Spontaneous Bacterial Peritonitis

Spontaneous bacterial peritonitis (SBP) is a frequent infection in patients who have cirrhotic ascites. The prevalence of SBP is 10-27% in patients hospitalized with ascites. Half of the cases of SBP will occur during a hospitalization course. The pathogenesis is probably related to transitory bacteremia, most often from the GI tract or urinary tract but also from skin, lungs, or after manipulation of the bowel in the case of endoscopy, or from transmural migration of bacteria, also known as intestinal translocation. The diagnosis is established by a polymorphonuclear cell count in ascitic fluid of >250 cells/mm3 and is confirmed by a positive culture of ascitic fluid obtained at the bedside with direct inoculation of blood culture bottles. There is a subgroup of patients who fulfill the criteria of abnormal polymorphonuclear cell count but have a negative culture (culture-negative neutrocytic ascites), and this may represent just a false-negative culture. The behavior of patients with culture-negative neutrocytic ascites is quite similar to that of patients with SBP.

In SBP, a single organism is found in 90% of the cases and bacteremia is present in 40-60% of patients. The most common signs and symptoms include leukocytosis in 65-80% of patients, portal systemic encephalopathy in 50-70%, fever in 50-70%, abdominal pain in 50-70%, abdominal tenderness in 40-50%, and hypotension in 40%. Rebound is extremely unusual (<10%) because of lack of contact of visceral against parietal peritoneum. The most common organisms are Gram-negative bacilli which are responsible for 70% of the cases, including E. coli (43%), Klebsiella pneumoniae (8%), and others. The other important group of pathogens are Gram-positive cocci, representing 10-20% of the cases. Of these, the most common is Streptococcus pneumoniae in 8%, as well as a-hemolytic streptococcus and group D streptococcus in 5% each. Enterococcus, Staphylococcus, anaerobes, and microaerophilic organisms such as Bacteroides, Clostridia, and Peptostreptococcus are found in <2% of the cases.

If the fluid contains multiple bacteria, fungal elements, or anaerobic bacteria, a bowel perforation should be suspected. The sensitivity of ascitic fluid culture obtained by inoculating blood culture bottles at the bedside is 91%, while sending the fluid to the laboratory gives a sensitivity of only 42%.

The mortality of infection without therapy is high but not necessarily related to the SBP. Other complications including renal insufficiency and encephalopathy results in a 78-100% death rate without therapy and 30% with adequate therapy. The recurrence of infections after successful therapy is 69% at 1 yr. For that reason, control of ascites is critical to avoid new infections. In addition to this, prophylactic therapy should be given to patients who have ascites with a protein of <1.5 g/dL while they are hospitalized (usually with a quinolone, e.g., norfloxacin 400 mg a day, or with trimethoprim-sulfamethoxazole DS one tablet a day for 5 d of each week). After discharge from the hospital prophylaxis is a little more controversial but 500 mg of ciprofloxacin twice a day one day of each week may be adequate. No definite increase in resistant organisms has been documented in SBP patients receiving prophylactic antibiotics.

Therapy for SBP is usually 2 g of cefotaxime three times a day (corrected according to renal function) as initial empirical therapy. Therapy should be changed once susceptibility of the microorganisms is known. A length of therapy of 5 d seems to be adequate. Response to therapy may be assessed by a new paracentesis 48 h after the initiation of therapy with the expectation of finding a decrease in polymorphonuclear count to less than half of the original count. In general, use of aminoglycosides is avoided in patients with cirrhotic ascites because of the high nephrotoxicity and mortality associated with the use of these drugs.

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