SECTION 6 INDIVIDUAL CHEMICAL WEAPON DETAILED QUICK REFERENCES Nerve Agents OVERVIEW37,39,40 This group consists of the highly toxic organophosphates tabun (GA), sarin (GB), soman (GD), cyclosarin (GF), VX, VE, VG, and VM. The V and G agents differ in that the V agents are about 10 times more toxic and are less volatile than the G agents. This reduction in volatility means the G agents produce more toxic vapor but the V agents persist longer on clothing and surfaces after release. All nerve agents produce their toxicity by inactivation of the enzyme acetylcholinesterase (AChE). This enzyme is responsible for the breakdown of the important neurotransmitter acetylcholine (ACh). In the absence of active AChE, there is an accumulation of ACh at nerve endings, producing the hyperexcitability of the nervous system that is the hallmark of the clinically observed effects of these agents. In a bioterrorist attack, these agents would likely be released as aerosol droplets for inhalation and dermal absorption. Any residual agent left on surfaces that may come in contact with bare skin is also highly toxic. Exposure to no more than a pinhead-sized drop of VX is lethal. When irreversible binding to the AChE or aging of the agent occurs, 2–PAMC1 is no longer an effective antidote. The aging time varies with each agent: GA (14 hr), GB (3–5 hr), GD (2–6 min), VX (48 hr).38 LATENT PERIOD The latent period is seconds to minutes via inhalation and minutes to hours via dermal absorption (up to 18 hr for GB). Symptoms may still occur after decontamination of the skin due to prior absorption and continued transit of the agent through the dermis. SYMPTOMS AND CLINICAL COURSE3,37,38,39,40 • Initial presentation depends on dose and route of exposure. DIAGNOSIS3,37,39,40 Clinical presentation of patients with gasping, miosis, copious secretions, sweating, and generalized twitching or fasciculations is very suggestive of nerve agent exposure. • Reduction of RBC-cholinesterase activity is suggestive of nerve agent intoxication, but normal RBC-ChE activity does not rule it out. • Administer atropine 2–6 mg (peds 0.02 mg/kg) IM or IV plus pralidoxime CI (2–PAMC1) 600–2000 mg (peds 20 mg/kg) IM or IV (military Mark 1 kits contain atropine 2 mg and 2–PAMC1 600 mg in separate autoinjectors). The initial dose (or number of Mark I kits administered) should be based on estimated exposure and severity of presenting symptoms. • Repeat atropine 2–4 mg and 2–PAMC1 600–1000 mg (1 Mark I kit) Q 2–5 min as needed. • Administer diazepam 10 mg (peds 0.1–0.3 mg/kg) IVP over 2–3 min as needed for seizures. • Administer supportive care with IV fluids, cardiac monitor, and mechanical ventilation as necessary. • Remove the patient’s clothing and any residual agent from the skin using soap and water or 1 part bleach (hypochlorite) in 9 parts water. ISOLATION PRECAUTIONS Isolation precautions depend on the level of patient contamination. Fully decontaminated patients require only standard precautions (gloves, hand washing, and splash precautions, as needed). Patients who may be partially contaminated (still wearing contaminated clothing or demonstrating obvious residual liquid agent) require the use of level C protection and butyl rubber gloves until fully decontaminated. Cyanides (Blood Agents) OVERVIEW Cyanide comes in four forms that may serve as chemical weapons. These are hydrogen cyanide (HCN), cyanogen chloride (CNC1), cyanogen bromide (CNBr), and cyanogen iodide (CNI). All forms may be released as a liquid, aerosol, or gas for inhalation; they may also be ingested or absorbed through the eyes and skin. Cyanide is rapidly lethal when used in enclosed areas, but its effectiveness out of doors is limited by its volatility, rapid dispersion, and relatively high concentrations required (LCt50). The victims of cyanide toxicity generally either rapidly die or fully recover. Through its binding to ferric iron in the mitochondrial cytochrome a3, cyanide blocks the cellular energy transport (cytochrome) system and prevents the use of oxygen as an electron receptor, producing cellular anoxia. Victim death occurs due to loss of central respiratory drive, which results in apnea. Contrary to what is popularly believed from television and films, the effects of cyanide are not irreversibly fatal, and victims may be successfully resuscitated by proper circulatory and respiratory support until the antidote can be administered. Cyanide has many industrial uses and may be produced by the combustion of many plastics. LATENT PERIOD The latent period is 10–15 seconds up to several minutes (depending on level of exposure) via inhalation and ingestion. SYMPTOMS AND CLINICAL COURSE3,37 • Initial presentation: • The initial presentation of cyanide poisoning can be differentiated from nerve agent intoxication by the lack of copious oral and nasal secretions and miosis, although this may be complicated by the lacrimation and airway secretions induced by cyanogen chloride. • Metabolic lactic acidosis is usually present and produces an unusually high anion gap. • Elevated blood cyanide concentration is noted. • Venous blood generally will appear unusually red and well oxygenated. • Supportive care with 100% oxygen, CPR, and respiratory support as needed with intubation and mechanical ventilation • Amyl nitrite: 1 ampule crushed and inhaled over 30 seconds. Repeat Q3 min until IV access is achieved and sodium nitrite can be administered. • Sodium nitrite: 300 mg (10 ml of a 3% solution) slow IVP over no less than 5 min. For pediatric patients, give 0.15–0.33 ml/kg of a 3% solution (up to 10 ml) slow IVP over no less than 5 min. Be certain to calculate peds dose correctly as overdose can be fatal. • Sodium thiosulfate: 12.5 g (peds 1.65 mL/kg of a 25% solution) IV over 10 min. • Repeat half the doses of sodium nitrite and sodium thiosulfate in 30 min if response is inadequate. • Treat acidosis if necessary with sodium bicarbonate 1–2 mEq/kg IV. ISOLATION PRECAUTIONS Decontamination is usually not needed. Remove any wet patient clothing with caution, as cyanide dissolves easily in water. Use standard precautions (gloves, hand washing, and splash precautions, as needed). Hydrogen Sulfide OVERVIEW38,42,43 Hydrogen sulfide (HS) is a colorless, heavier than air, extremely toxic gas that produces the well-known rotten-egg odor. Exposure occurs by inhalation of the gas and absorption through the lungs. An air concentration of only 100 ppm may be lethal. Like cyanide, it blocks the cellular energy transport (cytochrome) system and prevents the use of oxygen as an electron receptor, producing cellular anoxia. Death occurs due to loss of central respiratory drive, which results in apnea, but victims may be successfully resuscitated by proper circulatory and respiratory support. HS differs from cyanide in that it also produces direct irritation of skin, eyes, and mucous membranes. It has some industrial uses. LATENT PERIOD Immediate onset is noted for skin, eye, and mucosal irritation, and cyanide-like effect. Pulmonary effects may not become apparent for up to 72 hr. SYMPTOMS AND CLINICAL COURSE38,42,43 • Initial presentation: DIAGNOSIS3,37 There is no specific diagnostic test. • The initial presentation of hydrogen sulfide poisoning can be differentiated from nerve agent intoxication by the lack of copious oral and nasal secretions and miosis. • A history of a rotten egg-like odor may help to differentiate it from cyanide. • Metabolic lactic acidosis is usually present and produces an unusually high anion gap. • Supportive care with 100% oxygen, CPR, and respiratory support as needed, with intubation and mechanical ventilation, are the mainstays of therapy. • Amyl nitrite: 1 ampule crushed and inhaled over 30 seconds. Repeat Q 3 min until IV access is achieved and sodium nitrite can be administered. • Sodium nitrite: 300 mg (10 ml of a 3% solution) slow IVP over no less than 5 min. For pediatric patients, give 0.15–0.33 ml/kg of a 3% solution (up to 10 ml) slow IVP over no less than 5 min. Be certain to calculate peds dose correctly as overdose can be fatal. (The effectiveness of nitrites is anecdotal, unproven, and controversial.) • Sodium thiosulfate is not effective and should not be used. • Treat acidosis if necessary with sodium bicarbonate 1–2 mEq/kg IV. • Control bronchospasm, if present, with theophylline and albuterol. • Treat chemical burns as any thermal burns would be treated. ISOLATION PRECAUTIONS Decontamination is usually not needed. Remove any wet patient clothing with caution, as hydrogen sulfide dissolves easily in water. Use standard precautions (gloves, hand washing, and splash precautions, as needed). Pulmonary Agents OVERVIEW3,37,42 Pulmonary agents (chlorine, phosgene, diphosgene, nitrogen oxides, PFIB, and chloropicrin) are all liquids and gases, but they exert their major toxicity by inhalation as gases. They enter the lung and disrupt the alveolar-capillary membranes, reducing oxygen exchange, and allowing leakage of fluid into the interstitial tissues and alveoli. These agents have some differing physical properties and frequently produce other peripheral effects. Phosgene and differing diphosgene are colorless, volatile liquids that produce a heavier than air vapor with the odor of fresh mown hay. Chlorine is an extremely irritating greenish yellow, heavier than air gas, with an acrid odor. Nitrogen oxides are colorless liquids that produce an irritating vapor. Chloropicrin, an agricultural biocide, is an oily, colorless to light green liquid with an intense odor. It is extremely irritating to any body surface it contacts, and it degrades to phosgene and other toxic substances. It produces lung damage at an air concentration of only 20 ppm. PFIB (perfluoroisobutylene) is a combustion product of Teflon and other plastics and is 10 times more toxic than phosgene. All have important agricultural and industrial uses. LATENT PERIOD The latent period ranges from minutes to hours, depending on the agent and the level of exposure (occasionally days). Exertion tends to shorten the latent period. SYMPTOMS AND CLINICAL COURSE3,37,42 • Initial presentation:
Small inhalational exposure: miosis, blurry and/or dim vision, rhinorrhea, dyspnea, and/or chest tightness. Wheezing may also be present.
Small dermal exposure: localized sweating and muscle fasciculations, nausea, vomiting, and diarrhea. Miosis may also be present in medium dermal exposures.
Large inhalational exposure: sudden loss of consciousness and generalized seizures followed by apnea, flaccid paralysis, miosis, lacrimation, diarrhea, urination, copious oral, nasal, and respiratory secretions, and sweating.
Large dermal exposure: presentation same as large inhalational exposure, but onset may be delayed by up to 30 minutes following exposure.
Mild to moderate exposure: 10–15 seconds of gasping breaths and tachypnea, hypertension, tachycardia, flushing, giddiness, sweating, headache, and dizziness, rapidly followed by nausea, vomiting, confusion, agitation, and heart palpitations.
Severe exposure: 10–15 seconds of gasping breaths and tachypnea, hypertension, tachycardia, flushing, sweating, headache, and dizziness, rapidly followed by coma, apnea, seizures, shock, and bradycardia or other arrhythmias.
If untreated, death follows in 6–8 min from respiratory arrest.
Cyanogen chloride is a chlorine-like irritant and may also produce lacrimation, rhinorrhea, and irritation of the upper and lower respiratory system.
Cyanosis is an infrequent and very late finding in cyanide poisoning, and the skin may actually be cherry red initially.
Low to moderate exposure: skin irritation and erythema, nasal pain, sneezing, rhinorrhea, sore throat, cough, dyspnea, painful tracheobronchitis with bronchial and/or pulmonary hemorrhage and hemoptysis, eye pain, lacrimation, photophobia, blepharospasm, blurred vision, and keratoconjunctivitis with corneal clouding. Rarely, late pneumonitis or pulmonary edema can develop, which takes up to 72 hr to manifest.
Moderate to high exposure: rapid onset of gasping breaths, tachypnea, hypertension, tachycardia, flushing, sweating, headache, and dizziness, rapidly followed by nausea, vomiting, confusion, agitation, cyanosis, and finally coma.
Severe exposure: immediate onset of several gasping breaths followed by apnea, seizures, sudden collapse, and coma. If untreated, death follows in 6–8 min from respiratory arrest. Dermal irritation, blistering, and/or burns may also be noted.
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