Spontaneous Bacterial Peritonitis and Hepatorenal Syndrome

Pathogenesis of Spontaneous Bacterial Peritonitis

A pathologic bacterial translocation (BT) from intestinal lumen to mesenteric lymph node is the main character in the pathogenesis of SBP. This “pathologic BT” in cirrhosis is related to several factors, including quantity and quality of intestinal bacteria, increased intestinal permeability, and systemic and local defects in host immunity. The intestinal bacterial overgrowth plays a key role in BT in cirrhosis. It is the result, at least partly, of decreased small-bowel motility and the delayed intestinal transit. Autonomic dysfunction, increased nitric oxide (NO) synthesis, and the oxidative stress of the mucosa are the main causes for decreased intestinal motility. In patients with cirrhosis there is not only an increase in quantity of bacteria in the bowel but also a change in quality. In fact, a depletion of the beneficial phyla Lachnospiraceae and enrichment in the phyla Proteobacteria (mainly Enterobacteriaceae) and Enterococcaceae have been demonstrated in the microbiota of patients with cirrhosis. Interestingly, Enterobacteriaceae (e.g., Escherichia coli, Klebsiella pneumoniae ) and Enterococcaceae have been found to be the most adept at translocating from intestinal lumen to mesenteric lymph node, and they are the pathogens most frequently found in patients with SBP.

Patients with cirrhosis also demonstrate an alteration in the integrity of intestinal mucosal barrier. In fact, portal hypertension leads to ultrastructural changes of intestinal mucosa, such as widening of intracellular spaces, vascular congestion, wall thickening, and tight junctions disruption. These alterations lead to an increased intestinal permeability that facilitates pathologic bacterial translocation.

Finally, alteration of innate and acquired immunity has been observed in patients with cirrhosis. The detailed description of the alterations of immune response in cirrhosis is beyond the purpose of this chapter, but it plays a significant role in the development of SBP because of a lack of control of bacterial translocation.

Clinical Manifestations and Diagnosis of Spontaneous Bacterial Peritonitis

Patients with SBP may have classic symptoms of infections, such as fever, abdominal pain, and ileus, and lab data may show leukocytosis and an increase in acute phase protein ( Box 84.1 ). However, sometimes the clinical scenario may be more complex without clear signs of infection, and the appearance of hepatic encephalopathy, difficult to control ascites, and/or acute kidney injury (AKI) may be the only clinical signs of SBP. Thus a diagnostic paracentesis should be performed in all patients with ascites admitted for an acute decompensation of cirrhosis. SBP is diagnosed when polymorphonuclear (PMN) cells in ascitic fluid are higher than 250 cells/µL. In all patients, ascitic and blood samples should be collected for microbiologic cultures. Ascitic fluid should be inoculated at the bedside, using blood culture bottles, including aerobic and anaerobic media. Despite the use of sensitive methods, ascites cultures are negative in 60% of cases.