What is therapeutic hypothermia

Therapeutic hypothermia was also associated with lower rates of favorable neurological survival for the overall cohort hypothermia-treated group, Conclusions and Relevance Among patients with in-hospital cardiac arrest, use of therapeutic hypothermia compared with usual care was associated with a lower likelihood of survival to hospital discharge and a lower likelihood of favorable neurological survival. These observational findings warrant a randomized clinical trial to assess efficacy of therapeutic hypothermia for in-hospital cardiac arrest.

Quiz Ref ID Therapeutic hypothermia, or targeted temperature management, is recommended for comatose patients following both out-of-hospital and in-hospital cardiac arrest. To our knowledge, there have been no randomized trials conducted in the in-hospital setting. Two small observational studies comprising a total of treated patients have not shown a survival benefit, 4 , 5 and a third included only 42 treated patients with in-hospital cardiac arrest.

To address this gap in knowledge, this study was designed to evaluate the association of hypothermia treatment with survival to hospital discharge and with favorable neurological survival at hospital discharge among patients with in-hospital cardiac arrest. In addition, by linking this registry with Medicare files, the association between hypothermia treatment and 1-year survival was evaluated.

Question Is therapeutic hypothermia associated with better survival outcomes for patients with in-hospital cardiac arrest? Compared with untreated patients, those treated with therapeutic hypothermia had significantly lower rates of in-hospital survival Meaning Therapeutic hypothermia was not associated with improved survival or better neurological outcomes and was potentially harmful. Current use of therapeutic hypothermia for in-hospital cardiac arrest may warrant reconsideration.

The GWTG-Resuscitation registry is a large, prospective, national, quality improvement registry of in-hospital cardiac arrest sponsored by the American Heart Association.

Its design has been previously described. Cases are identified by hospital research staff through multiple methods, including centralized collection of cardiac arrest flow sheets, reviews of hospital paging system logs, and routine checks of code carts and pharmacy tracer drug records. For patients aged 65 years and older, GWTG-Resuscitation data have been previously linked with Medicare inpatient files.

For this study, as newer years of Medicare files were available, the deterministic linkage was repeated for Medicare data through This linkage was successful in The study included patients aged 18 years and older enrolled in GWTG-Resuscitation between March 1, after publication of hypothermia trials for out-of-hospital cardiac arrest 2 , 3 , and December 31, As this study evaluated therapeutic hypothermia, only patients with return of spontaneous circulation after an index in-hospital cardiac arrest were included.

For those aged 65 years and older, patients who were not linked to Medicare inpatient files no unique match or enrolled after were excluded to enable examination of postdischarge survival. To ascertain that hypothermia was available at each hospital, patients from hospitals with no cases of therapeutic hypothermia were excluded. Moreover, only cases occurring after the first documented use of therapeutic hypothermia for in-hospital cardiac arrest at each hospital were included.

Quiz Ref ID As therapeutic hypothermia is considered in comatose patients, the cohort was restricted to patients on mechanical ventilation at the time of cardiac arrest as documented by GWTG-Resuscitation or after cardiac arrest as documented by a Medicare International Classification of Diseases, Ninth Revision, Clinical Modification procedure code for mechanical ventilation [ Patients with missing information on survival to discharge and comorbidities for model adjustment were excluded.

Furthermore, patients with an initial out-of-hospital cardiac arrest followed by an in-hospital cardiac arrest were excluded. The independent exposure variable was active induction of therapeutic hypothermia, as documented within GWTG-Resuscitation.

The primary outcome was in-hospital survival ie, to hospital discharge. The secondary outcome was favorable neurological survival, defined as survival to hospital discharge with a Cerebral Performance Category score of 1 or 2 ie, without severe neurological disability. The last follow-up date was February 4, , for survival to discharge and favorable neurological survival and December 31, , for 1-year outcomes.

To evaluate the association between therapeutic hypothermia treatment and survival outcomes, propensity score analyses were conducted. This model included the hospital site and the following variables from GWTG-Resuscitation: age, sex, self-identified race by patients or families which is known to affect survival 15 and was categorized as white, black, and other , initial cardiac arrest rhythm asystole, PEA, ventricular fibrillation, and pulseless ventricular tachycardia , location of cardiac arrest, comorbid conditions prior heart failure or myocardial infarction, index admission heart failure or myocardial infarction, diabetes mellitus, baseline depression in central nervous system function, acute stroke, pneumonia, and metastatic or hematologic malignant neoplasm , medical conditions present within 24 hours of cardiac arrest renal insufficiency, hepatic insufficiency, respiratory insufficiency, hypotension, septicemia, and metabolic or electrolyte abnormality , and interventions in place at the time of cardiac arrest continuous intravenous vasopressor, implantable cardioverter-defibrillator, and hemodialysis.

The model also adjusted for duration of acute cardiopulmonary resuscitation, the time of day work hours [ am to pm ] vs after hours [ pm to am ] , and day of the week weekday vs weekend of the cardiac arrest. After deriving a propensity score for each patient, variable optimal matching for each hypothermia-treated patient was performed, with up to 4 controls without replacement for each treated patient, using an algorithm match with a caliper width no greater than 0.

Interaction analyses were conducted between therapeutic hypothermia and cardiac arrest rhythm to assess whether the association between therapeutic hypothermia and survival outcomes differed for patients with shockable ventricular fibrillation and pulseless ventricular tachycardia and nonshockable asystole and PEA cardiac arrest rhythms. For 1-year survival, a separate propensity score model was derived for patients aged 65 years and older.

Cumulative survival over the first year was compared between the propensity score—matched patients. In addition, a binomial model using a log link stratified by matched sets assessed overall rates of 1-year survival. Although use of a propensity score balances measured covariates between treatment groups, indication bias due to unmeasured confounding may exist.

To address this, a sensitivity analysis was conducted whereby all patients who died within the first 24 hours were excluded. If there was indication bias against therapeutic hypothermia treatment whereby sicker patients were more likely to receive therapeutic hypothermia , this analysis, from 24 hours onward, would result in a stronger survival benefit for therapeutic hypothermia treatment, as a greater proportion of patients treated with hypothermia would have died during the first 24 hours.

This sensitivity analysis was conducted after deriving new propensity scores for this cohort and reperforming the previous analyses. For each analysis, the null hypothesis was evaluated at a 2-sided significance level of. All analyses were performed using SAS version 9. Overall, patients 6. Patients treated with hypothermia were younger, less likely to have a cardiac arrest in the intensive care unit, and more likely to have an initial cardiac arrest rhythm of ventricular fibrillation Table 1.

The duration of resuscitation before return of spontaneous circulation was similar between patients treated with and without hypothermia, but patients with therapeutic hypothermia initiated were more likely to have a myocardial infarction prior to their cardiac arrest and less likely to have hypotension, respiratory insufficiency, renal insufficiency, hepatic insufficiency, pneumonia, acute stroke, and a metastatic or hematologic malignant neoplasm at the time of their cardiac arrest.

It is helpful only for people whose heartbeat returns after a sudden cardiac arrest. Therapeutic hypothermia can be a good choice if the heart restarted but you are still not responsive. It can raise the chance that you will wake up. The chemical reactions of the body slow down.

The lowered temperature may also lessen inflammation in the brain. Both of these factors may help reduce injury. Therapeutic hypothermia is very helpful for some people. But it has some rare risks. Some of these risks include:. This procedure is used only for people who are unconscious after cardiac arrest.

It can be helpful for family members to learn about the procedure. While your body temperature is lower, you may look, act, and feel lifeless. You may also have tubes and monitoring devices attached to you. This can be scary. Your family should know that the healthcare providers are working hard to give you the best possible chance of recovery. Sometimes, healthcare providers may do therapeutic hypothermia at the same time as other treatments.

For example, they might do heart catheterization after a cardiac arrest caused by a heart attack. The medical team will carefully watch you. You will be in the intensive care unit. You may be on a ventilator to help with breathing. Increased risk of infection, coagulopathy, cardiopulmonary compromise and risks of re-warming erode the clinical utility of systemic therapeutic hypothermia, offsetting any beneficial effects on neurological function and limiting the achievable depth of induced hypothermia 1,9.

Moreover, induction of systemic hypothermia exhibits a significant and unpredictable lag time from institution of therapy to achievement of target temperature Selective hypothermia, initially investigated in the s prior to the advent of effective cardiopulmonary bypass, has re-emerged as a potential solution to the logistical obstacles and systemic complications of whole body hypothermia Descriptions of different methods to selectively cool the central nervous system CNS are numerous; however few have been thoroughly tested in clinical practice Given the paucity of therapeutic options for many neurological injuries, translation of the beneficial effects of therapeutic hypothermia noted in the laboratory to effective clinical applications at the bedside remains an area of interest.

Selective therapeutic hypothermia offers a promising modality to realize the potential benefits of therapeutic hypothermia in the clinical arena. In this article, we review the published strategies of selectively cooling the CNS. Additionally, we will argue that one direction of future research holds particular promise.

We will consider separately noninvasive and invasive techniques of cooling. While the former enjoys obvious advantages, such as ease of implementation, most studies have shown very minimal ability to cool the parenchyma of the brain. In contrast, invasive methods of cooling remain a field in its infancy, with few human participant trials. This latter approach holds greater promise for the future of selective hypothermia.

The upper airway - The beneficial role of systemic, therapeutic hypothermia after resuscitation from cardiac arrest has been well established 12, However, cooling techniques remain suboptimal. In seminal trials establishing the role of mild hypothermia after cardiac arrest, systemic cooling was begun after return of spontaneous circulation, and associated with improved neurological outcomes.

In contrast, animal have shown that early, and even intra-arrest cooling is associated with better outcomes, and diminished reperfusion injury In recent years, the technique of transnasal-evaporative cooling TEC has emerged as a potential solution to the problem of delayed cooling. In TEC, a mixture of liquid coolant and oxygen is sprayed into the nasopharnyx, and the liquid undergoes rapid evaporation under the administration of high flow oxygen The device is portable and results in rapid cooling of the nasal passages and brain.

In animal studies, the device, when administered at the time of arrest, has been shown to result in a higher probability of restoration of spontaneous circulation, and improved neurological outcomes compared with cooling performed after resuscitation, applied systemically The randomized, multicenter trial pre-restoration of spontaneous circulation IntraNasal Cooling Effectiveness trial PRINCE sought to test whether TEC would improve neurological outcomes among victims of witnessed arrest compared to usual care.

Standard European resuscitation guidelines governed EMS actions. Tympanic membrane temperature was monitored as a surrogate for deep brain temperature. TEC reached this temperature minutes before usual care. Although the study was not powered to detect differences in survival, the authors note a trend toward improved survival among the subset of patients admitted to the hospital In a further subset of patients for whom cardiopulmonary resuscitation CPR was initiated within 10 minutes of arrest, intranasal cooling was associated with a significant benefit in survival to hospital discharge Fourteen and 13 patients survived to hospital discharge, and nine and 11 were neurologically intact at that point, respectively.

Thus, the raw numbers show no benefit. At least one reason for the null results may be that tympanic membrane temperature is likely not a valid surrogate for deep brain temperature Other groups have called into question whether externally measured temperatures have any correlation with deep brain ones Beyond evaporative methods, conductive cooling of the nasopharnyx has also been employed in the quest for selective hypothermia.

In rat models, flushing the nasopharnyx with cold saline 21 , or cold water passed through tygon tubing have both been attempted Others have extended these findings to large animal pig models At baseline the parenchymal brain temperature was After one hour of continuous cooling brain temperature was Three studies of high flow gas through the upper airways all yielded null results.

Einer-Jensen and Khorooshi 24 examine the effect of high flow oxygen though the nasopharnyx on brain temperature for 11 intubated adult rats. They noted a slight dose response of 0. Cooling was applied for more than two hrs. Mellegard observed at best a 0. Finally, Andrews and Harris 26 performed a trial of air delivered at rates equivalent to minute ventilation via bilateral nasal cannulae to 15 patients who had suffered trauma or hemorrhage.

No change in parenchymal or subdural temperature was observed. Surface cooling of the head - Studies of convective air-cooling of the brain have yielded unimpressive results. Wass and colleagues 27 utilized a forced air-cooling helmet for 16 anesthetized dogs. They found at best a 2 degree Celsius drop in intraparenchymal temperature at a depth of 2cm, with an average drop of 0.

Shiraki and colleagues 28 provide a case report of a single adolescent undergoing face fanning after surgery for a pineal tumor. Shiraki et al. Tooley and colleagues 29 investigate the role of the cooling cap in providing selective hypothermia.

Eight anesthetized newborn pigs underwent a hypoxia ischemia injury known to result in brain damage. They then were cooled with an externally placed cooling cap.

Temperature of the scalp, dura, deep brain measured in basal ganglia , and rectal temperature were monitored. The authors wanted to test the feasibility of selective brain cooling, while preserving core body temperature. The authors demonstrated that the deep brain temperature could be brought down to They also made the observation that scalp skin temperature did not correlate with deep brain temperature. This fact raises questions for other methods of intranasal cooling, which monitor only externally measured temperatures.

Such surface temperatures are likely unreliable. A similar technique of selective hypothermia via cooling cap was employed in a randomized trial of neonates with hypoxic-ischemic encephalopathy HIE Two hundred thirty-four babies with HIE were randomized to a cooling cap, and overhead heating for 72 hours within six days of birth or conventional care. Prespecified subgroup analysis, based on severity of amplitude integrated electroencephalography aEEG findings demonstrated a subset of children who benefited from therapy.

However, though the subgroups were prespecified, such an analysis does not avoid the limitations of subgroup analyses, most notably inflated false positive rates from multiple testing While these results are encouraging for neonatal care, they are not easily generalizable to an adult population given the unique anatomy and intracranial dynamics of newborns.

Harris and colleagues performed a randomized controlled trial of a cooling helmet among adults presenting with a traumatic brain injury TBI. The trial was hindered by poor enrollment, and ultimately twelve patients underwent treatment and thirteen served as controls. The authors report a measure of selective cooling called the intracranial-bladder temperature gradient, and make the observation that it did not differ significantly between groups. Finally no mortality benefit was noted, as six and four patients died in the treatment and control groups, respectively.

Certainly, the study was underpowered to detect changes in mortality, but it is notable that externally applied cooling did not result in significant differences in regional temperature gradients. Qui and colleagues 32 performed a larger trial using a cooling cap and neckband among patients with traumatic brain injury. Both groups had similar demographics, admission GCS, pupil examination, admission intracranial pressure ICP , rate of craniotomy and findings on head CT intracranial hematoma, diffuse brain injury and contusions and others.

Mechanisms of action, physiological effects, and complications of hypothermia. Qadir R, Kanjwal K. Severe bradycardia with a prominent J wave refractory to atropine: was it a cause or a result of a fall?

A case report and a brief review on the treatment of hypothermia. Am J Ther. Michelle E. Patricia R. Deckard has been aWebcast presenter for Medivance, Inc. This article was peer-reviewed for bias and none was found. Ebright and the planners of this CNE activity have disclosed no relevant financial relationships with any commercial companies pertaining to this activity. It gives excellent Scientific as well as wonderful general information also.

It clears many doubts in our mind also. Supplement post. The article has a lot of good information. It is related to the situation of which I am involved. Dale Cook. This beautifully complete article reminds me the debt of gratitude I owe to the RNs who made this possible for me. I died in a car, 3 blocks from St. What they did, how they did it places me in a rare class of humans. Thank you, authors. Dan Verbeck. Save my name, email, and website in this browser for the next time I comment.

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American Nurse American Nurse. Sign in. Forgot your password? Get help. Create an account. Password recovery. Therapeutic hypothermia after cardiac arrest. July 11, Author s :. What is therapeutic hypothermia? How does cardiac arrest cause neurologic deficits? How does therapeutic hypothermia help? Phases of therapeutic hypothermia Therapeutic hypothermia occurs in three phases—induction, maintenance, and rewarming. Induction phase The goal of the induction phase is to get the patient to target body temperature as quickly as possible.

Rewarming phase Temperature control remains important during rewarming. Duration Duration of therapeutic hypothermia depends on facility protocol.

Potential adverse effects Therapeutic hypothermia may lead to fluid and electrolyte imbalances, arrhythmias, insulin resistance, shivering, coagulation problems, and other adverse effects. Fluid and electrolyte imbalances Fluid and electrolyte shifts especially of potassium, magnesium, and calcium are common with therapeutic hypothermia. Arrhythmias Bradycardia, atrioventricular blocks, and atrial and ventricular fibrillation may occur.