Spontaneous bacterial peritonitis: from pathophysiology to prevention

摘要

Patients with cirrhosis present an increased susceptibility to bacterial infections, which are the cause of hospital admission in about 10% of patients and are present in about 40% of those admitted for ongoing complications. Lastly, about a third of patients develop nosocomial infections. Spontaneous bacterial peritonitis (SBP) is the most frequent infection in advanced cirrhosis; it is mostly caused by Gram-negative bacteria of intestinal origin, but Gram-positive cocci can be involved in nosocomial-acquired SBP. Its occurrence is associated with complications, such as renal and circulatory failure, cardiac dysfunction, coagulopathy, encephalopathy, and relative adrenal insufficiency, ultimately leading to multi-organ failure and death within a few days or weeks in about 30% of cases. The main mechanism underlying the development of SBP, as well as other bacterial infections in cirrhosis, is represented by bacterial translocation from the intestinal lumen to mesenteric lymph nodes or other extraintestinal organs and sites. This process is facilitated by several factors, including changes in intestinal flora, portal hypertension, and, mainly, impairment in local/systemic immune defense mechanisms. Bacterial infections in advanced cirrhosis evoke an enhanced systemic inflammatory response, which explains the ominous fate of PBS. Indeed, an exaggerated production of cytokines ensues, which ultimately activates vasodilating systems and generates reactive oxygen species. Primary antibiotic prophylaxis of PBS is warranted in those conditions implying an increased incidence of bacterial infections, such as gastro-intestinal bleeding and low protein content in ascites associated with severe liver and/or renal dysfunction. Fluoroquinolones are commonly employed, but the frequent occurrence of resistant bacterial strains make third generation cephalosporins preferable in specific settings. The high PBS recurrence indicates secondary antibiotic prophylaxis.