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The ancient Greeks around 400 B.C. first recognized that ascites was associated with liver disease. Abdominal paracentesis is one of the oldest medical procedures; the first report of this procedure is dated about 20 B.C. Yet the bulk of the literature regarding the diagnosis and management of ascites and the details of paracentesis has been published only since 1980.
The causes of ascites in the United States have changed over the past 90 years. At the turn of the century, patients with ascites were usually found to have cardiac or renal failure. Now more than 80% of patients with ascites seen by general internists and gastroenterologists-hepatologists have liver disease (Table 9-1). As we head into the next century, chronic parenchymal liver disease, including cirrhosis and alcoholic hepatitis, is the predominate cause of ascites.
A history, physical examination, and careful analysis of ascitic fluid (Table 9-2, Table 9-3, Table 9-4, Table
9-5) provide the diagnosis of the cause of ascites formation in most patients. Approaching the differential diagnosis of ascites aided by detailed analysis of ascitic fluid is cost effective. Therefore, diagnostic paracentesis is a very important procedure for these patients. It has become apparent that ascitic fluid infection, particularly spontaneous bacterial peritonitis, is a common complication of ascites. Paracentesis reveals that 10% to 27% of patients admitted to the hospital with ascites have infection at admission (Table 9-6). In addition, ascertaining which patients with ascites are at high risk for infection of ascitic fluid allows selective intestinal decontamination with effective prophylactic antibiotics. Routine admission paracentesis has become the standard at many institutions for rapid assessment of the cause of ascites formation and early detection of infection.
The serum-ascites albumin gradient (SAAG) has replaced ascitic fluid total protein concentration (AFTP) in the classification of ascites (see Table 9-3). Ascites is now characterized as high albumin gradient (1.1 g/dL) or low albumin gradient (<1.1 g/dL) rather than transudative or exudative (see Table 9-4). The efficacy of treatment of patients with ascites has been found to depend in large part on the cause of ascites formation. Patients with high-albumin-gradient (e.g., cirrhotic or cardiac) ascites respond to salt restriction and diuretics, whereas patients with low-albumin-gradient ascites (e.g., peritonitis or ovarian peritoneal carcinomatosis) do not respond to diuretics and need specific therapy.
Patients who seek medical attention late in the course of disease or who have disease refractory to medical management may have abdominal hernias from the weight of the fluid or even rupture of the hernia and leakage of ascitic fluid (Fig. 9-1, Fig. 9-2, Fig. 9-3, Fig. 9-4).
In recent years, therapeutic abdominal paracentesis has been investigated scientifically and has been found to be safe and effective in the management of ascites. However, because about 90% of patients with ascites respond to diuretics and because chronic therapeutic paracentesis is highly consumptive of physician hours, therapeutic paracentesis is reserved for patients with tense ascites who need urgent decompression and for patients with ascites refractory to diuretic therapy. Therapeutic paracentesis can be performed relatively rapidly with semirigid tubing (e.g., a blood collection set) and vacuum bottles.