Cerebral glucose and oxygen metabolism in patients with fulminant hepatic failure

Abstract

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 v 18.3 ؎ 5.5 and 28.5 ؎ 6.6 mol/100 g/min (P < .05) and 86 ؎ 18 v 164 ؎ 42 and 174 ؎ 27 mol/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 lactatepyruvate 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. (Liver Transpl 2003;9:1244-1252.) F ulminant hepatic failure (FHF) is a critical illness with multiorgan failure and hepatic encephalopathy (HE). Cerebral edema and intracranial hypertension are feared and often fatal complications. The pathophysiological background for these complications is not fully understood, but alterations in cerebral metabolism and cerebral blood flow (CBF) seem to be of importance. 1 Metabolism of the brain is different from most other tissues in several aspects. It uses glucose only as an energy source under normal physiological conditions, and in contrast to most other organs, brain cells are permeable to glucose and can use glucose without the intermediation of insulin. 2 However, when necessary, the brain can use other substrates as energy sources, such as ␤-hydroxybutyrate (␤-OHB) and acetoacetate. 3 Hyperammonemia is a consistent finding in FHF, and arterial ammonia concentration seems to correlate with the development of cerebral edema and intracranial hypertension in patients with FHF. 4 The exact biochemical mechanisms involved in cerebral ammonia toxicity are not fully established, but ammonia-induced alterations in cerebral glucose metabolism may be of importance. 5 In experimental studies of hyperammonemia, both reduced 6,7 and increased 8 cerebral glucose metabolism have been reported. Also, studies of patients with FHF reported both reduced, 9,10 normal, 10 and increased 11 cerebral glucose metabolism, whereas cerebral oxygen metabolism was reduced in all studies. [9][10][11][12] The a...

A physiological Intensive Control Insulin-Nutrition-Glucose (ICING) model validated in critically ill patients

“…This model has an additional insulin independent [56] central nervous system glucose uptake, CN S, with an experimental value between 0.29-0.38 mmol/min [56,57,58,59,60,61,62,63,64].…”

Fuelling Cerebral Activity in Exercising Man

“…During exercise, skeletal muscle releases ammonium (NH 4 + , which equilibrates rapidly with the readily diffusible The brain in exerciseammonia, NH 3 ) and cerebral uptake (Felipo and Butterworth, 2002) could alter MR (Tsacopoulos et al, 1997). The NH 3 may also affect neurotransmitter metabolism of glutamate and g-amino butyric acid (Guezennec et al, 1998;Sonnewald et al, 1997) and deteriorate cerebral function as surmised in hepatic encephalopathy and hyperammonaemia (Strauss et al, 2003).…”

Multimodal brain monitoring in fulminant hepatic failure

“…Studies in patients with FHF demonstrate that the monitoring of brain oxygenation provides valuable data for the clinical management of this population [62] . Oxygen and cerebral glucose consumption have been observed before signs of brain swelling, suggesting that cerebral oxygen metabolism is intact at this stage [62] . In another study, CMRO2 was found to be decreased in all patients with FHF [61] .…”

“…In the study, it was concluded that hyperemia alone was not related to the outcome, despite having occurred more frequently during elevated ICP. All patients with malignant intra cranial hypertension previously had hyperemia [62,63] . Nielsen et al [36] reported that both pressure and arterial oxygen saturation were maintained during infusion with norepinephrine.…”