• Alexandra S Reynolds, John Liang, Monica Raiss, Neha S Dangayach, and Thomas D Schiano.
• Department of Neurosurgery, Mount Sinai Hospital, New York, NY, United States of America; Department of Neurology, Mount Sinai Hospital, New York, NY, United States of America. Electronic address: Alexandra.Reynolds@mountsinai.org.
• J Crit Care. 2021 Feb 1; 61: 115-118.

PurposeUnlike patients with acute liver failure, patients with cirrhosis are not traditionally thought to be at risk for developing cerebral edema. In the largest case series to date, we document clinical characteristics of cirrhotic patients who develop cerebral edema.Materials And MethodsIn this retrospective case series, seventeen adult patients with acute-on-chronic liver failure (ACLF) were identified using Morbidity & Mortality data. Neurological decompensation was defined by focal neurological deficits or abnormal movements. Elevated ICP was diagnosed clinically by pupillary reflex change improving with hyperosmolar therapy, or by herniation on CT. Pulsatility indices >1.2 on transcranial Dopplers (TCDs) and/or optic nerve sheath diameter (ONSD) >0.5 cm were acceptable alternatives.ResultsMedian MELD-Na was 36 (IQR 31.5,43) compared with 20 (IQR 19,23) prior to admission. Neurological decompensation was associated with abnormal pupil reactivity in 76% and abnormal movements in 65%. Cerebral edema was diagnosed by CT (n = 14). For those too ill to transport, elevated ICP was confirmed with TCDs for three patients and ONSD for two. Mortality was 100% a median of 3 days (IQR 1.5,5) from neurologic decompensation.ConclusionsACLF patients with neurological decompensation exhibit distinct clinical changes. Noninvasive bedside techniques may serve as surrogate measures for ICP.Copyright © 2020 Elsevier Inc. All rights reserved.

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