1998;44:958–64.Kinoshita K, Kushi H, Sakurai A, Utagawa A, Saito T, Moriya T, et al.

Injury may result from impairment or local declines in cerebral blood flow (CBF) after a TBI. 2004;30:96–102.Nishikawa T, Edelstein D, Du XL, Yamagishi S, Matsumura T, Kaneda Y, et al. J Neurosci. A practical scale. Rappaport M, Hall KM, Hopkins K, et al. 1995;83:949–62.Rosner MJ, Daughton S. Cerebral perfusion pressure management in head injury. Prevention of venous thromboembolism: the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. As the primary insult, which represents the direct mechanical damage, cannot be therapeutically influenced, target of the treatment is the limitation of the secondary damage (delayed non-mechanical damage). J Clin Invest. Risk factors for intraoperative hypotension in traumatic intracranial hematoma. Parcell DL, Ponsford JL, Rajaratnam SM, et al. 1999;27:66–72.Flohé S, Lendemans S, Schade FU, Kreuzfelder E, Waydhas C. Influence of surgical intervention in the immune response of severely injured patients. Nickels JL, Schneider WN, Dombovy ML, et al.
Characterization of the cardiac effects of acute subarachnoid hemorrhage in dogs. Although this mismatch is induced by several different vascular and haemodynamic mechanisms as indicated earlier, the final common endpoint is brain tissue hypoxia. Cognition, Health-related Quality of life, and Depression Ten Years after Moderate to Severe Traumatic Brain Injury: a prospective cohort study.

Thus, the actions of preventing secondary brain injury are largely actions of maintaining normality. 1998;26:344–51.Latronico N, Beindorf AE, Rasulo FA, Febbrari P, Stefini R, Cornali C, et al. Jugular venous oxygen saturation monitoring; In: Narayan RK, Wilberger JE, Povlishock JT, editors. Diffuse axonal injury in head trauma. Pachet A, Friesen S, Winkelaar D, et al. The resulting dehydration and degraded hemodynamics lead to an unstable state and unanticipated hypotension. cerebrovascular constriction or dilation in response to increases or decreases in CPP) is impaired or abolished in most patients.Compared with CBF autoregulation, cerebrovascular COPost-traumatic cerebral vasospasm is an important secondary insult that determines ultimate patient outcome.Cerebral metabolism (as reflected by cerebral oxygen and glucose consumption) and cerebral energy state (as reflected by tissue concentrations of phosphocreatine and ATP or indirectly by the lactate/pyruvate ratio) are frequently reduced after TBI and present with considerable temporal and spatial heterogeneity.As an alternative pathophysiological event, hypermetabolism of glucose may occur.TBI is characterized by an imbalance between cerebral oxygen delivery and cerebral oxygen consumption.

1991;75:731–9.Sheinberg M, Kanter MJ, Robertson CS, Contant CF, Narayan RK, Grossman RG. Inflammatory leukocytic recruitment and diffuse neuronal degeneration are separate pathological processes resulting from traumatic brain injury. Neurosurgery. Additional feedback? McKee AC, Cairns NJ, Dickson DW, et al. While the clinical evidence indicates that high blood glucose levels following TBI are linked to a greater severity of injury and poor neurological outcome [It has been proposed that hyperglycemia may contribute to endothelial cell damage in brain ischemia models [In the clinical setting, however, a frequent post-hospitalization event in patients with severe brain injury is a rapid and large increase in blood glucose concentration that occurs in various situations.

Understanding the multidimensional cascade of secondary brain injury offers differentiated therapeutic options.Traumatic brain injury (TBI) still represents the leading cause of morbidity and mortality in individuals under the age of 45 yr in the world.
The second stage of the pathophysiological cascade is characterized by terminal membrane depolarization along with excessive release of excitatory neurotransmitters (i.e. J Crit Care.

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