Zaporizhzhya state medical university

Department of faculty surgery

Methodical recommendations

for a practical lesson in the discipline of

“Surgery”

To the students of 4 course

Speciality 222 «General Medicine», 228 «Pediatrics»

Topics:
ACUTE APPENDICITIS

ACUTE CHOLECYSTITIS

ACUTE PANCREATITIS

COMPLICATED GASTRIC AND DUODENAL ULCERS

ACUTE INTESTINAL OBSTRUCTION

PERITONITIS

BLUNT ABDOMINAL TRAUMA

SEPSIS SYNDROME

Zaporizhzhya 2020
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Application developers: Head of the Department, MD, Professor A.V. Klimenko;

Associate Professor, PhD, O.V. Cherkovska, Associate Professor, PhD, O.V.

Zakharchuk; Assistants - Ph.D. A.I. Bilay; Ph.D., A.S. Tuhushev; Ph.D., A.O.

Steshenko; Ph.D., O.M. Kiosov; Ph.D., D.V. Syvolap, Ph.D., O.V. Mamunchak.

REVIEWERS: Gubka V.O. – professor of the Department of Hospital

surgery, MD.
Gaidarzhi Y. I. – as. prof. of the Department of Hospital
surgery, PhD

Discussed at a meeting of the Department and recommended for approval

methodic commission surgical disciplines
« 16 » March 2020, protocol number 8.

Head. department Klimenko A.V.

Adopted by the Commission on cyclic methodical surgical disciplines and

recommended for use in the learning process
« 21 » may 2020, Protocol № 10

Head cyclic methodical commission MD, Professor Zavgorodniy S.M.

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Table of contents

Acute appendicitis .................................................................................................... 3

Acute cholecystitis .................................................................................................. 12
Cholecystitis ........................................................................................................... 13
Acute calculous cholecystitis.................................................................................. 14
Acute pancreatitis ................................................................................................... 17
Gastric ulcer ............................................................................................................ 24
Duodenal ulcer ........................................................................................................ 28
Ulcer stenosis.......................................................................................................... 32
Perforated gastroduodenal ulcers............................................................................ 34
Bleeding gastroduodenal ulcers .............................................................................. 37
Acute intestinal obstruction .................................................................................... 42
Peritonitis ................................................................................................................ 48
Sepsis syndrome ..................................................................................................... 60
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LECTURE ACUTE APPENDICITIS

Acute appendicitis till now is one of the most important surgical problems. It's enough to say, that
appendectomy constitutes about 20 -30% of all surgery. In Ukraine about 500.000 appendectomies are
performed annually without marked downtrend (A.A. Shalimov, 1989). Studies of appendix had passed
many stages before the modern system of etiology, pathogenesis, clinical picture and treatment was
created. This disease is insidious one. The existent conception about it as about of slight indisposition is
easily disproved by statistics. Lethality seems to be not high, taking into consideration the incidence of
the disease; it is rarely exceeds 0,2-0,3%, but these figures mean dozens of thousands lives.
The first appendectomies had been performed by Kronlein in 1883, by Malomed in 1884, and by
A.A. Troyanov in 1890.

Brief Anatomo-Topographic Sketch

Vermiform appendix (appendix vermiformis) is the constituent of the iliocaecal angle, which
presents morphological integrity of four intestinal departments: the caecum, terminal end of the ileum,
initial part of the ascending colon, and the vermiform process. All the constituents of the iliocaecal angle
are in strict correlation and perform the function of "internal analyzer", coordinating the most important
function of the intestine — conduction of chyme from the small to large intestine (A.M. Maximenkov,
1972).
The important element of iliocaecal angle is the iliocaecal (Bauhin's) valve (valva ileocaecalis)
with very intricate structure. Its function is to accomplish regulation in transition of intestinal content to
the caecum in little portions and to prevent its return from the caecum to the small intestine.
The iliocaecal angle is situated in the right ileac fossa. Fundus of the caecum is projected on the
distance of 4-5 cm upwards the center of the inguinal ligament; under condition of its filling, fundus of
caecum is located just above the center of the inguinal ligament or may even descend to the small pelvis.
Great variability in anatomo-topographic situation of the caecum and the vermiform process explains in
many respects such a diversity of clinical picture, which may be observed in acute appendicitis.

The most frequent and practically important deviations from the normal position of the caecum
are the following (V. I. Kolesov,1959):
1) high, or hepatic position, when the caecum and the vermiform process are situated high,
sometimes reaching the lower border of the liver;
2) low, or pelvic position, when the caecum and the vermiform process are situated below
normal, i.e. descends to the pelvis.
Other variants of it localization, such as its left-side position, location along the middle line of the
abdomen, in the umbilical region, in the left hypochondrium, in the hernial sac, etc. occur rather
infrequently.
The vermiform process is located intraperitoneally. It has its own mesentery (mesenteriolum),
which supplies it with vessels and nerves.
Blood supply of the iliocaecal angel is provided owing to the superior mesenteric artery — a.
ileocolica, which is subdivided into the anterior and posterior iliac arteries. The natural artery of
vermiform process — a. appendicularis, which may have a loose, arterial or mixed structure, branches
off from a. ileocolica or from its branch. Artery of the vermiform process goes through its mesenteries,
along its free edge, to the end of the process. Though its small caliber (from 1 to 3 mm), post-operative
hemorrhages from a. appendicularis may be very intensive, as a rule, they require relaparotomy.
Veins of the caecum and the vermiform process are the tributaries of the ileocolic vein (v.
ileocolica), which flows in the superior mesenteric vein (v. mesenterica superior).
Innervation of the iliocaecal angle is performed by the superior mesenteric plexus, which is
connected with the celiac (solar) plexus, which takes part in innervation of all digestive organs. The
iliocaecal angle is considered to be "the junction depot" of all abdominal organs innervation. Running
from here impulses influence functions of many organs. The peculiarity of innervation of the iliocaecal
angle and the vermiform process explains the onset of pain in the epigastrium and their spreading over
the abdomen in acute appendicitis.
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Lymph outflow from the vermiform process and from the iliocaecal angle performs entirely to the
lymphatic vessels, which are situated along the ileocolic artery. There is a chain of lymph nodes (10-20)
along this artery, which extends to the central group of mesenteric lymph nodes. Immediate proximity of
the mesenteric and iliac lymph nodes explains the similarity of clinical picture in inflammation of these
nodes (acute mesenteric adenitis) and in inflammation of the vermiform process.
Five variants of localization of the vermiform process with respect to the caecum are
distinguished: descending (caudal (is); lateral, internal (medial), anterior (ventral), and posterior
(retrocaecal). In descending, more frequent localization, the vermiform process, directing towards the
small pelvis, adjoins to certain extent the organs of the small pelvis. In lateral position, the process lies
from the outside of the caecum. Its apex is directed to the inguinal (Poupart's) ligament. Medial
localization is also rather frequent. In those cases the vermiform process lays medially to the caecum,
being localized between the loops of the small intestine; all these provide favorable conditions for extent
inflammation inside the abdominal cavity and give rise to abscesses. The anterior position of the
process, in which it lies in front of the caecum, occurs rarely. Such localization is favorable to anterior
parietal abscess. Some of the surgeons mark out ascending type of the process localization. Here, the
two variants are possible. The first one, in which the whole iliocaecal angle is located rather high, under
the liver, and then the term subhepatic position of the vermiform process is applied, or the second
variant, when the apex of the retrocaecal vermiform process is directed to ward the liver. Retrocaecal
position of the process, which is observed in 2-5% of the patients, two variants of its bedding with
respect to the peritoneum is characteristic: in some cases the process, being covered with the
peritoneum, lies in the iliac fossa behind the caecum, while in other cases it projects from the leaf of the
peritoneum and lies intraperitoneally. This position of the vermiform process is termed retrocaecal
(retroperitoneal) one. The latter is considered to be the most insidious variant, especially in suppurative
and destructive appendicitis, since in the absence of the peritoneal cover of the process the inflammatory
process extends to the paraumbilical fat, causing deep retroperitoneal phlegmon.

Etiology, Pathogenesis, Pathologic Anatomy, and Classification

There is no consensus of opinion about etiology of acute appendicitis. But there are some theories
explaining the causes of the disease and its pathogenesis. The most common of them is mechanical
(congestion), infectious, and aponeurotic theories. Besides that, at different periods a number of
conceptions, sometimes very original, were elaborated. All the theories and conceptions, reflecting one
or another etiological agent are not without logic and sense. At the same time, a variety of forms and
stages of acute appendicitis suggests the polyetiology of this disease, which results from the changed
correlation between the human body and microorganisms. It being known, acute appendicitis is a non-
specific inflammation of the vermiform process. The causative agents of infections may be
staphylococci, colon bacilli, and mixed and anaerobic flora. All the efforts on choosing a particular
pathogenic organism and to number acute appendicitis among specific inflammatory disease were not
successful.
Mechanical theory indicates the role of foreign bodies, infections and scary strictures of the
vermiform process in development of acute appendicitis. But these factors occur are far from being in all
the patients. Helmint invasion and angina (sore throat) are of great, but not absolute importance in
genesis of the disease. Infectious theory correctly indicates the role of infection and the primary affect,
but does not explain what stimulates an infection, which is permanently present in the lumen of the
vermiform process. And similar weak points take place among the other theories and conceptions.
Gained scientific and practical experience proves that taking into consideration the variety of clinical
and morphological forms of the disease, there may be several predisposing factors and their
combinations. For example, the following mechanisms and ways of development of acute appendicitis
are quite logical:
1. Obstruction of the lumen of the process and formation of a closed cavity filled with feces,
which contain toxins with highly reactive enzymes, gradually result in suppuration, lesion of the mucous
membrane, and infection penetrates inside the vermiform process wall. Development of exudative
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inflammation is accompanied by microcirculatory disturbances and degeneration of intramural neural

apparatus. But neurodystrophic changes together with the vascular factor constantly result in
inflammatory intensification and its progressing up to formation of phlegmon or gangrene.
2. Due to neurological disturbances, vascular stasis occurs in the vermiform process. It results in
trophopathy of the vermiform process and formation of necrotic foci. Pathologically changed tissues are
easily infected, i.e. secondary infection takes place. The following spread of the infectious process
causes more extensive pathologic changes with all possible severe consequences.
3. Primary formation of acute ulceration in the vermiform process, which had been observed by
Selye at general adaptation syndrome, is possible. It may be the result of neurogenic vasospasm.
4. In those cases, when abrupt clinical picture of the disease is followed very rapidly by gangrene of the
vermiform process, it is quite possible to consider primary thrombosis of a. appendicularis and its
branches. Inflammatory component and infection join secondarily.
Appendicular colic. It means a muscle spasm of the vermiform process, caused by any of
pathologic process and proved by pain in the right iliac area. A surgeon makes this diagnosis in those
cases, when clinical manifestations disappear quickly, or when at the time of operation he does not see
any inflammatory changes in the vermiform process.
Catarrhal (congestive) appendicitis. Exudate may be absent or it may be in very small amount. It
is transparent, odorless. The peritoneum is unchanged and is hyperemic a little. All changes are strictly
localized in the vermiform process. It is hyperemic along the whole length or at the limited site (usually
distal one), thick to the touch, slightly edematous. The lumen of the process may be either empty, or
may contain mucus, impacted feces, and foreign bodies. The mesentery is not changed, or may be
slightly edematous and hyperemic one. Microscopically: leukocyte infiltrations in the impaired sites of
the process. Sometimes it is possible to find out a defect of the mucous membrane (primary affect),
which is covered with fibrin and cellular elements.
Phlegmonous appendicitis. Exudate may be serous, serofibrous, seropurulent one. Fetid odor
appears at perforation of the vermiform appendix. In most of cases it is possible to speak about the local
peritonitis, but in advanced cases, when the process is not delimited, but the amount of exudates is
considerable and it baths the large sites of the abdominal cavity, it is possible to consider diffuse and
even general peritonitis. The omentum, the caecum, and adjacent loops of the small intestine may be
also involved in the pathologic process. They are hyperemic, thickened, are covered with fibropurulent
deposit and are fused by loose adhesions. The vermiform appendix is considerably enlarged in its sizes,
is of dark red color, strained is covered with mucous fibrin. The sites of white-yellowish pus may be
often seen through the transparent serous coat. Pus, which is inside the lumen of the organ, is gradually
stretching it, and empyema is formed. The mesentery is thickened, its leaves are hyperemic and
edematous, may be easily treated. Similar changes are frequently observed in the caecum cupola wall
and considerably complicate appendectomy. On microscopic examination it is possible to reveal
leukocyte infiltration of all the layers of the vermiform process; it is impossible to differentiate them due
to their saturation with pus. Apostematous appendicitis takes place in case of appearance of multiple
abscesses against a background of diffuse purulent inflammation of appendix. In case of ulceration of
the mucous membrane against a background of phlegmonous appendicitis, phlegmonous-ulcerative
appendicitis occurs.
Gangrenous appendicitis. Abdominal changes are similar to phlegmonous appendicitis, but they
are more pronounced. Exudate is turbid, with ichorous purulent odor. The vermiform process is partly or
completely of black, brown, brown-green, black-brown, or dirty-gray color. Its wall is flabby with
phlegmonous masses. Gangrenous appendicitis is frequently perforating one, and then it is possible to
see fetid feces pouring through the opening in its wall inside the abdominal cavity. As a rule, peritonitis
occurs. It may be local, diffuse, or general, but according to the nature of microflora, colibacillary,
anaerobic, and mixed types are distinguished. Extensive necrotic foci with bacteria colonies,
hemorrhages, and vascular thrombosis may be revealed on microscopic investigation. Somewhere it is
possible to see the foci of phlegmonous inflammation. The mucous membrane is ulcerated all along. As
a rule, destructive changes are pronounced up to perforation in the distal part of the organ.
Generalization of infection in a form of endotoxic shock occur in gangrenous appendicitis more
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frequently than in other forms of inflammation.

Appendicular infiltrate is one of the complications of acute appendicitis. The vermiform
appendix, being destructively changed, becomes an epicenter of adhesion process. A conglomerate of
chaotically fused neighboring organs and tissues is formed around it. The greater omentum, loops of the
small intestine, the caecum and ascending intestine, the peritoneum become involved in the pathologic
process. The wall of these organs are subjected to inflammatory infiltration, the boundaries between
them become gradually lost. Infiltrate rapidly increases in sizes, being compactly connected to the
anterior, posterior, and lateral walls of the abdomen. Sometimes infiltrate is of vast sizes, occupying the
whole right side of the abdomen.

Classification
But there are two classifications, which are used by the present and make it easier to choose the
policy of treatment. They are the classification according to A.I. Abrikosov (1946), in which he wanted
to reflect the problems of acute appendicitis pathologic anatomy, and the classification according to V.I.
Kolesov (1959), where he tried to reflect clinical forms of acute appendicitis and its complications.

Classification according to A.I. Abrikosov:

I Superficial appendicitis (primary affect);
II Phlegmonous appendicitis:
1) simple phlegmonous appendicitis;
2) ulcer phlegmonous appendicitis;
3) apostematous appendicitis;
a) with perforation;
b) without perforation;
c) empyema of the vermiform appendix;
III Gangrenous appendicitis:
1)primary gangrenous appendicitis;
a) with perforation;
b) without perforation;
2) secondary gangrenous appendicitis:
a) with perforation;
b) without perforation.

Classification according to V.I. Kolesov:

I. Acute simple (superficial) appendicitis;
A)Without general clinical signs, but with mild local, quickly disappearing, manifestations of the
disease.
B) With insignificant general clinical signs and local manifestations of the disease.
II. Destructive acute appendicitis (phlegmonous, gangrenous, perforating):
A)With clinical picture of moderate severity and the signs of local peritonitis;
B) With severe clinical picture and the signs of local peritonitis;
III. Complicated appendicitis:
A) With appendicular infiltrate;
B) With appendicular abscess;
C) With diffuse peritonitis.

The Main Principles of Medical Aid in Acute Appendices

1) On suspicion of acute appendicitis the patient is subjected to urgent hospitalization to the surgical
unit, he is to be under constant medical care and to undergo additional examination.
2) Recognized acute appendicitis requires an urgent surgical invention, irrespective to manifestation of
clinical picture, the age of a patient, duration of the disease (with the exception of delimited infiltrates).
3) In vague cases, in the presence of suspicion of acute appendicitis, it is necessary to perform
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laparoscopy or explorative laparotomy.

4) In the absence of changes in the vermiform appendix during the operation, or in case of not
corresponding of revealed changes with clinical picture, it is necessary to perform revision of the
abdominal cavity.

Clinical Picture, Diagnostics, and Treatment

Acute appendicitis is characterized by variety of clinical manifestations. I.I. Grekov figuratively
called it "a chameleon-like disease", and Y.Y. Dzhanelidze called it as insidious one. Almost all the
symptoms of acute appendicitis are non-specific, i.e. occur in many other abdominal diseases. That is
why the symptom is not important by itself, but its characteristics, combination with other symptoms
and the consequence of its appearance are very important in diagnostics. One and the same symptom at
different stages of the disease and at different forms of it has its own features.
There are three main forms of acute appendicitis: 1) early stage (up to 12 hours); 2) stage of
development of destructive changes in the vermiform appendix (from 12 to 48 hours); 3) stage of
complications (48 hours and more). This division at stages is rather relative one, and the disease may run
by its own, much more transient scenario, however, more frequently it proceeds exactly in such a way.
Pain is the first and most common symptom of acute appendicitis. It occurs predominantly at
night, becomes constant, gradually intensifying. Patients may characterize pain as piercing, cutting,
burning, dull, acute one. At the first stage of the disease the intensity of pain is not significant, it is quite
tolerable. Patients do not cry or moan, but also do not show superfluous motive activity, as jerky
movements of the body, for example, at cough (the cough shock symptom) intensify the pain. Cramping
pain occur very rarely.
Localization of pain is different. In typical cases it is localized at once in the right iliac area, but it
also may not be localized, but spreading all over the abdomen. Approximately in a half of patients it
locates at first it the epigastric area (Kocher — Volkovich's sign), and only in 1-2 hours descends to the
right iliac area. Sometimes this symptom lasts for more prolonged time, and it considerably hampers
differential diagnosis. At the second stage of the disease, on developing of destructive changes in the
vermiform process, pain increases, causing the patients to suffer. The most severe pain is in empyema,
when pressure increases in the lumen of the vermiform process. In those cases the patients rush about,
they could not find a place for themselves. On the background of constant pain a patient suddenly feels
the increase of pain — perforating symptom. But paradoxical reaction is rather frequent too, when
during the process of destruction pains subside up to their complete disappearance; this is associated
with gangrene of the vermiform appendix wall. Discrepancy of severe condition of the patient and
clinical picture is evident. At the third stage clinical picture of either appendicular infiltrate or abscess or
peritonitis is revealed.
Pain may radiate to different parts of the abdomen: to the umbilicus, to the epigastric area, and to
the loin. It depends on position of the caecum and the vermiform process.
Nausea and vomiting is observed in 60 -80% of patients (V.I. Kolesov, 1972). Nausea usually
precedes vomiting, but sometimes it may be an independent symptom. It is important that these
symptoms do not ever precede pains, but arises during the first or the second hour of the disease. At the
first stage vomiting is of reflex nature, with mucous and eaten food. At the second and third stages
vomiting occurs again, but now its frequency and nature depend predominantly upon expressiveness of
peritonitis, intoxication and developing dynamic (paralytic) intestinal insufficiency.
Gas and stools retention. They are immutable concomitants of acute appendicitis. At the first
stage of the disease retention of gas and stools occurs as physiologic, reflex reaction to outside
stimulants, but later it results from paralytic ileus in peritonitis. Loose stools is rather infrequent, it may
be observed mainly in children in case of spreading of inflammatory process on the sigmoid colon or the
large intestine. In case of pelvic location of the vermiform appendix and its contiguity with the urinary
bladder wall disuric disturbances are possible.
At the onset of the disease temperature averages 37-38°C. Pulse rate corresponds to the
temperature-80 -100 beats per minute. Only in destructive forms of appendicitis temperature may be
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38,5-39°C, but tachycardia becomes 130 -140 beats per minute. Thermometer readings under the armpit
and into the rectum are to be compared because of certain diagnostic importance. Revealing of
considerable difference (over 1/5°C) objectively testifies an acute pathology in the abdomen.
Examination of the abdomen. At an onset of the disease the abdomen usually of normal form,
moves with breathing, symmetrical. In lean patients it is possible to notice the lag of the right side of the
abdomen in respiratory movements due to muscular strain (Ivanov's symptom). In perforating of the
vermiform appendix the respiratory movements of the anterior abdominal wall disappear. In a man of
athletic type it is possible to notice the relief of strained abdominal muscles. Abdominal distention is the
late symptom. It testifies the development of peritonitis. Muscular tension (defanse musculare) is the
main symptom in acute appendicitis. In severe cases the site of the most tenderness and local tension of
the abdominal wall is in the right iliac area; the degree of the muscular tension increases in accordance
with intensity of the inflammatory process inside the peritoneum. Revealing of the symptom requires a
certain experience. Infrequently the patient strains the abdominal wall by himself, preventing the pain,
especially if the investigation is carried out unskillfully and crudely. At the first stage of the disease the
muscular tension may be absent. It may be frequently observed in elder and senile persons and in
women with flabby and dilated abdominal wall, who had experienced labors many times, and also at
retrocaecal, retroperitoneal and pelvic localization of the vermiform appendix.
Deep palpation of the most painful area is not expedient. It rarely gives additional information, as
it is usually prevented by muscular protection. But at soft abdomen deep palpation allows to diagnose
appendicular infiltrate, to determine its size and bounds, consistency, mobility. Sometimes it is possible
to feel the caecum, area of which is always painful in case of acute appendicitis. But it is almost
impossible to feel the vermiform appendix, and it is not necessary. Revealing of painful points
(McBurney's point, points of Lanz and Kummel) is not of great diagnostic value. In acute appendicitis
tenderness of the abdomen is rarely strictly localized. Blumberg's sign (guarding symptom) is a rebound
tenderness symptom. Already at the early stage of acute appendicitis, at mild catarrhal inflammation of
the parietal peritoneum it is usually positive. The following may check it. The tips of the fingers are
introduced very gently and gradually into the anterior abdominal wall, pressing it inside the abdomen.
Then the arm is abruptly taken away. In positive reaction the patient notes the increase of pain,
sometimes he shrivels and utters a scream.
Percussion of the abdomen allows to localize the area of the greatest tenderness more precisely
(Razdolsky's (abductor of femur sign). These are also rebound tenderness symptoms. A slight
percussion of the abdominal wall at its different sites is enough to determine this symptom. By means of
percussion, being oriented on the dullness of the percussion sound it is easy to estimate the bounds of
appendicular infiltrate, and in peritonitis — the presence of fluid in sloping places of the abdomen.
Auscultation of the abdomen allows to estimate the intestinal peristalsis. Already at an early stage
of the disease it is weakened, but survives for a long time. The absence of peristalsis is a threatening
symptom of peritonitis.
Appendicular symptoms. More than 100 symptoms of appendicitis had been already described.
We shall settle on only on some of them, which are the most pathognomonic, and gained popularity
among the surgeons.
Sitkovsky's sign. A patient is asked to turn on his left side. If at that the pain in the right iliac
region arises, the symptom will be considered to be positive one.
Bartomye's symptom is checked as Sitkovsky's one, but at the same time palpation of the right
iliac region is performed. At positive symptom palpatory tenderness increases.
Rovsing's symptom. In dorsal position of a patient, a surgeon presses the sigmoid colon to the
posterior abdominal wall with the fingertips of the left arm and fixes it. Simultaneously, a little above,
by means of balloting palpation, he shakes the abdominal wall in the sigmoid area. The onset of pain in
the right half of the abdomen is the evidence of a positive symptom.
Voskresensky's symptom. A shirt or T-shirt of a patient is tightened with the left arm and fixed
at the pubis. By fingertips of the right arm a surgeon slightly presses to the abdominal wall in the area of
the xiphisternum, and at time of expiration performs a quick uniform sliding motion at first towards the
left iliac-inguinal region, and then to the right one, but for all that the arm is held on the abdominal wall.
 9

In the presence of positive symptom a patient feels pain in the right side.
It is also necessary to remember some other appendicular symptoms, such as Corn's, Britten's,
Chugaev's, Cope's, Dumbadze's, Rizvash's, Gabay's, Yaure-Rozanov's, Punin's, Bulynin's, and
Promptov's symptoms.

Laboratory Diagnosis
Moderate leukocytosis is noted at an early stage of the disease. In catarrhal form of inflammation
it is from 10xl09/l to 12xl09 /I, in destructive forms it achieves 14xl09/l-18xl09/l, but sometimes it may
be even higher, It is dangerous when neutrophilic shift of differential blood count to the left takes place.
The increase of stab neutrophil up to 10-16% and appearance of juvenile forms is the evidence of high
degree intoxication.
Laboratory investigations of the blood may be widened by examination of C-reactive blood
protein (C-RP), phagocyte activity of neutrophils, investigation of alkaline phosphatase, peroxides,
oxidase, and cytochrome oxidase. However, non-specific character and considerable labor-consuming
nature of these reactions decreases their diagnostic value in urgent surgery. Urinary tests reveal
pathologic changes in severe intoxication and peritonitis.
In uncertain diagnosis of acute appendicitis, laparoscopy is of particular value; approximately in
90% of cases it puts an end to doubt in diagnosis. Especially often the necessity of laparoscopy occurs at
differential diagnosis with genital diseases and renal colic.
Complications in Acute Appendicitis
Appendicular infiltrate occurs in 0.9-2.9% of patients, who had been hospitalized in 48 hours and
later from the onset of the disease with evident prevalence of elder and senile patients.
Morphologic and clinical essence of infiltrate consists in the inflammatory focus in the vermiform
appendix is delimited from the free abdomen by the omentum, and the adjacent tissues and organs,
which are also involved in the inflammatory process, united into one conglomerate, which is connected
with the anterior, posterior or lateral abdominal wall.
The size of infiltrate may be different, from small one, with the size of a fist, to the giant one,
occupying the whole right side of the abdomen. The boundaries of infiltrate, as a rule, are distinct; their
mobility is usually limited.
As a whole, it takes about 2-5 days to form appendicular infiltrate; during this period it passes
several stages (A.I. Krakovsky and co-authors, 1986):

1 . Loose infiltrate. In typical cases it is located in front of the caecum, with mild peritoneal response,
purulent exudate in the small pelvis, with involvement of the caecum, phlegmonous or gangrenous
appendicitis, omentum, and the loops of the small intestine;
2. Dense infiltrate, which can be either resolved or form an abscess;
3. Periappendicular abscess.
Infrequently diagnosis is difficult. Before surgery it is possible to make a correct diagnosis only in
a half of patients. Sometimes there are quite forcible arguments, foe example, atypical position of the
vermiform appendix and, accordingly, of infiltrate in the small pelvis or behind the caecum; excessive
obesity of patients with abundant layer of fatty tissue; impossibility of deep palpation due to acute
tenderness and protective muscular tension. Insufficiently careful and full-value investigation is the
common reason of diagnostic pitfall.
In typical cases the delimitation of the process in phlegmonous appendicitis without any signs of
perforation must coincide with gradual improvement of the patient's general condition and control of
acute manifestations. The pains gradually cease up to their complete disappearance. Pulse becomes
normal. Temperature decreases, but, however, remains stably sub febrile. Signs of dynamic intestinal
obstruction disappear rapidly.
Subsequent course of the disease may be different. Three variants are possible. The most
favorable one is resorbtion under the influence of conservative treatment. Usually it takes approximately
from 2 weeks to 1 month. The second variant is the most dangerous of all, when peritonitis progresses
 10

simultaneously with the process of infiltrate formation. And, finally, the third variant — infiltrate
abscess formation, when in the presence of obviously localized process, clinical manifestations of
purulent septic process are evident: increase of pain in the infiltrate area, hectic fever with chills, and
intoxication.

General Appendicular Peritonitis

Difficulties and dangers of acute appendicitis at common appendicular peritonitis reach the
apogee. Incidence of this complication averages from 0,6 to 4,1%. It is necessary to note, that among the
causes of common peritonitis acute appendicitis takes the first position, achieving 50-55% (A.A.
Shalimov, 1990). Clinical picture, diagnosis and treatment of common peritonitis are expounded in the
appropriate lecture.

Pilephlebitis
Purulent trombophlebitis in the region of the superior mesenteric or portal vein is one of the most
severe complications of acute appendicitis. It occurs rather seldom, in 0,06-1,5% of cases from general
number of patients with this disease. The course of the disease is exclusively severe; with fatal outcome
in most cases. In 1986 V.S. Savelyev advanced the opinion that there were no reliable observations of
pilephlebitis. Information of N.V. Karamanov about successful treatment of 11 patients with
pilephlebitis seems to be more optimistic. Timeliness diagnostics is a guarantee of success. Appearance
on the background acute appendicitis clinical picture such symptoms as chill, hectic fever, pain in the
right hypochondrium, jaundice, etc., including laboratory data, proving severe intoxication, must put a
surgeon on his guard.
Treatment of Acute Appendicitis
Treatment is only operative; there is no choice. Delay of operation is dangerous by impetuous
course of the process and development of the severest complications. The only contraindication for
operation is the presence of dense appendicular infiltrate but only in those cases when there is no signs
of abscess formation and peritonitis.
Being dependable on clinical situation, the operation may be performed both under local and
general anesthesia. General anesthesia is preferable. Three main approaches to the vermiform appendix
are used: oblique (Volkovich-Dyakonov's), Lenander's (pararectal) incisions, and midline laparotomy.
In all cases of acute appendicitis with strictly localized clinical picture in the right iliac fossa an
oblique incision is applied. At typical position of the caecum and in other positions of the vermiform
appendix, optimal conditions are produced due to this incision.
Pararectal Lenander's incision is applied in case of vague diagnosis. It may be rapidly elongated
up and downwards. But in case of retrocaecal position of the appendix and at local periappendicular
abscesses Leander’s incision is not so suitable.
Mid-midline or low-midline laparotomy is applied in the presence of clinical signs of diffuse and
general peritonitis.
Operation technique for appendectomy is identical on principle in various forms of inflammation
of the vermiform appendix, but each of them introduces its own features and a number of additional
tricks in performance of operation. In catarrhal appendicitis before performance of operation it is
necessary to make certain that visible morphological changes correspond to clinical picture of the
disease and are not the secondary ones. In phlegmonous appendicitis, having evacuated the exudates
from the right iliac fossa, it is necessary to determine that the process inside the abdomen is localized;
for this purpose the surgeon examines the right lateral canal, right mesenteric sinus and cavity of the
small pelvis by means of a swab. If muddy exudate appears from these spaces of the lower abdomen, it
is necessary to suggest diffuse or general peritonitis. At the beginning of operation for appendectomy of
gangrenous appendix it is necessary to delimit carefully the area of the iliocaecal angle from the other
portions of the abdominal cavity by means of wide gauze towels. In case of perforation, one should
thoroughly wrap the vermiform appendix with wet towel, avoiding the appearance of intestinal content
inside the abdominal cavity. Operation in conditions of appendicular infiltrate is fraught with many
 11

dangers. In such a case it is necessary to exhibit a particular wisdom. It is on these conditions that
excessive activity of the surgeon may result in a number of serious complications and in the growth of
lethality (diffuse peritonitis, sepsis, intestinal fistula, thromboembolism, bleedings).
Retrograde appendectomy is performed in those cases, when it becomes impossible to draw out
both the caecum and appendix into the wound due to adhesions and inflammatory infiltration.
Ligation of the mesentery applying a purse-string suture and treatment of the appendicle stump
are the most important stages of appendectomy. It is prohibited to be in hurry. Everything must be done
carefully and safely. It is these stages of operation that may result in such complications as postoperative
abdominal hemorrhages, postoperative peritonitis, intestinal fistula, abdominal abscess, etc.
 12

ACUTE CHOLECYSTITIS

For the recent years in many countries of the world there is noted a considerable growth
of the bile-excreting system diseases, and, first of all, the diseases of the gallbladder. It is
explained by the fact, that life span had increased, and cholelithiasis declares itself mainly in
middle and elderly age. Besides that, consumption of animal protein rich of cholesterol is a
well-known fact. Gallstones are found in 15-20% of population, moreover, in 8% of cases they
cause to death. 25% of people over 60 and 30% of people over 70 have gallstones. The given
statistical data indicate the urgency of the problems of etiology, pathogenesis, diagnosis and
treatment of cholelithiasis and acute cholecystitis.
Both cholelithiasis and cholecystitis are closely related. When speaking of cholecystitis,
we mean the presence of inflammation in the gallbladder, either acute or chronic, regardless of
presence or absence of concrements in it. When speaking of cholelithiasis, we mean the disease
of the gallbladder, which had developed in the presence of calculi, which stimulated the
development of the disease itself. In the most cases calculi preceded the inflammatory process in
the gallbladder; if they had been there, they only paved the way for occurrence of infection.
In the most cases the clinical picture is identical both in the presence and absence of
calculi in the gallbladder. Similarity of symptoms of cholelithiasis and acalculous cholecystitis
allows analyzing problems of their clinical picture.

Brief Anatomy-Physiological Sketch Review

Anatomy of the gallbladder and bile ducts is variable. Classical anatomy of the bile-
excreting ducts is found only in 50% of cases.
The left and right hepatic ducts form the common hepatic duct at the point of their exit
out of lobes of the liver (with the length of about 3-4 cm). The common hepatic and cystic
duct form the common bile duct (with the length of 8-10 cm, and 3-10 mm in diameter). The
common bile duct is located laterally in respect to the common hepatic artery and forwards the
portal vein. The common bile duct has 4 portions: supraduodenal (from the point of confluence
of the common hepatic duct with the cyst duct to the external margin of the duodenum);
retroduodenal (from the external margin of the duodenum to the head of the pancreas);
pancreatic (which goes behind the head of the pancreas or its parenchyma); intramural (which
goes inside the duodenum). The duct opens into the duodenum on a Vater's papilla.
Here are the variants of junction of the bile and pancreatic ducts:
• they come to the duodenum as a common duct;
• the ducts are united inside the wall of the duodenum;
• the common bile and pancreatic ducts flow into the duodenum separately.
Oddi's sphincter of the common bile duct is located at the point of passage of the duct
through the ampula of the Vater's papilla; it regulates entry of bile into the duodenum.
Blood supply of the intrahepatic ducts is carried out directly from the hepatic ducts; blood
supply of the supraduodenal portion of the common bile duct is variable. In the most cases it is
directed from the hilus of the liver.
The gallbladder is in the vesical fossa on the lower surface of the liver. It is a landmark of
the border of the right lobe of the liver. There are several anatomical structures, which may be
distinguished in the gallbladder: gallbladder bottom (fundus of gallbladder), body of
gallbladder, Hartman's pouch, which is located between the gallbladder neck and body of
gallbladder (the portion of the gallbladder, located backwards) and the neck, which goes into the
cystic duct.
The arterial blood comes to the gallbladder through the cystic artery - one of the
branches of the right hepatic artery (infrequently through the proper hepatic artery), venous
outflow from the gallbladder takes place mainly through the cystic vein, which flows into the
 13

portal vein.
From the gallbladder lymph flows out both to the liver and to the lymph nodes of the liver
hilus.
The cystic duct, common hepatic duct and cystic artery form Calot's triangle. Biliary
tracts have sphincters, which regulate bile secretion: Lutkens' sphincter, which is in the
gallbladder neck; Mirizi's sphincter, which is in the point of fusion of the cystic and common bile
ducts. The branches of the celiac plexus innervate the gallbladder. Hanster's valves represent the
folds of the mucous membrane of the cystic duct, though they do not act as valves.
Secretion of bile in the liver. The vagus and celiac nerves, secretin, theophyllin,
phenobarbital, and steroid hormones stimulate bile secretion. Approximately 600 ml of bile
(250-1000 ml/per day) is secreted daily.
Composition of bile:
1) water and electrolytes;
2) bile pigment;
3) protein;
4) lipids (phospholipids, cholesterol, bile acids and their salts).
Functions of the gallbladder:
1) deposition of bile;
2) concentration of bile:
a) absorption of water and electrolytes by the mucous membrane of the gallbladder results
in 10-times increase of fats, salts, bile acids and bile pigment;
b) secretion of mucous, which prevents the mucous membrane from irritant action of bile
and makes easier its passage through the cystic duct.
3) bile flow:
a) evacuation of bile to the duodenum is the result of simultaneous contraction of the
gallbladder and Oddi's sphincter;
b) bile flow to the duodenum occurs mainly under the control of humoral factor
(cholecystokinin, in particular); neurohumoral regulation is accomplished by the vagus
and celiac nerves.

Cholecystitis
Cholecystitis is an inflammation of the gallbladder. In 85-95% of cases it arises in
patients with cholelithiasis. There may be another causes of the disease — cholestasis, bacterial
infection, and thrombosis of the cystic artery. Bacteria can invade the gallbladder from the
bowel, lymph and blood.
Chronic cholecystitis is a condition with recurrent subacute symptoms.

Clinical Picture
Mild periodical pains in the right hypochondrium and in the epigastric area radiating to
the right scapula; nausea; vomiting; heartburn; bitter eructation. Frequently symptoms arise
after eating of fat, fried or spicy food, possessing choleretic action.

Diagnosis
Laboratory findings in patients with chronic cholecystitis are within the normal limits.
Excretory cholecystography and ultrasound investigation are helpful in diagnostics.

Treatment
Treatment is surgical (cholecystectomy). At present 80-90% of operations it is
laparoscopic cholecystectomy.

Results
The disease regresses in 75% of patients. In 25% of patients residual symptoms of the
 14

disease are observed.

Acute Calculous Cholecystitis Etiology

In 90-95% of cases acute cholecystitis develops in obstruction of the gallbladder neck or
cystic duct with a calculus. Direct compression of the mucous membrane by a calculus results
in ischemia, necrosis of the mucous membrane and disturbances in venous outflow. Later
neutrophilic infiltration caused by a small amount of bacteria, which are inside the gallbladder,
occurs. Bacterial infection may also result in inflammation. According to clinic and pathologic
signs acute cholecystitis may be divided into:
- Acute catarrhal cholecystitis.
- Acute phlegmonous cholecystitis.
- Acute gangrenous cholecystitis.

Pathomorphology
1. Acute catarrhal cholecystitis is an inflammation, which is limited by the mucous and
submucous membranes.
2. Acute phlegmonous cholecystitis is a suppurative inflammation with infiltration of all layers
of the gallbladder wall. Ulceration of the mucous membrane with the subsequent exudation of
exudates into the paravesical space is possible.
3. Acute gangrenous cholecystitis is a partial or total necrosis of the gallbladder wall. In case of
perforation of the gallbladder wall the bile flows into the abdomen (gangrenous-perforative
cholecystitis). Gallbladder empyema is a suppurative inflammation of the gallbladder.

Clinical Picture
The age of patients is from 30 to 80. Women suffer more frequently. Most of the patients
have chronic cholecystitis in their past history. Attack of acute cholecystitis begins from colicky
pain in the right hypochondrium or in the epigastric region with possible radiation to the back
lower the angle of the right scapula.
Inflammation of the gallbladder is characterized by the following symptoms:
Murphy’s symptom — involuntary breath-holding during inspiration when pressing on
the right hypochondrium area;
Kerr's symptom — tenderness on palpation in the right hypochondrium, which
increases severely during inspiration;
Ortner's symptom — pain in knocking with the hand along the costal margin;
Mussy-Georgievsky's symptom (phrenicus symptom) — tenderness on pressing on the
Mussi's point (it is located between the cruses of the sternocleidomastoid muscle projections
onto the skin);
Local Blumberg's sign.
Leukocytosis, the increase of temperature, nausea, vomiting, retention of stool and gases
are possible. Jaundice develops in 20 % of patients. Rebound tenderness symptom is positive
more frequently in phlegmonous and gangrenous cholecystitis.

Differential Diagnosis
Differential diagnostics should be made against the following diseases:
• perforated or penetrating ulcer of the stomach or duodenum;
• myocardial infarction;
• pancreatitis;
• hiatus hernia;
• right-side pneumonia of the lower lobe;
• appendicitis;
• hepatitis;
 15

• infectious diseases.

Diagnosis
Diagnosis is suggested in the presence of characteristic clinical picture, especially in
patients with cholelithiasis.
1. Clinical and biochemical analyses of blood: high serum alkaline phosphatase is noted in 23%
of patients with acute cholecystitis, hyperbilirubinemia in 45%, AST in 40%, and amylase in
13%.
2. Ultrasonic investigation of the gallbladder reveals the presence of gallstones, allows
determining the sizes of the organ and its wall thickness, the presence of paravesical infiltrate
and consistency of the gallbladder contents.
3. Radiography is of low value. The most of gallstones are nonopaque and consist of
cholesterol; 10-15% of gallstones contain sufficient amount of calcium to be contrasted.
4. Radioisotope scanning. The absence of gallbladder visualization following intravenous
injection of iminodiacetic acid supposes obstruction of the cystic duct.
5. ECG and radiography of the chest for differential diagnostics.

Treatment
Cholecystectomy is indicated. Operations are distinguished by the term of performance.
Emergency operations are performed during 72 hours from the onset of the disease. Postponed
operations are carried out approximately in 6 weeks following the conservative treatment of
acute inflammatory signs (antibacterial, desintoxication infusion therapy). Early surgical
treatment of acute cholecystitis is preferable. Patients with acute cholecystitis complicated by
peritonitis are subjected to urgent operation. Emergency operation (1-2 days of observation and
conservative treatment) is performed in patients with lasting symptomatic on the background of
conservative treatment. Planned operation is carried out in case of effective conservative
treatment of acute cholecystitis attack.
Conservative treatment of acute cholecystitis includes the bed regimen, diet (water and
tea load), spasmolytics, and infusion therapy with the purpose of elimination of intoxication and
inflammation, water-electrolytic and power losses, bilateral paranephral block according to
Vishnevsky, and antibacterial therapy. Complications of acute cholecystitis require urgent
surgical treatment.
Emphysematous cholecystitis develops under the influence of metabolites of gas-
producing bacteria. Emphysematous cholecystitis afflicts men more frequently than women.
Diabetes mellitus is revealed in 20-30% of patients. Gas in the gallbladder is revealed
radiologically; communication between the gallbladder and gastrointestinal tract is absent.
Treatment of acute cholecystitis consists of early cholecystectomy, indication of antibiotics,
which act selectively on anaerobic microorganisms.
Obturative cholecystitis causes wedging-in of a concrements into the orifice of the
cystic duct. At first there is hydrops of gallbladder — accumulation of the serous fluid in its
lumen — develops. Then empyema — infection with development of acute purulent
inflammation of the gallbladder — occurs. Intoxication and high risk of perforation are
characteristic.
Gangrenous cholecystitis arises on the background of cystic artery thrombosis and
results in necrosis of the gallbladder. Antibacterial therapy with taking into consideration
susceptibility of bile microflora is necessary. Operation for gangrenous cholecystitis is
cholecystectomy.
Perforative cholecystitis occurs in case of necrosis of the gallbladder wall. Local
perforation appears during the period from several days till one week from the onset of acute
cholecystitis and results in paravesical abscess. Free perforation with bile outflow into the
subhepatic space results in development of general (diffuse) peritonitis with lethal outcome in
25% of cases; it appears at early stages of clinical course of the disease. Perforation into'
 16

adjacent organ — the duodenum, jejunum, colon or stomach — with formation of internal fistula
is possible. Passage of a big gallstone into the lumen of the intestine may cause intestinal
obstruction.
Cholecystectomy. In the absence of pronounced inflammation the cystic artery and cystic
duct are exposed, ligated and dissected at the beginning of the operation (cholecystectomy from
the neck). On performance of cholecystectomy from the bottom the artery and the duct are
transected after separation of the gallbladder from the liver.
Radiography of the common bile duct through the cystic duct with contrast study
(intraoperative cholangiography is made in suggestion for migration of gallstones into the
common bile duct or in case of impairment of its potency of other etiology. Cholecystectomy
may be performed by traditional or laparoscopic technique.
Cholecystostomy is the method of choice in treatment of patients with severe somatic
diseases of cardio-vascular and respiratory systems at decompensation stage. It is performed in
pronounced inflammatory process and in the presence of obstructive jaundice for biliar
decompression. The gallbladder bottom is opened, and bile with gallstones is evacuated. A probe
for evacuation of infected bile is introduced into the gallbladder. In laparoscopic
cholecystostomy puncture drainage is applied.
 17

ACUTE PANCREATITIS

The term "acute pancreatitis", as it agreed by S. V. Lobachov, G.M. Mazhdrakov and

some other authors, is in a certain sense a conditional concept, as not all morphological changes,
which take place in the pancreas in case of acute pancreatitis, correspond to generally accepted
manifestations of inflammatory process. In acute pancreatitis there not only the symptoms of
acute inflammation in the pancreas are present, but there are also the signs of hemorrhages and
necrotic processes, which are stipulated by auto-digestion of the glandular tissue by pancreatic
enzymes.

Etiology
The main factors causing the development of acute pancreatitis are:
• bile and digestive-pancreatic reflux;
• obstruction and hypertension of the biliar ducts;
• blood supply disturbance of the pancreas;
• allergic and infectious processes.
Theory of bile reflux into the biliary duct (E. Opie, 1901). Regurgitation of bile into the
system of the pancreatic ducts increases the intraductal pressure, which results in destruction of
the glandular cells. Z. Dragstedt had approved, that the cells of impaired parenchyma of the
gland, under the influence of the bile, secrete cytokynase, which has a destructive effect on the
tissues of the pancreas.
Theory of hypertension of the pancreatic duct (A. Rich, G. Duff, 1936). The authors
had approved, that the increase of pressure in the duct system of the pancreas results in rupture
of its acinoses and small ducts and leads to the damage of cells. As a result, cytokynase is
eliminated. Self-activation of enzymes and autodigestion of the glandular cells take place.
Blood supply disturbance of the pancreas (I.G. Rufanov, 1925; V.M. Voskresensky,
1951). Arterial blood supply disturbance of the pancreas may provoke acute pancreatitis. It may
be proved by the fact that edema and necrosis of the pancreas infrequently occurs in elderly and
obese patients, who suffer from extensive atherosclerosis.
Allergic theory. Role of allergy in development of acute edema and hemorrhagic necrosis
of the pancreas is noted by many authors (R. Gregroire, R. Couvelaire, 1937; P.D. Solovov,
1940; O.S. Kochnev, 1958). Abrupt course of its symptoms, rapid development of edema and
necrosis of the glandular tissue with subsequent development of shock phenomena and
infrequently appeared eosinophilia testify possible allergic nature of acute pancreatitis. The
allergic character of pathologic changes in acute pancreatitis is confirmed morphologically by
hemorrhagic nature of inflammation and the presence of fibrin thrombus in the pancreatic
vessels.
Role of infection in development of acute pancreatitis is confirmed by the fact, that acute
hemorrhagic pancreatitis may arise in acute inflammatory process in the gallbladder without
impairment of bile passage through the bile ducts, in acute parotitis, status typhosus and other
infectious diseases. Infection penetrates the pancreas through the blood and lymph vessels.
Thus, the essence of acute pancreatitis consists in that fact, that intracellular activation of
enzymes, which are produced by the pancreas with subsequent fermentative autolysis of acinar
cells with formation of necrotic foci with aseptic (bacterial) inflammation around them.
Infectious inflammation of the pancreas, as a rule, is a complication of pancreatonecrosis. It
develops at the latest stages of the disease due to microbial infection of necrosis.
Activation of enzymes inside the pancreas itself promotes: a) damage of acinar cells; b)
hypersecretion of the pancreatic layer; c) impediment of the pancreatic juice outflow with
development of acute hypertension inside the pancreatic ducts.
Damage of acinar cells may result from:
1) abdominal and pancreatic injury; 2) pancreas surgical intervention; 3) blood flow
 18

disturbance in the glandular tissue (thrombosis, embolism, ligation, etc); 4) exogenous

intoxication; 5) allergic reaction; 6) alimentary disorders.
2) Hypersecretion of the pancreas may be caused by:
1) alcohol abuse; 2) abundant, especially fatty food.
Difficulty in pancreatic blood outflow may be provoked by pathological processes,
localized in the area of excretory duct of pancreas, occlusion of ampula of the major duodenal
papilla with a gallstone, and edema of the duodenal mucous membrane in the area of the major
duodenal papilla.

Pathogenesis
The initial point of pathogenesis of acute pancreatitis is the process of activation of
proteolytic enzymes as a result of their interaction with cytokynase. In pathogenesis of acute
pancreatitis two stages are distinguished.
I. Tripsin stage.
Cytokynase activates tripsinogen, transforming it in tripsin. Tripsin activates tripsinogen
and chemotrypsinogen owing to cytokynase of digested tissues. Tripsin and tripsinogen affect
the interstitial tissue and vessels of the pancreas, which result in edema, stasis and hemorrhage.
In such conditions there is cell death and death of the glandular tissue and, accordingly, inflow
of cytokynase continue.
II. Lipase stage.
Salts of fatty acids activate lipase, which initiates the development of fat necrosis.
The presence of edema, hemorrhage and fat necrosis result in destruction of the pancreatic
tissue, extension of edema to surrounding tissues, to transudation of fluid into the abdominal
and pleural cavities, and sometimes into the pericardial cavity and into the retroperitoneal space.
Abdominal organs (peritonitis), organs of the retroperitoneal space (paranephritis) and
thoracic organs (pleurisy and pericarditis) are involved in the pathologic process. The so-called
pleurovisceral syndrome develops.
In the foci of fat necrosis binding of calcium by salts of fatty acids takes place, and by the
end of the 2-nd of 3-rd day hypocalcaemia may develop, which may be followed by tetany.
Progressive peritonitis with enteroparesis results in disturbance of water-electrolytic and
protein metabolism.
On the background of lipase stage of pancreatitis the conditions for development of
purulent pancreatitis are produced.
Thus, in acute pancreatitis the following "local" pathomorphological changes are noted:
1. Edema of the pancreas and surrounding tissues.
2. Fat necrosis.
3. Formation of hemorrhagic foci.
4. Necrosis of the pancreatic parenchyma.
5. Suppurative inflammation.
However, recently classification of acute pancreatitis adopted in 1992 in Atlanta is
introduced. According to this classification, acute pancreatitis is subdivided into the following
forms: edematic-interstitial, necrotic, pseudocyst of the pancreas, and abscess of the pancreas.
The following classification of acute pancreatitis, which underlay the form of pathologic process
at the period of progress of the disease, is proposed for estimation of a general state of a patient:
I. Clinical and anatomical forms:
• Edematous pancreatitis.
• Fatty pancreatitis.
• Hemorrhagic pancreatitis.
• Mixed pancreatitis.
II. Periods of the disease:
• The period of haemodynamic disturbances and pancreatogenic shock.
• The period of functional insufficiency of parenchimatous organs.
 19

• The period of degenerative suppurative complications.

III. Complications:
A. Toxic: pleural effusion (pancreatic lung), massive hepatic and kidney necrosis; erosive-
hemorrhagic gastritis; delirium; coma.
B. Necrotic and pancreatic: parapancreatic infiltration, abscess of the pancreas,
phlegmonous or apostematous pancreatitis, phlegmon of the retroperitoneal fat, pseudocyst of
the pancreas.
C. Visceral: External and internal fistula (pancreatic, biliar, gastric, intestinal,
pancreatobronchial, and pleural).
D. Arrosive hemorrhages.
E. Occlusive vascular impairments.

Clinical Picture
Clinical picture of acute pancreatitis depends on form of the pathologic process and stage
of the disease. Complaints of the patients with acute pancreatitis are reduced to description of
pain syndrome, clinical picture of dynamic intestinal obstruction, respiratory and cardiac
insufficiency. At late stages of the disease they are characterized by impaired function of basic
systems of the internal organs (pleurovisceral syndrome).
Pain in acute pancreatitis may be moderate in edematous form of pancreatitis and
unbearable in pancreonecrosis. It occurs most often after inaccuracy in diet. In most cases pain
appears suddenly, localizes in the epigastric area and along the projection of the pancreas.
In case, when pathologic process impairs the head of the pancreas, pain is usually localized
in the pit of the stomach or to the right of the median line of the abdomen. If body of the
pancreas is involved, pain is localized in epigastric area, and if the tail of pancreas is impaired, it
is felt in the left upper abdomen. In case of total impairment of the pancreas pain is felt through
the upper abdomen, infrequently it is girdle (Voskresensky-Lobachev's symptom).
Pain in acute pancreatitis may radiate to the lumbar area (Mayo-Robson's symptom), to
the right scapula (Mussi's symptom), to the left part of the chest.
The cause of pain in acute pancreatitis is compression of nerve plexuses, which are located
around the pancreas; they may occur in enlarged pancreas and in case when edema extends on
the parapancreatic fat.
Vomiting is a characteristic symptom of acute pancreatitis. It appears simultaneously with
pain or accompanies it, may be recurrent and persistent, and sometimes becomes uncontrollable.
Emesis contain mucous, food debris, and sometimes blood.
Some patients with acute pancreatitis note distention of abdomen and gas retention.
On examination of patients with acute pancreatitis patient's position in bed should be
taken into consideration. In mild and moderate clinical course the patients are active and quiet in
bed. In severe forms of pancreatitis during the attack of pain some patients are exited, toss in
bed, cry with pain, and others lie motionless with bending knees.
Body temperature in patients with acute pancreatitis either within normal limits, or sub
febrile one. In case of suppurative inflammation it may attain 38°C and higher.
When examining the skin integuments of patients with acute pancreatitis the following
may be revealed:
Mondor's symptom — violet spots on the body and face alternating with the sites of the
pale skin;
Halsted's symptom — cyanosis of skin of the abdomen;
Turner's symptom — cyanosis of the lateral surfaces of the abdomen and the lumbar
region;
Grunwald's symptom — petechial skin rash in the navel area.
Change in color of skin integuments is the result of dystonia of the skin vessels caused by
pain symptom, general hypoxia of tissues, raised number of histamine I blood.
The abdomen of the patient with acute pancreatitis may be distended. Intestinal peristalsis
 20

may be either increased, or sluggish. On percussion of the abdomen there may be revealed the
presence of fluid in the abdomen and clear percussion sound over the surface of the intestine.
Muscular tension is not defined on palpation. Even in peritonitis the degree of muscular tension
is insignificant. At the same time, its considerable regional tension in the epigastric area and
along the projection of pancreas (Korte's symptom) is pronounced on the background of
moderate general protective muscular tension. This symptom should be estimated as
visceromotor or axon-reflex.
On palpation of the abdomen in patients with acute pancreatitis there is pronounced skin
hyperesthesia, which area of location is associated with location of pathologic process in one or
another portion of the pancreas.
Deep palpation of the abdomen in the area of the pancreas reveals the absence of pulsation
of the abdominal aorta (Voskresensky's symptom). On palpation in the area of the left
costovertebral angle it is possible to establish the presence of rigidity or tenderness (Mayo-
Robson's symptom).
Laboratory diagnostics. Blood investigation is of great importance for diagnosis of acute
pancreatitis. In destructive forms ot acute pancreatitis in some patients hypochromic anemia is
revealed, though in abrupt fluid loss erythrocytosis may be noted in the first two days.
Leukocytosis is revealed in 60% of patients with acute pancreatitis. Deviation of the
differential count to the left due to increase of immature forms, lymphopenia, eonosinophilia,
and elevation of the erythrocyte sedimentation rate are characteristic.
Examination of urinary amylase (diastase) is of great practical importance. Increase of its
activity (over 128 units according to Volgemuth) is noted in 70% of patients. However, in case of
necrosis of the glandular tissue urinary amylase (diastase) is low.
In severe course of acute pancreatitis serum amylase, which count may be increased, should
be determined.
Estimation of serum potassium, sodium and especially calcium, blood sugar, total protein
fractions of blood allow to determine degree of severity of a patient's general state. As a rule, in
edematous form of acute pancreatitis and in fat necrosis hypercoagulation is observed, but in
hemorrhagic necrosis — hypocoagulation. Hyperfibrinogenemia and increased amount of C-
reactive blood protein are noted nearly always.
In pancreatonecrosis daily urine is decreased up to anuria. In urinalysis there revealed
proteinuria, microhaematuria and cylindruria.
Special methods of investigation. X-ray, CT, endoscopic examination
(gastoduodenoscopy and laparoscopy) is applied for diagnostics of acute pancreatitis.
X-ray examination does not give direct indications on affection of the pancreas, but only
reveals indirect signs, which may be helpful in diagnostics of acute pancreatitis. Indirect X-ray
signs of acute pancreatitis are the following: distension of the abdomen and the transverse colon,
sometimes the presence of air-fluid levels (Kloyberg’s cups) in the intestine, high position of the
left part of the diaphragm and the absence of well defined outlines of the left psoas muscle. In
isolated cases during the X-ray examination of the abdomen it is possible to reveal free fluid in
it.
Computer tomography is "a gold standard" in topical diagnostics and the most sensing
method of investigation in acute pancreatitis and its complications. It reveals the enlargement of
the pancreas, which shadow has well defined outlines edematous form of acute pancreatitis, but
in hemorrhagic, necrotic and suppurative pancreatitis the outlines of the pancreas become
blurred. By means of CT it is possible to reveal pancreatogenic abscesses and fluid masses in the
retroperitoneal space at early stage of the disease.
Ultrasonic tomography at present is the most rapid, available to all and rather reliable
special method of investigation, which allows to diagnose acute inflammatory process in the
pancreas.
Computer tomography and ultrasonic scanning of the pancreas allow distinguishing fluid
mass from dense inflammatory-necrotic masses, but do not give the possibility to determine the
 21

level of infection of the revealed cavity content. For differential diagnostics of sterile
pancreatonecrosis against its septic complications percutaneous puncture of discovered fluid
mass under the control of CT and US with subsequent immediate coloring of bio-substrate
according to Gram and bacteriologic investigation for determining the type of microbes and their
sensitivity to antibiotics is applied.
Gastroduodenoscopy reveals retro displacement of the pylorus and the posterior wall of
the stomach, hyperemia, edema and the presence of erosions of the mucous coat of the stomach
and the signs of gastroduodenitis and papillitis.
Laparoscopy is of great importance for diagnostics of acute pancreatitis, as it allows
diagnosing for sure the most severe form of the disease — pancreatonecrosis. Laparoscopic sign
of pancreatonecrosis is the presence of plaques of the fat tissue necrosis foci, which may be
located along the greater, and lesser omentum, gastrocolic ligament, on the peritoneum of the
anterior abdominal wall, the round ligament of the liver, and the transverse mesocolon.
In case of fat necrosis there may be revealed serous exudates in the abdominal wall;
amount of it may be different. On investigation of this exudates hyperactivity of pancreatic
enzymes may be found out.
Frequent sign of pancreatonecrosis is the serous impregnation of fatty tissue, the so-called
vitreous edema of fatty tissue.
In contrast to pancreatonecrosis, edematous pancreatitis does not have characteristic
laparoscopic signs, as pathologic process in this case does not exceed the bounds of the omental
bursa.

Treatment
Patients with acute pancreatitis have to be treated at the surgical unit only. Treatment mode
depends on intensity of clinical picture, severity of the patient's state, and data of laboratory and
instrumental investigation. Treatment of the seriously ill patients with pronounced toxemia is
necessary to carry out at the intensive care unit. As it is very difficult to eliminate the etiologic
factor during acute period of the disease, the main treatment of patients with acute peritonitis has
to be directed on different aspects of pathogenesis and include both conservative and surgical
methods of treatment.
Conservative treatment of acute pancreatitis consists of complex of measures directed
on:
1) elimination of pain;
2) decrease of exocrine function of the pancreas, and inactivation of enzymes;
3) infection prevention and fight against it.
Different types of novocaine blocks, which also have positive neurotrophic action, are used
for elimination of pain. Elimination of pain relieves the Oddy’s sphincter spasm, which results in
improvement of the pancreatic juice outflow. Besides that, the block promotes the decrease of
enzyme activity of the pancreas. Choice of type of novocaine block depends on localization of
pathologic process in the pancreas: The block of the round ligament of the liver is applied in
clolecystopancreatitis, left vagosympathetic block — in sterile form of acute pancreatitis,
bilateral paranephral block — in acute pancreatitis with marked signs of intestinal obstruction.
Intravenous injection of glucose-novocaine mixture (per 250 ml of 12% novocaine solution
and 5% glucose solution) is a good anesthetic.
To control the pain and to eliminate enteroparesis epidural anesthesia is widely used
nowadays.
To decrease the exocrine function of the pancreas a strict bed regimen, cold on the
abdomen, starvation, evacuation of gastric contents by means of a nasogastral tube is indicated.
The appliance of different preparations promotes the decrease of excretory function of the
pancreas.
Anticholinergic drugs, among which 1% atropine solution is used most frequently, are
widespread. Atropine blocks the endings of the vagus in the pancreas and inhibits the pancreatic
 22

secretion.
Preparations, which decrease the pancreatic secretion, include methylthiouracil, pentoxyl,
and azetazolamine. Recent years somatostatin and its synthetic analog ocreotid acetate
(sandostatin), which are the strongest inhibitors of basal and stimulated secretion of the pancreas,
stomach, and jejunum are used for decrease of pancreatic function.
Inhibition of excretory function of the pancreatic cells may be attained by appliance of
cytostatic drugs: 5-fluorouracil, cyclophosphane, and fluorofur. Action of these drugs is more
effective on their introduction through celiac trunk following its catheterization according to
Seldinger-Odman. It allows to taper a dose of the drug and to establish its high concentration in
the glandular tissue. The appliance of cytostatic drugs is indicated in destructive pancreatitis. In
case of total pancreatonecrosis and in suppurative complications of pancreatitis and hepato-renal
insufficiency their administration is unpractical.
Local hypothermia of the pancreas, which may be performed by continuous gastric lavage
with cold water or by means of special cooling apparatus, has a suppressive influence on the
excretory function of the pancreas.
Antienzym drugs, such as trasilol, gordox, contrical, zimophren, etc. are indicated to
inactivate pancreatic enzymes. Antienzym action is achieved by intravenous injection of fresh
frozen plasma (FFP) and albumin.
Elimination of active pancreatic enzymes from the body may be realized by means of
artificial (forced) diuresis, peritoneal dialysis and drainage of thoracic lymph duct.
Complex of therapeutic procedures in edematous pancreatitis includes saline infusions and
5% glucose solution.
Conservative treatment of pancreatonecrosis. At the intensive care unit it is necessary
to exercise constant control of diuresis and cardio-vascular system parameters. It is also
necessary to control the central venous pressure, haemoglobin level, haematocrit and glycaemia
data, and also serum and urinary amylase. For treatment the patients with pancreatonecrosis it is
important to determine the level of oxygen and acid-base balance in the blood.
The main aim of therapy of a patient with pancreatonecrosis is the treatment and
prophylaxis of severe inflammation of the upper abdomen consequences. For that first of all it
is necessary to suppress hypovolemic shock (volume of circulating fluid is restored by
intravenous infusion of 6% dextran solution — macrodex or polyglucin) and to fight pain
(epidural anesthesia).
Respiratory function is to be under the constant attention, and in case of lowering of oxygen
level in the blood it is necessary to carry out oxygen therapy. In severe cases a patient has to be
carried to artificial pulmonary ventilation.
An important place in treatment of pancreatonecrosis is occupied by desintoxication
(infusion) therapy and correction of acute metabolic disturbances, and hypoalbuminaemia,
hypocalcaemia and other electrolytes. Calcium gluconate, magnesium gluconate, potassium
gluconate, and 5% solution of bicarbonate are used for restoration of electrolyte balance.
Desintoxication therapy includes intravenous injection of physiologic saline, 5% glucose
solution.
In patients with pancreatonecrosis antibacterial prophylaxis and treatment of septic
complications is of great importance. Efficient fight against paralytic ileus (nasogastral
aspiration, medicamentous stimulation of intestinal motility) is traditional prophylaxis of
suppurative complications following acute pancreatitis. However, the right choice of
antibacterial drug and its right dosing regimen is of great importance in prophylaxis and
treatment of suppurative complications of pancreatitis. Here antibiotics with good penetration in
the pancreas have to be agents of choice. At present such antibiotics are the following ones:
cephalosporin’s of the IV generation (cephepim), piperacillin, ticarcilin, fluoroquinolones
(ciprophloxacin, ophloxacin, pephloxacin), carbopenems (imipenem, meropenem),
metronidazole.
Taking into consideration the role of translocation of interstitial bacteria in pathogenesis of
 23

suppurative complications of pancreatonecrosis, intestinal decontamination, which is carried out

by oral introduction of fluoroquinolones in combination with polymyxin, should be included in
antimicrobial treatment regimen.
In those cases, when the patient with acute pancreatitis is in grave condition (with the signs
of multiple organ failure) the method of nutritive (alimentary) assistance at early stage of the
disease through nasojejunal tube established distally to Treiz's ligament (duodenal-jejunum) by
means of gastroduodenoscopy.
Glutamine is used as nutriceutic strengthening the intestinal barrier, and pectin is used as
protector of the intestinal barrier.
Surgical treatment of pancreatonecrosis is absolutely indicated in:
1) infection of the glandular tissue;
2) in case of development of pancreatogenic abscess;
3) in septic phlegmon of retroperitoneal fat;
4) in purulent pancreatitis.
Surgical treatment of patients with pancreatonecrosis includes different drainage
operations, which provide conditions for proper drainage of the retroperitoneal space and the
abdomen depending on extent and character of pancreatic, retroperitoneal fat and abdominal
involvement.
Techniques of drainage operations on the omental bursa and retroperitoneal space in
pancreatonecrosis are divided into closed, open, and semiopen ones.
Closed techniques propose active drainage of the retroperitoneal fat, the omentum bursa
and retroperitoneal space by means of introduction of double- and three-lumen drains.
Introduction of drains is performed under the control of ultrasonic or computer tomography.
Antiseptic solutions are injected through drains, and liquid mediums are actively aspirated.
Semiopen technique includes introduction of "active" drainage constructions in
combination with Penrose drain in the suppurative foci during laparotomy. Laparotomy wound
is sutured closely. Drains are delivered through counter incisions located in the lumbar and
lateral lumbar regions of the abdominal wall.
Combined omentopancreatobursostomy and laparostomy regard to open drain technique
of pyogenic abscesses in pancreatonecrosis.
Lately methods of endoscopic drain and sanitation of peritoneal space through lumbar and
extraperitoneal approach had been elaborated.
Surgical treatment of patients with acute pancreatitis is used in those cases when
mechanical intestinal obstruction of major duodenal papilla and destructive cholecystitis set
conditions for development of pancreatitis. To eliminate barriers in outflow of pancreatic
secretion an endoscopic transduodenal papillosphincterotomy and choledocholithoextraction are
performed. In case of stenosis of the distal portion of the pancreatic duct an endoscopic
transduodenal pancreaticotomy is carried out. To eliminate the nidus of infection located in the
pancreas cholecystectomy is performed.
 24

GASTRIC ULCER

The gastric ulcer is a chronic disease. The main features of peptic ulcer are the presence of
ulcer defect in the mucosa. It forms the basis of pathology of many gastroenterological diseases.
Such phenomenon is explained by not only considerable distribution of disease but also the dan-
gerous complications which always accompany gastric ulcers.

Etiology and pathogenesis

Frequency of morbidity of the peptic ulcer among the adult population is about 4 %. It is
more frequently seen patients in age group between 50-60 years.
The mechanism of development of the disease is still not studied sufficiently. From a plenty
of different theories in relation to genesis of peptic ulcer no one is able to explain the disease. So,
each of such factors as neurogenic, mechanical, inflammatory, vascular is present in the mecha-
nism of development of peptic ulcer. Consider for today, that disturbance between the factors of
aggression and defense mechanism of mucosa leads to peptic ulcer. The first factors includes:
hydrochloric acid, pepsin, reverse diffusion of ions of hydrogen, products of lipid
hyperoxidizing. The second includes: mucus and alkaline components of gastric juice, property
of epithelium of mucosa to permanent renewal, local blood flow of mucosa and submucosa.
In the terminal stage of mechanism of origin of gastric ulcers peptic factor has an important
role and disturbance of trophism of gastric wall as a result of local ischemia. It confirmed by
decreasing the blood flow in the wall of stomach in patients with ulcers in 30-35 % compared to
the norm. It is proved, that a local and functional ischemia more frequently seen in lesser
curvature of stomach, in the areas of ectopy of the antral mucosa. The ulcers appear in these
areas.
Important part in ulcerogenesis is contributed by duodenogastric reflux and gastritis. Also,
gastrostasis can provoke hypergastrinaemia and hypersecretion and formed gastric ulcers.
Numerous scientific developments of the past testify to the important infectious factor in
the mechanism of origin of peptic ulcer, mainly, by helicobacter pylori.

Pathomorphology

Different stages of the disease have been distinguished: erosion, acute and chronic ulcers.
Erosions, mainly, are multiple. The floor as a result of formation of muriatic haematine is
black, the edges are infiltrated by leucocytes. The defect usually does not penetrate outside the
muscle layer of the mucosa. If necrosis spreads to deeper layers of the wall of the stomach, an
acute ulcer develops. The ulcer is funnel-shaped. The floor is black, edges are edematous.
Chronic ulcers are mainly single and sometimes reaches the serous layer. The floor is smooth,
sometimes indurated, edges are elevated and dense.

Classification

Today the most common classification of gastric ulcers by Johnson (1965). There are three
types of gastric ulcers: type I - ulcers of lesser curvature (3 cm higher than the pylorus); type
II— double localization of ulcers simultaneously in the stomach and duodenum; type III —
ulcers of pyloric end of stomach (not farther than 3 cm from the pylorus). 70,9 % of ulcer are
located on the lesser curvature of the stomach, on the posterior wall near the lesser curvature -
4,8 %, 12,9 % - in the cardial end and 11,4 — in the pyloric end of the stomach. The ulcer of the
greater curvature are rare.

Clinical management

The complaints of patients with the gastric ulcer always give valuable information about
 25

the disease. The detailed analysis of their anamnesis allows to pay attention to the possible
reasons of origin of ulcer, time of the first complaints, to the changes of symptoms.
Pain. The pain symptom in the peptic ulcer disease is very important. There are typical
staging for this disease: hunger - pain - food intake -facilitation - again hunger - pain - food
intake - facilitation (so during all days). Night pain for the gastric ulcer is not typical. Such
patients rarely wake up in order to take food. For diagnosis of ulcer localization it is important to
know the time of appearance of pain. Between acceptance of food and appearance of pain it is
the lowly placed, than the higher placed gastric ulcer. Thus, in patients with the cardial ulcer
pain arises at once after the food intake, with the ulcers of lesser curvature - in 50-60 minutes, in
pyloric localization - approximately in two hours. However this feature is relative and some
patients in general do not mark relation between food intake and pain. In other patients the pain
attack is accompanied by salivation.
The pain is usually located in the epigastric region (below the xiphoid process). The
radiation of pain is not usual for gastric ulcers. Radiation occur in patients with penetration of the
organ, in which an ulcer penetrates.
In the examination of patient with ulcer disease it is expedient to determine the special pain
points: Boas (pain on pressure lateral to the X-XII pectoral vertebrae), Mendel (pain on
percussion lateral to epigastric region). Vomiting, the sign of disturbance of gastric motility, is
the second typical symptom of gastric ulcer. More frequent gastrostasis arises as a result of
failure of stomach muscle, it's atony which can be due to organ ischemia. Vomiting could arise
both on empty stomach and after food intake. Heartburn is one of the early symptoms of gastric
ulcer, however in prolonged disease it can be hidden or disappear. Often it precedes pain (initial
heartburn) or accompanies a pain symptom. Mostly heartburn arises after the food intake, but
can appear independently, it is observed not only at hypersecretion of the hydrochloric acid, but
at normal secretion, even reduced acidity of gastric juice.
The belching at gastric ulcers is examined rarely, more frequent in patients with cardial and
subcardial ulcers. It is necessary to bind to disturbance of function of cardial valve.
The general condition of patients with the uncomplicated gastric ulcer is usually
satisfactory, and in a period between the attacks - even good. However for most patients loss of
body weight and pallor are typical. In the epigastric region hyperpigmented spots are observed
after the prolonged application of hot-water bottle. On palpation of stomach in this area it is
sometimes tender. It is also important to listen for "splash sound", the presence of which can be
the sign of possible gastrostasis.
On the examination of oral cavity the tongue has whitish-yellow incrustation. In patients with
penetrating ulcers and disturbances of evacuations from the stomach dryness of tongue is seen.
Stomach, as a rule, is regular and rounded in shape, however during the pain attack it is pulled
in. There is anti peristalsis arises during the pylorostenosis. The increased secretion of hy-
drochloric acid in patients with gastric ulcers is observed rarely and,
mainly, when ulcer is located in the prepiloric area. Mostly secretion is normal, and in some
patients it is even reduced.
X-Ray examination. The direct signs of ulcer at X-Ray examinations are: signs of
"Haudek's niche", ulcer cavity and convergence of folds of mucosa. Indirect signs: symptom of
"forefinger" (circular spasm of muscles), segmental hyperperistalsis, pylorospasm, delay of
evacuation from a stomach, duodenogastric reflux, disturbance of function of cardiac part
(gastroesophageal reflux).
Gastroscopy can give important information about localization, sizes, kind of ulcer,
dynamics of its cicatrisation, and also allow to perform biopsy with subsequent histological
examination.

Clinical variants and complication

The gastric ulcer can be acute and chronic. Acute ulcers arise as result of stress situations,
 26

related to the nervous overstrain, trauma, loss of blood, some infectious and somatic diseases.
The diameter of ulcer ranges from a few millimeters to centimeters, is round or oval in shape
with even edges. Thus in most cases clinically observed clear ulcer clinical signs. If
complications are absence (bleeding, perforation) such ulcers are treated medically and usually
heal.
G.J. Burchynsky (1965) distinguished such variants of clinical presentation:
1. Chronic ulcer which does not heal over long time.
2. Chronic ulcer which after the conservative therapy heals over relatively
easily, however inclined to relapses after the periods of remission of a different duration.
3. Ulcers, which are migrant in character. Observed in people with acute ulcer process of
stomach.
4. Special form of gastric ulcer seen after the already carried disease. Patient presents with
expressed pain syndrome. Characterized by the presence in place of ulcer defect of scars or
deformations and absence of symptom of "niche".
Certain complications can develop in patients with gastric ulcer: penetration, stenosis,
perforation, bleeding and malignant change.

Diagnosis program

1. Anamnesis and physical examination.

2. Endoscopy.
3. X-Ray examination of stomach.
4. Examination of gastric secretion by the method of aspiration
of gastric contents.
5. Gastric pH metry.
6. Multi position biopsy of edges of ulcer and mucosa of stomach.
7. Gastric Dopplerography.
8. Sonography of abdominal cavity organs.
9. General and biochemical blood analysis.
10.Coagulogram.

Differential diagnosis

Chronic gastritis, like gastric ulcer is characterized by the pain syndrome, which arises after
the food intake. In such patients it is possible to observe nausea and vomiting of gastric content,
heartburn and belching. However, unlike gastric ulcer, in gastritis typical symptom of "quick sa-
tiation by food" is seen. Unsteady emptying, diarrhea are also more inherent to gastritis. In
gastric ulcer frequently the delay in gastric empting leads to constipation for 4-5 days.
The cancer of stomach, it is comparative with gastric ulcer, has considerably shorter
anamnesis. The most typical clinical signs of this pathology are: absence of appetite, weight loss,
rapid fatigability, depression, unsociability, apathy. In such patients X-Ray examination expose
the "defect of filling", related to exophytic tumor and deformation of walls of organ. A final
diagnosis is set after the results of multiposition biopsy of shady areas of mucosa of stomach.
Differential diagnosis also needs to be conducted with the so called precancerous states:
gastritis with the achlorhydria; chronic, continuously recurring ulcers, poliposis and Addison-
Biermer anemia.

Tactic and choice of treatment method

Conservative treatment of gastric ulcer always must be complex, individually

differentiated, according to the etiology, pathogenesis, and localization of ulcer and character of
clinical signs (disturbance of functions of gastroduodenal organs, complication and
accompanying diseases).
 27

Conservative therapy must include: a) anticholinergic drugs (atropine, methacin,

platyphyllin) and myolitics (papaverine, halidor, nospanum); antiacid drugs - in accordance with
the results of pH-metry;
b) H2- blocker histamine receptor (ranitidine) - 150 mg in the evening, famotidine - 40 mg at
night, roxatidine - 150 mg in the evening,
c) Reparative drugs (dalargin, solcoseryl, actovegin) - for 2 ml 1-2 times per days; A)
antimicrobial drugs (de-nol, metronidazole, and semisynthetic antibiotic); e) vitamins of group B
and symptomatic medicine.

Treatment of patient with a gastric ulcer must continue for not less than 6-8 weeks.
Surgical treatment must be performed in cases:
a) of relapse of ulcer after the course of conservative therapy;
b) in the cases when the relapses arise during supportive antiulcer therapy;
c) When an ulcer does not heal during 1,5-2 months of intensive treatment, especially in
families with "ulcer anamnesis".
d) in relapse of ulcer in patients with complications (perforation or bleeding);
e) Suspected malignancy of ulcers, in case of negative cytological analysis.
The choice of method of surgical treatment of gastric ulcer depends on localization and
sizes of ulcer, presence of gastro- and duodenostasis, accompanying gastritis, complications of
peptic ulcer (penetration, stenosis, perforation, bleeding, and malignization), age of patient,
general condition and accompanying diseases. In patients with cardiac localization of ulcer the
operation of choice is the proximal resection of stomach, which, from one side allows removing
an ulcer, and from other -to save considerable part of organ, saving its functional ability.
In case with large cardiac ulcers, when the vagus nerves are pulled in the inflammatory
infiltrate and it is impossible to save integrity, operation needs to be complemented by
pyloroplasty. It will give possibility to warn pylorospasm and gastrostasis, which in an early
postoperative period can be the reason of insufficient anastomosis and other complications.
The choice of method of surgical treatment of gastric ulcers with subcardial localization on
lesser curvature without duodenostasis it is better to apply the methods of stomach resection
while preserving the passage through duodenum.
For this purpose we have developed the method of segmental resection of stomach with
addition selective proximal vagotomy. The redistribution of gastric blood flow between the
functional parts of stomach as an answer to medical vagotomy (intravenous introduction 1,0 ml
0,1 % solution of atropine of sulfate) is studied. Hyperemia of acid-forming part of stomach is
seen after the introduction of the preparation. The functional aspects of the parts of the stomach
are determined. The border between acid-forming and antral parts is the most frequent sites of
gastric ulcers.
In this operation a middle laparotomy is performed, intravenously 1,0 ml 0,1 % solution of
atropine is given, then the areas of functional parts of stomach are identified and by sutures is
marked the intermedial segment. Selective proximal vagotomy is performed. After mobilization
of greater curvature of the stomach within the limits of intermedial segment its resection is
performed. After that gastro-gastro anastomosis "end-to-end" is done.
The analysis of supervisions of the patients operated by such method in postoperative
period has good results. It allows recommendation of this operation for clinical practice, in case
of gastric ulcers of subcardial localizations, without duodenostasis, penetration, malignant
transformation, damage the nerves of Latarjet.
The operation of choice in patients with subcardial ulcers and duodenostasis is gastric
resection by Billroth II.

In the choice of method of surgical treatment of ulcers which are localized in the upper and
middle third of stomach, it is necessary to consider such factors, as absence of penetration into
the small omentum and absence of the duodenostasis. In such patients segmental resection of
 28

stomach with removal of ulcer with selective proximal vagotomy is performed. In case of
penetrating ulcer in the small omentum with infiltration of Latarjet nerves, such operation is
impossible because in future it can lead to spasm of pylorus and gastrostasis. If duodenostasis is
In patients -with duodenostasis better to perform gastric resection by Billroth II.
There can be spasm and gastrostasis in a post-operative period in the border of gastric
resection near the pyloric sphincter. Avoiding such complication is possible, if the area of gastric
resection passes no more than 1,5 cm from the pyloric sphincter (M.M. Risaev, 1986). So, during
resection, that passes higher than 2,0 cm from the pylorus, integrity of both loops is maintained.
In patients with antral ulcers without the duodenostasis the gastric resection by Billroth I is
performed, and in presence of duodenostasis -Billroth II.
Prepiloric ulcers are similar to the ulcers of duodenum. Such localization of gastric ulcers
without malignancy allow to performing selective proximal vagotomy.
However, with large prepyloric ulcers with penetration without duodenostasis it is better to
perform gastric resection by Billroth I and in the presence of duodenostasis - by Billroth II.
Contraindications to operations are decompensation pylorostenosis, functional gastrostasis
and duodenostasis. In such patients it is better to perform gastric resection by Billroth II.

Duodenal ulcer

The duodenal ulcer is the chronic recurrent disease which is characterized by ulcer defect
on a mucosa of the duodenum. Pathology often leads to development of complications.

Etiology and pathogenesis

There are some etiologic factors of the duodenal ulcer: Helicobacter pylori, emotional stress
and neuropsychic stress, overstrain heredity and genetic inclination, presence of chronic
gastroduodenitis, disturbance of diet and harmful habits (alcohol, smoking). In pathogenesis of
peptic ulcer a leading role is played by disturbance of equilibrium between aggressive and
projective properties of secretion of stomach and its mucosa. The aggressive factors are
hyperfunctioning vagus and hypergastrinaemia; hyperproduction of hydrochloric acid and
pepsin, and also reverse diffusion of the ions H+, action of bilious acids and isoleucine, toxins
and enzymes of helicobacter pylori (HP). There are factors which contribute to ulcerogenic
action like disturbance of motility of stomach and duodenum, ischemia of duodenum, and
metaplasia of the epithelium.
Pathomorphology

Morphogenesis of duodenal ulcer fundamentally does not differ from that of ulcer in the
stomach. Chronic ulcers are mainly single, is localized on the anterior or posterior wall of bulb
(taulbar ulcer) and only in 7-8 % cases - below it (postbulbar ulcer). Multiple ulcers of
duodenum are met in 25 % cases.

Classification
(By A.L.Hrebenev, A.O.Sheptulin, 1989)

The duodenal ulcer is divided: I. By etiology:

A. True duodenal ulcer.
B. Symptomatic ulcers.
II. By onset of disease:
1. Acute (first exposed ulcer).
2. Chronic: a) with the rare exacerbation;

b) with the annual exacerbation;

 29

c) with the frequent exacerbation (2 times per a year and

more frequent).
III. By the stages of disease:
1. Exacerbation.
2. Scarring: a) stage of "red" scar;
b) stage of "white" scar.
3. Remission.
IV. By localization:
1. Ulcers of bulb of duodenum.
2. Low postbulbar ulcers.
3. Combined ulcers of duodenum and stomach.
V. By sizes:
1. Small ulcers up to 0,5 cm.
2. Middle - up 1,5 cm.
3. Large - up to 3 cm;
4. Giant ulcers over 3 cm.
VI. By the presence of complications:
1. Bleeding.
2. Perforation.
3. Penetration.
4. Organic stenosis.
5. Periduodenitis.
6. Malignant transformation.

Clinical management

Pain in the epigastric region is the most common symptom of duodenal ulcer, often with
radiation to the right in the projection area of bulb of duodenum and gall-bladder. Also for this
pathology is typical the pain, that arises in 1,5-2 hours after food intake, "hunger" and nightly
pain. As a rule, it is acute, sometimes unendurable, and relived only by intake food or water.
Such patients complain of seasonal exacerbation, more frequent in spring and in autumn.
However exacerbation can be also in winter or in summer. In the acute phase of the disease
heartburn often increases. However heartburn is the frequent symptom of cardiac insufficiency
and gastroesophageal reflux. For a duodenal ulcer the acute burning feeling of acid in an
esophagus, pharynx and even in the cavity of mouth is especially typical. Often belching of air
or sour content, excessive salivation.
Vomiting is not a typical symptom for duodenal ulcer. More typical sign is nausea. Sometimes
for relief patients willfully cause vomiting. These symptoms, arises in the late periods of
duodenal ulcer.
Intensity of pain and dyspepsia syndromes depends both on the depth of penetration and
from distribution of ulcer and periulcer processes. Superficial ulceration within the mucosa, as a
rule, does not cause the pain because it does not have sensible receptors. However, more deep
layers of wall (muscular and especially serous) have many sensible vegetative receptors.
Therefore, on deepening and distribution of process arises visceral pain. Evident periulcer
processes and penetration of ulcers to neighboring organs and tissues usually a parietal
peritoneum that has spinal innervation is pulled in. Pain becomes viscerosomatic, more intensive.
Such a pain syndrome (with a radiation in the back) is typical for low postbulbar ulcers and
bulbous ulcers of back wall, which penetrates in a pancreas and hepatoduodenal ligament.
Usually such patients have good appetite. Some of them limit themselves in acceptance of
ordinary food, takes small intermitted feeds, and some - even hold back from a food, being afraid
to provoke pain, and as a result of which there's weight loss. Some of the patients feed more
intensively and often.
 30

The psychical status of patients often is changed as an asthenoneurotic syndrome: irritation,

decrease of working capacity, indisposition, hypochondria, and abusiveness.
Inspection as a rule, gives insignificant information. In many cases on the abdominal skin it
is possible to notice hyperpigmentation seen after application of hot-water bottle. During the
pain attack patients often occupy the forced position. On palpation of the abdominal wall
hyperesthesia can be determined in ulcer projection area. In the epigastric region, during deep
palpation, it is possible to define pain and muscular tension, mostly of moderate intensity. There
is an important symptom on local percussion (Mendel's symptom): percussion by fingers in the
symmetric epigastric areas provoke pain in the ulcer, which is increased after the deep breath.
The rentgenologic and endoscopic examination are main diagnostic methods. The sign of ulcer
crater is a classic rentgenologic sign. It is a depot of contrast agent, which is corresponds to the
ulcer defect, with clear contours and light edges to which are converged fold of mucosa.
Cicatricial deformation of the bulb of duodenum, narrowing, tube-like appearance of the
duodenum, diverticulum and other are forms the important sign of chronic ulcer process. The
roentgenogram is especially important for determination of configuration and sizes of stomach
and duodenum, and also for estimation of motility functions. X-Ray examination is the main
method in peptic ulcer complicated by stenosis with disturbance of evacuation, duodenostasis,
duodenal-gastric reflux, gastroesophageal reflux, and diverticulum. But by X-Ray examination it
is difficult to diagnose small superficial ulcers, acute ulcers, erosions, gastritis and duodenitis.
The most informative method of investigation in such cases is endoscopy. During endoscopy
examination it is possible to define localization, form, sizes and depth of ulcer. During bleeding
grumes, trickle or pulsating of blood is observed. By irrigation by styptic solutions, by
cryocoagulation, by laser coagulation endoscopy allows to secure hemostasis. Endoscopy allows
performing the biopsy of ulcer tissues for determination of possible malignization.

Clinical variants and complication

In patients with low postbulbar ulcers the clinical signs are more expressed. It characterized
by late (in 2-3 hours after food intake) and intensive "hunger" and night pains, that often irradiate
to the back and to the right hypochondrium. The postbulbar ulcers are inclined to more frequent
exacerbation, and also to more frequent complications, such as penetration, stenosis and
bleeding. Penetration, stenosis and malignization in patients with duodenal ulcers are observed
rarely.
Penetration is a frequent complication of "low" and postbulbar ulcers of duodenum, -which
are placed on posterior, posterior superior and posterior inferior walls. Deep chronic ulcers
usually penetrates through all layers of duodenum an into neighboring organs and tissues (head
of pancreas, hepatoduodenal ligament, small and large omentum, gall-bladder, liver). Such
penetration is accompanied by development of inflammatory process in the neighboring organs
and surrounding tissues and formation of cicatrical adhesions. The pain syndrome becomes more
intensive, permanent and often pain is irradiated to the back. Sometimes in the area of
penetration it is possible to palpate painful infiltrate.

Diagnosis program
1. Anamnesis and physical examination.
2. Endoscopy.
3. X-Ray examination of stomach and duodenum.
4. General and biochemical blood analysis.
5. Coagulogram.

Differential diagnosis

The duodenal ulcer must be differentiated from acute and chronic cholecystitis,
pancreatitis, and gastroduodenitis. Endoscopy helps to diagnose duodenal ulcer.
 31

Tactic and choice of treatment method

Conservative treatment.

In most patients after conservative treatment the ulcer heals in 4-6 weeks. Relapses can be
prevented by supportive therapy for many years.
The best therapy of duodenal ulcer is associated with the treatment of helicobacter infection
- the use of antagonists of H2- receptors of histamine (ranitidine- 300 mg in the evening or 150
mg twice daily; famotidine- 40 mg in the evening or 20 mg twice daily; nisatidine — 300 mg in
the evening or 150 mg twice daily; roxatidine — 150 mg in the evening) in combination with
sucralfate (venter) - for 1 gm trice daily and antacid (almagel, maalox or gaviscon - 1 table-
spoon 1 hour after food intake). To this treatment it is added antibacterial preparations (De-nol -
1 tabl. 4 times a day for 4-6 weeks + oxacylline 0,5 g 4 times a day for 10 days + Tryhopol
(metronidazole) for 0,5 g 4 times a day for 15 days).
In treatment of duodenal ulcer used chinolitics and myolitics (atropine, methacin,
platyphyllin), and also mesoprostol (200 mg 4 times a day) and omeprasole (20 or 40 mg daily).
Treatment of patients with the duodenal ulcer must be for 4-6 weeks. If complications are
absence there is no need of in the special diet.
Because of appearance of new pharmaceutical preparations and modern therapeutic
treatment need for the operative methods of treatment have decreased. But the number of acute
complications of duodenal ulcer has not decreased, especially bleeding and perforations which
require urgent surgery.

Indications to elective operation:

1. Staging of duodenal ulcer with the frequent relapses which could not be treated conservatively.
2. Repeated ulcer bleeding.
3. Stenosis of pyloric part of stomach.
4. Chronic penetration ulcers with the pain syndrome.
5. Suspicion malignant change.

Methods of surgical treatment.

In patients with the duodenal ulcer three types of operations are performed:
- organ-saving operations;
- organ-sparing operations;
- resection.

Among the best surgical methods are: organ-saving operations with vagotomy, excision of
ulcer and drainage operation.
Types of vagotomy: trunk (TrV), selective (SV), selective proximal (SPY). Selective
proximal vagotomy is optimal in the elective surgery of duodenal ulcer. However in urgent
surgery a trunk, selective or selective proximal is often used in combination with drainage
operations

Drainage of the stomach operations are: Heineke-Mikulicz pyloroplasty, Finney

pyloroplasty, submucous pyloroplasty by Diver-Barden-Shalimov, gastroduodenostomy by
Jaboulay, gastroenteroanastomosis.
It is necessary to mark that "clean isolated" SPV, performed in patients with duodenal
ulcer, often (in 15-20 % cases) results in relapses. Considerably less number of relapses (8-10 %)
is observed after SPV in combination with drainage operations. Especially dangerous is the
relapse of the ulcers located in the projection of large duodenal papilla, after
gastroduodenostomy by Jaboulay.
 32

If ulcer is located on the anterior surface of duodenal bulb it can be performed by the Jade
method (fig. 12) with subsequent pyloroplasty by Heineke-Mikulicz.
At patients with decompensate stenosis and expressed dilatation and atony of stomach the
classic resection of stomach by Billroth -I or Billroth -II is done.
The choice of subtotal resection of stomach needs to be done when there's suspicion of
malignancy or when there's histologically confirmed malignant ulcers. In a duodenum this
process happens very rarely.

Ulcer stenosis

Ulcer stenosis is complication of Peptic ulcer, which is characterized by narrowing of the

duodenum or pylorus.

Etiology and pathogenesis

Stenosis of pyloric part of the stomach and duodenum due to ulcers arise as a result of
scarring and common morphological changes around an ulcer. Narrowing, disturbance of the
coordinated motility of pylorus as a result of ulcer creates an obstacle to the normal movement
of stomach content to the duodenum.

Pathomorphology

Such pathology in the compensation stage leads to hypertrophy of the stomach walls. The
pyloric orifice is 0,5-0,7 cm in diameter. The mucosa of the pyloric part of stomach is thickened
with rough folds. Muscular fibers' are hypertrophied and solid. Histological hyperplasia of
pyloric glands is observed.
During decompensation the muscular layer of stomach becomes thinner and the pyloric
orifice narrows to a few millimeters. Microscopically
atrophy of mucosa and muscular fibers, vessels sclerosis is seen. The stomach collects the form
of the stretched sack which is pulled down to the level of the small pelvis.

Classification (by A.A. Shalimov and V.F.Saenko, 1987)

Three clinical stages of stenosis are distinguished:

I — compensated;
II - subcompensated;
III - decompensated.
The morphological changes in the initial part of stomach and duodenum are represented by
the classification offered by M.I. Kuzin (1985). On the basis of clinical, rentgenologic,
endoscopic, electrogastrographical and intraoperative methods the examinations distinguished
three stages of stenosis:
I - inflammatory;
II — cicatricial ulcer;
III - cicatricial.

In accordance with localization, by V.F.Saenko (1988) distinguished three types of

stenosis:
I - stenosis of pylorus;
II - stenosis of bulb of duodenum;
III - postbulbar duodenal stenosis.
First two types of stenosis are similar by functional and the organic changes and is called
pyloroduodenal or high duodenal stenosis. The second group is postbulbar duodenal stenosis. It
is impotents feature that the pylorus does not take part in the cicatricial- ulcer process and its
 33

function is maintained.

Clinical management

The first signs of stenosis can be seen after eight-ten years after the onset of the peptic ulcer
disease, mainly there are narrowing and rigidity and disturbance of retractive activity of the
pylorus, which creates a barrier for transition of stomach content to the duodenum.
In the stage of the compensated stenosis there is hypertrophy of the wall of stomach
develops. Thereupon gastric content does pass through the narrowed area of stomach but passes
slowly. In this stage patients usually complains a feeling of discomfort in the epigastric area after
food intake, periodic vomiting of sour gastric contents. On empting of the stomach by a stomach
tube 200-300 ml gastric content is removed.
In the subcompensated stage muscular layer of stomach becomes thinner. Evacuation
disorders are increased. In this stage of the disease patients usually complains of permanent
feeling of weight in epigastric region and regurgitation with an unpleasant "foul" smell of
sulphuretted hydrogen.
Vomiting becomes systematic (once or twice on a day) up to half liter per day. On empting
the stomach it is possible to aspirate more than 500 ml of food eaten the day before.
In the decompensation stage the clinical signs appear quickly. There are disturbances in the
general condition of the patient, considerable loss of weight (to 30-40 %), acutely expressed
dehydration, hypoproteinaemia, hypocalcaemia, azotaemia and alkalosis. In case of the
prolonged disease, as a result of progress of disturbances of metabolism, there can be convulsive
syndrome (gastric tetany). Vomiting in this stage is not always considered to be a typical sign, in
fact patients often stop eating, and the stomach considerable increase in size and become over
distended form, its tone is violated and atrophy of wall is seen. In such patients in the epigastric
region it is possible to define the contours of the stretched stomach, •with a slow peristalsis. In
the distance it is possible to hear the splash. With a gastric tube 1.5-2 liters of food with a putrid
smell are removed. There can be gastric tetany and considerable disturbances of electrolyte
metabolism.
A diagnosis is set according to a typical symptom, results of sounding of stomach,
rentgenoscopy, in which by contrasting with barium shows stenosis of initial part of stomach or
duodenum, determines it origin and estimate the degree.
Rentgenologically in the compensation stage stomach is normal in sizes, its peristalsis is
deep, increased, and evacuation of contents takes no more than 6 hours. In the stage of
subcompensation the stomach is megascopic, peristalsis is decreased, and evacuation takes up to
24 hours. During decompensation the stomach is considerably dilated like a sack and deformed,
the waves of anti peristalsis can take place; the contrast stays for long to more than 24-48 hours.
The method of the double contrasting by a barium and air considerably facilitates diagnosis.
Determination of stomach motility not only has diagnostic but also has a prognostic value
for the choice of method of operation.
In the stage of compensation motility the stomach is well-kept, often increased. With the
increasing degree of stenosis the motility disturbance is increased, leading to gastroplegia.
In the biochemical blood test there's marked decrease of content of albumen to 54-48 g/1;
potassium - to 2,9-2,5 mmol/1; chlorides - to 85-87 mmol/1. The changes of such indexes are
most expressed in patients with gastrogenous tetany.
The study of secretory function of stomach allows defining the degree of compensation of
stenosis and is important for choosing the appropriate method of operation.
Gastroscopy with biopsy is a very informative method of examination of such patients. By
this method it is possible to determine the reason and degree of stenosis and also the state of
mucosa of stomach.
 34

Diagnosis program

1. Complaints of patient and anamnesis of disease.

3. Sounding of stomach and examination of gastric content.
4. Fibergastroduodenoscopy, biopsy.
5. Intragastric pH-metry.
6. Study of motility of stomach.
7. X-ray examination of stomach and duodenum (structural features, passage).
8. Sonography.

Differential diagnosis

Stenosis of the pyloric part of stomach and duodenum as a result of ulcers there is a need to
differentiate from functional gastrostasis and narrowing of tumour and chemical genesis.
Functional gastrostasis is more frequently seen in women. In that there is absence of some
organic changes in the area of pyloric part of stomach or in a duodenum that can be exposed
during fibergastroscopy.
Differential diagnosis of stenosis of tumour genesis, as a rule also does not cause the
special difficulties. A diagnosis is finally confirmed by histological examinations of the biopsy
material taken during endoscopy.
Postburn stenosis of piloroantral area of stomach is observed from data of statistics in more
than 25 % of cases of patients with the burn of esophagus. Some diagnostic difficulties can arise
with isolated postburn stenosis of pyloric part of stomach. However carefully history taking and
professionally conducted endoscopic examination enables to set the correct diagnosis.

Tactic and choice of treatment method

Treatment of ulcer stenosis of pyloroantral part of stomach and duodenum must be

exclusion ally operative. The choice of method depends on many factors: degree of stenosis,
secretory and motility functions of stomach, age of patient, presence of accompanying diseases
and others like that. In the compensated and subcompensated stages of stenosis and when
functions of stomach is preserved it is possible to perform organ-saving operations (vagotomy
with drainage operations, minimal resection of stomach). With increase in the signs of stenosis
and disturbance of basic functions of stomach, the volume of operation must be increased to
resection by the Bilroth's second method.
An older age persons with severe accompanying pathology minimum surgery of
gastroenteroanastomosis is performed.
Preoperative preparation must be strictly individual.
In patients with insignificant disturbances of gastric motor activity (stage of compensation,
subcompensation) and with good level of metabolism indexes it is better to shorten preoperative
preparation in time. Such patients are usually, operated on 3-4 day. Preoperative preparation of
patients with decompensated pylorostenosis must be directed to the correction of metabolic
disturbances. Such patients must receive transfusion of fluids up to 2,5-3 1 per day which contain
the ions K+, Na+, Ca++, amino acid and glucose; plasma, albumen. Twice daily decompression
and washing of stomach with anti-ulcer therapy is done. Effective preoperative preparation in
such patients requires 5-7 days, sometimes even more.

Perforated gastroduodenal ulcers

The typical perforation of gastric or duodenum al ulcer is due to increase of necrotic

process in the area of ulcer with subsequent disturbance of integrity of the wall, that result in the
permanent flow of gastroduodenal content and air in the free abdominal cavity.
 35

Etiology and pathogenesis

50,7 % cases of duodenal ulcer perforates and 42,8 % ulcers of pyloric part of stomach, 4,8
% ulcers of lesser curvature of body of stomach and 0,7 % cardial ulcers lead to perforation.
Ulcers, which lie on the anterior wall of stomach and duodenum frequently lead to
perforation with general peritonitis, while ulcers on a posterior wall lead to perforation with
adhesive inflammation.
The causes of ulcers perforation are: exacerbation of peptic ulcer, harmful habits, stress,
professional, athletic overexertion, alcohol abuse.

Pathomorphology

In pathogenesis of acute perforation important: progressive necrotic processes in the area of

ulcer with activation by virulent infection; hyperergic type of local vaculostromal reaction with
the thrombosis of veins of stomach and duodenum; local manifestation of autoimmune conflict
with accumulation of mucopolysaccharides on the periphery of ulcer and
high coefficient of plasmatization of mucosa (K.I. Mishkin, A.A. Frankfurt, 1971).

Classification (by V.S. Savelev, 1986)

Perforated gastroduodenal ulcers are divided according to:

1. etiology:
2. localization:
a. gastric (lesser curvature, cardial, antral, prepyloric, pyloric ulcer, anterior
and posterior walls;
b. Ulcers of duodenum (anterior and posterior walls).
3. type of perforation:
a. perforated in an abdominal cavity;
b. covered perforations;
c. Atypical perforations.

Clinical management

The clinical picture of perforation is very typical and depends on distribution of

inflammatory process and infection of abdominal cavity. Clinically the perforations are
distinguished into three phases: shock, transitory phase and peritonitis (Mondor, 1939).
The phase of shock last for about 6 hours and the typical symptom is acute pain in the
epigastric region (Delafua compares it to pain due to stabbing with a dagger) with an radiation
to the right shoulder and collarbone, the face is pale, with expression of strong fear, lines
become acute (facies abdominalis), skin is cold and clammy. The pulse at first is slow (vagus
pulse), later becomes frequent. Sometime the reflex vomiting and delay of gases is seen. Arterial
pressure is reduced. On examination stomach is pulled in, and does not take part in respiration.
On palpation the stomach is "wooden belly", especially in an upper part, where usually there is
more pain. Positive Blumberg's sign. On percussion there is absence of hepatic dullness (the
Spizharny symptom). On rectal examination there is tenderness in the area of rectouterine or
rectovesical pouch (the Kulenkampff’s symptom).
The phase of shock is followed by transient recovery, when the reflex signs decrease: the
general condition of patient gets better, the pulse becomes normal, arterial pressure rises; the
stomach-ache diminishes partly. However tension of muscles of anterior abdominal wall is
present, positive Blumberg's sign.
 36

The phase of "recovery transition" lasts for 6-12 hours and then followed by the phase of
peritonitis where the pulse is rapid, the stomach is distended, bowel sounds are not audible, the
face acquires a specific look — facies Hippocratica - the eyes fall back, lips turn blue, the nose
becomes sharp, the tongue becomes dry and furred, breathing is superficial and frequent, the
temperature rises.

Clinical variants and complications

Covered perforation (A.M. Shnicler, 1912). In this pathology the perforation is closed by
fibrin, by omentum or sometimes - by food particle. After that some amount of stomach content
and air gets in into the abdominal cavity. This protective mechanism leads to relief from
stomachache, but tension of muscles of anterior abdominal wall, especially superior quadrant of
stomach persists. On percussion hepatic dullness is doubtful. During x-Ray examination it is not
always possible to mark gas in right hypochondrium (fig. 13).
Consequences of phase of the healed perforation: repeated perforations with development
of classic clinical signs; can lead to subdiaphragmatic or subhepatic abscess; complete closing of
defect by surrounding tissue with gradual convalescence of patient.
The atypical perforation is the perforation, at which gastric or intestinal content does not
enter the abdominal cavity, but enters the retro-peritoneal space (ulcers of posterior wall of
duodenum), large or small omentum (ulcers of lesser curvature of stomach), and hepatoduodenal
ligament.
In such patients during the perforation pain is not acutely expressed. During palpation
insignificant rigidity of muscles of anterior abdominal wall is observed. On occasion, especially
in the late stages of disease, there can be hypodermic emphysema and crepitation.

Diagnosis program

1. Anamnesis and physical examination.

2. Analysis of blood and urine, biochemical blood test, coagulogram.
3. X-Ray examination of abdominal cavity organs for presence of
free gas (pneumoperitoneum).
4. Pneumogastrography, contrasting pneumogastrography.
5. Fibergastroduodenoscopy.
6. Sonography of abdominal cavity organs.
7. Laparocentesis with the Neymark diagnostic test (to 2-3 ml of abdominal cavity
exudate add 4-5 drops of the 10 % solution of iodine. If the admixtures of gastric
content appear in exudate, then under action of iodine gastric content gets a dirty dark
blue color).
8. Laparoscopy.

Tactic and choice of treatment method

The diagnosed perforated gastric and duodenum ulcer is an absolute indication to operation.
Preoperative preparation must include: in I phase antishock treatment; in the II and III phases -
reanimation, introductions of antibiotics for 2-3 hours before operation, correction of
hypovolemia by salt blood substitutes (solution of chlorous sodium), solutions of dextran
(polyhlukine, reopolihlukine). Amount of liquid necessary for correction of hypovolemia, is
calculated after haematocrit by central vein pressure. Taking the normal of haematocrit as 40 %,
on each 5 % increase, 1000,0 ml of fluids is to be prescribed.

Conservative treatment (method of Taylor, 1946) can be justified when the refuses for
operation, or when surgery contraindicated.
Conservative management includes:
 37

- permanent nasogastral aspiration of gastric content;

- introduction of preparations which decrease gastric secretion (atropine,
H2- blockers and others like that);
- introduction of antibiotics;
- correction of metabolism;
- laparocentesis with drainage and closed lavage of the abdominal cavity.

In the decision of question about the choice of method of operative treatment of perforated
gastroduodenal ulcers the importance is given to the following factors: localization of ulcer,
clinicomorphological description of ulcer (perforation of acute or chronic ulcer), associated
complications of perforation of ulcer, like bleeding, cicatricial ulcer stenosis, penetration, degree
of risk of operation and feature of clinical situation.
Operative treatments of the perforated ulcer divide into palliative and radical.

Palliative operationsPalliative operations are: closure of the perforation of ulcer, tamponade of

the perforation by omentum by B.A. Oppel - P.N. Polikarpov - M.A.Pidhorbunskyy. Indications
and terms for their implementation are:

- perforation of acute duodenal ulcer in youth and young age without anamnesis;
- perforation of acute ulcer in the II-III phases;
- perforation of callous gastric ulcer in the II-III phases;
— high degrees of risk of operation.

Radical operations

The radical operations in perforated ulcers are: resection of stomach and excision of the
perforation in combination with pyloroplasty and StV, SV or SPY.
Indications and terms for implementation of resection of stomach are:
- perforation of callous gastric ulcer in I phase of clinical staging;
- repeated perforation of ulcer;
- perforation of ulcer in I phase of clinical staging in combination with stenosis and bleeding
of ulcer;
- perforation of duodenal ulcer in I phase of staging in combination with a gastric ulcer;
- unexpressed and moderate degree of risk of operation;
- Sufficient qualification of surgeon, availability of material resources for operating.
Indications for implementation of operation of excision of the perforation of ulcer with
pyloroplasty, StV, SV and SPV are: perforation of ulcer of anterior wall of duodenum or pyloric
part of stomach in the I-II phases;
- Perforation of ulcer of anterior wall of duodenum in the I-II phases of clinical staging in
combination with the bleeding ulcer of posterior wall;
- perforation of duodenal ulcer in the I-II phases of clinical staging in combination with the
compensated stenosis of pyloric part of stomach;
- increased gastric secretion;
- insignificant and moderate degree of risk of operation;
— Sufficient qualification and technical experience of surgeon.

Bleeding gastroduodenal ulcers

Bleeding gastroduodenal ulcers are due to bleeding in the gastrointestinal tract cavity as a
result of increasing necrosis in the ulcer area with blood vessels, with the subsequent damage of
their walls.
 38

Complication of peptic or duodenal ulcer by bleeding is critical situation which threatens

life of the patient and requires immediate and decisive actions for clarification of reasons of
bleeding and choice of tactic of treatment. The ulcer bleeding comprises of 60 % of the acute
bleeding from the upper parts of gastrointestinal tract.

Etiology and pathogenesis

The origin of the gastrointestinal bleeding in patients with gastric or duodenal ulcer almost
is always related to exacerbation of ulcer process. The reason of bleeding is an erosive vessel
that is on the floor of ulcer. The expressed inflammatory and sclerotic changes round the
damaged vessel decrease its constrictity that diminishes its ability to control bleeding.
Gastric ulcers as compared to duodenal, is frequently complicated by bleeding. Bleeding in
gastric ulcers are more expressed, profuse, and heavy.
In duodenal ulcers bleeding is more frequent with the ulcers of posterior wall, which
penetrates into the head of pancreas.
In men ulcer is complicated by bleeding twice as more, than in women. It’s important to
note that 80 % of patients, who had bleeding from ulcer and was treated by conservative
methods, are under permanent threat of recurrent bleeding.

Pathomorphology

Increase in the process of necrosis are leading factors in the development of the ulcer
bleeding in the area of ulcer crater with penetration into the vessel and subsequent damage of the
vascular wall; activation of fibrinolysis in tissues of stomach and duodenum; ischemia of tissues
of wall of stomach.

Classification

Bleeding gastroduodenal ulcers according to blood loss (by O.O. Shalimov and V.F.
Saenko, 1987) are divided into:
I degree - observed with loss at 20 % volume of circulatory blood (at a patient with weight
of body 70 kg it is up to 1000 ml);
II degree - is loss 20 to 30 % volume of circulatory blood (1000-1500 ml);
The III degree - is observed with blood loss of more than 30 % volume of circulatory blood
(1500-2500 ml).

Clinical management

In patients with peptic ulcer disease, bleeding starts, mainly at night. Vomiting can be the
first sign, mostly, with gastric localization of ulcers. Vomiting, as a rule, is "coffee-ground" in
appearance. Sometimes they are like fresh blood or grumes.
The black tar-like stools are the permanent symptom of ulcer bleeding, with an unpleasant
smell ("melena"), that can take place few times in a day.
Bloody vomiting and "melena" is accompanied by worsening of the general condition of
patient. An acute weakness, dizziness, noise in a head and darkening in eyes, sometimes - loss of
consciousness. A collapse with the signs of hemorrhagic shock can also develop. It is needed to
remember, that for diagnosis anamnesis is very important. But often, a patient with peptic ulcer
is already diagnosed once. It appears sometimes, that bleeding has occurred repeatedly or
patients have undergone surgery for perforated ulcer in the past. In some patients a gastric or
duodenum ulcer was not diagnosed before and attentively collected anamnesis revealed, that the
patient had stomach-ache. Thus its relation with food and seasonality is typical (more frequent
appears in spring and in autumn). Patients tell, that pain is in upper part of abdomen which
occurred a few days prior to bleeding, suddenly disappears the onset of bleeding (the Bergmann's
 39

symptom).
In patients with ulcer bleeding there are typical changes of haemodynamic indexes: the
pulse is rapid, weak filling and tension, arterial pressure is mostly reduced. These indexes need
to be observed in the dynamics, as they can change during the short interval of time.
There is pallor of skin and visible mucosa at a examination. The stomach sometimes is
moderately enlarged, but more frequently it is pulled in, soft on palpation. In upper part it is
possible to notice hyperpigmented spots - as a result of prolonged application of hot-water bottle.
Pain on deep palpation in the area of right hypochondrium (duodenal ulcer) or in a epigastric
area (gastric ulcer) is often observed in penetrated ulcers. Important symptom of Mendel also -
pain on percussion in the projection of pyloroduodenal area.
In the examination of patients with the gastrointestinal bleeding Digital examination of
rectum is obligatory. It needs to be performed at the first examination, because information about
the presence of black excreta ("melena") is important. Digital examination of rectum allows
revealing tracks of black excreta or blood. In addition, it is sometimes possible to expose the
tumour of rectum or haemorrhoidal nodes which are also the source of bleeding.
The deciding value in establishment of diagnosis is the endoscopic examination.
Fibergastroduodenoscopy enables not only to deny or confirm the presence of bleeding but also,
it is especially important, to set its reason and source. Often a negative result is obtained if the
stomach and duodenum content blood. In such cases it is necessary to remove blood or other
content by gastric lavage, and to repeat endoscopic examination. During the examination area of
bleeding with fresh blood from the bottom of ulcer or ulcer defect with one or a few erosive and
thrombosed vessels is revealed stopped bleeding). The floor of ulcer can be filled with blood.
Important information about such pathology is given by haematological indexes also.
Decreased number of red corpuscles and haemoglobin, decrease of haematocrit is observed in
such patients. However always remember, that initially after bleeding haematological indexes
can change insignificantly. Conducting of general analysis of blood in dynamics in every few
hours is more informative.

Clinical variants and complications

It is necessary always to remember that complication of peptic ulcer by bleeding happens

considerably more frequently, than it is diagnosed. Usually, 50-55 % of moderate bleeding
(micro bleeding) are unseen. In fact profuse bleeding with the loss 50-60 % of the volume of
circulatory blood could stop the heart and cause the death of patient.
The clinical signs and staging of disease depends on the degree of loss of blood (O.O.
Shalimov and V.F.Saenko, 1987).
For loss of blood I degree typically there is rabid pulse to 90-100, decrease of arterial
pressure of to 90/60 mm Hg. The excitability of patient changes by lethargy, however
consciousness is clear, breathing is frequent. After the bleeding stops and in absence of
hemorrhagic compensation the disturbances of circulation of blood are not observed.
In patients with the II degree of hemorrhage the general condition needs to be estimated as
average. Expressed pallor of skin, sticky sweat, lethargy. Pulse - 120-130 per min., weak filling
and tension, arterial pressure - 90-80/50 mm Hg. In the first few hours the spasm of vessels
(centralization of circulation of blood) arises after bleeding, that predetermines normal or
increased arterial pressure. However, as a result of the massive bleeding compensatory
mechanisms of arterial pressure are exhausted and can acutely go down at any point. Without the
proper compensation of hemorrhage such patients can survive, however almost always there are
considerable disturbances of blood circulation with disturbance of functions of liver and kidneys.
The III degree of hemorrhage characterizes clinical stage with heavy bleeding. The pulse in
such patients 130-140 per min., and arterial pressure — from 60 to 0 mm Hg. Consciousness is
almost always darkened acutely expressed adynamy. Central vein pressure is low. Oliguria is
observed, that can change to anuria. Without active and directed correction of hemorrhage the
patient can die.
 40

But, not always amount of bleeding and the degree of hemorrhage correspond to the general
condition of patient. On occasion with considerable loss of blood during a set time is
accompanied by the relatively satisfactory condition of patient, and vice versa (moderate
hemorrhage can bring to the considerable worsening of general condition). It can depend on
compensatory mechanism of the organism and the presence of accompanying pathology.
It is needed to remember, that the ulcer bleeding can accompany the perforation of ulcer.
During perforation, ulcers are often accompanied by bleeding. Correct diagnosis of these two
complications has important value in tactical approach and in the choice of method of surgical
treatment. In fact simple suturing of perforated and bleeding ulcer can lead to complications in
the postoperative period, as profuse bleeding and cause the necessity of repeat operation.

Diagnosis program

1. Anamnesis and physical examination.

2. Digital examination of rectum.
3. Gastroduodenoscopy.
4. General analysis of blood.
5. Coagulogram.
6. Biochemical blood test.
7. X-Ray examination of gastrointestinal tract.
8. Electrocardiography.

Differential diagnosis

With wide use of gastroduodenoscopy the question of differential diagnosis of bleeding is

less significant. However such a problem arises due to impossibility to use this method of
examination when the general condition of patient is bad or taking into account other reasons.
Differential diagnosis is conducted in bleeding of no ulcer origin, which can arise in different
parts of digestive tract.
For bleeding from the varicose veins of esophagus in patients with portal hypertension with
cirrhosis of liver the acute onset without pain is characteristic, like during exacerbation of ulcer
disease. This type of bleeding is massive and leading to considerable hemorrhage. Vomiting of
fresh blood, expressed tachycardia, falling of arterial pressure is observed. In such patients it is
possible to find the signs of cirrhosis of liver and portal hypertension ("head of jelly-fish",
hypersplenism, ascitis, icterus).
The cancer of stomach in the destruction stage can be also complicated by bleeding.
However, such bleeding is massive, and chronic character is carried mostly with gradual growth
of anaemia. In this pathology there is inherent worsening of the general condition of patient, loss
of weight of body, decrease of appetite and waiver of meat. At the rentgenologic examination the
"defect of filling" is seen in the stomach.
The gastric bleeding can be related to the diseases of the cardiovascular system
(atherosclerosis, hypertensive disease), however this is mainly seen in the older people. Clearly,
in such patients with endoscopic examination the source of bleeding can not be located.
Other diseases to be differentiated from ulcer bleeding are: the Mallory-Weiss syndrome,
benign tumors of stomach and duodenum (more frequent leiomyoma), hemorrhagic gastritis,
acute (stress) erosive defects of stomach, arteriovenous fistula of mucosa.
Often differential diagnosis performed according to the level of localization of source of
bleeding in different parts of gastrointestinal tract. For the upper parts of digestive tract
(esophagus and stomach) typical are: vomits like "coffee-ground" and stool is dark colored due
to "melena". During the bleeding from a small intestine excreta looks like "melena". In case of
such pathology of colon (polyps, tumors, unspecific ulcer colitis) the stool is usually contents
fresh red blood.
 41

Tactic and choice of treatment method

The conservative therapy is indicated for patients of I degree and whom bleeding has
stopped; for patients of II-III degrees with heavy accompanying pathology, because of operative
risk.
Conservative therapy must include:
- prescription of haemostatic preparations (intravenously the aminocapronic acid 5 % - 200-400
ml, chlorous calcium 10 % - 10,0 ml, vicasol 1 % - 3,0 ml);
- increase the volume of circulatory blood (gelatin, polyhlukine, salt blood substitutes);
- preparations of blood (fibrinogen - 2-3 r, cryoprecipitate);
- blood substitutes therapy (red corpuscles mass, washed red corpuscles, plasma of blood);
- antiulcer preparations - blocker of H2- receptor (ranitidine, roxatidine, nisatidine- for 150 mg
1-2 times per days);
- antacid and adsorbents (almagel, phosphalugel, maalox- for 1-2 dessert-spoons through 1 hour
after food intake).
It is important to wash stomach with ice water and the use 5 % solution of aminocapronic
acid 1 tablespoon every 20-30 minutes.
Absolute indications to surgical treatment are: 1) prolonged bleeding I degree; 2) recurrent
bleeding after hemorrhage I degree; 3) bleeding of the II-III degrees; 4) stopped bleeding with
hemorrhage of the II-III degrees with endoscopically exposed ulcer defect with the presence of
thrombosed vessels or erosive vessels filled with clotted blood, in the floor of the ulcer.
The choice of method of surgical treatment always needs to be decided individually. Today
the best tactic which gives advantage to organ saves and organ sparing methods of operations.
The removal of ulcer as a source of bleeding must be an obligatory condition.
Palliative operations (incision of ulcer, forming of roundabout anastomosis) can be justified
only by taking into account the general condition of patient.
In bleeding ulcers of duodenum it is better to excise the ulcer or exteriorize it with other
methods, developed by V.Zajtsev and Velihotsky. Operation complemented by one of types of
vagotomy, it is better by a selective proximal with pyloroplasty. The resection of stomach by the
second or first method of Billroth can be realized only if the general condition of patient is
stable. During the resection of stomach in case of low bleeding duodenal ulcers it is better to
execute mobilization of duodenum and suturing of its stump on the transcholedocheal drainage
which formed as transcholedocheal duodenotomy (Laqey, 1942). This method warns the
possible intraoperative damages of choledoch that are the possible at low duodenal ulcers.
Transcholedocheal duodenotomy by performing the decompression of stump of duodenum
warns insufficiency of its sutures that can arise up in an early postoperative period.
In case of bleeding gastric ulcers, the resection methods of operations can be performed.
Only occasionally, when patient’s general condition is grave, it is possible to perform the wedge
resection of ulcer.
 42

ACUTE INTESTINAL OBSTRUCTION

Intestinal obstruction is a complete or partial violation of intestinal function due to many

causes.

Etiology and pathogenesis

The principal causes of intestinal obstruction are:

1) adhesions of abdominal cavity after traumas, wounds, previous operations and inflammatory
diseases of organs of abdominal cavity and pelvis;
2) long mesentery of small intestine or colon, that predetermines considerable mobility of
their loops;
3) tumors of abdominal cavity and retroperitoneal space.
Such principal reasons can cause violation of intestinal function, disorder of adsorption
from the intestine and loss of plenty of electrolytes both by vomiting and in the intestine
cavity as a result of disorders of blood flow in its wall.

Pathomorphology

The morphological signs of dynamic intestinal obstruction are: slight thickening" of the
wall (with considerable paresis there is thinning), friability of tissue (the bowel perforates
easily) and presence of liquids and gases in lumen of bowel. In mechanical obstruction their is
always a causative factor like: adhesions, tumors, strangulated hernia, cicatricial strictures,
wrongly placed drainages, tampons and others like that. In place of compression strangulation
is present. Higher the strangulation the bowel is and distally - collapsed. In case of released
invagination on small distance two strangulation furrows are observed, and distally from the
second ring cylindrical expansion of bowel lumen is observed.

Classification (by D.P.Chuhrienko, 1958)

Acute intestinal obstruction is divided:

I. According to morphofunctorial signs.
1. Dynamic intestinal obstruction:
a) paralytic;
b) spastic;
c) haemostatic (embolic, thrombophlebitic).
2. Mechanical intestinal obstruction:
a) strangulated, volvulus, jamming;
b) obturation (closing of bowel lumen, squeezing from outside);
c) mixed (invagination, spike intestinal obstruction).
II. According to clinical features.
1. Acute.
2. Chronic.
III. According to the degree of loss of intestinal function.
1. Small intestinal.
2. Large intestinal:
a) high;
b) low.
IV. According to the passing of intestinal maintenance.
1. Complete.
2. Partial.
 43

V. According to the origin.

1. Innate.
2. Acquired.
VI. According to development of pathological process.
1. Stage of acute violation of intestinal motility.
2. Stage of haemodynamic disorders of bowel wall and its mesentery.
3. Stage of peritonitis.

Clinical management

The onset of clinical signs of intestinal obstruction is sudden and is seen within 1-2 hours
after taking the meal. The pain in the abdomen is intermittent and is seen in all forms of
mechanical intestinal obstruction. However, some types of strangulated intestinal obstruction
(node formation, volvulus of small intestine and colons) can be accompanied by permanent
pain. It is important to note that at the peak of intestinal obliteration, invagination and
obturation cramp-like pain can be considered as pathognomic sign of disease. For paralytic
intestinal obstruction more frequent is inherent permanent pain which is accompanied by
progressive.
In spastic obstruction of intestine the pain is mainly acute, the abdomen is not distended and
sometimes may be refracted.
Nausea and vomiting are present in 75-80 % patients with severe forms of high level
intestinal obstruction (node formation, volvulus of small intestine, obstruction). At obturation
obstruction and invagination they are not observed so often.
There is increased thirst which can be considered as an early symptom. Besides, the
higher intestinal obstruction, the greater is the complain of thirst.
Distension of abdomen, the delay of emptying and gases are observed in 85-90%
patients, mainly, with the high forms of obstruction (volvulus of small intestine, spike
intestinal obstruction).
Where as in invagination loose stools mixed with mucus and blood are more
characteristic.
During palpation the abdomen is soft sometimes - there is slight resistance over the
anterior abdominal wall, and at percussion - high tympanitis. On auscultation at the beginning of
the disease there is increased peristalsis, then gradually the peristalsis disappears (the Mondor's
symptom, "sounds of onset beginning, quietness of end").
There are other signs pathognomic for intestinal obstruction.
The Vala's sign is the elastic sausage-shaped deformity of the bowel.
The Sklarov's sign is the sound of intestinal splash.
The Kywul's sign is the sound above the exaggerated bowel.
The Schlange's sign is the peristalsis of bowel, that arises after palpation of abdomen.
The Spasokukotsky's sign is "sound of falling drop".
The Hochenegg's sign - incompletely closed anus in combination with balloon expansion
of ampulla of rectum.
On rentgenoscopy or –pornography of the abdominal cavity liquid and gas are observed in
bowels - the Kloyberg’s bowl.

Variants of clinical presentation and complications

Strangulated obstruction. The Ischemia is the characteristic feature of this form of intestinal
obstruction, that is due to presence investigation of constriction of mesenteric vessels, which
determines the dynamics of pathomorphologic changes and clinical signs of disease, and the basic
complaint is pain. Consequently, sudden appearance of disease, acuteness of pain syndrome
 44

and ischemic disorders in the wall of bowel cause necrotic changes in area of bowel affected by
the disease. It is accompanied by the progressive worsening of the patient condition and origin of
endotoxicosis.
Obturation intestinal obstruction, unlike strangulated, does not progress quickly. Clinically
the symptoms of violation of passage on the intestine (prolonged intermittent pain, flatulence),
instead of symptoms of bowel destruction and peritonitis.
For high, especially strangulated, intestinal obstruction progressive increase of clinical
signs of disease and violation of secretory function of intestine is inherent. Thus the volume of
circulatory blood diminishes, the level of haematocrit rises and leukocytosis increase. There is
violation of homeostasis (hypoproteinaemia, hypopotassaemia, hyponatraemia and hypoxia). In
patients with low intestinal obstruction features mentioned above- are less expressed, and their
progress more slow. Invagination of bowel which can be characterized by the triad of
characteristic signs is the special type of intestinal obstruction with the signs of both obturation
and strangulation: 1) periodicity of appearance of the intermittent attacks of pain in the
abdomen; 2) presence of elastic, insignificantly painful, mobile mass in an abdominal cavity;
3) appearance of blood in the stool or presence of blood in rectum (on rectal examination).
One of the special forms of obturation intestinal obstruction is the obstruction caused by
gall-stones. The stones reach the small intestine as a result of damage in the walls of gall-
bladder and bowel, that adjoins to it. It is needed to mention that intestinal obstruction can be
caused by calculus of considerably more small diameter than bowel lumen. The mechanism of
such phenomenon is related to irritating action of acids on the bile bowel wall. The last
explains this action by a spasm due to the dense wedging of stone in the bowel lumen.
In intestinal obstruction caused by gall-stones the features of colic and acute
cholecystitis always proceeds. Characteristically, that in the process of development of disease
the pain caused by acute cholecystitis calms down, whereas the pain characteristic of other
pathology like intestinal obstruction always reappears and persists.
Dynamic intestinal obstruction is divided into paralytic and spastic. Paralytic obstruction
often seen after various different abdominal operations, inflammatory diseases of organs of
abdominal cavity, traumas and poisonings. The spastic intestinal obstruction can be caused by
lead poisonings, poor-quality meal, neuroses, hysterias, helminthosis and etc. Clinical
presentation and signs of dynamic intestinal obstruction is always variable and depends on the
reason, that caused it. The disease is characterized by pain in the abdomen, delay of gases and
emptying. During palpation the abdomen is distended, painful, but soft. Diagnosis of this form
of intestinal obstruction is not difficult, especially, if its etiology is known.
Haemostatic intestinal obstruction develops after embolism or thromboses of mesenteric
arteries and thromboses of veins, or there can be mixed forms. Embolism of mesenteric arteries
is seen in patients with heart diseases (like mitral and aortic valve disease, myocardial
interaction, warty endocarditis) and usually damages, the superior mesenteric arteries. The
onset of disease, is acute, with nausea, sometimes — vomiting. At first there is a picture of
acute abdominal ischemic syndrome, that is often accompanied by shock (rapid pulse,
decrease of arterial and pulse pressure, cold and clammy skin, cyanosis of mucus membranes
and acrocyanosis). Patients become restless, uneasy, occupy the forced knee-elbow position or
lie on the side with legs flexed for relief.
During the examination of the abdomen it is symmetrical, abdominal wall is soft,
increased peristalsis is heard from the beginning to 1-2 hours (hypoxic stimulation of
peristalsis), which later decreases or disappears ("grave quiet"). According to the phenomena
of intoxication peritonitis grow quickly. At the beginning of disease the delay of gases and
emptying is observed, later there is diarrhea with the admixtures of blood in the stool. When it
is difficult to come to a diagnosis exploration of the intestine is necessary.

Investigations:

1. Anamnesis and physical methods of examination (auscultation, palpation of abdomen,

 45

percussion and others like that).

2. General analysis of blood, urine and biochemical blood test.
3. Plan rentgenography of organs of abdominal cavity.
4. Coagulogram.
5. Electrocardiography.
6. Irrigography.

Differential diagnosis

Intestinal obstruction must be differentiated from other acute diseases of organs of

abdominal cavity.
The perforation of gastroduodenal ulcer, as well as intestinal obstruction, arises acutely
with sudden intensive pain and increased tension of muscles of abdomen. However, in patients
with this pathology, unlike intestinal obstruction, the abdomen is not distended, it is retracted
on palpation it is rigid (heard like) due to tension of the muscles of anterior abdominal way.
There is also history of ulcer . Rentgenologic and by percussion pneumoperitoneum is observed.
Certain difficulties in conducting of differential diagnosis of intestinal obstruction can arise in
atypical cases and in case of healed perforations.
Acute pancreatitis almost always presents with the phenomena of dynamic intestinal
obstruction and symptoms of intoxication and repeated vomiting, with rapid progress. During
the examination of such patients, unlike intestinal obstruction, rigidity of abdominal wall and
painfulness is observed in the projections of pancreas and positive Korte's sign and Mayo-
Robson's. The examination of diastase in urine and amylase in blood have important value in
establishment of diagnosis.
Acute cholecystitis. Unlike intestinal obstruction, patients with this pathology complain of
pain in the right hypochondrium, that irradiate to the right shoulder-blade, right shoulder and
right subclavian area. Difficulties can arise, when the symptoms of dynamic intestinal
obstruction appear due to peritonitis.
The clinical presentation of renal colica similar to intestinal obstruction, however, attacks
of pain in the lumbar area with characteristic irradiation to genital region and the thigh and
disuric symptoms help to set the correct diagnosis. Certain difficulties in conducting of
differential diagnosis also can arise in difficult patients, who have frequent vomiting which
sometimes can be observed in patients with renal colic.

Techniques and choice of treatment method

In the first 1,5-2 hours after hospitalization of patient intensive conservative therapy is
started on lines of differential-diagnosis and simultaneously preoperative preparation is
conducted.
Treatment is directed to prevent the complications related to painshock, correction of
homeostasis and, simultaneously, an attempt to correct intestinal obstruction by inoperative
methods.
1. The measures directed against abdominal pain shock include use of neuroleptanalgesia, procaine
paranephral block and introduction of spasmolytics. In patients with the expressed pain syndrome
and spastic intestinal obstruction positive effect can be attained by epidural anesthesia also.
2. Correction of hypovolemia by correction of electrolyte, carbohydrate and albumin
exchange is achieved by introduction of salt blood substitutes, 5-10 % solution of glucose,
gelatinol, albumen and plasma of blood. There are a few methods suitable for use in the
calculation of amount of liquid necessary for correction of hypovolemia. Most simple and
accessible is calculation of the values of haematocrit. Consider 40 % as upper limit of
normal haematocrit end for every 5 % rise of haematocrit infuse 1000 ml of liquid.
3. Correction of haemodynamic indexes, microcirculation and desintoxication therapy is
achieved by intravenous infusion of Rheopolyglucin.
 46

4. Decompression of intestinal tract is achieved by nasogastral drainage and stomach wash,

and also by giving of siphon enema. It is important to note that technically the application of
siphon enema plays an important value in the attempt to correct intestinal obstruction by
conservative methods, therefore this manipulation must be conducted in the presence of
a doctor. For such enema special device with a rectal tip is used which is connected to a
PVC pipe with diameter of 1,5-2,0 cm and watering-can of very thin material. When
liquid enters into the colon the patient experiences pain , then the watering-can is
lowered below the level of patient who lies. The passage of gases and excrement is
looked after. As a rule, this manipulation is to repeat repeatedly with the use of plenty of
warm water (to 15-20 and more liters).
Correction of the intestinal obstruction by such conservative methods is successful in
50-60 % of the patients •with mechanical intestinal obstruction.
In patients with dynamic paralytic intestinal obstruction stimulation of peristalsis of intestine
is to be conducted, necessarily after infusion therapy and correction of hypovolemia. Many kinds
of stimulation of intestinal peristalsis are offered. Most common of them are: 1) hypodermic
introduction of 1,0 ml of 0,05 % solution of proserin; 2) through 10 min - 60 ml intravenously
stream of 10 % solution of chlorous sodium; 3) hypertonic enema.
Surgical treatment of intestinal obstruction must include the following important stages:
1. In middle laparotomy novocaine blockade of the mesentery of small and large intestine
is performed and operative exploration of organs of abdominal cavity is done during which
the cause of intestinal obstruction and the viability of intestines is looked for.
The revision in small intestinal obstruction begins with the Treitz' ligament to iliocaecal
corner. In large intestinal obstruction the hepatic, splenic and rectosigmoidal parts are
observed intently. Absence of pathological processes after revision must be fallowed by the
examination of other areas of the cavity sites of strangulation of internal hernia: internal
inguinal and femoral rings, obturator openings, pockets of the Treitz' ligament, Winslow's
opening, diaphragm and periesophageal opening.
2. Correction of causes of obstruction (release of adhesion, that compresses the bowel,
correction of volvulus and node formation of loops, desinvagination, removal of
obstructive tumors and others like that).
One should know that there's no unique method of correction of acute intestinal
obstruction. In the viability of bowel is lost then resection of nonviable area is performed
with 30-40 cm of afferent and 15-20 cm of efferent part with imposition of "end-to-end"
anastomosis.
3. Intubation. Decompression of intestine is carried out by passing an elastic probe of
thickness of 8-9 mm and length of 3-3,5 M with the multiply openings of diameter 2-2,5
mm all along probe, except in the parts, that will be in the esophagus, pharynx and
outside. A few methods of intubation are via the nose (nasogastral, trough gastrostomy,
trough caecostomy or trough an appendicostomy). The choice of the method is according to
the needs of the individual and the indication.
Each of them has its own the advantages and disadvantages. There's always a risk of
pneumonia while inserting the tube on older patient so in, entering an intubation probe to the
patients of old ages is better by means of gastrostomy. Most surgeons avoid the method of
introduction of probe through caeco- or appendicostoma because of technical difficulties of passing
in a small intestine through a Bauhin's valve. Today the most wide clinical application has
intubation of intestine extracted by the nasogastral method with the use of other thick probe as
explorer of the first (by L.J. Kovalchuk, 1981). Such method not only simplifies procedure of
intubation but also facilitates penetration through the pyloric sphincter and duodenojejunal
bend, and also warns passing of intestinal maintenance in a mouth cavity and trachea. Thus
probe is tried to be conducted in the small intestine as possible farther and deleted the next day
after appearance of peristalsis and passage of gases, however not later than on 7th days,
because more prolonged sign of probe carries the real threat of formation of bedsores in the wall
 47

of bowel.
4. Sanation and draining of abdominal cavity is performed by the generally accepted
methods of washing of antiseptic. Draining of the abdominal cavity it is needed from four
places: in both iliac areas and both hypochondrium, better by the coupled synthetic drainpipes.
 48

PERITONITIS

Peritonitis - is the acute or chronic peritoneal inflammation with characteristic local and
general changes in the organism and severe dysfunction of organs and vital systems.

Etiology and pathogenesis

The main causes of peritonitis are the acute inflammation of abdominal viscera,
discontinuity and disturbed permeability of their walls, open and closed traumas of the abdomen
with the damage of viscera with following microbial contamination of peritoneal space.
Despite the cause of peritonitis, the disease is characterized by a typical bacterial
inflammation. The infectious agents are represented by Escherichia colli, Staphylococcus and
Enterococcus, Proteus, Streptococcus and also nonclostridial anaerobes. At least in 30 % of
cases association of two or more agents occur.
Primary peritonitis occurs very rarely and results from pneumococcal, streptococcal and
staphylococcal infection.
Besides microbial peritonitis, caused by peritoneal contamination, distinguished also
aseptic peritoneal inflammation, which results from entering of different chemical noninfectious
agents into peritoneal cavity (blood, urine, bile, pancreatic juice, etc.). It's so called toxic
chemical peritonitis. But with the development of aseptic inflammation bacteria penetrate into
peritoneal space with transformation of peritonitis into bacterial.
Chronic peritonitis is mainly caused by tuberculosis, which agents are usually located
extraperitoneally (lungs, mediastinal lymph nodes) or in mesenteric lymph nodes and by
haematogenous way enter the peritoneum.

Classification

Peritonites are classified:

1. According to the character of microbial contamination: primary and secondary.
2. According to the clinical course: acute and chronic.
3. According to the etiological agents: peritonitis, caused by bacteria of digestive tract (E.
colli, staphylococci, streptococci, proteus, anaerobes, etc.) and also bacteria, which exist out of
gastrointestinal tube (gonococci, pneumococci, streptococcus haemolyticus, etc.). Also
distinguished septic (nonbacterial peritonites), resulting from irritation by blood, bile, ancreatic
juice or urine.
4. According to the character of exudate: serous, fibrinous, fibrin purulent, purulent,
hemorrhagic, "peritonitis sicca".
5. According to the extension of inflammatory process: local, diffuse nd generalized.

Dependent on duration and degree of pathological alterations in the clinical course of

peritonitis distinguished three stages:
• reactive (first 24 hours) — maximal manifestation of local signs of the disease;
• toxic (24-72 hours) — gradual reducing of local signs and increasing of internal intoxication.
• terminal (after 72 hours) - severe, often irreversible intoxication on the background of sharply
expressed local manifestation of peritoneal inflammation.

Symptomatology and clinical course

The clinical picture of acute peritonitis is determined by the character of primary causative
 49

lesion, duration of inflammatory process, its extension and also the stage of the disease.
Predominant clinical sign is the abdominal pain, which gradually increases. At first it is localized
in the region of the source of peritonitis and then extends all over the abdomen. Elderly patients
may experience lacking pain and even pay no attention on it, but general malaise, loss of
appetite, and weakness are evident. This course is also characteristic for postoperative
peritonitis, which results from parting of sutures (of anastomosis or site of perforation) or
leaking colon carcinoma. Simultaneously with the increase of pain also change the general
appearance. The patient looks anxious, with drawn features, hollowed-eyed. Further this is
accompanied by nausea and vomiting: on initial stages vomit consists of gastric contents, later -
duodenal and thereafter - intestinal contents. With progression of the disease vomiting becomes
constant, effortless and overcomes into frequent regurgitation by brown foul-smelling fluid.
Patient's lips and tongue are dry, with brown fur. Respiration is of thoracic type and is shallow
and rapid. In order to prevent pain the patient speaks very quite. Every change of position results
in increase of pain, thus the patient lies with the knee drawn up to relax the abdominal wall.
Often the vomiting is accompanied by hiccup, which results from irritation of
diaphragmatic peritoneum. This is considered to be an unfavorable prognostic sign. The patient
tries to retain distended abdomen by his hands during hiccup and thus provokes increase of pain.
During examination observed restricted movements of abdominal wall, which is mainly
expressed over the inflammatory focus. Abdominal percussion reveals the region of maximal
painfulness, which response the site of lesion, high tympanic sound as a result of intestinal
gaseous dilatation, but sometimes dullness, caused by cumulating of great amount of exudate.
On palpation revealed muscular tension of abdominal wall. Especially expressed the muscular
rigidity in case of perforation of hollow organs ("board-like abdomen"). Pelvic location of
peritonitis usually causes less clinical manifestations. In such cases a diagnostic value has digital
examination of the rectum and bimanual palpation of the pelvis and lower abdomen, which
reveals overhanging and painfulness of anterior rectal wall or posterior vaginal vault owing to
accumulation of the exudate.
The clinical manifestation of peritonitis is various and individual. It depends on the
character of primary lesion, extension of inflammatory process, and defensive properties of the
organism. In reactive stage of the disease the most common are the pain, muscular rigidity and
positive Shchotkin-Blumberg's symptom. The general state changed a little — the patient is
active, sometimes excite. A moderate tachycardia and hypertension are commonly observed. In
toxic stage of the disease the pain and muscular defense tends to dimmish, but on palpation the
muscular tenderness and Shchetkin-Blumberg's symptom retain on the same level. More evident
the signs of intestinal paresis (abdominal distension, absence of peristalsis). The general state is
worsened. The patient is apathetic, the skin is blanched or cyanotic. Observed progressing of
tachycardia, decreasing of blood pressure and rising of temperature. In blood analysis revealed
leukocytosis and deviation of the differential count to the left.
In terminal stage of the disease the feeling of pain disappears, but the patient suffers from
the uncontrollable vomiting by congested fecal contents. The patient is adynamic, with drawn
features and blanched or cyanotic skin. The pulse becomes increasingly rapid small and thready.
The arterial pressure tends to diminish. No peristalsis is evident and no bowel sounds are heard
on auscultation. Shchetkin-Blumberg's symptom is slightly expressed. The respiration is rapid,
with congested rales, and oliguria develops. This clinical pattern resembles a septic shock. The
prognosis in this stage is serious and the patient will die if the urgent treatment is not be applied.
Plain films of the chest and abdomen with the patient in both supine and the erect position
are essential. The chest x-ray examination assists in identifying thoracic causes of the acute
abdomen and sometimes reveals specific x-ray findings of intraabdominal catastrophes (e.g. free
air under the diaphragm associated with perforation of the gastrointestinal tract).
Laparoscopy is a rapid, direct, and often definitive method of identifying the cause of
peritonitis in difficult cases. Finally, for patients who have acute intraabdominal problem of
unknown nature and whose symptoms, signs, and laboratory findings are suggestive as treating
 50

life, exploratory laparotomy remains the most prudent diagnostic procedure.

Variants of clinical course and complications

Postoperative peritonitis is characterized by atypical and even asymptomatic course. This results
from administering of analgesics, antibiotics and anesthetics. The general state of the patient
after the operation is gradually worsens.
The most earliest and frequent sign of postoperative peritonitis is the increase of abdominal
pain on the background of the previous satisfactory condition, tachycardia, high temperature,
leukocytosis, deviation of the differential count to the left, elevation of erythrocyte sedimentation
rate. The pain and muscular rigidity usually expressed slightly or absent at all. Later (on the 5-6th
day) the general state continues to be worsened, which manifest by dry tongue, lack of
peristalsis, expressed nausea, vomiting, tachycardia and shallow breathing. General weakness,
adynamy, general intoxication and rebound tenderness symptoms progress. The outcomes of
postoperative peritonitis are usually unfavorable, and they prevented by early repeated operation.
The specific complications of acute peritonitis include inflammatory infiltrates and
abscesses of abdominal cavity (subphrenic, subhepatic, interintestinal and pelvic), dynamic ileus,
intestinal fistula, suppuration of postoperative wound, eventration, peritoneal adhesions, etc.

The patients with subphrenic abscess as a rule complain of the pain in epigastrium and
lower chest, which irradiates into the shoulder and increases during cough and deep breathing.
Sometimes revealed painfulness during digital pressing and swelling of soft tissues in the region
of VII-X intercostals space. The patients are suffering from nausea, hiccup, and high
temperature. Sometimes they must stay in forced position: supine or semi sedentary. The tongue
is dry, the abdomen is slightly bloated, and rebound tenderness symptoms are usually absent. In
blood revealed leukocytosis, deviation of the differential count to the left. The abscess requires a
surgical treatment. If the abscess is located near anterior abdominal wall, it is drained by means
of oblique access under the costal arch. The abscesses, which located in posterior subphrenic
space, are drained after the previous puncture through the access after resection of X rib.

Subhepatic abscess is characterized by the pain and presence of infiltrate below right
costal arch, positive Shchetkin-Blumberg symptom. The abscess is drained through the incision
along right costal arch.
The clinical pattern of interintestinal abscess is vague. It is formed mostly on the 12-14th
day after appearance of peritonitis. The patients complain of the high temperature and dull pain
in the site of its location. The abdomen is soft, but during palpation revealed dense, painful
infiltrate. In case of localization near to abdominal wall one can observe muscular tension and
positive Shchetkin-Blumberg symptom. The rentgenologic or ultrasound investigation often
reveals focal shadow with air-fluid level. The abscess is drained over the site of its localization,
dividing the bowel loops.
Abscesses of small pelvis mostly occur as a result of appendicitis or accumulation of the
exudate in Douglas space in diffuse peritonitis. Such patients complain of constant pain in the
lower abdomen, high temperature, painful urinary excretion and tenesmus. The palpation of the
abdomen usually reveals no pathology. But the digital rectal examination finds out a painful
infiltrate that drawn into the rectum. The mucosa over the infiltrate is edematous and immovable.
The vaginal examination of the female patients reveals overhanging of posterior vaginal vault
and painfulness of cervical shift. Often on the background of solid consistency of the infiltrate
the softened regions are palpated, which respond to accumulation of pus. The purulent sites of
small pelvis in males are drained through the anterior wall of the rectum and in females - through
the posterior vaginal vault. For this purpose the infiltrate is punctured by thick needle and under
its check the abscess is drained by means of scalpel incision. Then the incision is expanded by
clamp, the pus is aspirated and the abscess cavity is drained by rubber strap, which is fixed to
 51

perineum.

The diagnostic program

1. Complaints and history of the disease.
2. Physical findings.
3. General blood and urine analyses.
4. Biochemical blood analysis (protein and its fractions).
5. Examination of the exudate (bacteriological, cytological).
6. Laparoscopy.
7. Plain film of the abdomen.
8. Laparocentesis.

Differential diagnostics

The differential diagnostics in toxic and terminal stage of peritonitis when the typical signs
of the disease are present commonly makes no difficulties. But in initial (reactive) stage the sings
are similar to manifestation of causative disease (appendicitis, cholecystitis, pancreatitis, etc.).
But there are variety of disorders, which according to their manifestation resemble peritonitis,
renal colic for instance. A sharp pain, nausea, vomiting, intestinal paralysis, and false Shchetkin-
Blumberg symptom (peritonism) frequently lead to misdiagnosis. A periodical pain attack with
typical irradiation in thigh, perineum, dysuria, positive Pasternatsky's symptom, lack of
inflammatory changes in blood analysis, presence of erythrocytes in urine help to make correct
diagnosis. For its improvement applied x-ray film of the abdomen, urography and
chromocystoscopy.
A diffuse abdominal pain, muscular tension of abdominal wall and peritonism often
accompany hemorrhagic diatheses (Schonlein-Henoch's disease). This disorder mostly occurs in
young people and manifests by multiple small hemorrhages on skin (forearm, chest, and thigh),
mucous membranes of cheeks, tongue and peritoneum as well. The rectal examination reveals
tarry stool or melena. In blood thrombocytopenia is observed.
Myocardial infarction especially in its location on posterior wall (abdominal form) usually
accompanied by epigastric pain, nausea and vomiting. Also revealed abdominal wall tension
with phenomena of peritonism. But ischemic heart disease in history and characteristic ECG
changes can favor correct diagnostics.
Basal pleurisy and acute lower lobe pneumonia, causing the pain and muscular guard in
epigastrium, also resemble peritonitis. Only thorough clinical examination leads to correct
diagnostics.

Tactics and choice of treatment

The treatment of acute peritonitis should be always carried out with appreciation of clinical
form and stage of the disease, causative factor, extension of inflammatory process, degree of
metabolic disturbances and dysfunction of vital organs of the patient.
The complex of treatment of peritonitis should include:
1) early operative approach in order to liquidate the source of peritonitis;
2) sanation of peritoneal cavity by means of lavage, adequate drainage and antibiotic
therapy;
3) intubation and decompression of gastrointestinal tract and liquidation of paralytic ileus;
4) metabolic correction (acid-base balance, blood electrolytes, protein metabolism,
energetic metabolism);
5) restore and support of visceral function (kidney, liver, heart, lung) and prevention of
complications.
The preoperative preparation in patients with peritonitis should be individual and lasted at
least 2-3 hours. In extremely advanced cases, which associated with toxic shock and low arterial
 52

pressure it can last to 4-6 hours and must include nasogastral decompression of the stomach with
active aspiration, catheterization of two veins, one of which is central, catheterization of bladder
for diuresis control, infusion therapy.
The infusion therapy includes 5 % solution of glucose, solution of albumins, plasma,
rheopolyglucin, vitamins of B and C group, solution of sodium hydrocarbonatis. The volume of
fluid infusion should be at least 1.5-2 liters. If there are no improvement of patient's condition
before the operation, the infusion therapy must go on during operative approach.
The most common access in diffuse peritonitis is a median laparotomy, which is the most
suitable for abdominal revision. In case of localized peritonitis (acute appendicitis) oblique
incision may be used. The main goal of surgery must be elimination of infectious focus
(appendectomy, cholecystectomy) or closure of stomach opening (perforating ulcer) or
disrupture of hollow viscera. The exudate must be maximum removed and peritoneal cavity
washed up by antiseptic solutions and thereafter the intestinal decompression and draining of
peritoneal space is performed.
In diffuse peritonitis the peritoneal cavity is drained in right and left hypochondrium and
both left and right inguinal regions. It is better to use double or multiple polyethylene tubes,
which are the most suitable for peritoneal dialysis. Thus the infectious exudate and toxic
substances are eliminated and antibiotics and antiseptic solutions are flown into the abdomen
through these tubes. In 1.5-2 hours after the operation before the dialysis the patient takes a semi
sedentary position. Then the solutions flow in through the upper tubes and flow out through the
lower. This procedure is performed as far as the solution from the lower tubes becomes clear,
using for this purpose 10-25 liters of fluid.
In recent years instead of dialysis applied peritoneal lavage. Controllable peritoneostomy in
association with lavage, epidural anesthesia and intestinal intubation allow rather promptly to
carry out the sanation of peritoneal cavity and liquidation of inflammatory process. These
procedures are repeated in 1-2 days up to complete elimination of pus, fibrin and necrotic tissues.
After the last sanation the abdominal wall is closed (fig. 4).
Antibacterial therapy is performed by means of intraabdominal and parenteral
(intramuscular, intravenous, end lymphatic) administering of antibiotics. It is desirable to use
broad-spectrum antibiotics and after results of antibioticogram to apply their direct correction.
The antibiotics are advisable to use in combination with sulfanilamide, metrogyl,
immunostimulators.
A struggle against paralytic ileus is a very important in the complex of treatment of
peritonitis. It should begin during operation by means of intestinal decompression, mesenteric
blockade, gastric lavage, and detoxycation therapy. For restitution of peristalsis used proserin, 10
% solution of sodium chloride, hypertonic enema. One of the most important factors in the
treatment of peritonitis is the complete restore of the volume of circulating blood, correction of
acid-base balance, blood electrolytes, protein metabolism. The total amount of fluid is calculated
with account of its loss during vomiting, urinary excretion, drainage discharges and also
respiration. For energetic compensation infused concentrated solution of glucose, sorbitol and
lipid emulsion. Also plasma, erythrocyte and blood transfusions are used. In order to prevent
hypoxia oxygenotherapy or hyperbaric oxygenation are applied.
 53

BLUNT ABDOMINAL TRAUMA

The number of patients with blunt abdominal trauma is increasing annually, due to the
fact that each year an increasing number of vehicles on city streets, increasing traffic, increasing
the volume of construction work and level of industrialization in industry and agriculture, as well
as an increase in the number of people involved in sport.
Blunt abdominal trauma is a leading cause of morbidity and mortality. It is a leading
cause of intra-abdominal injuries. It is known that 19% of intra-abdominal injuries have no pain
(J.R.Varcelotti “Imaging in Blunt Abdominal Trauma” XIX Panamerican Trauma Congress). As
physical examination shows usually blunt abdominal trauma is more often in men than in
women.
In clinical practice we can distinguish two groups of abdominal trauma: closed (blunt)
and open injury.
Blunt abdominal trauma is divided into two groups: blunt abdominal trauma without injuries of
internal organs and the second is when there are injuries of internal organs.
It is very important while examining a patient to receive information about the nature of
trauma and treatment in the prehospital phase.
Physical examination of such patients is very important, but it is notoriously unreliable. It is due
to the fact that many patients can have altered mental state, drug and alcohol intoxication and
distracting injuries. So we need some additional information to indicate the diagnosis correctly.
For this purpose we use additional methods of examination.
Historical perspective shows that in the pre 1960’s the way of diagnose of abdominal
injuries was four quadrant paracentesis. During and after 1960’s the diagnostic peritoneal lavage
(DPL) was used. In 1980’s abdominal computed tomography scan (CT Scan) became the method
of diagnostics. In 1990’s focused abdominal sonography for trauma (FAST scan) was basically
used for diagnostics.
The choice of diagnostic method depends on some factors:
• patient’s clinical status

• accuracy of the study

• operator’s experience

• cost

• availability of procedure

Further evaluation requires the use of one or more of the following diagnostic modalities:

• Physical Examination (PE)

• Diagnostic Peritoneal Lavage (DPL)
• Ultrasound (FAST)
• CT Scan
• Laparoscopy
• Laparotomy

These different methods, each discussed below, are by no means equal. The decision on
which method, or combination of methods, to choose will depend primarily on hospital
factors such as trauma patient load, access to in-patient beds, availability of in-house surgical
teams, access to multislice CT scanners etc. Whichever decision tree is chosen should be
accepted at a hospital-wide level. The practice should not change from surgeon to surgeon
and day to day. The algorithm should be routinely audited for missed injuries, effectiveness
and use of resources.
 54

PE DPL FAST CT Laparoscopy Laparotomy

Scan
Sensitivity (%)
(for therapeutic 95-97 87-100 46-85 97 50-100 -
intervention)
Specificity (%) 100 52-89 48-95 98 74-90 -
NPV (%) 92 78-100 60-98 98 100 -

Requires awake,
cooperative + - - - - -
patient
Invasive - + - - + ++
Requires
+ - - - + +
admission
Evaluates
+/- - - + - +
retroperitoneum
High clinical
+ - - - +/- +/-
workload
Complication rate - +/- - - + ++

One of diagnostic method is abdominal X-Rays. It will help you to examine the patient, but it
is not the leading way of diagnostics. Abdominal X-Rays helps you to diagnose diaphragmatic
injury (especially useful with help of oral contrast or a nasogastric or orogastric tube),
pneumoperitoneum, retroperitoneal gas, rib fractures, spinal fractures and pelvic fractures. The
patient who has free air on abdominal x-ray needs rapid laparotomy, rather than an attempt to
localize the organ rupture. Similarly, the patient with hypotension, left upper quadrant pain, and
a positive peritoneal lavage needs surgery now. Assume a ruptured spleen. If it turns out to be a
bruised left abdomen and a laceration of the mesenteric blood vessels, so what? Your goal is to
identify the need for surgery.
The exam notes the location and relative severity of tenderness, and seeks any clues such as
broken ribs, or a steering wheel mark across the abdomen. If any evidence of injury is present,
make a decision about further evaluation after the secondary survey, when the patient’s other
problems are known. X-rays and peritoneal lavage may be used to screen for bowel laceration
or major bleeding.
Diagnostic peritoneal lavage (DPL) involves passing a small catheter into the peritoneal
cavity, usually at the umbilicus or just inferior to this. If blood can be aspirated through this
catheter, this is referred to as a positive 'tap' or aspiration (DPA). If no blood can be aspirated a
litre of warm crystalloid solution is run into the peritoneal cavity and then allowed to drain out.
This lavage fluid is then sent to the laboratory for analysis of red cell count, white cell count and
any bowel contents (faecal or food matter).
It is important to realise that the role of DPL in the haemodynamically stable patient is
diffierent from that in the unstable patient. In the unstable patient the problem is one of major
haemorrhage, and identifying the site of haemorrhage. DPL is used as an alternative to the FAST
scan to identify intra-peritoneal haemorrhage. In the unstable patient one is searching for a lot of
blood, so a positive DPL in this setting requires either a positive aspiration (DPA) or a high red-
cell count (>100,000/ml).
 55

If faecal or food matter is seen on microscopy this is diagnostic. However this is rarely the
case - and a decision to proceed to laparotomy is usually based on the red cell count. By
necessity this must be lower than that looking for gross haemorrhage, so the threshold for the red
cell count is set somewhere between 5000/ml and 20,000/ml. The lower the threshold, the more
sensitive the test, but the higher the non-therapeutic laparotomy rate. Contamination from the
insertion site of the DPL can lead to false positive results. Some units also use a white cell count
>500/ml as a positive result - this value is probably too low and 3000/ml is probably a better
threshold for gastrointestinal tract injury.
DPL can be done in two ways: open or closed. Open method is most secure in the following
situations: 1) pregnancy, 2) in the presence of multiple post-operative scarring of the anterior
abdominal wall, and 3) when the air is full of loops of small intestine (as seen, for example, in
resuscitation with ventilation of the lungs through a mask). It is seldom used in unstable patients.
In general DPL is used by infraumbilical approach (supraumbilical in pregnant patients or
patients with pelvic hematomas).
The primary disadvantages of DPL are that it is invasive, does not evaluate the retroperitoneum,
and has a signficiant false positive rate.

FAST (Focused Abdominal Sonogram for Trauma)

Ultrasound is used for any patient and is considered to be non invasive. It is used during the
initial assessment and resuscitation phase.
Ultrasound as yet cannot detect the small amounts of fluid which may be associated with a
hollow viscus injury. According to Branney, Morre FAST will detect minimum of 200cc of
fluid. According to Baulanger, Branney, Tso injures not associated with hemoperitoneum, may
not be detected by this modality.
Not a reliable method to exclude hollow visceral injury (Glasser, Buzzas, McKenney).
• A positive FAST indicates peritoneal penetration, but is poor at discriminating for injuries
requiring intervention
• A negative FAST does not exclude significant abdominal trauma.
FAST is non reliable in grading solid organ injury. Therefore in hemodinamically stable
patients, a follow up CT scan should be obtained if non op management is contemplated. It is
more cost effective when compare with DPL or CT.
Ultrasound transducer is placed in the pericardial area, right upper quadrant, left upper quadrant,
pouch of Douglas.
Therefore it is impossible to recommend FAST as the only investigation for the assessment of
blunt abdominal trauma. It MAY have a role in combination with other investigations.
CT Scan. As the technology has improved, CT scanning is finding more and more of a role in the
evaluation of blunt abdominal trauma. Most studies recommend a multidectector (multislice)
scanner with triple-contrast protocol (intravenous, oral and rectal), although it is not clear how
important the GI contrast is for the detection of bowel injury. Of all the diagnostic modalities
listed, CT gives the best assessment of retroperitoneal structures.
The CT features of bowel injury are:
• Signs of peritoneal violation
o Free intra-peritoneal air
o Free intra-peritoneal fluid
• Signs of bowel injury
o Bowel wall defect
o Bowel wall thickening
o Intra-luminal contrast leak
• Other signs of intra-peritoneal injury
o Intravenous contrast extravasation
o Diaphragmatic tear
The use of CT for blunt abdominal trauma remains in its infancy, and not all CT scanners have
 56

the resolution or software capabilities necessary to achieve the sensitivity and specificity rates.
Interpretation of the scans is also difficult and requires multiple passes on different 'window'
settings by a trained and experienced trauma radiologist.
Laparoscopy is also a technology somewhat in its infancy, and remains very user dependent. A
full trauma laparoscopy for the evaluation of blunt abdominal trauma requires general
anaesthesia and complete examination of intra-peritoneal contents, including visualisation of the
whole small bowel and intra-peritoneal colon. In most studies laparoscopy has a significant false
negative, primarily from missed bowel injuries. Laparoscopy is also limited in the evaluation of
retroperitoneal injury.
Laparoscopy is the diagnostic method of choice for the diagnosis of suspected diaphragmatic
injury. Many diaphragmatic lacerations can also be repaired via the laparoscope.
Laparoscopy may also have a role in patients who have localised tenderness or develop a white
cell count or fever without generalised peritonitis after a period of clinical observation.
Laparotomy
Exploratory laparotomy for all blunt abdominal trauma still has a role in resource-limited
environments, or occasionally in cases of multi-cavitary injuries. For most situations however
the non-therapeutic laparotomy rate will be unacceptable high. With the incidence of
complications with a negative laparotomy at of 12%-41%, with hospital stays of 4-8 days, , it is
difficult to support such a strategy where adjunctive methods such as CT or DPL are available
and physicial examination has such a low missed injury rate.

Blunt abdominal trauma without injuries of internal organs includes injuries of the anterior
abdominal wall. In these patients, during careful examination and palpation are often revealed
subcutaneous or intermuscular hematoma, indicating the rupture of anterior abdominal wall
muscles.
In cases where there is only damage to the anterior abdominal wall, such pathology is manifested
only minor pain in the anterior abdominal wall, the skin at the examination may be scratches or
bruises, while for severe injuries the anterior abdominal wall with subcutaneous ruptures of
muscles in patients have extreme pain, over the anterior abdominal wall muscles, belch, hiccup,
vomiting, bloating phenomena.
Method of physical examination helps to differentiate the subcutaneous ruptures of muscles in
patients from anterior abdominal wall injury without subcutaneous ruptures of muscles. During
PE we put hand on the front wall of the abdominal cavity and ask the patient to sit down. The
patient with subcutaneous ruptures of muscles is not able to sit down. DPL helps to indicate
internal organs injury in patients with anterior abdominal wall injury.
Treatment The contusion of anterior abdominal wall is treated conservatively. In cases of
muscle rupture the anterior abdominal wall with the presence of extensive hematoma – the drain
hematoma is used.

Parenchymatous organs injury.

The main cause of pathological changes and mortality in case of damage of parenchymatous
organs is blood loss. A possible additional source of pathological processes is products of
secretion of these bodies. Usually they are sterile and in the early period are less dangerous than
the loss of blood, which can be life-threatening. Therefore, immediate surgery to stop bleeding is
crucial. Intra-abdominal bleeding is accompanied by tachycardia and hypotension. If the
bleeding is limited to a certain space, the hematoma can be palpated or detected during
radiological examination. For isolated lesions of the spleen or liver often brings great benefit
reinfusion of blood during the operation.
 57

Liver Injury
The liver may be lacerated by either blunt or penetrating trauma. Liver laceration is common.
Biliary tract injury is unusual, and harder to diagnose.Liver injury can be divided into the
following types:
- Rupture of the liver capsule; - Subcapsular ruptures of parenchyma;
- - Capsule and parenchyma rupture;
- - Central ruptures of the parenchyma of the liver, leading to the formation of cysts
(posttraumatic) or hematobiliary fistula;
- - Porta liver injury;
- - Extensive injury of the liver.

Clinical Findings: In blunt trauma, there will often be fractures of the 7-9th ribs overlying the
liver. Right upper quadrant tenderness will be present. Pain can irradiate to the area of right
shoulder and right half of the neck. Rebound sensitivity and guarding will not be present until
blood has been in the abdomen long enough to cause peritoneal irritation — about two hours.
Very often liver injury accompanied bleeding (hemorrhagic shock): pale skin, cold clammy
sweat, tachycardia, increasing blood pressure).
Diagnosis: Suspect liver laceration when penetrating trauma involves the right lower chest or
right upper abdomen. While palpating tenderness in the right hypochondrium and muscular
tension in this area is revealed. Also the increasing of stomach volume is observed. Digital
investigation can show bulging of the anterior rectal wall. If the patient is stable, a CT scan of
the abdomen may demonstrate a laceration that can be managed non-operatively. If the patient is
in shock, or has other urgent injuries, DPL is used to confirm intraperitoneal hemorrhage.
Finding bile on peritoneal lavage means biliary tract injury.
Treatment: Many small lacerations can be followed conservatively. Large lacerations require
laparotomy and repair. Operation means final stop bleeding, removal of damaged and necrotic
liver tissue, liver wound closure and drainage of the abdominal cavity.
Complications: In the early postoperative period, the formation of gall fistula is possible. Fistulas
are usually close spontaneously with adequate drainage and the absence of obstruction in the
distal bile duct.
Sepsis, as a result of growing intrahepatic or peritoneal abscess is usually diagnosed with CT
scan and treated with drainage. This is done either during surgery or using percutaneous puncture
for CT or ultrasound control.
Another complication is injury of the vessels with formation of pseudoaneurysm and its
subsequent rupture and bleeding. This bleeding appears after several weeks or months after
injury, therefore particularly important to collect detailed medical history. Symptoms of this
syndrome include gastrointestinal bleeding, jaundice; abdominal colic, decreasing after
vomiting. For diagnosis angiography is used and it is used for embolization of fistula. Often
standard treatment is surgery, which means pseudoaneurysm resection.

Spleen Injury
The spleen is the most commonly injured organ in blunt abdominal trauma. Hypotension from
hemorrhage is the most common presenting finding.
Clinical Findings: The injury should be suspected when the 9-10th ribs on the left are fractured,
or when left upper quadrant tenderness and tachycardia, pale skin and mucous membranes,
increasing blood pressure are present. Pain can irradiate to the left shoulder and the left half of
the neck. Sometimes patients complain of nausea, vomiting. Commonly the patient complains of
pain in the left shoulder — but this is usually not present for an hour or two. Peritoneal signs
such as rebound sensitivity and guarding will be delayed until the blood has had time to cause
local irritation of the peritoneum.
Diagnosis: Any patient with tachycardia or hypotension and left upper quadrant tenderness is
assumed to have a ruptured spleen until proven otherwise. With percussion spleen borders may
 58

be expanded. Sometimes pain along back edge of muscle sternokleidomastoideus. In blood

analysis we can see decreasing of RBC and Hb, increasing of WBC. Establish the diagnosis by
peritoneal lavage in patients with evidence of significant hemorrhage, or by CT scanning in those
who are stable.
Treatment: Small lacerations may be observed in the hospital without repair. Larger lacerations
may be treated with oversewing, or by splenectomy.

Bowel Rupture
Most commonly, injuries that break the wall of the bowel are due to penetrating injury. In
penetrating trauma, the small bowel is most frequently injured, followed by the stomach and
large intestine.
Rupture also can occur when a localized crush occurs, such as when the steering wheel pinches
the duodenum against the spine. In blunt trauma, most commonly the duodenum is injured, due
to its location and its ligamentous attachments.
Clinical Findings: Symptoms are caused by the intestinal contents, rather than blood loss.
Stomach rupture causes rapid onset of burning epigastric pain, followed quickly by rigidity and
rebound sensitivity. Small bowel and colon injury may present only with vague generalized pain,
with peritonitis following after hours. Duodenal injury may cause back pain.
Diagnosis: The diagnosis of bowel rupture is made by finding free air on abdominal x-ray. Use a
decubitus or cross-table view for the patient who cannot stand for an upright view. Duodenal or
sigmoid colon injury may result in retroperitoneal air only. Peritoneal lavage will show WBCs
and intestinal content, except for retroperitoneal duodenal or sigmoid rupture. Contrast
examination may be required in equivocal cases, if surgery is not indicated for another reason.
Treatment: Surgical repair is required.

Pancreas Injury
Pancreatic injury is notoriously difficult to diagnose. Most cases are discovered only at surgical
exploration. The injury should be suspected after a localized blow to the mid-abdomen, such as
motorcycle handlebars or steering wheel. Pancreas injury has a high mortality. Duodenal or
biliary duct injury are often present as well.
Clinical Findings: Suspect the injury with any localized blow to the abdomen. The patient often
experiences vague upper and mid-abdominal pain that radiates into the back. Hours after the
injury, generalized peritoneal irritation may reveal the presence of traumatic pancreatitis.
Diagnosis: Serum amylase determinations are usually not helpful in the acute setting. A CT scan
establishes the diagnosis. Equivocal cases can be investigated with ERCP (endoscopic retrograde
canulation of the pancreas) once other injuries have been stabilized.
Treatment: Management may be surgical or conservative, depending on the degree of injury, and
on the presence of associated injuries. Surgical consultation is mandatory.

Kidney Injury
Kidney injury is common with falls and automobile accidents. Suspect it with fractures of the
11th-12th ribs or flank tenderness. If hematuria (to any degree) is present, the nature of the injury
must be determined. Kidney lacerations can bleed extensively into the retroperitoneal space.
Clinical Findings: The ruptured kidney usually presents with pain on inspiration in the abdomen
and flank, and CVA tenderness. Gross hematuria will almost invariably be present, but the injury
can still occur with only microscopic hematuria. Flank discoloration is a late finding that will
never be present in the emergency department. The contused kidney can present with identical
findings.
Diagnosis: Differentiating between the lacerated kidney and the contused kidney requires IVP
examination or CT scan. If a contrast study such as an aortogram is required for another reason,
the kidneys can be assessed during the course of that study. The lacerated kidney will show
leakage of dye, whereas the contused kidney will either be normal or show a “blush” of dye in
 59

the kidney stroma. A non-visualizing kidney implies severe rupture or avulsion of the renal
pedicle.
Treatment: The contused kidney is simply observed. Some kidney lacerations can be managed
non-operatively. Surgical consultation is mandatory for any kidney that shows extravasation of
dye.
 60

SEPSIS SYNDROME

Sepsis syndrome is a systemic response to infection that includes fever, tachycardia,

tachypnea, hypotension and organ dysfunction associated with compromised circulation.
Approximately 500,000 cases of sepsis occur annually in the United States, with mortality
ranging from 20-50% overall and as high as 90% when refractory hypoperfusion (shock)
develops. Bacterial superantigens, Gram-positive bacteria and even fungi can elicit sepsis.

- Common sites of infection are:

- Respiratory 25%.
- Urinary 25%.
- Soft tissues 15%.
- Gastro-intestinal 15%.
- Genital tract 10%.
- Foreign bodies 5%.
- Miscellaneous, including meningococcal 5%.
Bacterial, viral or fungal infection is confirmed in only 50% of cases of the systemic
inflammatory response syndrome (SIRS). Other causes of SIRS include trauma, burns,
pancreatitis and obstetrical catastrophe.
However the sepsis syndrome occurs most commonly in response to LPS from Gramnegative
bacteria (fig.1).

Fig.1.
Lipopolysaccharide (LPS) recognition occurs via the innate immune system.
LPS is a major constituent of Gram-negative bacterial cell walls and is essential for membrane
integrity. The toxic portion of LPS is referred to as endotoxin and has been localized to the
innermost and most highly conserved phosphoglycolipid, lipid A.
LPS is removed by macrophages through scavenger receptors (for example SR-A) which are
highly expressed in the liver and thus positioned to remove LPS from portal blood draining the
intestines, and by neutrophils through the primary granule protein, BPI, which is toxic to Gram-
negative bacteria.
Inflammation leads to widespread endothelial activation and organ dysfunction.
Cytokine production in the bloodstream results in widespread endothelial cell activation, with
expression of adhesion molecules, activation of the coagulation cascade and the production of
chemokines and cytokines by the endothelial cells themselves, thus amplifying the inflammatory
cascade. The adhesion and activation of circulating neutrophils at the endothelium results in both
oxidative and elastase-mediated damage, resulting in the loss of vascular integrity and
consequent failure to maintain adequate blood pressure. TNFα and IL-1 also depress myocardial
function directly. Refractory shock, with leakage of edema fluid, and the failure of organs with
 61

large capillary beds, such as the lung and kidney, leads to death (fig.2.).

Fig.2.
STAGES OF SEPSIS. CONSENSUS CONFERENCE DEFINITION

In 1991, a consensus conference in Chicago produced definitions of sepsis and its adverse
sequelae. Patients with sepsis are not all equally ill. Sepsis is a continuum of injury response
ranging from sepsis to septic shock to multiple organ dysfunction syndrome (MODS).
The term systemic inflammatory response syndrome (SIRS) defines the clinical manifestations
of the widespread inflammation that results from a variety of insults, including infection,
pancreatitis, trauma and burns. Sepsis was defined as the systemic inflammatory response to a
documented infection. Severe sepsis is associated with organ dysfunction, hypoperfusion or
hypotension (after excluding other causes of hypotension). Septic shock refers to those patients
who remain hypotensive despite adequate fluid resuscitation (fluid replacement) and who display
perfusion abnormalities such as lactic acidosis, oliguria and acute alteration in mental state.
MODS describes the presence of altered organ function such that haemostasis cannot be
maintained without intervention.

• Systemic Inflammatory Response Syndrome (SIRS).

Two or more of the following:
– Temperature of >38oC or <360C
– Heart rate of >90 beats/minute
– Respiratory rate of >20 breaths/minute, on blood gas a PaCO2 less than 32 mm Hg
(4.3 kPa) (tachypnea or hypocapnia due to hyperventilation).
– WBC count >12 x 109/L or <4 x 109/L or 10% immature forms (bands).
• Sepsis. SIRS plus a culture-documented infection.
• Severe Sepsis. Sepsis plus organ dysfunction, hypotension, or hypoperfusion (including
but not limited to lactic acidosis, oliguria, or acute mental status changes).
• Septic Shock. Hypotension (despite fluid resuscitation) plus hypoperfusion
• Multiple Organ Dysfunction Syndrome - dysfunction of 2 or more systems (Four or
more systems - mortality near to 100 percent)

Examples of end-organ dysfunction include the following:

1. Lungs
o acute lung injury (ALI) (PaO2/FiO2 < 300) or acute respiratory distress syndrome
(ARDS) (PaO2/FiO2 < 200)
2. Brain
encephalopathy
o symptoms:
 62

▪ agitation
▪ confusion
▪ coma
o etiologies:
▪ ischemia
▪ hemorrhage
▪ microthrombi
▪ microabscesses
▪ multifocal necrotizing leukoencephalopathy
3. Liver
o disruption of protein synthetic function: manifests acutely as progressive coagulopathy
due to inability to synthesize clotting factors
o disruption of metabolic functions: manifests as cessation of bilirubin metabolism,
resulting in elevated unconjugated serum bilirubin levels (indirect bilirubin)
4. Kidney
o oliguria and anuria
o electrolyte abnormalities
o volume overload
5. Heart
o systolic and diastolic heart failure, likely due to cytokines that depress myocyte
function
o cellular damage, manifest as a troponin leak (although not necessarily ischemic in
nature)

Factors Associated with Highest Mortality

• Respiratory > abdominal > urinary
• Nosocomial infection
• Hypotension, anuria
• Isolation of enterococci or fungi
• Gram-negative bacteremia, polymicrobial
• Body temperature lower than 38°C
• Age greater than 40
• Underlying illness: cirrhosis or malignancy

Predisposing Underlying Diseases

• Heart disease-rheumatic or congenital
• Splenectomy
• Intraabdominal sepsis
• Septic abortion or pelvic infection
• Intravenous drug abuse
• Immunocompromised

Organisms Responsible for Septic Shock in Relation to Host Factors

• Asplenia - Encapsulated organisms, Pneumococcus spp., Haemophilus influenzae,
Neisseria meningtidis, Capnocytophagia canimorsus, Babesiosis.
• Cirrhosis - Vibrio, Yersinia, and Salmonella spp., other Gram-negative rods (GNRs),
encapsulated organisms.
• Alcoholism - Klebsiella spp., Pnemococcus.
• Diabetes - Mucormycosis and Pseudomonas ssp., Malignant external otitis, Escherichia
coli.
• Steroids - Tuberculosis, Fungi, Herpes virus.
 63

• Neutropenia - Enteric GNR, Pseudomonas, Aspergillus, Candida, and Mucor spp.,

Staphylococcus aureus.
• T-cell abnortmalities - Listeria, Salmonella, and Mycobacteria spp., Herpes virus group
(herpes simplex virus, cytomegalovirus, varicella, zoster virus)

Bacteremia in the Preantibiotic Era

• Streptococcus pneumoniae
• Group A streptococcus
• Staphylococcus aureus
• Haemophilus influenzae
• Neisseria mennigitidis
• Salmonella spp.

Emergence of Gram-Negative Organisms

• Antibiotic pressure on normal flora
• Use of invasive devices
• Immune suppression

CLINICAL MANIFESTATIONS
• Fever, chills, hypotension
• Hypothermia, especially in the elderly
• Hyperventilation - respiratory alkalosis
• Diaphoresis, apprehension, change in mental status

History
• Community versus hospital-acquired
• Prior or current medications
• Recent manipulations or surgery
• Underlying diseases
• Travel history

Skin
• Furuncles, cellulitis, bullous lesions
• Intravenous sites, phlebitis
• Erythema multiforme
• Ecchymotic or purpuric lesions
• DIC, petechiae
• Ecthyma gangrenosum
• Purpura fulminans

Cardiovascular Signs
• Warm shock” -  CO,  SVR
• “Cold shock” -  CO,  SVR
• Anaerobic metabolism - lactic acidemia
• Myocardial depressant factor - ??

Pulmonary Signs
• Tachypnea
• Hyperventilation, respiratory alkalosis
• ARDS, respiratory failure
• Ventilation-perfusion mismatch
• Widened alveolar-arterial oxygen gradient
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• Reduced lung compliance

Hematologic Findings
• Neutrophilic leukocytosis
• Leukemoid reaction
• Neutropenia
• Platelet count < 80,000/mm3 or 50% drop from maximum in chronically
thrombocytopenic patients, OR
• International normalized ratio (INR) > 2
• Toxic granulations
• Disseminated Intravascular Coagulation

Renal Signs
• Acute tubular necrosis, oliguria, anuria
• Serum creatinine ≥ 2 times the upper limit of normal for age or 2-fold increase in
baseline creatinine in patients with chronic kidney disease.

Gastrointestinal Signs
• Upper gastrointestinal bleeding
• Total serum bilirubin ≥ 4 mg/dl, OR
• Alanine aminotransferase (ALT) ≥ 2 times the upper limit of normal
• Hypoglycemia

Neurologic dysfunction
• Glasgow Coma Score (GCS) ≤ 11, OR
• altered mental status with drop in GCS of 3 or more points in a patient with
developmental delay/mental retardation

LABORATORY STUDIES
• Blood cultures
• Infected secretions/body fluids
• Stool for WBC, Clostridium difficile
• Aspirate advancing edge of cellulitis
• Skin biopsy/scraping
• Buffy coat
• Procalcitonin

DIFFERENTIAL DIAGNOSIS OF FEVER AND SHOCK

A. Infectious
• Gram Negative sepsis
• Gram Positive Sepsis: Staphylococcal, Streptococcal, or Pneumococcal Bacteremia,
Toxic Shock Syndrome, Costridial Sepsis
• Atypical infection: Chlamydia psittici, Leionella, Typhoidal syndromes
• Viral Illness: Viral hemorrhagic fevers, Hantivirus syndrome
B. Idiopathic Vasculitides
• Polyarteritis Nodosa
• Giant Cell Arteritis
• ANCA-Related Vasculitides
• SLE - Systemic Lupus Erythematosus
• Cryoglovulinemia
• Serum Sickness
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C. Other Causes
• Pre-Eclampsia
• Anaphylactic Reactions: Drug reactions, Insect bites, Stevens Johnsons Syndrome (Toxic
Epidermal Necrolysis), Certain parasitic infections (as hydatid cyst)
• Microangiopathic Hemolytic Anemias (MAHA): Hemolytic Uremic Syndrome (HUS),
Thrombotic Thrombocytopenic Purpura (TTP), HELLP Syndrome (severe pre-
eclampsia)
• Severe Ulcerative Colitis
• Cholesterol Emboli Syndrome - eosinophilia may be present
• Adrenal Failure (Addisonian Crisis) - eosinophilia may be present

STANDARD TREATMENT

Approach to Septic Patient

• Seek primary site of infection
• Direct therapy to primary site
• Repeated examination

Routine management of the septic patient includes use of suitable antibiotics, taking into
account any positive microbiological culture results, the likely source of infection and likely
tissue uptake of the antibiotic.
In septic shock, there is an imbalance between oxygen supply and demand, resulting in cellular
and organ dysfunction. Fluid resuscitation attempts to reverse hypotension, which generally
refers to a mean arterial pressure below 65–70mmHg.
The choice of fluid is hotly debated: Europeans traditionally favor colloids, whereas
North Americans prefer crystalloids. In the presence of a dilated, high output circulation,
vasopressors, such as noradrenaline, are started if fluids fail to restore adequate arterial pressure
and organ perfusion. Noradrenaline preferentially acts on the alpha1-adrenoreceptor, thereby
causing vasoconstriction, which leads to an increase in systemic vascular resistance.
Myocardial depression is also a common sequela of sepsis and it can lead to a low cardiac
output (that is, less than 4L per minute). An inotrope, eg, adrenaline or dobutamine, is more
appropriate in myocardial depression.

Therapy of Septic Shock

• Correct pathologic condition
• Optimize intravascular volume
• Administer empiric antimicrobial therapy
• Administer vasoactive drugs
Empiric Antimicrobial Regimens for Sepsis Syndrome
• Community-acquired non-neutropenic
– Urinary tract: 3rd generation cepholosporin, piperacillin, quinolone +
aminoglycosides
– Non-urinary tract: 3rd generation cepholosporin + metronidazole, -lactam/ -
lactamase inhibitor + aminoglycosides
• Hospital-acquired
– Nonneutropenic: 3rd generation cephalosporin + metronidazole, -lactam / -
lactamase inhibitor, menopenem all + aminoglycosides
– Neutropenic: Timentin + aminoglycosides, meropenem + aminoglycosides;
ceftazidime + metronidazole + aminoglycosides
Immunotherapies for Septic Shock
• Corticosteroids
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• Vasopressin
• Methylene blue
• Antiendotoxin monoclonal antibodies E-5, HA-1A
• Anti-TNF antibodies
• IL-1 receptor antagonists
• Tissue factor pathway inhibitor (TFPI) is a naturally occurring anticoagulant and
antiinflammatory protein.
• Recombinant human activated protein C
Other Treatment Modalities
• Granulocyte transfusions
• Granulocyte-macrophage colony stimulating factor
• Diuretics
• Pentoxifylline, ibuprofen, naloxone
• Oral nonabsorbable antimicrobial agents

Prognosis
Prognosis can be estimated with the MEDS score. Approximately 20–35% of patients with
severe sepsis and 40–60% of patients with septic shock die within 30 days. Others die within the
ensuing 6 months. Late deaths often result from poorly controlled infection, immunosuppression,
complications of intensive care, failure of multiple organs, or the patient's underlying disease.
Prognostic stratification systems such as APACHE II indicate that factoring in the patient's age,
underlying condition, and various physiologic variables can yield estimates of the risk of dying
of severe sepsis. Of the individual covariates, the severity of underlying disease most strongly
influences the risk of dying. Septic shock is also a strong predictor of short- and long-term
mortality. Case-fatality rates are similar for culture-positive and culture-negative severe sepsis.

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