Medical Management

Management of a casualty with nerve agent intoxication consists of decontamination, ventilation, administration of the antidotes, and supportive therapy. The condition of the patient dictates the need for each of these and the order in which they are done.

Decontamination is described elsewhere in this manual. Skin decontamination is not necessary after exposure to vapor alone, but clothing should be removed because it may contain "trapped" vapor.

The need for ventilation will be obvious, and the means of ventilation will depend on available equipment. Airway resistance is high (50-70 cm of water) because of bronchoconstriction and secretions, and initial ventilation is difficult. The resistance decreases after atropine administration, after which ventilation will be easier. The copious secretions that may be thickened by atropine also impede ventilatory efforts and require frequent suctioning. In reported cases of severe nerve agent exposure, ventilation has been required from 0.5 to 3 hours.

Three drugs are used to treat nerve agent exposure, and another is used as pretreatment for potential nerve agent exposure. The three therapeutic drugs are atropine, pralidoxime chloride, and diazepam. The use of the pretreatment drug pyridostigmine bromide is discussed later in this chapter.

Atropine is a cholinergic blocking or anticholinergic compound. It is extremely effective in blocking the effects of excess acetylcholine at peripheral muscarinic sites. Under doses. When small amounts (2 mg) are given to normal individuals without nerve agent intoxication, atropine causes mydriasis, a decrease in secretions (including a decrease in sweating), mild sedation, a decrease in GI motility, and tachycardia. The amount in three MARK I Kits may cause adverse effects on military performance in a normal person. In people not exposed to nerve agents, amounts of 10 mg or higher may cause delirium. Potentially, the most hazardous effect of inadvertent use of atropine (2 mg, IM) in a young person not exposed to a cholinesterase inhibiting compound in a warm or hot atmosphere is inhibition of sweating, which may lead to heat injury. In the military, atropine is packaged in autoinjectors, each containing 2 mg.

Pralidoxime chloride (Protopam chloride, 2-PAMCl) is an oxime. Oximes attach to the nerve agent that is inhibiting the cholinesterase and break the agent-enzyme bond to restore the normal activity of the enzyme. Clinically, this is noticeable in those organs with nicotinic receptors. Abnormal activity in skeletal muscle decreases and normal strength returns. The effects of an oxime are not apparent in organs with muscarinic receptors; oximes do not cause a decrease in secretions, for example. They also are less useful after aging occurs, but with the exception of GD (soman) intoxicated individuals, casualties will be treated before significant aging occurs. Pralidoxime chloride (600 mg) is in an autoinjector for self-use along with the atropine injector. These atropine and pralidoxime chloride autoinjectors are packaged together in a MARK I Kit. Each soldier is issued three MARK I Kits.

Diazepam is an anticonvulsant drug used to decrease convulsive activity and reduce the brain damage caused by prolonged seizure activity. Without the use of pyridostigmine pretreatment, experimental animals died quickly after superlethal doses of nerve agents despite conventional therapy. With pyridostigmine pretreatment (followed by conventional therapy), animals survived superlethal doses of soman but had prolonged periods of seizure activity before recovery. They later had performance decrements and anatomic lesions in their brains. The administration of diazepam with other standard therapy to soman-poisoned animals pretreated with pyridostigmine reduced the seizure activity and its sequelae. Current military doctrine is to administer diazepam with other therapy (three MARK I Kits) at the onset of severe effects from a nerve agent, whether or not seizure activity is among those effects. Each soldier carries one autoinjector containing 10 mg of diazepam for his buddy to administer to him (if he could self-administer it, he would not need it). Diazepam should be administered with the three MARK I Kits when the casualty's condition warrants the use of three kits at the same time. Medical personnel can administer more diazepam to a casualty if necessary. The medical corpsman carries extra diazepam injectors and is authorized to administer two additional injectors at ten-minute intervals to a convulsing casualty.

The doctrine for self-aid for nerve agent intoxication states that if an individual has effects from the agent, he/she should self-administer one MARK I Kit. If there is no improvement in ten minutes, he/she should seek out a buddy to assist in the evaluation of his/her condition before further MARK I Kits are given. If a buddy finds an individual severely intoxicated (e.g., gasping respirations, twitching, etc.) so that the individual cannot self-administer a MARK I Kit, the buddy should administer three MARK I Kits and diazepam immediately. The discussion below is advice for medical assistance.

The appropriate number of MARK I Kits to administer initially to a casualty from nerve agent vapor depends on the severity of the effects. Systemic atropine will not reverse miosis (unless administered in very large amounts), and miosis alone is not an indication for a MARK I Kit. If the eye or head pain and nausea associated with the miosis are severe, topical application of atropine (or homatropine) in the eye will bring relief. Topical atropine should not be used without good reason (severe pain), because it causes blurred vision for a day or longer. A casualty with miosis and rhinorrhea should be given one MARK I Kit only if the rhinorrhea is severe and troublesome (he cannot keep his mask on because of fluid). A casualty with mild to moderate dyspnea should be given one or two MARK I Kits, depending on the severity of his distress and the time between exposure and therapy. Some of the respiratory distress from a mild exposure will spontaneously decrease within 15 to 30 minutes after termination of exposure, so if the casualty is not severely uncomfortable, only one MARK I Kit should be used initially. Atropine is quite effective, and care should be taken not to give too much in a casualty who does not need it.

A severe casualty from nerve agent vapor has miosis, copious secretions from the nose and mouth, severe difficulty breathing or apnea, possibly some degree of cyanosis, muscular fasciculations, and twitching or convulsive activity, and is unconscious. He should be given three MARK I Kits and diazepam immediately. Ventilation will be needed and should be done via an endotracheal airway if possible. Suctioning of the excessive airway secretions will be necessary to enhance air exchange and will make ventilatory efforts easier. Atropine, 2 mg, should be repeated at three to five-minute intervals and should be titrated to a reduction of secretions and to reduction of ventilatory resistance. When the IV preparation is available, the preferred route of atropine administration is via the IV route, but this route should be avoided until hypoxia is corrected, because intravenously administered atropine in hypoxic animals has produced ventricular fibrillation. In a hypotensive patient or a patient with poor veins, atropine might be given intratracheally, either via the endotracheal tube or directly into the trachea, for more rapid absorption via the peribronchial vessels.

The medical care provider might err in giving too much atropine to a mild to moderate casualty. More importantly, the care provider might err by giving too little atropine to a severe casualty. In a severe casualty, atropine should be pushed at frequent intervals until secretions are dry (or nearly dry) and until ventilation can be accomplished with ease. In reported cases this has required 10 to 20 mg of atropine within the first several hours. A conscious, less-severely exposed casualty should receive atropine until he is breathing comfortably, and he will be able to communicate this. Dry secretions need not be an endpoint in mild to moderate casualties.

The casualty with skin exposure to liquid is more difficult to evaluate and manage than is a vapor exposure casualty. Agent on the surface of the skin can be decontaminated, but agent absorbed into the skin cannot be removed. The initial effects from absorbed liquid agent can start two to three hours after thorough decontamination of agent droplets on the skin. A casualty from liquid exposure on the skin may continue to worsen because of continued absorption of the agent from the skin depot.

The first effects of a liquid droplet on the skin are sweating with or without blanching, and occasionally, muscular fasciculations at the site. Gastrointestinal effects (nausea, vomiting, and sometimes diarrhea) are the first systemic effects, and these may start from 0.5 to 18 hours after contact with the agent. If these effects occur within the first several hours after exposure, they may portend more severe effects, and initial therapy should be two MARK I Kits. If effects begin later, initial therapy should be one MARK I Kit.

A large amount of liquid agent on the skin will cause effects 1 to 30 minutes after contact, whether or not decontamination was done. Nevertheless, early decontamination may lessen the magnitude of the effects. After a 1 to 30-minute latent or asymptomatic period, the casualty will suddenly lose consciousness and begin seizure activity. The condition of the casualty and management are the same as described for a severe casualty from vapor exposure.

Further care of the severe casualty consists of atropine administration to minimize secretions and ventilation until spontaneous respiration resumes. Oxime administration should be repeated at hourly intervals for two or three additional doses. The preferred method of administration of the oxime is by IV drip of 1 gram over 20 to 30 minutes (more rapid administration will cause hypertension), but 3 additional oxime autoinjectors (total dose of 1.8 grams) may be given if the IV route cannot be used. The need for ventilation may continue for 0.5 to 3 hours. Unless prolonged hypoxia or other complications have occurred, the casualty will eventually begin having spontaneous muscular activity and make sporadic attempts to breathe. Muscles will become stronger and breathing more regular, and the casualty will have intermittent episodes of conscious behavior. Within an hour or two, he will be breathing, moving, and conscious, although he will be weak and intermittently obtunded.

Table III. Nerve Agent Effects. Vapor Exposure

Mild

Eyes: miosis, dim vision, headache

Nose: rhinorrhea

Mouth: salivation

Lungs: dyspnea ("tightness in the chest")

Time of onset: seconds to minutes after exposure

Self-aid: one MARK I Kit

Buddy-aid: stand by

Severe

All of the above, plus

Severe breathing difficulty or cessation of respiration

Generalized muscular twitching, weakness, or paralysis

Convulsions

Loss of consciousness

Loss of bladder, bowel control

Time of onset: seconds to minutes after exposure

Self-aid: None - soldier will be unable to help self

Buddy-aid: 3 MARK I Kits and diazepam immediately

Table IV. Nerve Agent Effects. Liquid on Skin

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