eMedicine Specialties > General Surgery > Abdomen

Peritonitis and Abdominal Sepsis

Author: Ruben Peralta, MD, FACS, Professor of Surgery, Anesthesia and Emergency Medicine, Senior Medical Advisor, Board of Directors, Program Chief of Trauma, Emergency and Critical Care, Consulting Staff, Professor Juan Bosch Trauma Hospital, Dominican Republic
Coauthor(s): Thomas Genuit, MD, Assistant Professor, Department of Surgery, Program in Trauma and Surgical Critical Care, University of Maryland School of Medicine; Lena M Napolitano, MD, FACS, FCCP, FCCM, Professor of Surgery, University of Michigan School of Medicine; Chief, Surgical Critical Care, Program Director, Surgical Critical Care Fellowship, Associate Chair, Department of Surgery, University of Michigan Health System; Sarah Guzofski, MD, Staff Physician, Department of Psychiatry, University of Massachusetts Medical School
Contributor Information and Disclosures

Updated: Aug 2, 2006

Introduction

Peritonitis is defined as inflammation of the serosal membrane that lines the abdominal cavity and the organs contained therein. Peritonitis is often caused by introduction of an infection into the otherwise sterile peritoneal environment through perforation of the bowel, such as a ruptured appendix or colonic diverticulum. The disease may also be caused by introduction of a chemically irritating material, such as gastric acid from a perforated ulcer or bile from a perforated gall bladder or a lacerated liver. In women, localized peritonitis most often occurs in the pelvis from an infected fallopian tube or a ruptured ovarian cyst.

For excellent patient education resources, visit eMedicine's Esophagus, Stomach, and Intestine Center, Liver, Gallbladder, and Pancreas Center, and Blood and Lymphatic System Center. Also, see eMedicine's patient education articles Abdominal Pain in Adults, Appendicitis, Diverticulosis and Diverticulitis, Cirrhosis, and Sepsis (Blood Infection).

History of the Procedure

Untreated cases of acute peritonitis may be fatal. In 1926, the fundamental role of operative therapy in the treatment of peritonitis was documented. Kirschner (1926) reported that the mortality rate from intra-abdominal infections decreased from more than 90% to less than 40% during the period from 1890-1924 with the introduction of operative management as an effective therapeutic modality.

Current treatment of peritonitis and peritoneal abscesses consists of a multimodality approach directed at correction of the underlying cause, administration of systemic antibiotics, and supportive therapy to prevent or limit secondary complications due to organ system failure.

Problem

Inflammation and/or infection of the peritoneal cavity are commonly encountered problems in the practice of clinical medicine today. In general, the term peritonitis refers to a constellation of signs and symptoms, which includes abdominal pain and tenderness on palpation, abdominal wall muscle rigidity, and systemic signs of inflammation. Patients may present with an acute or insidious onset of symptoms, limited and mild disease, or systemic and severe disease with septic shock.

The peritoneum 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 (ie, chemical or mechanical).

Peritoneal infections are classified as primary (ie, spontaneous), secondary (ie, related to a pathologic process in a visceral organ), or tertiary (ie, persistent or recurrent infection after adequate initial therapy).

The intra-abdominal infections are usually divided into generalized (peritonitis) and localized (intra-abdominal abscess). This article focuses on the diagnosis and management of infectious peritonitis and abdominal abscesses.

Frequency

The overall incidence of peritoneal infections and abscess formation is difficult to establish and varies with underlying abdominal disease processes.

The most common etiology of primary peritonitis is spontaneous bacterial peritonitis (SBP) due to chronic liver disease. Approximately 10-30% of all patients with liver cirrhosis who have ascites develop bacterial peritonitis over time.

The common etiologic entities of secondary peritonitis (SP) include perforated appendicitis; perforated gastric and duodenal ulcer disease; perforated (sigmoid) colon caused by diverticulitis, volvulus, or cancer; and strangulation of the small bowel (see Table 1).

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*Iatrogenic trauma to the upper GI tract, including the pancreas and biliary tract and colon, often results from endoscopic procedures; anastomotic dehiscence and inadvertent bowel injury (eg, mechanical, thermal) are common causes of leak in the postoperative period.

After elective abdominal operations for noninfectious etiologies, the incidence of SP (caused by anastomotic disruption, breakdown of enterotomy closures, or inadvertent bowel injury) should be less than 2%. Operations for inflammatory disease (ie, appendicitis, diverticulitis, cholecystitis) without perforation carry a risk of less than 10% for the development of SP and peritoneal abscess. This risk may rise to greater than 50% in gangrenous bowel disease and visceral perforation.

After operations for penetrating abdominal trauma, SP and abscess formation is observed in a small number of patients. Duodenal and pancreatic involvement, as well as colon perforation, gross peritoneal contamination, perioperative shock, and massive transfusion, are factors that increase the risk of infection in these cases.

Etiology

SBP occurs in the absence of an apparent intra-abdominal source of infection and is observed almost exclusively in patients with ascites formation 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 hematogenous seeding in the presence of bacteremia.

Approximately 10-30% of patients with cirrhosis and ascites develop this problem over time. The incidence rises with ascitic fluid protein contents 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%]) (see Table 2). Anaerobic microorganisms are found in less than 5% of cases, and multiple isolates are found in less than 10%.

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SP is, by far, the most common form of peritonitis encountered in clinical practice today. It is caused by perforation or necrosis (transmural infection) of a hollow visceral organ with bacterial inoculation of the peritoneal cavity. The list of potential differential diagnoses is complex (see Table 1).

The spectrum of pathogens depends to some degree on the site of the original disease. Gram-positive organisms predominate in the upper GI tract; however, a shift toward gram-negative organisms may be noticed 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 defenses 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 (see Table 2).

As many as 15% of patients who have cirrhosis with ascites who were initially presumed to have SBP have secondary peritonitis. In many of these patients, clinical signs and symptoms alone are not sensitive or specific enough to reliably differentiate the 2 entities. A thorough history, evaluation of the peritoneal fluid, and additional diagnostic tests are needed to establish the correct diagnosis and treatment in these patients.

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.

In general, the incidence of abscess formation after abdominal surgery is less than 1-2%, even when the operation is performed for an acute inflammatory process. This incidence increases with preoperative perforation of the hollow viscus, significant fecal contamination of the peritoneal cavity, bowel ischemia, delayed diagnosis and therapy of the initial peritonitis, the need for reoperation, and in the setting of immunosuppression. In these instances, the risk of abscess formation may be as high as 10-30%. Overall, abscess formation is the leading cause of persistent infection and development of tertiary peritonitis.

Tertiary peritonitis represents the persistence or recurrence of peritoneal infection following apparently adequate therapy of 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 patients with significant preexisting comorbid conditions and in patients who are immunocompromised. 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, and 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 less effective compared to all other forms of peritonitis.

Tuberculous peritonitis (TP) is a rare disease in the United States (<2% of all causes of peritonitis), but it continues to be a significant problem in underdeveloped countries and among patients with HIV disease. The presenting symptoms are often nonspecific and insidious in onset (eg, low-grade fever, anorexia, weight loss).

More than 95% of patients have evidence of ascites on imaging studies, and more than half of these patients have clinically apparent ascites. Most patients have evidence of cirrhosis, and the diagnosis of TP may be unsuspected. Chest radiograph findings are abnormal in most patients, but active pulmonary disease is present in fewer than 30% of patients. 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, lactate dehydrogenase (LDH) level greater than 90 U/mL, or predominantly mononuclear cell count greater than 500 cells/µL should raise suspicion but has limited specificity for the diagnosis. Laparoscopy and visualization of granulomas on peritoneal biopsy specimens, as well as positive results on cultures (requires 4-6 wk) may be needed for the definitive diagnosis; however, empiric therapy should begin immediately.

Chemical (sterile) peritonitis may be caused by irritant substances such as bile, blood, barium, and other substances or by transmural inflammatory processes 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

Peritonitis causes a reduction in the intra-abdominal fibrinolytic activity (increased plasminogen activator inhibitor activity) and fibrin sequestration with subsequent adhesion formation. The production of fibrinous exudates is considered an important part of the host defense, but large numbers of bacteria may be sequestered within the fibrin matrix. This may lead to retardation of spread and systemic dissemination 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 defibrinogenization and those of abdominal fibrin therapy, heavy peritoneal contamination uniformly led to severe peritonitis with early death ( <48 h) because of overwhelming sepsis.

Abscess formation has been viewed as a host defense strategy to contain the spread of infection; however, this process can lead to persistent infection and life-threatening sepsis.

The initiation of abscess formation involves the release of bacteria and an abscess-potentiating agent into a normally sterile environment. The host defense is unable to eliminate the infecting agent and attempts to control the spread by compartmentalization. This process is aided by a combination of factors that share a common feature, ie, impairment of phagocytotic killing. Some studies suggest that the number of bacteria present at the onset of abdominal infections is much higher than originally believed (approximately 2 X 10⁸ CFU/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 defense.

In minimal contamination, bacterial clearance was complete in nearly 100% of cases, and no differences in outcome were observed among fibrin-depleted, normal, and fibrin-treated groups. With moderate contamination, fibrin-treated animals demonstrated a significantly reduced early mortality rate but developed more abdominal abscesses. Finally, studies with adhesion-reducing devices (ie, bioresorbable membranes) increased the incidence of peritonitis and peritoneal infections in experimental peritonitis models.

Transient bacterial peritoneal contamination (caused by primary visceral disease and intentional or unintentional violation of the gut) is common. The resultant exposure to bacterial antigens has been shown to alter subsequent immune responses to recurrent peritoneal inoculation. This may lead to an increased incidence of later abscess formation, alteration of the bacterial content, and increased late mortality rates. More recent studies have shown that nosocomial infections at other sites (eg, pneumonia, line sepsis, wound infections) also increase the likelihood of subsequent abdominal abscess formation.

Bacterial virulence factors that interfere with phagocytosis and neutrophil-mediated bacterial killing are important mediators leading to persistence of infections and abscess formation. Among these 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 defense. 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 bacteremia 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.

The role of fungi in the formation of intra-abdominal abscesses is not fully understood. Abdominal infections, particularly with Candida species, are becoming increasingly common in critically ill patients. Studies suggest that the microbiology of intra-abdominal infections may be inherently different in severely ill patients. Candida albicans was the organism most commonly isolated from the peritoneum in critically ill patients with culture-proven intra-abdominal infections and preoperative APACHE II (acute physiology and chronic health evaluation) scores greater than or equal to 15, with an associated mortality rate of 52%. Additional common peritoneal organisms in this patient population were Enterococcus and Enterobacter species and Staphylococcus epidermidis. These data suggest that broader antimicrobial, and possibly antifungal, coverage may be warranted in patients with severe abdominal sepsis.

Some authors suggest that bacteria and fungi exist as nonsynergistic parallel infections with incomplete competition, allowing the survival of all organisms. In this setting, treatment of the bacterial infection alone may lead to an overgrowth of fungi, which may contribute to increased morbidity. Predisposing factors for the development of abdominal candidiasis include prolonged use of broad-spectrum antibiotics, gastric acid suppressive therapy, central venous catheters and intravenous hyperalimentation, malnutrition, diabetes, and steroids and other forms of immunosuppression.

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 has not been studied exhaustively, certain fiber analogues (eg, bran) and the contents of autoclaved stool have been identified as such abscess-potentiating agents. In animal models, these factors inhibited opsonization 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 (ie, 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.

Presentation

The diagnosis of peritonitis is usually clinical. Essentially, all patients present with some degree of abdominal pain. This pain may be acute or more insidious in onset. Initially, the pain is often dull and poorly localized (visceral peritoneum) and then progresses to steady, severe, and more localized pain (parietal peritoneum). If the infectious 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 frequently present and may precede the development of abdominal pain. Vomiting may occur because of the underlying visceral organ pathology (ie, obstruction) or secondary to the peritoneal irritation.

On physical examination, patients with peritonitis most often appear unwell and in acute distress. Fever with temperatures that can exceed 38°C is usually present, but patients with severe sepsis may present with hypothermia. Tachycardia is caused by the release of inflammatory mediators and intravascular hypovolemia caused by anorexia and vomiting, fever, and third-space losses into the peritoneal cavity. With progressive dehydration, patients may become hypotensive, they may demonstrate decreased urine output, and, with severe peritonitis. They may present in overt septic shock.

On abdominal examination, essentially 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 (ie, the site of maximal peritoneal irritation).

Nearly all 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 may lead to the differential diagnosis of pelvic inflammatory disease (eg, endometritis, salpingo-oophoritis, tubo-ovarian abscess), but the findings are often difficult to interpret in severe peritonitis.

When evaluating the patient with suspected peritoneal infection, performing 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 carefully 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 only vague symptoms and may be afebrile.

Indications

Early control of the septic source is mandatory and can be achieved by operative and nonoperative means. Nonoperative interventional therapies include percutaneous drainage of abscesses and percutaneous and endoscopic stent placements. 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.

Operative management addresses the need to control the infectious source and to purge bacteria and toxins. The type and extent of surgery depends on the underlying disease process and the severity of intra-abdominal infection. Open treatment allows for thorough drainage of the intra-abdominal infection, but the specific indications are not clearly defined.

Relevant Anatomy

The peritoneum is the largest and most complex serous membrane in the body. It forms a closed sac (ie, coelom) by lining the interior surfaces of the abdominal wall (anterior and lateral), by forming the boundary to the retroperitoneum (posterior), by covering the extraperitoneal structures in the pelvis (inferior), and by covering the undersurface of the diaphragm (superior). This parietal layer of the peritoneum reflects onto the abdominal visceral organs to form the visceral peritoneum. It thereby creates a potential space between the 2 layers (ie, the peritoneal cavity).

The peritoneum consists of a single layer of flattened mesothelial cells over loose areolar tissue. The loose connective tissue layer contains a rich network of vascular and lymphatic capillaries, nerve endings, and immune-competent cells, particularly lymphocytes and macrophages. The peritoneal surface cells are joined by junctional complexes, thus forming a dialyzing membrane that allows passage of fluid and certain small solutes. Pinocytotic activity of the mesothelial cells and phagocytosis by macrophages allow for clearance of macromolecules.

Normally, the amount of peritoneal fluid present is less than 50 mL, and only small volumes are transferred across the considerable surface area in a steady state each day. The peritoneal fluid represents a plasma ultrafiltrate, with electrolyte and solute concentrations similar to that of neighboring interstitial spaces and a protein content of less than 30 g/L, mainly albumin. In addition, peritoneal fluid contains small numbers of desquamated mesothelial cells and various numbers and morphologies of migrating immune cells (reference range is <300 cells/µL, predominantly of mononuclear morphology).

The peritoneal cavity is divided incompletely into compartments by the mesenteric attachments and secondary retroperitonealization of certain visceral organs. A large peritoneal fold, the greater omentum, extends from the greater curvature of the stomach and the inferior aspect of the proximal duodenum downward over a variable distance to fold upon itself (with fusion of the adjacent layers) and ascends back to the taenia omentalis of the transverse colon. This peritoneal fold demonstrates a slightly different microscopic anatomy, with fenestrated surface epithelium and a large number of adipocytes, lymphocytes, and macrophages, and it functions as a fat storage location and a mobile immune organ.

The compartmentalization of the peritoneal cavity, in conjunction with the greater omentum, influences the localization and spread of peritoneal inflammation and infections.

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