…And it Drags On – Ascites After Liver Transplantation

The diagnosis and management of ascites have always been central in our daily work as hepatologists. Ascites is one of the key symptoms in our field and its occurrence often has major implications for prognosis and therapy of the sick child. Although some cardiologists or nephrologists may disagree: ascites really is a liver problem. How to best deal with it, how much ascites to allow to just create enough space for the graft and when to prescribe albumin in these days of cost pressures and evidence-based medicine – these, almost emotional, questions are close to the heart of our profession. So it is disappointing to be reminded by Herzog et al. in this issue of Paediatric Transplantation that ascites persists after liver transplantation in 20–30% of patients. Historians tell us that the link between liver dysfunction and ascites was reported in the days of ancient Greece. To date, we are still unsure about the complex interplay between the development of ascites, renal function and the hyperdynamic circulation that characterize endstage liver disease. Several theories have tried to unravel the sequence of events. First, there is the overflow theory (1) that implicates renal sodium retention as a mechanism for expansion of plasma volume which leads to a hyperdynamic circulation. This hyperdynamic state increases the sinusoidal pressure in the liver parenchyma and lymph is secreted into the peritoneal cavity. In contrast the underfilling theory (2) assumes that it is the loss of circulating plasma volume in the first place that induces renal sodium retention. The increased circulating plasma volume then leads to increased microcirculatory pressure and the generation of ascites. Another hypothesis, the arterial vasodilation theory (3, 4), considers that the peripheral arterial vasodilatation is a consequence of the overproduction of nitric oxide and other vasodilators in cirrhotic patients, which is followed by a reflectory activation of the renin– angiotensin system and subsequent sodium retention. Although all three models have limitations they illustrate that the formation of ascites pretransplant is a complex reaction between liver, kidneys and vascular system. One feature all three models have in common is abnormal hepatic microcirculation with an increased sinusoidal pressure that leads to the leakage of lymph through the capsule of the liver (5). Given the lack of a basal membrane, the discontinuous endothelium and the large pore size within the hepatic sinusoids it is crucial to maintain low-pressure gradients within this system. Under normal conditions a low outflow resistance and sinusoidal baroreceptors to down regulate hepatic arteriolar inflow, maintain a consistently low pressure in the sinusoids of the healthy liver. In addition to this a relatively high oncotic pressure in the circulating plasma maintains the intrasinusoidal volume and avoids shifts of free fluid into the interstitium of the liver. The frequency of perioperative complications following liver transplantation has decreased with increasing medical and surgical expertise. Survival rates continue to improve throughout the world. However, ascites persists in some patients despite normal liver function and this has been published for adult patients. Cirera et al. (6) reported that 25 of 378 liver transplant recipients had ascitic losses of more than 500 mL/day for more than 10 days, related to surgical complications either associated with the surgical technique of the hepatic vein anastomosis or otherwise impaired hepatic venous outflow. There was a predominance of male recipients but no significant link between persisting ascites with perioperative or donor variables such as cold ischaemic time or donor age. A more recent report compares 25 historical patients from the Mayo clinic with persistent ascites 3 months after liver transplantation with a control cohort without ascites transplanted consecutively over a period of 2 yr. Pediatr Transplantation 2005: 9: 7–8. DOI: 10.1111/j.1399-3046.2004. 00281.x