bubble_chart Overview

Organophosphorus pesticides are highly effective insecticides commonly used in agriculture and are toxic to humans. Children are more sensitive to them than adults. Commonly used highly toxic ones include 1605 (parathion), 1059 (demeton), 3911 (phorate), fenthion, phoxim, omethoate, and dichlorvos, with only trichlorfon being relatively low in toxicity. Most organophosphorus pesticides are oily liquids and can volatilize. Except for trichlorfon, which decomposes into the more toxic dichlorvos under the action of alkaline solutions, the toxicity of the others decreases when they react with alkaline substances.

bubble_chart Etiology

Disease cause

Organophosphorus poisoning in children is often caused by accidental ingestion of food contaminated with organophosphorus; contact with toys tainted with toxic substances; or playing in fields or indoors where pesticides have been sprayed, leading to absorption through the digestive tract, skin, or respiratory tract.

Toxic mechanism

After absorption, organophosphorus is distributed via blood and lymph to various organs and tissues, exerting toxic effects. Its primary toxicity lies in inhibiting the activity of cholinesterase, rendering it unable to catalyze the hydrolysis of acetylcholine. This results in the accumulation of excessive acetylcholine in the body, leading to neurological dysfunction. (1) It stimulates the parasympathetic nervous system, causing smooth muscle contraction, increased glandular secretion, pupil constriction, slowed heart rate, and decreased blood pressure; (2) It excites motor nerves, inducing muscle tremors or even spasms. In grade III or advanced stages, muscle strength weakens or paralysis occurs; (3) It stimulates sympathetic ganglia and preganglionic fibers, exciting the cardiovascular system, leading to increased blood pressure and heart rate. In advanced stages, vasomotor nerve paralysis may result in circulatory failure; (4) Its effect on the central nervous system initially manifests as excitation, followed by inhibition, potentially causing respiratory center paralysis.

bubble_chart Clinical Manifestations

Acute intoxication usually manifests within 4–6 hours, with the fastest onset occurring within minutes and the slowest not exceeding 24 hours.

1. Muscarinic symptoms result from the stimulation of cholinergic receptors in postganglionic fibers of the parasympathetic nerves and sympathetic nerves distributed to sweat glands, leading to increased glandular secretion. This presents as profuse sweating, salivation, increased bronchial secretion, bronchospasm causing dyspnea and pulmonary edema, and contraction of the iris sphincter muscle leading to miosis and blurred vision. Excitation of gastrointestinal smooth muscles causes nausea, vomiting, abdominal pain, and diarrhea. Inhibition of the cardiovascular system results in bradycardia and hypotension, while contraction of the detrusor muscle of the bladder leads to urinary incontinence.
2. Nicotinic symptoms arise from the stimulation of cholinergic receptors at the neuromuscular junction of motor nerves, manifesting as muscle tremors or spasms, with advanced stages showing muscle weakness and paralysis. Involvement of respiratory muscles can exacerbate dyspnea. Excitation of preganglionic fibers of the sympathetic nerves and the adrenal medulla presents as elevated blood pressure, tachycardia, and increased body temperature.
3. Central nervous system symptoms result from the stimulation of cholinergic receptors at neuronal synapses, causing dysfunction of the CNS. This leads to headache, dizziness, agitation, restlessness, delirious speech, and in severe cases, transitions to inhibition with speech impairment, unconsciousness, and respiratory paralysis. Respiratory center paralysis is the primary fatal cause of organophosphorus poisoning.

bubble_chart Diagnosis

1. There is a clear history of ingestion, contact, or inhalation of organophosphorus toxic substances.
2. The typical clinical manifestations, especially sweating, salivation, muscle tremor, constricted pupils, and elevated blood pressure, are of great significance for diagnosis.
3. Vomitus or exhaled breath has a distinctive garlic-like odor.
4. Blood cholinesterase activity is decreased. If it drops to 70–50% of normal, it is classified as grade I poisoning; 50–30% as grade II; and below 30% as grade III.
5. If the diagnosis is uncertain, the vomitus or the first gastric aspirate can be tested for organophosphorus toxic agents.
6. For cases with unclear history or atypical clinical manifestations, attention should be paid to excluding toxic pneumonia, food poisoning, mushroom poisoning, and encephalitis B.

bubble_chart Treatment Measures

﹝Treatment﹞

(1) Removal of Poison

1. For oral poisoning, immediate induction of vomiting and gastric lavage is necessary. Generally, normal saline or 2% sodium bicarbonate (contraindicated for dipterex poisoning or when the poison is unknown) is used as the lavage solution, repeated multiple times until the lavage fluid is clear and odorless, followed by administration of magnesium sulfate for catharsis.
2. For poisoning via skin absorption, immediately remove contaminated clothing and thoroughly wash hair and skin with clean water or soapy water (soapy water is contraindicated for dipterex poisoning). Rinse the eyes with normal saline for at least 10 minutes.

(2) Removing Toxin Medication

1. Atropine is a cholinergic nerve inhibitor that can counteract the muscarinic effects of acetylcholine, particularly relieving bronchospasm, inhibiting bronchial secretions, preventing pulmonary edema, alleviating gastrointestinal symptoms, and stimulating the respiratory center. For Grade I poisoning, administer atropine intramuscularly at 0.02–0.03 mg/kg per dose, every 2–4 hours until symptoms disappear. For Grade II poisoning, administer 0.03–0.05 mg/kg intravenously, every 0.5–2.0 hours, reducing the dose as the condition improves. For Grade III poisoning with unconsciousness, use an early, sufficient, and repeated continuous dose of 0.05–0.1 mg/kg every 15–30 minutes until symptoms such as dilated pupils, facial flushing, dry mouth, and reduced sweating appear, then gradually reduce the dose and extend the dosing interval until symptoms disappear.
2. Cholinesterase reactivators can remove organophosphates bound to cholinesterase, significantly alleviating nicotinic symptoms and promoting consciousness recovery, but they cannot counteract the muscarinic effects of acetylcholine. Commonly used reactivators include pralidoxime or obidoxime. For Grade I poisoning, administer 15 mg/kg per dose, diluted in 10% glucose solution to form a 2.5% solution for intravenous drip, repeated every 2–4 hours until symptoms disappear. For Grade II poisoning, administer 15–30 mg/kg per dose, repeating half the dose every 2–4 hours, reducing the dose and extending the interval as the condition improves. For Grade III poisoning, administer 30 mg/kg per dose, repeating every half-hour, reducing the dose and extending the interval as symptoms improve.

Combining cholinesterase reactivators with atropine yields synergistic effects, but the atropine dose should be appropriately reduced. For Grade I poisoning, using one medication alone is sufficient. Pralidoxime and obidoxime should not be mixed with alkaline drugs, as hydrolysis may produce cyanide. Intravenous pralidoxime must not extravasate; obidoxime can be administered intramuscularly.
After symptoms disappear, continue observation for 1–2 days. If symptoms recur, promptly manage them and measure cholinesterase activity. If it remains low, continue using cholinesterase reactivators.
(3) General Therapy

1. Maintain airway patency, promptly clear respiratory secretions, and detect and treat respiratory failure early. Endotracheal intubation and positive-pressure oxygen supply may be employed.
2. Promptly manage cerebral edema and pulmonary edema. For convulsions, use phenobarbital; morphine is contraindicated.
3. Monitor and maintain water-electrolyte and acid-base balance.
4. Provide liver protection and safeguard renal function.
5. For critical cases, administer adrenal corticosteroids or transfuse fresh blood.
6. Use cytochrome c, coenzyme A, and ATP to support and protect the nervous system.
7. Administer antibiotics to prevent and treat infections.

bubble_chart Prevention

(1) Strengthen the management of organophosphorus pesticides; (2) Prohibit the use of organophosphorus pesticides for killing lice, mosquitoes, and flies. Clothing and bedding contaminated with organophosphorus pesticides must be thoroughly rinsed repeatedly; (3) Do not consume fish, poultry, or livestock that have died from organophosphorus pesticide dermatitis medicamentosa; (4) Nursing mothers exposed to organophosphorus pesticides must perform thorough cleaning before breastfeeding or caring for infants.