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  • Organophosphates inactivate the enzyme acetylcholinesterase, causing increased levels of acetylcholine at cholinergic receptor sites in muscles, glands, and neural ganglia.
  • The early muscarinic manifestations of organophosphate toxicity include salivation, lacrimation, diarrhea, vomiting, and miosis.
  • Although organophosphate exposure can often present with seemingly nonspecific respiratory, gastrointestinal, or neurologic manifestations, the combination of miosis and increased salivation should prompt serious consideration of the diagnosis.
  • The antidotes atropine and pralidoxime are used to treat organophosphate exposure, while atropine alone is used for carbamate toxicity.
  • Nicotinic manifestations are common in organophosphate exposure, but uncommon in carbamate toxicity.

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More than 50% of exposures to organophosphate and carbamate pesticides involve children younger than 6 years. Several factors make these pediatric cases difficult to diagnose. Often the child is too young to give a history, and the parents might not suspect that oral or topical pesticide exposure has occurred. In addition, the typical respiratory and gastrointestinal symptoms of the cholinergic syndrome may be mistaken for those of common childhood illnesses: bronchitis, pneumonia, upper respiratory infection, or gastroenteritis. Finally, some studies have indicated that well-recognized manifestations of cholinergic toxicity in adults—for example, bradycardia and muscle fasciculations—occur in only a minority of pediatric cases, whereas tonic-clonic seizures occur more frequently in children.1 A high index of suspicion allows early diagnosis, which will not only facilitate optimal treatment for the individual patient but may also provide early warning of contamination in the child's home or environment.2,3

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Acetylcholine is the chemical messenger at junctions where nerves connect to skeletal and smooth muscle, and to secretory glands. Organophosphates poison acetylcholinesterase; the enzyme breaks down and inactivates acetylcholine. This causes a buildup of acetylcholine and hyperstimulation of areas of the nervous system that contain cholinergic receptors.3 There are two major classifications of cholinergic receptors: (1) muscarinic receptors, found on glands and involuntary smooth muscle, and (2) nicotinic receptors, found on voluntary skeletal muscle and some autonomic ganglia. There are also central cholinergic receptors found within the brain. When thinking of the clinical presentation of organophosphate toxicity, it is helpful to break down the signs and symptoms according to the three different types of receptors: muscarinic, nicotinic, and central.

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The initial signs and symptoms of cholinergic toxicity are often muscarinic. A helpful mnemonic to remember these muscarinic manifestations is DUMBELS:

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  • Diarrhea, Diaphoresis
  • Urination
  • Miosis
  • Bronchorrhea, Bronchospasm
  • Emesis
  • Lacrimation
  • Salivation

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Although miosis and the overall increase in secretions—saliva, sweat, and tears—can help suggest the diagnosis, the life-threatening effects are really bronchospasm and bronchorrea—the so-called “killer Bs.” As the airway fills with secretory fluid and constricts, oxygenation and ventilation may be difficult or impossible unless adequate antidote is administered.

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Nicotinic effects of excess acetylcholine at the neuromuscular junction include muscle spasm and fasciculations, followed by weakness or paralysis as the muscle fatigues. Bronchorrhea, bronchospasm, and respiratory muscle weakness can combine to ...

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