Summary: Alterations in cerebral hemodynamics are postulated to contribute to brain herniation, a major cause of death in patients with severe hepatic encepha lopathy due to fulminant hepatic failure (PHP). In an ef fort to identify these changes in cerebral hemodynamics, regional and global cerebral blood flow (CBP) and CO2 reactivity were measured using stable xenon-enhanced computed tomography (Xe/CT) in 24 patients within 72 h of onset of severe hepatic encephalopathy. Regional vari ations in CBP, most notably, a relative decrease in CBP in the anterior circulation and an increase in CBP in the posterior circulation were found. CBP was significantly lower in PHP patients compared with controls, however, Abbreviations used: ABG, arterial blood gases; ACA, anterior cerebral artery; CMRoz, cerebral metabolic rate of oxygen; FHF, fulminant hepatic failure; HE, hepatic encephalopathy; MANOVA, multivariate analysis of variance; MCA, middle ce rebral artery; PCA, posterior cerebral artery; PET, positron emission tomography; ROI, region of interest; Xe/CT, xenon enhanced computed tomography.
329these values are well out of the established ischemic range. PHP patients also showed significant impairment in CBP response to hypoventilation, while the CBP re sponse to hyperventilation remained intact. This study suggests that PHP patients demonstrate early changes in both CBP patterns and CO2 reactivity. The relatively "normal" CBP values obtained in PHP patients in severe hepatic encephalopathy coupled with the lack of vasodi latation to hypo ventilation suggest a state of uncoupled CBP and metabolism or "luxury perfusion" that could theoretically contribute to vasogenic edema, brain swell ing, and cerebral herniation.