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Organophosphate and carbamate insecticides inactivate the enzyme acetylcholinesterase resulting in a cholinergic crisis with the immediate threat to life being respiratory failure.
The diagnosis is clinical with the history of exposure being key; the combination of miosis and increased salivation is relatively specific.
Immediate administration of very large doses of atropine is life saving.
Pralidoxime is an adjunctive antidote for organophosphate but not for carbamate poisoning.
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Historically, the commonest scenario for organophosphate and carbamate exposure in young children involved aerosol spray products available to the consumer for insect control in the home. This produced negligible morbidity because of low concentrations of active ingredients. Organophosphates and carbamates have been replaced by other active compounds in most of these products. However, organophosphate and carbamate insecticides intended for outdoor use and in particular for agricultural use are available in high concentrations typically dissolved in hydrocarbon solvents. They are diluted prior to use. Exposures to these concentrated insecticides are responsible for most significant organophosphate and carbamate poisonings.
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Organophosphates and carbamates inhibit acetylcholinesterase, the enzyme that inactivates acetylcholine. The resultant accumulation of this neurotransmitter produces ongoing cholinergic stimulation.1 Muscarinic cholinergic receptors are found in exocrine glands and smooth muscle while their nicotinic counterparts are found in skeletal muscle and autonomic ganglia. There are also central cholinergic receptors in the brain.
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These compounds inhibit acetylcholinesterase by occupying the acetylcholine binding site. The attachment by organophosphates is much more robust than for carbamates; the latter is often spontaneously reversible. Thus, organophosphate poisoning is usually more severe than its carbamate counterpart. In carbamate poisoning, functional enzyme activity is often largely restored within 8 hours, with red blood cell cholinesterase completely restored within 48 hours. Despite this, some carbamates such as aldicarb and carbaryl can be highly toxic.2
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Carbamate toxicity is primarily restricted to muscarinic effects. Carbamates are much less likely than organophosphates to cause CNS effects since they do not penetrate the blood–brain barrier well. Nicotinic manifestations are also uncommon. However, children with severe carbamate poisoning can develop mental status depression and occasionally seizures.
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The largest clinical series of organophosphate and carbamate poisoning in infants and children was published in 1988.3 The initial signs and symptoms of cholinergic toxicity are often muscarinic. “DUMBELS”(Table 131-1) is a helpful mnemonic. Nicotinic effects of excess acetylcholine at the neuromuscular junction include muscle spasm and fasciculations, followed by weakness or paralysis as the muscle fatigues. Central nervous system effects of organophosphate exposure range from agitation and delirium to seizures and coma.
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