Author(s): Raghavan M, Marik PE
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Abstract Severe intracranial hypertension (IH) in the setting of fulminant hepatic failure (FHF) carries a high mortality and is a challenging disease for the critical care provider. Despite considerable improvements in the understanding of the pathophysiology of cerebral edema during liver failure, therapeutic maneuvers that are currently available to treat this disease are limited. Orthotopic liver transplantation is currently the only definitive therapeutic strategy that improves outcomes in patients with FHF. However, many patients die prior to the availability of donor organs, often because of cerebral herniation. Currently, two important theories prevail in the understanding of the pathophysiology of IH during FHF. Ammonia and glutamine causes cytotoxic cerebral injury while cerebral vasodilation caused by loss of autoregulation increases intracranial pressure (ICP) and predisposes to herniation. Although ammonia-reducing strategies are limited in humans, modulation of cerebral blood flow seems promising, at least during the early stages of hepatic encephalopathy. ICP monitoring, transcranial Doppler, and jugular venous oximetry offer valuable information regarding intracranial dynamics. Induced hypothermia, hypertonic saline, propofol sedation, and indomethacin are some of the newer therapies that have been shown to improve survival in patients with severe IH. In this article, we review the pathophysiology of IH in patients with FHF and outline various therapeutic strategies currently available in managing these patients in the critical care setting.
This article was published in Neurocrit Care
and referenced in Journal of Addiction Research & Therapy