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Key Features

  • Tuberculous involvement of the peritoneum

  • Accounts for < 2% of all causes of ascites in the United States

  • Incidence higher among those with HIV disease, urban poor, nursing home residents, and immigrants from underdeveloped countries

  • In the United States, half have underlying cirrhosis and ascites from portal hypertension

Clinical Findings

  • Low-grade fever

  • Anorexia, weight loss

  • Abdominal distention and tenderness

  • Clinically apparent ascites or suggestion of abdominal mass

Diagnosis

  • Tuberculin skin tests positive in less than half (Table 9–13)

  • Chest radiographs abnormal in > 70%

  • Active pulmonary tuberculosis disease in < 20%

  • Ultrasonography or CT imaging of the abdomen

    • Reveals free or loculated ascites in > 80% of patients

    • May demonstrate lymphadenopathy or peritoneal, mesenteric, or omental thickening

  • Ascitic fluid total protein > 3.0 g/dL, lactate dehydrogenase > 90 units/L, or mononuclear cell-predominant leukocytosis > 500/mcL; each has a sensitivity of 70–80% but limited specificity

  • Ascitic fluid smears for acid-fast bacilli are usually negative; cultures are positive in only 35%

  • Ascitic fluid adenosine deaminase activity ≥ 36–40 international units/L has sensitivity > 100% and specificity of 97%, but limited predictive value in cirrhotic ascites or HIV disease

  • Laparoscopy establishes diagnosis

  • Characteristic peritoneal nodules are visible in > 90%

  • Peritoneal biopsy reveals granulomas

  • Peritoneal biopsy cultures are positive in < 66% and require at least 4–6 weeks

Table 9–13.Classification of positive tuberculin skin test reactions.1

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