Infectious Diseases in Critical Care Medicine

derived from the sum of the points for each of these five parameters. Patients with chronic liver

disease are placed in one of three classes (A, B, or C). Despite having some limitations the

modified Child–Pugh scoring system continues to be used by many clinicians to assess the risk

of mortality in patients with cirrhosis (Table 1).

SPONTANEOUS BACTERIAL PERITONITIS

Pathogenesis

Spontaneous bacterial peritonitis (SBP) is the infection of ascitic fluid with no identifiable

abdominal source for the infection. SBP is perhaps the most characteristic bacterial infection in

cirrhosis, occurring in as many as 20% to 30% of cirrhotic patients who are admitted to the

hospital with ascites (6,21,23). SBP occurs when normally sterile ascitic fluid is colonized

following an episode of transient bacteremia. Aerobic gram-negative bacilli, especially

Escherichia coli, cause approximately 75% of SBP infections. Aerobic gram-positive cocci,

includingStreptococcus pneumoniae,Enterococcus faecalis, other streptococci, andStaphylococcus

aureus, are responsible for most other SBP cases (25,26). Because enteric bacteria predominate

in SBP, it is thought that the gut is the major source of organisms for this infection. Several

mechanisms have been proposed to explain the movement of organisms from the intestinal

lumen to the systemic circulation (reviewed in Ref. 1). Cirrhosis-induced depression of the

hepatic reticuloendothelial system impairs the liver’s filtering function, allowing bacteria to

pass from the bowel lumen to the bloodstream via the portal vein. Cirrhosis also is associated

with a relative increase in aerobic gram-negative bacilli in the jejunum. A decrease in mucosal

blood flow due to acute hypovolemia or drug-induced splanchnic vasoconstriction may

compromise the intestinal barrier to enteric flora, thereby increasing the risk of bacteremia.

Finally, bacterial translocation may occur with movement of enteric organisms from the gut

lumen through the mucosa to the intestinal lymphatics. From there bacteria can travel through

the lymphatic system and enter the bloodstream via the thoracic duct. It is assumed that SBP

caused by non-enteric organisms also is due to bacteremia secondary to another site of

infection with subsequent seeding of the peritoneum and ascitic fluid (Fig. 1).

Decreased opsonic activity of ascitic fluid also increases the risk of SBP in patients with

cirrhosis. Immunoglobulin, complement, and fibronectin are important opsonins in ascitic

fluid, and patients with low protein concentrations in their ascitic fluid are especially

predisposed to SBP (27,28). Patients with ascitic fluid protein concentrations below 1 g/dL

have a sevenfold increase in the incidence of SBP when compared to patients with higher

protein concentrations in ascities (27).

Other risk factors have been associated with SBP, including gastrointestinal bleeding,

fulminant hepatic failure, and invasive procedures such as the placement of peritoneovenous

shunts for the treatment of ascites. An elevated bilirubin level also is correlated with a high risk

of peritonitis in patient with cirrhosis (28).

Table 1 Modified Child–Pugh Classification of Liver Disease Severity

Points Assigned

Parameter 1 2 3

Ascites None Slight Moderate/severe
Encephalopathy None Grade 1–2 Grade 3–4
Bilirubin (mg/dL) <2.0 2.0–3.0 >3.0
Albumin (mg/L) >3.5 2.8–3.5 <2.8
Prothrombin time (seconds increased) 1–3 4–6 >6.0

Total score Child–Pugh Class

5–6 A

7–9 B

10–15 C

342 Preheim