TASER-Conducted Electrical Weapon Injuries

Similar to fishhook injuries, the small barbs on the electrodes typically penetrate the dermal and epidermal layers of the skin, however because of the variation in dermal thickness, for example the dermis in the eyelid is 3mm whereas the dermis in the back is 3 cm, it is possible to injure hypodermal structures. The patient also may have superficial burns between the two barbs. For most tissue injuries, barbs can be removed by applying inward traction while the other hand grips the electrodes and pulls back firmly. Anesthesia is not necessary because of the small caliber of the barbs and its electrocautery effect to the tissue. Ocular injuries can include eyelid trauma, iritis, globe ruptures, macular cysts, and cataracts, and should therefore be emergently referred to an ophthalmologist.  Any retained electrodes in the eye should not removed by the ED physician. In addition to the eye, injuries to joints, cranium, or locations where there is a risk of the dart penetrating a body cavity should be removed with care and with the appropriate consultation if warranted. Tetanus prophylaxis should be offered to all patients.

Cardiac

The standard TASER delivers 5 seconds of low current with short pulses for a total of 2mA with each discharge of the weapon. The threshold to depolarize the cardiac membrane is approximately 100mA. Additionally, current flow takes the path of least resistance, preferring to spread within the superficial tissues and not penetrate to the organs. In 23 different trials in peer-reviewed journals with healthy human volunteers receiving 5 or 10-second CEW applications, ECG or echocardiogram monitoring, showed no ventricular arrhythmias and no changes to troponins, QRS, QT, or QTC. There was also no effect on blood pressure. There were some significant transient changes noted, including increases in heart rate (2.4-15 beats per minute), decreases in PR interval related to the increase in pulse, some nonspecific ST changes, and sinus arrhythmias. The limitation to the studies relying solely on ECGs is that the actual deployment interferes with ECG monitoring. The real-life limitations to relying on these studies is that while 5 seconds is the standard discharge time, in the field, 50% of discharges are “singles”, and 50% of the time discharges are “multiples”. Moreover, these studies were done in individuals without known structural heart disease, outside of a highly stressful environment, and without confounding factors such as drugs or psychosis. Critics of CEWs often cite a famous case of a 16 year-old male with ADD and asthma who immediately fell unresponsive after receiving two 5 second shots to the chest wall. The EMS ECG after 1.5 minutes of CPR showed Vfib and after 4 rounds of defibrillation, the subject was pronounced dead. Pathologists later noted a possible arrhythmogenic right ventricular cardiomyopathy in the patient as well as marijuana in his blood. In animal studies, when the “dart to heart” distance was less than 2 cm and the discharges were given for prolonged periods of time, fatal cardiac arrhythmias were noted in some subjects, for example after two 40 second CEW exposures 3 in 19 pigs in one study had fatal vfib. In 2009, TASER International updated their guidelines to “avoid chest shots” whenever possible as the estimated arrest-related death rate is 1 in 100,000 in “physiologically or metabolically compromised persons.“

In the emergency department, patients with CEW-related cardiac complications will have presented during their pre-hospital care and we will continue ACLS resuscitations. While there is a paucity of evidence for patients with pacemaker or defibrillator devices, most sources recommend interrogating the device prior to making a disposition. In asymptomatic individuals, routine ECG and troponins are not necessary.

Musculoskeletal

CEWs stimulate the A-α motor neurons causing muscle contractions, which can lead to muscle cell damage and the subsequent release of creatinine kinase. In numerous studies CK and myoglobin did increase significantly, but not to a level considered important clinically. Therefore CK is not part of routine laboratory testing.

Secondary Trauma

A CEW discharge induces muscle tetany and a loss of muscle tone which may result in two complications 1) falls and 2) tetany-induced bony fractures. Fall injuries often occur from the temporary loss of muscle control while the subject is running, jumping, or climbing. Moreover, the loss of voluntary muscle control may prevent them from maneuvering in such a way to lesson the impact of their fall, such as breaking their fall with an outstretched hand. A complete secondary survey must be conducted to evaluate for trauma.

Agitation Delirium

Agitation delirium is often precipitated by an extreme adrenergic state where an individual on drugs such as cocaine, PCP, or bath salts uses intense physical exertion to resist arrest. If the individual is apprehended, for example, by TASER, handcuffs, or chokehold, this furthers their adrenergic state. Agitation delerium is multifactorial, with alcohol or drugs seen in 70-100% of those with poor outcomes and extreme physical exertion found in 78%. Psychiatric illnesses such as mania or schizophrenia or systemic illnesses were also noted in case reports of patients with agitation delirium. An interesting study in the 1980s was the first of many studies to note that the average cocaine blood levels in patients who died from agitation delirium were lower than levels seen in typical cocaine overdose fatalities suggesting that while cocaine factored into the deaths of these individuals, their cause of death was not from the typical mechanism of a cocaine overdose. Both stimulants and stress trigger excessive dopamine release, which in turn triggers the autonomic hyperactivity seen in patients with agitation delirium, though the exact mechanism is incompletely understood. Many consider agitation delirium to be on the same spectrum as neuroleptic malignant syndrome (NMS). Like NMS, agitation delirium patients may display a sudden onset of paranoia, hyperactive behavior, hyperventilation, and hyperthermia. The mortality rate approaches 84%, with two-thirds dying on scene from respiratory failure or cardiac arrest. Those who survive long enough to reach the emergency department often suffer from complications such as rhabdomyolysis, DIC, and renal failure.

Management should start with rapid sedation. While we may instinctively reach for our trusty neuroleptics (Haldol) and benzodiazepines (Ativan), patients don’t have time to wait the 10-15 minutes for the onset of these medications. IM Ketamine (4-5mg/kg/dose with onset of action in 3-4 minutes) or IV Ketamine (1-2mg/kg/dose with onset of action of 30 seconds) quickly produces sedation and analgesia. Once sedation is achieved, IV, 02, and monitoring should rapidly be established. The autonomic hyperactivity must also be addressed and therapies such as Clonidine and Dantrolene should strongly be considered. Full labs including Creatinine Kinase and blood gases should be obtained.