Carbon dioxide reactivity, pressure autoregulation, and metabolic suppression reactivity after head injury: a transcranial Doppler study

Object. Contemporary management of head-injured patients is based on assump tions about CO., reactivity, pressure autoregulation (PA), and vascular rea ctivity to pharmacological metabolic suppression. In this study, serial ass essments of vasoreactivity of the middle cerebral artery (MCA) were per-for med using bilateral transcranial Doppler (TCD) ultrasonography. Methods. Twenty-eight patients (mean age 33 +/- 13 years, median Glasgow Co ma Scale score of 7) underwent a total of 61 testing sessions during postin jury Days 0 to 13. The CO, reactivity (58 studies in 28 patients), PA (51 s tudies in 23 patients), and metabolic suppression reactivity (35 studies in 16 patients) were quantified for each cerebral hemisphere by measuring cha nges in MCA velocity in response to transient hyperventilation, arterial bl ood 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 CO, reactivity, PA, and metabolic s uppression reactivity (p < 0.0001), respectively. Intracranial hypertension , classified as intracranial pressure (ICP) greater than 20 mm Hg at the ti me of testing, was associated with global impairment of CO, reactivity, PA, and metabolic suppression reactivity (p < 0.05). A low baseline cerebral p erfusion pressure (CPP) was also predictive of impaired CO, reactivity and PA (p < 0.01). Early postinjury hypotension or hypoxia was also associated with impaired CO, reactivity (p < 0.05), and hemorrhagic brain lesions in o r overlying the MCA territory were predictive of impaired metabolic suppres sion reactivity (p < 0.01). The 6-month Glasgow Outcome Scale score correla ted with the overall degree of impaired vasoreactivity (p < 0.05). Conclusions. During the first 2 weeks after moderate or severe head injury, CO, reactivity remains relatively intact, PA is variably impaired, and met abolic suppression reactivity remains severely impaired. Elevated ICP appea rs to affect all three components of vasoreactivity that were tested, where as other clinical factors such as CPP, hypotensive and hypoxic insults, and hemorrhagic brain lesions have distinctly different impacts on the state o f vasoreactivity. Incorporation of TCD ultrasonography-derived vasoreactivi ty data may facilitate more injury- and time-specific therapies for head-in jured patients.