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 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 is defined as inflammation of the serosa membrane that lines the abdominal cavity and the organs contained therein. The , 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 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 , 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 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 ). This article focuses on the diagnosis and management of infectious peritonitis and abdominal . 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 Anatomy of the abdominal Determine the topographic Physiology cavity features of the abdominal cavity

2. Pathomorphology Theory of inflammation Describe macroscopic and Pathophysiology and its morphological changes of inflamed signs, etiological factors peritoneum of disease

3. Propedeutics of Sequence of patient’s Determine the patients internal diseases survey and physical complaints, medical history examination of the of the disease, perform abdominal cavity superficial and deep palpation of the 4. Pharmacology Groups and Prescribe conservative representatives of treatment of patient with , spasmolytics, acute peritonitis analgesics, anti- inflammatory , colloid and crystalloid solutions 5. Radiology Efficiency of radiological Indications and description of investigation in patients x-ray, ultrasound, computed with acute tomography examination Future subjects Anaesthesiology and Clinical signs urgent Determine the symptoms of Critical Care conditions that occur in urgent conditions, differential Medicine patients with diagnosis and treatment complications of acute peritonitis, methods of diagnosis and pharmacotherapy

Interdisciplinary integration 1. Acute Clinical picture of acute Check Mondor’s, Grey- pancreatitis Turner’s, Cullen’s, Mayo- Robson’s signs 2. Acute Clinical picture of acute Check Ortner’s, Kehr’s, cholecystitis Merphy’s, Mussy’s signs 3. Peptic ulcer of Clinical picture of peptic Check Blumberg’s sign, and ulcer of stomach and describe plain abdominal film duodenum in patient with peptic ulcer perforation 4. Acute bowel Clinical picture of acute Describe x-ray signs of acute obstruction bowel obstruction

5. Renal colic Clinical signs of renal Check Pasternacky’s sign colic

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 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 (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 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 . This function explains the development of polymicrobial liver abscesses in patients with severe cases of 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 . Up to 30 % of all patients with liver 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, , 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, (40 %), (7 %), Pseudomonas species, Proteus species, other gram-negative species (20 %)) and gram-positive organisms (eg, 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. 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 , 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. 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 , 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, 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 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 .  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, ), 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 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. , 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 , ), the abdominal pain may be generalized from the beginning. Anorexia and 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 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 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 12 Other 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 (CAPD). SBP occurring in children is usually associated with nephrogenic or hepatogenic ascites. Group A Streptococcus, , 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, 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 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 ), 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 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 , 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 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

Learning Main stages of the objective in Methods of Time class, their # the levels teaching and Guidelines distributi function and of control on meaning mastering Preliminary stage 1. Arrangements 5 min. 2. Determining the 1. Relevance 5 min. relevance, 2. Educ. objectives educational objectives and motivation 3. Control of the 45 min. input level of knowledge, skills and abilities: 1. Aetiology and І Survey Questions pathogenesis 2. Clinical signs ІІ Survey, tests Questions, II level MCQs 3. Diagnosis ІІ Clinical Typical clinical cases, MCQs cases, II level MCQ 4. Treatment ІІ Clinical Typical clinical cases, MCQs cases, II level MCQ Main stage 4. Formation of ІІІ 95 min. students professional skills: 1. Master the skills Practical Patients with acute of the physical training peritonitis examination 2. Perform Practical Patients with acute physical training peritonitis, patients examination of cards the patient with acute peritonitis 3. Plan the patients laboratory and Practical Clinical cases, III instrumental training level MCQs examinations 4. Differential diagnosis Practical Diagnostic training algorithms, atypical clinical 5. Treatment cases schemes Practical Typical and training atypical clinical cases

Final stage 5. Correction of the ІІІ Personal Clinical cases and 30 m professional skills skills III level MCQs i and abilities control, n analysis and . evaluation of the results of clinical work, clinical cases, level III MCQs

6. Summarizing class Results of patients examination, MCQs and clinical cases solutions 7. Homework Oriented card for (recommendation independent work of basic and with literature additional 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 (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.