REGIONAL CEREBRAL BLOOD-FLOW AND CO2 REACTIVITY IN FULMINANT HEPATIC-FAILURE

Alterations in cerebral hemodynamics are postulated to contribute to b rain herniation, a major cause of death in patients with severe hepati c encephalopathy due to fulminant hepatic failure (FHF). In an effort to identify these changes in cerebral hemodynamics, regional and globa l cerebral blood flow (CBF) and CO2 reactivity were measured using sta ble xenon-enhanced computed tomography (Xe/CT) in 24 patients within 7 2 h of onset of severe hepatic encephalopathy. Regional variations in CBF, most notably, a relative decrease in CBF in the anterior circulat ion and an increase in CBF in the posterior circulation were found. CB F was significantly lower in FHF patients compared with controls, howe ver, these values are well out of the established ischemic range. FHF patients also showed significant impairment in CBF response to hypoven tilation, while the CBF response to hyperventilation remained intact. This study suggests that FHF patients demonstrate early changes in bot h CBF patterns and CO2 reactivity. The relatively ''normal'' CBF value s obtained in FHF patients in severe hepatic encephalopathy coupled wi th the lack of vasodilatation to hypoventilation suggest a state of un coupled CBF and metabolism or ''luxury perfusion'' that could theoreti cally contribute to vasogenic edema, brain swelling, and cerebral hern iation.