Pathophysiological basis of therapy of raised intracranial pressure in acute liver failure.
78 - 83.
In acute liver failure (ALF) patients that have raised increased intracranial pressure (ICP), mortality remains unacceptably high. There has been an explosion in the knowledge about the pathophysiological basis of raised ICP but treatment modalities are limited. Current therapy is aimed at reducing the circulating ammonia levels and attempts to reduce brain swelling which are only moderately effective. More recently, cerebral hyperemia has been suggested as being of major importance in the pathogenesis of increased ICP providing a new look at interventions such as hyperventilation, N-acetylcysteine, thiopentone sodium and propofol. More recently studies have focused upon the role of systemic inflammatory response in the pathogenesis of increased ICP and support the use of antibiotics prophylactically. The application of moderate hypothermia to treat uncontrolled intracranial hypertension seems promising and its exact place will be decided in a large trial being planned in USA and Europe. Early data from studies in an animal model suggests that albumin dialysis is a promising new tool to treat intracranial hypertension in patients with ALF. The recent advance in our understanding of the pathophysiological basis of intracranial hypertension has provided the platform for the discovery of new treatments. (c) 2005 Elsevier Ltd. All rights reserved.
|Title:||Pathophysiological basis of therapy of raised intracranial pressure in acute liver failure|
|Keywords:||acute liver failure, intracranial pressure, cerebral blood flow, ammonia, orthotopic liver transplantation, hepatic encephalopathy, FULMINANT HEPATIC-FAILURE, INDUCED BRAIN EDEMA, PROSPECTIVE CONTROLLED TRIAL, PORTACAVAL ANASTOMOSIS, MODERATE HYPOTHERMIA, CEREBRAL EDEMA, PROPHYLACTIC PHENYTOIN, TOTAL HEPATECTOMY, BODY-TEMPERATURE, OXYGEN-TRANSPORT|
Archive Staff Only