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Does anesthetic provide similar neuroprotection to therapeutic hypothermia after cardiac arrest?
Hong Zhang
Critical Care , 2010, DOI: 10.1186/cc8923
Abstract: Therapeutic hypothermia has been shown to provide neuroprotection against ischemic injury after cardiac arrest in in vitro and in vivo models. In the previous issue of Critical Care, Meybohm and colleagues [1] demonstrate that cardiac arrest triggers the release of cerebral inflammatory cytokines in pigs' cerebral cortex. Therapeutic hypothermia alters inflammatory response in cardiac arrest and subsequent cardiopulmonary resuscitation. The combination of hypothermia with sevoflurane post-conditioning does not confer additional anti-inflammatory effects compared with hypothermia alone.Cardiac arrest remains the leading cause of death in the US and Europe, with an out-of-hospital cardiac arrest survival-to-discharge rate of less than 10%. In-hospital cardiac arrest presents a dismal prognosis. According to a large in-hospital registry, the survival-to-discharge rate is 18%, whereas that of a developing country is 6.9% [2,3]. Without prompt care, the chance for meaningful survival falls dramatically within minutes of arrest onset. When immediate care is available and victims are successfully resuscitated, the majority of these initial survivors subsequently suffer crippling neurologic injury or die in the few days following the cardiac arrest event. Thus, improving survival and brain function after initial resuscitation from cardiac arrest remains a critical challenge. Therapeutic hypothermia, introduced more than six decades ago, remains an important neuroprotective factor in cardiac arrest. Laboratory studies have demonstrated that cooling after resuscitation from cardiac arrest improves both survival as well as subsequent neurologic and cardiac function and has few side effects. these findings have been reproduced using a variety of cooling techniques in different species, including rats, dogs, and pigs.However, physician use of hypothermia induction in patients resuscitated from cardiac arrest is low. In 2003, Abella and colleagues [4] reported that 87% of US phys
Therapeutic hypothermia post out-of-hospital cardiac arrest - more questions than answers?
Richard Lyon
Critical Care , 2011, DOI: 10.1186/cc10123
Abstract: Patients post out-of-hospital cardiac arrest (OHCA) are common admissions to the ICU. Therapeutic hypothermia has been shown to improve both survival and neurological outcome for OHCA patients surviving to reach the ICU and now forms part of routine post-resuscitation care. The Time to Target Temperature (TTTT) study group presents key observations on the relationship between body temperature and outcome following OHCA [1], yet ultimately are we left with more questions than answers on therapeutic hypothermia?Nearly a decade ago two landmark papers fundamentally changed the practice of post-resuscitation care. The Hypothermia after Cardiac Arrest study group [2] and Bernard and colleagues [3] not only demonstrated the benefit of cooling OHCA patients but also highlighted how hugely effective the therapy was, with a number needed to treat of seven patients and six patients, respectively, for survival. Such impressive therapeutic benefit is rarely seen in medical practice, let alone in critical care medicine. A key difference between these two studies was the time from return of spontaneous circulation (ROSC) to the onset of cooling. The time to reach the target temperature (<34°C) varied greatly from immediately post ROSC to over 16 hours post ROSC and yet the therapeutic benefit of cooling was still evident. The TTTT group demonstrated that the change in body temperature during the period from ROSC to cooling initiation has a direct relationship on survival [1].Since 2002 few studies have examined the optimum method, rate of cooling and timing of initiation. Little is known about the mechanism of action of therapeutic hypothermia. Whilst animal evidence strongly suggests that early cooling, especially intra-arrest, is beneficial, few human studies have demonstrated a benefit from early cooling. Early cooling, in the prehospital or emergency department setting, has significant technical challenges and may distract from the basic principles of resuscitation. Yet emerg
Blood levels of copeptin on admission predict outcomes in out-of-hospital cardiac arrest survivors treated with therapeutic hypothermia
Petr Ostadal, Andreas Kruger, Vladimira Zdrahalova, Marek Janotka, Dagmar Vondrakova, Petr Neuzil, Miroslav Prucha
Critical Care , 2012, DOI: 10.1186/cc11671
Abstract: A group of 40 out-of-hospital cardiac arrest survivors who were treated with endovascular hypothermia was analyzed. Copeptin levels were measured in blood samples taken at admission using a commercially available immunoassay. Neurological outcome was assessed at 30 days post admission according to the Cerebral Performance Category (CPC): CPC 1, no neurological deficit; CPC 2, mild to moderate dysfunction; CPC 3, severe dysfunction; CPC 4, coma; and CPC 5, death.Copeptin levels were significantly lower in patients with CPC 1 compared with CPC 2 or CPC 3 to CPC 5 (74.3 ± 14.4 pmol/l, 219.8 ± 33.9 pmol/l and 302.7 ± 52.1 pmol/l, respectively; P < 0.0001). Using an optimal cutoff value ≤ 217.9 pmol/l calculated from the receiver operating characteristic curve (area under curve = 0.801, 95% confidence interval = 0.644 to 0.910; P = 0.0001), the sensitivity of predicting survival with good neurological outcome was 78.6% and the specificity was 75.0%. Multiple logistic regression analysis revealed that a copeptin level > 217.9 pmol/l was an independent predictor of severe neurological dysfunction or death, with an adjusted odds ratio of 27.00 (95% confidence interval = 2.27 to 321.68; P = 0.009).The present study found that copeptin levels have a significant prognostic value at the time of hospital admission, and are a promising diagnostic tool for predicting outcomes in out-of-hospital cardiac arrest survivors.A large number of patients experience cardiac arrest each year, which is associated with high mortality and poor neurological outcomes [1,2]. In patients who survived to hospital admission, brain injury was the major cause of death; ischemic brain damage is responsible for approximately 70% of in-hospital deaths after out-of-hospital cardiac arrest [1,2]. Cerebral ischemia during cardiac arrest is also responsible for significant encephalopathy in many cardiac arrest survivors [1,2]. Before the introduction of therapeutic hypothermia into clinical practice, only 26
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
Successful use of therapeutic hypothermia in an opiate induced out-of-hospital cardiac arrest complicated by severe hypoglycaemia and amphetamine intoxication: a case report
Michael Busch, Eldar S?reide
Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine , 2010, DOI: 10.1186/1757-7241-18-4
Abstract: The cardiac arrest was not witnessed, no bystander CPR was initiated, the time interval from the call to ambulance arrival was 9 minutes and the initial cardiac rhythm was asystole. Eight minutes of advanced cardiac life support resulted in ROSC.Upon hospital admission, the patient's pupils were dilated. Her arterial lactate was 17 mmol/l, base excess -20, pH 6.9 and serum glucose 0.2 mmol/l. During the first 24 hours in the ICU, the patient developed maximally dilated pupils not reacting to light and became increasingly haemodynamically unstable, requiring both inotropic support and massive fluid resuscitation. After 1 week in the ICU, however, she made an uneventful recovery with a Cerebral Performance Category of 1 at hospital discharge and at a follow up examination at 6 months.According to most prognostic factors, the patient had a statistical chance for survival of less than 1%, not taking into account her severe state of hypoglyaemia. We suggest that this case exemplifies the need for more studies on the use of TH in non-coronary causes of OHCA.Most primary survivors of out-of-hospital cardiac arrest (OHCA) will succumb to anoxic-ischemic brain injury during their hospital stay [1].Among the factors known to predict a dismal prognosis are a non-cardiac cause of the OHCA, non-witnessed arrest, asystole as the initial ECG-rhythm, lack of bystander cardiopulmonary resuscitation (CPR) and time interval between distress call and arrival of the ambulance of more than 6 minutes [2]. Hypoglycaemic, anoxic-ischemic and amphetamine-caused brain injury share many pathophysiological pathways, such as oxidative stress, mitochondrial dysfunction, excitotoxicity, apoptosis, increased calcium influx, as well as increased seizure activity [3-7]. However, the role of therapeutic hypothermia (TH) in OHCA due to non-cardiac causes (e.g., asphyxia or drug overdose) is not widely studied [8].A 26-year old female sustained an OHCA after intentional poisoning. The cardiac arrest was
Are There Age-Related Differences in the In-Hospital Treatment of Victims from Out-of-Hospital Cardiac Arrest?  [PDF]
Martin Christ, Katharina Isabel von Auenmueller, Irini Maria Breker, Jeanette Liebeton, Michael Brand, Jan Peter Noelke, Hans-Joachim Trappe
International Journal of Clinical Medicine (IJCM) , 2015, DOI: 10.4236/ijcm.2015.66056
Abstract:
Objective: Hardly anything is known about reasons for age-related differences in surviving out-of-hospital cardiac arrest (OHCA) with worse surviving rates in elderly. Methods: 204 victims from OHCA who were admitted in our hospital between January 1st 2008 and December 31st 2013 were identified. According to their mean age (69.1 ± 14.2 years) we classified those patients (pts) who were younger than mean age minus standard deviation (SD) as young, and those victims from OHCA who were older than mean age plus SD as old. Results: Young victims from OHCA (n = 32 pts) presented more often with an initial shockable rhythm than the elderly (n = 38 pts) (50.0% vs. 21.1%; p = 0.014), received more often coronary angiography (71.9% vs. 18.4%; p < 0.001), more often percutaneous coronary intervention (46.9% vs. 13.2%; p = 0.003), more often mild therapeutic hypothermia (78.1% vs. 15.8%; p < 0.001) and could be more often discharged alive (65.6% vs. 21.1%; p < 0.001). Conclusion: At hospital admission, physiological data did not differ between young and old victims from OHCA. Less use of coronary angiography and mild therapeutic hypothermia in elderly victims from OHCA might suggest that the observed age-related differences in survival following OHCA might be caused by age-related differences in the in-hospital treatment.
Out-of-hospital cardiac arrests in children  [cached]
Kamarainen Antti
Journal of Emergencies, Trauma and Shock , 2010,
Abstract: Prehospital pediatric cardiac arrest is a rare event compared with adult cardiac arrest. Despite the recent advancements in postresuscitation care improving the outcome of adult patients, similar evidence is lacking in pediatric victims of cardiac arrest. In this brief article, the current data on pediatric cardiac arrest occurring in the prehospital setting are reviewed. The annual incidence of pediatric out-of-hospital cardiac arrest is approximately 8-10 cases per 100,000 persons. The outcome is generally poor, as only 2-9.6% of patients survive to hospital discharge. The neurologic outcome of survivors is good in 24-31% of patients. Current evidence is insufficient to strongly support or refute the use of mild therapeutic hypothermia during the postresuscitation phase in pediatric patients. The application of a goal-directed treatment protocol for pediatric cardiac arrest and postresuscitation syndrome needs to be evaluated.
Changes in S-100 protein serum levels in survivors of out-of-hospital cardiac arrest treated with mild therapeutic hypothermia: a prospective, observational study
Matthias Derwall, Christian Stoppe, David Brücken, Rolf Rossaint, Michael Fries
Critical Care , 2009, DOI: 10.1186/cc7785
Abstract: This was a prospective, observational study performed during a two-year period, involving medical emergency services and five collaborating hospitals at the city of Aachen, Germany. Sixty-eight subjects were enrolled by the emergency physician on duty by taking blood samples after successful attempts at resuscitation with return of spontaneous circulation (ROSC), followed by samples at 6, 12, 24, 72 and 120 hours post ROSC by the appropriate intensive care unit staff. Depending on the decision of the attending physician, subjects were cooled down to 33°C (n = 37) for 24 hours or were held at 37°C (n = 31). Patients were tracked for estimating mortality and gross neurological outcome for 14 days.S-100 levels in patients not receiving mild therapeutic hypothermia (normothermia (NT)) showed equivalent numbers as compared with cooled patients (mild therapeutic hypothermia (MTH)) on baseline (NT = 1.38 μg/l versus MTH = 1.30 μg/l; P = 0.886). S-100 levels on baseline were significantly lower in patients with a good neurological outcome at 14 days after the event in comparison to their peers with adverse outcome (P = 0.014). Although the difference in S-100 levels of MTH patients with adverse or favourable neurological outcome reached statistical significance, it did not in NT patients.Although the predictive power of S-100 levels were best on admission but not at later time points, MTH had no influence on S-100 serum levels in survivors of non-traumatic out-of-hospital cardiac arrest in the particular setting of this investigation.Sudden cardiac arrest (SCA) is the leading cause of death in the USA and Europe affecting about 750,000 people annually [1,2]. Because of improved public training of cardiopulmonary resuscitation (CPR) and advances in professional emergency medical response [3], the rate of return of spontaneous circulation (ROSC) has risen in the past decades. However, depending on the duration of the arrest, neurological survival is still a major concern [4].
Hypothermia and cardiac arrest: the promise of intra-arrest cooling
Roger A Band, Benjamin S Abella
Critical Care , 2008, DOI: 10.1186/cc6845
Abstract: In the previous issue of Critical Care, Bruel and colleagues report findings from a small, prospective, observational study in which they investigate the feasibility, efficacy and safety of intra-arrest therapeutic hypothermia (TH) for victims of out-of-hospital cardiac arrest (OHCA) [1]. From an initial pool of 412 cardiac arrest victims, the study enrolled 33 patients with a variety of presenting rhythms. This represents the first study of its kind to investigate the feasibility of intra-arrest cooling in the clinical setting, an approach that has shown significant promise in animal models of cardiac arrest and brain injury [2-4].Sudden cardiac arrest, defined as the abrupt loss of mechanical cardiac activity and concomitant global loss of blood flow, is a leading cause of death in the United States and Europe. Approximately 200,000 people suffer OHCA in the United States each year, and over 90% will succumb during resuscitation efforts or during subsequent hospitalization [5,6]. Survival to hospital discharge depends on a number of factors, including prompt delivery of cardiopulmonary resuscitation and defibrillation when indicated, the initial cardiac rhythm of arrest, and the quality of post-resuscitation care including provision of TH.Despite the significant effort that has been invested in this field, few therapeutic or pharmacologic interventions have yielded meaningful increases in overall survival from OHCA over the past 20 years [6,7]. The relatively new and evolving treatment modality of TH, however, has been associated with markedly decreased mortality and neurologic injury among patients who initially survive OHCA [8,9].TH reduces both the cerebral metabolic rate and oxygen demand, and it is thought to attenuate reperfusion injury, global inflammation and endothelial dysfunction – all consequences of cerebral and other organ ischemia [10,11]. Through such mechanisms, TH is thought to improve clinical parameters and outcomes. Two landmark multicenter ra
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