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
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.
Chelation
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.
Prevention
The key to preventing lead toxicity in children is identification and elimination of the major sources of lead exposure. 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.
Age of the housing is a major determinant of lead paint hazards. For housing built from 1978 to 1998, 2.7% contained one or more lead paint hazards, whereas the prevalence of residential hazards increased to 11.4% of housing built from 1960 to 1977, 39% of housing built from 1940 to 1959, and 67% of housing units built before 1940. In addition, the primary sources of lead in water is lead service lines, lead solder, and brass fittings that contain high concentrations of lead. Plumbing installed before 1986 (the year a federal ban was enacted), is likely to contain higher concentrations of lead. [20]
Lead-based paint is the major source of lead, but ingestions of lead-contaminated house dust and residential soil are the major pathways for exposure. House dust can be contaminated by small particles of lead-based paint or lead-contaminated soil can be tracked indoors leaving children who live in older, poorly maintained housing vulnerable to exposure. Ingestions of lead-contaminated house dust and soil are also the primary pathways of exposure for children who live in homes that were recently abated or renovated. [20]
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. [10, 21]
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.
