Choreoathetosis secondary to lead toxicity.

Dra. Mariana Spitz – Rua Paulo César de Andrade 200/402 22221-090 Rio de Janeiro RJ Brasil. E-mail: [email protected] Firearm projectiles have been described, albeit rarely, as a cause of lead toxicity. The usual route of lead exposure is oral ingestion, but toxicity secondary to retained bullet fragments has been well documented. Switz et al. described the first case in 1976 – a bullet was lodged in a patient’s left ankle and gastrointestinal symptoms emerged forty years after the wound. Since then several reports followed, including one by Goodheart et al., in 1999, in which the authors reported 25 patients with lead intoxication secondary to intentional petrol sniffing, among whom 8 presented with chorea, though the most common neurological complication was altered mental state, observed in all subjects. The major clinical manifestations of lead toxicity are gastrointestinal, hematological and neurological, namely abdominal cramps, anorexia, nausea, vomiting, constipation, anemia, headache, peripheral neuropathy and encephalopathy. This is characterized by delirium, seizures, somnolence, and even coma. Joint and muscle pain and nephropathy may also be part of the clinical picture. We herein describe an interesting case, where choreoathetosis was attributed to lead toxicity due to retained bullet fragments. CASE A 42-year-old right-handed man was shot in 1987 at the age of 23. He had been a drug addict since the age of 14 – he had used marijuana and inhaled cocaine, but denied intravenous drug use. He was shot in the left side of the abdomen, left shoulder and right thigh. At that time, he had undergone emergency surgery – there was no injury to internal organs, but one of the bullets could not be successfully removed because its location in the lumbar spinal column – in close proximity to the spinal cord – was considered too risky. The patient was discharged a week after the surgery. He remained asymptomatic until February 1994, when he started complaining of frequent abdominal cramps, nausea, vomiting and constipation. On that occasion he was referred to the Orthopedics Clinic of our hospital. On physical examination, he was pale, the abdomen was diffusely tender to palpation, but there were no signs of peritonitis. Neurological examination was normal. His blood exams showed normochromic normocytic anemia and blood lead levels were in the toxic range (112 μg/ dL), which was attributed to the retained bullet. He was diagnosed with lead toxicity and underwent chelation with dimercaprol and EDTA (ethylenediaminetetracetic acid). One month later, since the blood lead levels remained high (65 μg/dL), che-