Ascites and peritoneal disease: Viva

Branch 1: Recognising and classifying the ascites

The candidate should recognise that progressive abdominal distension with shifting dullness and a fluid thrill in a child with biliary atresia is ascites, and that its appearance marks the transition from compensated to decompensated cirrhosis. The key first investigation is ascitic fluid analysis, and the key calculation is the serum-ascites albumin gradient. A strong candidate would explain that the gradient is calculated by subtracting the ascitic albumin from the serum albumin, and that a gradient of 11 g per litre or more indicates portal hypertension. [2]

If the examiner presses on the significance, the candidate should explain that the gradient correctly classifies the cause in over 97 per cent of cases and has replaced the older transudate-exudate concept based on total protein. In this child, with underlying biliary atresia, the gradient should be 11 g per litre or more, confirming portal-hypertensive, cirrhotic ascites. The candidate should also send the fluid for cell count, culture, and total protein, and should request an abdominal ultrasound with Doppler to assess the liver architecture, portal vein patency, and splenomegaly. [2]

A strong candidate would acknowledge that while cirrhosis is the most likely cause, the gradient and the fluid analysis are what separate cirrhosis from cardiac ascites, Budd-Chiari syndrome, and the non-portal causes such as nephrotic syndrome and tuberculosis. This is why ascitic fluid analysis is never optional, even when the diagnosis seems obvious. [1]

Branch 2: Spontaneous bacterial peritonitis

If the examiner introduces fever or abdominal pain, the candidate should immediately raise spontaneous bacterial peritonitis and state that any cirrhotic child with ascites who develops fever, abdominal pain, or altered mental status must have a diagnostic paracentesis without delay. The candidate should name the diagnostic criterion confidently: a polymorphonuclear count of 250 or more per cubic millimetre makes the diagnosis, regardless of the culture result. [1]

If asked about treatment, the candidate should describe empirical third-generation cephalosporin therapy with cefotaxime or ceftriaxone at 50 to 100 mg per kg per day for 5 to 7 days, begun immediately after the diagnostic tap. The candidate should then state that intravenous albumin at 1.5 g per kg on day 1 and 1 g per kg on day 3 is added, citing the Sort trial, which showed that albumin reduces hepatorenal syndrome and mortality. Failing to mention albumin is a common and serious omission. [3]

If the examiner asks about the long-term implications, the candidate should explain that SBP carries a one-year mortality of 50 to 70 per cent and mandates transplant assessment, and that secondary prophylaxis with oral norfloxacin or trimethoprim-sulfamethoxazole is continued indefinitely until transplantation. The candidate should present this honestly as an ominous prognostic event that escalates the priority for liver transplantation. [1]

Branch 3: Stepwise management of cirrhotic ascites

If asked to construct the management plan, the candidate should present a clear stepwise approach. The foundation is dietary sodium restriction to 1 to 2 mmol per kg per day, paired with diuretic therapy using spironolactone at 1 to 3 mg per kg per day and furosemide at 0.5 to 1 mg per kg per day. The target weight loss is no more than 0.5 kg per day to avoid precipitating hepatorenal syndrome. [1]

If the ascites is tense or refractory, the candidate should describe large-volume paracentesis and should state that when more than 5 litres is removed, albumin is given at 6 to 8 g per litre of fluid drained to prevent paracentesis-induced circulatory dysfunction. For refractory ascites, the options are serial paracentesis or a transjugular intrahepatic portosystemic shunt, and the candidate should present refractory ascites as a firm indication for transplant assessment. [1]

A strong candidate would close by linking the management back to the underlying disease, explaining that all of these measures are palliative and that liver transplantation is the definitive treatment for decompensated cirrhosis. The PELD score for children under twelve and the MELD score for those twelve and older guide the transplant listing, and the appearance of ascites complications accelerates the priority. [1]