| ||||||||||||||
|
|
|||||||||||||

From the *Department of Critical Care, Logan Hospital, Griffiths University, Brisbane, Australia; and
Department of Intensive Care, Princess Alexandra and Wesley Hospitals, University of Queensland, Brisbane, Australia.
Address correspondence and reprint requests to Dr Hayden White, Logan Hospital, PO Box 4096, Loganholme DC, Queensland 4129, Australia. Address e-mail to hayden_white{at}health.qld.gov.au.
Abstract
It is now well recognized that low cerebral blood flow (and cerebral perfusion pressure (CPP)) is associated with poor outcome after traumatic brain injury. What is less clear is whether altering cerebral blood flow or CPP will lead to clinical improvement. Initial studies indicated that increasing CPP may be beneficial and the Brain Trauma Foundation acknowledged this by incorporating a target of 70 mm Hg in the 1996 guidelines. However, the lack of a demonstrable benefit and the increased complication rate associated with this approach led to a reduction in the CPP goal to 60 mm Hg. More recently, evidence that autoregulation may be disrupted after traumatic brain injury has led some authors to propose an individualized approach to CPP management. Furthermore, with the advent of advanced neuromonitoring techniques, clinicians are able to more closely monitor the effects of hemodynamic manipulations on cerebral metabolism. As yet, there is no strong outcome evidence to support this approach. Until then, the current debate over the optimal approach to CPP management is likely to continue.
|