Acute liver failure, also known as fulminant hepatic failure (FHF), embraces a spectrum of clinical entities characterized by acute liver injury, severe hepatocellular dysfunction, and hepatic encephalopathy. This is an uncommon, but not rare, condition with approximately 2,000 cases annually in the United States and a mortality rate ranging from 50% to 90%, despite intensive care therapy 1,2 . Cerebral edema leading to intracranial hypertension complicates approximately 50% to 80% of patients with severe FHF (grade III or IV coma), in whom it is the leading cause of death 2,3,4 . Brain edema in FHF patients is a relatively recent concept. In a 1944 report of 125 autopsies of military patients who had died from a condition he called fatal hepatitis (previously referred to as idiopathic acute yellow atrophy of the liver), Lucké 5 noted little alteration in the brain except for edema, but did not describe cerebral herniation. The first reports of brain edema and cerebral herniation as complications of FHF only emerged in the 1980s 6,7 . It is also noteworthy that brain edema and intracranial hypertension are not recognized common features of chronic liver failure, despite some case reports and small series 8,9 . The recent recognition of brain edema in FHF patients could be due to the advances in FHF patient care. Previously, FHF patients were dying from early hepatocellular insufficiency complications, mainly hemorrhage or sepsis
ABSTRACTIntracranial hypertension and brain swelling are a major cause of morbidity and mortality of patients suffering from fulminant hepatic failure (FHF). The pathogenesis of these complications has been investigated in man, in experimental models and in isolated cell systems. Currently, the mechanism underlying cerebral edema and intracranial hypertension in the presence of FHF is multi-factorial in etiology and only partially understood. The aim of this paper is to review the pathophysiology of cerebral hemodynamic and metabolism changes in FHF in order to improve understanding of intracranial dynamics complication in FHF.Keywords: hepatic insufficiency; intracranial hypertension; brain edema.
RESUMOO edema cerebral e a hipertensão intracraniana (HIC) são as principais causas de morbidade e mortalidade de pacientes com insuficiência hepática fulminante (IHF). A patogênese dessas complicações tem sido investigada no homem, em modelos experimentais e em sistemas celulares isolados. Atualmente, o mecanismo subjacente ao edema cerebral e HIC na presença de IHF é multifatorial em etiologia e pouco compreendido na literatura. O objetivo deste trabalho é revisar a fisiopatologia das alterações hemodinâmicas e metabólicas cerebrais na IHF, visando melhorar a compreensão da complicação da hemodinâmica encefálica na IHF.Palavras-chave: insuficiência hepatica; hipertenção intracraniana; edema encefálico.