CEREBRAL HEMODYNAMIC AND METABOLIC CHANGES IN FULMINANT HEPATIC-FAILURE - A RETROSPECTIVE STUDY

The purpose of this retrospective study was to determine cerebral hemo dynamic and metabolic changes in comatose patients with fulminant hepa tic failure. Computerized tomography of the brain and cerebral blood f low measurements by the xenon-computerized tomography scan or intraven ous xenon-133 methods were obtained in 33 patients with fulminant hepa tic failure. In a subgroup of 22 patients, arteriojugular venous oxyge n content difference and cerebral metabolic rate for oxygen were deter mined. Carbon dioxide reactivity was tested in 17 patients, and intrac ranial pressure was recorded by an epidural monitor in 8 patients. Cer ebral blood flow and arteriojugular venous oxygen content difference w ere adjusted to the average arterial carbon dioxide pressure of the sa mple (32 mm Hg). Adjusted cerebral blood flow varied from 16.5 to 94.7 ml/100 gm/min; 52% of the patients had reduced adjusted cerebral bloo d flows (less than 33 ml/100 gm/min), whereas 24% had hyperemic values (greater than 50 ml/100 gm/min). Patients with higher adjusted cerebr al blood flows showed cerebral swelling on computerized tomography sca n (p < 0.002), were in deeper coma (p < 0.05) and had greater mortalit y (p < 0.002). The adjusted arteriojugular venous oxygen content diffe rence was negatively correlated with adjusted cerebral blood flow (r = -0.61, p < 0.002). The majority of patients with reduced adjusted cer ebral blood flows had low adjusted arteriojugular venous oxygen conten t differences (less than 5 vol%), indicating hyperemia rather than isc hemia. The average cerebral metabolic rate for oxygen was 50% of norma l (1.6 +/- 0.4 ml/100 gm/min); even patients with low cerebral metabol ic rates for oxygen recovered neurologically. Carbon dioxide reactivit y was preserved in almost all patients, which argues for the effective ness of hyperventilation in reducing blood flow. All four patients wit h elevated intracranial pressures (greater than 24 mm Hg) had increase d adjusted cerebral blood flows; three of four patients with intracran ial pressures less than 20 had reduced adjusted cerebral blood flows. These findings suggest that cerebral swelling, intracranial hypertensi on and cerebral hyperemia are poor prognostic signs in patients with f ulminant hepatic failure.