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Lead is used in a variety of industrial and commercial products, such as firearms ammunition, storage batteries, solders, paints, pottery, plumbing, and gasoline and is found in some traditional Hispanic and Ayurvedic ethnic medicines. Lead toxicity usually results from chronic repeated exposure and is rare after a single ingestion. Lead produces a variety of adverse effects on cellular function and primarily affects the nervous system, gastrointestinal tract, and hematopoietic system.

CLINICAL FINDINGS

Lead poisoning often goes undiagnosed initially because presenting symptoms and signs are nonspecific and exposure is not suspected. Common symptoms include colicky abdominal pain, constipation, headache, and irritability. Severe poisoning may cause coma and convulsions. Chronic intoxication can cause learning disorders (in children) and motor neuropathy (eg, wrist drop). Lead-containing bullet fragments in or near joint spaces can result in chronic lead toxicity.

Diagnosis is based on measurement of the blood lead level. Whole blood lead levels above 5 mcg/dL warrant public health investigation. Levels between 10 and 25 mcg/dL have been associated with impaired neurobehavioral development in children. Levels of 25–50 mcg/dL may be associated with headache, irritability, and subclinical neuropathy. Levels of 50–70 mcg/dL are associated with moderate toxicity, and levels greater than 70–100 mcg/dL are often associated with severe poisoning. Other laboratory findings of lead poisoning include microcytic anemia with basophilic stippling and elevated free erythrocyte protoporphyrin.

TREATMENT

A. Emergency and Supportive Measures

The most critical intervention in the treatment of lead poisoning is identification of and removal from the source of exposure. For patients with encephalopathy, maintain a patent airway and treat coma and convulsions as described at the beginning of this chapter.

For recent acute ingestion, if a large lead-containing object (eg, fishing weight) is still visible in the stomach on abdominal radiograph, whole bowel irrigation, endoscopy, or even surgical removal may be necessary to prevent subacute lead poisoning. (The acidic gastric contents may corrode the metal surface, enhancing lead absorption. Once the object passes into the small intestine, the risk of toxicity declines.)

The United States Occupational Safety and Health Administration (OSHA) establishes workplace standards for lead exposure. Contact the regional office for more information. Several states mandate reporting of cases of confirmed lead poisoning.

B. Specific Treatment

The indications for chelation depend on the blood lead level and the patient’s clinical state. A medical toxicologist or regional poison control center (1-800-222-1222) should be consulted for advice about selection and use of these antidotes.

1. Severe toxicity

Patients with severe intoxication (encephalopathy or levels greater than 70–100 mcg/dL) should receive edetate calcium disodium (ethylenediaminetetraacetic acid, EDTA), 1500 mg/m2/kg/day (approximately 50 mg/kg/day) in four to six divided doses or as a continuous intravenous infusion. Most clinicians also add dimercaprol (BAL), 4–5 mg/kg intramuscularly every 4 hours for ...

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