Low Cerebral Oxygen Consumption and Blood Flow in Patients With Cirrhosis and an Acute Episode of Hepatic Encephalopathy

Background & AimsIt is unclear whether patients with hepatic encephalopathy (HE) have disturbed brain oxygen metabolism and blood flow.MethodsWe 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.ResultsNeither 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.ConclusionsThe 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.