ELEMENTAL MERCURY-POISONING

Three siblings with inhaled elemental mercury toxicity are described, and the signs and symptoms of mercury toxicity, interpretation of mercury concentrations, and management of elemental mercury exposure are reviewed. A 4-year-old girl was admitted to the hospital with a history of fever and increasing irritability, fatigue, malaise, insomnia, headache, anorexia, and ataxia. She was discharged two days later with a diagnosis of acute cerebellar ataxia. During the following 18 days, the child's condition worsened, and she was rehospitalized. Meanwhile her 11-year-old sister was hospitalized for evaluation of fatigue, weakness, lower back pain, and ataxia. The older girl's blood mercury concentration, at 5.5-mu-g/dL, was in the toxic range. Twenty-four-hour urine mercury screening confirmed mercury intoxication in both children. Questioning revealed that the girls' brother had recently spilled 0.5-1 oz of elemental mercury in the house. All family members underwent blood and urine mercury testing. The brother underwent a dimercaprol challenge to determine his tissue mercury burden, which was found to be > 2.4-mu-g/dL. The sisters underwent two courses of chelation therapy with dimercaprol. Symptoms persisted in all three children, and they underwent five 10-day cycles of N-acetyl-D,L-penicillamine (NAP) therapy; the youngest underwent a third dimercaprol regimen. All siblings continued NAP chelation therapy because of extensive tissue mercury burden until the results of repeated urine mercury concentration determinations were normal. The cases presented illustrate several challenges in diagnosing and managing mercury toxicity: lack of agreement upon toxic versus normal levels of blood and urine mercury, lack of correlation between symptomatology and blood and urine test results, and the absence of endpoints for initiation and cessation of chelation therapy. Treatment options include dimercaprol, penicillamine, and the investigational agents NAP and 2,3-dimercaptosuccinic acid (DMSA). DMSA may be the most effective agent available for mercury chelation therapy; however, further study is needed to determine toxic levels of blood and urine mercury and endpoints for initiation and cessation of therapy.