Paraquat poisoning

Introduction to paraquat poisoning It is a strong herbicide (herbicides) that kills weeds and has a strong toxic effect on humans and animals. Most of them are poisoned by oral administration or suicide, but they can also be killed by skin and respiratory absorption poisoning, which has become a common cause of pesticide poisoning death. The adult lethal dose is 5-15 ml (20-40 mg/kg) in a 20% aqueous solution. Paraquat is absorbed through the digestive tract, skin and respiratory tract. Toxicity affects multiple organs throughout the body. In severe cases, it can cause multiple organ dysfunction syndrome (MODS). The lung is the main target organ, which can lead to paraquat lung. Acute lung injury (ALI) or acute respiratory distress syndrome (ARDS), late alveolar and interstitial fibrosis, is the main cause of death caused by paraquat poisoning, the mortality rate is as high as 50% to 70%. basic knowledge The proportion of illness: 0.0083% Susceptible people: no specific people Mode of infection: non-infectious Complications: pulmonary fibrosis

The cause of paraquat poisoning

Paraquat absorbs quickly after oral administration, mainly accumulates in the lungs and muscles, and excretion is slow, so the toxic effect can persist. The lesion mainly occurs in the lungs, called paraquet lung, and the herbicide can produce peroxide ions. (O-2) damages type I and type II alveolar epithelial cells, causing swelling, degeneration and necrosis, inhibiting the production of pulmonary surfactant. The basic lesions are proliferative bronchiolitis and alveolitis. The morphological changes of the lung depend on the photometry. The length of survival after the entry, the death within 1 week, showing lung congestion, edema, increased lung weight, similar to oxygen poisoning, survival for more than 1 week, alveolar exudate (including abscisuous alveolar epithelial debris, giant Phagocytosis, erythrocyte and transparent membrane), mononuclear infiltration, hemorrhage and interstitial fibroblast proliferation, alveolar interstitial thickening, the result of extensive fibrosis, formation of honeycomb lung and bronchiectasis, paraquat Poisoning can cause tubular necrosis, central lobular cell damage, necrosis, myocarditis, pulmonary thickening, and adrenal cortical necrosis.

Paraquat poisoning prevention

prevention:

1. Strictly implement the relevant provisions on pesticide management, implement production licenses and sales franchise systems to avoid the spread of pesticides and random purchases.

2. Carry out safe use of pesticide education and improve anti-virus capabilities.

3. Improve production process and spraying equipment to prevent running, running, dripping and leaking.

4, follow the safe operating procedures, such as standing on the wind to retreat spray, wear long trousers, wear protective glasses, use plastic film apron, once the skin is contaminated, should be cleaned in time.

5, strict management, to avoid drug loss, individuals do not save medicine: add warning color, odor or emetic in the liquid to prevent accidental service.

Paraquat poisoning complications Complications pulmonary fibrosis

Oral lethal dose is about 14mg/Kg, and severe poisoning mortality is as high as 60%-80%. Survivors often leave severe pulmonary fibrosis.

Symptoms of paraquat poisoning Common symptoms Hematuria, abdominal pain, purpura, respiratory failure, dyspnea, protein urinary tract and pharyngeal burning sensation

Ingestion of herbicides can cause burning sensation in tongue, mouth and throat, esophagitis and gastritis, vomiting and abdominal pain. Excretion of drugs from the kidney can damage the renal tubules, produce proteinuria, hematuria, blood urea nitrogen, creatinine High performance of renal dysfunction, the respiratory system mainly manifests as progressive dyspnea and purpura, eventually leading to respiratory failure and death, chest X-ray findings: initially scattered scattered fine-spotted shadows, more of the following lung fields, rapid progress, lesions The fusion is characterized by severe pulmonary edema, pulmonary function is mainly characterized by carbon monoxide diffusion disorder, moderate airway obstruction and/or restrictive ventilation abnormalities, and heart, liver and adrenal intoxication can cause corresponding symptoms and signs.

Paraquat poisoning check

1, laboratory examination: peripheral blood white blood cell count is significantly increased; paraquat can be detected in hematuria; alveolar / pulmonary PaO2 difference increased, severe hypoxemia.

2, X-ray examination of the lungs: early poisoning (3 days - 1 week), mainly for increased lung texture, pulmonary interstitial inflammation, visible spots, flaky shadows, decreased lung translucency or frosted glass, medium term ( 1-2 weeks), lung consolidation or large consolidation, partial pulmonary fibrosis occurred, and pulmonary fibrosis and atelectasis occurred in the later stage (after 2 weeks).

Diagnosis and identification of paraquat poisoning

1. History of taking paraquat - a description of the patient or other insider.

2. Evidence of taking paraquat (suicide suicide note, empty paraquat package, residue, smell and color)

3, clinical signs, especially severe vomiting, mucosal redness and pain or ulceration (usually appear several hours after oral administration).

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