Volume 27, Issue 2 pp. 369-376
Original Article
Free Access

Cerebral blood flow and metabolism in patients with chronic liver disease undergoing orthotopic liver transplantation

Barbara J. Philips M.B.B.S., F.R.C.A.

Corresponding Author

Barbara J. Philips M.B.B.S., F.R.C.A.

Intensive Care Unit, Scottish Liver Transplantation Unit, Royal Infirmary of Edinburgh, Edinburgh, Scotland

Senior Registrar, Intensive Care Unit and Scottish Liver Transplantation Unit, Royal Infirmary of Edinburgh, Lauriston Place, Edinburgh, Scotland EH3 9YW. Fax: 44-131-536-1515===Search for more papers by this author
Ian R. Armstrong

Ian R. Armstrong

Intensive Care Unit, Scottish Liver Transplantation Unit, Royal Infirmary of Edinburgh, Edinburgh, Scotland

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Anthony Pollock

Anthony Pollock

Intensive Care Unit, Scottish Liver Transplantation Unit, Royal Infirmary of Edinburgh, Edinburgh, Scotland

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Alistair Lee

Alistair Lee

Intensive Care Unit, Scottish Liver Transplantation Unit, Royal Infirmary of Edinburgh, Edinburgh, Scotland

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First published: 30 December 2003
Citations: 46

Abstract

Changes in cerebral hemodynamics and metabolism associated with anesthesia and liver transplantation may present particular hazards for patients with cirrhosis. Fifteen patients undergoing liver transplantation were studied, 7 of whom had encephalopathy. Cerebral blood flow (CBF) was measured at the start of surgery, during veno-venous bypass and post reperfusion, using a method based on the Kety-Schmidt method. Cerebral metabolism was assessed by measuring the cerebral metabolic rate for oxygen (CMRO2) and the lactate oxygen index (LOI). The cerebral vascular reactivity to carbon dioxide (CO2) was studied during the preanhepatic and post reperfusion phases. During the preanhepatic period, the median CBF was 44 mL/100 g/min at an arterial carbon dioxide tension (PaCO2) of 3.8 kPa. After reperfusion the CBF increased (P < .02) to 102 mL/100 g/min, the arterial hydrogen ion concentration increased from 39 nmol/L to 53 nmol/L (P < .02) and the jugular venous oxygen saturation from 74% to 89% (P < .02). CBF was similar in patients with and without encephalopathy. The cerebral vascular reactivity to CO2 remained intact, although after reperfusion, the CBF for a given PaCO2 was greater, and the slope of the CBF/CO2 response curve diminished. The CMRO2was normal in patients without encephalopathy. In the encephalopathic patients, the CMRO2 was low during all stages of transplantation (0.54, 0.86, 1.24 mL/100 g/min, respectively). Patients with encephalopathy may be at increased risk of hypoxemic brain injury during transplantation. To minimize this possibility, more detailed neurological monitoring may be useful.

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