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Relationship between time to target temperature and outcome in patients treated with therapeutic hypothermia after cardiac arrest
Moritz Haugk, Christoph Testori, Fritz Sterz, Maximilian Uranitsch, Michael Holzer, Wilhelm Behringer, Harald Herkner, the Time to Target Temperature Study Group
Critical Care , 2011, DOI: 10.1186/cc10116
Abstract: Temperature data between April 1995 and June 2008 were collected from 588 patients and analyzed in a retrospective cohort study by observers blinded to outcome. The time needed to achieve an esophageal temperature of less than 34°C was recorded. Survival and neurological outcomes were determined within six months after cardiac arrest.The median time from restoration of spontaneous circulation to reaching a temperature of less than 34°C was 209 minutes (interquartile range [IQR]: 130-302) in patients with favorable neurological outcomes compared to 158 min (IQR: 101-230) (P < 0.01) in patients with unfavorable neurological outcomes. The adjusted odds ratio for a favorable neurological outcome with a longer time to target temperature was 1.86 (95% CI 1.03 to 3.38, P = 0.04).In comatose cardiac arrest patients treated with therapeutic hypothermia after return of spontaneous circulation, a faster decline in body temperature to the 34°C target appears to predict an unfavorable neurologic outcome.For patients who have been successfully resuscitated after cardiac arrest, therapeutic mild hypothermia increases the rate of a favorable outcome in comparison with standard life support. Randomized controlled trials, however, have not shown evidence of whether the time to target temperature correlates with neurological outcome [1-4]. Registries about the practical use of therapeutic hypothermia have also not found a significant association between the timing of therapeutic hypothermia and final outcome [5-7]. We expected a strong relationship between the time to target temperature (<34°C) and neurological outcome. Furthermore, we hypothesized that earlier achievement of target temperature would not necessarily improve outcome.The study was designed as a single-center retrospective cohort study on temperature data extracted from patients' charts by observers blinded to outcome. The protocol and consent procedures were approved by the ethics committee of the Medical University of
Spontaneous hypothermia on intensive care unit admission is a predictor of unfavorable neurological outcome in patients after resuscitation: an observational cohort study
Alexander W den Hartog, Anne-Cornélie JM de Pont, Laure BM Robillard, Jan M Binnekade, Marcus J Schultz, Janneke Horn
Critical Care , 2010, DOI: 10.1186/cc9077
Abstract: Demographics and parameters influencing neurological outcome were retrieved from the charts of all patients resuscitated for primary cardiac arrest and treated with induced mild hypothermia in our ICU from January 2006 until January 2008. Patients were divided into two groups according to their body temperature on ICU admission: a hypothermia group (< 35.0°C) and a non-hypothermia group (≥35.0°C). Neurological outcome after six months was assessed by means of the Glasgow Outcome Score (GOS), with GOS 1 to 3 defined as unfavorable and GOS 4 to 5 as favorable. A logistic regression model was used to analyze the influence of the different parameters on neurological outcome.The data of 105 consecutive patients resuscitated for primary cardiac arrest and treated with induced mild hypothermia were analyzed. Median ICU admission temperature was 35.1°C (interquartile range (IQR) 34.3 to 35.7). After six months, 61% of the patients had an unfavorable outcome (59% died and 2% were severely disabled), whereas 39% had a favorable outcome (moderate disability or good recovery). Among patients with spontaneous hypothermia on ICU admission, the percentage with unfavorable outcome was higher (69% versus 50%, P = 0.05). Logistic regression showed that age, acute physiology and chronic health evaluation (APACHE) II and sequential organ failure assessment (SOFA) scores and spontaneous hypothermia on ICU admission all had an increased odds ratio (OR) for an unfavorable outcome after six months. Spontaneous hypothermia had the strongest association with unfavorable outcome (OR 2.6, 95% CI (confidence interval) 1.1 to 5.9), which became even stronger after adjustment for age, presenting heart rhythm, APACHE II and SOFA scores (OR 3.8, CI 1.3 to 11.0).In this observational cohort study, spontaneous hypothermia on ICU admission was the strongest predictor of an unfavorable neurological outcome in patients resuscitated for primary cardiac arrest.A large number of patients resuscitated for c
The Practice of Therapeutic Hypothermia after Cardiac Arrest in France: A National Survey  [PDF]
Jean-Christophe Orban, Florian Cattet, Jean-Yves Lefrant, Marc Leone, Samir Jaber, Jean-Michel Constantin, Bernard Allaouchiche, Carole Ichai, for the AzuRéa group
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0045284
Abstract: Aims Cardiac arrest is a major health concern worldwide accounting for 375,000 cases per year in Europe with a survival rate of <10%. Therapeutic hypothermia has been shown to improve patients’ neurological outcome and is recommended by scientific societies. Despite these guidelines, different surveys report a heterogeneous application of this treatment. The aim of the present study was to evaluate the clinical practice of therapeutic hypothermia in cardiac arrest patients. Methods This self-declarative web based survey was proposed to all registered French adult intensive care units (ICUs) (n = 357). Paediatrics and neurosurgery ICUs were excluded. The different questions addressed the structure, the practical modalities of therapeutic hypothermia and the use of prognostic factors in patients admitted after cardiac arrest. Results One hundred and thirty-two out of 357 ICUs (37%) answered the questionnaire. Adherence to recommendations regarding the targeted temperature and hypothermia duration were 98% and 94% respectively. Both guidelines were followed in 92% ICUs. During therapeutic hypothermia, sedative drugs were given in 99% ICUs, mostly midazolam (77%) and sufentanil (59%). Neuromuscular blocking agents (NMBA) were used in 97% ICUs, mainly cisatracurium (77%). Numerous prognostic factors were used after cardiac arrest such as clinical factors (95%), biomarkers (53%), electroencephalography (78%) and evoked potentials (35%). Conclusions In France, adherence to recommendations for therapeutic hypothermia after cardiac arrest is higher than those previously reported in other countries. Numerous prognostic factors are widely used even if their reliability remains controversial.
Recent treatment of postischaemic anoxic brain damage after cardiac arrest by using therapeutic hypothermia
An?eli? Sla?ana
Srpski Arhiv za Celokupno Lekarstvo , 2008, DOI: 10.2298/sarh0810549a
Abstract: Organ injury caused by ischemia and anoxia during prolonged cardiac arrest is compounded by reperfusion injury that occurs when spontaneous circulation is restored. Mild hypothermia (32-35oC) is neuroprotective through several mechanisms, including suppression of apoptosis, reduced production of excitotoxins and free radicals, and anti-inflammatory actions. Experimental studies show that hypothermia is more effective the earlier it is started after return of spontaneous circulation (ROSC). Two randomized clinical trials show improved survival and neurological outcome in adults who remained comatose after initial resuscitation from prehospital VF cardiac arrest, and who were cooled after ROSC. Different strategies can be used to induce hypothermia. Optimal timing of therapeutic hypothermia for cardiac ischemia is unknown. In patients who failed to respond to standard cardiopulmonary resuscitation, intra-arrest cooling using ice-cold intravenous (i.v.) fluid improved the chance of survival. Recently, fasudil, a Rho kinase inhibitor, was reported to prevent cerebral ischaemia in vivo by increasing cerebral blood flow and inhibiting inflammatory responses. In future, two different kinds of protective therapies, BCL-2 overexpression and hypothermia, will both inhibit aspects of apoptotic cell death cascades, and that combination treatment can prolong the temporal 'therapeutic window' for gene therapy.
Mild therapeutic hypothermia shortens intensive care unit stay of survivors after out-of-hospital cardiac arrest compared to historical controls
Christian Storm, Ingo Steffen, Joerg C Schefold, Anne Krueger, Michael Oppert, Achim J?rres, Dietrich Hasper
Critical Care , 2008, DOI: 10.1186/cc6925
Abstract: A prospective observational study with historical controls was conducted at our medical ICU. Fifty-two consecutive patients (median age 62.6 years, 43 males, 34 ventricular fibrillation) submitted to therapeutic hypothermia after out-of-hospital cardiac arrest were included. They were compared with a historical cohort (n = 74, median age 63.8 years, 53 males, 43 ventricular fibrillation) treated in the era prior to hypothermia treatment. All patients received the same standard of care. Neurological outcome was assessed using the Pittsburgh cerebral performance category (CPC) score. Univariate analyses and multiple regression models were used.In survivors, therapeutic hypothermia and baseline disease severity (Acute Physiology and Chronic Health Evaluation II [APACHE II] score) were both found to significantly influence ICU stay and ventilator time (all P < 0.01). ICU stay was shorter in survivors receiving therapeutic hypothermia (median 14 days [interquartile range (IQR) 8 to 26] versus 21 days [IQR 15 to 30] in the control group; P = 0.017). ICU length of stay and time on ventilator were prolonged in patients with CPC 3 or 4 compared with patients with CPC 1 or 2 (P = 0.003 and P = 0.034, respectively). Kaplan-Meier analysis showed improved probability for 1-year survival in the hypothermia group compared with the controls (log-rank test P = 0.013).Therapeutic hypothermia was found to significantly shorten ICU stay and time of mechanical ventilation in survivors after out-of-hospital cardiac arrest. Moreover, profound improvements in both neurological outcome and 1-year survival were observed.Persistent coma is a common finding after cardiac arrest and has profound ethical and economic implications. In a significant proportion of patients, neurological status rather than specific treatment of the underlying disease affects the outcome after cardiac arrest [1]. Recent randomized controlled trials have demonstrated that therapeutic hypothermia is highly effective in
Prehospital therapeutic hypothermia after cardiac arrest - from current concepts to a future standard
Antti K?m?r?inen, Sanna Hoppu, Tom Silfvast, Ilkka Virkkunen
Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine , 2009, DOI: 10.1186/1757-7241-17-53
Abstract: The purpose of this review was to evaluate current clinical studies on prehospital induction of mild hypothermia after cardiac arrest. Most reported studies present data on cooling rates, safety and feasibility of different methods, but are inconclusive as regarding to outcome effects.Following successful resuscitation from cardiac arrest, induced mild therapeutic hypothermia (TH) at 32 to 34°C for 12 to 24 hours has been shown to improve overall survival and neurological outcome[1,2]. These results are derived from prehospital cardiac arrest victims resuscitated from ventricular fibrillation (VF), and current resuscitation guidelines of the International Liaison Committee on Resuscitation (ILCOR) promote induction of TH in this patient subgroup[3]. However, more recent evidence has now shown that the treatment is beneficial in cases with non-VF initial rhythm also[4]. Recently published Scandinavian guidelines recommend to consider TH in these cases as well if active treatment is chosen[5].The potential mechanisms of mild hypothermia as a protecting and preserving factor after cardiopulmonary resuscitation have been summarized by the Task Force on Scandinavian Therapeutic Hypothermia Guidelines[5]. Most of the deleterious reactions suppressed by TH are either initiated at or exacerbated rapidly after return of spontaneous circulation (ROSC) following successful resuscitation. There is experimental evidence showing that a delay in cooling results in lesser benefit [6] and, following successful resuscitation, TH is recommended to be induced as soon as possible[3,5]. Following prehospital cardiac arrest, rapid induction of mild hypothermia is best achieved by emergency medical service (EMS) personnel prior to and during transfer to hospital. In this article, we review the current evidence on prehospital induction of mild hypothermia in the context of sudden cardiac arrest.The databases PubMed, MEDLINE, CINAHL and EMBASE were searched for original articles in English t
Too cold may not be so cool: spontaneous hypothermia as a marker of poor outcome after cardiac arrest
Jakobea W?rner, Mauro Oddo
Critical Care , 2010, DOI: 10.1186/cc9270
Abstract: den Hartog and colleagues prospectively analyzed data from 105 consecutive comatose patients resuscitated from cardiac arrest (CA) and treated with therapeutic hypothermia (TH) over a 2-year period [1]. They observed that the percentage of patients with unfavourable outcome (including death, vegetative state and severe disability) was significantly higher in patients with spontaneous hypothermia (69%) than in those with a body temperature ≥35°C on admission to the ICU (50%, P = 0.05). Using multivariable analysis, and adjusting for age, initial arrest rhythm, and APACHE II and SOFA scores, the association between spontaneous hypothermia and outcome at 6 months was confirmed.In this single centre prospective cohort of more than 100 patients, spontaneous hypothermia remained significantly associated with long-term outcome, even when adjusted for APACHE II and SOFA scores. This indicates that low body temperature <35°C on admission after CA is a strong marker of neurological recovery.Previous studies have shown that spontaneous hypothermia is associated with increased mortality after severe trauma and haemorrhage [2]. TH has improved prognosis of hypoxic-ischemic encephalopathy [3], and might have an impact on our ability to predict final patient prognosis [4]. den Hartog and colleagues identify spontaneous hypothermia as a new prognostic marker of CA.However, in accordance with Utstein's style registry [5], arrest conditions (that is, witnessed versus un-witnessed arrest), initial arrest rhythm (that is, ventricular fibrillation versus non-ventricular fibrillation) and duration of circulatory arrest (that is, time from collapse to return of spontaneous circulation) are other well-known predictors of prognosis [6]. These parameters, and particularly time to return of spontaneous circulation, were not entered in the logistic regression; thus, it remains to be further established whether spontaneous hypothermia is an independent predictor of outcome. Furthermore, body te
Improved Survival with Therapeutic Hypothermia after Cardiac Arrest with Cold Saline and Surfacing Cooling: Keep It Simple  [PDF]
Cristina Granja,Pedro Ferreira,Orquídea Ribeiro,Jo?o Pina
Emergency Medicine International , 2011, DOI: 10.1155/2011/395813
Abstract: Aim. To evaluate whether the introduction of a therapeutic hypothermia (TH) protocol consisting of cold saline infusion and surface cooling would be effective in targeting mild therapeutic hypothermia (32–34°C). Additionally, to evaluate if TH would improve survival after cardiac arrest. Design. Before-after design. Setting. General Intensive Care Unit (ICU) at an urban general hospital with 470 beds. Patients and Methods. Patients admitted in the ICU after cardiac arrest between 2004 and 2009 were included. Effectiveness of the TH protocol to achieve the targeted temperature was evaluated. Hospital mortality was compared before (October 2004–March 2006) and after (April 2006–September 2009) the protocol implementation. Results. Hundred and thirty patients were included, 75 patients were not submitted to TH (before TH group), and 55 were submitted to TH (TH group). There were no significant differences concerning baseline, ICU, and cardiac arrest characteristics between both groups. There was a significant reduction in hospital mortality from 61% ( ) in the before TH group to 40% ( ) in the TH group. Conclusion. Our protocol consisting of cold saline infusion and surface cooling might be effective in inducing and maintaining mild therapeutic hypothermia. TH achieved with this protocol was associated with a significant reduction in hospital mortality. 1. Introduction The outcome after cardiac arrest is still poor [1], with only 7% to 30% of the patients being discharged from hospital with good neurologic outcome [1]. Therapeutic hypothermia (TH) can improve survival and the neurological outcome [2, 3] after cardiac arrest. Previous and current guidelines recommend TH in comatose survivors of cardiac arrest associated with nonshockable rhythms as well as shockable rhythms, acknowledging, however, the lower level of evidence for use after cardiac arrest from non-shockable rhythms [4, 5]. The effect of hypothermia on the neurological outcome would seem to be most beneficial when the treatment is initiated as early as possible after restoration of spontaneous circulation (ROSC) and maintained for 12–24?h [6]. A recent metanalysis [1, 7] and a revision of the literature [8] have confirmed the benefit of the TH even outside the scope of randomized controlled trials. While several methods of cooling are currently applied [6–14], there is no proof of superiority of any cooling method above others, and there are currently no formal cost-benefit analyses [1]. Surface cooling is generally considered the least expensive and is probably the most widely used [15–17].
Therapeutic hypothermia after cardiac arrest – the implementation of the ILCOR guidelines in clinical routine is possible!
Christian Storm, Joerg C Schefold, Lutz Nibbe, Frank Martens, Anne Krueger, Michael Oppert, Achim Joerres, Dietrich Hasper
Critical Care , 2006, DOI: 10.1186/cc5061
Abstract: However, recent studies have shown that only a minority of resuscitated patients are treated with therapeutic hypothermia in both American and European intensive care units [2-4]. A letter recently published in Critical Care reported the use of therapeutic hypothermia in Germany in only 38% of departments treating patients after cardiac arrest [5].To improve adherence to the ILCOR guidelines we developed a written standard operating procedure (SOP) for patients after cardiac arrest admitted to our 38-bed medical intensive care unit.Starting in December 2005 the SOP was to be applied to all comatose patients after cardiac arrest, irrespective of the initial rhythm. Since then the SOP has been applied in 28 out of 34 eligible patients. For four patients the physician in charge did not consider therapeutic hypothermia despite clear indication. In two other patients hypothermia was considered to be contraindicated because of extensive coronary vasospasm or massive pulmonary bleeding of a bronchial carcinoma, respectively. In all the remaining 28 patients surface cooling with technical devices (CritiCool from MTRE, Yavne Israel, and ArcticSun from Medivance, Louisville, KY, USA) was used to induce and maintain hypothermia for 24 hours. The target temperature of 33°C was reached in 6.0 ± 3.2 hours (mean ± SD).In none of the patients were serious adverse events potentially related to therapeutic hypothermia, such as clinically relevant bleeding episodes or arrhythmias, observed. In 12 out of 28 patients (42.9%) treated with therapeutic hypothermia a favourable neurologic outcome was reached (Cerebral Performance Category 1 or 2).Although our limited experience does not yet permit a valid statistical evaluation of the impact of therapeutic hypothermia on the neurological outcome of the patients, initial results are encouraging. We are currently trying to shorten the time to target temperature, which we feel was still too long in some patients. However, the simple availabili
Mild therapeutic hypothermia alters neuron specific enolase as an outcome predictor after resuscitation: 97 prospective hypothermia patients compared to 133 historical non-hypothermia patients
Ingo G Steffen, Dietrich Hasper, Christoph J Ploner, Joerg C Schefold, Ekkehart Dietz, Frank Martens, Jens Nee, Anne Krueger, Achim J?rres, Christian Storm
Critical Care , 2010, DOI: 10.1186/cc8975
Abstract: In this prospective observational cohort study the data of patients after cardiac arrest receiving MTH (n = 97) were consecutively collected and compared with a retrospective non-hypothermia (NH) group (n = 133). Serum NSE was measured 72 hours after admission to ICU. Neurological outcome was classified according to the Pittsburgh cerebral performance category (CPC 1 to 5) at ICU discharge.NSE serum levels were significantly lower under MTH compared to NH in univariate analysis. However, in a linear regression model NSE was affected significantly by time to return of spontaneous circulation (ROSC) and ventricular fibrillation rhythm but not by MTH. The model for neurological outcome identified NSE, NSE*MTH (interaction) as well as time to ROSC as significant predictors. Receiver Operating Characteristic (ROC) analysis revealed a higher cutoff value for unfavourable outcome (CPC 3 to 5) with a specificity of 100% in the hypothermia group (78.9 μg/l) compared to the NH group (26.9 μg/l).Recommended cutoff levels for NSE 72 hours after ROSC do not reliably predict poor neurological outcome in cardiac arrest patients treated with MTH. Prospective multicentre trials are required to re-evaluate NSE cutoff values for the prediction of neurological outcome in patients treated with MTH.Early prediction of neurological outcome in patients surviving cardiac arrest is a challenging problem. A combined approach using clinical assessment, electrophysiological studies and biochemical markers has been proven reliable in predicting poor outcome and is currently used in most centres [1-3].Neuron specific enolase (NSE) is a gamma isomer of enolase that is located in neurons and neuroectodermal cells. Several studies have evaluated the significance of NSE to predict neurological outcome in patients after cardiac arrest. However, the results are not unanimous regarding outcome prediction and the best cutoff value for NSE [3-5]. Most authors agree that the NSE serum level after 72 hours
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