Posthypothermic rewarming considerations following traumatic brain injury.
To date, considerable attention has been focused upon the use of hypothermia as a therapeutic strategy for attenuating many of the damaging consequences of traumatic brain injury (TBI). Despite the promise of hypothermic intervention following TBI, many questions remain regarding the optimal use of hypothermic intervention, including, but not limited to, the rewarming rates needed to assure optimal brain protection. In this review, we revisit the relatively limited literature examining the issue of hypothermia and differing rewarming rates following TBI. Considering both experimental and clinical literature, evidence is presented that the rate of posthypothermic rewarming is an important variable for influencing the protective effects of hypothermic intervention following TBI. In the experimental setting, posttraumatic hypothermia followed by slow rewarming appears to provide maximal protection in terms of traumatically induced axonal damage, microvascular damage and dysfunction, and contusional expansion. In contrast, hypothermia followed by rapid rewarming not only reverses the protective effects associated with hypothermic intervention, but in many cases, exacerbates the traumatically induced pathology and its functional consequences. While similar evaluations have not been conducted in the clinical setting, multiple lines of clinical evidence suggest the benefits of posttraumatic hypothermia are optimized through the use of slow rewarming, with the suggestion that such a strategy reduces the potential for rebound vasodilation, elevated intracranial pressure (ICP), and impaired neurocognitive recovery. Collectively, this review highlights not only the benefits of hypothermic intervention, but also the rate of posthypothermic rewarming as an important variable in assuring maximal efficacy following the use of hypothermic intervention.
Povlishock
John T
JT
Department of Anatomy and Neurobiology, Virginia Commonwealth University Medical Center, Richmond, Virginia 23298-0709, USA. jtpovlis@vcu.edu
Wei
Enoch P
EP
D000818:Animals; D001369:Axons / Q000378:metabolism / Q000473:pathology; D001831:Body Temperature / Q000502:physiology*; D001921:Brain / Q000098:blood supply / Q000378:metabolism / Q000503:physiopathology*; D001930:Brain Injuries / Q000378:metabolism / Q000503:physiopathology* / Q000628:therapy*; D006801:Humans; D006940:Hyperemia / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control; D007036:Hypothermia, Induced / Q000009:adverse effects / Q000379:methods* / Q000592:standards; D017694:Rewarming / Q000009:adverse effects / Q000379:methods* / Q000592:standards; D013997:Time Factors; D014855:Wallerian Degeneration / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control