Body Temperature in TBI Patients
Based on experimental and clinical studies, there is a general view that fever is detrimental to TBI patients (Thompson et al. 2003). An important goal in the treatment of these patients has therefore been to prevent or reduce fever. So far, we lack evidence-based consensus regarding how to reduce temperature in TBI patients. Fever can be reduced pharmacologically by affecting the thermostat or by active cooling of the patient. During the last 10–15 years, it has also been suggested that active cooling to subnormal temperatures (32–34°C) should be beneficial due to its well-known neuroprotective effect, as demonstrated in animal studies after brain ischaemia and also in humans after near-drowning and after active cooling following heart resuscitation, and the fact that hypothermia decreases an increased intracranial pressure (Polderman 2008; Grände et al. 2009). The mechanisms behind the hypothermia-induced neuroprotection are not clarified, but the reduced neuronal metabolism and the inflammatory response, and the reduction in toxic substances such as glutamate and a scavenging effect may be involved. It was therefore believed that active cooling should be beneficial in TBI patients, but we still lack studies giving support for active cooling in clinical practice. In this chapter, we give recommendations on how and when temperature should be reduced and the goal temperature in TBI patients, based on the results of the most recent studies and current knowledge in this field. It will be concluded that active cooling is associated with side effects and that we lack support for its use in TBI patients, and it can therefore not be recommended.
KeywordsBolus Dose Scavenge Effect Goal Temperature Active Cool Neuronal Metabolism
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