Sepsis in cirrhosis

Abstract

Patients with cirrhosis are at risk of developing sepsis and sepsis-induced organ failure as well as dying. Spontaneous bacterial peritonitis (SBP) is the most common site of severe infections. Bacterial infections are equally distributed among one of the following three categories: community-acquired, healthcare-associated and nosocomial. The incidence of sepsis caused by multiresistant bacteria is increasing. In patients with cirrhosis and severe sepsis, high production of pro-inflammatory cytokines seems to play a role in the development of organ failure (including worsening of liver function). The underlying molecular mechanisms that explain cytokine overproduction in cirrhosis are poorly understood. In patients with cirrhosis and sepsis, the identification of failing organs is assessed using the Sequential Organ Failure Assessment (SOFA) scale. Emergent empiric, broad-spectrum and non-nephrotoxic antibiotic therapy should be started. The choice of antibiotics depends on whether or not patients are at risk of developing infection due to extended-spectrum β-lactamase-producing Enterobacteriaceae. In patients with SBP without shock treated with antibiotics, intravenous albumin administration decreases the occurrence of hepatorenal syndrome and improves survival. Two randomized control studies on extracorporeal liver support systems have shown an improvement of hepatic encephalopathy but no benefit for survival. Bacterial sepsis is preventable by using norfloxacin in patients with variceal hemorrhage or in the setting of primary or secondary prophylaxis of SBP.