OBJECTIVES: Brain 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. METHODS: One 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. RESULTS: Six 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. DISCUSSION: A 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.
OBJECTIVES:Brain 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. METHODS: One 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. RESULTS: Six 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. DISCUSSION: A 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.
Authors: Rajannya Sen; Alexander V Zhdanov; Thomaz F S Bastiaanssen; Liisa M Hirvonen; Peter Svihra; Patrick Fitzgerald; John F Cryan; Stefan Andersson-Engels; Andrei Nomerotski; Dmitri B Papkovsky Journal: Sci Rep Date: 2020-11-04 Impact factor: 4.379