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Mercury Poisoning: Introduction |  |
| Mercury exists in a variety of organic and inorganic forms. The replacement of commercial mercurial compounds, including antiseptics (eg, mercurochrome), diuretics, and fungicides by other agents has decreased the likelihood of mercurial toxicosis; however, the possibility of exposure to environmental sources of organic methylmercury exists. |
| Inorganic Mercurials: |
| These include the volatile elemental form of mercury (used in thermometers) and the salted forms (mercuric chloride [sublimate] and mercurous chloride [calomel]). Ingested inorganic mercury is poorly absorbed and low in toxicity. Large amounts of these mercurials are corrosive and may produce vomiting, diarrhea, and colic. Renal damage also occurs, with polydipsia and anuria in severe cases. In rare cases of chronic inorganic mercurial poisoning, the CNS effects resemble those
of organic mercury poisoning. Mercury vapor from elemental mercury produces corrosive bronchitis and interstitial pneumonia and, if not fatal, may lead to neurologic signs as do organic forms. |
| Emesis followed by initiation of chelation therapy (see below) is recommended after acute oral ingestion. Oral administration of sodium thiosulfate to bind mercury still in the gut may be beneficial. |
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| Organic Mercury: |
| Inorganic mercury is converted to the organic alkyl forms, methylmercury and ethylmercury, by microorganisms in the sediment of rivers, lakes, and seas. Marine life accumulate the most toxic form, methylmercury, and fish must be monitored for contamination. There are reports of commercial cat food causing severe neurologic disturbances in cats fed an exclusive tuna diet for 7-11 mo. |
| The organic mercurials are absorbed via all routes and bioaccumulate in the brain and to some extent in the kidneys and muscle. Aryl mercurials (eg, phenylmercury fungicide) are slightly less toxic and less prone to bioaccumulation. Animals poisoned by organic mercury exhibit CNS stimulation and locomotor abnormalities after a lengthy latent period (weeks). Signs may include blindness, excitation, abnormal behavior and chewing, incoordination, and convulsions. Cats show hindleg
rigidity, hypermetria, cerebellar ataxia, and tremors. Mercury is also a mutagen, teratogen, and a carcinogen, and is embryocidal. Differential diagnoses include conditions with tremors and ataxia as predominant signs, such as ingestion of other metals and insecticides and cerebellar lesions due to trauma or feline parvovirus. |
| Histologic lesions include degeneration of neurons and perivascular cuffing in the cerebrocortical gray matter, cerebellar atrophy of the granular layer, and damage to Purkinje cells. Laboratory diagnosis must differentiate between normal concentrations of mercury in tissue (especially whole blood, kidney, and brain) and feed (<1 ppm) and concentrations associated with poisoning. |
| Neurologic signs may be irreversible once they develop. Chelation therapy with dimercaprol (3 mg/kg body wt, IM, every 4 hr for the first 2 days, qid on the third day, and bid for the next 10 days or until recovery is complete) has been beneficial. When available, the water soluble, less toxic analog of dimercaprol, 2,3-dimercaptosuccinic acid, is the chelator of choice for organic mercury poisoning. Penicillamine (15-50 mg/kg, PO) may be used only
after the gut is free of ingested mercury and renal function has been established. |
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