Cerebral hemodynamic and metabolic profiles in fulminant hepatic failure: Relationship to outcome

Authors

  • Shushma Aggarwal,

    Corresponding author
    1. Department of Anesthesiology/Critical Care Medicine, University of Pittsburgh Medical Center, Pittsburgh, PA
    • Department of Anesthesiology, University of Pittsburgh Medical Center, Room C220, 230 Lothrop Street, Pittsburgh, PA 15213

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    • Telephone: 412-647-6465; FAX: 412-647-6290

  • Walter Obrist,

    1. Department of Neurosurgery, University of Pittsburgh Medical Center, Pittsburgh, PA
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  • Howard Yonas,

    1. Department of Neurosurgery, University of Pittsburgh Medical Center, Pittsburgh, PA
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  • David Kramer,

    1. Department of Anesthesiology/Critical Care Medicine, University of Pittsburgh Medical Center, Pittsburgh, PA
    Current affiliation:
    1. Mayo Clinic Transplant Center, Jacksonville, FL
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  • Yoogoo Kang,

    1. Department of Anesthesiology/Critical Care Medicine, University of Pittsburgh Medical Center, Pittsburgh, PA
    2. Thomas Jefferson University, Jefferson Medical College, Philadelphia, PA
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  • Victor Scott,

    1. Department of Anesthesiology/Critical Care Medicine, University of Pittsburgh Medical Center, Pittsburgh, PA
    2. Med-Pro, Phoenix, AZ
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  • Raymond Planinsic

    1. Department of Anesthesiology/Critical Care Medicine, University of Pittsburgh Medical Center, Pittsburgh, PA
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Abstract

The purpose of this retrospective study was to examine the potential role of cerebral hemodynamic and metabolic factors in the outcome of patients with fulminant hepatic failure (FHF). Based on the literature, a hypothetical model was proposed in which physiologic changes progress sequentially in five phases, as defined by intracranial pressure (ICP) and cerebral blood flow (CBF) measurements. Seventy-six cerebral physiologic profiles were obtained in 26 patients (2 to 5 studies each) within 6 days of FHF diagnosis. ICP was continuously measured by an extradural fiber optic monitor. Global CBF estimates were obtained by xenon clearance techniques. Jugular venous and peripheral artery catheters permitted calculation of cerebral arteriovenous oxygen differences (AVDO2), from which cerebral metabolic rate for oxygen (CMRO2) was derived. A depressed CMRO2 was found in all patients. There was no evidence of cerebral ischemia as indicated by elevated AVDO2s. Instead, over 65% of the patients revealed cerebral hyperemia. Eight of the 26 patients underwent orthotopic liver transplantation—all recovered neurologically, including 6 with elevated ICPs. Of the 18 patients receiving medical treatment only, all 7 with increased ICP died in contrast to 9 survivors whose ICP remained normal (P < 0.004). Hyperemia, per se, was not related to outcome, although it occurred more frequently at the time of ICP elevations. Six patients were studied during brain death. All 6 revealed malignant intracranial hypertension, preceded by hyperemia. In conclusion, the above findings are consistent with the hypothetical model proposed. Prospective longitudinal studies are recommended to determine the precise evolution of the pathophysiologic changes. (Liver Transpl 2005;11:1353–1360.)

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