CEREBRAL BLOOD-FLOW, OXYGEN-METABOLISM AND TRANSCRANIAL DOPPLER SONOGRAPHY DURING HIGH-VOLUME PLASMAPHERESIS IN FULMINANT HEPATIC-FAILURE

Objective: The effect of high-volume plasmapheresis on hepatic encepha lopathy, cerebral blood flow (CBF) and cerebral metabolic rate for oxy gen (CMRO(2)) was investigated in patients with fulminant hepatic fail ure (FHF). Methods: Twelve consecutive patients (8 women, 4 men, media n age 34 years (range 19-51)) were studied before and after high-volum e plasmapheresis with 10-16 litres fresh frozen plasma, while PaCO2 an d body temperature were maintained at 30 (23-34) mmHg and 37.6 degrees C (36.6-38.4), respectively. Blood samples from the internal jugular vein and a radial artery allowed calculation of the cerebral arteriove nous oxygen difference (AVDO(2)) and oxygen extraction (AVDO(2) divide d by arterial oxygen content). CBF was determined by a xenon-133 clear ance method in eight patients and CMRO(2) calculated as AVDO(2) times CBF. Cerebral perfusion pressure (CPP) was determined as the differenc e between mean arterial and subdural pressures in eight patients. Resu lts: High-volume plasmapheresis was initiated 22 (6-168) h after the d evelopment of hepatic encephalopathy and 11 patients had grade 4 encep halopathy. Following high-volume plasmapheresis the grade of encephalo pathy improved in four patients. The CBF increased from a median of 31 (16-86) to 45 (18-97) ml/100 g/min and as oxygen extraction remained unchanged(32 (9-41) vs. 29 (7-39)%), CMRO(2) increased from 1.24 (0.96 -1.82) to 1.86 (1.00-2,07) ml/100 g/min (P < 0.05). The CPP increased from 62 (19-76) to 92 (50-105) mmHg (P < 0.01), whereas the intracrani al pressure remained unchanged (19 (3-45) vs. ii (5-33) mmHg). No stat istical difference was found between the relative changes in the above parameters in survivors compared to non-survivors. Conclusion: Althou gh the clinical status did not improve in all patients, both CBF and C MRO(2) increased after high-volume plasmapheresis. The alleviation of brain oxygen metabolism by high-volume plasmapheresis may reflect part ial removal of neuroinhibitory plasma factors.