Article

Successful resuscitation of a patient in asystole after a TASER injury using a hypothermia protocol

Case Report

Successful resuscitation of a patient in asystole after a TASER injury using a hypothermia protocol

Abstract

New studies have shown the benefit of initiating a hypothermia protocol in the survivors of cardiac arrest. Although the data have shown an improved neurologic end point in patients initially in ventricular fibrillation or pulseless ventricular tachycardia, there is still debate about whether patients initially in other rhythms would benefit from hypothermia after return of spontaneous circulation. This is a report of a 17-year-old male found to be in asystole after sustaining a TASER injury, who was treated with a hypothermia protocol after return of spontaneous circulation and left the hospital with intact neurologic function.

Excellence in resuscitation has always been a foundation of emergency medicine. This includes following standard Advanced cardiac life support and pediatric advanced life support (PALS) algorithms for patients in ventricular fibrillation, pulseless ventricular tachycardia, pulseless electrical activity, and asystole [1]. Recent focus has also included what other therapy can be offered once a return of spontaneous circulation is obtained [2-5]. We present a case of a pediatric patient in asystole after sustaining a TASER (Madison, Wisconsin) injury who was resuscitated with a hypothermia protocol.

A 17-year-old boy with bipolar disease and polysubstance abuse was at home with his mother. He became aggressive, and the police were called. When they arrived, he was still agitated and was subdued with a TASER. He was struck in the left side of his chest and fell to the ground without any other injury. Twenty minutes later, it was noticed that he was still on the ground, unconscious, and not moving.

Emergency medical services was called. When they arrived, they found him to be in asystole. Cardiopulmonary resuscitation was begun including intubation. He received epinephrine, atropine, and was defibrillated when he went into ventricular fibrillation. In the emergency department, he was initially in ventricular fibrillation and received epinephr- ine, defibrillation, amiodarone, atropine, and sodium bicar- bonate. After return of spontaneous circulation, ice packs were applied to his axilla and chest, and an Alsius cool line was inserted for implementation of a hypothermia protocol.

In the intensive care unit, he remained sedated with fentanyl and versed, and on a levophed drip. Monitors showed him to be in atrial fibrillation with intermittent runs of ventricular tachycardia. He was cooled to 33 degrees for 18 hours and paralyzed with cisatracurium. Initial labora- tory results showed rhabdomyolysis, acute renal failure, shock liver, hypernatremia, hyperphosphatemia, and car- diac ischemia (troponin I peaked to 160 ng/mL). In the intensive care unit, he went into Pulseless electrical activity twice but was successfully resuscitated. He slowly improved, and on hospital day 4, he opened his eyes and responded to stimuli. He moved all his extremities by day 5, followed purposeful commands by day 11, and had a tracheostomy and feeding tube placed on day 12. He was weaned from the ventilator and transferred to an inpatient rehabilitation center on hospital day 21, at which time it was noted that he could walk and did not have any noticeable focal neurologic deficits.

Hypothermia after cardiac arrest was first reported in the 1950s [5]. In the 1990s, hypothermia began to be studied again for post-cardiac arrest patients and has been evaluated in patients with severe stroke and other injuries [4]. Studies have shown the promise of hypothermia in patients initially in ventricular fibrillation or pulseless ventricular tachycardia [4,5]. A study by the Hypothermia After Cardiac Arrest Study Group found a risk ratio of 1.40 and a number needed to treat of 6 to prevent one unFavorable neurologic outcome (Pittsburgh cerebral per- formance category 3-5) in patients with ventricular fibrillation or a nonperfusing ventricular tachycardia [5]. Bernard et al [4] found 49% of patients enrolled in the hypothermia cohort vs 26% of patients in the normothermia group had a Good neurologic outcome. This study only included patients initially in ventricular fibrillation.

The data on patients initially in PEA or asystole have not been as promising. Studies, including only small numbers of patients, have shown little change in both mortality and neurologic function when a hypothermia protocol was used [3]. Patients in these studies had a mean age of 57 and age greater than 70 years, respectively [3]. Our patient was

17 years old, which may have contributed to his good outcome. PALS does not endorse induced hypothermia in these patients.

This case also involves the use of a TASER. Although studies have been done, they normally involve the use of

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animals or humans in possibly unrealistic situations [6]. Studies involving both pigs and live volunteers both insinuate that their use on the public is safe [7,8]. Idekar and Dosdall [9] deduced that the induction of ventricular fibrillation by a TASER was unlikely after calculating the mean current strength that was necessary to cause this phenomenon and comparing it to the stimuli delivered by a TASER. In a swine study by Jauchem et al [10], jugular venous samples drawn after TASER exposure showed a significant increase in lactate levels and a lower pH compared to pre-TASER levels. However, there were no reported incidents of ventricular fibrillation. Although one cannot simply conclude that the TASER caused the cardiac arrest because of the temporal relationship, it does raise the question if more research is needed concerning the device’s safety or if more stringent protocols need to be developed concerning its usage. This is particularly important because unlike what is displayed on television, a TASER should not cause Long-term disability. Once it has finished delivering its electricity, the person who was tasered should be able to move.

Evan S. Schwarz MD

Barnes Jewish Hospital Washington University School of Medicine Division of Emergency Medicine

660 South Euclid Avenue, Campus Box 8072

Saint Louis, MO 63110, USA E-mail address: [email protected]

Michael Barra MD

Barnes Jewish Hospital Washington University School of Medicine Division of Emergency Medicine

660 South Euclid Avenue, Campus Box 8072

Saint Louis, MO 63110, USA

Michael M. Liao MD Division of Emergency Medicine Denver Health Medical Center

777 Bannock St, Denver, CO 80204

doi:10.1016/j.ajem.2008.07.042

References

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  10. Jauchem JR, Sherry CJ, Fines DA, et al. Acidosis, lactate, electrolytes, muscle enzymes and other factors in the blood of Sus scrofa following repeated TASER exposures. Forensic Sci Int 2006;161:20-33.

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