Cerebral blood flow, oxygen metabolism and transcranial Doppler sonography during high-volume plasmapheresis in fulminant hepatic failure

Abstract

Objective: The effect of high-volume plasmapheresis on hepatic encephalopathy, cerebral blood flow (CBF) and cerebral metabolic rate for oxygen (CMRO₂) was investigated in patients with fulminant hepatic failure (FHF). Methods: Twelve consecutive patients (8 women, 4 men, median age 34 years (range 19–51)) were studied before and after high-volume plasmapheresis with 10–16 litres fresh frozen plasma, while PaCO₂ and body temperature were maintained at 30 (23–34) mmHg and 37.6°C (36.6–38.4), respectively. Blood samples from the internal jugular vein and a radial artery allowed calculation of the cerebral arteriovenous oxygen difference (AVDO₂) and oxygen extraction (AVDO₂ divided by arterial oxygen content). CBF was determined by a xenon-133 clearance method in eight patients and CMRO₂ calculated as AVDO₂ times CBF. Cerebral perfusion pressure (CPP) was determined as the difference between mean arterial and subdural pressures in eight patients. Results: High-volume plasmapheresis was initiated 22 (6–168) h after the development of hepatic encephalopathy and 11 patients had grade 4 encephalopathy. Following high-volume plasmapheresis the grade of encephalopathy 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)%), CMRO₂ increased from 1.24 (0.96–1.82) to 1.86 (1.00–2.07) ml/100 g/min (P2 increased after high-volume plasmapheresis. The alleviation of brain oxygen metabolism by high-volume plasmapheresis may reflect partial removal of neuroinhibitory plasma factors.