Suggestive paraclinical findings:
1. Hiperamilazemia (duodenal or pancreatic injury)
2. Pneumoperitoneum on plain radiography, extravasation of
contrast agent (gastrografin).
3. Abdominal CT with oral contrast is the most important
examination in diagnosis.
4. DPL: may indicate the laparatomy but does not specify the
injured organ.
Retroperitoneal rupture has a more subdued clinical
picture of reflex stop of bowel movements, restlessness
or dizziness associated with a febrile syndrome
(retroperitoneal effusion).
Intraoperatively, a retroperitoneal rupture of the duodenum
is suggested by the Winiwarter triad : the presence of
blood + bile + gas in the retroperitoneum.
The treatment of duodenal lesions varies depending on
location and severity of injuries:
– Gr. I: hematoma usually is treated conservatively. Laceration is
treated by simple suture.
– Gr. II: hematomas require evacuation and multiple suture.
Laceration of less than 50% of circumference is sutured in two
layers. An intestinal loop can be used to patch the parietal defect.
– Gr. III: in total duodenal transection distal duodenal segment can
be closed and the proximal segment is ansatomosed to a jejunal
loop. In large defects, after suturing, an intestinal loop can be used
to patch the parietal defect, or for anstomosis.
– Gr. IV:
For lesions without involvement of the bile duct or Vater’s
ampulla a duodeno-jejunal anastomosis is preferred.
For lesions of CBD without pancreatic lesions, reimplantation
of CBD (in duodenum or jejunum) is performed.
When pancreatic lesions are associated, cephalic duodeno-
pancreatectomy is the solution.
– Gr. V:
major duodeno-pancreatic injury requires cephalic duodeno-
pancreatectomy with a high mortality rate.
Traumatic duodenal lesions are frequently associated
with other intra-abdominal injuries particularly with
pancreas, they are difficult to diagnose and pose special
problems concerning surgical technique and therefore
they have a high postoperative mortality and morbidity.
 Small intestines and mesentery
trauma
Small intestine and mesentery are the most frequently
damaged organs during abdominal trauma. Small
intestines lesions occur in up to 50% of penetrating
abdominal wounds and in association with mesenteric
lesions in up to 70% of abdominal contusions.
Mechanisms of lesion include:
– Crushing
– Sudden explosion by increasing intralumenal pressure
– Rupture at site of the junction between fixed and mobile
segments
– Mesentery lesions with vascular impairment and
intestinal necrosis.
– Posttraumatic mesenteric thrombosis is rare but a
serious cause of intestinal venous infarction.
AAST classification of traumatic lesions of the small
intestine:
– Gr. I : contusion with hematoma without devascularization, parietal
incomplete rupture.
– Gr. II: complete parietal rupture (all layers) less than 50% of the
circumference.
– Gr. III : rupture over 50% of circumference without interrupting the
continuity of the intestine.
– Gr. IV : interruption of intestinal continuity.
– Gr. V : complete transsection of the intestine with loss of substance
or a devascularization of an intestinal segment.
There are three clinical syndromes associated to bowel
injuries:
1. Traumatic shock: caused by irritation of vegetative
plexuses with no visceral lesions (respond quickly to
treatment).
2. Internal bleeding syndrome.
3. Perforation syndrome (symptoms of peritonitis).
Frequently there are mixed forms, usually with the
preponderance of the internal bleeding syndrome.
Late posttraumatic manifestations:
– Peritonitis due to late perforations as a result of parietal necrosis.
– Intestinal obstruction due to incarcerated internal hernia or
compressive hematoma.
Surgical treatment:
– Gr. I: sero-muscular suture of the parietal defect, hematoma
evacuation.
– Gr. II: suture in two layers or resection.
– Gr. III: transverse suture to prevent stenosis, if intestinal vascular
supply is preserved. If not, resection is necessary.
– Gr. IV and V: resection with primary anastomosis.
Breaches of the mesentery should be sutured to prevent
internal hernias. If intestinal vascular supply is
compromised, resection is the solution with end-to-end or
latero-lateral anstomosis.
 Colon trauma
Colon injuries have a lower frequency than those of the
small bowel, up to 5%, but are of extreme gravity with a
mortality of up to 20% due to the septic content of the
colon.
AAST classification of traumatic lesions of the colon:
– Gr. I - contusion with hematoma without devascularization,
incomplete parietal rupture.
– Gr. II - complete parietal lesions (all layers) less than 50% of
the circumference.
– Gr. III - rupture over 50% of circumference without
interrupting the continuity.
– Gr. IV - interruption of continuity of colon.
– Gr. V - complete transsection of the colon with loss of
substance or devascularization of a colic segment.
 Clinical picture depends on the degree of laceration
and if it is located intra or retroperitoneal :
1. intraperitoneal rupture causes stercoral peritonitis
with toxic-septic shock. Pneumoperitoneum is
present in up to 70% of cases.
2. retroperitoneal rupture causes a retroperitoneal
abscess or phlegmon with nonspecific symptoms:
fever, ileus, local Celsian signs. Ultrasound and CT
scan facilitates the diagnosis and can guide the
puncture of the abscess.
The treatment of traumatic lesions of the colon is
different depending on location and the severity of
injuries, but requires mandatory association with
broad-spectrum antibiotics.
Possible types of operations are:
1. Suture of a simple lesion protected or not by a
superjacent colostomy or ileostomy.
2. Exteriorization of the injured segment as a loop
colostomy if a mobile segment of the colon is affected.
3. Segmental resection, when lesions are more serious,
followed by:
 Colo-colic ansatomosis – in mobile segments (transverse and
sigmoid colon) – is not recommended in stercoral peritonitis
due to the high incidence of fistula. The anstomosis can be
protected by a colostomy or ileostomy.
 Hartmann’s I procedure when the distal end is closed and the
proximal is exteriorized in terminal colostomy.
 Exteriorization of the both end of the colon in colostomy.

4. Right hemicolectomy when the right colon is affected –

may be followed by ileo-colic anastomosis or just
ileostomy and closure of the colic stump.
5. Left hemicolectomy usually followed by colostomy of
the proximal end and closure of the distal one, in left
colon injuries.
6. Subtotal colectomy with ileostomy and closure of the
distal end.
Performing a colostomy is indicated when:
1. The damage exceeds 50% of the circumference.
2. Massive intraperitoneal contamination.
3. Shocked patient with hypotension.
4. Patients requiring multiple blood transfusions.
5. Three or more colic lesions associated or association with a rectal
injury.
6. Ischemic necrosis of the colon.
7. Interventions performed at more than 6 hours after injury (major
septic risk).
8. Association with a retroperitoneal hematoma from a fractured
pelvis.
9. Association with a posttraumatic parietal defect.
 Rectal trauma
The mechanisms of rectal lesions are mainly endoluminal
during endoscopy or produced by foreign bodies. Another
possible mechanism is the rectal lesion by bone fragments
during pelvic fractures.
Rectum may be injured in its intraperitoneal segment
resulting in peritonitis or subperitoneal segment resulting in
abscess formation with a mortality rate up to 20%.
AAST classification of traumatic lesions of the rectum:
1. Gr. I : Contusion with hematoma without devascularization,
incomplete parietal rupture.
2. Gr. II : Complete parietal rupture (all layers) in less than 50% of the
circumference.
3. Gr. III : More than 50% of the circumference rupture without
breaking continuity.
4. Gr. IV : Lesion with perineal extension that interest all layers of the
rectum.
5. Gr. V : Devascularization of a rectal segment.
Clinical picture is variable depending on the involved rectal
segment, but rectal bleeding is the common element (but
not constant) .
– Intraperitoneal segment lesions are followed by rapidly evolving
stercoral peritonitis.
– Retroperitoneal lesions are followed by cellulites or pelvic abscess
manifested by fever, pain, local celsian signs.
– The association with uretro-bladder lesions is followed by leakage
of urine through the rectum and pneumaturia (presence of air in
the bladder), fecaluria (mixture of feces and urine that is passed
from the urethra) and severe ascending urinary infections.
Digital rectal examination is mandatory in these patients
and can highlight: rectal solutions of continuity, or
fluctuence of perirectal tissues, intrarectal or perirectal
foreign bodies (bone fragments), bleeding.
Diagnosis is confirmed by rectoscopy. Endorectal
ultrasound can detect incomplete lesions of the rectal wall
and the presence of perirectal collections.
Treatment
Grade I and II injuries can be primary sutured.
In more serious injuries, when suture is possible, an
upstream protective colostomy should be performed.
Injuries that can not be sutured require Hartmann’s I type
procedure.
Rectal injuries associated with pelvic collections require
drainage. In most cases the appropriate approach is through
an incision between the anus and coccyx.
Very rare perianal gun shot produces massive lesions with
devascularization of the rectum, requiring resection with
colostomy.
Intrarectal foreign bodies are extracted through the anus in
spinal anesthesia. After extraction recto-sigmoidoscopy is
required to assess any damage to the rectum. When the
foreign body cannot be extracted through the anus it will be
extracted by laparotomy through a colotomy.
Uretro-bladder injuries are treated by suture associated with
cystostomy.
 Pancreatic trauma
Although pancreatic traumas are rare (< 10%) they are
very serious due to frequent association with other
abdominal injuries, especially of the large vessels that
cause a high immediate mortality. Late mortality is mainly
due to infection complicating acute post-traumatic
pancreatitis.
Ethiopathogenesis: the most frequent causes are traffic
accidents (in frontal collisions when the abdomen is
crushed against the steering wheel), followed by gunshots.
Iatrogenic pancreatic lesions may appear during
abdominal surgery and endoscopic maneuvers (ERCP).
AAST classification of pancreatic trauma:
1. Gr. 1- Subcapsular hematoma or pancreatic tissue
laceration but without damage to the pancreatic ducts.
2. Gr. 2 - Complete transsection of the tail of the pancreas or
parenchymal injury with damage of the pancreatic duct.
3. Gr. 3 - Complete transsection of the head of the pancreas
or lesions of the Vater’s ampulla.
4. Gr. 4 - Massive destruction in the pancreatic head.
Clinical picture:
Abdominal wounds, especially the gunshots, where
pancreas lesions are suspected, are considered a major
emergency and are explored through laparotomy without
any other investigations.
In blunt abdominal trauma, pancreatic lesions are
frequently associated with other organ or vessels lesions
and the clinical picture is that of a traumatic shock with a
mixed syndrome of internal bleeding and pancreatitis.
Isolated pancreatic injuries are more difficult to diagnose,
and may evolve as a post-traumatic acute pancreatitis with
its early and late complications.
Surgery is adapted to lesion types:
– Gr. 1: hemostasis, infiltration with lidocaine, neighborhood
drainage to avoid a pancreatic pseudocyst in case of
unrecognized minor injuries of the pancreatic duct.
– Gr. 2: ductal lesions located to the left mesenteric pedicle
require caudal pancreatectomy with or without splenectomy.
– Gr. 3: ductal lesions located to the right of superior
mesenteric vein may be treated by subtotal pancreatectomy
or pancreatico-jejunal anastomosis with closure of the
cephalic stump duct.
– Gr.4 : are encumbered by the highest mortality due to
association with duodenal and vessels lesions. The first
concern is to stop bleeding and then, if the patient is stable,
cephalic duodeno-pancreatectomy is performed. If the
patient is unstable, just multiple drainage is performed after
hemostasis.
The most common postoperative complications are
fistulas and pancreatic pseudocysts and the overall
mortality is around 15%.
 Splenic trauma
Spleen is the most commonly injured organ in blunt
abdominal trauma, especially in traffic accidents
associated with left ribs fractures.
The spleen may be also injured during penetrating trauma
and surgery.
Lesions appeared on an pathological spleen in
splenomegaly of any etiology may occur after apparently
minor trauma.
AAST classification of traumatic lesions of the spleen:
– Gr. I: rupture of less than 1 cm of parenchyma without bleeding,
subcapsular hematoma in 10% of the splenic area.
– Gr. II: 1-3 cm parenchymal rupture with bleeding, subcapsular
hematoma of 10-50%.
– Gr. III: rupture more than 3 cm or involving the trabecular vessels,
subcapsular hematoma over 50% of the surface or
intraparenchymatous over 5 cm.
 – Gr. IV: broken intraparenchymatous hematoma blood vessels or
lesions involving the deep spleen hilum vessels and
devascularization of 25% of the parenchyma.
– Gr. V: spleen avulsion, parenchyma explosion.
Clinic picture:
Splenic trauma symptoms vary depending on the severity
of injury but the forefront syndrome is that of intraperitoneal
hemorrhage and hemorrhagic shock (tachycardia,
tachypnea, restlessness, anxiety).
In severe forms, associated with liver damage or large
vessels injuries, the patient can die in few minutes even
before applying of the first therapeutic measures.
In lesions with capsular rupture and hemoperitoneum, in
addition to general signs of acute anemia and hemorrhagic
shock, there are local signs of pain or left upper quadrant
defense and radiation of pain to left shoulder (Kehr sign).
 Saegesser’s splenic point of tenderness: it is an area of
tenderness on left side between scalenus medius and
sternocleidomastoid muscle.
Balance’s sign: on percussion unshifting dullness present on
left side of the abdomen due to subcapsular and coagulated
blood around the spleen.
The two-stage splenic rupture: the first stage is the
subcapsular and perisplenic hematoma (blocked by
adhesions) and the second stage, which may occur after
several days even weeks, is represented by the
intraperitoneal bleeding due to the rupture of the distended
capsule and perisplenic adhesions.
Paraclinical investigations
FAST (focused assessment with sonography for trauma)
(perihepatic, perisplenic, pelvis, pericardium) - reveals the
subcapsular or perisplenic hematoma, parenchymal rupture
and the presence of fluid in the peritoneal cavity.
Plain radiography: left ribs fracture, elevation of the left
hemidiaphragm, displacement of gastric fluid-air level.
DPL: reveals intraperitoneal bleeding and indicates the
surgical exploration.
CT with contrast highlights with high accuracy the
splenic lesions.
Angiography is performed after CT scan, more frequently
for primary therapeutic management by
angioembolization (gelfoam)
Although imaging explorations have a good diagnostic
index, some minor injuries may go unrecognized at initial
evaluation. Therefore all patients with trauma that may
be associated with splenic lesions require periodic
reassessment.
Treatment
Splenic injuries, depending on severity, can be managed
surgically or nonsurgical.
Surgical treatment of choice is splenic conservation
(hemostasis by electro-coagulation, plasma-coagulation,
local hemostatics, suturing, partial resection) whenever
possible to avoid post-splenectomy infections especially
in children. Splenectomy is the choice in severe and
multiple lesions of the spleen with hemodynamic
instability. Indications for splenectomy:
1. Parenchyma explosion
2. Vascular lesions in the hilum
3. Intra-parenchymal massive hematoma
4. Patients in critical condition or other severe inta-abdominal
injuries
5. Failure of conservative surgical techniques
Criteria for nonoperative management:
1. Patient in an intensive care unit with continuous monitoring of
vital functions.
2. Daily or even several times a day ultrasound assess of lesion
development (expanding hematoma or hemoperitoneum
requiring surgery).
3. Surgical team always available for secondary bleeding.
4. Hemodynamic stable patient.
5. Negative abdominal scan.
6. Absence of contrast extravasations on CT.
7. Absence of other indication for laparotomy.
8. Absence of other condition associated with high risk of bleeding
(coagulopathy, use of anticoagulants, etc).
 Liver and biliary tract injuries
The liver is interested in 10% of abdominal trauma. Its
lesions are associated with a rapid loss of important
quantities of blood and a high mortality rate (up to 80%)
due to its rich vascularization, its low resistance to
anoxia and difficult surgical approach.
AAST classification of liver trauma:
1. Gr. I: subcapsular hematoma in 10% of surface, less than 1 cm
capsular rupture without bleeding.
2. Gr. II: subcapsular hematoma in 10-50% of liver surface,
intraparenchymatous hematoma less than 10 cm diameter, 1-3
cm hepatic rupture.
 3. Gr. III: subcapsular hematoma over 50% of surface,
intraparenchymatous hematoma over 10 cm diameter, liver
wound deeper tahn 3 cm.
4. Gr. IV: broken intraparenchymatous hematoma with active
bleeding, destruction of 25-75% of a lobe or 1-3 segments.
5. Gr. V: lesions exceeding 75% or 3 segments of a lobe, liver
large vessels are interested.
6. Gr. VI: vascular avulsion of the liver.
Clinical picture
Major liver trauma with vascular injuries or liver
explosions are above the therapeutic resources,
patients dying at the scene, even before the first aid
measures can be applied.
The main syndrome is that of intraperitoneal hemorrhage
associated with intense acute anemia.
Finsterer triad in liver trauma: the paradoxical
bradycardia in a patient with hypotension, shock and
jaundice.
On local examination abdominal contracture may occur
due to extravazation of bile into the peritoneal cavity.
Liver lesions can be manifested as a two-stage clinical
picture: the initial liver trauma with subcapsular
hematoma and then the rupture of the capsule with
intraperitoneal hemorrhage.
Liver trauma can be associated with immediate or late
complications:
– Hemobilia: the penetration of blood into the biliary
tree manifested by Owen triad: colicky pain, upper
gastrointestinal bleeding and mechanical jaundice.
 – Biliragy (bile leakages) due to biliary tree injuries
– Hepatic necrosis due to vascular disruption leading to
liver abscess with abdominal pain, fever, jaundice
and progression to severe sepsis and hepato-renal
failure.
Paraclinical investigations:
Positive DPL impose the surgical exploration.
Abdominal ultrasound may reveal the liver rupture, the
subcapsular hematoma and the presence of fluid in the
peritoneal cavity, but lesions severity are difficult to be
assessed.
CT available for stable patients can more accurately
assess the severity of injuries.
Surgery:
In liver trauma the first aim of surgical treatment is to
stop the bleeding and then to repair the damages.
Clamping of the hepatic pedicle, also known as the
Pringle maneuver, allows surgeons to evaluate traumatic
liver injury. Pringle maneuver can be performed with
atraumatic vascular clamp or with fingers. It has also a
diagnostic value: if the bleeding comes from branches of
the portal vein or hepatic artery, after this maneuver, it
stops or significantly reduces in quantity, if bleeding
comes from suprahepatic vessels or vena cava, bleeding
will not stop. Pringle maneuver can be maintained up to
15 minutes in normothermia or 30 minutes under
hypothermia.
Other methods of hemostasis are the temporary manual
compression or compressive wound packing.
Temporary control of bleeding allows replacement of lost
fluid volume and provides conditions for achieving final
hemostasis.
Lesions of the suprahepatic veins or vena cava are
usually lethal. Making temporary hemostasis in these
cases is very difficult and can be performed in three
ways:
1. vascular isolation of the liver: clamping the subdiaphragmatic
aorta, clamping the vena cava suprahepatic and suprarenal,
associated with Pringle maneuver, is engraved with a high
mortality due to decreased venous return in an already
hypovolemic patient.
2. Performing an atrio-caval shunt: by introducing a catheter with
balloon through the atrium into the vena cava in suprarenal
position to maintain a sufficient venous flow to the heart.
3. The use of balloon Moore -Plicher: inserting a catheter through
the femoral vein into the vena cava and inflating the balloon in
the place of venous lesion (suprahepatic veins or cava vein) to
achieve haemostasis.
Whichever method is chosen mortality in these cases
exceeds 50%.
Definitive treatment methods of liver injuries are ranging
from haemostatic packing of liver wounds to liver
transplantation.
– Grade I and II: superficial lesions of the liver can be managed
by manual compression followed by hemostatic procedures:
electro-coagulation, argon plasma coagulation or application
of haemostatic sponges, sutures.
– Grade III-IV: may benefit from superficial haemostasis but
most often other methods are needed:
Haemostatic suture of liver parenchyma is the method of choice for
superficial wounds under 3 cm deep
Hepatotomy with elective ligation of injured pedicle
Atypical or anatomical (controlled) liver resections
Haemostatic packing is used for serious grade III-V injuries
especially in shocked patients to prevent further blood loss. It can be
performed in two ways: packing the tears with gauze or introducing a
high quantity of gauze into the hepato-phrenic space to achieve
compression and hemostasis. The main risk of doing this is that
severe sepsis may follow. If hemostasis was achieved, after 24-48
hours gauzes have to be extracted.
Biliary tract injuries are recognized by the presence of bile in
the peritoneal cavity.
Gallbladder lesions are solved by cholecystectomy unless
gallbladder will be used for a bilio-digestive bypass.
Injuries of the common bile duct are more serious because
their repair is engraved by late stenosis. In case of linear
lesions, without loss of substance, suturing can be performed
associated with a Kehr type drainage. Major injuries or
complete section can be solved only by choledochojejunal
anastomosis with a Roux-en-Y loop.
External biliary drainage is indicated in any important hepatic
laceration even without obvious biliary injury to prevent
postoperative biliary leakage.
Overall mortality of patients with liver injury is 10%. The main
cause of death is exsanguination.
Frequent postoperative complications in liver trauma surgery :
– postoperative bleeding (unrecognized injury or transfusion
coagulopathy).
– Infection, most commonly in ischemic territories due ligation or en
block suture.
– Biliary leakage
 Large vessels trauma
Traumatic lesions of the large abdominal vessels are
encumbered by a very high mortality rate (30-60%),
despite the all improvements of transportation and
resuscitation of patients.
The main cause is penetrating abdominal wounds and
the leading cause of death is hemorrhage.
Vascular lesions are usually associated with other intra-
abdominal injuries and in up to 40% of cases the damage
involves at least two major vessels.
Injury severity is directly influenced by three factors:
1. The number of injured vessels
2. Location
3. Mechanism
The most serious are those that involve the aorta, and
those produced by firearms.
From clinical point of view, two situation may be
encountered: patients with active bleeding or those with
retroperitoneal hematoma.
1. Patients with retroperitoneal hematoma present a
transitional shock with hypotension which responds
to volemic rebalancing, but hypotension reappears
when the hematoma is surgical explored or when the
hematoma breaks into the peritoneal cavity. The
bleeding usually comes from an injured vein.
2. Patients with active bleeding (often arterial) present
shock and hypotension refractory to resuscitation
associated with abdominal distension. A specific sign
is the absence of unilateral femoral pulse, suggestive
for a lesion of the common or external iliac artery.
Injury to major vessels requires emergency surgery. The
first goal is to stop the bleeding by various maneuvers of
temporary hemostasis (compression, clamping) followed
by final hemostasis either by suture, reconstruction or
sometimes vessel ligation.
Mortality in traumatic abdominal aorta injury ranges from
70-90%:
 Retroperitoneal hematoma
Various causes, but in order of frequency are:.
1. Lesions of the retroperitoneal organs (kidney,
pancreas)
2. Fractures of the pelvis or lumbar spine.
3. Lesions of retroperitoneal vessels
Retroperitoneal hematoma due to renal trauma has a
high-lateral topography but it can descend to the pelvi-
subperitoneal space.
Bleeding from large vessels lesions are associated with
a very high mortality (avg. 50%). Thus, aortic lesions:
40% -80%, vena cava 10-40% and iliac artery or vein 15-
40% mortality.
In terms of size they are considered:
– Very large, when extend from the upper pole of the kidney to the
Douglas;
– Large - do not exceed the lower renal pole;
– Medium and small - located only in the pelvis or around the
various organs (kidney, duodenum, pancreas, etc.).
By its presence, hematoma is a permanent cause of
irritation of the retroperitoneal nerve plexuses and may
result in ischemic necrosis of the intestine by
compression on mesenteric vessels. Paralytic ileus
causes serious fluid and electrolyte disorders, leading to
complex shock. The toxic component of the shock
results from the resorption of blood.
Diagnosis. A careful clinical examination may reveal
clinical signs of retroperitoneal hematoma: palpation of
the hematoma mass, abdominal distension and
muscular defense in lateral quadrants, dullness in the
lower parts of the abdomen on percussion.
The sequence of investigations could be the following:
1. Plain abdominal radiography – reveals bone lesions,
signs of paralytic ileus, decrease of psoas shadow
2. Abdominal ultrasound reveals fluid collections and
kidney lesions
3. Mounting a central vein catheter through the femoral
vein - for harvesting blood for laboratory
investigations and cavagrafy or urography and also
for fluid rebalancing
4. CT scan with contrast – is the most important
investigation
5. Other investigations as needed: cystography,
selective arteriography, etc
Complications
Evolution of post-traumatic retroperitoneal hematoma is
characterized by the occurrence of complications in a
high percentage of cases.
1. Resorption syndrome - is dominated by the development of
variable intensity jaundice resulting from blood resorption. The
most important aspect is however increasing of K + ion levels
very dangerous with concomitant development of the acute
renal insufficiency (source of hyper-potassium levels).
2. Suppuration of retroperitoneal hematoma can progress to a
diffuse cellulitis, with fatal outcome. Favorising circumstances
are coexisting organ damage (rectum, colon, etc.).
3. Lymphorrhagia and pancreatic fistula.
4. Retroperitoneal seroma- due to incomplete resorption. It
evolves like a retroperitoneal compressive tumor that may
rupture into the peritoneal cavity.
 5. Early rupture into the peritoneal cavity - explains the presence
of a concomitant haemoperitoneum without any lesions of
intraperitoneal organs.
6. Late rupture into the peritoneal cavity.
7. Retroperitoneal liposclerosis – intense adhesions around
retroperitoneal anatomical structures.
 Treatment
 The surgical indication will be established after
immediate resuscitation, aimed to control the traumatic
shock and hemorrhage and maintenance of the
important functions.
 Absolute surgical indication of surgery in emergency
is the retroperitoneal hematoma of vascular and renal
origin.
 Relative indication for surgery are the hematomas due
to bone fractures of the pelvis with no vascular or
visceral lesions.
Conservative treatment will be applied to small
hematomas, or hematomas without major vascular
lesions or visceral lesions.
Prognosis
There are three periods of evolution:
During the first 24-48 hours, the prognosis depends
mainly on: intensity of the shock (traumatic,
hemorrhagic) and involvement of the celiac plexus
(vagal-sympathetic irritation).
During the first 3-5 days, the prognosis may be
worsened or remains reserved because of: persistence
or recurrence of shock, occurrence of acute renal
failure, intestinal paresis.
The period of local complications, with lower
implications in vital prognosis.
 UPPER
GASTROINTESTINAL
BLEEDINGS
Acute gastrointestinal bleeding is
a major emergency for both
patients and doctors.
Definitions
 Upper gastrointestinal bleeding (UGIB) = bleeding
from a source proximal to the ligament of Treitz.
 Haematemesis = bleeding exteriorized through vomiting.
The blood is fresh of arterial or venous source.
 Melanemesis = vomiting of discolored black blood with
aspect of “used coffee grounds“. It appears when the
blood spent more time in the stomach (hemorrhage has
reduced or stopped) and the hemoglobin was converted to
haematin (of brown color) under the action of gastric acid.
 Hematochezia = fresh blood passage through the
rectum. Usually indicates a bleeding from the lower part of
the digestive tract, but may be the result of increased
amounts of upper gastrointestinal bleeding associated with
a rapid intestinal passage of blood (under 14 hours).
 Melena = black stools, typically indicating a higher
gastrointestinal source of bleeding, but bleeding source can
be as well the small intestine or the colon. To produce
melena, 150-200 ml blood are required, which is
transformed under the action of digestive juices and
intestinal bacteria. Melena may continue several days after
bleeding has stopped. Note that black stool, with negative
occult bleeding tests, may be due to ingestion of iron,
bismuth and a variety of foods.
 Massive gastrointestinal bleeding = when
gastrointestinal bleeding is accompanied by shock, or
orthostatic hypotension, the decrease in hematocrit is of 6-
8% or a minimum of 2 units of blood transfusion is
required.
 Occult bleeding = loss of small quantities of blood (less
than 50 ml) by stool, as evidenced by fecal occult blood
tests (HemoCult, HemoQuant).
Incidence and mortality
 For the U.S. it is estimated an incidence of 150 per
100,000 inhabitants per year. Ulcer disease is
responsible for 35.6% out of all bleeding episodes. For
Europe, the incidence is 48-145 per 100,000 inhabitants
per year.
 Digestive hemorrhage mortality remained unchanged
over the past 25 years, being 8-10%, but in severe
bleeding goes up to 25-50%.
 75% of bleeding cases are due to acid-peptic disease
(peptic ulcer, gastritis, esophagitis), 10-15% are
secondary to portal hypertension (esophageal and
gastric varices) and the remaining of 10-15% have
mixed causes (neoplasms, Mallory-Weiss syndrome, etc).
Etiology of upper gastrointestinal bleeding

 Ulcers or erosions
1. Peptic ulcer 2. Esophagitis
 Idiopathic  Peptic
 Induced  Infectious
– Aspirin – Candida albicans
– NSAIDS – Herpes simplex virus
 Infectious – Cytomegalovirus
– Helicobacter pylori – Other
– Cytomegalovirus b.  Induced
– Herpes simplex virus – Alendronate
 Stress ulcer – Tetracycline
 Zollinger Ellison syndrome – Qinidin
– Potassium chloride
– Aspirin
– NSAIDS
3. Portal hypertension 6. Tumors
 Esophageal varices  Benign
 Gastric varices  Leiomioame
 Duodenal varices  Lipomas
 Polyps (hyperplastic, adenomatous,
 Portal hypertension gastropathy hamartomatos)
4. Arterial or venous  Malignant
malformations  Adenocarcinoma
 Idiopathic angioma  Leiomyosarcoma
 Rendu-Osler-Weber syndrome  Lymphoma
 Dieulafoy lesions  Kaposi's sarcoma
 Antral vascular ectasia  Carcinoid
(watermelon stomach)  Melanoma
 Metastases
 Radiation induced teleangiectasia
 "Blue rubber bleb nevus 7. Other
syndrome“ (association between  Hemobilia
cavernous hemangiomas of the  Haemosuccus pancreaticus (It is
skin and similar lesions in the GI
tract.) caused by a bleeding source in the
pancreas, pancreatic duct, or
5. Traumatic or postoperative
structures adjacent to the pancreas,
 Mallory-Weiss syndrome
such as the splenic artery, that bleed
 Ingested foreign bodies
into the pancreatic duct, which is
 Surgical anastomosis
connected at the duodenum.)
 Enteric arterial fistula
Highlighting bleeding
 Medical history, color, amount of gastric aspiration or
vomit, or aspect of stools are suggestive and provide
important data. A positive gastric aspirate confirms the
upper gastrointestinal bleeding, but a negative aspirate
does not exclude a source of bleeding.
Quantitative assessment of bleeding
 Assessment of bleeding and replacing lost blood is the most
important acute aspects of the therapy of patients with
gastrointestinal bleeding.
 Usually, blood loss is underestimated. Assessment of blood
loss requires an accurate assessment of vital signs, central
venous pressure, hemoglobin and hematocrit and a degree
of clinical experience.
Indicators of a massive hemorrhage are:
1. Resting tachycardia (100 beats / min).
2. In standing position heart rate increases with over 20
beats/min, the systolic pressure decreases with over 20
mmHg, diastolic pressure decreases with over 10
mmHg.
3. Acidosis.
4. Azotemia (blood urea increased by over 40 mg/100 ml
without pre-existing renal disease).
5. Transfusion requirements of more than one unit at 8
hours or 6 units in total.
6. Hematochezia from upper gastrointestinal source.
7. Unable to clarify the fresh red blood in gastric lavage.
8. Continued bleeding or rebleeding during endoscopy.
 An increased risk is when there are met more
criteria :
1. age over 60 years,
2. significant comorbidities,
3. coagulopathy,
4. hemodynamic instability,
5. signs of active bleeding.
 These patients will be admitted in ICU and subjected to
emergency endoscopic diagnostic / therapeutic
maneuvers. Surgical and interventional radiology services
will be alerted for possible evaluation.
 Rockall score based on clinical and endoscopic criteria
in patients with a history of UGIB provides predictability
of recurrence and severity of bleeding.
 25% of patients hospitalized in ICU are low risk and can
be treated in other hospital departments
(gastroenterology, surgery).
 Rockall Severity Score
Score
The variable
0 1 2 3
Age <60 60-79 >80
•Without shock
•BP  100 mmHg
P •BP > 100 mmHg •BP  100 mmHg
•Pulse  100
•Pulse  100
•Renal impairment •Renal
•Ischemic cardiopathy failure
•Without major
Comorbidity •Digestive cancer •Liver
comorbidities
•Any other major failure
comorbidity •Metastases
•Mallory-Weiss
syndrome
•Any other
Diagnosis •Without highlighted
diagnostics
lesions and without
massive bleeding
Major signs of •Blood into the
•Without active
recent digestive tract, adherent
bleeding or just a
hemorrhage thrombus, visible
dark spot
at endoscopy bleeding vessel
 Patients with scores of up to 2 have a relapse rate of 5.3%
and mortality of 0.2%. They will be monitored for a short
time and will be discharged early from ICU.
 Patients with Rockall score 3 are likely to evolve unfavorably
and they require bleeding relapse prevention. Hemorrhagic
risk predictability allows the selection of cases that are
suitable for interventional endoscopic treatment and those
requiring continuous surveillance in ICU.
 Patients with signs of recent bleeding, such as active
bleeding, visible vessel or adherent clot on endoscopy, are
likely to rebleed in 50% of cases without an endoscopic
therapeutic intervention. Ulcers located on the small
curvature of the stomach and duodenum and those located
on the posterior wall are likely to produce an UGIB due to
the rich vascularization of those zones.
Resuscitation protocol for UGIB
1. Adequate venous access
1. Two large diameter intravenous cannula
2. Central vein catheterization if necessary
3. In case of myocardial infarction or severe ischemia,
pulmonary artery catheter
2. Bladder catheter
3. Hydroelecrtolytic rebalancing
4. Monitoring:
1. Blood pressure and its changes in standing (invasive
monitoring)
2. Pulse
3. Hematocrit
4. Flow of urine
5. Central venous pressure or cardiac output
5. Transfusion of blood and derivatives
6. Gastroenterology consult
7. Radiological or other investigations
Establishing the source of bleeding
 The presence of blood in the gastric aspirate after lavage,
indicates an UGIB. If gastric aspirate is negative, an upper
gastrointestinal endoscopic exploration could rule out the
superior digestive source of bleeding. Anyway, endoscopic
exploration should be performed also in cases with positive
gastric lavage.
 Intense bowel sounds indicate a superior source of
bleeding. The pain usually indicates a peptic ulcer, vomiting
before bleeding suggests Mallory-Weiss syndrome.
 If the patient has experienced a hemorrhage from a known
source, there are 70% chances to be a bleeding from the
same source.
 Particular attention is given to self-administration of drugs,
because there is a significant relationship between severe
bleeding and use of aspirin or other drugs.
 Physical examination may reveal an injury, bleeding
diathesis or stigmata of chronic liver disease.
Intensive care of patient with severe
gastrointestinal bleeding
Management of severe gastrointestinal bleeding

 Resuscitation and stabilization

 Assessment of onset and severity of bleeding
 Diagnostic endoscopy
 Therapeutic endoscopy – aims:
1. control of active bleeding or high-risk lesions
2. minimize complications related to endoscopic
treatment
3. treatment of persistent or recurrent bleeding
 Physical examination, history, gastric lavage will be
performed simultaneously with the initiation of
resuscitation.
 1-2 i.v. catheters with wide lumen, 14-16 G, will be
installed and blood samples will be harvested for laboratory
tests (Htc, Hgb, prothrombin time, partial thromboplastin
time, chemistry analysis, blood group and Rh).
 Saline will be rapidly infused to maintain systolic pressure,
above 100 mmHg and pulse under 100/min.
 Patients will be transfused with packed red blood cells,
platelets and plasma cryoprecipitate necessary to maintain
Htc over 24%, platelets over 50,000 and prothrombin time
less than 15 ".
 The surgeon and the gastroenterologist will examine the
patient as soon as possible to establish the diagnosis and to
indicate the appropriate therapy.
Criteria for a favorable prognosis:
(Bordley et al.)

1. Age under 75 years

2. Absence of concomitant unstable diseases
3. Absence of ascites
4. Normal prothrombin time
5. Systolic pressure over 100 mmHg at one hour after
admission
6. Gastric lavage without fresh blood at one hour after
admission
 Gastric lavage is used for 3 proposes: diagnosis,
preparation for endoscopy and hemostasis.
 The introduction of nasogastric tube should be done gently
to prevent the damage the nasal or digestive mucosa.
 Some authors contraindicate the introduction nasogastric
tube in cases of suspected esophageal varices due to the
risk of damage them and therefore bleeding. However,
atraumatic probe can be inserted gently in these cases also
without causing damage to the esophageal varices.
 The presence of blood in the gastric lavage fluid
demonstrates the UGIB. Blood characteristics can give us
information about the source of bleeding. If blood is bright
red, then very probable the source is a peptic ulcer. The
darker, venous, aspect of the blood indicates a source of
bleeding from esophageal or gastric varices.
 Nasogastric tube allows also the evaluation of the amount
of blood that is lost.
 The main purposes of gastric lavage are gastric emptying
and stop of bleeding.
 The first measure in stopping the bleeding from a peptic
ulcer is evacuation of blood from the stomach. A stomach
full of blood will still bleed.
 This maneuver also prevents the passage of the blood into
the intestines and its digestion and thus the increasing of
azotemia. In reducing azotemia, evacuation enema is also
useful.
 Gastric lavage may be performed with tap water or saline.
In most cases tap water is used. In many cases, iced cold
water is used for its vasoconstrictor effect, although there
are studies that deny the haemostatic effect of cold water
because of subsequent vasodilatation.
 Also, the lavage fluid may contain vasoconstrictor
(Adrenostazin), astringent and alkalizing agents.
 Lavage is repeated until the returning fluid shows no
further gastric content.
 In most cases of digestive hemorrhage due to ulcers or
drugs, bleeding can be stopped by this method after
using of about 2 liters of lavage fluid. Nasogastric tube
will remain in place because rebleeding is always possible.
 If after gastric lavage bleeding does not stop, endoscopic
hemostasis or other surgical methods are required.
 Bleeding from gastroduodenal ulcers
 Gastro-duodenal ulcers are the leading cause of upper
gastrointestinal bleeding (75% of cases)
 Bleeding may come either from small vessels of
inflammatory granulation tissue of the ulcer or from a
larger vessel, in the bottom of ulcer, as a result of its wall
erosion.
 Usually the massive bleeding is common in the posterior
duodenal ulcers, penetrating into the gastro-duodenal
(pancreatico-duodenal) artery.
 Ulcers with clean base is less likely to give a relapse, while
ulcers with a red or black spot on the base has a
recurrence rate of bleeding of 8%. When there are cloths
adherent to the ulcer’s base rebleeding occurs at a rate of
14%. Rebleeding has the highest rate (41%), and the
highest mortality, when there is visible vessel on its bottom.
 The following factors are known as a poor prognosis of
bleeding from gastro-duodenal ulcers associated with a
high morbidity and mortality:
1. Age over 60 years,
2. Coexisting medical illness,
3. Shock or orthostatic hypotension,
4. Coagulopathy,
5. Onset of the hemorrhage in the hospital,
6. Need for blood transfusion,
7. Evidence of fresh blood in the gastric aspirate,
8. High location of the gastric ulcer on the small
curvature (adjacent to the left gastric artery),
9. Posterior duodenal ulcer (adjacent to the gastro-
duodenal artery),
10.Endoscopic highlighted arterial type of bleeding or
visible vessel on the ulcer’s base.
Pharmacological therapy for those with acute
bleeding is a proton pump inhibitor (PPI) administered
immediately after endoscopic treatment. For example,
Pantoprazole i.v. 80 mg in bolus followed by an infusion of
8 mg per hour. If rebleeding does not occur within 24
hours, the patient will receive Pantoprazole 40 mg / day or
Omeprazole 20 mg / day.
 Somatostatin and its retard analogue Octreotide have the
advantage of reducing the splanchnic blood flow, inhibit
gastric acid secretion and have cytoprotective effects.
Somatostatin can be used as adjuvant therapy before
endoscopy in doses of 250 micrograms in bolus, followed
by hourly administration of the same dose for 3-7 days.
Octreotide dose is 50-100 micrograms in bolus followed by
25 micrograms per hour for 3 days.
Endoscopic therapy
 Endoscopic hemostasis is the most effective non-surgical
treatment of bleeding ulcers.
 Patients receiving endoscopic hemostasis are those who are
at high risk of rebleeding and those where endoscopy shows
active arterial bleeding, a visible vessel or adherent clot.
 Patients with clean ulcer base have a very low rate of
rebleeding and they can leave the intensive care unit soon
after endoscopy and can immediately start an oral diet.
 Endoscopic hemostasis aim is to coagulate the eroded vessel.
This can be achieved with various thermal devices:
– contact probe (monopolar, bipolar or multipolar electrocoagulation and
thermocoagulation)
– laser photocoagulation devices (yttrium-aluminum-granat laser-
NEODYN, Argon laser).
 These devices are effective in sealing arteries up to 2 mm
diameter, usually found in bleeding ulcers. Rebleeding: 10-
30%.
 Chemical hemostasis. Endoscopic hemostasis can be
achieved by injection of chemicals such as Adrenaline
(0.5 to 1 ml 1:10.000 - up to 10-15 ml- in and around
the bleeding point), Polidocanol or alcohol (98% total
volume less than 1 ml). It is an effective and inexpensive
method.
 Mechanical hemostasis. Endoscopic application of
clips (first introduced by Hayashi in Japan) on the
bleeding vessel has become popular in recent years. The
advantage of the method is that it does not produce
tissue damage and the risk of perforation is reduced.
Rebleeding risk is 2-20%.
 A relatively new method is endoscopic application of
fibrin glue to induce hemostasis and prevent bleeding
recurrence.
 Vessel Clips

Lesser curvature ulcer

Surgical therapy
 Absolute indications of surgical therapy are:
1. Failure of endoscopic therapy
2. Sustained hemodynamic instability despite resuscitation (more than three
units of blood transfused)
3. Recurrent bleeding after initial stabilization (up to two attempts of
endoscopic hemostasis)
4. Shock associated with recurrent bleeding
5. Reduced bleeding but persistent, requiring more than three units of blood
per day
 Relative indications of surgical treatment are:
1. A rare blood group
2. Refusal of transfusion
3. Emergency patient presenting shock
4. Advanced age
5. Severe associated disease
6. Chronic peptic ulcer known as the origin of bleeding
 These criteria also apply to elderly patients who do not bear prolonged
resuscitation, large amounts of transfusions and prolonged
hypotension.
Emergency surgical options:
1. Gastrotomy + suturing the bleeding vessel (in most cases located
on the posterior duodenal wall) + gastroraphy. It is the easiest way
to stop the bleeding, but because the ulcer remains in place,
bleeding can recur.
2. Excision of bleeding gastric ulcer + suture of the stomach. It can be
also an easy method when ulcer is in a facile location but it can be
difficult or impossible when it’s located on the posterior wall or under
the cardia.
3. Excision of the anterior duodenal ulcer + Pylorectomy /Pyloroplasty
(gastric drainage procedure) + troncular vagotomy (decreases the
acid secretion)
4. Bulb-antrectomy (with the removal of the ulcer) + troncular
vagotomy + gastro-duodenostomy (Pean procedure) – it seems to be
the best choice in duodenal ulcers and Johnson’s type III of gastric
ulcer. Vagotomy reduces the neurogenic stimulated acid secretion and
antrectomy reduces the secretion of gastrin.
5. In case of bleeding gastric ulcers Johnosn type II the procedure of
choice is gastric 2/3 gastric resection, including the ulcer, +
restoration of digestive continuity by gastro-duodenostomy (Pean) or
gastro-jejunostomy (Bilroth II) procedures.
6. In case of gastric ulcer Johnson type I (under the cardia), the easiest
and fastest solution is gastrotomy, visualization of bleeding source,
hemostasis by suture and gastroraphy. Other possibility is superior
gastric resection with eso-gastrostomy.

 In bleeding gastric ulcer the main problem is the

differential diagnosis between the benign and
malignant ulcer. Whenever possible, a biopsy specimen
should be obtain preoperatively.
 If surgery has to be performed in emergency condition,
two solutions are available depending on patient
condition:
1. In unstable patients, simple gastrotomy +
hemostatic suture + biopsy + gastroraphy. Then, if
the histopathologic diagnosis is cancer, the patient
should be reoperated (respecting the oncological
principles) when its general condition permits.
2. In stable patients, who can bear a more complex
operation, the ulcer should be considered as malignant
and resection whenever possible should be performed
with curative intention. Another possibility is to send a
specimen of ulcer tissue to frozen sections examination
and wait for result, and then continuing the operation
according to histopathological findings. (simple
resection or oncological resection)
 Bleeding from esophageal varices
 Four major issues are important in the prevention of
morbidity and mortality and for treatment in case of
esophageal varices:
1. Prediction of patients at risk
2. Primary prophylaxis against bleeding from varices in patients with
cirrhosis
3. Treatment of active bleeding
4. Prevent rebleeding
 Current definitions:
– time zero is the time of admission to a medical facility.
– clinically significant bleeding is defined as a necessary of blood
transfusion of two or more units within 24 hours from time zero,
together with a systolic blood pressure below 100 mmHg.
– acute bleeding episode is the event occurring within 48 hours
from time zero. Bleeding in this time interval is considered a
treatment failure.
 Esophageal varices develop when the gradient pressure
between the porta and hepatic veins is greater than 12
mmHg.
 Many clinical and physiological factors are useful in
predicting bleeding from varices in cirrhotic patients:
a) Location of varicose veins: distal esophagus, stomach.
b) The size of varicose veins: varices occupying more than 1/3 of the
esophageal lumen.
c) The endoscopic appearance of varicose veins: "red marks" (red
streaking or spotting).
d) Clinical signs: the degree of hepatic dysfunction according to Child-
Pugh classification.
e) Bleeding in patient’s history.
f) The pressure in varices. The incidence of bleeding according to the
pressure is:
 - 13 mmHg - 0%;
 - 14 mmHg - 9%;
 - 15 mmHg - 17%;
 - 16 mmHg - 50%;
 -> 16 mmHg - 72%.
Therapeutic options in bleeding varices
 Although there is no unanimity, most authors agree that
therapy begins with stabilizing the patient and
confirming the diagnosis. The patient will be monitored
in an intensive care unit.
 Resuscitation is initiated by volume rebalancing with
blood and blood substitutes.
 Irrational use of saline solutions should be avoided as
worsening ascites and portal hypertension due to
secondary hyperaldosteronism present in cirrhosis.
 Nasogastric lavage is beneficial in removal of blood and
for stomach decompression, decreasing the risk of
aspiration into the lungs and facilitating the endoscopic
exploration.
A. Medical treatment
 Use of isosorbide 5-mono-nitrate (20 mg 2X/zi) is safe
and effective in preventing first bleeding, administered for
at least 2 years.
 Vasopressin reduces portal pressure by constricting
mesenteric arterioles. 0.4 U in bolus is administered and
then continue with 0.4 to 1 U/min infusion. Vasopressin
has a high incidence of cardiac complications due to
nonspecific vasoconstriction.
 Terlipresin is a long acting congener of Lizin-vasopressin
which has less side effects.
 Somatostatin infusion results in a selective splanchnic
vasoconstriction without cardiac complications and it is
considered more effective than vasopressin. The dose of
Octreotide (Sandostatin) is 25-250 micrograms/hour.
 Somatostatin is considered as initial therapy until the
elective treatment. The effects are antisecretory
(inhibiting gastric acid, pepsin secretion and gastrin),
increases gastric mucus production, and decreased blood
flow in the azygos vein and esophageal varices in portal
hypertension. Somatostatin inhibits the release of
vasodilator hormones such as glucagon, producing
moderate vasoconstriction and thereby decreasing
splanchnic portal flow.
 If existing coagulopathy can not be adequately corrected
with FFP (fresh frozen plasma) then or/and rFVIIa
(recombinant human factor VIIa - NovoSeven) will be
given in a dose of 80 micrograms / kg in 30 minutes.
B. Balloon tamponade for esophageal varices
 There are three types of probes with balloon:
Sengstaken-Blakemore, Linton-Nicholas and Minnesota
probe, each with two balloons, gastric and esophageal of
different forms. It is considered that balloon tamponade
has a 85-98% initial success, but after removing the
balloon rebleeding rate is of 21-60%. This method has
an incidence of 30% severe complications such as
aspiration pneumonia, oesophageal rupture and airway
obstruction. There are no significant differences in
efficiency between balloon tamponade and vasopressin.
Esophageal balloon tamponade kit
C. Endoscopic procedures
1. Sclerotherapy of esophageal varicose veins
 The aim of sclerotherapy is the initial hemostasis
followed by sclerotherapy weekly until all varices are
obliterated.
 Esophageal varices are more suitable for endoscopic
therapy than those located in the stomach.
 Complications of endoscopic sclerotherapy are:
esophageal ulcers that can bleed or perforate,
esophageal strictures, mediastinitis, pleural effusion,
aspiration pneumonia, ARDS, chest pain and
suprainfection.
2. Rubber band ligation of esophageal varices
 Varices are suctioned into a cylinder and then, a
tensioned rubber band is downloaded at its pedicle.
The rubber band will strangulate the varices producing
hemostasis but also after a few days the varices will be
eliminated because the rubber band will slowly cut the
pedicle.
 It has been shown that the method is equally effective
in achieving haemostasis and preventing rebleeding as
sclerotherapy, but with fewer local complications
(mainly stricture). The technique is more difficult to
perform in active bleeding than sclerotherapy.
 I.v. administration of Ocreotide or Somatostatine
Emergency Endoscopic Variceal Band Ligation, or
Endoscopic ScleroTherapy

Bleeding stops Bleeding continue Early rebleeding

Early rebleeding

Blakemore tamponade ± Ocreotide or Somatostatine

TIPS (Transjugular Intrahepatic Portosystemic Shunt) or surgery

D. Surgical therapy of bleeding varices
1. Porto-systemic shunts were the most commonly
used therapy in the '70s, but were encumbered by a
mortality of 50%. Many types of porto-systemic shunts
have been applied to reduce portal hypertension.
2. Distal spleno-renal shunt (Warren-Zeppa) was
practiced in order to prevent certain complications,
particularly portal encephalopathy. This technique is
more difficult, produces a smaller decrease in portal
tension, but does not interfere with subsequent liver
transplantation.
 Compared with sclerotherapy, surgical shunts
significantly reduce bleeding recurrence rate, but does
not alter survival. Some authors suggest combining
shunts with sclerotherapy to improve survival.
3. There have been developed some surgical
procedures, without a portal-systemic shunt :
1. Esophageal transection with varying degrees of
devascularization
2. Esophageal transection with extended devascularization and
splenectomy
3. Procedures that include splenectomy or intrathoracic
transposition of the spleen.
 Esophageal transection by stapler is
recommended if rebleeding occurs after two sessions
of sclerotherapy.
 Sugiura proposed an emergency technique that is
extended devascularization of the esophagus plus
splenectomy, selective vagotomy and pyloroplasty. His
results were: 13.3% operative mortality rate and just
1.5% of bleeding relapse.
E. Transjugular intrahepatic porto-systemic
shunt (TIPS)
 It is an interventional radiology procedure in which a
metallic stent, of 8-10 cm length and up to 8-12 mm
diameter is placed percutaneously intrahepatic to
performed a portosystemic shunt and thus the gradient
pressure between portal vein and hepatic veins is
significantly decreased.
 The method is expensive, effective for short time control
of bleeding from varices, but stent obstruction, followed
by recurrence of bleeding, occurs in 59% of patients
after two years. In addition, it induces portal
encephalopathy in 10-20% of cases.
 This method does not interfere with subsequent liver
transplantation.
F. Liver transplantation
 Stress ulcers
Definition and clinical features
 Stress ulceration is the most common cause of
gastrointestinal bleeding in intensive care unit and it
increases mortality in those patients for up to five times.
The risk of stress ulcers complicated by significant
bleeding is estimated at 1.5 to 5% in patients from
intensive care unit.
 Stress ulcers are erosions of the digestive mucosa that
generally appear in the gastric fundus but sometimes also
in the antrum, duodenum and distal esophagus. Generally
erosions are superficial, the source of bleeding being the
capillaries, but deeper lesions can erode the submucosa
causing massive bleeding and /or perforation.
Pathogenesis
 Mucosal lesions occur when the effects of gastric acid and
pepsin exceed the gastric mucosal defense mechanisms:
1. by excessive production of acid and pepsin (aggressive factors)
2. by overcoming the defensive factors of gastric mucosa
1. Physiological mechanisms of gastric mucosa defense:
1. secretion of mucus and bicarbonate, which forms a protective
layer on the cell surface,
2. rapid regeneration of damaged cells,
3. endogenous prostaglandin production,
4. the maintenance of an adequate gastric mucosal blood flow.
 Breaking one of the mechanisms of mucosal defense will
result in the inability to maintain a pH gradient and allows
both acid and pepsin to produce mucosal lesions.
1. Mucus has three functions:
1. Mechanical protection of the epithelial surface
2. Prevents the retrodiffusion of pepsin
3. Focuses the bicarbonate secreted by gastric mucosa on the
epithelial cell surface.
 Neither mucus, nor bicarbonate alone can prevent the
diffusion of hydrogen ions to the surface of the mucosa.
The combination of the two mechanisms maintains a pH
of 7 to the lining surface when the intraluminal pH is 2.

1. Cell membranes are also part of the barrier to

hydrogen ions, being composed of phospholipids. These
phospholipids allow diffusion of soluble molecules but
prevent diffusion of hydrogen ions. Bile salts, which are
natural detergents, harm the cell membrane by dissolving
the lipid components.
 Gastric epithelial cells have the capacity for rapid
regeneration. Under normal conditions, epithelial cell
surface is completely replaced by the progenitor cells of
the basal lamina every 3 days. In acute injuries the
epithelium may be replaced in a few hours. Erosions
destroy the progenitor cells and stop reepitelization.

3. Endogenous prostaglandins do not have a direct

protective effect on gastric mucosa but they help
through other mechanisms: stimulating mucus and
bicarbonate production, increase the concentration of
phospholipids in cell membranes, decrease acid
secretion, stimulates cell regeneration and increase
blood supply of the mucosa.

4. Inadequate gastric mucosa blood flow is one of

the primary factors contributing to the "stress gastritis."
Decreased blood flow results in decreased oxygen and
nutrients to the gastric mucosa.
 There are two major risk factors for bleeding:
1. Mechanical ventilation for more than 48 hours, and
2. Coagulopathy.
 Other risk factors are: shock, sepsis, liver failure, renal
failure, multiple trauma, burns over 35% of body surface,
post-transplant, head and column trauma, history of peptic
ulcer or SDGB.
 As long mucosal blood flow is adequate, the bicarbonate is
available to neutralize the retrodiffused hydrogen ions into
the cells.
 Shock and hypoperfusion not directly cause erosion of the
gastric mucosa. Mucosal damage occurs as a result of
reperfusion. Reperfusion of ischemic cells after shock,
potentiates mucosal lesions by releasing oxygen free
radicals. These radicals attack the lipids increasing the
membrane permeability for acid.
 Neutralization of acid by the gastric mucosal cell depends
not only on the gastric mucosal blood flow, but also on
systemic acid-base balance. Systemic acidosis in shock
exacerbates the gastric mucosal lesions.
 There have been described several "barrier destroyers“:
aspirin, nonsteroidal antiinflammatory drugs (NSAIDs) and
alcohol. NSAIDs block the formation of prostaglandins
leading to changes in the layer of mucus and
polysaccharides. Alcohol lowers glutathione, which is a
"scrubber“ of free radicals. Urea, in chronic renal failure,
also compromises the barrier. Steroids decrease mucus
production and lead to changes in the composition of
polysaccharides.
 However gastric lesion does not occur in the absence of
intraluminal acid and pepsin.
Clinical picture
 Acute gastric mucosal erosions are found in 60-100% of
critical patients at endoscopy. In most cases they heal
spontaneously in 10-14 days in parallel with the
improvement of the primary disease.
 Patients in intensive care unit, with stress ulcers, do not
have pain or other gastrointestinal symptoms compared to
other patients with peptic ulcer. In addition, many patients
are unable to report symptoms because they are
mechanically ventilated or have mental status changes.
 Stress lesions become clinically apparent only when they
are complicated with hemorrhage or perforation.
 Generally bleeding is manifested by a gradually declining
of the hematocrit or occult blood loss, highlighted in
gastric aspirate or by positive Hemocult test from stool. An
active hemorrhage manifested as a frank haematemesis or
melaena, with tachycardia and hypotension, is a clear
indication for emergency endoscopy.
 Endoscopy is the "gold standard" for diagnosis of stress
ulcers. In addition, endoscopic treatment can be done to
stop an active bleeding or prevent a bleeding recurrence.
 Barium studies have no role in the diagnosis of stress
bleeding in intensive care patients.
 If the endoscopy is negative, angiography may
occasionally detect a lesion with active bleeding or a
little bleeding ulcer.
Prognosis
 Bleeding stops with medical treatment in most cases, but
2-6% of patients, who develop severe bleeding, require
surgery.
 Mortality in patients with gastric stress ulcers is usually
due to the underlying disease and not to bleeding. Only
12% of cases are assigned to hemorrhage, the
remaining of 88% are based on disease specific
mortality.
 Stress gastritis associated to multiple organ failure
syndrome is considered a poor prognostic sign.
Prophylactic treatment of bleeding from stress
ulcers

 Different agents were studied in an attempt to prevent

acute mucosal lesions in patients with critical stress:
1. Antacids
2. Histamine receptor antagonists
3. Proton pump inhibitors
4. Prostaglandin analogues
5. Sucralfate (citoprotector agent)
6. Enteral nutrition

 Antacids: neutralize the stomach acid, stimulate

prostaglandin synthesis in gastric mucosa and thus
improving its irrigation. Disadvantages are: short-term
effectiveness, osmotic diarrhea, acid secretion rebound by
hypergastrinemia, mucosal micro trauma by microcrystals
of aluminum, hypophosphatemia and hypomagnesemia.
 H2 receptors blockers increase the gastric pH and
decrease the stimulatory effects of histamine on parietal
cell acid secretion. H2 blockers administration in
continuous infusion allows a better control of gastric pH
but with notable complications such as interstitial
nephritis, confusion, and thrombocytopenia. Ranitidine
and Famotidine give less mental confusion and
antiandrogenic effects. It is reported an increased
incidence of nosocomial pneumonia in patients in
therapy with antacids: bacterial colonization of the
stomach was demonstrated in 100% of cases when
gastric pH was continuously maintained above 4.
 Anticholinergic drugs (pirenzepina) decrease the gastric
acid production by producing a vagal blockade, however,
achieving only a small increase in gastric pH. Side effects
are tachycardia and central nervous effects (agitation,
dizziness).
 Proton pump inhibitors (PPI): omeprazole, esomeprazole,
lansoprazole, pantoprazole, rabeprazol.
 Inhibition of acid secretion is achieved rapidly by iv
administration. A dose of 80 mg esomeprazole in bolus
over 30 minutes, followed by a continuous infusion of 8
mg/hr administered for 3 days (72 hours).
 PPI are more effective in stopping and preventing active
bleeding than H2 blockers because gastric pH control is
more accurate, and platelet aggregation and blood clot
formation is enhanced at pH values above 7.
 Prostaglandins: administration of endogenous
prostaglandin increases the irrigation of mucosa, the
mucus and bicarbonate secretion, stimulates epithelial cell
regeneration and inhibits gastric acid secretion. Analogues
of prostaglandin E1 and E2 were used in the prophylaxis
of stress ulcers. The Misoprostol, a prostaglandin E1
analogue, has an efficiency similar to antacids, but causes
diarrhea in 25% of cases and is more expensive.
 Sucralfate is a cell protector agent. It is an aluminum
salt of sucrose composed of 8 sulphate groups. At a
gastric pH below 3, dissociation of aluminum hydroxide
ions occurs forming polymerized viscous mass covering
gastro-duodenal mucosa. Thus, it protects the lining
against the action of hydrochloric acid, pepsin and bile
acids, and it improves the mucosal irrigation stimulating
prostaglandin release.
 It is not absorbable, does not modify the gastric pH and
it has a bactericidal effect. It is a drug of choice, given
the low incidence of nosocomial pneumonia compared
with other drugs.
 Sucralfate is also the drug of choice for prophylaxis of
bleeding and stress ulcers, in a dose of 3x2 g/day as a
suspension, in acute coronary syndromes, acute
myocardial infarction with thrombolytic therapy or
unstable angina.
 Early enteral nutrition is recommended by many authors in
the prevention of stress ulcers. Small amounts of foods
have a protective effect even in cases of ileus, or when
other medical conditions do not permit usually enteral
nutrition. Enteral nutrition is not important for increasing
gastric pH, but it can prevent depletion of energy needs in
gastric epithelium, thus avoiding necrosis and ulcer
formation.
Treatment of bleeding from stress ulcers
 In most cases, bleeding will stop under medical treatment.
The objectives of treatment are mainly targeted to the
underlying disease and to eliminate additional stress. If
the stress is removed, the digestive mucosa heal
spontaneously. Treatment aims primarily rapid
resuscitation of shock, rapid restoration of intravascular
blood volume, sepsis treatment, acid-base rebalancing,
correcting the coagulation defects, ventilator and
nutritional support.
 Gastric lavage is performed to empty the stomach and
prepare the patient for endoscopy.
 Early endoscopy is performed to determine the source of
bleeding. Endoscopic control of bleeding is rarely
possible due to the diffuse nature of bleeding from
stress gastritis.
 Angiographic embolization of bleeding sites is possible
but diffuse nature makes it difficult to control bleeding
permanently.
 Surgery is a last alternative therapy being less practiced
in recent years. Most reports of surgical therapy for
stress gastritis dates from the '70s. Suggested surgical
operations are : vagotomy and pyloroplasty with or
without haemostatic suture, vagotomy and antrectomy,
subtotal or total gastrectomy. The overall mortality was
55%.
 In conclusion, currently available data show that
prophylactic medical therapy, reduces bleeding in
patients with stress gastritis from 15% to 3%.
 Esophagitis
 Acute hemorrhage from esophagitis is treated by H2
receptor blockers or PPI medication in cases when the
patient has resumed eating. Endoscopy or surgery are not
a choice for the treatment of bleeding esophagitis.

Mallory-Weiss syndrome
 There are longitudinal lacerations of the mucosa at the
gastro-oesophageal junction. The pathogenesis is not yet
well understood. Lesions seem to be produced by increased
transmural pressure. The syndrome is linked to the effort of
vomiting, coughing, defecation, hiccups and seizures.
 Bleeding usually stops without therapy but in cases of
active bleeding endoscopic therapy is practiced successfully
with bipolar electrocoagulation, photocoagulation or
injection therapy. Relapse is rare after endoscopic therapy
and occurs more often in patients with portal hypertension.
 Dieulafoy lesion
 It is caused by a submucosal artery, large, aberrant, that
brakes into the gastric lumen and cause serious bleeding,
usually located at 6 cm from gastro-esophageal junction. It
is characterized by recurrent gastric bleeding without an
obvious source, unless the vessel is visible. There are no
ulcerative changes.
 Endoscopic treatment has an incidence of recurrence of
50%. Definitive treatment is surgical resection.
Upper gastrointestinal angiodysplasia
 Angiodysplasia is represented by enlarged submucosal
vessels, that appear like a spider-shaped lesion, of red color
at endoscopy. The cause is unknown. Some patients have
Rendu-Osler-Weber disease, chronic renal failure, cirrhosis
and aortic stenosis. Angiodysplasia can occur also in
intestines. Bleeding is usually self-limited or occult but may
be massive.
 Endoscopic therapy may stop bleeding thereby decreasing
the need for blood transfusions.
Endoscopic hemostasis
using hemoclips
 Upper gastrointestinal tumors
 Represent 1% of severe upper gastrointestinal bleedings.
Bleeding occurs from esophageal or gastric ulcerated
tumors.
 The endoscopic control of active bleeding allows the patient
hemodynamic stabilization before surgical resection.

Aorto-enteric fistula
 Most fistulas are associated with the placement of an
intraaortic prosthesis. Common location is in the 3rd portion
of duodenum while other segments of the small intestine or
colon may be affected as a consequence of erosion of the
intestinal wall. Typically, the patients with aorto-enteric
fistula have a small initial hemorrhage, known as heraldic
bleeding that occurs before a massive hemorrhage.
 Surgical treatment is to by-pass the affected artery and
repair of intestinal damage or removal of the prosthesis and
fistula and to make an axilo-femoral bypass.
 Watermelon stomach
 The anomaly is more common in women and is related to
severe liver disease and renal failure. Laser
photocoagulation was successful in many cases but
surgical resection is the treatment of choice.

Watermelon stomach
 Hemobilia and hemosuccus pancreaticus
 Hepatic arterio-portal fistulas may occur as a result of
trauma or rupture of a hepatic artery aneurysm.
Angiography is the diagnostic procedure of choice but
Doppler ultrasound is also used. Treatment is indicated
even in asymptomatic cases to prevent portal
hypertension. Embolization is performed for intrahepatic
fistulas and surgery for extrahepatic fistulas.
 Hemobilia may complicate liver transplantation at biliary
anastomosis level. If bleeding is early, Kehr drainage will
be performed. Angiographic embolization is indicated but
when it is not technically possible surgical treatment
should be applied.
 Hemosuccus pancreaticus occurs most frequently in
connection with the formation of pseudoaneurysm and
pancreatitis and are produced by hepatic and splenic
artery aneurysms. Although ultrasound, magnetic
resonance and CT scan reveal a pancreatic pseudocyst,
angiography is necessary to highlight the blood flow and
thus clarify the diagnosis. Temporary hemostasis is
performed before surgery through an arterial catheter.
 ARTERIAL PATHOLOGY

 Vessels anatomy and physiology

1. Arterial trauma
2. Arteriovenous fistulas
3. Arterial aneurysms
4. Acute peripheral ischemia
5. Chronic obstructive arterial disease
Anatomical and physiological aspects of the
vascular system
 Vascular system is represented by a network of blood
vessels that carry the blood from the heart to tissues and
vice versa, the heart being the main pump that moves the
blood.
 There are two vascular circuits: pulmonary and systemic.
 Pulmonary circuit leads venous (deoxygenated) blood
collected by the right heart to the lungs to be oxygenated,
and from there back to the left heart. In this circuit
oxygenated blood is carried by veins (returning vessels –
pulmonary veins) not by arteries like in systemic circuit.
 Systemic circuit carries oxygenated blood and nutrients
through the arteries to tissues where, at level of capillary
bed, takes place the exchange: blood releases oxygen and
nutrients towards tissues and is loaded with carbon dioxide
and waste.
 Deoxygenated blood is transported by veins to the right
heart (atrium and ventricle) and from there to the
pulmonary circuit. Wastes are transported by arteries to
the liver and kidneys where they are metabolized and
eliminated.
 Blood vessels leaving the heart are called arteries and
those arriving are called veins. The arterial and venous
system are interconnected by small vessels called
capillaries.
 In their journey from the heart towards tissues, the
arteries ramify and blood passes through vessels of six
principal types: elastic arteries, muscular arteries,
arterioles, capillaries, venules and veins.
 From heart towards tissues, arteries show a progressive
diminution in diameter from about 25 mm in the aorta to
0.3 mm in some arterioles.
Structure of the Artery Wall
 Blood vessels are not simply rigid pipes. They are active
organs, elastic, with a complex structure. The artery wall
consists of three layers:
1. Tunica Adventitia - the outer layer of arteries and veins.
It is composed of connective tissue, collagen and elastic
fibers. These fibers allow the arteries and veins to stretch
to prevent overexpansion due to the pressure that is
exerted on the walls by blood flow.
2. Tunica Media - t is composed of smooth muscle and
elastic fibers. This layer is thicker in arteries than in veins.
The structure also depends on the type of artery and
determines the mechanical properties of the arterial wall.
In larger arteries it consists of connective tissues, elastic
tissue and elastic fibers. In smaller arteries, smooth
muscle cells replace the elastic fiber layer.
3. Tunica Intima (endothelium) - the inner layer of arteries
and veins, an interface between circulating blood and
blood vessel wall. It is composed of an elastic membrane
lining and smooth endothelium (special type of epithelial
tissue).
 Endothelial cells are involved in many aspects of vascular
biology, including:
 Atherosclerosis
 Barrier function - controlling the passage of materials and white blood
cells into and out of the bloodstream.
 Blood clotting (thrombosis & fibrinolysis). The endothelium normally
provides a non-thrombogenic surface.
 Inflammation
 Angiogenesis
 Vasoconstriction and vasodilatation, and hence the control of blood
pressure
 Specialized 'filtering' functions in some organs (the renal glomerulus and
the blood-brain barrier)
 Impaired endothelial function causes hypertension and thrombosis
 The arterial system is also fundamentally involved in the
physiology of blood flow and homeostasis of blood
pressure, in coagulation and fibrinolysis, in achieving the
inflammatory and immune response and also in
lipoprotein metabolism.
 It seems that the endothelial cell due to the roles
assigned to it in various systems of regulation is the cell
with the most and perhaps most important functions in
the body.
 Because of the essential antithrombotic role of the
endothelial cells, vascular surgery is practiced with full
protection of the vascular endothelium.

 Although both carry blood, there are major differences

between the arterial and venous system both in terms of
anatomic structure and physiology, which must be
known to understand the pathology of blood vessels.
 Differences between arteries and veins
Arteries
1. Transport blood away from the
heart
2. Carry oxygenated blood
(except in the case of the
pulmonary artery)
3. Have relatively narrow lumen
4. Have relatively more
muscle/elastic tissue
5. Transports blood under higher
pressure than veins
6. Do not have valves (except for
the semi-lunar valves of the
pulmonary artery and the
aorta)
Veins
1. Transport blood toward the
heart
2. Carry de-oxygenated blood
(except in the case of the
pulmonary vein)
3. Have relatively wide lumen
4. Have relatively less
muscle/elastic tissue
5. Transports blood under lower
pressure (than arteries)
6. Have valves throughout the
main veins of the body.
Arteries are divided into four types:

1. Elastic Conducting arteries:

 Are represented by the largest arteries: aorta and its
branches
 They have a large diameter: 2.5 to 1 cm
 Because of the large diameter they have a low
resistance pathway
 Their wall contains most elastic fibers which enables
them to withstand high pressure. Muscular layer is not
active in vasoconstriction.
 Inside the artery the flow is pulsatile. They expand in
systole and recoil in diastole.

2. Muscular Distributing arteries:

 Their diameter is smaller (1 cm to 0.3 cm)
 They deliver blood to specific organs
 Their muscular layer is well developed being active in
vasoconstriction and vasodilatation
3. Arterioles:
 Their diameter is between 0.3 cm and 10 micrometer.
 Large arterioles have more smooth muscles but smaller
arterioles have a small amount of muscles.
 They constrict and dilate in response to neural and
chemical stimuli and represent the most important site of
resistance in the whole systemic circulation.

4. Metarterioles:
 They are short vessels that links arterioles and venules.
 The muscular layer is composed of smooth muscle cells
placed a short distance apart, each forming a
precapillary sphincter that encircles the entrance to that
capillary bed.
 Constriction of these sphincters reduces or shuts off
blood flow through their respective capillary beds. This
allows the blood to be diverted to elsewhere in the body.
 Capillaries have the endothelial layer placed on a
basement membrane. The more metabolically active the
cells, the more capillaries present in the tissue. They are
of three types: continuous (endothelial cells provide an
uninterrupted lining), fenestrated (have pores in the
endothelial cells) and sinusoidal (a special type of
fenestrated capillaries that have larger openings) (Ex. In
the liver, spleen)
 Arterial branches have anastomosis between them at
different levels so that a particular anatomical region
receives blood from several sources → vascular
collateral circulation.
 The degree of extension and function of collateral
circulation differs from one area to another (from one
organ to another), being the least well represented in
the coronary arteries, renal and retina where the
circulation is of terminal type ("end arteries").
 Development and functional status of collateral
circulation is an issue of utmost importance in case of
arterial occlusion. In such situations, the effectiveness of
collateral circulation depends on the type of occlusion:
acute or chronic occlusion.
Blood Flow
 The pumping action of the heart generates blood flow.
Blood flow and pressure are unsteady. The cyclic nature
of the heart pump creates pulsatile conditions in all
arteries. The blood flow that passes through a given
blood vessel depends directly on gradient of pressure
between the two ends of the blood vessel and indirectly
on the resistance of blood movement. Normal arterial
flow is laminar with secondary flows generated at curves
and branches.
 Turbulent flow induces:
1. An increase of platelet count near the intima layer of the vessel
2. Increased time of contact between platelets and endothelium
3. A decreased rate of clearance of procoagulant factors at interface
between endothelium blood stream
 Blood vessels are not simple pipes (they have the ability
to adapt to differences in pressure and also to adjust the
pressure by the action of their muscular layer). On the
other hand, blood is not a simple fluid but a liquid tissue
that has a certain viscosity and can, under certain
conditions to clot forming plugs that can obstruct the
vessels.
 In normal laminar flow all the blood cells and platelets
occupy the central (axial) stream. The periphery of the
blood stream, adjacent to the endothelium, moves more
slowly and is composed of blood plasma.
 Stasis and turbulence in this flow caused by vascular
disease, chronic congestion, external compression and
by a lack of movement of the muscles that normally
"pump" blood through the veins, may cause dysfunction
or damage to the endothelium and brings blood platelets
into contact with the endothelial cells permitting the
build-up of thrombi.
Blood pressure is the force exerted by blood flow on the
walls of blood vessels. (mmHg). The blood flows from
high to low pressure (gradient). Pressure results when
flow is opposed by resistance. Blood pressure always
refers to systemic arterial blood pressure in the large
arteries.
Pulse Pressure represents the difference between systolic
and diastolic blood pressure. Systolic = 120 mmHg,
Diastolic = 70 to 80 mmHg. Pulse pressure is felt as the
pulse: pulsation in an artery in systole.
Mean Arterial Pressure (MAP) represents the average
of blood pressure. Diastolic is more important because
diastole is longer than systole in a single cardiac cycle.
MAP = Diastolic Pressure + 1/3 (Pulse pressure)
Peripheral Resistance depends on:
1. Blood viscosity: plasma proteins and blood cells (RBC’s)
make blood viscous. It is normally constant. Blood is
approximately four times more viscous than water.
2. Blood vessel length: the longer the vessel the more
resistance (normally constant). Blood vessels can’t
become longer but can become shorter as a result of
arterio-venous shunts. This leads to decrease of
resistance but also to increase of venous flow and
pressure.
3. Blood vessel diameter is the most important in
determining peripheral resistance. The smaller the
diameter result in more friction and higher resistance.
Because arterioles can dilate and constrict they are the
major determinants of peripheral resistance.
 Blood pressure is highest in the aorta and decreases
steadily until the arterioles.
Methods of investigation and treatment in
surgical diseases artery
 Arterial surgical techniques developed and diversified
greatly in recent years, supported largely by modern
methods of diagnosis and preoperative evaluation of
surgical diseases of the arteries.
 Methods of investigation:
Non-invasive:
1. Oscillometry
2. Plethysmography
3. Determining the leg-arm index
4. Effort test
5. Ultrasound and Doppler ultrasound
6. Nuclear magnetic resonance and computed tomography in some cases
Invasive: angiography (arteriography).
 The gold standard in exploring arteries remains the
angiography, but it is not mandatory in all cases.
Oscillometry is now an outdated method which offers just
indicative data about peripheral arterial pathology.
 The principle of the method is the measurement of
transmitted intra-arterial pulsations to the occluding cuff
surrounding the limb. It measures the peak of oscillations
of the mean arterial pressure (oscillometric index). It
compare the amplitude of oscillations making
simultaneous measurement in different parts of the body.
 The instrument is called Pachon's oscillometer (1900)
which is an improvement over the oscillometer devised by
Heinrich von Recklinghausen (1867-1942). It was widely
used during World war I and between the world wars.
 Over the time, improvements were made represented by
automated instrumentation using plethysmographic
sensors, pulse-wave velocity sensors and ultrasonic
microphones.
Oscillometers
Plethysmography measures the changes in limb volume
induced by cardiac activity. It was, for a long period of
time, the main way of non-invasive investigation of
peripheral arteries, now replaced by direct imaging
methods.
The Ankle Brachial Pressure Index (ABPI), is the
ratio between the blood pressure in the lower limbs and
that in arms. Compared to the arm, lower blood pressure
in the leg is an indication of blocked arteries (peripheral
vascular disease). The ABI is calculated by dividing the
systolic blood pressure at the ankle by the systolic blood
pressures in the arm. The value is usually between 0.91-
1.3, the degree of alteration of its values quantifying the
degree of peripheral obstruction. Analysis can be
sensitized by performing measurements in an effort test.
 A Doppler ultrasound probe and a sphygmomanometer
are usually needed. The blood pressure cuff is inflated
proximal to the artery. Measured by the Doppler probe,
the inflation continues until the pulse in the artery ceases.
The blood pressure cuff is then slowly deflated. When the
artery's pulse is re-detected through the Doppler probe
the pressure in the cuff at that moment indicates the
systolic pressure of that artery.
 ABPI drawbacks:
1. Is unreliable on patients with arterial calcification which results in
less or incompressible arteries, as the stiff arteries produce falsely
elevated ankle pressure, giving false negatives.
2. Is time consuming.
3. Resting ABPI is insensitive to mild peripheral arterial disease
requiring testing during effort which is not suitable for patients
with co-morbidities.
4. Lack of protocol standardization.
5. Skilled operators are required.
 ABPI interpretation

Measurement Interpretation
>0.90 Normal
0.71-0.90 Mild obstruction
0.41-0.70 Moderate obstruction
0.00-0.40 Severe obstruction
Ultasonography (transthoracic echocardiography or
transoesophageal, Doppler ultrasound of peripheral
arteries, etc.) is the most common current method used
in diagnosis of vascular diseases.
 The ability to detect blood flow velocities and waveform
characteristics allow the surgeon to understand the
hemodynamic significance of a vascular disease.
 Advantages:
– Does not require intravenous or intra-arterial access
– Does not expose the patient to contrast substances
– The examination device is portable, which allows evaluation in
the emergency room, intensive care unit, and/or operating room
– Duplex scanning is also one-tenth of the cost of conventional
arteriography.
Standard computed tomography (CT-scan) is used in
the investigation of large vessels pathology when both
transesophageal ultrasonography and magnetic resonance
are unavailable (or if MRI is contraindicated). A variant of
this method, known as spiral CT, is more accurate but
more expensive.
Computed tomography angiography is a more sensitive
and specific method of investigation, with easy access
and excellent diagnostic capability. A CT angiography of
the lower extremity is obtained by injecting a bolus of
intravenous contrast through the peripheral venous
system. After an appropriate delay, a CT of the lower
extremities is obtained while the arteries fill with contrast.
The image can then be quickly reformatted to visualize
the appropriate vessels. Computed tomography findings
that suggest arterial injury include contrast extravasation,
pseudoaneurysm formation, abrupt narrowing of an
artery, loss of opacification of an arterial segment, and
arteriovenous fistula formation.
 CT angiography

Stent in SMA

Plaques
 CT angiography may give more precise anatomical detail
than magnetic resonance imaging (MRI), particularly in
small blood vessels.
 CT angiography has still some risks and limitations:
– Exposure to radiation. However, the benefit of an
accurate diagnosis far outweighs the risk.
– Allergy to x-ray contrast material.
– Extravasation of contrast can cause tissue damage.
– Contrast nephropathy.
– Very large patients may not fit into the opening of a
conventional CT scanner or may be over the weight
limit
 Nuclear magnetic resonance is a non-invasive
exploration which provides significantly better resolution,
but is expensive and rarely available in emergency. It is
indicated in long-term monitoring of large artery
pathology.
Angiography is a procedure which uses x-ray and contrast
substances to highlight arteries and veins and to observe
the blood flow through them.
 While performing this procedure a thin catheter is inserted
into a blood vessel and guided to reach the area to be
examined. Through that catheter a dye is injected and the
vessel appears highlighted when x-ray images are taken.
Images can be stored also as radiological film in a digital
form.
 Benefits
– It may eliminate the need for surgery.
– Catheter angiography presents a very detailed, clear and accurate
picture of the blood vessels.
– It offers the possibility to assess vessels in specific body sites
(superselective angiography).
– It makes possible to combine diagnosis and treatment in a single
procedure (angioplasty, placement of a stent, embolization).
 Risks:
– Heart attack
– Stroke
– Trauma to the catheterized artery
– Irregular heart rhythms (arrhythmias)
– Allergic reactions to the dye or
medication
– Perforation of heart or artery
– Kidney damage
– Excessive bleeding
– Infection
– Blood clots
– Radiation exposure from the X-rays
 Angiography

Complete
Obstruction Stenosis of popliteal artery
Of femoral a.

Collaterals
 Traumatic lesions of the
arteries
 The consequences of arterial injury depends on the
intensity and nature of injury, size and location of the
concerned artery, and degree of impairment.
 Traumatic lesions of the arteries have two major
clinical manifestations:
1. Peripheral acute ischemia.
2. Hemorrhage: is the defining characteristic of this type of
pathology.
 Their frequency is about 20% of all injuries. Leg
arteries are interested in 50-60% of cases. In most
cases the lesions affect both arteries and veins, but
can also affect other structures such as nerves, bones,
muscles, etc.
 The highest incidence of arterial injuries occurs during
armed conflicts, when very frequently extremities vessels
are affected. Extremities amputations (as an extreme
measure for life saving) due to vessels injury reached an
incidence of 40% during the Second World War. Newer
methods of reconstruction, including endovascular
surgery, are now applied to nearly half the vascular
injuries.
Etiopathogenesis
 In peacetime, causes of arterial lesions in order of
frequency are: car accidents, work accidents , sports
accidents, domestic accidents and aggressions.
 Vessels injuries may occur after two kinds of trauma:
blunt trauma and penetrating trauma. The most
common injuries occur as a result of wounds.
 The mechanism of injury:
1. Direct arterial lesions consecutive to blunt trauma or
penetrating trauma
2. Indirect lesions usually caused by fragments of bone fractures
3. Iatrogenic lesions during surgery, endovascular explorations
(catheter angiography)
Morphopathology:
Contusions: The structure of the arterial wall is only
partially affected, the continuity of the artery being
preserved. Most frequently is damaged the inner layer
(tunica intima), which is the most brittle. Usually the
tear is circular partial or complete.
 Broken endothelium may reflect and act as a damper
causing occlusion and distal ischemia.
 Sometimes, the tunica media breaks leading to a
weakening of the arterial wall and the appearance of
an aneurysm.
 A hematoma in the arterial wall can produce artery
occlusion with ischemia.
Partial rupture of the artery. The tear remains opened
because of intima layer retraction, favoring bleeding.
Bleeding may be exteriorized or may occur in a cavity or
hollow organ. The accumulation of blood around the
artery may causes compression or a pulsatile hematoma
and then a false posttraumatic aneurysm may occur. In
the early phase of false aneurysm, the risk of breaking
and of external hemorrhage is very high (80-90% of the
cases). After three weeks, in the next 6-8 weeks, the
fibrous organization of the pulsatile haematoma walls
occurs and it transforms into a false aneurysm, which
becomes stable, yet has progressive evolution.
 There are cases when both artery and satellite vein are
injured and an arteriovenous fistula may result.
Complete artery rupture or section usually is the
consequence of stab wounds or fire arms wounds.
Complete ruptures occur after extreme elongations
usually associated with bone fractures.
 Hemorrhage may be massive (exteriorized or into a
cavity) or may stop as a result of media layer
contraction, thrombus development at side of arterial
stumps or outside compression due to hematoma. Pulse
disappears shortly after trauma. Proximal and distal to
lesion an intravascular thrombosis occurs till the first
efficient collateral artery. Ischemic lesions extension
depend on collateral circulation efficiency.
Diagnosis is based on history, general and local
examination and paraclinical investigations. Depending on
patient’s status, severity of hemorrhage, and facilities of
investigation, CT angiography, Doppler ultrasound and
catheter angiography may be performed in supporting
the diagnosis. In any circumstances angiography or other
investigations shouldn’t delay the surgical restoration of
blood flow.
 Patient assessment is rapidly performed evaluating the
degree of hemorrhage and shock (pulse, faintness, low
blood pressure, sweaty cold skin, pallor, oliguria, etc.).
 History (co-morbidities) and important data regarding the
mechanism of trauma can be obtained from patient,
relatives or witnesses.
 Involved limb examination is performed compared to the
opposite limb. Instrumental exploration of the wound is
indicated to be performed only in the operating room.
 The standard care is represented by arteriogram in stable
patients and operative exploration in unstable or bleeding
patients.
 Classic direct signs of vascular injury include the following:
1. Observed pulsatile bleeding
2. Arterial thrill (vibration) by manual palpation
3. Bruit over or near the artery by auscultation
4. Signs of distal ischemia
5. Visible expanding hematoma
 Posttraumatic ischemia clinical picture has some specific
features:
– The pain is persistent, progressive and does not diminish after
antialgic drugs administration or reduction of bone fractures or joint
dislocation.
– Pulse may be present in contusions. On the other hand pulse may be
absent in bone fractures or joint dislocation and reappears after
reduction.
– Functional impairment of the limb may be due to bone, joint, muscle
or nerve lesions not necessarily to ischemia.
 The full clinical picture of peripheral ischemia appears at 4-
5 hours after trauma. Nerve lesions occur after 15-30
minutes an may be reversible till 8-12 hours. Anesthesia
and palsy and also muscles contracture (rigor mortis)
appeared at 6-8 hours are signs of severity and
irreversibility. After 12-14 hours the ischemia is completely
irreversible and the only chance to rescue the patient’s life
is limb amputation.
Treatment
 Bleeding is the main problem to be solved and requires
immediate surgical intervention in any elective or urgent
cases, because of the vital risk.
 The first main goal is to save the patient’s life. When the
hemorrhage is present, (almost in every cases), it must be
stopped to prevent anemia and shock.
 The other main aim of the treatment is to reestablish and
maintain an efficient blood flow in the affected limb to
prevent ischemia and amputation.
 Other therapeutic measures will be taken to prevent
thrombosis and other postoperative possible
complications.
 Hemostasis must be applied at site of accident. The most
effective method is the compressive dressing of the
wound. This is a temporary hemostasis but in some cases,
when the diameter of the artery is small it can become a
definitive hemostasis. Other temporary hemostasis
methods are: digital compression, vessel clamp with
forceps, haemostasis by tourniquet.
 There are a lot of controversies regarding haemostasis by
tourniquet. Negative aspects are: suppresses the venous
return, worsens the venous hemorrhage, worsens
ischemia, blocks collateral circulation and after removing
the tourniquet the shock may appear (tourniquet-shock
syndrome) as a result of passage into the bloodstream of
toxins from ischemic tissues.
 A temporary method in preserving blood flow in the
affected extremity is an improvised by-pass using different
kind of materials (catheter, drainage tubes, etc), followed
by definitive hemostasis and blood flow reestablish
performed in adequate conditions by specialists.
 Definitive hemostasis may be achieved in different ways
depending on injured vessel and its location.
1. Vessel stumps ligation could be a solution in non
important arteries or where collateral circulation ensures a
good blood supply. It cannot be applied in large arteries
due to consecutive downstream ischemia.
– In some cases, operative intervention is primarily
performed for life-saving hemorrhage control rather than
for operative repair with limb salvage. In severe cases
with multiple associated injuries, hemorrhage control by
ligation of actively bleeding arterial or venous vessels may
be all that is possible
2. Arterial reconstruction is the method used in large
and important arteries. Depending on type of lesion it
can be performed by:
1. Vessel’s wall suture
2. End-to-end suture
3. Patching the arterial defect (with autologous or prosthetic
material)
4. Interposition of graft
5. By-passing the affected area using prosthesis, vein or artery
fragment harvested from other location.
 Vascular reconstruction that occurs within 3 hours of
injury is generally accepted to have the best outcome.
 After reconstruction the surgeon should consider the
risk of reperfusion injury and the potential for
compartment syndrome (compression of nerves, blood
vessels, and muscle inside a closed space).
 When there is a marked edema of the limb decompression
fasciotomy (a surgical procedure where the fascia is cut
to relieve tension or pressure) is required.
 In case of trauma with complex lesions (bones, nerves)
most often mixed team of surgeons (vascular surgeon,
neurosurgeon, orthopedic) is required.
 In case of prolonged ischemia in which there are already
signs of irreversibility, surgeons should balance the desire
to save the limb with that of preserving the patient's life.
Limb amputation remains the single choice in advanced
cases of ischemia.
 Thrombosis of the graft remains the most common
complication of vascular injury and blood vessel repair. On
the other hand anticoagulation and antiplatelet agents
should be balanced with the risk of fatal hemorrhage from
other injuries (eg, head and chest injuries).
 Arterial aneurysms
 The aneurysm represents a localized permanent dilatation
of the vessel produced by decreased strength of its wall.
 The incidence increases with age, aneurysms being found
in about 10% of cases of autopsies.
 Approximately one in every 250 people over the age of 50
will die of a ruptured aortic aneurysm.
 Abdominal aneurysm affects as many as eight percent of
people over the age of 65.
 Males are four times more likely to have abdominal
aneurysm than females.
 Those at highest risk are males over the age of 60 who
have ever smoked and/or who have a history of
atherosclerosis.
 50 percent of patients with aortic aneurysm who do not
undergo treatment die of a rupture.
Etiology
 Congenital – are present at birth and they are due to
chromosomal abnormalities that induce degeneration
of the elastic and muscular fibers. Frequently
associated with endocrine disorders.
 Acquired – appear during lifetime and comprise the all
other aneurisms
1. Atherosclerosis – 95% of aortic aneurisms
2. Infectious due to nonspecific (gram positive or negative)
germs or specific agents (syphilis) and fungi, which produce
ulceration of the intima.
3. Rheumatic
4. Posttraumatic – unlike the true aneurysm, the false aneurysm
wall does not have a muscular or elastic layer. False
aneurysms usually present as a pulsatile mass.
5. Anastomotic - as a late complication of vascular surgery.
Morphology
 Aneurysms may be:
– Fusiform
– Sacular
 The aneurysm may contain clots as a result of
turbulent blood flow.
 Dissecting aneurysm: represents a special type of
aneurysm localized on thoracic or abdominal aorta in
which the wall rips (splits, dissects) longitudinally and
the blood flows between layers. The etiology and
pathogenesis is usually a degenerative process due to a
primary or secondary weakness of the vessel wall as in
Marfan’s disease, cystic medial necrosis, hypertension or
atherosclerosis.
 Less frequently it is seen after iatrogenic manipulations
(puncture, catheter interventions etc.), in coarctation
and trauma.
 Arteriovenous aneurysm results from a nearby vein
erosion and a direct vascular link between an artery and
a vein.

Arteriovenous aneurysms are

usually the result of
arteriosclerosis. Less
common causes include
trauma, inflammation of an
artery (arteritis), and
infection.
Arteriovenous aneurysms
occurs most commonly in
the arms and legs.
 Clinical picture. Symptoms depend largely on the
developing stage of the aneurysm, its complications and
its location.
 There are no symptoms in the early stages. As volume
increases, aneurysm produces compression on adjacent
structures causing various symptoms, pain being the
most important.
 Symptomatic aortic aneurysms present as lower back
pain and/or mid-abdominal pain together with prominent
aortic pulsation suggest rapid growth of aneurysm with
possible rupture.
 Severe back, abdominal or flank pain with hypotension
indicates a ruptured aneurysm. Up to 90% of patients
die before reaching hospital or during or immediately
after surgery.
 The cardinal manifestation of the aorta dissection is the
pain, present at onset in most cases, with acute onset and
high intensity, with posterior or anterior thoracic location
radiating anywhere in the chest or abdomen. In addition
to pain and pre-existing hypertension, circulatory disorders
related symptoms are caused by propagation of
dissection, proximal or distal.
 Propagation towards the ascending aorta can result in:
 Acute aortic insufficiency (30-50% of dissections of the ascending
aorta);
 Acute myocardial ischemia;
 Cardiac tamponade and sudden death in case of rupture of the aorta
in the pericardium;
 Hemothorax if rupture extends beyond the external layer;
 Neurological deficits to stroke, by direct spread to carotid arteries or
by reducing carotid blood flow;
 Horner's syndrome (superior cervical sympathetic ganglion
compression), vocal cord paresis with hoarseness (compression of left
recurrent nerve).
 Propagation of dissection in the descendending aorta can
cause:
 Splanchnic ischemia,
 Renal failure,
 Peripheral pulse deficit with varying degrees of peripheral ischemia,
 Focal neurological deficits due to spinal ischemia.
 Suspicion of aortic dissection includes some of the
following aspects in elderly patients with atherosclerosis
and hypertension long history:
1. Acute onset of violent chest pain;
2. Mediastinum widening on chest X-ray image;
3. Inequality of pulse and blood pressure between upper limbs.
 Differential diagnosis of pain is made with acute
myocardial infarction (can also develop early circulatory
failure), massive pulmonary embolism, acute pancreatitis
(some cases), pericarditis, etc. ..
Evolution
 Abdominal aneurysms grow an average of 0.3-0.4 cm /
year.
 Risk of rupture at 5 years depending on the size of
aneurysm:
– Very low risk for aneurysms less than 4 cm;
– 5% for aneurysms between 4-4.9 cm;
– 25% for aneurysms between 5-5.9 cm;
– 35% for aneurysms between 6-6.9 cm;
– 75% for aneurysms 7 cm or greater.
 Distal arteries aneurysms (femoral, popliteal) are
frequently associated with symptoms resulting from
thrombosis, embolisation or compression of adjacent
structures causing venous thrombosis or neuropathy.
Investigations
– Abdominal ultrasound as screening study and follow-up for small
<5 cm aneurysms.
– Aortography, MRI, CT scan.
– Full assessment of cardiovascular status and cardiovascular risk
factors.
– May need to consider vasculitis and connective tissue disorders
so an ESR, CRP and autoantibody profile may be indicated.
– Assessment of renal function if possibly compromised by aortic
aneurysm.
– Assessment of peripheral circulation using Doppler.
Ultrasound
CT scan MRI
Treatment
 Prophylaxis consists in atherosclerosis prevention and
treatment of hypertension.
 Elective surgical indication:
1. Abdominal aortic aneurysms larger than 5-5.5 cm diameter
2. Variation of diameter greater than 0.5 cm in 6 months

 In all patients with aneurysms which are not operated,

ultrasound monitoring should be made at every 6
months.
 Surgical possibilities:
1. Resection of the aneurysm and arterial reconstruction
2. By-passing the aneurysm
3. Resection of a portion of the artery with reconstruction
4. Endoluminal stenting (endovascular stent graft, graft
inclusion) through a percutaneous procedure
 The treatment of a dissecting aneurysm initially involves
lowering the blood pressure with drugs to reduce the
force on the tear in the aorta.
 Generally it is considered that the ascending aorta
dissections are surgical emergency and must be treated
by surgery, while the descending aorta dissections are
treated conservatively, unless there are signs of
progression of dissection or bleeding with hemodynamic
instability. The closer the dissection is to the heart, the
more likely it is that surgery will be performed.
 Surgical therapy, even aggressive (Ex. replacing the
aortic arch) or in unfavorable conditions (MI, stroke)
results in lower mortality than with conservative attitude
in the ascending aorta dissection (7-35% compared to
50% ), so all patients with DeBakey class I and II should
be treated surgically in emergency.
 Arteriovenous fistulas
 Arteriovenous fistulas are direct communications, through
a duct or network, between the venous and arterial
system which bypasses the microcirculation.
 The passage of the arterial blood (with higher pressure)
into the vein will induce an increased pressure in that vein
which becomes elongated, dilated, tortuous and pulsatile.
Other effect is the decrease of arterial irrigation distal to
fistula with possible ischemia.
 The general consequence is the increased blood flow into
the veins with increased blood return to the heart, that
will overload the heart with the consequence of increased
heart output and its dilatation. The heart may become
insufficient (heart insufficiency).
 Location of fistulas may be anywhere, in any artery,
central or peripheral.
Classification. Fistulas may be:
1. Congenital – generally they are located peripheral and
are a consequence of angiodysplasia. Their
appearance is that of hemangioma, looking red-purple,
soft to the touch, reducing their dimension under
compression. They may be locate on limbs, abdomen,
thorax, neck, head or in viscera.
 The Parks-Weber syndrome is a congenital disease
with multiple skin hemangiomas characterized by the
triad:
1. Elongation of the inferior limb
2. Diffuse angiodysplasia
3. Varicose veins
2. Acquired – with various etiology
1. Posttraumatic – (see above) Communication
between artery and vein may be unique or multiple.
They are locate in most cases on limbs but may be
present at neck, penis or intraabdominal.
2. Spontaneous intraabdominal – as a result of
evolution of a tumor or aneurysm.
3. Post-surgical – unintentional ( kidney surgery) or
intended, like in portal hypertension (portal-
systemic shunts) or in chronic renal failure (radio-
cubital shunt for hemodialysis). For hemodialysis,
special large core catheters are used. Performing an
arteriovenous shunt will result in venous dilatation
so that the vein will fit the catheter.
Clinical picture
 Functional symptoms: moderate local pain, muscular
fatigue, sometime intermitent claudication. Symptoms of
heart overload: tachycardia, dyspnoea, symtoms of heart
failure.
 Signs: venous dilatation, limb enlargement, dilated
capillary vessels (hemangiuomas), skin discoloration,
dystrophic skin lesions, soft tissue gangrene. At
palpation the tumor is soft, compressible, with elevated
local temperature and a thrill can be felt. At auscultation
a systolic or continuous sound (murmur) can be heard.
Digital compression of the fistula reduces tachycardia
(the venous return is reduced)
 Investigations: Doppler ultrasound, angiography and
CT scan are helpful.
 Complications: thrombosis, skin ulcerations and
gangrene, infections, heart failure, distal ischemia.
 Treatment. There are various methods depending on
fistula location, dimension and debit.
– Percutaneous embolization using Gelofoam
– Quadruple vascular ligation
– Vascular reconstruction
 Peripheral acute ischemia
 Peripheral arterial occlusion is an important cause of
morbidity and mortality, particularly in connection with
atherosclerotic disease, a pathological condition that can
generate any form of peripheral obstruction (on small,
large or medium vessels, acute or chronic).
 Acute peripheral arterial occlusion results in acute
peripheral ischemia syndrome which is due to suppression
or sudden decrease of blood flow to the limbs, followed
by tissue anoxia. This may happen when the artery is
broken or occluded.
 Ischemia is a condition of decreased tissue viability
caused by a lack of perfusion limiting the delivery of
oxygen and nutrients to the tissue. This causes both
physiological and biochemical changes in the tissue.
 The severity of the acute manifestation depends on the
site of occlusion, presence of collateral circulation, and
nature of the occlusion (thrombus or embolus). Emboli
are associated with a higher morbidity because the limbs
has not had time to develop collateral circulation.
 Arterial occlusion results in both, proximal and distal
thrombosis due to flow stagnation.
Etiology
 Acute peripheral ischemia syndrome may be caused by:
 Organic causes
1. Trauma with damage to arteries
2. Embolism
3. Acute arterial thrombosis
4. Arterial wall dissection
 Functional causes
1. Neuro-vascular reaction to different kind of agents (low temperature –
frost bite, or chemicals – ergotamine)
2. Massive venous thrombosis, with secondary ischemia (phlegmasia
coerulea dolens)
3. Arteriovenous fistula
4. General causes: eg. toxic shock with collapse
Embolism
 Emboli are the most common cause of acute ischemia.
 Their origin may be:
1. cardiac (80%)
2. proximal atheroma
3. tumors
4. foreign objects, gas embolism, fatty embolism
 Causes of cardiac embolism are: atrial fibrillation,
rheumatic valvular heart disease especially mitral, left
ventricular myocardial infarction with thrombosis, post-
myocardial infarction sequelae, valves, endocarditis
vegetations on native or prosthetic valves, cardiac tumos
fragments (atrial myxoma).
 Emboli tend to lodge at artery bifurcations or in areas
where vessels abruptly narrow. The femoral artery
bifurcation is the most common site (43%), followed by
the iliac arteries (18%), the aorta (15%), and the
popliteal arteries (15%).
 A special form of
embolism, is the
paradoxical embolism,
when a deep venous
thrombus reaches in the
arterial system. This can
happen when there is a
communication between
the right and the left
atrium (atrial septal
defect) and the
thrombus reached in the
right atrium from the
vein passes into the left
and then get in the
arteries.
Acute arterial thrombosis is most frequently
caused by atherosclerotic lesions of the artery. Other
causes may be: aneurysms, hypercoagulability
(thrombosis in situ), artery trauma with intima layer
injury. It may occur as a complication of diseases:
thrombangeitis obliterans, lupus erythematosus,
periarteritis nodoasa, polycythemia vera, scleroderma.
 Thrombosis can be initiated anywhere in the
cardiovascular system, isolated or in combination
conditions of the Virchow triad: endothelial injury,
blood stasis, hypercoagulability.
Pathophysiology
 Arterial occlusion will result in:
1. Sudden stop or important decrease of blood flow downwards
the occlusion in the affected artery and also collaterals
2. Extensive thrombosis downstream and upstream the occlusion
3. Arterial spasm to compensate the decrease of arterial pressure
resulting in increased peripheral resistance
 4. Decrease of cardiac debit
5. Extension of secondary thrombosis (vicious circle)
6. Capillary stasis with sludge
7. Cellular hypoxia
8. Transmineralization (Na+ enters the cells and K+ exits the cells
resulting in cell edema)
9. The metabolism switches from aerobe to anaerobe leading to
metabolic acidosis, lysosomal lysis and cell destruction.
 Tissues resist to ischemia depending on their type.
Nervous tissue after 15-30 minutes presents edema,
myelin degeneration and then the neuromuscular plate
is affected. Symptoms are pain, paresthesia, anaesthesia
and functional impotence of the limb. These changes are
reversible till 8-12 hours after attack.
 The muscular tissue after 8-12 hours presents edema,
capillary stasis, disappearance of myoglobin,
rhabdomyolysis, fibroblastic infiltration and Volkmann's
ischemic retraction or contracture.
 Fatty tissue and skin are more resistant to ischemia
modifications being reversible till 12 hours. Phlyctenas
and gangrene appear.
Clinical picture
 Symptoms appear suddenly and are usually violent.
 British authors describe them as the "6p" :
1. Pain
2. Pulselessness
3. Pallor
4. Poikilothermia (perishing cold)
5. Paresthesia
6. Paralysis
 Acute ischemia develops during 3 phases: initial phase,
phase of worsening and phase of tissue damage.
 The pain usually occurs suddenly, distal to lesion, it is
intense and does not disappear after the administration of
painkillers. Sometimes the pain may begin insidiously,
especially in older people with atherosclerosis. The pain
may be masked by nerve damage or shock in trauma.
 The abolition of tactile sensibility, the occurrence of
ischemic paralysis and muscle rigidity are signs of serious
(irreversible ischemia). Tactile sensibility disappears the
first and then the pain and thermal sensitivity.
 Skin pallor is distal to the occlusion and later turns in
purple-blackish color due to cyanosis and gangrene.
 Absence of pulse distal to the occlusion is an important
sign as long as it was present before the ischemic episode.
There are patients with chronic peripheral arterial disease
who do not have peripheral pulse in legs. It is also difficult
to assess the pulse if an important edema is present or the
anatomic region is modified by trauma.
 In the worsening stage the intravascular thrombosis is
extending leading to intense edema of the muscles
and cyanosis. The compartment syndrome is
worsening the ischemia. The success of surgical
treatment in this phase is doubtful.
 In the last stage rigor mortis of the limb appears, the
skin is intense cyanotic with phlyctens and gangrene.
The only solution in this stage is the amputation of the
limb.
 Determining the occlusion site is made clinically by:
1. The initial site of pain
2. The level where the pulse cannot be felt
3. Distribution and degree of circulatory disorders
Gangrene of the calf
 The clinical picture must correlated with patient’s history,
taking in account diseases that may cause embolic or
thrombotic acute ischemia.
 In case of thrombotic occlusion patients usually have prior
history of claudication, because acute thrombosis develops
most often on pre-existing atherosclerotic lesions.
 Patients with embolic occlusion suffer, in many cases, from
emboligene diseases. The onset of symptoms is more
brutal and clinical evolution is significantly more faster
when acute occlusion is of embolic origin.
 The most useful examinations are Doppler ultrasound and
arteriography. Arteriography can provide important
information about the site of arterial occlusion, collateral
circulation and status of the arteries in general.
 A series of other examinations have to be performed for
the underlying disease and laboratory measurements for
the patient's general condition.
Differential diagnosis is made with:
– Acute venous thrombosis at onset accompanied by arterial spasm
and pain and phlegmasia cerulea dolens (a severe form of deep
venous thrombosis which results from extensive thrombotic
occlusion of the main and collateral veins of an extremity which is
characterized by sudden severe pain, swelling, cyanosis and edema
of the affected limb. Foot gangrene may also occur. An underlying
malignancy is found in 50% of cases.)
– Arterial spasm due to poisoning (arsenic, ergotamine), arthritis or
peripheral neuropathy (sciatica) pain less violent, short duration
associated with hyperhidrosis.
Evolution
 Ischemic injury causes myoglobin release from muscle into
circulation, causing acute renal failure by precipitation in the
tubules. In late stages, marked by profound irreversible cell
injury, appear: hyperpotassemia, metabolic acidosis,
myocardial depression and other organs failure (MSOF) due
to toxic products released from ischemic necrotic area.
Treatment
 Therapeutic measures must be taken very sun after the
onset of ischemia. The interval of time when
desobstruction is considered useful is in the first 6-8
hours, with an optimum in the first 4-6 hours.
 The patient will be in absolute rest in bed, with the limb
in a lower position (not elevated) and without applying
any heat or cold on the leg.
 All medication will be given by vein.
 Medical treatment goals are:
1. Pain release – with major painkillers (opioids)
2. Suppression of arterial spasm – with vasodilators (Papaverine,
Lydocaine, Pentoxifylline)
3. Prevention of thrombosis extension – with anticoagulants
4. Metabolic rebalancing and treatment of the underlying disease
 Anticoagulant treatment is routinely established
preoperatively in acute arterial obstructions to prevent
thrombosis extension and is continued postoperatively,
depending on the underlying pathology.
 Current methods of treatment have improved prognosis
by introducing surgical desobstruction with Fogarty
catheter and thrombolytic therapy with streptokinase.
 If the desobstruction is successful, in postoperative
period a tourniquet-shock like syndrome (reperfusion
syndrome) may appear threatening the life of the
patient. Patients presents hyperazotaemia, acidosis and
hyperkalemia. After revascularization a decrease of blood
pressure may appear. Stasis and swelling are worsened
because of existing vasoplegia. Kalium brutally released
into the blood stream may induce cardiac arrest.
Sometimes amputation is required between two dialysis
sessions.
 Surgical procedures
1. Direct or indirect embolectomy with Fogarty catheter
2. Thrombectomy followed by angioplasty
3. Bypasses or arterial grafting
4. Lumbar sympathectomy - in thrombosis of smaller vessels
5. Fasciotomy
6. Limb amputation – if there are irreversible damages under
protection of dialysis.

 Amputations after embolectomy - up to 15%

 Postoperative mortality rate - up to 34% due to:
– Cardiac complications
– Pulmonary complications - pneumonia, pulmonary embolism
– Acute renal failure
– Recurrent embolism
Fogarty probes
 Peripheral chronic ischemia

 Chronic peripheral obstructive arteriopathies, regardless

of the underlying anatomical changes, etiology and
pathogenesis are manifested by chronic peripheral
ischemic syndrome.
 The disease is more common in men (6 / 1), over the age
of 50, although it can occur under 40. All kind of arteries
may be affected (large-caliber, middle or small arteries).
Lower limbs are more often affected than the upper.
Etiology
Determinant factors:
 Genetic – genetic metabolic disorders that affect the arteries wall
 Infectious - typhus, syphilis, typhoid fever - may cause arterial
damage
 Allergic - exogenous and endogenous antigens inducing antigen-
antibody reaction altering the endothelium.
 Metabolic - hyperglycemia, hypercholesterolemia, hypertriglyceridemia
 Endocrine – pituitary gland, suprarenal gland, endocrine pancreas
 Physical and mechanical: cold, humidity, repeated microtrauma
 Nervous – may induce vascular spasm
 Chemicals: increased ratio of Ca / Na and lack of microelements (I, Br,
Mg) in food, favor arterial wall swelling and thrombosis
 Toxic - nicotine, alcohol, arsenic, lead, chromium
 The neighborhood venous thrombosis may cause inflammation of the
satellite artery
 Predisposing factors are considered male gender, age
over 40 years, sedentary lifestyle, hyperglucidic and
hyperlipidic diet.
 Risk factors are: Cigarette smoking is the most
important. Seventy to 90% of patients with arterial
insufficiency are smokers. Risk remains increased for up
to 5 years after smoking cessation. Other risk factors
include hyperlipidemia, diabetes mellitus, obesity and
hypertension.
Etiologic classification
– Atherosclerosis in 90% of cases.
– Other causes:
 Thrombangeitis obliterans (Burger’s disease)
 Temporal arteritis Horton
 Raynoud phenomenon,
 Arterial inflammation.
 Atherosclerosis is a condition in which an artery wall
thickens as a result of the accumulation of cholesterol. It is
promoted by low-density lipoproteins and caused by the
formation of multiple plaques within the arteries.
 Atherosclerosis is one of the top causes of mortality in the
world with 17 million deaths per year. Of these, 20% are
caused by ischemic heart disease. In Europe, Romania
ranks third, after Russia and Bulgaria, in terms of death rate
caused by cardiovascular disease. Atherosclerosis causes
the narrowing of any vessels in the body.
 Macroscopically. There is a hardening of the arteries and
increased consistency with rigidity. The lumen has an
uneven caliber, with plaque buildup and thrombosis area.
Sclerosis can affect the whole arterial wall and may extend
to the surrounding tissues.
 Peripheral arterial occlusive disease (PAD) is characterized
by intermittent claudication, consisting of exercise-
induced lower extremity pain relieved by rest. Claudication
occurs when the blood supply is inadequate to meet the
demand of lower limb muscles, usually resulting from
atherosclerotic arterial stenosis.
 Depending on the intensity of this cardinal symptom,
Leriche and Fontaine quantify the severity of chronic
arterial obstruction as follows:
– Stage I: the absence of any signs of ischemia, vascular obstruction
is diagnosed only by clinical or laboratory tests
– Stage II: effort ischemia, intermittent claudication (IIa – appears
at more than 200 m of walking, IIb - claudication at less than 200
m of walking);
– Stage III: ischemic rest pain without trophic disorders;
– Stage IV: ischemia at rest with trophic disorders.
 A more recent classification by Rutherford consists of three
grades and six categories:
1. Mild claudication
2. Moderate claudication
3. Severe claudication
4. Ischemic pain at rest
5. Minor tissue loss
6. Major tissue loss

Clinical picture
 About 20% of patients may be asymptomatic. Other symptoms
include:
 Claudication - pain, weakness, numbness, or cramping in muscles
due to decreased blood flow
 Sores, wounds, or ulcers that heal slowly or not at all
 Noticeable change in color (blueness or paleness) or temperature
(coolness) when compared to the other limb (termed unilateral
dependent rubor; when both limbs are affected this is termed
bilateral dependent rubor)
 Diminished hair and nail growth on affected limb and digits.
Clinical evaluation of claudication
 Patients should be asked about the intensity of
claudication , its location, and the distance they have to
walk before it begins.
 Evaluation consists of determining the location, extent,
and severity of disease and the degree of functional
impairment. The key clinical feature of claudication is the
reproducibility of muscular pain after a given level of
activity and cessation of pain after a period of rest.
 Aortoiliac disease is manifest by discomfort in the
buttock and/or thigh and may result in impotence and
reduced femoral pulses.
 Leriche's syndrome occurs when impotence is
associated with bilateral hip or thigh claudication.
 Iliofemoral occlusive disease is characterized by
thigh and calf claudication. Pulses are diminished from
the groin to the foot.
 Femoropopliteal disease usually causes calf pain.
Patients have normal groin pulses but diminished pulses
distally.
 Tibial vessel occlusive disease may lead to foot
claudication, rest pain, non-healing wounds, and
gangrene.
 Rest pain consists of severe pain in the distal portion of
the foot due to ischemic neuritis. The pain is deep and
unremitting, and it is exacerbated by elevation of the
foot, and the pain is relieved by dangling the affected
foot over the side of the bed.
Other clinical tests to assess chronic obstruction:
 Buerger test consists in lifting the inferior limb at 60-75
degree with the patient in dorsal decubitus and
performing movements of ankle joints and toes till the
onset of fatigue. If there is a deficiency in blood flow,
the foot becomes intensely pale and the leg dorsal veins
are collapsed.
 Moskowicz test consists in lifting the limb to vertical
position, wrapping it with elastic bands and remaining in
that position for 5 minutes. After that, set the foot on
the ground and loosen the bands. The column of blood
will descend till the level of obstruction, recoloring the
foot except the affected area;
 Cosăcescu test: on the affected limb perform scratches
on the skin from top to bottom. In the well irrigated
area, the dermographism is positive, while in the less
irrigated area is negative and the skin is pale.
Paraclinical investigations
 The gold standard investigation of arteries is
arteriography. The main disadvantage of this
investigation is that it is an invasive one but it offers the
most comprehensive information about arteries
morphology. It is indicated mainly in patients who are
candidates for surgery.
 A noninvasive procedure is the Ankle Brachial Pressure
Index (ABPI). It may be performed as a primary
investigation but it has also drawbacks. (see above)
 Doppler ultrasound investigation is very useful prior to
angiography because it is not invasive and can highlight
the stenotic zone of artery. It has also some limitations.
 CT scan angiography is useful especially to highlight the
relations of the arteries with the surrounding structures.
Etiological forms:
 atherosclerosis
 non-atherosclerotic peripheral chronic occlusion is
represented mainly by Takayasu's disease and Buerger’s
disease.
 Takayasu disease (a form of arteritis with giant cells)
is a rare pathological entity (most common in the Far
East), which is found mainly in young women aged 20-
40 and mostly affects the aortic origin. To the aortic
inflammatory lesions, stenosis and aneurysms of the
aorta and its branches are also associated.
 Clinically there is unilateral or bilateral absence of pulse,
signs of cerebral ischemia, transient amaurosis, crisis of
angina pectoralis, abdominal angina, renal hypertension,
etc..,
 A particular form of giant-cell arteritis is represented by
Horton’s disease which usually affects the cephalic
arteries being most common in females. The main
symptoms are headaches, visual disturbances, weight
loss, fatigue. Chewing causes pain in the jaw. It is
treated with anti-inflammatory (cortisone). Without
treatment, patients risk blindness
 Buerger disease (thromangiitis obliterans) is a
segmental inflammatory-proliferative vasculopathy,
usually with self-limited evolution, which occurs mainly in
young patients, male, smokers. It is characterized by the
absence or minimal presence of atheromas and
involvement of small- and medium-sized arteries and
veins of the upper and lower extremities.
 Cardinal clinical manifestation is pain unremitting
ischemic ulcerations, and gangrene of the fingers and
toes and as the disease evolves, the patients may require
several surgical amputations. The treatment is rarely
surgical, as there are distant and diffuse arterial
damages. Sometimes successfully react to surgical
sympathectomy.
Buerger disease
DIFFERENTIAL DIAGNOSIS OF THE 2 LEADING CAUSES OF PERIPHERAL
ARTERIAL CHRONIC OCCLUSION
ATEROSCLEROSIS
- predominantly affects men
who are around the age of
CLINIC 60 years
- mainly large and medium
size vessels are affected
- continuous lesions
- irregular contour of the
artery
- asymmetrical lesions,
more advanced in the
ANGIO-
GRAPHIC affected limb
- well developed collateral
circulation, with separation
of collaterals at right angles
from the main artery
THROMBANGIITIS
OBLITERANS
- predominantly affects young
men between 20-40 years,
heavy smokers
- small and medium sized
arteries are interested
- segmental lesions
affected arterial segments
have smooth walls thin,
filiform, with the aspect of
“loss in the rain “ to the ends
- lesions frequently
symmetrical
collateral network consists of
thin vessels that come off
from the main trunk in sharp
angle
 Another etiologic form of chronic peripheral occlusion of
the small vessels is the diabetic foot caused by
diabetes mellitus. The clinical picture is that of ischemic
lesions of the leg going to wet gangrene. Ulceration and
necrosis appear and are infected, the infection spreading
along the fascia and tendons causing cellulite. Usually
patients have diabetic neuropathy and so lesions may
not be painful.
Treatment
 Prevention: smoking cessation, rational nutrition
(reduced lipids and carbohydrate intake), avoidance of
general infections, treatment of associated morbidities
(diabetes, hypertension, obesity), physical activity,
prophylactic medication with antiplatelet and
hypolipemiant drugs if the persons are over 50 years old,
with risk factors.
Medical treatment:
 General measures: smoking and alcohol cessation,
rational alimentation, avoiding exposure to cold and wet,
wearing comfortable shoes and appropriate clothing,
proper local hygiene.
 Physiotherapy: medical gymnastics, carbonated baths,
thermal cures.
 Medicines: administration of antiplatlet drugs (Aspirin)
vasodilators, anticoagulants, anti-atherosclerotic, pain
relievers, etc..
Surgical treatment:
 Surgery is indicated in stage III-IV of the disease
 Functional operations: lumbar sympathectomy or
thoracic splanchnicectomy or adrenalectomy (especially
useful in thrombangiitis), and combinations of these.
 Because, in addition to atherosclerosis which causes
mechanical obstruction, in chronic peripheral ischemia,
increased sympathetic tone with vascular spasm is also
involved (intricated mechanism of atherogenesis),
surgical sympathetic denervation is often an adjuvant
treatment with good result.
 Reconstructive surgery:
– Angioplasty
 Open - arterial patch application,
 Endovascular procedures
– Balloon angioplasty
– Stenting angioplasty
– Laser angioplasty
– Bypasses (with own saphena magna vein or prosthesis)
– Endarterectomy
– Segmental arterial resection (restoration of continuity with the autograft
or prosthesis)
 Operations of necessity: amputations, necrectomies.
Endarterectomy is a surgical procedure to remove the
atheromatous plaque material, or blockage, in the lining
of an artery constricted by the buildup of soft/hardening
deposits. It is carried out by separating the plaque from
the arterial wall.
Endovascular angioplasty.
It uses a catheter and a balloon to open up blocked
arteries.
The catheter is passed into a main artery, often in the
groin, and pushed along until it reaches the narrowed
vessel. The balloon at the tip of the catheter is then
inflated so that it pushes any build-up of plaque in the
artery against the vessel's wall – allowing a freer flow of
blood.
Angioplasty is less radical alternative to open or bypass
surgery.
Stenting
The stent is inserted in the
area where the artery is
narrowed to keep it open.
Some stents are "coated"
with medication to prevent
the artery from forming
clots and stenosing again.
Stents are used in most
angioplasties except when
an artery is too small for a
stent to fit.
 Laser vaporization of atherosclerotic plaque, or
laser angioplasty.
 A special balloon angioplasty catheter is used which
contains a fiberoptic channel through which a laser is
passed. The laser is used to vaporize the plaque and the
balloon then stretches the zone.
 Ao

Aorto-Bifemoral prosthesis
 Sympathectomy increases peripheral blood flow by
vasodilatation of arterioles in cutaneous vascular beds.
Some patients may receive sufficient increases to help
heal superficial ischemic ulcers and relieve rest pain.
 Usually 2 lumbar ganglia are excised: L2 and L3
ganglionectomy usually sufficient.
 Because of abolishing basal and reflex constriction of
arterioles and precapillary sphincters, flow increases with
10-200%. Also it produces a relief of ischemic rest pain
due to loss of attenuation of painful stimulus
transmission but sympathectomy does not improve
claudication.
SURGICAL PATHOLOGY OF
THE INFERIOR LIMB VEINS

Anatomy
1. Varicose veins
2. Thrombophlebitis
Anatomy
Veins are vessels which collect blood from tissues and
lead it toward the right heart.
Veins of the inferior limb may be classified in four
types:
1. Superficial veins – under the skin
2. Deep veins – under the muscular fascia
3. Connecting veins - connect veins in the same fascial plane
4. Perforator veins – connect the superficial veins to the deep
veins (crossing fascial plane)
Superficial veins
The superficial venous system is a subcutaneous
extremely variable weblike network of interconnecting
veins. A few larger superficial veins are fairly constant
in location.
The superficial venous system of the leg caries 20% of
blood and the deep veins 80%.
 Superficial veins do not accompany the arteries and they
drain into the two main superficial venous collectors: the
great (or internal) saphenous vein and the small (or
external) saphenous vein.
Digital veins of the leg flow into the dorsal venous arch of
the foot. From the medial end of the arch starts the internal
saphenous vein and from the external side the small
(external) saphenous vein.
The internal saphenous vein (the great saphenous, the
long saphenous, vena saphena magna) starts in the front
of the tibial malleolus, and then ascends on the medial side
of the calf and thigh towards the saphenous hiatus located
approximately 4 cm below the inguinal ligament in the groin
and passes through this hiatus, of the fascia lata, to drain
into the common femoral vein.
Vena saphena magna receives two tributary veins
below the knee in the posterior medial region:
the superficial anterior saphenous vein and
the posterior crural arch (described by Leonardo da
Vinci) which sometimes communicates with the
lesser saphenous vein (saphena parva).
There are three relatively constant veins that drain into
the great saphenous vein arch at level of saphenous
hiatus, near the saphenofemoral junction:
1. The superficial inferior epigastric vein
2. The superficial external pudendal veins (2)
3. The superficial circumflex iliac vein
Other tributary veins are the anterolateral branch and
posteromedial branch called the vein of Giacomini
Many patients have a duplicated great saphenous trunk
in the thigh, which parallel the main trunk and either
reconnect with it, usually just above or below the knee,
or traverse more superficially in the distal thigh.
From a surgical point of view, the most important
variations occur at the saphenofemoral junction in the
groin. The anatomical arrangement of the individual
tributaries can be very different from one leg to another.
External or small saphenous vein (vena saphena parva)
starts from behind the external (peroneal) malleolus and
follows the straight ascending median axis of the
posterior aspect of the calf. Initially it is located
superficially in the subcutaneous tissue and then enters
a splitting of the gastrocnemius fascia in the muscle. It
flows into the popliteal vein, in the popliteal space,
between the two heads of the gastrocnemius muscles.
In two-thirds of cases, it joins the popliteal vein above
the knee joint, and in one-third of cases, it joins with
other veins (most often the great saphenous vein or the
deep muscular veins of the thigh). In some patients, the
vein may have two or three different termination sites.
In only 50 to 70 % of the cases the saphenopopliteal
junction is located in the popliteal fossa, whereas in
about 10 % it is found below it.
The great and small saphenous veins are interconnected
by multiple anastomoses.
The great anastomotic vein of Giacomini is one of the
most important which descends in scarf obliquely on the
back of the thigh.
Deep veins
– Posterior tibial vein carries blood from the posterior compartment of
the leg and joins the peroneal veins to form the tibioperoneal trunk
– Peroneal vein carries blood from the lateral compartment of the leg
and joins the posterior tibial veins to form the tibioperoneal trunk
– Tibioperoneal trunk Is formed by the confluence of the peroneal
veins and the posterior tibial veins.
– Anterior tibial vein carries blood from the anterior compartment of
the leg and joins the tibioperoneal trunk to form the popliteal vein.
– Popliteal vein
– Femoral vein a continuation of the popliteal vein that begins at the
adductor canal.
– Deep femoral vein (profunda femoris vein) carries blood from the
posterior aspect of the thigh and joins the femoral vein to form the
common femoral vein
– Common femoral vein
– External iliac vein is the continuation of the common femoral vein
above the inguinal ligament
Perforator veins
There are about 150 perforator veins but only a few have
clinical importance. They “perforate” the muscular
aponeuroses throughout the leg linking the two systems
anatomically and hemodynamically.
A few named perforating veins are fairly constant in
location and are named only as vague groupings. The
old nomenclature included:
– Hunter’s perforator in the mid thigh,
– Dodd’s perforator in the distal thigh,
– Boyd’s perforator at the knee,
– Cockett’s perforators in the distal medial calf and ankle.
Other perforators:
– Bassi perforators: located posterior link the great saphenous
vein to peroneal vein
– Hach perforators: located posterior link the femoral vein with the
superficial system
– Linton and Kosinski are located near the junction between the
lesser saphenous vein and popliteal vein
– May perforators and gastrocnemius perforating group
The extrasaphenous dermal plexus has also a complex
connection with the deep venous system through the
Delater perforators.
Perforator veins in the foot are avalvulated but in the calf
they have 2-3 valves that prevent reflux of blood from the
deep veins into the superficial system.
Healthy perforator veins have continent one-way valves
which lead the blood flow from the surface to depth.
When valves are insufficient or incontinent the blood
may flow abnormally from depth toward surface (reflux).
Perforators veins play an important role in the
hemodynamic of the leg. They regulate the blood flow
between the two systems: deep (high pressure) and
superficial (low pressure) helping to maintain an efficient
evacuation of blood from the leg.
Perforator veins insufficiency is caused by their
enlargement and so valves become insufficient or
because of fragile valve leaflets destruction as a
consequence of thrombosis.

There is an intimate relation between the great

saphenous vein and the saphenous nerve and also
between the small saphenous vein and the sural nerve in
the lower leg which may result in nerve damage during
operations for varicose veins.
Lower limb venous circulation physiology
The main functions of the venous system are: transport
blood to the heart, blood storage and thermoregulation.
The superficial collecting veins can dilate to
accommodate large volumes of blood with little increase
in back pressure, so that the volume of blood
sequestered within the venous system can vary at any
moment without interfering with the normal function of
the veins.
The correct functioning of the venous system depends
on a complex system formed by valves and muscles
(which act like pumps = the peripheral heart) that are
individually prone to malfunction or fail, yet the system
as a whole performs remarkably well under extremely
adverse conditions.
Physiology of venous legs circulation is complex and
varies greatly depending on conditions such as:
standing, lying, limb elevation.
Motor factors that ensure the circulation of venous return
are:
1. Left ventricular propulsion force (vis-a-tergo)
2. Aspiration force of the heart and respiratory muscles
(vis-a-fronta)
3. Leg muscle pump and especially calf muscles
(peripheral heart)
4. Pulse transmitted by paravenous arteries
5. Autonomous tone of the vein wall
6. Unidirectional venous valves that prevent backflow
The calf muscle pump
The passage of blood upward from the feet against
gravity depends on a complex array of valves and
pumps. Squeezing of the vein segment occurs when
muscle contraction increases the pressure within a
fascial muscle compartment.
With normal cycles of contraction and relaxation, the
veins are alternately compressed and decompressed
( "pumped").
Inflow to a segment of deep vein is through intake
valves from perforating veins as well as from the
deep vein segment below. Outflow is through an
outflow valve to the deep vein segment above.
 Opposing factors of the venous circulation are:
1. Gravity
2. Blood viscosity
3. Abdominal pressure
The imbalance between the two categories of factors
leads to venous stasis in the legs and consecutively
varicose veins developing and trophic modifications of
the skin.
 VARICOSE VEINS
It is a chronic disease of the lower limb venous system
characterized by:
1. Alterations of the venous walls and valvular apparatus
2. Reflux of blood from the deep venous system towards the
superficial
3. Dilated superficial veins
Pathophysiology – Hydrostatic varices
In orthostatic position blood stasis induces a higher
pressure in the lower limb veins. This will lead in the first
stage to a slightly dilatation of the deep veins sufficient to
dilate the junctions sites between the superficial and deep
venous system.
At junction level between the femoral vein and saphenous
veins, ostium saphenae, there are one-way valves. When
ostium enlarges the valve becomes incompetent allowing
the backflow into the superficial veins.
The reflux will induce a higher pressure into the
superficial veins leading to their dilatation.
A vicious circle occurs. The superficial veins valves
become insufficient as they cannot close completely and
so the blood column cannot be fragmented (by valves)
further increasing the hydrostatic pressure into the vein.
This will lead to further dilatation of veins which become
also elongated and tortuous (varices). The high
hydrostatic pressure will force the perforator veins,
especially in the calf, where the pressure is higher. The
perforator veins will expand leading to their valves
incompetence and reflux from the deep to the surface
system at this level too.
Intravenous high pressure will determine lesions of the
endothelium which associated with stasis and turbulent
flow will favor the occurrence of thrombosis.
The stasis is worsening especially in the lower third of
the calf. As venous (deoxygenated) blood stagnates
here too much time, the tissues become less oxygenated
and trophic changes of the skin and subcutaneous
tissues appear culminating with leg venous ulcers.

Venous ulcer
Morphopathology
Varicose veins are elongated, tortuous, dilated veins, in
most cases located along the trajectory of the
saphenous veins and/or their tributaries.
Venous valves are atrophied, with zones of verrucous
endo-phlebitis, parietal sclerosis and connective tissue
dysplasia, as evidenced microscopically.
These changes are circumscribed by a zone of sclerosis
of the subcutaneous tissue, lymphatics and adjacent
skin.
Etiology
Many factors have been incriminated:
Endogenous factors:
– Anthropological factor - bipedal position
– Anatomo-physiological factor - the superficial venous network
less valvulated and uninfluenced by muscle contractions
– Genetic factor – deficiency of collagen and elastin fibers in the
venous wall (frequently associated with hemorrhoids and flatfoot)
– Constitutional type
– Sex - most common in women
– Age - 20 - 40 most frequently
– Endocrine factor - disorders of pituitary, ovarian, thyroid, adrenal
gland and endocrine pancreas function
– Pregnancy
– Obesity
Exogenous factors
– profession, prolonged standing or sitting, heat, humidity, dietary
factors, infections.
Classification
In terms of etiopathogenesis varicose veins can be
classified into:
Congenital varicose veins
– Klippel - Trenaunay syndrome - characterized by the triad of
varicose veins, hypertrophic elongation of the limb, tuberous
haemangioma
– Parkes - Weber syndrome - congenital arteriovenous fistulas
– Venous angioma –tumors containing excess of venous
structures
Primitive varicose veins – the cause is unknown but
predisposing factors are present
Secondary varicose veins – the etiology is known
– Post-thrombotic syndrome
– Compression on the main venous trunks
– External and internal venous trauma
– Arteriovenous fistulas
Klippel - Trenaunay syndrome
The CEAP classification of venous disease is widely
recognized, and was developed in 1994 by an
international ad hoc committee of the American Venous
Forum (JOURNAL OF VASCULAR SURGERY, 1250 Eklöf et al December 2004).
The severity scoring system was based on 3 elements:
number of anatomic segments affected, grading of
symptoms and signs, and disability.
CEAP means:
– Clinical severity
– Etiology or cause
– Anatomy
– Pathophysiology
For the initial assessment of a patient, the clinical severity
is the most important and can be made by simple
observation. Classification starts with the patient’s initial
visit, but can be better defined after further investigations.
A final classification may not be complete until after
surgery and histopathologic assessment.
There are 3 levels of testing, depending on the severity
of the disease: (JOURNAL OF VASCULAR SURGERY, 1250 Eklöf et al December
2004)

– Level I: office visit, with history and clinical

examination, which may include use of a hand-held
Doppler scanner.
– Level II: noninvasive vascular laboratory testing,
which now routinely includes duplex color scanning,
with some plethysmographic method added as
desired.
– Level III: invasive investigations or more complex
imaging studies, including ascending and descending
venography, venous pressure measurements,
computed tomography (CT), venous helical scanning,
or magnetic resonance imaging (MRI).
Grades of increasing clinical severity:(JOURNAL OF VASCULAR
SURGERY, 1250 Eklöf et al December 2004)

– C0 No visible or palpable signs of venous disease.

– C1 Telangiectasies or reticular veins.
– C2 Varicose veins; distinguished from reticular veins by a
diameter of 3 mm or more.
– C3 Edema.
– C4 Changes in skin and subcutaneous tissue secondary to
chronic venous dfisease,
C4a Pigmentation or eczema.
C4b Lipodermatosclerosis or atrophie blanche.
– C5 Healed venous ulcer.
– C6 Active venous ulcer.
S: symptomatic, including ache, pain, tightness, skin irritation,
heaviness, and muscle cramps, and other complaints attributable to
venous dysfunction
A: asymptomatic
Terminology (JOURNAL OF VASCULAR SURGERY, 1250 Eklöf et al December
2004)

Atrophie blanche (white atrophy) = localized, often

circular whitish and atrophic skin areas surrounded by
dilated capillaries and sometimes hyperpigmentation -not
to be confused with healed ulcer scars.
Corona phlebectatica = Fan-shaped pattern of numerous
small intradermal veins on medial or lateral aspects of
ankle and foot. Synonyms include malleolar flare and
ankle flare.
Eczema = Erythematous dermatitis, which may progress
to blistering, weeping, or scaling eruption of skin of leg.
Most often located near varicose veins, but may be
located anywhere in the leg.
Edema = Perceptible increase in volume of fluid in skin
and subcutaneous tissue, characteristically indented with
pressure. Venous edema usually occurs in ankle region,
but may extend to leg and foot
 Atrophie blanche Ankle flare

Eczema Edema
Lipodermatosclerosis = localized chronic inflammation
and fibrosis of skin and subcutaneous tissues of lower
leg. It must be differentiated from lymphangitis,
erysipelas, or cellulitis by their characteristically different
local signs and systemic features.
Pigmentation = Brownish darkening of skin, resulting
from extravasated blood. Usually occurs in ankle region,
but may extend to leg and foot.
Reticular vein = Dilated bluish subdermal vein, usually 1
mm to less than 3 mm in diameter. Usually tortuous.
Excludes normal visible veins in persons with thin,
transparent skin. Synonyms include blue veins,
subdermal varices, and venulectasies.
Lipodermatosclerosis

Reticular vceins

Spider veins

Pigmentation
Telangiectasia = Confluence of dilated intradermal
venules less than 1 mm in caliber. Synonyms include
spider veins, hyphen webs, and thread veins.
Varicose vein = Subcutaneous dilated vein 3 mm in
diameter or larger, measured in upright position. May
involve saphenous veins, saphenous tributaries, or
nonsaphenous superficial leg veins. Varicose veins are
usually tortuous, but tubular saphenous veins with
demonstrated reflux may be classified as varicose veins.
Synonyms include varix, varices, and varicosities.
Venous ulcer = Full-thickness defect of skin, most
frequently in ankle region, that fails to heal
spontaneously.
Varicose veins
 Examples of classification:
Etiologic classification
Classification according
– Ec: congenital
to basic CEAP:
– Ep: primary
C6,S, Ep,As,p,d, Pr.
– Es: secondary (postthrombotic)
Classification according
– En: no venous cause identified
to advanced CEAP:
Anatomic classification C2,3,4b,6,S, Ep,As,p,d,
– As: superficial veins Pr2,3,18,13,14 (2004-05-
– Ap: perforator veins 17, L II).
– Ad: deep veins
– An: no venous location identified
Pathophysiologic classification
– Pr: reflux
– Po: obstruction
– Pr,o: reflux and obstruction
– Pn: no venous pathophysiology
identifiable

(JOURNAL OF VASCULAR SURGERY Volume 40, Number 6

Eklöf et al 1251)
Diagnosis
Venous disease diagnosis requires a careful history, a
proper clinical examination and laboratory investigations.
History
Genetic aspects
– Family history of varicose veins, of thrombophlebitis,
arterial or lymphatic disease.
– The personal physiological antecedents – for women
regarding the number of pregnancies and evolution.
– The personal pathological antecedents -
thrombophlebitis, drugs (anticoagulants, diuretics, birth
control pills), nicotine intake, diabetes,
hyperlipidaemia, arteriopathies, dehydration, varicose
veins surgery, fractures, immobilization diseases at
risk of thrombosis with stasis. Important are also heart,
kidney or liver diseases for differential diagnosis of
edema.
 Professions requiring prolonged standing and/or effort
and those with exposure to heat are accompanied by
varicose veins and their complications - teachers,
workers, trade, cooks, builders, athletes (volleyball
players, weightlifters).
Patient age, height, weight.
Detail about the disease evolution: onset (acute, chronic,
insidious), initial symptoms and their evolution.
Clinical examination
Inspection of the legs is standing and lying position.
Appreciate the differences of thickness (by swelling) or
length (congenital diseases present) of the legs. Other
findings: edema, dilated veins, corona phlebectatica,
skin pigmentation and trophic disorders (hair loss, leg
ulcer).
Sicard’s test. The patient is lied in supine position and
asked to cough. Suddenly a bulge appears in the groin at
level of great saphenous vein arch. It demonstrates the
ostial insufficiency at saphenous-femoral junction.
By palpation, dilated veins and the presence of thrombosis
are estimated. Assessment of dilated veins in obese
patients is more difficult, both on inspection and palpation
because they are hidden in the thigh fat.
Percussion and palpation. Schwartz’s sign: in supine
position, percussion of the great saphenous vein above the
internal malleolus will produce a wave that can be felt in
the groin portion of the saphena magna. It demonstrates
that valves are incompetent allowing the transmission of
wave through a continuous column of blood.
On auscultation systolic-diastolic sounds are present only
in secondary varicose veins due to arteriovenous fistulas.
Clinical functional tests are still useful in assessing
lower limb veins, although they lost importance due to the
new paraclinical non-invasive explorations.
Brodie - Trendelenburg – Troianov test: is used to determine
the site of valvular incompetence. The patient is lied down.
The leg is elevated and so veins are emptied. A tourniquet
is applied in the upper thigh. Ask the patient to stand. If the
tourniquet prevents the veins from re-filling rapidly (under 30
seconds), the site of the incompetent valve must be at the
sapheno-femoral junction. If the veins re-fill faster with the
tourniquet in place, the incompetence must be lower down.
(Mahorner Ochsner test 3 tourniquets)
Proceed with the same protocol down the leg:
– above the knee - to assess the mid-thigh perforator
– below the knee - to assess competence between the
short saphenous vein and popliteal vein
If re-filling cannot be controlled, the communication is
probably by one or more distal perforating veins.
Clinical tests for the deep venous system
Perthes test: The patient is in supine position. The calf is
bandaged with elastic bands so that only the superficial
veins to be collapsed and not the deep, and then he
walks 10 to 15 min. In case of deep veins occlusion, pain
in the calf will appear in this period of time.
Delbet – Macquot test: A tourniquet is applied above the
knee, making sure the it does not interfere with the deep
venous circulation. The patient is invited to walk,
watching the changes of varicose veins. If varicose veins
reduce it means that there is an insufficiency of internal
saphenous vein, but the perforators veins are
competent. The persistence of varicose veins without
modification denotes perforator veins incompetence. If
varicose veins increase, it means that there is a deep
venous system insufficiency.
Linton test: The tourniquet is applied below the knee.
Patient in supine position with the leg elevated will
present a fast draining of varices when deep venous
system is permeable.
Pratt test: – highlights the areas of reflux in the
communicating veins. Patients is in supine and a
tourniquet is applied on the upper part of the thigh to
eliminate the possibility of reflux from femuro-saphenous
junction. A bandage with elastic bands is also applied
running from the ankle to the groin. In standing position
as the bandage is removed from thigh towards the ankle,
there is a refill of varicose veins, when perforator veins
are incompetent.
Symptoms
During the onset, usually there are no symptoms. As the
varicose veins develop patient complains of pain in the
leg especially in the form of tension, muscle cramping
and burning. Pain is worsened after sitting or standing
for a long time. The patient notices after prolonged
standing the edema which usually disappears after rest
with the leg elevated. In advanced stages trophic skin
disorders appear going to ulcer.
Acute complications:
– Varicoflebitis (thromboflebitis of the superficial veins) -
inflammation and thrombosis of varicose veins that become
swollen, painful with redness of skin and fever.
– Bleeding from varicose veins (spontaneous or posttraumatic) or
from venous ulcer.
Chronic complications – chronic venous insufficiency
with all its consequences: eczema, loss of hair, edema,
liposclerosis, pigmentation, ulcer.
Paraclinical investigations
Ultrasound and Doppler ultrasound are the most useful
investigation and also noninvasive. They highlight the
dilated veins and also the reflux sites. They can asses
the superficial and also the deep venous system.
Phlebography is rarely indicated, only in cases of deep
venous system thrombosis or other pathology is
suspected.
Differential diagnosis is made between
etiopathological types of varicosities. In advanced stages
of chronic insufficiency the differential diagnosis is more
difficult and should be performed with:
– Swelling of the legs of different etiologies
– Dermatitis of legs
– Dermathologic etiology of leg ulcers
– Ischemic ulcer
– Mal perforans ulcer
– Erythema Induratum (Nodular Vasculitis) Bazin
– Ulcers in hemolytic disease
– Post-thrombotic ulceration
The treatment is prophylactic and curative.
Prophylactic treatment aims to eliminate factors
incriminated in the occurrence of varicose veins:
– Avoid prolonged sitting and standing
– Wearing compression stockings
– Exercise daily
– Elevate legs when possible, keeping them positioned higher than
heart level
– Maintain an ideal body weight
– Avoid excessive heat
Curative treatment consists of:
1. Physiotherapy
2. Medication – Phlebotropic drugs
3. Sclerotherapy
4. Minimally invasive procedures (endovenous ablation)
5. Surgery
1. For the varicose veins
2. For perforator veins
3. For venous ulcers
Sclerotherapy: is a method indicated for small veins only
(reticular veins).
A sclerosant (irritant for the endothelium) solution is injected into the
varicose veins or spider veins in order to cause their disappearance.
The most frequent used substance is polidocanol (aethoxysklerol)
which causes localized destruction of the intima layer and fibrosis of
the vein, occluding the lumen of the vessel, and reducing its
appearance.
Sclerotherapy is an outpatient procedure and is performed in several
sessions which are carried out at 4-8 week intervals. The solution
must be injected strictly intravenously otherwise it may cause
perivenous tissue necrosis and skin pigmentation. Another condition
for success is that the vein must be completely emptied of blood
before injecting the sclerosant agent. Patients are told to walk
immediately after each treatment session and graduated compression
must be applied. Class II (30-40mmHg) compression hose or elastic
stocking are most commonly used for this purpose.
 Possible complications of sclerotherapy:
1. Hyperpigmentation - this is a common occurrence after
sclerotherapy of veins of all sizes in approximately 10-80% of
patients
2. Swelling
3. Telangiectatic matting or "postsclerotherapy neovascularization”.
Matting is the name given to networks of fine red blood vessels
which develop near the site(s) of previous injections.
4. Pain
5. Localized urticaria
6. Folliculitis
7. Localized hirsutism
8. Cutaneous necrosis
9. Systemic allergic reactions
10. Superficial thrombophlebitis
11. Arterial injection
12. Deep venous thrombosis
13. Nerve damage
 Suggested Sclerosant/Concentrations
for Treatment of Telangiectasia/Reticular veins

VESSEL TYPE SCLEROSANT CONCENTRATION

Telangiectasia Hypertonic saline 11.7%

< 1mm
Sodium tetradecol sulfate STS 0.2%

Polidocanol (Aethoxysklerol) 0.25%

Venulectasia Sodium tetradecol sulfate STS 0.25%

1-2mm
Hypertonic saline 23.4%

Hypertonic glucose/saline The formula for Hypertonic

(Sclerodex) glucose/saline is 200mg/ml
dextrose 100mg/ml sodium chloride
100mg/ml propylene glycol 8mg/ml
phenoxyalcohol

Polidocanol (Aethoxysklerol) 0.5%

Reticular veins Hypertonic saline 23.4%

>2mm
Hypertonic glucose/saline

Sodium tetradecyl sulfate STS 0.25%

Polidocanol 0.5-1.0%
Laser therapy for superficial small veins (spider veins)
works by sending strong bursts of light onto the vein,
through the skin which makes the vein slowly fade and
disappear. No incisions or needles are used.
Minimal invasive procedures are catheter-assisted
procedures (endovenous procedures). In these
procedures a thin catheter is introduced percutaneously
into the vein and advanced as necessary. In most cases
the procedure is performed under ultrasound guidance.
As the catheter is pulled out, the heat provided by laser
or ultrasound destroys the vein by causing it to collapse
and seal shut. This procedure is usually done for larger
varicose veins. It can be performed in local anaesthesia
on an outpatient.
Surgical treatment
It has three main objectives:
1. Suppression of the ostial reflux at junction level between deep
and superficial system of the saphena magna and parva if
necessary
2. Suppression of reflux through the perforator veins (highlighted
by ultrasound)
3. Removing the varicose veins and heal the lesions (ulcers)
There are two major types of surgery:
1. Addressed directly to veins
2. Addressed to complications (bleeding, ulcers)

There are many types of procedures which are applied

considering the degree of varicose veins development.
The traditional technique is that of subcutaneous
stripping of the great saphenous vein – Babcock
procedure.
Babcock procedure starts with a skin incision of 2-4 cm at
groin level where the great saphenous vein flows into the
femoral vein. The great saphenous vein is discovered and
isolated. Then all tributaries of the saphenous arch
(external pudendal, circumflex iliac, inferior epigastric,
anterior accessory veins) are ligated and resected. The
saphena vein is ligated and resected just above the
junction with femoral vein. Then Giacomini vein is ligated
and resected. The next step is a small incision above and
anterior to the internal malleous where the origin of
saphena vein is discovered. The vein is isolated and
separated from the sapnenous nerve, then resected. A
stripper is introduced into the upper end of the saphena
and advanced upstream till the saphenous arch in the
groin. The tip of the stripper is ligated to the vein and the
vein is tripped out in an anterograde or retrograde way.
If the stripper cannot progress till the saphenous arch,
extra skin incisions have to be performed and the
saphneous vein is stripped out in two or more segments.
During avulsion of the great saphenous vein, collaterals
and perforator veins are broken (interrupted).
Retrograde stripping is more recommended because of
less saphenous nerve damage.
Other clusters of varices are removed through separate
incisions.
If necessary the small saphenous vein arch is also
resected and the vein removed.
Possible complication after stripping:
– Soreness and bruising (subcutaneous bleeding and hematoma
formation)
– Numbness due to nerves lesions
– Suppuration
– Chronic leg swelling from damaged lymphatic tissue
– Incision scars
Other surgical procedures:
Terrier-Alglave procedure: removes the saphenous arch
and also the entire great saphenous vein through a
continuous linear incision from the groin till the
malleolus. The very long incision is time consuming and
also may result in an unaesthetic scar. The main
indication remains the case of great saphenous vein
thrombosis when stripping is impossible.
Operations addressed to perforator veins:
In advanced stages of venous insufficiency with trophic
lesions of the skin and ulcers, interrupting the blood
reflux through the perforator veins is indicated for skin
lesions healing. It can be achieved in different ways.
There are two main very similar operations : Felder’s and
Linton’s technique. In both, a longitudinal incision is
performed in the posterior or postero-lateral aspect of
the calf sectioning the skin and the fascia. The perforator
veins are intercepted under the fascial plane, ligated and
resected. Then the fascia and skin are sutured.
New less invasive techniques have been developed in
recent years. One of these is the subfascial endoscopic
perforator vein surgery.
For endoscopic approach two ports (10 mm and 5
mm) are placed in the subfascial space of the calf
remote from the area of venous ulceration. A dissector
balloon is introduced and inflated to improve access.
Carbon dioxide is then insufflated to facilitate
dissection. The incompetent perforating veins are
clipped and divided using endoscopic scissors or
alternatively, coagulated and divided using an
ultrasonic coagulator (harmonic scalpel).
Deep venous occlusion and/or infected ulcers are
usually contraindications to subfascial perforator veins
surgery
Treatment of venous ulcers
There are surgical and non surgical treatments.
Conservative treatments use different types of ointments
with epithelisant effect. Ulcers must be kept free of
infection, absorbing any excess discharge, maintaining a
moist wound environment and the edema must be also
controlled. The patient will wear compression garments,
physical activity will be encouraged and also elevated
position of the leg during rest.
Conservative treatment of venous ulcers can be
frustrating and lengthy and recurrences are frequent.
Surgery provides faster healing of ulcers. The primary
condition is to ensure a normal local metabolism of the
skin. Causes of venous stasis that produces hypo-
oxygenation and edema must be first resolved
(saphenectomy and ligation of perforator veins).
In many cases, eliminating the causes of venous stasis
results in ulcer healing with conservative methods.
For large ulcers there are many surgical methods but the
most used are those of plastic surgery using skin grafts.
Unfortunately skin grafts have a high rate of failure.
Topical therapy with growth factors (platelet-derived
growth factor and epidermal growth factor) is also an
alternative but more expensive.
ACUTE VENOUS THROMBOSIS
(AVT)
AVT is represented by blood clotting inside the veins
with an acute onset.
– Venous thrombosis = blood clotting inside the veins without
signs of acute inflammation.
– Thrombophlebitis = thrombosis + symptoms and signs of acute
inflammation
– Venous thromboembolism = migration of the thrombus from
deep veins along the blood stream causing obstruction of
pulmonary vessels and in many cases the death of the patient.
– Superficial venous thrombosis = thrombosis is affecting only the
superficial veins or varices (varicophlebitis)
– Deep venous thrombosis = deep veins (of the calf or thigh) are
affected – these are the most dangerous and the cause of
thrombembolism
Etiopathology
Three factors are involved in intravascular blood clotting
(Virchow’s triad):
1. Stasis/turbulence
2. Endothelial lesions
3. Hypercoagulability
Factors associated with an increased risk of venous
thrombosis are:
– Age > 40 years, male gender, obesity and cancer
– A history of thrombosis or pulmonary embolism
– Operations (orthopedic, neurosurgical, urological, any operation
lasting more than 2 hours)
– Pregnancy
– Use of oral contraceptives
– Nephrotic syndrome
– Dysfibrinogenemia
– Hereditary deficiency or abnormal synthesis of protein C, protein
S, antithrombin III, plasminogen
Venous endothelial injury
– As a result of prolonged compression of the vein or after trauma
– Prolonged immobilization of the legs on a solid surface
– Intravenous injections or catheter
– Hypoxia due to stasis
– Endothelial infection
Venous stasis and turbulence
– Prolonged standing
– Prolonged immobilization after surgery or trauma
– Any increase in abdominal pressure situations: pregnancy, abdominal
tumors, ascites, obesity
– Irregular dilated veins (varices) with turbulent flow
Hypercoagulability
– A postoperative or posttraumatic decrease of antithrombin III
– Congenital deficiency of antithrombin III
– Increased of inhibitor factor of plasminogen activation
– Still unexplained circumstances related to duration of surgery, obesity,
advanced age, sepsis
– Polycytemia and thrombocytosis
– Malignant tumors (Trousseau syndrome) - procoagulants factors
synthesized by the tumor cells and peritumoral inflammatory infiltrate
 Superficial trombophlebitis of
the lower limbs – varicophlebitis
Most superficial thrombophlebitis of the legs occur in the
varicose veins due to venous stasis and blood circulation
disorders with turbulent flow. In addition, local trauma may
be another cause.
In most cases the clinical manifestation is that of an acute
thrombophlebitis with symptoms and local signs of
inflammation.
The onset is sudden with pain along the involved vein. The
great saphenous vein or other superficial veins and
varices are affected in variable lengths.
Examination of the lover limb reveals the Celsian local
signs: swelling over the affected veins and redness of the
skin. On palpation the skin is warm, and the thrombosed
vein feels like a painful hard cord under the skin.
The differential diagnosis should include lymphangitis
and cellulitis.
Superficial thrombophlebitis rarely is a life threatening
condition, but a thorough investigation of the patient is
mandatory because of occult deep vein thrombosis
which may be associated and carries high rates of
morbidity and mortality.
The goal of treatment of superficial thrombophlebitis, is
to stop the spread of the thrombotic process and to
reduce the local inflammatory reactions.
Conservative treatment consist of:
– Anticoagulants (heparin and then long term oral anticoagulants)
– Antiplatelet - Dipyridamole, Aspirin
– Local ointments with heparin
– Non-steroidal anti-inflammatory drugs, such as: ibuprofen,
aspirin, acetaminophen, naproxen sodium etc.
– Antibiotics
– Wearing compression bandages or stockings
 After resolution of inflammatory phenomena, in most
cases, an organized superficial vein thrombosis remains
that can be the site from where bacteria are discharged
into the bloodstream or phlebitis may relapse. In few cases
the inflammatory process evolves to abscess formation.
These are the reasons why, thrombosed varicose veins
should be surgically removed.
Surgical treatment is addressed not only to the complication
of varicose veins, the superficial trombosis, but also to the
underlying disease: the varicose veins disease itself. The
thrombosed vein is removed, if necessary with the overlying
skin (due to inflammation there may be an intense adhesion
of the vein to the skin) through an incision along the vein
taking care not to open the vein as the thrombus is
considered to be infected.
Great saphenous vein
arch thrombosis

Crossectomy
Thrombosed saphena magna
Deep venous thrombosis (DVT)
It is a very dangerous condition as it endangers the
patient's life by possible evolution to pulmonary
embolism.
The vast majority of cases of deep vein thrombosis and
pulmonary embolism are found in patients receiving
surgery.
The annual worldwide incidence of DVT of the leg is 1
case per 1000 population.
The etiopathogenesis of deep thrombophlebitis in
surgical patient, involves many factors of which the most
important is the venous stasis due to immobilization. In
addition to this tissue factors resulting from surgical
trauma are released into the blood stream contributing to
increased platelets adhesion and blood coagulability.
Obese patients, those with cancer disease, those with
venous insufficiency of the lover limbs (varicose veins),
those operated for bone fractures and pelvic pathology
and are at the highest risk of developing postoperative
deep venous thrombosis.
Based on these facts, all patients are encouraged to
postoperative early ambulation (to avoid stasis) and they
are treated with anticoagulants as needed.
Most commonly, thrombosis begins in the veins of the calf
and pelvis. The thrombosis process extends from distal
(peripheral) to central veins (popliteal, femoral, iliac).
Occluded veins induce a high retrograde intravenous
blood pressure manifested by edema of which extension
depends on thrombosis extension.
Steps of thrombosis process are:
1. White thrombus formation – platelets are the main
components - platelet adhesion and activation and then
aggregation to form the platelet plug.
2. The red thrombus (mixed thrombus) – a fibrin gel network that
includes red cells and white cells, which fuse with the platelet
plug.
3. Retraction of the thrombus
4. Organized thrombus – the fibrinolysis process dissolves the
clot.
After fibrinolysis the thrombus may dissolve completely or partially
resulting the total or partial (like a sieve) recanalization of the
vein. In this last situation, the blood flow is slowed with
peripheral stasis. After prolonged standing, edema and cyanosis
of the affected lower limb occur.
The major risk for embolism is on the second and third
phase (between days 2-12 after surgery) and the most in
the shrinking (retraction) phase of the thrombus.
Clinical picture
General signs:
– Michaelis Sign - gradual increase of temperature to 38 C in the
absence of an obvious cause
– Mahler’s "climbing pulse rate" - the scale of pulse in contrast to
that of temperature
– Unexplained anxiety and restlessness
Local signs:
– Swelling of the whole inferior limb or only the calf. There is an
increased diameter of the calf (and thigh sometimes) compared
to the opposite inferior limb. More then 2 cm difference,
measured at the same level, between the two legs is suggestive
for deep venous thrombosis.
– The skin is stretched, glossy with high local temperature and
slightly cyanotic
– On palpation - tenderness of the calf with high consistency of
muscular tissue due to edema.
Right calf swelling
 Clinical signs:
1. Pratt’s sign = dilated pretibial vein which remains dilated
even when the leg is elevated (sign of deep femoral vein
thrombosis)
2. Payr sign = pain at palpation of the median muscular region
of the sole
3. Bisgaard sign = retromalleolar pain
4. Tschmarke sign = pain on calf compression
5. Ducuing sign = pain at shaking the calf musculature
6. Homans sign = pain in the calf induced by passive
dorsiflexion of the leg
7. Lowenberg sign = calf pain produced by compression with
blood pressure cuff at higher values than 100 mmHg.
8. Meyer sign = tender points in calf over the affected vein
Clinical forms by location:
– Thrombosis of the calf’s veins is manifested by
increased consistency of the calf but not excessive
edema
– Thrombosis of the popliteal and femoral vein – there
is a calf edema extended till the knee
– Thrombosis of the ilio-femoral vein – there is an white
edema of the calf and thigh called “ phlegmatia alba
dolens”
– Very extended ilio-femoral thrombosis may result in
“phlegmatia cerulea dolens” - a very painful edema of
the whole inferior limb. There is an associated spasm
of the arteries with cyanotic cold skins, weak femoral
pulse and alteration of general status of the patient.
Foot gangrene can occur.
phlegmatia cerulea dolens
 – Thrombosis extended to the hypogastric veins is
manifested by: pain in the lower abdominal quadrant,
lumbar pain dysuria, acute urinary retention, rectal and
genital pain.
– Thrombosis of the inferior cava vein will result in edema
of the both inferior limbs, low arterial blood pressure and
shock.
Thrombosis may occur also simultaneously in both lower
limbs. Other less frequent possible sites of thrombosis are:
upper limbs, portal and splenic vein.
Unfortunately there are many cases without any symptoms
of acute inflammation (just thrombosis and not
thrombophlebitis) or just with slight symptoms as moderate
calf pain, which evolve directly to pulmonary embolism and
death, before any measure can be taken.
Diagnosis of acute phase is based on clinical picture
and other investigation of which the Doppler ultrasound
is the most useful and uninvasive.
Evolution under treatment goes to remission of
symptoms. In convalescence the edema disappears in
supine but reappears in standing position. During
stabilization phase symptoms disappear. The last phase
is that of sequelae with postthrombotic syndrome and
different kinds of possible complications.
Complications:
– Pulmonary embolism
– Venous gangrene
– Post-thrombotic syndrome
– Chronic venous insufficiency (edema, cellulitis, leg ulcers)
 PULMONARY EMBOLISM

Is the most dangerous complication. The thrombus starts

from the deep leg veins and carried by the blood stream to
the heart. If the clot is big enough it will occlude the
pulmonary artery resulting in sudden death. If the clot is
small or there are many fragments of clots, these will pass
into the smaller pulmonary arteries occluding them and
leading to pulmonary infarction.
Symtoms
In massive thromboembolism the onset is acute with
anxiety, violent retrostrernal pain, cyanosis, dyspnea,
tachycardia and death in few minutes or evolution to
cardiogenic shock.
In less massive embolism the thrombi reach till the lungs
where they occlude some arteries leading to pulmonary
infarction manifested at 24-48 hours by: chest pain,
cough, hemoptysis, dyspnea. Fever till 38 C degree is
present for 2-3 days. Thoracic radiography and CT scan
reveal a wedge-shape pulmonary condensation.
Pulmonary infarction may also develop serohematic
pleural effusion which persists 2-3 weeks.
In case of small and repeated pulmonary
thrombembolism there are short episodes of dyspnea,
tachycardia, arrhythmia, cough and hemoptysis.
 Pulmonary infarction

Chest X-ray

CT scan

wedge-shaped pulmonary condensation

Physical signs
– Tachypnea (respiratory rate >16/min) - 96%
– Pulmonary rales - 58%
– Accentuated second heart sound - 53%
– Tachycardia (heart rate >100/min) - 44%
– Fever (temperature >37.8°C) - 43%
– Diaphoresis - 36%
– S3 or S4 gallop - 34%
– Clinical signs and symptoms suggesting thrombophlebitis - 32%
– Lower extremity edema - 24%
– Cardiac murmur - 23%
– Cyanosis - 19%
Approximately 10% of patients who develop pulmonary
embolism die within the first hour and approximately one
third of patients who survive an initial pulmonary
embolism die from a subsequent embolic episode.
 Late complication of pulmonary thromboembolism is
chronic pulmonary hypertension.
POST-THROMBOTIC SYNDROME
Evolution of venous thrombus may be:
1. To complete resolution – this is a rare possibility
2. Recanalization through a single canal but with valves destruction
3. Recanalization through multiple canals as a sieve
4. Repermeabilization through collateral avalvulate veins
5. Fibrous organization as a hard cord
There are five types of post-thrombotic syndrome:
1. Obstructive – there is a persistent obstruction of the venous axis
2. Substitution – the blood flow finds other ways to avoid the
occlude vein
3. Restrictive – veins loose their elasticity and the capacity of
stoking blood
4. With reflux – due to valves lesions hydrostatic pressure rises and
reflux towards superficial veins appears
5. Combinations of the above types
As a consequence of difficult blood flow, venous stasis
and high hydrostatic pressure will develop downstream
the affected veins. This will lead to edema initially
reducible and then irreducible, trophic alterations of the
skin, pigmentation, cellulitis and ulcer. Venous ulcer
develops more rapidly (1-2 years) then after varicose
veins (10-20 years).
Treatment of DVT
Untreated DVT will lead to embolism in 50% of cases
and to death in 10-38%. The risk lowers in treated
patients to 5-20% for embolism and <8% for mortality.
The most important treatment is prophylaxis.
Preventive measures must be applied to all surgical
patients especially to those obese, with varicose veins,
those with cancer, operated for bone fractures or for
pelvic organs pathology:
1. Applying compression stockings or elastic bandages on the
legs prior to operation and wearing it after.
2. Using of pneumatic socks (sequential compression device)
during operation and in the first days after in obese patients
3. Early ambulation
4. Using anticoagulant drugs (heparine or fractionated heparine
such as Clexane, Fraxiparine, Fragmin, etc)
5. Antiplatelet drugs – Dextrane, Aspirin, etc
Treatment of the acute phase
Once the deep vein thrombosis is diagnosed, the patient will
be put at rest in bed for 7-10 days with the leg elevated at
20-25 degrees. Walking is not permitted to prevent
thrombus mobilization and embolia.
Anticoagulant treatment will be started with intravenous
administration of unfractionated heparin 5000 iu and then
500-1300 U/h for 7-10 days. Oral anticoagulant tablets will
be given simultaneously for three days and then continued
3-6 month just with tablets in doses that keep the value of
plasmatic thrombin time 2-3 folds higher than normal values
or the INR in the range of 2.0 to 3.0. Heparin may be
discontinued when the international normalized ratio (INR) is
stable and greater than 2.0
Anticoagulant treatment does not directly restore venous
patency or vascular function, it just prevent thrombus
developing. On the other hand even in patients who are fully
anticoagulated, however, DVT and pulmonary embolism can
and often do recur.
 In addition anti-inflammatory and antibiotics will be
associated.
Walking will be permitted after the resume of
inflammatory fenomena and edema.
Thrombolysis (dissolves the clots) is reserved for
extensive forms (phlegmatia cerulea dolens) of DVT
and iliofemoral thrombosis. Patients selection:
1. Patients with an expected long-term survival
2. Massive DVT or phlegmasia cerulea dolens
3. Iliofemoral DVT
4. Multiple segment DVT
5. Patients who remain symptomatic despite anticoagulation
6. Recent onset DVT (<10d)
7. No previous DVT
8. Younger patient, few co-morbidities
 Contraindications for thrombolysis are:
1. Active bleeding
2. Cerebrovascular accident (within 2 months)
3. Major surgery (within 10 days)
4. Pregnancy or recent delivery
5. Metastatic cancer to brain or spinal cord
There are two types of thrombolysis: systemic and direct
catheter guided. Systemic is more expensive and less
accurate. Catheter guided uses less quantities, has less
adverse effects and a higher rate of success.
Catheter thrombolysis is performed under imaging
guidance, the fibrin-specific thrombolytic agent being
delivered directly to the clot through a catheter inserted in
the vein.
Ultrasound (US)-accelerated thrombolysis, involves
simultaneous delivery of low intensity US and thrombolytic
agent into a thrombosed vessel, and so accelerates the
thrombolysis and reduces the time of infusion and risk of
bleeding.
Thrombolytic agents
Thrombolytic agents can be classified in two categories:
1. Fibrin-specific agents (alteplase, reteplase, and
tenecteplase) which produce limited plasminogen
conversion in the absence of fibrin.
2. Non–fibrin-specific agents such as streptokinase.

– Streptokinase (the first used agent 1933) – extracted from

beta-hemolytic streptococci, is the cheapest but also the
most antigenic and it has many adverse reactions (fever,
hypotension, etc) - the usual dose regimen is an IV bolus of
250,000 U followed by a maintenance drip at 100,000 U/h.
The drip is continued for 1-3 days, until clinical or laboratory
investigation shows thrombus resolution.
– Urokinase (1947) - unlike streptokinase, it is not antigenic
and directly activates plasminogen to form plasmin. It is
produced by renal parenchymal cells. It is indicated in case
of massive pulmonary embolism.
For systemic treatment the dose is 4,400 U/kg Urokinase as an
IV bolus, followed by a maintenance drip of 4,400 U/kg/h. The
drip is continued for 1-3 days, until clinical or laboratory
investigations demonstrate thrombus resolution. For
intrathrombus delivery the dose is a loading dose of 250,000 U
IV, followed by an infusion of 500 U/kg/h. If clot lysis is
inadequate, the infusion rate can be increased gradually up to
2,000 U/kg/h.
– Alteplase (1st generation), the first recombinant tissue-type
plasminogen activator. It is fibrin specific effective only at
the surface of fibrin clot. It is not antigenic. Catheter-
directed infusion of 1-1.5 mg/h for 12-24 hours.
– Reteplase (2nd generation) - works more rapidly and has a
lower bleeding risk. It is also not antigenic. Catheter-
directed infusion of 1 U/h is maintained for 18-36 hours.
– Tenecteplase (TNKase) (3rd generation) produced by
recombinant DNA technology. It has the advantage for a
single bolus administration and decreased bleeding side
effects.
Venous thrombectomy is applied in rare cases,
especially in iliac vein thrombosis using the Fogarty
catheter.
In case of pulmonary embolism the first who tempted to
surgically remove the clot from the pulmonary artery was
Trendelemburg but the first who reported a success was
Kirschner in 1919. The method implies thoracotomy and
extracorporeal circulation and it has a high burden of
mortality.
Other methods have been developed such as catheter
removal and thrombolysis.
Thrombolytic treatment is accepted in case of
hemodynamic instability or right ventricular dysfunction
being suggested in select high-risk patients who do not
have hypotension and are at low risk for bleeding.
Every patient with an episode of pulmonary embolism
should receive oral anticoagulant therapy for at least 3
months.
In patient with high risk of recurrent thrombembolism
(and for those whom the anticoagulant therapy is
contraindicated) inferior vena cava filter (Greenfield filter)
may be useful.
Treatment in chronic phase (pos-thrombotic
syndrome)
– Elevation of extremity at rest and at night
– Compression stockings grade 2 should be worn
during the day, while standing but not needed to be
worn at night
– Weight loss and behavior modifications
– Increased exercise with strengthening of extremity
muscles
– Pain management
– Compression pump
– Vascular interventional radiology procedure: balloon
opening and stenting of narrowed vein
INDICATIONS FOR
SPLENECTOMY
 Splenectomy is the most widely used technique in
surgery of the spleen.
 Splenectomy means total ablation of splenic tissue,
namely the spleen and any accessory spleen.
 Segmental (partial) splenectomy means the removal of
one or more segments of the spleen.
Anatomy
 Size of spleen is about 12 x 7 x 3 cm. The average
weight is 150 g, (80 to 300 g).
 It has a dark purplish color being a soft organ of very
friable consistence, highly vascular which makes it very
difficult to sewn. Also because of its friability, the spleen
breaks easily during direct or indirect abdominal or left
thoracic trauma.
 The spleen is located in the deep left hypochondrium. It
lies between the fundus of the stomach and the
diaphragm. Its projection is between the left ribs 9 and
11.
 It has two surfaces (convex and visceral concave) and
two borders. The anterior border has a few clefts. The
posterior border is more rounded and blunter than the
anterior.
 The concave surface comes into direct contact with: the
stomach, the pancreas, the left kidney and the splenic
flexure of the colon.
 The spleen is covered by peritoneum, which is firmly
adherent to its capsule. It is held in position by two
peritoneal folds: the phrenicolienal ligament and the
gastrolienal ligament. The lower end of the spleen is
supported by the phrenicocolic ligament. The most cases
of iatrogenic lesions of the spleen is due to this ligament
(phrenicocolic) which frequently adhere to the inferior pole
of the spleen. During operations like left hemicolectomy or
gastrectomy, traction exerted on this ligament results in
avulsion of the spleen capsule with consecutive bleeding.
 Accessory spleens are frequently present in the
neighborhood of the spleen in the gastrolienal ligament
and greater omentum. They are small nodules of splenic
tissue of variable size from that of a pea to that of a plum.
 Vascularization: The arterial supply comes from the
lienal artery, a branch of the celiak trunk from the aorta.
The lienal artery divides in the hilum of the spleen in
several branches and provides a segmental
vascularization. The venous blood is collected by the
lienal (splenic) vein which joins with the superior
mesenteric vein to form the portal vein. The inferior
mesenteric vein flows into the splenic vein.
 Lymphatic vessels have their origin in the white pulp
forming a network around vessels and flowing into the
lymph nodes located in the hilum of the spleen.
 Because the very close relations between the tail of the
pancreas and the hilum of the spleen, there is a
possibility to injure the tail of the pancreas during
splenectomy (when ligating and resecting the vessels)
that may result in an iatrogenic pancreatitis.
•The spleen is coated by a thin capsule which in the hilum
is reflected inward upon the vessels in the form of
sheaths.
•The spleen is composed of two pulps: the red pulp and
the white pulp. The white pulp is lymphoid tissue that
usually surrounds splenic blood vessels. The red pulp is a
network of channels (sinuses) filled with blood.
 Spleen has a major hematopetic function till the 5th
intrauterine month life. The most important function of
the spleen is the mechanical filtration, that removes
senescent red blood cells and control of infection.
Abnormal blood components will be trapped in the spleen
and ingested by splenic phagocytes.
 The spleen is a major site of production for the opsonins,
properdin and tuftsin. Opsonin are molecules that target
an antigen for an immune response. Properdin is a
globulin protein that acts like a pathway of complement
activation important for destruction of bacteria, foreign
and abnormal cells. It also helps to neutralize some
viruses. Tuftsin binds to specific receptors on the surface
of macrophages and polymorphonuclear leukocytes,
stimulating their migration, phagocytic, bactericidal, and
tumoricidal activity. It also influences antibody formation.
 In non-traumatic cases the indication for splenectomy
arises from an interdisciplinary collaboration: surgeon,
internist, hematologist, gastroenterologist, parasitologist,
pediatrician, etc.
 Taking into account the important role of the spleen in
immunity, the indication of splenectomy must be very
well documented to avoid situations that can lead to
unwanted complications or worsening of diseases.
Splenectomy for spleen abnormalities
 Abnormalities of position (spleen "displaced" in other site
than splenic lodge) may be congenital ("ectopic") or
acquired and are often accompanied by abnormal splenic
mobility which can cause twisting or volvulation around
the elongated pedicle with secondary splenic infarction
or compression on neighboring viscera.
 Abnormalities of number: the presence of
supernumerary spleens (accessory spleen) may require
splenectomy in context of hypersplenism.
 Abnormalities of shape: splenectomy is indicated in case
of complications (infarction, spontaneous or traumatic
rupture, compression on the neighborhood organs).
Splenectomy for vascular abnormalities
 Splenic infarction. Single or multiple lesions secondary to
emboligene cardiovascular disease or other diseases (hematologic,
inflammatory, septic, vasculopathies) clinically silent or manifest by
complications: splenomegaly accompanied by pathological
phenomena, splenic rupture with / without intraperitoneal bleeding,
infection with abscesses.
 Splenic artery aneurysm (the second most frequent location after
the aorta) - considering the risk of rupture with vital risk, large
aneurysms should be surgically treated immediately after the
discovery of the aneurysm by splenectomy (if distal location) or
aneurysm excision with restoration and preservation of spleen artery
(if troncular location).
 Arteriovenous splenic fistula which may cause a portal
hypertension syndrome. In case of intrasplenic arteriovenous large
shunt, splenectomy is also indicated.
 Spontaneous rupture of splenic vessels – a rare clinical
condition with acute onset of intraperitoneal hemorrhage.
 Volvulus of the spleen around its vascular pedicle, rarely
reversible spontaneously, with mixed infarction (arterial and
venous) of the spleen, with symptoms of acute abdomen requiring
emergency laparotomy with splenectomy.
 Splenectomy in portal hypertension indicated in the following
conditions:
1. As single gesture:
– In case of segmental portal hypertension with thrombosis of the
splenic vein
– Il hypertension associated with splenomegaly and hypersplenism (in
the absence of esophageal varices, upper gastrointestinal bleeding
and ascites)
– In case of portal hypertension due to arteriovenous fistula
2. As associated procedure complementary to different types of
portal hypertension surgery: distal spleno-renal bypass,
azygoportal deconnection Sugiura-Futagawa or Hassab operation.
3. Completing a previous intervention (such as a non-selective porto-
caval shunt without splenectomy leaving the possibility of further
development of splenomegaly accompanied by mechanical
consequences and hypersplenism).
Parasitic splenopathies
 Splenic echinococcosis (primitive or secondary): splenectomy is
the only resonable therapeutic solution.
 Malaria manifested by intermittent febrile accesses, associated with
splenomegaly and anemia (hypersplenism predominantly on red-
cells line). The splenomegaly develops in two phases (acute,
congestive, reversible and chronic phase sclerous irreversible). The
treatment is complex, medical and surgical, splenectomy being
indicated to control and prevent complications such as mechanical,
vascular, infectious and hematologic.
 Visceral leishmaniasis - manifested with fever, anemia and
splenomegaly. The treatment is medication and eventually surgical
(splenectomy is indicated if there are risks of complications and to
eliminate an important reservoir of parasites).
 Schistosomiasis (bilharziasis, Egyptian splenomegaly) manifested
by portal hypertension with splenomegaly and hypersplenism.
Splenectomy is a step of eso-gastric devascularization during
Hassab operation.
Septic and viral splenopathies
 Splenic abscess (single or multiple) of variable
etiology: microbial (digestive bacteria) or parasitic
(Entamoeba histolytica, Plasmodium) by hematogenous,
from neighborhood or direct inoculation. Diagnosis is
based on clinical picture, lab investigations and imaging.
In most cases splenectomy is the optimal therapeutic
approach.
 Other infectious splenopathies: typhoid fever,
endocarditis, tuberculosis, infectious mononucleosis, can
benefit from splenectomy during a complex treatment.
Splenic tumors
 The main reasons for establishing the indication for
splenectomy are symptoms and the risk or complications
(tumor size plays an important role in risk especially for
cystic hemangiomas).
Splenopathies during hematologic
diseases
 Benign haematological conditions which benefit from
splenectomy are:
 Thalassemia - inherited autosomal recessive blood
disorder which results in reduced rate of hemoglobin
synthesis or formation of abnormal hemoglobin
molecules, thus causing anemia. Severe associated
splenomegaly is an indication for splenectomy.
 Sickle-cell anemia or drepanocytosis, is an
autosomal recessive genetic blood disorder characterized
by abnormal, rigid, sickle shape red blood cells. Sickle-cell
disease may lead to various acute and chronic
complications, several of which have a high mortality rate.
Indications for splenectomy in patients with sickle cell
disease include: acute splenic sequestration crisis (rapid
enlargement of spleen, anemia), hypersplenism, splenic
abscess.
 Hereditary spherocytosis, is an autosomal dominant
disease that results from a deficiency of spectrin, a red
blood cell cytoskeletal protein. This defect causes
membrane abnormality in the red blood cells that are
small, spherical, and rigid with increased osmotic
fragility. It is manifested by hemolytic anemia,
occasionally jaundice, and splenomegaly. Splenectomy
decreases the rate of hemolysis and usually leads to
resolution of the anemia. It is usually performed in
childhood shortly after diagnosis but is delayed until
after the 4th year of life to preserve immunologic
function of the spleen in young children.
 Aplastic anemia is a condition where bone marrow
does not produce sufficient new cells (red blood cells,
white blood cells, and platelets) termed pancytopenia.
Splenectomy helps some patients with severe
thrombocytopenia.
 Immune thrombocytopenic purpura (idiopathic
thrombocytopenic purpura, Werlhof disease) is characterized by low
platelet count, a normal bone marrow, and the absence of other
causes of thrombocytopenia. There is an increased platelet
destruction due to autoantibodies to platelet membrane. Indication
for splenectomy are:
– refractory severe thrombocytopenia
– toxic doses of steroids
– relapse after initial steroids
– >6 weeks of steroids and continue to have a platelet < 10,000/mm 3
– >3 months with incomplete response to primary therapy platelet <
30,000/mm 3
– 2nd trimester of pregnancy with medical refractory platelet
<10,000/mm 3 or who have platelet <30,000/mm 3 and bleeding
problems.
 The success rate (complete and permanent response) is about 65%.
 The cause of failure to respond to splenectomy or relapse after an
initial response, in many cases, is represented by accessory spleen
which also must be surgical excised.
 Thrombotic thrombocytopenic purpura (TTP,
Moschcowitz disease) is a rare disorder of the blood-
coagulation system, causing extensive microscopic clots
in the small blood vessels. It is manifested by neurologic
symptoms (alteration in mental status, seizures,
hemiplegia, paresthesias, visual disturbance, and
aphasia), fever, dark urine, pallor, jaundice, and
petechiae due to anemia and thrombocytopenia. The
exact etiology of TTP is not clear. The therapy of choice
is plasma exchange with fresh frozen plasma and
corticosteroids. Splenectomy is indicated in refractory
cases of TTP.
 Storage diseases (Gaucher disease , Niemann-Pick
disease, etc.) manifested mainly by hepatomegaly and
splenomegaly with hypersplenism.
 Haematological malignancies in which
splenectomy may be associated in a complex
treatment: chronic lymphocytic leukemia (CLL), hairy
cell leukemia, malignant lymphoma (Hodgkin or non-
Hodgkin), myeloproliferative syndromes, (chronic
myeloid leukemia (CML), myelofibrosis with myeloid
metaplasia, etc..).
Splenectomy for spleen trauma
 Splenectomy is the choice in severe and multiple
lesions of the spleen with hemodynamic instability.
Indications for splenectomy:
1. Parenchyma explosion
2. Vascular lesions in the hilum
3. Intra-parenchymal massive hematoma
4. Patients in critical condition or other severe intra-abdominal
injuries
5. Failure of conservative surgical techniques
Other classification for splenectomy
indications: (according Angelescu et al.)
A. Absolute indications
 In emergency (Vital)
– Splenic trauma
– Splenic abscess with septic syndrome
– Ruptured arteriovenous aneurysms
– Splenic infarction (torsion of the opedicle, embolism)
– Intestinal obstruction (compression, colic volvulus)
– Splenic vein thrombosis with ruptured gastric varices
 Elective
– Hereditary spherocytosis
– Immune thrombocytopenic purpura
– Splenic hydatid cyst
– Benign splenic tumors
– Primary malignant tumors
 B. Relative indications
– Autoimmune hemolytic anemia
– Other congenital hemolytic anemia
– Thrombotic thrombocytopenic purpura
– Splenic neutropenia
– Splenic pancytopenia
– Felty syndrome
– Myeloid metaplasia
– Chronic myeloid leukemia
– Chronic lymphocytic leukemia
– Hairy cell leukemia
– Gaucher disease
– Nieman-Pick disease
– Cirrhosis with portal hypertension and hypersplenism
– Splenic tuberculosis
– Splenic syphilis
– Malaria
– Uncomplicated aneurysms
– Splenic metastatic tumors
 Splenectomy for diagnosis
– Undiagnosed splenic tumors
– Hodgkin's lymphoma (stage I, IIB)
– non Hodgkin lymphoma
 Tactical splenectomy
– Pancreatectomy (total or left)
– Total gastrectomy
– Spleno-renal shunt
– Esophagoplasty
– Left hemicolectomy
– Left nephrectomy
Indications for partial splenectomy
 Partial splenectomy (segmentectomy, ablation of a splenic pole,
hemisplenectomy, subtotal splenectomy) is considered for
preservation of immune functions of the spleen.
 1.For haemostasis – partial spleen trauma
 2. For localized spleen lesions
– Cysts (pseudocyst, hydatid cyst)
– Benign solid tumors
– Partial infarctions
– Localised abscess
 3. For reduction of the spleen volume
– Gaucher disease (in children)
– Severe hypersplenism (in children)
– Myelofibrosis
– Schizostomiasis
 4. For diagnosis purpose
– Hodgkin's lymphoma
– Unspecified tumors
– Isolated splenomegaly
Contraindications for splenectomy
 There are cases when splenectomy may lead to
negative effects in the absence of any beneficial
therapeutic outcome for the patient:
1. Limited spleen infarction, uncomplicated and asymptomatic
2. Portal hypertension: splenectomy without any other procedures
lowering the portal pressure is contraindicated (spleen serves
as a buffer organ in portal system)
3. Splenomegaly in systemic sepsis
4. Congestive splenomegaly in malaria
5. Hereditary hemolytic anemia of low or medium grade
6. Acute leukemias (splenomegaly appears in the stage of
generalization of malignancy)
7. Non-Hodgkin systemic lymphoma (advanced evolutionary
stage)
8. Splenomegaly in polycythemia vera
9. Essential haemorrhagic thrombocythaemia
10. Spleen sarcomas in generalized sarcomatosis stage (stage III).
11. Spleen metastatic tumors
Surgical technique of splenectomy.
 Splenectomy can be performed via laparotomy (open
approach) or by laparoscopic approach.
 In certain cases splenectomy can be also perform via a
left thoracotomy through the left diaphragm. This last
approach is reserved especially for polytrauma or stab
wounds when there are intrathoracic lesions (more life
threatening) associated with diaphragmatic and spleen
lesions but with no other intra-abdominal lesions.
Splenectomy can be easily performed through this
approach and is followed by diaphragmatic repair and
thoracic drainage.
 Laparotomy can be a left subcostal approach or a median
laparotomy. The subcostal approach ensure a better and
direct access to the spleen but it has also some
disadvantages: it does not afford a thorough exploration
of the entire abdominal cavity and is followed by paralitic
incisional hernia due to intercostal nerves lesions.
 The subcostal aproach is performed especially in cases
where the spleen is the single abdominal organ affected
established by investigations.
 Median laparotomy is performed especially in emergency
cases when a thorough exploration of the abdominal
cavity is necessary such as abdominal trauma (blunt or
penetrating) with hemoperitoneum when other organs
may be involved. This approach offers the best view
over the all organs and can be split in any direction.
 There are two strategies to remove the spleen:
– Anterior approach - starting from the spleen hilum – gastro-colic
and gastro-splenic (short gastric vessels) ligament are divided,
the tail of the pancreas and the hilum of the spleen are exposed,
splenic vessels are ligated and resected, and spleen is extracted
after resection of persplenic adesions and ligaments.
– Posterior approach – starts from the posterior aspect of the
spleen with the incision of the spleno-parietal reflection of the
peritoneum; the spleen and the tail of the pancreas are
mobilised to the surface and vessels are legated and resected.
 Laparoscopic approach is a minimal invasive
procedure which requires a laparoscopic unit, special
instruments and a skilled surgeon. It has advantages
over the open procedure. It can be performed through
either a lateral or an anterior approach. The steps are
almost the same as in open procedure but the spleen
must be removed using a special bag in which the
spleen is first chopped (fragmented).
 Hand-assisted laparoscopic surgery refers to a
laparoscopic approach performed with the aid of one
surgeon’s hand introduced into the abdomen through a
plastic device inserted in a 7.5 to 10 cm wound. By this
procedure the splenectomy is much easier and also the
extraction but the minimal invasive principle is violated.
 Robotic splenectomy - The main advantages are a
better tridimensional view and an increased versatility of
the surgical instruments.
Hand assisted splenectomy
Robotic surgery
Contraindications for laparoscopic approach
 Absolute
1. Contraindications of general anesthesia (severe
cardiopulmonary disease and other co-morbid conditions
making laparoscopic or even open splenectomy impossible to
perform.)
 Relative
1. Uncontrolled coagulopathy
2. Advanced myeloproliferative syndromes
3. Spleen larger than 20 cm
4. Aneurysms of splenic pedicle
5. Cirrhosis with portal hypertension
6. Pregnancy
Possible complications after splenectomy
 Immediate complications
– Bleeding from the spleen bed or other sources
– Spleen lodge hematoma and abscess
– Postoperative infections
– Fever
– Acute pancreatitis
– Thromboembolic complications
– Left pleural effusions
 Late complications
– Minor infections
– Fulminant life-threatening systemic sepsis
– Hernia at the incision site
 Given the important role of the spleen in immunity,
whenever possible, surgeons try to preserve a normal
spleen or to perform limited resections. This became
possible with the development of hemostatic materials
(TachoSil and others) or special instruments (harmonic
scalpel, LigaSure, laser, argon plasma, etc.) which ensure
a proper hemostasis.
THORACIC TRAUMA
Surgical anatomy considerations

 Thorax is the part of the body between the neck and

abdomen. It consists of the rib cage, an osteocartilaginous
structure (which houses the vital organs like lungs, heart
and large vessels) and soft tissues (muscles, fascia,
tendons, skin). On the front of the chest mammary glands
are located.
 The osteoacartilaginous elements are represented by
twelve thoracic vertebrae, sternum and ribs with costal
cartilages. Between ribs there are 11 intercostal spaces,
which are occupied by the Intercostal muscles and
intercostal vessels and nerves. The role of this cage is to
protect vital organs and also to confer the rigidity
necessary for ventilation.
 During trauma, any of these anatomical structures can
suffer injuries. The less likely are the vertebrae, which
are protected by the paravertebral muscles. The most
fragile are the ribs and cartilages, structures that break
most often. Types of bone lesions and their location
depend much on the nature, strength and direction of the
traumatic force.
 Bone fractures have two important consequences:
broken edges may injure the nearby anatomic structures
(intercostal vessels, pleura, lung, heart) and also alter
the most important function of the thorax, namely the
respiratory function, endangering the patient's life.
 The thorax cage is like a rigid box, feature which is very
important in respiration. Altering the rigidity of the cage
especially after ribs fractures will alter the respiratory
function also.
 The thoracic cavity is separated from the abdominal
cavity by the diaphragm which is the most important
respiratory muscle. It acts like a piston. During its
contraction it lowers decreasing the intra-thoracic
pressure allowing the inspiration. During relaxation the
diaphragm moves upward leading to a higher pressure in
the thoracic cavity, inducing expiration.
 Intercostal muscles are the other respiratory muscles
which by contraction elevate the ribs and increase the
thoracic diameter and the depth of inspiration.
 Accessory muscles of breathing are considered: the
sternocleidomastoid, scalene, serratus, pectoralis,
trapezius, latissimus dorsi, and others. If a breathing
disorder exists, the accessory muscles of inspiration may
become overused.
 Expiration is a passive action based on elastic recoil of
the lungs. In forced expiration as well in certain condition
when lung elasticity is affected the abdominal muscles
and the internal intercostal muscles help expel air.
 Another important aspect that must be understand is that
between the two pleural layers (parietal and pulmonary)
there is a virtual space with negative pressure (lower
than the atmospheric pressure) so that traumatic lesions
of these layers and beneath anatomical structures will be
followed by rapid accumulation of fluids or gas (or both)
into the pleural space which will lead to lung collapse
and possible mediastinum dislocation. All these will
impair more or less rapidly or dramatically the respiratory
and cardiac function.
 Often there is no direct relationship between the extent
of injury and the physiopathological disorders.
 There are many cases when minimal gestures such as
thoracocentesis, with fluid or gas evacuation, can save
the patient’s life.
 Traumas represent a principal cause of deaths in
peacetime but especially in wartime. Chest and head
trauma are the most dangerous. Chest trauma
represents about a quarter of trauma in general, and
greatly contributes (9-10%) to the general mortality of
about 25%-50%.
 In most cases, chest injuries are part of polytrauma.
 Nowadays the most common injuries are caused by road
traffic accidents. Thoracic trauma is estimated to be
responsible for approximately 16,000 deaths per year in
the United States.
 Estimates of thoracic trauma frequency indicate that
injuries occur in 12 persons per million population per
day. Approximately 33% of these injuries require hospital
admission.
 Early deaths due to thoracic trauma which occur within
30 minutes to 3 hours after the injury are secondary to
cardiac injury with/without tamponade, great vessels
injury, airway obstruction and aspiration.
 Two thirds of these patients reach the hospital prior to
die. Only 10-15% of blunt trauma require thoracic
surgery, and 15-30% of the penetrating chest trauma
require open thoracotomy. 85% of patients with thoracic
trauma, can be managed by simple lifesaving
maneuvers that do not require surgical treatment.
 Optimal treatment requires a through knowledge of the
pathophysiology of the thorax and expertise the
therapeutic interventions.
 Improved prehospital care and rapid transportation have
increased the survival, but the mortality remains high.
CLASSIFICATION
A. Blunt trauma
 Blunt trauma are closed thoracic trauma (there is no
solution of continuity on the skin).
 Blunt chest trauma may affect any component of the
chest wall and thoracic cavity (bony skeleton, lungs and
pleurae, tracheobronchial tree, esophagus, heart, great
vessels of the chest, and the diaphragm).
 Kinetic forces act in different ways or mechanism:
 Blast – the pressure wave can produce:
 Tissue disruption
 Vascular lesions
 Disruption of alveolar tissue
 Disruption of tracheobronchial tree
 Traumatic diaphragm rupture
 Direct impact by a blunt object
 A hard object that hit the thorax can produce bone
fractures, especially ribs and through the fractured
edges, lesions of the nearby anatomical structures
(pleura, intercostal vessels, lungs, etc).
 Crush - compression
 The thorax is compressed between two hard surfaces.
Direct injury of chest wall and internal structures
occurs. It causes a marked increase in blood pressure
within the veins of the upper thorax and may result in
traumatic asphyxia. Anterior-posterior compression
forces place indirect pressure on the ribs, causing
lateral, mid-shaft fractures. Lateral compression forces
applied to the shoulder are common causes of
sternoclavicular joint dislocation and clavicle fractures.
 Deceleration
 The body in motion strikes a fixed object. For
example during frontal collision in car crashes (the
sternum hits the steering wheel), or a fall from
height. A blunt trauma to chest wall is produced,
but after the contact with the hard surface the
internal structures continue in their motion being
crushed to the internal chest wall and also
anatomical structures of fixation will be broken or
even organs will be broken.
 The degree of external trauma may not fully predict
the severity of internal injuries and clinical
suspicion of cardiac and vascular trauma should be
heightened.
 Consequences of closed chest trauma are highly
dependent on many factors. The first is the force
intensity. Then the direction and site of action is also
important. It should also be considered if injury
occurred during inspiration or expiration. Last but not
least should be considered patient’s age and existing
co-morbidities. (The younger thorax is more flexible and
better resist to deformation while in elderly fractures
occur more easily).
B. Penetrating Trauma – there is a skin solution of
continuity. Depth of penetration may be limited only to
the soft tissues of the chest wall but penetration maybe
deeper affecting the pleural cavity and internal organs.
When the traumatic agent penetrates the whole thorax,
being present an opening for entry and one of exit, we
talk about transfixing trauma.
 1. Low energy forces (arrows, knives, handguns) cause
injury by direct contact and cavitation.
2. High energy forces (military guns, high powered
hunting rifles) – produce extensive cavitation injury
due to high pressure. Tissue destruction is much
higher due to bone fragments driven by traumatic
agent.
 Penetrating wounds consequences depend primarily on
penetration depth and the affected organs. If
mediastinal organs as the heart or great vessels are
affected, the chances of quickly death are very high.
Affecting other organs (pleura, lungs, esophagus) are
also life threatening but there is an interval of time when
investigations could be performed and rescue measures
can be taken.
 Classification according to pathophysiological
criteria:
1. Without pathophysiological disorders
2. With pathophysiological disorders:
1. Acute respiratory insufficiency
2. Acute cardiocirculatory insufficiency
3. Acute cardiorespiratory insufficiency
4. With temporary stop of cardiorespiratory function

 Classification according to pathogenesis

1. Closed chest trauma (blunt trauma)
2. Open chest trauma (wounds)
1. Blind or transfixiant wounds
2. Nonpenetrating or penetrating wounds
3. With or without effusions
4. Mixed
 Classification based on anatomical criteria
 Without anatomical lesions
 With anatomical lesions:
 Parietal non-skeletal lesions
 Parietal skeletal lesions
 Diaphragmatic
 Endothoracic lesions
 Single organ affected, multiple organ affected
 Associated with other trauma
 Ribs fractures
Sternum fractures
Parietal lesions
Flail chest (free-floating
segment of the chest wall)
Simple pneumothorax
Open pneumothorax
Pleural space
Tension pneumothorax
Hemothorax
Contusions
Pulmonary parenchyma
Lacerations
Trachea and bronchi
Mediastinum Heart and great vessels Lesions of these organs
Esophagus
Diaphragm Diaphragmatic lesions
 Potential physiological consequences in
thoracic trauma:
1. Hypoxia
2. Hypercapnia
3. Hypovolemic shock
4. “Obstructive" shock
5. Acidosis
 The 6 types of rapidly fatal chest injuries (found on
primary examination):
1. Airway obstruction
2. Suffocating pneumothorax
3. Open pneumothorax
4. Massive hemothorax
5. Flail chest - free-floating segment of the chest wall
6. Cardiac tamponade
 The 6 types of potentially lethal chest trauma (found at
secondary examination):
 Rupture of the aorta (dissection)
 Myocardial contusion
 Tracheobronchial rupture
 Rupture (perforation) of esophagus
 Pulmonary contusion
 Diaphragmatic rupture (hernia)
 The 8 types of thoracic injury free of fatal potential
(identified at secondary examination):
 Simple pneumothorax or reduced hemothorax
 Sternoclavicular joint dislocations
 Sternal fracture
 Clavicle fracture
 Scapular fracture
 Traumatic asphyxia
 Simple rib fractures
 Chest wall contusion
Some aspects of pathophysiology
 Chest trauma may affect vital functions: ventilation and
circulation by several mechanisms manifested by the
following syndromes:
1. Compression syndrome (compression exerted on
intrathoracic organs by pleural or pericardial effusions)
 Air: Pneumothorax
 Fluid: blood = Hemothorax, lymphatic fluid = Chylothorax
 Mixed – Fluidopneumothorax
2. Chest wall instability - when the chest wall looses its
rigidity as a consequence of multiple ribs fractures in two
or more places (free-floating segment of the chest wall)
the ventilatory dynamics is deeply affected, resulting in
acute respiratory failure.
 The following four disturbances of respiratory dynamics
may appear:
 Paradoxical respiration – the floating area of the chest wall
moves in during inhalation and out during exhalation causing
poor ventilation of the lungs, oxygen depletion and severe and
even fatal cardiovascular disturbances.
 Pendular motion of the mediastinum - still further hampers the
heart and great vessels and reduces the already impaired
oxygenating power of the lungs.
 The "pendulum air” – it appears when injury crushes only one
side of the chest. On inhalation, the air is pulled out of the flailing
side and exhalation pushes the healthy side's stale air back into
the flailing lung. The paradoxical air "pendulum" only switches
stale air from one lung to the other.
 Bronchial hypersecretion
 There are two important vicious circles:
 COURNAND - hypoxia  pulmonary hypertension  alveolar
hypersecretion  hypoxia
 POISVERT - paradoxical respiration  hypoxia 
hyperventilation  increased paradoxical respiration.
• When several ribs are broken on the both sides
and chest loses its rigidity and becomes soft (flail chest),
the situation is more critical because the patient can not
breathe. In this case the only solution is mechanical
ventilation by orotracheal intubation .
3. Obstructive syndrome - accumulation of fluids in
tracheo-bronchial tree will occlude the lumen impairing
ventilation, gas exchanges and promoting infection.
Causes:
 Bronchial hypersecretion
 Bleeding into the tracheobronchial tree
 Pulmonary hypertension
 Aspiration in the airway of saliva or gastric contents by vomiting
 Shock lung (wet lung) - insidious onset of rapid superficial
breathing, dyspnea, and productive cough; rales and wheezes;
refractory cyanosis. Xray appearance of enlarging interstitial
and alveolar infiltrates which extend until the entire lung is
enveloped in a diffuse haze.
4. Fluid, electrolytes and acid-base imbalance: Loosing
electrolytes can be caused by bleeding, sweating,
tachypnea. Acidosis has a respiratory component and a
metabolic component. Initially respiratory acidosis is
followed by metabolic acidosis.
5. Diaphragmatic syndrome:
 Phrenic nerve injury will lead to paralysis of the diaphragm and
so it will not participate in respiratory movements.
 Laceration of the diaphragm can cause the ascension into the
chest of the abdominal organs.
6. The infectious syndrome - although not the most
important, must always be considered.
7. Traumatic shock - refers to pulmonary shock or ARDS
(Acute Respiratory Distress Syndrome) which is
characterized by inflammation of the lung parenchyma
leading to impaired gas exchange with concomitant
systemic release of inflammatory mediators causing
inflammation, hypoxemia and frequently resulting in
multiple organ failure.
8. Pain is also an important element. Because of pain
patients can not breathe well and that will lead to
hypoventilation with bronchial hypersecretion and hypo-
oxygenation and so oxygenation will decrease even
more.
 Hemorrhagic shock – appears as a consequence of blood
loss. The most severe and acute forms are due to cardiac
and great vessels injury (hemomediastinum) but most
often it is due to intercostal vessels lesions (produces by
broken costal edges) and lung wounds. The blood
accumulates into the pleural space (hemothorax) that may
also dangerously reduce the vital capacity by compressing
the lung on the involved side. In lung wounds the pleural
space contains blood and also gas giving a characteristic
image on thoracic X-ray (hemo-pneumothorax) with a
horizontal line delimitation between fluid and gas.
 Right Fluido-pneumothorax

Pneumothorax

Collapsed
Lung

horizontal line delimitation between fluid and gas

 The pathophysiological mechanisms (acting alone or in
combination) can lead to two life threatening syndromes:
acute posttraumatic respiratory failure and acute
posttraumatic heart failure.
The mechanism of acute respiratory failure in thoracic
trauma:
1. Ventilation deficiency - may be caused by:
 Disturbances of chest wall dynamics:
 Flail chest
 Limitation of respiratory movements due to pain
 Cancellation of tightness of chest wall:
 Pneumothorax
 Disturbances of diaphragm movements:
 Traumatic diaphragmatic rupture or phrenic nerves lesions
 Exclusion from ventilation of lung parenchyma areas:
 Compression by pleural effusions or herniated abdominal viscera
 Airway obstruction
 Aspiration of foreign bodies, blood, tracheobronchial hypersecretion
2. Impairment of air distribution in the lung parenchyma:
 Paradoxical breathing
 Pendular mediastinal movements
3. Alterations of gas diffusion:
 Posttraumatic pulmonary edema
 Pulmonary shock

The mechanism of acute heart failure in thoracic trauma:

 Compression and dislocation of the large venous trunks
 Mediastinum emphysema and hematoma
 Compression on atria (massive pleural effusions)
 Heart trauma
 Cardiac tamponade
Symptoms and signs of acute respiratory
failure:
 As a result of hematosis (venous blood oxygenation)
deficiencies:
 Polypnea or tachypnea (accelerated respiratory frequency)
appears at the onset of the interstitial pulmonary edema and the
frequency increases as respiratory failure progresses.
 Dyspnea is increasing progressively
 Cyanosis (due to hypoxemia) occurs when the de-oxygenated
Hb reaches at least 5 g/dl. It is a late sign when anemia is
associated.
 Cardiovascular signs (in advanced stages):
 Tachycardia, (bradycardia in end stages)
 Hypotension
 Neurological signs:
 Impaired sensitivity
 Altered consciousness (dizziness, coma)
 Signs of end stages:
 Shallow breathing or agony breathing
 Cyanosis
 Sweating
 Hypotension, bradycardia
 Oliguria, anuria

 Laboratory signs
 Decreased oxygen saturation (SaO2) - normal 97.5%
 Respiratory acidosis - decreased PaO2 and increased PaCO2,
decreased blood pH.
 Radiological signs - according to respiratory failure causes
Examination of patient with thoracic trauma
 The evaluation of patient with chest trauma is
performed in three stages:
1. At site of accident (the primary evaluation) where vital
function are assessed and also the first life-saving
measures are taken.
2. Then, at hospital level in the emergency receiving unit
(the secondary evaluation) where further investigations
(radiography, tomography, laboratory, etc.) are carried
out and measures of stabilization and resuscitation are
applied.
3. In the department of surgery or intensive care unit if
patient requires hospitalization for surgery or
surveillance. If surgery is required the exploration and
assessment of damages are continued intraoperatively.
 The initial management of the patient with thoracic
trauma is frequently the responsibility of the emergency
physician who is not a thoracic surgeon. It is therefore
mandatory that the emergency physician should be able
to recognise the thoracic injuries that are or will be
dramatic if not treated properly.

 Patient’s history - collect data from the patient (where

possible) and/or environment (when patient can not
communicate).
 Circumstances of injury
 Traumatic agent nature
 Conditions which acted
 Injury time (time elapsed from the occurrence of trauma)
 Patient’s co-morbidities and previous treatment
 Patient's symptoms (pain, dyspnea, bleeding, etc.)
 In unstable and critical circumstances, quick decisions
and adequate maneuvers based on recordings of vital
signs and a right interpretation of clinical and
diagnostic pattern are required.
Patient examination
 On inspection:
1. Parietal lesions (wounds, deformities, bruising, hematoma)
2. Abnormal movements or limitation of thoracic respiratory
movements (rib fractures with floating regions of the chest
wall, paradoxical respiration - flail chest)
3. Breathing disorders – polypnea, dyspnea, tirage = inspiratory
sinking of the intercostal spaces due to airway obstruction
4. Signs of bleeding (pallor, hemoptysis, external bleeding)
5. Disorders of hematosis (cyanosis, sweating)
6. Other signs (ecchymotic mask – a dusky discoloration of the
head and neck occurring when the trunk has been subjected
to sudden and extreme compression, mental disorders, other
associated lesions, etc)
 On palpation:
 Pain
 Signs of rib or sternal fractures (focal pain, bone discontinuity,
bone crepitations)
 Possible floating regions of chest wall
 Subcutaneous emphysema (subcutaneous crepitation –
accumulation of gas in the subcutaneous tissue)
 On percussion:
 Hypersonority in pneumothorax
 Dull sound in pleural effusions
 Enlargement of cardiac area
 On auscultation:
 Reduction or abolition of lungs vesicular murmur (pleural
collection)
 Auscultatory asymmetry between the two hemithorax
 Pleural or pericardial friction rub sounds
 Blurred heart sounds (In the event of cardiac tamponade)
 Digestive sounds of intestinal movements (In case of traumatic
diaphragmatic hernia)
Primary evaluation
 The evaluation of the patient's chest trauma is only a
part of the total assessment. A general examination
should also be performed to observe any associated
lesions (abdominal, limb, head, spine).
 Because thoracic injuries are severe and potentially
lethal, the diagnosis and therapy go hand in hand.
 In unstable and critical patients quick decisions based
on check of the following vital signs are required:
Airway patency:
 Ensuring a free airway is a major priority in emergency
resuscitation, patient’s life depending largely on it.
Foreign bodies must be removed from the month and
specific maneuvers are applied to prevent backwards
fall of the tongue.
 All the airway manipulations must be performed with
respect to potential cervical spinal injuries.
 Chin lift maneuver Jaw trust maneuver Head-tilt/chin-lift maneuver

 Before starting any maneuver for airway patency some

basic parameters should be assessed:
1. If patient is conscious or not
2. Breathing is appropriate or not - check respiratory movement,
and their extension
3. Duration of hypoxia - cyanosis appears very late
4. Airway patency
5. Need for administration of neuromuscular blocking agents
(muscle tension, teeth clenching, severe obstructive
pulmonary disease or asthma)
6. Stability of cervical spine
The circulation status is evaluated by assessing patient's
pulses (radial, carotideal or femoral). In hypovolemic
shock radial pulse becomes small and may be absent
when blood pressure is below 60 mm/Hg.
 The neck veins are distended when there is cardiac
tamponade, if it is associated with hypovolemic shock
distension of the neck veins may be absent.

Airway

Breathing

Circulation
 BLUNT THORACIC TRAUMA
Chest wall lesions
Contusions
1. Simple contusions
 May be of variable severity, but often they are mild.
Contusion is the effect of a direct or indirect, frontal or
tangential action of the traumatic agent.
 Clinic picture is represented by: pain, respiratory
discomfort, dyspnea associated with different chest wall
lesions at the site of impact (abrasions, bruising,
hematoma, effusions, etc..).
 Radiological examination is required but in most cases
nothing pathological is found.
 Treatment is symptomatic with painkiller, myorelaxants,
non-steroidal anti-inflammatories.
2. Muscular ruptures:
 Rarely due to the action of a blunt object, often as a result
of accidents, sports, etc..
 Clinically is manifested by violent pain with limitation of
mobility. At the site of rupture initially a depression may be
noticed followed by a hematoma.
 Chest X-Ray shows nothing special but ultrasound
examination can highlight the muscular rupture and
hematoma.
 Treatment is symptomatic with bed rest (immobilization),
myorelaxants, non-steroidal anti-inflammatories and in
rare cases surgical repair.
3. Chest compression:
 It occurs when the chest is compressed between two
forces which leads to a sudden increase of pressure in the
chest. The pressure exert a high force on the intra-thoracic
organs (lungs, heart) which are squeezed and then
transmitted then to vessels (veins, arteries).
 MORESTIN - acute thoracic compression syndrome - is
characterized by: cervico-facial cyanosis, petechiae and
edema in the upper thoracic region and conjunctival and
retinal hematic extravasation (ecchymotic mask) plus
neurological signs of cerebral edema with Cheyne-
Stockes breathing type.
 In addition to symptomatic treatment, oxygen therapy is
needed and/or assisted ventilation and also cardiac and
renal treatment may be necessary.

Ecchymotic mask
Fractures
1. Simple rib fractures: are the most common lesions
in the thoracic contusion.
 They are produced either directly - at site of impact, or
indirectly - by antero-posterior chest compression.
Fractures may be complete or incomplete (Greenstick
fractures).
 Rib fractures are not always simple. Depending on
traumatic agent and its force, more than one rib may
be fractured. There are many cases when rib fractures
are complicated with lesions of the nearby tissues or
organs due to the dislocation of the fractured edges.
 The most frequent associated lesions are those of intercostal
vessels and parietal pleura resulting in hemothorax.
 If the lung is also perforated hemothorax will be associated
with pneumothorax too.
  Rarely other intrathoracic organs (heart, aorta) are injured by
fractured rib edges.
 In 20% of cases trauma and fractures of left ribs 9,10, and 11 are
associated with spleen rupture and consecutive hemoperitoneum.
 Even if rib fractures are not complicated, due to the intense
pain exacerbated by every respiration, the respiratory
function of the patient may be impaired especially in those
with pulmonary co-morbidities. Pain prevents the patient to
breathe deeply enough which will lead to alveolar hypo-
oxygenation and bronchial hypersecretion. Because the
patient can not cough effectively and expectorate,
secretions accumulate and lead to airway obstruction,
stasis and infection. That’s the reason why treating pain in
rib fractures is very important.
 Diagnosis is based mainly on clinical criteria: pain at the
site of fracture, bone crepitations, limitation of respiration,
decreased breath sounds on the affected side.
 Complications of rib fracture may include the following:
 Hypoventilation
 Hypercapnia
 Hypoxia
 Atelectasis
 Pneumonia
 Damage to underlying visceral organs
 Pneumothorax (immediate or delayed)
 Hemothorax (immediate or delayed)
 Aortic injury (immediate or delayed)
 Pulmonary contusion
 Intra-abdominal organ injury
 First rib fractures have often been associated with serious head
injury, cervical spine injury, delayed subclavian vessel
thrombosis, aortic aneurysm, tracheobronchial fistula, thoracic
outlet syndrome, and Horner's syndrome.
 Chest X-ray in two incidences help much in diagnosis of
rib fractures and associated complications (hemo-
pneumothorax).

Multiple rib fractures

 Cpllapsed lung

Rib fracture with right pneumothorax

 Other useful investigations are: ultrasonography
especially when spleen rupture is suspected, and CT
scan which is not indicated for every simple case, just for
those associated with complications or in polytrauma
and unconscious patients.

Pneumo

Fracture Heart

Lung

CT scan – right pneumothorax

 Costochondral disjunction may exist alone or in
combination with the broken ribs. Without associated rib
fracture the condition is not life-threatening and nothing
special must be done, but in association with ribs
fractures it causes a free-floating area of the chest wall
(flail chest) which may be very dangerous impairing the
ventilation.
 Simple rib fractures without complications, may be
managed on an outpatient basis. Pain killers, myorelaxants
and anti-inflammatory drugs will be prescribed and a chest
X-ray will be repeated at 24-48 hours. If pain is very
intense, intercostal nerve block (first described by Braun in
1907) is indicated. It can be performed with Lidocain but it
has a short effect, or with Lidocain associate with absolute
alcohol (9/1) in which case the effect is longer. Respiratory
parameters typically show impressive improvements upon
removal of pain. Blockade of two dermatomes above and
two below the level of fracture is required.
 Rib belts or binders do not control pain and are not
recommended as they will limit the respiratory movements.
 When there are complications such as hemo-
pneumothorax, the patient should be admitted in the
hospital and properly monitored and treated. Also consider
admission for elderly and patients with underlying lung
disease or decreased pulmonary reserve.
The injection needle with bevel faced cephalad is inserted to the rib, then
redirected until the point just clears the inferior margin of the same rib. It
is then advanced 0.5 cm., and if aspiration is negative for blood, the
anesthetic solution is injected.
2. Sternal fractures:
 Sternal fracture occurs as a consequence of a direct
impact on the sternum such as the wheel steering during
car accidents (deceleration mechanism).
 In most cases the fracture line is transversal but rarely it
can be longitudinal. The fracture may be with or without
displacement, with or without overlapping of fractured
edges. In case of displacement there is a high risk of
cardiac lesion or compression.
 The main symptom is the local pain. The pain must be
differentiated from angina or cardiac infarction. On
palpation there is a local tenderness, and a deformation
as a step of scale when fractured parts are overlapping.
 The diagnosis is based on physical examination and
imaging explorations.
 The lateral radiograph is usually the most valuable view
for detecting sternal fractures and for determining the
degree of displacement.
 CT is particularly useful for assessing for associated
injuries such as pulmonary contusion, pneumothorax, or
retrosternal hematoma.
CT scan

lateral radiograph
 Treatment – as in rib fractures, treatment is aimed at
achieving analgesia and optimization of respiration. In
case of displacement with cardiac compression surgical
reduction and fixation of the sternum may be considered.
3. Flail Chest – represents a segment of the chest that is
free-floating with the pressure changes of respiration. It
appears when there are three or more adjacent rib
fractures in two or more places or rib fractures are
associated with costochondral disjunction or longitudinal
fracture of the sternum.
 Variations include posterior flail segments, anterior flail
segments, and flail including the sternum with ribs on
both sides of the thoracic cage fractured, mixed forms
and “soft chest” (totally crushed chest).
 Incidence: 20% of chest trauma in most cases
representing a serious chest wall injury with underlying
pulmonary injury.
 Effects of flail chest are:
 Paradoxical respiration
 Pendulum air
 Pendulum mediastinum
Clinical picture.
 The major symptom is the pain caused by fractures.
 The degree of respiratory insufficiency is related to the
underlying lung injury. The worst respiratory insufficiency
is seen when the chest is totally crushed because the
patient cannot breathe at all. In this case there are
multiple bilateral rib fractures and the thorax looses it
rigidity becoming soft. For saving patient’s life it must be
intubated and ventilated with positive pressure (internal
pneumatic stabilization).
 Tachypnea is present due to the pain.
 Paradoxical movements of the affected segment of the
chest wall can be observed.
 Other symptoms and signs may be present depending
on the associated lesions and the severity of respiratory
insufficiency.
 Diagnosis relies on physical examination (clinical
observation), imaging studies and arterial blood gas
measurements (helpful to assess the need for
mechanical ventilation and to monitor the patient).
Treatment
 Severity of respiratory insufficiency is less a result of the
paradoxical motion of the chest wall but rather a result of
pulmonary and other associated lesions.
 Priorities:
 Airway patency – remove the foreign bodies, blood cloths,
secretions. If necessary orotracheal intubation or even
tracheostomy may be performed.
 Oxygenation through mask or intubation.
 Remove pleural collections to ensure lungs expansion – by
thoracocentesis or thoracostomy (pleurostomy).
 Cardiocirculatory support – fluid rebalancing, replace lost blood.
 Analgesia
 Stabilization of the chest wall or early intubation and mechanical
ventilation for poor gas exchange
 Stabilization of chest wall to eliminate the paradoxical
respiration can be achieved by:
1. Non surgical procedures.
2. Surgical procedures which are most commonly performed in
patients requiring a thoracotomy for other reasons.
3. Internal pneumatic stabilization indicated in massive crash of
the chest (soft chest wall).
 For most patients with acceptable respiratory function
the simple immobilization of the flail segment is
sufficient. It can be done using bandages or better
adhesive tapes applied only on the affected
hemithorax not to impair the respiratory movements.
 External fixation – uses a metal plate whose ends lie on
the rigid thoracic wall. Flail ribs are suspended by
threads passed under the ribs and fixed to that plate.
 Advantages of ribs fixation:
 Decreased pain
 Improved mechanics
 Decreased need of mechanical ventilation
 Decreased hospital stay

Surgical fixation of fractures

 OPEN CHEST TRAUMA
 Nonpenetrating trauma - presumes a solution of
continuity in the skin with varying degrees of damage to
the anatomical structures of the thoracic wall but without
penetration into the chest cavity. The vast majority are
due to weapons or accidents.
 Wounds are treated like any other wounds
(decontamination, suture, etc..)
 Penetrating trauma
 Low Energy (arrows, knives, handguns) - Injury caused by direct
contact and cavitation.
 High Energy (military, hunting rifles & high powered hand guns) -
extensive injury due to high pressure cavitation.
 Shotguns - Injury severity based upon the distance
between the victim and shotgun & caliber of shot:
 Type I: >7 meters from the weapon - Soft tissue injury
 Type II: 3-7 meters from weapon - Penetration into deep fascia and
some internal organs
 Type III: <3 meters from weapon - Massive tissue destruction
 Penetrating chest wounds can cause damage to any
intrathoracic organ but most frequently lungs and heart are
affected. Extent of lesions depends on kinetic energy and
type of the traumatic agent. Some injuries are simple
perforations, others are so massive that are incompatible
with life.
 Intrathoracic organ injuries would cause accumulation of
fluids (air, blood, lymph, digestive content) into the
pleural cavity, mediastinum or pericardium.
 Most of these are life-threatening injury, surgical repair
being mandatory for life rescue. Surgical gestures can
be very simple but there are situations in which complex
interventions are required.
 Pneumothorax
 It represents the presence of air into the pleural cavity
which is an abnormal situation because the parietal and
visceral pleura loose their intimate contact which is
necessary for a good expansion of the lungs in
inspiration.
 There are two possible sources from where the
atmospheric air may enter the pleural cavity:
 through an opening of the chest wall (wound), or
 through an opening in the lung or bronchial tree (wound or leak)
 Mechanisms:
1. Spontaneous – Usually on an emphysematous lung during an
intense efforts or cough when emphysematous bubbles burst.
2. Traumatic
1. Closed chest trauma due to lung, bronchial or tracheal rupture or tear
2. Open chest trauma - penetrating wounds which may affect lungs
3. Iatrogenic – during subclavian vein catheter insertion or cardiac
resuscitation maneuvers.
Simple post-traumatic pneumothorax
 In most cases, is the consequence of lung perforation by
fractured ribs edges during blunt trauma. More rarely the
tracheobronchial tree lesions are the cause of
pneumothorax in which case this is associated with
pneumomediastinum. Simple pneumothorax may be also
a consequence of penetrating chest trauma (wounds)
with lesions of the lungs and/or thracheobronchial tree
but, if the parietal wound is large enough, an open
pneumothorax will develop.
 Accumulation of gas into the pleural space in most cases
is associated with accumulation of blood resulting in
hemo-pneumothorax.
 Depending on how much gas and fluid are accumulated
into the pleural space, the lung will collapse more or less
and respiratory function will be affected accordingly.
 Lung

Left pneumothorax
 If there are no adhesions between the two pleura:
parietal and pulmonary, the lung will collapse entirely. If
there are adhesions, gas and fluid will be trapped in
some pleural spaces and lung won’t collapse. In this last
eventuality if there is a tear in the parietal pleura the air
will spread between anatomical layers of the thoracic
wall till the subcutaneous plane resulting in
subcutaneous emphysema. The air will spread in all
directions especially in the upper part of the body (chest,
neck, face) but it may reach in the lower part also
(abdomen, scrotum). Air can also spread in fatty tissue
of the mediastinum (pneumomediastinum) and the
irritation of recurrent laryngeal nerves will cause
hoarseness.
 A simple pneumothorax may progress to a tension
pneumothorax.
 Symptoms may vary very much depending on
pneumothorax extension and associated lesions. In small
pneumothorax there are no symptoms except those
caused by chest trauma (pain exacerbated by respiration).
In larger pneumothorax associated with blood collection
symptoms of respiratory insufficiency are intricated with
those of anemia with tachycardia, pallor, hypotension, cold
sweats.
 In subcutaneous emphysema swelling of the neck, chest,
face, eyelids can be observed. This can induce pain,
difficulty of swallowing, wheezing and difficulty of
breathing.
 Skin marks of thoracic trauma may be evident or not.
 On percussion of the affected side there is a tympanic
sound and on auscultation vesicular murmur is
diminished or absent. In hemopneumothorax, on
percussion, two zones are found: the upper of sonority
and a lower of dullness, separation line between them
being horizontal.
 Diagnosis is based on clinical and imagistic
investigations. On a postero-anterior chest X-ray the
pneumothorax can be seen, the lung being collapsed
more or less. In hemopneumothorax the superior level of
fluid is highlighted by a horizontal line. In simple fluid
collections without pneumothorax this line is not
horizontal but convex downward. Subcutaneous
emphysema has also a specific image on X-ray. CT scan
is helpful in assessing associated lesions.
 Treatment. All patients with pneumothorax should be
admitted, investigated, treated and monitored.
 Small simple pneumothorax (not tension pneumothorax !)
often resolve on their own by gas resorption. Gas
reabsorbs from the pleural space at a rate of 1.25% of
the trapped volume per day. Therefore, a pneumothorax
occupying 30% of the hemithorax would require 24 days
to resolve with the patient breathing room air. Additional
oxygen administration increases the rate of resorption.
 Medication consists of painkillers, anti-inflammatory
drugs, O2, myorelaxants, antibiotics, fluid rebalancing,
administration of blood if necessary.
 Surgical therapy consists of thoracostomy with pleural
drainage which in most cases is sufficient for lung
reexpansion and blood evacuation. In certain cases when
pneumthorax does not resolve with this procedure or
bleeding is massive, thoracotomy and lesions treatment
(aerostasis and hemostasis) becomes necessary.
 If not massive, the subcutaneous emphysema is
reabsorbed by itself in a few days. To remove the gas
from subcutaneous layer there are several methods:
insertion of large bore needles, small skin incisions or
subcutaneous drainage tubes.
 Pleural drainage if performed will eliminate the source of
the air entering the subcutaneous space.
Open pneumothorax with traumatopnea

 Traumatopnea = passage of respiratory air in and out

through a wound of the chest wall.
 Due to the gradient of pressure between the pleural
space and atmosphere during respiration, the air passes
through the open thoracic wound into the pleural cavity
during inspiration and leaves it during expiration through
the same opening (sucking chest wound).
 Air will be drawn through wound if wound is 2/3 diameter
of the trachea or larger.
 Chest wound may be associated with pulmonary lesions
so that air can enter the pleural space also from the lung.
 The consequences are :
1. Acute respiratory failure with reduced tidal volume
and vital capacity caused by lung collapse and
oscillation (pendulation) between the two lungs of the
deoxygenated air.
2. Circulatory failure by pendulation of mediastinum
toward the healthy hemithorax during inspiration and
toward affected hemithorax during expiration which
affects the return of venous blood by vena cava
compression.
 Tidal volume is the lung volume representing the normal volume of air
displaced between normal inspiration and expiration when extra effort is
not applied. Typical values are around 500ml
 Vital capacity is the maximum amount of air a person can expel from the
lungs after a maximum inspiration. It is equal to the inspiratory reserve
volume plus the tidal volume plus the expiratory reserve volume.
 Symptoms are represented by dyspnea with cyanosis.
On inspection the penetrating wound is found through
which air enters and exits. On percussion of the affected
side there is a tympanic sound and on auscultation
vesicular murmur is absent being replaced by the sound
produced by flowing air through the thoracic wound.
 Chest X-ray will show a total collapse of the lung.
 Treatment of open pneumothorax.
 The first aid intention is to close (seal) the wound to
prevent further pendulum air and mediastinum. It can be
done by dressing the wound with an impermeable gauze
(soaked with ointment) and the patient must be
transported urgently to the hospital. High-flow oxygen
will be administered and aggressive hemodynamic and
respiratory resuscitation should be initiated.
 Patients with severe respiratory insufficiency should be
intubated and ventilated. As long the thoracic wound is
opened there is no risk of tension pneumothorax.
 In hospital a chest tube drainage will be applied through
thoracostomy (or toracotomy if necessary) into the
pleural cavity to evacuate collections and allow the lung
reexpension. The thoracic wound will be closed. The
patient will be monitored and lung reexpansion will be
assessed by auscultation and chest X-ray.
Tension pneumothorax
 Represents the progressive accumulation of air (with
every inspiration) into the pleural cavity, air which
remains trapped into the cavity and gradually
compresses the lung and shifts the mediastinum to the
opposite side. It is a high life-threatening condition but
life can be saved by simple maneuvers.
 The mechanism is due to a lesion of the thoracic wall
(external pneumothorax) or lung (internal pneumothorax)
that acts like a one-way valve letting the air to enter the
pleural cavity but not to exit.
 Major vessels such as the vena cava, pulmonary artery,
and aorta become kinked or compressed, and severe
hypoxemia ensues. Cardiovascular compromise
develops because the return of venous blood to the right
ventricle is severely impaired, as is the cardiac output.
Circulatory collapse shortly follows.
 General condition is rapidly altered and the patient can
die in few minutes.
 Tension pneumothorax can be a progression of a simple
or open pneumothorax.
 Sympyoms and signs:
 Dyspnea with tachypnea is the first symptom. As
pulmonary atelectasis by compression progresses
dyspnea becomes more and more intense with cyanosis.
 On inspection a thoracic wound may be noticed in
external pneumothorax and the flow of air through the
opening may be heard. The affected hemithorax is
distended with intercostal spaces bloating. Other signs
are: tachycardia, tachypnea, and diminished breath
sounds, hyperresonance to percussion, and decreased
tactile fremitus on the ipsilateral side. A significant
volume of gas in the pleural space causes tracheal
deviation and mediastinal shift toward the contralateral
lung, hypotension, distended neck veins, and respiratory
distress.
 Tension pneumothorax is a major emergency - rarely
there is enough time available to conduct investigations.
The diagnosis relies on clinical symptoms and signs.
 When possible, anteroposterior chest radiography while
the patient assumes a Fowler's or semi-Fowler's position
shows:
 Collapse of the lung
 Mediastinal shift to the healthy side
 Descend of the affected side diaphragm
 Widening of intercostal spaces
 Treatment
 Pleural decompression is needed urgently before patient
reaches the hospital.
 If this diagnosis is suspected, do not delay treatment in
the interest of confirming the diagnosis. Immediately
place the patient on 100% oxygen.
 Decompression can be easily performed by inserting a
14-16-gauge needle into the 2nd intercostal space along
the mid-clavicular line or into the 5th intercostal space
along the mid axillary line. When the needle enters the
pleural space, the sound of gas escaping is generally
perceived. The needle should be placed just above the
cephalad border of the rib to avoid the intercostal
vessels.
 A catheter can be introduced through the needle and
then the needle may be withdrawn.
 This maneuver actually establishes a communication
between the pleural space and atmosphere converting a
tension penumothorax into an open pneumothorax.
 After needle decompression (if it is not performed in the
hospital) the patient will be transported urgently to the
hospital. All patients with pneumothorax will be admitted.
• If a patient is to be ventilated with positive pressure
following needle aspiration, whether fluid, air or nothing
was encountered, a chest drain should be inserted.
• In hospital conditions treatment will be continued by
inserting a pleural drainage, although this maneuver can
be performed at site of accident by specialized rescue
team. The site of insertion depends on coexisting of fluid
accumulation (blood, effusions, lymph) into the pleural
cavity. In case of pure pneumothorax the drain may be
inserted into the 2nd intercostal space on mid-clavicular
line. If there is fluid collection too, the drain should be
inserted into the 5th-6th intercostal space on mid axillary
line, or associated to that in the 2nd space.
Steps for a correct
insertion of pleural
drainage tube:
A. Incision
B. Dissection
C. Finger exploration
D. Inserting the tube with the
forceps
E. Advancing the tube into the
pleural cavity
F. Fixation of tube
 The chest tube will be attached to a Heimlich valve with
drainage bag or sealed underwater (simple Bulau or
Beclaire or aspiration drainage).
 Mild aspiration can be applied through the drainage tube
in order to reexpand the lung but suction should be seen
as the exception rather than the rule.

Heimlich valve
 Most chest drains need no suction. An effective cough can
generate a much higher pressure than can safely be
produced with suction. Thoracic suction should only be
used on wards where the staff are familiar with chest drain
suction. A drain is safer with no suction than suction which
is not working correctly.
 Aggressive aspiration could maintain open an air leak, the
better solution instead of aspiration being the surgically
closure of the air fistula (aerostasis).
 After drainage obtain a follow-up chest x-ray to assess for
lung reexpansion and thoracostomy tube positioning.
 Monitor the patient continuously for arterial oxygen
saturation.
 In case of an external tension pneumothorax the cause
can be very easily removed by suturing the wound chest.
 In case of internal pneumothorax due to lung perforation,
lung reexpansion against the internal chest wall and
adhesions formation will seal the perforation in a few
days.

Hemothorax

 Represents the accumulation of blood into the pleural

space.
 The source of blood may be any anatomical structure of
the thorax but in most cases after trauma it comes from
intercostal vessels injured by rib fracture and lung
lesions.
 The quantity of blood into the pleural cavity may be
small, medium or large. Blood loss can be sudden and
massive like in large vessels injuries or slow and
progressive.
 Symptoms and hemodynamic changes vary depending
on the amount of bleeding and the rapidity of blood loss.
1. Blood loss of up to 750 mL should cause no significant
hemodynamic change.
2. Loss of 750-1500 mL will cause the early symptoms of shock
(ie, tachycardia, tachypnea, and a decrease in pulse pressure).
3. Significant signs of shock with signs of poor perfusion occur
with loss of blood volume of 30% or more (1500-2000 mL).
 Exsanguinating hemorrhage can occur without external
evidence of blood loss.
 Dyspnea is often the predominant complaint associated
to those caused by chest trauma and hypovolemia.
 On general examination pallor, tachycardia, cold
sweats, and tachypnea can be noticed. On chest
examination beside the traumatic lesions of the skin
(bruising, hematoma, wounds, etc..) on percussion dull
sound over the affected side may be noticed. The upper
margin of the dull depends on blood quantity in the
pleural cavity.
 On auscultation breath sounds are diminished if there is
a large hemothorax. In many traumatic cases
hemothorax is associated with pneumothorax.
 The main imagistic investigation is the upright chest
radiography. CT scan is a valuable method in assessing
lungs and other intrathoracic organs.

Hemothorax Hemopneumothorax
 Possible evolution of hemothorax:
1. Accumulation in large quantities endangering the patient’s life.
Needs evacuation or thoracotomy and hemostasis and also
blood replacement.
2. Lysis and resorbtion if small hemothorax.
3. It causes a pleural reaction with exudate and increases the
volume of the pleural fluid.
4. Infection with thoracic empyema.
5. Transformation in fibrothorax causing lung adhesions which
prevent a good lung expansion reducing their capacity.
 Differential diagnosis should be made with other
pleural collections – Hydrothorax, Pleurisy, Empyema,
Chylothorax. In thoracic trauma context the
chylothorax is more likely to be produced or blood can
come from abdominal cavity through a diaphragmatic
rupture.
 Treatment depends on the size of hemothorax, its
speed of developing and the source of bleeding. In most
cases patients will be admitted for treatment and
surveillance.
 Indications for thoracotomy after trauma:
 A. >1500 mL blood from chest tube on insertion.
 B. >200 mL blood/hour from chest tube thereafter (for 2-4 hours).
 C. Massive air leak such that lung will not re-expand after a
properly placed and functioning chest tube has been inserted.
 The medical treatment will be common as for thoracic
trauma plus blood replacement if necessary and
antibiotherapy. In small hemothorax aspiration of blood
by thoracocentesis can be performed. In medium and
large hemothorax pleural drainage through thoracostomy
is the method of choice. If bleeding continues or pleural
drainage is not effective thoracotomy should be
performed for hemostasis (intercostal vessels ligation,
lung suture, etc).
 Cardiac tamponade
 It is a highly life threatening condition.
 Accumulation of fluid (blood in most traumatic cases)
into the pericardial sac will lead to cardiac movements
limitation with cardiocirculatory insufficiency and cardiac
arrest.
 The pericardial space normally contains 20-50 mL of
fluid. Pericardial effusions can be serous,
serosanguineous, hemorrhagic, or chylous.
 In chest trauma intrapericardial fluid is represented by
blood which may come from:
1. A penetrating (stab, shot) wound which produces a lesion of the
cardiac vessels (coronary vessels) or heart wall (heart
perforation)
2. A contusion of the heart with consecutive heart wall necrosis
and rupture
3. Contusion of the heart with rupture of its wall
 The pathophysiologic mechanism is represented by
diminished diastolic filling because ventricles cannot
distend sufficiently to overcome the increased
intrapericardial pressures. Tachycardia is the initial
cardiac response to these changes to maintain the
cardiac output.
 The rate of fluid accumulation into the pericardial sac is
very important. Rapid accumulation of about 150 ml will
develop an increased pressure that opposes filling the
heart with blood. The rapid accumulation is more likely to
occur during chest trauma. In other conditions, when
accumulation produces over a long period of time, more
than 1000 ml of fluid won’t have significant effect due to
adaptive stretching of the pericardium.
 Symptoms: tachycardia, tachypnea, palpitations,
dyspnea, restless body movements, unusual facial
expressions, sense of impending death, dizziness,
drowsiness.
 Signs: distended jugular veins, hepatomegaly, enlarged
cardiac dullness on percussion, diminished heart sounds,
pericardial friction rub, weak pulse, hypotension and also
other signs related to chest trauma.
 The Beck triad:
1. increased jugular venous pressure
2. hypotension
3. diminished heart sounds
 Kussmaul’s sign: Decrease or absence of jugular vein
dilatation during inspiration
 Imaging studies:
 Chest X-Ray – enlargement of the heart shadow as a tent, with
disappearance of heart contours (plus other possible associated
modifications due to trauma)
 Ultrasound reveals fluid accumulation in the pericardial sac
limiting the amplitude of cardiac movements)
 CT scan – may reveal fluid accumulation in pericardial sac and
other lesions but in most cases there is not sufficient time to
perform the examination
 Cardiac tamponade

Shape of tent
 Electrocardiogram will show: sinus tachycardia, low-
voltage QRS complexes and PR segment depression.
 Differential diagnosis in chest trauma should include:
 Tension pneumothorax – distended jugular veins is also present !
 Cardiogenic shock
 Pulmonary embolism
 Treatment
 Cardiac tamponade during chest trauma is a very serious
condition with a high mortality. Life saving depend on rapid
recognition of it and rapid pericardial decompression. After
decompression the treatment must be continued for the
underlying cause that means in majority of cases
thoracotomy or sternotomy, opening the pericardial sac
and hemostasis either by cardiac suture or vascular
suture.
 Pericardial puncture
1. Epigastric approach – Marfan’s point at the tip of
xiphoid appendix.
2. Chest approach - may be performed on the right or left
side of the sternum
 The left approach:
 In the 4th or 5th intercostal space very close to the sternum to avoid
the internal mammary artery. The needle is inserted perpendicularly.
 Dieulafoy point – in the 5th intercostal space at 6 cm beyond the
sternum
 Delorme’s point – in the 6th intercostal space at the edge of sternum
 Rendu’s point - in the 6th intercostal space at 8 cm beyond the
sternum
 Huchard’s point – in the 7th intercostal space at 8 - 9 cm from sternal
midline (below the Dieulafoy point)
 The righ approach
 Roth’s point – in the 6th intercostal space, very close to the sternum.
The needle is inserted to the left and up.
 The patient will be in a semi-seated position in a 45
degree inclination of the thorax.
 After the needle passes the skin it is driven cephalad
and obliquely to the left, following the posterior face of
the sternum. Then it passes the diaphragm and after a
trajectory of 4 cm for patients younger than 5 years and
6 cm for those over 15 years it enters the pericardial sac
in its lowest region.
 Advantages of this technique is that it avoids the pleura
and the internal mammary vessels and may be used in
small pericardial collections. The epigastric approach is
contraindicated in sternum deformities.
• The possible complications of pericardial puncture:
1. Coronary artery damage
2. Laceration of the myocardium
3. Penetration in the lung
• Echocardiograpic guidance increases the success
rate of pericardiocentesis by reducing these
complications.
 Lesions of the intrathoracic organs
Lungs
Pulmonary contusion – is represented by an
intraparenchymatous hematoma surrounded by
atelectasis. It is manifested by pain, dyspnea, cough,
hemoptysis. In case of extensive contusion hypo-
oxygenation and low blood oxygen saturation may occur
with cyanosis.
 The severity ranges from mild to very serious. Pulmonary
contusion is the most common type of potentially lethal
chest trauma. Estimated mortality rate ranges between
14% and 40%.
 It occurs in 30–75% of severe chest injuries.
 On chest X-ray a zone of pulmonary condensation
(characteristic white region) is seen. The presence of
hemothorax or pneumothorax may obscure the contusion
on a radiograph.
 CT scanning is a more sensitive for pulmonary contusion.
Contusion can be detected almost immediately after the
injury. However, in both X-ray and CT a contusion may
become more visible over the first 24–48 hours after
trauma.
 Differential diagnosis. If the consolidation lasts longer than
72 hours, consider:
 Aspiration
 Pneumonia
 ARD
 Treatment in most cases is just supportive. In severe
extended pulmonary lesions with hypoxia mechanical
ventilation with oxygen supplementation is needed.
Mechanical ventilation with moderate positive pressure is
indicated when:
 Partial pressure of oxygen is less than 60 mm Hg at a concentration
of 50% oxygen in the inspired air
 Respiratory rate> 24/minut
 Maximum vital capacity <10 ml / kg
 Antibiotherapy is used to prevent pulmonary infection.
 Pulmonary contusion can progress to complete
resorption in 5-10 days or with complications such as
infection and abscess formation. It can also permanently
reduce the compliance of the lungs.
Pulmonary laceration
 Pulmonary laceration is produced in most cases by
penetrating chest wounds (stab or shot) but also it can
occur during very intense blunt thoracic trauma or as a
consequence of rib fractures. The injury is more serious
when is closer to the pulmonary hilum (in these cases
large vessels and bronchi are damaged too).
 Symptoms and signs are the same as in thoracic
contusions or penetrating wounds with hemothorax or
hemopneumothorax plus hemoptysis.
 Radiological images are similar to those of lung contusion
+ hemothorax or hemopneumothorax.
 Treatment - in patients with small lesions without
respiratory failure thoracostomy and pleural cavity drainage
with mild aspiration for lung reexpansion is sufficient.
 In case of important penumothorax or hemoptysis,
bronchoscopy would be necessary for diagnosis of
tracheobronchial tree lesions.
 Patients requiring mechanical ventilation may develop
broncho-pleural fistulas, sometimes requiring two
independent lung ventilation.
 In more serious lesions thoracotomy is necessary for
saving the life of the patient. Lungs lesions are surgically
resolved, aerostasis and hemostasis is checked and two
drainage tubes are placed in the pleural cavity. In most
cases this patients are monitored in the intensive care unit.
 Tracheo-bronchial tree lesions
 Lesions can be axial or circular, complete or incomplete.
 Symptoms are dependent on the size and permeability of
the affected bronchus (fragments of lung parenchyma or
blood clots can obstruct airways).
 Characteristic features on which diagnosis relies are
hemoptysis accompanied by tension pneumothorax,
pneumomediastinum or subcutaneous emphysema.
 Suspected bronchial rupture arises whenever in a
pneumothorax the lung does not reexpand under proper
suction drainage.
 Bronchoscopy should be carried out promptly since it is the
most reliable means of establishing the diagnosis.
 Surgical treatment is represented by thoracotomy and
suture of the ruptured bronchus or trachea under ventilatory
support using double lumen tubes and selective bronchial
intubation.
 Cardiac lesions
 Cardiac lesions may be a consequence of blunt thoracic
trauma (most often in traffic accidents when the steering
wheel hit the sternum) or penetrating trauma (stab,
gunshot, puncture, etc).
 Types of lesions and their severity depend on traumatic
agent type, its force and coexisting cardiac diseases.
Survival depends much on the type of cardiac lesion and
time elapsed between the accident and establishment of
treatment.
Blunt trauma are represented by myocardial contusion and
myocardial rupture. The rupture may interest the walls or
septum ( interventricular / interatrial) and valves.
 The right atrium and ventricle are the most frequently
injured due to their anterior position followed by the left
atrium and left ventricle. The survival rate with 1-
chamber rupture is about 40%. Two-chamber rupture
has a mortality of 100%.
 A sudden rise in blood pressure during compression of
the chest may injure the cardiac valves or lacerate the
ventricular wall or septum.
 Myocardial contusion is represented by patchy areas of
muscle necrosis and hemorrhagic infiltrate.
 Les extended heart muscle contusion induces cardiac
arrhythmias that usually improves with time but injury to
a coronary artery can lead to myocardial infarction.
 Regurgitation and cardiac insufficiency due to traumatic
lesions of valvular system tends to worsen with time
within in few weeks or years.
 Diagnosis
 A patient with angina-like chest pain or progressive
dyspnea after trauma must be suspected of having a
cardiac injury. Arrhythmias are not very specific.
Systemic hypotension and elevated venous pressure are
important signs of cardiogenic shock or tamponade.
 Paraclinical investigations comprise:
 Thoracic X-ray – reveals sternal and ribs fracture, hemothorax,
enlarged cardiac shadow ,but cannot offer information about
heart.
 CT scan – offer more detailed aspects concerning the pleural
spaces, lungs and mediastinum, but not very much about cardiac
contusion.
 Ultrasound – echocardiography is an important diagnostic tool
that can be used to detect anatomical anomalies (pericardial
effusion, areas of ventricular dyskinesia, and valvular
dysfunction) and physiologic anomalies of the heart (abnormal
blood-flow patterns).
 12-lead EKG – may show abnormalities.
 CPK (Creatine phosphokinase) values may be elevated, but also
in skeletal and muscular trauma – so they are not very specific.
 Troponins (a complex of three regulatory proteins: troponin C,
troponin I and troponin T – found in skeletal and cardiac muscle,
but not smooth muscle) are more specific.
 Treatment
 In stable patients without evident lesions on echocardiography
the evolution is good and only a close monitoring for several
hours is required. If their condition remains stable and the ECG
reveals no or only minor changes they can be admitted to a
regular ward.
 A patient with angina-like chest pain, elevated enzyme levels or
minor arrhythmias should be monitored in an intermediate care
unit.
 A patient with progressive dyspnea, ischemic patterns on ECG,
or complex arrhythmias should be treated in an intensive care
unit, receive specific therapy, and be investigated further.
 A patient in cardiogenic shock due to cardiac tamponade will be
quickly investigated and treated accordingly (see cardiac
tamponade).
 In case of ventricular akinesia the patient may benefit from
inotropic support or intraaortic balloon counterpulsation.
 More serious injuries of intracardiac septa and valves require
surgery and extracorporeal circulation.
Most penetrating cardiac injuries are secondary to assaults
or accidents (industrial, traffic). Penetration with sharp
objects is associated in general with a better outcome
than penetration resulting from gunshot. Iatrogenic
causes are represented by lesions produced secondary
to cardiopulmonary resuscitation (fractured sternum or
ribs may penetrate the heart), central venous
catheterization, or percutaneous cardiac procedures.
 Survival after such lesions is very low (6-17%), very few
patients reaching the hospital alive but from those who
reach alive almost ¾ can be saved.
 Patients with small wounds of the heart will develop
cardiac tamponade but those with extensive lacerations
die almost immediately, as a result of rapid and
voluminous blood loss.
 To prevent exsanguination, any stabbing weapons still
present in the chest should not be removed before
reaching the hospital.
 If there are suspicions of penetrating cardiac lesion a
pericardial window can be performed by subxiphoid
approach.
 Penetrating cardiac trauma must be surgically resolved.
The approach can be through a left thoracotomy or by
sternotomy. The pericadial sac is opened, the blood and
cloths removed and the cardiac wound is assessed.
Digital compression direct on the wound is the procedure
for temporary hemostasis. Cardiac suture can be
performed with the finger still in place on the wound or
using a balloon catheter introduced into the cardiac
cavity for temporary hemostasis. Larger injured coronary
arteries will require either direct repair or bypass.
 Aortic injury
 The two most common causes of this type of lesion are
traffic accidents and stab or shot wounds. In the first
case the mechanism is deceleration (heart displacement
will put under tension the aorta) and in the second the
direct action of the traumatic agent.
 Aortic rupture is very deadly, about 90% of patients die
within minutes. Of those who arrive at the hospital alive,
another 90% die.
 Many patients have little external evidence of serious
chest trauma.
 Aortic injury should be suspected on chest radiographs
when the mediastinum is enlarged more than 8 cm and
aortic knuckle is disappeared.
 CT scan reveals mediastinal hematoma but not
necessarily from aortic rupture.
 When the diagnosis is suspected on basis of chest
radiography or clinical findings it can be confirmed by
means of contrast-enhanced aortography.
 Treatment is only surgical but unfortunately with a very
high mortality rate.
 Esophageal rupture
 The esophagus is located in the posterior mediastinum
being a well protected organ against traumatic agents.
However, there are rare cases when esophagus may be
injured during thoracic trauma especially during
penetrating trauma caused by stab wounds or shot gun
wounds. On the other hand, iatrogenic lesions are not
very rare (85-90% of cases) occurring during endoscopic
procedures, gastric tubing or during abdominal or
thoracic operations. There are also self induced
esophageal lesions caused by foreign bodies, corrosive
or drug ingestion and postemetic trauma.
 Esophageal lesions are a potentially devastating
condition. Rapid diagnosis and therapy provide the best
chance for survival but delay in diagnosis is common,
resulting in substantial morbidity and mortality.
 Spontaneous esophageal rupture is a rare entity, which is
known as Boerhaave syndrome (rupture of the
esophageal wall due to vomiting).
 The estimated mortality is approximately 35%, making it
the most lethal perforation of the digestive tract. The best
outcomes are associated with early diagnosis and
definitive surgical management within 12 hours of rupture.
If intervention is delayed longer than 24 hours, the
mortality rate (even with surgical intervention) rises to
higher than 50% and to nearly 90% after 48 hours.
 As a result of a tear or rupture of the esophagus, its
content (saliva, food, air) will enter the mediastinum
resulting in mediastinitis.
 Clinical picture is represented by retrosternal pain,
dysphagia, hematemesis, subcutaneous emphysema,
pleural effusion, fever, septic shock.
 The Mackler triad:
1. vomiting
2. lower chest pain
3. cervical subcutaneous emphysema
 Chest radiography and CT scan may show: enlargement
of the mediastinum, pneumomediastinum, pleural effusion
especially on the left side, subcutaneous emphysema. A
water-soluble contrast (Gastrografin) can be used to
highlight the extravasation of contrast and location and
extent of rupture/tear.
 Esophagogastroduodenoscopy is not recommended for
acute esophageal rupture.
 Treatment.
 Patients will be admitted to ICU
 Nothing by mouth
 Parenteral nutritional support
 Nasogastric suction
 Broad-spectrum antibiotics
 Criteria for nonoperative treatment :
 Recent iatrogenic or postemetic esophageal perforation with
minimal symptoms and absence of sepsis.
 No malignancy, obstruction, or stricture in the region of the
perforation
 Isolation of the leak within the mediastinum and drainage of
perforation into the esophagus
 Medical contraindications to surgery (eg, severe emphysema,
severe coronary artery disease)
 The aims of surgery for esophageal rupture are:
 Prevent further mediastinal contamination
 Drainage of the medistinum and pleural cavity
 Ensure enteral nutrition
 Reestablish the esophageal integrity or replace a portion of it
(esophagoplasty)
 Surgical techniques include the following:
 Tube thoracostomy (alone or associated to other techniques)
 Primary repair (suture plus reinforcement) of the rupture either
by thoracic or abdominal approach or by thoracoscopic
approach.
 Diversion (cervical esophagostomy)
 Diversion and exclusion (cervical esophagostomy + esophagus
ligation above the cardia + feeding gastrostomy or jejunostomy)
 Esophageal resection (+ cervical diversion + feeding
jejunostomy)
 Esophageal stent
 Endoscopic placement of fibrin sealant
 Esophagoplasty (using stomach or colon) in a second phase
after mediastinitis resolution
 Diaphragmatic rupture
 It may be a consequence of blunt or penetrating thoracic
and abdominal trauma.
 The diaphragm is the main respiratory muscle which
separates the abdominal cavity from the thoracic cavity.
Between those two cavities there is a gradient of pressure:
the intra-abdominal pressure is higher then the
intrathoracic, and this is the reason why abdominal organs
tend to protrude into the thoracic cavity when there is a
solution of continuity (rupture) of the diaphragm.
 The right diaphragm is better protected against rupture
during blunt trauma by the liver while the left diaphragm
ruptures more frequently (70-90%) especially at level of
the central tendon.
 More frequently the rupture is the consequence of a
sudden rise of the intra-abdominal pressure during blunt
abdominal trauma then during thoracic trauma because
the thoracic wall is more rigid.
 On the other hand during blunt thoracic trauma, especially
from lateral side, the diaphragm (and also the nearby
organs – spleen, liver) may be injured by fractured ribs.
 Penetrating trauma, either thoracic or abdominal, may
produce tears in the diaphragm and organs from both
cavities. Even though they are not injured, abdominal
organs can protrude into the pleural cavity resulting in
diaphragmatic hernia with the possibility of strangulation
and necrosis of herniated organs. Visceral herniation
occurs in 30-50% of patients with diaphragmatic tears, and
the stomach is the most common abdominal organ to
become herniated, but there are not rare cases when the
transverse colon, spleen or small intestines are involved in
herniation.
 In large diaphragmatic ruptures the herniated abdominal
organs produce a dislocation of the lung and heart
leading to ventilatory, respiratory and cardiocirculatory
dysfunction with dyspnea, cyanosis and cardiac rhythm
disturbances.
 Other symptoms may be: sharp shoulder pain, digestive
symptoms (dysphagia, vomiting, intestinal obstruction)
and associated symptoms depending on the associated
traumatic lesions.
 The small diaphragmatic ruptures are frequently
unrecognized in the first days as they do not give any
specific symptoms and may be overlooked at chest x-ray
investigation. Diagnosis may be delayed in as many as
two thirds of all patients.
 The plain chest radiograph is abnormal in 77% of
patients, but the findings are nonspecific and the
diagnosis is initially missed in most cases.
 On physical examination of the thorax the most important
sign that rises the suspicion of diaphragmatic rupture is
the bowel movements heard on auscultation.
 There are 3 clinical phases of diaphragmatic injuries
(described by Grimes).
 1. Acute phase - in the same day with the trauma.
 2. The second or latent phase if the injury is not recognized in the
early phase. It is an asymptomatic phase but intra-abdominal
viscera evolve into gradual herniation.
 3. The third phase is that of complications (obstruction,
incarceration, strangulation, perforation, peritonitis, pleural
effusions, etc).
 Radiographic findings include apparent elevation of the
hemidiaphragm, loss of the normal contour, distortion of
the normal shape or mediastinal shift away from the injury.
The pathognomonic findings are the intrathoracic intestinal
fluid-air levels and bowel or gastric movements observed
during fluoroscopy. Administered Gastrographin will fill the
herniated stomach or intestines.
 Left diaphragmatic rupture

Colon
Gastric gas bubble
 CT findings of diaphragmatic rupture include the
followings:
 Discontinuity of the diaphragm
 Herniation of abdominal organs into the chest
 Pneumothorax and/or hemothorax and/or hemoperitoneum
 The mortality rate in unrecognized cases is 30% as a result
of delayed herniation of abdominal viscera and bowel
strangulation. Early recognition and repair of diaphragmatic
tears improves the prognosis.
 Most often the patients are polytraumatized and
unconscious.
 The first taken measures are those for life support, but
concomitant good clinical and paraclinical evaluation must
be carried out.
 Intrathoracic organs lesions are more life threatening than
those intra-abdominal, and therefore the initial approach
should be the thoracotomy in this cases. The abdominal
organs can be assessed somewhat through the
diaphragmatic rupture and if there are no intra abdominal
lesions the diaphragm will be sutured without laparotomy.
Some abdominal organs lesions can be managed through
the thoracic approach (splenectomy). If necessary,
laparotomy can be associated.
 PLEUROPULMONARY
SURGICAL PATHOLOGY
1. Pleural effusions - Pleurisy
 Lungs anatomy
2. Hydatid cyst of the lungs
3. Lung abscesses
4. Lung cancer
Pleural effusions
Between the two pleura layers: the parietal and the
visceral one, there is a virtual space which contains a
small quantity of fluid (1ml) which ensure a sliding
plane and also keeps the two pleura in contact. This
liquid is produced continuously but also reabsorbed so
its quantity remains constant under the control of
oncotic and hydrostatic pressure and lymphatic
drainage.
The pleural effusion represents an abnormal collection
of fluid into the pleural cavity as a result of excess fluid
production or reduced absorption.
Pleural effusions are classified as:
1. Transudates which results from an imbalance in oncotic and
hydrostatic pressures, generally as a result of systemic factors
impairment.
2. Exudates which is the result of inflammation of the pleura or
decreased lymphatic drainage – local factors.
3. Combination of these
 Mechanisms:
1. Alteration of pleural permeability - inflammation,
malignancy, pulmonary embolus
2. Increased capillary permeability - trauma, malignancy,
inflammation, infection, pulmonary infarction, drug
hypersensitivity, uremia, pancreatitis
3. Reduction of oncotic pressure - hypoalbuminemia,
cirrhosis, cashexia
4. Increased hydrostatic pressure in the systemic and/or
pulmonary circulation - congestive heart failure,
superior vena cava syndrome
5. Decreased lymphatic drainage - including thoracic duct
obstruction or rupture
6. Migration of fluid - from pulmonary edema across the
visceral pleura - migration across the diaphragm via
the lymphatics or structural defects - cirrhosis,
peritoneal dialysis
 Causes
Transudates
1. Congestive heart failure
2. Cirrhosis (hepatic hydrothorax)
3. Atelectasis
4. Hypoalbuminemia
5. Nephrotic syndrome
6. Peritoneal dialysis
7. Myxedema
8. Constrictive pericarditis
9. Urinothorax - Usually due to obstructive uropathy
10. Rare cases ( cerebrospinal fluid leaks to the pleura, intra-
pleural migration of central venous catheter)
 Exudates – inflammatory fluid with elevated protein
content
1. Pneumonia (Parapneumonic)
2. Malignancy - lung or breast cancer, lymphoma, leukemia,
sarcomas, melanoma
3. Pulmonary embolism
4. Systemic diseases - collagen-vascular conditions -
rheumatoid arthritis, systemic lupus erythematosus
5. Tuberculosis (TB)
6. Trauma – thoracic trauma, postcardiac injury syndrome,
esophageal perforation
7. Radiation pleuritis
8. Sarcoidosis
9. Fungal infection
10. Intra-abdominal pathological processes – abscess (especially
subdiaphragmatic), pancreatitis, pancreatic pseudocyst,
stomach cancer, ovarian cancer, Meigs syndrome (benign
pelvic neoplasm with associated ascites and pleural effusion)
11. Status-post coronary artery bypass graft surgery
12. Pericardial disease
13. Ovarian hyperstimulation syndrome - iatrogenic complication
of ovarian stimulation for assisted reproduction technology
14. Drug-induced pleural disease
15. Asbestos-related pleural disease
16. Yellow nail syndrome (genetic disorder - yellow nails,
lymphedema, recurrent pneumonia, pleural effusions)
17. Uremia
18. Trapped lung (unexpandable lung due to visceral pleural
localized scarring with the formation of a fibrin peel leading to
pleural effusion)
19. Chylothorax (elevated triglycerides in pleural fluid, traumatic
causes, non-traumatic causes – idiopathic, congenital)
20. Pseudochylothorax (chronic condition with elevated
cholesterol in pleural fluid)
21. Fistula (ventriculopleural, biliopleural, gastropleural, etc)
Prognosis
It depends on the underlying condition, the moment of
beginning the treatment and its accuracy.
In many cases, complete healing is possible with
removal of the cause which led to the pleural effusion.
However, untreated or inappropriately treated, effusions
may lead to empyema, constrictive fibrosis, sepsis and
other complications.
Sometimes, unfortunately, the cause can not be cured
completely such as in cancer, systemic or congenital
diseases. In these cases the goal of treatment is to
prolong life and maintain a good quality of life.
Mortality depends primarily on the underlying disease,
but pleural effusion may endanger life by itself due to
mechanical and septic complications.
 Clinical picture
Anamnesis is very important in diagnosis. Patients should
provide information about associated known illnesses
(pneumonia, cancer, cirrhosis, cardiac insufficiency,
renal impairment, trauma, etc) and underwent treatment.
Also occupational history aspects may be important
(asbestosis). Patients will describe the onset and
evolution of symptoms.
Symptoms
Dyspnea - is the most frequent and constant symptom
but its degree depends much on the quantity of fluid
accumulated. Dyspnea may be caused by the condition
producing the pleural effusion or associated co-
morbidity, such as lung or heart disease, obstructing
endobronchial lesions, or diaphragmatic paralysis, rather
than by the effusion itself.
Chest pain – is very variable in intensity and sometimes
absent. On the debut of a pleural effusion due to pleuritis
(inflammation, exudate) the pain is intense, sharp or
stabbing, exacerbated by respiratory movements due to
pleural irritation. Generally, pain is absent in transudates.
Pain may be caused by the underlying disease: cancer,
pulmonary infarction, pneumonia, etc.
Cough – is frequently present but unproductive. When it
is productive with purulent or bloody sputum the
underlying cause may be pneumonia, pulmonary
infarction or cancer.
Other symptoms depending on the underlying disease.
Signs - Generally, there are no physical findings for
effusions smaller than 300 mL.
On inspection – in small and medium collections nothing
special can be noticed. In large collections on the
affected side, the thoracic wall is distended and also the
enlarged intercostal spaces are bulging between ribs.
The patient is lying on the affected side. This position
reduces the movements of the affected side and so the
pain, permitting better expansion of the opposite
hemithorax. Orthopnea is seen especially in patients with
cardiac insufficiency.
On palpation – the pectoral fremitus is diminished.
On percussion – dullness with superior margin convex
downward (Ellis Damoiseau line). Decreased
diaphragmatic excursions. Mediastinal shift away from
the effusion.
On auscultation – diminished or inaudible breath sounds.
Investigations
Chest radiography – it is the most often performed
investigation. Performed in upright position it shows a
basal opacity on the affected side. Small volume of fluid
(175 ml) will just blunt of the costophrenic angle. Large
volumes will compress the lung and shift the
mediastinum to opposite side.
PLEURAL EFFUSION

small medium large

To detect small effusions more reliable is lateral
decubitus chest X-Ray. Layering of an effusion on lateral
decubitus films defines a freely flowing fluid and, if the
layering fluid is 1 cm thick, indicates an effusion of
greater than 200 mL.

Chest radiography in
many cases also offers
information about the
underlying condition
such as: pneumonia,
pulmonary infarction,
lung tumors, cardiac
enlargement, etc.
CT scan, usually is the next investigation ordered. It is
more accurate, offers a better resolution and more
details regarding the effusion and other co-morbidities. In
many cases effusions are found on CT performed for
other illnesses.
It is very useful especially
in cases of loculated
effusion pleural effusion,
complete opacification of
hemithorax, or
associated lung
parenchymal
abnormalities and for
CT scan
guiding the interventional
procedures.
Ultrasound examination – has certain advantages: does
not use radiations, can be performed at bedside, is
faster, is cheaper and can detect small quantities of
pleural fluid.
MRI is performed especially for diagnosing tumoral
masses associated with pleural effusions.

Once the fluid was highlighted by imagistic investigations

the next step in diagnosis is to determine the nature of
the fluid and what is causing it. Sometimes, especially in
transudates, the underlying cause is obvious and
treatment may be applied without necessity of
performing a diagnostic Thoracentesis (eg. congestive
heart failure)
Thoracentesis is performed for two reasons: 1. for
diagnosis and, 2. as a treatment procedure for fluid
evacuation.
In most cases it is performed based only on physical
examinations but it can be guided by imagistic
investigation also.
Diagnostic Thoracentesis is indicated only when there is
sufficient liquid accumulated (over 200 ml) and in case of
new and unexplained pleural effusions.
It can be performed using a simple intramuscular needle
attached to a syringe. In obese patients with thick
thoracic wall a longer puncture needle is needed.
The most appropriate position of the patient is sitting on a
chair with back turned to the doctor. The superior margin
of the fluid is located by percussion and marked on skin.
Puncture will be always performed in full dullness
preferable on the posterior axillary line in the 6th
intercostal space. During procedure the patient will be
assisted by a nurse or another doctor. After skin
disinfection a local anesthesia will be performed. The
puncture needle attached to the syringe will be advanced
till the resistance of the rib is encountered. Then the
needle is reoriented above the rib and advanced 1-2 cm
maintaining a negative pressure in the syringe.
The needle is inserted above the rib to avoid damaging of
intercostal vessels. The patient is advised not to move,
cough, or take a deep breath during the procedure.
The syringe is filled with fluid, withdrawn (the needle
also) and sent for bacteriologic and chemical analysis.
If the intention is also to evacuate the fluid, before
insertion, an intermediate tube will be attached between
the needle and the syringe. The fluid can be withdrawn
by gravity drainage or by suction. The quantity and
aspect of evacuated fluid will be documented.
After thoracentesis a control chest radiography will be
performed.
 Precautions:
1. Identifying the correct landmarks – if the needle is inserted too
low the liver or the spleen may be damaged. Too high
insertion can result in lung perforation and iatrogenic
pneumothorax.
2. Never insert the needle through an area with an infection.
3. Patients who are on anticoagulant drugs should be carefully
considered for the procedure.
4. Ask the patient not to move, cough or deep breathing during
the procedure.
5. Assess the patient during the procedure (difficulty breathing,
dizziness, faintness, chest pain, nausea, pallor or cyanosis,
weakness, sweating, cough, alterations in vital signs, oxygen
saturation levels, or cardiac rhythm)
6. Avoid rapid suction and don’t evacuate more than 1500 ml of
fluid because of the risk of reexpansion (ex vacuo) pulmonary
edema with a mortality rate of 20%.
The gross aspect of extracted fluid:
– Aqueous aspect is characteristic for transudate -
Hydrothorax
– Serocitrine aspect is characteristic for exudate
– Bloody aspect is frequently due to malignancy,
pulmonary infarction, post-traumatic
– Frankly purulent is characteristic for empyema
– A putrid odor suggests an anaerobic empyema
– Milky, opalescent fluid suggests a chylothorax

Extracted liquid will be sent for laboratory tests:

– cytology
– bacteriological and sensitivity (antibiogram)
– biochemistry analysis
 Other investigations:
1. Surgical thoracoscopy plus biopsy – the procedure
is burdened by the risks of general anesthesia.
2. Medical thoracoscopy plus biopsy – is performed on
a conscious sedated patient.
3. Closed-needle pleural biopsy.
These procedures are indicated in undiagnosed cases
of pleural effusion especially when malignancy or TB
are suspected.
 PLEURISY
Pleuritis represents an inflammation of the pleura in most
cases due to infection. Pleurisy means a pleuritis
associated with pleural effusion. The accumulated fluid is
an exudate.
Depending on fluid character pleurisy can be:
– Serofibrinous pleurisy (pulmonary tuberculosis, etc.);
– Purulent pleurisy (Empyema) (pulmonary tuberculosis,
pneumopathies);
– Hemorrhagic pleurisy (heart infarction, lung cancer or pulmonary
tuberculosis).
The inflamed pleural layers rub against each other every
time the lungs expand and this causes severe sharp pain
with inhalation (pleuritic chest pain).
Serofibrinous pleurisy
Is characterized by a fibrinous exudate on the surface of
the pleura and an extensive effusion of serous fluid into
the pleural cavity.
Etiopathogenesis: Pulmonary tuberculosis is still the most
common cause (50-55%). Other possible causes may
be: cancerous pleurisy (25-30%), viral pleurisy,
associated to a pulmonary infarction, rheumatismal
pleurisy, secondary a serious bacterial pneumonia
treated with antibiotics, pleurisy from subdiaphragmatic
collections, liver cirrhosis, collagenosis (especially lupus
erythematosus).
In tuberculosis it appears in patients aged between 16
and 35 years and it may be the first manifestation of the
disease.
 In TB the pleural cavity is seeded by hematogenous route
or by contiguity from lung or lymph nodes TB process.
Favorising factors are: exposure to cold, humidity,
malnutrition, immunity impairment.
The disease starts with a pleuritis (without fluid collection).
The pleura is swollen, erythematous and covered with
fibrin deposits. If the process progresses the exudate (a
clear yellow liquid) appears. In TB miliary tubercles are
present in pleura. Inflammation can heal without sequelae
but in many cases adhesions between the two pleural
layers appear representing pleural symphysis which can
involve just some regions or the entire pleural cavity
(fibrothorax).
Clinical picture
The onset of symptoms is acute in most cases (but it may
be also silent) with thoracic pain intensified by respiratory
movements radiating in shoulder or abdomen. Pain
reduces in intensity when the pleural collection appears.
In the next days the fever (39-40 C degrees) and chills
appear.
 The fever evolves constantly for 5 days till 3 weeks and
pain reduces gradually. Associated symptoms are: pallor,
dyspnea and unproductive cough.
Physical examination. Usually physical signs will be absent
when fluid accumulation is small.
On palpation the tactile vocal fremitus is diminished and
local tenderness can be identified on the affected side.
On percussion in pleural effusion there is a dull sound and
the location of the upper level of the dullness depends on
how much fluid is accumulated in the pleural space.
On auscultation in pleuritic phase pleural friction rub
(leathery/creaking sounds during inspiration and expiration)
may be heard and when there is a pleural collection the
breath sounds will be reduced on the affected side.
 Chest radiography reveals the pleural collection as an
homogeneous basal opacity and possible pulmonary TB
process or pneumonia.
Exploratory pleural puncture will extract fluid which is an
exudate rich in proteins with positive Rivalta reaction
containing many lymphocytes. Koch bacillus is found
exceptionally, but inoculation of mice can cause TB
infection when TB is the cause.
ESR is constantly accelerated, and leukocytosis appears
in the early days.
Clinical forms
1. Tuberculosis pleurisy – may evolve as an acute-fibrinous
pleurisy, as a subacute pleurisy, or become prolonged as
chronic pleurisy. It may be complicated by pericardial or
peritoneal tuberculosis. Treatment consists in administration of
tuberculostatics. Immediate prognosis is generally good, but the
remote is reserved as tuberculosis recurs frequently, especially
in the first three years after the disease.
1. Pleurisy which accompanies or follows bacterial pneumonia
occurs either in the first week of evolution process (parapneumonic)
or in the recovering period (metapneumonic). Exudate is rich in
polynuclear cells. It may resolve spontaneously and under
antibiotherapy, but sometimes tends to progress to empyema.
Indications for urgent drainage of parapneumonic effusions include:
1. Frankly purulent fluid
2. A pleural fluid pH of less than 7.2
3. Loculated effusions
4. Presence of bacteria on Gram stain or culture
2. Rheumatic pleurisy occurs in children and adolescents. It coexist
with rheumatic fever. Exudate is reduced and contains much fibrin,
albumin and endothelial cells.
3. Malignant pleurisy usually occurs in a patient over 50 years,
evolving without fever. Exudate often is bloody and cancerous cells
can be detected at cytological examination. Fluid collection
reappears soon after evacuation. Prognosis is bad due to the
underlying disease (mean survival of less than 1 year).
 Chylothorax
Is the presence of lymphatic fluid in the pleural space
secondary to leakage of the thoracic duct or one of its
main tributaries.
Because the thoracic duct transports up to 4 L of chyle
per day, a tear in this duct allows a rapid and large
accumulation of fluid in the chest.
Etiology
1. Malignant etiologies account for more than 50% of
chylothorax diagnoses and are separated into
lymphomatous and nonlymphomatous. Lymphoma is
the most common cause, representing about 60% of
all cases. Non-Hodgkin lymphoma are more likely to
cause a chylothorax than Hodgkin lymphoma.
2. Frequent (25%) causes of ductus thoracicus lesions
are thoracic trauma and different kind of surgeries
(thoracic, cardiac, esophageal) – iatrogenic lesions.
3. Congenital chylothorax is seen in neonates.
4. Miscellaneous causes include: cirrhosis, tuberculosis,
sarcoidosis, amyloidosis, and filariasis.
5. Idiopathic – the cause is knot known.

Pseudochylothorax (cholesterol pleurisy) results from

accumulation of cholesterol crystals in a chronic
existing effusion. The most common cause of
pseudochylothorax is chronic rheumatoid pleurisy,
followed by tuberculosis and poorly treated empyema.
Symptoms and signs are those of classical pleural
effusions without fever.
Mortality and morbidity rates are approximately 10% in
major clinical medical centers.
Diagnosis
The fluid extracted by Thoracentesis looks milky. Pleural
fluid analysis for triglyceride content helps to confirm a
diagnosis of chylothorax. A level greater than 110 mg/dL
has a 99% chance that the fluid is chyle.
The diagnosis is simple in case of posttraumatic
(accidental or surgical) duct lesion. More difficult is to
establish the location of lesion.
When the cause of chylothorax is not obvious other
investigations are needed to rule out a malignancy: CT,
MRI, lymphography.
Treatment. The principles of treatment are:
– Treatment of the underlying cause of chylothorax
– Decrease the chyle production
– Draining the collection
– Obliterating the pleural space
– Fluid and nutritional rebalancing
 In large volumes of pleural collection the first intention
is to decompress the lung. This can be achieved by
thoracostomy. This is not a suitable measure for a long
period of time due to the consecutive nutritional
depletion and metabolic complications.
Conservative treatment can be considered because
the thoracic duct leak closes spontaneously in nearly
50% of patients.
Reduction of chyle production may be achieved by
several methods:
1. Total parenteral nutrition or a fat-restricted oral diet
2. Chemoradiation in patients with malignant
chylothorax who are not surgical candidates
3. Somatostatin administration
Indications for surgical intervention include the
followings:
1. Drainage of more than 1 L of chyle per day for 5 days
or a persistent leak for more than 2 weeks despite
conservative management.
2. Nutritional or metabolic complications.
3. Loculated chylothorax, fibrin clots, or trapped lung
4. Postesophagectomy chylothorax

When traumatic lesion of the thoracic duct is the cause,

the best treatment is duct ligation. This is performed by a
right thoracotomy or laparoscopic approach and the duct
is discovered and ligated just above the aortic hiatus.
Other surgical methods are:
– Pleuro-peritoneal shunt (the chyle is driven into the
peritoneal cavity through a siliconated tube)
– Pleurodesis – obliterating the pleural space can be
achieved chemically (talcum which produces
inflammation and fibrosis) or surgically (pleural
abrasion or pleurectomy).
Varieties of pleurisy by location:
– Diaphragmatic pleurisy – the diaphragmatic pleura is
affected. The effusion is small in quantity and may be
either sero-fibrinous or purulent. Frequently occurs in
intra-abdominal subdiaphragmatic septic processes
(abscesses). The pain is located at the base of the
affected hemithorax being exacerbated by respiration.
Nausea and vomiting often occur. If effusion is purulent,
there may be bulging of the intercostal spaces. The
temperature is high and the patient presents a septic
status.
– Interlobar pleurisy - The inflammatory process affects
the interlobular pulmonary pleura. The effusion is
trapped into the interlobar space due to adhesions
which separate this space from the pleural cavity. It is
found more frequently in the right side than in the left,
and between the upper and lower lobus, of the lung.
Symptoms are not characteristic. Abscesses located
here can perforate and evacuate into a bronchus.
According to localization, pleurisy may be:
1) costal-diaphragmatic;
2) diaphragmatic;
3) costal;
4) interlobe;
5) paramedistinal;
6) apical.
Encysted pleurisy is the result of adhesions between
parietal and visceral pleura which delimit enclosed
spaces in various positions. Symptoms are not
characteristic. Collection is found on chest radiography
but is difficult to differentiate from other pleuro-
pulmonary condensations. The exact position of
collection is better established under flouroscopy and CT
or MRI scan which can also guide the exploratory
puncture.
Thoracic empyema. Empyema is a collection of pus in a
natural cavity of the body unlike abscess which is a
collection of puss in an newly formed cavity.
The puss accumulation may occupy the entire pleural
cavity (generalized purulent pleurisy) or it may be
trapped in smaller cavities (encysted purulent pleurisy).
Most commonly it is a consequence of parapneumonic
exudative pleurisy but it may develop after any bacterial
inoculation, from any source, of the pleural cavity. It may
progress to pleural sclerosis and may lead to lung
entrapment and then to trapped lung, conditions in which
the lung is unexpandable due to visceral pleural
restriction. The inability of the lung to fully expand and fill
the thoracic cavity after drainage is associated with a
chronic pleural effusion. Another cause of lung entrapment
may be malignancy. Patient may be asymptomatic or
dyspnea is the main symptom with restriction on
pulmonary function testing.
Typical symptoms of thoracic empyema include cough,
fever, chest pain, sweating and shortness of breath. Digital
clubbing may be present in cases of chronic evolution.
Diagnosis is based on history, symptoms and signs and
also on imaging studies and Thoracentesis when puss is
extracted.
Empyema
Digital clubbing
Pleural effusion treatment depends very much on
the underlying condition that induced the effusion and
it is addressed especially to that condition but also to
effusions complications: lung compression, encysted
pleurisy, thoracic empyema, lung entrapment.
Surgical treatment may be represented by:
1. Fluid evacuation by repeated Thoracentesis or by
thoracostomy
2. Thoracotomy or thoracoscopic approach for thoracic duct
ligation in chylothorax or for pleuro-peritoneal shunt
3. Pleural abrasion or pleurectomy to seal the pleural cavity
(pleurodesis)
4. Decortication for trapped lungs to remove a thick, inelastic
pleural peel that restricts ventilation and produces progressive
or refractory dyspnea.
5. Thoracoplasty (removal of some portions of the ribs) alone or
with muscle flaps in the treatment of chronic thoracic
empyema without remaining pulmonary tissue to obliterate the
pleural space.
SURGICAL PATHOLOGY OF THE
LUNGS
Surgical anatomy
The lungs, two in number, are the essential organs of
respiration. They are located one on either side within
the thorax, being separated from each other by the
mediastinum.
The right lung usually weighs about 625 gr. and the left
567 gr. Their shape is conical and present an apex, a
base, three borders, and two surfaces.
– The apex – extends into the base of the neck reaching from 2.5
to 4 cm. above the level of the sternal end of the first rib. In
emphysema the apex exceeds collarbone filling the
supraclavicular fossa. It has close relationships with brachial
plexus and subclavian vessels so that tumors (Pancoast-Tobias)
at this level can easily invade these anatomical structures.
– The base is concave, and rests upon the diaphragm, which
separates the right lung from the right lobe of the liver, and the left
lung from the left lobe of the liver, the stomach, and the spleen.
Lungs (especially the right) may be interested in intra-abdominal
pathologic processes. Examples are bilio-bronchial fistulas due to
liver hydatid cysts or abscesses.
– The costal surface is convex, in contact with the costal pleura, and
ribs. This surface is most common interested in pathological
thoracic processes, traumatic (contusions, chest wounds,
iatrogenic) and non-traumatic (pleurisy, pleural tumors, etc.).
– The mediastinal surface is concave being oriented towards the
mediastinum entering into direct contact with the heart and large
vessels. Here is located the pulmonary hilum, where the vessels,
airways and nerves and enter or leave the lung.
– Borders
The inferior border is thin and sharp
The posterior border is broad and rounded and comes in contact with
the esophagus aorta and ductus thoracicus
The anterior border is thin and sharp, and overlaps the front of the
pericardium
Segmentation
Lungs are divided by fissures in lobes and lobes are divided
in segments separated by connective tissue. Each
bronchopulmonary segments have their own tertiary
bronchi and arterial supply (two arteries) and a vein.
The left lung is divided into two lobes, an upper and a
lower which is the largest of the two, by an interlobular
fissure (oblique fissure), which extends from the costal to
the mediastinal surface of the lung both above and below
the hilus.
The left lung has 8-10 segments
– superior lobe
apico-posterior (merger of "apical" and "posterior")
anterior
lingula of superior lobe
inferior lingular
superior lingular
– inferior lobe
superior
anteromedial basal (merger of "anterior basal" and "medial basal")
posterior basal
lateral basal
Lungs topography
The right lung is divided by two fissures into three
lobes: superior, middle and inferior. There are 10
segments:
– superior lobe The bronchopulmonary segment:
apical
posterior 1. Has a pyramidal shape, with the apex
anterior at the lung hilum;
– middle lobe 2. Is the largest subdivision of a lobe;
lateral 3. Is surrounded by connective tissue;
medial 4. Has separate arterial supply from
– inferior lobe other segments and receives its own
superior
segmental (tertiary) bronchus;
medial-basal
anterior-basal 5. Is drained by intersegmental veins
lateral-basal that lie in the connective tissue around
posterior-basal the segment;
6. Can be removed surgically without
affecting the function of other
segments.
Bronchial tree
The bronchi branch from the trachea. There are two main bronchi:
the left and the right. Bronchi divide into lobar bronchi which divide
into tertiary bronchi, also known as segmental bronchi, each of
which supplies a bronchopulmonary segment.
The right bronchus is wider and shorter than the left bronchus and
branches into three secondary bronchi, one passing to each of the
three lobes of the right lung.
The left bronchus is smaller in diameter and about twice as long as
the right bronchus. It is also more horizontal and more susceptible to
obstruction. It branches into the secondary bronchi for the inferior
and the superior lobes of the left lung.
The segmental bronchi divide into many primary bronchioles which
divide into terminal bronchioles, each of which then gives rise to
several respiratory bronchioles, which go on to divide into 2 to 11
alveolar ducts. There are five or six alveolar sacs associated with
each alveolar duct. The alveolus is the basic anatomical unit of gas
exchange in the lung.
Arterial supply
The lungs have two arterial systems: one functional that
brings deoxygenated blood to lungs and which belongs to
the lesser circulation and the another one that provides
lung nutrition belonging to the systemic circulatory system.
The functional arterial blood (deoxygenated) comes from
the right heart directed by the pulmonary trunk, which
divides into the two pulmonary arteries. These arteries
follow a similar branching pattern to the bronchi,
accompanying them as they divide. They continue
branching and terminate as capillaries in the walls of the
alveoli.
Oxygenated blood supply is derived from the bronchial
arteries which arise from the descending aorta.
It is important not to confuse the pulmonary arteries with
bronchial arteries. The former carry the deoxygenated
blood from the right side of the heart in order to pick up
oxygen. The latter are systemic, carrying oxygenated blood,
like all systemic arteries, to supply the tissues of the
bronchi.
Venous drainage
There are also two types of venous drainage:
One functional, which carries the oxygenated blood from
the alveolar capillaries towards larger pulmonary veins
and then into the left atrium. Each lobe of the lung is
drained by a pulmonary vein. Veins do not accompany
the artery and bronchus in segments, but instead run in
the segmental boundaries.
One systemic represented by the bronchial veins which
are much smaller, and drain blood from the regions
supplied by the bronchial arteries. The left vein drains
into the hemiazygos vein, which then crosses behind the
carina to empty into the azygos vein and thereby the
superior vena cava. The right bronchial vein drains
directly into the azygos vein.
Lymphatics
The lymphatic drainage of the lung is important in
oncology because it represents a route of spread for
cancerous cells.
There are two lymphatic plexuses: one superficial just
beneath the pleura and a deep plexus which
accompanies the bronchi.
The deep plexus drains lymph into subsegmental,
segmental, interlobar and bronchial lymph nodes. The
superficial plexus usually has no nodes. The two
plexuses combine at hilum, where tracheobronchial
nodes are located (station 10R/10L). In general, lymph
will pass to superior tracheobronchial nodes from the
upper lobes, and to the inferior tracheobronchial nodes
from the lower lobes, but there are anastomoses
between the lymphatic channels which may cause
unexpected spread. The lymph is drained then into the
mediastinal lymph nodes.
 Intercongress Meeting of
the European Soc. of Pathology in Prague, Czech; 8.9 - 12.9.2012

Mediastinal nodes have numerous stations to allow surgical and radiological

correlation.
ation Location Description

Right - Bounded superiorly by the apex of the lung, laterally by the pleura, medially by the trachea, inferiorly by the
2R / Upper
intersection of the caudal border of the brachiocephalic artery and trachea.
2L Paratracheal
Left – As for right, except the inferior boundary is formed by the superior part of the arch of aorta

4R / Lower Right – Bounded above by station 2R, inferiorly by the caudal margin of the azygos vein.
4L Paratracheal Left – Bounded superiorly by station 2L, laterally by the ligamentum arteriosum, and inferiorly by the carina

Aortopulmonar
5 Located lateral to the ligamentum arteriosum and above the pulmonary artery / trunk
y

Anterior
6 The space located anterior to the trachea, pulmonary arteries, aorta and ligamentum arteriosum
mediastinum

7 Subcarinal The mediastinum beneath the carina, medial to station 9

Paraoesophage
8 The mediastinum posterior to the trachea, on either side of the oesophagus
al

9R / Pulmonary
Located within the pulmonary ligament, inferior to the root of the lung
9L Ligament

Right - Superior to the carina / right main bronchus, medial to the origin of the right upper lobe bronchus, and
10R / Tracheobronchi inferior to station 4R
10L al Left – Lateral and superior to the carina / left main bronchus, medial to the origin of the left upper lobe bronchus,
and inferior to station 4L

11R /
Interlobar Located between the junction of the lobar bronchi
11L

12R /
Lobar Located along the lobar bronchi
12L

13R /
Segmental Located along segmental bronchi
13L

14R /
Subsegmental Located along subsegmental bronchi
14L
 Innervation
Sympathetic nervous fibers com from the paravertebral
ganglia. They produce bronchodilation, vasoconstriction
and reduce secretion of mucous glands in the bronchi.
Parasympathetic fibers are derived from the vagus nerve
(X) and produce bronchoconstriction, vasodilatation and
increase the mucous secretion.
Nervous fibers form plexuses which enter the lung at hilum
and accompany the bronchial tree and the vessels.
Lungs function
The lungs are part of the body's respiratory system which
is one of the most important system in preserving life. A
person can live for weeks without food and a few days
without water but only a few minutes without oxygen.
The principal function of the lungs is to exchange gases
between the air and the blood. In the lungs, carbon dioxide
is removed from the blood and oxygen from inspired air
enters the bloodstream (hematosis = the arterialization of
the blood in the lungs).
A person at rest breathes about 6 liters of air a minute.
Heavy exercise can increase the amount to over 75
liters per minute. The lungs have the greatest surface
exposed to air of about 28 sqm at rest (but up to 93 sqm
during a deep breath) compared to the skin with its
surface area of approximately 1.9 sqm.
The lungs are spongy organs which in inspiration are
filled with oxygenated air and during expiration the air
loaded with carbon dioxide is exhaled. Air movement in
and out the lungs is called ventilation and several
anatomical structures participate in this process.
Inspiration is an active process produced by the
respiratory muscles and exhalation is a passive process
based on lung elasticity and compliance. Gas exchange
occurs through the alveolar-capillary membrane as
oxygen moves into and carbon dioxide moves out of the
bloodstream.
 The most common parameters of lungs function are:
1. Tidal Volume (TV):, the volume of air that is inhaled
or exhaled with each normal breath.
2. Expiratory Reserve Volume (ERV): the maximal
amount of air forcefully exhaled after a normal
inspiration. The amount of exhaled air will be more
than was just inhaled.
3. Inspiratory Reserve Volume (IRV): the maximal
amount of air forcefully inhaled after a normal
inhalation.
4. Residual Volume (RV): the amount of air remaining
in the lungs after the deepest exhalation possible.
6. Vital Capacity (VC): The maximum amount of air that
can be exhaled after the fullest inhalation possible.
Vital capacity is the sum of the tidal volume, the
inspiratory reserve volume, and the expiratory reserve
volume.
7. Total Lung Capacity (TLC): the sum of the vital
capacity and the residual volume. The average total
lung capacity of an adult human male is about 6 litres
of air.
 Average lung volumes in healthy adults

Value (litres)
Volume
In men In women
Inspiratory reserve volume 3.3 1.9
Tidal volume 0.5 0.5
Expiratory reserve volume 1.0 0.7
Residual volume 1.2 1.1

Lung capacities in healthy adults

Average value (litres)

Volume Derivation
In men In women
Vital capacity
4.6 3.1 IRV plus TV plus ERV

Inspiratory capacity 3.8 2.4 IRV plus TV

Functional residual
2.2 1.8 ERV plus RV
capacity
Total lung capacity 6.0 4.2 IRV plus TV plus ERV plus RV
LUNG ABSCESSES
 Lung abscess is a localized infection as a consequence
of liquefactive necrosis of the lung characterized by a
pus-filled cavitary lesion. The formation of multiple small
(< 2 cm) abscesses is occasionally referred to as
necrotizing pneumonia or lung gangrene.
In the pre antibiotic era lung abscesses were a
devastating disease with a mortality over 30%.
Etiology
1. The most frequent cause of abscess is pulmonary
aspiration of content from oral cavity, esophagus or
stomach. This was demonstrated by the presence of the
same types of bacteria in the wall of the abscess, as in
mouth.
2. A less frequent cause is hematogenous seeding of the
lungs due to suppurative thromboembolism. In this case
usually there are multiple small abscesses in lungs.
3. Also rare cases are when lung abscess develops as a
secondary abscess spread from an extrapulmonary
organ or bronchiectasis.
4. Other causes may be infected pulmonary cysts, or
hydatid cysts, or infected necrotized lung tumor.

Lung abscesses can be classified as:

– Based on pathogenesis:
Primary abscesses
Secondary abscesses
– Based on evolution
Acute - less than 4-6 weeks
Chronic
– Based on etiologic agent
The etiologic agent
The most common aerobe pathogens are streptococci
and staphylococci. Staphylococcus aureus (MRSA)
causes a very serious and fulminant necrotizing
pneumonia in young adults and children.
Anaerobe negative germs are represented especially by
Actinomyces sp. and Bacteroides sp., Fusobacteria.
The most frequent gram-negative bacteria is Klebsiella.
Patients immunocompromised may have infection with
Nocardia, Mycobacteria sp, or fungi.
Some people, especially those from developing
countries, are at risk of developing TB abscess. There
are rare cases due to amebic infection (eg, with
Entamoeba histolytica), paragonimiasis, or Burkholderia
pseudomallei.
Pathogenesis
The most common cause of lung abscess is aspiration of
digestive content. This is possibly accidentally, without
any prior condition, or is favored by a number of
conditions such as:
Loss of cough reflex:
– Cerebral vascular accidents
– Drug overdose
– Alcoholism
– Post-op state or coma from any cause
Trouble with deglutition:
– Neurological disorders
– Esophageal diseases (DIverticulum, achalasia, GERD)
Post obstructive pneumonia:
– Lung cancer
– Foreign body aspiration
85% of abscesses are located in the superior segments
of right lower lobes, left lower lobes and axillary
subsegments of anterior and posterior segments of the
right upper lobe.
Gravitational forces determine the site of aspiration.
Position of the patient at time of aspiration determines
the segment the aspiration is most likely to occur.
The right lower lobe is the most common site for
aspiration in sitting position. In this position gravity
facilitates lodging of the aspirate to basal segments of
the right lower lobe due to the straight line with the
trachea of the right main bronchus while the left takes of
at an angle.
In supine position with the patient on back, superior
segment of right lower lobe is the most dependent
segment.
Clinical Picture
The onset and symptoms depend largely on the etiologic
agent. In most cases, especially produced by anaerobic
bacteria, the onset is insidious and may go even 3-4
weeks until the patient seeks medical attention.
Sometimes the onset is acute with a pneumonia which
then progresses to cavitation and formation of an
abscess.
Symptoms:
– Cough
– Low grade fever
– Anorexia
– Weight loss
– Expectoration of foul smelling sputum (lack of foul smell does not
exclude lung abscess, as 50% of anaerobic infections do not
produce a foul smell)
– Patients may develop hemoptysis or pleurisy
Physical findings
Physical signs are variable depending on the severity
and extent of the disease, and the patient's health status
and co-morbidities.
On inspection – on clinical general examination can be
observed: fever, pale skin, edentation and gingival
problems, purulent sputum, fetid halitosis, digital
clubbing and signs depending on the associated
pathology.
On palpation – pectoral fremitus diminished in coexisting
pleurisy.
On percussion – dullness over the area of abscess or
basal when associated with pleurisy.
On auscultation - decreased breath sounds, bronchial
breath sounds, course inspiratory crackles, or when
pleural effusion is associated the absence of breath
sounds over the effusion.
Investigations
Imagistic and bacteriologic investigations are the most
important in diagnosis and therapeutic conduit.
Chest radiography. The typical radiographic
appearance is of an irregularly shaped cavity with an air-
fluid level inside.

Basket like shape

air

fluid

Chest radiography
 Evacuated
Lung abscess

Chest radiography
This typical image must be differentiated from other
similar images in case of : cavitating cancer, TB, simple
cyst, hydatid cyst, esophageal diverticulum, encysted
pleural effusion, empyema, etc.
Embolic pulmonary disease often causes multiple
cavitations, and TB typically involves the apices.
The wall thickness of a lung abscess progresses from
thick to thin and from ill-defined to well-circumscribed as
the surrounding lung infection resolves. The wall of the
abscess is typically thick and the inner surface irregular
but is less commonly nodular, which raises the possibility
of cavitating carcinoma.
CT scan is not routinely needed but may be useful in
differential diagnosis.
CT scan
Bacteriologic diagnosis
To accurately detect the causative germ, harvested
material must not be contaminated.
Unfortunately the expectorated sputum does not yield
useful results for anaerobic culture because the oral
cavity is extensively colonized with anaerobes.
Uncontaminated material may be obtained for
anaerobic culture from the followings:
1. Blood culture – in rare cases blood cultures are positive
2. Pleural fluid (if empyema is present) –not every abscess is
associated with empyema
3. Transtracheal aspirate
4. Transthoracic pulmonary aspirate FNA guided by CT – invasive
method
5. Surgical specimens – invasive method
6. Fiberoptic bronchoscopy with protected brush – limited
experience
7. Bronchoalveolar lavage with quantitative cultures
 On the other hand if antibiotherapy was initiated most
likely the culture will not be positive.
Flexible fiberoptic bronchoscopy is performed to
exclude a bronchopulmonary carcinoma.
Differential diagnosis
Cavitary pulmonary lesions are not always caused by
infection. Noninfectious causes include the followings:
– Bullae with air-fluid level
– Bronchiectasis
– Lung cancer
– Lung infarction
– Nodular silicosis, nodule with central necrosis
– Pulmonary embolism
– Pulmonary sequestration
– Sarcoidosis
– Wegener's granulomatosis
Treatment
Antibiotic therapy. If uncontaminated cultures can be
obtained, then antibiotic therapy will be guided by
atibiogram. Traditionally, penicillin alone was used and
produced satisfactory results but due to the developing
of germs resistance it is no longer recommended.
Clindamycin is the most popular antimicrobial due to its
good intracellular uptake and its stability in low pH and
poor vascularity. Imipenem also has excellent activity
against anaerobes. Antibiotics must be given for several
weeks.
As in any other abscesses evacuation of puss is very
important in healing. Pulmonary abscesses may be
drained by various methods.
1. Postural drainage is the most often used and in
association with antibiotics is sufficient. The patient
should be trained to obtain the optimal position for an
efficient drainage. Bronchodilators and aerosols
facilitate the evacuation of puss.
2. Drainage by bronchoscopy is very efficient but it cannot
be used daily. It is reserved when postural drainage is
not efficient and the cavity is enlarging.
3. Percutaneous chest tube drainage. To avoid spilling of
pus into pleural cavity the tube must be inserted through
a region where the parietal and pulmonary pleura are
sealed together (as a consequence of inflammatory
processes or surgically induced by different kind of
procedures - pleurodesis).
Surgery
Surgery in now days is very rarely indicated. The
patients will be operated only in case of complications
such as massive hemoptysis, airway obstruction,
empyema, pulmonary gangrene or if there is a
suspected neoplasm, or congenital lung malformation.
The surgical procedure performed is either lobectomy or
pneumonectomy.

Lung abscess complications may include spread of

infection to other lung segments, bronchiectasis,
empyema, and bacteraemia with metastatic infection
such as brain abscess.
PULMONARY HYDATID CYST
Hydatid cyst of the lungs is a parasitic disease caused
by infestation with larvae of the dog tapeworm
Echinococcus granulosus. Infestation is produced by
ingestion of tapeworm eggs that contaminate the water,
vegetables or other foods, or when hands are lead to
mouth without washing them after handling soil or petting
a dog whose fur contains the parasite.
The larva hatches out of the egg in the intestines and
migrates through the portal vein into liver and then to
lungs and other organs where it will remain as a large
larval tapeworm cyst (hydatid cyst).
Some authors suggest that lungs should be the favorite
location of hydatid cyst because through the lung is the
route of the entire blood of the body, whereas other
authors claim that the liver is the most frequent location
because this is the first filter for blood coming from
intestines.
 The portal circulation and so liver may be by-passed if the
hexacanth embryos enters a lacteals in the intestinal villi
and then via the lymphatic duct into the cava vein.
Morphopathology
The cyst is a kind of round tumor of variable size (up to
15 or even 20 cm in diameter) bordered by a thick wall
and filled with a liquid more or less clear and scolices
(tapeworm heads).
Hydatid cysts of the lung can be central or peripheric. The
latter, through their ever increasing growth, can come into
contact with the pleura.
There are 3 phases of evolution:
1. The initial phase - between infestation moment and
diagnosable pulmonary lesion. At 6 hours after infestation
a catarrhal alveolitis develops, then at 48 hours a
pulmonary condensation appears and at 10 days a
pulmonary nodule called echinococcus pseudo-tubercle
(a nodule that resembles a tuberculosis granule but is caused by a
microorganism other than Mycobacterium tuberculosis).
2. The phase of constituted cyst – when it is detectable
by chest radiography. In this phase the pericyst is
formed by mechanical compression on the lung tissue
and by local allergic reaction. The pericyst consists of
three layers:
1. The inner is formed by hyaline tissue
2. The middle formed by connective tissue vessels and many
eosinophils
3. The external layer much thicker formed by alveoli
condensation.
Between the cyst and the pericyst there is a virtual
space that allows the enucleation of the hydatid
membrane.
As the cyst continue to grow it will compress other
pulmonary structures such as bronchi leading to fistula
formation.
3. The phase of complications – The most frequent
complication is the rupture of the cyst and evacuation of
its content into the bronchial tree. Rupture is also
possible into the pleural cavity.
Clinical picture
There are no symptoms for a very long period of time, in
many cases the cyst being found incidentally on a chest
radiography. Symptoms depend on many factors such
as: location, number, volume, evolution stage and
patient’s age.
In uncomplicated stage symptoms may be:
– Chest pain – inconstant symptom present mostly in large
volume cyst.
– Dyspnea – in large or multiple cysts
– Cough rare in this stage but when appears it announces a
complication
– Hemoptysis is also rare in this phase
– Allergic reactions – urticaria (hives)
Physical signs in this stage are also poor and they are
represented by the same findings as in any pulmonary
condensation.
In the complicated phase the most frequent symptoms
are caused by cyst rupture.
The main symptom of rupture into the bronchial tree is
the vomica when the content of the cyst is expelled. The
vomica is an acute episode preceded and associated
with intense cough. The volume of fluid expelled
depends on volume of the cyst. The fluid is watery clear
and may contain the whole hydatid membrane or just
part of it. If the entire membrane is expelled spontaneous
healing of the disease may occur. If only the fluid is
eliminated, the membranes will remain in the adventitial
cavity where the retraction of the cavity's walls and the
narrowness of the bronchial opening make the expulsion
of the membrane almost impossible (incarcerated
membrane)
 Vomica may induce more complications such as:
– Aspiration of the fluid into the bronchial tree followed by
Mendelson syndrome and even death.
– Anaphylactic shock that must be treated urgently with
corticosteroids
– Hemoptysis more or less important
– Infection of the remnant cavity which is usually the rule
Diagnosis is established based on three elements:
anamnesis (occupation, endemic zones and previous
operation for liver hydatid cyst, are important), clinical
picture (vomica is the most characteristic) and paraclinical
examinations.
Imagistic investigations are represented especially by
chest radiography and the more reliable radioscopy that
may highlight the “cyst respiration” sign (Brjovschi-Linberg
sign) – the cyst modifies its diameters during respiration.
Radiologic investigation remains the milestone in
diagnosis. It can specify the number, location, size
complication of cysts.
The simple hydatid
cyst is represented
by a round or
polylobed mass of
2-20 cm diameter
with well defined
borders.
Calcifications are
exceptional.
The complicated
cyst has many
stages with different
radiological aspects.
Simple hydatid cyst of the left Multiple pulmonary hydatid cysts
superior lobe
Ruptured right hydatid cyst with “water lily “ sign – the floating membrane
CT examination bring more information about the
pulmonary mass specifying its cystic nature, studying the
membranes and complications.
Ultrasound examination may be useful especially in
peripheral location of the cyst asserting the liquid content
and observing the hydatid sand and the daughter cysts.
Abdominal ultrasound examination is also useful in
diagnosis of an associated liver hydatid cyst.

cyst

CT scan
Laboratory tests: are not always necessary in
positive diagnosis. In uncertain cases it may be helpful
the following:
– Eosinophilia over 5%
– The indirect hemagglutination test and the enzyme-
linked immunosorbent assay (ELISA) have a
sensitivity of 40% in pulmonary echinococcosis and
are the initial screening tests of choice.
– Immunodiffusion and immunoelectrophoresis
demonstrate antibodies to antigen 5 and provide
specific confirmation of reactivity.
– The ELISA test is useful in follow-up to detect
recurrence.
Differential diagnosis is made with other pulmonary or
mediastinal masses such as:
– Pulmonary TB – tuberculum and especially TB
cavern. Patient’s history, nodular images,
calcifications, PPD skin test and bacteriology help the
diagnosis.
– Bronchopulmonary cancer – CT scan and
bronchoscopy with biopsy are helpful in diagnosis.
– Simple or contaminated pulmonary cysts
– Lung abscess
– Encysted pleurisy
– Esophageal diverticulum
– Aortic aneurism
– Mediastinal tumors
Treatment
The single efficient treatment is the surgical one.
In case of uncomplicated cyst the aims of surgical
treatment are: to eradicate the parasite and remove the
hydatid membrane and to treat the residual cavity
preserving as much lung tissue as possible.
The approach is through a thoracotomy.
There are many possible surgical techniques. Part of
them remove the membrane by opening the cyst and
other remove the entire cyst without opening it.
– ARCE procedure – the fluid is slowly evacuated by puncture.
– FINOCHETO procedure – the fluid is rapidly evacuated by
aspiration and then the membrane is removed.
– BARRET procedure – evacuates a small quantity of fluid and
then opens the cyst, evacuates the rest of liquid and the
membrane.
Hydatid membrane
– Incision of the pericyst and removing the intact cyst (Barret)
– Segmentectomy or lobectomy are applied in rare instances only
when the pulmonary parenchyma is very affected (advanced
pericystic pneumonitis). The most conservative treatment should
be used to save as much lung tissue as possible.

The most difficult decision is the attitude toward the

residual cavity. There are a lot of procedures, some of
them do not close the cavity, other close or collapse the
cavity using different techniques of suture or seal the
cavity using intercostal muscular flaps. The cavity is
thoroughly irrigated. The bronchial openings, with or
without capitonnage (the folding of the pericystic zone by
sutures) of the residual cavity, are then closed and the
pleural space is drained.
Choosing one of this techniques depend on surgeon
experience, location of the cyst and other important
features of the cyst.
 The WHO guidelines recommend chemotherapy with
albendazole (ABZ) and mebendazole (MBZ) for inoperable
primary liver or lung echinococcosis and for patients with
multiple cysts in two or more organs.
Preoperative chemotherapy may reduce the risk for
recurrence of echinococcosis and facilitate the operation.
Postoperative is recommended in cycles of 1 month with
2-weeks interval between cycles.
Prognosis
With appropriate treatment, the prognosis is excellent.
Postoperative complications (12% and 19%) are
influenced by the size and number of cysts and the type of
operation. The most common complications are pleural
infection and prolonged air leakage.
The operative mortality in large series doesn't exceed 2%.
The recurrence rate is also very low (0% - 3%).
BRONCHOPULMONARY
CANCER
Epidemiology
Cancer of the lung is the most common cancer in the
world.
It is a very life-threatening cancer and one of the most
difficult cancers to treat.
The bronchial tree and also the pulmonary parenchyma
are the sites where tumors may develop as primary
tumors or secondary tumors (metastases). Lung cancer
is one of the most frequent location of cancerous
disease, being in many countries the leading cause of
death in men as well as in women. It was responsible for
1.3 million deaths in 2004. Estimated new cases and
deaths from lung cancer (non-small cell and small cell
combined) in the United States in 2012: 226,160 and
death: 160,340.
According to the U.S. National Cancer Institute,
approximately one out of every 14 men and women in
the U.S. is diagnosed with cancer of the lung.
For both sexes Hungary has the highest rate of lung
cancer, followed by French Polynesia and the United
States of America. About 55 per cent of lung cancer
cases occur in less developed countries. The lowest
incidence in Eastern, Western and Middle Africa. For
women the United States of America has the highest
rate of lung cancer, followed by Denmark and Canada.
(http://globocan.iarc.fr/ )
Lung cancer occurs predominantly in elderly. Almost
70% of people diagnosed with lung cancer are over 65
years of age, while less than 3% of lung cancers occur in
people under 45 years of age.
 The incidence of lung cancer is greater in men than in
women, but in women the lung cancer is accounting for
almost twice as many deaths as breast cancer. Women
tend to be slightly younger, by an average of two years,
at the age of diagnosis than men. Unlike men, a great
percentage of women that develop lung cancer have
never smoked ( 20% occur in lifelong nonsmokers).
Blacks are much more likely than whites to get lung
cancer from smoking cigarettes.
Higher incidence and mortality rates are reported among
men from lower socio-economic groups.
Risk factors
Tobacco smoke is by far the most important risk factor.
Radon is a radioactive gas that cannot bee seen,
smelled, or tasted. People who work in mines may be
exposed to radon.
Asbestos (construction) and other substances (arsenic,
chromium, nickel, soot, tar etc. - chemical industries)
have an increased risk of lung cancer.
Air pollution slightly increases the risk of lung cancer.
Family history of lung cancer.
Personal history of lung cancer.
Age over 65.
Morphopathology
Lung cancer may be primary (derived from cells of the
lung parenchyma or bronchial tree) or secondary
represented by metastases from variable other primary
tumors.
The most frequent primary tumors are represented by
those derived from bronchial tree. The vast majority of
lung cancers are carcinomas that arise from epithelial
cells. The cells of origin may be: basal cells, secretory
cells and endocrine cells.
There are a multitude of histological types. The World
Health Organization in 2004, reviewed the histological
classification of malignant lung tumors establishing
two major groups, with important clinical practice,
evolution and different treatment:
1. Non small cell lung carcinoma (NSCLC),
2. Small cell lung carcinoma (SCLC)

Histological types of bronchopulmonary cancer

Carcinoma with squamous cells
(epidermoid)
Carcinoma with small cells
(micro cell)
Large-cell carcinoma
(macro-cell)
Papillary carcinoma
Carcinoma with clear cells
Carcinoma with small cells
Basaloid carcinoma
Carcinoma with small mixed cells
Large-cell neuroendocrine carcinoma
– Combined large cells
neuroendocrine carcinoma
Basaloid carcinoma
Lymphoepithelioma-like carcinoma
Carcinoma with clear cells
Large-cell carcinoma with rhabdoid
phenotype
Adenocarcinoma Acinar adenocarcinoma
Papillary adenocarcinoma
Mixed adenocarcinoma
Bronchioloalveolar carcinoma
–Mucinous
–Non-mucinous
–Combined
Mucus producing solid carcinoma
–Fetal adenocarcinoma
–Mucinous adenocarcinoma
–Mucinous cystadenocarcinoma
–Signet cells adenocarcinoma
–Adenocarcinoma with clear cells
Adenosquamous
carcinoma
Sarcomatoid Pleomorphic carcinoma
carcinoma Spindle cell carcinoma
Giant cell carcinoma
Carcinosarcoma
Pulmonary blastoma
Carcinoid Typical carcinoid
Atypical carcinoid
Salivary gland tumors Mucoepidermoid carcinoma
Adenoid cystic carcinoma
Epithelial-myoepithelial carcinoma
Pre-invasive lesions Squamous carcinoma in situ
Atypical adenomatous hyperplasia
Diffuse idiopathic pulmonary neuroendocrine cell
hyperplasia
The most common type is adenocarcinoma (40%),
followed by squamous cell carcinoma (25%), small cell
carcinoma (20%) and large cell carcinoma (10-15%),
other types representing about 5%.
In Romania, on the first place is epidermoid carcinoma
(45%), followed by adenocarcinoma (25%), large cell
carcinoma (10%) and small cell carcinomas (20%).
Morphological features
Lung cancer appears mostly in the right lung (6/4
compared to the left lung) more frequently in the superior
lobes and in ventral segments.
The macroscopic appearance of the carcinoma with
central location is that of a solid tumoral mass, with
irregular shape, variable in size, generally smooth, with
gray or white aspect on section. The endobronchial
surface is typically ulcerated. By grows it produces
partial or complete obstruction of the bronchial lumen,
producing atelectasis, bronchiectasis and secondary
pulmonary suppurations.
Carcinoma with peripheral location looks hard, irregular
and presents a clear separation from the surrounding
pulmonary tissue. It has a homogeneous aspect on
section surface. Unlike small lesions, the large tumors
produce central necrosis with cavitation.
Epidermoid cancer: two thirds appear in the central
zone of the lung, grow slowly and metastasize late.
Those located at periphery produces cavitation.
Adenocarcinoma: 70% are located in the peripheral
zone of the lung. Appears on lung scars and interstitial
fibrosis. It has a medium rate of grows and rarely
cavitates. Metastasize early.
Large-cell carcinoma: can be located centrally or
peripherally; metastasize rapidly; the peripheral forms
produce cavitation and the prognosis is bad.
Small-cell carcinoma: are located mostly in the central
region rapidly invading the hilum and mediastinal lymph
nodes. It is the most aggressive form.
Bronchial carcinoids : are generally small (3 cm-4 cm
or less) tumors when diagnosed and occur most
commonly in people under 40 years of age.
Spread of the lung cancer
There are three ways of spread: direct extension,
lymphatic and via the blood vessels.
By direct extension the tumor invades the nearby
anatomical structures: lung parenchyma, bronchial tree,
pericardium, esophagus, pleura, thoracic wall and other
structures. The bronchial extension of the tumor is about
1.9 cm above the tumor and that is the reason for
resecting the bronchus more than 2-2.5 cm above the
macroscopic limit of the tumor.
Lymphatic extension depends on histological type and
the size of the tumor. The small-cell carcinoma
metastasize predominantly on this way and less the
epidermoid carcinoma. In case of tumors less then 1 cm
in diameter metastases in lymph nodes were not found
but for tumors between 1 and 2 cm the lymph node
metastases were found in 12% of cases.
 Hematogenous spread is due to blood vessels invasion.
Invasion of great vessels is a bad prognosis factor.
The most frequent sites of metastases are: brain, liver,
bones and adrenal glands. Less frequent sites are:
kidney, pancreas and other organs.
Stadialization:
Primary Tumor (T)
TX – Primary tumor cannot be assessed or tumor proved by the
presence of malignant cells in sputum or bronchial washings but not
visualized by imaging or bronchoscopy
T0 - No evidence of primary tumor
Tis - Carcinoma in situ
T1 - Tumor 3 cm or less in greatest dimension, surrounded by lung
or visceral pleura, without bronchoscopic evidence of invasion more
proximal than the lobar bronchus* (i.e., not in the main bronchus)
T2 - Tumor with any of the following features of size or extent:
– More than 3 cm in greatest dimension
– Involves main bronchus, 2 cm or more distal to the carina
– Invades the visceral pleura
– Associated with atelectasis or obstructive pneumonitis that extends to
the hilar region but does not involve the entire lung
 T3 - Tumor of any size that directly invades any of the following: chest
wall (including superior sulcus tumors), diaphragm, mediastinal pleura,
or parietal pericardium; or tumor in the main bronchus less than 2 cm
distal to the carina but without involvement of the carina; or associated
atelectasis or obstructive pneumonitis of the entire lung
T4 - Tumor of any size that invades any of the following: mediastinum,
heart, great vessels, trachea, esophagus, vertebral body, or carina; or
tumor with a malignant pleural or pericardial effusion or with satellite
tumor nodule(s) within the ipsilateral primary tumor lobe of the lung
Regional Lymph Nodes (N)
NX - Regional lymph nodes cannot be assessed
N0 - No regional lymph node metastasis
N1 - Metastasis to ipsilateral peribronchial and/or ipsilateral hilar
lymph nodes and intrapulmonary nodes involved by direct extension of
the primary tumor
N2 - Metastasis to ipsilateral mediastinal and/or subcarinal lymph
node(s)
N3 - Metastasis to contralateral mediastinal, contralateral hilar,
ipsilateral or contralateral scalene, or supraclavicular lymph node(s
Distant Metastasis (M)
MX - Presence of distant metastasis cannot be assessed
M0 - No distant metastasis
M1 - Distant metastasis present‡. Specify sites
Pre-invasive lesions:
A) mild dysplasia
B) moderate dysplasia
C) severe dysplasia
D) carcinoma in situ
E) atypical adenomatous hyperplasia
F) diffuse idiopathic neuroendocrine cells hyperplasia
Clinical picture
Clinical manifestations of lung cancer have a great
diversity in relation to anatomo-clinical form,
histological type and stage. In some asymptomatic
patients the tumor is discovered accidentally on chest
radiographs, but most cancers are diagnosed by the
development of new or worsening of existing signs or
symptoms.
There are no pathognomonic symptoms or signs for
lung cancer, but they can be classified into 4
categories:
1. Clinical manifestations due to local tumor growth and
intrathoracic spread
2. Signs and symptoms due to distant metastases
3. Unspecific general symptoms
4. Paraneoplastic syndromes
Symptoms Frequency (%)
Small-cell Non-small-cell
lung carcinoma lung carcinoma
(SCLC) (NSCLC)

Cough 50-76 40
Dyspnea 34-40 30-40
Chest pain 35-36 25-40
Hemoptysis 15-23 15-35
Pneumonia 21-25 13-24
Vocal cord paralysis 15 unusal
Superior cava vein syndrome 12 < 10
Pleurysis 10-15 15
Pancoast-Tobias syndrome rare 3
Pericarditis unusual rare
Cough - is the most frequent symptom in lung cancer
especially in those with central location. A new cough or a
change in the character of the cough in a smoker or a
former smoker should raise concern for lung cancer. A
cough that persists more than a few weeks and worse
over time should be suspected as caused by a lung
cancer.
Hemoptysis - cough up blood or sputum streaked with
blood. Lung cancer accounts for up to 20% of cases of
hemoptysis.
Dyspnea - usually is due to the blockage to the flow of air
in part of the lung, pleural effusion or the spread of the
tumor throughout the lungs.
Chest pain - appears in about 25% of people with lung
cancer. The pain is dull, aching, and persistent. Lung
cancers may press on nerves, resulting in pain in
shoulder, chest, back or arm even before they cause
cough or dyspnea.
Wheezing or hoarseness - may be signs of tracheo-
bronchial compression due to a tumor.
Repeated respiratory infections, such as bronchitis or
pneumonia, can be a sign of lung cancer due to
obstruction that predisposes to infections.
Vocal cord paralysis is due to recurrent laryngeal nerve
compression or invasion by tumor.
Superior cava vein syndrome - is the result of the
direct obstruction of the superior vena cava by right lung
upper lobe tumors and/or mediastinal lymphadenopathy.
It is manifested by dyspnea, facial swelling, head
fullness, cough, arm swelling, chest pain, dysphagia,
orthopnea, distorted vision, hoarseness, stridor,
headache, nasal stuffiness, nausea, pleural effusions,
venous distension of the neck and chest wall, upper
extremity edema, mental changes, plethora, cyanosis,
papilledema, stupor, and even coma.
Esophageal compression by lung cancer is manifested
by difficulty of swallowing or pain with swallowing.
Heart function disorders represented by abnormal heart
rhythms, blockage of blood flow through the heart, or fluid
in the pericardial sac may be other symptoms of lung
tumor extension into the mediastinum.
Pancoast-Tobias syndrome - caused by an apical
(superior pulmonary) malignant neoplasm of the lung
which invades the surrounding tissues and produces: an
ipsilateral invasion of the cervical sympathetic plexus
leading to Horner's syndrome (miosis, enophthalmia,
palpebral ptosis), shoulder and arm pain (brachial plexus
invasion C8-T2) leading to wasting of the intrinsic hand
muscles and paraesthesiae in the medial side of the arm.
Less commonly unilateral recurrent laryngeal nerve palsy
producing unilateral vocal cord paralysis (hoarse voice ±
bovine cough), and/or phrenic nerve involvement. There
may be arm oedema secondary to the compression of
blood vessels.
Pancoast-Tobias tumor
It is estimated that approximately 60-70% of patients with
lung cancer have metastases at presentation and 1/3 of
them have symptoms due to these metastases, that has
an unfavorable prognostic significance. Unspecific
symptoms related to advanced stages of cancer are:
anorexia, weight loss, fatigue, fever, anemia.
Paraneoplastic syndromes occur in approximately 10-
20% of patients. They are represented by a series of non-
specific disorders in relation with various organs and
systems, produced in relatively early stages of the
disease. These syndromes are not related to the size or
location of the lung cancer and do not necessarily indicate
that the cancer has spread outside the chest. They are
due to secretion of hormones or other substances by the
tumor tissue and so may disappeared after tumoral
resection or may recur in case of relapse or metastasis.
Paraneoplastic symptoms occur more frequently in
small-cell carcinoma and rarely in epidermoid carcinoma
and adenocarcinoma. Include the following major
categories: endocrine, neurological, cardiovascular,
musculoskeletal and skin manifestations.
– Endocrine
Bartter syndrome (a rare inherited defect in the thick ascending limb
of the loop of Henle in kidney characterized by hypokalemia,
alkalosis, and normal to low blood pressure) – appears in 5-10% of
cases exclusively in small-cell carcinoma.
Hypercalcemia – in squamous cancer
Gynecomastia – in clear-cell carcinoma
Others
– Neurological
Eaton-Lambert syndrome - a rare autoimmune disorder that is
characterized by muscle weakness of the limbs. It is the result of an
autoimmune reaction, where antibodies are formed against
presynaptic voltage-gated calcium channels in the neuromuscular
junction. It appears exclusively in small-cell carcinoma.
Subacute sensory neuropathy - there is a degeneration of the dorsal
root ganglia manifested by ataxia, but with little development of
motor weakness. This is common in SCLC and there is no cure.
Subacute cerebral degeneration - progressive arm and leg bilateral
ataxia and other neurological signs (dementia, nystagmus,
ophthalmoplegia, extensor plantar signs, dysarthria and arm
involvement). This degeneration is progressive and disabling. The
condition can precede cancer by weeks or years appearing most
commonly in breast and ovarian cancer. Improvement is possible
following successful cancer treatment.
Limbic encephalopathy – is a form of autoimmune disease caused
by auto-antibody against the limbic system of the brain (Anti-Hu,
which is associated with small-cell carcinoma of the lungs). It is
manifested by memory deficits, headache, irritability, sleep
disturbance, delusions, hallucinations, agitation, seizures and
psychosis.
Visual paraneoplastic syndrome - Loss of visual acuity and loss of
visual field, impaired color vision. Most often occurs with small cell
carcinoma of lung.
Subacute necrotizing myelopathy - ascending motor and sensory
loss, which are very rapid due to the loss of gray and white matter of
the spinal cord. This leads to paraplegia. It may be shown on an
MRI.
– Cardiovascular and blood
Thrombotic endocarditis
Migratory thrombophlebitis
Hypercoagulation
– Renal
Glomerulonephritis
Nephrotic syndrome
– Skin and musculoskeletal
Hypertrophic pulmonary osteoarthropathy - clubbing - an abnormal
proliferation of skin and bone tissue, primarily in the hands and feet,
most commonly associated with NSCLC (especially adenocarcinoma)
Acanthosis nigricans - brown to black hyperpigmentation of the skin
usually found in body folds such as the posterior and lateral folds of
the neck, the axilla, groin, umbilicus, forehead, and other areas.
Dermatomyositis - The main symptoms include skin rash and
symmetric proximal muscle weakness which may be accompanied by
pain.
 Clubbing

Acanthosis nigricans

Dermatomyositis
Paraclinical investigations are aimed to:
1. Confirm the diagnosis
2. Determine the histological type
3. Determine the stage and extension
Imaging investigations (X-ray, computed tomography,
MRI) and bronchoscopy provide the maximum
information to assess lung cancer.
In most cases, conventional chest radiography is the
first that suggests the diagnosis of lung cancer.
Computed tomography (CT) is extremely useful in
determining tumor extension, to highlight adenopathies
(only 64% of cases are identified by standard radiologic
examination, but 95% by CT) and the presence of
metastases (liver, adrenal, brain, etc).
Newer techniques, such as positron emission
tomography (PET) and helical (spiral) CT, are improving
the ability to detect small cancers. Oncologists frequently
use PET-CT scanners, which combine the PET and CT
technology in one machine, to evaluate patients with
suspected cancer.

PET

PET-CT
After a lung cancer is suspected based on imaging, a
sample of tissue is required to confirm the diagnosis and
determine the type of cancer.
Sputum cytology is the easiest way to do this, but its use is
limited to those tumors that extend into the airways.
Sputum cytology is not always accurate and can miss
some cancer cells. Almost always, a sample of tissue
directly from the tumor is needed.
A way to obtain the tissue sample is with bronchoscopy.
If the tumor is too far away from the major airways the
specimen can be obtained by percutaneous needle biopsy
under CT guidance.
Sometimes, a specimen can only be obtained by a
thoracotomy, thoracoscopy or Thoracentesis (associated
effusions).
Mediastinoscopy, offers the possibility to take samples of
enlarged lymph nodes to determine if inflammation or
cancer is responsible for the enlargement.
Bronchoscopy
Virtual bronchoscopy – is a 3D reconstruction of the
tracheobronchial tree based on data acquired from CT
and/or MRI scanning. The advantage is that it is not
invasive but the limitation is that it cannot perform
biopsy.
Magnification bronchovideoscopy is a combination of two
systems: a video system for high magnification and a
fiber optic for scope's direction. The system allows
differentiation between dysplasia and other pre-invasive
lesions.
Endobronchial ultrasonography appreciates the tumor
extension, being used to analyze small lesions.
Optical Coherence Tomography (OCT) is a way of
obtaining images with high resolution in real time. OCT
identifies microscopic characteristics of cells, glands,
crypts, lymphatics and vessels. Unlike endobronchial
ultrasonography image is limited in depth about 2 mm
compared to about 5 mm in case of ultrasound 30 MHz.
Anatomo-clinical forms of lung cancer

THE SQUAMOUS CARCINOMA

It is the most frequent histopathological form
encountered in Romania (45%) compared to Western
countries where it represents only 25-30%.
The cancerous cells are derived from the ciliated cells of
the bronchial epithelium as a result of local irritation and
carcinogenic effects of smoking. The tumoral growth is
relatively slow (doubling time of 90-130 days).
The macroscopic aspect on sections is gray-whitish, with
keratinized areas. It can be well or poor differentiated.
The tumor is located in central region on large bronchi in
80% of cases and cavitation is relatively frequent.
The tumor produces cough and hemoptysis.
Bronchoscopy and sputum cytological examination are
the main methods of diagnosis. It produces bronchial
obstruction with consecutive pneumonia. The main route
of spread is through lymphatic vessels and less through
blood vessels. Paraneoplastic syndromes are rare
represented by hypercalcemia and clubbing.
Squamous cell carcinoma may benefit from radical
surgery but it is not responding to radio and
chemotherapy.
 ADENOCARCINOMA

Ranks second as frequency in Romania (25%) but it

represents the main subtype in U.S. and European
Union (30-45%). The incidence has increased by 10% in
the last 25 years in Europe.
It appears predominantly in young men (<50 years) and
females regardless of age, in non-and ex-smokers.
Tumor growth is relatively slow, the doubling time being
160 days. It appears as a white-gray lobulated mass,
usually located peripherally often affecting the pleura
and producing metastases in the pleural cavity.
Sometimes is associated with a scar impregnated by
anthracotic pigment.
Peripheral adenocarcinomas originate from epithelium or
glands of the mucosa of small bronchi included in areas
of fibrosis or old scars. The tumor may contain
calcospherites (tiny, spheroidal, concentrically laminated body
containing accretive deposits of calcium salts, probably as the result
of degenerative changes in the fibrovascular stroma).
Adenocarcinomas tend to metastasize early to regional
lymph nodes and remotely to brain.
A history of chronic interstitial lung disease
(scleroderma, sarcoidosis, tuberculosis, interstitial
pneumonia, etc) is frequently associated with this type of
cancer and this is the reason why the term of "scar
carcinoma” is given to lung adenocarcinomas.
Usually peripheral adenocarcinoma is asymptomatic
being diagnosed incidentally by imagistic methods of
investigation. On chest radiography the aspect area is as
a bipolar lesion represented by the tumoral nodule and
the enlarged regional lymph nodes. Bronchoscopy can
detect only tumors with central location.
Local development is without cavitation but frequently
invading the pleura and the thoracic wall.
The tumor has a low sensitivity to chemotherapy and
radiotherapy.
BRONCHIOLO-ALVEOLAR CARCINOMA
(BAC)

It is a subtype of adenocarcinoma, which has been

extensively studied in recent years due to rising
incidence especially among younger non-smoking
women. BAC is more likely to affect non-smokers,
women, and Asians than other forms of lung cancer.
BAC has 3 subtypes: mucinous, non-mucinous or mixed.
While bronchiolo-alveolar non-mucinous carcinomas are
usually manifested as solitary nodules and favorable
prognosis, the mucinous type tends to spread and form
satellite nodules or pneumonic condensations and have
a poor prognosis. Most patients with solitary BAC, non-
invasive, and size <2 cm, can be treated by only
resection.
The clinical picture is represented by irritative cough and
severe respiratory failure. Radiological bronchiolo-
alveolar carcinoma may be peripheral (single node,
multiple nodules, diffuse), condensation pneumonia-like
or disseminated carcinomatosis. These aspect tumors
are suitable for differential diagnosis with metastatic
adenocarcinoma of the pancreas, colon, breast, stomach,
kidney. It is not uncommon for BAC to be mistaken for
pneumonia or other lung diseases before it is diagnosed.
Peripheral located BAC determines bronchial
hypersecretion (> 500 ml / day), explaining bronchogenic
dissemination.
A diagnosis of BAC requires a sample of tissue, and fine-
needle aspiration biopsy.
The solitary well differentiated BAC, have a better
prognosis than other forms, while diffuse or multinodular
form does not respond to therapy.
 LARGE CELL CARCINOMA
It is a rare histological type, representing approximately
9% of all lung cancers. The origin of this tumor is found
in bronchial mucous glands, especially in the peripheral
bronchi. It appears as a large necrotic mass, most
commonly peripheral invading the pleura and
neighboring structures.
Over 90% of giant cell carcinoma is associated with
other histological types such as: adenocarcinoma or
epidermoid carcinoma.
Evolution is similar to squamous cell carcinoma, with
cavitation and hematogenous relatively late
dissemination. Occasionally it is associated with
neuroendocrine syndromes, which seems to respond
better to chemotherapy.
SMALL LUNG CELL CARCINOMA (SCLC)

It represents 20 to 25% of lung cancers.

The of origin of tumoral cells are represented by
Kulchitzky cells which have neuroendocrine activity
(peptide hormones and growth factors ) and are
located into the submucosal layer of the bronchial tree.
SCLC is considered a distinct pathological entity due
to its aggressive biological features (growth rate with a
fast duplication time of approximately 30 days), with
early metastatic potential and rapid dissemination via
lymphatic and blood vessels.
The presence of neuroendocrine activity explains the
high frequency of endocrine paraneoplastic
syndromes.
Small cell carcinoma occurs in 90% of cases as a central
mass, soft, friable, whitish, with necrosis, which may
produce bronchial obstruction. Less than 5% of cases
have peripheral locations.
It has rapid growth with early metastases in the liver,
CNS, bone, adrenal glands, pancreas and kidney.
Even if the tumor has an increased sensitivity to
chemotherapy the prognosis unfavorable due to early
metastases. Up to 80% of patients die in the first year
after the positive diagnosis.
Treatment
Treatment is based on histologic type, stage of disease
(particularly in NSCLC), associated diseases and
prognosis. Bronchopulmonary cancer treatment includes
surgery, radiotherapy, chemotherapy, curative or
palliative.
Chemotherapy and radiotherapy are most widely used
in both non-small cell and small cell lung cancers. In a
small number of cases they may lead to a cure. These
therapies result in shrinking of the tumor and are
effective in relieving symptoms prolonging the life of
patients.
Chemotherapy is sometimes coupled with radiation
therapy, especially for small cell lung cancer which is
aggressive and has often spread to distant parts of the
body by the time of diagnosis.
 The brain is sometimes treated with radiation even if no
tumor is present there, called prophylactic cranial
irradiation.
In recent years, new molecular therapies for the treatment
of NSCLC have been added - epidermal growth factor
receptor inhibitors (EGFR), agents that target vascular
endothelial cells, farnesyl transferase inhibitors, retinoids,
proteosome inhibitors and inhibitors of raf / MAP kinase
(activated mitotic protein-kinases).
Surgery
At the time of diagnosis, only about 20–25% of lung
cancers can potentially be cured, primarily by surgery.
NSCLC are good candidates for surgery which is the
treatment of choice in early-stages, but surgically removal
of tumor does not always result in a cure. Unfortunately
relapses are very frequent.
In general, surgery is not used for SCLC, because this
aggressive cancer requires chemotherapy and radiation
therapy and because in most cases the cancer has
spread beyond the lungs at time of diagnosis.
Possible operations, aimed to remove the lung tumor are
represented by more or less extensive lung resection,
such as segmentectomy, lobectomy or pneumectomy,
mainly depending on tumor location.
Even if the tumor is in early stage, having a small size,
being in a good location, and could be technically easily
removed, in many cases the operation cannot be
performed due to associated diseases. The Pulmonary
Function Testing (PFT)) must be performed prior to
operation to determine whether the amount of lung
remaining after surgery will be able to provide enough
oxygen and breathing function.
Most patients with a preoperative forced expiratory
volume in one second of greater than 2.5 L are able to
tolerate pneumonectomy. With a forced expiratory
volume in one second of 1.1-2.4 L, a lobectomy is
possible. With a forced expiratory volume in one second
of less than 1 L, patients are not considered candidates
for surgery.
Following lung volume reduction surgery, mortality rates
are between 5% and 9%. The perioperative mortality
rate is 6% for pneumonectomy, 3% for lobectomy, and
1% for segmentectomy. These rates reflect
improvements in anesthesia and surgical techniques.
In recent years new palliative endoscopic treatment has
been developed prolonging and improving the life quality of
this patients.
Different endoscopic techniques can be classified as
follows: (from http://annonc.oxfordjournals.org/ by guest on May 15, 2012, 248)
1. Techniques enabling rapid removal of obstruction (e.g.
mechanical debulking/resection, ND:YAG-laser resection,
electrocautery) in case of life-threatening obstruction.
2. Techniques enabling delayed removal of obstruction (e.g.
cryotherapy, endobronchial irradiation, photodynamic
therapy) in cases of non-critical stenosis.
3. Techniques enabling maintenance of airway patency (e.g.
stenting).
4. Techniques enabling symptom control such as hemoptysis
(e.g. argon plasma coagulation, electrocautery, ND:YAGlaser
therapy,).
5. Techniques for increased local tumor control (e.g.
intratumoral injection of gene therapy vectors).
 Indications for interventional bronchoscopic procedures
in lung cancers are:
1. Life-threatening obstruction of the central airways
(trachea, carina, main bronchi)
2. Central airway obstruction causing symptoms
(dyspnea, atelectasis, post-obstructive pneumonia,
hemoptysis or reducing the airway lumen >50%)
3. Inoperable early lung cancer amenable to
endoscopic treatment
Light-amplified stimulated emission of radiation (LASER)
has been used for several decades for airway disorders.
Nd:YAG (neodymium-yttrium aluminum garnet) laser,
using an infrared wavelength of 1064 nm. The primary
indication for this technique is palliation of airway
obstruction by either primary or metastatic malignancies.
Electrocautery has the same indications but its major
advantages compared with laser therapy are its very low
cost, despite equal levels of efficiency, and probably
superior levels of safety.
Cryotherapy is the application of extreme cold for local
destruction of living tissue. The main indications are
treatment of non-critical malignant airway obstruction,
hemoptysis and treatment of superficial early lung cancer.
Argon plasma coagulation (APC) is a new method using
ionized argon plasma delivered through special probes
with flexible bronchoscope to obtain airway patency and
haemostasis.
Airway stenosis can be managed also by stent insertion.
A large variety of stents have been used in the last two
decades but the common problems associated include
migration, granulation tissue formation and mucus
plugging.
Endobronchial irradiation (brachytherapy) is currently
achieved by placing a highly radioactive source (iridium
192 probe) by means of a flexible bronchoscope at the
desired location. It can be used for curative intent
treatment of early superficial lung cancer, for treatment
of primary non-resectable bronchial carcinoma and for
palliative treatment involving the removal of obstruction
for primary or recurrent endoluminal lung cancer.

Despite all current efforts in prevention (smoking

cessation), early detection and early treatment,
development of new chemotherapeutic agents and
combined modality of treatments, the overall prognosis
of lung cancer is still dismal, with 5-year survival
remaining at about 13% over the last few decades.