Rethinking autoregulation in traumatic brain injury: a majority of patients with disruptive dynamic autoregulation do not respond to an elevated cerebral perfusion pressure

Authors: Peterson EC, Tozer K, Cohen W, Lam AM, Chesnut RM.

INTRODUCTION: It is widely accepted that pressure autoregulation is often disrupted after traumatic brain injury, based on studies using dynamic testing. The response to cerebral blood flow augmentation in such patients has not been evaluated. We hypothesized that augmenting systemic blood pressure with pressors would not change cerebral blood flow in patients that had disrupted dynamic autoregulation by TCD.
METHODS: We conducted autoregulation testing on a consecutive series of severe TBI patients treated at Harborview Medical Center from 2009 to 2010. All patients nderwent placement of a Licox intracranial pressure monitor and brain tissue oxygen probe. Each patient underwent dynamic testing with TCD (thigh-cuff method) and static autoregulation testing with CT perfusion. A CTP was performed at a baseline CPP and then repeated at an elevated CPP of 20mmHg above baseline. The two CTP blood flow maps were compared to assess the cerebrovascular response to the CPP challenge.
RESULTS: Autoregulation testing was performed in 81 patients. Eighty-four percent were performed in the first 48 hours, and 56% in the first 24 hours. Three patterns of CPA disruption emerged: 48% had intact static CPA but disrupted dynamic CPA, 40% had disrupted static and dynamic CPA, and 12% had intact static and dynamic CPA. The pattern of disrupted static and intact dynamic CPA was not seen.
CONCLUSION: Testing both static and dynamic CPA in the same patient suggests that the global CPA reflex has separate components and that dynamic CPA testing can demonstrate an impaired latency while static CPA testing may show that the overall capacity of CPA is intact. The majority of patients with disrupted dynamic autoregulation by TCD testing do not demonstrate improved perfusion when CPP was increased. This suggests the traditional concept of autoregulation in TBI needs to be reconsidered in light of at least two underlying mechanisms.

Full text and source: PubMed

 2012 Aug;71(2):E560.

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