• Michael Louis Smith, George J Counelis, Eileen Maloney-Wilensky, Michael F Stiefel, Kathy Donley, and Peter D LeRoux.
• Department of Neurosurgery, Hospital of the University of Pennsylvania, Philadelphia, PA 19104, USA.
• Neurol. Res. 2007 Oct 1;29(7):755-9.

ObjectivesBrain death is a clinical diagnosis often confirmed with supplementary tests. In this study, we examined the relationship between brain death and the partial pressure of brain tissue oxygen (PbtO(2)). We hypothesized that a sustained PbtO(2) of 0 is associated with brain death.MethodsOne hundred and twenty-six patients (Glasgow coma scale < or = 8, median age: 50 years) who underwent PbtO(2) monitoring were studied prospectively during a 2 year period in the neurointensive care unit at a university-based level I trauma center. PbtO(2), intracranial pressure (ICP), mean arterial pressure (MAP), cerebral perfusion pressure (CPP) and brain temperature (BT) were compared before and after the diagnosis of brain death.ResultsSix patients (median age: 52 years) experienced brain death. In these patients, PbtO(2) decreased toward 0 mmHg as ICP increased and CPP decreased. PbtO(2) reached 0 only when there was clinical evidence for brain death. During the subsequent 12 hours until the second brain death examination, PbtO(2) remained 0 mmHg and did not respond to oxygen challenge. In addition, TCD examination demonstrated a 'to and fro' pattern consistent with brain death and cerebral circulatory arrest. PbtO(2) of 0 mmHg was observed in five non-brain dead patients. These episodes were transient (>30 minutes) and responded to an oxygen challenge, directed treatment or catheter replacement.DiscussionA sustained (>30 minutes) brain PbtO(2) of 0 is consistent with brain death. We suggest that a sustained 'zero' PbtO(2) may be used to determine when a brain death examination is appropriate in the pharmacologically suppressed patient.

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