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ACUTE EXPOSURE INFORMATION
- Amiton is an organophosphate compound. The following are signs and symptoms from organophosphates in general, which are due to the anticholinesterase activity of this class of compounds. All of these effects may not be documented for amiton, but could potentially occur in individual cases.
- USES: Amiton, an insecticide, is not registered for use in the United States; it may be available in other countries. It has also been used as a miticide.
- TOXICOLOGY: Organophosphates competitively inhibit pseudocholinesterase and acetylcholinesterase, preventing hydrolysis and inactivation of acetylcholine. Acetylcholine accumulates at nerve junctions, causing malfunction of the sympathetic, parasympathetic, and peripheral nervous systems and some of the CNS. Clinical signs of cholinergic excess develop.
- EPIDEMIOLOGY: In general, organophosphate exposure is common, but serious toxicity is unusual in the US. Common source of severe poisoning in developing countries.
- WITH POISONING/EXPOSURE
- MILD TO MODERATE POISONING: MUSCARINIC EFFECTS: Can include bradycardia, salivation, lacrimation, diaphoresis, vomiting, diarrhea, urination, and miosis. NICOTINIC EFFECTS: Tachycardia, hypertension, mydriasis, and muscle cramps.
- SEVERE POISONING: MUSCARINIC EFFECTS: Bronchorrhea, bronchospasm, acute lung injury. NICOTINIC EFFECTS: Muscle fasciculations, weakness, respiratory failure. CENTRAL EFFECTS: CNS depression, agitation, confusion, delirium, coma, seizures. Hypotension, ventricular dysrhythmias, metabolic acidosis, pancreatitis, and hyperglycemia also develop.
- DELAYED EFFECTS: It is not known if amiton produces delayed effects. The following is based on general information regarding organophosphate exposure. Intermediate syndrome is characterized by paralysis of respiratory, cranial motor, neck flexor, and proximal limb muscles 1 to 4 days after apparent recovery from cholinergic toxicity, and prior to development of delayed peripheral neuropathy. Manifestations can include inability to lift the neck or sit up, ophthalmoparesis, slow eye movements, facial weakness, difficulty swallowing, limb weakness (primarily proximal), areflexia, respiratory paralysis. Recovery begins 5 to 15 days after onset. Distal sensory-motor polyneuropathy may rarely develop 6 to 21 days following exposure to some organophosphate compounds, however, it has not yet been reported in humans after exposure to amiton. Characterized by burning or tingling followed by weakness beginning in the legs which then spreads proximally. In severe cases may result in spasticity or flaccidity. Recovery requires months and may not be complete.
- CHILDREN: May have different predominant signs and symptoms than adults (more likely CNS depression, stupor, coma, flaccidity, dyspnea, and seizures). Children may also have fewer muscarinic and nicotinic signs of intoxication (ie, secretions, bradycardia, fasciculations and miosis) as compared to adults.
- INHALATION EXPOSURE: Organophosphate vapors rapidly produce mucous membrane and upper airway irritation and bronchospasm, followed by systemic muscarinic, nicotinic and central effects if exposed to significant concentrations.
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