Intracranial hypertension in acute liver failure: Pathophysiological basis of rational management.
SEMIN LIVER DIS
271 - 282.
Increased intracranial pressure (ICP) in patients with acute liver failure (ALF) remains a major cause of morbidity and mortality. Conventional methods of ammonia reduction such as the use of lactulose do not improve outcome, and metabolic substrates such as L-ornithine L aspartate may offer more promise. Mannitol remains the mainstay of therapy. An important role for cerebral hyperemia in the pathogenesis of increased ICP has led to a reevaluation of established therapies such as hyperventilation, N-acetylcysteine, thiopentone sodium, and propofol. Recent studies have focused on the role of systemic inflammatory response in the pathogenesis of increased ICP and support the use of antibiotics prophylactically. Moderate hypothermia reduces ICP in patients with uncontrolled intracranial hypertension and prevents increases in ICP during orthotopic liver transplantation (OLT). Advances in understanding the pathophysiological basis of intracranial hypertension in ALF have outstripped appropriate testing of the newly generated ideas in appropriate clinical trials, and more effort should be mounted at a national level to organize the appropriate multicenter studies required.
|Title:||Intracranial hypertension in acute liver failure: Pathophysiological basis of rational management|
|Keywords:||acute liver failure, intracranial pressure, cerebral blood flow, ammonia, orthotopic liver transplantation, hepatic encephalopathy, FULMINANT HEPATIC-FAILURE, CEREBRAL-BLOOD-FLOW, INDUCED BRAIN EDEMA, PROSPECTIVE CONTROLLED TRIAL, PORTACAVAL ANASTOMOSIS, MODERATE HYPOTHERMIA, TOTAL HEPATECTOMY, BODY-TEMPERATURE, N-ACETYLCYSTEINE, OXYGEN-TRANSPORT|
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