Regional Cerebral Blood Flow and CO₂ Reactivity in Fulminant Hepatic Failure

Abstract

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.

Regional cerebral blood flow autoregulation in patients with fulminant hepatic failure

“…This finding supports 2 previous studies of regional cerebral perfusion in patients with FHF that used computed tomographic scans 4 and single-photon emission tomography, 10 showing that frontal perfusion is low compared with both other brain regions, as well as compared with healthy controls. This impaired perfusion was speculated to increase the risk for frontal hypoxia during prolonged arterial hypotensive episodes, which could critically restrict blood flow to this brain region.…”

“…2 In the later stages of fulminant hepatic failure (FHF), but before intracranial hypertension is manifest, cerebral hyperemia often prevails and seems to precede herniation. 3,4 Therefore, the genesis of cerebral hyperemia may be of crucial importance not only to elucidate why brain edema occurs so frequently, but also to secure rational critical care management of patients with liver failure.…”

Brain edema in liver failure: Basic physiologic principles and management

“…Studies of CBF in patients with ALF indicate that increased CBF precedes high ICP and cerebral herniation. 25,[39][40][41] The genesis of this high CBF is not fully settled. 10,29,40,42 However, at least two distinct mechanisms may be of importance for development of high CBF.…”

Acute changes in cerebral blood flow and metabolism during portasystemic shunting

“…8 Cerebral hyperemia has been suggested as an important factor in the development of cerebral edema by a number of workers, but this has been in the context of acute liver failure. [9][10][11][12][13] Conversely, patients with chronic liver disease show an increase in cerebral vascular resistance and a concomitant decrease in CBF. 14 It is likely that an acute stress, introduced by uncontrolled variceal bleeding and hypotension, and TIPSS insertion may have contributed to the seemingly contradictory observation of increased CBF.…”