Professional Documents
Culture Documents
Surgical Pathology
2013
Surgical Pathology
Table of Contents
Chapter Title
Page
Introduction .
45
Bariatric Surgery..
109
127
151
Rectal Cancer...
203
Anoperineal Pathology.
217
240
263
299
332
Peritonitis..
364
Intestinal Occlusions
374
388
394
Abdominal Trauma...
417
445
495
Breast Pathology...
520
562
584
604
Thoracic Traumas.
612
640
INTRODUCTORY COURSE
About General Surgery
Just like other teachers would say that their specialty is the most important, so I
would also say that surgery is probably the most important medical specialty in saving
lives and cure many illnesses.
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 a better cure, a
number of other surgical subspecialties have emerged from surgery specialty, 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 of cure or in combination with other methods.
Basic skills of general surgery are necessary to any doctor or nurse regardless their
specialty. The third year college students, in classes of semiology and surgical practice
acquire most of these skills. 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
in classes of surgery. Maneuvers as injections, hemostasis, airway release,
cardiopulmonary resuscitation, and thoracocentesis should be known by any doctor.
These are only few aspects that make surgery one of the most important medical
specialties.
Just think how many young patients would die because of acute appendicitis in the
absence of surgical treatment!
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, etc.) with the patient's biological products, which may
contain pathological germs such as HIV, hepatitis viruses, bacteria, TB,
Echinococcus, and 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. Surgery produces irreversible effects - In most cases, surgery produces
irreversible effects on bodys 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 patients 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 patients condition (eg. gastric sleeve or gastric by-pass
for morbid obesity). Surgery may produce changes in patients psychological
status and fortunately, in most cases changes are good. Some irreversible
changes are very apparent especially in plastic surgery influencing deeply the
patients psyche. When changes are made, especially on the patients 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 patients psyche and quality of life
(eg. total mastectomy, rectal amputation, etc.) but these are performed just when
necessary.
7. Surgery 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.
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 the 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 others mistakes than from yours. 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. Not always, the surgeon can guide his actions based
on protocols. There are many cases when improvisations are necessary, making
surgery an art.
10. Surgery presumes work in team - For best results, well-trained teams are
necessary. Depending on operation type, two or three surgeons, a scrub nurse,
anesthesiologist, and auxiliary staff form the team (totally about 7-8 persons in
an operating room). Every member of the team should know its responsibilities.
11. Surgery has a high judicial risk - Surgery is one of the specialties with the
highest judicial 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 should be reserved
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 records. 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 high performance,
minimal invasive with minimum damages to the patient, special and very costly
devices and instruments are necessary. In addition, the consumption of sanitary
materials during operation and after it 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.
Other important aspects in surgery:
1. Never forget that the patient is the most important for us doctors!
2. There are no illnesses outside the patients! 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 dont 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.
Surgical anatomy
Esophageal syndrome
Achalasia
Esophageal diverticula
Esophageal cancer
Esophageal varices
1. Surgical Anatomy
The esophagus is a segment of the digestive tract being represented by a musculomembranous tubular organ, located between the pharynx and the stomach. Its average
length is 25 cm and its diameter is about 1.5-2 cm.
The esophagus has three segments depending on which anatomical region it
crosses: cervical, thoracic and abdominal. (Figure 1) It also has two main curves: one
in sagital plane, with convexity oriented posterior, and the other with convexity oriented
to the right in frontal plane. (Figure 2) These curves guide the surgical approach to the
left or to the right. Thus, in cervical region, the approach is preferred on the left side.
For the first two thirds of intrathoracic esophagus the approach is easier via the right
thoracotomy, because the esophagus is located at the right of the aorta, whereas the
lower third of intrathoracic esophagus is easier accessed via a left thoracotomy.
The esophagus has three physiological straits important in the development of
postcaustic strictures: (Figure 3)
Cricoidian strait - at 15 cm from the dental arch
Bronchoaortic strait - at 25 cm from the dental arch
Diaphragmatic strait - at 40 cm from the dental arch
Innervation
is
sympathetic
(from
paravertebral, celiac and semilunar ganglia) and
vagal. There are two intramural plexuses:
Auerbach and Meissner important in
esophageal contractions for swallowing.
Alterations of these structures will lead to
esophageal motor dysfunction explaining for
example the achalasia.
Physiology
The main function of the esophagus is in
swallowing. (Figure 8) Factors contributing to
the swallowing process are gravity and
esophageal peristaltic waves. There must be
coordination between peristaltic waves and opening of the cardia. The LES (low
esophageal sphincter) opens on a pressure of 20 cm water column. Missing of this
coordination will lead to esophageal functional syndromes such as achalasia.
2. Esophageal Syndrome
Causes of this syndrome can be either organic or/and functional, and includes:
1. Dysphagia (difficulty in swallowing). Sometimes, dysphagia may have a short
onset and evolution especially when functional disorders are the cause. If there
are anatomical lesions, dysphagia is usually progressive manifested initially for
solids and then for fluids. In achalasia, the reverse situation exists, the so-called
"paradoxical dysphagia.
2. Pain located retrosternal and in epigastrium.
3. Regurgitation. Not to be confused with vomiting. The content of regurgitation
is represented by undigested food coming from esophagus not from the stomach
like in vomiting. It may occur early in upper stenosis, or late in lower stenosis.
4. Hypersalivation (sialorrhea) is caused by the vagus nerves irritation produced
by esophageal distension.
10
3. Achalasia (Cardiospasm)
Achalasia is represented by three elements: the incomplete lower esophageal
sphincter (LES) relaxation when the alimentary bolus reaches at this level, increased
LES tone, and aperistalsis (lack of peristaltic waves) 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.[1,2]
Epidemiology [2-6]
The prevalence is of less than 1/10.000, and the incidence between 0.03 and
1/100.000 inhabitants per year.
The sex ratio is: male/female = 1/1
The most affected ages are between 25 and 60 years. Less than 5% of cases
occur in children.
Achalasia seems to be less common among some Asian and African populations.
Causes
1. Idiopathic (the cause is not known). Perhaps a viral infection results in
myenteric plexus inflammation that leads to an autoimmune response with
subsequently destruction of the inhibitory myenteric ganglion cells resulting in
the clinical syndrome of idiopathic achalasia. [1]
2. Trypanosoma Cruzii infection (Chagas disease)
3. Tumors in this area
4. Degeneration of vagus nerves nuclei
5. Pharmacological disorders of chemical mediators from the neuromuscular
endplate in the lower esophageal sphincter (LES)
Three criteria are defining the achalasia:
1. The spasm of the lower esophageal sphincter
2. Abnormal esophageal peristalsis
3. Weak esophageal contractions or nonexistent, aperistaltic, biphasic or
multiphasic contractions.
Morphopathology
The dimension of abdominal esophagus is normal but the thoracic esophagus is
much dilated and the dilatation does not depend on the duration of disease.
The esophageal wall may be very thin with a bold or thin (atrophic) mucosa,
with esophagitis.
The cardia has no modifications.
The intramural Meissners plexuses are altered, especially in the lower part of
the esophagus.
Physiopathology
Food accumulates in the esophagus
leading to its expansion and dilatation.
After a while, the food manages to pass into
the stomach according to the Hurst law.
According to this law, the LES will open
only when the intra-esophageal pressure is
higher than the LES contraction force of 20
11
13
Park W, Vaezi MF. - Etiology and pathogenesis of achalasia: the current understanding. - Am. J. Gastroenterol. 2005;
100(6):1404-1414.
2.
3.
Mayberry JF. - Epidemiology and demographics of achalasia. - Gastrointest. Endosc. Clin. N. Am. 2001; 11:235-248.
4.
Ho KY, Tay HH, Kang JY. - A prospective study of the clinical features, manometric findings, incidence and prevalence
of achalasia in Singapore. - J. Gastroenterol. Hepatol. 1999; 14:791-795.
5.
6.
Mayberry JF, Atkinson M. - Studies of incidence and prevalence of achalasia in the Nottingham area. - Q. J. Med. 1985;
56:451-456.
7.
Cecconello I, Zilberstein B, Ishioka S, Pollara WM, Lemos AM, Venco FE. - Precancerous esophageal lesions. - Dig.
Dis. Sci. 1986; 31(10supl):80S.
8.
9.
The
Merk
Manual
For
Health
Care
Professionals
(online
edition)
http://www.merckmanuals.com/professional/gastrointestinal_disorders/esophageal_and_swallowing_disorders/motility_
disorders.html
10. Dughera L, Battaglia E, Maggio D, et al. - Botulinum toxin - Treatment of oesophageal achalasia in the old old and
oldest old: a 1-year follow-up study. - Drugs Aging 2005; 22:779-783.
11. Pohl D, Tutuian R. - Achalasia: an Overview of Diagnosis and Treatment - Journal of gastrointestinal and liver diseases
2007; 16:297-303.
14
15
4. Esophageal Diverticula
Diverticulum is a sacciforme dilatation of the esophageal wall with various
locations, at different levels, which communicates with the esophageal lumen through
an opening of various calibers. (Figure 15) The main locations are cervical and thoracic.
Based on physiopathological criteria, there are two main types of esophageal
diverticula: diverticula of pulsion or of pressure, and diverticula of traction.
16
17
18
Morales-Divo C, Jecker P, Lippert B, Mann WJ. - Extraesophageal reflux in patients suffering from Zenker's
diverticulum. - W.J. HNO. 2007; 55(7):546-50.
2.
Sturdza VR, Sturdza M. - Zenker's diverticulum. - Rev. Med. Chir. Soc. Med. Nat. Iasi. 1989; 93(4):759-61.
3.
Stafford ND, Moore-Gillon V, McKelvie P. - Handedness and the side on which pharyngeal pouches occur. - B.M.J.
1984; 288:815816.
4.
Jill DSouza - Zenkers Diverticulum. - Grand Rounds Presentation, University of Texas Medical Branch, Department of
Otolaryngology , May 28, 2010 (http://www.utmb.edu/otoref/grnds/divert-zenk-100526/divertic-zenk-100526.pdf)
5.
Bradley PJ, Kochaar A, Quraishi MS. - Pharyngeal pouch - carcinoma: real or imaginary risks? - Ann. Otol. Rhinol.
Laryngol. 1999; 108:10271032.
19
5. Esophageal Cancer
Esophageal cancer is the most deadly cancer of the alimentary tract, even more
than pancreatic cancer. It ranks on the forth place after gastric, colon and rectal cancer,
as frequency. The main features of esophageal cancer, which makes it one of the most
lethal cancers, are:
1. It is very extended in surface and depth
2. It is difficult to treat
3. Treatment is followed by modest results
Epidemiology [1,2]
There are two main histological types of esophageal cancer: squamous and
adenocarcinoma. Squamous cell carcinoma is most frequently encountered in Asian
countries, the Middle East and in South Africa. In recent years the incidence of
adenocarcinoma has increased dramatically especially in Western countries. Based on
race, squamous cancer incidence is three times higher in black people, while
adenocarcinoma is more common in whites. Geographical distribution shows an
incidence of 20-30 times higher in China and Asia in general than in the U.S. and
Europe. Distribution by sex groups shows a three to five-fold higher incidence in males
than in the females. The average age of patients who develop esophageal cancer is 6970 years. Only two thirds of treated patients survive at 2 years and about 15% to 20% of
survive at least 5 years after diagnosis.[3]
Etiology and risk factors
The exact etiology of esophageal cancer is unfortunately unknown. Despite great
efforts in elucidating the disease, we follow the empirical observations, which establish
risk factors associated with esophageal cancer. Their presence does not mean that the
individual will develop esophageal cancer, but
the probability is higher. The following are the
risk factors most often incriminated:
1. Age over 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-Vinson syndrome
7. Tylosis (palmoplantar keratoderma)
8. Esophageal diverticula
9. Benign stenosis
10. Local radiations
Morphopathology
Based on its location, esophageal cancer
can be classified as: (Figure 23)
Of the upper third
Of the mid third (thoracic)
Of the lower third
20
21
T stage
TX: Primary tumor cannot be assessed
T0: No evidence of primary tumor
Tis: Carcinoma in situ
T1: Tumor invades lamina propria (T1a)
or submucosa (T1b)
T2: Tumor invades muscularis propria
T3: Tumor invades adventitia
T4: Tumor invades adjacent structures
N stage
NX: Regional lymph nodes cannot be
assessed
N0: No regional lymph node metastasis
N1: Regional lymph node metastasis
N1a: One to three nodes involved
N1b: Four to seven nodes involved
N1c: More than seven nodes involved
Stages
Stage 0 - Tis, N0, M0
Stage I - T1, N0, M0
Stage IIA - T2, N0, M0, T3, N0, M0
Stage IIB - T1, N1, M0, T2, N1, M0
Stage III - T3, N1, M0, T4, any N, M0
Stage IV - Any T, any N, M1
Stage IVA - Any T, any N, M1a
Stage IVB - Any T, any N, M1b
22
Symptoms. The onset is insidious and that is the main reason why many patients are
diagnosed in advanced stages of evolution. The patient with esophageal cancer usually
is a man in the 6th - 7th decade of age, smoker, with the habit of alcohol consumption,
who complains of retrosternal discomfort in early phases and then of all symptoms of
the esophageal syndrome. The main symptoms are:
1. Dysphagia is the main symptom being permanent, progressive, and generally
has a short duration of evolution. At first manifested for solid foods and then for
liquids and finally complete when the patient can no longer feed and die of
starvation.
2. There is an important weight loss
3. Retrosternal and epigastric pain
4. Superior digestive bleedings
5. Other symptoms from invaded or compressed organs such as hoarseness,
hematemesis, hemoptysis, esotracheal or esobronchial fistula, which are
characteristic for the period of complications due to loco-regional extension,
usually meaning the overcoming of curative surgery stage.
Physical examination reveals an asthenic patient, underweighted, with nicotine skin
impregnation. Particular attention should be given to supraclavicular lymph nodes
palpation. The presence of lymph node metastases at this level contraindicates surgery
with radical intent. Physical signs are poor especially in the early stages.
Workup
The most important is endoscopy because of direct visualization and the
possibility of performing biopsies. (Figure 26)
23
Differential diagnosis should include benign stenosis, achalasia, diverticula, and reflux
esophagitis.
Treatment of esophageal cancer is complex and multimodal - mainly surgical plus
preoperative radio-chemotherapy in patients over 75 years for tumor conversion, also
applied in the postoperative period. Recent studies show that using either chemotherapy
or chemoradiotherapy before surgery is better than surgery alone.[6,9,10] Other
modalities of treatment are :
Laser tumor vaporization
Electrocoagulation
Application of stents
Preoperative preparation. The patient must be carefully investigated and
prepared before surgery. Besides the above-mentioned investigations, required for
primary diagnosis, further investigations are needed. Routine laboratory tests including
blood group and proteinemia will be performed. Cardiac function will be explored
establishing the necessary medication. Respiratory function will also be explored by
spirometry, since thoracotomy and manipulation of the lung reduce the ventilation
capacity of the lungs. Hepatic and renal function will also be evaluated. Gastroscopy (if
possible) and contrast imaging will explore the stomach to assess its availability for
esophagoplasty. The patient should undergo preoperative mechanical bowel preparation
by purgation (washout) considering that the colon may be used for esophagoplasty.
Electrolyte and protein deficits will be corrected. If the level of proteins is low, below
3.4 g%, the risk of anastomotic fistulas and infections is very high. In cachectic patients,
the best approach is to perform a preoperative feeding jejunostomy for enteral nutrition.
Jejunostomy may be useful in postoperative period or may be a definitive solution in
unresectable cases.
Following these investigations, the patient will be classified in one of the
anesthesia risk groups according to the scale ASA (American Society of
Anesthesiologists). (Table 2)
Table 2 - American Society of Anesthesiologists (ASA) Risk Classification
I A normal healthy patient
II A patient with mild systemic disease
III A patient with severe systemic disease
IV A patient with severe systemic disease that is a constant threat to life
V A moribund patient who is not expected to survive without the operation
VI A declared brain-dead patient whose organs are being removed for donor purposes
24
25
When the stomach is not suitable for esophagoplasty (small stomach, previous
operations on stomach, etc.), the most frequently used organ is the colon (ascending or
transverse colon especially). The colon should be mechanically prepared before
operation. When the right colon is used, the ileocolic and the right colic vessels are
resected and appendectomy is also performed. The arterial supply will be ensured by the
middle colic artery or left colic artery. The cecum is ascended to the cervical region
28
29
30
References
1.
2.
3.
4.
Shields TW, LoCicero J, Ponn RB, Rusch VW. - Less Common Malignant Tumors of the Esophagus. - Lippincott
Williams & Wilkins. 2005; pp. 23252340.
5.
6.
Ajani J, D'Amico TA, Hayman JA, Meropol NJ, Minsky B. - National Comprehensive Cancer Network - Esophageal
cancer. Clinical practice guidelines in oncology. - J. Natl. Compr. Canc. Netw. 2003; 1(1):14-27.
7.
Ahmed
A,
David
J.
A,
Thomas
R.
Esophageal
Cancer
http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/hematology-oncology/esophageal-cancer/
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Ellis FH Jr, Watkins E Jr, Krasna MJ, Heatley GJ, Balogh K. - Staging of carcinoma of the esophagus and cardia: a
comparison of different staging criteria. - J. Surg. Oncol. 1993; 52(4):231-235.
9.
Cancer.Net Guide - Esophageal Cancer - Treatment - Printed October 4, 2012 from http://www.cancer.net/cancertypes/esophageal-cancer/treatment
10.
Medical Research Council Oesophageal Cancer Working Group. - Surgical resection with or without preoperative
chemotherapy in oesophageal cancer: a randomised controlled trial. - Lancet 2002; 359:1727-1733.
11.
DAmico TA. - Surgery for Esophageal Cancer. - Gastrointest. Cancer Res. 2008; 2(4 Supplement 2):S6S9.
12.
Ando N. - Future perspectives on the standardization of surgical treatment for esophageal cancer. - Nihon Geka Gakkai
Zasshi 2003; 104:390-394.
13.
Low DE. - Open versus minimally invasive esophagectomy: what is the best approach? Frame the issue. - J. Gastrointest.
Surg. 2011; 15:497-499.
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Kunisaki C, Kosaka T, Ono HA, Oshima T, Fujii S, Takagawa R, Kimura J, Tokuhisa M, Izumisawa Y, Makino H,
Akiyama H. - Significance of thoracoscopy-assisted surgery with a minithoracotomy and hand-assisted laparoscopic
surgery for esophageal cancer: the experience of a single surgeon. - Endo. I. J. Gastrointest. Surg. 2011; 15:1939-1951.
15.
Bresadola V, Terrosu G, Cojutti A, Benzoni E, Baracchini E, Bresadola F. - Laparoscopic versus open gastroplasty in
esophagectomy for esophageal cancer: a comparative study. - Surg. Laparosc. Endosc. Percutan. Tech. 2006; 16:63-7.
16.
Atkins BZ, Shah AS, Hutcheson KA, Mangum JH, Pappas TN, Harpole DH Jr, D'Amico TA. - Review Reducing
hospital morbidity and mortality following esophagectomy. - Ann. Thorac. Surg. 2004; 78(4):1170-6.
17.
18.
Martin LW, Hofstetter W, Swisher SG, Roth JA. - Management of intrathoracic leaks following esophagectomy. - Adv.
Surg. 2006; 40:173-190.
19.
Schweigert M, Dubecz A, Stadlhuber RJ, Muschweck H, Stein HJ. - Treatment of intrathoracic esophageal anastomotic
leaks by means of endoscopic stent implantation. - Interact. Cardiovasc. Thorac. Surg. 2011; 12:147-151.
20.
Feith M, Gillen S, Schuster T, Theisen J, Friess H, Gertler R. - Healing occurs in most patients that receive endoscopic
stents for anastomotic leakage; dislocation remains a problem. - Clin. Gastroenterol. Hepatol. 2011; 9(3):202-210.
21.
van Heijl M, Gooszen JA, Fockens P, Busch OR, van Lanschot JJ, van Berge Henegouwen MI. - Risk factors for
development of benign cervical strictures after esophagectomy. - Ann. Surg. 2010; 251(6):1064-1069.
31
Honkoop P, Siersema PD, Tilanus HW, Stassen LP, Hop WC, van Blankenstein M. - Benign anastomotic strictures after
transhiatal esophagectomy and cervical esophagogastrostomy: risk factors and management. - J. Thorac. Cardiovasc.
Surg. 1996; 111(6):1141-1146.
23.
Rice TW. - Anastomotic stricture complicating esophagectomy. - Thorac. Surg. Clin. 2006; 16(1):63-73.
24.
Mine S, Udagawa H, Kinoshita Y, Makuuchi R. - Post-esophagectomy chylous leakage from a duplicated left-sided
thoracic duct ligated successfully with left-sided video-assisted thoracoscopic surgery. - Interact. Cardiovasc. Thorac.
Surg. 2008; 7:1186-1188.
32
6. Esophageal Varices
Esophageal varices are dilated veins in the esophageal wall under the mucosa
layer, produced by the increased pressure in portal vascular system. Wolf has first
described them in 1928. Due to the gravitational forces, varices are located mainly in
the lower third of the esophagus. Varices are also frequently found in the upper portion
of the stomach. (Figure 42)
Portal vein, with a caliber of 6-8 mm,
forms by the confluence of the superior
mesenteric vein with the splenic vein behind the
head of the pancreas. The blood flow into the
portal vein is about 1.5 l/min representing one
forth from cardiac output. Portal vein supplies
75% of blood volume that passes through the
liver and 60% of its oxygen.[1] Normal portal
vein pressure is 5 mm Hg.[2] The first
consequences of pressures above this value are
splenomegaly and thrombocytopenia. The
esophageal varices are a later complication that appears at values above 10-12 mmHg in
portal pressure.[3] The rupture risk of varices is 9% at a pressure of 13 mmHg and it
rises up to 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 from
ruptured esophageal varices in the last few decades has decreased from 42% in 1981 [4]
to 15-20% in present days.[5,6] Bleeding will stop spontaneously in about 40-70% of
cases.[3] However rebleeding will occur in 40% of cases in the next 72 hours. Every
bleeding episode will shadow more and more the prognosis. If patients survive the
variceal rupture, there is approximately a 70% risk that they will have a further bleed
within the following 2 year.[7] The high mortality rate comes from some factors such as:
Liver insufficiency
Sepsis
Exsanguination
Brain edema
Complications of the anemia
Superior digestive bleeding is the most difficult to treat when 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 raises the risk because the cirrhotic patient will bleed two times more frequently
than the patient without ulcer and three times more than those with ulcer but without
cirrhosis. Hematemesis in patients with liver cirrhosis may occur from three main
sources:[8]
1. Esophageal varices - 50% of cases
2. Gastric varices - 30% of cases
3. Gastro-duodenal ulcer - 9% of cases
However, association of the main three sources has been encountered.
33
34
Factor
Serum bilirubin
3
>51
>3.0
< 3.0
>6
>2.3
Poorly controlled
Advanced
37
Endoscopic treatment
Rubber band ligation
Sclerosing substances (Sodium Tetradecyl Sulfat, Cyanoacrylat)
Coagulation with Argon plasma
Maintenance treatment
Pharmacological therapy
Lifestyle changes
Diet
Liver transplant
Another classification is:
1. Primary prophylaxis
2. Secondary prophylaxis - the therapy that prevents relapses of bleeding
I. Primary prophylaxis
Primary prophylaxis is considered the first therapy that prevents bleeding from
esophageal varices. In the same category enter the surgical portosystemic and
transjugular shunts, sclerotherapy and variceal ligation, but because of the risks and side
effects, especially of shunts, in nowadays, the pharmacotherapy is considered as a first
intention in primary prevention.
Cirrhotic patients should be examined endoscopically every 2-3 years and those
with high-risk of esophageal varices bleeding will benefit from primary prevention
methods.
The most used drugs are beta-blockers. Propranolol, blocking the beta-receptors,
will induce an alpha-adrenergic overactivity with the consequence of splanchnic
vasoconstriction and thus reducing the portal flow and pressure. Also reduces cardiac
output. Use of beta-blockers can reduce the risk of bleeding by 45% and deaths by 50%
from variceal bleeding. Propranolol dosage should induce a decrease of heart rate by
25% but not less than 55-60 beats / min.
When the effect of beta-blockers is unsatisfactory (20%) or there are
contraindications (20%), long-acting nitrates can be used. They produce vasodilatation
with decreased venous return and post-sinusoidal resistance and thus, consecutive
decrease of portal pressure. In high doses, produce a decrease of tension that will induce
splanchnic vasoconstriction with the consequent decrease in portal pressure.
Endoscopic ligation is the only invasive procedure recommended as primary
prophylaxis especially for varices with high risk of bleeding.
II. Treatment of superior digestive bleeding in emergency condition
The primary goal is to stop the bleeding and rebalance the patient (procedures are
performed simultaneously). Actions:
A. Rapid clinical evaluation of the patient
1. Collect biological specimens (blood, urine)
2. Clinical assessment (blood pressure, heart rate, temperature, blood
oxygenation, central venous pressure, diuresis, etc.)
3. A central venous catheter insertion for fluids administration and other drugs
4. Urinary catheter
5. Orotracheal intubation if the patient is unconscious
38
39
3. Endoscopic procedures
Endoscopic procedures for definitive hemostasis should be applied as soon as
possible if bleeding can be controlled by pharmacotherapy.
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 Vasopressin and Octreotide increases the success rate in these
maneuvers.
4. Hemostatic surgery
If bleeding could not be stopped by tamponade or/and pharmacotherapy, or the
hospital does not have endoscopy facility, or bleeding could not be solved by repeated
endoscopic maneuvers, hemostatic surgery is required.
The less extensive operation is exploratory laparotomy followed by longitudinal
gastrotomy and hemostasis by ligation of sight bleeding varices usually located in the
fornix or around the cardia.
Other more laborious maneuvers such
as portal-systemic shunts or azygoportal
disconnection are burdened by high mortality
in emergency. However, when there are no
other solutions, they can also be performed
in emergency condition too.
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 intraabdominal perigastric associated with
ligation of short gastric vessels, splenectomy,
40
42
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 the portal vein to the gastric veins lowers
2. The blood flows from the varices through the splenic (portal circulation)
vein into the left renal vein (systemic circulation)
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 transplantation remains the surgical option for cure. (Figure 48)
43
Curtney S. Liver - Chapter 48 - Surgery: Basic Science and Clinical Evidence, second edition. 2008 Springer, edited by
Jeffrey A. Norton, Philip S. Barie, Ralph R. Bollinger, Alfred E. Chang, Stephen Lowry, Sean J. Mulvihill, Harvey I.
Pass, Robert W. Thompson.
2.
Burroughs AK. - CHAPTER 9, The Hepatic Artery, Portal Venous System and Portal Hypertension: the Hepatic Veins
and Liver in Circulatory Failure - Sherlocks Diseases of the Liver and Biliary System, Twelfth Edition. Edited by James
S. Dooley, Anna S.F. Lok, Andrew K. Burroughs, E. Jenny Heathcote. - Published 2011 by Blackwell Publishing Ltd.
3.
4.
Graham DY, Smith JL. - The course of patients after variceal hemorrhage. - Gastroenterology 1981; 80:800-809.
5.
Chalasani N, Kahi C, Francois F, Pinto A, Marathe A, Bini EJ, et al. - Improved patient survival after acute variceal
bleeding: a multicenter, cohort study. - Am. J. Gastroenterol. 2003; 98:653-659.
6.
Carbonell N, Pauwels A, Serfaty L, Fourdan O, Levy VG, Poupon R. - Improved survival after variceal bleeding in
patients with cirrhosis over the past two decades. - Hepatology 2004; 40:652-659.
7.
McKay Rebecca, Webster NR. - Variceal bleeding. - Oxford Journals Medicine, BJA: CEACCP - 7(6):191-194
http://ceaccp.oxfordjournals.org/content/7/6/191.full
8.
Odelowo OO, Smoot DT, Kim K. - Upper gastrointestinal bleeding in patients with liver cirrhosis. - J. Natl. Med. Assoc.
2002; 94(8):712715.
2008
9.
10.
Child CG, Turcotte JG. - Surgery and portal hypertension. In: The liver and portal hypertension. Edited by CG Child.
Philadelphia: Saunders 1964:50-64.
11.
Pugh RN, Murray-Lyon IM, Dawson JL, Pietroni MC, Williams R. - Transection of the oesophagus for bleeding
oesophageal varices. - Br. J. Surg. 1973; 60(8):646649.
12.
Spech HJ, Wrdehoff D. - Classification of esophageal varices - endoscopic and clinical aspects. - Leber Magen Darm
1982; 12(3):109-14.
13.
Yong H. Hahn - Portal hypertension - CHORUS Collaborative Hypertext of Radiology - 2 February 1995 Last updated:
1 September 2006, http://chorus.rad.mcw.edu/doc/00863.html
14.
Ritter DM, Rettke SR, Hughes Jr. RW, Burritt Mary F, Sterioff S, Ilstrup DM. - Placement of Nasogastric Tubes and
Esophageal Stethoscopes in Patients with Documented Esophageal Varices - Anesth. Analg. 1988; 67:2833.
15.
Cook D, Laine L. - Indications, technique, and complications of balloon tamponade for variceal gastrointestinal bleeding.
- J. Intensive Care Med. 1992; 7(4):212-218.
16.
Conn HO, Simpson JA. - Excessive Mortality Associated With Balloon Tamponade of Bleeding Varices. - A Critical
Reappraisal - JAMA 1967; 202(7):587-591.
17.
Freedman AM, Sanyal AJ, Tisnado J. - Complications of transjugular intrahepatic portosystemic shunt: a comprehensive
review. - Radiographics 1993; 13(6):1185-210.
44
1. Surgical Anatomy
The stomach
The stomach is the most dilated portion of the digestive tract, being located
between the esophagus and the small intestine. It is an intra-peritoneal organ. Its
capacity is about of 1000-1500 ml.
The stomach has several ligaments, anatomical structures more or less loose,
which give it certain mobility. (Figure 1) The most fixed parts of the stomach are the
cardia, which continues the esophagus, and the pylorus, continuing with the duodenum.
Excessive laxity of these ligaments may cause gastric volvulus.
The stomach has two faces (anterior and posterior), two curves (lesser and
greater) and two openings (cardia and pylorus). (Figure 2) On the lesser curvature of the
stomach the lesser omentum is inserted and on the greater curvature, the greater
omentum.
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.). (Figure 3) Small intestines may enter
the foramen of Winslow and incarcerate (the internal hernia of Treitz).
45
The anterior surface of the stomach, easily accessible, comes against the chest,
the abdominal wall, and the left and quadrate lobe of the liver. The posterior surface,
more difficult to surgical exploration, represents the anterior wall of bursa omentalis
through which the stomach comes in relation with the pancreas, splenic vessels, spleen,
left kidney and left adrenal gland and the transverse mesocolon.
Arterial supply
The stomach has a very good vascular supply. (Figure 5) It has four arterial
sources, all coming from the celiac trunk. These arteries form two vascular arcades
along the two gastric curves. The main arterial sources are:
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
In addition to these sources, should also be mentioned the short gastric arteries
from the splenic artery and the diaphragmatic inferior artery, which irrigates the gastric
fornix.
Venous drainage
Gastric veins have the same routes as the arteries and they flow into the portal
system. Left and right gastric veins flow directly into the portal vein, the left
gastroepiploic via the splenic vein, and the right gastroepiploic vein via the superior
mesenteric vein.
46
Lymphatic drainage
The stomach has a very well represented lymphatic network. There are two
lymphatic networks: one submucous that drains the lymph through the muscular layer
toward the other plexus located in subserosa layer, from where extragastic lymphatic
vessels are starting.
There are four areas of lymphatic drainage of the stomach: (Figure 6)
1. Area I- the superior region of the lesser curvature from where the lymph is
drained towards the lymph nodes located around the gastric artery and
celiac trunk and toward the right paracardial lymph nodes.
2. Area II- the antral region of the lesser curvature is drained towards
suprapyloric and hepatic pedicles nodes.
3. 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 nodes.
4. Area IV- the 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.
Initially, Japanese specialists [1] described
16 groups of lymph nodes draining the stomach,
of particular importance in lymphatic excision in
surgical treatment of gastric cancer. (Figure 7)
1. Right paracardial
2. Left paracardial
3. Along the lesser curvature
4. Along the grater curvature
5. Right suprapyloric
6. Subpyloric
7. Along the left gastric artery
8. Along the common hepatic artery
9. At celiac trunk
10. From splenic hilum
47
48
This special structure of gastric wall (resistant serosa, thick muscular layer and
the well-represented vascular supply) makes it a particularly good material for
anastomosis with low risk of developing anastomotic fistulas.
Types of cells encountered in the mucosa layer are:
1. Mucus producing cells
2. Parietal cells - producing HCl
3. Zymogene cells - producing pepsin
4. Endocrine cells
G cells producing gastrin being best represented in the antral mucosa
ECL (enterochromaffin-like cells) producing histamine
Delta cells producing somatostatin
Others
Physiology
The stomach has motor and secretory functions, 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 after 3-4 hours. Motor activity of gastric emptying ("antro-pyloric
pump") is ensured by gastric antral peristaltic waves with a regularity of 3/minute. The
function is controlled by vagus and sympathetic autonomic nerves and by some
hormones.
The secretory function of the stomach is exocrine and endocrine.
Exocrine function is represented by the gastric juice, with intense acid pH,
secreted in volume of 1.5-3 L/24 hours. It is composed of hydrochloric acid, enzymes
(pepsinogen) and mucus.
Digestive enzymes are:
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.[2]
3. Gastric lipase, which acts on short chain fatty acids, being important in
infants.
4. Cathepsin, a proteolytic enzyme that plays a role especially in infants.[2]
5. Gelatinase, is a proteolytic enzyme that hydrolyses gelatin with more
intense activity than that of pepsin.
6. Other enzymes are carbonic anhydrase, lysozyme and gastric urease.
49
50
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). (Figure 11)
Duodenum is a secondary retroperitoneal organ being covered by peritoneum (the
coalescence fascia of Treitz). Due to its retroperitoneal position, it is difficult to access
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: (Figure 12)
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
51
Japanese Classification of Gastric Carcinoma - 2nd English Edition - Japanese Gastric Cancer Association - Gastric
Cancer, 1998; 1:10-24.
2.
Kelly EJ, Newell SJ, Brownlee KG, et al. - Gastric acid secretion in preterm infants. - Early Human Dev. 1993; 35:215220.
52
2. Peptic Ulcer
Peptic ulcer represents 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, peptic ulcer was considered 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 termed under the generic name of "ulcerous
disease" or gastro-duodenal ulcer. As knowledge progressed, it was found that gastric
ulcer and duodenal ulcer are two distinct diseases, which have many similarities but also
differences. For this reason, the two conditions will be treated separately.
A. Gastric Ulcer
Epidemiology
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 higher. Only in Japan,
the gastric ulcer is more common than duodenal ulcer.[1-3]
Etiopathogenesis
The predominant role in the etiology of gastric ulcer is the less efficiency of local
defense factors resulting in an imbalance between aggression and defense factors of the
gastric mucosa.
Gastric mucosal defense factors are:
The viscous alkaline mucus
The tight connection between gastric epithelial cells
The renewal of epithelium lining every 3 days
Aggression factors are:
Acid-peptic hypersecretion - is less important than for duodenal ulcer
Gastric motility disorders with gastric stasis or delayed emptying
Duodenal-gastric reflux which impairs the mucus barrier
Helicobacter pylori infection, is less important in the genesis of gastric
ulcers than in the duodenal ulcer.[4] The bacteria colonize the antral region
of the stomach, causing chronic active gastritis (type B). This chronic
gastritis results in increased secretion of gastrin and therefore the
hydrochloric acid and peptic secretion too. In addition, H. pylori has a direct
ulcerogenic effect by releasing cytotoxic enzymes such as phospholipase and
proteases and also because of its spiral shape and flagella. The presence of
genes associated with cytotoxic effect (cag A) was isolated in 60% of cases.
Exogenous factors, such as: treatment with nonsteroidal anti-inflammatory
drugs (NSAIDs), intra-arterial chemotherapy, cortisone, excessive use of
laxatives. Non-steroidal anti-inflammatory drugs block the formation of
local prostaglandins responsible for the production of protective mucus by
blocking the cyclooxygenase 1 (cox 1) essential in the production of these
prostaglandins. Therefore, new non-steroidal anti-inflammatory drugs act
only on cox-2, less important in the secretion of these prostaglandins.
53
Glucocorticoids lead to atrophy of all epithelial cells, but it seems that their
role is still minor.
Smoking and stress
Zollinger Elisson syndrome
Genetic factors - blood group O seems to be more relate to duodenal
ulcer.[5,6]
Morphopathology
Gastric ulcer appears as a lack of substance in the gastric mucosa, usually single
but may be multiple and may be located anywhere from the cardia to the pylorus. Ulcer
margins are perpendicular and associated with chronic gastritis signs.
Depending on its depth, we can distinguish acute and chronic ulcers.
Acute ulcer may be represented either by a gastric erosion (exulceratio
simplex) limited to the mucosa, being of small size, which heals without
scars, or by a larger ulcer (about 1 cm diameter) that penetrates all gastric
layers, surrounded by swelling and redness, which heals leaving a visible
scar.
Chronic ulcer reaches 2-5 cm in diameter, has a round or oval shape, with
well-defined edges where there is always a chronic inflammatory infiltrate.
Because of this inflammatory reaction, the stomach may become adherent to
adjacent organs facilitating ulcer progression representing the ulcer
penetration. During the active phase, the ulcer has four zones: inflammatory
exudate, fibrinoid necrosis, granulation tissue and fibrous tissue. Fibrous
base of the ulcer may contain vessels with thin walls or thrombosis.
Classification
The most frequent location is the lesser curvature. Then follows, in order: anterior
wall, posterior wall, pre-pyloric region and grater curvature. Almost half of gastric
ulcers are located in the antral region.
Johnsons classification of gastric ulcers depending on location and secretory
status: (Figure 13) [6]
Type I: ulcer with high location on the upper part of the lesser curvature.
Acid secretion is reduced to normal value. Gastritis and duodenal reflux is
common. 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.[6]
Type III: ulcer located in antrum, pre-pyloric, which acts as a symptomatic
duodenal ulcer. It 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, after consumption of aspirin or NSAIDs.
54
Symptoms
In recent years, symptoms have lost much of specificity so that the clinical picture
is no longer as characteristic as it was described in classical treaties. The evolution is in
acute episodes interrupted by asymptomatic periods.
The main symptom is the pain, usually with epigastric location, but other
locations are possible depending on lesions position. The pain is as if burning,
cramping, twisting or stabbing, 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 has a calming effect on pain. Retrosternal heartburn
occurs mainly in ulcers located in a higher position or in those associated with
gastroesophageal reflux. Other symptoms are related to complications.
Diagnosis
Diagnosis relies on three elements: anamnesis, physical examination and
investigations. Physical examination offer poor elements for positive diagnosis. The
most important are investigations especially those endoscopic.
X-ray with contrast (barium or water-soluble
substances) may indicate the diagnosis in 80% of
cases. The direct radiological sign is the niche (ulcer
crater) that appears as a filling defect on gastric
contour and takes several forms: small, triangular,
pedunculated. The niche may be of medium size,
large with three levels inside: barium, fluid and air
(the Haudek niche) or giant. After evacuation, the
contrast remains inside the niche as a "persistent
spots." Sometimes, ulcerous niche is surrounded by
a halo of edema giving the aspect of target sign(en
cocarde). Indirect radiological signs are represented
by deformation of the lesser curvature, a ring of
spastic contraction of the greater curvature in
ulcerous region ("finger showing the lesion") and
the convergence of mucosal folds toward the ulcer.
(Figure 14)
Gastroscopy is the main investigation for
diagnosis. It directly visualizes the ulcer and allows
lesion biopsy sampling. (Figure 15) A single biopsy
sampling has an accuracy of 70% for malignant
ulcer, while seven biopsies taken from the ulcer base
and margins increase the accuracy to 99%.[7-9]
55
56
57
58
B. Stress Ulcers
(See also the chapter of upper gastrointestinal bleeding)
Stress ulcers are special clinical forms of ulcers appeared on a normal mucosa due
to extreme stressful 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 (avoiding causal conditions) and curative
consisting in gastric emptying (nasogastric tube), local hemostatics, proton pomp
inhibitors, and replacement of lost blood. When these conservative measures prove
ineffective, surgical hemostasis including vagotomy and in rare cases even total
gastrectomy become necessary.
References
1.
Kurata JH, Haile BM. - Epidemiology of peptic ulcer disease. - Clin. Gastroenterol. 1984; 13(2):289-307.
2.
Watanabe Y, Kurata JH, Kawamoto K, Kawai K. - Epidemiological study of peptic ulcer disease among Japanese and
Koreans in Japan. - J. Clin. Gastroenterol. 1992; 15(1):68-74.
3.
Lam SK. - Differences in peptic ulcer between East and West. - Baillieres Best Pract. Res. Clin. Gastroenterol. 2000;
14(1):41-52.
4.
5.
Beasley WH. - Blood Groups of Gastric Ulcer and Carcinoma. - Br. Med. J. 1960; 1(5180):1167-1172.
6.
Johnson D. - Gastric ulcer: classification, blood group characteristics, secretion patterns and pathogenesis. - Ann. Surg.
1965; 162(6):996-1004.
7.
8.
Llanos O, Guzmn S, Duarte I. - Acuracy of the first endoscopic procedure in the differential diagnosis of gastric lesions.
- Ann. Surg. 1982; 195(2):224-226.
9.
Yeowon Choi, Hyo Sun Choi, Woo Kyu Jeon, Byung Ik Kim, Dong Il Park, Yong Kyun Cho, Hong Joo Kim, Jung Ho
Park, and Chong Il Sohn - Optimal Number of Endoscopic Biopsies in Diagnosis of Advanced Gastric and Colorectal
Cancer - http://dx.doi.org/10.3346/jkms.2012.27.1.36 - J. Korean. Med. Sci. 2012; 27:36-39.
10. Finsterer H. - Malignant Degeneration of Gastric Ulcer. - Proc. R. Soc. Med. 1939; 32(3):183-196.
11. Rubin E, Reisner H. - Essentials of Rubins Pathology 5Th Edition 2008.
12. Hansson LE, Nyrn O, Hsing AW, Bergstrm R, Josefsson S, Chow WH, Fraumeni JF, Adami HO. - The Risk of
Stomach Cancer in Patients with Gastric or Duodenal Ulcer Disease. - N. Engl. J. Med. 1996; 335:242-249.
13. Jamieson GG. - Current Status of Indications for Surgery in Peptic Ulcer Disease. - World J. Surg. 2000; 3(24): 256-258.
59
C. Duodenal Ulcer
Epidemiology
Duodenal ulcer occurs more frequently in adulthood, being about four times more
common than gastric ulcer. The maximum incidence is between the forth and fifth
decade of live, and the ratio between men and women is 4/1-6/1.
The incidence of duodenal ulcer decreased in last decades due to the development
of new antisecretory drugs, but still remains at 1-2%.[1] In nowadays, admission in
hospital is required only in complicated cases of duodenal ulcer. Duodenal ulcer never
turns malignant.
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 ulcerous disease and an important risk factor in gastric
cancer. The presence of bacteria was found in 90% of patients with duodenal
ulcer.[2,3] The lifetime risk of peptic ulcer in a person infected with H. pylori
ranges from 3 % in the United States to 25% in Japan.[4,5]
Predisposing (exogenous) factors:
External factors incriminated in duodenal ulcer: smoking, alcohol
consumption, poor nutrition, chronic intake of inflammatory drugs,
psychological factors
Genetic factors are also important because the disease frequently occurs in
members of the same family and in those with O (I) blood type.[6,7]
Morphopathology
Duodenal ulcer appears as a single or
multiple ulcerations located with predilection in
the duodenal bulb (D1).
The ulcer crater has an inflammatory
reaction around it, which over the time turns into
fibrosis, 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. (Figure 20)
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 during night or morning and it gives the feeling of "hunger pain". The pain
relieves after the ingestion of milk or alkali. The picture above is the so-called the
small periodicity in duodenal ulcer (pain-ingestion-relief-pain). Symptoms usually are
exacerbated in spring and autumn - the great periodicity or seasonal periodicity. 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.
60
61
62
63
64
65
66
Treatment
Upper gastrointestinal bleeding is a surgical emergency, the patient being
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 purposes of treatment are to stop bleeding, rebalance the patient and
prevent rebleeding. Treatment may be pharmacologic, 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 aspiration 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 PPI in bolus over 30 minutes, followed by a continuous infusion
of 8 mg/h administered for 3 days) and hemostatics (Adrenostazin, K vitamin,
Calcium).[17,18]
Somatostatin and its analogue Octreotide reduce splanchnic blood flow, inhibit
gastric acid secretion and have a cytoprotective effect. They can be used as adjunctive
therapy before and after endoscopy.[19] Somatostatin is used in dose of 250 micrograms
iv bolus followed by hourly administration of the same dose infusion for 3-7 days.
Octreotide dose is 50-100 micrograms in bolus followed by 25 micrograms per hour for
3 days.
Gastric aspiration with lavage and medication can stop the bleeding if it is not
produced by an important vessel (gastroduodenal artery). Emptying the stomach is very
important in hemostasis. Lavage is performed with cold, alkaline and hemostatic
solutions (adrenostazin) until clarification of lavage fluid.
Nasogastric aspiration is important for:
1. Diagnosis purposes. The absence of blood in the stomach in a patient with
melena raises the suspicion of a postbulbar ulcer or other sources located
downstream the duodenum.
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68
B. Perforation
Despite all progresses in medical treatment of peptic ulcer, perforation remains
one of the most important complications burdened by a high (8-42%) mortality risk.[2224]
The first cases of perforation were reported in 1817 by Traves, and in 1884,
Mikulicz first described treatment methods.[25] In the past, the incidence of perforation
was about 10% but it decreased after introduction of modern antacid drugs.
Helicobacter pylori is involved in 70-92% of all perforated duodenal ulcers. The
second most common cause (40-50%) of perforated duodenal ulcer is the ingestion of
anti-inflammatory non-steroidal (AINS) drugs. The least common cause is pathologic
hypersecretory status, such as Zollinger-Ellison syndrome.[25]
In half of cases, the perforation takes place in the free peritoneal cavity, when the
ulcer is located on the anterior duodenal wall. In about 40-50% of cases the perforation
is sealed (covered) by neighboring organs: the liver, gall bladder or omentum, as a
defense reaction of the body that tries to isolate the pathologic process.[25]
Clinical picture is dominated by symptoms and signs of generalized peritonitis. First,
there is a chemical and then bacterial peritonitis develops. The onset is sudden with
intense epigastric pain (as a knife stabbing") that can migrate into the right iliac fossa
and then quickly generalized. Initially epigastric pain and then located in the right iliac
fossa, lead to confusion with acute appendicitis. The pain may radiate to shoulder (Kehr
sign) because of the diaphragmatic peritoneum irritation, transmitted along the phrenic
nerve.
General signs may be fever, tachycardia, pallor, superficial tachypnea and signs
of acute dehydration. After several hours symptoms fade away, as hypovolemic shock
sets up. Abdominal wall contraction is replaced by abdominal distension, nausea and
69
70
71
72
D. Penetration
Ulcer penetration is actually a perforation in an area of the duodenum covered by
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 common bile duct and fistulas between duodenum and these
organs may appear.
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.
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 based on radiologic and endoscopic explorations.
Treatment is only surgical. In most cases, the ulcerous 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 by Bilroth I, Bilroth II or Roux anastomosis.
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Wang YR, Richter JE, Dempsey DT. - Trends and outcomes of hospitalizations for peptic ulcer disease in the United
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Paptheodoridis GV, Sougioultzis S, Archimandritis AJ. - Effects of Helicobacter pylori and nonsteroidal antiinflammatory drugs on peptic ulcer disease: A systematic review. - Clin. Gastroenterol. Hepatol. 2006; 4:130-142.
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pylori. - In: Achtman M, Suerbaum S, eds. Helicobacter pylori: molecular and cellular biology. - Wymondham, United
Kingdom: Horizon Scientific Press, 2001:29-51.
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Schlemper RJ, van der Werf SD, Biemond I, Lamers CB. - Seroepidemiology of gastritis in Japanese and Dutch male
employees with and without ulcer disease. - Eur. J. Gastroenterol. Hepatol. 1996; 8:33-39.
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Doll R, Drane H, Newell AC. - Secretion of blood group substances in duodenal, gastric and stomal ulcer, gastric
carcinoma, and diabetes mellitus - Gut. 1961; 2(4):352-359.
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Edgren G, Hjalgrim H, Rostgaard K, Norda R, Wikman A, Melbye M, Nyrn O. - Risk of Gastric Cancer and Peptic
Ulcers in Relation to ABO Blood Type: A Cohort Study. - Am. J. Epidemiol. 2010;172(11):1280-1285.
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Kill J, Andersen D. - X-Ray Examination and/or Endoscopy in the Diagnosis of Gastroduodenal Ulcer and Cancer. Scand. J. Gastroenterol. 1980; 15(1):39-43.
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Dragstedt LR, Owens FM. - Supradiaphragmatic section of vagus nerves in the treatement of duodenal ulcer. - Proc. Soc.
Exp. Biol. Med. 1943; 53:152.
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Ohmann C, Thon K, Hengels KJ, Imhof M. - Incidence and pattern of peptic ulcer bleeding in a defined geographical
area. DUSUK Study Group. - Scand. J. Gastroenterol. 1992; 27(7):571-581.
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Lee YC, Liou JM, Wu MS, Wu CY, Lin JT. - Eradication of Helicobacter Pylori to Prevent Gastroduodenal Diseases:
Hitting more than One Bird with the Same Stone. - Therap. Adv. Gastroenterol. 2008; 1(2):111-120.
12.
Van Leerdam ME - Epidemiology of acute upper gastrointestinal bleeding. - Best Pract. Res. Clin. Gastroenterol. 2008;
22:209-224.
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Sadic J, Borgstrm A, Manjer J, Toth E, Lindell G. - Bleeding peptic ulcer - time trends in incidence, treatment and
mortality in Sweden. - Aliment Pharmacol. Ther. 2009; 15;30(4):392-398.
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Del Piano M, Antonia Bianco M, Cipolletta L, Zambelli A, Chilovi F, Di Matteo G, Pagliarulo M, Ballar M, Rotondano
G. - The "Prometeo" Study: Online Collection of Clinical Data and Outcome of Italian Patients With Acute Nonvariceal
Upper Gastrointestinal Bleeding. - J. Clin. Gastroenterol. 2013; 47(4):e33-37.
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Holster IL, Kuipers EJ. - Management of acute nonvariceal upper gastrointestinal bleeding: Current policies and future
perspectives. - World J. Gastroenterol. 2012; 18(11):1202-1207.
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Laine LA. - Review Helicobacter pylori and complicated ulcer disease. - Am. J. Med. 1996; 100(5A):52S-57S;
discussion 57S-59S.
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Keyvani L, Murthy S, Leeson S, Targownik LE. - Pre-endoscopic proton pump inhibitor therapy reduces recurrent
adverse gastrointestinal outcomes in patients with acute non-variceal upper gastrointestinal bleeding. - Aliment
Pharmacol. Ther. 2006; 24(8):1247-1255.
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Barkun AN. - The role of intravenous proton pump inhibitors in the modern management of nonvariceal upper
gastrointestinal bleeding. - Drugs Today (Barc) 2003; 39 Suppl A:3-10.
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Choi CW, Kang DH, Kim HW, Park SB, Park KT, Kim GH, Song GA, Cho M. - Somatostatin adjunctive therapy for
non-variceal upper gastrointestinal rebleeding after endoscopic therapy. - World J. Gastroenterol. 2011; 17(29):34413447.
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En-Ling Leung Ki1, James Y W - New Endoscopic Hemostasis Methods. - Clin. Endosc. 2012; 45(3):224-229.
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Van Leerdam ME, Vreeburg EM, Rauws EA, Geraedts AA, Tijssen JG, Reitsma JB, Tytgat GN. - Acute upper GI
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1993/1994 and 2000. - Am. J. Gastroenterol. 2003; 98(7):1494-1499.
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Kingdom - Digestive and Liver Disease, 2002; 34(5):322-327.
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perforation. - J. Gastroenterol. Hepatol. 2007; 22(4):565-570.
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Morbidity and Mortality. - World J. Surg. 2003; 27(7):782-787.
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Cellan-Jones CJ. - A rapid method of treatment in perforated duodenal ulcer. - B.M.J. 1929; 36:1076-1077.
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Lui FY, Davis KA. - Gastroduodenal perforation: maximal or minimal intervention. - Scand. J. Surg. 2010; 99(2):73-77.
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Siu WT, Leong HT, Law BK, Chau CH, Li AC, Fung KH, Tai YP, et al.- Laparoscopic repair for perforated peptic ulcer:
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Lunevicius R, Morkevicius M. - Management strategies, early results, benefits, and risk factors of laparoscopic repair of
perforated peptic ulcer. - World J. Surg. 2005; 29(10):1299-1310.
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Lunevicius R, Morkevicius M. - Systematic review comparing laparoscopic and open repair for perforated peptic ulcer. Br. J. Surg. 2005; 92(10):1195-1207.
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Bhogal RH, Athwal R, Durkin D, Deakin M, Cheruvu CN. - Comparison between open and laparoscopic repair of
perforated peptic ulcer disease. - World J. Surg. 2008; 32(11):2371-2374.
74
Duodenum
A. Epithelial:
Adenoma (tubular, villous,
tubulovillous)
Brunners Gland Adenoma
B. Mesenchymal:
Leiomyoma
Leiomyoblastoma
Lipoma
Vascular
Fibroma
Neurogenic
C. Others:
Familial Adenomatous Polyposis
Gardners Syndrome
Peutz-Jeghers Syndrome
Duodenal Gangliocytic
Paraganglioma
Symptoms
Most patients will not have any symptoms for a long period. Symptoms are
produced by tumoral complication, being represented mostly by upper gastrointestinal
bleeding and gastric outlet obstruction. Nonspecific symptoms as abdominal pain,
nausea, and weight loss may be present. Periampullary tumors can manifest with
jaundice, cholangitis, and pancreatitis. On physical examination, the bulky tumors may
be palpable.
Diagnosis
Endoscopic examinations (gastroduodenoscopy and endoscopic ultrasound) are
the most important because they directly visualize the tumor and are able to perform
biopsies. In certain cases, endoscopic procedures (stenting) may be applied as an
intermediate or definitive treatment.
CT and MRI scans are important in assessing the degree of tumoral penetration
and spread outside the digestive wall.
The most common benign tumors in the stomach are polyps (75%) and
leiomyomas. In the duodenum, the most common benign lesion is adenoma followed by
leiomyomas and lipomas.
75
2.
Goh PMY, Lenzi JE - Benign tumors of the duodenum and stomach - Surgical Treatment: Evidence-Based and ProblemOriented. Holzheimer RG, Mannick JA, editors. - Munich: Zuckschwerdt; 2001.
3.
Halpin R, Thomson S, Catterall N, Haffejee A. - Smooth muscle tumors of the stomach: clinicopathological aspects. - J.
R. Coll. Surg. Edinb.1993; 38:23-27.
4.
Orlowska J, Jarosz D, Pachlewski J, Butruk E. - Malignant transformation of benign epithelial gastric polyps. - Am. J.
Gastroenterol.1995; 90:2152-2159.
5.
Schoenberg M, Treistschke F, Harada N, Beger H. - Benign tumor of the ampulla of Vater: surgical treatment and
prognosis. - Eur. J. Surg.1998; 164:765-770.
77
4. Gastric Cancer
The stomach is one of the most common sites of cancer in the digestive tract,
ranking second after colon and rectum. Gastric cancer mortality rates have remained
relatively unchanged over the past 30 years, and gastric cancer continues to be one of
the leading causes of cancer-related death.[1] 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 to 2-3 decades ago, the stomach cancer ranks first in the hierarchy of digestive
cancers before colorectal cancer. As knowledge about etiopathogenesis and treatment
methods developed, gastric cancer incidence decreased constantly. However, stomach
cancer was the fourth most common malignancy in the world in 2008, with an estimated
989,600 new cases. Approximately 72% of new cases occurred in developing countries.
Stomach cancer incidence rates vary widely across countries, ranging from less than
1/100,000 inhabitants in areas such as Botswana to about 62/100,000 in Korea for men
and from less than 1/100,000 in Botswana to about 26/100,000 in Guatemala for
women. In general, the highest incidence rates are in Asia (particularly in Korea, Japan,
and China) and many parts of South America, and the lowest rates are in North America
and most parts of Africa with the exception of Mali and Western Sahara.[2]
Age most affected is 50-60 years. Gastric cancer occurs rarely under the age of 30
and is two to three times more common in men than in women. After the age of 40,
there is a linear increase of carcinogenic risk. In United States the mean age at time of
diagnosis is 72 years, the lifetime risk of gastric cancer is approximately 1% and that of
dying from gastric cancer is 0.6%.[3]
Gastric cancer mortality, although decreasing, remains high. It is the third leading
cause of cancer death in men and the fifth leading cause in women. The disease
prognosis remains reserved and the 5-years survival rate in Europe is about 25%. In
Japan, the five-year relative survival has increased with 20% (up to 50% survival)
between 1975 and 1999.[2]
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:
1. Helicobacter pylori infection
2. Certain gastric diseases
3. Diet
4. Socio-economic conditions
Infection with Helicobacter pylori seems to increase the risk of gastric cancer by
three to six times, in association with gastric mucosal atrophy. More than 50% of new
stomach cancer cases are attributed to H. pylori infection.[4-7] H. pylori infection is
linked to gastric lymphomas and regression of such tumors often follows its
eradication.[8-10]
78
6. Previous gastric resection - Balfour was the first surgeon who in 1922 made
the correlation between gastric cancer and previous operations on the
stomach for benign diseases. Patients with distal gastric resection and/or
vagotomy (mostly for duodenal ulcer) in their history have a four to sevenfold greater risk of developing gastric cancer on the remaining stump, caused
by the duodenal-gastric reflux.[13-16] The average time between resection
and cancer onset is 20-25 years.
7. Gastroesophageal reflux disease (GERD) is doubling in the risk of gastric
cardia adenocarcinoma.[17] The risk of cardia cancer remains high even after
antireflux surgery.[18] People diagnosed with Barrett's esophagus have an
eighteen-fold risk of cancer.[19]
In 8% to 10% of cases, gastric cancers have an inherited familial component [20]
(Li-Fraumeni syndrome, hereditary nonpolyposis colon cancer, familial adenomatous
polyposis and Peutz-Jeghers syndrome).
Diet is considered a major factor in gastric cancer. This 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 foods have a
carcinogenic role compared to those preserved by cold. Smoked foods, salted meat or
fish and pickled vegetables are mostly incriminated. High fruit and vegetable intake is
associated with a reduced risk of gastric cancer. Mediterranean-style of diet reduces the
risk of gastric cancer.[21]
Smokers have a 50% to 60% increased risk for stomach cancer compared to
nonsmokers.[22-24]
Morphopathology
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 (Borrmanns classification 1926):
Type I: polypoid
Type II: fungoid
Type III: ulcerative
Type IV: infiltrative
Unclassifiable
A very common classification is that of Marson and Dawson:
Vegetative with variable extent, located mostly in the fundus and body of
stomach
79
o
o
o
o
o
o
A. Epithelial tumors
o carcinoma with signet ring cells
intraepithelial neoplasia -adenoma
o adenosquamuos carcinoma
carcinoma
o Adenocarcinoma (95%)
o squamous cell carcinoma
o small cell carcinoma
intestinal type
o undifferentiated carcinoma
80
o
o
o
C. Malignant lymphomas
cell lymphoma of MALT type marginal zone
mantle cell lymphoma
large cell lymphoma Diffuse B
D. Others
81
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 stomach 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 gastric openings. In
pyloric location vomiting appears late after food intake, whereas in case of cardial
location dysphagia is the main symptom and vomiting is manifested as regurgitation. In
evolution, vomiting becomes more frequent, and may contain dark digested blood in
small quantities. Upper gastro-intestinal bleeding is rarely massive and less important
than in peptic ulcer.
82
83
84
86
87
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47.
Lundegardh G, Adami HO, Helmick C, Zack M. - Risk of cancer following partial gastrectomy for benign ulcer disease.
- Br. J. Surg. 1994; 81:1164-1167.
91
5. Gastric Sarcomas
Sarcomas are malignant tumors of mesenchymal origin representing about 1-3%
of malignant tumors of the stomach, with an increased malignancy. The most frequent
way of spreading is via the blood vessels. They can be localized or diffuse, intra- or
extra-gastric, pedicled or sessile, fast growing and with high tendency to bleeding and
perforation. Gastric tissue sarcomas are classified by provenance in:
1. lymphomas
2. leiomyosarcomas
3. fibrosarcomas
4. neurosarcomas
5. angiosarcomas
Leiomyosarcomas represent 25% of all gastric sarcomas developing from
muscular gastric layers. Their location may be inside or outside the stomach and may
have a pedicle. During evolution, they ulcerate and bleed. Histologically consist of
elongated muscle cells with abundant cytoplasm with large nuclei. Symptoms depend
on location of tumor, its size and the presence of ulceration. Often is diagnosed during a
bleeding episode. Diagnosis is difficult because there are no pathognomonic signs. Even
endoscopic biopsy may be negative due to submucosal location of the tumor.
Fibrosarcomas develop from connective tissue within submucosa layer, where
otherwise they remain confined. They can be pedicled or sessile and large forms
become ulcerated. Histologically they are composed of elongated cells arranged in
plaques or of spherical and polygonal cells. The only effective treatment is surgical.
Malignant Schwannomas are rare, 90% of them being benign. They are
developed from nerve tissue and can take two forms of evolution: a very malignant one,
rapidly evolving and the other one with reduced malignancy that can get healing even
after simple excision.
Angiosarcomas have the starting point the blood vessels. Those typical are rarely
located in the stomach, and those atypical are represented by Kaposi's sarcoma and
hemangiopericytoma.
o Kaposi's sarcoma is characterized by the presence of multiple visceral lesions,
rarely gastric, preceded or followed by characteristic skin lesions. The
incidence is higher following renal transplantation and immunosuppression,
and in AIDS patients. When the lesion is present on the stomach, it appears as a
round ulcerated growth without affecting gastric peristalsis and without
stiffening the gastric wall. Frequently are hemorrhagic. Of more than 450
reported cases, only eight instances have been documented until 2002.[1] The
therapeutic approach to gastrointestinal bleeding includes injection therapy,
heat coagulation, sclerotherapy, H2 blocker, sucralfate, and general supportive
care. Surgical excision, angiographic embolization, and systemic chemotherapy
are also considered choices of treatments.[1]
o Hemangiopericytoma occurs as a proliferation of peripheral cells located in
the arteriovenous capillary network (Rougiet pericytes). Their appearance is of
tumors formed by clews of capillary outside the basement membrane,
sometimes forming hematic cysts on the stomach wall. Tumors betray their
presence by gastrointestinal bleeding. Treatment is surgical. Until 1995, only
29 cases were reported.[2]
92
Gastric Lymphoma
Gastric lymphoma can be primitive or secondary in a systemic disease (Hodgkin's
disease, Brill-Symmers disease) and may be reticulosarcoamas or lymphosarcomas.
However, the stomach is the most common extranodal site of lymphoma, representing
4-20% of all extranodal lymphomas [3] and the most common site in the gastrointestinal
tract.
Gastric lymphomas are encountered mostly at ages over 50 and two to three times
more frequently in males than in females.[4]
Morphopathology
Most gastric lymphomas are developing from the so-called mucosa-associated
lymphoid tissues (MALT), which usually develop after chronic inflammation induced,
by H. pylori infection. The association between H. pylori chronic gastritis and MALT
lymphoma has been confirmed in large population based studies.[5-7]
The origin of majority of gastric MALT lymphomas is the B-cells non-Hodgkins
type (NHLs). Other rare forms of gastric lymphomas are non-MALT type, and in rare
cases, tumors may be of T cell origin.
Grading has been classified into low, intermediate and high grade.
Macroscopically, tumors are large, developed primary in the submucosa layer. In
1/3 of cases, the lesions are larger than 10 cm at time of presentation. 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 gastric body or
there is a multifocal location.[8]
Risk factors:
o Helicobacter pylori
o Long-term immunosuppressant drug therapy
o HIV infection
Symptoms
In most patients symptoms are vague and nonspecific debuting with 4-10 months
prior the diagnosis. Upper abdominal pain and early satiety are the most common
symptoms. Other symptoms may be nausea, vomiting, weight loss, abdominal fullness,
night sweat, jaundice, fever and dysphagia. In advanced cases, hematemesis and melena
are present, manifested especially by occult bleeding and gastric obstruction.
Frequently the tumor is palpable in the epigastrium.
Diagnosis
Preoperative diagnosis of lymphoma is important because it allows an accurate
assessment of patients for staging with a high therapeutic importance.
The diagnosis can be established only by histological examination and
immunohistochemical staining of tissue samples, which are typically obtained by biopsy
at the time of endoscopy. Other possibility is the biopsy during the laparoscopic
exploration of the peritoneal cavity.
Imaging investigations such as CT scans and endoscopic ultrasound are useful to
stage disease. Thoracic X-ray examination, CT scan, MRI and ultrasound examination
permit assessment of nodal involvement located above and below the diaphragm, and
extension of the tumor outside the stomach.
An elevated LDH level may be suggestive of lymphoma.
93
94
Gastric Carcinoid
The original description of carcinoid tumors was made by Langhans, in 1867.
Gossett and Massion in 1914 showed the affinity of certain granules in the cytoplasm of
the cells for silver salts. These were designated argentaffin cells and hence the lesions
were called argentaffinomas.[10] The term "carcinoid" was introduced by Oberndorfer
[11] first in 1907 and in 1923 Askanazy [12] reported the first gastric carcinoid.[13]
Carcinoid tumors are neuroendocrine tumors developed from fundal
enterochromaffin-like (ECL) cells of Kulchitsky, which are considered neural crest cells
situated at the base of the crypts of Lieberkuhn's glands. They either develop as a result
of chronic stimulation of enterochromaffin like cells by high concentrations of serum
gastrin or may occur sporadically.[14-16]
Epidemiology
The incidence of gastric carcinoid tumors have steadily increased over the last 50
years from 0.3% to 1.8% among all gastric cancers representing 8.7% of all enteric
carcinoids.[17] Reasons of this situation may be the improvement of diagnostic
procedures and the increasingly use of gastric acid inhibitors that induces higher levels
of gastrin secretion.
Gastric carcinoid can occur at any age between 20 and 90 years, being
encountered with a slightly higher frequency in women compared to men.
The occurrence of carcinoid tumors of clinical importance according to the
location of origin: [18]
28.5% small intestine
5% appendix
14% rectum
28% bronchial system of the lungs
5-7% colon
4% stomach
1% pancreas
>1% liver
8% other
Symptoms
Patients with gastric carcinoid tumors have nonspecific symptoms represented by
pain or a palpable abdominal mass. These types of tumors secret serotonin and other
histamine like substances being able to induce the carcinoid syndrome when the level of
secreted serotonin and histamine exceeds the metabolizing capacity of monoamine
oxidase present in the liver and lung.[10] Over 85% of patients are asymptomatic and
only 10% present carcinoid syndrome manifested primarily by transient erythema and
diarrhea.
Classification of gastric carcinoid tumors: [19,20]
Type I (75%) - Associated with chronic atrophic gastritis with or without
pernicious anemia. In autoimmune gastritis, a progressive destruction of
parietal cells leads to atrophy, intestinal metaplasia, and hypergastrinemia.
95
Cheng-Hui Lin, Chao-Wei Hsu, Yan-Jen Chiang, Kwai-Fong Ng - Cheng-Tang Chiu, MD. - Esophageal and Gastric
Kaposi's Sarcomas Presenting as Upper Gastrointestinal Bleeding- Chang Gung Med. J. 2002; 25(5).
http://memo.cgu.edu.tw/cgmj/2505/250506.pdf
2.
Guadagni S, Gianfelice F, Pistoia MA, et al. - A case of gastric hemangiopericytoma. - Minerva Chir. 1995; 50(7-8):693698.
96
Al-Akwaa AM, Siddiqui N, Al-Mofleh IA. - Primary gastric lymphoma. - World J. Gastroenterol. 2004; 10(1):5-11.
http://www.wjgnet.com/1007-9327/10/5.asp
4.
Danzon A, Belot A, Maynadi M, Remontet L, Dupont AC, Carbonnel F. - Incidence and survival of gastric nonHodgkin's lymphoma: a population-based study from the Association of the French Cancer Registries (FRANCIM). Acta Oncol. 2009; 48(7):977-983.
5.
Farinha P, Gascoyne RD. - Helicobacter pylori and MALT lymphoma. - Gastroenterology 2005; 128:1579-1605.
6.
Montalban C, Norman F. - Treatment of gastric mucosa associated lymphoid tissue lymphoma: Helicobacter pylori
eradication and beyond. - Expert Rev. Anticancer Ther. 2006; 6:361-371.
7.
Parsonnet J, Hansen S, Rodriguez L, et al. - Helicobacter pylori infection and gastric lymphoma. - N. Engl. J. Med, 1994;
330 (18):1267-1271.
8.
Kitamura K, Yamaguchi T, Okamoto K, Ichikawa D, Hoshima M, Taniguchi H, Takahashi T. - Early gastric lymphoma:
a clinicopathologic study of ten patients, literature review, and comparison with early gastric adenocarcinoma. - Cancer.
1996; 77(5):850-857.
9.
Speranza V, Lomanto D. - Primary gastric lymphoma.- Surgical Treatment: Evidence-Based and Problem-Oriented.
Holzheimer RG, Mannick JA, editors. Munich: Zuckschwerdt; 2001. http://www.ncbi.nlm.nih.gov/books/NBK6966/
10. Kaur S, Goyal R, Juneja H, Sood N, Bajaj P. - Carcinoid Of The Stomach -A Rare Tumour. - Ind. J. Radiol. Imag. 2006;
16(4):545-547.
11. Oberndorfer S. - Karzinoide Tumoren des Dunndarms. - Frankf. Z. Pathol. 1907; 1:425-429.
12. Askanazy M. - Zur Pathogenese der Magen-krebse und uber inhren gelegentlichen Ursprung aus angeboren epithelialen
Keimen in der Magenwand. - Dtsch. Med. Wochenschr. 1923; 49:49-51.
13. Abby Mulkeen, Charles Cha - Gastric carcinoid. - Curr. Opin. Oncol. 17:1-6. 2004 Lippincott Williams & Wilkins.
14. Berger MW, Stephens HD. - Gastric carcinoid tumors associated with chronic hypergastrinemia in a patient with
Zollinger - Ellison syndrome. - Radiology 1996; 201:371-373.
15. Hkanson R, Sundler F. - Proposed mechanism of induction of gastric carcinoids: the gastrin hypothesis. - Eur. J. Clin.
Invest. 1990; 20 Suppl 1:S65-71.
16. Solcia E, Rindi G, Silini E, Villani L. - Enterochromaffin-like (ECL) cells and their growths: relationships to gastrin,
reduced acid secretion and gastritis. - Baillieres Clin. Gastroenterol. 1993; 7(1):149-165.
17. Modlin IM, Lye KD, Kidd M. - A 50-year analysis of 562 gastric carcinoids: small tumor or larger problem? - Am. J.
Gastroenterol. 2004; 99(1):23-32.
18. A Review of Carcinoid Cancer - July 2012 (updated) - http://www.carcinoid.org/content/review-carcinoid-cancer
19. Rindi G, Luinetti O, Cornaggia M, et al. - 3 Subtypes of gastric argyrophil carcinoid and the gastric neuroendocrine
carcinoma a clinicopathological study.- Gastroenterology 1993; 104:994-1006.
20. Kloppel G, Anlauf M. - Epidemiology, tumour biology and histopathological classification of neuroendocrine tumours of
the gastrointestinal tract. - Best Pract. Res. Clin. Gastroenterol. 2005; 19:507-517.
21. Gergics P, Dabasi G, Csoregh E, et al. - Regression of metastatic gastric carcinoid associated with atrophic gastritis and
after octreotid treatment. - European Congress of Endocrinology 2007, Budapest, Hungary, Endocrine Abstracts;
(2007)14:485.
22. Odashima M, Otaka M, Jin M, Horikawa Y, Matsuhashi T, Ohba R, Mimori N, Koizumi S, Kinoshita N, Takahashi T,
Watanabe S. - Rapid Regression of Multiple Gastric Carcinoid Tumors with Hypergastrinemia and Atrophic Gastritis
after Renal Transplantation. - Dig. Dis Sci. 2008; 53(3):865-866.
23. Kurt Borch, Bo Ahrn, Hkan Ahlman, Sture Falkmer, Gran Granrus, Lars Grimelius - Gastric Carcinoids Biologic
Behavior and Prognosis After Differentiated Treatment in Relation to Type. - Ann. Surg. 2005; 242(1):64-73.
24. Kvols LK, Moertel CG, OConnell MJ, Schutt AJ, Rubin J, Hahn RG. - Treatment of the malignant carcinoid syndrome:
evaluation of a long-acting somatostatin analogue. - N. Engl. J. Med.1986; 315:663-666.
25. Kvols LK. - Metastatic carcinoid tumors and the malignant carcinoid syndrome. - Ann. N. Y. Acad. Sci.1994; 733:464470.
26. Modlin IM, Kidd M, Latich I, Zikusoka MN, Shapiro MD. - Current Status of Gastrointestinal Carcinoids. Gastroenterology 2005; 128:1717-1751.
27. Adachi Y, Shiraishi N, Kitano S. - Modern treatment of early gastric cancer: review of the Japanese experience. - Dig.
Surg. 2002; 19:333-339.
97
6. Gastric Volvulus
Gastric volvulus means partial or complete twisting of the stomach around of its
one axis. (Figure 40) The most frequently used classification is that proposed by
Singleton: [1]
1. Organoaxial (59% of cases)
2. Mesentericoaxial (29% of cases) and
3. Combined
Another classification:
1. Subdiaphragmatic, or primary (one
third of all cases) which is not
associated with diaphragmatic defects,
and
2. Supradiaphragmatic, or secondary,
associated with diaphragmatic defects.
The degree of twisting varies between 180 degree and 360 degree.
Consequences of this twisting are:
1. Variable loss of blood supply (ischemia) and possible gastric wall necrosis,
and
2. Gastric occlusion
According to etiology, gastric volvulus can be classified as:
1. type 1 - idiopathic, or
2. type 2 - congenital or acquired
Etiology
Determinant factors:
1. Excessive laxity of the stomach fixing ligaments
2. Hiatal hernias - gastric volvulus is the most common complication of
paraesophageal hernias
3. Gastric adhesions
4. Other rare causes
Contributory factors:
1. Increased intragastric pressure by intrinsic or extrinsic benign or malignant
obstacles
2. Motility disorders of the stomach
3. Low insertion of esogastric junction
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 symptoms.
In cases of acute onset, symptoms are of an acute surgical abdomen, with rapid
progress to shock. In these cases, Borchardt describes the clinical triad:
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
Intra-abdominal gastric volvulus manifests as a sudden severe epigastric or left
upper quadrant pain. Intra-thoracic gastric volvulus manifests as sharp chest pain
radiating to the left side of the neck, shoulder, arms, and back.[2]
98
99
2.
3.
Tanner NC. - Chronic and recurrent volvulus of the stomach with late results of "colonic displacement". - Am. J. Surg.
1968; 115(4):505-515.
4.
Palanivelu C, Rangarajan M, Shetty AR, Senthilkumar R. - Laparoscopic suture gastropexy for gastric volvulus: a report
of 14 cases. - Surg. Endosc. 2007; 21(6):863-866.
5.
Katkhouda N, Mavor E, Achanta K, Friedlander MH, Grant SW, Essani R, et al. - Laparoscopic repair of chronic
intrathoracic gastric volvulus. - Surgery. 2000; 128(5):784-790.
100
7. Postgastrectomy Syndromes
Under this generic name, a number of specific late complications affecting 20%
of patients after gastric surgery are gathered. Vagotomy and ablation or bypass of the
pylorus are the most significant factors contributing to postgastrectomy syndromes.[1]
Gastric surgery may result in mechanical and functional disorders by two
mechanisms:
1. Mechanical disorders of digestive transit are represented by: stenosis,
efferent or afferent loop syndrome, bilio-gastric or esophageal reflux, all of
which are relatively easy to correct by surgical procedures.
2. Functional disorders, occurring in patients who received the correct surgery
but cannot 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: [2]
Esophageal
2. Dumping syndrome
1. Gastroesophageal reflux
3. Bacterial contamination
2. Dysphagia
syndrome
Gastric
4. Pancreatic insufficiency,
1. Delayed gastric
celiac disease, lactase
emptying
deficiency
2. Bezoars
5. Weight loss and
3. Anastomosis stenosis
malabsorption of:
4. Stoma inflammation
1. Metals
5. Gastric stump gastritis
2. Folic Acid
6. Recurrent peptic ulcer
3. Vitamin B12
7. Gastric stump cancer
4. Calcium
8. Afferent loop syndrome
5. Fats
9. Efferent loop syndrome
6. Anemia
Small intestine
Gall bladder
1. Postvagotomy diarrhea
1. Gallstones
All these conditions occurring late after gastric surgery have some common
characteristics:
Most cases occur after operations for duodenal ulcer
The condition is not influenced by the stage of the initial disease for what the
patient was operated
Disturbances are more intense when surgery produced profound
modification of the regional anatomy
Many postoperative complaints are often associated, and may be represented
by local, general or mixed symptoms
A. Functional disorders of the esogastric junction
Reflux esophagitis is caused by the alteration of the antireflux mechanisms at
level of cardia, followed by reflux of the gastric content into the esophagus and
consecutive esophagitis. This complication can occur after:
Surgical interventions that remove the cardia such as upper and total
gastrectomy,
Lower gastric resections because the Hiss angle becomes widened or is
abolished,
101
Any other gastric surgery after which the stomach evacuation is impaired.
The onset of symptoms may be rapid or after a period up to 5 years after surgery.
The clinical picture is dominated by heartburn, acid or bilious regurgitation, belching.
Initially, symptoms have a postural character appearing mainly in supine position. Then,
symptoms become permanent caused by local morphological changes of the reflux
esophagitis, and can be associated with anemia and dysphagia subsequent to repeated
bleeding and esophageal stenosis.
Diagnosis is based on radiological examination including Trendelemburg
position, endoscopic examination, manometry of the esophagus and pH-measurements.
Treatment may be prophylactic and curative. Surgical prophylaxis of esophagitis
should be performed during the primary operation.[3] Prophylaxis means a correct
surgical technique avoiding unnecessary detachments and mobilization of the stomach
during distal resection and vagotomy. Another method to prevent biliopancreatic
content of the duodenum to reach up into the esophagus is to remove the duodenum
from the normal digestive route, aim that can be achieved by restoring the digestive
tract after gastric resection using a gastro-jejunal anastomosis, either with a Roux-en-Y
loop or with an omega loop with Braun fistula. Curative surgery is indicated when
symptoms are severe and do not respond to usual therapeutic methods (postural
drainage, antisecretory drugs, etc.). The surgical procedure depends on the previous
operation. After inferior gastric resection, a fundoplication can be performed or the
gastroduodenal anastomosis is transformed into a gastrojejunal anastomosis using a
Roux-en-Y intestinal loop. If the initial operation was a superior gastric resection,
possible alternatives are pylorotomy and antro-jejunostomy with a Roux-en-Y loop.
After total gastrectomy, the aim is to divert the duodenal content far away from the
ascending intestinal loop that goes to the esophagus and the procedure depends on what
kind of montage was used initially.
Early postoperative dysphagia is usually caused by intraoperative trauma of the
esophagus and periesophageal hematoma. Causes of late postoperative dysphagia are
esophagitis and esophageal anastomotic stenosis.
B. Anastomosis disorders
In this category are included late complications resulting from inflammatory
reactions present at site of anastomosis and clinically manifested by superior digestive
bleedings and occlusive phenomena.
Gastritis is the inflammation of the gastric stump generally caused by duodenogastric reflux. The pathogenesis may be represented by either chemical alkaline
irritation or microbial colonization of the gastric mucosa. Morphological aspects can be
hypertrophic or atrophic gastritis or even ulcerative gastritis. Symptoms are represented
by pain, belching, and vomiting, postprandial fullness and in about 20% of cases by
upper gastrointestinal bleeding. The diagnosis is established by endoscopy, which
reveals the edematous mucosa with hyperemia or ulcers. Treatment in most cases is
conservative using medication. Severe bleedings that cannot be resolved by medication
or endoscopic procedures require a surgical solution. This consists in either a total
gastrectomy or other different kinds of gastrojejunal montages (Roux-en-Y
gastrojejunostomy) accompanied by vagotomy.[4,5]
Anastomotic inflammation is caused, in many cases, by nonabsorbable sutures.
A reject type reaction appears around the suture threads with ulceration of the mucosa
or even polypoid mucosal hypertrophy that can interfere with the flow through the
102
103
105
106
Eagon JC, Miedema BW, Kelly KA. - Postgastrectomy syndromes. - Surg. Clin. North. Am. - 1992; 72(2):445-465.
2.
3.
Ermolov AS, Dzhumabaev SU, Urinov AIa, Kharitonov LG. - Postoperative reflux esophagitis and its sequelae. - Vestn.
Khir. Im. I. I. Grek. 1994; 152(5-6):33-35.
4.
Van Heerden JA, Phillips SF, Adson MA, McIlrath DC. - Postoperative reflux gastritis. - Am. J. Surg. 1975; 129(1):8288.
5.
Sawyers JL, Herrington JL Jr, Buckspan GS. - Remedial operation for alkaline reflux gastritis and associated
postgastrectomy syndromes. - Arch. Surg. 1980; 115(4):519-524.
6.
John G. Kral - Effects of truncal vagotomy on body weight and hyperinsulinemia in morbid obesity. -Am. J. Clin. Nutr.
1980; 33:416-419.
7.
Deller DJ, Witts LJ. - Changes in the blood after partial gastrectomy with special reference to vitamin B12. I. Serum
vitamin B12, haemoglobin, serum iron, and bone marrow. - Q. J. Med.1962; 31:71-88.
8.
Miwa H, Sakaki N, Sugano K, et al. - Recurrent peptic ulcers in patients following successful Helicobacter pylori
eradication: a multicenter study of 4940 patients. - Helicobacter. 2004; 9(1):9-16.
9.
Stabile BE, Passaro E Jr. - Recurrent peptic ulcer. - Gastroenterology, 1976; 70(1):124-135.
10.
Turnage RH, Sarosi G, Cryer B, Spechler S, Peterson W, Feldman M. - Evaluation and management of patients with
recurrent peptic ulcer disease after acid-reducing operations: a systematic review. - Journal of Gastrointestinal Surgery,
2003; 7(5):606-626.
11.
Setlacec D, Popovici A, Medianu D, Horvat T. - Recurrent postoperative ulcer. - Revista de Chirurgie Oncologie
Radiologie ORL. Oftalmologie Stomatologie Chirurgie, 1981; 30(5):351-364.
107
108
Bariatric Surgery
BARIATRIC SURGERY
The word "Bariatric" was derived from a Greek word Baros meaning heavy
and Iotrics meaning medical treatment.
Bariatric surgery, or obesity surgery, includes several surgical procedures applied
to obese patients to lose weight and thereby improve their health condition. This kind of
surgery is not applied for aesthetic reasons.
Even though obesity is not a primary disease of the digestive system, this topic is
included in this volume because the vast majority of bariatric surgical procedures are
applied on the stomach.
Obesity
Background
Body weight is a feature that determines the individual physical appearance,
mental health, and quality of life.
Obesity is currently defined as an excess accumulation of body fat so that it can
affect the health. Obesity is the result of a positive energy balance protracted over time,
due to an increase in caloric supply and/or a decrease in caloric expenditure.[1]
Humans have been described as being among the fattest of all mammals.[2] In
fact, mammals embrace a wide range (1%-45%) of body mass across a wide range of
body size, and humans from pre-industrial societies are lying roughly within the middle
of the range for their weight.[3]
The ability to accumulate energy reserves, as fat in conditions of abundant food
was an evolutionary advantage necessary for survival in conditions of insufficient or
lack of food, so the chance of survival of obese individuals was higher during famine.
This tendency to store fat, however, is inadequate in today's developed societies, which
ensure a stable food supply.
From other point of view, we must not forget that until recently, obesity was
considered as a sign of distinction. Relevant are the paintings of Rubens, and other
artists, where overweight is the symbol of beauty. Opinion about obesity in nowadays,
has changed radically, not only from aesthetical point of view, but from medical as well.
Today is a certain relationship between obesity and diseases with the highest
mortality rate such as cardiovascular diseases, dyslipidemia, diabetes etc. Thus, 85-95%
of diabetics have been or are obese and over 60% of dyslipidemia patients are obese.
Obesity is rather a health problem then a problem of image. It becomes a major
cause of morbidity and mortality through diverse diseases (cardiovascular disease
diabetes and joint pain, etc.).
Obesity, first emerged as a major public health problem in western populations,
but rapidly has spread to countries undergoing nutritional transition and became the
primary global nutritional problem.[4] In the last decade, obesity and overweight have
become a global problem - according to the World Health Organization (WHO), back in
2005, approximately 1.6 billion adults over the age of 15 were overweight, at least 400
million adults were obese and at least 20 million children under the age of 5 years were
overweight. Experts believe that if the current trends continue by 2015, approximately
2.3 billion adults will be overweight and more than 700 million will be obese. The
109
Bariatric Surgery
extent of the obesity problem causes serious consequences for individuals and
government health systems.
Formulas to establish the degree of obesity and risk of associated illnesses
Classically, obesity was considered as being the overcoming of the ideal weight
by 15 - 20% calculated after the Brocas index (Weight=Height-100). A more exact
formula to calculate the ideal weight was introduced by Lorentz in 1029:
Weight = Height - 100 [(Height - 150) x 0.25]
The formula is complicated and therefore not much used in practice.
Nowadays, the most commonly used is the Body Mass Index (BMI), for
classifying people's weight relative to an ideal weight for their height. Adolphe Quetelet
was who proposed this index formula and it was termed the Body Mass Index in 1972
by Ancel Keys.[5]
110
Bariatric Surgery
Waist-to-hip ratio is an index which provides information on fat distribution, and
it seems to correlate better than BMI with cardiovascular risk.[11] It is used mainly to
classify obesity as gynoid (gluteo-femoral type) or android (abdominal type). (Figure 2)
Persons with abdominal obesity, "apple-shaped", are at higher risk of metabolic and
cardiovascular diseases than those with "pear-shaped" bodies who carry more weight
around the hips.
Based on the index there are two clinical forms of obesity: gynoid and android.
Gynoid type obesity (Rubensian type) is seen more frequently in women, but it
can occur in male adults and children of both sexes. Skeletal muscles are poorly
developed, and adipose tissue is localized in the lower parts of the body, the lower
abdomen, flanks, hips, thighs, knees, calves. Patient moves with difficulty, tiring easily
and quickly gain weight. Consumes fewer calories, but weakens hard. Complications
such as respiratory, heart, bones, muscles, etc., occur rapidly. Some forms retain more
water and salt and do not respond to diet or diuretic therapy. A special form is the
Dercum cellulite, in which body fat infiltration is painful (adiposis dolorosa) and it has a
hereditary character.
Android type obesity (Falstaff type - Sir John Falstaff is a fictional character who
appears in three plays by William Shakespeare as a companion to Prince Hal, the
future King Henry V.) is found more frequently in men. Adipose tissue develops in the
upper part of the body, neck, shoulders, upper abdomen. The musculature is strong and
adipose tissue less developed than in the previous form. These, are people who always
complain of hunger and they eat more. Complications such diabetes, hyperuricemia,
dyslipidemia and atherosclerosis are the most frequent.
None of the formulas presented so far indicate, in fact, what is the percentage of
fat in the body. A more precise and individualized way to determine the ideal weight is
a test to assess the percentage of fat in the body. Fat percentage is an index that takes
into account that body fat percentage is generally 10% higher in women for the same
BMI and that body fat percentage is higher at more advanced ages even if weight
remains the same. Test accuracy is 4%. Formula is:
Fat % = 1.2 * BMI + 0.23 * age 5.4 10.8 * sex (where, sex =0 for woman and
sex=1 for man) The higher the fat percentage, the higher the risk of metabolic diseases.
(Table 2)
Table 2 Risk category according to fat percentage
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
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Utility of obesity indexes. Formulas represent the foundation for medical interventions
and nutrition in obesity. There are situations when medical interventions are
significantly based on these formulas: for example the decision to establish an enteral
nutrition, can objectively be sustained by calculating an index called Buzby. Body mass
index is used in some protocols as a landmark in establishing therapeutic attitudes (for
example, most surgeons do not perform obesity surgery for MBI below 40). Nutritional
risk index, called index Buzby, is used to stratify degrees of nutritional state of the
patient. The formula is: NRI (Nutritional Risk Index) = 1.519 x serum albumin (g / l) +
41.7 x (current weight / usual weight). The interpretation is:
1. NRI 97.5: no denutrition
2. NRI 83.5 - 97.5: moderate denutrition
3. NRI 83.5: severe denutrition
Dysmetabolic Syndrome
The metabolic syndrome is a cluster of the most dangerous heart attack risk
factors: diabetes and elevated fasting plasma glucose, abdominal obesity, high
cholesterol and high blood pressure.[12,13] Recently, the IDF (International Diabetes
Federation) issued a new set of criteria definition focusing on abdominal obesity as a
mandatory element of the syndrome. Dysmetabolic syndrome is represented by:
Abdominal obesity (defined by abdominal circumference > 94 cm for European
men and > 80 cm for European women - for other specific ethnic values, see the source
document) plus at least two of the four elements listed 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>130 mmHg or diastolic> 85 mmHg), or
treatment for previously diagnosed hypertension,
4. Elevated fasting glucose level (>100 mg/dL), or previously diagnosed type 2
diabetes.
Anatomy of the adipose tissue
Since childhood, there is a difference in terms of body fat and its distribution
between the two sexes prevailing in girls. Differences are maintained in terms of the
number of adipocytes (fat cells), which is higher in women. The number of fat cells
once established (possibly hereditary), remains permanently. The ratio between the
number and volume of fat cells causes two types of obesity: a form of hypertrophic
and another of hyperplastic obesity. Certain hormones also affect the body distribution
of fat. Androgen (testosterone) and glucocorticoids determine a prevalent distribution of
fat in the upper part of the body (android obesity) whereas the estrogen in the lower part
(gynoid obesity).
Hyperplastic obesity is represented by an 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 occurs in adults caused by reduced physical activity
without a proportional reduction of food intake. With age, physical activity
reduces and the caloric surplus is turned into triglyceride reserves, increasing
the volume of adipocytes.
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Besides hyperplastic and hypertrophic obesity, there are the mixed forms of
obesity, which associate an increased number of adipocytes with an increase in volume
that occurs at any time during life. It is more common in women.
Losing weight means lowering the volume, not the number of adipocytes, which
is a fixed value.
Adipose tissue is not an inert tissue; it regulates the uptake of fatty acids and
circulating triglycerides, the endogenous synthesis of glycerides starting from glucose,
the catabolism of fatty acids, the release of fatty acid into circulation, etc.
Regarding the feelings of hunger and satiety, regulation is done by:
Glucose (hunger during hypoglycemia and sensation of fullness during
hyperglycemia)
Digestive factors (glucose entering the duodenum is followed by a decrease
in hunger)
Neurological factors that act on the hypothalamus and cortex. Endogenous
obesity is the expression of a neuroendocrine disease.
Body fat is classified as:
1. Subcutaneous fat, and
2. Visceral (intra-abdominal or central fat)
In women the amount of fat is higher (about 1/5) but is mainly subcutaneous and
less visceral than in males. 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).
Problems arise when the fat exceeds a certain amount and constant release too
many fatty acids in portal circulation. As a consequence, hyperinsulinemia occurs
preventing normal suppression of glucose release from the liver and causing insulin
resistance (type 2 diabetes), increase of triglycerides and high-density lipoprotein
suppression (HDL) - See metabolic syndrome.
Epidemiology
Obesity is a problem that currently affects civilized world, where 25% to 50% of
population suffers from overweight or obesity.[14] (Figure 3) It is a medical and social
problem, reaching epidemic proportions worldwide. In 2008, more than 1.4 billion
adults, 20 years and older, were overweight. Of these, over 200 million men and nearly
300 million women were obese. More than 40 million children under the age of five
were overweight in 2010. Obesity medical costs account for 2-7% of total medical costs
in developed countries.[15]
In USA, 65% of adults are overweight or obese, and obesity represents the second
cause of preventable death. Direct health costs attributable to obesity have been
estimated to $52 billion in 1995 and $75 billion in 2003.[16]
It is generally believed that overweight is less prevalent than undernutrition in the
developing world, particularly in rural areas, and that it is concentrated in higher
socioeconomic status (SES) groups.
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The highest rate of obesity has been reported in the Pacific Islands and the lowest
rates have been seen in Asia. The rates in Europe and North American are generally
high, while the rates in Africa and Middle Eastern countries are variable.[17,18]
Obesity etiology
The vast majority of authors agree that the positive energy balance between
excessive food intake and reduced energy expenditure is the primary cause of obesity.
In a small number of cases, the high consumption of foods is due to genetic, medical, or
psychiatric disorders. Obesity is caused by a complex interaction between the
environment, genetic predisposition, and human behavior. The main causing factors are:
1. Diet
2. Lifestyle
3. Genetic factors
4. Socioeconomic factors
5. Medical and psychiatric diseases
6. Intestinal flora
7. Others
Diet is the principal factor in the development of obesity. It acts through the
composition of the macronutrients and eating behavior. Nutrients with high calorie
count per gram affect the accumulation of excess energy; fats are deposited in the
adipose tissue with about 96% efficiency. Food taste is also important; it is easy to eat
too much palatable foods.
Eating behavior: eating disorders such as consumption of large quantities of food
but not very frequently or excessive consumption in the late afternoon or evening
(night eating syndrome) predispose to obesity.[1,19]
Physical activity: this is the most variable element of the energy balance,
representing from 20 to 50% of the total energy expenditure. In western countries, there
is a close correlation between low levels of physical activity and obesity. The risk of
obesity is more than 5 times greater in children who watch television for five hours or
more per day, compared to those who watch it for less than two hours.[20]
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Social influences: population studies confirm the influence of the society in
which we live on the development of obesity. The body weight trend differs greatly
between people who emigrate to rich, western societies and those with the same genetic
patrimony who remain in their conditions of origin. There is a tendency to gain weight
after marriage and as parity increases. Environmental factors are a very important
component in the genesis of the behaviors that aid excess weight and are among those
called into question to explain the global epidemic obesity.
Genetic factors seem to be important having a role equal to 40% of cases.[1] The
ascertainment that obesity is present in entire families could appear to prove the genetic
hypothesis. Up to now, researchers verified about forty genes or loci in different
chromosomes apparently linked to the obese phenotype or, in any case, connected to the
amount of adipose tissue. The main genetic syndromes associated with obesity are the
'Trader-Willi syndrome" and the "Laurence-Moon-Bardet-Biedl syndrome" but other 25
conditions that associate obesity with genetic mutations have been described.
Educational level: the incidence of obesity is significantly greater in persons with
an elementary level of education or no formal education compared to graduates (15.4%
against 4.4%).[1,21,22]
Other factors
Easy access to palatable foods
Car culture
Mechanized manufacturing
Insufficient sleep
Psychological factors, meaning refuge in food satisfaction after a failure or
different emotional delusions
Endocrine disorders, which interfere with lipid metabolism
Decreased variations in ambient temperature
Lowering the percentage of smokers (smoking reduces appetite)
Excess of drugs that can lead to weight gain
Pregnancy in advanced ages
Positive natural selection of individuals with higher BMI
Expanding distribution of ethnic groups and other population groups that
tend to obesity
Associative tendency of obese people (marriages, etc.)
Neurobiological mechanisms implicated in obesity
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., have
been 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 resistance
developed against this mediator. Leptin acts on the arcuate nucleus of the hypothalamus
so that the deficiency or resistance to this mediator leads to overeating, and represents
possible mechanism in some genetic or acquired forms of obesity.
Ghrelin is a 28 amino acid peptide hormone, structurally similar to motilin,
produced mainly by the stomach and, to a lesser degree, by other tissues.[23,24] Its
activity is mediated by the growth hormone (GH) activating the GH-secretagogue
(GHSla) receptors which are concentrated at the hypothalamic-hypophyseal level.[25]
Ghrelin also has many other endocrine effects. Ghrelin, unlike leptin has an orexic
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effect. The body weight gain caused by ghrelin is due to an increase in fat mass without
changes in skeletal musculature.[26]
Consequences of obesity:
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
21.
22.
23.
24.
25.
26.
27.
Headaches
Swelling of the legs
Varicose veins
Hemorrhoids
Chronic gastritis
Reflux esophagitis
Nervous system disorders: insomnia,
increased appetite for food, increased
thirst, vegetative disorders
Impaired potency
Affecting the menstrual cycle
Infertility (female extra pounds, make
the pregnancy difficult and sometimes
causes abortions)
Hydro-saline metabolism disorders
Complications after infectious diseases
Susceptibility to pneumonia
Recommendations:
Obese patients should be evaluated by a medical specialist (because obesity should be
considered a disease) to provide necessary and relevant information, to make the right
choice of treatment.
Available methods in treating the obesity and its consequences are:[27,28]
Diet - Reduce caloric intake by 500 to 1,000 kcal per day to produce a
weight loss of 1 to 2 lb per week. Whatever diet is recommended, do not
forget that what matters are calories! (1200 kcal/day for women and 1500
kcal/day for men are considered as normal intake). Nutritional needs should
take into account the individuals age, sex, height. The diet should last about
six months. Then, follows a period of 12-18 months, in which the loss should
be maintained. Only after that, a new diet starts again. To combat obesity
both, dietary and behavior attitude toward the physical activity should be
changed. Food should provide the principal nutrients, but also trace elements
(Ca, Mg, Na, K, etc.) and vitamins. Usually it is a mild hypocaloric diet,
with reduced fat (especially saturated fat) and salt, rich in fiber.
Physical activity - Obese patients should start with moderate levels of
physical activity (e.g., brisk walking) for 30 to 45 minutes, three to five days
per week. All patients should accumulate at least 30 minutes or more of
moderate intensity physical activity on most, and preferably, all days of the
week.
Changing lifestyle - Use multiple strategies (e.g., combine cognitive
restructuring, self-monitoring, social support, stimulus control and stress
management).
SPA
Alternative medicine (acupuncture)
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therapy of obesity: diet and behavior modification, physical activity and
pharmacotherapy.
Evaluation of the subject requires the assessment of the degree of weight gain, the
level of health risk and the entity of the motivation to lose weight. The following points
should be considered:[1]
the reasons that inspire weight loss,
the history of previous attempts, whether successful or not,
the presence of support from family, friends and in the work
environment,
the subject's knowledge about the causes of obesity,
the attitude towards physical activity,
the ability to engage in physical activities,
the availability of time for treatment,
economic considerations.
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 is
scientific evidences regarding mortality reduction.
Effects of bariatric surgery on the main endocrine and metabolic alterations
caused by obesity. The majority of data in the literature concerns insulin. In fact,
bariatric surgery significantly reduces insulin resistance, insulin secretion and the
connected alterations in glucose tolerance and lipid metabolism, most likely because of
the reduction in adipose mass. It is also believed that weight loss re-establishes normal
GH secretion in the obese person.
Conditions for the best result of bariatric surgery are:
1. Surgery should be performed by an experienced surgeon who works in a
suitable environment
2. Hospital environment must ensure a multidisciplinary pre-and postoperative
approach, with postoperative follow-up for life
3. The patient must be well informed, highly motivated and with minimal
operative risks
4. Patient selection must be made by a multidisciplinary team internist,
endocrinologist, surgeon, psychiatrist and nutritionist
5. Postoperative dietary supervision is required.
Surgical procedures may be:
Restrictive - reduce the food intake. The role of gastric resection is to induce
early satiety, to limit the food intake and so inducing the weight loss. Restrictive
procedures are:
o 1. Intragastric balloon
o 2. Gastric banding
o 3. Vertical banded gastroplasty
o 4. Gastric sleeve
Malabsorptive - reduce food absorption surface in terms of food consumption
almost unchanged. Weight loss is based on fat and protein malabsorption. These
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procedures improve lipid status and glucose control in patients with
dyslipidemia and diabetes. On the other hand, it may produce Iron (Fe)
deficiency anemia, deficiency of fat-soluble vitamins (A, D, E, K), bone
demineralization and very smelly flatulence due to steatorrhea.
Mixed procedures - restrictive and malabsorptive
o 5. Gastric bypass
o 6. Biliopancreatic diversion (Scopinaro)
o 7. Duodenal switch (Marceau)
All these procedures (except intragastric balloon, which is an endoscopic
procedure) can be performed by open surgery or laparoscopic approach, but almost all
cases are performed in nowadays by laparoscopic approach due to its well-known
advantages, being a minimal invasive procedure.
1. Intragastric balloon procedure (Figure 4)
The procedure is based on lowering the stomach capacity after introducing of a
foreign body (balloon) into the stomach that induces thus the feeling of fullness. The
first experiences were performed in the 80s, but the results were disappointing due
complications. In 1986, Gau introduced the use of a silicone
balloon that could be inflated with saline solution, this
technique being used in nowadays. The procedure is
reversible.
The balloon is placed endoscopically into the stomach
and filled with saline dyed with methylene blue. About 400700 ml of solution is introduced, the balloon occupying about
40% of stomach capacity. Antisecretory medication is
associated. The balloon must be removed after a maximum
period of six months. Unfortunately, after removal, the lost
weight is generally regained. The weight loss is 25%-40% of extra pounds.
The procedure can be useful for preparing the patient for a later bariatric surgery,
reducing the anesthesiological and surgical risk thanks to the achieved weight loss.
Contraindications of the procedure are:
previous surgery on the stomach
severe esophagitis or gastritis
peptic ulcer
hiatal hernia >5 cm
hemorrhagic diathesis
drug or alcohol addiction
treatment with anticoagulants or cortisone
pregnancy
psychiatric disorders
Possible complications are nausea and vomiting, colicky pains, gastric ulceration
and perforation, bowel occlusion due to balloon disinflation and balloon rupture.
2. Gastric banding (Figure 5) is also a gastric restrictive procedure, which may be
reversible. It is performed by laparoscopic approach. An adjustable band is set around
the stomach just below the cardia and inflated in order to produce a narrowing and thus
dividing the stomach into two segments. The superior segment has a very limited
capacity (20-30 ml) inducing a very rapid satiety after food intake. There are several
types of rings (bands) but the most used are those of silicone, equipped with a port that
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allows inflating the ring to produce the desired narrowing of the stomach. The ring is
inflated with saline solution, under fluoroscopic guidance.
The procedure was widely applied, but because of its poor results and possible
complications, is less applied in nowadays, when other methods (gastric sleeve) proved
to have better results.
The procedure is indicated for patients with BMI of 40-50. The weight loss is
about 50% of extra pounds but in 20% of
cases, it has no apparent effect.
Complications may appear in up to 20% of
cases being represented by: ring slippage,
ulceration and perforation of the stomach,
intragastric migration of the band,
enlargement of the upper segment of the
stomach, and port infection.
The
main
contraindication
for
adjustable
gastric
banding
is
the
nonacceptance on the patients part of
dietetic restrictions, with lack of compliance
with the long-term follow-up and behavioral disorders.
3. Vertical banded gastroplasty (Figure 6)
This procedure is a restrictive one and weight loss is caused by early satiety
consecutive to reduction of the functional volume of the stomach. Two procedures are
combined in this operation. Initially the stomach is partially divided into two segments
using two types of staplers: circular and linear. The upper segment will represent the
new small stomach (gastric pouch), which will communicate with the other segment of
the through a narrow outlet created by the circular stapler. The narrow communicating
part of the stomach is then calibrated using a
ring represented by a nonadjustable band
used also to prevent gastric dilatation of this
segment.
Early postoperative complications are
represented by those common to any
operation (pulmonary embolism, respiratory
insufficiency, sepsis, etc.) or specific, like
bleeding,
perforations,
pouch-emptying
delays. The most frequent late postoperative
complication is caused by poor patient
compliance and intolerance to solid foods,
with excessive vomiting, outlet stenosis,
gastroesophageal reflux, gastric pouch
dilatation and weight loss failure.
If weight loss after this operation is unsatisfactory, it can be easily transformed
into a gastric Roux-en-Y bypass operation.
4. Gastric sleeve procedure (Figure 7) is an irreversible procedure based on the same
principle of reducing the capacity of the stomach that induces rapid satiety.
This procedure was originally published by Marceau in 1993 as a restrictive part
of the duodenal switch operation. It is widelly used in Europe.
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Bariatric Surgery
It is a simple procedure performed by laparoscopic approach. The stomach is
divided into two parts using linear staplers. The larger part of the stomach, represented
by the greater curvature, gastric fundus and a part of the body, is removed. The
remaining part of the stomach is represented by a narrow gastric tube (sleeve) formed
by the lesser curvature of the stomach and the antrum. Special devices such as LigaSure
and staplers with hemostatic strips simplified very much this operation (the mean
operating time is 60-90 minutes).
The procedure does not affect digestion.
The weight loss is about 60% of extra pounds
in the first year. The patient may regain weight
after 4-5 years due to the enlargement of the
remaining stomach.
Gastric sleeve may represent the first
stage in treating super- or hyper-obese patients.
This operation will ensure a weight loss, which
will make more confortable the next operation
(gastric bypass or duodenal switch) and will
reduce the anesthesiological and surgical risks.
A second step procedure is proposed after a
mean of 12-16 months if the patient regains
weight or after stabilization of weight loss.
The main indications of this procedure
are:
BMI of > 40
Patients who are not in appropriate physical condition to undergo gastric
bypass surgery or other more radical weight loss surgeries
Patients who cannot return for the follow-up visits required by gastric
banding
Males with android obesity
Age > 60 years
Intraoperative unexpected technical or anatomical difficulties during more
radical intended operations
Adolescents
Down staging ASA score as a first step of other more radical bariatric
procedure
The advantages of sleeve gastrectomy are as follows:[1]
The stomach is reduced without loss of function
The chance of ulcer occurrence is minimized
Pyloric preservation prevents dumping
It requires only few days of hospitalization
It provides an effective first-stage procedure for super obese patients
It is useful in patients with disorders such anemia or Crohns disease
No foreign materials are left inside the body
5. RouxenY gastric bypass (RYGBP) (Figure 8) is a more radical operation, which
combines two principles: that of gastric volume reduction with that of malabsorption
produced by the reduction of intestinal absorption of alimentary nutrients. There is also
an important hormonal mechanism, which contribute to the weight loss.
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In 1966, Mason, starting from observations that patients operated with gastric
subtotal resection for peptic ulcer had a rapid postprandial satiety and had lost weight,
began the restrictive surgery for obesity using gastric bypass.
This is the bariatric operation most spread
in USA.
The restrictive procedure is achieved by
dividing the stomach into two segments: the upper
one, the gastric pouch, which will represent the
new stomach of small volume (15-20 ml) and
the lower one, which will be left on site. The
gastric pouch will be anastomosed to a Roux-enY jejunal loop ascended in supramesocolic region
in front of the transverse colon or retrocolic
through the transverse mesocolon. This will be the
alimentary limb of the Y loop. The jejunum will
be transected at a distance of about 50 cm from
the duodenal Treitz angle (this will be the
biliopancreatic limb) and reinserted into the
jejunal loop (which will be ascended) at about 100
cm from the resection line of the intestine. Distances where the jejunum will be divided
and reinserted may vary according to many factors but especially considering the BMI
of the patient. Therefore, the smaller the gastric pouch and the more distal the intestinal
segment anastomosed to it, the more effective the procedure is.
The effects of this operation will be:
Restrictive - rapid satiety after food intake due to the small capacity of
the gastric pouch
Malabsorptive - food will meet the biliopancreatic juice and digestion
will start only after the alimentary limb of the Y intestinal loop (the
common loop). In this way digestion will be impaired and the absorption
as well.
Hormonal - exclusion of the food transit of the stomach, in particular of
the fundus and duodenum, where ghrelin (orexic hormone) is produced,
would lead to the stimulation of the secretion of ghrelin which, through
an override inhibition, would result in the suppression of ghrelin
production, with the effect of decreasing the feeling of hunger and
relative reduction in food intake and frequency of meals.[1] It is still
unclear whether or not and how ghrelin plays a role in this complex
hormonal mechanism.
Indications:
BMI>50
Failure of a previous restrictive bariatric procedure
Metabolic disorders: RYGBP is more likely to be effective in patients
with metabolic disorders in the presence of significant imbalances, where
malabsorption is the only possible solution and gives a guarantee of long
term success (for example, dyslipidemia of particular significance)
Eating disorders: patients with reduced compliance with diets
Sweet eaters: a restrictive operation is not effective for these patients but
in RYGBP procedure there is a reduced sweet intake over the long term,
especially when dumping syndrome is present
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Bariatric Surgery
The procedure is more laborious and burdened by possible intraoperative
complications then the previous presented operations.
Early postoperative complications are represented by:
Anastomotic dehiscence with an incidence that varies from zero to 7%, is
the most severe complication, being the major cause of death
Intestinal obstruction
Digestive hemorrhages from anastomotic bleeding
Peritonitis caused by intestinal perforation undiagnosed during operation
The most frequent late postoperative complications are stenosis of the
gastrojejunal anastomosis, anastomotic ulcer and intestinal obstructions caused by band
adhesions or internal hernias.
6. Biliopancreatic diversion (Scopinaro procedure) (Figure 9)
It is a mixed restrictive and malabsorptive method. Stomach volume is reduced by
distal gastrectomy. Digested food absorption is reduced by intestine anastomosis close
to the cecum. Bile and pancreatic juice will be in direct contact with food only in the
terminal portion of the intestine (the last 50 cm of ileum). A long (250 cm) Roux-en-Y
limb is used for reconstruction, where the enetroenteral anastomosis is performed at 50
cm distance from the cecum. Cholecystectomy is associated in most cases because of
the risk of developing gallstones.
With this operation a greater weight loss is obtained (80% of surplus) but with the
risk of hypoalbuminemia, hypovitaminosis and
dumping syndrome.
The essential weight loss is based on the
limitation of intestinal absorption. The absorption
of fats being conditioned by the presence of bile
salts, takes place only in the common limb (the
last 50 cm). Proteins and starches are absorbed in
the entire intestine. Mono and disaccharides, short
chain triglycerides and alcohol, which do not
require digestion, continue to be absorbed after
this procedure.
Unfortunately, there are many side affects
after this type of operation such as increased
frequency of bowel movements (two to four per
day) with foul-smelling stools and flatulence.
Dumping syndrome with diarrhea is also frequent.
Late specific complications include:
Anemia - the exclusion from the alimentary limb of the primary iron
absorption site inevitably leads to hypoferremia. Oral supplementation
with iron and folates reduces anemia incidence.
Post anastomotic ulcer - responds well to medical treatment and has a
low tendency to recur if the operated subject refrains from smoking and
alcohol.
Gastrojejunal anastomosis stenosis requires balloon dilatations or
surgical revision with deconstruction of the existing gastrojejunal
anastomosis.
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Bariatric Surgery
Bone demineralization - the duodenum and the proximal jejunum are the
sites of choice for calcium absorption.
Protein malnutrition - hypoalbuminemia, anemia, edemas, asthenia, and
alopecia are the most serious specific late complication and usually
require two to four weeks of parenteral nutrition.
Peripheral neuropathy requires administration of B complex and E
vitamins.
Biliopancreatic diversion is unanimously
considered the most effective operation for
obesity. Like any other powerful weapon, it can
be very dangerous if used incorrectly.[1]
7. Duodenal Switch (Marceau Procedure)
(Figure 10) is a variation of biliopancreatic
diversion.
The main differences consist in preserving
the antropyloric region to prevent dumping
syndrome and a longer digestive intestinal loop
for a better digestion and absorption. It is
considered a hybrid technique, which combines
the restrictive effect of gastric sleeve with that of
moderate intestinal malabsorption. The
alimentary loop has a length of 250 cm and the
common loop of 100 cm. The procedure primarily
induces malabsorption of fats due to the diversion of bile and pancreatic enzymes to the
distal portion of the alimentary limb (common limb).
Surgical treatment of type 2 diabetes (metabolic surgery)
The first intention of bariatric surgery was to treat obesity but over years,
remarkable metabolic effects, especially the improvement of type 2 diabetes, were
observed. Almost every obese patient with type 2 diabetes who underwent such surgery
had normalized their glucose levels and thus they were able to quit pharmacological
treatment.[30-33] Further, non-obese diabetic patients, who underwent gastric surgery for
diverse causes had noticed a better glycemic control.[34-36] These observations were
also confirmed by animal experiments.[37]
Improvement of glycemic control observed especially after gastrointestinal
bypass procedures (Roux-en-Y gastric bypass and biliopancreatic diversion are the most
effective procedures in controlling diabetes) offered the opportunity to treat and
understand type 2 diabetes and thus, surgery becomes a viable alternative to
conservative treatment of type 2 diabetes especially in obese patients. The antidiabetic
effect of bariatric surgery is also long lasting.
It is not known exactly yet all the mechanisms by which these interventions cure
type 2 diabetes, but there are several theories that have been confirmed by experiments.
Further research on this topic is needed.
The evolution of bariatric surgery to metabolic surgery for type 2 diabetes and
metabolic syndrome is represented by the change in title of American Society of
Bariatric Surgery to American Society of Metabolic and Bariatric Surgery.
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Jonathan CK Wells - The evolution of human fatness and susceptibility to obesity: an ethological approach - Biol. Rev.
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Guidelines
on
Overweight
and
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Wei M, Gaskill SP, Haffner SM, Stern MP. - Waist circumference as the best predictor of noninsulin dependent diabetes
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Han TS, van Leer EM, Seidell JC, Lean ME. - Waist circumference action levels in the identification of cardiovascular
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Electronic
Textbook
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126
Surgical anatomy
Intestinal volvulus
Intussusceptions
Crohn disease
Meckels diverticulum pathology
Tumors of the small intestine
1. Surgical Anatomy
The small intestine is the longest segment of the digestive tract extending
between pylorus and ileocecal valve, occupying most of the peritoneal cavity. Its length
is about 4-7 meters, with variations between 3 and 10 meters, depending on the tonicity
and constitutional type. It develops from the primitive intestine of endodermic origin,
which, communicates with the umbilicus during intrauterine life through the
omfaloenteric canal, which is completely reabsorbed
at birth.
The small intestine is composed of three
segments: duodenum, jejunum and ileum.
The intestinal diameter is of 2-4 cm. Intestines
form 15 to 16 U shaped loops of which the first 8 to
10 are horizontally positioned, belonging to the
jejunum, and the remaining in vertical position,
belonging to the ileum. (Figure 1)
The small intestine is neighboring with the
majority of abdominal viscera: superior with the
transverse colon and mesocolon, inferior 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 posterior abdominal wall. The root of mesentery
has a fix base of 15-18 cm length and it extends
obliquely from the duodenojejunal flexure (L2
vertebra) to the cecum. Inside the mesentery, there are
vessels (branches of superior mesenteric artery and
veins), nerves and lymphatics, all of them covered by
fatty tissue.
The distal portion of the mesentery is much
longer than the proximal one and forms folds. Its
greater length in the last ileal loops explains why
127
128
Small intestine innervation originates in the celiac and mesenteric artery plexuses,
from where fibers are distributed through the perivascular network to the myenteric
plexus (Auerbach) and submucous plexus (Meissner).
Small intestine structure
Inside, the small intestine has circular valves (Kerkring's plicae) with an initially
height of 7-10 mm, which decrease gradually towards the ileum, covered by intestinal
villi that gives the soft appearance of the mucosa. All these elements significantly
increase the contact surface with the intestinal content for a better absorption of
nutrients.
The small intestine has four layers: serosa, muscular, submucosa and mucosa.
Mucosa is the best represented; it occupies two thirds of wall thickness. Mucosa
epithelium is composed of enterocytes, Goblet cells, Paneth cells, stem cells,
enterochromaffin cells, and undifferentiated cells.
The main functions of the small intestine are digestion and absorption.
129
2. Intestinal Volvulus
Intestinal volvulus represents a distinct clinical form of intestinal obstruction
characterized by the twisting of the whole intestine or just a segment of it, at least 360
around its mesenteric axis.
Classification
The pathological process can involve the entire intestine, the total volvulus,
which frequently occurs in children. In these cases it is often involved the right colon as
well (common mesentery). In segmental volvulus, only a segment of the bowel is
twisted, and it occurs mainly in adults, with predilection in men. (Figure 7)
Another classification based on etiopathogenesis is:
1. Primary volvulus, mainly due to congenital anomalies (common mesentery).
2. Secondary volvulus, caused by extrinsic obstructions or compressions (adhesion
bands, tumors, etc.).
Morphopathology
The aspect of the intestinal segment and its
mesentery, interested in the pathological process,
is very similar to the aspect of the mesenteric
infarction. In the initial phase, the intestine is
enlarged, with thickened wall, edematous and redpurple color. Then, the segment becomes brown,
inert, non-peristaltic, looking like a "dead leaf"
and has gangrenous areas or macroscopic
perforations. (Figure 8) At the base (root) of the
twisted bowel, there is a ring of torsion where the
most serious lesions are found, caused by
compression and ischemia. The fluid in peritoneal
cavity looks bloody with fetid smell.
Clinical picture
The clinical picture is dominated by
symptoms of intestinal occlusion installed more or
less acutely, followed by rapid onset of the
hypovolemic shock. Symptoms are represented by
violent pain, which does not respond to treatment.
Intestinal transit stops being accompanied by
nausea and vomiting. On inspection, asymmetrical
abdominal distension can be observed.
Workup
Although, there are no pathognomonic
signs for volvulus of small intestine, plain abdominal X-ray can be useful in
highlighting signs of occlusion, with multiple fluid-air levels.
Diagnosis
The diagnosis of certainty in most cases is not possible. The preoperative
diagnosis will be that of intestinal occlusion, which presumes surgical intervention. The
supposition of volvulus is based mainly on the sudden onset of violent continuous
abdominal pain localized around the umbilicus in a patient with possible previous
130
131
3. Intussusceptions
Intussusception is produced when a segment of intestine invaginates into the
adjoining intestinal lumen, causing bowel obstruction. (Figure 9)
Epidemiology
Intussusception occurs mostly in children and
rarely in adults. Two thirds of children with
intussusception are younger than 1 year.
Intussusception is the most common cause of
intestinal obstruction in patients aged 5 months to 3
years.
Overall, male-to-female ratio is approximately
3:1. With advancing age, gender difference becomes
marked. In patients older than 4 years, the male-tofemale ratio is 8:1.[1]
Classification
There are two types of intussusceptions:
1. Primary or functional (idiopathic), which occurs on an unaffected bowel. There
are no evident causes of the intussusception.
2. Secondary or organic, when a mechanical obstacle (polyp, tumor, stenosis, etc.),
is the cause of intussusception.
Morphopathology
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. (Figure 10)
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, and
2. Complex, with 5 or 7 cylinders
At the neck of intussusception, venous stasis
and swelling of the invaginated loop occur, which
will result in vascular elements compression,
responsible for the intestinal necrosis.
Clinical picture
Symptoms differ according to whether intussusception occurs in newborn,
infants, older children or adults.
In infants, intussusceptions begin suddenly with violent paroxysmal abdominal
pain; the infant becomes agitated, screams out, shakes hands and feet, and has a wry
face. The infant refuses food, or vomits the last meal. The bowel movements can be
abolished or bloody diarrhea may appear. The initial crisis lasts 5-10 minutes, and then
132
133
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Lam AH, Firman K. - Value of sonography including color Doppler in the diagnosis and management of long-standing
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ultrasonography in intussusception. - J. Ultrasound Med. 1997; 16:141-144.
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Liu KW, Maccarthy J, Guiney EJ, Fitzgerald RJ . - Intussusception-current trends in management. - Archives of Disease
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Hilal A, MacMahon P, Cosgrove JF. - Outcome of acute intussusception in a regional paediatric centre. - Ir. Med. J.
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Kaiser AD, Applegate KE, Ladd AP. - Current success in the treatment of intussusception in children. - Surgery 2007;
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Parashar UD, Holman RC, Cummings KC, Staggs NW, Curns AT, Zimmerman CM, Kaufman SF, Lewis JE, Vugia DJ,
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140(6):17041712.
2.
Dessein R, Chamaillard M, Danese S. - Innate Immunity in Crohns Disease. - Journal of Clinical Gastroenterology,
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Marks DJ, Rahman FZ, Sewell GW, Segal AW. - Crohn's disease: An immune deficiency state. - Clinical reviews in
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Bernstein CN, Wajda A, Svenson LW, MacKenzie, A, Koehoorn M, Jackson M, Fedorak R, Israel D et al. - The
Epidemiology of Inflammatory Bowel Disease in Canada: A Population-Based Study. - Am. J. Gastroenterol. 2006;
101(7):15591568.
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Lotfus EV Jr . - Clinical epidemiology of in ammatory bowel disease: incidence, prevalence, and environmental in
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14. Bernstein CN, Orr K, Blanchard JF, Sargent M, Workman D. - Development of an assay for antibodies to
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A. BENIG TUMORS
Etiology
The etiology is unknown. In some forms, there is a clear genetic determinism
(Peutz-Touraine-Jeghers and Gardner syndrome) but for the others there are many
theories, which partially explain the etiology (food theory of proliferative agents,
infectious theory, theory of biliopancreatic juice action, etc.).
Morphopathology
Benign tumors are represented by:
Adenoma is the most common benign tumor of the small intestine. It appears
under three pathological aspects: polypoid, insular and of Brunners glands.
Polypoid adenoma, whether tubular or villous type, can be unique or
multiple, located mainly in the proximal portion of the intestine. It may reach
or even exceed three cm in diameter. It can be pedunculated or sessile. The
risk of malignant transformation is lower than that of colic polyps. More
commonly villous polyps, especially sessile forms, larger than four cm, turn
malignant.[1] Insular adenoma develops from ectopic pancreatic tissue
islands, causing endocrine syndromes such as Zollinger-Ellison syndrome,
Werner-Morrison syndrome, hypoglycemic syndromes. Brunnerian adenoma
is the most frequent benign tumor present in the duodenum, located in the
proximity of the papilla. Its dimension is below one cm and is usually
asymptomatic.
Leiomyoma occurs at ages between 40 and 70 years. It develops either from
the muscularis mucosae or from the muscular layer of the intestine. The
tumor reaches sizes up to 2 cm, and can be located intraluminal, submucosal
or subserosal.
Fibroma develops from connective tissue. It may be pedunculated or sessile,
usually less than 2 cm in diameter and grows in submucosa layer.
142
Clinical picture
Symptoms of benign tumors depend on their location, volume and their
development relative to the intestinal lumen. Endoluminal development of tumors
causes obstruction or intussusception. Intraparietal tumors produce intestinal stenosis
and tumors developed into the subserosa layer may produce intestinal volvulus. Colicky
pains of variable intensity, gastrointestinal bleeding and intestinal occlusion represent
the most frequent symptoms.
Physical examination reveals no changes unless tumors reach very large volume
becoming accessible to palpation as mobile tumors.
Workup
Radiological examination of the small intestine is difficult. Plain radiography
shows fluid-air levels when intestinal occlusion is present. Contrast radiologic
examination may highlight the site of intestinal obstruction or intussusception.
Enteroclysis is a fluoroscopic X-ray of the small intestine. The contrast material is
administered directly into the duodenum through a tube and images are taken in real
time as the contrast moves through the intestines.
Endoscopic examination has become more commonly used in exploring small
intestine. Double-balloon enteroscopy, also known as push-and-pull enteroscopy was
developed by Hironori Yamamoto in 2001.[5] It is the first endoscopic technique that
allows the entire gastrointestinal tract visualization in real time.[6]
Ultrasound examination is a harmless, cheap, portable, flexible investigation that
can reveal intestinal tumors. The method has limitations in obese patients and with
intestinal air impairing image quality. The small intestine is the most difficult part to
examine of the gastrointestinal tract because of its length and tortuous course.
Wireless capsule endoscopy is a relatively new noninvasive method of
examination, developed especially for the small intestine and obscure causes of
intestinal bleeding. One of the drawbacks of the method is that often is difficult to
discern the exact anatomic location of the lesion because the small bowel looks similar
through-out its length.[7-9]
CT scan is widely used for diagnosis with a specificity of 97%.
Laparoscopy and laparotomy are invasive methods of diagnosis.
143
144
T-cell lymphoma
neoplasm)
o enteropathy associated
o Gastrin cell tumor, functioning
o unspecified
(gastrinoma) or non-functioning
Others
o Somatostatin cell tumor
Secondary tumors
o EC-cell, serotonin-producing
neoplasm
o L-cell, glucagon-like peptide and
PP/PYY producing tumor
Mixed carcinoid-adenocarcinoma
Gangliocytic paraganglioma
Others
Adenocarcinomas
Adenocarcinomas are the most common malignant tumors of the small intestine
(30%-50%) localized with predilection in duodenum (54%) around the ampulla of
Vater, and more rarely in jejunum (28%) and ileum (18%).[14]
As with almost any cancer, etiology is unknown but there are some predisposing
factors or underlying conditions that increase the risk of adenocarcinomas such as
Crohn's disease, celiac disease, ulcerative colitis and familial adenomatous
polyposis.[15] It is not very clear if elevated body mass index (BMI), cigarette use and
alcohol consumption increase the risk of small bowel cancer.[16-19]
Clinical picture of small bowel adenocarcinoma is related to the size and location
of the tumor. Tumor located in jejunum and ileum, manifests with periumbilical colicky
pains accompanied by nausea, vomiting, weight loss, asthenia, and intermittent
obstructive episodes. Chronic bleeding manifests as iron-deficiency anemia, but
massive bleeding are rare. In large tumors a mobile palpable mass can be felt.
Complications may be represented by intestinal occlusion and perforation with
generalized peritonitis. In duodenal location, tumors can induce jaundice due to biliary
obstruction.
The diagnosis can be established by the same investigations presented at benign
tumors of the small intestine or by laparoscopy or laparotomy.
Adenocarcinoma develops from the Lieberkuhn glands and includes the entire
intestinal wall, accompanied by a fibrous reaction that gives its schirous aspect.
Carcinomas may be polypoid, infiltrating or stenosing. Duodenal carcinomas are usually
145
Lymphosarcomas
These tumors arise predominantly from the lymphatic structures of the terminal
ileum and frequently are lymphomas of mucosa-associated lymphoid tissue (MALT).
Lymphomas constitute a significant proportion (30-50%) of all malignant small
intestine tumors.[15] The majority of intestinal lymphomas involving the small bowel
are B-cell lymphomas of MALT type, including both low-grade and aggressive types.
The macroscopic aspect is that of a vegetant (fungating) tumor, multiple or infiltrative.
146
147
Carcinoid tumors
Carcinoid tumors represent well-differentiated neoplasms of the diffuse endocrine
system. Other neuro-endocrine tumors of the small intestine are small cell carcinomas
(poorly differentiated endocrine neoplasms) and malignant large cell neuroendocrine
carcinomas. This tumor has endocrine activity secreting different kind of hormones
(serotonin, bradykinin, substance P and other vasoactive substances) which may
produce the so-called carcinoid syndrome manifested by flushing, diarrhea,
bronchoconstriction, and cardiac disease.
Carcinoid tumors account for some 35%-42% of neoplasms in the small intestine,
most of which occur in the ileum and rarely in the duodenum. The average annual
incidence rate is about one case per 100,000 inhabitants [13] but with an occurrence rate
of 1 case per 300 autopsies.[31]
Tumoral cells commonly spread to loco-regional lymph nodes, paraaortic lymph
nodes and to the liver. With distant spread, especially to the liver, carcinoid syndrome
can develop. Patients with the syndrome almost invariably have hepatic metastases.
Clinical picture is common to other small intestinal tumors manifested by
intermittent abdominal pains, and in more advanced cases, by intermittent intestinal
occlusion and a palpable abdominal mass. Most patients with carcinoid tumors do not
develop carcinoid syndrome. Only 40-50% of patients experience the syndrome.
In the presence of carcinoid syndrome, the diagnosis is easier. The main
investigation is represented by urinalysis which in patients with carcinoid syndrome,
shows high levels of urinary 5-Hydroxyindoleacetic acid (5-HIAA), usually more then
five times the normal values in a 24-hour.
Because carcinoid tumors are well vascularized, noncontrast CT scan is used to
highlight the tumor. In addition, OctreoScan may highlight the tumor. For this
examination, Ocreotide labeled with a radioactive isotope is injected. Because carcinoid
tumors have Somatostatin receptors, the radiolabeled Ocreotide binds to the tumor and
radiography thus shows the tumor.
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Emedicine
Surgical anatomy
Investigation methods of the colon
Megacolon
Colonic polyps
Colon cancer
1. Surgical Anatomy
The colon, or the large bowel, extends between the ileocecal valve of Bauhin, and
the rectum, describing a frame around the small intestines. Its length is about 1.6-1.7 m,
with large variations from individual to individual, and it has a 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 that of the small bowel and its 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
vascularization. The anastomotic risk is higher than for other segments of the digestive
tract.
Another important aspect is that the content of the colon is very septic, reason
why a good preoperative preparation is necessary in most cases. Septic risk is much
higher in colon surgery.
From anatomical point of view, the colon is divided into four segments: (Figure
1A)
1. Ascending colon (cecum, and ascending colon)
2. Transverse colon (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. (Figure 1B)
151
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colon takes about 10 minutes. Expect the entire virtual colonoscopy procedure to take 20 to 30 minutes."
http://en.wikipedia.org/wiki/Virtual_colonoscopy
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157
3. Megacolon
Megacolon represents an abnormal dilatation of the colon often accompanied by a
paralysis of the peristaltic movements of the bowel. Dolichocolon represents an
abnormal length of the colon. The combination of these two conditions is called
megadolichocolon (abnormal long and dilated colon).
Classification
According to its etiology, megacolon can be classified as:
Congenital
Idiopathic
Acquired
Toxic
Symptomatic
Congenital megacolon
The disease is also known as aganglionic megacolon or Hirschsprung's disease.
The disease is named after Harald Hirschsprung, a Danish physician who first described
two infants who died of this disorder in 1888.[1]
Etiopathogenesis: it is a congenital disorder of the colon in which ganglion cells of the
myenteric or Auerbach's plexus, of the terminal sigmoid and rectum walls are absent.
The length of bowel that is aganglionic varies. In most cases the distal part is affected
(the short-segment form) but there are cases when aganglionosis extends proximal to the
sigmoid.[2] Total colonic and total intestinal aganglionosis also occur. The macroscopic
aspect reveals a narrowing of the affected colon and distension of the superjacent,
containing giant fecaloma. Histological examination reveals the absence of the
intramural ganglionic plexus.
Hirschsprung's disease is frequently associated with other malformations or
genetic mutations such as Down syndrome in 2-15%.[3-5]
Epidemiology
Hirschsprung's disease occurs in approximately 1% of 5000 live births being
more frequently encountered in males and often has a familial character.[5,6]
Symptoms
Symptoms appear few days after birth and go through several successive periods:
In neonatal period, the newborn fails to pass meconium within 24-48 hours
after birth;[7] the abdomen becomes distended associated with pain and
postprandial vomiting, which, are signs of low intestinal incomplete or
chronic obstruction.
In infant period, the child has a big belly giving the grotesque appearance,
and also the same complaints as above, especially chronic constipation since
birth, are present.
In the period of childhood and adolescence, constipation and abdominal
distension are persisting; defecation is possible only with enema (1 stool at
5-10 days).
On rectal digital examination, the rectal ampulla is found empty! This aspect is
important for differential diagnosis.
158
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 insufficiency. The appearance is that of an underweight child, always
tired, pale, inert, with tachypnea and polypnea, and in advanced stages even cachectic.
Rarely acute occlusive episodes appear. Colonic perforation is also a rare (2%)
complication.[5] Enterocolitis may appear in 10%-26% of cases manifested by diarrhea,
being the main source of mortality and morbidity in Hirschsprung's disease.[5,9-11]
Treatment is purely surgical. If occlusion does not appear, operation is not indicated
under the age of one 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 first step is a diverting loop colostomy above
the affected zone, or diverting loop ileostomy, procedures that allow the colon
emptying. After a period, when the child is in a better condition, colon resection
followed by different types of anastomosis can be performed. Contraindications to a
one-stage procedure include:[7]
massively dilated proximal bowel
severe enterocolitis
perforation
malnutrition
inability to accurately determine the transition zone by frozen section
159
Idiopathic megacolon
It appears in children aged between three and seven years and causes are
unknown. Symptoms are represented by chronic constipation, moderate abdominal
distension. On rectal examination, the rectal 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.[18,19] 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 in one-third of cases to the destruction of digestive tract ganglia cells producing
a clinical picture of a congenital megacolon installed in adulthood. Destruction of
autonomic system cells may eventually result in megaesophagus, megacolon and
accelerated dilated cardiomyopathy.[20] The parasite can be detected by microscopic
examination of fresh anticoagulated blood. In the early, acute stage, symptoms are mild
and usually produce no more than local swelling at the site of infection. The initial acute
phase is responsive to antiparasitic treatments, with 6090% cure rates. After 48
weeks, individuals with active infections enter the chronic phase of Chagas disease that
160
Toxic megacolon
Toxic megacolon is a potentially lethal condition and means a nonobstructive
colonic dilatation larger than 6 cm and signs of systemic toxicity (fever, tachycardia,
leukocytosis, dehydration, hypotension, confusion).[23]
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.[23] Although
recognized as a complication of ulcerative colitis, toxic megacolon may occur in other
types of colitis, volvulus, diverticulitis and colon cancer. Risk factors in the
development of severe colitis include infection with C. difficile, malignancy,
immunosuppression, chemotherapy, renal failure, radiation colitis, etc.
Rapid distension of the colon may cause the following symptoms: painful
abdominal distension, fever, dehydration, tachycardia and cardiovascular shock.
Perforation with subsequent peritonitis is the most frequent complication.
Treatment addresses the underlying disease. It consists of reducing colonic
distension to decrease the risk of perforation, correcting dehydration through
administration of fluids and electrolyte solutions and treating toxemia and risk factors.
The mortality rate for toxic megacolon decreased in the past few decades from 20% to
4% due to early recognition and diagnosis, improved general and surgical treatment. If
perforation occurs, the mortality rate is approximately 20%.[25]
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.
Dolichocolon is another pathological entity of the colon different from
megacolon, represented by a very long colon, which is not enlarged. This condition
affects especially the mobile segments of the colon: the transverse and sigmoid colon.
Chirays typical triad dominates the clinical picture and is represented by constipation,
abdominal distension and pain. Sometimes, the long and mobile colic segment may
become volvulated producing intestinal occlusion. Diagnosis relies on barium enema
that shows a long colic loop and a delay in evacuation of barium (after 2-5 days).
Nonsurgical treatment is common in these cases (proper diet, laxatives
/purgatives). In case of occlusion (volvulus), surgery is required (segmental colectomy).
161
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system progenitor cells. - Gut. 2007; 56(4):489-496.
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162
Updated:
Aug
3,
4. Colonic Polyps
Polyps are tumors that may occur on the inner surface of the entire
gastrointestinal tract, mostly in the colon and rectum and have a potential of malignant
transformation. The word derives from the Latin "polypus" which means "multiple
legs". (Figure 13)
Polyps may be of different sizes and shapes (sessile or
pedunculated) (Figure 14); they are congenital or acquired,
benign or malignant, symptomatic or asymptomatic, singular
localized or multiple, spread throughout the entire colon.
Colonic polyps can occur as part of inherited polyposis
syndromes. In this case, their number is greater and the risk
for malignant transformation is much greater than with
isolated colonic polyps. Polyposis syndromes are hereditary
conditions that include familial adenomatous polyposis
(FAP),
hereditary
nonpolyposis
colorectal
cancer
(HNPCC)/Lynch syndrome, Gardner syndrome, Turcot
syndrome, Peutz-Jeghers syndrome, Cowden disease,
familial juvenile polyposis, and hyperplastic polyposis.[1]
These syndromes should be taken into account when
polyps are detected in young patients, in case of two or more
polyps detected, when colic cancer is detected in young
patients (under the age of 40) and when there are
extraintestinal manifestations associated to polyps. In these patients, even genetic
counseling is important, considering the hereditary transmission, and the high
possibility of malignant transformation.[2,3]
Epidemiology
Contradictory statistics for the incidence of polyps have been reported. Autopsy
studies performed in US suggest that about 30% of middle-aged or elderly individuals
have colonic polyps.[1] Other studies reported an incidence of 51%-69%, and that the
incidence increases with advancing years up to 88% in centenarians.[4,5] Estimated
prevalence of asymptomatic polyps in the general population ranges from 1.6% to12%,
while in population over 70 years, may reach 40%.[6-9] Because the highly prevalence
with increasing age, they confer an important predisposition to colon cancer.
The risk for cancer development depends on the size of the polyp, villous
histology, and its association with polyposis syndromes. In FAP, cancer inevitably
develops 10-20 years after the initial appearance of colonic polyps.[1]
Males seem to have a moderately higher incidence of polyps compared to
females.[10]
Classification. There are two main types of polyps from histopathological point of
view: non-neoplastic and neoplastic polyps. The most important difference between
these two groups is that the non-neoplastic polyps rarely turn malignant where as
neoplastic polyps are considered the precursors of colon cancer.
1. Non-neoplastic polyps
Hyperplastic polyps
Submucosal polyps represented by benign lymphoid polyps
Inflammatory polyps
Hamartomatous polyps
163
164
166
167
168
170
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17. Desai DC, Neale KF, Talbot IC, et al. - Juvenile polyposis. - Br. J. Surg. 1995; 82:14.
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173
5. Colon Cancer
Colon cancer represents the location of the neoplastic process along the colic
frame, from the ileocecal valve to the rectosigmoid junction. Although, from anatomical
and ontogenetic points of view, the two portions of the large intestine, the colon and the
rectum are different, in most treaties, colon and rectal cancer are studied together as
colorectal cancer. There are many similarities of tumoral etiopathogenesis between the
two segments, but there are also significant differences regarding symptoms, methods of
investigation and especially of surgical treatment. Peculiarities of surgical treatment for
rectal tumors are dictated by the special anatomy of the rectum, which has very intimate
relations with pelvic organs, and by the intention of surgeons to preserve, whenever
possible, the anal sphincter during operations for rectal cancer.
Remember that there may be more simultaneous tumors located in different
segments of the colon and/or rectum, and these tumors are called synchronous tumors.
They usually occur as a result of malignization of colorectal polyps. Metachronous
cancer is the occurrence of another (or more) tumor along the colon (usually away from
the primary tumor) after a period of time (of 6 months) following the removal of the
primary tumor. These cases occur most often because of malignization of remaining
colic polyps. These tumors should not be confused with local recurrences caused by
multiplication of remnant tumor cells in the area of primary tumor.
If diagnosed in the early stages, colon cancer is curable offering high rates of long
survival.
Although the etiology of colorectal cancer is not yet known and treatment
methods remained the classical surgery and chemoradiotherapy, in recent years progress
have been made in different fields such as: better understanding of the molecular basis
of carcinogenesis, endoscopic investigation and less toxic treatments.
Incidence
About 608,000 deaths from colorectal cancer are estimated worldwide,
accounting for 8% of all cancer deaths, making it the
fourth most common cause of death from cancer.[1]
Of 57 million global deaths in 2008, 7.6 million
(13%) was caused by cancer in general. The most
important causes of cancer death in 2008 are shown in
the table below (Table 1) according to the WHO.[2]
Colorectal cancer mortality is declining in the
last 15 years (at an average rate of 1.6% per year) due
to modern methods of detection and better therapeutic
methods.[3]
Geographical spread. Colorectal cancer
incidence is variable depending on geographical, socio-economic profile, eating habits,
etc. Almost 60% of the cases occur in developed regions. Incidence rates vary 10-fold in
both sexes worldwide, the highest rates being estimated in Australia/New Zealand and
Western Europe, the lowest in Africa (except Southern Africa) and South-Central Asia,
and are intermediate in Latin America. In the United States, colorectal cancer is the
second cause of death after lung cancer. Estimated new cases and deaths from colon and
rectal cancer in the United States in 2012 was: 143,000 (103,170 colon and 40,290
rectal) and respectively 51,690 (colon and rectal combined).[4]
174
177
178
179
To reduce dietary fat content at less than 30% of total caloric intake
value,
To eat a greater amount of vegetables, fruits, and cereals,
To reduced the consumption of alcohol,
To avoid smoked and fried foods.
2. Cigarette smoking: A person who smokes cigarettes may be at increased risk
of developing polyps and colorectal cancer.[46,47]
3. Ureterosigmoidostomy. Patients with such surgery are at increased risk of
cancer. Tumors appear around the anastomosis, with a latency period of less
than 20 years.[48-51]
Morphopathology
To grow up from 10 microns to 1 cm, a cancerous cell needs thirty divisions.
Considering that doubling time is 109 days, a 1 cm tumor evolves over nine years
before it can be detected as a small tumor. Even with a high growth potential of 34 days
of doubling time, the tumor will need at least 30 months to reach a diameter of one cm.
Tumor growth rate varies depending on its developmental stage. As the tumor increases
its volume, nutrition supply is more limited and hence there is a deceleration of tumor
growth.
Macroscopic appearance. There are four types of colorectal cancers. (Figure 23)
1. Ulcerative form (or endophytic/ulcerative) - the tumor looks like a crater
with irregular raised edges, often with necrotic base. Lesions tend to
infiltrate deep the colic wall increasing the risk of perforation.
2. Polypoid (vegetative or exophytic/fungating) form - the lesion protrudes into
the intestinal lumen having a cauliflower aspect. Sometimes the surface is
ulcerated (the ulcero-vegetative form). These types of tumors are located
most commonly in the cecum and ascending colon.
3. Infiltrative form - it is an annular tumor with circumferential involvement of
the colorectal wall and constriction of the lumen. The circular stenosing
lesion varies in size, with tendency to ulceration. It occurs most commonly
in the left colon, leading to intestinal occlusions. In the diffuse infiltrative
form, the cancer infiltrates the intestinal wall for at least 5-8 cm. It is rarely
encountered, being similar to the gastric linitis plastica.
4. The colloid form is described only by some authors. These tumors produce
large amounts of mucin that gives them a gelatinous appearance.
Pathways of dissemination
Colon cancer spreads by contiguity, through lymphatic or blood vessels, along
nerve fibers, into the peritoneal cavity by gravitation or by surgical insemination.
180
181
182
Malignant melanoma
Others
Malignant lymphomas
Marginal zone B-cell lymphoma of
MALT Type
Mantle cell lymphoma
Diffuse large B-cell lymphoma
Burkitt lymphoma
Burkitt-like /atypical Burkittlymphoma
Others
Secondary tumors
Polyps
Hyperplastic (metaplastic)
Peutz-Jeghers
Juvenile
185
187
Workup
The most important investigation for colorectal cancer diagnosis is colonoscopy
(Figure 26) with biopsy. Colonoscopy has the advantages that directly visualizes
the tumor and can perform biopsies. Colonoscopy is not a simple procedure and
not free of any risks (perforation, bleeding) and requires a good preparation of
the bowel by purgation and even
sedation of the patient. Sigmoidoscopy
is an easier endoscopic investigation,
which does not require patient sedation
being useful for diagnosis of most
colorectal cancers considering that
two-thirds of tumors are located on the
left colon. It is also a good screening
investigation.
Barium enema is the second choice in
nowadays being applied especially in
188
190
192
Left hemicolectomy. After ligation of the colon below and above the tumor, the
next maneuver will be the ligation and resection of the inferior mesenteric vein. This
vein can be easily discovered in the retroperitoneum, left to the Treitz angle of the
194
195
196
197
198
Postoperative complications
In colon cancer surgery, postoperative complications are more frequent and
severe than after other abdominal operations, due to the neoplastic disease, relatively
poor blood supply of the colon, and its septic content. Surgery of the colon is a risky
surgery (infectious, anastomotic and oncologic risk).
The most dangerous and life threatening
complication is the anastomotic dehiscence with
severe peritonitis and respiratory, heart, and
kidney complications. In most cases, reoperation
is necessary as soon as possible. Other possible
early complications are wound suppuration,
bleedings, evisceration, intestinal occlusion, colon
prolapse, and others.
Possible late complications are incisional
hernia, intestinal occlusion caused by intraabdominal adhesions, colostomy prolapse (Figure
46), local recurrence, and others.
Prognosis
A large number of studies tried to identify the specific and most significant
prognostic factors for colon cancer, establishing that the most important are: depth of
the tumoral penetration, number of lymph nodes with metastases, the degree of
histological tumor differentiation, blood or lymphatic vessels invasion and residual
tumor following surgery with curative intent.[75-77]
The higher stage of tumor, the more reserved is the prognosis, making early
detection through screening programs the best currently way to improve this prognostic.
(Table 4)
Table 4 - The five-year survival rates prognosis depending on colorectal stage. [78]
Stage
TNM Group Group Dukes
Prognosis
5 year survival
Stage I
T1
N0
M0
Dukes A
>90%
T2
N0
M0
Stage II
T3
N0
M0
Dukes B
70-85%
T4
N0
M0
55-65%
Stage III any T
N1
M0
Dukes C
45-55%
any T N2, N3
M0
20-30%
Stage IV any T any N
M1
Dukes D
< 5%
199
Colorectal Cancer Incidence and Mortality Worldwide in 2008, Summary - GLOBOCAN 2008 (IARC) , Section of
Cancer Information (12/11/2012) http://globocan.iarc.fr/factsheets/cancers/colorectal.asp
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3.
Robert
J
Fingerote
Colon
Cancer
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5.
Tomislav
Dragovich
Colon
Adenocarcinoma
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De Cosse JJ, Ngoi SS, Jacobsen JS et al. - Gender and colorectal cancer. - Eur. J. Cancer Prev. 1993; 2:105-115.
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Keating J, Pater P, Lolohea S, Wickremesekera K. - The epidemiology of colorectal cancer: what can we learn from the
New Zealand Cancer Registry? - The New Zealand Medical Journal, 2003; 116(117416):1-8.
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Efremidou EI, Liratzopoulos N, Papageorgiou SM, Romanidis K, Tourlis T, Kouklakis G, Manolas KJ. - Colorectal
carcinoma: correlation between age, gender and subsite distribution. - Chirurgia (Bucur). 2008; 103(6):659-663.
10.
Copotoiu C. - Tratat de patologie chirurgical, sub redacia N. Angelescu, 2001, Ed. Med., Vol II.
Medscape
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a district general hospital: is there a true "rightward shift"? - Postgraduate Medical Journal, 2004; 80:667-669.
12.
Ponz de Leon M, Marino M, Benatti P. et al. - Trend of incidence, subsite distribution and staging of colorectal
neoplasms in the 15-year experience of a specialised cancer registry. - Annals of Oncology, 2004; 15:940-946.
13.
Zhang S, Cui Y, Weng Z, Gong X, Chen M, Zhong B. - Changes on the disease pattern of primary colorectal cancers in
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200
201
202
Rectal Cancer
RECTAL CANCER
1. Surgical anatomy of the rectum
2. Rectal cancer
203
Rectal Cancer
The anal canal is the terminal portion of the alimentary tract. It has a length of 23 cm. It is a straight, the shortest and the most fixed part of the terminal bowel.
Anatomical aspects of the inner surface of the lower rectum and anal canal are
represented by:
Morgagnis columns, varying in number from 6 to 14
Anal valves (semilunar envelopes) with anal papillae
Anal sinuses or cripts
Pectinate or dentate line separating the anal canal from the rectum
Linea alba (white line) of Hilton, a delineation between the internal and external
anal sphincters
Anal musculature is represented by:
The internal anal sphincter (smooth muscle), a thickening of the rectal circular
muscular layer, which surrounds the anorectal junction. It ends at the white line.
204
Rectal Cancer
The external anal sphincter (striated muscle), which surrounds the completely
the anal canal and consists of three parts: subcutaneous, superficial and deep.
The upper half of the anal canal is lined by mucosa and the lower half is lined by
stratified squamous non-keratinized epithelium. This explains the different kind of
histological types of cancers between those two segments.
Arterial supply of the rectum (Figure 3) is
represented by:
Superior
rectal
(hemorrhoidal)
artery, terminal branch of the inferior
mesenteric artery, which divides into
two branches
Middle rectal arteries, coming from
the internal iliac artery
Inferior rectal arteries, below the
levator ani muscles, come from the
internal pudendal artery
Middle sacral artery, arising from the
back of the aorta at one centimeter
above the bifurcation and goes in
front of the sacrum and coccyx
Rectal arteries anastomosize between
them, forming thus an intra- and extraparietal anastomotic system, 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, venules start crossing the muscular layer thus creating the rectal or
hemorrhoidal veins.
1. Superior rectal vein collects the blood from the rectal ampulla and flows into the
inferior mesenteric vein (portal
system).
2. Middle rectal veins are thin, leaving
the lower portion of the rectal
ampulla and flowing into the
internal iliac veins toward the
inferior cava vein.
3. 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 established through
these rectal veins (see the portal
hypertension). (Figure 4)
205
Rectal Cancer
There are four physiologic portacaval shunts:
1. Between the superficial and inferior epigastric veins, represented by the
paraumbilical veins. Dilatation of these veins gives the aspect of caput
medusae in portal hypertension.
2. Between the superior rectal vein and the inferior and middle rectal veins. In
portal hypertension, the consequence could be the developing of symptomatic
hemorrhoids.
3. Between small posterior veins of the colon and lumbar veins and renal venous
branches.
4. Between the azygos system (dependant to the superior cava vein) and the gastroesophageal veins belonging to the portal system with the consequence of gastroesophageal varices in case of portal hypertension.
Lymphatic drainage (Figure 5)
The lymph is drained from the mucous and submucous plexuses towards three
pedicles:
1. Superior lymphatic pedicle which
has four lymph node stations:
a. The first station is located on the
posterior rectal wall, described by
Gerota
b. The second station located at the
bifurcation
of
superior
hemorrhoidal artery, described by
Mondor, also receiving short
lymphatic pathways from the
anus
c. The third station (Bacon) is
located in front of rectosigma at
the
junction
between
hemorrhoidal and sigmoidian
arteries, also known as the
"lymphatic mesenteric hilum "
d. The fourth station is located at the
origin of the left colic artery.
2. Lateral lymphatic pedicle includes all the lymph nodes of the pelvis, as follows:
a. Inferior lymph-node-station, located near the middle and lateral sacral
vessels
b. Lateral lymph-node-station, consisting of nodules along the middle
hemorrhoidal and hypogastric vein
c. 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 (Figures 6 and 7)
Sympathetic fibers of the rectum are derived from the first three lumbar spinal
segments, which pass through the sympathetic ganglion chains and leave them as
lumbar sympathetic nerve reaching the preaortic plexus. From here, there is an
206
Rectal Cancer
extension along the inferior mesenteric artery called the inferior mesenteric plexus,
which reaches the lower portion of the rectum.
Presacral or hypogastric nerve comes from the aortic plexus and lateral lumbar
splanchnic nerves. The trunk thus formed is divided into two branches, which pass on
either side of the pelvis where branches meet the sacral parasympathetic nerves to form
the pelvic plexus. 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.
Innervation of the anal canal
Motor innervation
Internal sphincter has both sympathetic and parasympathetic nerve supply.
Sympathetic system has a stimulatory effect whereas the parasympathetic an
inhibitory effect of the sphincter.
External sphincter is innervated by the inferior rectal branch of the internal
pudendal nerve and by the perineal branch of the fourth 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.
207
Rectal Cancer
2. Rectal Cancer
The incidence, epidemiology, and etiopathogenesis of rectal cancer are the same
as for colon cancer. For the etiology of the anal cancer, some special features should be
highlighted. Squamous cell carcinoma (SCC) of the anal canal is frequently associated
with chronic HPV infection (sexually transmittable human papillomaviruses).[1-5] A
strong association with tobacco smoking has been established in women, but the role of
smoking in men is less clear.[1,5-7] Hemorrhoids, anal fissures, fistulae, abscesses and
Crohns disease of long duration in the anal region are no longer considered
predisposing factors.
The macroscopic aspect of the tumor can be ulcerative, infiltrative or vegetative.
Penetration into adjacent organs is rapid and more frequent as in colon cancer due
to the close relations with these organs.
From histopathological point of view, most cases are represented by
adenocarcinomas, (98%) but other forms are also possible, such as carcinoid (0.1%),
lymphoma (1.3%), sarcomas (0.3%). Epithelioma (squamous cell carcinoma) and
melanoma appear especially in anoperineal region.[1]
The TNM classification (AJCC):
Primary tumor (T) (Figure 8)
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
208
Rectal Cancer
whereas the T category of anal canal cancer is defined by tumor size. The N category of
colorectal cancers is defined by number of affected nodes, whereas the N category for
anal cancers is defined by the location of affected nodes.[8]
Symptoms
The clinical picture of the rectal cancer depends on tumors development stage. In
the initial stage, the patient is asymptomatic for a long period. The tumor can be
discovered incidentally on endoscopic or rectal examination. In the phase of state,
symptoms are represented by:
Rectal bleeding which is the most frequent symptom (60% of cases). Other
pathological rectal discharge may be associated such as mucus and pus.
Confusion is often made with bleeding from hemorrhoids. Bleeding from
rectal cancer is rarely massive and the blood is mixed with stool. Sometimes
bleeding manifests as blood clots like a jelly or the fecal bolus is marked by
a trail of blood. Chronic bleeding will lead to anemia.
Pain is manifested initially as a local rectal embarrassment, intrarectal foreign
body sensation, or incomplete evacuation. In advanced stages, pain becomes
more and more intense associated with tenesmus.
Change in bowel habits is represented by diarrhea, particularly if the tumor
has a large villous component. Some patients experience a change in caliber
of the stool (thinner) and the large tumors can cause obstructive symptoms.
. In advanced stages, symptoms are represented by:
Intense pain - caused by sacral penetration
Colicky pain - caused by tumoral obstruction
Hypogastric and perineal pain - caused by penetration in the pelvic
organs
Anal incontinence
Recto-vaginal, recto-bladder or recto-uterine fistula
Jaundice due to liver metastases
Neoplastic impregnation signs (asthenia, malaise, anemia, weight loss,
etc.)
Compressive edema of the legs and genital organs
Physical examination
Digital rectal examination is one of the most important methods of diagnosis in
rectal cancer and the cheapest. Remember that 75% of rectal tumors can be detected by
digital rectal examination! (tumors located up to 10-12 cm from anal verge). However,
one study considers that digital rectal examination is an inaccurate procedure and a poor
predictor for palpable rectal tumor.[9]
The following features of the tumor, found at rectal digital examination, should be
described:
The distance from the anal verge of the lower margin
The exact position on the rectal wall (anterior, posterior, lateral or circular)
Tumor dimensions (extension)
Tumor sensitivity
The surface of the tumor (ulcerated ?)
Tumor delimitation
Tumor mobility - very important to asses the penetration
Bleeding or not- look at the finger glove
209
Rectal Cancer
Groin lymph nodes should be palpated because in lower location of the cancer,
these lymph nodes could be enlarged because of metastases.
In women, vaginal digital examination is of important value in assessing the
penetration of rectal cancer into the posterior wall of the vagina.
Investigations
Rectoscopy with biopsy is the most important investigation (for tumor with
higher location, rectosigmoidoscopy would be necessary).
Endorectal (transrectal) ultrasonography (EUS) (Figure 9) is useful for the
assessment of penetration through
the rectal wall, tumor relations with
surrounding organs and lymph
nodes metastases. It is 72-94%
accurate. [10-12]
CT or MR scan are performed for
the same reasons as above being
more precise but also more
expensive. Endorectal ultrasound
and magnetic resonance tomography
(MR) are the most adequate for
determining tumoral stage. MR is
highly accurate in predicting the
circumferential resection margin. Accurate node staging remains however
difficult with both EUS and MR. [13,14]
Abdominal ultrasound is useful especially for liver metastases and ascites.
Chest radiography is useful for detecting lung metastases.
Intravenous urography or cystoscopy is performed when a fistula with the
bladder or compression on ureters are suspected.
Carcinoembryonic antigen (CEA) test, even though is not specific for rectal
cancer, is performed in all patients. A baseline level is obtained before surgery
and then a follow-up level after surgery. If a previously normalized CEA begins
to rise (over 100 ng/mL) in the postoperative period, usually indicates metastatic
disease or local recurrence.
Differential diagnosis should include other anorectal diseases such as:
Hemorrhoids
Anal fissure
Ulcerative recto-colitis
Rectal syphilis
Crohn disease
Genitourinary diseases, and others
Treatment
The treatment is complex (multimodal): surgical and adjunctive oncotherapeutic.
The therapeutic priority depends on tumor location, stage and size.
In cancers located in the lower part of the rectum, initially preoperative
radiotherapy is indicated for tumoral reduction and then, after 4-6 weeks, follows the
surgery. Some authors advocate also for neoadjuvant chemotherapy for locally
advanced tumors.[15-17]
210
Rectal Cancer
The operative technique varies depending on many factors among which tumor
location is primary. Other factors considered for the operative strategy are: tumoral
stage, age of the patient, other associated illnesses of the patient and the patient's
wishes.
The most important dilemma of the rectal surgery is to choose between a radical
operation and an anal sphincter preserving operation. Of course, surgeons will try
whenever possible to save the anal sphincter but without compromising oncologic
principles.
Surgical treatment implies:
1. the removal (excision) of the tumoral rectum, and
2. lymphadenectomy (total mesorectal excision) for tumors in stage II-III
Extension of resection. It was found that the tumor does not infiltrate more than 2
mm from the macroscopic edge. 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 tumor and the 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, up to the inferior margin of the
tumor. Under this limit, in most cases, the anal sphincter cannot be saved and a rectal
amputation is the major surgical indication. An important step forward in sphincter
preserving surgery was made by the
introduction of staplers for colorectal
anastomosis that enabled lowering as much
as possible the anastomosis line near the
anus.
In anorectal cancers, the only
operation indicated is abdominoperineal
resection (rectal amputation).
Types of operations
Radical operations (Figure 10)
Low anterior resection with colorectal
anastomosis (Dixons operation) with or
without temporary colostomy or
ileostomy for anastomosis protection.
(Figure 11)
Ultralow resection with peranal or
intersphincterian anastomosis (Parks
operation).
Abdominoperineal resection or rectal
amputation (Miles operation) with
definitive left iliac anus (terminal
colostomy). (Figure 12)
Pull-through operations (Babckoc,
Bacon, Mandache, Chiricuta). (Figure
13)
Hartmanns operation
Endoluminal excision (in early stages)
211
Rectal Cancer
Palliative operations
Colostomy, cecostomy, ileostomy
Palliative resection (Hartmann I step)
Approaches may be:
Classic - median laparotomy, or transsacral (rarely applied)
Laparoscopy
Endoluminal (endoscopic)
Stapled anastomosis
The evolution of mechanical suture technology experienced a continuous
improvement over the 40 years of history. The use of staplers facilitated the anastomosis
technique allowing a lower rectal resection and anastomosis, avoiding rectal
amputations in many patients. Staplers can be used for any anastomosis but they are the
212
Rectal Cancer
most useful in rectal tumors. For sphincter preserving procedures, tumors should be
located above 5-6 cm from the anal verge. Resecting 2 cm below the tumor will leave
an anorectal stump of only 3-4 cm, the minimum length necessary for mechanical
colorectal anastomosis. For tumors located under 5-6 cm the options could be
represented by:
Abdominoperineal resection
Colo-anal anastomosis (intersphincteric)
Pull-through procedures
Technical details: the same principles as in conventional surgery must be
respected (anastomosis without tension and a good arterial supply of the colon) to
prevent anastomotic leaks. It is important to verify the integrity of anastomosis by
verifying the integrity of the tissue ring of the cut edges, direct visualization, hydropneumo 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 and endoscopic visualization. (Figure 15)
213
Rectal Cancer
Postoperative complications after Low Anterior Resection
Anastomotic fistula is the most dangerous and life threatening due to septic
shock after peritonitis. To prevent peritonitis, temporary colostomy or
ileostomy can be performed.
Wound suppuration, bleedings, etc., are not so difficult to treat but may
endanger the patients life.
Intestinal obstruction mostly caused by adhesions or internal hernias.
Transient urinary dysfunction secondary to weakening of the detrusor
muscle.
Sexual dysfunction is more prominent and includes retrograde ejaculation
and impotence. In the past, this complication occurred in 5-70% of men, but
recent reports indicate that the current incidence is lower. [21,22]
Abdominoperineal resection - Rectal Amputation - Miles operation (Figure 16)
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. Usually, 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: the abdominal one, when the rectum and mesorectum are
prepared down to the levator ani muscles, and the perineal approach, when the
anorectum will be completely freed up and removed.
Complex operations
Unfortunately there are many cases with advanced cancers when the tumor
invades other organs being necessary multiple visceral resections (when possible) the
so-called complex operations.
214
Rectal Cancer
Transanal excision of rectal tumor (Figure 17) can be performed only if: [23-26]
1. The tumor is in stage 0 or I (Tis, T1)
2. The tumor does not occupy more than one third of the circumference of the
rectum
3. There are no pathological lymph nodes (verified by endorectal ultrasound)
4. The tumor does not involve the anal sphincter
5. Preferably the tumor to be of polypoid form
6. Rectal wall is excised in its entire thickness at least at 1 cm away from the
lesion being followed or not by suture of the subperitoneal rectum.
References
1.
Hamilton SR, Aaltonen LA. - Pathology and Genetics of Tumours of the Digestive System - WHO Classification of
Tumours, IARC Press, Lyon, 2000.
2.
Stanley MA, Winder DM, Sterling JC, Goon PK. - HPV infection, anal intra-epithelial neoplasia (AIN) and anal cancer:
current issues. - BMC Cancer, 2012 8; 12:398.
3.
Machalek DA, Poynten M, Jin F, Fairley CK, Farnsworth A, Garland SM, Hillman RJ, Petoumenos K, Roberts J, Tabrizi
SN, et al. - Anal human papillomavirus infection and associated neoplastic lesions in men who have sex with men: a
systematic review and meta-analysis. - Lancet Oncol. 2012; 13(5):487-500.
4.
Centers for Disease Control and Prevention (CDC). - Human papillomavirus-associated cancers - United States, 20042008. - MMWR Morb. Mortal. Wkly, Rep. 2012; 61:258-261.
5.
Daling JR, Madeleine MM, Johnson LG, Schwartz SM, Shera KA, Wurscher MA, Carter JJ, Porter PL, Galloway DA,
McDougall JK. - Human papillomavirus, smoking, and sexual practices in the etiology of anal cancer. - Cancer 2004;
101(2):270-280.
6.
Daling JR, Sherman KJ, Hislop TG, Maden C, Mandelson MT, Beckmann AM, Weiss NS. - Cigarette smoking and the
risk of anogenital cancer. - Am. J. Epidemiol. 1992; 135:180-189.
7.
Frisch M, Glimelius B, Wohlfahrt J, Adami HO, Melbye M. - Tobacco smoking as a risk factor in anal carcinoma: an
antiestrogenic mechanism? - J. Natl. Cancer Inst. 1999; 91:708-715.
8.
Compton CC. - Colorectal Carcinoma: Diagnostic, Prognostic, and Molecular Features. - Mod. Pathol. 2003; 16(4):376
388.
9.
Ang CW, Dawson R, Hall C, Farmer M. - The diagnostic value of digital rectal examination in primary care for palpable
rectal tumour. - Colorectal Disease 2008; 10 (8):789-792.
10.
Ren JH, Guo FJ, Dai WD, Han XJ, Ma N. - Study of endorectal ultrasonography in the staging of rectal cancer. - Chin.
Med. J. (Engl). 2012; 125(20):3740-3743.
11.
Kav T, Bayraktar Y. - How useful is rectal endosonography in the staging of rectal cancer? - World J. Gastroenterol.
2010; 16(6):691-697.
12.
215
Rectal Cancer
13.
Juchems MS, Aschoff AJ. - Current imaging for rectal cancer. - Chirurg. 2009; 80(4):274-280.
14.
Ho ML, Liu J, Narra V. - Magnetic resonance imaging of rectal cancer. - Clin. Colon Rectal Surg. 2008; 21(3):178-187.
15.
Aliev II, Guliaev AV, Pravosudov IV, Karachun AM. - Current principles and approaches to the treatment for patients
with locally advanced rectal cancer. - Vopr. Onkol. 2012; 58(2):203-206.
16.
Sauer R, Liersch T, Merkel S, Fietkau R, Hohenberger W, Hess C, Becker H, Raab HR, Villanueva MT, Witzigmann H,
Wittekind C, Beissbarth T, Rdel C. - Preoperative versus postoperative chemoradiotherapy for locally advanced rectal
cancer: results of the German CAO/ARO/AIO-94 randomized phase III trial after a median follow-up of 11 years. - J.
Clin. Oncol. 2012; 30(16):1926-1933.
17.
Glynne-Jones R, Kronfli M. - Locally advanced rectal cancer: a comparison of management strategies. - Drugs 2011;
71(9):1153-1177.
18.
Heald B. - Autonomic nerve preservation in rectal cancer surgery --the forgotten part of the TME message a practical
"workshop" description for surgeons. - Acta Chir Iugosl. 2008; 55(3):11-16.
19.
Maurer CA. - Urinary and sexual function after total mesorectal excision. - Recent Results Cancer Res. 2005; 165:196204.
20.
Faucheron JL. - Pelvic anatomy for colorectal surgeons. - Acta Chir. Belg. 2005; 105(5):471-474.
21.
Havenga K, Maas CP, DeRuiter MC, Welvaart K, Trimbos JB. - Avoiding long-term disturbance to bladder and sexual
function in pelvic surgery, particularly with rectal cancer. - Semin. Surg. Oncol. 2000; 18(3):235-243.
22.
Hojo K, Vernava AM 3rd, Sugihara K, Katumata K. - Preservation of urine voiding and sexual function after rectal
cancer surgery. - Dis. Colon Rectum 1991; 34(7):532-539.
23.
Amann M, Modabber A, Burghardt J, Stratz C, Falch C, Buess GF, Kirschniak A. - Transanal endoscopic microsurgery
in treatment of rectal adenomas and T1 low-risk carcinomas. - World J. Surg. Oncol. 2012; 10(1):255.
24.
Lonard D, Remue C, Kartheuser A. - The transanal endoscopic microsurgery procedure: standards and extended
indications. - Dig. Dis. 2012; Suppl 2:85-90.
25.
Langer C, Liersch T, Markus P, Sss M, Ghadimi M, Fzesi L, Becker H. - Transanal endoscopic microsurgery (TEM)
for minimally invasive resection of rectal adenomas and "Low-risk" carcinomas (uT1, G1 - 2). - Z. Gastroenterol. 2002;
40(2):67-72.
26.
Dias AR, Nahas CS, Marques CF, Nahas SC, Cecconello I. - Transanal endoscopic microsurgery: indications, results and
controversies. - Tech. Coloproctol. 2009; 13(2):105-111.
216
Anoperineal Pathology
ANOPERINEAL PATHOLOGY
1.
2.
3.
4.
5.
217
Anoperineal Pathology
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 columns of Morgagni. Two adjacent columns are connected below at the
pectinate line by anal valves (Ball). Morgagni's crypts (or anal crypts, or sinuses, or
saccules of Harner) are small pockets between the lower ends of columns with the same
name. These sinuses may be of some surgical significance as some foreign bodies may
lodge into them with resulting infection or trauma.
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 (Figure 2)
Perineopelvic spaces are directly concerned in surgical therapy especially of
perianal abscesses and fistula in ano. The perineopelvic spaces are:
1. The perianal space surrounds the anus and the lower third of the anal canal.
Laterally it continues with the ischiorectal fossa. Posterior, 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. The ischiorectal space, located on the both sides of the anal canal and below the
pelvic diaphragm. Its base is oriented downwards to the surface and the apex
upwards. It contains ischiorectal fat, inferior hemorrhoidal veins and nerves
crossing transversely. Posterior, it is
crossed by the perineal and
perforating branches (coetaneous) of
the pudendal plexus and anterior by
the posterior scrotal or labial vessels
and nerves.
4. The
supralevator
(pararectal)
spaces located above the levator
muscle and below the peritoneal
reflections of the abdominal cavity.
5. The retrorectal (presacral) space
lies posterior to the rectum and
anterior to the sacrum and coccyx.
218
Anoperineal Pathology
PATHOLOGY
The prevalence of anal diseases in the general population is probably much
higher than that detected in clinical practice because most patients do not seek medical
care because of shame.[1] The common anoperianal lesions are presented in the table
bellow (Table 1)[2]
Table 1 - Anoperineal lesions
2. Anal Fissure
The anal fissure is a tear in the mucocutaneous layer of the anal canal. (Figure 3)
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
the
anal
thermometer, enema cannula, ultrasound
probe, other foreign bodies, 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) [3]
Leukemia
Tuberculosis
Viral infections: cytomegalovirus
219
Anoperineal Pathology
or herpes, syphilis, gonorrhea, Chlamydia, chancroid (Hemophilus ducreyi),
and human immunodeficiency virus (HIV)
Some drugs (antiparkinsonian) may induce constipation and others
(Nicorandil - vasodilator) directly anal ulceration.[4]
Fissures usually occur in stressed people or psychologically labile and sedentary.
Also, people who travel a lot (drivers, sales representatives, 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. Anterior location is not as
frequent and more common in women (10%)
than in men (1%).[5] Multiple fissures are
also
possible.
Explanations
for
predominantly posterior location of the anal
fissure are: the weaker muscles and the
poorer arterial supply in this region.[6] At the lower end of fissure a tag of skin may
form, called the sentinel pile. (Figure 4)
Pathophysiology
Most acute anal fissures heal spontaneously or with appropriate treatment but
there are cases that do not have any tendency to heal and rather become chronic. The
ulceration penetrates deeper and deeper through the layers of the anal canal and a series
of complications appear such as bleeding and intersphincteric abscess. The reason why
these fissures do not 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 during defecation and fissure
open with each bowel movement.
There are two forms of anal fissure: acute and chronic (Figure 5)
Acute anal fissure appears as a tear of the anal skin continued into 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. Sphincter spasm in advanced
forms is permanent due to muscle infiltration
with fibrous tissue and scar. Local
inflammatory changes can evolve to the
formation of abscesses with further
development of fistula. In most cases,
surgery is the only way to cure the 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 with the
220
Anoperineal Pathology
next stool. After defecation, the pain recurs with greater intensity and can last for
several hours. 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.
Anal bleedings are also possible, the patient observing the presence of bright red
blood.
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 been
reported in some people with labile psyche.
Diagnosis
The diagnosis of anal fissure is not difficult being based on anal pain features and
clinical observations.
The
diagnosis
is
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, Cronhs disease,
ulcerative colitis, etc). (Figure 6)
Treatment
The goal of treatment for anal fissures is to break the vicious circle of anal
sphincter spasm that maintains the repeated tearing of the anoderm.
General measures
In acute fissures, medical therapy is successful in the majority of patients. Most
(80-90%) acute anal fissures will heal with conservative measures whereas only 40% of
chronic will heal with these methods.[7,8]
Preventing and treating constipation with proper diet with more vegetables and
fruits, with minimum 1.5 L of fluids intake per day, avoiding spicy foods, and
possibly mild laxative (stool softeners) 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.[9]
221
Anoperineal Pathology
222
Anoperineal Pathology
References
1.
Gopal DV. - Diseases of the rectum and anus: a clinical approach to common disorders. - Clin. Cornerstone. 2002;
4(4):34-48.
2.
Gupta PJ. - A review of proctological disorders - European Review for Medical and Pharmacological Sciences 2006; 10:
327-335.
3.
Williams DR, Coller JA, Corman ML, Nugent FW, Veidenheimer MC. - Anal complications in Crohn's disease. - Dis.
Colon. Rectum. 1981; 24(1):22-24.
4.
Colvin HS, Barakat T, Moussa O, Babu H, Slaughter T, Palmer JG, Hinson FL. - Nicorandil associated anal ulcers: an
estimate of incidence. - Ann. R. Coll. Surg. Engl. 2012; 94(3):170-172.
5.
Petros JG, Rimm EB, Robillard RJ. - Clinical presentation of chronic anal fissures. - Am. Surg. 1993; 59(10):666-668.
6.
Van Outryve M. - Physiopathology of the anal fissure. - Acta Chir. Belg. 2006; 1 06(5):517-518.
7.
Wray D, Ijaz S, Lidder S. - Anal fissure: a review. - Br. J. Hosp. Med (Lond). 2008; 69(8):455-458.
8.
Dhawan S, Chopra S. - Nonsurgical approaches for the treatment of anal fissures. - Am. J. Gastroenterol. 2007;
102(6):1312-1321.
9.
Gupta PJ. - Effects of warm water sitz bath on symptoms in post-anal sphincterotomy in chronic anal fissure--a
randomized and controlled study. - World J. Surg. 2007; 31(7):1480-1484.
10. Svendsen CB, Matzen P. - Treatment of chronic anal fissure with topically applied nitroglycerin ointment. A systematic
review of evidence-based results. - Ugeskr. Laeger. 2002; 164(33):3845-3849.
11. Ehrenpreis ED, Rubin DT, Ginsburg PM, Meyers JS. - Treatment of anal fissures with topical nitroglycerin. - Expert
Opin. Pharmacother. 2001; 2(1):41-45.
12. Yiannakopoulou E. - Botulinum toxin and anal fissure: efficacy and safety systematic review. - Int. J. Colorectal Dis.
2012; 27(1):1-9.
13. Madalinski M, Kalinowski L. - Novel options for the pharmacological treatment of chronic anal fissure-role of botulin
toxin. - Curr. Clin. Pharmacol. 2009; 4(1):47-52.
14. Nelson RL, Chattopadhyay A, Brooks W, Platt I, Paavana T, Earl S. - Operative procedures for fissure in ano. Cochrane Database Syst Rev. 2011; (11):CD002199.
15. Lockhart-Mummery HE. - Fissure-in-ano. - In: Rob C, Smith R, editors. Operative Surgery. London: Butterworth; 1957.
pp. 113.
16. Boulos PB, Araujo JG. - Adequate internal sphincterotomy for chronic anal fissure: subcutaneous or open technique? Br. J. Surg. 1984; 71(5):360-362.
17. Oh C, Divino CM, Steinhagen RM. - Anal fissure. 20-year experience. - Dis. Colon Rectum. 1995; 38(4):378-382.
18. Floyd ND, Kondylis L, Kondylis PD, Reilly JC. - Chronic anal fissure: 1994 and a decade later-are we doing better? Am. J. Surg. 2006; 191(3):344-348.
19. Abd Elhady HM, Othman IH, Hablus MA, Ismail TA, Aboryia MH, Selim MF. - Long-term prospective randomised
clinical and manometric comparison between surgical and chemical sphincterotomy for treatment of chronic anal fissure.
- S. Afr. J. Surg. 2009; 47(4):11211-4.
20. Oueidat D. - A comparative study in anal fissure treatment. - J. Med. Liban. 1999; 47(3):164-168.
223
Anoperineal Pathology
3. Hemorrhoids (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
may become pathological with various
complications when they increase in
volume.
The anorectal canal is not like a pipe
with smooth inner surface. It has
overlapping folds (cushions) created by
physiological hemorrhoids 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. (Figure 8)
Frequency
Ten million people in the United States have hemorrhoids, which represents a
prevalence rate greater than 4%.[1] The true epidemiology of this disease is unknown
because patients have a tendency to use self-medication rather than to seek proper
medical attention.[2]
Etiology
The genetic factor is determinative. The main cause of hemorrhoids is a decreased
resistance of the venous walls, which become weaker leading to venous dilatations.
There is a genetic disorder of collagen and elastic fibers with decreased vein wall
elasticity. Usually it has a familial character and is frequently associated with other
diseases such as varicose veins and flat feet.
Predisposing factors are: [2-4]
Constipation: by forcing the passage of stool, the increased intra-abdominal
pressure causes increased pressure in the hemorrhoidal veins. There are
authors who do not agree that constipation is a risk factor.[5]
Diarrhea and laxatives are actually more important factors than constipation,
causing mucosa irritation.[4,5]
Occupational factors: prolonged standing or sitting (accountants, drivers,
pilots, etc).
Rectal cancer - symptomatic hemorrhoids
Increased intra-abdominal pressure
o Pregnancy
o Obesity
o Ascites
o Tumors
Increased venous pressure
o Portal hypertension (symptomatic hemorrhoids)
224
Anoperineal Pathology
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. (Figure 9)
Internal hemorrhoids are classified into
four grades:
Grade I: No prolapse.
Grade II: Prolapse upon defecation
but spontaneously reduce.
Grade III: Prolapse upon defecation
and must be manually reduced.
Grade IV: Prolapsed hemorrhoids,
which cannot be manually reduced.
Prolapsed hemorrhoids are internal
hemorrhoids that are so distended that they
are pushed outside the anus. (Figure 10)
Symptoms
Uncomplicated
asymptomatic.
hemorrhoids
are
Complications
Bleeding is the most frequent
complication and it is the major 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 colorectal cancer. Chronic bleeding will lead to iron
deficiency anemia.
Hemorrhoidal prolapse occurs in advanced stages of hemorrhoids (the fourth
stage). 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 partial or complete, circular.
Inflammation can progress to necrosis, ulceration, bleedings, and suppuration. (Figure
11)
Hemorrhoidal thrombosis occurs more frequently in the external hemorrhoids. It
is due to blood clotting in the hemorrhoidal veins (phlebothrombosis) and if
inflammatory processes are associated, it is called thrombophlebitis. The patient notices
a swelling on the anal ring that becomes increasingly painful. 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.
(Figure 11)
225
Anoperineal Pathology
Thrombosed hemorrhoid may progress to regression and resorption with
decreasing 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.
Anoperineal Pathology
Treatment
It is preventive and curative.
Depending on the stage of hemorrhoids, the choice of the patient and physicians
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
option is surgical treatment.
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 (Figure 12) is
performed on an outpatient basis. It is a
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. The internal hemorrhoid is
sucked into the tubular device and the two
rubber rings are downloaded at the root of
the
hemorrhoid.
Thus
hemorrhoid
vascularization is interrupted inducing its
necrosis and detach within 5-7 days.
Remaining scar will heal completely in
about 2-3 weeks. The procedure is performed in several sessions depending on the
number and size of hemorrhoids. Elastic ligation is applied only to internal
hemorrhoids.
Surgery is indicated in advanced stages with complications of hemorrhoids and
for external hemorrhoids. The goal is to remove hemorrhoidal packages.
Indications for elective hemorrhoidectomy include the followings:[6]
1. Failure of medical and nonoperative therapy
2. Symptomatic third degree, fourth-degree, or mixed internal and external
hemorrhoids
3. Symptomatic hemorrhoids in the presence of a concomitant anorectal
condition that requires surgery
4. Patient preference, after discussion of treatment options with the referring
physician and surgeon
There are several methods of surgical treatment
Removal (hemorrhoidectomy)
Stapling (hemorrhoidopexy)
Blood clot (thrombus) removal. The external hemorrhoid is incised and
the blood clot removed.
Transanal hemorrhoidal dearterialization (THD) and rectal mucopexy
227
Anoperineal Pathology
Operations can be performed under
local or general anesthesia, but in most cases
spinal or epidural anesthesia is preferred.
External hemorrhoidal thrombosis can
be treated by removing the blood clots and
excision of the underlying veins under local
anesthesia, (Figure 13) but remember that
acute thrombosis resolves spontaneously in
10-14 days, thus, a patient who presents late
and has diminishing pain should not be
operated.
Resection is usually reserved for patients with hygiene deficiency caused by
large skin tags, a history of multiple external
thromboses, or hemorrhoidal complications.
Milligan-Morgan Technique (Figure 14)
was developed by Drs. Milligan and Morgan
in the United Kingdom, in 1937.[7] The three
major hemorrhoidal cushions 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 and is considered the gold
standard by which most other surgical
hemorrhoidectomy techniques are compared.
Ferguson Technique (Figure 15) was
developed in the United States, in 1952 by
Dr. Ferguson. This is a modification of the
Milligan-Morgan technique whereby the
incisions are totally or partially closed with
absorbable running sutures. The Ferguson
method has no advantage in terms of wound
healing because of the high rate of suture
breakage during bowel movement.[8]
Stapled Hemorrhoidopexy (Figure 16), also known as Procedure for Prolapse &
Hemorrhoids (PPH), Stapled Hemorrhoidectomy, or Circumferential Mucosectomy, is a
technique developed in the early 90's [9] that reduces the prolapse of hemorrhoidal
tissue by excising a band of the prolapsed anal mucosa using a circular stapling device.
This restores the hemorrhoidal tissue back to its original anatomical position.
228
Anoperineal Pathology
Whitehead Hemorrhoidectomy (Figure 17) described in 1882 by the author, with
good results, but is responsible for the most serious postoperative complications: anal
stenosis, ectropion and anocutaneous sensitivity disappearance.[10] A circular sleeve of
anal mucosa with hemorrhoidal packages is excised, the skin being sutured to the rectal
mucosa. In Romania, the operation was
introduced and developed by Vercescu. In
1998, Wolff and Culp improved the
calibration technique with flaps sutured to
the dentate line that prevents stenosis of the
anal canal.[11] 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.
Radiofrequency ablation and suture fixation
of hemorrhoids, bipolar diathermy hemorrhoidectomy, LigaSure and Starion
hemorrhoidectomy with submucosal dissection are newer methods which use special
devices to remove the hemorrhoids with less intraoperative bleeding and postoperative
complications.[12-14]
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 after hospital discharge are:
Warm sitz bathes
Ointments with healing effect
Avoid constipation and diarrhea
Avoid spicy food
Paraffin oil to facilitate stool evacuation
Wound dressing is not always necessary
Control at 3-4 weeks after surgery including a digital rectal examination to
assess anal stenosis occurrence and patency of the anal sphincter.
Postoperative complications [15-17]
Early: severe postoperative pain lasting 2-3 weeks, wound infection, acute
urinary retention, hemorrhage, anal incontinence
Late: secondary hemorrhage, anal stenosis, ectropion, anal fissure, skin
tags, recurrence
References
1.
Johanson JF, Sonnenberg A. - The prevalence of hemorrhoids and chronic constipation. An epidemiologic study. Gastroenterology 1990; 98(2):380-386.
2.
Varut Lohsiriwat - Hemorrhoids: From basic pathophysiology to clinical management. - World J. Gastroenterol. 2012;
18(17): 20092017.
3.
Loder PB, Kamm MA, Nicholls RJ, Phillips RK. - Review Haemorrhoids: pathology, pathophysiology and aetiology. Br. J. Surg. 1994; 81(7):946-954.
4.
Delc F, Sonnenberg A. - Associations between hemorrhoids and other diagnoses. - Dis. Colon Rectum 1998;
41(12):1534-1542.
5.
Johanson JF, Sonnenberg A. - Constipation is not a risk factor for hemorrhoids: a case-control study of potential
etiological agents. - Am. J. Gastroenterol. 1994; 89(11):1981-1986.
229
Anoperineal Pathology
6.
American Gastroenterological Association medical position statement: Diagnosis and treatment of hemorrhoids. Clinical Practice Committee, American Gastroenterological Association - Gastroenterology. 2004; 126(5):1461-1462.
http://faculty.ksu.edu.sa/Al-Amri/Guidelines/AGA%20statement%20dx%20hemorroids.pdf
7.
Milligan ET, Morgan CN, Jones LE, Officer R. - Surgical anatomy of the anal canal and operative treatment of
haemorrhoids. - Lancet 1937; 11:11191194.
8.
Agbo SP. - Surgical Management of Hemorrhoids. - J. Surg. Tech. Case Rep. 2011; 3(2): 6875.
9.
Longo A. - 6th world congress of Endoscopy Surgery. Naples: Mundozzi Editore; 1998. - Treatment of haemorrhoidal
disease by reduction of mucosa and haemorrhoidal prolapse with a circular stapling device: A new procedure; pp. 777
784.
10. Maria G, Alfonsi G, Nigro C, Brisinda G - Whitehead's hemorrhoidectomy. A useful surgical procedure in selected
cases. - Tech. Coloproctol. 2001; 5(2):93-96.
11. Sands LR., Sands Dana R. - Ambulatory colorectal surgery - 2009 by Informa Healthcare USA, Inc.Informa Healthcare
is an Informa business.
12. Gupta PJ. - Radiofrequency ablation and plication of hemorrhoids. - Tech. Coloproctol. 2003; 7(1):45-50.
13. Andrews BT, Layer GT, Jackson BT, Nicholls RJ. - Randomized trial comparing diathermy hemorrhoidectomy with the
scissor dissection Milligan-Morgan operation. - Dis. Colon Rectum 1993; 36(6):580-583.
14. Chen CW, Lai CW, Chang YJ, Chen CM, Hsiao KH. - Results of 666 consecutive patients treated with LigaSure
hemorrhoidectomy for symptomatic prolapsed hemorrhoids with a minimum follow-up of 2 years. - Surgery 2013;
153(2):211-218.
15. Sayfan J. - Complications of Milligan-Morgan hemorrhoidectomy. - Dig. Surg. 2001; 18(2):131-133.
16. Wolff BG, Culp CE. - The Whitehead hemorrhoidectomy. An unjustly maligned procedure. - Dis. Colon Rectum. 1988;
31(8):587-590.
17. Mirzaei R, Mahjoubi B, Kadivar M, Azizi R, Zahedi-Shoolami L. - Anal sphincter injuries during hemorrhoidectomy: a
multi center study. - Acta Med. Iran. 2012; 50(9):632-634.
230
Anoperineal Pathology
4. Anoperineal Abscesses
Etiology
Staphylococci, Streptococci, E. coli, Proteus and anaerobes such as clostridium
welchii and bacteroides are frequently responsible for these abscesses.
In 10-20% of cases, the site of entry of the infective organisms is obvious.
Perianal abscess may develop after:
Dorsal anal fissure
Anal hematoma
Thrombosed hemorrhoids
Following injection of a anesthetic solution or alcohol in perianal or
ischiorectal space in the treatment of perianal pain
Following injections (sclerotherapy) of the internal hemorrhoids
Injury to anal or rectal mucosa
As a complication of hemorrhoidectomy or sphincterotomy
Pathophysiology
Anorectal abscess is a cryptoglandular 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 stages it presents as
fistula in ano.[1,2]
According to this theory, the first step
is the formation of the intersphincteric
abscess located between the internal
sphincter
and
the
longitudinal
intersphincteric fibers, caused by the
infection of anal glands. Subsequently the
pus may force its way downward along the
longitudinal fibers 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 and developing the 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 (or supralevator) abscess.
(Figure 18)
According to their location abscesses
may be: (Figure 19)
Intersphincteric
Submucous
Perianal
Ischiorectal
High intermuscular
Supralevator
231
Anoperineal Pathology
Clinical picture
Perianal abscesses manifest with symptoms
and signs of an acute perianal inflammatory
process. Celsian signs: tumor, dolor, calor, rubor
and functio laesa are present.
Patient complains of pain, becoming more
and more intense. The patient cannot sit and in
most cases is feverish.
The classical signs of a perianal abscess
are: (Figure 20)
on inspection, a perianal swelling with
stretched, shiny, flushing skin
on palpation, a painful in duration with high local temperature. In advanced
stages, fluctuance may be felt. In more advanced stages, the ulcerated skin
with fistula and pus discharge appears.
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 maneuver is painful.
Natural evolution of perianal abscesses
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.
Intersphincterian abscess may spontaneously drain into the anal canal, or may
progress to other sites (perianal, submucous, ischiorectal, etc.).
Ischiorectal abscess evolves with symptoms of sepsis, or intrarectal fistulization is
possible in advanced stages.
Supralevator abscess, being very deep, is difficult to diagnose. Also evolves with
sepsis, and usually fistulization takes place into the rectum.[3]
In rare cases, the abscess can progress to a very serious form of necrotizing
fasciitis that extends to the genitals, the Fourniers gangrene.
Diagnosis
Diagnosis is usually 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:
Bartholins abscess
Hemorrhoidal thrombophlebitis
Douglas sac abscess
Gynecological inflammatory disease
Rectal tumors
232
Anoperineal Pathology
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. Surgical
treatment consists of incision, evacuation, debridement, lavage and drainage or
swabbing with hydrogen peroxide, in spinal or general anesthesia. Packing may be
beneficial at the time of abscess drainage by providing hemostasis of the inflamed,
hypervascular abscess cavity.[39]
Perianal and submucous abscesses are easily incised. Incision is made in the
maximum fluctuance.
In case of ischiorectal abscesses, perianal skin incision is guided by the finger
introduced into the rectum to find the collection.
In case of intersphincterian 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 into the rectum 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.[2,4,5] 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.
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. Pelvis CT
scan and ultrasound examination are useful
in diagnosis.
Horse shoe abscess (Figure 21)
appears in neglected cases of ischiorectal
abscess when puss spreads from one side to
the other via the retroanal or preanal space
thus giving rise to a bilateral ischiorectal
abscess, the so-called horse shoe abscess.
This type of abscess is not uncommon
(10-11%) and in most cases, the infection
starts from a posterior anal crypt.
Fournier's Gangrene (Figure 22) is a
specific form of necrotizing fasciitis.
Classically, it involves the penis and
scrotum, but it also can affect genitalia in
females.[6] 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
233
Anoperineal Pathology
destruction in necrotizing infections tend to spread along these planes. Pathognomonic
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. Associated diseases that
compromise the immune system have been incriminated as necessary predisposing
factors for the development of Fournier gangrene. The following are common
predisposing co-morbidities:
Diabetes mellitus (cited most often)
Morbid obesity
Cirrhosis
Vascular disease of the pelvis
Malignancies
High-risk behaviors (eg. alcoholism, intravenous drug abuse)
Immune suppression due to systemic disease or steroid administration
Early aggressive treatment of the underlying conditions is essential. Surgery
consists in large debridement, copious wounds lavage with hydrogen peroxide, removal
of necrotic tissues and hyperbaric oxygen. Risk of death is around 16%, and is related to
the patient's condition at presentation.[6]
Supralevator abscess is a rare condition and the most difficult to diagnose.
The patient presents with 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 fingertip. When the abscess fistulizes into the rectum and stools contain a large
quantity of pus, the diagnosis becomes easier. CT scan reveals the collection in the
supralevator space. Surgical treatment consists of a transanal incision of the rectal wall
in the maximum fluctuance. A drainage tube is placed in the abscess cavity and
exteriorized through the anal orifice.
References
1.
Parks AG. - Pathogenesis and treatment of fistula-in-ano. - Br. Med. J. 1961; 1:463469.
2.
Whiteford MH. - Benign Anorectal Conditions. Perianal Abscess/Fistula Disease. - Clin. Colon Rectal Surg. 2007; 20(2):
102109.
3.
Prasad ML, Read DR, Abcarian H. - Supralevator abscess: diagnosis and treatment. - Dis. Colon Rectum 1981;
24(6):456-461.
4.
Vasilevsky CA, Gordon PH. - The incidence of recurrent abscesses or fistula-in-ano following anorectal suppuration. Dis. Colon Rectum 1984; 27(2):126-130.
5.
Henrichsen S, Christiansen J. - Incidence of fistula-in-ano complicating anorectal sepsis: a prospective study. - Br. J.
Surg. 1986; 73(5):371-372.
6.
Eke N. - Fournier's gangrene: a review of 1726 cases. - Br. J. Surg. 2000; 87(6):718-728.
234
Anoperineal Pathology
Frequency: The prevalence rate is 8.6 cases per 100,000 individuals. The male-tofemale ratio is 1.8:1. The mean age of patients is 38.3 years.[1,2]
Causes:
Primary
The most common cause is the obstruction of the anal gland that leads to
stasis and infection with perianal abscess formation, which was previously
operated, or with spontaneous fistulization to the skin surface.
Secondary
Iatrogenic (hemorrhoidal surgery)
Inflammatory bowel diseases (Crohn's disease more common than
ulcerative colitis)
Infections (viral, fungal or TB)
Malignancy
Radiation
Clinical picture
Patients often provide a reliable history of previous pain, swelling, and
spontaneous or planned surgical drainage of an anorectal abscess. Symptoms are:
Perianal discharge (puss) through the external opening of the fistula
Pain
Swelling
Anal bleeding
Diarrhea
Skin excoriation
Physical examination. An external opening that appears as an open sinus or
elevation of granulation tissue can be observed on the perianal skin. Spontaneous
discharge via the external opening may be apparent or expressible upon digital rectal
examination. (Figure 23)
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
235
Anoperineal Pathology
and voluntary squeeze pressure should be assessed before any surgical intervention to
delineate whether preoperative manometry is indicated.
Investigations
Anuscopy is usually required to
identify the internal opening.
Ultrasound, fistulography and MRI
investigations are not performed routinely
but they are helpful in highlighting an occult
cause of fistula recurrence. In recent years,
endoanal ultrasound (EUS) has been widely
used in the assessment of fistula and, in most
cases, shows the position of the internal
opening.[3]
When describing a fistula, it is
important to mention the following aspects:
Position of the skin opening on axial images (using the anal clock)
Distance of the opening to the anal verge
Secondary fistulas or abscesses
Several techniques have been described to help locate the trajectory of the fistula
and more important: to identify the internal opening. One of these is the instrumental
exploration of fistula tract. Care should be taken to not use excessive force and create
false passages. If internal orifice cannot be detected, blue dye or hydrogen peroxide may
be injected through the external orifice under direct visualization of the interior aspect
of the anal canal.
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
Classification
The most widely used is the Parks
classification, which distinguishes four
kinds of fistula: (Figure 24)[4]
1. Intersphincteric (25%)
2. Transsphincteric (69.2%)
3. Suprasphincteric (5%)
4. Extrasphincteric (3.8%)
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.
236
Anoperineal Pathology
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 which is not related to the sphincter or the perianal
glands and is not part of the Parks
classification. These are more often due to
Crohn's disease or anorectal procedures such
as hemorrhoidectomy or sphincterotomy.
Goodsalls rule (Figure 25)
This rule 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 posterior. 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.
Principles of treatment
Anal fistulas never heal spontaneously. The inner wall of the fistula develops
fibers and pyogenic membrane that does not allow spontaneous healing. Only surgical
treatment can heal the fistula. There are three main surgical procedures:
1. Fistulotomy (cutting/opening the fistula tract)
2. Fistulectomy (excision the whole fistula tract)
3. Seton placement
There are many other techniques including laser coagulation of the fistula tract,
sealing with fibrin glue, collagen plugs, etc.[3,5]
In simple cases, fistulotomy is preferred to fistulectomy because it does not
involve excision of a portion of the sphincteric muscle. Seton placement is rarely used
because it is a very painful procedure.
Fistulotomy (Figure 26)
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.
237
Anoperineal Pathology
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. (Figure
27)
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. (Figure 28)
Postoperative care
Sitz baths, analgesics, and stool bulking e are recommended. It is important to
ensure that the wound does not close prematurely, causing a recurrent fistula. Wound
healing usually occurs within 6 weeks.
Complications
Early postoperative
Urinary retention
Bleeding
Fecal impaction
Hemorrhoidal thrombosis
Delayed postoperative
Recurrence
Anal incontinence
Anal stenosis
Delayed wound healing
238
Anoperineal Pathology
/Outcome and Prognosis
Following standard fistulotomy, the reported rate of recurrence is 0-18% and the
rate of any stool incontinence is 3-17%.[6-8] There are no major difference between the
various techniques as far as recurrence rates are concerned.[9]
There are cases with multiple recurrences or complex fistulas that sometimes
require making a temporary loop colostomy, to divert the feces from anorectum and to
allow healing after fistulectomy or fistulotomy.
To prevent recurrences several conditions are necessary:
Fistula tract must be removed entirely (fistulectomy) that is more difficult in
complex fistulas. Fistula track can be marked with methylene blue dye.
Internal orifice should be discovered
Wound healing must happen from the depth toward the surface
References
1.
2.
Sainio P. - Fistula-in-ano in a defined population. Incidence and epidemiological aspects. - Ann. Chir. Gynaecol. 1984;
73(4):219-224.
3.
Helena Tabry, Farrands PA. - Update on anal fistulae: Surgical perspectives for the gastroenterologist. - Can. J.
Gastroenterol. 2011; 25(12):675680.
4.
Ozkavukcu E, Haliloglu N, Erden A. - Frequencies of perianal fistula types using two classification systems. - Jpn. J.
Radiol. 2011; 29(5):293-300.
5.
Whiteford MH. - Benign Anorectal Conditions. Perianal Abscess/Fistula Disease. - Clin. Colon Rectal Surg. 2007;
20(2):102109.
6.
Garcia-Aguilar J, Belmonte C, Wong WD, Goldberg SM, Madoff RD. - Anal fistula surgery. Factors associated with
recurrence and incontinence. - Dis. Colon Rectum 1996; 39(7):723-729.
7.
Vasilevsky CA, Gordon PH. - Results of treatment of fistula-in-ano. - Dis. Colon. Rectum 1985; 28(4):225-231.
8.
van Tets WF, Kuijpers HC. - Continence disorders after anal fistulotomy. - Dis. Colon Rectum 1994; 37(12):1194-1197.
9.
Jacob TJ, Perakath B, Keighley MR. - Surgical intervention for anorectal. - Cochrane Database Syst. Rev. 2010;
(5):CD006319.
239
Surgical anatomy
Acute appendicitis
Chronic appendicitis
Tumors of the appendix
1. Surgical Anatomy
Appendix begins to develop in the fifth month of intrauterine life. It is a
cylindrical hollow organ, worm-like (hence the Latin name "appendix vermicularis"),
with a length ranging between 2 and 30 cm and a diameter of about 0.5 to 0.8 cm. It is
located at the bottom of the cecum (Figure 1) at the convergence of the three tenia coli
(omental, mesenteric and free). This last aspect is of particular importance in detecting
the base of the appendix through a small laparotomy. Another constant landmark is the
implantation of the appendix in cecum at approximately 2.5 cm medial and posterior to
the ileo-cecal valve. (Figure 2)
240
2. Acute Appendicitis
Despite progresses in antibiotic therapy and surgery, acute appendicitis remains a
surgical emergency being the main cause of admissions in emergency for acute surgical
abdomen. The only rational therapeutic approach remains the appendectomy. 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 in every five appendicitis is misdiagnosed, especially in
women, and the incidence of normal (unmodified) appendix during appendectomy is
estimated at 10-40% of all cases.[3-7]
History
The appendix was probably recorded for the first time in Egyptian civilization
(3000 BC) during mummification. Although appendicitis was a common disease, only
at the beginning of the 9th century the appendix was identified as an organ capable of
producing disease.[8]
241
242
243
245
247
appendicitis. Diarrhea and the absence of anorexia, nausea, and vomiting favor
differential diagnosis but are not sufficient to exclude an acute appendicitis. In many
cases, regional enteritis is diagnosed during the operation for a supposed
appendicitis.
Other conditions of the colon. Perforated diverticulitis of the ascending colon, or
more often of a long sigmoid loop set in the right iliac fossa, or perforated tumor of
the cecum may be indistinguishable from a perforated appendicitis and are usually
intraoperative surprises. History is of great importance in these cases.
Ureteral stones. A stone in the ureter near the appendix can simulate retrocecal
appendicitis. Radiation of pain to the labia, scrotum, or penis, the positive sign of
Giordano, hematuria and/or the absence of fever or leukocytosis suggest the renal
colic. Ultrasound examination or pyelogram usually confirms stones.
Urinary infection. Acute pyelonephritis, especially on the right side, can mimic
acute retrocecal appendicitis. Chills, pains in the costo-vertebral angle as well the
presence of bacteriuria in urinalysis allow differentiation of the two diseases.
Primitive peritonitis. It rarely mimics a simple acute appendicitis; in turn, symptoms
are similar to those of the secondary peritonitis caused by appendicular perforation.
Diagnosis is set by bacteriological analysis of peritoneal fluid obtained by puncture.
Monomicrobial flora indicates a primitive peritonitis and it will be treated
medically, whereas a polymicrobial flora suggests secondary peritonitis.
Henoch-Schonlein purpura (anaphylactoid purpura, or purpura rheumatica). This
syndrome usually occurs in 2-3 weeks after a streptococcal infection. Abdominal
pain may be prevalent but associated purpura and nephritic syndrome are usually
present.[24,25]
Gynecological pathology. Acute appendicitis diagnosis errors are most common in
young women. 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.
Other conditions occurring in both sexes and at any age: bowel perforation caused
by foreign body, mechanical bowel obstruction, mesenteric infarction, lower right
pleurisy, acute cholecystitis, acute pancreatitis and abdominal wall hematoma.
251
252
253
Sequences:
Preparation of the operative field: skin disinfection is not limited to the right
iliac fossa but extended to the entire anterior abdominal wall, because there
are cases (generalized peritonitis) when the McBurney incision must be
converted into a more extended laparotomy.
Opening the peritoneal cavity: skin incision, subcutaneous hemostasis, cutting
the Scarpa's fascia, longitudinal incision of the external oblique muscle
aponeurosis, dissociation of internal oblique and transverse muscles fibers,
incision of fascia transversalis, opening the peritoneum and isolation of the
peritoneal cavity. On opening the peritoneal cavity usually, the first
anatomical element that appears in the operative field is the greater omentum
attracted there by the inflammatory process. Particular attention should be
paid to the peritoneal fluid that may be purulent, fetid, denoting a perforated
appendicitis. A turbid odorless liquid is not a sign of perforation.
Finding the appendix is the next step and not always a very easy task. The
exploration is performed with two anatomical forceps. Finding the cecum is
easier and then, following the tenia leads us to the base of the appendix. In
difficult cases digital exploration of the abdominal cavity helps in finding the
appendix, which is felt as an
increased consistency cord.
Appendectomy.(Figure 10) Once
the
appendix
found,
the
appendectomy can be conducted in
an anterograde or retrograde way.
When the tip of the appendix is
easily found and available in the
operative field, the anterograde
appendectomy is the choice. The
mesoappendix containing blood
vessels is cut and ligated between
two forceps. The base of the appendix is ligated near the cecum. A purse
string is applied on the cecum serosa around the base of the appendix. The
appendix is cut and removed (this represents the septic phase of the operation
and care must be taken to avoid contamination of the operative field). The
remaining appendicular stump is sunken (clogged) into the cecum using the
purse string (some authors consider this maneuver as a stump inversion but it
is not a real inversion because the appendicular stump is just covered by
254
256
257
3. Chronic Appendicitis
Chronic appendicitis is represented by micro- and macroscopic lesions of the
appendix resulted after (repeated) inflammatory processes of moderate acute
appendicitis that evolved towards resolution.
The macroscopic appearance of appendix can be:
Without obvious changes
Sclero-hypertrophic. The appendix is enlarged, thickened, well
vascularized with infiltrated mesoappendix and enlarged lymph nodes.
Sclero-atrophic. The appendix is small or thin with areas of stenosis or
uniform caliber and thickened mesoappendix.
Atrophic processes affecting mucosa, submucosa and muscular layers often
dominate histopathology.
Along with appendicular lesions, there is a regional lymphangitis. Often, the
appendix is adherent to neighboring organs (cecum, ileum, the right adnexa, omentum,
mesentery, sigmoid colon, etc.). Multiple membranes (Jackson) sometimes cover the
appendix.
Symptoms and signs
There are no specific symptoms for chronic appendicitis. The clinical picture may
vary greatly, mimicking almost any abdominal pathology.
The main complaints are:
Abdominal pain mainly located in the right iliac fossa, flank, and right upper
quadrant. The pain has nothing specific.
Dyspeptic phenomena manifested by bloating, nausea, belching and
frequently constipation.
Neuropsychological complaints represented by fatigue, insomnia, headache.
Clinical examination usually reveals a diffuse abdominal tenderness with
moderate pain within the right iliac fossa. Otherwise, there are no other pathological
changes unless an associated pathology is present.
Diagnosis and treatment
Except for histopathology, no other investigation can specify with certainty the
diagnosis of chronic appendicitis.
The diagnosis of chronic appendicitis is actually made by exclusion of other
conditions that may cause the patients symptoms. Usually these patients have multiple
admissions to various medical services, especially gastroenterology, and numerous
investigations, which do not reveal any obvious changes justifying symptoms. Most
often patients undergo conservative treatment, that brings temporary relief of symptoms,
but finally they will reach in a surgical department. Thorough medical history may be
helpful in diagnosis.
Treatment is represented by appendectomy preferable by laparoscopic approach,
which offers the possibility of general visual exploration of the abdominal cavity. In
many cases, although appendectomy was performed, complaints may persist after
surgery, and is good for the patient to be informed preoperatively on that eventuality.
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259
Appendicular mucocele
Mucocele is a rare appendicular tumor (0.3% of all appendectomies) represented
by a unique or multiple cystic dilatation of the appendix, with a mucoid content.
There are four histopathologic forms: simple appendiceal mucocele, mucocele
with epithelial hyperplasia, cystadenoma and cystadenocarcinoma; the last two
subgroups represent neoplastic forms.[55]
Benign mucocele is an accumulation of mucus produced by Goblet cells into the
appendicular lumen, caused by 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 in classical appendectomy
with caution not to disseminate the tumor content by breaking the appendicular wall. As
long as there is no preoperative certainty of benign origin, most authors contraindicate
laparoscopic appendectomy in these cases because of the risk to break the appendix
during manipulation and intraperitoneal dissemination of cancer.
Malignant mucocele (one case of nine) actually represents a first degree of
mucous papillary adenocarcinoma. The mucus contains muciparous cells that can
260
261
Medscape
reference
Emedicine
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2012; 203(4):503-507.
40. Berry J Jr, Malt RA. - Appendicitis near its centenary. - Ann. Surg. 1984; 200(5):567-575.
41. Ricci MA, Trevisani MF, Beck WC. - Acute appendicitis: A 5-year review. - Am. Surg. 1991; 57:301305.
42. Grleyik G, Grleyik E. - Age-related clinical features in older patients with acute appendicitis. - Eur. J. Emerg. Med. 2003;
10(3):200-203.
43. Barquist E, Zinner M. - Chapter 102 Neoplasms of the Small Intestine, Vermiform Appendix, and Peritoneum. - Holland-Frei
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44. Schmutzer KJ, Bayar M, Zaki AE, Regan JF, Poletti JB. - Tumors of the appendix. - Dis. Colon Rectum. 1975; 18(4):324-331.
45. Chang P, Attiyeh FF. - Adenocarcinoma of the appendix. - Dis. Colon Rectum. 1981; 24(3):176-180.
46. Gilhome RW, Johnston DH, Clark J, Kyle J. - Primary adenocarcinoma of the vermiform appendix: report of a series of ten
cases and review of the literature. - Br. J. Surg. 1984; 71(7):553-555.
47. Modlin IM, Lye KD, Kidd M. - A 5-Decade Analysis of 13,715 Carcinoid Tumors. - Cancer 2003; 97(4):935-959.
48. Plckinger U, Rindi G, Arnold R, et al. - Guidelines for the Diagnosis and Treatment of Neuroendocrine Gastrointestinal
Tumours A Consensus Statement on Behalf of the European Neuroendocrine Tumour Society (ENETS) - Neuroendocrinology
2004; 80:394424.
49. Mein C, Vasile I, Vlcea ID, Paalega M, Calot F, Enache DS, Dumitrescu T, Mirea C, Mogoanta S. - Carcinoid tumour of
the appendix: problems of diagnosis and treatment. - Chirurgia (Bucur). 2011; 106(2):239-245.
50. Collins DC. - 71,000 human appendix specimens. A final report summarizing forty years study. - Am. J. Proctol. 1963;
14:365.
51. Moertel CG, Dockerty MB, Judd ES. - Carcinoid tumors of the vermiform appendix. - Cancer 1968; 21:270.
52. Ramage JK, Ahmed A, Ardill J, et al; UK and Ireland Neuroendocrine Tumour Society. - Guidelines for the management of
gastroenteropancreatic neuroendocrine (including carcinoid) tumours (NETs). - Gut 2012; 61(1):6-32.
53. Goede AC, Caplin ME, Winslet MC. - Carcinoid tumour of the appendix. - Br. J. Surg. 2003; 90(11):1317-1322.
54. Fornaro R, Frascio M, Sticchi C, De Salvo L, Stabilini C, Mandolfino F, Ricci B, Gianetta E. - Appendectomy or right
hemicolectomy in the treatment of appendiceal carcinoid tumors? - Tumori 2007; 93(6):587-590.
55. Caracappa D, Gull N, Gentile D, Listorti C, Boselli C, Cirocchi R, Bellezza G, Noya G. - Appendiceal mucocele. A case
report and literature review. - Ann. Ital. Chir. 2011; 82(3):239-245.
56. Jandu Gomes De Abreu Filho; Erivaldo Fernandes De Lira - Mucocele of the appendix : appendectomy or colectomy? - J.
Coloproctol. (Rio J.) 2011; 31(3).
57. Esquivel J, Sticca R, Sugarbaker P, Levine E, Yan TD, Alexander R, et al. - Cytoreductive surgery and hyperthermic
intraperitoneal chemotherapy in the management of peritoneal surface malignancies of colonic origin: a consensus statement. Ann. Surg. Oncol. 2007; 14(1):128-133.
58. Gonzlez Moreno S, Sugarbaker PH. - Right hemicolectomy does not confer a survival advantage in patients with mucinous
carcinoma of the appendix and peritoneal seeding. - Br. J. Surg. 2004; 91(3):304-311.
262
1. Surgical Anatomy
The pancreas is a mixed gland. It has two components:
1. The exocrine component, composed of glandular acini and ducts of
pancreatic juice excretion, and
2. The endocrine component, represented by pancreatic insulin secreting
islands of Langerhans, and other pancreatic hormones, which are released
directly into the blood stream.
The length of pancreas is about 15-18
cm and it weights 70-90 g. The pancreas was
divided arbitrary in 5 segments: (Figure 1)
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-Grgoire 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 duodenopancreatic posterior mobilization (the Kocher maneuver) during surgery in this region.
The pancreas is located across, from duodenal horseshoe (to the right) towards the
hilum of the spleen (to the left), being a fixed organ.
Anatomical relations
The root of the transverse mesocolon attaches on the anterior surface of the
pancreas dividing it into two regions: one inframesocolic and the other supramesocolic.
The head and neck of the pancreas (Figure 2)
The head of the pancreas is attached to the 2nd and 3rd portion of the duodenum (the
duodenal horse shoe) by the biliopancreatic confluence which flows into the
duodenum through the Vaters ampulla at level of papilla major (the papilla minor is for
the Santorini duct). The common bile duct (choledocus) passes through the posterior
surface of the pancreas.
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265
Lesser duct of Santorini is an accessory duct that drains the superior portion
of the head of the pancreas and empties separately into the second portion of
the duodenum through the papilla minor. In 30 % of cases, Santorini duct is
blind, and in 10 % of cases, it bears the entire pancreatic secretion. (Figure 6)
The pressure inside the pancreatic ducts is higher than in CBD (15 - 30 mm Hg,
versus 7 - 17 in CBD), thus preventing the reflux of bile and damage of the pancreatic
ducts, that can lead to an acute pancreatitis.
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 highest in the tail of the pancreas.
Islet cells are of several types:
Cells A or (20%, produce glucagon)
Cells B or (75%, produce insulin)
Cells D or (produce somatostatin)
Cells non- (PP cells, produce pancreatic polypeptid )
Cells D1 (produce vasoactive intestinal polypeptid VIP)
Cells G (produce gastrin)
Cells C (clear cells without secretory granules), etc.
Insulin secretion starts from the fifth intrauterine month.
Arterial supply of the pancreas is ensured by three main sources: (Figure 7)
1. Common hepatic artery
2. Splenic artery (from celiac trunk)
3. Superior mesenteric artery
266
2. Acute Pancreatitis
Acute pancreatitis represents the anatomo-clinical expression of the acute
syndrome of pancreatic and peripancreatic autodigestion.
Acute pancreatitis is an acute pancreatic inflammation, usually with rapid onset of
pain, accompanied by vomiting and systemic inflammatory response syndrome (SIRS)
with high levels of pancreatic enzymes in blood and urine (in urine not always present).
Epidemiology
Annual incidence is ranging from 5 to 80 per 100,000 inhabitants.[1-5]
In Europe and other developed nations, more patients tend to have gallstone
pancreatitis, whereas in the United States, alcoholic pancreatitis is the most common.[1]
Mortality and morbidity
The overall mortality rate of patients with acute pancreatitis ranges between 2%
and 15% but values depend very much on author.[1-3,6] 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.[3,7]
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.[8]
Race. Pancreatitis incidence is three times higher in blacks than in whites. These
racial differences are more visible for males than females.[1,9]
Sex. In general, acute pancreatitis affects males more often than females. The
etiology in males is more often related to alcohol, whereas 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:[10]
Alcohol related - 39 years
Biliary tract related - 69 years
Trauma related - 66 years
Drug induced etiology - 42 years
Endoscopic retrograde cholangiopancreatography 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.[1]
Classification
Histopathological classification:
Edematous acute pancreatitis
Necrotic acute pancreatitis
Suppurated acute pancreatitis
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269
270
271
272
Laboratory
Hyperamylasemia (normal values of amylasemia are 8-32 Wolgemuth u, or <150.
Somogy u, or <300 Phadebas u) becomes positive at 2-12 hours after the onset, reaches
a maximum at 24 hours and returns to normal after 4-7 days in mild pancreatitis. The
273
274
CT Grade Points
0 points
1 point
2 points
3 points
4 points
Points
0 points
2 points
Necrosis Percentage
30 to 50% necrosis
Over 50% necrosis
Points
4 points
6 points
275
276
Within 48
hours:
Criteria
Age in years
White blood cell count
Blood glucose
Serum AST (Aspartate
transaminase)
Serum LDH (Lactate
dehydrogenase)
Serum calcium
Hematocrit fall
Oxygen
BUN
Base deficit
Sequestration of fluids
Interpretation. Each positive Ranson parameter is noted with 1 point, so the score
can vary between 0 and 11 points. A score higher than 3 already announces the
possibility of evolving to a severe pancreatitis.
If the score 3, severe pancreatitis is likely
If the score < 3, severe pancreatitis is unlikely
Or
Score 0 to 2 : 2% mortality
Score 3 to 4 : 15% mortality
Score 5 to 6 : 40% mortality
Score 7 to 8 : 100% mortality
Complications
Pancreatic sequesters (sequestrum/sequestra) represent delimitated fragments of
necrotic pancreatic and peripancreatic tissue, which appear in about the second week
after the debut of pancreatitis. Almost 50% of sterile necrosis will evolve to resorption.
Effusions are represented by necrosis of peripancreatic tissues (especially fat
tissue) with tendency to expand into the root of the mesentery and retroperitoneum
278
279
Medical treatment
Aggressive treatment for preventing and treating hypovolemia and shock
Fighting respiratory failure: patients with acute pancreatitis should be closely
monitored by pulse oximetry and blood gas analysis, in order to act immediately in
case of respiratory insufficiency. Arterial pO2 below 70 mmHg requires nasal
oxygen, while decreasing below 60 mmHg is an indication for tracheal intubation
with assisted mechanical ventilation.
Putting at rest the pancreas is achieved by absolute food abstention and establishing
a continuous nasogastric aspiration. The aim is to suppress exo- and endogenous
stimuli of pancreatic secretion.
Nutritional support: it is important to achieve a high protein (1.5 g/kg/day) and
caloric (25-30 cal/kg/day) intake.[24] Classical parenteral nutrition is supplemented
with modern enteral nutrition achieved through a jejunal tube placed endoscopically
or by minilaparotomy in order to avoid the occurrence of intestinal mucosal atrophy
accompanied by bacterial translocation.
Restoring electrolyte and acid-base balance by administration of sodium,
potassium, magnesium, calcium.
Analgesia is a primary objective, given the severity of pain. The continuous epidural
anesthesia has a benefic role.
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 used for cure if infection is set, being
conducted based on antibiogram, or for prophylactic purpose.
Corticosteroid therapy is beneficial in the initial phase of the disease, both by
protecting cell membranes and due to its antishock, anti-inflammatory, antitoxic and
anti allergic effects.
Inhibitors 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:
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281
2.
Sekimoto M, Takada T, Kawarada Y, et al. - JPN Guidelines for the management of acute pancreatitis: epidemiology,
etiology, natural history, and outcome predictors in acute pancreatitis. - J. Hepatobiliary Pancreat. Surg. 2006; 13(1):10
24.
3.
Spanier BW, Dijkgraaf MG, Bruno MJ. - Epidemiology, aetiology and outcome of acute and chronic pancreatitis: An
update. - Best Pract. Res. Clin. Gastroenterol. 2008; 22(1):45-63.
4.
Appelros S, Borgstrm A. - Incidence, aetiology and mortality rate of acute pancreatitis over 10 years in a defined urban
population in Sweden. - Br. J. Surg. 1999; 86(4):465470.
5.
Banks PA. - Epidemiology, natural history, and predictors of disease outcome in acute and chronic pancreatitis. Gastrointest. Endosc. 2002; 56(6 Suppl):S226230.
6.
De Bolla AR, Obeid ML. - Mortality in acute pancreatitis. - Ann. R. Coll. Surg. Engl. 1984; 66(3):184186.
7.
Lund H, Tnnesen H, Tnnesen MH, Olsen O. - Long-term recurrence and death rates after acute pancreatitis. - Scand. J.
Gastroenterol. 2006; 41(2):234-238.
8.
Renner IG, Savage WT, Pantoia JL, Renner VJ. - Death due to acute pancreatitis: a retrospective analysis of 405 autopsy
cases. - Dig. Dis. Sci. 1985; 30:1005-1018.
9.
Fagenholz PJ, Fernndez-del Castillo C, Harris NS, Pelletier AJ, Camargo CA. - National study of United States
emergency department visits for acute pancreatitis, 19932003. - BMC Emerg. Med. 2007; 7:1.
10.
Chang MC, Su CH, Sun MS, Huang SC, Chiu CT, Chen MC, Lee KT, Lin CC, Lin JT. - Etiology of acute pancreatitis -a
multi-center study in Taiwan. - Hepatogastroenterology 2003; 50(53):1655-1657.
11.
Banks PA. - A new classification system for acute pancreatitis. - Am. J. Ggastroenterol. 1994; 89:151-152.
12.
Guo-Jun Wang, Chun-Fang Gao, Dong Wei, Cun Wang, Si-Qin Ding. - Acute pancreatitis: Etiology and common
pathogenesis. - World J. Gastroenterol. 2009; 15(12):14271430.
13.
Lankisch PG, Assmus C, Pflichthofer D, Struckmann K, Lehnick D. - Which etiology causes the most severe acute
pancreatitis? - Int. J. Pancreatol. 1999; 26(2):55-57.
14.
Lankisch PG, Assmus C, Lehnick D, Maisonneuve P, Lowenfels AB. - Acute pancreatitis: does gender matter? - Dig.
Dis. Sci. 2001; 46(11):2470-2474.
15.
Agarwal N, Pitchumoni CS, Sivaprasad AV. - Evaluating tests for acute pancreatitis. - Am. J. Gastroenterol. 1990;
85(4):356-366.
16.
Treacy J, Williams A, Bais R, Willson K, Worthley C, Reece J, Bessell J, Thomas D. - Evaluation of amylase and lipase
in the diagnosis of acute pancreatitis. - ANZ J Surg. 2001; 71(10):577-582.
17.
Balthazar EJ. - Acute Pancreatitis: Assessment of Severity with Clinical and CT Evaluation. - Radiology 2002; 223:603613.
18.
Balthazar EJ, Robinson DL, Megibow AJ, Ranson JH. - Acute pancreatitis: value of CT in establishing prognosis.
Radiology 1990; 174(2):331336.
19.
Fiocca F, Santagati A, Ceci V, Donatelli G, Pasqualini MJ, Moretti MG, Speranza V, Di Giuli M, Minervini S, Sportelli
G, Giri S. - ERCP and acute pancreatitis. - Eur. Rev. Med. Pharmaco. Sci. 2002; 6(1):13-17.
20.
Fan ST, Lai EC, Mok FP, Lo CM, Zheng SS, Wong J. - Early treatment of acute biliary pancreatitis by endoscopic
papillotomy. - N. Eng. J. Med. 1993; 328(4):228-232.
21.
22.
Corfield AP, Cooper MJ., Williamson RC, et al. - Prediction of severity in acute pancreatitis: prospective comparison of
three prognostic indices. - Lancet 2, 1985; (8452):403407.
23.
Ranson JH, Rifkind KM, Roses DF, Fink SD, Eng K, Spencer FC. - Prognostic signs and the role of operative
management in acute pancreatitis. - Surgery, Gynecology & Obstetrics 1974; 139(1):6981.
24.
Ong JP, Fock KM. - Nutritional support in acute pancreatitis. - J. Dig. Dis. 2012; 13(9):445-452.
282
283
284
3. MRI has no additional advantages over the CT scan except the fact that it does
not irradiate. Unfortunately, it cannot be applied to very obese patients, to those bearing
aneurism clips or cardiac pacemaker or to patients suffering of claustrophobia.
4. CT or MR cholangiography is a CT or MRI investigation associated with
intravenous or oral biliary contrast agent. (Figure 26) It provides noninvasive
information about the morphology of the biliary tract. The main limitation of these
contrast agents is that the rate of allergic reactions and of renal or hepatic toxicity (or
both) is relatively high.[30]
5. Endoscopic retrograde cholangiopancreatography (ERCP) can differentiate
cephalic pancreatic tumor from other periampullary tumors producing obstructive
jaundice. It offers the possibility to perform biopsies and to introduce stents into the
common bile duct in cases of inoperable patients. It is an invasive method being
associated with some risks and complications
(complications rate ranges from 0.5% to 5%).[31]
6.
Percutaneous
transhepatic
cholangiography (PTC) is also an invasive
method. A fine needle is introduced
percutaneously under ultrasound guidance
transhepatic into a biliary duct and a contrast
agent is injected. The anatomy of the biliary tract
is very well delineated. PTC is more useful in
tumors of the CBD than in those of the pancreas
where ERCP is superior. It can be also followed
by an external biliary drainage by introducing a
drainage tube into the intrahepatic biliary duct.
287
288
Staging [35]
Primary Tumor (T)
TX
Minimum requirements cannot be met
Limited to pancreas, less than 2.0 cm in diameter
T1
T2
Limited to pancreas, 2 to 6 cm in diameter
T3
Over 6 cm in diameter
T4
Extrapancreatic direct extension to contiguous structures
Nodal Involvement (N)
NX
Minimum requirements cannot be met
N0
No metastatic nodes
N1
One regional group involved at laparotomy
N2
Two or more regional groups involved at laparotomy
N3
Clinical evidence of regional node involvement (no laparotomy)
N4
Involvement of juxtaregional nodes
Distant Metastasis (M)
MX
Not assessed
M0
No (known) distant metastasis
M1
Distant metastasis present
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 and multimodal (surgery, oncology,
pain therapy, etc.).
Tumors located in the head of the pancreas may have the chance to benefit from
radical surgery because they produce early mechanical jaundice and so the tumor can be
diagnosed in an earlier phase of development. However, only 10-20% of pancreatic
cancers benefit from radical surgery.[36] In most cases, tumor cannot be removed
because it penetrates the major vascular structures (portal vein, superior mesenteric
artery) or other organs. In these cases, only palliative surgery can be performed.
Usually, there is an important peritumoral inflammatory process even though on CT
scan images the tumor seems to be resectable.
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 need bypass surgery but duodenal stenting in nowadays is also possible.[3739]
289
290
291
Intraoperative 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.[40] During the 1980s, however, many centers reported
mortality rates around 5% and a morbidity of 25% to 60%.[41,42] In high-volume
centers, with a substantial experience, mortality decreased below 5% and morbidity
below 40%.[43]
Many early local complications (more than 45 types) may appear in the
postoperative period. Anastomotic fistulas or leaks (at site of
292
293
294
In patients who do not support any surgery or stenting cannot be performed, the
percutaneous drainage of the biliary tract may be a solution. (Figure 37) It is
performed under ultrasound and eco-doppler guidance. A catheter is placed into a
biliary duct and bile is diverted outside.
Resolving the duodenal stenosis
About 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 Rouxen-Y loop. (Figure 38) A non-surgical procedure is the endoscopic duodenal stenting.
(Figure 39)
295
Fighting pain
Chemoneurolysis represents the infiltration of the celiac plexus with 50% phenol
or alcohol during palliative surgery with net improvement in pain for several months
(Figure 40), either before or after surgery by percutaneous approach (Figure 41) under
radiological or ultrasound guidance. This nerve block may last for up to 3 or 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 the external beam radiation
therapy. The radiation beam is directed at the tumor and may provide fast onset of pain
relief.
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20. Tascilar M, van Rees BP, Sturm PD, Tytgat GN, Hruban RH, Goodman SN, Giardiello FM, Offerhaus GJ, Tersmette
AC. - Pancreatic cancer after remote peptic ulcer surgery. - J. Clin. Pathol. 2002; 55(5):340-345.
21. Olson SH. - Selected medical conditions and risk of pancreatic cancer. - Mol. Carcinog. 2012; 51(1):75-97.
22. Ye W, Lagergren J, Nyrn O, Ekbom A. - Risk of pancreatic cancer after cholecystectomy: a cohort study in Sweden. Gut 2001; 49(5):678-681.
23. Chow WH, Johansen C, Gridley G, Mellemkjaer L, Olsen JH, Fraumeni JF Jr. - Gallstones, cholecystectomy and risk of
cancers of the liver, biliary tract and pancreas. - Br. J. Cancer 1999; 79(3-4):640-644.
24. Borch K, Kullman E, Hallhagen S, Ledin T, Ihse I. - Increased incidence of pancreatic neoplasia in pernicious anemia. World J. Surg. 1988; 12(6):866-870.
25. Karlson BM, Ekbom A, Wacholder S, McLaughlin JK, Hsing AW. - Cancer of the upper gastrointestinal tract among
patients with pernicious anemia: a case-cohort study. - Scand. J. Gastroenterol. 2000; 35(8):847-851.
26. Permuth-Wey J, Egan KM. - Family history is a significant risk factor for pancreatic cancer: results from a systematic
review and meta-analysis. - Fam. Cancer 2008; 8(2):109-117.
27. Jacobs EJ, Chanock SJ, Fuchs CS, et al. - Famly history of cancer and risk of pancreatic cancer: A pooled analysis from
the pancreatic cancer cohort consortium (PANSCAN). - Int. J. Cancer 2010; 127(6):1421-1428.
28. Dieter Birk and Hans G Beger. - Pancreatic cancer. - Surgical Treatment: Evidence-Based and Problem-Oriented.
Holzheimer RG, Mannick JA, editors. Munich: Zuckschwerdt; 2001. Bookshelf ID: NBK6961.
http://www.ncbi.nlm.nih.gov/books/NBK6961/
29. Tseng JF, Warshaw AL, Sahani DV, et al. - Serous Cystadenoma of the Pancreas. Tumor Growth Rates and
Recommendations for Treatment. - Ann. Surg. 2005; 242(3):413421.
30. Ott DJ, Geland DW. - Complications of gastrointestinal radiologic procedures. II. Complications related to biliary tract
studies. - Gastrointest. Radiol. 1981; 6:47-52.
31. American Society for Gastrointestinal Endoscopy - Complications of ERCP - Gastrointestinal Endoscopy, 2012; Volume
75, 3:467-474 http://www.asge.org/WorkArea/showcontent.aspx?id=14602
32. Powis ME, Chang KJ. - Endoscopic Ultrasound in the Clinical Staging and Management of Pancreatic Cancer: Its Impact
on Cost of Treatment. - Cancer Control 2000; 7(5):413-420.
33. Rosch T, Lorenz R, Braig C, et al. - Endoscopic ultrasound in pancreatic tumor diagnosis. - Gastrointest. Endosc. 1991;
37:347-352.
34. Yasuda K, Mukai H, Fujimoto S, et al. - The diagnosis of pancreatic cancer by endoscopic ultrasonography. Gastrointest. Endosc. 1988; 34:1-8.
35. International Union against cancer (1997) - TNM classification of malignant tumors. - WileyLiss, New York .
36. Li D, Xie K, Wolff R, Abbruzzese JL. - Pancreatic Cancer. - Lancet 2004; 363:10491057.
37. Frdrique Maire, Pascal Hammel, Philippe Ponsot, et al. - Long-term Outcome of Biliary and Duodenal Stents in
Palliative Treatment of Patients with Unresectable Adenocarcinoma of the Head of Pancreas. - Am. J. Gastroenterol.
2006; 101(4):735-742.
38. Moura EG, Ferreira FC, Cheng S, Moura DT, Sakai P, Zilberstain B. - Duodenal stenting for malignant gastric outlet
obstruction: prospective study. - World J. Gastroenterol. 2012; 18(9):938-943.
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298
Segmentation
Functionally, the right and left lobe are of about equal size and are separated by a
line extending from the inferior vena cava (posterior) to the middle of the gallbladder
fossa (anterior). This is the most important
topographic line for orientation in liver surgery.
(Figure 2)
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. Segment 4 is sometimes
divided into segment 4a and 4b according to
Bismuth classification. The numbering of
segments is in a clockwise manner. (Figure 3)
299
Anatomical relationships
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. It is completely covered by peritoneum
except along the line of attachment of the falciform ligament. The falciform ligament
defines anatomically the right and left lobes. On the right lobe, costal arch impressions
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. Pathological processes located
here (especially hydatid cyst and abscesses) may affect the pleural cavity (pleurisy,
empyema) and even the lung (biliobronchial fistula).
2) The inferior surface is divided into four lobes by five fossas arranged in the
form of the letter H. (Figure 1)
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 behind, the fossa for the Arantius ligament, which was a venous duct
connecting the umbilical vein to the inferior cava vein in the intrauterine life.
The right limb of the H is formed in front by the fossa for the gall bladder, and
rear by the fossa for the inferior vena cava. These two fossas are separated by a band of
liver substance, termed as caudate process. The bar connecting the two limbs of the H
is the liver hilum where the portal vein separates into two branches (transverse fissure)
entering the liver. The quadrate lobe lies in front of it and the caudate lobe behind it.
The transverse fissure contains the liver hilum formed by hepatic pedicle consisting of
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.
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 liver surface. The surface is almost completely covered by peritoneum.
Quadrate lobe comes against the pyloric portion of the stomach, the duodenum, and
transverse colon. Caudate lobe has relations with the diaphragm, cava vein, esophagus,
celiac trunk, the upper edge of the pancreas and the lesser curvature of the stomach.
3) The posterior surface of the liver 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 or
area nuda) and is in direct contact with the diaphragm.
300
301
302
2. Liver Abscesses
Liver abscess are represented by purulent collections developed inside the liver
parenchyma surrounded by a liver tissue transformed fibrously.
Classification. Liver abscesses can be classified according to four criteria:
According to etiology:
1. Pyogenic abscess (produced by microbial pathogens)
2. Parasitic abscess (amebic abscess)
3. Fungal abscess, most often caused by Candida species, account 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 and chronic abscesses.
Fever, which is the most constant sign associated or not with chills. In many
cases, the first diagnosis is fever of unknown origin.
Anorexia, and malaise
Right upper quadrant pain
Right diaphragmatic irritation may induce reflected pain to the right shoulder
due to the phrenic nerve irritation, cough and hiccoughs
On physical examination, fever and tender hepatomegaly are the most common
signs. Jaundice is present in some cases associated with biliary tract disease, or in case
of multiple liver abscesses.
The topography of the liver abscess influences symptoms, being almost
asymptomatic in deep and posterior location. Pleuropulmonary symptoms may be
present (pleurisy, cough, chest pain) when the abscess in located on the hepatic dome.
The left hepatic lobe abscess can be confused with left subphrenic abscess or perforated
peptic ulcer.
Untreated liver abscess evolve to serious life threatening complications. The most
common are:
Breaking into the peritoneal cavity with peritonitis
Fistulization into the bile ducts with cholangitis
Rupture into the pleural cavity with pleural effusion
Fistulization into the pericardium with pericarditis or cardiac tamponade
Fistulization into a hollow organ (digestive system), when symptoms may
improve
Laboratory tests show an increase of leukocytosis, transaminases, bilirubin, ESR and
alkaline phosphatase. Of high importance in establishing microbiologic diagnosis is the
blood culture drawn during chills.
Imaging studies
Ultrasonography (US) reveals hypoechoic masses with irregular borders and
internal inhomogeneity or cavity debris. Ultrasonography can evaluate the biliary tree
morphology and guide the aspiration of the abscess cavity. The sensitivity of the method
depends on operators experience.
Computed tomography (CT) scan with contrast has a higher sensitivity than US
and also is very helpful in detecting associated intra-abdominal pathology. CT can guide
the percutaneous aspiration and drainage. Liver abscess appears as a relatively welldemarcated hypodense area (Figure 8) of irregular shape (not as round as a hydatid
cyst). Gas can be seen inside the abscess in 20% of cases.
Chest radiography may reveal basal atelectasis, right hemidiaphragm elevation,
and right pleural effusion when the abscess is
located on the liver dome. (Figure 9)
Positive diagnosis relies on the triad described by
Fontan:
1. Pain
2. Fever
3. Hepatomegaly, plus the rest of the
symptoms and investigations mentioned.
Differential diagnosis should include other
processes associated with fever, chills and sepsis.
Often the diagnosis is not easy, patient being
304
305
306
307
Branum GD, Tyson GS, Branum MA, Meyers WC. - Hepatic abscess. Changes in etiology, diagnosis, and management.
- Ann. Surg. 1990; 212(6):655-662.
2.
Zibari GB, Maguire S, Aultman DF, McMillan RW, McDonald JC. - Pyogenic liver abscess. - Surg. Infec. (Larchmt),
2000; 1(1):15-21.
3.
Chen SC, Wu WY, Yeh CH, et al. - Comparison of Escherichia coli and Klebsiella pneumoniae liver abscesses. - Am. J.
Med. Sci. 2007; 334(2):97-105.
4.
Cerwenka H. - Pyogenic liver abscess: differences in etiology and treatment in Southeast Asia and Central Europe. World J. Gastroenterol. 2010; 16(20):2458-2462.
5.
Trcoveanu E, Vlad N, Moldovanu R, Georgescu St, Bradea C, Lupau C, Crumpei F, Vasilescu A, Strat V. - Pyogenic
liver abscesses. - Chirurgia (Bucur). 2008; 103(4):417-427.
6.
Alkofer B, Dufay C, Parienti JJ, Lepennec V, Dargere S, Chiche L. - Are Pyogenic Liver Abscesses Still a Surgical
Concern? A Western Experience. - HPB Surg. 2012; 2012:316013. http://www.hindawi.com/journals/hpb/2012/316013/
7.
Karatassas A, Williams JA. - Review of pyogenic liver abscess at the Royal Adelaide Hospital 1980-1987. - Aust. N. Z.
J. Surg. 1990; 60(11):893-897.
8.
Wuerz T, Kane JB, Boggild AK, Krajden S, Keystone JS, Fuksa M, Kain KC, Warren R, Kempston J, Anderson J. - A
review of amoebic liver abscess for clinicians in a nonendemic setting. - Can. J. Gastroenterol. 2012; 26(10):729-733.
9.
Congly SE, Shaheen AA, Meddings L, Kaplan GG, Myers RP. - Amoebic liver abscess in USA: a population-based
study of incidence, temporal trends and mortality. - Liver Int. 2011; 31(8):1191-1198.
10.
Salles JM, Moraes LA, Salles MC. - Hepatic amebiasis. - Braz. J. Infect. Dis. 2003; 7(2):96-110.
11.
12.
13.
Ralston KS, Petri WA Jr. - Tissue destruction and invasion by Entamoeba histolytica. - Trends Parasitol. 2011;
27(6):254-263.
14.
Acuna-Soto R, Maguire JH, Wirth DF. - Gender distribution in asymptomatic and invasive amebiasis. - Am. J.
Gastroenterol. 2000; 95(5):1277-1283.
15.
Merens A, Rapp C, Fabre R, Cavallo JD. - Utility and limitations of laboratory diagnosis of amebiasis. - Med. Trop.
(Mars). 2005; 65(2):167-75.
16.
Haque R, Kabir M, Noor Z, Rahman SM, Mondal D, et al. - Diagnosis of amebic liver abscess and amebic colitis by
detection of Entamoeba histolytica DNA in blood, urine, and saliva by a real-time PCR assay. - J. Clin. Microbiol. 2010
Aug; 48(8):2798-801.
17.
Hoenigl M, Valentin T, Seeber K, Salzer HJ, Zollner-Schwetz I, Flick H, Raggam RB, Wagner J, Grisold AJ, Spreizer C,
Krause R. - Amoebic liver abscess in travellers: indication for image-guided puncture? - Wien Klin. Wochenschr. 2012
Nov; 124 Suppl 3:31-4.
18.
Choudhuri G, Rangan M. - Amebic infection in humans. - Indian J. Gastroenterol. 2012 Jul; 31(4):153-62.
19.
Cosme A, Ojeda E, Zamarreo I, Bujanda L, Garmendia G, Echeverra MJ, Benavente J. - Pyogenic versus amoebic liver
abscesses. A comparative clinical study in a series of 58 patients. - Rev. Esp. Enferm. Dig. 2010 Feb; 102(2):90-9.
308
309
Parasitic eggs are released from the last proglottid into the carnivores intestine
(especially canine animals, domestic or wild) which are the definitive host, and via the
feces into the environment. The intermediate host animal is represented usually by a
livestock animal species (e.g. sheep, cow, goat, horse, donkey, pig, and camel) or an
omnivorous or herbivorous wild animal species (e.g. marsupial, wild cattle, wild sheep,
wild goat, deer, moose, and caribou). These animals consume 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. This is the life cycle of Echinococcus. (Figure 13)
Humans are "paratenic host- essentially an accidental host - not a normal part
of the parasite's usual life cycle.
Morphopathology
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 are:
1. 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)
310
311
312
Clinical examination
When the cyst is small, or with 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 can 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. Investigations - the most important
Imaging investigations
The most important are the imaging
investigations, which easily detect the cyst(s)
in the liver, and 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
investigators
experience. Some features suggest the
echinococcus etiology: the fine debris
(hydatid "sand), septae and daughter cysts, floating germinal membrane (the endocyst),
etc. (Figure 16)
Ultrasound classification of hydatid cysts (WHO): [6]
a. Cystic lesion - there is a simple cyst in the affected organ - not suggestive
for echinococcosis.
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.
313
Intra-abdominal sepsis
Portal hypertension
Tuberculosis
315
316
317
Pedrosa I, Saz A, Arrazola J, Ferreirs J, Pedrosa CS. - Hydatid Disease: Radiologic and Pathologic Features and
Complications. - RadioGraphics 2000; 20:795-817.
2.
3.
Vlad DC, Neghina AM, Dumitrascu V, Marincu I, Neghina R, Calma CL. - Cystic Echinococcosis in Children and
Adults: A Seven-Year Comparative Study in Western Romania. - Foodborne Pathog. Dis. 2013 Jan 21.
4.
Moldovan R, Neghina AM, Calma CL, Marincu I, Neghina R. - Human cystic echinococcosis in two south-western and
central-western Romanian counties: a 7-year epidemiological and clinical overview. - Acta Trop. 2012; 121(1):26-29.
5.
Megherbi MT, Oulmane D, Hireche L, Abid L, Benabadji R. - Multiple hydatid cyst of the liver: indication for a
conservative treatment in uncomplicated univesicular localizations. Apropos of 19 cases. - J. Chir. (Paris) 1988;
125(5):358-363.
6.
WHO Informal Working Group. - International classification of ultrasound images in cystic echinococcosis for
application in clinical and field epidemiological settings. - Acta Trop. 2003; 85(2):253-261.
7.
8.
de Diego J, Lecumberri FJ, Franquet T, Ostiz S. - Computed tomography in hepatic echinococcosis. - Am. J. Roentgenol.
1982; 139:699-702.
9.
Holman
Jackson
HH.
Hepatic
Cysts
http://emedicine.medscape.com/article/190818-workup
Workup.
Medscape
Reference,
Emedicine
10. PAIR: Puncture, Aspiration, Injection, Re-Aspiration An option for the treatment of Cystic Echinococcosis WHO/CDS/CSR/APH/2001.6 http://whqlibdoc.who.int/hq/2001/WHO_CDS_CSR_APH_2001.6.pdf
11. Burlui D, Roca Monica - Chirurgia chistului hidatic hepatic - Editura Medical Bucureti, 1977.
319
4. Liver Tumors
A. BENIGN TUMORS
Benign tumors can develop from liver parenchyma cells (adenoma, cholangioma)
or from the 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
represented by mild pain in the upper right abdominal quadrant especially when tumors
are large.
Surgical treatment is not needed in most cases. Indications for surgical removal of
benign tumors are:
High volume tumors with persistent symptoms
If the tumor compresses surrounding anatomical structures (vessels, bile
ducts, etc)
If there is no possibility to differentiate from a malignant tumor
Based on histological criteria, the classification of benign liver tumors is:
Epithelial tumors: adenoma, cystadenoma, papilloma
Mesenchymal tumors: cavernous hemangioma, capillary angioma
Mixed tumors: teratoama
Tumor-like lesions: focal nodular hyperplasia, anoxic necrosis,
hamartoma
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.[1-5]
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:
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 over 10 cm in diameter are of
therapeutic interest due to possible compression on liver pedicle.
Lecene solitary adenoma (liver simple dysembryonic tumor). The tumoral
epithelial cells are similar to hepatocytes and grouped in the form of lobules. They are
well encapsulated that allows an easy surgical removal.
Trabecular adenoma. Tumoral cells are arranged in trabeculae, without any
lobular organization and without any capsule; out of all adenomas they have the greatest
tendency to turn malignant.
Forms less frequent are cholangiomas - benign tumors, usually of 1-2 cm
diameter, multiple, grouped or disseminated in one or both lobes, discovered
incidentally, difficult to differentiate from secondary liver metastases.
320
Hemangioma
It is the most common liver tumor after liver metastases. It can be seen in both
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
teleangiectasia.
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: [6-8]
intense symptoms,
changes in shape and volume of the tumor,
repeated intratumoral hemorrhage or subcapsular rupture,
central necrosis,
benign-malignant uncertainty
Stage I: T1, N0, M0: There is a single tumor (any size) that has not grown into any blood
vessels. The cancer has not spread to nearby lymph nodes or distant sites.
Stage II: T2, N0, M0: Either there is a single tumor (any size) that has grown into blood
vessels, OR there are several tumors, and all are 5 cm (2 inches) or less across. The cancer
has not spread to nearby lymph nodes or distant sites.
Stage IIIA: T3a, N0, M0: There is more than one tumor, and at least one is larger than 5 cm
(2 inches) across. The cancer has not spread to nearby lymph nodes or distant sites.
323
Stage IIIB: T3b, N0, M0: At least one tumor is growing into a branch of a major vein of the
liver (portal vein or hepatic vein). The cancer has not spread to nearby lymph nodes or
distant sites.
Stage IIIC: T4, N0, M0: A tumor is growing into a nearby organ (other than the
gallbladder), OR a tumor has grown into the outer covering of the liver. The cancer has not
spread to nearby lymph nodes or distant sites.
Stage IVA: Any T, N1, M0: Tumors in the liver can be any size or number and they may
have grown into blood vessels or nearby organs. The cancer has spread to nearby lymph
nodes. The cancer has not spread to distant sites.
Stage IVB: Any T, Any N, M1: The cancer has spread to other parts of the body. (Tumors
can be any size or number, and nearby lymph nodes may or may not be involved.)
Although the TNM system defines the extent of liver cancer in some detail, it
does not consider the liver function. Several other staging systems have been developed
that include both of these factors and others - the Okuda classification, French
classification, the Cancer of the Liver Italian Program (CLIP) score, The Chinese
University Prognostic Index (CUPI), The Japan Integrated Staging (JIS).[16] The
Barcelona Clinic Liver Cancer staging system (BCLC) is the most common used and it
includes four stages:[17,18]
A. Includes patients with asymptomatic early tumors
B. Patients with asymptomatic multinodular HCC
C. Patients with symptomatic tumors and/or invasive tumor pattern
D. End stage disease
Patients at stage A are candidates for radical therapies (resection, liver
transplantation or percutaneous treatments). Those at stage B with intermediate HCC
may benefit from chemoembolization. Patients at stage C with advanced HCC may
receive new agents in the setting of randomized controlled trials, and patients at stage D,
with end-stage, disease will receive only symptomatic treatment.[16,19]
Diagnosis
The main biological data on a possible HCC are: accelerated ESR, increased
serum bilirubin, increased LDH, decreased albumin (announce a poor prognosis). In
addition, alpha-fetoprotein and GTP may be increased. The screening for HCC includes
the alpha-fetoprotein level and ultrasonography.[20]
Imaging studies are of particular importance and are represented by ultrasound
CT, MRI, scintigraphy (with technetium, colloidal gold or Gallium for differential
diagnosis from liver metastases) and selective angiography. The sensitivity of
ultrasound for HCC detection is low since small nodules can be missed in a cirrhotic
liver.[20]
On CT imaging, the HCC has three distinct patterns of growth: (Figure 26)
1. A single large tumor
2. Multiple tumors
3. Poorly defined tumor
with
an
infiltrative
growth pattern
The key characteristic on CT is
the hypervascularity in the arterial
phase scans, with an early arterial
uptake followed by washout in the
portovenous or late, equilibrium phase.
324
Cholangiocarcinoma (CCA)
The tumor originates from the epithelium of intrahepatic bile ducts. In terms of
etiology, in addition to the factors referred to CHC, sclerogenic cholangitis lesions have
an important role.
In terms of morphological 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 based on immunohistochemical profile, by
highlighting specific epithelial membrane antigen, cytokeratin and impregnation of
biliary canaliculi with polyclonal antibody for carcinoembryonic antigen. Frequently
used tumor markers are the Carbohydrate antigen 19-9 (CA 19-9), Carcinogenic
Embryonic antigen (CEA), and Cancer Antigen 125, which in combination have shown
sufficient sensitivity and specificity to detect and monitor CCA.[23]
The differential diagnosis with liver metastases from gastrointestinal carcinomas
is sometimes impossible, even after immunohistochemistry tests and laparotomy; in this
case, the differential diagnosis relies on 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 are 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.
325
Liver metastases
By far the most common malignant liver tumors are metastases. The liver is an
important blood filter especially for gastrointestinal tract. Three major types of liver
metastases are more often met:
colorectal cancer metastases
liver metastases from endocrine cancers, and
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:
synchronous,
when
they
occur
simultaneously with the primary tumor
or shortly after primary tumor removal,
and
metachronous, they occur at a distance
greater than five years after primary
tumor removal
In synchronous metastases, symptoms overlap
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) (Figure 27), biopsy and elevated levels of CEA (carcinoembryonic
antigen).
Principles of treatment of hepatic malignancies
Important tumoral features that guide treatment include:
size
spread
involvement of liver vessels
presence of a tumoral capsule
presence of extrahepatic metastases
presence of daughter nodules
vascularity of the tumor
When liver cancer is diagnosed in early stages, the liver transplantation is the first
line of treatment.
The Milan criteria (based on Mazzaferro et al. studies in 1996) state that a patient
is selected for transplantation when:[24]
1. Only one lesion smaller than 5 cm in present
2. Up to 3 lesions smaller than 3 cm
3. No extrahepatic manifestations
4. No vascular invasion
Because the Milan criteria were considered too restrictive and acceptable
outcomes can still be achieved using more liberal tumor criteria [25-27], researchers at
the University of California at San Francisco (UCSF) proposed the following criteria for
tumor size:
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327
Wound infection
Intra-abdominal sepsis
General complications
Pleural effusion
Pneumonia
Deep vein thrombosis/pulmonary embolism
Cardiac failure, myocardial infarction
Prognosis
Liver resection of colorectal metastases is associated with 3 and 5-year survival
rates close to 40% and 30%, respectively. After resection, recurrences are observed in
two-thirds of the patients.[31,42]
Postoperative survival rates in HCC are in the range of 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.[43,44]
In cholangiocarcinoma, unfortunately, curative resection is possible in only about
30% of patients due to locally advanced disease, distant metastases or co-morbidities in
elderly patients. Even after resection, the recurrence rate is approximately 60%,
resulting in a low 5-year overall survival.[30]
When transplant or resection is not possible, chemoembolization and radiofrequency ablation are the treatments of choice. These therapies can be applied alone or
in association.
Chemoembolization 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
(embolizing agent is mixed with anticancer drugs such as doxorubicin, mitomycin or
cisplatin). Second, it cuts off the tumors 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. (Figure 30) 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. 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.[45] Side effects are represented by fever,
abdominal pain and elevated transaminases.
Patients should be carefully chosen as the
procedure may produce liver failure and death in
those with cirrhosis. Chemoembolization may
also be used to shrink liver tumors while the
patient awaits a donor organ.
An alternative to embolization is intraoperative ligation of the hepatic artery or its
branches.
Many local ablative therapies have been developed for unresectable liver cancer
including percutaneous ethanol injection (PEI), percutaneous acetic acid injection,
329
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National
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10. Jemal A, Bray F, Center MM, Ferlay J, Ward E, Forman D. - Global cancer statistics. - CA Cancer J. Clin. 2011;
61(2):69.
11. El-Serag HB. - Hepatocellular carcinoma: an epidemiologic view. - J. Clin. Gastroenterol. 2002; 35(5 Suppl 2):S72-8.
12. WHO - Cancer health topic - Global Alert and Response (GAR), Hepatitis B - http://www.who.int/cancer/en/index.html
13. Michielsen PP, Francque SM, van Dongen JL. - Viral hepatitis and hepatocellular carcinoma - World J. Surg. Oncol.
2005; 3:27.
14. Liver Cancer - How is liver cancer staged? - http://www.cancer.org/cancer/livercancer/detailedguide/liver-cancer-staging
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The
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https://www.thieme-
18. Llovet JM, Burroughs A, Bruix J. - Hepatocellular carcinoma. - Lancet 2003; 362:19071917.
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20. Bolog N, Andreisek G, Oancea I, Angelica Mangrau - CT and MR Imaging of Hepatocellular Carcinoma. - J.
Gastrointestin Liver Dis. 2011; 20(2):181-189.
21. Tanimoto A, Kuribayashi S. - Application of superparamagnetic iron oxide to imaging of hepatocellular carcinoma. Eur. J. Radiol. 2006; 58(2):200-216.
22. Robinson P. - Hepatocellular carcinoma: development and early detection. - Cancer Imaging. 2008; 8 Spec No A:S12831.
23. Malaguarnera G, Paladina I, Giordano M, Malaguarnera M, Bertino G, Berretta M. - Serum markers of intrahepatic
cholangiocarcinoma. - Dis. Markers 2013; 34(4):219-228.
24. Mazzaferro V, Regalia E, Doci R, Andreola S, PulvirentiA BF, et al. - Liver transplantation for the treatment of small
hepatocellular carcinomas in patients with cirrhosis. - N. Engl. J. Med. 1996; 334:693699.
25. Patel SS, Arrington AK, McKenzie S, et al. - Milan Criteria and UCSF Criteria: A Preliminary Comparative Study of
Liver Transplantation Outcomes in the United States. - International Journal of Hepatology 2012; 2012:253517.
26. Silva MF, Sherman M. - Criteria for liver transplantation for HCC: What should the limits be? - J. Hepatol. 2011;
55(5):1137-1147.
27. Decaens T, Roudot-Thoraval F, Hadni-Bresson S, et al. - Impact of UCSF criteria according to pre- and post-OLT tumor
features: analysis of 479 patients listed for HCC with a short waiting time. - Liver Transpl. 2006; 12(12):1761-1769.
28. Schwartz M, Sasan Roayaie, Konstadoulakis M. - Strategies for the Management of Hepatocellular Carcinoma. - Nat.
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29. Dhanasekaran R, Hemming AW, Zendejas I, George T, Nelson DR, Soldevila-Pico C, Firpi RJ, Morelli G, Clark V,
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32. Popescu I. - Chirurgia ficatului, Rezectia hepatica - Ed. Univ. Carol Davila, Buc. 2004
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35. Asiyanbola B, Chang D, Gleisner AL, Nathan H, Choti MA, Schulick RD, Pawlik TM. - Operative mortality after
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37. Thon-Than-Tung - Les resections majeures et mineures du foie. -Masson. Paris, 1979
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331
Surgical anatomy
Pathology of the gallbladder - lithiasis
Common bile duct lithiasis
Non tumoral stenosis of the biliary ducts
Tumors of the biliary ducts
1. Surgical Anatomy
Bile ducts represent a system of ducts that drain the bile from the liver secreting
cells toward the duodenum. Biliary tree is divided into two regions: (Figure 1)
1. Intrahepatic bile ducts - inside the liver, and
2. Extrahepatic bile ducts - outside the liver
Extrahepatic bile ducts are formed by:
Right and left hepatic ducts
Common hepatic duct - ductus hepaticus
Gallbladder
Cystic duct
Common bile duct or choledochus (CBD)
which in the duodenal wall joins the main
pancreatic duct of Wirsung forming thus the
ampulla of Vater, which opens into the
duodenum through the papilla major.
The anatomically normal length of the CBD
is 10-12 cm and the thickness of 6 mm.
The common hepatic duct has posterior
relations with the portal vein and the right branch
of the hepatic artery. Hepatic artery is located on
the left side of the duct. (Figure 2)
There are many anatomical variations of the
liver pedicle. 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 has four portions:
(Figure 3)
1. Supraduodenal portion which, is
bordered rear by the portal vein and on
the left side by the proper hepatic
artery.
332
333
334
335
336
337
Mechanical complications
Gallbladder hydrops, happens when the biliary stones clog the cystic duct. Intense
prolonged colicky pains manifest it initially and 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 (transparent).
Migration into the common bile duct. Small stones are more dangerous as they could
migrate through the cystic duct into the common duct. If stones are less than 3 mm
in diameter, they can pass through the papilla major into the duodenum. Symptoms
are represented by intense and prolonged colicky pain associated with transient
jaundice. If stones are larger, they will remain stocked into the common bile duct
and will produce periodically jaundice associated with colicky pains and fever
(acute cholangitis). In most cases, CBD stones are the cause of an associated acute
pancreatitis as a result of bile reflux into the Wirsung duct.
Cholecysto-choledochus fistula usually appears when a large biliary stone develops
inside the Hartmanns gallbladder pouch. Compression on gallbladder and common
bile duct walls and associated inflammatory processes will erode the walls
developing a communication between the gallbladder and CBD. Due to
compression, the most frequent clinical manifestation is the jaundice. Smaller stones
can also migrate through the fistula into the common bile duct.
Cholecysto-digestive fistulas are represented in most cases by cholecysto-duodenal
fistula and in rare cases, the stomach or even the colon may be involved. 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 enough, it can produce
intestinal obstruction, the so-called biliary ileus. On abdominal radiography, air can
be observed in the gallbladder (pneumobilia) and on barium swallow, the contrast
passes into the gallbladder.
Inflammatory complications
Acute cholecystitis is the result of stasis and infection of the bile inside the
gallbladder most often caused by 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 hypochondrium and frequently
associated with fever, nausea and vomiting. Fever and chills are signs of cholangitis
or abscess formation. On palpation, an intense pain is found in the right
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343
344
345
346
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Possibilities:[28]
Primary closure of the choledocus after choledochotomy (choledochorrhaphy),
without a biliary drainage procedure. It is rarely performed because of the risk of
biliary leak (during interdigestive periods the Oddi sphincter contracts and the
pressure inside the biliary tree will rise forcing the suture).
External drainage of the CBD using a T-tube (Kehr drainage) is the most frequent
solution for choledochus less than 1.5 cm in diameter. The drainage will prevent
the biliary leak but also will allow the radiological exploration of biliary tree in
the postoperative period. If the cholangiography shows no remnant stones and a
good passage of the contrast into the duodenum, the tube can be removed after
few weeks. If remnant stones are found, ERCP is the solution for removing them.
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349
could be affected in any segment but most often, the choledochus and right
hepatic duct are injured. The main causes of injuries are inability to recognize
local anatomy and inexperienced surgical team.
Abdominal trauma
Stones with repeated episodes of cholangitis and Mirizzi syndrome
(obstructive jaundice due to a bulky stone in the Hartmanns pouch which
compresses the CBD)
Repeated episodes of acute pancreatitis
Chronic pancreatitis
Sclerosing cholangitis (stenosis of intra and extrahepatic bile ducts)
Chgolangiopathy during HIV infection [29,30]
Clinical picture
Lesions usually remain undetectable until the
stenosis is sufficient to produce mechanical jaundice.
Rarely other symptoms such as right upper quadrant
pain occur before jaundice, or the illness begins
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. Patients 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.
Investigations are the same as for CBD lithiasis.
(Figure 22)
Classification
The Bismuth's classification (1982) [31] is based on the lowest level at which
healthy biliary mucosa is available for anastomosis and is intended to help the surgeon
to choose the appropriate technique for repair. (Figure 23)
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
350
Prognosis
Treated before the onset of chronic complications (biliary cirrhosis) the disease
has a favorable prognosis, but depending on the underlying cause. Patients with stenosis
or sclerosing cholangitis occurring in HIV infection, have a poor outcome.
351
352
Morphopathology
Even though there are many histopathological forms, gallbladder cancer is
represented in 80% -95% of cases of by adenocarcinoma [42] and less frequently by
other types (undifferentiated carcinomas - 7%, squamous carcinoma - 3%, mixed
carcinoma - 1%).
WHO classification is most comprehensive including the following types of
tumors:[44]
Epithelial tumors
Carcinoma in situ
Adenocarcinoma
Papillary adenocarcinoma
Adenocarcinoma, intestinal type
Mucinous adenocarcinoma
Clear cell adenocarcinoma
Signet ring cell carcinoma
Adenosquamous carcinoma
Squamous cell carcinoma
Small cell carcinoma (oat cell carcinoma)
Undifferentiated carcinoma
Endocrine tumors
Carcinoid tumor
Mixed carcinoid-adenocarcinoma
Paraganglioma
Nonepithelial tumors
Rhabdomyosarcoma
Kaposi sarcoma
Leiomyosarcoma
Malignant fibrous histiocytoma
Angiosarcoma
Miscellaneous tumors
Carcinosarcoma
Malignant melanoma
Malignant lymphomas
Unclassified tumors
Secondary tumors
Tumor-like lesions
Because gallbladder cancers are mostly infiltrative with high aggressiveness and
frequent metastases, there are many inoperable forms.
Gallbladder carcinoma usually produces asymmetric thickening of the gallbladder
wall with infiltration of surrounding structures. Most cancers originate in the gallbladder
fundus. As the tumor progresses, the gallbladder may fill with tumor or may contain
pus, mucus, or stones.[42]
The first organ usually invaded is the liver but spread can be over the bile ducts.
Cancer can extend through hepato-duodenal ligament to the duodenum, colon, stomach,
and pancreas. Tumoral cells spread via the lymphatic system to the Mirizzi lymph node,
around the choledochus, pancreatico-duodenal lymph nodes and so on. Spread over the
venous system involves the liver and other organs. Peritoneal spread will lead to
peritoneal carcinomatosis.
AJCC classification (the sixth edition) [45,46]
Primary tumor (T)
TX Primary tumor cannot be assessed
T0 No evidence of primary tumor
Tis Carcinoma in situ
T1 Tumor invades lamina propria (T1a) or muscle layer (T1b)
T2 Tumor invades perimuscular connective tissue; no extension beyond serosa or into liver
T3 Tumor perforates the serosa (visceral peritoneum) and/or directly invades the liver
and/or 1 other adjacent organ or structure, such as the stomach, duodenum, colon, pancreas,
omentum, or extrahepatic bile ducts.
353
T4 Tumor invades main portal vein or hepatic artery or invades multiple extrahepatic
organs or structures.
Regional lymph nodes (N)
NX Regional lymph nodes cannot be assessed
N0 No regional lymph node metastasis
N1 Regional lymph node metastasis
Distant metastasis (M)
MX Distant metastasis cannot be assessed
M0 No distant metastasis
M1 Distant metastasis
Stage III
Stage IV
Tis N0 M0
T1 N0 M0
T2 N0 M0
T3 N0 M0
T1 N1 M0
T2 N1 M0
T3 N1 M0
T4 Any N M0
Any T Any N M1
1.
2.
3.
4.
5.
In situ carcinoma
Mucosal or muscular invasion
Transmural direct liver invasion
Cystic lymph node metastasis
Contiguous or/and distant liver
metastasis or metastasis to any
other organs
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 classical
right upper quadrant pain of gallstone disease. Jaundice, anorexia, and weight loss often
indicate disease that is more advanced.
Physical signs in gallbladder cancer are present only in advanced cases and may
be represented by:
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 (Virchows node)
Pelvic seeding: masses palpated on digital rectal examination (Blumers shelf).
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.
Urea, creatinine and urinalysis assess renal function prior to enhanced CT scan
examination.
CBC (Complete Blood Count): anemia may be an indicator of more advanced
disease.
Imaging Studies
Ultrasonography represents usually the first imaging investigation, which
highlights abnormalities of the gallbladder wall raising the suspicion of cancer.
A mass can be identified in 50-75% of patients with gallbladder cancer.[40]
Liver metastasis can be also seen on ultrasound.
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357
359
In patients in whom the inoperability of the tumor is well established and in those
with associated comorbidities where surgery is contraindicated minimal invasive
procedures are the best solution. These procedures are represented by biliary stenting
via ERCP or biliary decompression via the percutaneous cholangiostomy.
Prognosis is poor with an overall survival rate at 5 years of less then 5% of cases. A
better survival rate was reported by Japanese authors (10% to 44% depending on tumor
stage) in distal resectable tumors.[59,60]
360
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Cancer
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What
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the
risk
factors
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http://www.cancer.org/cancer/gallbladdercancer/detailedguide/gallbladder-risk-factors
gallbladder
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is not associated with gallbladder carcinoma. - Am. Surg. 2001; 67(1):7-10.
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2013;17(6):1161-1168.
40. Mary
Denshaw-Burke
Gallbladder
Cancer
Clinical
http://emedicine.medscape.com/article/278641-clinical#a0218
Presentation.
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42. Sunita Singh, Mumtaz Ahmad Ansari, Gopeshwar Narayan - Pathobiology of gallbladder cancer. - Journal of Scientific
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43. Nath G, Gulati AK, Shukla VK. - Role of bacteria in carcinogenesis, with special reference to carcinoma of the
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Extrahepatic Bile Ducts A Commentary on the Second Edition. - Cancer 1992; 70(2):410-414.
45. Fong Y, Wagman L, Gonen M, et al. - Evidence-Based Gallbladder Cancer Staging. Changing Cancer Staging by
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363
Peritonitis
PERITONITIS
1. Anatomical aspects
2. Peritonitis, generalities
3. Etiologic forms of primary peritonitis
a. Streptococcus peritonitis
b. Pneumococcal peritonitis
c. Gonococcal peritonitis
d. Chlamydia peritonitis
e. Tuberculous peritonitis
4. Acute localized peritonitis
1. Anatomical Aspects
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 square meters).
The intraperitoneal cavity is the space located within the abdomen and wrapped
by peritoneum. It is divided arbitrary by anatomical structures in some compartments
and recesses creating an interconnecting network that allows the spread and
sequestration of intraperitoneal effusions.
The transverse mesocolon divides the
peritoneal cavity in two spaces: (Figure 1)
1. Supramesocolic space, and
2. Inframesocolic space
The small bowel mesentery divides the
inframesocolic space into two compartments:
1. The right infracolic, and
2. The left infracolic
The right and left paracolic gutters are formed
between the lateral aspect of the ascending and
descending colon and the peritoneal reflection on the
abdominal
wall.
These
gutters
represent
communications between the supramesocolic and
pelvic area.
The falciform ligament separates the right from the left subphrenic space.
Normally, the amount of intraperitoneal fluid is less than 50-100 mL.
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Peritonitis
2. Peritonitis - Generalities
Peritonitis represents an inflammation of peritoneal serosa, generalized or
localized, of bacterial or chemical etiology. Peritonitis is a serious life threatening
condition, a surgical emergency in most cases.
Classification
Classification by origin of germs:
1. Primary, when the source of contamination is extraperitoneal, the
infection being produced via the blood or lymphatic circulatory system.
This type is very rare (5%) and is monobacterial (a single germ is
responsible for peritonitis).
2. Secondary peritonitis are the most frequent (95% of cases) having a
plurimicrobial etiology. There is an intraperitoneal source of
contamination, such as: perforations of intra-abdominal hallow organs,
inflammation of abdominal organs or postoperative.
3. Tertiary peritonitis is represented by persistent or recurrent infection
after adequate initial therapy.
Classification by evolution:
1. Acute peritonitis, which are the most frequent.
2. Chronic peritonitis (rare) caused in most cases by recurrent inflammatory
disease of the intraperitoneal organs (pelvic), intraperitoneal presence of
foreign substances (talcum, barium) or tuberculosis.
Classification by extension:
1. Generalized (diffuse) - extended to the entire 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 - produced by gastric juice from a perforated peptic
ulcer, bile, pancreatic enzymes (pancreatitis), etc.
The most common bacteria identified in peritonitis are gram-positive germs (E.
coli, Enterobacter, Klebsiela), gram-negative germs (Enterococci), anaerobic
(Bacteroides, Clostridium) and fungi (Candida).
Pathophysiology
In secondary septic peritonitis, which is the most common type, intra-abdominal
sepsis results from a perforated viscus with direct spillage of luminal content into the
peritoneal cavity (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,
contaminate the peritoneal cavity. Germs multiply producing different kind of toxins
leading to local inflammatory reaction and tissue damages. Toxins will enter the blood
stream inducing a general inflammatory response also affecting the functionality and
structure of important organs such as cardio-vascular system, kidneys, lungs, and so on.
Not just toxins but germs themselves spread over the vascular system resulting in
metastatic abscesses. Defense mechanisms of the body try to limit the effects of
infection but in most cases, they are outweighed by the massive infection.
The most dangerous toxins are endotoxins produced by gram-negative bacteria,
which lead to the release of cytokines that induce cellular and humoral cascades,
365
Peritonitis
resulting in cellular damage, septic shock, and multiple organ dysfunction syndrome
(MODS). Massive quantities of toxins are released also by bacterial destruction
produced by antibiotics, so antibiotherapy, which otherwise is very important in limiting
bacterial multiplication, cannot be considered the single therapy in these cases. The
most efficient therapy is represented by surgical removal of septic peritoneal content
(abundant lavage) and resolving the cause of contamination. Both methods surgery and
antibiotherapy (and other measures too) should be applied together for the best
outcome.
The gravity and evolution of peritonitis depends on two factors: 1. the number
and virulence of germs, and 2. the particular reactivity of the patient.
Chemical (sterile) peritonitis is caused by irritants such as gastric juice, bile,
blood, or other substances without bacterial inoculation of the peritoneal cavity. The
most intense abdominal 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.
The primary defense reaction of the peritoneum to the contamination is to isolate,
by different kinds of mechanisms, the infection. Chemotactic and plastic proprieties of
the greater omentum and other mobile intra-abdominal organs, especially the small
intestine, contribute to isolation of the infection by compartmentalization, but in most
cases fail to completely eliminate the infection resulting in intraperitoneal abscess
formation. 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 caused by
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 ascites. In adults, primary peritonitis develops in
up to 25% of patients with alcoholic cirrhosis.[1]
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 are represented by abdominal pain, vomiting, stop of bowel movements,
hiccups, fever, impaired general condition and others.
The onset of pain may be sudden, violent like a knife stab, when a hollow organ
is perforated (such as the stomach, duodenum, or colon) or it 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. Initial location of pain depending on
the affected organ:
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, especially in perforations, with maximum of intensity in
the causing organ region and the patient takes an antalgic position, any movement
exacerbating the pain.
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Peritonitis
Vomiting is initially reflex (sometimes may be absent as in perforated peptic
ulcer) but as peritonitis progresses to paralytic ileus it becomes more frequent with
fecaloid content. According to Stokes law, the smooth muscles paresis produced by
peritoneal serosa irritation will lead to paralytic ileus and the abdomen becomes
distended.
Hiccups are caused by the diaphragmatic irritation.
General and local signs
Patients position is generally on lateral decubitus with legs folded as an antalgic
position.
The facial aspect of the patient has some special features, the so-called peritonitic
or Hippocratic face described by Hippocrates as follows: 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.[2]
Fever (38-390 C) is present in most case but may be absent at the debut, in
elderly, children and immunosuppressed patients. In postoperative peritonitis, fever may
represent the first alarming sign drawing the surgeons attention to an imminent intraabdominal complication.
The 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 contraction, diaphragmatic irritation and
abdominal distension. Sudden postoperative dyspnea is a very important sign in surgery
for patients operated on the abdomen because it may represent the first symptom of an
intra-abdominal complication with peritonitis, especially in unreactive elderly patients,
where pain is also faded by analgesic medication.
Signs of hypovolemic and/or septic shock are represented by pale skin, cold and
sweaty, hypotension, tachycardia, and oligo-anuria.
Local signs
On 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. This aspect is seen in early phases of generalized
peritonitis, especially in chemical peritonitis caused by perforations.
Pain is the cardinal sign of peritonitis. It can be observed on superficial and deep
palpation and on percussion.
Palpation is the most important physical examination. Depending on type and
etiology of peritonitis there are many signs and maneuvers very helpful in diagnosis. On
superficial palpation, the cutaneous hyperesthesia can be noticed, representing the
increased sensitivity to sensory stimuli, such as pinch or touch (Voskresenski maneuver
in appendicitis, Dieulafoy sign). Abolition of cutaneous reflexes (abdominal muscles
will not contract on skin stimuli) can be also observed. Induced pain on profound
palpation has the maximum intensity in the region of the causing organ.
Muscular guarding represents the reflex contraction of the abdominal wall
muscles on palpation that resumes after palpation is finished, but reappears in a new
attempt. It is present in the early phases of the peritonitis.
Muscular contracture is not induced by palpation, the abdominal wall muscles
being permanently contracted. It is a painful contraction, initially localized and then
367
Peritonitis
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.
Even gentle abdominal percussion can induce abdominal pain in acute peritonitis,
the so-called Bell sign. In case of perforated peptic ulcer, the prehepatic dullness
disappears on percussion due to the intraperitoneal gas (from stomach). Shifting
dullness is present in intraperitoneal effusions.
On auscultation, in initial phases, intestinal movements can be heard but later
these disappear (the abdominal silentium) as intestines enter in paresis.
On rectal and/or vaginal digital examination the pain is induced by finger
palpation of the Douglass pouch and the patient screams of pain, the so-called
Douglass pouch screaming sign.
Diagnosis
In most cases, the diagnosis relies on anamnesis and physical examination. Lab
and other investigations serve to determine the cause of the peritonitis and the patients
status.
Lab tests will show hyperleukocytosis and other modifications depending on
status of the patient.
Plain abdominal radiography may show pneumoperitoneum in case of hollow
organs (stomach, duodenum, colon) perforation, and fluid-air levels when paralytic ileus
is installed.
Abdominal ultrasound examination can reveal intraperitoneal collections
(effusions) and other pathological changes suggestive for the underlying disease.
Paracentesis 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 can be performed in uncertain cases, and may represent a way of
approach for surgical treatment.
CT scan is performed in uncertain cases or uncertain underlying disease. It is very
useful to determine the presence of isolated intraperitoneal effusions (intraperitoneal
abscesses).
Differential diagnosis will include other conditions manifested by intense abdominal
pain, such as:
Acute medical abdomen:
o Biliary and renal colic - the pain is colicky, not continuous, being
calmed by antispastic drugs
o Saturnine colic is produced by lead poisoning
o Tabes pain, "tabes dorsalgia", is a related back pain produced by
advanced syphilis
o Intense abdominal pains can manifest acute porphyria, a rare autosomal
dominant metabolic disorder affecting the production of heme, the
oxygen-binding prosthetic group of hemoglobin
368
Peritonitis
369
Peritonitis
drainage will also provide clues on the integrity of anastomoses (drains shall be placed
in the vicinity of lesion and in declivities such as Douglas pouch, paracolic and
subphrenic spaces).
Postoperative evolution may be shadowed by some complications such as:
Death in the first 2-5 days caused by toxic-septic shock
Intraperitoneal abscesses formation
Intestinal occlusion due to intraperitoneal adhesions
Wound infection and evisceration or later incisional hernias
Prognosis
In case of uncomplicated peritonitis, the mortality rate is less than 5%, but this
rate may increase in severe infections. Factors that independently predict worse
outcomes include:[3]
advanced age
malnutrition
presence of cancer
preoperative organ dysfunction
The development SIRS (systemic inflammatory response syndrome) and MSOF
(multiple system organ failure) can increase the mortality rate to greater than 70%80%.[3]
370
Peritonitis
develop perihepatic adhesions. The ultrasound examination is normal and Pap smears
confirm infection with Chlamydia.
e. Tuberculous peritonitis
Peritoneal tuberculosis is an uncommon site of extrapulmonary infection caused
by Mycobacterium tuberculosis. It appears more frequently in young people up to 40
years old.
The infection spreads via hematogenous route from active pulmonary TB or less
frequently, directly from an infected small bowel or salpinx.[4] In most cases, these
patients have an impaired immunity because of associated comorbidities such as cancer,
cirrhosis, diabetes, AIDS or are treated with corticosteroids.
The onset is insidious with unspecific misleading abdominal symptoms, the
diagnosis being delayed with several months, in part because it is not suspected.
There are three possible intraoperative aspects:
1. Wet peritonitis, or the ascitic form, characterized by transparent, yellowish
peritoneal fluid and tendency to coagulation. On the peritoneal surface,
there are numerous miliary granules, whitish nodules, small as needle pins
with discontinuous distribution. In this case, surgical treatment is
represented by fluid evacuation abundant lavage without drainage.
2. Dry peritonitis, the fibrocaseous, adhesives or plastic form, characterized
by reduced volume of ascites, but plurivisceral conglomerates with
median location. Frequently patients are operated for an intestinal
occlusion or tumoral mass of obscure origin. The solution is represented
by adhesiolysis (bands of adhesions are divided) freeing up all intestines
followed or not by enteroplication. Enteroplication represents a surgical
technique by which adjacent loops of intestine are sutured to each other to
prevent further intestinal occlusion. If necessary, segments of affected
intestines can be resected followed by intestinal tract reconstruction.
3. Purulent form, characterized by a cold abscess filled with by tuberculous
pus surrounded by adherent intestine and omentum. External fistulization
may appear to the skin, or internal into the bowel. Surgical solution is
represented by adhesiolysis, evacuation of the abscess, or if necessary,
segmental resection of the affected intestines.
371
Peritonitis
Abscesses occur thanks to the defense role of the peritoneum, which seeks to limit
the infection, but cannot totally defeat it. They are less serious than acute diffuse
peritonitis, but may cause severe complications such as rupture into the large peritoneal
cavity, and sepsis.
Topographically, purulent collections may be located anywhere but the most
common are those located under the diaphragm and in the Douglas pouch.
Initially, collections walls are formed by surrounding anatomic structures but
thereafter they become fibrous, hard and thick.
Clinical picture
Symptoms vary by location of collection, but general signs, especially septic
fever are those that attract attention to the existence of a septic process.
1. Interhepatophrenic abscess manifests with pain in the right upper quadrant
and hemithorax. Tachypnea is associated with polypnea. Hiccups and pain on the
phrenic nerve route (shoulder) represent the phrenic irritation syndrome.
2. Left subphrenic abscess (collection of pus located between the left diaphragm
and sustentaculum lienalis) is manifested by spontaneous pain in the left upper
quadrant, hemithorax and shoulder, pain on palpation of intercostal space and parietal
edema.
3. Subhepatic abscess manifests with diffuse abdominal pain or fixed (Carnot),
painful muscular guarding (not a true contracture) and painful dullness in the right
upper quadrant.
4. Abscess in the bursa omentalis manifests with nonspecific, misleading
symptoms (epigastric pain, fever, digestive disorders, nausea and vomiting).
4. Inframesocolic abscesses manifest with local pain, abdominal guarding, bowel
disorder (especially constipation) offering a clinical picture of an intestinal febrile
occlusion.
5. Pelvic abscess is manifested by a deep suppuration syndrome with signs of
pelvic irritation: rectal and bladder tenesmus, polyuria, dysuria, diarrhea. Digital rectal
or vaginal examination is relevant finding the Douglas pouch bulging and very painful
(the Douglas scream").
Investigations
Establishing the diagnosis is not always an easy task because small abscesses are
difficult to be visualized by various imaging procedures the more if they are located
between intestinal loops.
372
Peritonitis
Standard abdominal X-ray offers limited information. The only positive sign is
the presence of fluid-air levels, which can be confused with or even may represent an
intestinal occlusion.
Ultrasound examination of the abdomen is useful in most cases because it can
highlight the collection, describe the wall and the contents of collection, allowing
guided puncture.
Computer tomography with contrast is the preferred examination that confirms
the diagnosis in almost all cases and also can guide the puncture.
Laboratory investigations are not useful for diagnosis except the microbiologic
examination of the extracted fluid, which is important for conducting an etiologic
treatment based on antibiogram.
Treatment
Percutaneous drainage, guided by ultrasound or tomography is the treatment of
choice in many cases. Effectiveness of the method is 85% but there is a rate of 0-15%
possible complications represented especially by gastrointestinal, pleural or vascular
perforation.
Surgical approach is performed in case of percutaneous drainage failure, or when
additional surgical gestures are required. Abscesses between intestinal loops or deep and
multiple collections require laparotomy. The parietal approach should be as direct as
possible to avoid contamination of the pleura or peritoneum. Douglas pouch abscesses
can be evacuated and drained through the vagina in women and through the rectum in
men.
References
1.
Radojkovic M, Stojanovic M, Zlatic A, Ljiljana Jeremic-Savic, Danijela Radojkovic, Mirjana Radisavljevic - Primary
peritonitis. - Acta Fac. Med. Naiss 2008; 25:133-138.
2.
Jane M. Orient - Sapira's Art and Science of Bedside Diagnosis, chapter 9, pp 161 - Lippincott Williams & Wilkins, Mar
28, 2012.
3.
Daley BJ. - Peritonitis and Abdominal Sepsis - Medscape reference, Emedicine http://emedicine.medscape.com/article/180234-overview#aw2aab6b2b6aa
4.
Valerie Byrnes, Sanjiv Chopra - Tuberculous peritonitis - UpToDate, Inc. updated: Oct 18, 2012,
http://www.uptodate.com/contents/tuberculous-peritonitis
373
Intestinal Occlusion
INTESTINAL OCCLUSION
Intestinal occlusion represents the stop of the intestinal transit produced by
various causes, being one of the most common abdominal surgical emergencies.
Classification
There are two main criteria of classification, which are used with immediate
practical implication, such as:
1. Etiopathogenic criteria
a. Mechanical occlusions - by obstruction or by strangulation
b. Dynamic occlusions - paralytic or spastic
c. Vascular causes of occlusions - embolic or thrombotic
2. Topographic criteria
a. High-level occlusions - pylorus, duodenum, jejunum
b. Intermediate occlusions - ileum, transverse and right colon
c. Low-level occlusions - left colon, sigmoid, and rectum
374
Intestinal Occlusion
Functional occlusions do not require surgical therapy except peritonitis.
Treatment is represented by correction of metabolic imbalances and other measures
such as nasogastric aspiration, enemas, drugs that stimulate intestinal peristalsis.
375
Intestinal Occlusion
376
Intestinal Occlusion
Pathophysiology
Intestinal obstruction produces superjacent digestive segment distension by
accumulation of air from swallowed air, bacterial fermentation processes, diffusion
from blood and accumulation of fluid from digestive secretions and food intake.
Obstruction will induce increased peristaltic contractions that contribute to
increased intraluminal pressure and small-bowel distention causing compression on
parietal lymphatic vessels, leading to bowel wall lymphedema with wall thickening.
Compression on submucous venous network accelerates the edema. Finally, the
continuous increase in bowel wall pressure blocks the arterial vessels, leading to
ischemic necrosis and perforation. This sequence may occur more rapidly in a closedloop obstruction with no proximal escape for bowel contents. (Figure 2)
377
Intestinal Occlusion
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.
Vomiting is less constant than pain. It is 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. Nausea, hiccups and eructation (gastric stasis
signs) always accompany vomiting. In high occlusions, vomiting is early, less abundant
but common, and the content is food or bile. It is produced mainly by reflex mechanism.
In low occlusions, vomiting is abundant and repeated at some intervals. It is produced
by stasis and retrograde peristaltic waves. Fecaloid vomiting has a serious prognosis.
Bloody vomiting is a sign of extreme gravity (parietal necrosis).
The stop of intestinal transit for gases and feces defines the occlusion, but there
are situations in which transit is not completely abolished (high-level occlusions) and
sometimes even false diarrhea may appear.
Signs
On inspection, the abdominal distension can be observed in most cases but in
high occlusion, it may be absent leading to errors of diagnosis. In small bowel
occlusions, distension is located particularly around the umbilicus, whereas in large
bowel occlusions, abdominal distension is located predominantly in epigastric region
and flanks (the colic frame).
In strangulation, distension occurs suddenly, is asymmetrical, immobile, elastic
on touch and tympanic on percussion, these features representing the Von Wahl sign. In
sigmoid volvulus, bloating is ovoid, oriented from left iliac fossa toward the right upper
quadrant - the Bayer sign.
In thin patients, the peristaltic waves can be seen through the abdominal wall
progressing toward a fixed point (where the obstacle is located) - the Knig sign.
On palpation, the abdomen is usually 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 (the Boudin sign), successive contraction and relaxation of
the underlying loop (the Besges sign) or points of painful hernia (umbilical, inguinal,
femoral). Unfortunately, hernial regions are often overlooked on physical examination.
Sensitivity located at 2 cm above the umbilicus in the small bowel occlusions represents
the Thevenard sign.
On percussion, excessive sonority (because of intestinal gas distension) and
shifting dullness (the Gangolphe sign of ascites) can be found.
On auscultation, the so-called steam spout sound can be heard being caused by
gases crossing the intestinal narrowed zone - the Knig syndrome. Rapid succession of
Knig syndrome is characteristic for multilevel stenosis - the Keberle syndrome. Due to
hyperperistalsis, bowel sounds are strong, metallic, interrupted by crackling that mimics
the release of an intestinal loop from a stenosis - the Schlange sign. In most cases,
auscultation reveals total silence - "silent abdomen" described by Mondor.
Digital rectal examination may highlight the stenosing rectal tumor or a distended
intestinal loop in the Douglas pouch - the Gold 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 evolving to death.
378
Intestinal Occlusion
Investigations
Abdominal plain radiography, for best result, is usually performed in supine
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 usually ruled out, but distended loops and air-fluid levels
may be absent with an obstruction of the upper jejunum or with closed-loop
strangulating obstructions.
In case of small bowel occlusion, air-fluid images are numerous, relatively
small, arranged centrally in the vertical axis and appear as "organ pipes",
"swallow nests" or "stairs. (Figure 3)
379
Intestinal Occlusion
380
Intestinal Occlusion
Table 2 - Differences between occlusion by strangulation and by obstruction
Criteria
By strangulation
By obstruction
Sudden onset Continuous
Insidious onset - colicky
Pain
Rapidly altered
Slow alteration
General condition
Relatively frequent and rapid due Is possible but in advanced and
Peritonitis
to intestinal necrosis and
complicated cases especially due
perforation
to diastatic perforations
381
Intestinal Occlusion
2. Nasogastric tube, for emptying the stomach and thus preventing aspiration
and for monitoring the quantity and quality of lost digestive fluids
3. Urinary catheter, for monitoring the urine output
Even though the most efficient method of treatment is the surgical solution,
before any surgical intervention, the patient should be reanimated. Duration of
reanimation depends on hypovolemic shock severity and associated illness, but it cannot
last long especially in upper digestive occlusions and occlusions with "closed intestinal
loop" (strangulation). The reanimation should be short and effective. In low intestinal
occlusion such as those caused by tumors of the colon (without peritonitis) emergency
surgery can be postponed and preoperative investigations and preparation carried out for
a longer period.
For volume rebalancing, which is the most important because in occlusion there is
a hypovolemic shock, the loss of fluids (gastric aspirate, diuresis, vomiting) must be
correctly assessed. Fluids such as 5% dextrose and saline will be administered until the
resumption of normal diuresis (1 ml/minute). If the patient is shocked, administration of
blood or plasma might be necessary.[2] High quantities of fluids will be administered
with caution in elderly because of the risk of cardiac insufficiency and acute pulmonary
edema.
Electrolyte rebalancing is based on administration of electrolyte solutions (NaCl,
KCl, Ringer, saline, etc.). In case of acidosis, serum bicarbonate will be administered.
For alkalosis with hypochloremia caused by abundant vomiting (loss of HCl), 5%
arginine hydrochloride will be used.
Because the patient cannot be fed orally, nutritional rebalancing will be carried
out by parenteral administration of 10% glucose (dextrose) solution buffered with
insulin (one unit/2 g of glucose), amino acid solutions, and solutions of soluble lipids or
combined solutions.
Depending on clinical picture severity, oxygen and antibiotics will be
administered. Associated diseases (heart, lung, liver) will be treated.
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 postoperatively too.
Surgery is aimed to remove the intestinal obstacle, intestinal content and
peritoneal effusions and to prevent relapses. Specific surgical measures depend on the
etiology of the occlusion, the status of the affected intestines and the general status of
the patient. Generally, surgical measures can be classified as:
1. For the small bowel occlusions
a. Adhesiolysis in case of adhesions
b. Devolvulation in case of volvulus
c. Reduction of internal strangulated hernias
d. Removal by enterotomy of biliary stone or other foreign body
e. Bowel resection (when the loop is not viable)
f. Ileostomy or intestinal bypass (when lesions cannot be removed)
g. Enteroplication (in patients with intense adhesive syndrome or
recurrent occlusions) to prevent further relapses of occlusion
2. For large bowel occlusions
a. In case of volvulus of the sigmoid colon (which is the most common),
the procedure is devolvulation and sigmoidopexy (suturing the loop to
the abdominal wall to prevent recurrences) when the colon is viable. If
382
Intestinal Occlusion
there are ischemic lesions, segmental resection of the sigmoid colon is
the solution followed by end-to-end anastomosis or by Hatmann's
operation (the distal end is closed and the proximal end is exteriorized
in terminal colostomy). The second stage of the Hartmann's operation
(re-intervention and end-to-end anastomosis) can be performed after a
few months.
b. When occlusion is caused by stenosing colon tumor, there are many
possibilities depending on which side of the colon the tumor is, the
extension of the tumor and the general status of the patient. These
procedures were mentioned in colon pathology chapter. Mainly there
are two types of procedures: those that remove the tumor (with or
without radical intention) and those that do not remove the tumor but
perform an external or internal diversion (palliative surgery).
If patient's general condition is very impaired, seriated operation can be
performed. The first operation is a minimal invasive one being represented in most
cases by external diversion (colostomy or ileostomy), which resolves the occlusion. The
second operation, after patients recovery, is represented by the radical surgery, which is
more extensive than the first one, but the general condition of the patient is significantly
improved.
Prognosis
Intestinal occlusion is a surgical emergency, potentially lethal. Prognosis depends
very much on patient's age, comorbidities and degree of shock. Negative prognostic
factors in the evolution of intestinal occlusion are:
The high-level of obstruction
Occlusion by strangulation
Associated intestinal perforation
Patients history (associated illnesses)
Elapsed time between onset of occlusion and surgery
If untreated, strangulated obstructions cause death in 100% of patients. If surgery
is performed within 36 hours, the mortality rate decreases to 8%. The mortality rate is
25% if the surgery is postponed beyond 36 hours in these patients.[1]
PARTICULAR FORMS OF INTESTINAL OCCLUSION
Intestinal intussusception and small intestine volvulus are described in chapter about
the 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 (60-80%), followed by the cecum (15%), transverse colon (3%), and
splenic flexure (2%).[3,4]
Volvulus of the Sigmoid Colon
The mechanism of volvulus is the twisting of colon around its axis. (Figure 7)
Patients with a long and mobile sigmoidian loop are prone to volvulus. The cause of
torsion may be a congenital or acquired postoperative adhesion band (strap) or the
Meckels diverticulum. The presence of a pelvic mass also increases the risk of
developing sigmoid volvulus. The mass displaces the sigmoid colon sufficiently to
383
Intestinal Occlusion
result in torsion of the mesosigmoid and a resultant
volvulus. Pregnancy and large ovarian tumors may
induce sigmoid volvulus.[5]
The condition is more common in men aged over
50 and a higher incidence is observed in patients with
Parkinson disease, multiple sclerosis, or spinal cord
injury.[3,6-8]
Torsion can be partial or complete (360). The
complete volvulus leads to the development of a closed
loop obstruction. 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 X-ray images, the twisted loop forms two large
compartments with a central double wall ending at the point of the twist, the so-called
"coffee bean" sign. (Figure 4) CT scanning is not often needed, since the plain
radiographic findings are typical for sigmoid volvulus.
Urgent endoscopic detorsion should be considered as the first choice of treatment
with a success rate up to 90% of patients.[9-11] The endoscope is advanced into the
rectum under direct visualization, the rectum is insufflated and 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 under direct visualization. The tip of the endoscope can also be used to apply
constant pressure at the apex, which can lead to detorsion and decompression.[3]
Unfortunately endoscopic detorsion has a high recurrence rate (>60%)[11] and it should
be followed in most cases by elective definitive surgery. Resection of the redundant
sigmoid colon is the gold standard operation.[12]
Surgical treatment is indicated in the following situations:
In emergency when there are signs and symptoms of intestinal loop
necrosis and / or peritonitis
When detorsion failed at endoscopic approach
When ischemic lesions are found at endoscopy
Procedures are represented by:
Detorsion and colopexy when the sigmoid loop is viable
Hartmanns procedure when there are ischemic lesions and anastomosis is
dangerous due to peritonitis (Figure 8)
Resection followed by colo-rectal anastomosis (hand sewn or stapled)
The overall mortality in recent studies is < 5%.[12]
384
Intestinal Occlusion
385
Intestinal Occlusion
small bowel is distended, whereas the distal colon is decompressed. A fold like
termination may be observed at the point of obstruction in the ascending colon at
barium enema examination.[14]
In most cases, plain radiograph is insufficient to confirm cecal volvulus.[15]
Endoscopic decompression is successful in rare cases, the most frequent
performed procedure being the right hemicolectomy. Other possible procedure is
devolvulation followed by cecopexy when the cecum wall is viable.
Biliary Ileus
It is produced by the passage of a big biliary stone into the digestive tract through
a biliodigestive fistula (cholecysto-duodenal in most cases). The biliary stone stops
more frequently in the duodenum (Bouveret syndrome), in the Treitz angle, the terminal
ileum or more rarely in the jejunum, producing obstructive occlusion. (Figure 11)
Biliary ileus is a rare condition, being reported in 0.06% of patients with
gallstones.[16]
Symptoms have three distinct phases:
1. Biliary history with colicky pains, fever and jaundice, characteristic for
biliodigestive fistula
2. Free interval
3. Occurrence of occlusive syndrome
with violent abdominal colicky pains
Abdominal X-ray image highlights the fluidair levels (sign of occlusion) and sometimes
pneumobilia (the presence of air into the biliary
tree). In most cases, biliary ileus is an
intraoperative surprise.
Treatment is represented by enterotomy,
removal of the stone and enterorraphy (closure of
the intestine by sutures), or segmental bowel
resection. Hepatobiliary region must be explored
and lesions (fistula) treated as necessary
(cholecystectomy and duodenorraphy).[17]
Postoperative Occlusions
One of the most frequent postoperative complications, especially after open
abdominal surgery, is the intestinal occlusion. Depending on when it appears after the
surgery, occlusion can be classified as:
1. Immediate occlusions. Almost all of these occlusions are exclusively
mechanical, produced by breaches in the transverse mesocolon, mesentery, or
omentum. Intestinal loops intrude through these breaches producing an
incarcerated internal hernia. It is very difficult to establish the etiology of these
occlusions before reintervention. In most cases, the confusion is made with acute
gastric dilatation.
2. Early occlusions occur within the first 4-7 days after surgery being caused by
adhesions or internal hernias. Unfortunately, they are burdened by a high rate of
mortality. Symptoms are diminished especially by pain medication, and general
condition of patient alters rapidly.
386
Intestinal Occlusion
3. Late occlusions are always mechanical being produced by adhesions, tumor
recurrences, incisional hernias or morphological bowel changes after
radiotherapy (enteritis radica).
References
1.
Nobie
BA.
Small-Bowel
Obstruction
Medscape
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2.
Talbot CH. - Volvulus of the small intestine in adults. - Gut, 1960; 1:76-80.
3.
Thornton
SC.
Sigmoid
and
Cecal
Volvulus.
http://emedicine.medscape.com/article/2048554-overview#showall
4.
Jones IT, Fazio VW. - Colonic volvulus. Etiology and management. - Dig Dis. 1989; 7(4):203-209.
5.
Kolusari A, Kurdoglu M, Adali E, Yildizhan R, Sahin HG, Kotan C. - Sigmoid volvulus in pregnancy and puerperium: a
case series. - Cases Journal 2009; 2:9275.
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Avots-Avotins KV, Waugh DE. - Colon volvulus and the geriatric patient. - Surg. Clin. North Am. 1982; 62(2):249-260.
7.
Rosenthal MJ, Marshall CE. - Sigmoid volvulus in association with parkinsonism. Report of four cases. - J. Am. Geriatr.
Soc. 1987; 35(7):683-684.
8.
Toebosch S, Tudyka V, Masclee A, Koek G. - Treatment of recurrent sigmoid volvulus in Parkinson's disease by
percutaneous endoscopic colostomy. - World J. Gastroenterol. 2012; 18(40):5812-5815.
9.
Martnez Ares D, Yez Lpez J, Souto Ruzo J, Vzquez Milln MA, Gonzlez Conde B, Surez Lpez F, Alonso
Aguirre P, Vzquez Iglesias JL. - Indication and results of endoscopic management of sigmoid volvulus. - Rev. Esp.
Enferm. Dig. 2003; b95(8):544-548, 539-543.
10.
Renzulli P, Maurer CA, Netzer P, Bchler MW. - Preoperative colonoscopic derotation is beneficial in acute colonic
volvulus. - Dig. Surg. 2002; 19(3):223-229.
11.
Tan KK, Chong CS, Sim R. - Management of acute sigmoid volvulus: an institution's experience over 9 years. - World J.
Surg. 2010; 34(8):1943-1948.
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Raveenthiran V, Madiba TE, Atamanalp SS, De U. - Volvulus of the sigmoid colon. - Colorectal Dis. 2010; 12(7
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13.
Agko M, Gociman B, Keilani ZM, Mukherjee A. - Cecal volvulus: a rare complication of colonoscopy. - Int. J.
Colorectal Dis. 2012; 27(2):265-266.
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Swenson BR, Kwaan MR, Burkart NE, Wang Y, Madoff RD, Rothenberger DA, Melton GB. - Colonic volvulus:
presentation and management in metropolitan Minnesota, United States. - Dis. Colon Rectum. 2012; 55(4):444-449.
16.
Rojas-Rojas DJ, Martnez-Ordaz JL, Romero-Hernndez T. - Biliary ileus: 10-year experience. Case series. - Cir. Cir.
2012; 80(3):228-322.
17.
Martnez Ramos D, Daroca Jos JM, Escrig Sos J, Paiva Coronel G, Alcalde Snchez M, Salvador Sanchs JL. Gallstone ileus: management options and results on a series of 40 patients. - Rev. Esp. Enferm. Dig. 2009; 101(2):117120, 121-124.
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Assar AN, Zarins CK. - Acute mesenteric ischaemia: facts and perspectives. - British Journal of Hospital Medicine,
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Bassiouny HS, Desai TR. - Diagnosis and treatment of nonocclusive mesenteric ischemia. - In: Rutherford RB, ed.
Vascular Surgery. 6th edn. 2005, Elsevier, Philadelphia: 172831.
3.
Yasuhara H. - Acute mesenteric ischemia: the challenge of gastroenterology. - Surg. Today 2005; 35(3):185-195.
4.
Oldenburg WA, Lau LL, Rodenberg TJ, Edmonds HJ, Burger CD. - Acute mesenteric ischemia: a clinical review. Arch. Intern. Med. 2004; 164(10):10541062.
5.
Boley SJ, Sprayregan S, Siegelman SS, et al. - Initial results from an aggressive roentgenological and surgical approach
to acute mesenteric ischaemia. - Surgery 1977; 82:848-855.
6.
Kumar S, Sarr MG, Kamath PS. - Mesenteric venous thrombosis. - N. Engl. J. Med. 2001; 345(23):16831688.
7.
Kieny R, Batellier J, Kretz JG. - Aortic reimplantation of the superior mesenteric artery for atherosclerotic lesions of the
visceral arteries: sixty cases. - Ann. Vasc. Surg. 1990; 4(2):122-125.
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Cormier JM, Fichelle JM, Vennin J, Laurian C, Gigou F. - Atherosclerotic occlusive disease of the superior mesenteric
artery: late results of reconstructive surgery. - Ann. Vasc. Surg. 1991; 5(6):510-518.
9.
Aouini F, Bouhaffa A, Baazaoui J, Khelifi S, Ben Maamer A, Houas N, Cherif A.- Acute mesenteric ischemia: study of
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Shanley CJ, Weinberger JB. - Acute abdominal vascular emergencies. - Med. Clin. North Am. 2008; 92(3):627647.
11.
Schoots IG, Levi MM, Reekers JA, Lameris JS, van Gulik TM. - Thrombolytic therapy for acute superior mesenteric
artery occlusion. - J. Vasc. Interv. Radiol. 2005; 16(3):317-329.
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Kassahun WT, Schulz T, Richter O, Hauss J. - Unchanged high mortality rates from acute occlusive intestinal ischemia:
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14.
Aliosmanoglu I, Gul M, Kapan M, Arikanoglu Z, Taskesen F, Basol O, Aldemir M. - Risk factors effecting mortality in
acute mesenteric ischemia and mortality rates: a single center experience. - Int. Surg. 2013; 98(1):76-81.
15.
Park WM, Gloviczki P, Cherry KJ Jr, et al. - Contemporary management of acute mesenteric ischemia: Factors
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Harnik IG, Brandt LJ. - Mesenteric venous thrombosis. - Vasc. Med. 2010; 15(5):407-418.
393
394
Peptic ulcer
Idiopathic
Induced
Aspirin
NSAIDS
Infectious
Helicobacter pylori
Cytomegalovirus b.
Herpes simplex virus
Stress ulcer
Zollinger Ellison syndrome
Esophagitis
Peptic
Infectious
o Candida albicans
o Herpes simplex virus
o Cytomegalovirus
o Other
Induced
o Alendronate
o Tetracycline
o Qinidin
o Potassium chloride
o Aspirin
o NSAIDS
Portal hypertension
Esophageal varices
Gastric varices
Duodenal varices
Portal hypertension gastropathy
Arterial or venous malformations
Idiopathic angioma
Rendu-Osler-Weber syndrome
Dieulafoy lesions
Antral vascular ectasia (watermelon
stomach)
Radiation induced teleangiectasia
"Blue rubber bleb nevus syndrome
(association between cavernous
hemangiomas of the skin and similar
lesions in the GI tract.)
Traumatic or postoperative
Mallory-Weiss syndrome
Ingested foreign bodies
Surgical anastomosis
Enteric arterial fistula
Tumors
Benign
o Leiomyomas
o Lipomas
o Polyps (hyperplasic,
adenomatous, hamartomatos)
Malignant
o Adenocarcinoma
o Leiomyosarcoma
o Lymphoma
o Kaposi's sarcoma
o Carcinoid
o Melanoma
o Metastases
Others
Hemobilia
Haemosuccus pancreaticus
Highlighting bleeding
Medical history, color and amount of gastric aspiration or vomit, or the 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 aspects of
the therapy of patients with gastrointestinal bleeding. Usually, blood loss is
underestimated.[2] 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:
Resting tachycardia (100 beats /min)
In standing position heart rate increases by more than 20 beats/min, the
systolic pressure decreases by more than 20 mmHg, and diastolic pressure
decreases by more than 10 mmHg.
Acidosis
395
Azotemia (blood urea increased by over 40 mg/100 ml without preexisting renal disease)
Transfusion requirements of more than one unit at 8 hours or six units in
total (10 units or more of red cells in a 24 hour period)
Hematochezia from upper gastrointestinal source
Unable to clarify the fresh red blood in gastric lavage
Continued bleeding or rebleeding during endoscopy
An increased risk is when there are met more criteria:[11,12]
Age over 60 years
Significant comorbidities
Coagulopathy
Hemodynamic instability
Signs of active bleeding
These patients will be admitted in ICU and subjected to emergency endoscopic
diagnostic and therapeutic maneuvers. Surgical and interventional radiology services
will be alerted for possible evaluation. About 25% of patients hospitalized in ICU are
low risk patients and can be treated in other hospital departments (gastroenterology,
surgery).
In order to standardize and improve care, various scoring systems (Rockall,
Blatchford and Baylor) have been developed to identify those individuals at high risk
requiring treatment (transfusion, endoscopic or surgical intervention) or at risk of
rebleeding and death.[10]
Rockall score, [13] (Table 1) based on clinical and endoscopic criteria in patients
with a history of UGIB, provides predictability of recurrence and severity of bleeding.
The variable
Age
P
Co-morbidity
Without major
comorbidities
Diagnosis
Mallory-Weiss
syndrome
Without
highlighted lesions
and without
massive bleeding
Without active
bleeding or just a
dark spot
Major signs of
recent
hemorrhage
at endoscopy
Renal impairment
Ischemic cardiopathy
Digestive cancer
Any other major comorbidity
Renal
failure
Liver
failure
Metastases
Any other
diagnostics
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 after endoscopy
with the recommendation to continue treatment at home.[14]
396
Ulcers located on the lesser curvature of the stomach and duodenum and those
located on the posterior wall are more likely to produce an UGIB due to the rich
vascularization of those zones.
Resuscitation protocol for UGIB
Adequate venous access
o Two large-bore intravenous catheter
o Central vein catheterization if necessary
o In case of myocardial infarction or severe ischemia, pulmonary artery
catheter
Bladder catheter
Hydroelectrolytic rebalancing
Oxygen
Monitoring:
o Blood pressure and its changes in standing position (invasive monitoring)
o Pulse
o Hematocrit
o Flow of urine
o Central venous pressure or cardiac output
Transfusion of blood and derivatives
Gastroenterology consult
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 in most cases. Anyway, endoscopic
exploration should be performed in cases with positive gastric lavage.
Intense bowel sounds indicate a superior source of bleeding. The pain usually
indicates a peptic ulcer and vomiting before bleeding suggests Mallory-Weiss
syndrome.
397
399
400
401
402
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.
Portal hypertension is defined as portal pressure gradient exceeding 5 mm Hg.[59]
Esophageal varices develop when the gradient pressure between the portal and hepatic
vein is greater than 10 mmHg and bleed only when the gradient exceeds 12 mm
Hg.[60,61]
Many clinical and physiological factors are useful in predicting bleeding from
varices in cirrhotic patients, such as:[59]
Location of varicose veins: distal esophagus, stomach
The size of varicose veins: varices occupying more than 1/3 of the
esophageal lumen
The endoscopic appearance of varicose veins: "red marks" (red streaking or
spotting)
The degree of hepatic dysfunction according to Child-Pugh classification
Bleeding in patients history
The presence of ascites
The pressure in varices. The incidence of bleeding according to the pressure
is:[62]
13 mmHg - 0%;
14 mmHg - 9%;
15 mmHg - 17%;
16 mmHg - 50%;
16 mmHg - 72%.
Therapeutic options in bleeding varices (see also the esophageal varices in chapter:
surgical pathology of the esophagus)
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.
403
404
405
406
Stress ulcers
Definition and clinical features
Stress ulcer 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.[84]
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 capillary vessels, but
deeper lesions can erode the submucosa causing massive bleeding and /or perforation.
There are two major risk factors for bleeding:[85]
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 upper digestive bleedings.
Pathogenesis
Mucosal lesions occur when the effects of gastric acid and pepsin exceed the
gastric mucosal defense mechanisms:
by excessive production of acid and pepsin (aggressive factors), and/or
by overcoming the defensive factors of gastric mucosa
Physiological mechanisms of gastric mucosa defense are represented by:[86-88]
secretion of mucus and bicarbonate, that form a protective layer on the
cell surface
rapid regeneration of damaged cells
endogenous prostaglandin production
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.
The gastric mucus has three main functions:[89,90]
1. Mechanical protection of the epithelial surface
2. Prevents the retrodiffusion of hydrogen ions
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.
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 of 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 reepithelialization.[91]
407
408
409
410
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 is not a
choice for the treatment of bleeding esophagitis.
Mallory-Weiss syndrome
There are longitudinal lacerations of the mucosa at the gastroesophageal junction.
The pathogenesis is not yet well understood but it seems that lesions are 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 (local injection, hemoclipping, or multipolar electrocoagulation) can be applied
successfully. Relapse is rare after endoscopic therapy and occurs more often in patients
with portal hypertension.
Dieulafoy lesion
A submucosal, large, aberrant, artery causes bleeding into the gastric lumen. The
lesion is usually located at 6 cm below the gastro-esophageal junction but other
locations are possible (body or fundus of stomach, cardia, esophagus, duodenum,
etc).[105] It is characterized by recurrent gastric bleeding without an obvious source,
unless the vessel is visible. There are no ulcerative changes. Angiography helps to find
the source of bleeding.
Advances in endoscopy and angiography have increased the detection of
Dieulafoy lesions and decreased the mortality from 80% to 8.6%.[106] Endoscopic
treatment combining different kinds of methods are becoming more and more effective
but rebleeding is possible.[107] Bleeding arrest is also possible by embolization.[108,109]
Definitive treatment is represented by surgery (gastric resection) by open or
laparoscopic approach.
411
Aortoenteric fistula
Most fistulas are associated with the placement of intraaortic prosthesis
(secondary fistula) or abdominal aortic aneurysm (primary fistula). Common location is
in the third portion of the 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 aortoenteric fistula have a small initial hemorrhage, known as heraldic
bleeding that occurs before a massive hemorrhage.
Surgical solution is to by-pass the affected artery and repair of intestinal damage
(duodenorrhaphy) or removal of the prosthesis and fistula, and performing an axilofemoral bypass.
Watermelon stomach
The pathognomonic endoscopic pattern of gastric mucosa is of red stripes
arranged radially, departing from pylorus resembling the aspect of watermelon. When
red stripes are arranged in a diffused-way, is the so called honeycomb stomach.[112]
Autoimmune disorders, mainly represented by Reynauds phenomenon and
sclerodactyly, are co-present in about 60% of patients.[112] The anomaly is more
common in women and is related to severe liver disease and renal failure. Laser
photocoagulation was successful in many cases [113,114] but surgical resection
(antrectomy) is the treatment of choice.[115]
412
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416
Abdominal Trauma
ABDOMINAL TRAUMA
Background
Injuries resulting from traffic collisions, drowning, poisoning, falls or burns and
violence from assault, self-inflicted violence or acts of war, kill more than five million
people worldwide annually accounting for 9% of global mortality.[1]
In 2004, cumulative mortality through intentional and unintentional injuries
ranked sixth after cardiovascular diseases, infectious and parasitic diseases, cancers and
respiratory diseases.[2]
Estimations indicate that by 2020, 8.4 million people will die yearly from injuries,
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.[3]
On the other hand, injuries represent a major public health and economic problem
due to the high costs of treatment and to the temporary or permanent disabilities.
Injuries affect mostly young people, the mortality produced by injuries
representing 22%-29% of all death at ages 1559, except in Africa, where it is 13%.[2]
In US mortality produced by unintentional injuries in 2010, ranked first in the group age
of 1-44 years.[4]
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.[3]
In Romania, injuries are the fourth leading cause of death. The rates for
unintentional injuries and for all the intentional injuries are lower than the regional
averages but higher than the European Union (EU) values. The leading causes of
unintentional injury-related death are road traffic injuries, followed by falls, poisoning,
drowning and fires. The leading causes of intentional injury-related death are suicide
followed by homicide.[5]
The abdomen is one of the most involved parts of the body in trauma, requiring
surgical exploration in up to 20% of cases.
Abdominal cavity can be divided into four areas where organs are more or less
protected by anatomical structures from external injuries.
1. The upper abdomen beneath and protected by ribs cage containing the liver,
gallbladder esophagus, stomach, duodenum and spleen
2. The lower or pelvic abdomen, protected by pelvic bones containing the:
bladder, uterus with annexes, rectum and 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 and part of the stomach
Classification
Abdominal trauma may be classified as blunt (contusions) and penetrating
(wounds).
Blunt trauma (contusions):
o Traffic accidents (most common 50-75%)
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Abdominal Trauma
o Falls
o Aggressions
o Accidents
o Sport (recreational) and domestic accidents
o Iatrogenic (resuscitation, Heimlich maneuver)
Penetrating trauma (Wounds):
o Stab wounds
o Gunshot wounds
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Abdominal Trauma
419
Abdominal Trauma
b. The two-stage peritonitis. The first stage is represented by the organ
trauma and then, the peritonitis as the second stage that may occur as a
result of:
Eschar of a hollow organ wall (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 represented by intraperitoneal abscess.
d. Intestinal obstruction produced by internal hernia (for example a breach
in the mesentery as a result of the abdominal trauma - see at hernia
chapter).
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Abdominal Trauma
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:
missile speed
missile shape (irregularly shaped splinters cause more serious injuries)
occurrence of secondary missiles (the missile fragments or fragments of
tissue displaced by it)
shooting distance
In penetrating abdominal trauma due to gunshot, the most commonly injured
organs are as follows: small bowel (50%), colon (40%), liver (30%) and abdominal
vascular structures (25%).[6]
Wounds caused by weapons (stab wounds) are more common, and generally,
intra-abdominal organ injuries are more predictable. Usually a single organ is affected
but 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: liver (40%), small bowel (30%), diaphragm (20%) and colon
(15%).[6]
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
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 laparotomy
5. Completion of secondary examination (laboratory tests) to detect occult
lesions
6. Frequent reassessment to follow the evolution of the patient considering
the possibility of undetected lesions or to detect late lesions (2 or 3 stages
lesions).
History is sometimes impossible or difficult in dizziness or unconscious patients.
Important information refers to:
The nature and circumstances of injury
The time when it occurred
The status of the patient at the time of trauma:
o physiological (food, stool, urination, pregnancy)
o pathological (associated diseases, allergies, previous interventions,
ingestion of medicines or drugs)
Pain: timing, location and radiation, the evolution in time.
Other symptoms or signs: hematemesis, melena, rectal bleeding,
hematuria.
Physical examination
A. Primary survey
Any penetrating abdominal trauma represents a surgical emergency because is
burdened by certain risk of death. Therefore, these patients will be evaluated and will be
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Abdominal Trauma
given first aid in the emergency service. Patient health status brought to the emergency
room can vary greatly depending on the severity of injuries. Some patients are in good
condition, hemodynamically stable, but others are unstable and comatose. Polytrauma
patients are a challenge for doctors in evaluation and stabilization of their vital
functions. On the other hand, a penetrating abdominal wound may have a lower risk of
death from abdominal vascular injuries.
Evaluation and stabilization measures must be made quickly and simultaneously.
The primary survey will not take more than 20-30 seconds. Vital functions should be
evaluated first according to the mnemonic ABCDE: Airway, Breathing, Circulation,
Disability, and Exposure/Environment.
A. First airway patency should be checked. If foreign bodies or secretions
are found, they will be removed.
B. Breathing is assessed and if necessary, orotracheal intubation will be
performed.
C. Assessment of circulation begins by assessing the patient's mental status,
skin color and temperature. Pulse and blood pressure are not very
characteristic of hemorrhagic shock and will be evaluated in secondary
survey if there is cardiac activity.
D. Disability is assessed for neurologic deficits before giving sedation or
paralytics. The Glasgow Coma Score and the gross motor and sensory
status of all four extremities should be determined and recorded.
E. 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.
B. Secondary survey and injury assessment
After primary evaluation, first measures, including surgery if necessary, are
aimed to save the patient's life. Blood samples will be collected for laboratory tests and
including blood group. If necessary, the patient will be intubated, and an intravenous
access will be established. In pure abdominal trauma, the most dangerous is the
hemorrhagic shock caused by intraperitoneal bleeding and surgical measures are
addressed to stop bleeding.
Secondary survey presumes a complete head-to-toe physical examination that can
be delayed until the patient is stabilized but performed as soon as possible.
On inspection, skin lesions may guide the prediction of injured intra-abdominal
organs. In gunshot wounds, skin lesions may represent either entrance or exit wounds.
In transfixiante wounds, the exit lesion is 2-3 times larger than the entrance lesion, and
frequently does not overlap the entrance wound because the bullet was deflected by the
skeletal structures. In the so-called blind wounds, represented only by the entrance
lesion, multiple missiles or foreign objects are retained within the body. Pathological
fluids (blood, intestinal content, urine) may be observed leaking through wounds.
Abdominal distention may mean a bowel obstruction or hemoperitoneum. A
visible mass may represent a massive abdominal hematoma, a traumatic hernia or intraparietal collection.
On palpation, a reducible swelling confirms the traumatic hernia, the presence of
fluctuance confirms a parietal collection. Pain is the most important sign. Abdominal
guarding or contracture reveals the peritoneal irritation. There is a lack of signs of
peritoneal irritation in patients with severe shock, coma, poisoning by drugs or alcohol.
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Abdominal Trauma
In other circumstances, signs of peritoneal irritation may be misleading such as in case
of false acute abdomen produced by injuries of the spinal cord, of the base of thorax or
properitoneal hematoma.
On percussion, the shifting dullness in lateral quadrants is a sign of
intraperitoneal fluid collection, most often blood. Tympanic sound means possible
bowel obstruction. Induced pain on percussion (Mandel positive maneuver), means
peritoneal irritation.
On auscultation, the absence of bowel sounds is observed in peritonitis and
exacerbation in mechanical bowel obstruction. Bowel sounds heard over the thorax are
present in diaphragmatic rupture. Arterial murmurs can be heard in large vessel lesions.
Rectal and vaginal finger examination is mandatory and can detect pain induced
by palpation of the Douglas bag that confirms pathological peritoneal fluid collection.
Local deformations produced by fractures of the pelvic bones can be detected.
Wounds located on the anterior abdomen can be explored locally (using sterile
instruments) to determine whether they penetrate the peritoneum. On the flank and back
areas, exploration is more difficult and less reliable. Imagistic explorations (ultrasound,
CT) are indicated in these cases.[8]
Repeated physical examination is the most important element of observation.[9,10]
Investigations
Three tests are the most important in diagnosis (of course in adjunction to history
and physical examination): CT scan, ultrasound examination and the diagnostic
peritoneal lavage. In Europe in the first preferred examination is the abdominal
ultrasound.
Laboratory tests. Blood count and blood group are 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 hemorrhage. 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 hematuria. Blood glucose, urea and creatinine, electrolytes and routine tests are to
be interpreted in evolution. Sometimes, detection of medicines and drugs levels in
biological fluids is necessary.
Abdominal ultrasound (US) is important because it can be done at bedside in
unstable patients.[11] Abdominal US is a useful and valuable diagnostic tool after
clinical evaluation in patients with blunt abdominal trauma.[12,13] The main
disadvantage is the lack of sensitivity especially in penetrating trauma.[11] 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 (pericardial, right upper quadrant, left upper quadrant, pelvis).
Ultrasound signs of lesions are:
1. The presence of free liquid in the Douglas pouch or Morrison (under the
liver) space
2. The presence of fluid in the pleural sinuses or pericardium
3. Parenchymal lesions such as spleen or liver rupture with hematoma
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Abdominal Trauma
Radiological explorations. Even in cases of pure abdominal wounds, a chest
radiograph should be performed (except when a CT scan was performed initially) to
rule out the penetration of the thoracic cavity.
Plain abdominal X-ray highlights the pneumoperitoneum in hallow organ
perforation, fluid-air levels in occlusions, foreign bodies (bullets) or disappearance of
psoas muscles shadow in retroperitoneal effusions. X-ray of pelvis and spine is used to
highlight fractures but CT scan and MRI are more reliable.
In patients with a good status and clinical course, investigations that are more
complex can be performed: examination of the digestive tract with hydrophilic contrast,
urography, and angiography.
CT scan can provide important data regarding the presence of intra-peritoneal
fluid and about its source but the diagnosis of significant penetrating injury should not
be delayed by routine CT. It is the standard examination for the detection of
parenchymatous organ damage. The indications for CT scan are:[14]
Patients hemodynamically stable, but with equivocal clinical examination
Spinal cord injuries (back and flank trauma)
Hematuria in stable patients
Head trauma
Pelvic fractures
CT requires a hemodynamically stable patient. In modern services spiral CT is
performed in all cases of severe injuries.
Diagnostic peritoneal lavage (DPL) shall be performed only after inserting a
nasogastric tube and a bladder catheter for decompression. It is indicated in:
Blunt abdominal trauma :
o Unstable patient
o Stable patients with inconclusive clinical examination
Penetrating abdominal trauma:
o Stabbed abdominal wound with no signs of peritoneal irritation
o Chest wound under the nipples level (possible diaphragmatic
injury)
o Stabbed wound in the flanks.
Contraindications are:
In penetrating stab wounds to the abdomen or flank, if the patient is
hemodynamically instable or has signs of peritonitis, diagnostic testing
should not delay laparotomy.[15]
Open abdominal surgeries in patients history (risk to damage the bowel
loops adherent to the abdominal wall)
Advanced pregnancy
DPL can be performed in two ways: 1. via the
open method, when the catheter is inserted into the
peritoneal cavity under direct visualization through a
small infraumbilical incision, or 2. via the closed
method when the catheter is inserted blindly over a
guide wire through a trocar.
Aspiration of gross blood (Figure 4) or food
particles is positive for peritoneal penetration and organ
injury. If aspiration is negative, one liter of warm
normal saline is infused rapidly and allowed to return by
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Abdominal Trauma
placing the bag on the floor. The fluid is then sent for analysis.
Indications for laparotomy are:[15,16]
1. 10 ml gross blood on initial aspiration
2. More than 100,000 red blood cells/ml, (30 ml of blood in the peritoneum
is enough to return a positive lavage)
3. More than 500 leukocytes/ml
4. The presence of bile, amylase, intestinal or fecal content, bacteria, fiber, or
urine
5. Failure to recover the fluid is considered positive point
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, and
therefore the patient will be monitored and resuscitated (if necessary) in the emergency
room. After the primary evaluation, priority will be given to support vital functions.
Airways will be released and if necessary, the patient will be intubated to ensure
appropriate oxygenation or ventilation. If there are intrathoracic lesions (ie
pneumothorax, hemothorax) these will be treated with priority to ensure respiratory
function. Airway protection and ventilatory support are followed by circulatory
resuscitation with fluid infusion.
Immediate laparotomy is indicated when the patient is instable hemodynamically,
in cases of evisceration, peritonitis or gunshot. However, in less serious cases, selected
patients may be managed expectantly [8] or an exploratory laparoscopy can be
performed.
Surgical treatment of abdominal trauma in hospital setting is adapted to specific
lesions but there are some general principles:
Diagnostic maneuvers and then surgery is associated with concomitant rebalancing maneuvers.
The patient should be placed on a cardiac monitor, pulse oximeter, and 100%
nonrebreather oxygen mask.
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).
Tetanus prophylaxis (Tetanus Toxoid), if five years have passed since the last
immunization.
Major painkillers 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, nasogastric tube, bladder catheter and tracheal intubation (if
necessary).
Nasogastric aspiration is useful because:
Ensures the stomach decompression
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Abdominal Trauma
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
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 stomach is injured in most cases during anterior abdominal penetrating
trauma and its anterior wall is the most affected. In blunt trauma, a full stomach may
explode due to sudden increase of pressure.
Extravasation of gastric content is followed by 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:[17]
Grade
I
II
III
IV
V
Lesion
Contusion/hematoma
Partial thickness laceration
Laceration
- <2cm in GE junction or pylorus
- <5cm in proximal 1/3 stomach
- <10cm in distal 2/3 stomach
Laceration
- >2cm in GE junction or pylorus
- >5cm in proximal 1/3 stomach
- >10cm in distal 2/3 stomach
Tissue loss or devascularization <2/3 stomach
Tissue loss or devascularization >2/3 stomach
Contusions without rupture of the gastric wall can be treated conservatively with
nasogastric aspiration, symptomatic treatment and frequent reassessment. If laparotomy
is necessary, surgery can be grouped as follows:
For grade I and II: - Hematoma evacuation, hemostasis and suture.
For grade III: - Lesion excision and suture, or lesion excision and
gastroentero- anastomosis. (GEA)
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Abdominal Trauma
Duodenal Trauma
Duodenal trauma is a very serious, life threatening condition and represents 1-2%
of all abdominal traumas. It is usually discovered during laparotomy for hypotension or
peritoneal irritation. The mechanism depends on the anatomical region involved. For the
D3 portion, crushing against the spine is main mechanism. Traction can cause the
rupture in duodenal extremities. The explosion of a full duodenum by compression is
another possibility.
Pathological classification of duodenal lesions according to AAST:[17]
Grade
I
II
III
IV
Lesion
Hematoma - Involving single portion of duodenum
Laceration - Partial thickness, no perforation
Hematoma - Involving more than one portion
Laceration - Disruption <50% of circumference
Laceration
- Disruption 50%-75% of circumference of D2
- Disruption 50%-100% of circumference of D1,D3,D4
Laceration
- Disruption >75% of circumference of D2
- Involving ampulla or distal common bile duct
Laceration - Massive disruption of duodenopancreatic complex
Vascular - Devascularization of duodenum
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Abdominal Trauma
defects, after duodenal suture, an intestinal loop can be used to patch the
parietal defect, or for anastomosis.
For grade IV: - When lesions are not involving the bile duct or Vaters
ampulla, a duodeno-jejunal anastomosis is preferred. For lesions of the CBD
without pancreatic lesions, reimplantation of CBD (in duodenum or jejunum)
is performed. When pancreatic lesions are associated, cephalic duodenopancreatectomy is the solution.
For grade V: - Major duodeno-pancreatic injury requires cephalic duodenopancreatectomy unfortunately burdened by a high mortality rate.
Traumatic duodenal lesions are frequently associated with other intra-abdominal
injuries particularly of the pancreas; they are difficult to diagnose and pose special
problems concerning surgical technique and therefore they have a high postoperative
morbidity and mortality.
Lesion
Hematoma - Contusion or hematoma without devascularization
Laceration - Partial thickness, no perforation
Laceration <50% of circumference
Laceration > 50% of circumference without transection
Laceration - Transection of the small bowel
Laceration - Transection of the small bowel with segmental tissue loss
Vascular - Devascularized segment
Abdominal Trauma
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 about 5% due to the septic content of the
colon.[18,19]
The most frequent causes are the abdominal stab wounds, gunshot wounds and
colonoscopies (1 in 1400 for overall colonoscopies and 1 in 1000 for therapeutic
colonoscopies).[20,21]
AAST classification of traumatic lesions of the colon:[17]
Grade
I
II
III
IV
V
Lesion
Hematoma - Contusion or hematoma without devascularization
Laceration - Partial thickness, no perforation
Laceration <50% of circumference
Laceration > 50% of circumference without transection
Transection of the colon
Transection of the colon with segmental tissue loss
Devascularized segment
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Abdominal Trauma
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:[17]
Grade
I
II
III
IV
V
Lesion
Hematoma - Contusion or hematoma without devascularization
Laceration - Partial-thickness laceration
Laceration < 50% of circumference
Laceration > 50% of circumference
Full-thickness laceration with extension into the perineum
Devascularized 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 urethral and 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 through the urethra) and severe ascending urinary
infections.
Digital rectal examination is mandatory in these patients and can highlight: rectal
solutions of continuity, fluctuance of perirectal tissues, intrarectal or perirectal foreign
bodies (bone fragments) and bleeding.
Diagnosis is confirmed by rectoscopy. Endorectal ultrasound can detect
incomplete lesions of the rectal wall and the presence of perirectal collections.
Surgical treatment varies according to severity of lesions.
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Abdominal Trauma
The grade I and II of injuries can be primary sutured. In more serious injuries,
when rectal sutures are possible, an upstream protective colostomy should be
associated. Injuries that cannot be sutured require Hartmanns 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 gunshot produces massive lesions with devascularization of
the rectum, requiring resection with colostomy.
Intrarectal foreign bodies are extracted through the anus in spinal or general
anesthesia. After extraction, rectosigmoidoscopy 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.
Urethral and bladder injuries are treated by suture associated or not with
cystostomy.
The mortality rate of rectal injuries caused by blunt trauma is more than 50%,
which is higher than the mortality rate of colon injuries caused by blunt trauma
(17%).[23]
Pancreatic Trauma
Although pancreatic traumas are rare (< 10%) they are very serious due to
frequent association with other abdominal lesions, especially of the large vessels that
cause a significant morbidity (3660%) and mortality (1823%).[25-28] Early mortality
usually results from uncontrolled or massive bleeding due to associated vascular and
adjacent organ injuries. Late mortality is mainly due to infection complicating acute
post-traumatic pancreatitis.
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:[17]
Grade
I
II
III
IV
V
Lesion
Hematoma - Minor contusion without duct injury
Laceration - Superficial laceration without duct injury
Hematoma - Major contusion without duct injury or tissue loss
Laceration - Major laceration without duct injury or tissue loss
Laceration - Distal transection or parenchymal injury with duct injury
Laceration - Proximal transection or parenchymal injury involving
ampulla
Laceration - Massive disruption of pancreatic head
Clinical picture. Isolated pancreatic injuries are difficult to diagnose, and may
evolve as a post-traumatic acute pancreatitis with its early and late complications. 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. Increased amylasemia and visible
lesions on CT scan facilitate diagnosis. In blunt trauma by frontal collision, a high index
of suspicion of pancreatic lesion should be present.
Surgery is adapted to lesion types.
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Abdominal Trauma
Abdominal wounds, especially the gunshots, where pancreas lesions are
suspected, are considered a major emergency and are explored through laparotomy
without any other investigations.
Pancreatic injuries should be treated by debridement and simple drainage unless
there is clinically obvious duct involvement.[25]
In grade I and II lesions the surgical measures are represented by hematoma
evacuation and hemostasis, infiltration with lidocaine, and neighborhood drainage to
avoid a pancreatic pseudocyst in case of unrecognized minor injuries of the pancreatic
duct.
Grade III of severity with lesions located to the left mesenteric pedicle requires
caudal pancreatectomy with or without splenectomy.
Grade IV 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.
In grade IV with ampulla lesions and massive disruption of the pancreatic head,
cephalic duodenopancreatectomy can be a solution but it is encumbered by a high
mortality rate considering the general status of the patient with multiple lesions and
hemorrhagic shock. The first concern is to stop bleeding and then, if the patient is
stable, cephalic duodenopancreatectomy is performed. If the patient is unstable, only
multiple drainages are performed after hemostasis and the resulting fistula dealt with at
a later operation, if necessary.[25,29]
The most common postoperative complications are fistulas and pancreatic
pseudocysts and the overall mortality is around 15%.
Splenic Trauma
The spleen is the most commonly injured parenchymatous organ in blunt
abdominal trauma, especially in traffic accidents associated with left ribs fractures. It
may be also injured during penetrating trauma and surgery. The consequence is the
intraperitoneal bleeding with hemoperitoneum and hemorrhagic shock.
Lesions on a pathological spleen in splenomegaly of any etiology may occur after
apparently minor trauma.
AAST classification of traumatic lesions of the spleen:[17]
Grade
I
II
III
IV
V
Lesion
Hematoma - Subcapsular <10% surface area
Laceration - Capsular tear <1cm parenchymal depth
Hematoma - Subcapsular, 10%-50% surface area; intraparenchymal, <5 cm in
diameter
Laceration - Capsular tear, 1-3cm parenchymal depth that does not
involve a trabecular vessel
Hematoma - Subcapsular, >50% surface area or expanding; ruptured
subcapsular or parecymal hematoma; intraparenchymal hematoma > 5 cm or
expanding
Laceration - >3 cm parenchymal depth or involving trabecular vessels
Laceration - Laceration involving segmental or hilar vessels producing
major devascularization (>25% of spleen)
Laceration - Completely shattered spleen
Vascular - Hilar vascular injury with devascularized spleen
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Abdominal Trauma
Clinical 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 addition to general signs of acute anemia and hemorrhagic shock, there are
local signs of pain or left upper quadrant guarding and referred pain to the left shoulder
(the Kehr sign). Saegessers splenic point of tenderness is an area on left side between
scalenus medius and sternocleidomastoid muscle.
There are cases when the spleen ruptures under the intact capsule developing a
subcapsular hematoma. As the hematoma develops in the following days, the capsule
becomes more and more tensioned and suddenly it ruptures (spontaneously or after
minor trauma) leading to hemoperitoneum. This is the so-called two-stage splenic
rupture. It may occur after several days or even weeks.
In subcapsular hematoma and coagulated blood around the spleen, fixed dullness
on the left flank on percussion can be noticed representing the Balances sign.
Obliteration of the resonant note in the Traube's space can be also observed on
percussion.
In lower left hemithorax and left flank contusions, the surgeon should have a high
degree of suspicion regarding spleen rupture even if the patient is in a good condition
without signs of internal bleeding and should proceed to investigations such as
ultrasound and chest X-ray. 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.
The most used investigation for detecting spleen rupture and hemoperitoneum is
the ultrasound examination, which is fast, noninvasive, cheap, and can be performed at
bedside. Focused assessment with sonography for trauma (FAST) is a rapid bedside
ultrasound examination performed as a screening test for blood around the liver, in the
pericardium, around the spleen and in the pelvis. Ultrasonography reveals the
subcapsular or perisplenic hematoma, parenchymal rupture and the presence of fluid in
the peritoneal cavity.
Plain radiography of the abdomen and chest can show the left ribs fracture,
elevation of the left hemidiaphragm and the displacement of gastric fluid-air level.
In uncertain cases, the diagnostic peritoneal lavage (DPL) can be performed but it
is less used in nowadays when ultrasound and CT scan are available in most medical
centers.
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).
Treatment of splenic injuries, depending on severity, can be managed surgically
or nonsurgical.
The surgical treatment of choice is spleen conservation (hemostasis by electrocoagulation, plasma-coagulation, local hemostatics, suturing, partial resection)
whenever possible to avoid post-splenectomy infections especially in children. Spleen
has an important role in immunity.[30,31] Splenectomy is the choice in severe and
multiple lesions of the spleen with hemodynamic instability.
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Abdominal Trauma
Indications for splenectomy are:[32]
Parenchyma explosion
Vascular lesions in the hilum
Intra-parenchymal massive hematoma
Patients in critical condition or other severe intra-abdominal injuries
Failure of conservative surgical techniques
Criteria for nonoperative management are:[33-35]
Patient in an intensive care unit with continuous monitoring of vital
functions. Daily or even several times a day ultrasound assess of lesion
development (expanding hematoma or hemoperitoneum requiring
surgery)
Surgical team always available for secondary bleeding
Hemodynamic stable patient
Negative abdominal scan
Absence of contrast extravasations on CT
Absence of other indication for laparotomy
Absence of other condition associated with high risk of bleeding
(coagulopathy, use of anticoagulants, etc)
Contraindications to nonoperative management are:[36]
Patients with hemodynamic instability
Generalized peritonitis
Other intra-abdominal injuries requiring surgical exploration
Portal hypertension
Higher-grade splenic injury with large volume hemoperitoneum
Refusal of blood transfusion
Altered neurologic status
Angiographic splenic embolization was first applied in 1981. It requires
specialized imaging facilities and an experienced vascular interventionalist. It is most
useful when employed selectively in hemodynamically stable patients who have CT
findings that include active contrast extravasation, splenic pseudoaneurysm, or large
volume hemoperitoneum.[36-39] The success rate is 57 to 93 percent.[36]
Lesion
Hematoma - Subcapsular, <10% surface area
Laceration - Capsular tear, <1cm parenchymal depth
Hematoma - Subcapsular, 10% to 50% surface area: intraparenchymal <10 cm in diameter
Laceration - Capsular tear 1-3 parenchymal depth, <10 cm in length
Hematoma - Subcapsular, >50% surface area of ruptured subcapsular or parenchymal
hematoma; intraparenchymal hematoma > 10 cm or
Laceration - expanding >3 cm parenchymal depth
434
Abdominal Trauma
IV
V
VI
Laceration - Parenchymal disruption involving 25% to 75% hepatic lobe or 1-3 Couinauds
segments
Laceration - Parenchymal disruption involving >75% of hepatic lobe or >3 Couinauds
segments within a single lobe
Vascular - Juxtahepatic venous injuries; ie, retrohepatic vena cava/central major hepatic veins
Vascular - Hepatic avulsion
Clinical picture of liver trauma depends very much on the severity of injury.
Major liver trauma with vascular injuries or liver explosion is 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's triad in liver trauma is represented by:
1. The paradoxical bradycardia in a patient with hypotension
2. Shock
3. Jaundice
On local examination, abdominal contracture may occur due to extravasation 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
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
The diagnosis is based especially on imaging explorations.
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. Recent advancement of contrast-enhanced sonography improved the
diagnostic accuracy.[41] Furthermore, contrast-enhanced ultrasound can be used in the
follow-up of patients who are managed with nonoperative treatment, avoiding radiation
and iodinated contrast medium exposure.[42] The hemodynamically unstable patient
with a positive ultrasound is moved directly to the operating room without further
imaging.[40]
CT scan is the standard imaging study for stable patients assessing more
accurately the severity of liver injuries. It plays an important role in the nonoperative
management of liver injuries and it can guide the percutaneous drainage of biloma (a
collection of bile inside the abdomen that has become encapsulated) and intraabdominal collections.
Angiography is performed after CT scan if this highlights extravasation of
contrast in stable patients. Angioembolization is an important method of conservative
treatment in hemodynamically stable patients. The success rate is about 6893%.[43-45]
Positive DPL impose the surgical exploration.
The treatment of patients with liver trauma depends much on the severity of
lesions, hemodynamic status and associated intra-abdominal lesions.
435
Abdominal Trauma
If the patient, with hepatic laceration, intrahepatic or subcapsular hematoma, is
hemodynamically stable continuously from the trauma through evaluation, the choice
will be the conservative management with frequent imaging and laboratory
reassessment. Conservative management is not contraindicated even if the patient is
unconscious after an associated head injury if he is hemodynamically stable.[40] If the
CT scan shows extravasation of contrast, angiographic embolization is recommended if
it is available.
Contraindications to nonoperative management include the following:
1. Hemodynamically unstable patient
2. Associated intra-abdominal injuries that require laparotomy
3. Extravasation of intravenous contrast when angiographic embolization is
not available or unsuccessful
4. AAST grade III, IV, or V hepatic laceration and large hemoperitoneum
In liver trauma, the first aim of surgical treatment is to stop the bleeding and then
to repair the damages.
The most preferred approach is the median laparotomy that can be extended in
any direction as needed for a better access. It is the fastest way to reach into the
peritoneal cavity and offers the best access over the whole cavity. In delayed emergency
or scheduled operations the right subcostal incision is preferred (extended to the left if
necessary or the so-called "Mercedes" incision) because it confers the best access to the
liver.
Surgical procedures depend very much on lesions type, but generally, hemostasis
is the first concern. One of the fastest ways to reduce liver bleeding is the compression
of the affected lobe between two hands. This maneuver will confer the time necessary
for intraoperative volume rebalancing and temporary hemodynamic stabilization and
provides conditions for achieving final hemostasis. However, it does not help when
large vessels such as hepatic, portal or cava veins are damaged. Another method of
temporary hemostasis is the compressive wound packing.
Clamping the hepatic pedicle (stops the hepatic inflow), also known as the Pringle
maneuver (in1908 J. Hogarth Pringle described first the maneuver), allows surgeons to
evaluate traumatic liver injury. Pringle maneuver can be performed with atraumatic
vascular clamp or with fingers. (Figure 5) 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
veins or cava vein, bleeding will not stop.
Continuous Pringle maneuver can be maintained up
to one hour in normothermia without major effects
on a normal liver.[46,47] Intermittent clamping
(clamping periods of 10 to 15 minutes are
separated by 5-minute periods of declamping) is a
useful maneuver for cumulative periods exceeding
120 minutes without major intraoperative blood
loss or complications.[48,49]
Total vascular exclusion of the liver (TVE) (Figure 6) means: clamping of the
inferior vena cava (IVC) above and below the liver always preceded by inflow
occlusion (the Pringle maneuver). The right adrenal vein must be ligated and divided.
The phrenic veins (usually three) draining into the IVC should be also clamped or
436
Abdominal Trauma
ligated. This will completely exclude the liver from
the splanchnic and systemic circulations. However,
this maneuver is associated with significant
decrease of volume return to the heart, which can
severely complicate the post-operative course.
A less drastic clamping procedure is
represented by the selective clamping of the hepatic
veins themselves, leaving the caval flow
undisturbed.
Lesions of the suprahepatic veins or vena
cava are usually lethal. In suprahepatic veins lesions
the inflow clamping is not sufficient because the
hepatic veins remain patent and bleeding may
continue. Air embolism may be significant with a
low central venous pressure. Making temporary
hemostasis in these cases is very difficult but can be
performed in several ways. The total vascular
exclusion of the liver (TVE) is one of the choices.
To maintain a sufficient venous flow to the heart an
atrio-caval shunt can be performed by introducing a
catheter with balloon through the atrium into the
vena cava in suprarenal position. (Figure 7) Another
solution is the use of the Moore-Plicher balloon. A
catheter is inserted through the femoral vein into the
vena cava and the balloon is inflated in the place of
venous lesion (suprahepatic veins or cava vein) to
achieve hemostasis.[50]
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.
The grade I and II represented by superficial lesions of the liver can be managed
by manual compression followed by hemostatic procedures such as electro-coagulation,
argon plasma coagulation or application of haemostatic sponges or sutures.
The grade III and IV of lesions may benefit from superficial hemostasis but most
often, other methods are needed such as:
Haemostatic suture of liver parenchyma for superficial wounds less than 3
cm deep
Hepatotomy with elective ligation of injured pedicles
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 hepatophrenic space to
achieve compression and hemostasis. The main risk is that of severe sepsis that may
follow. If hemostasis was achieved, after 24-48 hours gauzes have to be extracted. If
bleeding restarts after removing the gauze, the angioembolization could be a less
invasive method of hemostasis.
Biliary tract injuries are recognized by the presence of bile in the peritoneal
cavity.
437
Abdominal Trauma
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 may be
complicated by late stenosis. In case of linear lesions, without loss of substance,
suturing can be performed associated with Kehr type (T-tube) drainage. Major injuries
or complete section can be solved only by choledochojejunal anastomosis with a Rouxen-Y loop.
External biliary drainage is recommended in any important hepatic laceration
even without obvious biliary injury to prevent postoperative biliary leakage.
Overall mortality of patients with liver injury is around 10%-20%.[51-55] The
main cause of death is exsanguination. Frequent postoperative complications in liver
trauma surgery are postoperative bleeding (unrecognized injury or transfusion
coagulopathy), infection (most commonly in ischemic territories due to ligation, en
block suture or embolization [53]) and biliary leakage.
438
Abdominal Trauma
thoracic aorta lesions) because vascular lesions are frequently associated with other
internal organs lesions, which require laparotomy. Choosing an open surgical repair
versus an endovascular stent graft depends upon physician expertise, clinical status of
the patient and clinical setting.
Mortality in traumatic abdominal aorta injury ranges from 70 to 90%.[63-66]
Retroperitoneal Hematoma
Retroperitoneal hematoma represents the accumulation of blood into the
retroperitoneal space. Sources of bleeding are various, but in order of frequency, they
are:
Lesions of the retroperitoneal organs (kidney, pancreas)
Fractures of the pelvis or lumbar spine
Lesions of retroperitoneal vessels
Retroperitoneal hematoma due to renal trauma has a high lateral topography but it
can descend to the pelvic-subperitoneal space.
Bleeding from large vessels (aorta or cava) is associated with a very high
mortality rate.
In terms of size, retroperitoneal hematoma is considered:
Very large, when it extends from the upper pole of the kidney to the
Douglas
Large, when it does not exceed the lower renal pole
Medium and small, when is located only in the pelvis or around the
various organs (kidney, duodenum, pancreas, etc.)
By its presence, the 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 relies especially on imagistic findings but a careful clinical
examination may reveal some clinical signs suggestive for retroperitoneal hematoma
such as palpation of the hematoma mass, abdominal distension and muscular guarding
in lateral quadrants and dullness in the lower parts of the abdomen on percussion.
Imagistic investigations, which help the diagnosis, are:
Plain abdominal radiography which, may reveals bone lesions, signs of
paralytic ileus, and decrease of psoas shadow
Abdominal ultrasound, which reveals fluid collections and kidney lesions
CT scan with contrast is the most important investigation
Other investigations as needed: cystography, selective arteriography, etc.
A central venous catheter placed into the femoral vein is useful in
performing the cavagraphy but also for urography, harvesting blood for
laboratory investigations and for fluid rebalancing.
Evolution of post-traumatic retroperitoneal hematoma may be complicated in
many cases. Complications could be represented by:
The resorption syndrome is dominated by the development of variable
intensity jaundice resulting from blood resorption. The most important
439
Abdominal Trauma
aspect is however, the increasing of K+ ion levels very dangerous with
concomitant development of the acute renal insufficiency (source of
hyper-potassium levels).
Suppuration can progress to diffuse cellulites, with fatal outcome.
Favoring circumstances are the coexisting organ damages (rectum, colon,
etc.).
Lymphorrhagia and pancreatic fistula are other possible complications.
Retroperitoneal seroma develops due to incomplete resorption. It evolves
like a retroperitoneal compressive tumor that may rupture into the
peritoneal cavity.
Early rupture of hematoma into the peritoneal cavity explains the
presence of the concomitant hemoperitoneum without any lesions of
intraperitoneal organs.
Late rupture into the peritoneal cavity is also possible.
Retroperitoneal liposclerosis is represented by intense adhesions around
retroperitoneal anatomical structures.
Treatment may be surgical or conservative (observational or angioembolization).
In 1984, Sheldon [67] introduced a treatment principle founded on a locationbased classification of traumatic retroperitoneal hematoma as central-medial (zone I)
flank or perirenal (zone II) and pelvic (zone III). (Figure 8)
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 origin.
Relative indication for surgery is the hematoma
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.
The judgment of whether and when to
explore the retroperitoneal hematoma is guided
by the mechanism of injury (blunt or penetrating)
and the location of the hematoma. Usually
hematoma localized to the upper central area after penetrating trauma implies injury to
the great vessels and always requires urgent surgical exploration.[68-70] Exceptions
include isolated lateral perirenal hematomas that have been carefully staged by CT and
some lateral pericolonic hematomas.[68] Retrohepatic hematomas without obvious
active hemorrhage are not opened. For zone III of retroperitoneal hematoma, associated
with pelvic fracture the attitude is no exploration in blunt pelvic trauma and surgery for
penetrating trauma.
Some ongoing hemorrhage may respond to therapeutic embolization.[71]
440
Abdominal Trauma
Prognosis depends on the period of evolution as follows:
1. During the first 24-48 hours, the prognosis depends mainly on intensity of
the shock (traumatic, hemorrhagic) and the involvement of the celiac plexus
(vagal-sympathetic irritation).
2. 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.
3. The local complications period affects less the vital prognosis.
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444
Definitions
Hernia - represents the protrusion of an organ or a part of it, outward the
abdominal cavity (under the skin or into 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 parietal defect located in any region of the abdominal
wall, most often as a consequence of the destruction its integrity such as after abdominal
surgery.
Evisceration - represents the extrusion of an organ or 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.
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2. Hernias - Generalities
Internal hernia represents an exception from the definition of "hernia represents
the protrusion . outward the abdominal cavity", because it represents the penetration
(or intrusion) of the intestines through preformed or acquired holes or cavities, inside
the peritoneal cavity.[1,2] (Figure 6)
Examples of intra-abdominal preformed
holes or cavities that may cause internal hernias
are:
Through the foramen of Winslow - the
TREITZ hernia
Inside the small pouches formed by the
peritoneal
folds
(periduodenal,
periappendicular,
retrocecal
or
intersigmoidian) - the RIEUX hernia
Acquired internal hernias appear when
intestines engage through the unclosed holes of
the mesocolon or mesentery intentionally
performed during different kind of operations. For
example, the PETERSEN internal hernia appears
when intestine passes through the mesocolon
defect. That loop is at risk for incarceration and
strangulation with intestinal occlusion.
Etiopathogenesis.
Abdominal wall hernias occur due to an imbalance between the intra-abdominal
pressure (Figure 7) and the abdominal wall strength. From this point of view, hernias
can be classified as hernias of force (caused by
excessive intra-abdominal pressure) and hernias
of weakness (due to the impaired strength of the
abdominal wall). Factors that lead to high intraabdominal pressure acting against the abdominal
wall are:
Voluntary factors - physical effort
Involuntarily factors - obesity
Physiological factors - pregnancy
Pathological factors
o Intra-abdominal - ascites, tumors, etc.
o Extra-abdominal - trauma
Abdominal wall strength and structural
integrity depend on factors such as:
Constitutional (genetic) - congenital hernias
Nutritional - obesity, vitamin deficiencies, etc.
Educational - sports
Pathological - trauma, subnutrition, paralysis, etc.
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Depending on the position of the sac inside the hernial canal (the degree of
protrusion) hernias are: (Figure 16)
Hernial point - the sac protrudes
into the canal being located at the
internal ring
Interstitial hernia - the sac is
contained inside the canal
between the internal and external
openings
Complete hernia - the sac
protrudes under the skin. It has
exceeded the external ring
The content of the sac could be any intraabdominal organ except the pancreas,
which is a retroperitoneal organ well, anchored to the posterior wall. Depending on
which organ is contained inside the sac, hernia may be:
Enterocele - the sac contains intestines
Epiplocele - the sac contains greater omentum
Littre hernia - the sac contains the Meckel's diverticulum
Garengoff hernia - the sac contains the vermiform appendix
Littre hernia - the sac contains Meckel's diverticulum
Depending on evolution, hernias can be classified as:
Uncomplicated hernias (simple, reducible hernia)
Complicated hernias (irreducible, incarcerated, strangulated, etc.)
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On palpation, the bulge is of soft elastic consistency, painless, and can be reduced
by taxis into the abdominal cavity on a trajectory through a hole of the abdominal wall.
Asking the patient to cough, the examiner feels that the hernial sac pushes the fingers
that are still in the hernial canal. This is the impulsion sign of the hernia. After removing
the fingers, the hernial sac bulges again under the skin spontaneously or after coughing.
This is the expansion sign of the uncomplicated hernia.
On auscultation of the hernial zone, nothing or intestinal sounds can be heard.
Symptomatic hernias are hernias that represent a symptom of another disease,
usually more serious, which produces an increase of intra-abdominal pressure (cirrhosis
with ascites, intra-abdominal mass, tumors of the colon, prostate adenoma, chronic
cough, etc.) (Figure 18)
Coercible hernia is the hernia whose content remains inside the abdominal cavity
in standing position after reduction maneuvers.
Incoercible hernia is the hernia that immediately restores after taxis (usually
hernias with wide opening).
The positive diagnosis of an uncomplicated hernia is easy, based on history and
physical examination. Usually there is no need for other investigations. Clues for
diagnosis are:
A recurrent bulging tumor under the skin, which usually appears after physical
effort, and gradually increases in volume (especially during physical effort), but
reduces itself or disappears in supine position or by taxis,
The presence of a tumor in a region of low resistance of the abdominal wall,
which after digital reduction presents the signs of impulsion and expansion
during coughing effort
Differential diagnosis could be difficult sometimes, especially in complicated femoral,
perineal, obturator hernias and posterior hernias. Differential diagnosis should include
other tumors of the respective anatomical region. In difficult cases, complementary
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B. Complicated Hernias
The most frequent complications are represented by:
Incarceration - appears when intestinal loops (or other organs) are unable to
return into the abdominal cavity (are trapped inside the sac) due to a
compression at level of internal or external ring, but the blood supply of the
organs inside the sac is not particularly affected. However, a bowel obstruction
will develop (when intestines are interested) and eventually will lead, through
distension, to ischemic lesions (similarity to a jailed prisoner who has not yet
been sentenced to death by hanging).
Strangulation - appears when, besides the fact that the bowel (or other organ)
can not return into the abdominal cavity, the compression at level of
strangulation ring is so intense that it affects the vascularization and the
intestinal loop "dies" (similarity to a jailed one convicted to death by
strangulation - hanging).
Other complications are:
Hernias with adhesions
Voluminous hernias with loss of domain ("lost their right of domicile)
Tumors in the hernial sac
Peritonitis in the hernial sac
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The Hesselbachs triangle is an important area of weakness as it is the site for direct
hernias. The triangle has the following borders: (Figure 30)
Medial - the border of rectus abdominis muscle
457
The spermatic cord begins at the deep inguinal ring located lateral to the
epigastric vessels, then passes into the inguinal canal and exits at the superficial inguinal
ring and finally ends in the scrotum at testis. 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: (Figure 31)
Ductus deferens (and its artery)
Testicular artery
Cremasteric artery
Panpiniform plexus
Genital branch of the genitofemoral nerve
Sympathetic nerve fibers
Lymphatic vessels
The fibrous vestige of the processus vaginalis
Classification
Depending on the degree of progression of the sac through the inguinal canal,
inguinal hernias can be classified as: (Figure 32)
1. Hernial point
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Interstitial hernia
Inguino-pubian (bubonocele)
Inguino-funicular
Inguino-scrotal (labial)
Looking from inside the abdominal cavity to the hypogastric region, three folds of
peritoneum can be noticed: one median determined by the urachus, two medial
produced by umbilical arteries, and two laterals produced by inferior epigastric vessels.
These three folds delimit between them three fossae: lateral, medial, and supravesical,
which are sites of weakness favorable for development of three types of inguinal
hernias, respectively external oblique, direct and internal oblique hernias. (Figure 33)
Indirect (congenital) hernia is the most common type of inguinal hernias. The hernial
sac is outpunching lateral to the inferior epigastric vessels. Abdominal content enters
the deep inguinal ring via the hernial sac, a congenital abnormality, represented by the
persistent processus vaginalis. The sac is elongated, pear shaped. The hernia then passes
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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.
461
Type 2 hernias (the most common indirect hernia) have a peritoneal sac coming through a 1fingerbreadth 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 Hyhuss based on transabdominal aspect,
classified hernias as:
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
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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. (Figure 38) 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 veins is ensured by small one-way
valves that prevent backflow. Defective valves, or compression of the vein by a nearby
structure, can cause stasis and reflux with dilatation of the veins near the testis, leading
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The Prolene Hernia System (PSH) (1997) is an innovation that uses a special type
of mesh with a shape of "H" letter, a mesh composed of two layers connected between
them by cylinder mesh. One layer is introduced through the internal ring into the
preperitoneal space and the other, resting on the transversalis fascia, is fixed to the
conjoint tendon and inguinal ligament. In this way a double curtain reinforcement is
performed. The connecting component of the two layers clogs the internal inguinal ring
preventing thus the relapse of oblique hernias. (Figure 52)
ProGrip Mesh is a self-fixating mesh, which has small, absorbable grips on one
side to secure to the abdominal wall tissues eliminating the need to suture the mesh into
place. It is used with Lichtensteins technique. (Figure 53)
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In recent decades new minimally invasive approaches for hernia repair have been
developed. The main benefit is the faster recovery of the patient. However, there are
still controversies over the cost-efficiency in laparoscopic approach. Laparoscopy 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.[15]
2. Plug and patch repair
3. Intraperitoneal onlay mesh repair (uses a silicone mesh)
4. Transabdominal preperitoneal mesh repair (TAPP)
5. Total extraperitoneal repair (TEP)
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, and
prior groin irradiation.
Laparoscopic total extraperitoneal approach
(TEP) was first described by Arregui in 1991. The
principle is the same as in Stoppas 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. (Figure
54) An inflatable balloon is used to dissect the
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B. Femoral Hernia
Femoral hernias occur just below the inguinal ligament, through a naturally
weakness called the femoral canal. (Figure 56) 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 and a more horizontalized position of the female pelvis.
Anatomy (Figure 57)
The femoral canal is a short (2 cm) conical
shape canal bordered:
superiorly by the inguinal
ligament
inferiorly by the pectineal
ligament lying anterior to the
superior pubic ramus
medially by the lacunar
ligament of Gimbernat
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Ectasia of the saphena magna vein arch - produces a bulge in the groin,
which can be reduced on a perpendicular direction, presenting also the sign
of cough expansion. On palpation, during cough effort a thrill can be felt,
caused by the blood reflux from the femoral vein into the dilated saphenous
vein. Eco-Doppler highlights the ectatic vein and the reflux.[4]
Lipomas - are benign tumors of the fatty tissue, which have a soft
consistency but are not reducible nor present coughing expansion sign.
Inguino-femoral lymphadenopathy - are inflammatory or tumoral enlarged
lymph nodes in the groin region. They are not reducible, nor present
coughing expansions sign. Ultrasound examination highlights the lymph
nodes.
Differential diagnosis of incarcerated femoral hernia (painful bulge and local
inflammatory signs) includes lymphadenitis of the Cloquet lymph node and phlebitis of
the greater saphenous vein arch.
Anatomoclinical types of femoral hernias: (Figure 59)
1. Laugier hernia - through the Gimbernarts
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 or Hesselbach hernia - through the
lacuna muscularis (psoas muscle)
Treatment
Goals are the same as in inguinal hernia repair:
finding and dissecting the sac, treating the content,
resecting the sac and reinforcement of the region to
prevent relapse. There are two possible approaches:
classical by open surgery and laparoscopic. Incisions in
open surgery are (depending on surgical technique):
(Figure 60)
Femoral - for a minimal invasive procedure
Extended femoral - for double curtain
procedure
Inguinal - for Ruggi Parlavecchio procedure
Laparotomy - the Lawson Tait procedure,
when laparotomy is recommended for other
intra-abdominal pathology
Procedures (most of them just of historical interest):
1. By femoral approach (Figure 61)
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
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3. 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 Henles ligament and inguinal ligament to the
Coopers ligament. (Figure 63) RUGGI - PARLAVECHIO is the procedure
most often used but there are also other procedures (CODIVILA, ROBINEAU,
etc.).
4. Plastic procedures
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, etc)
Procedures that use meshes
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C. Umbilical Hernia
The umbilicus represents another weak zone of the anterior abdominal wall. At
the umbilicus, the peritoneum makes a condensed fold, the so called Richets fascia,
which determines two types of umbilical hernia direct hernia (in the absence of
Richets fascia) and indirect umbilical hernia (oblique inferior or superior). (Figure 64)
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D. Epigastric Hernia
Epigastric hernias represent 0.5-5 % of all operated abdominal hernias and are 2-3
times more common in men, with a higher incidence in patients from 20 to 50 years.[20]
This type of hernia appears on the midline of the epigastric region through the
fibers of the linea alba. The first to protrude is the properitoneal fatty tissue, the socalled prehernial lipoma, which produces a cone of the peritoneum, which will become
the future hernial sac.
Usually hernias are of small dimensions, 1-2 cm in diameter, and difficult to
diagnose in obese patients. On palpation, a small, painful bulge can be felt under the
skin of the epigastric region. There are two clinical forms: a painful form and an
asymptomatic form. Frequently epigastric hernias are associated with other pathology of
the supramesocolic organs (peptic ulcer, gastric cancer, gall stones, etc.). This is the
reason why pre- and intraoperative 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.
E. Spigelian Hernia
Spigelian hernia appears under the aponeurosis layer between the rectus
abdominis muscle medially, and the semilunar line laterally, at or below the linea
arcuata site.
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 consists in abdominal wall repair through a classical open approach
or by laparoscopic approach. In open approach, the incision is placed on the hernial
area. The muscular layer is dissected and the sac is found and reduced into the
abdominal cavity or resected. Then, the posterior rectal sheath is reinforced and the
other layers re-approximated. Using a mesh is another possible way to reinforce the
abdominal wall. By laparoscopic approach, the parietal defect is covered by a siliconecoated mesh kept in place using tacks and threads. The procedure is similar to that
applied in umbilical hernia. Laparoscopic approach ensures a very fast recovery of the
patient who in most cases is discharged in the next day after the operation. (Figure 70)
F. Obturator Hernia
The obturator canal contains the obturator nerve and vessels. It has rigid walls,
which explains why hernias through this canal incarcerate so frequently.
Incarceration or strangulation is manifested by intestinal occlusion signs and
symptoms so that usually the patient is operated in emergency by open approach
(laparotomy) and the hernia is an intraoperative finding.
The Rombergs sign observed in this type of hernia is caused by the compression
of the obturator nerve exerted by the hernial sac. The thigh is flexed in abduction with
external rotation of the knee (antalgic position). The patient feels the pain in a region
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4. Incisional Hernias
Incisional hernia represents a special type of hernia, which appears after invasive
surgical procedures (incisions) that involve and destroy the integrity of the abdominal
wall. Compared to common hernias, incisional hernias represent the total or partial
protrusion of abdominal viscera, under the skin, through a defect in the abdominal
wall. - (until here the definition is almost the same as in common hernia.) but
.the integrity of the anatomical structure of the abdominal wall is being affected (in
most cases by surgery). Another difference is that incisional hernias may appear in any
zones of the abdominal wall not just in hernial zones as in case of common hernias
(where the abdominal wall is naturally weaker).
They are called incisional because appear most often after surgeries that require
laparotomy. However, the term of "incisional" hernia does not include the full spectrum
of pathology to which it relates. A better term is evntration, which besides hernia,
caused by surgical incisions, includes as well those produced by trauma (aggressions,
accidents, etc) and also the abdominal wall relaxation.
Classification
Traumatic hernias are those caused by abdominal wall trauma. In this case,
there is a breach in the abdominal wall through which the hernial sac is
protruding under the skin. The hernial sac is present and incarceration is
whenever possible. (Figure 71)
Postoperative - these are the true incisional hernias
Non surgical - accidentally, as a consequence of a blunt or penetrating
trauma of the abdomen
Non-traumatic hernias are actually relaxations of the abdominal wall
produced by various factors. There is no true hernial sac and no breach in the
abdominal wall. The wall is weakened, relaxed, and thus bulges in the
affected region. These types of hernias never lead to incarceration.
Various deficiencies (protein, vitamins, etc.) and other pathologies that
affect the abdominal muscles or their innervation.
Obstetrical hernias, the so-called diastasis of the rectus abdominis
muscles represent a weakening of the fascial membrane (linea alba)
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5. Eviscerations
Evisceration represents the extrusion of the viscera outside the peritoneal cavity,
in direct contact with atmosphere, through a solution of continuity in the abdominal
wall. There is no sac like in hernia and the skin is opened.
Causes that might produce evisceration are: (Figure 75)
1. Postoperative disruption (dehiscence) of the wound
2. Posttraumatic, in case of penetrating wounds (accidental or by aggression)
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6. Diaphragmatic Hernias
The diaphragm is a fibro-muscular structure that separates the thoracic cavity
from the abdomen. Between the two cavities, thoracic and abdominal, there is a gradient
of pressure. The higher pressure in the abdominal cavity will determine the migration of
abdominal viscera into the thoracic cavity through a defect of the diaphragm.
The diaphragm develops from three anatomical structures, which merge to form
the diaphragm: the septum transversarium (for the fibrous part of the diaphragm), and
two Ustkovs folds (for the muscular part of the diaphragm). (Figure 76) Deficiencies of
diaphragm development, will lead to congenital diaphragmatic hernias.
Weak zones of the diaphragm are all diaphragmatic holes through which diverse
anatomical structures are passing from, or towards the abdominal or thoracic cavity
(aortic hiatus, esophageal hiatus, inferior cava vein, ductus thoracicus, splanchnic
nerves, azygos veins, etc.). (Figure 77)
Diaphragmatic hernia is a defect or hole in the diaphragm that allows the
abdominal contents to move into the chest cavity.
maldevelopment
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Congenital hernias
The most frequent congenital
diaphragmatic defects through which
abdominal viscera herniate into the
thoracic cavity are: the MorgagniLarreys orifice and the Bochdaleks
costo-vertebral foramen.
Large congenital hernias are
manifested shortly after birth.
Clinical picture is represented by
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 is the most common diaphragmatic hernia in children with a
frequency of about one of every 2,500 live births. About 85% of Bochdalek
hernias occur on the left side, about 10% on the right, and approximately 5% are
bilateral.[35] It is twice as common in male as in female neonates. Mortality
ranges from 45% to 50%. [36,37]
There is a classic triad is represented by:[38] (Figure 78)
1. respiratory distress - the principal symptom
2. apparent dextrocardia, and
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.[39] 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 (Morgagni-Larrey) hernia is the maldevelopment of the septum
transversum, which failed to merge to the sternal and costal elements. It
comprises approximately 2% of all congenital diaphragmatic hernias and is
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Hiatal Hernia
Hiatal hernia represents the protrusion of the superior portion of the stomach into
the thoracic cavity through the esophageal hiatus.
Normally, the cardia and the stomach are located within the abdominal cavity
being maintained in this position by various anatomical structures and physiological
processes. Between the esophagus and the
diaphragm, there is interposed connective tissue
(the membrane of Leimer-Bertelli Treitz) and
muscle fibers that are drawn from the diaphragm
and dissolve into the esophageal wall (Rougets
muscle). (Figure 79) The visceral peritoneum and
the phrenoesophageal membrane cover the
abdominal esophagus. The phrenoesophageal
ligament is a fibrous layer of connective tissue
bridging the space between the esophageal wall
and the margins of the esophageal hiatus. The
ligament plays an important role in anchoring the
lower esophagus and maintaining gastroesophageal competence.[40] The cardia and part
of the gastric fundus is ancored by various ligaments and membranes to the
retroperitoneal plane, which provide adequate stability to the esophagogastric junction.
The size of the hiatus narrows whenever intra-abdominal pressure rises.[41]
With advancing in age, collagen fibers replace elastic fibers loosing thus elasticity
and loosening attachments. Large accumulation of adipose tissue between the
phrenoesophageal membrane and the cardia may
cause the loose of anchorage of the cardia. All
these factors associated with an enlarged hiatus
and high intra-abdominal pressure (obesity,
pregnancy, physical efforts) are contributing
factors in developing hiatal hernia.
The gastroesophageal junction acts as a
barrier to prevent reflux of the stomach content
into the esophagus and the consequent
esophagitis (GERD gastro esophageal reflux
disease). Components of this barrier are the diaphragmatic crura, the lower esophageal
sphincter, and the angle of Hiss. (Figure 80) The consequence of intrathoracic
protrusion of the cardia and/or the stomach is the loss of antireflux mechanisms.
Types of hiatal hernia (Figure 81)
1. Short esophagus (brachyesophagus) - the esophagus is shortened, and 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 inside the thorax.
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CT scan with oral contrast offers detailed information about the position of the
cardia and the stomach and about the size of hernia. (Figure 82)
Esophagogastroscopy has the advantage that it directly visualizes the esophageal
mucosa highlighting the esophagitis and can take biopsies. (Figure 83)
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:
Lifestyle changes
Antacid medications
Stimulation of gastric motility and evacuation
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).[47] Surgery is
recommended especially for paraesophageal hernias. Goals of treatment are:
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7. Diaphragmatic Ruptures
The diaphragm is a musculo-membranous structure, relatively thin, which
represents the upper wall (ceiling) of the abdominal cavity. It separates two cavities
with different pressures: the thoracic cavity with low pressure and the abdominal cavity
with high pressure. The movement of diaphragm by contraction and relaxation changes
the pressure inside those two cavities having the main role in ventilation (inspiration
and expiration). Diaphragmatic rupture, according to the extent and localization leads to
two important consequences:
1. Protrusion of the abdominal organs into the thorax, and
2. Impairment of the ventilatory function
The mechanisms by which the diaphragm may
break are: (Figure 88)
Closed trauma or blunt abdominal trauma,
produces a sudden increase of the intraabdominal
pressure
leading
to
diaphragmatic rupture
Open or penetrating trauma represented by
wounds (stab, gunshot, etc.), which can be:
o Transabdominal wounds or/and
o Transthoracic wounds
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7. Diaphragmatic Relaxations
The phrenic nerves, which are the only motor
supply to the diaphragm, arises from C3,4,5 roots. It lies
on the scalenus anterior muscle and enters the thorax.
The right phrenic nerve passes through the diaphragm
close to the inferior vena cava in the central tendon. The
left phrenic passes through the muscular part of the
diaphragm. (Figure 90)
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. (Figure 91)
491
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Takeyama N, Gokan T, Ohgiya Y, Satoh S, Hashizume T, Hataya K, Kushiro H, Nakanishi M, Kusano M, Munechika H.
- CT of internal hernias. - Radiographics 2005; 25:997-1015.
3.
Dabbas N, Adams K, Pearson K, Royle GT. - Frequency of abdominal wall hernias: is classical teaching out of date? JRSM Short Rep. 2011; 2(1): 5.
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10. Gilbert AI, Graham MF, Voigt WJ. - Inguinal Hernia: Anatomy and Management Classification of Groin Hernias. Medscape General Surgery - http://www.medscape.org/viewarticle/420354_4
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Tuberculosis
Diagnosis
&
Management
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493
494
496
Lymphatic drainage of the thyroid gland. (Figure 6) Lymphatics are arranged in two
networks: one around the thyroid follicles and the other subcapsular. Most of lymphatic
vessels have an upward trajectory draining towards the deep jugular lymph nodes
groups. Other lymphatic vessels drain the lymph downward, towards pretracheal and
mediastinal groups. Other lymph nodes groups are: perilaryngeal, deep lateral, and
submandibular. Lymphatic vessels may cross the midline draining into the contralateral
lymph nodes. These lymphatic groups should be known and removed by surgeons
during operations of neck dissection.
Innervation. The thyroid gland receives autonomic sympathetic fibers from the cervical
sympathetic chain, and parasympathetic fibers from the vagus nerves.
Histology. The histological structure of the gland is composed of many small globular
sacs called follicles. Follicles are lined by follicular cells and are filled with a fluid
known as colloid that contains a gelatinous substance consisting of proteins, mainly the
prohormone thyroglobulin and other iodoproteins and serum albumin. Between
follicles, there are fibroblasts, endothelial cells and C cells or parafollicular cells derived
from the neural crest. They secrete calcitonin.
Physiology. The thyroid is an endocrine gland that secretes several hormones of which
the most important are thyroxine (T4), triiodothyronine (T3) and calcitonin.
Calcitonin is secreted by C cells in response to the increase in calcium levels,
decreasing the bone resorption.
The thyroid gland has the ability to uptake iodine supplied by food and using it in
the synthesis of thyroid hormones. The thyroid cells, under the action of the TSH
(thyroid - stimulating hormone) and PRL (prolactin) hormones assimilate the inorganic
blood iodine. Iodine is mostly concentrated in thyroid gland. The thyroid iodine
concentration is 30-50 times higher than in blood.[2,3] The follicular cells, using some
enzymes, synthesize the thyroglobulin, which is stored in colloid. When thyroid
hormones are needed, thyroglobulin is reabsorbed from the colloid into the cells, where
it is split into its component parts, including the two thyroid hormones thyroxine (T4)
497
498
499
Thin needles, generally of 25-gauge, are used for FNAB (Cyba, Westcott,
Franseen, etc.). (Figure 10) The procedure can be performed without anesthesia or
under local anesthesia and under ultrasound guidance. (Figure 11) Fluid and cells, not
tissue samples, are extracted by this method. Usually a syringe is attached to the needle.
To extract cells from the thyroid nodule, active aspiration is applied, although there are
methods that are not using a syringe and nor aspiration. More types of vacuum devices
exist on the market but the principle is the same: creating a negative pressure into the
syringe. Six to ten smears are prepared from each nodule (harvested fluid is thinly
distributed across the slide) and then examined microscopically (cytology).
500
501
502
503
505
506
507
B. Acute thyroiditis
Thyroid gland infection occurs via blood or by direct seeding from upper
respiratory infections. Patient complains of sudden onset pain, fever and swelling of the
anterior region of the neck. Gross appearance is that of a normal or slightly enlarged
painful thyroid gland with Celsian signs, and suppurative areas may be present.
Treatment consists in antibiotherapy, and in case of abscess formation incision
and drainage.
508
5. Hyperthyroidism
Hyperthyroidism represents the over activity of the thyroid gland which produces
excessive thyroid hormones and accelerates metabolism in the peripheral tissues.
Clinical picture
The clinical picture depends on the stage of the disease. There are described four
stages:
1. Neurogenic with nonspecific symptoms
2. Neurohormonal with all specific symptoms due to increased thyroid
hormone secretion
3. Visceral stage - with complications especially cardio-vascular
4. Cachectic stage
GRAVES' DISEASE, which is the most common form or cause of hyperthyroidism, is
an autoimmune disorder with thyrotoxicosis. Out of all patients, 85% are women,
usually aged between 20-40 years.
Classical clinical presentation was described by Graves Basedow and
characterized by the triad:
1. Goiter
2. Exophthalmos
3. Tachycardia
The condition starts with neuro-psychological symptoms manifested by emotional
lability, irritability, psychomotor instability, hyperactivity, agitation, loss of memory.
Cardiovascular symptoms and signs are the most important being early and
constant, manifested by palpitations, tachycardia, arrhythmias, heart failure, and toxic
myocarditis. Tachycardia usually exceeds 100 beats/min and is persistent during sleep
and worse at efforts. On auscultation, functional systolic murmur can be heard. Systolic
pressure increases and diastolic pressure decreases.
Thyroid hypertrophy is almost constant. The gland consistency is elastic, the
surface is smooth and on auscultation, thyroid thrills and bruits could be heard. In
thyroid toxic adenoma (TTA) a hypersecretory solitary nodule is found.
Changes of skin and appendages are also present manifested by pink, warm,
moist, smooth skin with increased sweating. Other signs are: perithyroidian red spots
(Maranon sign), presternal red spots (spots of "shame"), pretibial myxedema. Diffuse
pigmentation disorders may appear such as: melasma (also known as "Chloasma
faciei), vitiligo, alopecy, white hairpiece (Sabouraud sign), axillary hair loss (Williams
sign). The nails are brittle with longitudinal and transverse striations.
Due to the increased metabolism, the patient presents weight loss despite of
increased appetite. Bowel movements are accelerated.
The patient also presents termophobia (heat intolerance) and increased tolerance
to cold.
509
510
6. Thyroid Cancer
Epidemiology. Thyroid cancer is the most common endocrine malignancy, accounting
for 1 % of all new malignant tumors.[61,62] In the last decades, thyroid cancer incidence
has continuously and sharply increased all over the world.[63,64] The increase mainly
regards papillary cells type tumors. It is estimated that 60,220 men and women (14,910
men and 45,310 women) will be diagnosed with, and 1,850 men and women will die of
cancer of the thyroid in 2013.[65] In 2008 there were an estimated 33,600 new cases of
thyroid cancer diagnosed in the European Union (EU-27). The highest incidence rate
was estimated to be in France, where the female rate was five times higher than the rate
of the lowest ranking country, Greece (18.6 versus 3.3 per 100,000 females).[66]
Female/male ratio is about 3:1. In about 80-90% of cases, cancer appears on a
preexisting nodular goiter. The disease is most frequent at ages between 30 and 60.
Etiology. Causing factors are not known but radiation exposure significantly increases
the risk of developing thyroid malignancies, particularly papillary thyroid carcinoma
(after the nuclear accident at Cernobil the incidence raised significantly).[63,67] Medical
radiation exposure of the thyroid at a young age is a recognized risk factor for the
development of differentiated thyroid cancer lasting for four decades and probably for a
lifetime after exposure.[68] Hashimotos chronic thyroiditis is considered a preneoplastic
condition.
Classification. From histological point of view, thyroid cancers are classified as
follows:[69,70]
Papillary carcinoma the most frequent encountered (60-86%), derived
from follicular cells
Follicular carcinoma (9-15%) - also derived from follicular cells
Anaplastic carcinoma (1-5%)- the most aggressive form
Medullary carcinoma (2-8%) derived from neuro-endocrine calcitonin
producing cells (C cells)
Lymphoma - derived from intra-thyroid lymphoid tissue
Sarcoma - derived from connective tissue
Histological type is an important determinant of prognosis in thyroid cancer.
TNM staging [71-74]
Primary tumor (T)
TX Primary tumor cannot be assessed
T0 No evidence of primary tumor is found
512
513
Preclinical clandestine life of the tumor may last more than 20 (5-35) years [75]
and without any treatment, the clinical evolution may last 12-18 months. About 10-15%
[76] (in some series 50-90%) [77,78,82] of patients with papillary and follicular cancers,
present with lymph node or lung metastases at diagnosis. Anaplastic cancer has a rapid
course and early dissemination.
Symptoms are few and unspecific. The patient observes an accelerated growth in
volume of the gland with appearance and accentuation of compressive symptoms
(dysphonia, hoarseness, dysphagia, etc.).
On physical examination, nothing special can be noticed or, the patients or
physicians, on routine palpation of the neck discover a painless, palpable, solitary
thyroid nodule. Other pathological findings may include:
Increased consistency of the gland
Palpable cervical lymph nodes
Palpable metastases
Penetrating in the surrounding tissue
Skin ulceration in very advanced cases (Figure 20)
Signs of compression on anatomical structures (eg. Claude Bernard H.
syndrome)
Investigations
Imaging:
Ultrasound - cannot distinguish benign from malignant nodules
CT and MRI scans - evaluate soft-tissue and extension of large or
suspicious thyroid masses
Radioiodine imaging - can determine the functional status of a nodule but
carcinoma cannot be excluded based on radioiodine scans.
Laboratory:
Elevated serum calcitonin is highly suggestive of medullary thyroid
carcinoma
514
515
10-year
survival
5-year survival
Stage I
100%
100%
100%
(always stage
IV)
Stage II
100%
100%
98%
Stage III
93%
71%
81%
Stage IV
51%
50%
28%
Overall
96% - 97%
91%
80% - 86%
Overall
93%
85%
75%
7%
7% - 14%
(no data)
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Roeher HD, Wahl R, Goretzki P, Branscheid D. - Surgery for hyperthyroidism: indications, pretreatment, operative
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Breast Pathology
BREAST PATHOLOGY
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and latissimus dorsi muscle. (Figure 3)
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 lymphadenopathy, 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 pectoral fascia by fibrous strips
called Coopers ligaments.
External appearance. Breasts look like 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 areolas 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.
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.
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. Upper outer (superolateral or superoexternal - SE) - over 50% of breast
cancers are located in this quadrant.
2. Lower outer (inferolateral or inferoexternal - IE)
3. Upper inner (superomedial or superointernal - SI)
4. Lower inner (inferomedial or inferointernal - II)
Two more quadrants are added: one central (C) corresponding to retroareolar area
and another, which is the axillary extension quadrant (AE) of the gland.
The structure of the breast
The breast is composed of four types of tissues:
1. Milk-producing mammary gland,
2. Milk ducts,
3. Fatty tissue, and
4. Connective and fibrous tissue, blood vessels, lymphatics and nerves
The gland is compartmentalized in 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 (Coopers ligaments), which on palpation give the feeling of a granular surface.
Do not confuse these fatty lodges with tumors.
522
Breast Pathology
The gland itself is fixed to the internal surface of the derma 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 represents a clinical sign for
cancer.
The retromammary layer is a fatty space by which the mammary gland can slide
over the surface of the pectoral major fascia. Invasion by cancer of this layer and
penetration into the pectoral muscle, leads to fixation of the gland to the underlying
muscular plane. Fixation can be highlighted by the Tillaux maneuver.
In very rare cases, the glandular tissue may cross through the retromammary fatty
layer penetrating into the pectoral muscle. This was the reason why Halsted radical
mastectomy removed the pectoral muscles along 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 septa 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 separately at the surface of the nipple. 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. The lining of the ducts is
composed of a double layer epithelium formed by cuboidal cells at the level of lobules
and cylindrical shape cells in the extra-lobular space. In the external layer,
myoepithelial cells are present. 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. The breast fibrocystic disease has also the starting point in these
ducts.
Vascularization and innervation
Breasts have a good arterial supply from many sources represented by:
Internal mammary artery (emerging from subclavian artery)
Lateral thoracic artery ( emerging from axillary artery)
Intercostal artery branches (from thoracic aorta)
Other sources such as: thoracica suprema artery, arteries for pectoral
muscles, thoracoacromial artery, subscapular artery, thoracodorsal artery
and superficial thoracic artery.
The venous drainage of the breast is organized into two networks: one superficial
and another one deep. The superficial network forms around the areola a venous plexus
called the Hallers 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.
Brachial cutaneous nerve and branches from the intercostal nerves 4, 5, 6, provide
breast skin innervation. 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 because the
tumoral spread 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 networks, there are two areas of
connection, one at the areola, where there is a superficial lymphatic plexus and one
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Breast Pathology
retroareolar (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:
1. External mammary route (axillary route) - it drains the lymph to the
ipsilateral axillary lymph nodes and 75%-97% of cancerous cells are
carried through this route. On the trajectory of the route there is a lymph
node (called Sorgius) located at the edge of the greater pectoral muscle.
2. 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.
The next lymph nodes stations are:
Supraclavicular lymph nodes
Cervical lymph nodes
On the left side toward the thoracic duct and left lymphatic duct
On the right side toward the right lymphatic duct
The Pirogoff jugulo-subclavian confluence
The mediastinal lymph nodes and broncho-aortic nodes
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 Rotters 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 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 cancer to reach the lymph nodes from contralateral axilla
5. Inferior route - described by Gerota (Romanian physician and anatomist),
which drains the lymph towards the epigastric region and diaphragmatic
nodules
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 four walls. The
content of the axilla is represented by:
Arteries:
o Axillary artery,
o Lateral thoracic artery,
o Subscapular artery,
o Thoracodorsal artery
Nerves:
o Brachial plexus,
o Intercostobrachial nerve,
o Thoracicus longus (Charles Bell - respiratory) nerve,
o Subscapular nerve,
o Thoracodorsal nerve,
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Breast Pathology
o Intercostal nerves
Fatty tissue
Lymph nodes
Anglo-American surgeons use Bergs axillary lymph nodes classification that
divides lymph nodes into three main levels based on prognosis importance and their
relations with the pectoralis minor muscle:
1. Level 1 - are lymph nodes located under the lateral edge of the pectoralis
minor (lateral posterior and anterior)
2. Level 2 - are lymph nodes lying underneath the muscle between the
medial and lateral edge
3. Level 3 - lymph nodes located medial or above the medial edge of the
muscle (apical, subclavian)
In fact, this classification is also used in the TNM system for malignant breast
tumors. To this group, called regional lymph nodes (N), in the TNM classification is
also added 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.
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Breast Pathology
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 in volume of the breast. This aspect is often observed in
phyllodes tumors.
The shape of the breast. As long the tumor is small enough no changes in
breast shape will be noticed. As it grows, alteration of breast shape will
appear as irregular elevations (bulges) or as depressions (skin retraction).
The aspect of the skin. The color can be normal. In some advanced cases
and in acute inflammatory breast cancer, the color turns to reddish as in an
inflammatory process making possible confusions with acute mastitis.
Skin surface may look as an orange peel (peau dorange) very suggestive
for breast cancer. It is caused by lymphatic stasis in the derma as the
lymph ducts are blocked by the tumoral process. Ulceration of the skin
appears in advanced cases. Venous network becomes visible being
augmented in advanced cases, and in phyllodes tumors. Nodules of
permeation appear also in advanced neglected cases.
The aspect of the areola. Tumoral processes like Pagets disease may
affect the areola. The aspect is similar to eczema.
The aspect of the nipple. Very suggestive for cancer is the unilateral
recently installed retraction of the nipple.
Pathological discharge from the nipple. Discharge could be serous,
brownish, lactescent, purulent, and hemorrhagic. The most suggestive for
cancer is the unilateral spontaneous hemorrhagic discharge, which appears
especially in case of intraductal papilloma.
Then, the patient rises up her arms 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 other modifications become more visible.
The patient bent forward with hands on hips. In this position breasts are hanging
and pathological changes can be observed in the breast bearing a malignant process. The
breast hangs less if the tumor is fixed to the pectoral muscles or chest wall.
Breast palpation. There are some rules to be considered during palpation:
The optimal period for breast palpation is between the fifth and the
seventh day after the onset of menstruation
Always start with the breast considered normal
Palpation is performed with the palmar surface of outstretched fingers 2-5
Palpation must be gentle
Palpation must explore the entire breast area
Both axillae and cervical lymph nodes should be palpated
There are four stages of palpation:
1. Gross palpation described by Velpeau. The clinician is trying to detect
any abnormal changes in the breast thickness. It is only an indicatively
palpation.
2. Palpation of finesse follows a certain scheme (circular - concentric, spiral,
or radial) not to omit any breast areas. No matter which method is chosen,
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Breast Pathology
the breast tissue should be compressed against the chest wall and all
quadrants should be explored.
3. Palpation of the tumor to determine the following features:
Number of tumors
Precise location (most tumors are located in the SE quadrant)
Dimensions of the tumor - 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.
Form of the tumor can be spherical or irregular
Consistency - generally, breast cancer is of hard consistency
Sensitivity - malignant tumor is not painful on palpation, at least in
the early stages and if there is no inflammatory process associated
Tumor surface is irregular in cancer but smooth in fibroadenoma
Tumor delimitation - cancer is poorly demarcated from the
surrounding tissues
Tumor mobility - breast cancer in first stages is mobile, without
having the mobility of a breast fibroadenoma. As it develops, it
becomes more and more fixed because of tissue invasion.
4. 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.
Assessing the tumoral penetration. Adherence to the skin can be appreciated by
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.
Penetration in the pectoral muscles can be explored by the Tillaux maneuver. The
doctor opposes to the adduction movement of the patients arm (the pectorals 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 lymph nodes. The following lymph nodes stations should be
examined in every case:
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
4. Malformations
Classification
Malformations can be classified as congenital and acquired. Another
classification considers the abnormalities of number, volume and shape of the breast.
527
Breast Pathology
A. Abnormalities of number
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
considered complete if both the areola and the nipple are absent.
Athelia - is represented by the absence of the nipple associated or not with the absence
of the areola. It may occur in a normal located breast but are more frequent in
supernumerary breast.
B. Abnormalities of volume
Anisomastia - is caused by the uneven development of breasts and their asymmetrical
location. If the aesthetic defect is important, it can be corrected by various operations of
mammoplasty.
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Breast Pathology
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.
C. Abnormalities of shape
Inverted nipple - 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: flattening, umbilication and
invagination. Han and Hong (in 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.
Breastfeeding is not contraindicated in inverted nipple, but it can pose 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:
most often, a neoplastic process, especially if the retraction is
circumferential
an inflammatory process underlying the nipple
a duct ectasia associated with periductal fibrosis
Breast ptosis
Because the only supports of breasts are the skin and the suspensory ligaments of
Cooper, they tend to descend over time due to their own weight. Ptosis is mainly caused
by the weakening of supportive fibrous breast elements (Coopers ligaments) as a result
of deficiencies in the structure of collagen and elastic tissue, or idiopathic (frequently is
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Breast Pathology
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 represented only by surgery 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 only the skin in mild forms, but in
forms with hypertrophy, a glandular reduction is also necessary.
530
Breast Pathology
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 fluctuance. In untreated forms, infection may extend to
the entire breast (panmastitis) with spontaneously fistulization to the skin.
Breast abscesses are localized breast suppurations probably related to obstruction
of lactiferous ducts. They can be located:
Subcutaneous
Retroareolar - the most frequent
Interlobular (periductal inflammation),
Retromammary
Central (simple or multiple)
Diagnosis is generally simple based on history (pregnancy or breast-feeding),
symptoms and signs (pain, redness, local swelling, and hyperthermia). Drained fluid
from the nipple after compression leaves a yellow stain (Budin sign). Axillary
inflammatory adenopathy is also present. Ultrasound investigation of the breast
highlights the presence of the abscess and may guide surgery.
Acute mastitis should be differentiated from other diseases with similar
symptoms such as:
Paramastitis
Breast engorgement (due to expansion and pressure exerted by the
synthesis and storage of breast milk)
Breast sarcoma
Inflammatory breast cancer
Treatment
The prophylaxis is represented by the compliance with local hygiene measures
and complete emptying of breast milk at each feeding.
Curative treatment differs depending on evolution stage of the mastitis. In
congestive phase, broad-spectrum antibiotics are used with favorable evolution in 96%
of cases. Additional measures are represented by:
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 (abscess formation), surgery is the main treatment associated with
antibiotherapy. General anesthesia is usually preferred. Incision of the abscess is
followed by pus evacuation, debridement, drainage and dressing. Pus samples are sent
for antibiogram. In superficial abscess, the skin incision may be arcuate, parallel with
the Langer lines of the skin, for a better aesthetic effect, but in profound abscesses radial
incisions are recommended to avoid sectioning the milk ducts.
Chronic breast abscess is the consequence of an unresolved acute mastitis.
Clinical picture is represented by:
A hard lump in the breast, which infiltrates the surrounding tissues
The lump is painful to touch and on compression, sometimes associated
with purulent nipple discharge
Peu d'orange and retraction of the nipple may be present
531
Breast Pathology
Old scars may be present on the skin (previous surgery)
Axillary lymph nodes are enlarged
After incision, thick sterile pus is observed surrounded by fibrous tissue
Because of its local features, the chronic abscess is very difficult to differentiate
from a breast cancer. A thorough history of the patient could reveal an acute mastitis
treated years ago. In addition, the skin scar present on the breast may help to make the
difference. Histological examination of the infiltrated tissue will rule out the
malignancy.
The treatment consists incision or excision with histopathological examination.
532
Breast Pathology
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 make it easy
to diagnose and differentiate from other tumors. There is a tumor 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.
Diagnosis is usually easy, based on clinical features of the tumor.
Useful 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 as mobile as fibroadenoma or is quite fixed in advanced stages, its
surface is irregular and frequently is associated with enlarged axillary lymph nodes.
Other affections for differential diagnosis are:
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.
Sclerocystic mastopathy - the condition gives the feeling of lead shots"
under the skin on palpation; ultrasound shows multiple small cystic
formations of various sizes; it is usually symmetrical, often painful, and
sometimes with greenish nipple discharge.
Breast lipogranulomas - are represented by poorly delimitated mass with
reduced mobility due to chronic inflammatory process, possibly associated
with axillary inflammatory adenopathy.
Lipomas - have a softer consistency and are more superficial that
fibroadenomas.
Other tumors of the breast
Treatment
Simple fibroadenomas are tumors well encapsulated which can be easily
enucleated. The operation of election is the 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, and 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 should be considered the fact 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%.
533
Breast Pathology
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, cysts are mobile with smooth surface and of elastic consistency.
They may be or not painful.
Cysts are related to papilloma tumor type. The histological features are of
apocrine metaplasia (the inner lining layer of large cysts is composed of apocrine cells).
Intraoperative they look dark ("blue dome cysts").
Breast 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, cytological examination is nod needed, because there is no
suspicion of cancer, but when blood is present, smears are examined microscopically.
In most cases, cyst evacuation by aspiration is the definitive treatment method.
Galactocele
Galactocele is 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.
534
Breast Pathology
Intracanalicular papilloma
Intracanalicular papillomas are cell proliferation in the mammary ducts.
The gross appearance is that of intraductal vegetations (like polyps) of a few mm,
red multi ramified epithelium developed in the ducts, located in the center of the gland
and retroareolar region. Intraductal papillomas are classified into central and peripheral
types. The ducts are enlarged but with thin walls and contain a brownish fluid.
The papilloma consists of a vascular axis covered by cylindrical epithelium. At
the periphery, hyperplastic alterations are present. Focal areas of hemorrhage and
necrosis are also present. It can accommodate atypical hyperplasia and ductal
carcinoma in situ. If the epithelium is double layer columnar cell, it becomes
noninvasive papillary carcinoma.
Clinical picture
The condition is common in women aged between 30-50 years. The patients
claims serous or serosanguinous discharge for long periods of time. On palpation, a
small, round tumor under the nipple that does not adhere to the skin can be felt. Traction
of the nipple mobilizes the tumor (related to milk duct). On nipple compression, serous
or serosanguinous discharge appears. There are no enlarged axillary lymph nodes.
Multiple intraductal papillomas occur in approximately 10% of cases, tend to
occur in the younger patients and are less often associated with nipple discharge.
Inverstigations
Ultrasound examination - high-resolution ultrasound examination can reveal
the dilated duct that contains a well-defined, smooth-walled, solid, hypoechoic mass.
Mammography - in small papillomas is not very helpful. When imaging
findings are present, the dilated duct can be seen in the retroareolar region
containing a benign-appearing mass
Galactography - usually reveals a filling defect
Mammary ductoscopy - directly visualizes the papilloma and guides the duct
excision surgery.
Cytological examination of nipple discharge - is used to detect malignant
cells
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, microdoctectomy 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 retroareolar
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.
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Breast Pathology
7. 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. It is
often associated to ductal ectasia and/or fibrocystic changes in the mammary gland.
Changes are often bilateral.
A less common noncancerous etiology is the ductal ectasia 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.
Subclinical nipple discharge occurs more frequently in women who use birth
control pills and substitutive hormone therapy.
Epidemiology
Nipple discharge can occur in both sexes but is more common in women. The
frequency is about 3-8% of all women and there are no differences between races. The
disease can occur at any age.
Clinical picture
In most cases, nipple discharges are bilateral. The aspect of the discharge may be:
Clear (aqueous)
Serous (yellowish)
Lactescent (white)
Serosanguinous
Sanguinolent
To be considered a nipple discharge, discharges must take place outside the
period of lactation, to be spontaneous and persistent.
Suspicion of cancer increases if the discharge appears only at one breast, from a
single pore and is sanguinolent. In addition, if a tumor can be felt on palpation and if the
patient is over 50 years old the risk of cancer is higher. Breast cancer is more common
in men with nipple discharge.
After investigations, when suspected lesions are not malignant, in 73% of cases,
nipple discharge regress spontaneously within 5 years.
Investigations
Mammography - is not always relevant but it may highlight modifications
suggestive for cancer (clusters of microcalcifications)
Galactography (ductography) is performed by injecting a contrast iodine
solution through a pore followed my 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
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Breast Pathology
cranio-caudal and latero-lateral mammograms are performed. Galactography
is not indicated when:
o Nipple discharge is bilateral
o Secretion is not spontaneous or it cannot be obtained by compression
of the nipple and so neither the pore can be observed
o Secretion occurs from many pores
Breast ultrasonography - may visualize the intracanalicular papilloma or
other breast gland modifications
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.
Ductoscopy - allows direct visual access to the mammary ducts, using
fiberoptic microendoscopes inserted through the ductal opening onto the
nipple surface
Galactorrhea is the spontaneous flow of milk from the breast, unassociated with
childbirth or breast feeding and usually not associated with breast cancer and the more,
when it is bilateral. Galactorrhea may occur due to:
local stimulation of the nipple
chest wall trauma
consumption of various drugs (contraceptives fenotiazide, antihypertensive,
etc.)
hypoparathyroidism
pituitary adenomas
amenorrhea
Treatment
Surgery is indicated when the discharge is from a single pore, unilateral.
Additional argument for surgery is palpable tumors, lesions found after investigations,
and age over 40 years.
Indication of surgical treatment is supported by the suspicion of an existing
cancer.
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.
Prognosis
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.
8. Breast Cancer
Unfortunately, we not know yet the cause of breast cancer and yet we cannot
prevent it, but history does not stop there.
Features of breast cancer:
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
womens psyche and personality.
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Breast Pathology
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 and mortality
Breast cancer ranks among the most common 3 diseases in the world. A new case
appears at every 30 seconds. One death occurs at every 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%
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. One percent 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.
Etiopathogenesis
Risk factors for breast cancer can be classified as:
A. Factors that can not be modified
B. Factors that can be modified (depend on our willing)
A. Factors that cannot be modified
Gender is 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. On the other hand, the latter are usually
diagnosed in more advanced stages with lower survival rate. 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.
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Breast Pathology
1 out of 1,760
1 out of 229
1 out of 69
1 out of 42
1 out of 29
1 out of 27
Lifetime
1 out of 8
Source: Among those cancer free at age interval. Based on cases diagnosed 2000-2002. "1 in" are
approximates. Source: American Cancer Society Breast Cancer Facts & Figures, 2008-2009.
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Breast Pathology
among flight attendants (stewardesses), incriminated factor being the more
intense cosmic radiation at higher altitudes.
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.
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:
o The existence of genetic markers of susceptibility (BRCA 1, BRCA 2)
o Family history of breast cancer unilateral or bilateral, especially in first
degree relatives
o Personal history of breast cancer
o History of hyperplastic mastopathy
o Hormone replacement therapy (to treat postmenopausal symptoms),
o History of ovarian or endometrial cancer
Moderate risk:
o Age
o Family history of breast cancer occurred before menopause
o Radiation of the chest
o Small and repeated breast trauma
Low risk:
o History of breast cancer occurred after menopause
o Nuliparity
o First birth at an older age than 30
o Early menarche before age 12
o Late menopause, occurring over the age of 55
o Obesity occurred after menopause (increases risk by 80%)
o Daily consumption of alcohol
o Diet rich in fat and carbohydrates
o Oral contraceptive used more than 10 years
Recommendations for primary prevention of breast cancer:
Avoid exposure to radiation (avoid unnecessary radiological examinations,
avoid prolonged exposure to ultraviolet radiation)
Physical activity has beneficial effects through several mechanisms
Limitation or exclusion of alcohol consumption
Maintaining an ideal weight through diet and exercise especially after
menopause
Hypocaloric, low fat diet rich in vegetables, fruits, trace elements and
vitamins, especially in adolescence
Avoid as much as possible hormone replacement therapy and birth control
pills
Giving birth and breastfeeding at a young age would be beneficial
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Breast Pathology
American Cancer Society recommends the following steps to detect early
breast tumors:
A. Women aged over 20 years - breasts self-examination should be performed
every month
B. Women between 20 and 39 years - should be clinically examined at least
once every three years
C. 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. They have the ability to spread in various ways in any region of the body. The
immune system cannot cope with this invasion and metastases appear.
The underground life of breast cancer 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 (one
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. Pain (continuous or
intermittent, localized or irradiated) occurs rarely, in 10% of patients. 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 tissue septa, along ducts and invasion of lymphatic and blood
vessels.
Local extension
Cancer extends to the skin by invasion of Duret crests and Cooper ligaments. In
this stage the skin becomes fixed, infiltrated and cannot be folded (the Ianisevskis
sign). By side displacement maneuver of the tumor, a depression appears behind it (the
Dupuytrains sign).
In a later stage, the tumor blocks the local lymphatic circulation producing a local
lymph edema. The skin pores become more evident and the aspect of orange peel (peau
dorange) appears.
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Breast Pathology
Then, the tumor directly invades the skin producing ulceration, which has
irregular and endured borders, purple color and necrotic tissue on the bottom. Bleeding
and infectious complications are common in this stage.
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
(pathognomonic sign) through invasion of milk ducts and connective tissue septa.
Retraction is fixed, irreducible, unilateral and acquired.
Ducts invasion also causes nipple discharge (serous, sanguinolent or lactescent)
either spontaneously or on compression.
Extension may progress in depth to the pectoral muscles and chest wall. Invasion
of these structures can be demonstrated by the Tillaux maneuver (during pectoral
muscle contraction in forced adduction the tumor becomes fixed to the chest wall).
Regional extension 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 lymph node can be found and removed for
examination by methods using radiotracers and dye tracers. Histopathological findings
from this are very important in choosing the type of surgery, which will be applied (with
or without axillary lymphadenectomy).
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 the upper
limb.
Lymphatic invasion extends to the subclavian and supraclavicular lymph nodes
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 the internal
mammary lymph nodes, which cannot be detected by clinical examination.
Remote extension is achieved by both lymphatic and venous routes. Tumor cells
invade the microcirculation and are transported by venous bloodstream towards superior
cava vein. From here, they follow the natural path to the right heart and then to the
lungs, which represent the first major systemic, filter. Liver represents the second filter.
Most tumor cells remain stuck in the first filter (the lung) and start to develop
lung metastases. Lung metastases are manifested initially by decreasing exercise
capacity, dyspnea on effort, and then even on rest. In advanced forms, irritating cough
and dyspnea is increasing more and more, leading to death, by both reducing the lungs
hematosis surface to and paraneoplastic pleurisy.
Tumor cells escaped from the lung filter 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 produce symptoms like weight loss, loss of appetite, digestive
problems and eventually jaundice. The dull pain under right costal margin is produced
by Glissons capsule distension. Liver metastases can be detected by ultrasound
examination of the liver or by CT scan.
Bone metastases are the most common sites of metastasis in breast cancer. They
are present in approximately 25% of cases. These metastases are manifested mainly by
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Breast Pathology
early pain. The most frequent complication of bone metastases is pathological fractures.
Bone metastasis can be observed on bone radiograms, which reveal bone circumscribed
demineralization, and/or on radioscintigraphy, or CT scan and PET scan.
Other regions of metastasis are the brain, spine, spinal cord, but never the
kidneys.
In conclusion, although in early stages the breast cancer does not cause pain,
other symptoms (such as those listed below) should be warning signs for women and to
determine them to contact a doctor.
The appearance of a breast tumor and/or axillary enlarged lymph nodes
Changes in breast shape and size, and nipple symmetry
Changes of skin surface (orange peel, tumor nodules, ulceration, increased
vascular drawing)
Nipple discharge, especially sanguinolent
Recent nipple retraction
Workup in breast cancer
Before treating a breast cancer, doctors are facing two important problems: the
first is to determine if the breast lesion is really a cancer and the second is to determine
the exact location and extension of the tumoral process. Several important investigation
methods are very helpful.
I. Imaging examinations
Mammography and breast ultrasound are the most frequent investigations used in
this field.
A. Mammography. It can find breast tumors in an early stage, about 2 years before
they can be detected by palpation but it does not prevent breast cancer!
Mammography uses X-rays with very low levels (0.1 Gy). Each breast is
compressed horizontally and then obliquely and x-rays are taken in each position.
There are two types of mammographies:
o Screening mammography, which is performed in women with no
complaints in the breast area, and
o Diagnostic mammography, for women who has some complaints or
modification in breast area
An improvement in this field is the digital mammography which stores and analyzes
the information on a computer. Detectable tumor size on mammography is an
average of one cm diameter. In the table below are given for comparison the
approximate sizes of mammary tumors detected by mammography and by palpation.
Mammographic features of a malignant tumor are:
Irregular whitish mass with marginal spicule
Clusters of microcalcification
Calcification less than 0.5 mm diameter
Deformation of local architecture
Density asymmetry
Skin retraction
Peritumoral edema
Mammographic features of a benign tumor are:
Circumscribed mass
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Breast Pathology
Fat-containing lesion
Macrocalcifications
Round, uniform density, large, coarse
Widely scattered
Interpretation of mammograms. Standardization system BI-RADSTM (Breast Imaging
Reporting and Database System) to characterize the mammographic images:
Category 0 - image inconclusive, it is necessary to carry out other imaging
Category 1 - negative
Category 2 - benign character changes
Category 3 - probably benign but require tracking changes
Category 4 - suspicious for cancer changes - requires biopsy
Category 5 - highly suggestive of cancer changes
B. Breast ultrasonography
Indications:
To investigate tumors detected by mammography or palpation and for biopsy
guidance.
To differentiate the cystic from solid tumors.
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)
To explore the axillary lymph nodes.
To explore the breast tissue in mastitis abscess formation
To guide the biobpsy
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
Isnt 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
C. Nuclear magnetic resonance imaging (MRI)
It provides valuable information about tumor extension. The main drawback is the
price far above the mammography examination.
Indications:
Preoperative staging in breast cancer for possible or multi-focal disease
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BRCA mutation
First-degree relative of BRCA carrier, but untested
Lifetime risk 2025% 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)
D. 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 and penetration into the chest wall structures
or distant metastases detection.
E. CTLM (Computed Tomography Laser Mammography)
This method 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 perform
images through implants and dense breast tissue easily, unlike mammography.
F. 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
such as:
For patients with dense breast tissue difficult to investigate with other imaging
methods
When a breast tumor can be felt but it cannot be detected by mammography or
ultrasound
Breast implants
When multiple, multifocal tumors are suspected
When after mastectomy tumors appear at the level of postoperative scar
To explore the axilla in detecting metastatic lymph nodes or for sentinel node
biopsy
G. P.E.T. - Positron Emission Tomography
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Breast Pathology
The principle is the same as in Sestamibi. Post-therapy is particularly useful for
detecting any remnant cancer and active areas and to detect lymph node or distant
metastases.
H. Other imaging investigations such as:
Chest radiograph is used to highlight the pulmonary metastases
Bone radiography and scintigraphy - for bone metastases
Thermography is based on the principle that the area around the cancer tissue
has a higher temperature because of rich blood supply and more intense
metabolism
Electrical impedance scanning (EIS) is based on differences of electrical
impedance between the normal tissue and the tumoral one.
ER/PR
(estrogen/
progesteron
receptor)
Description
Estrogen receptors bind to cancer cells stimulating their proliferation and
differentiation. Progesterone is also a mitogenic factor stimulating the
mammary 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.
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BRCA1
(breast cancer 1)
Chromozom 17q
BRCA2
(breast cancer 2)
Chromozom 13q,
HER-2/neu
(human epidermal
growth factor
receptor 2)
Gene ERBB2
localised on
chromozom 17q21.1
CA 15-3
(Carbohydrate
Antigen 15-3)
(Cancer Antigen 153) Antigen oncofetal
(from blood)
CA-125 also known
as mucin 16
CA 27-29
Breast Pathology
After aspiration, the tumor mass does not disappear completely
In case of a recurrent cyst
There is a suspicion for cancer on mammogram
b. Tru-cut biopsy is also a percutaneous method. The essential differences from fine
needle aspiration biopsy are:
It uses a thick needle, specially fitted with a cutting mechanism
The process of obtaining biopsy material is cutting not aspiration
The material obtained is a cylinder of tissue, enough to differentiate
between invasive and noninvasive type of cancer
Core needle biopsy is not suitable for cystic lesions
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.
c. 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.
d. 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. It is
carried out only with stereotactic equipment. Rarely used in now days.
SURGICAL BIOPSIES
a. Excisional biopsy. It is the most commonly used type of biopsy. The surgeon will
remove the tumor with a safety margin of normal tissue around it.
b. 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. The surgeon will harvest only a portion of the tumor 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.
Staging of breast tumors - TNM classification (American Joint Committee on Cancer)
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
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Breast Pathology
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
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
Stage grouping
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
Treatment of breast cancer is a complex and multimodal one. The arsenal includes:
1. Surgical
2. Adjuvant
3. Radiotherapy
4. Chemotherapy
5. Hormonal therapy
6. Immunotherapy
7. Others
Selection of local and systemic treatment modalities and priorities of application
depends on a number of factors and prognostic predictors including:
Tumor histology
Clinical and pathological features of tumor
Lymph nodes status
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Breast Pathology
Tumor hormone receptor
HER2 marker level
Distant metastases
Existing co-morbidities
Age of patient
Menopausal status of the patient
Patient preferences
Breast cancer in men is treated in the same way as in postmenopausal women.
TREATMENT STRATEGIES BASED ON STAGE GROUPS
1) Non-invasive carcinoma (stage 0)
a) ductal carcinoma (DCIS)
b) lobular carcinoma (LCIS)
2) Operable invasive carcinomas
a) stage I
b) stage II
c) some of stage IIIA
3) Inoperable invasive cancers
a) stage IIIB
b) stage IIIC
c) some stage IIIA
d) 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 patients 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 breastconserving therapy requiring radiation therapy (RT) include:
Absolute:
Prior RT to the breast or chest wall
RT during pregnancy
Diffuse suspicious or malignant appearing microcalcifications
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Breast Pathology
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 will remove the level I and II of lymph nodes. Sentinel node
biopsy may be considered in the following cases:
Nonpalpable axillary lymph nodes
Tumor less than 5 cm diameter
Without having had breast surgery on the same breast
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 (T4, any N, M0) and IIIC (any
T, N3, M0)
Treatment begins with preoperative chemotherapy followed by mastectomy with
lymphadenectomy if remission is obtained. 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. Recurrences
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:
Mastectomy or excision of recurrences with the purpose of "cleaning" the
ulcerated lesions which has become infected.
Oophrectomy (ovarectomy) in premenopausal patients
Bone marrow transplantation (autologous) or stem cell transplantation
combined with high dose radio-chemotherapy.
SURGICAL TREATMENT
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Breast Pathology
1) Tumor removal (+ / - Lymphadenectomy)
a) Conservative surgery
i) Lumpectomy
ii) Quadrantectomy
iii) Extended quadrantectomy
b) Mastectomy
i) Simple mastectomy
ii) Skin sparing mastectomy
iii) Mastectomy with axillary lymphadenectomy
Maden
Patey
Halsted - limited indications (tumor infiltration of the pectoral
muscles)
iv) Heroic" operations (Ugon, Dubau, etc.) have no indication in now
days
2) Surgery to remove the lymph nodes
a) Sentinel node biopsy
b) Axillary lymphadenectomy
c) Internal mammary lymphadenectomy
3) Breast reconstruction surgery
4) Endocrine surgery (oofrectomy)
Lumpectomy is a surgical method applied for early stages of cancer, which removes
the tumor with surrounding healthy tissue. Usually 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) means the removal of a quadrant of
mammary gland.
Partial mastectomy (or extended quadrantectomy) means 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 is almost the same as in Madden procedure but the pectoraslis minor
insertion is sectioned for a better access to the axilla.
Radical mastectomy or amputation of the breast (Halsted operation) presumes
mastectomy plus a wide excision of the pectoral muscles and axillary lymph nodes. In
nowadays this type of operation is no longer performed, just in cases when muscles are
invaded by tumor.
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Breast Pathology
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. These are the reasons why the lymphatic mapping prior operation
is important. Mapping is useful also for guiding the radiation therapy.
Possible locations of sentinel lymph node are:
Axillary level I, II and III
Internal mammary chain
Supraclavicular and cervical
Intramammary
Interpectoral (Rotter)
Other locations
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.
The excised node will be sent to histological 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
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Breast Pathology
important in preventing associated complications (seroma, shoulder and upper limb
pain, lymphedema, scars, etc.).
Postoperative complications
Post-mastectomy
Subcutaneous hematoma
Wound infection
Skin necrosis
Chest paresthesia
Postoperative local pain
Seroma
Lymphedema - the reported prevalence rate of lymphedema is
approximately 11%. Extensive surgery, RT, and advanced age are
recognized risk factors for arm edema
Keloid scars
Granulomas
Tumor recurrence
After axillary lymph node dissection:
Lesions or thrombosis of the axillary vein
Seroma
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
Post-therapy follow-up program for patients with breast cancer
Clinical examination
Chest radiography
Mammography
Year 1
4 month
Initial
12 month
Year 2
4 month
If necessary
12 month
Years 3-5
6 month
If necessary
12 month
> 5 Years
12 month
If necessary
12 month
Bone scintigraphy
Initial
If necessary
If necessary
If necessary
Breast Pathology
erythema and edema, increased local temperature. The aspect is that of peau dorange
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 anti-inflammatory 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 receptors 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.
Breast Pathology
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Breast Pathology
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.
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.
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.
Prognosis. For the benign forms, the prognosis is very good. In malignant forms
recurrences are more aggressive as the primary tumor. Most frequently 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.
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Breast Pathology
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 investigations 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.
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Breast Pathology
Inflammatory carcinoma
Paget's disease of the breast.
Lobular carcinoma in situ has not been found in breast cancer in men.
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 and treatment are the same as for women.
Tamoxifen hormone therapy is also indicated in men especially in forms of cancer
with ER / PR positive receptors.
Prognosis. 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.
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Breast Pathology
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 is 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.
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Veins
Transport blood toward the heart
Carry de-oxygenated blood
(except in the case of the pulmonary vein)
Have relatively wide lumen
Have relatively less muscle/elastic tissue
Transports blood under lower pressure (than
arteries)
Have valves throughout the main veins of the
body.
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Kidney damage
Excessive bleeding
Infection
Blood clots
Radiation exposure from the X-rays
569
4. 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. Half of patients with aortic
aneurysm who do not undergo treatment die of a rupture.
Etiology
Congenital aneurysms are present at birth and they are due to chromosomal
abnormalities that induce degeneration of the elastic and muscular fibers. It is frequently
associated with endocrine disorders.
Acquired aneurysms appear during lifetime and comprise the all other
aneurisms
Atherosclerosis 95% of aortic aneurisms
Infectious due to nonspecific (gram positive or negative) germs or specific
agents (syphilis) and fungi, which produce ulceration of the intima
Rheumatic
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.
Anastomotic - as a late complication of vascular surgery
Morphology
Aneurysms may be fusiform or saccular.
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 Marfans 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 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
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573
5. Arteriovenous Fistulas
Arteriovenous fistulas are direct communications, through a duct or network,
between the venous and arterial system that 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:
Congenital Generally, they are located peripheral and are a consequence of
angiodysplasia. The appearance is that of hemangioma, looking red-purple, soft to the
touch, reducing their dimension under compression. They may be located 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
Acquired with various etiology
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.
Spontaneous intraabdominal as a result of evolution of a tumor or aneurysm.
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 are represented by moderate local pain, muscular fatigue,
sometime intermittent claudication. Symptoms of heart overload such as tachycardia,
dyspnea, symptoms of heart failure may be present.
Physical examination reveals venous dilatation, limb enlargement, dilated
capillary vessels (hemangiomas), skin discoloration, dystrophic skin lesions, and soft
tissue gangrene. On palpation, the tumor is soft, compressible, with elevated local
temperature and a thrill can be felt. On auscultation, a systolic or continuous sound
(murmur) can be heard. Digital compression of the fistula reduces tachycardia because
reduces the venous return.
Investigations: Doppler ultrasound, angiography and CT scan are helpful.
Complications: thrombosis, skin ulcerations and gangrene, infections, heart failure,
distal ischemia.
574
Embolism
Emboli are the most common cause of acute ischemia. Their origin may be:
cardiac (80%), proximal atheroma, tumors, foreign objects, gas embolism, and fatty
embolism.
Causes of cardiac embolism are: atrial fibrillation, rheumatic valvular heart
disease (especially mitral), left ventricular myocardial infarction with thrombosis, postmyocardial infarction sequelae, valves, endocarditis vegetations on native or prosthetic
valves, cardiac tumor fragments (atrial myxoma).
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581
Angiographic
continuous lesions
irregular contour of the artery
asymmetrical lesions, more
advanced in the affected limb
well developed collateral circulation,
with separation of collaterals at right
angles from the main artery
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
A. 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.
B. Medical treatment
General measures: avoiding exposure to cold and wet, wearing
comfortable shoes and appropriate clothing, proper local hygiene.
Physiotherapy: medical gymnastics, carbonated baths, thermal cures.
Medication: administration of antiplatlet drugs (Aspirin) vasodilators,
anticoagulants, anti-atherosclerotic, pain relievers, etc..
C. 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:
o Angioplasty
Open - arterial patch application,
Endovascular procedures
Balloon angioplasty
Stenting angioplasty
Laser angioplasty
o Bypasses (with own saphena magna vein or prosthesis)
o Endarterectomy
o Segmental arterial resection (restoration of continuity with the
autograft or prosthesis)
Operations of necessity: amputations, necrectomies.
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Anatomy
Lower limb venous circulation physiology
Varicose veins
Acute venous thrombosis
1. 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.
2.
3.
4.
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 greater (or internal) saphenous vein and the lesser (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
lesser (external) saphenous vein.
The internal saphenous vein 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. The magna saphenous
vein 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 greater saphenous vein
arch at level of saphenous hiatus, near the saphenofemoral junction:
1. The superficial inferior epigastric vein
2. The superficial external pudendal veins (two veins)
3. The superficial circumflex iliac vein
Other tributary veins are the anterolateral branch and posteromedial branch called
the vein of Giacomini.
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3. Varicose Veins
The condition represents a chronic disease of the lower limb venous system
characterized by:
Alterations of the venous walls and valvular apparatus
Reflux of blood from the deep venous system towards the superficial
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.
Morphopathology
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Terminology
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
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.
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
589
Ec - congenital
Ep - primary
Es - secondary (postthrombotic)
En - no venous cause identified
Anatomic classification
As - superficial veins
Ap - perforator veins
Ad - deep veins
An - no venous location identified
Pathophysiologic classification
Pr - reflux
Po - obstruction
Pr,o - reflux and obstruction
Pn - no venous pathophysiology identifiable
Examples of classification:
Classification according to basic CEAP: C6,S, Ep,As,p,d, Pr.
Classification according to advanced CEAP: C2,3,4b,6,S,
Pr2,3,18,13,14 (2004-05-17, L II).
Ep,As,p,d,
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Sclerotherapy can bed applied 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) (Table 1) 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 are:
Hyperpigmentation - this is a common occurrence after sclerotherapy of
veins of all sizes in approximately 10-80% of patients
Swelling
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.
Other complications (pain, localized urticaria, folliculitis,
localized
hirsutism, skin necrosis, systemic allergic reactions , superficial
thrombophlebitis, deep venous thrombosis, nerve damage)
Table 1 - Suggested sclerosant/concentrations for treatment of telangiectasia/reticular veins
VESSEL TYPE
Telangiectasia
< 1mm
Venulectasia
1-2mm
Reticular veins
>2mm
SCLEROSANT
CONCENTRATION
Hypertonic saline
Sodium tetradecol sulfate STS
Polidocanol (Aethoxysklerol)
Sodium tetradecol sulfate STS
Hypertonic saline
Hypertonic glucose/saline
(Sclerodex)
Polidocanol (Aethoxysklerol)
Hypertonic saline
Hypertonic glucose/saline
Sodium tetradecyl sulfate STS
Polidocanol
11.7%
0.2%
0.25%
0.25%
23.4%
The formula for Hypertonic
glucose/saline is 200mg/ml dextrose
100mg/ml sodium chloride 100mg/ml
propylene glycol 8mg/ml phenoxyalcohol
0.5%
23.4%
0.25%
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 that makes the vein slowly fade and
disappear. No incisions or needles are used.
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C. Pulmonary Embolism
It 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 large 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.
Symptoms
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 the lungs where they occlude some
arteries leading to pulmonary infarction manifested at 24-48 hours by: chest pain,
cough, hemoptysis, and dyspnea. Fever up to 380C degree is present for 2-3 days.
599
D. Post-Thrombotic Syndrome
Evolution of venous thrombus may be:
To complete resolution - this is a rare possibility
Recanalization through a single canal but with valves destruction
Recanalization through multiple canals as a sieve
Permeabilization through collateral avalvular veins
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 occluded 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 (1020 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.
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C. 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 esogastric devascularization during Hassab operation.
E. 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).
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Total gastrectomy
Spleno-renal shunt
Esophagoplasty
Left hemicolectomy
Left nephrectomy
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THORACIC TRAUMA
1. Considerations about anatomy and physiology of the chest
2. Chest trauma - generalities
3. Blunt thoracic trauma
a. Simple contusions
b. Muscular ruptures
c. Chest compression
d. Simple rib fractures
e. Sternal fractures
f. Flail chest
4. Open chest trauma
a. Pneumothorax
b. Open pneumothorax with traumatopnea
c. Tension pneumothorax
d. Hemothorax
e. Cardiac tamponade
5. Lesions of the intrathoracic organs
a. Lungs lesions
b. Tracheo-bronchial tree lesions
c. Cardiac lesions
d. Aortic injury
e. Esophageal rupture
f. Diaphragmatic rupture
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Thoracic Trauma
most important function of the thorax, namely the respiratory function, endangering the
patient's life.
The thorax cage is like a rigid box, feature that 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 is the fact that between the two pleural layers (parietal
and pulmonary) there is a virtual space with negative pressure (lower than the
atmospheric pressure). This explains why 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 patients life.
Thoracic Trauma
open thoracotomy. About eighty percent 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.
Classifications
A. Blunt trauma
Blunt traumas 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:
1. 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).
2. 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.
3. 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. Finally yet
important should be considered patients age and existing co-morbidities. The younger
thorax is more flexible and better resist to deformation while in elderly fractures occur
more easily.
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Thoracic Trauma
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.
Low energy forces (arrows, knives, handguns) cause injury by direct contact and
cavitation.
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:
Without pathophysiological disorders
With pathophysiological disorders:
o Acute respiratory insufficiency
o Acute cardiocirculatory insufficiency
o Acute cardiorespiratory insufficiency
o With temporary stop of cardiorespiratory function
Classification according to pathogenesis
Closed chest trauma (blunt trauma)
Open chest trauma (wounds)
o Blind or transfixiant wounds
o Non-penetrating or penetrating wounds
o With or without effusions
o Mixed
Classification based on anatomical criteria
Without anatomical lesions
With anatomical lesions:
o Parietal non-skeletal lesions
o Parietal skeletal lesions
o Diaphragmatic
o Endothoracic lesions
Single organ affected, multiple organ affected
Associated with other trauma
Parietal lesions
Pleural space
Pulmonary parenchyma
Simple pneumothorax
Open pneumothorax
Tension pneumothorax
Hemothorax
Contusions
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Lacerations
Mediastinum
Diaphragmatic lesions
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Thoracic Trauma
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:
1. 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.
2. Pendular motion of the mediastinum - still further hampers the heart and
great vessels and reduces the already impaired oxygenating power of the
lungs.
3. 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.
4. Bronchial hypersecretion
There are two important vicious circles:
1. COURNAND - hypoxia pulmonary hypertension
alveolar
hypersecretion hypoxia
2. 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 cannot
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.
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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 hypooxygenation and so oxygenation will decrease even more.
9. 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.
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:
Ventilation deficiency - may be caused by:
o Disturbances of chest wall dynamics:
o Flail chest
o Limitation of respiratory movements due to pain
o Cancellation of tightness of chest wall:
o Pneumothorax
Disturbances of diaphragm movements:
o Traumatic diaphragmatic rupture or phrenic nerves lesions
o Exclusion from ventilation of lung parenchyma areas:
o Compression by pleural effusions or herniated abdominal viscera
o Airway obstruction
o Aspiration of foreign bodies, blood, tracheobronchial
hypersecretion
Impairment of air distribution in the lung parenchyma:
o Paradoxical breathing
o Pendular mediastinal movements
o Alterations of gas diffusion:
o Posttraumatic pulmonary edema
o 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
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Thoracic Trauma
Conditions which acted
Injury time (time elapsed from the occurrence of trauma)
Patients 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:
Parietal lesions (wounds, deformities, bruising, hematoma)
Abnormal movements or limitation of thoracic respiratory movements
(rib fractures with floating regions of the chest wall, paradoxical
respiration - flail chest)
Breathing disorders polypnea, dyspnea, tirage = inspiratory sinking of
the intercostal spaces due to airway obstruction
Signs of bleeding (pallor, hemoptysis, external bleeding)
Disorders of hematosis (cyanosis, sweating)
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, and 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:
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Thoracic Trauma
Airway patency. Ensuring a free airway is a major priority in emergency
resuscitation, patients 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.
Before starting any maneuver for airway patency, some basic parameters should
be assessed:
If patient is conscious or not
Breathing is appropriate or not - check respiratory movement, and
their extension
Duration of hypoxia - cyanosis appears very late
Airway patency
Need for administration of neuromuscular blocking agents (muscle
tension, teeth clenching, severe obstructive pulmonary disease or
asthma)
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.
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, and nonsteroidal anti-inflammatories and in rare cases surgical repair.
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3. Chest compression
It occurs when the chest is compressed between two forces, which lead to a
sudden increase of pressure in the chest. The pressure exerts a high force on the intrathoracic 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.
B. Fractures
4. Simple rib fractures are the most common lesions in the thoracic contusion.
They are produced either directly - at site of impact, or indirectly - by anterior-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 cannot cough effectively and expectorate, secretions accumulate
and lead to airway obstruction, stasis and infection. That is 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
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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 helps much in diagnosis of rib fractures and
associated complications (hemo-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.
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. Painkillers, 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
Lidocaine but it has a short effect, or with Lidocaine 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, because 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.
5. 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 and rarely 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.
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Thoracic Trauma
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.
6. Flail Chest
It 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 patients 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
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1. 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:
1. through an opening of the chest wall (wound), or
2. through an opening in the lung or bronchial tree (wound or leak)
Mechanisms:
Spontaneous Usually on an emphysematous lung during an intense
efforts or cough when emphysematous bubbles burst.
Traumatic
o Closed chest trauma due to lung, bronchial or tracheal rupture or
tear
o Open chest trauma - penetrating wounds which may affect lungs
Iatrogenic during subclavian vein catheter insertion or cardiac
resuscitation maneuvers.
Simple post-traumatic pneumothorax
In most cases, simple post-traumatic pneumothorax 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 tracheobronchial
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.
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 will not 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.
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Thoracic Trauma
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 pneumothoraxes (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, and 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
pneumothorax 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.
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Thoracic Trauma
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
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 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
thoracotomy if necessary) into the pleural cavity to evacuate collections and allow the
lung reexpansion. The thoracic wound will be closed. The patient will be monitored and
lung reexpansion will be assessed by auscultation and chest X-ray.
3. 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.
Symptoms 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
fermiums on the ipsilateral side. A significant volume of gas in the pleural space causes
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Thoracic Trauma
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 second intercostal space along the mid-clavicular line or into the fifth 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 pneumothorax 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 second 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 second space.
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.
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 is 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.
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Thoracic Trauma
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.
4. 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.
Blood loss of up to 750 mL should cause no significant hemodynamic change.
Loss of 750-1500 mL will cause the early symptoms of shock (ie, tachycardia,
tachypnea, and a decrease in pulse pressure).
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, the traumatic lesions of the skin (bruising, hematoma,
wounds, etc.) can be noticed. On percussion, dull sound over the affected side may be
heard. 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.
Possible evolution of hemothorax:
Accumulation in large quantities endangering the patients life - needs
evacuation or thoracotomy and hemostasis and blood replacement
Lysis and resorption if small hemothorax
It causes a pleural reaction with exudate and increases the volume of the
pleural fluid.
Infection with thoracic empyema
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, and chylothorax. In thoracic trauma context, the
chylothorax is more likely to be produced or blood can come from abdominal cavity
through a diaphragmatic rupture.
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Thoracic Trauma
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:
>1500 mL blood from chest tube on insertion
>200 mL blood/hour from chest tube thereafter (for 2-4 hours)
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).
5. 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 movement limitation with cardiocirculatory insufficiency and cardiac
arrest.
The pericardial space normally contains 20-50 mL of fluid. Pericardial effusions
can be serous, serosanguinous, hemorrhagic, or chylous.
In chest trauma, intrapericardial fluid is represented by blood, which may come
from:
A penetrating (stab, shot) wound which produces a lesion of the cardiac
vessels (coronary vessels) or heart wall (heart perforation)
A contusion of the heart with consecutive heart wall necrosis and rupture
Contusion of the heart with rupture of its wall
The pathophysiological 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, more than 1000 ml of
fluid will not 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
Kussmauls sign: Decrease or absence of jugular vein dilatation during inspiration
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Thoracic Trauma
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
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 by either cardiac suture or vascular suture.
Pericardial puncture
1. Epigastric approach Marfans point at the tip of xiphoid appendix.
2. Chest approach - may be performed on the right or left side of the
sternum
a. 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
Delormes point in the 6th intercostal space at the edge
of sternum
Rendus point - in the 6th intercostal space at 8 cm
beyond the sternum
Huchards point in the 7th intercostal space at 8 - 9 cm
from sternal midline (below the Dieulafoy point)
b. The righ approach
Roths 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.
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Thoracic Trauma
Advantages of this technique are 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:
Coronary artery damage
Laceration of the myocardium
Penetration in the lung
Echocardiographic guidance increases the success rate of pericardiocentesis by
reducing these complications.
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Thoracic Trauma
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 pneumothorax 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.
3. 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 traumas 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.
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Thoracic Trauma
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.
Investigations
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
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Thoracic Trauma
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 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 pericardial 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.
4. 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.
5. 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 (8590% 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).
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Thoracic Trauma
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 mediastinum 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)
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Thoracic Trauma
6. 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 intraabdominal 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
because 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
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Thoracic 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.
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 these 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.
639
1. 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 (about 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.
Classification. Pleural effusions are classified as:
1. Transudate,s 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 two
The mechanisms of pleural effusions production:
Alteration of pleural permeability inflammation, malignancy,
pulmonary embolus
Increased capillary permeability - trauma, malignancy, inflammation,
infection, pulmonary infarction, drug hypersensitivity, uremia, pancreatitis
Reduction of oncotic pressure - hypoalbuminemia, cirrhosis, cachexia
Increased hydrostatic pressure in the systemic and/or pulmonary
circulation - congestive heart failure, superior vena cava syndrome
Decreased lymphatic drainage - including thoracic duct obstruction or
rupture
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
o Congestive heart failure
o Cirrhosis (hepatic hydrothorax)
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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. In addition, occupational
history aspects may be important (asbestosis). Patients will describe the onset and
evolution of symptoms.
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642
A. PLEURISY
Pleuritis represents an inflammation of the pleura in most cases due to infection.
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645
B. Chylothorax
It 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
Malignant etiologies account for more than 50% of chylothorax diagnoses and
are separated into lymphomatous and non-lymphomatous. Lymphoma is the
most common cause, representing about 60% of all cases. Non-Hodgkin
lymphoma is more likely to cause a chylothorax than Hodgkin lymphoma.
Traumatic. Frequent (25%) causes of ductus thoracicus lesions are thoracic
trauma and different kind of surgeries (thoracic, cardiac, esophageal)
iatrogenic lesions.
Congenital chylothorax is seen in neonates.
Miscellaneous causes include cirrhosis, tuberculosis, sarcoidosis, amyloidosis,
and filariasis.
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
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C. Thoracic empyema
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Tracheobronchial
11R / 11L
Interlobar
12R / 12L
Lobar
13R / 13L
Segmental
14R / 14L
Subsegmental
Innervation
Sympathetic nervous fibers come from the paravertebral ganglia. They produce
bronchodilation, vasoconstriction and reduce secretion of mucous glands in the bronchi.
Parasympathetic fibers are derived from the vagus nerves (X) and produce
bronchoconstriction, vasodilatation and increase the mucous secretion.
Nervous fibers form plexuses, 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 systems 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 lung 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:
Tidal Volume (TV):, the volume of air that is inhaled or exhaled with each
normal breath.
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.
Inspiratory Reserve Volume (IRV): the maximal amount of air forcefully
inhaled after a normal inhalation.
Residual Volume (RV): the amount of air remaining in the lungs after the
deepest exhalation possible.
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
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Volume
Volume
Vital capacity
Inspiratory capacity
Functional residual capacity
Total lung capacity
In men
In women
3.3
0.5
1.0
1.2
1.9
0.5
0.7
1.1
1.8
4.2
ERV plus RV
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
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.
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.
In addition, in rare cases lung abscess develops as a secondary abscess spread
from an extrapulmonary organ or bronchiectasis.
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Differential diagnosis is made with other pulmonary or mediastinal masses such as:
Pulmonary TB tuberculum and especially TB cavern. Patients 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. Parts 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.
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 these 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.
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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 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 locations 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
are. 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 socioeconomic 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.
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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 is 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:
4. Non small cell lung carcinoma (NSCLC),
5. Small cell lung carcinoma (SCLC)
Histological types of bronchopulmonary cancer
Carcinoma with squamous cells
Papillary carcinoma
(epidermoid)
Carcinoma with clear cells
Carcinoma with small cells
Basaloid carcinoma
Carcinoma with small cells
Carcinoma with small mixed cells
(micro cell)
Large-cell carcinoma
Large-cell neuroendocrine carcinoma
(macro-cell)
Mucinous
Non-mucinous
Combined
Mucus producing solid carcinoma
Fetal adenocarcinoma
Mucinous adenocarcinoma
Mucinous cystadenocarcinoma
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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 four 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
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Symptoms
Frequency (%)
Cough
Dyspnea
Chest pain
Hemoptysis
Pneumonia
Vocal cord paralysis
Superior cava vein syndrome
Pleurysis
Pancoast-Tobias syndrome
Pericarditis
Small-cell
lung carcinoma
(SCLC)
50-76
34-40
35-36
15-23
21-25
15
12
10-15
rare
unusual
Non-small-cell
lung carcinoma
(NSCLC)
40
30-40
25-40
15-35
13-24
unusal
< 10
15
3
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-
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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
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