Approach to persistent ascites after liver transplantation

Abstract

Persistent ascites (PA) after liver transplantation (LT), commonly defined as ascites lasting more than 4 wk after LT, can be expected in up to 7% of patients. Despite being relatively rare, it is associated with worse clinical outcomes, including higher 1-year mortality. The cause of PA can be divided into vascular, hepatic, or extrahepatic. Vascular causes of PA include hepatic outflow and inflow obstructions, which are usually successfully treated. Regarding modifiable hepatic causes, recurrent hepatitis C and acute cellular rejection are the leading ones. Considering predictors for PA, the presence of ascites, refractory ascites, hepato-renal syndrome type 1, spontaneous bacterial peritonitis, hepatic encephalopathy, and prolonged ischemic time significantly influence the development of PA after LT. The initial approach to patients with PA should be to diagnose the treatable cause of PA. The stepwise approach in evaluating PA includes diagnostic paracentesis, ultrasound with Doppler, and an echocardiogram when a cardiac cause is suspected. Finally, a percutaneous or transjugular liver biopsy should be performed in cases where the diagnosis is unclear. PA of unknown cause should be treated with diuretics and paracentesis, while transjugular intrahepatic portosystemic shunt and splenic artery embolization are treatment methods in patients with refractory ascites after LT.

Management of Established Small-for-size Syndrome in Post Living Donor Liver Transplantation: Medical, Radiological, and Surgical Interventions: Guidelines From the ILTS-iLDLT-LTSI Consensus Conference

“…Overall, the approach should be similar to the pretransplant setting focused on diuretics use and sodium restriction for moderate volume of ascites, whereas large volume paracentesis followed by plasma expansion would be appropriate for large volume or refractory ascites. 50 Patients with high output loss of ascitic fluid via drainage tubes present significant issues with regard to maintaining volume and sodium homeostasis. The sodium content in the drain fluid is similar to plasma and represents an obligate sodium loss.…”