الفهرس 
Pathophysiology of Pediatric Traumatic Brain Injuries TBIOnly 14 pages are availabe for public view
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Abstract
Traumatic brain injury is the leading cause of death among infants and children. The majority of TBI is classified as mild, and around 8–10% is classified as moderate or severe. Patients with mild TBI have a good prognosis providing treatable complications are not missed. Overall mortality in this group is around 0.1% and is associated with missed intra-cranial hemorrhage (Yates et al., 2007).
Traumatic brain injury has been divided into two distinct periods: primary and secondary brain injury. The primary injury is the result of the initial, mechanical forces, resulting in shearing and compression of neuronal, glial, and vascular tissue. Axonal tissue is more susceptible to the injury than vascular tissue. Thus, focal injuries are usually superimposed upon more diffuse neuronal injury. The consequences of the initial injury include physical disruption of cell membranes, infrastructure, and disturbance of ionic homeostasis secondary to increased membrane permeability. This in turn may lead to astrocytic and neuronal swelling, hypoperfusion, and a cascade of neurotoxicevents because of increased intracellularcalcium. The secondary injury is described as the consequence of further physiological insults, suchasischaemia, re-perfusion and hypoxia, to areas of ‘at risk’ brainafter the initial injury (Werner and Engelhard, 2007).
Traumatic brain injury combines mechanical stress to brain tissue with imbalance between CBF and metabolism, excitotoxicity, oedema formation, and inflammatory and apoptotic processes. Understanding cascade of injury offers therapeutic options as 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 patient (Werner and Engelhard, 2007).
Despite decades of research, there are still few data to define the best practice for TBI. Hypotension, hypoxia, hyper- and hypocapnia, hyper- and hypoglycaemiaall remain avoidable insults, which are associated with worse outcome. Adherence to guidelines is associated with improved outcome (Moppett, 2007).
Most clinicians are agreed on the general principles of early management: maintenance of adequate and stable cerebral perfusion, adequate oxygenation, avoidance of hyper- and hypocapniaandavoidance of hyper- and hypoglycaemia, while avoiding iatrogenic injury (Moppett, 2007).
As improved monitoring techniques, such as brain tissue monitors and advanced imaging methods are being further developed, the ability to recognize adverse events and identify the pathophysiological processes occurring in a given individual will improve. This may allow a more individualized approach to interventions, help refine protocols and more effective targeted guidelins. Theymay also help to develop effective therapies to add to protocolized management strategies in the hope that this will translate into an improvement in outcome after TBI (Helmy et al., 2007).