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  1. Pharmacology. Oximes reverse acetylcholinesterase (AChE) inhibition (thus reversing cholinergic excess at both muscarinic and nicotinic receptors) by reactivating the phosphorylated AChE and protecting the enzyme from further inhibition. The role of oximes in human poisoning is uncertain, as there are few controlled studies and these have provided conflicting results. A study in 2009 and an accompanying editorial suggested that oximes may improve outcome in low-dose agricultural exposures but may be harmful in deliberate self-poisoning in which the ingested dose is much greater. However, oximes are the only agents available capable of reactivating AChE and reversing the excess acetylcholine (Ach) at the nicotinic receptors of the neuromuscular junction, the ganglia of the parasympathetic and sympathetic nervous system, and the CNS. Although this effect is most pronounced with organophosphate (OP) insecticides, positive clinical results have been seen with carbamate insecticides that have nicotinic toxicity and variably with cholinesterase inhibitors formulated as “nerve gas” chemical weapons.

    1. Pralidoxime chloride (2-PAM) is the only oxime currently approved for use in the United States. Oximes differ in their effectiveness against specific agents, recommended doses, and side-effect profiles. Oximes commonly used in other countries include obidoxime, trimedoxime, and HI-6.

    2. Oximes are more effective when given before AChE has been bound irreversibly (“aged”) by the organophosphate. The rate of aging varies considerably with each OP compound. For dimethylphosporylated AChE (eg, from dichlorvos or malathion poisoning), the aging half-life is approximately 3.7 hours, whereas for diethylphosphorylated AChE (eg, from diazinon or parathion poisoning), the aging half-life is approximately 33 hours. For some chemical warfare agents, aging may occur in several minutes (eg, with soman, the phosphorylated AChE aging half-life is about 2–6 minutes). However, late therapy with 2-PAM is appropriate (even several days after exposure), especially in patients poisoned with diethyl compounds and with fat-soluble compounds (eg, fenthion, demeton) that can be released from tissue stores over days, causing continuous or recurrent intoxication.

    3. “Nerve” agents prepared as chemical warfare weapons, such as sarin, soman, tabun, and VX, are mechanistically similar to AChE-inhibiting insecticides. However, they are far more potent and responsive only to certain oximes. Pralidoxime is not effective against tabun, for example, but HI-6 has been found to be effective. Current oxime research seeking agents with broader activity against nerve agents is evaluating oximes HI-6, K027, K048, K074, and K075.

    4. Inadequate dosing of 2-PAM may be a contributing cause of “intermediate” syndrome, which is characterized by prolonged muscle weakness.

    5. Peak plasma concentrations are reached within 5–15 minutes after intravenous 2-PAM administration. Pralidoxime is eliminated by renal excretion and hepatic metabolism, with a half-life of 0.8–2.7 hours.

  2. Indications

    1. Oximes are used to treat poisoned patients who exhibit nicotinic receptor–associated symptoms caused by intoxications with cholinesterase inhibitor insecticides and nerve agents, including organophosphates, mixtures of organophosphorus and carbamate insecticides, and pure carbamate insecticides. Pralidoxime has low toxicity, is able to reverse nicotinic as well as muscarinic effects, and may reduce atropine requirements. For these reasons, pralidoxime should be considered early and empirically for suspected cholinesterase inhibitor poisoning, ...

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