Cases of Note

Cases of Note features peer-reviewed case reports and case series that document clinically relevant findings from critical and high acuity care environments. Cases that illuminate a clinical diagnosis or a management issue in the treatment of critically and acutely ill patients and include discussion of the patient’s experience with the illness or intervention are encouraged. Proposals for future Cases of Note articles may be e-mailed to [email protected].


Abstract Therapeutic hypothermia is an important and successful treatment that has been endorsed only in specific clinical settings of cardiac arrest. Inclusion criteria thus far have not embraced drug-induced cardiac arrest, but clinical evidence has been mounting that therapeutic hypothermia may be beneficial in such cases. A 59-year-old man who experienced a cocaine-induced cardiac arrest had a full neurological recovery after use of therapeutic hypothermia. The relevant pathophysiology of cocaine-induced cardiac arrest is reviewed, the mechanism and history of therapeutic hypothermia are discussed, and the clinical evidence recommending the use of therapeutic hypothermia in cocaineinduced cardiac arrest is reinforced. (American Journal of Critical Care. 2014; 23:89-92)


herapeutic hypothermia remains a relatively new immediate treatment option for patients who have had return of spontaneous circulation after cardiac arrest but remain unresponsive. In several studies,1 therapeutic hypothermia has been definitively shown to improve neurological recovery when used after the return of spontaneous circulation. These studies, however, excluded survivors of drug-induced cardiac arrest.2 As a result, evidence supporting the use of therapeutic hypothermia in drug-induced cardiac arrest has been absent despite clinical suspicion of its benefits. We report a second unique published instance of successful use of therapeutic hypothermia in the setting of cocaine-induced cardiac arrest.2 ©2014 American Association of Critical-Care Nurses doi:

Case Report A 59-year-old man was found to be unresponsive and pulseless by his girlfriend, who noted his only complaint had been chest discomfort 2 hours before she found him. She called emergency medical services, and the paramedics found the patient was in ventricular fibrillation. He was defibrillated 3 times in the field and endotracheally intubated. Once the patient was in the emergency department at Mercy Catholic Medical Center, refractory ventricular tachycardia was detected and the patient was defibrillated once more. Correct placement of the endotracheal tube was confirmed at this time. Resuscitation attempts in the field and hospital followed Advanced Cardiac Life Support (ACLS) 2012 guidelines. Initial electrocardiography (ECG) in the emergency department showed ST-segment elevations in the anterior, septal, and lateral leads (see

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Figure A, Initial electrocardiogram obtained when patient arrived in the emergency department shows ST-segment elevation in anterior, septal, and lateral leads. B, Electrocardiogram obtained 3 hours after resuscitation no longer shows ST-segment elevation.

About the Authors Dane Scantling is a fourth year medical student at The Philadelphia College of Osteopathic Medicine, Philadelphia, Pennsylvania. Emily Klonoski is an internal medicine resident a St Luke’s University Health Network in Bethlehem, Pennsylvania. Dominic J. Valentino III is the medical director of critical care at Mercy Fitzgerald Hospital in Darby, Pennsylvania. Corresponding author: Dane Scantling, The Philadelphia College of Osteopathic Medicine, 4170 City Avenue, Philadelphia, PA 19131 (e-mail: [email protected]).


Figure, part A), and the patient was emergently taken to the cardiac catheterization laboratory. The catheterization did not show any significant coronary artery disease. The patient did not have any significant past medical or surgical history. His social history was unknown. At this time, the patient was started on a therapeutic hypothermia protocol with a goal temperature of 33°C (91.4°F) and range of 32°C to 34°C (89.6°F-93°F). His initial arterial blood gas analysis

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indicated metabolic acidosis and yielded a pH of 7.30, PCO2 of 35.0 mm Hg, bicarbonate level of 16 mEq/L, and PO2 of 390 mm Hg. A complete blood cell count and blood chemistry laboratory results were otherwise within acceptable limits. His ECG 3 hours after resuscitation showed no retained STsegment abnormalities (see Figure, part B). Cooling lasted 24 hours and gradual controlled rewarming was subsequently initiated by using the Alsius (Zoll Medical Corp) invasive targeted temperature management system. Subsequently, a urine drug screening was positive for cocaine. Following rewarming, the patient was noted to be alert and following commands and was extubated. He then admitted to use of a large amount of intranasal cocaine the night before and in the late morning hours during the morning of his cardiac arrest. Initially, he complained of a subjectively weak and ataxic gait. Progressive neurological improvement and return of ability to ambulate followed, and he was discharged several days later with no significant residual deficits of any kind.

Discussion The current literature lacks direction on the generalized benefits of therapeutic hypothermia in cases of cocaine-induced cardiac arrest. One previous report of therapeutic hypothermia in such a cardiac arrest was published in 2008.2 In that instance, a 28-year-old woman had a cardiac arrest after ingestion of crack cocaine.2 Resuscitation efforts varied in that our patient did not receive atropine, he did not experience prolonged asystole, and his course instead followed 2012 ACLS protocols. Therapeutic hypothermia, studied initially almost 75 years ago by using profound cooling to combat cancer,3 remains relatively underused. Only recently has it been accepted as routine practice in major medical centers. After a 2002 study published in the New England Journal of Medicine,4 therapeutic hypothermia begin to gain traction in the medical community. The following year, the International Liaison Committee on Resuscitation endorsed guidelines for use of therapeutic hypothermia in cases of out-of-hospital arrest with an initial rhythm of ventricular fibrillation and later extended this to such cases with ventricular tachycardia without a pulse.1 Contemporary ACLS guidelines recommend use of therapeutic hypothermia in unconscious adult patients upon return of spontaneous circulation after an out-of-hospital cardiac arrest when the initial rhythm was ventricular fibrillation and direct cooling to 32°C to 34°C for 12 to 24 hours.5 Although additional populations of patients have long been believed to gain from such therapy, official exclusion criteria have been relatively slow to recede. The expanding use of therapeutic hypothermia

has often been due to a lack of other treatment options rather than the presence of specific studies declaring its effectiveness in narrowly defined situations. Indeed, exclusion criteria maintain that patients in a coma that could be due to drug intoxication not have therapeutic hypothermia started. However, it can be deduced that the benefits of therapeutic hypothermia would extend to patients with cocaineinduced cardiac arrest for a variety of reasons. Although treatment of cocaine-induced cardiac arrest with hypothermia has not been thoroughly studied, the potential for neurological recovery after cocaine-induced cardiac arrest has been studied. Cocaine can be a complicated cause of cardiac arrest as it may induce myocardial infarction and block either sodium or potassium channels.2 It should be noted, however, that cocaine-related cardiac arrest may have potential for superior neurological outcomes compared with cardiac arrest not related to cocaine6 and that cocaine has become the second most common cause of drug-related visits to emergency departments in the United States.7 Accordingly, expansion of treatment for complications should be a priority. In a 2001 study of adults who had used cocaine more than 10 times in their life, the incidence of myocardial infarction was 6 times the incidence in the general population, 25% of nonfatal myocardial infarctions were attributable to frequent cocaine use, and about 1% of such users have a myocardial infarction during their lifetime.8 Prevalence of cocaine use within the population of persons having a cardiac arrest is unknown, but the possibility to benefit such patients certainly exists. A potential factor in the benefit of therapeutic hypothermia in cocaine-induced cardiac arrest is the direct effect of cocaine on cerebrovascular circulation. Indeed, cocaine is a known cause of ischemic and hemorrhagic stroke. Effects may be transient or permanent and occur as a result of decreases in mean arterial blood pressure, glucose utilization, blood volume, tissue oxygenation, and cerebral blood flow due to vasoconstriction in addition to an independent increase in intracellular calcium concentration associated with cell death.9 Conversely, therapeutic hypothermia has long been believed to be capable of reducing primary brain injury and preventing secondary inury,10 and its use even in stroke patients is an area of ongoing study and scientific interest without definitive conclusions.11 Therapeutic hypothermia is theorized to combat global ischemia in several unique ways. Global ischemia, defined as perfusion less than a twentieth of the baseline, induces selective neuronal death

Cocaine-related cardiac arrest may have better neurologic outcomes than noncocaine-related cardiac arrest.

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even if reperfusion occurs within 30 minutes12 and drives poor outcomes despite the return of circulation. Importantly, animal experiments show definitive protective effects if hypothermia is induced quickly.12 Cells injured by ischemia essentially have 3 options: become necrotic, undergo apoptosis, or recover.12 The theoretical benefit of therapeutic hypothermia is that it combats injury by reducing cerebral edema, disruption of the blood brain barrier,13 and free radical production as well as by stabilizing membranes.10,14 Therapeutic hypothermia is also thought to reduce excitatory neurotoxic effects caused by impaired glutamate reuptake10,15,16 and inflammatory cytokine release, specifically interleukins 1 and 6 and tumor necrosis factor–α.17 In keeping with existing research, therapeutic hypothermia has a variety of applications,18 possibly because of the multitude of effects that it exerts on the brain after cardiac arrest. Our clinical result, like that reported in 2008, was complete neurological recovery by the time of discharge after a successful use of therapeutic hypothermia. As such clinical evidence grows, so too can the use of therapeutic hypothermia. FINANCIAL DISCLOSURES None reported. eLetters Now that you’ve read the article, create or contribute to an online discussion on this topic. Visit and click “Respond to This Article” in either the full-text or PDF view of the article.

REFERENCES 1. Nolan JP, Morley PT, Hoek TL, Hickey RW; Advanced Life Support Task Force of the International Liaison Committee on Resuscitation. Therapeutic hypothermia after cardiac arrest: an advisory statement by the Advanced Life Support Task Force of the International Liaison Committee on Resuscitation. Resuscitation. 2003;57:231-235. 2. Fuller ET, Milling TJ Jr, Price B, Spangle K. Therapeutic hypothermia in cocaine-induced cardiac arrest. Ann Emerg Med. 2008;51:135-137.


3. Smith LW, Fay T. Temperature factors in cancer and embryonal cell growth. JAMA. 1939;113(8):653-660. 4. The Hypothermia after Cardiac Arrest Study Group. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med. 2002;346:549-556. 5. Neumar RW, Otto CW, Link MS, et al. 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science: Part 8: Adult Advanced Cardiac Life Support. Circulation. 2010; 122:5729-5767. 6. Hsue P, McManus D, Selby V, et al. Cardiac arrest in patients who smoke crack cocaine. Am J Cardiol. 2007;99:822-824. 7. Goldstein R, DesLauriers C, Burda A. Cocaine: history, social implications and toxicity—a review. Dis Mon. 2009;55:6-38. 8. Qureshi AI, Suri MF, Guterman LR, Hopkins LN. Cocaine use and the likelihood of nonfatal myocardial infarction and stroke: data from the Third National Health and Nutrition Examination Survey. Circulation. 2001;103:502-506. 9. Du C, Yu M, Volkow ND, Koretsky AP, Fowler JS, Benveniste H. Cocaine increases the intracellular calcium concentration in brain independently of its cerebrovascular effects. J Neurosci. 2006;26:11522-11531. 10. Yenari MA, Han HS. Neuroprotective mechanisms of hypothermia in brain ischemia. Nature Rev Neurosci. 2012;13(4):267-278. 11. Song SS, Lyden PD. Overview of therapeutic hypothermia. Curr Treat Options Neurol. 2012;26:541-548. 12. Polderman KH. Application of therapeutic hypothermia in the ICU: opportunities and pitfalls of a promising treatment modality. Part 1: indications and evidence. Intensive Care Med. 2004;30:556-575. 13. Huang ZG, Xue D, Preston E, et al. Biphasic opening of the blood-brain barrier following transient focal ischemia: effects of hypothermia. Can J Neurol Sci. 1999;26:298-304. 14. Globus MY, Alonso O, Dietrich WD, Busto R, Ginsberg MD. Glutamate release and free radical production following brain injury: effects of posttraumatic hypothermia. J Neurochem. 1995;65:1704-1711. 15. Siesjö BK, Bengtsson F, Grampp W, Theander S. Calcium, excitotoxins and neuronal death in brain. Ann N Y Acad Sci. 1989;568:234-251. 16. Warren DE, Bickler PE, Clark JP, et al. Hypothermia and rewarming injury in hippocampal neurons involve intracellular Ca2+ and glutamate toxicity. J Neurosci. 2012;207:| 316-325. 17. Hayashi N, Bullock R, Dietrich DW, Maekawa T, Tamura A, eds. Hypothermia for Acute Brain Damage: Pathomechanism and Practical Aspects. Tokyo, Japan: Springer-Verlag; 2004. 18. Andrzejowski J. Clinical applications of induced hypothermia. Contin Educ Anaesth Crit Care Pain. 2006;6(1):23-27.

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Use of Therapeutic Hypothermia in Cocaine-Induced Cardiac Arrest: Further Evidence Dane Scantling, Emily Klonoski and Dominic J. Valentino III Am J Crit Care 2014;23:89-92 doi: 10.4037/ajcc2014299 © 2014 American Association of Critical-Care Nurses Published online Personal use only. For copyright permission information:

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Use of therapeutic hypothermia in cocaine-induced cardiac arrest: further evidence.

Therapeutic hypothermia is an important and successful treatment that has been endorsed only in specific clinical settings of cardiac arrest. Inclusio...
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