Andreas Bacher

Acute liver failure is a very complex type of disease with a mortality of up to 90%, leading to numerous severe disturbances of the whole organism. Bleeding because of absent synthesis of various coagulation factors and disseminated intravascular coagulation, acute kidney failure, circulatory failure with vasopressor dependence, respiratory failure with adult respiratory distress syndrome, neurological failure up to coma because of hepatic encephalopathy, and a very high risk of infection and sepsis frequently result from the initial state of isolated liver failure. High urgency liver transplantation is a highly efficient therapy if performed in time. However, increasing the rate of spontaneous recovery of the patients' own liver, and reducing the need for liver transplantation is preferable and would further improve the outcome of acute liver failure. Extracorporeal liver support by multipass albumin dialysis or plasmapheresis and filtering systems may offer a possibility to fulfill these aims of therapy. A prospective study in 88 patients with acute liver failure has shown a nonsignificant trend in improvement of survival after acute liver failure by multipass albumin dialysis and filtering. Other retrospective studies have shown benefits in improving hepatic encephalopathy and brain oedema. Further, an increase in the rate of spontaneous recovery of liver function has been described. With regional citrate anticoagulation for multipass albumin dialysis and filtering, the need for systemic anticoagulation – a potentially very harmful measure in these patients – can be eliminated and the rate of filter clotting can extremely effectively be reduced.

Introduction: Liver failure is associated with reduced synthesis of clotting factors, consumptive coagulopathy, and platelet dysfunction. The aim of the study was to evaluate the effects of liver support using a molecular adsorbent recirculating system (MARS) on the coagulation system in patients at high risk of bleeding. Methods: We studied 61 MARS treatments in 33 patients with acute liver failure (n = 15), acute-on-chronic liver failure (n = 8), sepsis (n = 5), liver graft dysfunction (n = 3), and cholestasis (n = 2). Standard coagulation tests, standard thromboelastography (TEG), and heparinase-modified and abciximab-fab-modified TEG were performed immediately before and 30 minutes after commencement of MARS, and after the end of MARS treatment. Prostaglandin I₂ was administered extracorporeally to all patients; 17 patients additionally received unfractioned heparin. Results: Three moderate bleeding complications in three patients, requiring three to four units of packed red blood cells, were observed. All were sufficiently managed without interrupting MARS treatment. Although there was a significant decrease in platelet counts (median, 9 G/l; range, -40 to 145 G/l) and fibrinogen concentration (median, 15 mg/dl; range, -119 to 185 mg/dl) with a consecutive increase in thrombin time, the platelet function, as assessed by abciximab-fab-modified TEG, remained stable. MARS did not enhance fibrinolysis. Conclusion: MARS treatment appears to be well tolerated during marked coagulopathy due to liver failure. Although MARS leads to a further decrease in platelet count and fibrinogen concentration, platelet function, measured as the contribution of the platelets to the clot firmness in TEG, remains stable. According to TEG-based results, MARS does not enhance fibrinolysis.