Carbon dioxide reactivity, pressure autoregulation, and metabolic suppression reactivity after head injury: a transcranial Doppler study.
OBJECTIVE
Contemporary management of head-injured patients is based on assumptions about CO2 reactivity, pressure autoregulation (PA), and vascular reactivity to pharmacological metabolic suppression. In this study, serial assessments of vasoreactivity of the middle cerebral artery (MCA) were performed using bilateral transcranial Doppler (TCD) ultrasonography.


METHODS
Twenty-eight patients (mean age 33 +/- 13 years, median Glasgow Coma Scale score of 7) underwent a total of 61 testing sessions during postinjury Days 0 to 13. The CO2 reactivity (58 studies in 28 patients), PA (51 studies in 23 patients), and metabolic suppression reactivity (35 studies in 16 patients) were quantified for each cerebral hemisphere by measuring changes in MCA velocity in response to transient hyperventilation, arterial blood pressure elevation, or propofol-induced burst suppression, respectively. One or both hemispheres registered below normal vasoreactivity scores in 40%, 69%, and 97% of study sessions for CO2 reactivity, PA, and metabolic suppression reactivity (p < 0.0001), respectively. Intracranial hypertension, classified as intracranial pressure (ICP) greater than 20 mm Hg at the time of testing, was associated with global impairment of CO2 reactivity, PA, and metabolic suppression reactivity (p < 0.05). A low baseline cerebral perfusion pressure (CPP) was also predictive of impaired CO2 reactivity and PA (p < 0.01). Early postinjury hypotension or hypoxia was also associated with impaired CO2 reactivity (p < 0.05), and hemorrhagic brain lesions in or overlying the MCA territory were predictive of impaired metabolic suppression reactivity (p < 0.01). The 6-month Glasgow Outcome Scale score correlated with the overall degree of impaired vasoreactivity (p < 0.05).


CONCLUSIONS
During the first 2 weeks after moderate or severe head injury, CO2 reactivity remains relatively intact, PA is variably impaired, and metabolic suppression reactivity remains severely impaired. Elevated ICP appears to affect all three components of vasoreactivity that were tested, whereas other clinical factors such as CPP, hypotensive and hypoxic insults, and hemorrhagic brain lesions have distinctly different impacts on the state of vasoreactivity. Incorporation of TCD ultrasonography-derived vasoreactivity data may facilitate more injury- and time-specific therapies for head-injured patients.
Lee
J H
JH
Brain Injury Research Center, University of California at Los Angeles, USA.
Kelly
D F
DF
Oertel
M
M
McArthur
D L
DL
Glenn
T C
TC
Vespa
P
P
Boscardin
W J
WJ
Martin
N A
NA
D000293:Adolescent; D000328:Adult; D001783:Blood Flow Velocity / Q000502:physiology; D001930:Brain Injuries / Q000000981:diagnostic imaging* / Q000503:physiopathology*; D002245:Carbon Dioxide / Q000502:physiology*; D002560:Cerebrovascular Circulation / Q000502:physiology; D005260:Female; D015600:Glasgow Coma Scale; D006706:Homeostasis / Q000502:physiology*; D006801:Humans; D007427:Intracranial Pressure / Q000502:physiology*; D008297:Male; D008875:Middle Aged; D020768:Middle Cerebral Artery / Q000000981:diagnostic imaging* / Q000503:physiopathology*; D017063:Outcome Assessment, Health Care; D011237:Predictive Value of Tests; D017585:Ultrasonography, Doppler, Transcranial; D014664:Vasodilation / Q000502:physiology*
D002245:Carbon Dioxide