Organophosphates and carbamates are often insecticides that inhibit cholinesterase activity, muscarinic acute manifestations (eg. As salivation, lacrimation, urination, diarrhea, vomiting, Bronchorrhö, bronchospasm, bradycardia, miosis) and some nicotinic symptoms leads, including muscle twitching and Schwächgefühl. Neuropathy dates may change to weeks after exposure to develop. Diagnosis is clinical and sometimes after a trial with atropine, a measurement of the erythrocyte acetylcholinesterase levels, or both. Bronchorrhö and bronchospasm be treated with high-dose titrated atropine. A neuromuscular toxicity with i.v. Pralidoxime treated.

Organophosphates and carbamates are chemically structurally different, but both inhibit cholinesterase activity. Some will be used therapeutically, to make a neuromuscular blockade reversed (z. B. neostigmine, pyridostigmine, edrophonium) or in the treatment of glaucoma, myasthenia gravis, and Alzheimer’s disease (z. B. echothiophate, pyridostigmine, tacrine, donepezil).

Organophosphates and carbamates are often insecticides that inhibit cholinesterase activity, muscarinic acute manifestations (eg. As salivation, lacrimation, urination, diarrhea, vomiting, Bronchorrhö, bronchospasm, bradycardia, miosis) and some nicotinic symptoms leads, including muscle twitching and Schwächgefühl. Neuropathy dates may change to weeks after exposure to develop. Diagnosis is clinical and sometimes after a trial with atropine, a measurement of the erythrocyte acetylcholinesterase levels, or both. Bronchorrhö and bronchospasm be treated with high-dose titrated atropine. A neuromuscular toxicity with i.v. Pralidoxime treated. Organophosphates and carbamates are chemically structurally different, but both inhibit cholinesterase activity. Some will be used therapeutically, to make a neuromuscular blockade reversed (z. B. neostigmine, pyridostigmine, edrophonium) or in the treatment of glaucoma, myasthenia gravis, and Alzheimer’s disease (z. B. echothiophate, pyridostigmine, tacrine, donepezil). Some organophosphates were developed as nerve gases. One of them, Sarin was used by terrorists. Organophosphates and carbamates are common insecticides (see Table: symptoms and treatment of specific poisons). The substances most frequently involved in poisoning of people are carbamates: aldicarb and methomyl organophosphates: chlorpyrifos, diazinon, Dursban, fenthion, malathion and parathion organophosphates and carbamates are most common causes of poisoning and toxic-induced deaths. Pathophysiology organophosphates and carbamates are absorbed by the gastrointestinal tract, lungs and skin. They inhibit the plasma and coated erythrocytes cholinesterase and prevent the breakdown of acetylcholine, resulting in an accumulation in the synapses. Carbamate spontaneously anaktiveirt within about 48 hours after exposure. However, organophosphates can irreversibly bind to cholinesterase. Symptoms and signs of acute treatment organophosphates and carbamates cause similar initial findings such as acute muscarinic cholinergic and nicotinic Toxidrome (see Table: Common Toxic Syndromes (Toxidrome)). Muscle twitching and weakness are typical. Respiratory findings include shortness of breath, wheezing and hypoxia, which can be severe. Most patients have bradycardia and, in severe poisoning, hypotension. CNS toxicity is common, sometimes, often associated with cramps and irritability with lethargy and coma. Pancreatitis is possible and organophosphates can cardiac arrhythmias such as AV block and QTc interval prolongation führen.Verzögerte findings weakness, in particular the proximal, skull and respiratory muscles can be 1-3 days after exposure to organophosphates or, rarely, opposite carbamates develop, even under treatment (advanced disease). These symptoms disappear after 2-3 weeks. Some organophosphates (eg. As chlorpyrifos, Triorthocresylphosphat) can lead to neuropathy, which can use 1-3 weeks after exposure. The mechanism is probably independent of the erythrocyte cholinesterase and the risk is independent of the severity of the poisoning. Long-term, sustained effects of organophosphate poisoning can be cognitive deficits or Parkinson’s disease. Diagnosis muscarinic Toxidrome with prominent Atemwegbefunden, pinhead large pupils, muscle twitching and weakness Sometimes erythrocyte cholinesterase levels The diagnosis is usually based on the characteristic muscarinic Toxidrom in patients with neuromuscular and respiratory findings, especially in patients with suspected exposure. If the findings are not unique, a reversal or reduction of muscarinic symptoms after a dose of 1 mg atropine (0.01-0.02 mg / kg in children) can confirm the diagnosis. The specific poison should, if possible, be identified. Many organophosphates smell characteristically garlic or mineral oil. The erythrocyte cholinesterase activity, which can be measured by some laboratories, indicates the severity of the poisoning. If it can be determined rapidly, the values ??can be used to monitor the effectiveness of treatment, but the patient’s clinical response is the most important indication. Treatment Supportive treatment atropine in respiratory symptoms decontamination pralidoxime in neuromuscular manifestations hospital treatment Supportive treatment is most important. Patients should be monitored because of the weakness of the respiratory muscles closely for respiratory failure. Atropine is given in amounts sufficient to relieve the bronchospasm and the Bronchorrhö, and not primarily to normalize the pupil size or heart rate. The initial dose is 2-5 mg i.v. (0.05 mg / kg in children); the dose may be every 3-5 minutes continuously doubled. Several grams of atropine may be needed to treat severely poisoned patients. A decontamination is initiated as soon as possible after the stabilization. Caregivers should be careful while taking care not to be contaminated themselves. For external contamination, the clothing is removed and rinsed thoroughly the body surface. At a dose, the back is less than 1 hour, activated carbon can be used. A gastric emptying is not usually applied. If it is still made, then, to prevent aspiration only after Intbation. Pralidoxime (pyridin-2-aldoximmethoxyiodid, 2-PAM) is added after the atropine to alleviate neuromuscular symptoms. 2-PAM (1-2 g in adults, 20-40 mg / kg in children) is about 15-30 min i.v. administered after exposure to organophosphate or carbamate, for frequently the identity of the poison is initially unclear. An infusion can be given (8 mg / kg / h for adults, 10-20 mg / kg / h in children). After bolus Benzodiazepines are used for seizures. Prophylactic given Diazepam can help apply neurocognitive late effects of moderate to severe organophosphate poisoning to verhindern.Behandlung at the scene people had with these poisons contact and are not near a hospital, may have low doses of atropine by available in pharmacies, self-injection products made specifically for use (2 mg for adults and children> 41 kg; 1 mg for children aged 19-41 kg, 0.5 mg for children <19 kg). The self-injection of 10 mg Diazepam is also recommended for persons who are victims of a chemical weapons attack were. Summary organophosphates are used as insecticides, medical drugs and biological weapons. A tentative diagnosis when patients have a muskarinartiges, cholinergenes Toxidrom with significant respiratory and neuromuscular findings Solte be found. The diagnosis is made by the response to atropine and sometimes by determining the erythrocyte cholinesterase levels. The treatment is supported with atropine to alleviate bronchospasm and Bronchorrhö and 2-PAM to control the neuromuscular symptoms.

Health Life Media Team

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