Pediatric Lead Toxicity Medication

  • Author: Mohamed K Badawy, MD, FAAP; Chief Editor: Timothy E Corden, MD   more...
 
Updated: Nov 8, 2011
 

Medication Summary

In patients with lead toxicity, the use of chelating agents is not recommended for blood lead levels (BLLs) less than 45 μg/dL. In 2005, the AAP Committee on Environmental Health issued the following guidelines for screening and treatment of elevated BLLs.[2]

BLL less than 10 μg/dL

No action is required

BLL 10-14 μg/dL

Obtain a confirmatory venous lead level within 1 month. If the BLL is still within this range, patient education about lead exposure is needed, and the BLL test should be repeated in 3 months

BLL 15-19 μg/dL

Obtain a confirmatory venous lead level within 1 month. If the BLL is still within this range, patient education about lead exposure is needed, and the BLL test should be repeated in 2 months

BLL 20-44 μg/dL

Obtain a confirmatory venous BLL in 1 week, and if the BLL is still within this range, assess complete medical, nutritional, and environmental hazards. Environmental evaluation by the local health department is also needed.

A large-scale study reported no improvement in neurologic and behavioral test scores after succimer chelation of children with BLL in this range.[10]

BLL 45-69 μg/dL

Obtain a confirmatory BLL within 2 days, and if the level is still within this range, the patient should undergo the same complete evaluation as would patients with a BLL of 20-44 μg/dL. At 45-69 μg/dL, chelation therapy is recommended. Treatment should be in a lead-free environment. If this is not possible, hospitalization is necessary.

Chelation can be started with oral succimer, or, if the patient is hospitalized, calcium disodium edetate (calcium EDTA) can be used. These agents have potential toxicities, and monitoring of the CBC count, electrolytes, and liver function test results is necessary.

BLL 70 μg/dL or higher

Hospitalize the patient, obtain a confirmatory venous BLL, and initiate chelation with dimercaprol and calcium 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.

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Chelating Agents

Class Summary

Chelating agents are the criterion standard for the treatment of patients with lead poisoning according to the blood lead levels (BLLs) discussed above. These agents bind to lead and promote its excretion. Patients receiving chelation therapy must be closely monitored because of the agents' potential toxicities.

Dimercaprol (BAL in oil)

 

Dimercaprol was first developed as an antidote for lewisite toxicity. It is water soluble and rapidly crosses the blood-brain barrier. Dimercaprol forms a nonpolar compound with lead that is excreted in bile and urine. It is the drug of choice in patients with acute lead encephalopathy, in whom the first dose is given and then the second dose is given combined with calcium EDTA after a 4-hour interval.

Edetate calcium disodium (Calcium Disodium Versenate)

 

This agent decreases blood lead concentration, reverses the hematologic effects of lead, and enhances the excretion of lead in urine.

Succimer (Chemet)

 

Dimercaptosuccinic acid (DMSA) is a water-soluble analog of dimercaprol. It causes a rapid decline in lead level and replenishes many of the sulfhydryl-dependent enzymes. In the absence of encephalopathy, patients may be treated with DMSA.

D-penicillamine (Cuprimine, Depen)

 

D-penicillamine is also known as D-dimethyl cysteine. It offers an alternative for oral treatment of lead poisoning. This agent is not approved by the US Food and Drug Administration (FDA) for use in lead poisoning, but has nonetheless been in use for more than 20 years.

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Contributor Information and Disclosures
Author

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

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

Disclosure: Nothing to disclose.

Coauthor(s)

Gregory P Conners, MD, MPH  Chief, Division of Emergency Medical Services, 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 is a member of the following medical societies: Academic Pediatric Association, American Academy of Pediatrics, American College of Emergency Physicians, American Pediatric Society, and 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, and Wisconsin Medical Society

Disclosure: Nothing to disclose.

Additional Contributors

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.

References
  1. Murata K, Iwata T, Dakeishi M, Karita K. Lead Toxicity: Does the Critical Level of Lead Resulting in Adverse Effects Differ between Adults and Children?. J Occup Health. Nov 6 2008;[Medline].

  2. American Academy of Pediatrics Committee on Environmental Health. Lead exposure in children: prevention, detection, and management. Pediatrics. Oct 2005;116(4):1036-46. [Medline]. [Full Text].

  3. American Academy of Pediatrics Committee on Environmental Health. Lead. In: Handbook of Pediatric Environmental Health. American Academy of Pediatrics. Elk Grove, IL: AAP; 1999:131-43.

  4. Canfield RL, Henderson CR Jr, Cory-Slechta DA, et al. Intellectual impairment in children with blood lead concentrations below 10 microg per deciliter. N Engl J Med. Apr 17 2003;348(16):1517-26. [Medline].

  5. Koller K, Brown T, Spurgeon A, Levy L. Recent developments in low-level lead exposure and intellectual impairment in children. Environ Health Perspect. Jun 2004;112(9):987-94. [Medline].

  6. CDC. Preventing Lead Poisoning in Young Children. CDC, United States Department of Health and Human Services:1991. [Full Text].

  7. CDC. Screening Young Children for Lead Poisoning. Guidance for State and Local Public Health Officials. Atlanta, GA: United States Department of Health and Human Services; 1997:[Full Text].

  8. Lanphear BP, Winter NL, Apetz L, Eberly S, Weitzman M. A randomized trial of the effect of dust control on children's blood lead levels. Pediatrics. Jul 1996;98(1):35-40. [Medline].

  9. Lanphear BP, Hornung R, Ho M. Screening housing to prevent lead toxicity in children. Public Health Rep. May-Jun 2005;120(3):305-10. [Medline].

  10. Rogan WJ, Dietrich KN, Ware JH, et al. The effect of chelation therapy with succimer on neuropsychological development in children exposed to lead. N Engl J Med. May 10 2001;344(19):1421-6. [Medline].

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