Restoration of cerebral blood flow autoregulation and reactivity to carbon dioxide in acute liver failure by moderate hypothermia

Authors

  • Rajiv Jalan,

    Corresponding author
    1. Institute of Hepatology, University College London Medical School, London, England
    2. Liver Unit and Scottish Liver Transplantation Unit, Royal Infirmary of Edinburgh, Scotland
    • Institute of Hepatology, University College London Medical School, 69-75, Chenies Mews, London WC1E 6HX, UK. fax: (44) 2073800405
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  • Steven W. M. Olde Damink,

    1. Liver Unit and Scottish Liver Transplantation Unit, Royal Infirmary of Edinburgh, Scotland
    2. Department of Surgery, University of Maastricht, Maastricht, the Netherlands
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  • Nicolaas E. P. Deutz,

    1. Department of Surgery, University of Maastricht, Maastricht, the Netherlands
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  • Peter C. Hayes,

    1. Liver Unit and Scottish Liver Transplantation Unit, Royal Infirmary of Edinburgh, Scotland
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  • Alistair Lee

    1. Department of Anaesthetics and the Intensive Care Unit, Royal Infirmary of Edinburgh, Scotland.
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Abstract

In patients with acute liver failure (ALF) and uncontrolled intracranial hypertension, moderate hypothermia (32°C) reduces intracranial pressure (ICP) and cerebral blood flow (CBF), and can be used as a bridge to liver transplantation. The purpose of this study was to test the hypothesis that moderate hypothermia reduced ICP by restoring CBF autoregulation. Nine patients with uncontrolled intracranial hypertension and ALF who fulfilled the criteria for poor prognosis were studied. CBF autoregulation and reactivity to carbon dioxide were evaluated before and 4 hours after cooling (32°C). Significant reductions were observed in the ICP (median, 46 [range, 27-54] mm Hg to 19 [15-22] mm Hg; P < .01) and CBF (median, 111 [69-134] to 56 [38-67] mL/100 g/min; P < .05). The defective CBF autoregulation and the absence of reactivity to carbon dioxide that was observed in all patients was restored with cooling. The results of our study suggest that the improvement in ICP observed with hypothermia may be the result of its effects on CBF autoregulation and provides a tool to explore the mechanisms associated with the deranged CBF autoregulation in ALF.

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