title: Cerebral blood flow in severe clinical head injury.
abstract: Following severe head injury, derangements of the cerebral vasculature and cerebral blood flow (CBF) often occur, rendering the brain at risk of secondary ischemia. Therefore, monitoring of CBF in head-injured patients is considered useful for understanding the pathophysiology and effects of therapy, although such monitoring has not yet become part of routine patient management in most centers. In this article, we review the current research on CBF in head injury. Understanding of the physiologic relationship between CBF and cerebral oxygen metabolism (CMRO2) is crucial in the interpretation of CBF values obtained in comatose head injured-patients. Although CMRO2 is reduced with coma, there is ample evidence to suggest that vulnerability of the brain to ischemia is in fact enhanced after traumatic injury. It is now well established that cerebral ischemia (CBF < or = 18 mL/100 g/min) is present in approximately 30% of cases within the first 6 hrs postinjury. In addition, early ischemia has been found to correlate with poor outcome and early mortality. Notably, early ischemia was present even with normal or restored blood pressure and arterial oxygenation, which suggests that other, nonsystemic causes of cerebral ischemia after traumatic brain injury exist. Although spasm of the larger cerebral arteries has been postulated as a possible cause of ischemia, recent measurements of cerebral blood volume are more compatible with compromise of the microcirculation, possibly due to perivascular swelling, with endothelial injury and leukocyte stasis. Disturbances of cerebrovascular CO2 reactivity and autoregulation appear to be less frequent than previously assumed. However, when present, such derangements do have consequences for therapy, in particular the management of blood pressure and cerebral perfusion pressure. Potential implications for patient management are discussed.
mesh_terms: D001921:Brain / Q000378:metabolism*; D002545:Brain Ischemia / Q000503:physiopathology* / Q000517:prevention & control / Q000628:therapy; D002560:Cerebrovascular Circulation / Q000502:physiology; D006259:Craniocerebral Trauma / Q000378:metabolism / Q000503:physiopathology*; D006706:Homeostasis / Q000502:physiology; D006801:Humans; D006973:Hypertension / Q000628:therapy; D008991:Monitoring, Physiologic / Q000379:methods; D011379:Prognosis