ABSTRACT
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.
KEYWORDS
Acute liver failure - intracranial pressure - cerebral blood flow - ammonia - orthotopic
liver transplantation - hepatic encephalopathy
