Journal: AANA Journal 76(2):95-97, 2008. 9 References
Reprint: Dept of Anesthesia, McLeod Regional Medical Center, Florence, South Carolina (PK Hrobak, CRNA, MSN) TT.05 SP0815/255 ©2008
Faculty Disclosure: Abstracted by T. Tilton, who has nothing to disclose.
In today’s world, the possibility for biological or chemical attacks is a fact of life. Chemical attack with nerve agents is a remote possibility. Anesthesia providers are considered airway experts who deal with nerve agents and may be called to help manage any such attack. An understanding of the effect of nerve agents on the neuromuscular junction and autonomic receptors is essential when time is of the essence.
Organophosphate nerve agents (ONA) are the most toxic; tabun (known as GA) and sarin (GB) were developed in Germany during 1936-45 but not used until the Gulf War, 1981-87, by Iraq against Iran. Sarin was released over the city of Matsumoto, Japan on June 27, 1994, resulting in more than 600 casualties and 7 deaths, and released as a vapor in a Tokyo subway in March 1995, resulting in 12 deaths. Thousands of people presented to the emergency departments for evaluation or treatment. Only a small dose of ONA can cause death.
ONA inhibit acetylcholinesterase leading to excess acetylcholine at autonomic (muscarinic and nicotinic) receptors. The muscarinic receptors stimulate defeca¬tion, urination, miosis, bronchospasm, bronchorrhea, bradycardia, emesis, lacrimation, and salivation, which can best be remembered with the pneumonic "DUMBBBELLS" because it contains the 3 "Bs" that are the most life-threatening. Nicotinic receptors are present in both the sympathetic and parasympathetic nervous systems; excitation will produce hyperten¬sion and tachycardia at low doses and hypotension and neuromuscular weakness at higher doses. Central nicotinic stimulation can cause seizures, coma, and respiratory center depression. The mnemonic for excessive nicotinic stimulation is "MTWHF" for mydriasis, tachycardia, weakness, hypertension, and fasciculation). Someone poisoned with high-dose ONA may experience fasciculations followed by paralysis similar to the depolarizing block seen after succinylcholine administration.
Initial presenting symptoms following ONA exposure depend on the dose and route and may include miosis leading to blurred vision, bronchospasm, dyspnea, rhinorrhea, sweating and fasciculations. The patient may exhibit either bradycardia or tachycardia. Practitioners should remember that the dose causing symptoms is only slightly less than the lethal dose and all victims should be treated as having been exposed to a lethal dose.
ONA are fairly easily and inexpensively synthesized. G-type agents (sarin, soman, tabun) are colorless, clear, tasteless liquids easily water soluble; sarin (most volatile) is odorless, tabun has a fruity odor, and soman has a camphor-like odor. All are heavier than air. Nerve agent VX is least volatile but most persistent. It is an oily liquid that can be absorbed through the skin with minimal contact time, and is more easily absorbed in higher temperatures.
Treatment involves the immediate and rapid removal from the area of contamination and all clothing. Use soap and water or 0.5% sodium hypochlorite solution (dilute household bleach) to decontaminate the skin. With inhalation exposures, the victim should be moved to an area with adequate ventilation.
Healthcare providers involved in the initial care and rescue must wear personal protective equipment to prevent secondary exposure, which may include respiratory protection. Atropine controls life-threatening muscarinic symptoms such as broncho¬constriction, bronchorrhea, and bradycardia. Dosing is 1-2 mg, IV or IM, or up to 6 mg for severe exposures followed by 2 mg every 5-10 minutes until symptoms are improved. Treatment for nicotinic symptoms is supportive and involves ventilatory support and vasopressors for hypotension. Seizures are usually controlled with diazepam. More definitive treatment consists of the use of an oxime such as pralidoxime chloride.
Nerve agents deactivate acetylcholinesterase enzyme activity with a set window of time before the bond becomes covalent and irreversible, which is called aging. Once aging occurs, acetylcholinesterase com¬plexes no longer can metabolize acetylcholine. Oximes remove the organophosphoryl moiety of the nerve agent from the acetylcholinesterase enzyme, which allows the enzyme to spontaneously regene¬rate. Unfortunately, the rate of aging varies widely among nerve agents and the likelihood of knowing the agent used is small. Patients should be promptly treated with an oxime to prevent aging. Pralidoxime chloride, 15 mg/kg, is given in a 1-2 g loading dose over 5-10 min up to a maximum adult dose of 12 g/24 hr. Unfortunately, dosing requirements depend on the nerve agent used and the severity of exposure.
Successful treatment of patients exposed to ONA requires quick recognition of the signs and symptoms of poisoning and swift implementation of basic life support. Pralidoxime chloride should be given as soon as possible, not waiting for confirmation of exposure. Atropine should be titrated until secretions have dried and breathing is easier. Diazepam treats seizures; vasoactive drugs are used to stabilize vital signs, and ventilatory support is used as needed. |
