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Traumatic Brain Injury: Clinical Studies

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Therapeutic Hypothermia

Part of the book series: Molecular and Cellular Biology of Critical Care Medicine ((MCCM,volume 4))

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Abstract

The treatment of traumatic brain injury (TBI) using hypothermia was first described by Temple Fay in 1943 (1). In the 1950s, Sedzimir noted “better than expected” outcomes in several patients with TBI after lowering their body temperatures to between 27° and 30°C for 1 to 5 days (2). Reports of contemporaneous research suggest that this pioneering use of hypothermia was based on the premise that TBI causes a hypermetabolic state, and that an increase in cerebral blood flow in response to the increased metabolic demand is responsible for the brain swelling associated with TBI. In uninjured dogs, for example, Rosomoff found that both cerebral blood flow and the cerebral metabolic rate for oxygen fell 6.7% for every 1°C reduction in body temperature between 35° and 25°C (3, 4). Stone and co-workers reported that cooling to 30°C in a primate model produced a 50% reduction in the cerebral metabolic rate for oxygen and a significantly lower rate of adenosine triphosphate depletion (5). According to Lundberg in 1959, hypothermia was as effective as osmotic diuretics for reducing elevated intracranial pressure (ICP) and had a more prolonged ICP-reducing effect than hyperventilation (6). James and colleagues found that hypothermia lowered the ICP in 20 of 40 patients with severe TBI; the ICP reduction averaged 51% (7).

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Marion, D.W. (2005). Traumatic Brain Injury: Clinical Studies. In: Tisherman, S.A., Sterz, F. (eds) Therapeutic Hypothermia. Molecular and Cellular Biology of Critical Care Medicine, vol 4. Springer, Boston, MA. https://doi.org/10.1007/0-387-25403-X_6

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  • DOI: https://doi.org/10.1007/0-387-25403-X_6

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-0-387-25402-9

  • Online ISBN: 978-0-387-25403-6

  • eBook Packages: MedicineMedicine (R0)

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