Electrical weapons, hematocytes, and ischemic cardiovascular accidents

Highlights

• An electrical weapon exposure acutely increases lymphocyte and monocyte counts.

• The platelet count and neutrophil levels were also increased at 5 min.

• The acute changes at 5 min remained within the normal reference ranges.

• An electrical weapon exposure did not cause clinically significant changes in hematocytes.

• Reported ischemic events do not appear to be caused by the electrical weapon exposure.

Abstract

Background

There have been case reports following the use of a conducted electrical weapon (CEW) suggesting that these devices might affect coagulation or thrombosis in at-risk individuals. The aim of this manuscript therefore is firstly to explore this hypothesis by reviewing each of these cases and secondly to report the results of a prospective study exploring a priori the effects of electrical weapons on hematocytes in a group of human volunteers.

Methods

First, we systematically reviewed all cases of adverse outcomes following CEW discharge that could be due to an effect on coagulation or thrombosis, with particular focus on the clinical scenario and its relationship with the weapon discharge. Second, we assessed hematocyte levels in venous blood from 29 volunteers before, 5 min after, and 24 h after receiving a full-trunk 5-s TASER® X26(E) CEW exposure.

Results

Following extensive review of the literature, we found 3 relevant case reports of possible vascular thromboembolic clinical events after CEW exposure, specifically a case of ischemic stroke, and 2 cases of ST-segment elevation myocardial infarctions. Review of these published cases failed to establish a plausible linkage to the CEW beyond a temporal association with significant emotional and physiological stress from a violent struggle.

Our prospective study of biomarker change following CEW discharge revealed acutely increased values for WBC (white blood cells), specifically lymphocytes and monocytes, and a raised platelet count. Neutrophil levels decreased as a percentage of WBC. While these changes were statistically significant at 5 min, all results remained within established reference ranges. At 24 h, all values had returned to baseline except total WBC which decreased to slightly below baseline but was still within the normal reference range.

Conclusions

A review of clinical cases, of ischemic or thrombotic events revealed no direct association with the CEW discharge. A full-trunk electrical weapon exposure did not lead to hematocyte changes beyond normal clinically expected variations in similar acute response scenarios. The case report and biomarker data do not support the hypothesis that a CEW discharge is associated with changes likely to promote coagulation or thrombus formation.

Introduction

The handheld conducted electrical weapon (CEW) deploys small probes to deliver short-duration (50–100 μs) electrical pulses to control skeletal muscle contractions. This typically leads to a loss of regional muscle control and a fall to the ground to end a violent confrontation or suicide attempt. The benefits and primary complications of the CEW are well established in numerous large studies and papers as summarized in Table 1. The aim of the present report is to review and summarize reported cases of thrombotic or ischemic vascular events in people receiving a CEW discharge. There is substantial literature describing the possibility of electrocution (CEW-induced ventricular fibrillation) and this will not be reviewed in this paper.1, 2, 3, 4 We also present the results of a biomarker study that explored whether changes in hematocytes might underlie any temporal relationship between a CEW discharge and ischemic or thrombotic events occurring in the field.

We have reviewed each of the 3 case reports of unexpected vascular sequelae temporally related to the use of a CEW and summarized them:

Case 1: Bell reported on a 32-year-old male who developed an ischemic stroke following electronic control.⁵ He presented to the emergency department following a CEW discharge to the forehead during an altercation with the police. The patient became briefly nonresponsive during the incident. Upon arrival to the emergency department, the patient had a persistent change in mental status with speech difficulty. Physical examination revealed abrasions on the forehead from the probe and generalized right-sided weakness. The past medical history was significant only for bipolar and schizoaffective disorder. The initial work-up included normal electrolytes and normal sinus rhythm on electrocardiogram (EKG). Upon further evaluation, a computed tomogram (CT) of the head demonstrated a non-hemorrhagic acute infarct along the left middle cerebral artery (MCA) territory with surrounding edema and associated mass effect. CTA and MRI/MRA of the head and neck were subsequently performed which demonstrated filling defects in the distal M1 and proximal M2 segments of the left middle cerebral artery with restricted diffusion in the MCA territory. There were no other intracranial or cervical vessel abnormalities. Subsequent work-up including tests for infections, inflammatory states, drug screening and coagulation abnormalities were normal except for mildly decreased protein S levels. Transesophageal echocardiogram was normal and HbA1c and lipid studies were negative. History of tobacco use was the only relevant cardiovascular risk factor. Heart rhythm monitoring during the hospitalization was normal. Bell suggested that the temporal relationship of the development of a stroke and probe discharge on the head in an otherwise young healthy individual presented the possibility of electrical injury-induced stroke from a combination of vasospasm and endothelial thermal injury.

Case #2: Belen reported a 37-year-old male patient with no prior cardiac history who, after an altercation with the security personnel of a hotel, collapsed after application of a CEW in probe mode to the anterior thoracic wall with pain in all parts of the body and spasms.⁶ One CEW probe entrance wound was 1 cm left of the left midclavicular line on the 6th intercostal space, and the other was 2 cm right of the anterior axillary line near the nipple level. While the patient was able to stand up with support, a crushing-like pain in the chest lasted for approximately 30 s following CEW application. The patient was admitted to the emergency service. EKG showed elevated ST segment in leads II, III and AVF, and reciprocal ST depression in leads I and AVL. The patient was conscious and had no past medical history or family history of relevance for ischemic heart disease. Physical examination showed no signs of traumatic injury or bleeding. The patient was transferred to coronary intensive care. Early laboratory tests were all normal including a drug screen. The patient was treated with aspirin, clopidogrel, isosorbide dinitrate, metoprolol, and diazepam (for sedation), and transferred for coronary angiography. Coronary angiography, 3 h after the CEW discharge, was normal and his further recovery was uncomplicated. The chest pain lasted for a total of 5 h, and the EKG normalized completely, while echocardiography showed minimal levels of inferior wall hypokinesia. The patient's cardiac markers peaked at 12 h: CK (1250 U/L), CK-MB (150 U/L), and troponin I (9 ng/mL). The patient was discharged on medication for secondary prevention and remained without symptoms at follow-up. In this case, it is possible that the effects of extreme stress could have led to a form of stress-related cardiomyopathy (similar to Takutsubo syndrome).⁷

Case # 3: Baldwin reported a case of a 20-year-old man involved in a brawl who received a TASER® X26 discharge to the upper right posterior part of the thorax and in the right buttock consisting of two 5-s activations of the device.⁸ The man did not sustain a significant fall, but was brought to the hospital in custody an hour later to have the probes removed whereupon, having initially been pain free, he developed burning retrosternal pain accompanied by dyspnea. He was treated with aspirin and nitroglycerin paste, and his symptoms subsided. The initial EKG showed ST elevation in the inferior leads. Urgent coronary arteriography revealed normal coronary arteries but left ventriculography showed hypokinesis of the distal inferior wall, and a normal ejection fraction. Four hours after the onset of chest pain, the EKG showed evolution of an inferior infarct. The initial serum troponin was 0.66 ng/mL and peaked at 10.73 (reference < 0.04); serum creatine kinase (CK) was 373 U/L and peaked at 1016 (reference < 230); and CK-MB was 7.3 ng/mL and peaked at 52.5 (reference < 7.7). The patient was taking no prescribed medications, and a drug screen was normal, but he reported regular use of Finaflex (Redefine Nutrition), an over-the-counter anabolic steroid supplement for muscle building. There were no other risk factors for ischemic heart disease although throughout his hospitalization, his blood pressure was elevated in the range of 146/90–190/98 mmHg. He had no further symptoms, and he was discharged with secondary prevention medications and was advised to stop taking the anabolic steroid supplement.

This subject had been engaged in a physical altercation prior to his myocardial infarction.⁹ Although a 10-s TASER exposure can lead to nominal cardiovascular response, this is much less than simulated combat and fleeing.⁹ Furthermore, anabolic steroid use and other fat-burning supplements are associated with premature cardiovascular complications including acute myocardial infarctions or coronary vasospasm.¹⁰ Nevertheless, the latter 2 reports hint at the possibility of acute myocardial injury due to coronary vasospasm in the presence of normal coronary arteries.

In addition to a case review, we also wanted to establish whether there are any effects on blood contents, specifically hematocytes, as a result of a CEW discharge that might predispose at-risk individuals to sustain coagulation or thrombotic-related sequelae.