Tragic injuries in high-profile sports can grab the national attention shine a spotlight on both the hazards and the treatment. This was the case when Kevin Everett of the Buffalo Bills football team suffered a spinal injury during a routine play. Damage to the spinal cord is often devastating, because it serves as a pipeline for sensory information coming into the brain from the body, and for motor commands going out from the brain to the body. Doctors did not expect Everett to walk again.
But now he is showing hopeful signs, such as wiggling his toes. Doctors cannot say which of the treatments they are using deserves the credit for keeping the spinal damage to a minimum. (This is not an experiment, after all. They are trying several things at once, rather than deliberately manipulating only the variable they are interested in.) But the most intriguing possibility is that they have controlled the damage by controlling Everett’s body temperature.
Therapeutic hypothermia has grown substantially in popularity as a procedure for preventing collateral damage and complications after serious trauma. The procedure is relatively simple and purportedly effective in quite a few cases. Nevertheless, there are several stumbling blocks: the relationship between mild hypothermia and the increased odds of recovery is questionable, and there are health risks associated with the procedure.
Kevin Everett’s case is one the first in which therapeutic hypothermia was used on a spinal cord injury. Although his recovery was miraculous by any standard, there is no consensus as to whether it was a result of therapeutic hypothermia. For one thing, Everett was tended for immediately after the injury occurred, which increased his odds of survival. Also, he was administered steroids just as quickly (Dunham, 2007). This is significant because steroids – methylprednisolone sodium succinate, for example, very common for spinal cord injuries – have been shown to reduce the likelihood for permanent paralysis if treatment occurs within 8 hours of injury (Bracken, 2002). It is not that therapeutic hypothermia had no effect on Everett, but that the effect is very much speculative.
Patients with cardiac arrests are another, much larger group for which therapeutic hypothermia is used, but in all of those cases therapeutic hypothermia is usually compounded with standard treatments. This, of course, makes sense: serious treatment should under no condition be considered as an opportunity for the kind of investigation that would theoretically take place to determine the effects of mild hypothermia on recovery. In Everett’s case, a useful study would compare recovery rates from using steroids only to those of using both steroids and therapeutic hypothermia.
Now, some studies have been conducted on the effectiveness of therapeutic hypothermia aiding recovery in brain injury subjects. One such study by the University of Ottawa of 1,069 head injury cases revealed surprisingly positive statistics about recovery rates associated with the intervention of therapeutic hypothermia, namely that the risk for mortality was reduced by 19% while that for unfavorable results by 22%. But the primary author of the study did clarify that the study was not “a primary randomized controlled trial,” but merely reviews of dated literature (Zucker, 2003). Another more recent study that appeared in the Cochrane Database of Systematic Reviews indicates that there is absolutely no evidence that therapeutic hypothermia has any positive effect on neurological recovery. Granted, this study was almost identical to the aforementioned one in terms of its procedure; but this conveys my point exactly – that starkly similar types of studies on the effectiveness of hypothermia are expressing completely opposing findings (Alderson, Gadkary, Signorini, 2004). These studies, in the end, do not amount to much.
In terms of health risks, therapeutic hypothermia has been linked in some circumstances with several serious conditions. Coming back to Everett’s story, his recovery from the spinal chord injury was spectacular but not altogether definite: he still faced the risk of having fatal blood clots and a stroke at the time of the article’s publishing. Nothing was mentioned of infection in the article. Once again, however, this is a singular matter. While victims of cardiac arrest under comatose are allegedly the best candidates for therapeutic hypothermia, they do not escape the risk for infection, impairments in blood clotting, and pneumonia. Why infection? Because a cooled body has a hindered inflammatory response. A similar explanation applies to blood clotting: at lower temperatures, coagulation and heart-conduction abnormalities are magnified as issues (Zucker, 2003; Alderson, Gadkary, Signorini, 2004). These nuances are not limited to targeting the heart, but may also go after Everett’s area of injury, or slightly broadly the central nervous system.
My intention with these explanations is not to spread blatant, stubborn skepticism about therapeutic hypothermia as a practice. There are many case studies that offer a detailed account of how this procedure is a wonderful, beneficial thing for someone in a critical condition. The ultimate reality, though, is that a procedure like therapeutic hypothermia should remain a very last resort at this point.
References:
http://www.reuters.com/article/healthNews/idUSMAR48026920070914?feedType=RSS&feedName=healthNews&pageNumber=2
http://www.cochrane.org/reviews/en/ab001048.html
http://www.cochrane.org/reviews/en/ab001046.html
http://www.pulmonaryreviews.com/sep03/pr_sep03_hypothermia.html
Comment by Evgeny Bulat — September 20, 2007 @ 8:44 am