IMPORTANCE Hospital cooling improves outcome after cardiac arrest, but prehospital cooling immediately after return of spontaneous circulation may result in better outcomes. OBJECTIVE To determine whether prehospital cooling improves outcomes after resuscitation from cardiac arrest in patients with ventricular fibrillation (VF) and without VF. DESIGN, SETTING, AND PARTICIPANTS A randomized clinical trial that assigned adults with prehospital cardiac arrest to standard care with or without prehospital cooling, accomplished by infusing up to 2 L of 4°C normal saline as soon as possible following return of spontaneous circulation. Adults in King County, Washington, with prehospital cardiac arrest and resuscitated by paramedics were eligible and 1359 patients (583 with VF and 776 without VF) were randomized between December 15, 2007, and December 7, 2012. Patient follow-up was completed by May 1, 2013. Nearly all of the patients resuscitated from VF and admitted to the hospital received hospital cooling regardless of their randomization. MAIN OUTCOMES AND MEASURES The primary outcomes were survival to hospital discharge and neurological status at discharge. RESULTS The intervention decreased mean core temperature by 1.20°C (95% CI, -1.33°C to -1.07°C) in patients with VF and by 1.30°C (95% CI, -1.40°C to -1.20°C) in patients without VF by hospital arrival and reduced the time to achieve a temperature of less than 34°C by about 1 hour compared with the control group. However, survival to hospital discharge was similar among the intervention and control groups among patients with VF (62.7% [95% CI, 57.0%-68.0%] vs 64.3% [95% CI, 58.6%-69.5%], respectively; P = .69) and among patients without VF (19.2% [95% CI, 15.6%-23.4%] vs 16.3% [95% CI, 12.9%-20.4%], respectively; P = .30). The intervention was also not associated with improved neurological status of full recovery or mild impairment at discharge for either patients with VF (57.5% [95% CI, 51.8%-63.1%] of cases had full recovery or mild impairment vs 61.9% [95% CI, 56.2%-67.2%] of controls; P = .69) or those without VF (14.4% [95% CI, 11.3%-18.2%] of cases vs 13.4% [95% CI,10.4%-17.2%] of controls; P = .30). Overall, the intervention group experienced rearrest in the field more than the control group (26% [95% CI, 22%-29%] vs 21% [95% CI, 18%-24%], respectively; P = .008), as well as increased diuretic use and pulmonary edema on first chest x-ray, which resolved within 24 hours after admission. CONCLUSION AND RELEVANCE Although use of prehospital cooling reduced core temperature by hospital arrival and reduced the time to reach a temperature of 34°C, it did not improve survival or neurological status among patients resuscitated from prehospital VF or those without VF. TRIAL REGISTRATION clinicaltrials.gov Identifier: NCT00391469.
"The research reviewed in this article illustrates the potential for improved outcomes, and as Nielsen et al. (2013) recently demonstrated the lack of harm from pre-hospital cooling, the field may now shift focus from determining whether cooling might improve patient outcomes to how best to implement and standardize cooling procedures to minimize post-CPR reperfusion injury on return of spontaneous circulation (Rittenberger and Callaway, 2013). Some problems associated with early clinical studies of pre-hospital cooling appear method dependent, such as transient pulmonary edema in patients cooled with a 2L 4 • C saline infusion (Kim et al., 2013), again indicating that optimization of currently used methods or experimentation into new methods of cooling would be beneficial. There have already been calls to open up such optimization with more and larger trials, especially with respect to better defining neurological outcomes in myocardial infarct cases by instituting a protocol for withdrawal of care (Rittenberger and Callaway, 2013). "
[Show abstract][Hide abstract] ABSTRACT: Brain temperature, as an independent therapeutic target variable, has received increasingly intense clinical attention. To date, brain hypothermia represents the most potent neuroprotectant in laboratory studies. Although the impact of brain temperature is prevalent in a number of common human diseases including: head trauma, stroke, multiple sclerosis, epilepsy, mood disorders, headaches, and neurodegenerative disorders, it is evident and well recognized that the therapeutic application of induced hypothermia is limited to a few highly selected clinical conditions such as cardiac arrest and hypoxic ischemic neonatal encephalopathy. Efforts to understand the fundamental aspects of brain temperature regulation are therefore critical for the development of safe, effective, and pragmatic clinical treatments for patients with brain injuries. Although centrally-mediated mechanisms to maintain a stable body temperature are relatively well established, very little is clinically known about brain temperature's spatial and temporal distribution, its physiological and pathological fluctuations, and the mechanism underlying brain thermal homeostasis. The human brain, a metabolically "expensive" organ with intense heat production, is sensitive to fluctuations in temperature with regards to its functional activity and energy efficiency. In this review, we discuss several critical aspects concerning the fundamental properties of brain temperature from a clinical perspective.
Frontiers in Neuroscience 10/2014; 8(307). DOI:10.3389/fnins.2014.00307 · 3.66 Impact Factor
"Guidelines suggest cooling as soon as possible after ROSC (Pederby et al., 2010) and only recently, the potential additional benefit of pre-hospital cooling has been investigated (Diao et al., 2013; Kim et al., 2014). Heterogeneity in T core measurement location has been highlighted (Diao et al., 2013); measurement and monitoring have been performed pre-hospitally with epitympanic and esophageal probes (Kim et al., 2014) and intra-hospitally with esophageal , rectal, bladder, brain, or pulmonary artery probes (Karibe et al., 2000; Abou-Chebl et al., 2011). During therapeutic hypothermia protocols, it is mandatory not only to assess the target T core , but also to maintain the target temperature within a narrow range. "
[Show abstract][Hide abstract] ABSTRACT: Abstract Strapazzon, Giacomo, Emily Procter, Peter Paal, and Hermann Brugger. Pre-hospital core temperature measurement in accidental and therapeutic hypothermia. High Alt Med Biol 15:000-000, 2014.-Core temperature (Tcore) measurement is the only diagnostic tool to accurately assess the severity of hypothermia. International recommendations for management of accidental hypothermia encourage Tcore measurement for triage, treatment, and transport decisions, but they also recognize that lack of equipment may be a limiting factor, particularly in the field. The aim of this nonsystematic review is to highlight the importance of field measurement of Tcore and to provide practical guidance for clinicians on pre-hospital temperature measurement in accidental and therapeutic hypothermia. Clinicians should recognize the difference between alternative measurement locations and available thermometers, tailoring their decision to the purpose of the measurement (i.e., intermittent vs. continual measurement), and the impact on management decisions. The importance of Tcore measurement in therapeutic hypothermia protocols during early cooling and monitoring of target temperature is discussed.
High Altitude Medicine & Biology 06/2014; 15(2). DOI:10.1089/ham.2014.1008 · 1.28 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: IMPORTANCE Fever is common in critically ill neurologic patients. Knowledge of the indicators of central fever may allow greater antibiotic stewardship in this era of rapidly developing super-resistant microorganisms. OBJECTIVE To develop a model to differentiate central from infectious fever in critically ill neurologic patients with fever of an undetermined cause. DESIGN, SETTING, AND PARTICIPANTS Retrospective data collection from January 1, 2006, through December 31, 2010, at a 20-bed neurologic intensive care unit of a large teaching hospital. Consecutive patients 18 years and older admitted for 48 hours or longer with a core body temperature higher than 38.3°C on at least 1 measurement for 2 consecutive days. Patients with alternative identified causes of noninfectious fever were excluded. In total, 526 patients were included in the final analysis. MAIN OUTCOMES AND MEASURES Percentage incidence and odds ratios of variables associated with central fever. Fever was classified as infectious if there was culture growth of a pathogenic species or documented clinical diagnosis of infection treated with antibiotics. Remaining patients were considered to have central fever. Continuous fever lasting longer than 6 hours for 2 or more consecutive days was considered persistent. RESULTS Fever was central in 246 patients (46.8%). Patients with infectious fever were older (mean, 57.4 vs 53.5 years; P = .01) and had a longer length of stay in the neurologic intensive care unit (mean, 12.1 vs 8.8 days; P < .001). Central fever was more likely to occur within 72 hours of admission to the neurologic intensive care unit (76.4% vs 60.7%; P < .001) and tended to be persistent (26.4% vs 18.6%; P = .04). Blood transfusion (odds ratio [OR], 3.06; 95% CI, 1.63-5.76); absence of infiltrate on chest x-ray (3.02; 1.81-5.05); diagnosis of subarachnoid hemorrhage, intraventricular hemorrhage, or tumor (6.33; 3.72-10.77); and onset of fever within 72 hours of hospital admission (2.20; 1.23-3.94) were independent predictors of central fever on multivariable analysis. The combination of negative cultures; absence of infiltrate on chest radiographs; diagnosis of subarachnoid hemorrhage, intraventricular hemorrhage, or tumor; and onset of fever within 72 hours of admission predicted central fever with a probability of .90. CONCLUSIONS AND RELEVANCE We provide a reliable model to differentiate central fever from infectious fever in critically ill neurologic patients, allowing clinicians to select patients in whom antibiotics may be safely discontinued despite ongoing fever.
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