Body temperature changes are associated with outcomes following in-hospital cardiac arrest and return of spontaneous circulation
University of Pittsburgh, Pittsburgh, PA, United States. Resuscitation
(Impact Factor: 4.17).
10/2009; 80(12):1365-70. DOI: 10.1016/j.resuscitation.2009.08.020
Spontaneous changes in body temperature after return of circulation (ROSC) from cardiac arrest are common, but the association of these changes with outcomes in hospitalized patients who survive to 24h post-ROSC is not known. We tested the hypothesis that adults who experience temperature lability in the first 24h have worse outcomes compared with those who maintain normothermia.
A prospective observational study from a multicenter registry of cardiac arrests (National Registry of Cardiopulmonary Resuscitation) from 355 US and Canadian hospitals. 14,729 adults with return of circulation from a pulseless cardiac arrest. We excluded those who died or were discharged before 24h post-event, those made Do-Not-Resuscitate (DNR) within 24h of event, those that had a preceding trauma, and those with multiple cardiac arrests. Finally, we included only subjects that had both a lowest (T(min)) and highest (T(max)) body temperature value recorded during the first 24-h after ROSC, resulting in a study sample of 3426 patients.
After adjustment for potential covariates, there was a lower odds of survival in those having an episode of hypothermia (adjusted odds ratio [OR], 0.62; 95% confidence interval [CI], 0.48-0.80), those having an episode of hyperthermia (OR, 0.67; 95% CI, 0.48-0.80), and those having an episode of both (OR, 0.59; 95% CI, 0.39-0.91). Among those who survived to discharge, there was also a lower odds of favorable neurologic performance in those who had an episode of hyperthermia (OR, 0.71; 95% CI, 0.51-0.98).
Episodes of temperature lability following in-hospital resuscitation from cardiac arrest are associated with lower odds of surviving to discharge. Hyperthermia is also associated with fewer patients leaving the hospital with favorable neurologic performance. Further studies should identify whether therapeutic control over changes in body temperature after in-hospital cardiac arrest improves outcomes.
Available from: Ericka L Fink
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ABSTRACT: Brain injury is the leading cause of death in our pediatric ICU [Au et al. Crit Care Med 36:A128, 2008]. Clinical care for brain injury remains largely supportive. Therapeutic hypothermia has been shown to be effective in improving neurological outcome after adult ventricular-arrhythmia-induced cardiac arrest and neonatal asphyxia, and is under investigation as a neuroprotectant after cardiac arrest and traumatic brain injury in children in our ICU and other centers. To induce hypothermia in children comatose after cardiac arrest we target 32-34 degrees C using cooling blankets and intravenous iced saline as primary methods for induction, for 24-72 h duration with vigilant re-warming. The objective of this article is to share our hypothermia protocol for cooling children with acute brain injury.
Neurocritical Care 02/2010; 12(3):414-20. DOI:10.1007/s12028-010-9334-5 · 2.44 Impact Factor
Available from: Gareth R Clegg
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ABSTRACT: Out-of-hospital cardiac arrest (OHCA) is a significant cause of death and severe neurological disability. The only post-return of spontaneous circulation (ROSC) therapy shown to increase survival is mild therapeutic hypothermia (MTH). The relationship between esophageal temperature post OHCA and outcome is still poorly defined.
Prospective observational study of all OHCA patients admitted to a single centre for a 14-month period (1/08/2008 to 31/09/2009). Esophageal temperature was measured in the Emergency Department and Intensive Care Unit (ICU). Selected patients had pre-hospital temperature monitoring. Time taken to reach target temperature after ROSC was recorded, together with time to admission to the Emergency Department and ICU.
164 OHCA patients were included in the study. 105 (64.0%) were pronounced dead in the Emergency Department. 59 (36.0%) were admitted to ICU for cooling; 40 (24.4%) died in ICU and 19 (11.6%) survived to hospital discharge. Patients who achieved ROSC and had esophageal temperature measured pre-hospital (n=29) had a mean pre-hospital temperature of 33.9 degrees C (95% CI 33.2-34.5). All patients arriving in the ED post OHCA had a relatively low esophageal temperature (34.3 degrees C, 95% CI 34.1-34.6). Patients surviving to hospital discharge were warmer on admission to ICU than patients who died in hospital (35.7 degrees C vs 34.3 degrees C, p<0.05). Patients surviving to hospital discharge also took longer to reach T(targ) than non-survivors (2h 48min vs 1h 32min, p<0.05).
Following OHCA all patients have esophageal temperatures below normal in the pre-hospital phase and on arrival in the Emergency Department. Patients who achieve ROSC following OHCA and survive to hospital discharge are warmer on arrival in ICU and take longer to reach target MTH temperatures compared to patients who die in hospital. The mechanisms of action underlying esophageal temperature and survival from OHCA remain unclear and further research is warranted to clarify this relationship.
Resuscitation 07/2010; 81(7):867-71. DOI:10.1016/j.resuscitation.2010.03.017 · 4.17 Impact Factor
Available from: Joshua W Lampe
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ABSTRACT: Historically, hypothermia was induced prior to surgery to enable procedures with prolonged ischemia, such as open heart surgery and organ transplant. Within the past decade, the efficacy of hypothermia to treat emergency cases of ongoing ischemia such as stroke, myocardial infarction, and cardiac arrest has been studied. Although the exact role of ischemia/reperfusion is unclear clinically, hypothermia holds significant promise for improving outcomes for patients suffering from reperfusion after ischemia. Research has elucidated two distinct windows of opportunity for clinical use of hypothermia. In the early intra-ischemia window, hypothermia modulates abnormal cellular free radical production, poor calcium management, and poor pH management. In the more delayed post-reperfusion window, hypothermia modulates the downstream necrotic, apoptotic, and inflammatory pathways that cause delayed cell death. Improved cooling and monitoring technologies are required to realize the full potential of this therapy. Herein we discuss the current state of clinical practice, clinical trials, recommendations for cooling, and ongoing research on therapeutic hypothermia.
Annual review of medicine 02/2011; 62(1):79-93. DOI:10.1146/annurev-med-052009-150512 · 12.93 Impact Factor
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