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Neurosurg Focus 12 (3):Article 3, 2002, Click here to return to Table of Contents

Common chemical agent threats

RANDALL R. MCCAFFERTY, M.D., AND PETER J. LENNARSON, M.D. Neurosurgical Services, Wright-Patterson Air Force Base, Ohio

The events of September 11, 2001, highlight the fact that we live in precarious times. National and global aware- ness of the resolve and capabilities of terrorists has increased. The possibility that the civilian neurosurgeon may con- front a scenario involving the use of agents has heightened. The information reported in this paper serves as a primer on the recognition, decontamination, and treatment of trauma patients exposed to chemical war- fare agents.

KEY WORDS • chemical warfare • terrorism • casualties • war

Prior to , chemical agents were considered tion to choking, , and blood agents, nerve agents but were infrequently used or ineffective products of war- were being produced in mass quantities. Despite signifi- fare. The Chinese used as early as 1000 cant efforts by all parties to garner intelligence on the B.C. The Spartans used noxious smokes during the Pelo- capabilities of opposition forces, the magnitude of chemi- ponnesian War. During the American Civil War, numer- cal weapons programs was not fully understood until after ous proposals for the use of , , , the war. and hydrochloric and sulfuric were developed; how- Throughout the remainder of the 20th century, chemical ever, most proposals were likely never acted upon. weaponry continued to be developed and used in major With the onset of World War I, few people believed that wars around the world. Those involved in international the proposals and research into chemical weapons would organizations and treaties continued to define and restrict result in any significant battlefield operations. Initial at- various aspects of chemical weapons programs as well as tempts at chemical warfare were ineffective against oppo- in the more recently developing atomic and biological sition forces. In April and May of 1915, German forces programs. As recently as the Persian Gulf War, the alleged successfully deployed large stores of chlorine by wind use of nerve and mustard agents by Iraqi troops has been drift against Allied forces defending Ypres. Within the reported. Following that war, there have been reports of next 2 years, the chemical warfare techniques practiced chemical agent use ordered by Saddam Hussein against by German and Allied forces evolved into the use of Kurd and Shiite Muslims as well as proliferation of chem- gas, , and vesicants. In addition, both ical weapons development in Libya. forces were supplied with chemical protective devices, Finally in 1993, the long awaited Chemical Weapons including gas masks. By Armistice Day in 1918, 26 mil- Convention was finalized. This treaty prohibited the de- lion casualties were recorded, approximately 1 million of velopment, production, stockpiling, and use of chemical which were attributable to gas warfare. weapons and provided for the verification and destruction In the years between World War I and World War II, of known stockpiles. Although 130 countries signed the new chemical weapons and protective and deployment ca- treaty, notable exceptions included Iraq and North Korea.3 pabilities were developed. All of the major nations in- Despite diplomatic efforts, chemical weapons will remain volved in World War I and several other countries devel- a threat in warfare and more recently have become a oped chemical weapons programs. Participants involved potential weapon of the terrorist. In 1994, a religious cult, in international conferences and treaties attempted to Aum Shinrikyo, released nerve gas in a residential area in define, limit, and/or prohibit the storage, development, Matsumoto, Japan, and in 1995 a attack occurred in and training in the use and deployment of chemicals in a Tokyo subway. warfare. The ease with which chemical weapons can be obtained At the start of World War II, training in the use, storage, and manufactured increases the concern that nonmilitary and deployment of, and protection from chemical warfare people may be exposed to chemical agents. These agents was high. Although there was no major event involving are most effectively employed against individuals who the use of chemical agents during World War II, the capa- lack knowledge of their properties as well as to protect bilities of participating countries were impressive. In addi- against themselves and personnel against them. Cities, ports, and airfields are especially vulnerable civilian tar- gets. Following terrorist activity against the Pentagon and Abbreviations used in this paper: CNS = central nervous system; World Trade Center on September 11, 2001, President US = . Bush established a Homeland Defense program in the US.

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In light of these recent events, there is a real possibility in which groups of patients experience symptoms such as that civilian medical personnel may be exposed to patients runny nose, blurred vision, drooling, stomach cramps, and and circumstances involving chemical weapons. The fol- chest tightness, medical personnel must consider that mild lowing is a brief synopsis of those chemicals and their exposures have occurred as well as the possibility of a effects that a neurosurgeon may need to recognize and be contaminated working area, equipment, or clothing. able to treat when managing victims in a mass-casualty The first principle in treating patients exposed to a scenario. Chemical weapons may be classified in a variety is to protect the medical personnel from expo- of different ways. For this discussion, the common nerve sure. This may require the donning of a protective mask agents, vesicants, blood agents, choking agents, and riot and hood, gloves, and impermeable clothing as the situa- control agents will be discussed. In addition, basic protec- tion dictates. Second, the source of nerve agent exposure tive mechanisms and decontamination procedures will be must be terminated. This may require that the patient be addressed. removed from a contaminated scene, as well as removal of clothing and personal items, cleansing of the patient, and/ NERVE AGENTS or placement of a protective mask. Ideally decontamina- tion would involve the use of diluted household bleach or The biological primary effect of nerve agents is their charcoal and resorptive resins. If these are not available, inhibition of the enzyme acetylcholinesterase.1 Although large amounts of may be used to wash skin surfaces these agents are commonly used as insecticides and may and dilute the exposure, or tissue paper can be used to also be used in medicine, the chemicals of military impor- wipe away nerve agent resins. Care must be used to con- tance tend to be more potent and longer lasting. Nerve tain contaminated items to avoid exposure to other people. agents can be divided into G and V agents. (GA), Third, an airway should be established (or maintained). sarin (GB), (GD), and VX are examples of these Suction of large secretions and supplemental agents. Nerve agents are frequently clear and colorless in may be all that is necessary. Endotracheal intubation or a pure state and tend to liquify at moderate temperatures, cricothyroidotomy may be required in more critically ill although G agents much more likely than V agents can patients. present a vapor hazard. Nerve agents can be absorbed through any body surface Chemical Agent Antidotes area or through the gastrointestinal and respiratory tracts.3 The US military recognizes the following antidotes in The effects of nerve agents occur extremely rapidly when the treatment of nerve agent exposure: atropine, prali- inhaled as a vapor, but cutaneous absorption of liquid doxime chloride, and diazepam.2 Certain troops deployed nerve agents can take several minutes. Holding one’s in combat may be provided with antidote-containing au- breath and donning an effective mask can prevent expo- toinjectors for self- or buddy administration.3 In general sure to vaporized nerve agent. The liquid form of nerve medical treatment of the nerve agent–exposed patient agent can penetrate regular clothing extremely quickly. should be directed at combating the physiological effects Rapid removal of permeable clothing and decontamina- of the nerve agent, as well as those effects of the medica- tion of exposed body surfaces can markedly reduce the tions given to treat the patient. amount of the compound that is absorbed cutaneously. Atropine blocks the effects of acetylcholine at mus- These agents are rapidly inactivated by alkali and chlori- carinic receptors. Thus, atropine decreases secretions and nating compounds. Diluted chlorinating compounds may reverses the contraction of smooth muscle (that is, it re- be used to decontaminate patients and healthcare person- lieves bronchoconstriction and gastrointestinal hyper- nel, and stronger solutions may be used to clean clothing motility). Except in very high doses, atropine does not and equipment. resolve miosis. Field troops are given autoinjectors that Because the action of nerve agents is to inhibit acetyl- supply a 2-mg dose of atropine. In a civilian healthcare cholinesterase enzymes, symptoms are produced when setting, 2 mg of atropine should be given every 5 to 10 acetylcholine accumulates at muscarinic and nicotinic minutes until secretions and dyspnea are minimized. Pra- receptors throughout the body. These symptoms can occur lidoxime chloride or 2-PAM CL is an oxime that is effec- locally at a site of exposure or systemically. Following ex- tive against some of the nerve agents. The drug can either posure to small amounts of vapor, miosis may result, block inhibition of cholinesterase and/or reactivate acetyl- secretions increase, and the patient may have slight bron- choline at muscarinic receptors. Oximes must be adminis- choconstriction. When exposed to a small dose of liquid, tered early in the course of treatment because it becomes increased sweating and muscular fasciculation at the site ineffective over short periods of time that are different for of exposure may occur. As doses of the nerve agent in- each nerve agent. Initially, 1 to 1.5 g of oxime should be crease, nausea, diarrhea, and generalized fatigue or weak- give over 20 to 30 minutes and, if effective, may be re- ness may begin. , lacrimation, salivation, and peated one to two times over 60 to 90 minutes. In severe dyspnea may become more intense. Exposure to large cases of nerve agent exposure, seizures may result. Di- amounts of any form of nerve agent may quickly induce azepam has been shown to be effective against these loss of conciousness, seizures, flaccid paralysis, and apnea. seizures and can also be effective in sedating a patient dur- To be able to recognize and thus diagnose cases involv- ing resuscitation. Ten-milligram doses may be adminis- ing exposure to nerve agents practioners must be aware of tered until the desired effect is achieved. Transient arryth- the aforementioned signs and symptoms.2 No other chem- mias can occur after exposure to either nerve agent or ical agent can produce the characteristic muscular fascic- during administration of atropine. Beta adrenergic block- ulations, pinpoint pupils, and autonomic and CNS symp- ing agents may be effective at controlling the tachycardia toms like the acetylcholinesterase inhibitors. In scenarios and ST segment changes associated with atropine.

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VESICANTS (BLISTER AGENTS) the eye should be liberally irrigated periodically. The use of topical analgesic and antibiotic agents may be neces- The vesicants, also known as blister agents, can be le- 1 sary. Vaseline should be placed on edges of the eyelids to thal. Vesicants burn or blister any part of the body they prevent the lids from adhering to each other and reduce contact. They have been used militarily to disable troops, scarring. A topical mydriatic can be administered to pre- contaminate equipment, and thus degrade fighting capa- vent synechia formation. Supplemental oxygen, obtaining bility. The common blister agents include the mustards, and maintaining an airway, and/or , and . Mustard and lewisite both may be necessary depending on the extent of exposure. induce fluid-filled . Phosgene oxime, which is not For lewisite exposure, a specific antidote (BAL [dimer- a true , forms a solid wheal. The weapons- caprol]) that binds to the in lewisite and can re- grade property of these compounds is typically an oily liq- duce its systemic effects; BAL can cause hypertension uid, although phosgene oxime can be disseminated in a and tachycardia. crystalline form. Protection from these agents requires both a mask and protective overgarments.3 The pain, as well as the clinical tissue effects associat- ed with mustard exposure will take hours to commence.2 BLOOD AGENTS The mildest and earliest sign of cutaneous mustard expo- Blood agents are distributed by the blood and generally sure is erythema, which may be accompanied by burning, enter the body via inhalation. They inhibit the ability of itching, and stinging. If exposure is extensive enough, blood cells to utilize and transfer oxygen. Thus, blood small blisters will begin to develop within the erythema- agents are that effectively cause the body to suf- tous region and will eventually coalesce. If the eye is ex- focate. Examples of blood agents include cy- posed to mustard vapor, pain, blepharospasm, conjunc- anide, chloride, and . tivitis, corneal damage, and will result. In At room temperature, hydrogen is a colorless cases of mild exposure of the airways, rhinorrhea, sneez- liquid. The most important route of poisoning is through ing, epistaxis, and a hacking begin. As the exposure inhalation. Both gaseous and liquid , as increases, the cough may become productive and the pa- well as cyanide salts in solution, can also be absorbed tient may experience severe dyspnea. Immunosuppres- through the skin. Its high volatility makes hydrogen cyan- sion may also occur. In addition to timing of symptoms, ide difficult to use outdoors.3 On the other hand, the con- exposure to mustards may be diagnosed by measuring and centration of it may rapidly reach lethal levels if it is noting a significant amount of thiodiglycol in the urine of released in confined spaces. an exposed patient. Cyanide poisoning–related effects are those of progres- The pain, erythema, and blister formation associated sive tissue hypoxia.1 The symptoms, signs, and physical with lewisite exposure occurs much more rapidly than in findings are directly related to the dose of cyanide, the cases of mustard exposure.2 Pain will often commence in route of exposure, and the type of cyanide compound. In seconds to minutes. Additionally the lesions that do occur addition to the effects we will describe, tend to heal much faster, and secondary infection is much also produces irritation of the eyes and mucous mem- less common. Although eye-related vapor exposure may branes similar to that produced by agent used in riot con- cause pain and irritation, the onset of blepharospasm is so trol agents. rapid that severe eye injury is much less likely. Shock may Within seconds of exposure to high concentrations of ensue in cases of exposure to large amounts of lewisite cyanide gas an initial hyperpnea is followed by a loss of because the resultant capillary-related and plasma consciousness (30 seconds postexposure).2 This progress- leakage causes hemoconcentration and . The es to apnea (3–5 minutes postexposure), cessation of car- rapid onset of symptoms can help differentiate lewisite diac activity (5–8 minutes postexposure), and death. After exposure from mustard exposure, but additional data will exposure to lower concentrations, or exposure to lethal be needed to distinguish this from a phosgene exposure. amounts via the oral or percutaneous routes, the effects Development of a blister compared with a wheal may be develop more slowly. For example, after ingestion of a helpful in this differential diagnosis. Additionally arsenic of a cyanide salt, the patient might survive 15 may be present in the urine of a lewisite-exposed patient. to 30 minutes during which an antidote could be adminis- Phosgene causes immediate pain and irritation to ex- tered. Prominent early signs and symptoms of cyanide posed body parts.2 Within 5 to 30 minutes, skin edema poisoning include a transient hyperpnea, headache, dysp- may form around an erythematous wheal and the center nea, and findings of general CNS excitement, including of the lesion may become necrotic. Painful anxiety, personality changes, and agitation progressing and may ensue. The major lesion of phosgene to seizures. Diaphoresis, flushing, weakness, and vertigo expose is and thrombosis caused by may also be present. Late-appearing indications of CNS pulmonary venules. depression, such as coma and dilated, unresponsive pu- Decontamination is the mainstay of treatment of vesi- pils, are prominent signs of cyanide intoxication. The tell- cant exposure.1 Patients should be thoroughly decontami- tale of bitter almonds cannot be used as a guide be- nated before allowing contact with unexposed patients. cause up to 60% of people are unable to detect the odor. Decontamination may be performed using either a dilute Relevant laboratory findings include an early decreased hypochlorite solution or water. Skin lesions should be kept arteriovenous difference in the partial pressure of oxygen clean to avoid secondary infection. Calamine or another with progressive lactic acidosis. Although cyanide levels soothing lotion may relieve burning or itching. Analgesic in blood, urine, and various tissues (for example and medication may be necessary for severe pain. Lesions of liver) can be measured, results are generally not available

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Unauthenticated | Downloaded 10/02/21 04:36 PM UTC R. R. McCafferty and P. J. Lennarson during the treatment phase. The first principle of treatment effectively disseminated in an aerosolized form. These is to eliminate any source of continued poisoning by re- compounds produce temporary disability because the ex- moving the victims from the offending environment, re- treme ocular irritation and blepharospasm cause the eyes moving their clothing, and washing their skin with soap to close temporarily, and the irritation of the airways caus- and water. For ingested sources, activated charcoal lavage es coughing, , and sometimes retching is indicated. General supportive measures may be all that or vomiting.3 These agents are also characterized by their are required in the conscious patient. Specific therapies rapid onset of effects (seconds to several minutes), a rela- are based on encouraging and accelerating the body’s own tively brief duration (15–30 minutes) of effects once the ability to excrete cyanide and to bind cyanide in the blood. victim has escaped the contaminated atmosphere and has Antidotes include sodium thiosulphate, sodium nitrite, di- been decontaminated (that is, removed the material from methylaminophenol, and hydroxycobalamin.1 his clothing), and a high safety ratio (the ratio of the lethal The most likely arsenic-containing compound to be dose to the effective dose).2 In contrast to human beings, used in chemical warfare is lewisite. Lewisite is a co- animals generally have low sensitivity to tear . Dogs lorless liquid that causes injuries similar to the mustard and horses can therefore be used by police for agents, although the onset of its effects is much more even when is used. rapid. Lewisite was more described in detail in the previ- The mainstay of tear gas exposure–related treatment is ous section (see Vesicants). A specific antidote, dimercap- removal from the contaminated environment and the use topropanol, more commonly called British Anti Lewisite, of soap and water to wash the skin and clothes. No long- protects against injuries to the skin and mucous mem- term effects of tear gas exposure have been documented. branes as well as systemic poisoning. CONCLUSIONS CHOKING AGENTS Recent national and international events have increased Choking agents inflict injury mainly on the respiratory the possibility of civilian healthcare organizations having tract including the nose, throat, and especially the . to care for an injured patient who has been exposed to a Victims typically inhale these agents, which can all lead to chemical agent. In this paper we briefly described chemi- pulmonary edema and . Examples of cal agents that civilian healthcare personnel may need to choking agents include chlorine, phosgene, , have knowledge to provide treatment to exposed patients. and .1 Basic principles of delivering care in an affected environ- Chlorine is a dense, pungent, greenish-yellow gas that ment include the following. 1) Protect medical and sup- is easily recognized by both color and odor. Because of its portive personnel from chemical exposure. 2) Decontam- tendency to settle in low-lying areas, this gas is especially inate the patient and the surrounding environment to limit hazardous in closed spaces. Symptoms of chlorine expo- the effects of the exposure and avoid additional exposure. sure include ocular and nasal irritation, spasmodic cough- To treat the victim, this may require placement of a mask, ing, and a feeling of suffocation. Signs of pulmonary removal of clothing, and washing of skin surfaces or sur- edema develop with continued exposure. Treatment is rounding surfaces. Care must be taken to prevent con- symptomatic, because there is no specific antidote. Al- tamination of medical equipment transport vehicles, and though not clinically proven, administration of cortico- rooms (for example, ambulances and hospital rooms). 3) steroid agents, as soon as possible after exposure, has been Finally, a specific treatment must be provided based on recommended to lessen the severity of pulmonary edema.3 the patient’s type of exposure and manifesting symptoms. Whereas the majority of chlorine exposure–induced The following references will serve as a more compre- deaths occur in the first 24 hours, victims who survive the hensive resource for in-depth reading on the aforemen- initial insult may live with minimal pathological or phys- tioned topics. iological sequelae.1 Phosgene, a gas heavier than air, generally appears as a white cloud, and at low concentrations has an odor of References freshly mown hay. Symptoms of exposure range from mild cough, chest tightness, and dyspnea to those of se- 1. Sidell FR, Takafuji ET, Franz DR (eds): Medical Aspects of Chemical and Biological Warfare. Washington, DC: Office vere, rapidly developing pulmonary edema. Treatment of the Surgeon General , 1997 and prognosis are similar to those in cases of chlorine 2. United States Armed Forces: Medical Management of Chem- exposure. ical Casualties Handbook. , MD: United States Army, 1999 3. United States Armed Forces: Treatment of Chemical Agent RIOT CONTROL AGENTS Casualties and Conventional Military Chemical Injuries. Riot control agents are defined as any chemicals not Washington DC: United States Army, 1995 listed in a specific chemical warfare schedule that can rapidly produce sensory irritation or disabling physical Manuscript received January 18, 2002. effects that disappear within a short time following ter- Accepted in final form February 20, 2002 The views expressed in this article are those of the author(s) and mination of exposure. The four compounds of most do not reflect the official policy or position of the US Air Force, significance are o-chlorobenzylidene , 1- Department of Defense, or the US Government. chloroacetophenone also known as , dibenz (b,f)- Address reprint requests to: Randall R. McCafferty, M.D., 74th 1,4-oxazepine, and diphenylaminearsine.1 At room tem- Medical Group/SGOSN, 4881 Sugar Maple Drive, Wright-Patter- perature all agents tend to be white powders that are most son Air Force Base, Ohio 45433.

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