Ascites and peritoneal disease: SAQ

This boy with known biliary atresia and chronic liver disease presents the classic picture of spontaneous bacterial peritonitis complicating cirrhotic ascites. The fever, abdominal pain, and increasing drowsiness in a cirrhotic child with ascites are the cardinal triggers for SBP, and they should never be attributed to a minor viral illness without a diagnostic paracentesis. The ascitic polymorphonuclear count of 480 per cubic millimetre is above the diagnostic threshold of 250 per cubic millimetre and confirms the diagnosis. The serum-ascites albumin gradient of 16 g per litre, calculated as 24 minus 8, confirms that the ascites is portal-hypertensive and therefore cirrhotic in origin. ^[1]

Question 1 (10 marks)

Outline your immediate management of this child, including the diagnosis, antibiotic therapy, and the role of albumin. ^[1]

The diagnosis is spontaneous bacterial peritonitis, made by the ascitic fluid polymorphonuclear count of 250 or more per cubic millimetre. The diagnostic paracentesis has already been performed, and the result of 480 per cubic millimetre is diagnostic regardless of the culture result, which may take days to return. The child should not wait for the culture before treatment is started, because delay increases mortality. ^[1]

Empirical antibiotic therapy is begun immediately with a third-generation cephalosporin. Cefotaxime or ceftriaxone at 50 to 100 mg per kg per day covers the typical enteric organisms that translocate from the cirrhotic gut, and it is continued for 5 to 7 days, guided by the clinical response and the culture and sensitivity results when they return. The fever, tachycardia, and prolonged capillary refill indicate early circulatory compromise, so intravenous access is secured and fluid resuscitation is given judiciously, because the cirrhotic child tolerates both overfilling and underfilling poorly. ^[1]

Intravenous albumin is a critical adjunct, not an optional extra. The landmark randomised trial by Sort and colleagues demonstrated that albumin at 1.5 g per kg on day 1 and 1 g per kg on day 3 reduces the incidence of hepatorenal syndrome and improves survival in SBP. The mechanism is expansion of the effective circulating volume and restoration of oncotic pressure in a child whose splanchnic vasodilation has reduced the effective arterial blood volume. The child's renal function and urine output are monitored closely, because hepatorenal syndrome is the feared renal complication. ^[2]

The paediatric hepatology and intensive care teams are involved early, because SBP carries a one-year mortality of 50 to 70 per cent and is an independent indication for liver transplant assessment. The family is counselled honestly about the seriousness of the event and the need for transplantation as the definitive treatment. After recovery, secondary prophylaxis is commenced. ^[2]