Cerebral glucose and oxygen metabolism in patients with fulminant hepatic failure

Hyperammonemia and hyperventilation are consistent findings in patients with fulminant hepatic failure (FHF), which may interfere with cerebral glucose and oxygen metabolism. The aim of the present study is to evaluate whether cerebral oxidative metabolism is preserved early in the course of FHF and whether hyperventilation has an influence on this. We included 16 patients with FHF, 5 patients with cirrhosis of the liver, and 8 healthy subjects. Concomitant blood sampling from an arterial catheter and a catheter in the jugular bulb and measurement of cerebral blood flow by the xenon 133 wash-out technique allowed calculation of cerebral uptake of glucose (CMR gluc) and oxygen (CMRO 2). Both CMR gluc and CMRo 2 were reduced in patients with FHF compared with those with cirrhosis and healthy subjects, i.e., 11.8 ±2.7 ± 18.3 ± 5.5 and 28.5 ± 6.6 μol/100 g/min ( P < .05) and 86 ± 18 ±v 164 ± 42 and 174 ± 27 μol/100 g/min ( P < .05). Arteriovenous difference in oxygen and oxygen-glucose index were normal in patients with FHF. Institution of mechanical hyperventilation did not affect glucose and oxygen uptake and hyperventilation did not affect lactate-pyruvate ratio or lactate-oxygen index. In conclusion, we found that cerebral glucose and oxygen consumption are proportionally decreased in patients with FHF investigated before clinical signs of cerebral edema. Our data suggest that cerebral oxidative metabolism is retained at this stage of the disease without being compromised by hyperventilation.