What Is Organophosphate Poisoning?

Organophosphorus pesticides (OPS) are the most widely used pesticides in China. It mainly includes dichlorvos, parathion (1605), parathion (3911), systemic phosphorus (1059), dimethoate, trichlorfon, and malathion (4049). Acute organophosphorus pesticide poisoning (AOPP) refers to a series of injuries mainly caused by nervous system damage caused by a large amount of organophosphorus pesticides entering the human body for a short time. Clinically, it mainly includes cholinergic excitement or crisis in patients with acute poisoning. Post-intermediate syndrome (IMS) and delayed peripheral neuropathy (OPIDPN). Every year millions of people around the world develop AOPP, of which about 300,000 people die, and most of them occur in developing countries.

Basic Information

English name

acute organophosphorus pesticide poisoning, AOPP

Visiting department

Emergency Department

Common causes

Ingested by mistake or taken orally, organic phosphorus falling on the skin when spraying pesticides, or organic phosphorus in the air caused by breathing into the body

Common symptoms

Cholinergic nerve excitement, crisis, intermediate syndrome, organophosphate delayed neuropathy, etc.

Contagious

no

Causes of acute organophosphorus pesticide poisoning

Organophosphorus poisons quickly combine with cholinesterase in the body after entering the body to generate phosphorylated cholinesterase, which makes cholinesterase lose the function of hydrolyzing acetylcholine, resulting in a large accumulation of cholinergic neurotransmitters and acting on the bile Alkali receptors cause severe neurological dysfunction, especially respiratory dysfunction, which affects life activities. The M-like effect caused by parasympathetic nerve excretion causes a large number of glands in the respiratory tract of the patient, causing severe pulmonary edema, exacerbating hypoxia, and the patient may die due to respiratory failure and hypoxia.

AOPP can also cause heart damage and can even lead to sudden cardiac death. The cause may be toxic myocarditis caused by direct damage to the heart, coupled with hypoxia, electrolyte disturbances, acidosis, etc., which can indirectly aggravate heart damage. At the same time, patients with sympathetic and parasympathetic nerves become dysfunctional during AOPP, causing arrhythmias. In addition, if the amount of atropine is too large during treatment, the patient's heart rate will be too fast and blood supply will be insufficient. At the same time, the heart's oxygen consumption will increase, leading to myocardial ischemic damage, and the stability of the ECG activity will be affected. Therefore, it is prone to malignant arrhythmias and even sudden death. .

Clinical manifestations of acute organophosphorus pesticide poisoning

Acute organophosphorus pesticides often develop rapidly after entering the human body, and patients quickly develop the following conditions:

1. Cholinergic nerve excitation and crisis

(1) Muscarinic symptoms are mainly smooth muscle spasm and increased glandular secretion caused by parasympathetic nerve terminal excitement. Clinical manifestations include nausea, vomiting, abdominal pain, sweating, tearing, runny nose, drooling, diarrhea, frequent urination, urinary incontinence, slowing heartbeat and pupil reduction, bronchospasm and increased secretions, cough, shortness of breath, and pulmonary edema in severe patients .

(2) Nicotinic symptoms Acetylcholine accumulates and stimulates excessively at the striated neuromuscular junction, causing muscle fibers to tremble in the face, eyelids, tongue, limbs, and systemic striated muscle, and even systemic muscle tonic spasm. Patients often have tightness and pressure throughout the body, followed by muscle weakness and paralysis. Severe cases may have respiratory muscle paralysis, causing peripheral respiratory failure. In addition, since the sympathetic ganglion is stimulated by acetylcholine, the catecholamine released from the end of the sympathetic nerve fibers after the festival causes the blood vessels to constrict, resulting in increased blood pressure, accelerated heartbeat and arrhythmia.

(3) Symptoms of the central nervous system The central nervous system has symptoms of dizziness, headache, fatigue, ataxia, irritability, delirium, convulsions, and coma.

Intermediate syndrome

Intermediate syndrome (IMS) refers to delayed release of organophosphorus poisons, redistribution in the body, or insufficient medication, which causes cholinesterase to be inhibited for a long time and accumulated in the synaptic space. High concentrations of acetylcholine continue to stimulate the postsynaptic membrane A series of symptoms caused by impaired transfer of nicotine receptors and impaired transmission at the neuromuscular junction. Generally, after the symptoms of acute poisoning are alleviated 1 to 4 days after acute poisoning, the patient suddenly appears clinical features characterized by respiratory muscles, muscles dominated by cerebral neuromotor movements, and weakness of the proximal muscles of the limbs. The patient developed paralysis of the neck, upper limbs and respiratory muscles. Involved cranial nerves, drooping eyelids, eye abduction disorders and facial paralysis. Myasthenia can cause peripheral respiratory failure. At this time, immediate respiratory support is needed, and if there is no timely intervention, it may easily lead to death.

3. Organophosphorus delayed neuropathy

Acute poisoning of organophosphorus pesticides generally has no sequelae. Individual patients may develop delayed neuropathy 2 to 3 weeks after the symptoms of acute poisoning disappear, mainly involving the extremities of the limbs, and neurological symptoms such as paralysis of the lower limbs and muscle atrophy of the extremities may occur. At present, it is believed that this lesion is not caused by the inhibition of cholinesterase, and may be caused by the organophosphorus pesticide inhibiting and aging the neural target esterase.

4. Other performance

Dichlorvos, trichlorfon, parathion, and systemic phosphorus can cause allergic dermatitis after contact with the skin, and blisters and peeling can occur. In severe cases, chemical skin burns can occur, affecting the prognosis. Organophosphorus pesticide drops into the eyes can cause conjunctival hyperemia and pupil shrinkage.

Examination of acute organophosphorus pesticide poisoning

Clinical examination

(1) Corresponding signs of AOPP have been checked by the system .

(2) Respiratory system examination Signs of pulmonary edema (wet lungs covered with wet snoring).

2. Laboratory inspection

(1) Determination of cholinesterase activity It is a specific marker enzyme for organophosphorus pesticide poisoning, but the degree of decrease in enzyme activity is not completely consistent with the condition and prognosis.

(2) Determination of creatine kinase (CK) and troponin (cTnI) can reflect the degree of myocardial damage when AOPP.

(3) Miscellaneous early detection of blood, urine, and gastric juice poisoning is of guiding value for diagnosis and treatment.

Diagnosis of acute organophosphorus pesticide poisoning

Medical history

Patients have a history of exposure to organophosphorus pesticides, such as oral, skin contact or inhalation of organophosphorus pesticide droplets during agricultural production. The onset time of poisoning is closely related to the poison species, dose and invasive route.

2. Clinical manifestations and laboratory tests

The patient's condition met the clinical and laboratory characteristics of AOPP.

3. Degree of acute poisoning

(1) Mild poisoning Symptoms include dizziness, headache, nausea, vomiting, sweating, chest tightness, blurred vision, weakness, and dilated pupils. Cholinesterase activity is generally 50% to 70%.

(2) Moderate poisoning In addition to the above symptoms, there are muscle fiber tremor, marked reduction of pupils, mild dyspnea, salivation, abdominal pain, staggering gait, and clear consciousness. Cholinesterase activity is generally 30% to 50%.

(3) Severe poisoning In addition to the above symptoms, coma, pulmonary edema, respiratory paralysis, and cerebral edema occurred. Cholinesterase activity is generally below 30%.

Differential diagnosis of acute organophosphorus pesticide poisoning

Since one of the typical symptoms of organophosphorus poisoning is pulmonary edema, it is easy to be confused with cardiogenic pulmonary edema (heart failure), and clinical identification is needed. Medical history can be used as a powerful identification point. Patients with cardiogenic pulmonary edema often have a history of severe heart disease, while those with AOPP have a history of toxic exposure.

Treatment of acute organophosphorus pesticide poisoning

On-site first aid

Removing poisons as quickly as possible is the key to saving patients' lives. For those who have skin poisoning, they should immediately remove the contaminated clothes in time, and repeatedly rinse with plenty of water at the scene. For those who are aware of oral poisons, they should immediately induce repeated vomiting at the scene. Never take the patient directly to the hospital without doing anything, otherwise it will increase the absorption of poisons and aggravate the condition.

2. Clear the body of poison

(1) Gastric lavage Thorough gastric lavage is the most effective way to cut off the continued absorption of poisons. Oral poisoning uses clean water, 2% sodium bicarbonate solution (dipterex should not be used) or 1: 5000 potassium permanganate solution (parathion (Do not use) Repeat gastric lavage until it is clear. Because the poison is not easy to be drained, the gastric tube should be retained and the gastric lavage should be repeated regularly.

(2) Enema The organophosphorus pesticide is severely poisoned, and when breathing is inhibited, magnesium sulfate cannot be used for drainage, to avoid large absorption of magnesium ions and aggravate respiratory depression.

(3) Adsorbent After gastric lavage, the patient is injected with activated carbon orally or intragastrically. Activated carbon will not be broken down and absorbed in the gastrointestinal tract, which can reduce the absorption of toxicants, reduce the metabolic half-life of toxicants, and increase their excretion rate.

(4) Blood purification has significant effects in the treatment of severe poisoning, including hemoperfusion, hemodialysis, and plasma exchange. It can effectively remove organophosphorus pesticides released from the blood and tissues, and improve the cure rate.

3. Combined use of antidote and revitalizer

(1) Atropine The principle is to promptly, adequately and repeatedly administer until atropine is achieved. Atropine should be given immediately, intravenously, and then every 10-20 minutes depending on the condition. When conditions permit, it is best to use a continuous injection of atropine with a micropump to avoid the peak and valley phenomenon of intermittent intravenous drug concentration.

(2) Atropine The pupil gradually enlarges and no longer shrinks, but there is a light reaction, salivation, runny nose stops or decreases significantly, cheek flushing, dry skin, fast and powerful heart rate, and lung snoring is significantly reduced or disappeared. After achieving atropine, the dose should be gradually reduced or the interval between medications should be extended to prevent atropine poisoning or repeated illness. If the patient has dilated pupils, blurred consciousness, restlessness, convulsions, coma, and urinary retention, it is suggested that atropine poisoning should be stopped.

(3) Intramuscular injection for patients with severe poisoning, once every 4 to 6 hours.

(4) Penhexyl ether injection (Chang Toning) is a new type of long-acting anticholinergic drug that is safe, effective, and low toxicity. The amount is given as mild poisoning, moderate poisoning, and severe poisoning. After 30 minutes, half of the first dose can be applied. In the late stage of poisoning or after the aging of cholinesterase, atropine can be maintained by changtonin at intervals of 8-12 hours. ChangTonin is superior to atropine in many aspects in the treatment of organophosphorus pesticide poisoning. It is an ideal substitute for atropine, and it is the first choice for treating severe organophosphorus pesticide poisoning or combined atropine poisoning.

4. Other treatments

Keep the airway open; give oxygen or use a respirator; use booster drugs for patients with shock; apply dehydrating agents and adrenal corticosteroids for cerebral edema; use barbiturate for patients with local and systemic muscle tremors and convulsions; For respiratory failure patients, naloxone can be used in addition to the ventilator; for critically ill patients, blood transfusion and blood exchange therapy can be used.

Note: It is not advisable to enter a large amount of glucose, CoA, ATP in the early stage of poisoning, because they can increase the synthesis of acetylcholine and affect the activity of cholinesterase. Vitamin C injection is not conducive to the decomposition of toxicants, which affects the increase of cholinesterase activity, and it is not suitable for early use. 50% magnesium sulfate, which can stimulate the duodenal mucosa after oral administration of bile-drugs, causes the gallbladder to contract, and organophosphorus pesticides retained in the gallbladder are discharged with the bile, causing 2 poisoning. Metoclopramide, cisapride, morphine, hibernating spirit, quinolone, citicoline, vitamin B ₅ , aminophylline, and reserpine can aggravate the symptoms of poisoning and should be disabled.

Prevention of acute organophosphorus pesticide poisoning

Establish and improve a series of pesticide sales, transportation and storage systems. At the same time, safety publicity and education should be strengthened so that the masses can take good care of organophosphorus pesticides and do not mix them with daily necessities to avoid being mistakenly taken.