Continuous assessment of cerebrovascular autoregulation after traumatic brain injury using brain tissue oxygen pressure reactivity.
OBJECTIVE
To evaluate whether two newly developed indexes of brain tissue oxygen pressure reactivity (ORx and bPtio2) provide information on the status of cerebrovascular autoregulation after traumatic brain injury. This was accomplished by analyzing the relationship between these indexes and an index of cerebrovascular pressure reactivity (PRx). PRx is an established parameter for estimation of cerebrovascular autoregulation.


METHODS
Retrospective analysis of prospectively collected data.


METHODS
Neurosurgical intensive care unit of a university hospital.


METHODS
Twenty-seven patients suffering from severe traumatic brain injury.


METHODS
Continuous monitoring of mean arterial blood pressure, intracranial pressure, cerebral perfusion pressure, and partial pressure of brain tissue oxygen (Ptio2) was performed for an average of 6.5 days. ORx was calculated as a moving correlation coefficient between values of cerebral perfusion pressure and Ptio2. The bPtio2 was calculated as a moving value of the slope of the linear regression function between cerebral perfusion pressure and Ptio2. PRx was calculated as a moving correlation coefficient between values for intracranial pressure and mean arterial blood pressure. Outcome was assessed at 6 months after traumatic brain injury (Glasgow Outcome Scale).


RESULTS
Both ORx and bPtio2 correlated significantly with PRx (r=.55 for ORx, r=.52 for bPtio2, p<.01). PRx and ORx showed a significantly negative correlation to the monitored Ptio2 values (r=-.42 for PRx, r=-.41 for ORx, p<.05) and outcome (r=-.52 for PRx, r=-.62 for ORx, p<.01), whereas bPtio2 did not.


CONCLUSIONS
ORx and, to a lesser extent, bPtio2 correlated with the autoregulatory marker PRx and provide additional information about the status of cerebrovascular autoregulation after traumatic brain injury. The data also suggested that patients with impaired autoregulation are at increased risk for secondary cerebral hypoxia.
Jaeger
Matthias
M
Department of Neurosurgery, University of Leipzig, Leipzig, Germany. jaem@medizin.uni-leipzig.de
Schuhmann
Martin U
MU
Soehle
Martin
M
Meixensberger
Jürgen
J
D000293:Adolescent; D000328:Adult; D000368:Aged; D001794:Blood Pressure; D001930:Brain Injuries / Q000175:diagnosis / Q000378:metabolism / Q000503:physiopathology*; D002560:Cerebrovascular Circulation; D005260:Female; D005500:Follow-Up Studies; D006706:Homeostasis / Q000502:physiology*; D006801:Humans; D007427:Intracranial Pressure / Q000502:physiology*; D008297:Male; D008875:Middle Aged; D008991:Monitoring, Physiologic; D010101:Oxygen Consumption / Q000502:physiology*; D012189:Retrospective Studies; D015599:Trauma Severity Indices