الفهرس 
Pathogenesis of Traumatic Brain InjuryOnly 14 pages are availabe for public view
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Abstract
Traumatic brain injuries are major causes of disability and death in nonpenetrating trauma accidents. This is true of severe TBIs, which are associated with high unfavorable morbidity and mortality . The pathogenesis of TBI can be grossly divided into primary and secondary insults. The primary insult is unpredictable and unpreventable, whereas the secondary insult is preventable and treatable to a certain degree. The prevention of the secondary insult can therefore significantly improve outcomes in traumatic brain-injured patients.
TBI combines mechanical stress to brain tissue with an
imbalance between CBF and metabolism, excitotoxicity, oedema formation, and inflammatory and apoptotic processes. Understanding the multidimensional cascade of injury offers therapeutic options including the management of CPP, mechanical (hyper-) ventilation, kinetic therapy to improve oxygenation and to reduce ICP, and pharmacological intervention to reduce excitotoxicity and ICP. Yet, the unpredictability of the individual’s pathophysiology requires monitoring of the injured brain in order to tailor the treatment according to the specific status of the patient.
Traditional monitoring in the NICU relegates physicians and nurses to treating patients reactively, only after the patients have declined neurologically and a physiologic process has become abnormal. Real-time monitoring of brain oxygen tension, brain temperature, ICP, CPP, CBF, and cerebral metabolism in addition to TCD ultrasonography, cEEG, and cardiovascular parameters gives the neurointensivist immediate insight in the physiologic and metabolic state of brain regions at risk for ischemia and injury and enhances the potential of early effective interventions to reverse pathologic states on an individual basis. Specifically, the combination of ICP/CPP monitoring, complemented by brain oxygen tension and lactate/pyruvate ratio monitoring, may distinguish areas of the brain at risk that might respond to manipulations of MAP or CPP.