Journal of Emergencies, Trauma, and Shock
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 Table of Contents    
EDITORIAL  
Year : 2016  |  Volume : 9  |  Issue : 3  |  Page : 93-94
What's new in emergencies, trauma, and shock: Intentional or accidental hypothermia in intensive care unit patients: Time to strike the colors?


Department of ICU, Universitair Ziekenhuis Brussel, Vrije Universiteit Brussel, Brussels, Belgium

Click here for correspondence address and email

Date of Submission23-Feb-2016
Date of Acceptance14-Mar-2016
Date of Web Publication4-Jul-2016
 

How to cite this article:
Honore PM, Jacobs R, Hendrickx I, Troubleyn J, De Waele E, Spapen HD. What's new in emergencies, trauma, and shock: Intentional or accidental hypothermia in intensive care unit patients: Time to strike the colors?. J Emerg Trauma Shock 2016;9:93-4

How to cite this URL:
Honore PM, Jacobs R, Hendrickx I, Troubleyn J, De Waele E, Spapen HD. What's new in emergencies, trauma, and shock: Intentional or accidental hypothermia in intensive care unit patients: Time to strike the colors?. J Emerg Trauma Shock [serial online] 2016 [cited 2020 May 30];9:93-4. Available from: http://www.onlinejets.org/text.asp?2016/9/3/93/185277




For centuries, scientists have been intrigued by the concept of hibernation as a means to preserve bodily functions. Over the years, intentional lowering of core temperature has evolved as the strongest neuroprotective intervention in clinical medicine. Hypothermia basically acts by blunting the excess oxidative stress, glutamate release, calcium influx, and cytotoxic edema that accompany neuronal injury.[1] As such, targeting temperatures as low as 32°C has been promoted as a part of standard medical care in traumatic brain injury, neonatal hypoxic-ischemic encephalopathy, and in patients remaining comatose after resuscitation from cardiac arrest.[2] However, unconditional belief in the benefit of hypothermia started to falter as the results of large randomized trials comparing induced hypothermia with “standard” temperature or fever control (i.e. targeting temperatures of 36–37°C) failed to show improved outcome in all of the aforementioned populations.[3],[4],[5] Moreover, some of these studies were prematurely suspended owing to safety reasons.[4],[5]

In this context, the study of Balvers et al. published in this Journal's issue is interesting. The authors describe that unintentional hypothermia, defined as a core temperature ≤ 35°C, is common in trauma patients upon admission in the Intensive Care Unit (ICU). Hypothermia was identified as the most important independent physiological predictor of both early and late mortality. A late worse outcome was also determined by the evidence of coagulopathy or presence of brain injury.[6] In contrast with intentional hypothermia, its accidental counterpart is inherently more complex but also to some extent “induced”! In the prehospital setting, the body may quickly lose heat after prolonged exposure to a cooler ambient temperature. Alcohol and certain medications can impair the body's ability to control heat loss. Weeping skin or burn wounds may provoke cooling of the body as well. If the injured patient is in shock, hypoperfusion will add to failing temperature regulation. In the hospital, resuscitation manoeuvres enhance the problem by infusing large amounts of cold isotonic solutions or insufficiently warmed up blood. Finally, prompt “injury-to-incision” decisions result in rapid transport of the patient to a “chilly” operation room.

The study of Balvers et al. once more underpins that trauma-associated hypothermia is far from being a physiological adaptation mechanism to protect the body from ongoing harmful stress but rather a life-threatening exponent of unanticipated exposure in an inadequately prepared person. Hypothermia, acidosis, and coagulopathy indeed have been repeatedly recognized as a “lethal triad” propelling trauma patients into a deadly vicious cycle.[7] Based on the findings of Balvers et al., one may wonder whether the outcome of trauma patients with hypothermia on ICU admission could be beneficially influenced by active rewarming. Unfortunately, clinical studies looking specifically at the effect of aggressive rewarming in accidental hypothermia on ICU mortality are scarce and of low methodological quality. One relevant recent study found no difference in the neurological outcome and mortality in patients with severe traumatic brain injury randomized to either prolonged therapeutic hypothermia with slow rewarming or to temperatures kept between 35.5°C and 37°C.[8] Moreover, attempting to rewarm a hypothermic trauma is potentially deleterious as vasodilation and mobilization of pooled peripheral blood may flood the tissues with waste and acidosis.

Taken together, we must humbly adapt our thinking that a better outcome is guaranteed when arousing humans from intentional hypothermia. In addition, accidental hypothermia definitely is a “bad sign” in trauma victims and probably requires early but gentle correction and at the least, close monitoring within the “golden hour (s)” of acute trauma care. Future research in this population should focus on prehospital temperature preservation, optimal time to initiate rewarming (immediately after arrival in the emergency ward or upon ICU arrival), rewarming speed (slow or aggressive), and most adequate rewarming techniques (intravenous or external).

 
   References Top

1.
Polderman KH. Mechanisms of action, physiological effects, and complications of hypothermia. Crit Care Med 2009;37 7 Suppl: S186-202.  Back to cited text no. 1
    
2.
Varon J, Marik PE, Einav S. Therapeutic hypothermia: A state-of-the-art emergency medicine perspective. Am J Emerg Med 2012;30:800-10.  Back to cited text no. 2
    
3.
Nielsen N, Wetterslev J, Cronberg T, Erlinge D, Gasche Y, Hassager C, et al. Targeted temperature management at 33°C versus 36°C after cardiac arrest. N Engl J Med 2013;369:2197-206.  Back to cited text no. 3
[PUBMED]    
4.
Andrews PJ, Sinclair HL, Rodriguez A, Harris BA, Battison CG, Rhodes JK, et al. Hypothermia for intracranial hypertension after traumatic brain injury. N Engl J Med 2015;373:2403-12.  Back to cited text no. 4
[PUBMED]    
5.
Shankaran S, Laptook AR, Pappas A, McDonald SA, Das A, Tyson JE, et al. Effect of depth and duration of cooling on deaths in the NICU among neonates with hypoxic ischemic encephalopathy: A randomized clinical trial. JAMA 2014;312:2629-39.  Back to cited text no. 5
[PUBMED]    
6.
Balvers K, Van der Horst M, Graumans M, Boer C, Binnekade JM, Goslings JC, et al. Hypothermia as a predictor for mortality in trauma patients at admittance to the Intensive Care Unit. J Emerg Trauma Shock 2016;9:99-103.  Back to cited text no. 6
    
7.
Mikhail J. The trauma triad of death: Hypothermia, acidosis, and coagulopathy. AACN Clin Issues 1999;10:85-94.  Back to cited text no. 7
    
8.
Maekawa T, Yamashita S, Nagao S, Hayashi N, Ohashi Y; Brain-Hypothermia Study Group. Prolonged mild therapeutic hypothermia versus fever control with tight hemodynamic monitoring and slow rewarming in patients with severe traumatic brain injury: A randomized controlled trial. J Neurotrauma 2015;32:422-9.  Back to cited text no. 8
    

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Correspondence Address:
Patrick M Honore
Department of ICU, Universitair Ziekenhuis Brussel, Vrije Universiteit Brussel, Brussels
Belgium
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0974-2700.185277

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