Anesthesia for Liver Transplantation in Patients with Fulminant Hepatic Failure under Intracranial Pressure and Jugular Venous Oxygen Saturation Monitoring.
10.4097/kjae.2002.43.2.165
- Author:
Eun Ha SUK
1
;
In Sook CHO
;
Kyu Sam HWANG
;
Kyu Taek CHOI
Author Information
1. Department of Anesthesiology, Asan Medical Center, College of Medicine, University of Ulsan, Korea. qtek@amc.seoul.kr
- Publication Type:Original Article
- Keywords:
Fulminant hepatic failure;
transplantation;
intracranial pressure;
jugular venous oxygen saturation
- MeSH:
Anesthesia*;
Brain Edema;
Brain Injuries;
Cause of Death;
Furosemide;
Hemodiafiltration;
Hemodynamics;
Hepatorenal Syndrome;
Humans;
Hypoventilation;
Intracranial Hypertension;
Intracranial Pressure*;
Jaundice;
Liver Failure;
Liver Failure, Acute*;
Liver Transplantation*;
Liver*;
Mannitol;
Oxygen*;
Perfusion;
Retrospective Studies;
Thiopental;
Transplantation;
Vasodilation
- From:Korean Journal of Anesthesiology
2002;43(2):165-173
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Fulminant hepatic failure is characterized by rapid progressive liver failure with the onset of encephalopathy within a few weeks of the appearance of jaundice. This illness is frequently complicated by hemodynamic instability, multiple organ dysfunction and intracranial hypertension associated with cerebral edema, which is the most common cause of death in this condition. We reviewed 8 cases of liver transplantation with fulminant hepatic failure with respect to anesthetic management and neurologic monitoring. METHODS: We analyzed anesthetic management, intracranial pressure (ICP), cerebral perfusion pressure (CPP), jugular venous oxygen saturation (SjvO2) and hemodynamics retrospectively during liver transplantation in 8 patients with fulminant hepatic failure. Intracranial hypertension was defined as an ICP >or= 20 mmHg for at least 5 minutes. The goal of management is to keep the CPP above 40 - 50 mmHg and ICP below 30 - 40 mmHg. There were 3 cases of hepatorenal syndrome and continous veno-venous hemodiafiltration (CVVHD) was used in 2 cases. RESULTS: All patients showed characteristic hyperdynamic circulation with severe vasodilation and vasopressive drugs were needed to maintain CPP. The episodes of intracranial hypertension occurred in all patients during transplantation. To decrease ICP, medical therapy with mannitol, furosemide and thiopental infusion were required. Intracranial hemorrhagic complications occurred in 3 cases. SjvO2 decreased transiently below 60% in 3 cases. However, it was improved with an increase of PaCO2 by hypoventilation and maintained above 60 - 80% in all cases. CONCLUSIONS: This data suggests that there is a risk of brain injury secondary to elevated ICP and low CPP during liver transplantation. ICP, CPP and SjvO2 monitoring in patients with fulminant hepatic failure can be useful for the prompt recognition of intracranial hypertension and for guiding therapy. However, correction of the coagulopathy before placement of the ICP tranducer must be performed to prevent hemorragic complications.
