Peritonitis and Abdominal Sepsis

Updated: Jan 11, 2017
  • Author: Brian J Daley, MD, MBA, FACS, FCCP, CNSC; Chief Editor: Praveen K Roy, MD, AGAF  more...
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Peritonitis is defined as an 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 various 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). Intra-abdominal sepsis is an inflammation of the peritoneum caused by pathogenic microorganisms and their products. [1] The inflammatory process may be localized (abscess) or diffuse in nature. (See Pathophysiology.)

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. (See Etiology.)

Peritoneal infections are classified as primary (ie, from hematogenous dissemination, usually in the setting of an immunocompromised state), secondary (ie, related to a pathologic process in a visceral organ, such as perforation or trauma, including iatrogenic trauma), or tertiary (ie, persistent or recurrent infection after adequate initial therapy). Primary peritonitis is most often spontaneous bacterial peritonitis (SBP) seen mostly inpatients with chronic liver disease. Secondary peritonitis is by far the most common form of peritonitis encountered in clinical practice. Tertiary peritonitis often develops in the absence of the original visceral organ pathology. (See Clinical Presentation.)

Infections of 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 image below.

A 35-year-old man with a history of Crohn disease 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.

The diagnosis of peritonitis is usually clinical. Diagnostic peritoneal lavage may be helpful in patients who do not have conclusive signs on physical examination or who cannot provide an adequate history; in addition, paracentesis should be performed in all patients who do not have an indwelling peritoneal catheter and are suspected of having SBP, because results of aerobic and anaerobic bacterial cultures, used in conjunction with the cell count, are useful in guiding therapy. (See Workup.)

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. (See Treatment and Management and Medication.)

Early control of the septic source is mandatory and can be achieved operatively and nonoperatively. Nonoperative interventions include percutaneous abscess drainage, as well as percutaneous and endoscopic stent placements. 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.



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 the 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/μ L, 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.



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, as indicated by the Acute Physiology and Chronic Health Evaluation II [APACHE II] score), and elements of the local environment, such as necrotic tissue, blood, or bile. [2]

Intra-abdominal sepsis from a perforated viscus (ie, secondary peritonitis or suppurative peritonitis) results from direct spillage of luminal contents into the peritoneum (eg, perforated peptic ulcer, diverticulitis, appendicitis, iatrogenic perforation). With the spillage of the contents, gram-negative and anaerobic bacteria, including common gut flora, such as Escherichia coli and Klebsiella pneumoniae, enter the peritoneal cavity. Endotoxins produced by gram-negative bacteria lead to the release of cytokines that induce cellular and humoral cascades, resulting in cellular damage, septic shock, and multiple organ dysfunction syndrome (MODS).

The mechanism for bacterial inoculation of ascites has been the subject of much debate since Harold Conn first recognized it in the 1960s. Enteric organisms have traditionally been isolated from more than 90% of infected ascites fluid in spontaneous bacterial peritonitis (SBP), suggesting that the GI tract is the source of bacterial contamination. The preponderance of enteric organisms, in combination with the presence of endotoxin in ascitic fluid and blood, once favored the argument that SBP was due to direct transmural migration of bacteria from an intestinal or hollow organ lumen, a phenomenon called bacterial translocation. However, experimental evidence suggests that direct transmural migration of microorganisms might not be the cause of SBP.

An alternative proposed mechanism for bacterial inoculation of ascites suggests a hematogenous source of the infecting organism in combination with an impaired immune defense system. Nonetheless, the exact mechanism of bacterial displacement from the GI tract into ascites fluid remains the source of much debate.

A host of factors contributes to the formation of peritoneal inflammation and bacterial growth in the ascitic fluid. A key predisposing factor may be the intestinal bacterial overgrowth found in people with cirrhosis, mainly attributed to decreased intestinal transit time. Intestinal bacterial overgrowth, along with impaired phagocytic function, low serum and ascites complement levels, and decreased activity of the reticuloendothelial system, contributes to an increased number of microorganisms and decreased capacity to clear them from the bloodstream, resulting in their migration into and eventual proliferation within ascites fluid.

Interestingly, adults with SBP typically have ascites, but most children with SBP do not have ascites. The reason for and mechanism behind this is the source of ongoing investigation.


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.

Whether fibrin ultimately results in containment or persistent infection may depend on the degree of peritoneal bacterial contamination. In animal studies of mixed bacterial peritonitis that examined 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

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 × 108 CFU/mL, much higher than the 5 × 105 CFU/mL inocula routinely used for in vitro susceptibility testing). This bacterial load may overwhelm the local host defense.

Bacterial virulence

Bacterial virulence factors [3] 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 Bacteroides fragilis and gram-negative bacteria, particularly E coli (see the image below) , where co-inoculation significantly increases bacterial proliferation and abscess formation.

Gram-negative Escherichia coli. Gram-negative Escherichia coli.


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. Nevertheless, the role of Enterococcus organisms in uncomplicated intra-abdominal infections remains unclear. Antibiotics that lack specific activity against Enterococcus are often used successfully in the therapy of peritonitis, and the organism is not often recovered as a blood-borne pathogen in intra-abdominal sepsis.


The role of fungi in the formation of intra-abdominal abscesses is not fully understood. 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.

Abscess formation

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 inhibit opsonization and phagocytotic killing by interference with complement activation.


The role of cytokines in the 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 few 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.



The etiology of disease depends on the type, as well as location, of peritonitis, as follows:

  • Primary peritonitis
  • Secondary peritonitis
  • Tertiary peritonitis
  • Chemical peritonitis
  • Peritoneal abscess

Primary peritonitis

Spontaneous bacterial peritonitis (SBP) is an acute bacterial infection of ascitic fluid. 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.

SBP can occur as a complication of any disease state that produces the clinical syndrome of ascites, such as heart failure and Budd-Chiari syndrome. Children with nephrosis or systemic lupus erythematosus who have ascites have a high risk of developing SBP. The highest risk of SBP, however is in patients with cirrhosis who are in a decompensated state. [4] In particular, decreased hepatic synthetic function with associated low total protein level, low complement levels, or prolonged prothrombin time (PT) is associated with maximum risk. Patients with low protein levels in ascitic fluid (< 1 g/dL) have a 10-fold higher risk of developing SBP than those with a protein level greater than 1 g/dL. Approximately 10-30% of patients with cirrhosis and ascites develop SBP. [5] The incidence rises to more than 40% with ascitic fluid protein contents of less than 1 g/dL (which occurs 15% of patients), 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, E coli [40%], K pneumoniae [7%], Pseudomonas species, Proteus species, other gram-negative species [20%]) and gram-positive organisms (eg, Streptococcus pneumoniae [15%], other Streptococcus species [15%], and Staphylococcus species [3%]) (see Table 1). However, some data suggest that the percentage of gram-positive infections may be increasing. [6, 7] One study cites a 34.2% incidence of streptococci, ranking in second position after Enterobacteriaceae. [7] Viridans group streptococci (VBS) accounted for 73.8% of these streptococcal isolates. A single organism is noted in 92% of cases, and 8% of cases are polymicrobial.

Anaerobic microorganisms are found in less than 5% of cases, and multiple isolates are found in less than 10%.

Secondary peritonitis

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.

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 1).

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.

Table 1. Common Causes of Secondary Peritonitis (Open Table in a new window)

Source Regions Causes
Esophagus Boerhaave syndrome


Trauma (mostly penetrating)


Stomach Peptic ulcer perforation

Malignancy (eg, adenocarcinoma, lymphoma, gastrointestinal stromal tumor)

Trauma (mostly penetrating)


Duodenum Peptic ulcer perforation

Trauma (blunt and penetrating)


Biliary tract Cholecystitis

Stone perforation from gallbladder (ie, gallstone ileus) or common duct


Choledochal cyst (rare)

Trauma (mostly penetrating)


Pancreas Pancreatitis (eg, alcohol, drugs, gallstones)

Trauma (blunt and penetrating)


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



Ulcerative colitis and Crohn disease


Colonic volvulus

Trauma (mostly penetrating)


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.

Common organisms cultured in secondary peritonitis are presented in Table 2, below. [8]

Table 2. Microbial Flora of Secondary Peritonitis (Open Table in a new window)

Type Organism Percentage
Gram negative Escherichia coli 60%
  Enterobacter/Klebsiella 26%
  Proteus 22%
  Pseudomonas 8%
Gram positive Streptococci 28%
  Enterococci 17%
  Staphylococci 7%
Anaerobic Bacteroides 72%
  Eubacteria 24%
  Clostridia 17%
  Peptostreptococci 14%
  Peptococci 11%
Fungi Candida 2%


Other rare, nonsurgical causes of intra-abdominal sepsis include the following:

  • Chlamydia peritonitis
  • Tuberculosis peritonitis
  • Acquired immunodeficiency syndrome (AIDS)-associated peritonitis

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 are 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.

Tertiary peritonitis

Tertiary peritonitis (see Table 3, below) 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%.

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) infection. The presenting symptoms are often nonspecific and insidious in onset (eg, low-grade fever, anorexia, weight loss). Many patients with TP have underlying cirrhosis. 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/μ L should raise suspicion of TP 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.

Table 3. Microbiology of Primary, Secondary, and Tertiary Peritonitis (Open Table in a new window)



Etiologic Organisms Antibiotic Therapy


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


Triazoles or amphotericin (considered in fungal etiology)

(Alter therapy based on culture results.)

Gram-positive Staphylococcus species
Fungal Candida species

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. [9]

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 occur subsequent to SP. Abscess formation may be a complication of surgery. 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.



The overall incidence of peritoneal infection and abscess is difficult to establish and varies with the underlying abdominal disease processes. SBP occurs in both children and adults and is a well-known and ominous complication of cirrhosis. [5] Of patients with cirrhosis who have SBP, 70% are Child-Pugh class C. In these patients, the development of SBP is associated with a poor long-term prognosis.

Once thought to occur only in those individuals with alcoholic cirrhosis, SBP is now known to affect patients with cirrhosis from any cause. In patients with ascites, the prevalence may be as high as 18%. This number has grown from 8% over the past 2 decades, most likely secondary to an increased awareness of SBP and heightened threshold to perform diagnostic paracentesis.

Although the etiology and incidence of hepatic failure differ between children and adults, in those individuals with ascites, the incidence of SBP is roughly equal. Two peak ages for SBP are characteristic in children: one in the neonatal period and the other at age 5 years.



Over the past decade, the combination of better antibiotic therapy, more aggressive intensive care, and earlier diagnosis and therapy with a combination of operative and percutaneous techniques have led to a significant reduction in morbidity and mortality related to intra-abdominal sepsis.

Spontaneous bacterial peritonitis

The mortality rate in SBP may be as low as 5% in patients who receive prompt diagnosis and treatment. However, in hospitalized patients, 1-year mortality rates may range from 50-70%. [10] This is usually secondary to the development of complications, such as gastrointestinal bleeding, renal dysfunction, and worsening liver failure. [11] Patients with concurrent renal insufficiency have been shown to be at a higher risk of mortality from SBP than those without concurrent renal insufficiency.

Mortality from SBP may be decreasing among all subgroups of patients because of advances in its diagnosis and treatment. The overall mortality rate in patients with SBP may exceed 30% if the diagnosis and treatment are delayed, but the mortality rate is less than 10% in fairly well-compensated patients with early therapy. As many as 70% of patients who survive an episode of SBP have a recurrent episode within 1 year, and in these patients, the mortality rate approaches 50%. Some studies suggest that the recurrence rate of SBP may be decreased to less than 20% with long-term antibiotic prophylaxis (eg, quinolones, trimethoprim-sulfamethoxazole); however, whether this improves long-term survival without liver transplantation is unclear.

Secondary peritonitis and peritoneal abscess

Uncomplicated SP and simple abscesses carry a mortality rate of less than 5%, but this rate may increase to greater than 30-50% in severe infections. The overall mortality rate related to intra-abdominal abscess formation is less than 10-20%. Factors that independently predict worse outcomes include advanced age, malnutrition, presence of cancer, a high APACHE II score on presentation, preoperative organ dysfunction, the presence of complex abscesses, and failure to improve in less than 24-72 hours after adequate therapy.

In severe intra-abdominal infections and peritonitis, the mortality rate may increase to greater than 30-50%. The concurrent development of sepsis, SIRS, and MOF can increase the mortality rate to greater than 70%, and, in these patients, more than 80% of deaths occur with an active infection present.

Soriano et al found that cirrhotic patients with SP who underwent surgical treatment tended to have a lower mortality rate than did those who received medical therapy only (53.8% vs 81.8%, respectively). [12] Among the surgically treated patients with SP, the survival rate was greater in those with the shortest time between diagnostic paracentesis and surgery. These researchers 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.

Tertiary peritonitis

In comparison with patients with other forms of peritonitis, patients who develop tertiary peritonitis have significantly longer ICU and hospital stays, higher organ dysfunction scores, and higher mortality rates (50-70%).

Other factors affecting prognosis

Several scoring systems (eg, APACHE II, SIRS, multiple organ dysfunction syndrome [MODS], Mannheim peritonitis index) have been developed to assess the clinical prognosis of patients with peritonitis. Most of these scores rely on certain host criteria, systemic signs of sepsis, and complications related to organ failure. Although valuable for comparing patient cohorts and institutions, these scores have limited value in the specific day-to-day clinical decision-making process for any given patient. In general, the mortality rate is less than 5% with an APACHE II of less than 15 and rises to greater than 40% with scores above 15. Rising APACHE II scores on days 3 and 7 are associated with an increase of mortality rates to greater than 90%, whereas falling scores predict mortality rates of less than 20%.

The mortality rate without organ failure generally is less than 5% but may rise to greater than 90% with quadruple organ failure. A delay of more than 2-4 days in instituting either medical therapy or surgical therapy has been clearly associated with increased complication rates, the development of tertiary peritonitis, the need for reoperation, multiple organ system dysfunction, and death.

Outcomes are worse in patients requiring emergent reoperations for persistent or recurrent infections (30-50% increase in the mortality rate); however, patients undergoing early planned second-look operations do not demonstrate this trend.

Persistent infection, recovery of enterococci, and multidrug-resistant gram-negative organisms, as well as fungal infection, are related to worse outcomes and recurrent complications.

Patients older than 65 years have a threefold increased risk of developing generalized peritonitis and sepsis from gangrenous or perforated appendicitis and perforated diverticulitis than younger patients and are 3 times more likely to die from these disease processes. Older patients with perforated diverticulitis are 3 times more likely than younger patients to have generalized rather than localized (ie, pericolic, pelvic) peritonitis. These findings are consistent with the hypothesis that the biologic features of peritonitis differ in elderly persons, who are more likely to present with an advanced or more severe process than younger patients with peritonitis.

Overall, studies suggest that host-related factors are more significant than the type and source of infection with regard to the prognosis in intra-abdominal infections. [13]