Spontaneous bacterial peritonitis (SBP) is a bacterial infection of ascitic fluid that occurs in the absence of an identifiable, intraabdominal, surgically treatable source such as a perforation.  Escherichia coli and Klebsiella pneumoniae are the most commonly associated pathogens.  The source of infection is believed to be secondary to either bacteremic seeding of the ascitic fluid or translocation of bacteria from an intestinal source to the surrounding ascites via the mesenteric lymph nodes.  The decreased ability of the cirrhotic patient/ascitic fluid to prevent infection (depressed phagocytic activity, low ascitic fluid opsonic activity, and neutrophil dysfunction) contributes to the development of SBP.  SBP is associated with an increased mortality if the diagnosis is not established and appropriate therapy begun in a timely manner.  Patients who have had an episode of SBP should be considered at risk for recurrence (20-40% recurrence rate over the first year after an initial episode), and prophylactic therapy should be started and the patient should be evaluated for liver transplantation.  Other risk factors for SBP include severe underlying liver disease, an ascitic fluid total protein level less than 1.5 gm/dL, esophageal varices, intestinal overgrowth, and gastrointestinal bleeding.

     Any patient with new onset ascites or any patient with chronic ascites who develops sudden diuretic resistance, deterioration in clinical status, progressive laboratory abnormalities (azotemia, leukocytosis or acidosis) or abdominal pain or fever should be evaluated for SBP.  Other symptoms associated with SBP include: hepatic encephalopathy, vomiting, diarrhea, shock and hypothermia.  Diagnosis is established by demonstrating an ascitic fluid absolute neutrophil count (ANC) of greater than or equal to 250 cells/mm3.  The ANC should be adjusted when the ascitic fluid RBC count is high by subtracting one from the ANC for every 250 RBCs.  Ascitic fluid should also be cultured in blood culture bottles (10 ml of ascitic fluid in each blood culture bottle) in an attempt to identify a pathogen.  Cirrhotic patients who should be considered at risk to develop SBP include:  those with severe liver disease (Child-Pugh class C), those with concomitant gastrointestinal hemorrhage, those who have had a prior episode of SBP, and those patients whose ascitic fluid protein content is less than or equal to 1 g/dL.

     SBP is diagnosed when the ANC is greater than or equal to 250 cells/mm3 and culture isolates a single organism (when multiple organisms are isolated consider acute secondary bacterial peritonitis due to perforation).  Culture negative neutrocytic ascites is diagnosed when the ANC is consistent with infection (> 250 cells/mm3) and the ascitic fluid cultures are negative.  This is considered consistent with infection and is treated the same as SBP.  Other causes of culture negative neutrocytic ascites include:  prior antibiotic therapy, hepatocellular carcinoma (HCC), hemorrhage into the ascitic fluid, peritoneal carcinomatosis, tuberculous carcinomatosis, and pancreatitis.  Monomicrobial nonneutrocytic bacterascites describes the condition where the ANC is less than 250 cells/mm3 but the culture grows a single organism.  Only patients who presented with symptoms of infection at the time of the paracentesis require therapy as asymptomatic cases resolve spontaneously.  Asymptomatic cases should have a repeat ANC and culture performed before a decision is made to initiate therapy.  It is important to exclude secondary acute bacterial peritonitis is all cases as these patients will require surgical evaluation and possible intervention.  Secondary peritonitis should be considered when ascitic fluid analysis reveals two or more of the following criteria:  polymicrobial infection, total protein >1g/dL, glucose <50 mg/dL, or LDH >225mU/mL.  Also, secondary peritonitis should be considered in patients diagnosed with SBP who display persistent symptoms, an increasing ANC, or a persistently positive ascitic fluid culture despite appropriate antibiotic therapy for 48 hours.

     Acute therapy entails intravenous cefotaxime (2 gm IV Q 8-12 hours) until infection has cleared (usually 5 days).  Prophylactic therapy entails norfloxacin (400 mg/day) or trimethoprim/sulfamethoxasole double strength (1 tablet daily).  Even with prophylaxis, the long term prognosis for patients who have survived SBP is poor.  Patients generally survive less than 2 years after infection even with prophylaxis.  Therefore, every patient should be evaluated for liver transplantation after their acute infection has resolved.