Extracorporeal renal and liver support in pediatric acute liver failure.

Abstract

The liver is the only organ which can regenerate and, thus, potentially negate the need for transplantation in acute liver failure (ALF). Cerebral edema and sepsis are leading causes of mortality in ALF. Both water-soluble and protein-bound toxins have been implicated in pathogenesis of various ALF complications. Ammonia is a surrogate marker of water-soluble toxin accumulation in ALF and high levels are associated with higher grades of hepatic encephalopathy, raised intracranial pressure, and mortality. Therefore, extracorporeal therapies aim to lower ammonia and maintain fluid balance and cytokine homeostasis. The most common and easily available modality is continuous kidney replacement therapy (CKRT). Early initiation of high-volume CKRT utilizing an anticoagulation regimen minimizing treatment downtime and delivering the prescribed dose is highly desirable. Ideally, extracorporeal liver-assist devices (ECLAD) should perform both synthetic and detoxification functions of the liver. ECLAD may temporarily replace lost liver function and serve as a bridge, either to spontaneous recovery or liver transplantation. Various bioartificial and biologic liver-assist devices are described in specialty literature, including molecular adsorbent recirculating system (MARS), single pass albumin dialysis (SPAD), and total plasma exchange (TPE); however, clinicians commonly use modalities easily available in intensive care units. There is a lack of standardization of indications for ECLAD, availability of different extracorporeal devices with varied technical approaches, and, of note, the differences in doses of ECLAD provided in clinical practice. We review the practicalities and evidence regarding these four artificial liver support devices in pediatric ALF.