Weapons of Terror: Chemical Weapons

Chemical Weapons

Agents that may potentially be used in chemical warfare are overt agents in that the effects are more apparent and occur more quickly than those caused by biological weapons. Agents are avail-able and well-known, result in major mortality and morbidity,and cause panic and social disruption. There are many agents, including those that affect nerves (sarin, soman), those that affect blood (cyanide), those that are vesicants (lewisite, nitrogen and sulfur mustard, phosgene), heavy metals (arsenic, lead), volatile toxins (benzene, chloroform), pulmonary agents (chlorine), and corrosive acids (nitric acid, sulfuric acid) (Table 72-3). Chlorine, phosgene, and cyanide are widely used in industry and therefore are readily available.

CHARACTERISTICS OF CHEMICALS

Volatility.

Volatility is the tendency for a chemical to become avapor. The most volatile agents are phosgene and cyanide. Most chemicals are heavier than air, except for hydrogen cyanide. Therefore, in the presence of most chemicals, the victim should stand up to avoid heavy exposure (because the chemical will sink toward the floor or ground).

Persistence.

Persistence means that the chemical is less likely tovaporize and disperse. More volatile chemicals do not evaporate very quickly. Most industrial chemicals are not very persistent.

Weaponized agents (chemicals developed as weapons by the mil-itary) are more likely than industrial chemicals to penetrate and cause secondary exposure as well.

Toxicity.

Toxicity is the potential of an agent to cause injury tothe body. The median lethal dose (LD50) is the amount of the chemical that will cause death in 50% of those who are exposed. The median effective dose (ED50) is the amount of the chemical that will cause signs and symptoms in 50% of those who are ex-posed. The concentration time (CT) is the concentration released multiplied by the time exposed (mg/min). For example, if 1000 mg of a chemical were released and the time of exposure to this amount of chemical was 10 minutes, then the concentration time would be 10,000 mg/min.

Latency.Latency is the time from absorption to the appearanceof symptoms. Sulfur mustards and pulmonary agents have the longest latency, whereas vesicants, nerve agents, and cyanide pro-duce symptoms within seconds.

LIMITING EXPOSURE

Evacuation is essential, as are removal of clothing and decontam-ination as close to the scene as possible and before transport of the person exposed. Soap and water are effective means of deconta-mination in most cases. Staff involved in decontamination efforts must wear PPE and contain the runoff after decontamination procedures.

VESICANTS

Vesicants are chemicals that cause blistering and result in burning, conjunctivitis, bronchitis, pneumonia, hematopoietic suppres-sion, and death. Examples of vesicants include lewisite, phosgene, nitrogen mustard, and sulfur mustard. In World War I and in the Iran–Iraq conflict of 1980–1988, vesicants were used to disable the opponent. Vesicants were the primary incapacitating agents, resulting in minimal (less than 5%) death but large numbers of injured (Brennan, Waeckerle, Sharp, & Lillibridge, 1999). Liquid sulfur mustard was the most frequently used vesicant in these conflicts. It is an oily liquid with a garlic odor, has a long latent period, and penetrates the skin if not rapidly removed. The skin damage is irreversible but is seldom fatal (2% to 3% mortality).

The initial presentation after exposure to a vesicant is similar to that of a large superficial to partial-thickness burn in the warm and moist areas of the body (ie, perineum, axillae, antecubital spaces). There is stinging and erythema for approximately 24 hours, followed by pruritus, painful burning, and small vesicle formation after 2 to 18 hours. These vesicles can coalesce into large, fluid-filled bullae. Lewisite and phosgene result in immediate pain after exposure. Tissue damage occurs within minutes.

If the eye is exposed, there is pain, photophobia, lacrimation, and decreased vision. This progresses to conjunctivitis, blepharo-spasm, corneal ulcer, and corneal edema.

Respiratory effects are more serious and often are the cause of mortality with vesicant exposure. Purulent fibrinous pseudo-membrane discharge leads to obstruction of the airways. Gastro-intestinal exposure includes nausea and vomiting, leukopenia, and upper gastrointestinal bleeding.

Appropriate decontamination includes soap and water. Scrub-bing and the use of hypochlorite solutions should be avoided, because they increase penetration. Once the substance has pene-trated, it cannot be removed. Eye exposure requires copious irri-gation. For respiratory exposure, intubation and bronchoscopy to remove necrotic tissue are essential. With lewisite exposure, dimercaprol (BAL in oil) is administered intravenously for systemic toxicity and topically for skin lesions. All persons with sul-fur mustard exposures should be monitored for 24 hours for de-layed (latent) effects.

NERVE AGENTS

The most toxic agents in existence are the nerve agents such as sarin, soman, tabun, VX, and organophosphates (pesticides). They are inexpensive, effective in small quantities, and easily dis-persed. In the liquid form, nerve agents evaporate into a colorless, odorless vapor. Organophosphates are similar in nature to the nerve agents used in warfare and are readily available. Nerve agents can be inhaled or absorbed percutaneously or subcuta-neously. These agents bond with acetylcholinesterase, so that acetylcholine is not removed; the adverse result is continuous stimulation (hyperstimulation) of the nerve endings. Carbamates, which are insecticides originally extracted from the Calabar bean, are derivatives of carbamic acid; they are nerve agents that specif-ically inhibit acetylcholinesterase for several hours and then spontaneously become unbound from the acetylcholinesterase. Organophosphates, however, require the formation of new en-zyme (acetylcholinesterase) before function can be restored.

A very small drop of agent is enough to result in sweating and twitching at the site of exposure. A larger amount results in more systemic symptoms. Effects can begin anywhere from 30 minutes up to 18 hours after exposure. The more common organophos-phates and carbamates that are used in agriculture (sevin and malathion) result in less severe symptoms than do those used in warfare.

Signs and symptoms of nerve gas exposure are those of cholin-ergic crisis and include bilateral miosis, visual disturbances, in-creased gastrointestinal motility, nausea and vomiting, diarrhea, substernal spasm, indigestion, bradycardia and atrioventricular block, bronchoconstriction, laryngeal spasm, weakness, fascicu-lations, and incontinence. The patient must be examined in a dark area to truly identify miosis. Neurologic responses include insomnia, forgetfulness, impaired judgment, depression, and ir-ritability. A lethal dose results in loss of consciousness, seizures, copious secretions, fasciculations, flaccid muscles, and apnea.

Decontamination with copious amounts of soap and water or saline solution for 8 to 20 minutes is essential. The water is blot-ted, not wiped, off. Fresh 0.5% hypochlorite solution can also be used. The airway is maintained, and suctioning is frequently re-quired. One must be aware that plastic airway equipment will absorb sarin gas, resulting in continued exposure to the agent.

Treatment.Intravenous atropine 2 to 4 mg is administered, fol-lowed by 2 mg every 3 to 8 minutes for up to 24 hours of treat-ment. Alternatively, intravenous atropine 1 to 2 mg/hr may be administered until clear signs of anticholinergic activity have re-turned (decreased secretions, tachycardia, and decreased gastro-intestinal motility). Another medication is pralidoxime; which allows cholinesterase to become active against acetylcholine. Pralidoxime 1 to 2 g in 100 to 150 mL of normal saline solution should be administered over 15 to 30 minutes. Pralidoxime has no effect on secretions and may have any of the following side effects: hypertension, tachycardia, weakness, dizziness, blurred vision, and diplopia.

Diazepam (Valium) or other benzodiazepines should be ad-ministered for seizures, to decrease fasciculations, and to alleviate apprehension and agitation. The military provides all military personnel with Mark I autoinjectors, which contain 2 mg atro-pine and 600 mg pralidoxime chloride. Diazepam is administered by a partner.

BLOOD AGENTS

Blood agents have a direct effect on cellular metabolism, result-ing in asphyxiation through alterations in hemoglobin. Examples include hydrogen cyanide and cyanogen chloride. Cyanide is an agent that has profound systemic effects. It is commonly used in the mining of gold and silver and in the plastics and dye indus-tries. In 1984, the Union Carbide pesticide plant in Bhopal, India, released large amounts of cyanide in an industrial disaster, and hundreds of deaths occurred.

A cyanide release is often associated with the odor of bitter al-monds. In house fires, cyanide is released during the combustion of plastics, rugs, silk, furniture, and other construction materials. There is a significant correlation between blood cyanide and carbon monoxide levels in fire victims, and most often the cause of death is cyanide.

Cyanide can be ingested, inhaled, or absorbed through the skin and mucous membranes.

Cyanide is protein bound and inhibits aerobic metabolism, leading to respiratory muscle failure, respiratory arrest, cardiac arrest, and death. Inhalation of cyanide results in flushing, tachy-pnea, tachycardia, nonspecific neurologic symptoms, stupor, coma, and seizure preceding respiratory arrest.

Emergency Treatment.

Rapid administration of the followingmedications is essential to the successful management of cyanide exposure: amyl nitrate, sodium nitrite, and sodium thiosulfate. First, the patient is intubated and placed on a ventilator. Next, amyl nitrate pearls are crushed and placed in the ventilator reser-voir to induce methemoglobinemia. Cyanide has a 20% to 25% higher affinity for methemoglobin than it does for hemoglobin; it binds methemoglobin to form either cyanomethemoglobin or sulfmethemoglobin. The cyanomethemoglobin is then detoxified in the liver by the enzyme rhodanase. Next, sodium nitrite is ad-ministered intravenously, also to induce the rapid formation of methemoglobin. Sodium thiosulfate is then administered intra-venously; it has a higher affinity for cyanide than methemoglobin does and stimulates the conversion of cyanide to sodium thio-cyanate, which can be renally excreted. There are side effects of these emergency medications: sodium nitrite can result in severe hypotension, and thiocyanate can cause vomiting, psychosis, arthralgia, and myalgia.

The production of methemoglobin is contraindicated in pa-tients with smoke inhalation, because they already have decreased oxygen-carrying capacity secondary to the carboxyhemoglobin produced by smoke inhalation. An alternative suggested treat-ment for cyanide poisoning is hydroxycobalamin (vitamin B₁₂a). Hydroxyocobalamin binds cyanide to form cyanocobalamin (vitamin B₁₂). It must be administered intravenously in large doses. Administration of vitamin B₁₂a can result in transient pink discoloration of mucous membranes, skin, and urine. In high doses, tachycardia and hypertension can occur, but they usually resolve within 48 hours.

PULMONARY AGENTS

Pulmonary agents such as phosgene and chlorine destroy the pul-monary membrane that separates the alveolus from the capillary bed. Hence, the person exposed cannot release carbon dioxide or acquire oxygen. Capillary leak results in fluid-filled alveoli. Phos-gene and chlorine both vaporize, rapidly causing this pulmonary injury. Phosgene has the odor of fresh-mown hay.

Signs and symptoms include pulmonary edema with shortness of breath, especially during exertion. Cough starts as a hackingcough followed by frothy sputum production. A mask is the only protection required. Phosgene does not injure the eyes.