INTRODUCTION

Ascites is excessive fluid in the peritoneal space. It is suggested clinically by the finding of shifting dullness and confirmed by imaging such as ultrasonography. Causes can be broadly categorised as portal hypertension-related or non-portal hypertension-related (Table 31.1). The latter include reduced plasma oncotic pressure, peritoneal inflammation, disruption to lymphatic drainage and increased vascular permeability. Despite this diversity in possible cause and mechanism, portal hypertension due to cirrhosis accounts for approximately 80% of cases in Western countries. Peritoneal malignancies and right heart failure account for most of the remaining cases. Tuberculosis is a common cause in patients from endemic areas. Although acute portal vein thrombosis commonly results in transient ascites, chronic portal vein obstruction does not usually cause ascites in the absence of underlying liver disease.

TABLE 31.1 Causes of ascites

Spontaneous bacterial peritonitis (SBP), an infection of ascitic fluid with a single bacterial species in the absence of any primary intra-abdominal source, may complicate the clinical course of patients with preexisting ascites, often resulting in an exacerbation of peritoneal fluid accumulation. Less commonly, ascites develops de novo as a consequence of SBP. Most instances of SBP occur in cirrhotic patients and clinical studies have identified several subgroups at particularly high risk (Table 31.2). Overall, SBP is present in up to 20% of all cirrhotic patients undergoing paracentesis, although the incidence is notably lower in recent outpatient-based series. SBP is also well recognised to occur in patients with acute liver failure and those with nephrotic syndrome and other hypoproteinaemic states.

TABLE 31.2 Proven risk factors for the development of spontaneous bacterial peritonitis in patients with cirrhosis