All patients with cirrhosis and ascites have a high risk of developing SBP; therefore a paracentesis should be performed to rule out SBP for all hospitalized patients with cirrhosis and ascites (Fig. 68.2). This has been proven to reduce mortality [1, 6, 7]. There are several additional criteria which suggest an increased risk of developing SBP and in these patients, the suspicion for SBP should be even higher: ascitic fluid total protein level of <1.0 g/dl, prior history of SBP, a serum total bilirubin >2.5 mg/dl, concomitant variceal bleeding, and recent use of a proton pump inhibitor [1, 3, 8].

The ascitic fluid should be sent for aerobic and anaerobic cultures, cell count and differential, and fluid chemistries (albumin, protein, glucose, lactate dehydrogenase, amylase, and in some cases bilirubin). It is important that diagnostic paracentesis be performed prior to the administration of antibiotics. The yield of the ascitic fluid cultures is greatly reduced even with the administration of a single dose of broad-spectrum antibiotics within 6 h prior to the paracentesis [1, 2, 7]. Appropriate handling of the ascitic fluid is crucial to minimize the risk of skin flora contaminating the cultures, and to avoid obtaining a false-positive culture. When culturing ascitic fluid, immediate bedside inoculation of the ascitic fluid into routine blood culture bottles with at least 10–20 ml of fluid has been shown to increase the sensitivity of cultures and to avoid false negative results [1, 9].

A total absolute neutrophils count of >250 cells/mm³, a positive ascitic fluid bacterial culture and absence of secondary causes of peritonitis (i.e. bowel perforation) usually confirm the diagnosis of SBP [1]. However, different variants of spontaneous ascitic infections exist which may not present with the classic neutrophil count. These are depicted in Table 68.1.

It is imperative to rule out secondary bacterial peritonitis, such as due to bowel perforation or intra-abdominal abscess, prior to diagnosing SBP. Failure to correctly diagnose secondary bacterial peritonitis from a surgical etiology can be catastrophic. Several findings can help differentiate SBP from a secondary bacterial peritonitis caused by perforation. SBP is often associated with less abdominal pain, lower ascitic fluid total protein levels, a lower ascitic fluid neutrophil count (<1000 cells/mm), lower ascitic fluid bilirubin levels (<6.0 mg/dl), normal or low ascitic fluid amylase levels (higher levels correlate with a perforation), and the presence of a monomicrobial culture result [10]. The presence of two of the three following “Runyon criteria” is very sensitive for the diagnosis of secondary bacterial peritonitis: ascitic fluid total protein >1.0 g/dl; glucose of <50 mg/dl; and an elevated serum LDH in the presence or absence of a polymicrobial blood culture [1, 10]. In the event that a patient that was initially diagnosed as having SBP is not clinically improving, a repeat paracentesis may be helpful as a rising ascitic fluid neutrophil count is highly concerning for secondary bacterial peritonitis. The presence of less common pathogenic bacteria (see below) or fungal growth in the ascitic cultures should also prompt a search for an intraabdominal abscess leading to secondary peritonitis.

Marked peripheral leukocytosis (or neutrophilia) does not seem to have an effect on the leukocyte (or neutrophil) count in ascitic fluid [11]. However, a traumatic paracentesis leading to hemorrhagic ascites fluid may alter the neutrophil count. The commonly used correction factor is to subtract 1 neutrophil for each 250 red blood cells/mm³ in the ascitic fluid [12].

Several explanations exist for how bacteria enter the ascitic fluid and lead to infection. The most widely accepted mechanism is that of translocation of gut bacteria across the leaky intestinal wall of cirrhotic patients into the mesenteric lymph nodes with subsequent seeding of the ascites [3, 13]. Intestinal bacterial overgrowth, either due to decreased intestinal motility or through the use of proton pump inhibitors has also been proposed but remains controversial [1, 3, 8, 14]. The bacteria that usually result in SBP are those that require a functionally intact immune system with adequate complement levels for opsonization and removal. Advanced cirrhosis certainly reduces the function of the complement system and phagocyte activity [3, 15].

Most cases of SBP are due to gut bacteria such as Escherichia coli and Klebsiella; however Streptococcus pneumonia, Enterobacteriaceae, Staphylococcus and Pseudomonas infections can also occur. Additional bacterial pathogens have geographic prevalence such as Aeromonas hydrophila, which is seen in Korea [16]. The presence of more than one type of bacteria in the ascitic fluid should prompt a consideration for a secondary peritonitis. Additionally, unusual organisms such as fungi found on culture analysis of the ascitic fluid can also suggest a secondary bacterial peritonitis from an abscess. There have also been case reports of spontaneous fungal peritonitis [17] and SBP due to Listeria monocytogenes [18], in immune-suppressed and elderly patients, respectively.

All patients with SBP should be started on broad spectrum antibiotics as soon as the diagnosis is suspected. Appropriate and timely treatment has been shown to significantly decrease morbidity and mortality [1, 7, 14]. Figure 68.3 is a useful table to help guide therapy in patients with suspected or confirmed SBP.