Journal of hepatology
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Journal of hepatology · Aug 1995
Analysis of prognostic variables in the prediction of mortality, shunt failure, variceal rebleeding and encephalopathy following the transjugular intrahepatic portosystemic stent-shunt for variceal haemorrhage.
The aim of this study was to analyse prognostic variables predicting mortality, shunt insufficiency, variceal rebleeding and encephalopathy following transjugular intrahepatic portosystemic stent-shunt for variceal haemorrhage. ⋯ The results of this study suggest that patients with severe liver disease and hyponatraemia are liable to die early, and the presence of encephalopathy prior to transjugular intrahepatic portosystemic stent-shunt independently determines long-term survival. Patients in these groups should be considered high risk and worked up for orthotopic liver transplantation early. Shunt function in patients with an initial portal pressure gradient of > 18 mmHg requires close supervision. Encephalopathic patients should have smaller shunts and prophylactic measures to prevent worsening encephalopathy.
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Journal of hepatology · Aug 1995
Functional loss of cerebral blood flow autoregulation in patients with fulminant hepatic failure.
In management of patients with fulminant hepatic failure, it is recommended that mean arterial pressure should be raised if cerebral perfusion pressure is lower than 50 mmHg, but the influence of such therapy on cerebral blood flow is unknown. We examined cerebral blood flow autoregulation in seven consecutive patients with fulminant hepatic failure during treatment of imminent insufficient cerebral perfusion pressure. Cerebral perfusion was evaluated by transcranial Doppler assessed mean flow velocity in the middle cerebral artery and by the arterio-venous difference for oxygen. ⋯ The mean flow veolocity increased from 68 (30-134) to 108 (48-168) cm s-1 and the arterio-venous difference for oxygen by 46 (10-82)% (p < 0.05). Both mean flow velocity (r = 0.63) and arterio-venous difference for oxygen (r = 0.71) were correlated to mean arterial pressure (p < 0.001), and a lower blood pressure limit of autoregulation could not be identified in any of the patients. These data suggest that the cerebral blood flow is not autoregulated in patients with fulminant hepatic failure and therefore cerebral blood flow should be "clamped" within the normal physiologic range by manipulation of arterial blood pressure in order to avoid cerebral hypoxia and/or hypertensive induced cerebral oedema.