Lead Poisoning
Lead Poisoning: Excerpt from The 5-Minute Pediatric Consult
Carla Campbell, MD, MS
Lead Poisoning - BASICS
Lead Poisoning - description
- One of the most common pediatric environmental health problems, involving a systemic intoxication by the heavy metal lead; most commonly this is with inorganic lead.
- The CDC considers a blood lead level (BLL) of ≥10 ์g/dL to represent undue lead exposure and absorption, and to be elevated.
- The CDC has recently reported on adverse health effects at lower BLLs, with no clear threshold.
- Lead poisoning, an older term that is less specific than an actual BLL.
- CDC classifcation, by BLL in mcg/dL:
- Class I (0–9); Class IIa (10–14)
- Class IIb (15–19); Class III (20–44)
- Class IV (45–69); Class V (≥70)
Lead Poisoning - general prevention
- Primary prevention: Removal of potential environmental lead hazards prior to exposure:
- The CDC now recommends that states and cities include primary prevention activities to reach the Healthy People 2010 goals of eliminating elevated BLLs in children.
- Provide anticipatory guidance to all parents about lead exposure pathways and the prevention of these exposures.
- Secondary prevention as screening for elevated BLLs:
- Minimum screening recommendations are a blood lead test for children at ages 1 and 2 years and for those 36–72 months old who have not had previous screening.
- Tertiary prevention: Case management and environmental remediation for children with lead poisoning
- Control measures:
- Abatement of building-based (residential) lead hazards by removal, encapsulation, or enclosure of lead-containing structures
- Control of environmental lead dust exposure and ingestion by good housekeeping (wet dusting and mopping of household dust) and personal hygiene (cleaning of child’s hands, toys, personal items)
- Removal of any other known lead source from the child’s environment
Lead Poisoning - epidemiology
- ~83% of American pre-1978 privately owned units contain some lead-based paint.
- A recent national survey estimates that 38 million and 24 million housing units have lead-based paint and significant lead-based paint hazards, respectively.
Lead Poisoning - prevalence
- Prevalence of elevated lead levels and geometric mean BLLs have decreased significantly in the past 20 years.
- ~310,000 American children ages 1–5 years (1.6% of a representative national sample) are estimated to have BLLs of ≥10 mcg/dL
Lead Poisoning - pathophysiology
- Lead adversely affects many organ systems including neurologic, hematologic, GI, renal, and reproductive systems. Many of the toxic effects result from inhibition of enzymes involved in heme biosynthesis, as the electropositive metal binds to the negatively charged sulfhydryl groups on the active sites of δ-aminolevulinic acid dehydratase (ALA-D), ferrochelatase, porphobilinogen synthase, coproporphyrinogen oxidase, and other enzymes. Divalent lead also acts competitively with calcium in various biologic systems.
- Children absorb lead more efficiently from the GI tract and are more likely than adults to ingest lead through hand-to-mouth activities.
- Because the developing, immature CNS is susceptible to the toxic effects of lead, the neuropsychologic effects of lead poisoning on young children have been of particular concern.
Lead Poisoning - DIAGNOSIS
Lead Poisoning - signs & symptoms
Lead Poisoning - history
- Etiology: The most common sources of lead:
- Ingestion of lead-based paint or contaminated dust or soil through residence in or visitation of older (pre-1980), deteriorated housing
- A parental occupation or hobby involving lead exposure (construction or battery plant work, stained glass window or pottery making)
- Use of remedies, cosmetics, or pottery containing lead
- Ingestion of contaminated water, food, or beverages
- Typical symptoms:
- Most children are asymptomatic.
- Although many of the clinical manifestations of symptomatic lead poisoning are nonspecific, a cluster of complaints including anorexia, intermittent abdominal pain, constipation, sporadic vomiting, change in mental status (such as irritability or lethargy), decreased play activity, and change in developmental status (particularly with regression of developmental milestones) may herald this condition.
- Lead encephalopathy:
- Can present with change in consciousness, ataxia, persistent vomiting, seizures, and coma
- Often this presents after a prodrome of symptoms mentioned above.
Lead Poisoning - physical exam
- Not generally helpful at lower lead levels. Symptomatic and/or encephalopathic patients may have acute GI, neurologic, hematologic, and systemic manifestations.
- Assess for clinical evidence of developmental delay.
Lead Poisoning - tests
Lead Poisoning - lab
- Blood lead test, either venous or capillary:
- Results may be reportable to local health authorities.
- The test result is a measure only of recent lead exposure and does not indicate total body burden of lead.
- CBC: To assess for anemia:
- Anemia is seen in lead poisoning starting at lead levels of ~60 mcg/dL from globin and heme synthesis inhibition and hemolysis.
- Iron deficiency anemia is often seen concomitantly.
- Anemia related to lead toxicity is typically normocytic and normochromic; a microcytic, hypochromic anemia may be seen with a mixed etiology.
- Basophilic stippling is sometimes seen on peripheral blood smear.
- Free erythrocyte protoporphyrin:
- Marker of lead-induced inhibition of heme synthesis
- Can be useful clinically to follow the recovery from heme synthesis inhibition during management
Lead Poisoning - imaging
- Abdominal radiograph: Look for radiopaque foreign material suggestive of ingestion of lead paint chips or other lead-containing foreign body, when ingestion of such is suspected in the history.
- Long-bone radiographs, not recommended for routine use:
- Look for lead lines or metaphyseal sclerosis, characterized by increased density along transverse lines in the metaphyses of growing long bones, representing increased mineralization owing to interference with the metabolism of the boney matrix. If present, lead lines imply chronic lead exposure.
Lead Poisoning - differencial diagnosis
- Lead encephalopathy should be considered in the differential diagnosis of a child presenting with seizures, altered mental status, and/or coma.
- Lead poisoning should also be considered in the differential diagnosis of mental retardation, behavioral disorders, and anemia.
- Failure to diagnose from:
- Delay in checking a blood lead test in the presence of clinical signs, symptoms of lead poisoning, or neuropsychologic disorders
- Failure to inquire about lead exposure possibilities, especially when approaching urban children
Lead Poisoning - TREATMENT
Lead Poisoning - general measures
Environmental management:
- Includes removing children from the lead source(s)
- Should occur when venous lead levels are recurrently 15–19 mcg/dL (CDC class IIB) and when levels are ≥20 mcg/dL (CDC class III). Could be done for lower BLLs as resources allow.
Lead Poisoning - medication
- Chelation therapy:
- Should complement environmental management in all children with venous levels of ≥45 mcg/dL (CDC class IV) or higher, using parenteral calcium disodium ethylenediamine tetra-acetate (EDTA; also calcium disodium versenate) or oral agents such as meso 2,3-dimercaptosuccinic acid (DMSA, succimer, Chemet)
- Chelation of children with levels <45 mcg/dL not recommended, as evidence suggests it does not reverse or diminish neuropsychological effects of lead.
- Outpatient therapy can take place if a lead-safe environment has been identified and compliance is expected.
- Succimer is given at 10 mg/kg/dose (or 350 mg/m2/dose) q8h for 5 days, then q12h for 14 more days. Weekly monitoring for neutropenia, platelet abnormality, and increased liver enzymes is recommended. Succimer is more lead-specific than other chelators and causes less mineral depletion.
- Children with symptomatic lead poisoning or with levels of ≥70 mcg/dL (CDC class V) should be admitted immediately to a hospital for parenteral chelation with both intramuscular dimercaprol (British antilewisite, BAL) and IV or IM calcium disodium EDTA. Because there are many issues involved with administration of both chelating agents, consultation of appropriate guidelines and pharmacologic information are recommended.
- Children with encephalopathy constitute a medical emergency and should receive the preceding treatment in an intensive care setting with attentive neurosurgical support. Consultation with a clinician experienced in lead toxicity treatment is advised for these patients.
- Ingested lead-containing foreign bodies should be evacuated with whole-bowel irrigation using a high-molecular-weight glycol solution.
Lead Poisoning - general measuress
Lead Poisoning - diet
- Nutritional support with calcium and iron supplementation should be given if intake is inadequate; deficiencies of these increase lead absorption from the gastrointestinal tract.
- Iron supplementation should be withheld during chelation therapy.
Lead Poisoning - special therapy
IV fluids: In general, maintain good hydration as lead is excreted by the kidneys. Close monitoring needed in cases where encephalopathy or increased intracranial pressure is present.
Lead Poisoning - FOLLOW UP
Lead Poisoning - disposition
Lead Poisoning - admission criteria
Admit all symptomatic children, those with BLLs ≥70, and those with BLLs ≥45 for which one cannot ensure a lead-safe environment and/or compliance with oral medication.
Lead Poisoning - discharge criteria
Consider discharge when symptoms have resolved, BLL has significantly declined, and a lead-safe discharge environment has been identified.
Lead Poisoning - issues for referral
- Close communication with the local health department is essential before, during and after admission.
- Referral may be made to early intervention or development assessment programs, social workers, therapists, neurologists or other specialists, as needed.
Lead Poisoning - prognosis
- In general, there is an increased risk for long-term neuropsychological sequelae, which increases with lead exposure and absorption that is more intense, of longer duration, and begins at an early age when the central nervous system is still developing.
- Recurrent episodes of symptomatic lead poisoning increase the risk for permanent sequelae.
- More subtle effects may not be detected until school entry.
Lead Poisoning - complications
- Acute encephalopathy
- Seizures
- Coma
- Death (predominantly owing to cerebral edema)
- Mental retardation
- Cognitive, behavioral, attentional, and neurodevelopmental impairment
- Anemia
- Fanconi syndrome
- Abdominal colic
- Adverse reproductive outcomes
Lead Poisoning - patient monitoring
- Prompt environmental follow-up of current lead exposure situations and investigation for additional exposure (e.g., with family moves, visitation of new residences) should occur.
- Follow-up venous lead levels should be performed for those with levels from 10–19 mcg/dL (CDC class IIA, IIB) approximately every 1–3 months; with less frequent follow-up after levels decline.
- Follow-up venous levels should be performed for those with levels of ≥20 mcg/dL at 1–2-month intervals until no additional lead exposure is present and levels have decreased.
- Follow-up venous levels should be performed 1–3 weeks following chelation therapy, with frequent monitoring thereafter.
Lead Poisoning - bibliography
- American Academy of Pediatrics Committee on Environmental Health. Lead exposure in children: Prevention, detection and management. Pediatrics. 2005;116:1036–1046.
Centers for Disease Control and Prevention. Preventing Lead Poisoning in Young Children. Atlanta: CDC, 2005.
- Centers for Disease Control and Prevention. Blood lead levels—United States, 1999–2002. MMWR Morb Mort Wkly Rpt. 2005;54:513–516.
- Lanphear BP, Matte TD, Rogers J, et al. The contribution of lead-contaminated house dust and residential soil to children’s blood lead levels. Environ Res. 1998;79(Oct):51–68.
- 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. 2001;344:1421–1426.
Lead Poisoning - CODES
Lead Poisoning - icd9
- 984.9 Toxic effect of unspecified lead compound
- 984.9[323.7] Lead encephalitis
- V15.86 Exposure to lead
Lead Poisoning - FAQ
- Q: What is lead abatement?
- A: Lead abatement is removal of a lead hazard from the environment either by replacing it (e.g., installing a new window), enclosing the area with the lead source (e.g., installing paneling), removing the lead-based paint from a surface (burning or dry sanding methods should never be used), or encapsulating the area (placement of a specific coating over the lead-containing surface, which prevents access to the lead hazard).
- Q: Is lead abatement permanent?
- A: Often the lead paint that is chipping or peeling is removed from a home. Any areas with intact lead-based paint may become deteriorated with aging, leading to new lead hazards, although ongoing maintenance and repair may prevent this.
- Q: Why didn’t my child’s brother and sister get lead poisoning at the same age since they lived in the same house?
- A: Children are different; some do much more hand-to-mouth activity than others, which is the main way that children get lead into their bodies. Also, your home may not have had the same lead dangers (hazards) when the siblings were younger.
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Book Source Details
- Book Title: The 5-Minute Pediatric Consult
- Author(s): M. William Schwartz MD; et al.
- Year of Publication: 2008
- Copyright Details: The 5-Minute Pediatric Consult, Copyright © 2008 Lippincott Williams & Wilkins.
More About Lead poisoning
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Medical Books Excerpts
- Poisoning
- "Professional Guide to Diseases (Eighth Edition)" (2005)
- [ read ]
Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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More About This Book:
Title: The 5-Minute Pediatric Consult
Authors: M. William Schwartz MD; et al.
Publisher: Lippincott Williams & Wilkins
Copyright: 2008
ISBN: 0-7817-7577-9
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