Raised intracranial pressure in hepatic encephalopathy
Mukherjee, K.K.; Chhabra, R.; Khosla, V.K.
Indian Journal of Gastroenterology Official Journal of the Indian Society of Gastroenterology 22 Suppl. 2: S62-S65
2003
ISSN/ISBN: 0254-8860 PMID: 15025259 Document Number: 9745
Intracranial hypertension secondary to cerebral edema is the cause of death in 50%-80% of patients with fulminant hepatic failure (FHF). This is rarely seen in chronic hepatic failure. The genesis of cerebral edema in FHF is poorly understood. The grade of encephalopathy and coagulopathy are the most important predictors of outcome in FHF. However, it is important to emphasize that intracranial pressure (ICP) may not reflect clinical course. Decerebrate posturing may be seen with ICP recording of 16 mmHg, while a quarter of the patients may have brain damage without clinical signs of raised ICP. ICP monitoring is therefore vital. The gold standard for ICP monitoring is the intraventricular method. Non-invasive methods like computerized tomography scan and magnetic resonance imaging have poor correlation with ICP. Other methods like transcranial Doppler and jugular venous oximetry measurement of brain metabolites need evaluation. The main indications for ICP monitoring in FHF are (a) patients in grade III or IV encephalopathy and (b) patients undergoing liver transplantation. Generally, patients with an ICP >40 mmHg with cerebral perfusion pressure <50 mmHg for over 2 hours are poor subjects for liver transplant.
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