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Ann Thorac Surg 1999;68:1452-1453
© 1999 The Society of Thoracic Surgeons
University of Ottawa Heart Institute, Ottawa, Ontario, Canada
Address reprint requests to Dr Nathan, University of Ottawa Heart Institute, H341, 40 Ruskin St, Ottawa, ON, Canada K1Y 4W7
e-mail: hnathan{at}ottawaheart.ca
Presented at Outcomes ’99, "The Key West Meeting," Key West, FL, May 26–30, 1999.
Interest in hypothermia as a neuroprotective strategy has received renewed interest with the recent appreciation that, in laboratory studies, modest reductions in brain temperature (2°C to 5°C) can have marked neuroprotective effects [1]. The benefit of these small temperature reductions is unlikely to be from the associated decrease in cerebral oxygen consumption, and possible mechanisms include inhibition of neurotransmitter release (eg, glutamate), reduction of calcium-mediated cell injury, reduction of free radical formation, and attenuation of the inflammatory response [2].
Despite the dramatic effect of hypothermia as a neuroprotective strategy in laboratory studies, conclusive proof of efficacy in patients is still lacking. Perhaps the most convincing evidence to date is from Marion and associates [3], who demonstrated improved outcome in patients with severe closed head injury who were cooled to 33°C for 24 hours compared with conventional treatment. In the cardiac surgical literature, there has been some debate provoked by the contrasting results of two studies of normothermic versus hypothermic bypass. Investigators at Emory [4] studied 1,001 patients and observed a stroke rate of 3.1% in the warm cohort compared with 1.0% in the cold. The Warm Heart Investigators [5] studied 1,732 patients and found stroke rates of 1.6% in the warm group and 1.5% in the cold. It is possible that the high stroke rate in the former study may have been due to the more frequent use of retrograde cardioplegia and more aggressive rewarming with inadvertent cerebral hyperthermia [6]. Thus, the results at Emory are not considered to be proof of a neuroprotective effect of hypothermia.
Proving efficacy of hypothermia for stroke will be extremely difficult in patients not only because of logistic and safety considerations but also because the clinical manifestations of stroke are often more dependent on the location of the injury rather than on the mass of neuronal necrosis. These difficulties have led researchers to turn to cognitive deficits in patients after cardiac surgery as an experimental model. Deterioration in intellectual function after cardiac surgery is common and is believed to be due, in part, to a diffuse brain injury caused by microembolization during cardiopulmonary bypass (CPB),hemodilution, hypotension, and other unphysiologic features of CPB [7]. Numerous studies document postoperative cognitive deficits (POCD) using neuropsychometric tests [8]. Although some would consider POCD a surrogate for stroke, one might argue that these deficits represent a brain injury syndrome and an independent adverse outcome.
Wong and McLean [9] were the first to address the question of the effect of CPB temperature on POCD and found no benefit of CPB at 28°C compared with 34°C. Mora and associates [6] reported the results of neuropsychologic testing of a subset of the patients at Emory reported by Martin and associates [4]. The incidence of neurological deficits was significantly higher in the warm group, and there was a trend toward better performance on some neuropsychologic tests at 7 to 10 days in the hypothermic group. Regragui [10] randomized 93 patients undergoing coronary artery bypass grafting (CABG) to one of three temperatures on CPB, 37°C, 32°C, or 28°C. Results of neuropsychologic testing suggested a benefit of hypothermic perfusion. Recent studies by Plourde and associates [11] and Heyer and associates [12] found no benefit of hypothermic CPB on neuropsychologic outcome of CABG. A characteristic all these studies have in common is that there is a temperature difference between groups only for a portion of the time patients are on CPB, and then the hypothermic groups are rewarmed. Thus, the duration of exposure to the possible beneficial effect of hypothermia is brief, and these patients are still exposed to the possibly deleterious effects of rewarming [13, 14]. We have recently completed a study where 223 patients undergoing CABG were all cooled to 32°C on commencement of CPB and then, before release of the aortic cross-clamp, were randomly allocated to rewarming either to 37°C or 34°C. A temperature gradient remained until after transfer to the recovery room, where surface warming began. This strategy both extended the exposure to hypothermia and avoided the possibility of hyperthermia on rewarming. The results of neuropsychological testing have yet to undergo peer review, however, we believe that the data suggest a significant benefit of hypothermia. There was no excess bleeding or infection in the hypothermic group.
The three most serious adverse consequences of mild perioperative hypothermia are bleeding, infection, and cardiovascular events [15, 16]. Further research is needed to better quantify the risk of these outcomes.
Conclusions
Mild hypothermia is the most promising neuroprotective strategy yet found in laboratory investigations. Because of the remarkable benefit demonstrated in the laboratory, there is great enthusiasm among clinicians for implementation of hypothermia when caring for patients at risk of neural injury. This enthusiasm must be tempered by a recognition of the potential for adverse effects and the limited evidence of efficacy in patients. What seems clear now is that body temperature is a variable that can affect patient outcome and should always be measured and controlled in the perioperative period.
References
This article has been cited by other articles:
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  A. M Karaskov, C S. Kitchlu, and V. N Lomivorotov Cardiac Surgery Under Perfusionless Hypothermia: Siberian Experience Asian Cardiovasc Thorac Ann, March 1, 2002; 10(1): 3 - 7. [Abstract] [Full Text] [PDF]
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 S. E. Kasner, T. Wein, P. Piriyawat, C. E. Villar-Cordova, J. A. Chalela, D. W. Krieger, L. B. Morgenstern, S. E. Kimmel, J. C. Grotta, and H.-C. Koennecke Acetaminophen for Altering Body Temperature in Acute Stroke: A Randomized Clinical Trial * Editorial Comment: A Randomized Clinical Trial Stroke, January 1, 2002; 33(1): 130 - 135. [Abstract] [Full Text] [PDF]
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