eMedicine Specialties > General Surgery > Abdomen
Peritonitis and Abdominal Sepsis
Updated: Jan 28, 2010
Introduction
Peritonitis is defined as inflammation of the serosal 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 (ie, 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 (ie, from hematogenous dissemination, usually in the
setting of immunocompromise), secondary (ie, related to a pathologic process in a visceral organ, such as perforation, trauma, or postoperative), or tertiary (ie, 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.
A 35-year-old man with a history of Crohn disease presented with pain and swelling in the right abdomen. In figure A, a thickened loop of terminal ileum is evident adherent to the right anterior abdominal wall. In figure B, the right anterior abdominal wall is markedly thickened and edematous, with adjacent inflamed terminal ileum. In figure C, a right lower quadrant abdominal wall abscess and enteric fistula are observed and confirmed by the presence of enteral contrast in the abdominal wall.
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, acute peritonitis may be fatal. The fundamental role of operative therapy in the treatment of peritonitis was documented in 1926 when Kirschner 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. Other elements, such as advances in the understanding of damage control surgery, novel antibiotics, and improvements in intensive care unit (ICU) treatment have now reduced mortality to approximately 20%.
The current approach to peritonitis and peritoneal abscesses targets correction of the underlying process, administration of systemic antibiotics, and supportive therapy to prevent or limit secondary complications due to organ system failure.
Frequency
The overall incidence of peritoneal infection and abscess is difficult to establish and varies with the underlying abdominal disease processes. The most common etiology 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 SBP.1
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.
SP also occurs, albeit infrequently, in patients with cirrhosis. In a retrospective analysis, Soriano et al compared the clinical characteristics and prognosis of SP with SBP in cirrhotic patients (24 patients with SP vs 106 episodes of SBP).2 The authors found that SP accounted for 4.5% of peritonitis cases in the study's cirrhotic patients. They also determined that in patients whose SP had been confirmed by surgery or autopsy, the diagnostic sensitivity and specificity of Runyon's criteria was 66.6% and 89.7%, respectively, with Runyon's criteria and/or polymicrobial ascitic fluid culture found in 95.6% of the patients. Abdominal computed tomography (CT) scanning was diagnostic in 85% of these patients.
The local inflammatory response in the study's patients with SP was significantly more severe than it was in patients with SBP, and the mortality rate during hospitalization was higher for SP than for SBP patients (66% vs 26.4%, respectively).
However, patients with SP who underwent surgical treatment tended to have a lower mortality rate than did those who received only medical therapy (53.8% vs 81.8%, respectively). Among the surgically treated patients with SP, the survival rate was greater in those with the shortest time between diagnostic paracentesis and surgery (3.2+/-2.4 days in survivors vs 7.2+/-6.1 days in nonsurvivors, p=0.31). Soriano and colleagues concluded that the prognosis of cirrhotic patients with SP could be improved via a low threshold of suspicion on the basis of Runyon's criteria and microbiologic data, prompt use of abdominal CT scanning, and early surgical evaluation. Table 1. Common Causes of Secondary Peritonitis
Open table in new window
Table
| Source Regions | Causes |
|---|---|
| Esophagus | Boerhaave syndrome Malignancy Trauma (mostly penetrating) Iatrogenic* |
| Stomach | Peptic ulcer perforation Malignancy (eg, adenocarcinoma, lymphoma, gastrointestinal stromal tumor) Trauma (mostly penetrating) Iatrogenic* |
| Duodenum | Peptic ulcer perforation Trauma (blunt and penetrating) Iatrogenic* |
| Biliary tract | Cholecystitis Stone perforation from gallbladder (ie, gallstone ileus) or common duct Malignancy Choledochal cyst (rare) Trauma (mostly penetrating) Iatrogenic* |
| Pancreas | Pancreatitis (eg, alcohol, drugs, gallstones) Trauma (blunt and penetrating) Iatrogenic* |
| Small bowel | Ischemic bowel Incarcerated hernia (internal and external) Closed loop obstruction Crohn disease Malignancy (rare) Meckel diverticulum Trauma (mostly penetrating) |
| Large bowel and appendix | Ischemic bowel Diverticulitis Malignancy Ulcerative colitis and Crohn disease Appendicitis Colonic volvulus Trauma (mostly penetrating) Iatrogenic |
| Uterus, salpinx, and ovaries | Pelvic inflammatory disease (eg, salpingo-oophoritis, tubo-ovarian abscess, ovarian cyst) Malignancy (rare) Trauma (uncommon) |
| Source Regions | Causes |
|---|---|
| Esophagus | Boerhaave syndrome Malignancy Trauma (mostly penetrating) Iatrogenic* |
| Stomach | Peptic ulcer perforation Malignancy (eg, adenocarcinoma, lymphoma, gastrointestinal stromal tumor) Trauma (mostly penetrating) Iatrogenic* |
| Duodenum | Peptic ulcer perforation Trauma (blunt and penetrating) Iatrogenic* |
| Biliary tract | Cholecystitis Stone perforation from gallbladder (ie, gallstone ileus) or common duct Malignancy Choledochal cyst (rare) Trauma (mostly penetrating) Iatrogenic* |
| Pancreas | Pancreatitis (eg, alcohol, drugs, gallstones) Trauma (blunt and penetrating) Iatrogenic* |
| Small bowel | Ischemic bowel Incarcerated hernia (internal and external) Closed loop obstruction Crohn disease Malignancy (rare) Meckel diverticulum Trauma (mostly penetrating) |
| Large bowel and appendix | Ischemic bowel Diverticulitis Malignancy Ulcerative colitis and Crohn disease Appendicitis Colonic volvulus Trauma (mostly penetrating) Iatrogenic |
| Uterus, salpinx, and ovaries | Pelvic inflammatory disease (eg, salpingo-oophoritis, tubo-ovarian abscess, ovarian cyst) Malignancy (rare) Trauma (uncommon) |
*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.
The most common cause of postoperative peritonitis is anastomotic leak, with symptoms generally appearing around postoperative days 5-7. 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.
Peritonitis is also a frequent complication and significant limitation of peritoneal dialysis.3 Peritonitis leads to increased hospitalization and mortality rates.
Etiology
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 hematogenous seeding in the presence of bacteremia.
Approximately 10-30% of patients with cirrhosis and ascites develop SBP.1 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%]) (see Table 2). Anaerobic microorganisms are found in less than 5% of cases, and multiple isolates are found in less than 10%.
Table 2. Microbiology of Primary, Secondary, and Tertiary PeritonitisOpen table in new window
Table
| Peritonitis (Type) | Etiologic Organisms | Antibiotic Therapy (Suggested) | |
|---|---|---|---|
| Class | Type of Organism | ||
| Primary | Gram-negative | E coli (40%) K pneumoniae (7%) Pseudomonas species (5%) Proteus species (5%) Streptococcus species (15%) Staphylococcus species (3%) Anaerobic species (<5%) | Third-generation cephalosporin |
| Secondary | Gram-negative | E coli Enterobacter species Klebsiella species Proteus species | Second-generation cephalosporin Third-generation cephalosporin Penicillins with anaerobic activity Quinolones with anaerobic activity Quinolone and metronidazole Aminoglycoside and metronidazole |
| Gram-positive | Streptococcus species Enterococcus species | ||
| Anaerobic | Bacteroides fragilis Other Bacteroides species Eubacterium species Clostridium species Anaerobic Streptococcus species | ||
| Tertiary | Gram-negative | Enterobacter species Pseudomonas species Enterococcus species | Second-generation cephalosporin Third-generation cephalosporin Penicillins with anaerobic activity Quinolones with anaerobic activity Quinolone and metronidazole Aminoglycoside and metronidazole Carbapenems Triazoles or amphotericin (considered in fungal etiology) (Alter therapy based on culture results.) |
| Gram-positive | Staphylococcus species | ||
| Fungal | Candida species | ||
| Peritonitis (Type) | Etiologic Organisms | Antibiotic Therapy (Suggested) | |
|---|---|---|---|
| Class | Type of Organism | ||
| Primary | Gram-negative | E coli (40%) K pneumoniae (7%) Pseudomonas species (5%) Proteus species (5%) Streptococcus species (15%) Staphylococcus species (3%) Anaerobic species (<5%) | Third-generation cephalosporin |
| Secondary | Gram-negative | E coli Enterobacter species Klebsiella species Proteus species | Second-generation cephalosporin Third-generation cephalosporin Penicillins with anaerobic activity Quinolones with anaerobic activity Quinolone and metronidazole Aminoglycoside and metronidazole |
| Gram-positive | Streptococcus species Enterococcus species | ||
| Anaerobic | Bacteroides fragilis Other Bacteroides species Eubacterium species Clostridium species Anaerobic Streptococcus species | ||
| Tertiary | Gram-negative | Enterobacter species Pseudomonas species Enterococcus species | Second-generation cephalosporin Third-generation cephalosporin Penicillins with anaerobic activity Quinolones with anaerobic activity Quinolone and metronidazole Aminoglycoside and metronidazole Carbapenems Triazoles or amphotericin (considered in fungal etiology) (Alter therapy based on culture results.) |
| Gram-positive | Staphylococcus species | ||
| Fungal | Candida species | ||
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. (See Table 1 for differential diagnoses.)
The pathogens involved in SP differ in the proximal and distal 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 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 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 preexisting 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.4
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 (eg, APACHE II score), and the elements of the local environment, such as necrotic tissue, blood, or bile.5
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 defense, 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 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.
Bacterial virulence factors3 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 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.
Abscess formation occurs when the host defense 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, ie, 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 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 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 (ie, 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 (ie, 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.
Indications
Early control of the septic source is mandatory and can be achieved by operative and nonoperative means.
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.
Nonoperative interventions include percutaneous abscess drainage, as well as percutaneous and endoscopic stent placements. If an abscess is accessible for percutaneous drainage and if the underlying visceral organ pathology does not clearly require operative intervention, percutaneous drainage is a safe and effective initial treatment approach.
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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Further Reading
Clinical guidelines:
ACR Appropriateness Criteria® acute abdominal pain and fever or suspected abdominal abscess. American College of Radiology - Medical Specialty Society. 1996 (revised 2006). 7 pages. NGC:005138
ACR Appropriateness Criteria® blunt abdominal trauma. American College of Radiology - Medical Specialty Society. 1996 (revised 2005). 8 pages. NGC:004602
Management of adult patients with ascites due to cirrhosis: an update. American Association for the Study of Liver Diseases - Private Nonprofit Research Organization. 1998 Jan (revised 2009 Jun). 21 pages. NGC:007373
Practice management guidelines for small bowel obstruction. Eastern Association for the Surgery of Trauma - Professional Association. 2007. 42 pages. NGC:006546
Practice parameters for the surgical management of Crohn's disease. American Society of Colon and Rectal Surgeons - Medical Specialty Society. 2007 Nov. 12 pages. NGC:006461
Clinical trials:
A Pharmacokinetic Study of Cefepime After Administration Into Dialysate in Patients With Continuous Ambulatory Peritoneal Dialysis (CAPD) Peritonitis
Clinical, Inflammatory, and Economic Impact of Dextran 70 in Treating Spontaneous Bacterial Peritonitis
Functional Genomic Influences on Disease Progression and Outcome in Sepsis
Randomized Comparison of Two Albumin Administration Schedules for Spontaneous Bacterial Peritonitis (SBP)
SIS Multicenter Study of Duration of Antibiotics for Intraabdominal Infection
Keywords
peritonitis, abdominal sepsis, appendix, appendicitis, peritoneal dialysis, spontaneous bacterial peritonitis, ruptured appendix, burst appendix, spontaneous peritonitis, peritonitis symptoms, acute peritonitis, peritonitis dialysis, peritoneal abscess, secondary peritonitis
