Abstract
Trauma, subarachnoid hemorrhage (SAH), cerebrovascular occlusive disease, and spontaneous intracranial hemorrhage all can cause significant brain injury. It is increasingly clear that two distinct phases of injury result in the ultimate neurologic dysfunction suffered by the patient. The first phase involves direct physical damage to the brain tissue, either from the percussive effects of trauma to the head, or compression and tearing of the brain tissue from an enlarging blood clot. The second phase, often called secondary brain injury, is due to a variety of metabolic and physiologic processes initiated by regional cerebral ischemia. These processes include breakdown of the blood-brain barrier, disruption of cerebral autoregulatory mechanisms, the accumulation of toxic extracellular levels of excitatory amino acids and free radicles, the cellular inflammatory response, and regional hyperthermia. Ultimately, the result of secondary injury is cytotoxic and vasogenic edema, elevated intracranial pressure, and cell death.
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Marion, D.W. (2003). Therapeutic Moderate Hypothermia and Fever. In: Cerebral Blood Flow. Update in Intensive Care Medicine, vol 37. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-56036-1_20
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DOI: https://doi.org/10.1007/978-3-642-56036-1_20
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