Traumatic brain injury induced temperature dysregulation: What is the role of β blockers?
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Asmar, SamerBible, Letitia
Chehab, Mohamad
Tang, Andrew
Khurrum, Muhammad
Castanon, Lourdes
Ditillo, Michael
Douglas, Molly
Joseph, Bellal
Affiliation
Division of Trauma, Critical Care, Emergency Surgery, and Burns, Department of Surgery, College of Medicine, University of ArizonaIssue Date
2021-01
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Lippincott Williams & WilkinsCitation
Asmar, Samer MD; Bible, Letitia MD; Chehab, Mohamad MD; Tang, Andrew MD; Khurrum, Muhammad MD; Castanon, Lourdes MD; Ditillo, Michael DO; Douglas, Molly MD; Joseph, Bellal MD Traumatic brain injury induced temperature dysregulation: What is the role of β blockers?, Journal of Trauma and Acute Care Surgery: January 2021 - Volume 90 - Issue 1 - p 177-184 doi: 10.1097/TA.0000000000002975Rights
Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved.Collection Information
This item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at repository@u.library.arizona.edu.Abstract
BACKGROUND: Traumatic brain injury (TBI) is associated with sympathetic discharge that leads to posttraumatic hyperthermia (PTH). Beta blockers (ββ) are known to counteract overactive sympathetic discharge. The aim of our study was to evaluate the effect of ββ on PTH in critically-ill TBI patients. METHODS: We performed retrospective cohort analysis of the Medical Information Mart for Intensive Care database. We included all critically ill TBI patients with head Abbreviated Injury Scale (AIS) score of 3 or greater and other body region AIS score less than 2 who developed PTH (at least one febrile episode [T > 38.3°C] with negative microbiological cultures (blood, urine, and bronchoalveolar lavage). Patients on preinjury ββ were excluded. Patients were stratified into (ββ+) and (ββ-) groups. Propensity score matching was performed (1:1 ratio) controlling for patient demographics, injury parameters and other medications that influence temperature. Outcomes were the number of febrile episodes, maximum temperature, and the time interval between febrile episodes. Multivariate linear regression was performed. RESULTS: We analyzed 4,286 critically ill TBI patients. A matched cohort of 1,544 patients was obtained: 772 ββ + (metoprolol, 60%; propranolol, 25%; and atenolol, 15%) and 772 ββ-. Mean age was 63.4 ± 15.4 years, median head AIS score of 3 (3-4), and median Injury Severity Score of 10 (9-16). Patients in the ββ+ group had a lower number of febrile episodes (8 episodes vs. 12 episodes; p = 0.003), lower median maximum temperature (38.0°C vs. 38.5°C; p = 0.025), and a longer median time between febrile episodes (3 hours vs. 1 hour; p = 0.013). On linear regression, propranolol was found to be superior in terms of reducing the number of febrile episodes and the maximum temperature. However, there was no significant difference between the three ββ in terms of reducing the time interval between febrile episodes (p = 0.582). CONCLUSION: Beta blockers attenuate PTH by decreasing the frequency of febrile episodes, increasing the time interval between febrile episodes, and reducing the maximum rise in temperature. ββ may be a potential therapeutic modality in PTH. LEVEL OF EVIDENCE: Therapeutic, level IV. Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved.Note
12 month embargo; published 01 January 2021EISSN
2163-0763PubMed ID
33332783Version
Final accepted manuscriptae974a485f413a2113503eed53cd6c53
10.1097/TA.0000000000002975
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