Diagnosis

A thorough history, including occupational exposures, and typical physical findings, especially tremor or a constellation of signs and symptoms suggesting erethism or acrodynia, may alert the emergency physician to mercury toxicity. Ingestion of mercuric chloride can produce a rapidly fatal course and should be considered in any patient presenting with a corrosive gastroenteritis. Often, however, the diagnosis of mercury toxicity is subtle, arrived at only after many other diagnoses have been investigated.

For all forms of mercury except short-chained alkyls, a 24-h urinary measurement of mercury should be performed. Most unexposed individuals will have levels of 10 to 15 pg/L or less. A level of greater than 20 pg/dL either before or after therapy indicates meaningful exposure. In cases of chronic toxicity, this measurement may be falsely low. Whole-blood mercury levels are less reliable diagnostically. A seafood meal (contaminated with mercury) can temporarily elevate the blood level to the toxic range until the mercury is eliminated.

Short-chained alkyl mercury compounds are predominantly excreted via the bile, rendering urinary measurements invalid. Laboratory diagnosis rests on finding elevated whole-blood mercury levels, since these compounds concentrate in erythrocytes. Whole-blood mercury levels are normally less than 1.5 pg/dL.

Magnetic resonance imaging (MRI) findings in methyl mercury toxicity from ingestion of contaminated seafood include marked atropy of the visual cortex, cerebellar vermis and hemispheres, and the postcentral cortex.27

The differential diagnosis of mercury toxicity depends on the form ingested. Hypothyroidism, apathetic hyperthyroidism, metabolic encephalopathy, senile dementia, adverse effects of therapeutic drugs (such as lithium, theophylline, phenytoin), Parkinson disease, delayed neuropsychiatric sequelae of carbon monoxide poisoning, lacunar infarction, cerebellar degenerative disease or tumor, and ethanol or sedative-hypnotic drug withdrawal may produce behavioral changes or tremor similar to those caused by elemental mercury. Causes of corrosive gastroenteritis such as iron, arsenic, phosphorus, acids, or alkalis should be considered in the differential diagnosis for mercury salts. Many of the differential diagnoses for elemental mercury also apply to the organic mercury compounds. Cerebral palsy, intrauterine hypoxia, and teratogenic effects of therapeutic and illicit drugs and environmental contaminants should be considered when evaluating an infant thought to be affected in utero by the short-chained alkyl mercury compounds.

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