Less Lethal Force


Christopher B. Colwell, MD, FACEP, Director, Department of Emergency Medicine, Denver Health Medical Center, Denver, CO.

Aaron Eberhardt, MD, Department of Emergency Medicine, Denver Health Medical Center, Denver, CO.

Peer Reviewer:

Gina Piazza, DO, FACEP, Associate Professor of Emergency Medicine, Georgia Health Science University, Augusta, GA.

My hospital has a contract to provide medical care to the county jail. At any one time, there are more than 10,000 inmates in the county jail facilities supervised by the sheriff's office. We often see patients who are in custody and have sustained trauma, sometimes from less than lethal weapons. In my humble opinion, these devices reduce the risk of injury to the law enforcement officer when attempting to arrest or control a violent individual, and they greatly reduce the risk of serious injury or even death to the violent individuals themselves. However, even these less than lethal force weapons can cause significant damage when used at close range or on individuals with underlying medical conditions that render them vulnerable to the effects of these weapons. Like other conditions we see, the challenge to the emergency physician is to detect the uncommon patient with serious injuries among the large population of walking wounded.

— J. Stephan Stapczynski, MD, FACEP, Editor


The local team has just won the national championship at home, and the city-wide celebration has begun. Things have quickly gotten out of hand, and groups of celebrants have turned violent and are assaulting people in the street and setting cars on fire. Law enforcement has been called in to help control the situation. Law enforcement officers have deployed pelargonic acid vanillylamide (PAVA) balls, pepper spray, 40 mm rubber and wooden bullets, and conducted electrical devices on several groups of rioters, and EMS has been called to evaluate those in custody. Scene safety for EMS providers continues to be an issue, and EMS can no longer stay on scene with the patients. Forty patients are now coming to you complaining of various pains, and some are short of breath. How are you going to prepare for their arrival? What injuries are you most concerned about, and who will need your attention first when they arrive? How can you best triage these patients to ensure their safety while still maintaining control of your emergency department?


The use of less lethal force by civilian law enforcement personnel originated during the 1960s during the civil rights and anti-war movements. These movements helped to create situations in which large gatherings of people were coming into contact with law enforcement officers. Given the emotional undertones to many of these situations, violent encounters were becoming more prevalent. As such, less lethal methods of crowd/riot control became a greater focus of attention for law enforcement. At the time, chemical irritants were the most prominently used method of riot control. These methods were essentially the civilian by-product of military research and chemical weapons programs.1 Other weapons, including wooden, rubber, and "bean bag" bullets, were also being introduced, but given constraints on civilian law enforcement budgets, these suffered from the lack of testing before being used.2 Electric shock devices based on the cattle prods used in livestock control were also initiated.

The increased use of these weapons during well-publicized events helped drive early policy makers to call for limiting the use of lethal weapons and developing alternatives to lethal weapons. In 1968, The Report of the National Advisory Commission on Civil Disorders recommended that local officials, "Develop guidelines governing the use of control equipment and provide alternatives to the use of lethal weapons. Federal support for research in this area is needed."3

In 1985, a landmark Supreme Court decision placed significant attention on the subject of less lethal force. The Supreme Court case (Tennessee v. Garner) involved a 15-year-old who was killed fleeing the scene after stealing $15. The decision limited the permissible use of deadly force against fleeing suspects and helped to push progress in the area of less lethal force.4

In response to this decision, Attorney General Edwin Meese convened a conference in 1986 focusing on less lethal force. After this conference, the National Institute of Justice established a less lethal technologies program. This program expanded over the years to include research, development, and testing of less lethal weapons. The incident between law enforcement and the Branch Davidians in Waco, TX, in 1993 served to further accelerate efforts in the development of less lethal weapons technology. Private industry also began to develop and market less lethal force weapons for both law enforcement and as personal protective weapons for private citizens, which is now a multi-million dollar industry, with TASER International reporting $22.9 million in net sales for the fourth quarter of 2010.5 With this increasing availability and use of less lethal weapons, the practicing emergency medical provider can expect to see patients that have been subjected to these devices.

Historically, the term "non-lethal" has been used to describe these weapons. It is important to recognize that the term "less lethal" is more appropriate, as there have been reported deaths following the use of these weapons. While in most cases less lethal options offer a safer alternative to traditional use of force, it would be difficult to establish any weapon as non-lethal under all circumstances, given the variety of situations these methods may be used in. As an example, less lethal means are now being recognized as a preferable alternative, when possible, in subduing a person who may be suffering from excited delirium, a condition that some have argued is potentially fatal regardless of how it is managed, where commonly more lethal methods may have been used.

Common misconceptions about less lethal methods include that they are or should be painless. They are not. All less lethal systems use discomfort to encourage submission and compliance. Another misconception is that they are harmless. Because less lethal systems are distance and target sensitive, they are capable of causing blunt or penetrating traumatic injury, even when used appropriately. When used as an alternative to more lethal force, less lethal methods almost certainly provide a preferable alternative.

In general, less lethal methods fall into three broad categories: conducted electrical devices (CEDs), riot control agents, and specialized projectiles. This paper will discuss the basic science behind these weapons, some of the controversy surrounding use of these weapons, and a practical clinical approach when encountering a patient in the ED who has come into contact with these weapons.

Conducted Electrical Devices

Figure 1: CED Barb

weapons fig1.pdf

Image courtesy of Christopher Colwell, MD.

Figure 2: CED Barbs

weapons fig2.pdf

Image courtesy of Christopher Colwell, MD.

Description. Some of the most common less lethal devices used by law enforcement agencies in this country are CEDs, with the most common of these being the products made by TASER International, commonly referred to as the TASER®. These devices work by delivering a series of pulsed electrical shocks and can deliver these shocks in two ways. In the first method, two metal barbs that are propelled toward a target deliver the pulsed shocks. The barbs remain connected to the deployment device by two insulated wires. (See Figures 1 and 2.) When engaged, the device delivers pulsed electrical shocks of 0.36 joules at up to 50,000 volts. The 0.36 joules delivered per second is about 1/100th of what is considered dangerous to the human body. This method is commonly referred to as the "probe mode." (See Figure 3.) The probe mode has a distinct advantage of being able to be deployed up to 35 feet away from the subject, although greatest accuracy is in the range of 12 to 15 feet.6 This has the benefit of potentially reducing the amount of physical contact between officer and subject. This can be beneficial for both the law enforcement officer and the subject. Shocks of the same strength can also be delivered in the "stun mode," in which direct contact is made between the front of the device and the subject. (See Figure 4.)

Figure 3: CED in Probe Mode

weapons fig5.pdf

Image courtesy of TASER International

Figure 4: CED Stun Mode

weapons fig6.pdf

The goal of the CED is to induce skeletal muscle contraction, rendering the subject motionless, or, in other words, temporary incapacitation by "electro-muscular disruption" without inducing loss of consciousness. The ultimate objective is to assist in the submission of a subject without causing any permanent or long-term damage. While the device is capable of being deployed on any part of the body, it is commonly recommended that the face and genitals be avoided. TASER International describes the suggested target zones for CEDs as low center of mass (below the chest) when shooting the front of the suspect, and below the neck and away from the spine when shooting the suspect from behind, taking care to avoid the head, chest, genitals, or known injury sites when operationally feasible.5

Epidemiology. As described in the introduction, there is increasingly widespread use of CEDs in both law enforcement agencies as well as for personal use. It is estimated that approximately 15,500 law enforcement agencies from 40 countries currently use CEDs.7 Many thousands of CEDs have also been sold to private citizens for personal use.5 Given the widespread use of these devices and the variance in how they are medically evaluated, it seems reasonable to assume that the practicing emergency physician may be called upon to evaluate a patient after coming into contact with one of these devices.

Physics of the Conducted Electrical Device. Understanding the basics physics of how CEDs work will help in the overall understanding of the potential physiological effects on patients. Deaths have occurred after shocks delivered from common household electrical sockets, which are 110 volts or less, while CEDs can deliver up to 50,000 volts to a subject and appear not to directly induce bodily injury or death. If voltage were the only determinant of injury severity, birds would not perch themselves on 10,000-volt high power lines. A common adage in physics states, "It's not voltage that kills, its current!" While this is essentially correct, a little more explanation is needed.

Figure 5: Ohm's Law

Voltage = Current × Resistance

The basic concepts of electrical injury are based in Ohm's Law. (See Figure 5.) Voltage is a measure of how much potential energy exists to move electrons from one point to another within a circuit. The actual movement of the electrons is the current, measured in amperes. The resistance is the force in the circuit that opposes the flow of electrons. A commonly used analogy to help understand these concepts is to think about a contained plumbing system. The voltage is equivalent to the water pressure that can be created by a water pump, the current is equivalent to the actual flow rate of the water, and the resistance is equivalent to the size of the pipes.

Figure 6: Rearranging Ohm's Law

Current = Voltage / Resistance

Image courtesy of TASER International

Rearranging Ohm's Law and expressing it in terms of current results in the formula found in Figure 6. Essentially, the amount of current flowing through a body is equal to the amount of voltage applied to the body divided by the electrical resistance offered by the body.8 Table 1 shows current levels as they relate to probable effects on the human body.

Table 1: Electrical Current Levels and Probable Effects on the Human Body9

Current Level (Milliamps)

Probable Effect on the Human Body

Source: www.osha.gov/SLTC/etools/construction/electircal_incidents/electrical.html

1 mA

Perception level

Slight tingling sensation

5 mA

Slight shock felt, not painful but disturbing

The average individual can let go.

6-16 mA

Painful shock; person begins to lose muscle control

Commonly referred to as the "let go range."

17-99 mA

Extreme pain, respiratory arrest, severe muscle contraction Individual cannot let go.

100-2000 mA

Ventricular fibrillation threshold

> 2000 mA

Cardiac arrest

Internal organ damage and severe burns

Death is probable.

Most CEDs on the market today deliver approximately 50,000 volts. However, the current these units deliver is only 2.1 to 3.9 milliamps.5 To put this into perspective, common household outlets are around 110 volts and create about 16 amps of current, which is at least 4000 times larger than the 2.1 to 3.9 milliamps delivered by a CED. This is only a fraction of the current required to induce a ventricular fibrillation.9

The Controversy. Manufacturers of CEDs assert that the devices provide law enforcement officers with a safer alternative to the use of lethal force.5 This is supported by statistics showing a decrease in injuries to both suspects and law enforcement officers. The city of Orlando, FL, reported a 67% reduction in suspect injuries when they added CEDs to their police force.10 Ventura County, CA, reported deputy injuries were down 70% in the first year of deployment.11 The Durham, NC, police department reported a 75% reduction in physical contacts.12 Statistics similar to these are replicated across many agencies. In fact, no agency has reported an increase in either suspect- or officer-related injury. Furthermore, a recent Department of Justice study concluded that the odds of a suspect being injured are decreased 60% when a CED is used when compared to the more traditional use of force.13 There have, however, been well-documented cases in which people have died after being exposed to a CED. It should be noted that a causal relationship has not been established between the use of the CED and the death of the subject. In many of these reports, the patient died many minutes or even hours after exposure to the CED, raising significant doubt as to whether electricity was the cause.

The occasional high-profile cases will likely continue to call into question the safety of CEDs. This occurs in spite of the fact that an estimated 640,000 criminal suspects and human volunteers have been exposed to CEDs.14 The public controversy has helped fuel scientific interest in conducting research into the safety of CEDs. In the past five years, a number of studies, case series, and case reports have helped to address the safety of CEDs.

Emergency Department Evaluation

It is common in some areas to have patients brought to the emergency department for "medical clearance" after being exposed to a CED. Many articles have researched potential injuries related to the use of conducted electrical devices and, from a clinical standpoint, there are only a few main concepts that need to be understood in order to manage these patients. These can largely be distilled down to three main questions: Does exposure to a CED cause clinically significant cardiorespiratory abnormalities? Does exposure to a CED cause clinically significant metabolic abnormalities? And, lastly, does exposure to a CED lead to significant traumatic injuries that require urgent or emergent medical evaluation and treatment?

CED and Cardiorespiratory Abnormalities. A majority of the case reports and police reports that have involved the death of a subject proximate to exposure to a CED have noted that death has occurred anywhere from 5 to 40 minutes after the exposure.15 If the shock itself induced cardiac instability leading to a lethal dysrhythmia, it would be expected to do so within seconds, not minutes, of the CED exposure.

A number of studies have looked at whether exposure to a CED induces dysrhythmias.16-21 None of these studies found dysrhythmias or any other clinically significant ECG changes, including ectopy, QT prolongation, or interval changes, in ECG findings. Additionally, a number of studies have trended troponin levels after CED exposure and found no troponin elevation, with one exception.17,14,20,22 The one patient who had an elevated troponin had a one-time increase at the 24-hour draw of 0.6 ng/mL (from a baseline negative of value of < 0.3 ng/mL). The patient received an extensive cardiac evaluation, including treadmill testing and myocardial perfusion studies. Both tests were interpreted as normal, and the patient's troponin level was back to 0.3 ng/mL 8 hours after the elevated lab draw.14 Ho et al, in a study published in the Journal of Emergency Medicine in 2009, looked at 25 human volunteers who exercised to exhaustion and then were subjected to a 15-second CED application. The researchers concluded that prolonged application in exhausted individuals did not produce a detectable change in the ECG.23 Some studies have also looked at delayed ECG changes and have found no significant changes after 60 minutes or more.15,14,20 Lastly, two studies had patients connected to echocardiography to analyze if there were any apparent functional abnormalities in the heart during CED exposure; they found none.18,19 It should be noted that most of these studies look at CED exposures of 15 seconds or less.

Based on the current literature, routine ECG, telemetry monitoring, and cardiac ischemia evaluation with troponin measurement are not warranted in the awake and asymptomatic patient who has received 15 seconds or less of CED exposure.

CED Exposure and Metabolic Abnormalities. Many of the early studies that evaluated the physiologic changes seen after relatively short exposures to CEDs were performed on healthy volunteers or animals, mostly swine.20,24 The changes seen during these studies include a mildly elevated lactate, as well as a decrease in pH and bicarbonate. These metabolic derangements all returned to baseline within 30 minutes (human) to a few hours (swine). While these studies seem to indicate clinically insignificant changes in physiology, the fact that the subjects were clinically healthy volunteers and animals raises the question of how applicable these results are to the population of often agitated and/or intoxicated individuals on whom these devices are used. Healthy individuals under normal circumstances can handle large physiologic and metabolic stress without significant clinical consequences. Do these weapons cause physiologic alterations that, while clinically insignificant in healthy individuals, may be harmful in at-risk populations?26

Some studies have attempted to better simulate these conditions by analyzing the effects of CED exposure of physically exhausted human volunteers and have found that the metabolic derangements remain clinically insignificant.23,25 Furthermore, a large, prospective, multicenter analysis of 1,201 "real life" exposures to CED in 2009, which primarily looked at traumatic injury, yielded only one patient with rhabdomyolysis that was not clearly linked to CED exposure, and no other apparent significant physiological changes manifested in this population.27

The conclusions of these studies are that while some metabolic derangements do occur after CED exposure, they are transient and not clinically significant. Therefore, in an asymptomatic patient, there is no evidence to support routine laboratory evaluation of patients based solely on CED exposure.

CED Exposure and Traumatic Injuries. Exposure to the CED itself causes very little traumatic injury. The most common traumatic injuries seen after CED exposure are the puncture wounds caused by the barbs that are fired from the device. Commonly, providers are called on to remove the bards from the CED that remain embedded in the skin. The barbs are relatively easy to remove. First, ensure that the electrical device is no longer engaged. Second, cut the insulated wires connecting the barbs to the device. Next, stabilize the skin around the barb with your non-dominant hand. Firmly grab the barb at the base close to where it enters the skin. With a quick, firm movement, pull the barb out of the skin. After removal, inspect the barb to ensure that you have removed the entire barb and that no foreign body remains embedded in the patient. If you are unsure, a quick X-ray may be helpful. Finally, provide local wound care to the affected area.

It is important to keep in mind that there is always the possibility of traumatic injury secondary to falls or as a result of physical altercations with police. These injuries should be treated as clinically indicated. There is also a case report of thoracic compression fractures in a healthy volunteer who did not fall after exposure to a CED.28 The etiology of these fractures was thought to be the extensive muscle contraction induced by the device, so if a patient has significant orthopedic complaints following exposure, appropriate clinical evaluation is warranted. It should be noted that falls after exposure to CEDs have resulted in significant injury and even death. Strote et al published the experience of the Seattle police department with CEDs over 6 years in the Journal of Trauma in 2010 and concluded that significant injuries were rare and admissions to the hospital were not related to law enforcement restraint. They did find one patient who had a positive troponin I. This patient was contacted by police after exhibiting very strange behavior (agitation and eating dirt). Furthermore, on medical evaluation, the patient was noted to have a toxicology screen that was positive for cocaine and methamphetamines, suggesting that this patient's elevated troponin was possibly multifactorial.29 Bozeman et al did find two intracranial injuries resulting from falls after exposure to CEDs, but went on to conclude the 99% of subjects do not experience significant injuries after CED use.27

In summary, deaths that have occurred following exposure to CEDs do not appear to be electrical deaths, nor does there appear to be a significant metabolic effect or direct trauma from the device itself. While some combination of toxic, metabolic, genetic, and environmental components cannot be absolutely excluded, no causal relationship can be identified based on current research. Some articles did note the high frequency of excited-delirium-related fatalities in patients who died after application of a CED, highlighting the importance of evaluating patients for the underlying cause of the behavior that resulted in the use of the CED.30

In terms of addressing concerns related specifically to the CED exposure, a recent review of the literature concluded that the current medical literature does not support routine performance of laboratory studies, electrocardiograms, or prolonged ED observation or hospitalization for ongoing cardiac monitoring after CED exposure in an otherwise asymptomatic awake and alert patient.31

Riot Control Agents

Riot control agents, sometimes referred to as chemical munitions, are highly potent sensory irritants that are designed to produce dose- and time-dependent acute site-specific toxicity. They are chemicals that interact pharmacologically with sensory nerve receptors associated with mucosal surfaces and can be delivered by spray, aerosol, or projectile ball. The desired effect of riot control agents is to temporarily disable individuals through intense irritation of the mucous membranes and skin without causing permanent damage or sequelae. Chemical munitions focus on the areas of the body where sensory irritation occurs, namely the eyes, skin, and respiratory tract. Although military experience with harassing agents had prompted the utilization of these agents by law enforcement as a means of riot control, many of the military agents were not suitable for law enforcement use due to concerns about the potential to produce total incapacitation or even fatalities. Unlike what may be called for in some military situations, riot control agents are intended to induce temporary disablement that is safe, effective, and can be disseminated readily. Commonly used riot control agents include chemical irritants such as oleoresin capsicum (OC) (also known as pepper spray), 1-chloroacetphenone (CN) (otherwise known as Mace), chlorobenzylidene malononitrile (CS), Adamsite (DM), and dibenz 1:4-oxazepine (CR).

Diphenylaminochloroarsine was developed as a chemical variant of diphenylchloroarsine and is commonly known as Adamsite, with the military designation DM. It was produced worldwide until it was superseded by the CN-series (Mace).32 Mace was first synthesized in 1871, was used in World War I, and was the primary tear gas used by law enforcement and the military through the 1950s. CS stands for Corson and Stoughton, who first synthesized it in 1928 and replaced CN in military use in the 1950s. By the 1990s, oleoresin capsicum (OC) had become the standard chemical munition used.

Oleoresin capsicum (pepper spray) has been increasing in use since the 1980s, with numerous commercial pepper spray products available over-the-counter for personal use as well as for law enforcement. It is a mixture of fat-soluble phenols called capsinoids and is derived from the natural oily extract from pepper plants in the genus Capsicum. Capsaicin makes up 80-90% of these capsinoids that make up OC. OC acts as a direct nerve irritant (pain) and stimulant for the release of peripheral neuropeptides. It binds with pain receptors that are responsible for sensing heat and initiates a response that results in the sensation that heat is being released at the site of contact. Capsinoids have been shown to produce a neurogenic inflammatory response in human skin that is accompanied by a concomitant increase in sensitivity to elevated temperature, sensations of stinging and burning, and the development of erythema.33 It is not flammable and can be delivered by spray (5-15 feet) or projectile ball (30 feet or more). The Denver Police Department has used pelargonic acid vanillylamide (PAVA), a synthetic pepper derivative, instead of OC with its Pepperball devices since 2001. There are seven levels of heat within the capsinoids, and PAVA represents the hottest of the seven. We are not aware of any studies comparing outcomes of the synthetic compounds to OC.

The clinical effects result from irritation and inflammation of the skin, eyes, and mucous membranes and include a burning sensation of the skin, eyes, and mucous membranes as well as increased lacrimation and mucous production. Specifically, at the biochemical level, capsinoids stimulate chemoreceptors in primary afferent nerve endings, resulting in immediate pain and burning sensation over exposed areas of the skin, ocular, nasal, and oropharyngeal tissues. They also cause the release of peripheral neuropeptides, including substance P, a neurotransmitter involved in neurogenic inflammation that can cause vasodilation, capillary leakage of plasma fluids, and pain sensation. Some have reported temporarily being unable to speak after exposure to pepper spray. No causal relationship with deaths in custody has ever been shown from the use of pepper spray. In 2000, Zollman et al looked at the effects of oleoresin capsicum on the human cornea and conjunctiva and found no serious or permanent ocular sequelae.34 This is in contrast, however, to other case reports that have noted more serious and, in some cases, permanent anterior eye damage as a result of being exposed to OC.35,36

Treatment is focused on relief of the burning sensation associated with exposure to these agents, including cool water to the affected areas, fresh air, and management of any underlying conditions that may have been exacerbated by exposure to the agent. In particular, exacerbations of asthma, COPD, and sickle cell disease have been described in association with exposure to riot control agents. A number of topical therapies have been proposed to treat acute pain from exposure to pepper spray. In a study published in 2008, Barry et al looked at five treatment regimens for pain from topical exposure to OC, including Maalox, 2% lidocaine gel, baby shampoo, milk, and water and found no significant difference in the pain relief provided by any of the five regimens. Time after exposure appeared to be the best predictor for decrease in pain.37

In summary, substantial evidence suggests that riot control agents are safe when used as intended. Medical management will most often focus on symptomatic relief and management of underlying medical conditions. Much like when managing patients who have been exposed to CEDs, it is important to consider what underlying condition or issue may exist that led to exposure to the riot control agent. It is this condition that may pose the greatest risk to your patient.

Specialized Projectiles

Specialized projectiles, also called impact rounds, are projectiles that are shot out of a gun and are designed to provide stopping power by inducing pain through blunt trauma without inducing serious injuries. Specialized projectiles are used by law enforcement to incapacitate individuals or as a riot control/crowd dispersal device.

Impact rounds are broadly classified into two categories: direct fire and indirect fire. Direct fire rounds are shot directly at the target, while indirect fire rounds are designed to be fired into the ground in front of the target and to rebound or bounce into the target. This design allows for dissipation of the projectiles' energy prior to striking the target.

Despite being shot from relatively high-powered guns, specialized projectile weapons are designed to employ the concept of kinetic energy to provide a less lethal means of incapacitation or subject control.

The kinetic energy of an object is the energy that the object possesses because of its motion. The kinetic energy of a point of mass is represented by the following equation:

Kinetic energy = 1/2 mv2

An object in motion can do "work" on anything that it hits. The kinetic energy equation quantifies the amount of work that the object can do as a result of its motion. Considering a specialized projectile shot out of a weapon, the impact round carries a certain amount of kinetic energy. The impact round can do "work" on the subject that it hits. In this case, the "work" done is infliction of pain by blunt trauma. The material used to make these impact rounds is typically less dense (less mass) than the lead normally used in bullets. The impact rounds are also fired at less velocity than traditional firearms. Looking at the equation, an object of less mass fired more slowly will have less kinetic energy and, therefore, do less "work" than a traditional bullet from a firearm. Impact rounds are also generally larger than traditional bullets and, therefore, have a greater surface area of contact, which further dissipates the energy, preventing penetration. Practically, these features of impact rounds lead to blunt trauma rather than a penetrating injury.

Types of Specialized Projectiles. Law enforcement agencies employ a number of different specialized projectiles by a number of different weapons, or launchers. While an in-depth discussion of every type is beyond the scope of this review, an emergency medicine provider should be familiar with the general categories of these projectiles.

Baton Rounds. Baton rounds are the most similar in shape and size to traditional metallic bullets. Baton rounds are cylindrical objects that are the full bore of the firearm and are typically made of plastic, rubber, foam, or wood. (See Figures 7 and 8.) In general, harder rounds are designed for indirect fire (otherwise referred to as "skip," as they are often aimed to skip off the ground before hitting the subject), while rounds made of softer material can be used for direct fire. Some baton rounds can be fired from certain launchers from as far as 75 feet away from the subject.

Figure 7: Rubber Baton

rubber baton_0001.jpg

Figure 8: Wood Baton

wood baton_0001.jpg

Bean Bag Rounds. Bean bag rounds consist of a fabric bag filled with small pellets. The fabric bag is flexible, which allows it to spread out against the target during contact. This increases the surface area of contact and dissipates the energy. Wide and flat bean bags can be shot at close range. Drag-stabilized bean bags are elliptical shaped bags with fabric tails that can be shot over longer ranges. (See Figure 9.)

Figure 9: Bean Bag Rounds

bean bag rounds_0001.jpg

Rubber Buckshot. Rubber buckshot rounds, commonly referred to as "stinger" rounds, consist of a number of small rubber pellets. By firing a number of smaller rubber pellets, each individual pellet contains much less kinetic energy than an entire baton round. (See Figures 10 and 11.)

Figure 10: Rubber Buckshot

rubber buckshot_0001.jpg

Figure 11: Rubber Buckshot Balls

rubber buckshot balls_0001.jpg

PepperBall™. PepperBall™ is a less lethal agent delivery system that uses high-pressure air launchers to deliver chemical agents from a distance. These can be used on individuals as well as large groups of people for riot and crowd control. This system combines the kinetic impact (pain) with the discomfort and panic associated with the chemical munitions. The devices will typically fire lightweight plastic spheres at high velocity (up to 400 feet per second) and can be fired from more than 30 feet away.38

Medical Evaluation. Specialized projectiles have the goal of inducing submission by inflicting a level of painful blunt trauma to the victim without permanent damage. While marketed as less-lethal weapons, there have been some notable deaths following use of these weapons. In October 2004, Emerson College junior Victoria Snelgrove, 22 years old, was killed when a round made of plastic powdered OC and bismuth, a mineral commonly confused with lead, fired by an FN 303 launcher from a police weapon struck her in the eye. The projectile was being used by Boston Police to disperse a rioting crowd after the Red Sox game. While tragic deaths like these do occur, most emergency providers will be evaluating patients who have sustained blunt trauma as a result of being struck by a projectile.

Management of these injuries will largely depend on the location of injury as well as extent of blunt trauma caused. One case series describes two patients subjected to rubber projectiles. In one case, the patient only sustained abdominal and lower extremity contusions and could be discharged relatively quickly. The other case, however, involved a patient who was shot in the low anterior chest from approximately 6 feet after the man began to mutilate himself with a knife. This patient suffered cardiac and pulmonary contusions requiring hospitalization.39 A number of significant facial injuries have also been described in the literature.40 These cases highlight the range of blunt trauma that patients can suffer. It is important for the emergency medical practitioner to understand that, while less lethal than traditional firearms, these weapons can inflict serious injuries. Management should be directed by patients' clinical presentation in accordance with accepted standards of management of blunt trauma.

Excited Delirium

Excited delirium, also referred to as excited delirium syndrome or agitated delirium, is now a well-recognized disease process seen most often by EMS providers and emergency physicians. Many patients suffering from excited delirium come into contact with law enforcement officers and, therefore, into situations where less lethal force, CEDs in particular, may be used.41 Given this, special mention of excited delirium is important to include in a discussion of the medical evaluation of patients after the use of less lethal force.

The pathophysiology of excited delirium is poorly understood. Despite the lack of a clear-cut unifying pathophysiological hypothesis, post-mortem studies of patients with excited delirium have provided some insight into the disease process. Excited delirium is commonly associated with stimulant abuse, especially cocaine. However, patients who have died of cocaine-associated excited delirium have been noted to have similar cocaine concentrations as those found in recreational users and cocaine overdoses. This suggests a different mechanism of death than simple cocaine overdose.42

Post-mortem studies of patients who have died of cocaine-associated excited delirium have demonstrated a decrease in the number of dopamine transporters in the striatum that potentially leads to dopamine dysfunction in this portion of the brain.43,44 Furthermore, these postmortem studies have found elevated levels of heat shock proteins in these patients. While this may help explain the profound hyperthermia noted in patients with excited delirium, how this dysfunction leads to the development of this disease process remains unclear.

Given the uncertainty about the exact pathophysiological basis of the disease, excited delirium is commonly defined by its clinical presentation. At a minimum, a patient with excited delirium must present with delirium and evidence of psychomotor and physiologic excitation.42

The common scenario that has been described in published cases of excited delirium involves acute drug intoxication, often a history of mental illness (especially those conditions involving paranoia), a struggle with law enforcement, physical or noxious chemical control measures or CED application, sudden and unexpected death, and an autopsy that fails to reveal a definite cause of death from trauma or natural disease.45

Given the continued uncertainty as to the exact cause and pathophysiology of excited delirium, treatment remains largely speculative and focused on supportive care and reversal of obvious clinical and laboratory abnormalities.42 Based on the usual clinical presentation of these patients, the main factors that need to be aggressively managed include agitation, acidosis, and hyperthermia.

Many excited delirium deaths follow a significant physical struggle. This physical struggle may be a significant contributor to the catecholamine surge and metabolic acidosis often seen in these patients.46 As such, physical restraint should be limited to only what is absolutely necessary to keep the patient, law enforcement officer, and the medical provider safe, taking care to avoid placing the patient in a prone position or "hog-tying" the patient. The cessation of struggling in an agitated patient should be considered an ominous sign. The initial decompensation in some situations may be respiratory arrest as opposed to cardiac arrest, so airway management and advanced cardiac life support measures may be life-saving in these circumstances.47 There are cases, however, in which the patient cannot be resuscitated even when the cardiopulmonary arrest occurs in the setting of a well-staffed and well-equipped emergency department, suggesting that cardiac arrest, in at least some of these patients, is a terminal event despite optimal management.42

Agitation should be managed with aggressive chemical restraint. The IV route of administration is preferable to the IM or IN route; however, these alternative routes of administration may be required to help calm the patient and facilitate IV placement. Commonly used agents for the control of agitation include benzodiazepines (midazolam, lorazepam, diazepam), antipsychotics (haloperidol, droperidol), or ketamine.45

Acidosis should be anticipated and managed accordingly. In cases where the acidosis may be related to hypovolemia, management should be initiated with judicious IV fluid resuscitation. Depending on the level of acidosis, bicarbonate may be given, although there has been no proven benefit in these situations. In extreme circumstances, patients may need to be chemically paralyzed and mechanically sedated. Finally, hyperthermia should also be anticipated and managed accordingly. Cooling techniques, such as those that might be used in cases of suspected heat stroke or exhaustion, are appropriate and include removal of the patient's clothes, reducing the temperature in the treatment room, and evaporative cooling techniques. Ice packs or infusion of cold saline can also be used.


There are many less lethal options available now to law enforcement officers, and it is likely that emergency physicians will be called upon to evaluate patients who have been subjected to less lethal force. Much like when air bags where first initiated in motor vehicles, there are injury patterns that do exist with each method of less lethal force, but the overall impact has been positive. The incidence of injuries associated with law enforcement use-of-force can be reduced dramatically when agencies responsibly employ less lethal weapons in lieu of more traditional uses of physical force. The overall impact of less lethal technology has been a decrease in suspect injuries, a decrease in law enforcement officer injuries, and decreased use of lethal force.48 Knowing what type of force your patient was subjected to and the specific issues related to that technology will be important when managing these events. Most deaths associated with less lethal force in the medical literature have been attributed to issues such as cocaine and methamphetamine intoxication and pre-existing underlying health conditions. Medical management will often need to focus on identifying and treating the underlying cause for the behavior that led to the use of less lethal force, such as excited delirium, acute psychosis, or drug intoxication. In addition to identifying and treating the underlying problem, medical attention may include an assessment of respiratory status, irrigation of eye and skin contacts, and wound care as appropriate. An understanding of what less lethal options can cause, and what they are unlikely to cause, will help the emergency physician focus assessment and treatment in these often difficult situations.


1. Coates J. Non-lethal police weapons. Technology Review 1972;June:49-56.

2. Ackroyd C, Margolis K, Rosenhead J, et al. The Technology of Political Control, second edition. London: Pluto Press; 1980: 205-212.

3. National Advisory Commission on Civil Disorders Report of the National Advisory Commission on Civil Disorders. New York: Bantam Books; 1969:1-29.

4. U.S. Supreme Court Tennessee v. Garner, 471 U.S. 1 (1985) Tennessee v. Garner No. 83-1035. Argued October 30, 1984. Decided March 27, 1985.

5. Taser web site. http://taser.com.

6. Meyer G. Conducted electrical weapons: A user's perspective. In: Kroll MW, Ho JD, eds. TASER® Conducted Electrical Weapons: Physiology, Pathology, and Law. Springer; 2009: 2.

7. National Institute of Justice. Police Use of Force, Tasers and Other Less Lethal Weapons. U.S. Department of Justice. Accessed at https://www.ncjrs.gov/pdffiles1/nij/232215.pdf. May 2011.

8. Herman S. Delmar's Standard Textbook of Electricity, 5th edition. Cengage Learning; 2010.

9. Occupational Safety and Health Administration construction etool: Electrical incidents. http://www.osha.gov/SLTC/etools/construction/electrical_incidents/mainpage.html.

10. Smith MR, Kaminski RJ, Alpert GP, et al. A multi-method evaluation of police use of force outcomes. University of South Carolina web site. http://www.cas.sc.edu/crju/pdfs/taser_summary.pdf.

11. "Editorial: Tasers prove their worth." Ventura County Star. March 27, 2008. http://www.vcstar.com/news/2008/mar/27/tasers-prove-their-worth/?print=1.

12. Chambers SB Jr. "TASERS cut injuries, N.C. police say." News and Observer. November 30, 2008. Accessed at www.policeone.com/police-products/less-lethal/articles/1761121-TASERS-cut-injuries-N-C-police-say.

13. Smith MR, et al. A multi-method evaluation of police use of force outcomes: Final report to the National Institute of Justice. Document Number 231176 July 2010. http://www.ncjrs.gov/pdffiles1/nij/grants/231176.pdf.

14. Ho JD, Miner JR, Lakiredy DR, et al. Cardiovascular and physiologic effects of conducted electrical weapon discharge in resting adults. Acad Emerg Med 2006;13;589-595.

15. VanMeenen KM, Cherniack NS, Bergen MT, et al. Cardiovascular evaluation of electronic control device exposure in law enforcement trainees: A multisite study. J Occup Environ Med 2010;52:197-201.

16. Bozeman WP, Barnes DG Jr, Winsolow JE 3rd, et al. Immediate cardiovascular effects of the Taser X26 conducted electrical weapon. Emerg Med J 2009;26: 567-570.

17. Ho JD, Dawes DM, Bultman LL, et al. Respiratory effect of prolonged electrical weapon application on human volunteers. Acad Emerg Med 2007;14:197-201.

18. Ho JD, Dawes DM, Reardon RF, et al. Echocardiographic evaluation of a Taser-X26 application in the ideal human cardiac axis. Acad Emerg Med 2008;15:838-844.

19. Levine SD, Sloane CM, Chan TC, et al. Cardiac Monitoring of human subjects exposed to the taser. J Emerg Med 2007;33;112-117.

20. Vilke GM, Sloane CM, Bouton KD, et al. Physiological effects of conducted electrical weapon on human subjects. Ann Emerg Med 2007 50;5:569-574.

21. Vilke GM, Sloane CM, Levine SD, et al. Twelve-lead electrocardiogram monitoring of subjects before and after voluntary exposure to the Taser X26. Am J Emerg Med 2008;26:1-4.

22. Sloan CM, Chan TC, Levine SD, et al. Serum troponin I measurement of subjects exposed to the Taser X-26. J Emerg Med 2008;35:29-32.

23. Ho JD, Dawes DM, Bultman LL, et al. Prolonged TASER use on exhausted humans does not worsen markers of acidosis. Am J Emerg Med 2009;27: 413-418.

24. Esquivel AO, Dawe EJ, Sala-Mercado JA, et al. The physiological effects of a conducted electrical weapon in swine. Ann Emerg Med 50;5:576-583.

25. Vilke GM, Sloan CM, Suffecool A, et al. Physiologic effects of the TASER after exercise. Acad Emerg Med 2009;16: 704-710.

26. Strote J, Hutson HR. Taser safety remains unclear. Editorial regarding: Vilke GM, Sloane CM, Bouton KD, et al. Physiological effects of conducted electrical weapon on human subjects. Ann Emerg Med 2007;5:569-574.

27. Bozeman WP, Hauda II WE, Heck JJ, et al. Safety and Injury profile of conducted electrical weapons used by law enforcement officers against criminal suspects. Ann Emerg Med 2009;4:480-489.

28. Winslow JE, Bozeman WP, Fortner MC, et al. Thoracic compression fractures as a result of shock from a conducted energy weapon: A case report. Ann Emerg Med 50;5:584-586.

29. Strote J, Walsh M, Angelidis M, et al. Conducted electrical weapon use by law enforcement: An evaluation of safety and injury. J Trauma 2010;68:1239-1246.

30. Strote J, Hutson HR. Taser use in restraint-related deaths. Prehosp Emerg Care 2006;10:447-450.

31. Vilke GM, Bozeman WP, Chan TC. Emergency department evaluation after conducted energy weapon use: Review of the literature for the clinician. J Emerg Med 2011;40:598-604.

32. Olajos EJ, Salem H. Riot control agents: Pharmacology, toxicology, biochemistry and chemistry. J Appl Toxicol 2001;21:355-391.

33. Pershing LK, Reilly CA, Corlett JL, et al. Assessment of pepper spray product potency in Asian and Caucasian forearm skin using transepidermal water loss, skin temperature and reflectance colorimetry. J Appl Toxicol 2006;26:88-97.

34. Zollman TM, Bragg RM, Harrison DA. Clinical effects of oleoresin capsicum (pepper spray) on the human cornea and conjunctiva. Ophthamology 2000;107:2186-2189.

35. Das S, Chohan A, et al. Capsicum spray injury of the eye. Int Ophthalmol 2005;26:171-173.

36. Kinestedt C, Fleischhauer J, et al. Pepper spray injuries of the anterior segment of the eye. Klin Monbl Augenheilkd 2005;222:267-270. (German)

37. Barry JD, Hennessy R, McManus JG. A randomized controlled trial comparing treatment regimens for acute pain for topical oleoresin capsaicin (pepper spray) exposure in adult volunteers. Prehosp Emerg Care 2008;12:432-437.

38. Pepperball web site. http://www.pepperball.com. Accessed Aug. 22, 2011.

39. Wahl P, Schreyer N, Yersin B. Injury pattern of the Flash-Ball, a less lethal weapon used for law enforcement: Report of two cases and review of the literature J Emerg Med 2006;31:325-330.

40. Khonsari RM, Fleuridas G, Arzul L, et al. Severe facial rubber bullet injuries: Less lethal but extremely harmful weapons. Injury Int J Care Injured 2010;41:73-76.

41. Jauchem JR. Deaths in custody: Are some due to electronic control devices) including TASER devices) or excited delirium. J Forensic Legal Med 2010:1-7.

42. Vilke GM, De Bard ML, Chan TC, et al. Excited delirium syndrome (EXDS): Defining based on a review of the literature. J Emerg Med In press. 8/10/11.

43. Mash DC, Duque L, Pablo J, et al. Brain biomarkers for identifying excited delirium as a cause of sudden death. Forensic Sci Int 2009;190:e13-19.

44. Mash DC, Pablo J, Ouyang Q, et al. Dopamine transport function is elevated in cocaine users. J Neurochem 2002:81:292-300.

45. American College of Emergency Physicians Excited Delirium Task Force.White Paper Report on Excited Delirium Syndrome. September 10, 2009.

46. Ho J, Dawes D, Ryan F, et al. Catecholamines in simulated arrest scenarios. Australasian College of Emergency Medicine Winter Symposium; June 25, 2009.

47. Sztajnkrycer MD, Baez AA. Excited delirium and sudden unexpected death. American College of Emergency Physicians web site (www.ACEP.org), Tactical Emergency Medicine Section. Accessed 8/15/2011.

48. MacDonald JM, Kaminshi RJ, Smith MR. The effect of less-lethal weapons on injuries in police use-of-force events. Am J Public Health 2009;99:2268-2274.