MINISTRY OF HEALTHCARE OF UKRAINE

DANYLO HALYTSKY LVIV NATIONAL MEDICAL UNIVERSITY

DEPARTMENT OF SURGERY #1

ACUTE PERETONITIS. ETIOLOGY AND PATHOGENESIS.

CLASSIFICATION. CLINICAL PRESENTATION. TREATMENT

Guidelines for Medical Students

LVIV – 2019

Approved at the meeting of the surgical methodological commission of Danylo

Halytsky Lviv National Medical University (Meeting report № 56 on May 16, 2019)

Guidelines prepared:

GERYCH Igor Dyonizovych – PhD, professor, head of Department of Surgery

#1 at Danylo Halytsky Lviv National Medical University

VARYVODA Eugene Stepanovych – PhD, associate professor of Department of

Surgery #1 at Danylo Halytsky Lviv National Medical University

STOYANOVSKY Igor Volodymyrovych – PhD, assistant professor of

Department of Surgery #1 at Danylo Halytsky Lviv National Medical University

CHEMERYS Orest Myroslavovych – PhD, assistant professor of Department of

Surgery #1 at Danylo Halytsky Lviv National Medical University

Referees:

ANDRYUSHCHENKO Viktor Petrovych – PhD, professor of Department of

General Surgery at Danylo Halytsky Lviv National Medical University

OREL Yuriy Glibovych - PhD, professor of Department of General Surgery at

Danylo Halytsky Lviv National Medical University

Responsible for the issue first vice-rector on educational and pedagogical affairs at

Danylo Halytsky Lviv National Medical University, corresponding member of

National Academy of Medical Sciences of Ukraine, PhD, professor M.R. Gzegotsky

I. Background

Peritonitis is defined as inflammation of the serosa membrane that lines the

abdominal cavity and the organs contained therein. The peritoneum, which is an

otherwise sterile environment, reacts to a variety of pathologic stimuli with a fairly

uniform inflammatory response. Depending on the underlying pathology, the

resultant peritonitis may be infectious or sterile (i.e., chemical or mechanical).

Peritonitis is most often caused by introduction of an infection into the

otherwise sterile peritoneal environment through organ perforation, but it may also

result from other irritants, such as foreign bodies, bile from a perforated gall bladder

or a lacerated liver, or gastric acid from a perforated ulcer. Women also experience

localized peritonitis from an infected fallopian tube or a ruptured ovarian cyst.

Patients may present with an acute or insidious onset of symptoms, limited and mild

disease or systemic and severe disease with septic shock.

Peritoneal infections are classified as primary (i.e., from haematogenous

dissemination, usually in the setting of immunocompromise), secondary (i.e., related

to a pathologic process in a visceral organ, such as perforation, trauma, or

postoperative), or tertiary (i.e., persistent or recurrent infection after adequate initial

therapy).

Infections in the peritoneum are further divided into generalized (peritonitis)

and localized (intra-abdominal abscess). This article focuses on the diagnosis and

management of infectious peritonitis and abdominal abscesses. An abdominal abscess

is seen in the images below.

II. Learning Objectives

1. To study the etiological factors of disease, classification of acute peritonitis,

clinical signs, diagnostic methods, treatment and complications (α = I).

2. To know the main causes of the disease, typical clinical course and

complications, diagnostic value of laboratory and instrumental methods of

examination and the principles of the modern conservative and surgical treatment (α

= II).

3. To be able to collect and analyse the complaints and disease history,

thoroughly perform physical examination, determine the order of the most

informative examination methods and perform their interpretation, establish clinical

diagnosis, justify the indications for surgery, choose adequate method of surgical

intervention (α = III).

4. To develop creativity in solving complicated clinical tasks in patients with

atypical clinical course or complications of acute peritonitis (α = ІV).

III. Purpose of personality development

Development of professional skills of the future specialist, study of ethical and

deontological aspects of physicians job, regarding communication with patients and

colleagues, development of a sense of responsibility for independent decision

making. To know modern methods of treatment of patients with acute peritonitis and

its complications.

IV. Interdisciplinary integration

Subject To know To be able

Previous subjects

1. Anatomy and

Physiology

Anatomy of the abdominal

cavity

Determine the topographic

features of the abdominal

cavity

2. Pathomorphology

and Pathophysiology

Theory of inflammation

and its morphological

signs, etiological factors

of disease

Describe macroscopic

changes of inflamed

peritoneum

3. Propedeutics of

internal diseases

Sequence of patient’s

survey and physical

examination of the

abdominal cavity

Determine the patients

complaints, medical history

of the disease, perform

superficial and deep palpation

of the abdomen

4. Pharmacology Groups and

representatives of

antibiotics, spasmolytics,

analgesics, anti-

inflammatory drugs,

colloid and crystalloid

solutions

Prescribe conservative

treatment of patient with

acute peritonitis

5. Radiology Efficiency of radiological

investigation in patients

with acute appendicitis

Indications and description of

x-ray, ultrasound, computed

tomography examination

Future subjects

Anaesthesiology and

Critical Care

Medicine

Clinical signs urgent

conditions that occur in

patients with

complications of acute

peritonitis, methods of

diagnosis and

pharmacotherapy

Determine the symptoms of

urgent conditions, differential

diagnosis and treatment

Interdisciplinary integration

1. Acute pancreatitis Clinical picture of acute

pancreatitis

Check Mondor’s, Grey-

Turner’s, Cullen’s, Mayo-

Robson’s signs

2. Acute cholecystitis Clinical picture of acute

cholecystitis

Check Ortner’s, Kehr’s,

Merphy’s, Mussy’s signs

3. Peptic ulcer of

stomach and

duodenum

Clinical picture of peptic

ulcer of stomach and

duodenum

Check Blumberg’s sign,

describe plain abdominal film

in patient with peptic ulcer

perforation

4. Acute bowel

obstruction

Clinical picture of acute

bowel obstruction

Describe x-ray signs of acute

bowel obstruction

5. Renal colic Clinical signs of renal

colic

Check Pasternacky’s sign

V. Content of the topic and its structuring

Anatomy of the Peritoneal Cavity

The peritoneum is composed of a layer of polyhedral-shaped squamous cells

approximately 3 mm thick and may be viewed anatomically as a closed sac that

allows for the free movement of abdominal viscera. Adherent to the anterior and

lateral abdominal walls, the peritoneum invests the intraabdominal viscera in such a

way as to form the mesentery for the small and large bowel, a peritoneal diverticulum

posterior to the stomach (the lesser sac) and a number of spaces or recesses in which

blood, fluid, or pus can localize in response to various disease processes

Fluid can therefore collect in the right and left subphrenic spaces (left more

commonly than right), the subhepatic space (posterior to the left lobe of the liver),

Morrison’s pouch the lesser sac (usually in response to pancreatitis or pancreatic

injury), the left and right gutters (lateral to the left and right colon respectively), the

pelvis, and the interloop spaces (between the loops of intestine).

The Omentum

The omentum is a membranous adipose tissue within the peritoneal cavity

forming the roof of the lesser sac between the greater curvature of the stomach and

the transverse colon (lesser omentum) and a veil-like structure suspended from the

transverse colon covering the small intestine (the greater omentum).

Surgeons have referred to the omentum as “the policeman of the abdomen”

because of its role in walling off intraabdominal abscesses and preventing free

peritonitis. However, there is no evidence that there is any intrinsic omental

movement. The precise mechanism by which the intraabdominal viscera and the

omentum wall off collections of pus is not known. The omentum also contains areas

with high concentrations of macrophages called “milky spots” which play a major

role in the immune response to peritoneal infection.

The Retroperitoneum

The liver, duodenum, and the right and left colon are all partially invested by the

peritoneal membrane so that portions of these structures are actually located in the

retroperitoneum. The pancreas, kidneys, ureters, and bladder are located entirely in

the retroperitoneum. A long retrocecal appendix may be considered as a

retroperitoneal structure. These anatomical considerations are important because

injuries, diseases, or perforations of these structures in their retroperitoneal location

usually produce subtle early symptoms and signs that are often more difficult to

diagnose than intraperitoneal infections owing to delay in the onset of peritoneal

irritation.

Physiology of the Peritoneum

The major function of the peritoneal membrane is the maintenance of

peritoneal fluid balance. The bidirectional semipermeable membrane has an exchange

surface area of 1 m2. Normally the peritoneal cavity contains less than 100 ml of

serous fluid. Although the parietal peritoneum of the anterolateral abdominal wall

behaves as a passive semipermeable membrane, the diaphragmatic peritoneum is

capable of absorbing bacteria. Von Recklinghausen in 1863 described intercellular

gaps called stomata in the diaphragmatic peritoneum that serve as portals to the

diaphragmatic lymphatic pools, called lacunae. Lymph flows from the lacunae via

subpleural lymphatics to the regional lymph nodes and then to the thoracic duct. As

the diaphragm relaxes during exhalation, the stomata open and a negative pressure

develops, drawing bacteria into the stomata, which vary in size from 4 to 23 μm7

When the diaphragm contracts on inhalation, the stomata close and the increased

pressure propels the lymph through the mediastinal lymphatic channels. Peritoneal

fluid travels cephalad toward the diaphragm by action of the “diaphragmatic pump”.

The concept of the diaphragmatic pump is useful in explaining several clinical

phenomena observed in patients with peritoneal infection. Septicaemia in patients

with peritonitis may in part be explained by the rapid clearance of bacteria from the

peritoneum by the diaphragmatic lymphatics. The propensity for the development of

subphrenic abscess after peritonitis and the perihepatitis of the Fitz–Hugh–Curtis

syndrome related to pelvic inflammatory disease is probably related to the cephalad

flow of peritoneal fluid.

Peritoneal Response to Infection

The peritoneum responds to infection in three ways: rapid absorption of

bacteria via the diaphragmatic stomata and lymphatics; opsonisation and destruction

of bacteria via the complement cascade; and localization of bacteria within fibrin to

promote abscess formation. Two intraabdominal organs, the liver and spleen, filter

bacteria and serve to isolate the infected peritoneal cavity from the rest of the body.

The liver filters the portal circulation draining the gastrointestinal tract. This function

explains the development of polymicrobial liver abscesses in patients with severe

cases of diverticulitis and appendicitis. The spleen filters the systemic circulation and

plays an important adjuvant role in bacterial opsonisation during bacteraemia.

Frequency

The overall incidence of peritoneal infection and abscess is difficult to

establish and varies with the underlying abdominal disease processes. The most

common aetiology of primary peritonitis is spontaneous bacterial peritonitis (SBP)

caused by chronic liver disease. Up to 30 % of all patients with liver cirrhosis

with ascites develop SBC.

The common etiologic entities of secondary peritonitis (SP) include

perforated appendicitis; perforated gastric or duodenal ulcer; perforated (sigmoid)

colon caused by diverticulitis, volvulus, or cancer; and strangulation of the small

bowel (see Table 1). Necrotizing pancreatitis can also be associated with peritonitis in

the case of infection of the necrotic tissue.

Aetiology

Primary peritonitis

SBP occurs in the absence of an apparent intra-abdominal source of infection

and is observed almost exclusively in patients with ascites from chronic liver disease.

Contamination of the peritoneal cavity is thought to result from translocation of

bacteria across the gut wall or mesenteric lymphatics and, less frequently, via

haematogenous seeding in the presence of bacteraemia.

Approximately 10-30 % of patients with cirrhosis and ascites develop SBP.

The incidence rises with ascitic fluid protein contents of less than 1 g/dL (which

occurs 15 % of patients) to more than 40 %, presumably because of decreased ascitic

fluid opsonic activity.

More than 90 % of cases of SBP are caused by a monomicrobial infection. The

most common pathogens include gram-negative organisms (eg, Escherichia coli

(40 %), Klebsiella pneumoniae (7 %), Pseudomonas species, Proteus species, other

gram-negative species (20 %)) and gram-positive organisms (eg, Streptococcus

pneumoniae (15 %), other Streptococcus species (15 %), Staphylococcus species

(3 %)). Anaerobic microorganisms are found in less than 5 % of cases, and multiple

isolates are found in less than 10 %.

Secondary peritonitis

SP is by far the most common form of peritonitis encountered in clinical

practice. It is caused by perforation or necrosis (transmural infection) of a hollow

visceral organ with bacterial inoculation of the peritoneal cavity.

The pathogens involved in SP differ in the proximal and distal gastrointestinal

(GI) tract. Gram-positive organisms predominate in the upper GI tract, with a shift

toward gram-negative organisms in the upper GI tract in patients on long-term gastric

acid suppressive therapy. Contamination from a distal small bowel or colon source

initially may result in the release of several hundred bacterial species (and fungi);

host defences quickly eliminate most of these organisms. The resulting peritonitis is

almost always polymicrobial, containing a mixture of aerobic and anaerobic bacteria

with a predominance of gram-negative organisms.

As many as 15 % of patients who have cirrhosis with ascites who were initially

presumed to have SBP have SP. In many of these patients, clinical signs and

symptoms alone are not sensitive or specific enough to reliably differentiate between

the 2 entities. A thorough history, evaluation of the peritoneal fluid, and additional

diagnostic tests are needed to do so; a high index of suspicion is required.

Peritoneal abscess Peritoneal abscess describes the formation of an infected fluid collection

encapsulated by fibrinous exudate, omentum, and/or adjacent visceral organs. The

overwhelming majority of abscesses occurs subsequent to SP. Approximately half of

patients develop a simple abscess without loculation, whereas the other half of

patients develop complex abscesses secondary to fibrinous septation and organization

of the abscess material. Abscess formation occurs most frequently in the subhepatic

area, the pelvis, and the paracolic gutters, but it may also occur in the perisplenic

area, the lesser sac, and between small bowel loops and their mesentery.

The incidence of abscess formation after abdominal surgery is less than 1-2 %,

even when the operation is performed for an acute inflammatory process. The risk of

abscess increases to 10-30 % in cases of preoperative perforation of the hollow

viscus, significant fecal contamination of the peritoneal cavity, bowel ischemia,

delayed diagnosis and therapy of the initial peritonitis, and the need for reoperation,

as well as in the setting of immunosuppression. Abscess formation is the leading

cause of persistent infection and development of tertiary peritonitis.

Tertiary peritonitis Tertiary peritonitis represents the persistence or recurrence of peritoneal

infection following apparently adequate therapy for SBP or SP, often without the

original visceral organ pathology. Patients with tertiary peritonitis usually present

with an abscess, or phlegmon, with or without fistulization. Tertiary peritonitis

develops more frequently in immunocompromised patients and in persons with

significant pre-existing comorbid conditions. Although rarely observed in

uncomplicated peritoneal infections, the incidence of tertiary peritonitis in patients

requiring ICU admission for severe abdominal infections may be as high as 50-74%.

Patients who develop tertiary peritonitis demonstrate significantly longer

lengths of stay in the ICU and hospital, higher organ dysfunction scores, and higher

mortality rates (50-70 %). Resistant and unusual organisms (eg,

Enterococcus, Candida, Staphylococcus, Enterobacter, Pseudomonas species) are

found in a significant proportion of cases of tertiary peritonitis. Most patients with

tertiary peritonitis develop complex abscesses or poorly localized peritoneal

infections that are not amenable to percutaneous drainage. Antibiotic therapy appears

to be less effective in tertiary peritonitis than in all other forms of peritonitis, and up

to 90 % of patients will require reoperation for additional source control.

Tuberculous peritonitis (TP) is rare in the United States (<2 % of all causes of

peritonitis), but it continues to be a significant problem in developing countries and

among patients with human immunodeficiency virus (HIV). The presenting

symptoms are often nonspecific and insidious in onset (eg, low-grade fever, anorexia,

weight loss). Many patients with TP have underlying cirrhosis and more than 95 % of

patients with TP have evidence of ascites on imaging studies, and more than half of

these patients have clinically apparent ascites. In most cases, chest radiographic

findings in patients with TP peritonitis are abnormal; active pulmonary disease is

uncommon (<30 %). Results on Gram stain of ascitic fluid are rarely positive, and

culture results may be falsely negative in up to 80 % of patients. A peritoneal fluid

protein level greater than 2.5 g/dL, a lactate dehydrogenase (LDH) level greater than

90 U/mL, or a predominantly mononuclear cell count of greater than 500 cells/µL

should raise suspicion but have limited specificity for the diagnosis. Laparoscopy and

visualization of granulomas on peritoneal biopsy specimens, as well as cultures

(requires 4-6 wk), may be needed for the definitive diagnosis; however, empiric

therapy should begin immediately.

Chemical peritonitis Chemical (sterile) peritonitis may be caused by irritants such as bile, blood,

barium, or other substances or by transmural inflammation of visceral organs (eg,

Crohn disease) without bacterial inoculation of the peritoneal cavity. Clinical signs

and symptoms are indistinguishable from those of SP or peritoneal abscess, and the

diagnostic and therapeutic approach should be the same.

Pathophysiology

In peritonitis caused by bacteria, the physiologic response is determined by

several factors, including the virulence of the contaminant, the size of the inoculum,

the immune status and overall health of the host, and the elements of the local

environment, such as necrotic tissue, blood, or bile.

Alterations in fibrinolysis (through increased plasminogen activator inhibitor

activity) and the production of fibrin exudates have an important role in peritonitis.

The production of fibrin exudates is an important part of the host defence, but large

numbers of bacteria may be sequestered within the fibrin matrix. This may retard

systemic dissemination of intraperitoneal infection and may decrease early mortality

rates from sepsis, but it also is integral to the development of residual infection and

abscess formation. As the fibrin matrix matures, the bacteria within are protected

from host clearance mechanisms.

The ultimate effect (containment vs. persistent infection) of fibrin may be

related to the degree of peritoneal bacterial contamination. In animal studies of mixed

bacterial peritonitis examining the effects of systemic defibrinogenation and those of

abdominal fibrin therapy, heavy peritoneal contamination uniformly led to severe

peritonitis with early death (<48 h) because of overwhelming sepsis.

Bacterial load and the nature of the pathogen also play important roles. Some studies

suggest that the number of bacteria present at the onset of abdominal infections is

much higher than originally believed (approximately 2 X 108CFU/mL, much higher

than the routinely used 5 X 105 CFU/mL inocula for in vitro susceptibility testing).

This bacterial load may locally overwhelm the host defence.

Bacterial virulence factors that interfere with phagocytosis and with

neutrophil-mediated bacterial killing mediate the persistence of infections and

abscess formation. Among these virulence factors are capsule formation, facultative

anaerobic growth, adhesion capabilities, and succinic acid production. Synergy

between certain bacterial and fungal organisms may also play an important role in

impairing the host's defence. One such synergy may exist between B fragilis and

gram-negative bacteria, particularly E coli, where co-inoculation significantly

increases bacterial proliferation and abscess formation.

Enterococci may be important in enhancing the severity and persistence of

peritoneal infections. In animal models of peritonitis with E coli and B fragilis, the

systemic manifestations of the peritoneal infection and bacteraemia rates were

increased, as were bacterial concentrations in the peritoneal fluid and rate of abscess

formation. This is more important in light of the difficulties in

eradicating Enterococcus faecalis with conventional antimicrobial therapy. The role

of Enterococcus organisms in uncomplicated intra-abdominal infections remains

unclear. Antibiotics that lack specific activity against Enterococcus organisms are

often used successfully in the therapy of peritonitis, and the organism is recovered

uncommonly as a blood-borne pathogen in intra-abdominal sepsis.

Abscess formation occurs when the host defence is unable to eliminate the

infecting agent and attempts to control the spread of this agent by

compartmentalization. This process is aided by a combination of factors that share a

common feature, i.e., impairment of phagocytotic killing. Most animal and human

studies suggest that abscess formation occurs only in the presence of abscess-

potentiating agents. Although the nature and spectrum of these factors have not been

studied exhaustively, certain fiber analogues (eg, bran) and the contents of autoclaved

stool have been identified as abscess-potentiating agents. In animal models, these

factors inhibited opsonisation and phagocytotic killing by interference with

complement activation.

The role of cytokines in mediation of the body's immune response and their

role in the development of the systemic inflammatory response syndrome (SIRS) and

multiple organ failure (MOF) have been a major focus of research over the past

decade. Comparatively little data exist about the magnitude of the

intraperitoneal/abscess cytokine response and implications for the host. Existing data

suggest that bacterial peritonitis is associated with an immense intraperitoneal

compartmentalized cytokine response. Higher levels of certain cytokines (i.e., tumor

necrosis factor-alpha [TNF-alpha], interleukin [IL]-6) have been associated with

worse outcomes, as well as secondary (uncontrolled) activation of the systemic

inflammatory cascade.

Laboratory Studies

CBC with differential - Most patients will have leucocytosis (>11,000

cells/µL), with a shift to the immature forms on the differential cell count.

Patients with severe sepsis, who are immunocompromised, or who have certain

types of infections (eg, fungal, cytomegalovirus) may demonstrate absence of

leucocytosis or leukopenia. In cases of suspected SBP, hypersplenism may

reduce the polymorphonuclear leukocyte count.

Blood chemistry - May reveal dehydration and acidosis

PT, PTT, and INR

Liver function tests - If clinically indicated

Amylase and lipase - If pancreatitis is suspected

Urinalysis (UA) - To rule out urinary tract diseases (eg, pyelonephritis, renal

stone disease); however, patients with lower abdominal and pelvic infections

often demonstrate WBCs in the urine and microhematuria.

Stool sample - In patients with diarrhoea, evaluate a stool sample —

employing a Clostridium difficile toxin assay, a WBC count, and a specific

culture (i.e., Salmonella, Shigella, cytomegalovirus [CMV]) — if the patient's

history suggests infectious enterocolitis.

Aerobic and anaerobic blood cultures

Peritoneal fluid (i.e., paracentesis, aspiration of abdominal fluid collections,

intraoperative peritoneal fluid cultures)

o Diagnostic peritoneal lavage (DPL) may be helpful in patients who do

not have conclusive signs on physical examination or who cannot

provide an adequate history. A DPL with more than 500 leukocytes/mL

is considered positive and suggests peritonitis.

o Evaluate the sample for pH, glucose, protein, lactate dehydrogenase

(LDH), cell count, Gram stain, and aerobic and anaerobic cultures.

o Include analysis if pancreatitis or pancreatic leak is suspected.

o Test for bilirubin when a biliary leak is suspected and for fluid creatinine

level when a urinary leak is suspected.

o Compare the peritoneal levels to the respective serum levels.

Imaging Studies

Radiographs

o Plain films of the abdomen (eg, supine, upright, and lateral decubitus

positions) are often the first imaging studies obtained in patients

presenting with peritonitis. Their value in reaching a specific diagnosis

is limited.

o Free air is present in most cases of anterior gastric and duodenal

perforation but is much less frequent with perforations of the small

bowel and colon and is unusual with appendicular perforation. Upright

films are useful for identifying free air under the diaphragm (most often

on the right) as an indication of a perforated viscus. Remember that the

presence of free air is not mandatory with visceral perforation and that

small amounts of free air are missed easily on plain films.

Ultrasonography

o Abdominal ultrasonography may be helpful in the evaluation of right

upper quadrant (eg, perihepatic abscess, cholecystitis, biloma,

pancreatitis, pancreatic pseudocyst), right lower quadrant, and pelvic

pathology (eg, appendicitis, tubo-ovarian abscess, Douglas pouch

abscess), but the examination is sometimes limited because of patient

discomfort, abdominal distension, and bowel gas interference.

o Ultrasonography may detect increased amounts of peritoneal fluid

(ascites), but its ability to detect quantities of less than 100 mL is

limited. The central (perimesenteric) peritoneal cavity is not visualized

well with transabdominal ultrasonography. Examination from the flank

or back may improve the diagnostic yield, and providing the

ultrasonographer with specific information of the patient's condition and

the suspected diagnosis before the examination is important. With an

experienced ultrasonographer, a diagnostic accuracy of greater than 85%

has been reported in several series.

o Ultrasonographically guided aspiration and placement of drains has

evolved into a valuable tool in the diagnosis and treatment of abdominal

fluid collections

CT scanning

o If the diagnosis of peritonitis is made clinically, a CT scan is not

necessary and generally delays surgical intervention without offering

clinical advantage. CT scans of the abdomen and pelvis remain the

diagnostic study of choice for peritoneal abscess and related visceral

pathology. CT scanning is indicated in all cases in which the diagnosis

cannot be established on clinical grounds and findings on abdominal

plain films. Whenever possible, the CT scan should be performed with

enteral and intravenous contrast. CT scans can detect small quantities of

fluid, areas of inflammation, and other GI tract pathology, with

sensitivities that approach 100%.

o Peritoneal abscesses and other fluid collections may be aspirated for

diagnosis and drained under CT guidance; this technique has become a

mainstay of therapy.

Nuclear medicine scans (eg, gallium Ga 67 scan, indium In 111–labeled

autologous leukocyte scan, technetium Tc 99m-iminoacetic acid derivative

scan).

o These diagnostic studies have little use in the initial evaluation of

patients with suspected peritonitis or intra-abdominal sepsis. They are

most frequently used in the evaluation of fever of unknown origin or in

patients with persistent fever despite adequate antibiotic treatment and

negative CT scan findings.

Magnetic resonance imaging (MRI)

o MRI is an emerging imaging modality for the diagnosis of suspected

intra-abdominal abscesses. Abdominal abscesses demonstrate decreased

signal intensity on T1-weighted images and homogeneous or

heterogeneous increased signal intensity on T2-weighted images;

abscesses are observed best on gadolinium-enhanced, T1-weighted, fat-

suppressed images as well-defined fluid collections with rim

enhancement.

o Limited availability and high cost, as well as the need for MRI-

compatible patient support equipment and the length of the examination

currently limit its usefulness as a diagnostic tool in acute peritoneal

infections, particularly for patients who are critically ill.

Contrast studies

o Conventional contrast studies (i.e., Gastrografin swallow, upper GI tract

study with follow-through, colorectal contrast enema, fistulogram,

contrast studies of drains and stents) are reserved for specific indications

in the setting of suspected peritonitis or peritoneal abscess.

Presentation

The diagnosis of peritonitis is clinical. Abdominal pain, which may be acute or

insidious, is the usual chief complaint. Initially, the pain may be dull and poorly

localized (visceral peritoneum) and often progresses to steady, severe, and more

localized pain (parietal peritoneum). If the underlying process is not contained, the

pain becomes diffuse. In certain disease entities (eg, gastric perforation, severe acute

pancreatitis, intestinal ischemia), the abdominal pain may be generalized from the

beginning.

Anorexia and nausea are frequent symptoms and may precede the development

of abdominal pain. Vomiting may be due to underlying visceral organ pathology (i.e.,

obstruction) or be secondary to peritoneal irritation. On physical examination,

patients with peritonitis generally appear unwell and in acute distress. Many of them

have a temperature that exceeds 38° C, although patients with severe sepsis may

become hypothermic. Tachycardia is caused by the release of inflammatory

mediators, intravascular hypovolemia from anorexia vomiting and fever, and third-

space losses into the peritoneal cavity. With progressive dehydration, patients may

become hypotensive, as well as oliguric or anuric; with severe peritonitis, they may

present in overt septic shock.

On abdominal examination, almost all patients demonstrate tenderness to

palpation. (When examining the abdomen of a patient with peritonitis, the patient

should be supine. A roll or pillows underneath the patient's knees may allow for

better relaxation of the abdominal wall.) In most patients (even with generalized

peritonitis and severe diffuse abdominal pain), the point of maximal tenderness or

referred rebound tenderness roughly overlies the pathologic process (i.e., the site of

maximal peritoneal irritation).

Most patients demonstrate increased abdominal wall rigidity. The increase in

abdominal wall muscular tone may be voluntary in response to or in anticipation of

the abdominal examination or involuntary because of the peritoneal irritation.

Patients with severe peritonitis often avoid all motion and keep their hips flexed to

relieve the abdominal wall tension. The abdomen is often distended, with hypoactive-

to-absent bowel sounds. This finding reflects a generalized ileus and may not be

present if the infection is well localized. Occasionally, the abdominal examination

reveals an inflammatory mass.

Rectal examination often elicits increased abdominal pain, particularly with

inflammation of the pelvic organs, but rarely indicates a specific diagnosis. A tender

inflammatory mass toward the right may indicate appendicitis, and anterior fullness

and fluctuation may indicate a cul de sac abscess.

In female patients, vaginal and bimanual examination findings may be

consistent with pelvic inflammatory disease (eg, endometritis, salpingo-oophoritis,

tubo-ovarian abscess), but exam findings are often difficult to interpret in severe

peritonitis.

A complete physical examination is important. Thoracic processes with

diaphragmatic irritation (eg, empyema), extraperitoneal processes (eg, pyelonephritis,

cystitis, acute urinary retention), and abdominal wall processes (eg, infection, rectus

hematoma) may mimic certain signs and symptoms of peritonitis. Always examine

the patient for the presence of external hernias to rule out intestinal incarceration.

Remember that the presentation and the findings on clinical examination may be

entirely inconclusive or unreliable in patients with significant immunosuppression

(eg, severe diabetes, steroid use, posttransplant status, HIV), in patients with altered

mental state (eg, head injury, toxic encephalopathy, septic shock, analgesic agents),

in patients with paraplegia, and in patients of advanced age. With localized deep

peritoneal infections, fever and/or an elevated WBC count may be the only signs

present. As many as 20 % of patients with SBP demonstrate very subtle signs and

symptoms. New onset or deterioration of existing encephalopathy may be the only

sign of the infection at the initial presentation. Most patients with TP demonstrate

vague symptoms and may be afebrile.

Manheim peritonitis index

Risk factors Points

Age > 50 5

Female 5

Organ insufficiency 7

Malignant tumor 4

Duration of peritonitis > 24 hours 4

Colon as a source of infection 4

Diffuse peritonitis 6

Excudate:

Fecal-purulent

Other

12

6

Max score 47

Severity of peritonitis: І – 12-20 points, prognostic mortality rate – 0

ІІ – 21-29 points, prognostic mortality rate – up to 29 %

ІІІ – 30-47 points, prognostic mortality rate – 100 %

The Bacteriology and Antibiotic. Therapy of Peritonitis

The classification of peritonitis as primary peritonitis, secondary peritonitis, or

tertiary peritonitis is useful when considering its bacteriology and antibiotic therapy.

Primary peritonitis refers to an extraabdominal source of hematogenously transmitted

bacterial infection such as spontaneous bacterial peritonitis (SBP), tuberculosis

peritonitis, or peritonitis associated with chronic ambulatory peritoneal dialysis

(CAPD). SBP occurring in children is usually associated with nephrogenic or

hepatogenic ascites. Group A Streptococcus, Staphylococcus aureus, and

Streptococcus pneumoniae are the most common organisms. In adults, SBP is most

often associated with liver cirrhosis. Aerobic enteric flora such as Escherichia coli

and Klebsiella pneumoniae are the most common organisms.

Secondary bacterial peritonitis refers to infections arising as a result of

intraperitoneal processes such as hollow viscus perforation, biliary tract disease,

bowel ischemia, and pelvic inflammatory disease. There is a gradient of bacterial

concentration (organisms/ml) within the gastrointestinal tract ranging from 100 to

102 for the stomach, 104 to 106 for the distal small bowel, and 105 to 108 for the

colon. The consequences of perforation of different parts of the gastrointestinal tract

relate, in part, to these differences in bacterial concentration.

The primary treatment of secondary bacterial peritonitis is surgical correction

of the anatomical pathology and peritoneal toilet. Empiric antibiotic therapy for

established secondary bacterial peritonitis plays an important supplemental role. The

goals of antibiotic therapy are the prevention and treatment of both the systemic

inflammatory response syndrome (caused predominantly by facultative gram-

negative bacteria) and intraabdominal abscesses (caused predominantly by

anaerobes). For community-acquired infections of mild to moderate severity, single

drug therapy with a second-generation cephalosporin with activity against anaerobes

(e.g., cefotetan, cefoxitin) or a semisynthetic penicillin in combination with a

lactamase inhibitor (e.g., ticarcillin-clavulinic acid, ampicillin- sulbactam, or

piperacillin-tazobactam) is reasonable. For severe infections, coverage with an

aminoglycoside (e.g., gentamicin, tobramycin) and an antibiotic with anaerobic

coverage (e.g., metronidazole, clindamycin) is an excellent choice. Adjustments may

be made for concerns about nephrotoxicity or penicillin allergy. The newer

quinolones (e.g., levofloxacin) will probably assume an increasingly important role in

the management of intraabdominal infection because of their anaerobic coverage.

Antibiotics are recommended for 5 to 7 days for generalized peritonitis,13 although

therapy up to 14 days is reasonable for patients with severe faecal peritonitis.

Antibiotics should be stopped if the patient becomes afebrile and leucocytosis

resolves. If signs of infection persist despite a course of antibiotics, a search for an

intraabdominal abscess or other source of infection is necessary.

Ill-advised prolonged use of antibiotics, particularly in patients with persistent

sources of intraabdominal infection,

can lead to so-called tertiary peritonitis, opportunistic infection with normally

nonpathogenic gut flora such as Candida albicans, Enterococcus, and even

Staphylococcus. The development of tertiary peritonitis is a serious occurrence and a

poor prognostic sign.

Antibiotic therapy

Spontaneous bacterial peritonitis (SBP)

Untreated SBP has a mortality rate of up to 50 %, but with prompt diagnosis and

treatment of the condition, this figure may be reduced to 20 %. Empiric therapy with

a third-generation cephalosporin must begin promptly and can subsequently be

narrowed according to the culture results. Avoid aminoglycosides in patients with

liver disease, because these patients are at an increased risk for nephrotoxicity. The

optimal duration of therapy is not known; traditionally, a course of 10 days is

recommended, although studies have suggested that 5 days of therapy (with

documentation of a decrease of peritoneal fluid WBC count to <250 cells/μ L) may

be sufficient in most cases.

The patient with SBP is also likely to require attention to changes in

hemodynamic function related to inflammatory pathways, as well as resultant renal

function impairment, although a discussion of this is beyond the scope of this chapter.

There is a high risk of relapse after SBP (40-70 % in 12 months); a variety of

prophylactic antibiotic regimens are available. A preliminary study of norfloxacin for

primary prophylaxis of SBP was positive.

Secondary and tertiary peritonitis

In secondary and tertiary peritonitis, systemic antibiotic therapy is the second

mainstay of treatment. Several studies suggest that antibiotic therapy is not as

effective in the infection's later stages and that early (preoperative) systemic

antibiotic therapy can significantly reduce the concentration and growth rates of

viable bacteria in the peritoneal fluid. Antibiotic therapy begins with empiric

coverage (effective against common gram negative and anaerobic pathogens) and

should be initiated as soon as possible, with a transition made to narrower spectrum

agents as culture results become available.

Perforations of upper GI tract organs are associated with gram-positive bacteria,

whereas the distal small bowel and colon perforations involve polymicrobial aerobic

and anaerobic species.

Culture results may be especially important in tertiary peritonitis, which is more

likely to involve gram-positive bacteria (enterococci); antibiotic-resistant, gram-

negative bacteria; and yeast. In community-acquired infections, a second- or third-

generation cephalosporin or a quinolone with or without metronidazole provides

adequate coverage, as do broad-spectrum penicillins with anaerobic activity (i.e.,

ampicillin/sulbactam) and newer quinolones (i.e., trovafloxacin, clinafloxacin). Most

studies suggest that single-drug therapy is as effective as dual or triple combination

therapy in mild to moderate abdominal infections.

For peritoneal dialysis – associated infections, Cochrane reviews of all published

randomized, controlled trials have not found significant differences between

antimicrobial agents or combinations, with similar response and relapse rates for

glycopeptide regimens and first-generation cephalosporins. Intraperitoneal antibiotics

had a lower failure rate than intravenous regimens. Risk for early peritonitis is

reduced with perioperative intravenous antibiotics; other prophylactic approaches are

not yet proven.

In severe and hospital-acquired intra-abdominal infections, imipenem,

piperacillin/tazobactam, and a combination of aminoglycosides and metronidazole

are often effective. A study of nearly 400 patients documented that ertapenem, a

novel carbapenem with a half-life that allows once-a-day dosing, was effective

(86.7% success rate) compared to piperacillin/tazobactam (81.2 % success rate) in the

treatment of complicated intra-abdominal infection and was well tolerated.

Additional clinical antimicrobial studies are underway investigating the efficacy of

new quinolones in the treatment of intra-abdominal infection.

With persistence of the infection (i.e., tertiary peritonitis) and prolonged critical

illness, obtaining peritoneal fluid and/or abscess cultures with sensitivities at

operation or drainage is important to properly treat unusual (eg, gram-positive

organisms, fungi) and resistant organisms (eg, Enterococcus, Staphylococcus,

Pseudomonas, resistant Bacteroides, and Candida species). Certain preexisting

conditions, immunocompromise, gastric acid suppression therapy, and recent

antibiotic use may also influence the spectrum of microorganisms. Consultation with

infectious disease specialists is warranted in these cases.

The optimal duration of antibiotic therapy must be individualized and depends on

the underlying pathology, severity of infection, speed and effectiveness of source

control, and patient response to therapy. In uncomplicated peritonitis in which there

is early, adequate source control, a course of 5-7 days of antibiotic therapy is

adequate in most cases. Mild cases (eg, early appendicitis, cholecystitis) may not

need more than 24-72 hours of postoperative therapy. Inadequate initial therapy has

been linked to worse outcomes, and these outcomes could not be significantly

changed by later specific or prolonged therapy. Antimicrobial therapy should

continue until signs of infection (eg, fever, leucocytosis) have resolved; when signs

of infection continue, persistent infection or the presence of a nosocomial infection

should be investigated.

Some patients demonstrate persistent signs of inflammation without a defined

infectious focus. In these patients, continued broad-spectrum antibiotic therapy may

be more harmful than beneficial (eg, emergence of resistant organisms, C

difficile colitis), and a trial of antibiotic therapy cessation under close surveillance

may be warranted.

Complicated persistent infections and infections in patients who are

immunocompromised may warrant a prolonged course of antibiotic therapy. In these

cases, continuously seeking and aggressively treating all new extraperitoneal and new

or persistent intra-abdominal sources is important. The length of the individual course

of treatment is variable and is often linked to signs of resolution of the inflammatory

process (eg, lack of fever for >24-48 h, return of the WBC count to reference range

levels).

Of note, antibiotics alone are seldom sufficient to treat intra-abdominal abscesses,

and adequate drainage of the abscess is of paramount importance. For most of the

commonly used antibiotics, abscess fluid antibiotic levels are generally below the

minimum inhibitory concentration-90 (MIC90) for B fragilis and E coli, and repeated

dosing or high-dose therapy does not improve penetration significantly.

Nonoperative drainage

CT scan – and ultrasonographically guided percutaneous drainage are well

established as effective source controls and may in some cases decrease the need for

surgical therapy. In some instances, success also includes the ability to delay surgery

until the acute process and sepsis are resolved and a definitive procedure can be

performed under elective circumstances.

For primary percutaneous management of intra-abdominal abscesses, the

aetiology, location, and morphology of the abscess must be defined; evaluate for the

presence of an ongoing enteric leak or fistula formation. With proper indication, most

studies have reported success rates of greater than 80% (range 33-100%) for drainage

of localized nonloculated abscesses; however, the success rates depend to some

degree on the underlying pathology. In these studies, no significant differences were

found between operative and primary nonoperative management with regard to the

overall morbidity or length of hospital stay (mean duration of drainage 8.5 d).

Common reasons for failure of primary nonoperative management include enteric

fistula (eg, anastomotic dehiscence), pancreatic involvement, infected clot, and

multiple or multiloculated abscesses. Procedure-related significant complications are

reported to occur in less than 10% of cases (range 5-27%), with less than a 1%

attributable mortality rate with experienced physicians.

In peritoneal abscess formation caused by subacute bowel perforation (eg,

diverticulitis, Crohn disease, appendicitis), primary percutaneous management with

percutaneous drainage was successful in most patients. Patients with Crohn disease

whose abscesses were drained percutaneously had significantly fewer associated

fistulae. Failure in these patients was related to pre-existing fistulisation and

extensive stricture formation.

Concerns regarding the transgression of small or large bowel with drainage

catheters in deep abscesses or ileus have been addressed in animal studies, which

have found no increase in abscess formation, independent of whether catheters

remained for 5 days or longer. Similar data are not available for human patients.

In summary, percutaneous and surgical drainage should not be considered

competitive but rather complementary. If an abscess is accessible to percutaneous

drainage and the underlying visceral organ pathology does not clearly require an

operative approach, percutaneous drainage can be used safely and effectively as the

primary treatment modality. In these cases, patients must be closely monitored, and

improvement should be observed in less than 24-48 hours. With lack of

improvement, patients must be reevaluated aggressively (eg, repeat CT scan) and the

therapeutic strategy should be altered accordingly.

Surgical Therapy

Surgery remains a cornerstone of treating peritonitis. Any operation should

address the first 2 principles of the treatment of intra-peritoneal infections: early and

definitive source control and elimination of bacteria and toxins from the abdominal

cavity. The issue of timing and adequacy of surgical source control is paramount

because an improper, untimely, or incorrect operation may have an overwhelmingly

negative effect on outcome (compared to medical therapy).

The operative approach is directed by the underlying disease process and the

type and severity of the intra-abdominal infection. In many cases, the indication for

operative intervention will be clear, as in cases of peritonitis caused by ischemic

colitis, a ruptured appendix, or colonic diverticula. The surgeon should always strive

to arrive at a specific diagnosis and delineate the intra-abdominal anatomy as

accurately as possible prior to the operation.

However, in severe abdominal sepsis, delays in operative management may

lead to a significantly higher need for reoperations and to worse outcomes overall;

early exploration (i.e., prior to completion of diagnostic studies) may be indicated.

Surgical intervention may include resection of a perforated viscus with re-

anastomosis or creation of a fistula. To reduce the bacterial load, a lavage of the

abdominal cavity is performed, with particular attention to areas prone to abscess

formation (e.g., paracolic gutters, subphrenic area).

Among the causes of peritonitis, pancreatitis is unique in several ways. Patients

may present with significant abdominal symptoms and a severe systemic

inflammatory response, yet they may have no clear organ-specific indications for

emergent exploration. Not all cases of severe (i.e., necrotizing) pancreatitis and

peripancreatic fluid collections are associated with a superinfection.

These patients may best be served by a period of 12-24 hours of observation

and intensive medical support. Deterioration of the patient's clinical status or

development of organ-specific indications (eg, intra-abdominal bleed, gas-forming

infection of the pancreas) should lead to prompt operation. Percutaneous treatment is

reserved for the management of defined peripancreatic fluid collections in stable

patients. Pancreatic abscess or infected pancreatic necrosis generally should be

treated with surgical debridement and repeated exploration. If an anastomotic

dehiscence is suspected, percutaneous drainage is of limited value, and the patient

should be treated surgically. The images below demonstrate the results of an

anastomotic dehiscence following colon cancer surgery.

Open-abdomen technique and scheduled reoperation In certain situations, staging the operative approach to intraperitoneal

infections is appropriate. Staging may be performed as a scheduled second-look

operation or through open management, with or without temporary closure (eg, mesh,

VAC technique).

Second-look operations may be used in a damage control fashion. In these

cases, the patient at initial operation is severely ill and unstable from septic shock or

coagulopathy (eg, mediator liberation, disseminated intravascular coagulation). The

goal of the initial operation is to provide preliminary drainage and to remove

obviously necrotic tissue. Then, the patient is resuscitated and stabilized in an ICU

setting for 24-36 hours and returned to the operating room for a more definitive

drainage and source control.

In conditions related to bowel ischemia, the initial operation aims to remove all

frankly devitalized bowel. The second-look operation serves to re-evaluate for further

demarcation and decision-making regarding reanastomosis or diversion.

In severe peritonitis, particularly with extensive retroperitoneal involvement

(eg, necrotizing pancreatitis), open treatment with repeat reexploration, debridement,

and intraperitoneal lavage has been shown to be effective.

Temporary closure of the abdomen to prevent herniation and contamination from the

outside of the abdominal contents can be achieved using gauze and large,

impermeable, self-adhesive membrane dressings, mesh (eg, Vicryl, Dexon),

nonabsorbable mesh (eg, GORE-TEX, polypropylene) with or without zipper or

Velcro-like closure devices, and vacuum-assisted closure (VAC) devices. Advantages

of this management strategy include avoidance of abdominal compartment syndrome

(ACS) and easy access for reexploration. The disadvantages include significant

disruption of respiratory mechanics and potential contamination of the abdomen with

nosocomial pathogens.

For delayed primary closure (permanent), our experience with the use of

human acellular dermis (commercially known as AlloDerm) has been satisfactory,

although this option has the disadvantage of being more expensive than others.

The decision to perform a series of reexplorations may be made during the

initial surgery if additional debridement and lavage is needed beyond that which can

be achieved in the first procedure. Indications for planned relaparotomy may include

failure to achieve adequate source control, diffuse faecal peritonitis, hemodynamic

instability, and intra-abdominal hypertension.

Multiple reoperations may be associated with significant risks, including from

a substantial inflammatory response, fluid and electrolyte shifts, and hypotension;

however, these must be balanced against the risks of persistent necrotic or infectious

abdominal foci. The open-abdomen technique allows for thorough drainage of the

intra-abdominal infection, but the specific indications are not clearly defined. Many

trials lack control groups or use historical controls; outcome variables (eg, mortality)

are often not specific enough, and data on resource use are limited.

To date, no conclusive data suggest a clear advantage for the open-abdomen

versus the closed-abdomen technique in the treatment of severe abdominal sepsis;

however, in the author's experience, bowel edema and subsequent inflammatory

changes limit the use of the closed-abdomen technique. Secondary abdominal

compartment syndrome (secondary ACS) may ensue if abdominal closure is

performed before the inflammatory process has resolved.

In some cases, staged operative interventions will be planned. In other cases,

patients may present continued peritonitis or abscess formation requiring "on

demand" relaparotomy. A 2004 study suggested that the mortality rate of on-demand

laparotomy is higher for those patients receiving intervention more than 48 hours

after their index operation.

Laparoscopy

Laparoscopy is gaining wider acceptance in the diagnosis and treatment of

abdominal infections. As with all indications for laparoscopic surgery, outcomes vary

depending on the skill and experience of the laparoscopic surgeon.

Initial laparoscopic examination of the abdomen can assist in determination of

the aetiology of peritonitis (eg, right lower quadrant pathology in female patients).

Laparoscopic surgery is commonly used in the treatment of uncomplicated

appendicitis, although in preliminary studies, outcomes for complicated appendicitis

have generally been positive. For complicated and uncomplicated appendicitis, the

laparoscopic approach is associated with a shorter length of stay and fewer wound

infections than the open approach; however laparoscopic surgery may be associated

with a higher rate of intra-abdominal abscess.

Laparoscopic diagnosis and peritoneal lavage in patients with peritonitis

secondary to diverticulitis has been shown to be safe and has helped to avoid the need

for colostomy in many patients in small clinical trials. In a prospective study

comparing laparoscopic peritoneal lavage to an open Hartmann’s procedure for

perforated diverticulitis with generalized peritonitis, peritoneal lavage without

operative intervention was found to be feasible, with a comparable mortality rate and

a low risk of short-term recurrence. Successful laparoscopic repair of perforated

gastric and duodenal ulcers has also been reported.

No definitive guidelines have been established regarding the optimal selection

of patients for successful laparoscopic repair. Studies have been investigating scoring

systems (eg, APACHE II, Boey score) for patient risk stratification to better select

appropriate patients for laparoscopic repair.

The treatment of perihepatic infections via laparoscopic approach has been

well established in acute cholecystitis, where laparoscopic cholecystectomy has

become the mainstay of therapy. More recently, primary treatment of subphrenic

abscesses and laparoscopic, ultrasonographically assisted drainage of pyogenic liver

abscesses have been performed successfully.

Individual reports also describe successful drainage of peripancreatic fluid

collections and complicated intra-abdominal abscesses that are not amenable to CT

scan – or ultrasonographically guided percutaneous drainage.

As minimally invasive procedures continue to advance technologically, use of

these approaches is likely to increase, reducing the need for the open surgical

approach for peritoneal abscess drainage.

Complications

Complications related to percutaneous drainage Percutaneous drainage procedures carry a risk of related significant

complications of less than 10 % (range 5-27 %) depending on the underlying

pathology and abscess location. These complications include bleeding, injury,

erosion, transgression of small and large bowel, fistula formation, and others.

Strategies to prevent these problems include correction of coagulation problems and

determination of the exact aetiology, location, and anatomic relationships of the

abscess. Indication for percutaneous treatment of complex abscesses and patients

with a persistent enteric leak should be reviewed critically, and operative treatment

should not be delayed with lack of adequate patient improvement.

Tertiary peritonitis Persistence of intra-abdominal infection (i.e., tertiary peritonitis) is a

complication that may occur following the treatment of primary or secondary

peritonitis and peritoneal abscess. The details of this problem are described in the

different sections of this article.

Complications related to the open-abdomen technique One of the complications related to treatment of severe intra-abdominal

infections with the open-abdomen technique and multiple reoperations is the

development of enterocutaneous fistulae..

A study of trauma patients found that morbidity due to wound complications

(wound infections, abscess, and/or fistula) from the open abdomen remained high at

25 %. Enterocutaneous fistulae can lead to ongoing (potentially large) volume,

protein, and electrolyte losses; inability to use the gut for nutritional support; and

associated long-term complications of intravenous alimentation. Patients with small,

low-output, and distal fistulae often can be fed enterally with elemental diets. A

proportion of these fistulae close spontaneously as the patient's overall status and

nutritional status improve.

High-output and proximal fistulae often require a delayed surgical repair.

Optimal timing of this repair is critical. Initial inflammatory adhesions and dense scar

formation may make safe reexploration impossible. Maturation of the scar tissue

occurs over 6-12 months. Close observation of the patient's overall condition and

nutritional status is important during that time. Deterioration of the patient's condition

may force an earlier reoperation.

For an extended time after operations for intra-abdominal infections, patients are

at a several-fold increased risk of developing bowel obstruction related to intra-

abdominal scar formation. While in some patients this obstruction may be partial and

reversible and may improve with cessation of enteral intake and gastric

decompression, most patients require reoperation over time.

VI. Plan and structure of class

#

Main stages of the

class, their

function and

meaning

Learning

objective in

the levels

of

mastering

Methods of

teaching and

control

Guidelines

Time

distributi

on

1.

2.

Preliminary stage

Arrangements

Determining the

relevance,

educational

objectives and

motivation

1. Relevance

2. Educ. objectives

5 min.

5 min.

3. Control of the

input level of

knowledge, skills

and abilities:

1. Aetiology and

pathogenesis

2. Clinical signs

3. Diagnosis

4. Treatment

І

ІІ

ІІ

ІІ

Survey

Survey, tests

Clinical

cases, MCQs

Clinical

cases, MCQs

Questions

Questions, II level

MCQs

Typical clinical

cases, II level

MCQ

Typical clinical

cases, II level

MCQ

45 min.

4. Main stage

Formation of

students

professional skills:

1. Master the skills

of the physical

examination

2. Perform

physical

examination of

the patient with

acute peritonitis

3. Plan the patients

laboratory and

instrumental

examinations

4. Differential

diagnosis

5. Treatment

schemes

ІІІ

Practical

training

Practical

training

Practical

training

Practical

training

Practical

training

Patients with acute

peritonitis

Patients with acute

peritonitis, patients

cards

Clinical cases, III

level MCQs

Diagnostic

algorithms,

atypical clinical

cases

Typical and

atypical clinical

cases

95 min.

5.

Final stage

Correction of the

professional skills

and abilities

ІІІ

Personal

skills

control,

analysis and

evaluation of

Clinical cases and

III level MCQs

30 mi

n

.

6.

7.

Summarizing class

Homework

(recommendation

of basic and

additional

literature)

the results of

clinical

work,

clinical

cases, level

III MCQs

Results of patients

examination,

MCQs and clinical

cases solutions

Oriented card for

independent work

with literature

VII. Materials for classes

Questions (α =І, α =ІІ)

1. Aetiology and pathogenesis of acute peritonitis.

2. Classification of acute peritonitis.

3. Clinical signs of acute peritonitis.

4. Laboratory diagnosis of acute peritonitis.

5. Role of localization procedures in diagnosing of acute peritonitis.

6. Differential diagnosis of acute peritonitis.

7. Treatment of acute peritonitis.

8. Complications of acute peritonitis.

MCQs (α =ІІ)

1. Which statement is wrong concerning primary microbial peritonitis?

A. Occurs without perforation of a hollow viscus;

B. Occurs with perforation of a hollow viscus;

C. Caused by direct seeding of microorganisms;

D. Seeding of microorganisms via bacterial translocation from the gut;

E. Seeding of microorganisms via haematogenous dissemination.

Correct answer: D

2. Specify the main microorganisms, which are identified in the abdominal cavity of

patients with purulent peritonitis:

A. Monomicrobial;

B. Gram-positive microorganisms domination;

C. Gram-negative microorganisms domination;

D. Staphylococcus;

E. Streptococcus

Correct answer: B

3. Choose a reason for the use of metronidazole as a component of antibacterial

therapy of patients with diffuse peritonitis?

A. Elimination of anaerobic bacteria;

B. Elimination of gram-positive flora;

C. Elimination of gram-negative flora;

D. Elimination of fungal infections;

E. Antiprotozoal antibiotic

Correct answer: A

4. One of the listed below diseases didn’t cause secondary peritonitis:

A. Acute cholecystitis;

B. Destructive appendicitis;

C. Acute cholangitis;

D. Bowel obstruction;

E. Mesenteric infarction

Correct answer: E

5. Which sign is characterized by rebound tenderness over the site of abnormality in

patients with peritonitis?

A. Kocher’s sign;

B. Blumberg's sign;

C. Murphy’s sign;

D. Pasternatski’s sign;

E. Cullen’s sign.

Correct answer: B

Typical clinical cases (α =ІІ)

1. A 58-year-old woman is admitted with an acute surgical abdomen. After

resuscitation with IV crystalloids fluids and administration of antibiotics, she is taken

for an immediate laparotomy. Perforated diverticulitis of the sigmoid colon is found.

The sigmoid colon is inflamed but mobile and the mesentery contains a perforated

abscess. The best operation for this patient would be?

Answer: Sigmoid resection and end sigmoid colostomy and oversew the

rectum (Hartmann procedure)

2. A 63-year-old woman is admitted to the hospital with severe abdominal

pain of 3-hour duration. Abdominal examination reveals board-like rigidity,

guarding, and rebound tenderness. Her blood pressure is 90/50 mmHg, pulse 110

b/pm (beats per minute), and respiratory rate is 30 breaths per minute. After a

thorough history and physical, and initiation of fluid resuscitation, what diagnostic

studies should be performed?

Answer: Upright chest X-ray

Atypical clinical cases (α =ІIІ)

1. A 62-year-old patient admitted to the surgical department with complaints

of abdominal pain, repeated vomiting, which does not bring relief. The pain starts 2

hours before admission, after consumption of large amount of food. Patient anxious,

pale skin, acrocyanosis, pulse 120 bpm, BP 90/60 mmHg. Abdomen moderately

distended in the epigastric region, in the lower parts – sink in. On palpation -

tenderness of the abdominal wall. On percussion: tympanic sound in the epigastric

region, increased peristalsis. On plain abdominal film dilated small intestinal loops.

Make diagnosis?

Answer: Small intestine volvulus

2. A 76-years-old patient, who suffers from mitral stenosis and atrial

fibrillation, 6 hours ago appeared severe abdominal pain, vomiting, diarrhoea. On

examination: tenderness in mesogastrium, positive Blumberg sign. CBC: Leukocytes

– 21*109/l. What is the diagnosis?

Answer: Acute mesenteric occlusion

VIII. Literature

1. Textbook of Surgery / J. J. Tjandra, G.J.A. Clunie, A. H. Kaye [etc.] –

Massachusetts: Blackwell Publishing, 2006. – 708 p.

2. Essential Practice of Surgery/ J. A. Norton, R. R. Bollinger, A. E. Chang, S.

F. [etc.] – New York: Springer-Verlag, 2003. – 761 p.

3. Silen W. Cope’s Early Diagnosis of the Acute Abdomen. Oxford: Oxford

University Press, 1996.

4. Gypta H, Dupuy DE. Advances in imaging the acute abdomen. Surg Clin

North Am 1997;77:1245–1283.

5. Nathan AB, Rotstein OD, Marshall JC. Tertiary peritonitis: clinical features

of a complex nosocomial infection. World J Surg 1998;22:158–163.