Clinical paperAssessment of risk factors for post-rewarming “rebound hyperthermia” in cardiac arrest patients undergoing therapeutic hypothermia☆
Introduction
Mild induced hypothermia (MIH), also known as therapeutic hypothermia (TH), is increasingly becoming the standard of care in certain cardiac arrest patients who have been successfully resuscitated with return of spontaneous circulation (ROSC). TH was first introduced in the cardiac arrest realm in 2002 and was shown to decrease mortality and improve neurologic outcomes.1, 2 Additionally, in 2003, the International Liaison Committee on Resuscitation (ILCOR) recommended that cardiac arrest patients with ventricular fibrillation (VF) or ventricular tachycardia (VT) be cooled to a core body temperature between 32 °C and 34 °C for 12–24 h. ILCOR further suggested that TH may also be beneficial for other cardiac rhythms, such as pulseless electrical activity (PEA) and asystole.3
Although TH has led to significant improvements in terms of neurologic outcomes and survival in cardiac arrest patients, there are questions about its direct effects on patients. Previously described complications of TH include increased infection risk, electrolyte disturbances, impaired drug metabolism, cold diuresis and hypovolaemia, mild coagulopathy, and insulin resistance.4 A newly described phenomenon is known as “rebound hyperthermia”, which is defined as a core body temperature of 38.5 °C or greater within 24 h of cessation of TH. One study reported that as much as 74% of patients experienced rebound hyperthermia.5 A similar study reported 22% of their patients experienced rebound hyperthermia and emphasized the need for further investigation into the implications of rebound hyperthermia.6 At the current time, it is unclear if rebound hyperthermia is a direct complication of therapeutic hypothermia or if it is a surrogate marker of some other pathophysiologic process.
Prior to the widespread implementation of TH, post-cardiac arrest patients were well-known to be predisposed to developing fever in the days following cardiac arrest, and this was associated with higher risk for mortality and neurologic morbidity.7 However, there is relatively sparse data describing how the subset of TH patients fits into this picture, in particular when describing the relationship between rebound hyperthermia and survival or neurologic morbidity. Identifiable risk factors for rebound hyperthermia have not been investigated either. The purpose of this study was to describe the relationship between rebound hyperthermia and short-term survival and neurologic morbidity, as well as to identify any risk factors that may be related to the incidence of rebound hyperthermia.
Section snippets
Study design
This study was designed as a retrospective, observational study and included patients who suffered from out-of-hospital cardiac arrest of any type and were admitted to the intensive care unit for administration of a TH protocol. All patients were admitted through the emergency department with management by emergency medicine and intensive care physicians and were quickly transferred to the medical intensive care unit. Four hospitals were utilized: Spectrum Health Butterworth and Mercy Health
Results
During the four year study period, 2580 patients were identified as having had cardiac arrest from the electronic database. As summarized in Fig. 1, a total of 2439 patients were excluded for not meeting inclusion criteria or meeting exclusion criteria. The vast majority of the excluded patients either had in-hospital cardiac arrest or never underwent therapeutic hypothermia as decided by emergency or intensive care physicians. Ten patients were excluded based on presence of trauma, three of
Discussion
The main findings in this study may be summarized as follows: (1) no potential risk factors were found to be associated with the development of rebound hyperthermia, (2) rebound hyperthermia is associated with increased risk for in-hospital mortality and neurologic morbidity at discharge, and (3) rebound hyperthermia is not associated with an increased length of stay.
The aetiology of rebound hyperthermia has not been a significant focus of research study in the past, and there are numerous
Conclusions
Rebound hyperthermia is a marker for increased mortality and worsened neurologic morbidity in cardiac arrest patients who have underwent therapeutic hypothermia. At the current time, it is unclear if rebound hyperthermia directly impacts mortality and morbidity, or if it is simply a result of a deeper pathophysiologic process. Further research is warranted to evaluate this relationship, in particular whether TH masks early infection development. The presence or absence of rebound hyperthermia
Conflict of interest statement
No authors involved have any financial or personal relationships with other people or organizations that could inappropriately bias their work. This includes employment, consultancies, stock ownership, honoraria, paid expert testimony, patent applications/registrations, and grants or other funding.
Funding
There are no study sponsors involved in the study design, in the collection, analysis and interpretation of data, in the writing of the manuscript, or in the decision to submit the manuscript for publication.
Disclaimers
The authors have no institutional or financial disclaimers to report.
Sources of support
No support in the form of grants or equipment was utilized in this study.
Acknowledgements
The investigators would like to acknowledge Sango Otieno and Jacob Boehmer at the Grand Valley State University Statistical Consulting Centre for their statistical support and expertise. Appreciation is extended to the research staff at Grand Rapids Medical Education Partners, Spectrum Health, and St. Mary's Hospital.
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A Spanish translated version of the abstract of this article appears as Appendix in the final online version at http://dx.doi.org/10.1016/j.resuscitation.2013.03.027.