Organophosphorus poisoning

Introduction Common pesticides belonging to organophosphorus poisoning include organophosphorus (3911), internal phosphorus (1059), parathion (1605), dichlorvos, dimethoate, trichlorfon, malathion (4049). The general cause of poisoning is direct skin contact, respiratory inhalation and misuse, misuse. Adsorption through the skin, slow progress; inhalation through the mouth and respiratory tract, rapid progress.

Cause

Organophosphorus pesticides are poisoned by absorption in the body or mucous membranes. The toxicity of organic phosphate insecticides to humans and animals is mainly the inhibition of acetylcholinesterase, causing the accumulation of acetylcholine, causing the cholinergic nerve to be sustained, leading to a series of excitatory and post-depletion. The muscarinic, nicotinic and central nervous system symptoms.

an examination

Related inspection

Cholinesterase serum cholinesterase (CHE)

Examination and diagnosis of organophosphate poisoning

I. Acute poisoning: The onset time of acute poisoning is closely related to the variety, dose and route of invasion. Poisoning through the skin, usually within 2 to 6 days of exposure, oral toxicity within 10min to 2h symptoms. Once the symptoms of poisoning appear, the condition develops rapidly.

1. The symptoms of muscarinic symptoms are the earliest, mainly caused by the excitability of parasympathetic nerve endings, similar to muscarinic effects, which are characterized by increased smooth muscle spasm and glandular secretion. Clinical manifestations include nausea, vomiting, abdominal pain, excessive sweating, tearing, salivation, salivation, diarrhea, frequent urination, incontinence, slow heartbeat, and dilated pupils. Increased bronchospasm and secretions, cough, shortness of breath, pulmonary edema in severe patients.

2. Nicotinic symptoms Acetylcholine is excessively accumulated and stimulated at the striated muscle neuromuscular junction, causing muscle fibrillation in the face, eyelids, tongue, limbs, and whole body striated muscles, and even tonic muscle spasm. Patients often have tight muscles and pressure, and then muscle weakness and paralysis occur. Respiratory muscle paralysis causes peripheral respiratory failure.

The sympathetic ganglia are stimulated by acetylcholine, and the release of catecholamines from the sympathetic nerve fibers at the end of the ganglia causes the blood vessels to contract, causing an increase in blood pressure, an increase in heart rate, and arrhythmia.

3. Central nervous system symptoms The central nervous system is dizzy, headache, fatigue, ataxia, irritability, paralysis, convulsions and coma after being stimulated by acetylcholine.

Second, local damage: dichlorvos, trichlorfon, parathion, and endogenous phosphorus can cause allergic dermatitis after contact with the skin, and blisters and peeling can occur. Dropping of organophosphate insecticides into the eye can cause conjunctival hyperemia and pupil dilation.

Differential diagnosis

Differential diagnosis

a. Mild poisoning: There are dizziness, headache, nausea, vomiting, sweating, chest tightness, blurred vision, weakness and other symptoms, the pupil may shrink. The whole blood cholinesterase activity is generally 50%~70%.

b. Moderate poisoning: The above symptoms are aggravated, there are fasciculation, dilated pupils, mild dyspnea, salivation, abdominal pain, diarrhea, gait, clear or blurred consciousness. Whole blood cholinesterase activity is generally 30%. ~50%.

c. Severe poisoning: In addition to the above symptoms, there are pulmonary edema, coma, respiratory paralysis or cerebral edema. Whole blood cholinesterase activity is generally below 30%.

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