Approach

The primary mode of treatment of lead poisoning is removing the source of exposure.

Any detectable lead level is consistent with exposure to lead. A blood lead reference value of ≥0.17 micromoles/L (3.5 micrograms/dL) is used to identify children with the highest blood lead levels (within the top 2.5 % of US children aged 1-5 years from 2015-2016 and 2017-2018 National Health and Nutrition Examination Survey [NHANES] cycles).[47] A case definition for an elevated blood lead level in an adult (person ≥16 years of age) is ≥0.24 micromoles/L (5 micrograms/dL).[2][3] In an adult, the US Occupational Safety and Health Administration considers a blood lead level of ≥1.2 micromoles/L (25 micrograms/dL) to be serious, requiring inspection.[2]

Need for chelation therapy is determined on an individual case basis, and in consultation with clinicians experienced in the management of lead poisoning. The lead exposure must be discontinued before initiating chelation therapy. Chelation therapy is controversial in cases of asymptomatic and mildly symptomatic intoxication.[67]

Lead encephalopathy is a medical emergency and requires aggressive lead chelation in an intensive care unit (ICU). Much of the toxicity of lead poisoning is not reversible by medical therapy, and lead resides in bone for decades after exposure has ceased. Lead poisoning is therefore a chronic illness.

Removal of source of exposure

Evaluating sources of exposure is necessary in cases of non-occupational exposure.

For most children, deteriorating lead-based paint and soil and dust contaminated by lead paint are the primary sources.[6] However, household interventions for removal or amelioration of lead sources in children with lesser elevations of blood lead are difficult and of limited effectiveness.[42][68]​​[69]​ In the absence of primary sources, alternatives must be evaluated, particularly foods, folk medicines, lead-painted toys, and consumer products.​[10][11][15][16][18][70]​ The water supply may also need to be evaluated, particularly if water is acidic.[17] Some hobbies may expose the hobbyist to high levels of airborne lead.[6][13]​ A detailed list of exposure sources is available from the US Centers for Disease Control and Prevention (CDC).[6]

The source of the exposure should be removed. However, if this is not possible, precautions should be introduced to protect against exposure. It may be necessary for the patient to change home or occupation in severe cases.

Gastrointestinal decontamination following ingestion

For solid lead objects known to be in the stomach (e.g., bullets, lead pellets, jewellery), removal is recommended to prevent potentially severe or fatal poisoning. Methods of removal can include endoscopic procedures, surgery, or whole bowel irrigation. The decision on the approach should be made on each patient basis, following discussion with specialist teams.[71]

Chelation therapy

Chelating agents remove lead from the blood and soft tissues. Need for chelation therapy is determined on an individual case basis, and in consultation with clinicians experienced in the management of lead poisoning.

Chelation therapy may be considered:[13][70][71]​​[72][73]​​

  • in patients who develop symptoms

  • in asymptomatic children with a blood lead level ≥2.2 micromoles/L (≥45 micrograms/dL)

  • in adults with a blood lead concentration >3.4 micromoles/L (>70 micrograms/dL).

Chelation therapy is controversial in cases of asymptomatic and mildly symptomatic intoxication.[67]

Patients usually require hospital admission if chelation therapy is given.[68][74] Dose is tailored to the size and age of the treated patient, as well as the severity of the case.

Lead chelation agents

Available agents include sodium calcium edetate and dimercaprol, which are given parenterally, and succimer and penicillamine, which are given orally.

Oral succimer or intravenous sodium calcium edetate are first-line options for asymptomatic patients. In symptomatic patients, sodium calcium edetate is usually given in combination with dimercaprol to prevent the worsening of symptoms during therapy.

Penicillamine is considered third-line in non-pregnant adults due to the overall toxicity and lack of demonstrated effectiveness associated with its use.

2,3 dimercapto-1-propane sulfonate (DMPS) is a commonly used agent for heavy metal intoxication in Europe and Asia, but is not available in the US. Other chelation agents may be available.

Efficacy and monitoring

The efficacy of chelation therapy should be monitored by measuring 24-hour urine. A lead-to-chelant ratio >1 microgram lead per 1 milligram chelant indicates effective lead chelation; chelation therapy should be discontinued if this is not achieved. The yield will fall with each subsequent day of chelation as the chelatable pool is depleted. The usual course of initial therapy is 5 days of sodium calcium edetate or 19 days of succimer. To evaluate for rebound (as lead stored in soft tissues and bone is released) and to determine whether additional chelation is indicated, a blood lead level should be taken 2 to 4 weeks after completion of chelation therapy.[71] This interval may be shorter in patients with high initial blood lead concentrations.[71] 

Chelating agents may be effective in alleviating acute symptoms (including central nervous system symptoms and abdominal pain [lead colic]), but their effectiveness at improving outcomes is limited. One major randomised clinical trial of succimer chelation for children reported transient declines in blood lead, but no short- or long-term improvement in neurological outcome.[75] There is no evidence that chelation improves blood pressure in lead-exposed children.[76]

Chelation therapy in pregnancy

Women with confirmed blood lead levels of ≥2.2 micromoles/L (≥45 micrograms/dL) should be treated in consultation with clinicians experienced in the management of lead toxicity and high-risk pregnancy.[65]

Chelation is usually contraindicated in pregnancy because succimer is a likely human teratogen, and there is considerable risk that redistribution of lead during chelation may lead to transiently increased exposure of the fetus to lead.

However, if a pregnant patient develops lead encephalopathy, the risks of chelation therapy must be carefully weighed against the threat to the life of the mother and fetus posed by the encephalitis itself, and chelation therapy may be appropriate in this setting.[71]

Management of encephalopathy

Both children and adults may develop symptoms of an acute encephalopathy. In children, this often manifests as altered sensorium and seizures and may progress to coma and death. Cerebellar signs are often prominent.

Aggressive combined chelation therapy with parenteral sodium calcium edetate and dimercaprol should be instituted in an ICU; combined therapy dramatically improves outcome.[77]​ Additional supportive care may include circulatory and electrolyte support, endotracheal intubation and mechanical ventilation, prevention and management of secondary bacterial infections, deep venous thrombosis prophylaxis, and gastrointestinal (ulcer) prophylaxis.

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