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Pediatric Lead Toxicity Treatment & Management

  • Author: Mohamed K Badawy, MD, FAAP; Chief Editor: Timothy E Corden, MD  more...
Updated: Jun 22, 2016

Approach Considerations

Treatment of lead toxicity involves the prevention of further lead exposure, decontamination, chelation, and supportive therapy.

Outpatient treatment seems to be a good option for asymptomatic children with blood lead levels (BLLs) in the range of 45-69 μg/dL. However, be absolutely sure that the environment in which the child is placed is safe and lead free. If this is impossible to ensure, inpatient treatment is needed until the environmental situation is investigated in collaboration with social services and the local health department.

For patients with a BLL 70 μg/dL or higher, hospitalize the patient, obtain a confirmatory venous BLL, and initiate chelation with dimercaprol and calcium disodium edetate (EDTA). Because calcium EDTA does not cross the blood-brain barrier, its use as the only agent in this situation is not recommended because of the possibility of lead redistribution from the soft tissues to the central nervous system (CNS). Pretreatment with dimercaprol (which crosses the blood-brain barrier) is recommended.

When children have lead encephalopathy, the best approach is to transfer them to a children's hospital where pediatric intensivists and other resources are available.

All children being treated for lead poisoning need close follow-up care. Monitoring their BLLs is important. Closely monitor cardiovascular and mental status in patients with lead poisoning, maintain an adequate urine output, and assess renal and hepatic functions.



Decontamination may be performed in patients with acute lead ingestion in whom lead paint chips are identified on plain abdominal radiographs.

Gastric lavage may be performed. Secure the airway before the initiation of gastric lavage in an obtunded child with acute lead ingestion. The use of gastric lavage is controversial because lead paint chips, being large in size, are believed to be poorly absorbed and mainly excreted in stools. In 1997, the American Academy of Clinical Toxicology (AACT) stated that no evidence indicates that gastric lavage use improves clinical outcomes.

Although whole-bowel irrigation (WBI) may be performed to decrease the bioavailability of paint chips, it remains a theoretical option for lead ingestion because insufficient data support or exclude its use. Charcoal binds poorly to lead, and no evidence supports its use in acute lead ingestion.



Use of chelating agents is recommended for children with venous lead levels of 45 μg/dL or higher. These include oral succimer and parenteral  calcium disodium edetate (calcium EDTA) and British antilewisite (BAL; dimercaprol).

Significant intravascular hemolysis may occur in patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency who are receiving BAL as a chelating agent. Iron supplementation should be avoided in patients receiving BAL chelation therapy because BAL forms a complex with iron, leading to toxicity. Diphenhydramine may help to alleviate the adverse effects of British antilewisite (BAL).


Supportive Therapy

Most children with lead poisoning are asymptomatic and are identified by screening. However, certain children may develop acute lead encephalopathy. In such circumstances, protection of the airway via endotracheal intubation may be necessary.

In the event of seizures, benzodiazepines are indicated. Maintenance of seizure control with phenobarbital may be needed. If seizures are difficult to control, presume the presence of increased intracranial pressure and pursue measures to decrease it (eg, hyperventilation, mannitol, steroids).

Maintain an adequate urinary flow to promote excretion of the lead-chelated complex. Once urinary flow is established, restrict fluids to maintenance and losses to prevent cerebral edema.


Deterrence and Prevention

Primary prevention

The 2020 Healthy People objective to eliminate childhood lead poisoning can be achieved through primary prevention. Pediatricians and family practitioners provide a fundamental role with anticipatory guidance about potential sources of lead exposure and its hazards for the development of children. A successful primary prevention plan should focus on the two main exposure sources for children in the United States: (1) lead in housing and (2) nonessential uses of lead in certain products, such as imported and domestically manufactured toys, eating and drinking utensils, cosmetics, and traditional medicines.

Parents should be educated about sources of lead, the common behavior involved (ie, pica), and the hazards associated with lead exposure on children's development.[8, 13]

Nutritional assessment is of particular importance because lead absorption is enhanced by improper dietary intake, especially in the presence of high fat intake and/or deficiency of certain elements, such as calcium and iron.

Secondary prevention

The Centers for Disease Control and Prevention (CDC) and AAP have issued recommendations regarding screening for lead poisoning. They recommend universal screening in areas where at least 27% of houses were built before 1950 and in places where the prevalence of elevated blood levels in children aged 1-2 years is 12%.

The CDC and AAP recommend targeted screening in all other areas in which a positive response is received to one or more of the following screening questionnaire items issued by the CDC:

  • Does your child live in or regularly visit a house that was built before 1950?
  • Does your child live in or regularly visit a house that was built before 1978 with recent or ongoing renovations or remodeling (within the past 6 mo)?
  • Does your child have a sibling or a playmate that has or did have lead poisoning?
Contributor Information and Disclosures

Mohamed K Badawy, MD, FAAP Assistant Professor of Emergency Medicine and Pediatrics, University of Texas Southwestern Medical School; Associate Medical Director, Division of Emergency Medicine, Children's Medical Center Dallas

Mohamed K Badawy, MD, FAAP is a member of the following medical societies: Academic Pediatric Association, Society for Academic Emergency Medicine, American Academy of Pediatrics

Disclosure: Nothing to disclose.


Gregory P Conners, MD, MPH, MBA Director, Division of Emergency and Urgent Care, Children's Mercy Hospital; Vice Chair of Pediatrics for Emergency and Urgent Care; Professor of Pediatrics and Emergency Medicine, University of Missouri-Kansas City School of Medicine

Gregory P Conners, MD, MPH, MBA is a member of the following medical societies: Academic Pediatric Association, American College of Emergency Physicians, American Pediatric Society, American Academy of Pediatrics, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Timothy E Corden, MD Associate Professor of Pediatrics, Co-Director, Policy Core, Injury Research Center, Medical College of Wisconsin; Associate Director, PICU, Children's Hospital of Wisconsin

Timothy E Corden, MD is a member of the following medical societies: American Academy of Pediatrics, Phi Beta Kappa, Society of Critical Care Medicine, Wisconsin Medical Society

Disclosure: Nothing to disclose.


Jeffrey R Tucker, MD Assistant Professor, Department of Pediatrics, Division of Emergency Medicine, University of Connecticut School of Medicine, Connecticut Children's Medical Center

Disclosure: Merck Salary Employment

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

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