Cerebral blood flow and metabolism in fulminant liver failure

TLDR

Fulminant liver failure often causes cerebral edema and increased intracranial pressure, and cerebral blood flow has been reported variably as high or low. The study measured cerebral blood flow and cerebral metabolic rate for oxygen in 30 grade‑4 encephalopathy patients and evaluated changes after hyperventilation and infusions of mannitol, epoprostenol, and acetylcysteine. Cerebral blood flow and CMRO₂ were quantified in 30 patients before and after hyperventilation and infusions of mannitol, epoprostenol, and acetylcysteine. Cerebral blood flow varied widely (14–71 ml/100 g min) while CMRO₂ was uniformly low (0.16–2.03 ml/100 g min); 21 of 30 patients showed anaerobic metabolism, hyperventilation lowered both CBF and CMRO₂, mannitol and acetylcysteine increased them, prostaglandin I₂ raised CMRO₂ without affecting CBF, and the low CMRO₂ was inappropriate for metabolic needs, supporting mannitol as the primary treatment. Abstract truncated at 250 words.

Abstract

Fulminant liver failure is a syndrome that is frequently complicated by cerebral edema and increased intracranial pressure. Cerebral blood flow has been reported as high in some studies but low in others. This study undertook to measure cerebral blood flow and cerebral metabolic rate for oxygen in 30 patients with fulminant liver failure in grade 4 encephalopathy and to assess these parameters after intervention with hyperventilation and infusions of mannitol, epoprostenol and acetylcysteine. Cerebral blood flow varied widely, from 14 to 71 ml/100 gm/min (normal range, widely, from 14 to 71 ml/100 gm/min (normal range, 41 to 66), whereas the cerebral metabolic rate for oxygen was low in all patients, 0.16 to 2.03 ml/100 gm/min (normal range, 3.12 to 3.96). Twenty-one of the 30 patients had evidence of anaerobic metabolism with cerebral lactate production. Hyperventilation resulted in a significant decrease in both cerebral blood flow (median, 36 to 28 ml/100 gm/min) and cerebral metabolic rate for oxygen (median, 0.92 to 0.65 ml/100 gm/min); mannitol and acetylcysteine infusions resulted in significant increases in both of these parameters. Prostaglandin I2 infusion did not significantly after cerebral blood flow, but there was a significant increase in cerebral metabolic rate for oxygen. The depressed cerebral metabolic rate for oxygen in patients with fulminant liver failure is inappropriate to metabolic requirements, as demonstrated by both cerebral lactate production and the increase in cerebral oxygen consumption after improvement in cerebral blood flow. Mannitol infusion should remain the main treatment of the cerebral complications of fulminant liver failure. (ABSTRACT TRUNCATED AT 250 WORDS)