CS (o-chlorobenzylidenemalononitrile)

CS has been an object of study in multiple animal studies. Systemic absorption of CS is primarily through the respiratory tract. After exposure of radiolabeled CS in rats, the tracer was seen mainly in the gastrointestinal tract, urinary bladder, mouth, and esophagus at one-hour post-exposure. By 24 hours, most of the residual radioactivity presented at the mouth, salivary glands, gastrointestinal tract, and urinary bladder.[14] There are two metabolic pathways for CS. Most will be hydrolyzed (approximately 90%) to 2-chlorobenzaldehyde and malononitrile, or it can be reduced (approximately 10%) to 2-chlorobenzyl malononitrile.[15] In humans, the half-life of CS, 2-chlorobenzaldehyde, and 2-chlorobenzyl malononitrile was found to be 5, 15, and 660 seconds respectively.[15] The liver is thought to be involved in the metabolism of CS as half-lives increased in rats with their hepatic circulation excluded.[16] No changes in half-life occurred when the kidney’s circulation was excluded in rats. Studies of elimination of CS showed that 50 to 60% disappeared by unknown means.[14] No similar studies are available in humans. The rest of the radiolabeled CS in rats was found mostly (44 to 100%) in the urine, 1 to 23% in feces and less than 1% recovered in respiratory CO.[16]

CN (chloroacetophenone)

There is very little data on the kinetics of CN. The metabolism of CN has not received thorough study. Though it is known that CN is eventually converted to an electrophilic metabolite. It can act as an SN2 alkylating agent and will react with the SH groups and nucleophilic sites of macromolecules, which can result in the disruption of cellular processes.[6] There is limited data on the absorption, distribution, and elimination of CN.

OC (Oleoresin Capsicum)

The gastrointestinal tract readily absorbs capsaicin. Intravenous infusion of capsaicin in animals resulted in rapid central nervous system uptake.  Subcutaneous administration resulted in a slow diffusion from the site of administration. Metabolism of capsaicin occurs mostly within the liver, with a small contribution by the kidney, lungs, and small intestine.[6] On the skin, capsaicin’s major metabolic pathway is via hydrolysis, which produces vanillylamine and vanillic acid. When metabolized by the liver, the three major metabolites were 16-hydroxycapsaicin, 17-hydroxycapsaicin, and 16,17-dihydrocapsaicin.[17] Capsaicin and its metabolites get excreted in the urine.[6]

Patients exposed to riot control agents often present reporting exposure to a noxious gas or spray. Symptom onset occurs within 20 to 60 seconds of exposure, usually beginning with ocular and respiratory symptoms.[1][6]  Other symptoms include burning pain, irritation, inflammation of the eyes, respiratory tract, and skin. Systemic symptoms may include cough, shortness of breath, chest pain, headache, dizziness, or syncope.[5][1]  Patients exposed to high concentrations or in poorly ventilated areas may have more severe symptoms. These severe symptoms include bronchospasm, hemoptysis, chemical pneumonitis, pulmonary edema, asphyxia, and even death.[1]

Physical findings of the eyes may include lacrimation, conjunctival injection, blepharospasm, photophobia, conjunctivitis, and periorbital edema. Riot control agents typically do not cause significant ocular injury, but they can occur.[2][3]  Reported ocular injuries include hyphemia, uveitis, necrotizing keratitis, coagulative necrosis, secondary glaucoma, cataracts, and traumatic optic neuropathy and loss of sight.[5][1]  Some of these injuries can be due to explosive devices, an organic solvent vehicle, or unintentional self-injury from the forceful rubbing of the eyes. Skin manifestations could include erythema, rashes, purpura, desquamation, vesicles, blistering, 1st, 2nd, or 3rd-degree burns, scaling and subcutaneous edema.[6][1][5] The severity of skin effects gets exacerbated by moisture. CN has been noted to cause more severe dermal injuries compared to CS [3]. Delayed dermal manifestations like allergic contact dermatitis and acute generalized pustulosis can appear about 12 to 24 hours or more after exposure.[1][6]

In most cases, symptoms are self-limited and resolve spontaneously within 10 to 30 minutes after removal from the source.[6] Cough and shortness of breath may persist, especially of patients have intrinsic lung disease. In animal studies, a significant reduction in minute ventilation was noted in both CS and OC exposure but may also be due to the organic solvent.[3] Visual acuity typically returns to normal within this same time frame. Erythema of the lid margins and photophobia could last longer.[6] Runny nose and salivation may last for about 12 hours, and headaches can remain for up to 24 hours. Erythema of the skin typically resolves within an hour, while blistering and more severe lesions usually resolve within four days.[1]

Hazardous materials management principles apply with initial decontamination by copious irrigation first to both treat the victim and prevent responders and healthcare professionals from becoming contaminated. It is unlikely but possible depending on the setting that workers could be exposed to riot control agents and become symptomatic. Providers will need to exercise reasonable judgment, unless other traumatic injuries demand immediate resuscitation, the patient needs decontamination before entering the healthcare environment. After initial stabilization, decontamination may be considered depending on the setting; this can initially start in the field if a patient is presenting via EMS. Aerosolized gases are heavier than the surrounding air, which is why an incapacitated patient should get lifted off of the ground, EMS vehicles should also try to park in higher areas than where the dispersion of gases occurred.Initial on-scene irrogation of the eyes especially is important. Use of topical ophthalmic anesthetic drops, such as proparicaine, helps with the ability to perform adequate eye irrigation.

Hospital workers can use customary personal protective equipment. Removal of contaminated clothing and prompt decontamination may be performed, including flushing the eyes and skin with copious amounts of water. If explosive devices were used to disperse agents, a close inspection of the skin and eyes should be performed to evaluate for foreign bodies, lesions, and shrapnel. Depending on the extent of ocular symptoms, a more detailed ophthalmologic exam with corneal fluroscein staining could be an option.[1]  If there are concerning pulmonary signs or symptoms, pulse oximetry, arterial blood gas analysis, and chest radiography can be obtained to evaluate for acute lung injury. There are no routinely available laboratory tests for identification or confirmation of riot control agent exposure.

Management of patients exposed to riot control agents should begin with the customary resuscitative priorities of securing the airway, ensuring adequate oxygenation and ventilation, and supporting hemodynamics. The face should be wiped with a moist towel to remove any particles before being washed. Copious water irrigation with soap should be used to remove contaminants. If there is significant skin breakdown, saline irrigation is the best choice.[1] Other solutions (milk, baby shampoo, antacids) have been investigated and have had mixed data regarding their benefit, but do no further harm. Diphoterine, a chelating compound, in research models appears to be effective in decontaminating a variety of chemical splashes to the skin or eyes, but is generally not available in many clinical settings, and decontamination with water should not be delayed while searching for alterantive decontamination fluids .[2]

Management of ocular exposures involves copious irrigation with water or saline. Irrigation should occur for at least 10 to 20 minutes but can continue longer if the patient continues to have ocular symptoms. Remove contact lenses before irrigation. A topical anesthetic should be used to reduce pain and blepharospasm, and improve irrigation.[1] With CS exposures, soap or shampoo can be added to irrigation since CS is sparingly soluble in water. Diphoterine has also been noted to be effective for ocular irrigation and may prevent further chemical injuries to the eye. In patients with severe chemical injuries, systemic corticosteroids can reduce inflammation.[18] For significant corneal injuries, there should be consultation with ophthalmology.

The majority of respiratory symptoms following exposure to these agents are mild and self-limited, most resolve within 10 to 20 minutes after removal from exposure. Management of respiratory symptoms is largely supportive. Suctioning is an option for patients with copious secretions. If bronchospasm is present beta-agonists agonists and steroids can be administered. Patients with asthma, emphysema, or bronchitis may present with an acute exacerbation. Very rarely, these agents can precipitate laryngospasm, causing respiratory failure, requiring intubation and mechanical ventilation. Late findings are rare but may include reactive airway dysfunction and pulmonary edema. Treatment of acute lung injury is supportive and may include supplemental oxygen, non-invasive ventilation, or mechanical ventilation depending on the severity.[1]

Gastrointestinal symptoms are uncommon, but some patients will have nausea and vomiting. If oral exposure to the spray occured this may increase the liklihood of gastrointestinal symptoms. Symptomatic treatment with intravenous rehydration, antiemetic agents, and electrolyte replacement is generally adequate. Given that the gastrointestinal symptoms are typically minor and self-limited, decontamination techniques including gastric lavage or charcoal is not necessary.[1]

In law enforcement or military training environments, diphoterine may be useful as pre-treatment. In one study, police officers prophylactically exposed to diphoterine solution had less facial pain after entering a CS cloud and returned to action sooner.[12]

Most exposures to either pepper spray or tear gas will present with a history of exposure to one of these agents and will have typical symptoms. Unknown exposures will be much less likely. Other agents that may have similar presenting symptoms could include cholinergic toxins, pulmonary irritants, or aerosolized caustics.

Tear gas and pepper spray usually are nonlethal agents and therefore usually have an excellent prognosis. In the vast majority of cases after removal from the exposure, resolution of symptoms will occur within 10 to 20 minutes. In some cases of prolonged exposures, patients can have more serious injuries and respiratory complications. In most of these cases, patients typically improve relatively quickly. Patients repeatedly exposed to these agents may develop slight diminihsed lung function by formal pulmonary testing.

Death after exposure is extremely rare, but reports do exist. Post-mortem findings in patients examined after prolonged exposure to lacrimator agents included pulmonary edema, focal intra-alveolar hemorrhage, and necrosis of the respiratory mucosa with pseudomembrane formation, early bronchopneumonia, serosal petechiae, cerebral edema, and hepatic fatty metamorphosis.[19]

The majority of exposures to lachrymator agents are benign with their irritant effects revolving within 30 minutes.[6] Rarely serious exposure can lead to more severe injuries to the eyes, dermis, and respiratory tract. Acute injuries of the eye can include hyphemia, uveitis, necrotizing keratitis, cataracts, and traumatic optic neuropathy, which can ultimately result in decreased or lost vision.[5][1]  Injuries to the dermis can range from a mild rash, up to severe full-thickness burns.[6][1][5] Severe respiratory injuries include bronchospasm, chemical pneumonitis, pulmonary edema, and asphyxia requiring intensive care. Death is rare.[19]

 Consultation with a medical toxicologist and/ or regional poison center in the United States can occur by calling (800) 222-1222.

While the use of the lacrimator agents has been banned in warfare for many years, they are still in use by law enforcement and civilians for personal protection.[14] Increasing use to disperse crowds has occured during protests in the U.S. and elsewhere, to the point where exposure to these agents can be anticipated in advance. Educate patients by offering reassurance that the vast majority of symptoms will resolve within 10 to 20 minutes, and most do not need medical treatment. If the patient is likely to be exposed while engaged or observing a protest event, medical aid stations with adequater supplies of water and anesthetic eye drops can be set up to start field treatment early. Asthmatics should carry a rescue inhaler with them if participating in such events. Only 25% of lacrimator exposures undergo evaluation in healthcare facilities.[10] Persistent ocular symptoms should undergo a formal eye examination.

Most exposures will be clinically stable and can undergo decontamination prior to direct medical treatment. Recognizing the excellent prognosis of most lacrimator exposures may help emergency departments, poison control, nurses, and pharmacists deal with mass casualty events. All these various disciplines need to collaborate across interprofessional lines to deliver optimal care.[Level V] The majority of patients will have self-limited symptoms; however, those with persistent respiratory or ocular symptoms will need further evaluation and treatment [Level V].