CEREBRAL BLOOD-FLOW AND METABOLISM IN FULMINANT LIVER-FAILURE

Citation
Ja. Wendon et al., CEREBRAL BLOOD-FLOW AND METABOLISM IN FULMINANT LIVER-FAILURE, Hepatology, 19(6), 1994, pp. 1407-1413
Citations number
30
Categorie Soggetti
Gastroenterology & Hepatology
Journal title
ISSN journal
02709139
Volume
19
Issue
6
Year of publication
1994
Pages
1407 - 1413
Database
ISI
SICI code
0270-9139(1994)19:6<1407:CBAMIF>2.0.ZU;2-7
Abstract
Fulminant liver failure is a syndrome that is frequently complicated b y cerebral edema and increased intracranial pressure. Cerebral blood h ow has been reported as high in some studies but low in others. This s tudy undertook to measure cerebral blood flow and cerebral metabolic r ate 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 acetylcys teine, Cerebral blood how varied widely, from 14 to 71 ml/100 gm/min ( normal range, 41 to 66), whereas the cerebral metabolic rate for oxyge n 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 resulte d in significant increases in both of these parameters. Prostaglandin I-2 infusion did not significantly alter cerebral blood flow, but ther e was a significant increase in cerebral metabolic rate for oxygen. Th e depressed cerebral metabolic rate for oxygen in patients with fulmin ant liver failure is inappropriate to metabolic requirements, as demon strated by both cerebral lactate production and the increase in cerebr al oxygen consumption after improvement in cerebral blood how. Mannito l infusion should remain the main treatment of the cerebral complicati ons of fulminant liver failure. Acetylcysteine has a beneficial effect that is not restricted to fulminant liver failure after acetaminophen overdose and has a role in the management of patients, regardless of cause of illness. The use of prostaglandin I, appears to be safe and m ay be beneficial. Acute hyperventilation causes decreases in both cere bral blood flow and cerebral metabolic rate for oxygen and has the pot ential to worsen cerebral ischemia.