INTRODUCTION	Section 2 of 10
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Background: Spontaneous bacterial peritonitis (SBP) is an acute bacterial infection of ascitic fluid. Generally, no source of the infecting agent is easily identifiable, but contamination of dialysate can cause the condition among those receiving peritoneal dialysis (PD). SBP occurs in both children and adults and is a well-known and ominous complication in patients with cirrhosis. 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.

Children with nephrosis or systemic lupus erythematosus who have ascites have a high risk of developing SBP.

SBP can occur as a complication of any disease state that produces the clinical syndrome of ascites, such as congestive heart failure and Budd-Chiari syndrome.

Pathophysiology: 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 are isolated from more than 90% of infected ascites fluid in 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 contribute 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.

Frequency:

• In the US: 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.

Mortality/Morbidity: The SBP mortality rate ranges from 40-70% in adult patients with cirrhosis and is lower in children with nephrosis.

• Patients with concurrent renal insufficiency have been shown to be at a higher risk of mortality from SBP than those without concurrent renal insufficiency.

• Recent reports show that mortality from SBP may be decreasing among all subgroups of patients because of advances in its diagnosis and treatment.

Race: No race predilection is known.

Sex: In patients with ascites, both sexes are affected equally.

Age: While 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.

	CLINICAL	Section 3 of 10
Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Bibliography

History: A broad range of signs and symptoms are seen in SBP. A high index of suspicion must be maintained when caring for patients with ascites, particularly those with acute clinical deterioration.

• Completely asymptomatic cases have been reported in as many as 30% of patients.

• Fever and chills occur in as many as 80% of patients.

• Abdominal pain or discomfort is found in as many as 70% of patients.

• Worsening or unexplained encephalopathy

• Diarrhea

• Ascites that does not improve following administration of diuretic medication

• Worsening or new-onset renal failure

• Ileus

Physical:

• Abdominal tenderness is found in more than 50% of patients with SBP. Findings on the abdominal examination can range from mild tenderness to overt rebound and guarding. In some cases, the abdominal examination mimics an acute intra-abdominal catastrophe requiring emergency surgical evaluation.

• Hypotension (5-14%)

• Signs of hepatic failure such as jaundice and angiomata

Causes:

• Etiologic agents (>90% intestinal flora)

• Traditionally, three fourths of SBP infections are caused by aerobic gram-negative organisms (50% of these being Escherichia coli), and one fourth of these infections are due to aerobic gram-positive organisms (19% streptococcal species). However, recent data suggest the percentage of gram-positive infections may be increasing. This increase may be due to quinolone resistance among gram-positive bacteria.

• Anaerobic organisms are rare because of the high oxygen tension of ascitic fluid.

• Single organism (92%)

• Polymicrobial (8%)

• Risk factors

• Patients with cirrhosis who are in a decompensated state are at the highest risk of developing SBP.

• Low complement levels are associated with the development of SBP. Patients at greatest risk for SBP have decreased hepatic synthetic function with associated low total protein or prolonged prothrombin time (PT).

• Patients with a 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.