• Eric Peterson and Randall M Chesnut.
• Department of Neurological Surgery, Harborview Medical Center, University of Washington Medical Center, Seattle, Washington 98104, USA. ericpete@u.washington.edu
• J Trauma. 2009 Nov 1;67(5):944-9.

BackgroundThe management of severe traumatic brain injury (sTBI) patients with and without intact cerebral pressure autoregulation (CPA) varies markedly. Recent studies, analyzing beat-to-beat interactions between intracranial pressure (ICP) and systolic blood pressure, or transcranial Doppler velocity changes during a rapid drop in cerebral perfusion pressure (CPP), suggest that CPA is disrupted after sTBI. We use computed tomography perfusion (CTP) to guide blood pressure manipulation in sTBI and have found CPA results that differ with this literature. We present these results here and suggest modifying our basic concepts of CPA disruption.MethodsWe tested CPA in 24 consecutive sTBI patients using CTP. ICP was monitored intraparenchymally and blood pressure with an arterial line. After a CTP study at baseline, a phenylephrine infusion was used to raise the CPP by 20 mm Hg, and a second CTP was performed immediately thereafter. Quantitative analysis of cerebral blood flow (CBF) was done offline. CPA was considered intact if CBF was unchanged despite the increase in CPP and disrupted if CBF rose after CPP manipulation.ResultsCPA was intact in 25 of 33 patients (75.7%) and disrupted in 8 of 33 patients (24.3%). The mean age was significantly different for the 2 groups; 52 years for the disrupted group, 29 years for the intact group (p < 0.0003). The mean ICP change was also statistically different; 3.8 for the disrupted group and 1.5 for the intact group (p < 0.006). Injury Severity Score (ISS), Glasgow Coma Scale, and CPP were not statistically different between the two groups.ConclusionBy using direct measurement of CBF in response to a CPP challenge, we found CPA disruption to be much less common than reported in similar groups of sTBI patients. This difference reflects potentially important separate aspects of CPA. We suggest that CPA measurement using beat-to-beat interactions and transcranial Doppler measurements reflect dynamic CPA processes (dynamic autoregulation), whereas our method reflects steady-state conditions (static autoregulation). If the major disruption of CPA after sTBI involves dynamic vascular responsiveness, perhaps we need more focus on this aspect and less on static-CPP manipulation in terms of pathophysiology and treatment.

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