Mercury poisoning treatment3/21/2024 Oral succimer follows this treatment at a dose of 10 mg/kg per dose orally 3 times a day for 5 days, then twice daily for 14 days. The dosing regimen for dimercaprol starts at 5 mg/kg per dose every 4 hours for 48 hours, followed by 2.5 mg/kg per dose every 6 hours for 48 hours, and then 2.5 mg/kg per dose every 12 hours for 7 days. Inorganic mercury and elemental mercury can be treated with an initial course of intramuscular dimercaprol and then followed by oral succimer. Chelation should be initiated early in mercury exposure cases as it may decrease the toxic effects. Charcoal which is not a highly effective binding metal should still be attempted, in addition to whole bowel irrigation, even if only minimally effective. GI decontamination should be attempted if possible, although there are risks of perforation. Monitor and manage any complications of the toxicity, such as respiratory distress, gastrointestinal bleeding, renal failure, and bowel perforation. After the patient and department are safe from exposure, supportive measures should begin, including oxygen and intravenous (IV) fluids. Initial treatment in the emergency department consists of removal from the exposure and decontamination of the patient. In addition to the severe neurologic findings, patients also develop mild renal, GI, and respiratory distress. More severe cases can progress to ataxia, blindness, movement disorders, and dementia. Early findings of orofacial paresthesias, headaches, tremors, and fatigue can occur. The related toxic symptoms typically occur weeks to months after exposure. Organic mercury toxicity is primarily neurologic and is usually permanent. Subacute mercury salt ingestion can lead to a wide array of GI, neurologic, and renal symptoms, including loose teeth, salivation, burning sensation in the mouth, tremors, erethism, nephrotic syndrome, proteinuria, neurasthenia, and acrodynia. The most common findings of significant ingestion include abdominal pain, hemorrhagic gastroenteritis, acute tubular necrosis, and shock. Acute ingestion of organic salts typically will cause a metallic taste and a graying of the oral mucosa. Ingested elemental mercury can be metabolized to inorganic mercury salts and can also develop those symptoms. Severe exposure may lead to respiratory distress and failure. Primary absorption of elemental mercury is through inhalation, which causes shortness of breath, cough, fever, nausea, vomiting, diarrhea, headache, metallic taste, salivation, and visual disturbance. Neurologic findings on MRI of atrophy of the cerebellar hemisphere, postcentral gyri, and calcarine area correlate with ataxia, sensory neuropathy, and visual field constriction. The organic mercury deposits in the CNS are thought to be converted to inorganic mercury, causing toxicity. Organic mercury, such as methylmercury, is lipophilic and distributes across all tissues, including the central nervous system. Inorganic salts have low lipid solubility, so they have poor penetration of the blood-brain barrier, but due to slow elimination, there is some accumulation. This damage is from the direct oxidative effects of mercuric ions. Mercury salts cause damage to the gastrointestinal tract mucosa and proximal renal tubules early after exposure. Inhibition of enzymes such as choline acetyltransferase and catechol O-methyltransferase can lead to acetylcholine deficiency, hypertension, and tachycardia. Therefore, mercury can cause significant dysfunction of enzymes, membranes, transport mechanisms, and structural proteins. Mercury primarily binds to sulfhydryl groups and secondarily to amide, carboxyl, and phosphoryl groups, which interrupt cellular enzymes and protein systems throughout the body. Freshwater fish, including pike, walleye, muskellunge, and bass, should be eaten in moderation. These fish include shark, king mackerel, tilefish, swordfish, and tuna. Since the fetal brain is more susceptible to toxicity, the FDA recommends pregnant or breastfeeding women, as well as children, avoid fish with high mercury content. The primary source of dietary ingestion is the consumption of contaminated fish. In Iraq, over 6000 people developed toxicity from eating bread baked with grain that was treated with methylmercury-based fungicide.Ĭhildren and fetuses have a higher susceptibility to mercury toxicity and, therefore, more severe clinical manifestations. Mercury was dumped into Minamata Bay, and members of the community developed toxicity from eating the fish containing methylmercury. Two major toxic incidents occurred in Minamata Bay, Japan, and Iraq. However, internationally, there are much higher rates of exposure, including mercury mining in China, small-scale gold mining, and food contaminated with mercury. In the United States, a 2013 report documented 1300 single mercury exposures, and only 24 had moderate to major effects.
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