Low Cerebral Oxygen Consumption and Blood Flow in Patients With Cirrhosis and an Acute Episode of Hepatic Encephalopathy
Background & Aims
It is unclear whether patients with hepatic encephalopathy (HE) have disturbed brain oxygen metabolism and blood flow.
Methods
We measured cerebral oxygen metabolism rate (CMRO2) by using 15O-oxygen positron emission tomography (PET); and cerebral blood flow (CBF) by using 15O-water PET in 6 patients with liver cirrhosis and an acute episode of overt HE, 6 cirrhotic patients without HE, and 7 healthy subjects.
Results
Neither whole-brain CMRO2 nor CBF differed significantly between cirrhotic patients without HE and healthy subjects, but were both significantly reduced in cirrhotic patients with HE (P < .01). CMRO2 was 0.96 ± 0.07 μmol oxygen/mL brain tissue/min (mean ± SEM) in cirrhotic patients with HE, 1.34 ± 0.08 in cirrhotic patients without HE, and 1.35 ± 0.05 in healthy subjects; and CBF was 0.29 ± 0.01 mL blood/mL brain tissue/min in patients with HE, 0.47 ± 0.02 in patients without HE, and 0.49 ± 0.03 in healthy subjects. CMRO2 and CBF were correlated, and both variables correlated negatively with arterial ammonia concentration. Analysis of regional values, using individual magnetic resonance co-registrations, showed that the reductions in CMRO2 and CBF in patients with HE were essentially generalized throughout the brain.
Conclusions
The observations imply that reduced cerebral oxygen consumption and blood flow in cirrhotic patients with an acute episode of overt HE are associated with HE and not cirrhosis as such, and that the primary event in the pathogenesis of HE could be inhibition of cerebral energy metabolism by increased blood ammonia.
Abbreviations used in this paper: CBF, cerebral blood flow, CMRO2, cerebral metabolic rate of oxygen, FDG, 18F-fluoro-deoxyglucose, FWHM, full width at half maximum, HE, hepatic encephalopathy, MR, magnetic resonance, MRI, magnetic resonance imaging, PET, positron emission tomography, pO2, partial pressure of oxygen, pCO2, partial pressure of carbon dioxide, VOI, volume of interest
Conflicts of interest The authors disclose no conflicts.
Funding Supported by the Danish Medical Research Council (271-06-0357, 271-07-0267), the Alfred Benzon Foundation, the Carlsberg Foundation, Aarhus University, and the Helga and Peter Kornings Foundation.
PII: S0016-5085(08)01895-7
doi:10.1053/j.gastro.2008.10.057
© 2009 AGA Institute. Published by Elsevier Inc. All rights reserved.


