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Preservation of cerebral oxidative metabolism in fulminant hepatic failure: An autoregulation study
Author(s) -
Larsen Fin Stolze,
Ejlersen Ellen,
Clemmesen Jens Otto,
Kirkegaard Preben,
Hansen Bent Adel
Publication year - 1996
Publication title -
liver transplantation and surgery
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.814
H-Index - 150
eISSN - 1527-6473
pISSN - 1074-3022
DOI - 10.1002/lt.500020504
Subject(s) - cerebral blood flow , cerebral edema , medicine , mean arterial pressure , middle cerebral artery , anesthesia , fulminant hepatic failure , intracranial pressure , blood pressure , cerebral arteries , cardiology , endocrinology , ischemia , liver transplantation , transplantation , heart rate
Under normal conditions cerebral blood flow (CBF) is regulated to secure oxidative brain metabolism, but in patients with fulminant hepatic failure (FHF), insufficient CBF has been suggested to precede cerebral edema and intracranial hypertension. In order to determine if insufficient CBF and hypoxia are present in patients with FHF we increased the mean arterial pressure and measured cerebral metabolism. In six patients with FHF CBF determined by 133 Xenon injection technique, transcranial Doppler mean flow velocity in the middle cerebral artery (V mean ) and cerebral metabolism were determined, before and after an increase in mean arterial pressure by norepinephrine infusion. Mean arterial pressure was measured in a radial artery, and blood samples from the radial artery and internal jugular vein allowed calculation of the cerebral arteriovenous oxygen (AVD o2 ), —glucose (AVD gl ), and —lactate (AVD lac ) differences. Cerebral metabolic rates (CMR o2,‐gl,‐lac ) were calculated as AVD o2,‐gl,‐lac times CBF. Mean arterial pressure was raised from 70 (54–105) to 111 (93–128) mm Hg during intravenous infusion of norepinephrine. CBF increased from 34 (12–55) to 47 (27–81) mL · 100g −1 · min −1 ( p < 0.05) and V mean from 53 (42–60) to 67 (61–79) cm · s −1 ( p < 0.05), whereas CMR o2 (1.4 (0.9–2.4) mL · 100g −1 · min −1 ), CMR gl (11 (4.8–20) μmol 100g −1 · min −1 ), and CMR lac (3.2 (0–8.9) μmol · 100g −1 · min −1 ) remained unchanged. Our finding indicates that cerebral oxidative metabolism is preserved in patients with FHF. Cerebral autoregulation is absent, however, and neuroprotective critical care is suggested to be guided by internal jugular vein oxygen saturation to secure appropriate cerebral oxygenation. Copyright © 1996 by the American Association for the Study of Liver Diseases.