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Childhood lead poisoning: Management

Childhood lead poisoning: Management
Literature review current through: Jan 2024.
This topic last updated: Jan 09, 2024.

INTRODUCTION — The management of lead poisoning in children will be reviewed here.

Clinical manifestations, diagnosis, exposure, and prevention of childhood lead poisoning are discussed separately. (See "Childhood lead poisoning: Clinical manifestations and diagnosis" and "Childhood lead poisoning: Exposure and prevention".)

GENERAL MANAGEMENT — The identification of a neonate, infant, or child who has been exposed to lead must be viewed as a public health emergency. The only effective long-term treatment is ending further lead exposure by eradication of environmental lead contamination. Because of the cognitive and behavioral effects of lead toxicity, primary prevention of lead exposure is the single most important strategy in the management of childhood lead poisoning. (See "Childhood lead poisoning: Exposure and prevention", section on 'Prevention'.)

Children at risk because of lead in their environment are often not found until elevated blood lead levels (BLLs) are detected during routine screening. At that point, secondary prevention of further lead exposure becomes the main treatment (table 1). Unfortunately, by the time a child is found with an elevated BLL, the neurodevelopmental harm from the exposure may have already occurred [1].

Chelation therapy may be necessary depending upon the degree of blood lead elevation (see 'Lead level 45 to 69 mcg/dL' below and 'Symptomatic lead poisoning' below). However, it has limited efficacy. With chronic ingestion or inhalation, lead can be incorporated into the skeletal system, which becomes an endogenous reservoir of lead that is resistant to elimination. While chelating agents can bind to lead in blood, they are ineffective in removing lead from the deep bone stores.

Approach — Because there is no known safe threshold for lead exposure, certain actions should be taken in all children with BLLs greater than the United States reference value (97.5th percentile of blood levels, 3.5 mcg/dL [0.17 micromol/L] since 2021); the timing, urgency, and setting of the interventions vary depending upon the severity of lead toxicity (table 2) [2,3] (see 'Asymptomatic lead exposure and poisoning' below and 'Symptomatic lead poisoning' below):

Patient assessment – The clinician should perform a complete history and physical examination that focus on identifying the source of lead exposure, symptoms of lead toxicity, and additional persons at risk. (See "Childhood lead poisoning: Clinical manifestations and diagnosis" and "Childhood lead poisoning: Exposure and prevention", section on 'Exposure'.)

During this assessment, clinicians should take a careful history to identify potential non-traditional sources of lead exposure (eg, cosmetics, ethnic products, folk medicines such as Ayurvedic medicines, and jewelry) and strongly encourage repeat investigations to assess for these sources if the original home inspection is negative [4]. Special care should be taken for children in foster care since the management of their lead exposure can be difficult as they may be moving from home to home frequently and may have frequent changes in caregiver [5]. Additionally, foster homes are not evaluated for lead risks prior to child placement, and children may have increased BLLs while in a foster home.

Children with lead poisoning are at risk for developmental delay and may be eligible to receive Early Intervention Services. Appropriate referrals should be made as indicated. Developmental surveillance should continue throughout childhood, particularly at critical transition points (eg, first, fourth, and sixth/seventh grades) [6]. (See "Developmental-behavioral surveillance and screening in primary care".)

Investigation for iron deficiency – Laboratory screening to determine the presence of concurrent iron deficiency is appropriate in all children with detectable or elevated BLLs (see "Iron deficiency in infants and children <12 years: Screening, prevention, clinical manifestations, and diagnosis", section on 'Evaluation for suspected iron deficiency anemia'):

-Complete blood count

-Serum ferritin

-C-reactive protein

Additional iron studies are suggested in children undergoing chelation. (See 'Lead level 45 to 69 mcg/dL' below and 'Initial evaluation' below.)

Nutritional interventions – Adequate nutritional intake of calcium, vitamin C, and iron along with regular meals should be routinely recommended to minimize lead absorption and prevent pica [7]. Fasting should be avoided because it increases intestinal lead absorption [8,9].

Calcium and vitamin C – In most patients, two daily servings of dairy or other calcium-rich foods and two servings of fruit or fruit juice provide sufficient calcium and vitamin C in the diet [6]. Supplementation of these nutrients is typically not necessary.

Iron intake and supplementation – Adequate iron intake is important in all children because iron deficiency causes neurocognitive deficits whether or not lead toxicity is present [10]. (See "Iron deficiency in infants and children <12 years: Screening, prevention, clinical manifestations, and diagnosis", section on 'Clinical manifestations of iron deficiency anemia'.)

Iron supplementation should not occur during chelation therapy.

The role of iron supplementation in children with lead poisoning who are not receiving chelation is unclear. Like calcium, dietary iron is thought to decrease the intestinal absorption of lead. This theory is supported by epidemiologic studies that demonstrate an increased prevalence of iron deficiency among children with lead poisoning [11,12]. However, the association is not present consistently [13]. Iron supplementation in children with iron deficiency and lead poisoning improves developmental assessment scores independent of BLL [14,15]. Evidence for such an effect in iron-replete children is lacking [16,17]. Until further data clarify the effect of iron supplementation on lead excretion and the benefit of iron supplementation in iron-replete children with lead toxicity, the decision regarding iron supplementation should be individualized [16].

Because elevated lead levels may cause constipation and decreased elimination, a diet with adequate fiber should be encouraged to ensure proper evacuation of the bowel and enable rapid clearing of any lead before it can be absorbed. Fresh fruits and vegetables are healthy ways to provide adequate fiber.

Lead education for the family – The family requires education including sources of lead exposure, prevention of exposure, and ways to decrease intestinal absorption of lead (table 3). (See "Childhood lead poisoning: Exposure and prevention", section on 'Education and dust control' and "Childhood lead poisoning: Exposure and prevention", section on 'Prevention'.)

Testing of other children at risk – Siblings and other children should be tested for lead poisoning by their primary care providers if they live in the same household or attend the same school/daycare that has been identified as a source of lead exposure. Venous blood testing is recommended. Regional public health personnel, regional poison control centers, and, if available, Pediatric Environmental Health Specialty Units can assist with interpreting test results and recommending further measures. (See 'Additional resources' below.)

Notification of appropriate public health authority – Public health department notification may require that the clinician make a mandated report to a regional health department (eg, city, county, state, or province), depending upon the jurisdiction. More often, the laboratory in which the testing was performed reports the elevated BLL. Clinicians should be aware of the reporting practices of the laboratories they use. However, for those pediatric practices who perform point-of-care testing, all results should be shared with the health department. Central reporting of lead toxicity helps to identify new risk categories for exposure. Ideally, the health department can arrange for inspection of the home and other environments where the child spends time so that remediation can begin.

Lead abatement – Many government health departments no longer have funding for lead inspection services. Limited funding has resulted in the inability to identify the lead source for some affected patients. The health care provider should still work with the public health departments to find qualified home inspectors and lead abatement contractors in the region. If a home assessment can be completed, the BLL that triggers a home inspection varies with the jurisdiction, but the Centers for Disease Control and Prevention (CDC) recommends that the home inspection and lead hazard reduction (abatement) occur for all children with levels above the reference level of 3.5 mcg/dL (0.17 micromol/L) with anticipatory guidance, at minimum, for children with any detectable BLLs [7,18]. Given the decrease in the lead reference level and the recognition that there is no safe lead level, the BLL that triggers specific environmental action may be lower in some jurisdictions. (See "Childhood lead poisoning: Exposure and prevention", section on 'Additional resources'.)

The health care provider should also inform parents/caregivers that any abatement work must be performed by a contractor licensed to do lead abatement if such licensing is performed in the jurisdiction. Families should not attempt abatement themselves for fear that they could make the environment more dangerous.

Follow-up lead testing – The child and siblings should have follow-up lead levels. The schedule for these tests varies depending upon the original level (table 2).

ASYMPTOMATIC LEAD EXPOSURE AND POISONING — Categories of lead poisoning have been defined by the Centers for Disease Control and Prevention (CDC) [19]. However, given that there is no safe blood lead level (BLL), all children with a detectable lead level warrant education and an environmental investigation. (See 'Approach' above.)

As levels increase, hospitalization and chelation may also be necessary depending upon symptoms, chronicity of lead exposure, and whether lead-safe housing for the child can be assured. When lead-safe housing cannot be assured, hospitalization will remove the child from the lead source and is a key component of successful treatment. Our recommendations below regarding management of elevated BLLs in asymptomatic children are largely consistent with the guidelines provided by the CDC [20].

When screening for lead poisoning, venous samples are preferred because they more accurately represent the child's current exposure to lead. Nevertheless, capillary samples are frequently obtained because of the convenience and immediate results provided by point-of-care testing. Because environmental lead contamination on the skin can lead to falsely elevated lead levels in capillary samples, they require confirmation of positive results using venous blood testing. However, capillary samples do serve as an indicator of lead in the environment. Thus, even if a venous sample does not confirm an elevated BLL, the elevated capillary level indicates that education should be provided. Hair and urine samples should not be used for diagnosis of lead poisoning. (See "Childhood lead poisoning: Clinical manifestations and diagnosis", section on 'Lead levels'.)

The approach to screening for lead poisoning is discussed separately. (See "Screening tests in children and adolescents", section on 'Lead poisoning'.)

Undetectable BLL <3.5 mcg/dl (current reference level) — A BLL below the current reference level is found in 97.5 percent of children aged one to five years, according to National Health and Nutrition Examination Survey (NHANES) data. However, no level of blood should be considered acceptable, and the clinician may need to reassess the child's environment in the future. The limit of detection for lead can vary by lab and is typically between 1 and 3.3 mcg/dL [2]. The child may need to be retested depending upon age or other risk factors for lead exposure (table 4). (See "Screening tests in children and adolescents", section on 'Lead risk assessment'.)

Detectable BLL 3.5 to 14 mcg/dL — A result between 3.5 and 5 mcg/dL, the 2021 and 2012 reference levels, may be within the variability of the test and present uncertainty as to the accuracy of the result. Clinicians should retest to establish a trend: a confirmed BLL at or above 3.5 mcg/dL is found in 2.5 percent of children aged one to five years.

Children with detectable BLLs 3.5 to 14 mcg/dL (0.17 to 0.68 micromol/L) should have a confirmatory venous BLL within one to three months (table 2). Retesting should be performed even if the original specimen was a venous sample to make sure that the BLL is not increasing rapidly. If the level remains the same or is decreasing, then monitoring of the level should occur every three months until it is <3.5 mcg/dL (0.17 micromol/L).

Once the BLL is confirmed, children with detectable BLLs that are <14 mcg/dL (0.68 micromol/L) warrant the following management (table 2) [19] (see 'Approach' above):

History and physical examination with emphasis on possible sources of lead exposure and screening for iron deficiency anemia.

Family education regarding the sources of potential lead exposure (table 3).

Home inspection for the source of lead exposure. Home inspection may not be available for all children at this level due to local and state resources. Thus, the pediatrician should gather the necessary information from the families to inform them of possible sources.

Nutrition assessment and anticipatory guidance.

Annual blood lead testing until six years of age.

Testing of BLL more often than once per year may be appropriate in selected patients [21-25]:

Children younger than two years of age – For children screened at age <12 months, retesting in three to six months is warranted because lead exposure may increase as mobility increases.

Patients tested before the onset of warm weather – BLL tend to be increased during the warm months, perhaps related to increased exposure to lead in dust and soil. Thus, patients with detectable BLL in the fall or winter may warrant retesting during the following summer.

Children at high risk for continued lead exposure – Such patients may reside or have care in a house built before 1978, have exposure to other lead sources (eg, leaded water pipes), or have recently moved to a setting where lead exposure is a concern.

Interpretation of BLLs <5 mcg/dL (0.24 micromol/L) is complicated by an increased risk of specimen contamination arising from blood collection equipment (eg, needles, blood collection tubes, or cryogenic vials) causing false positives and the inability for many laboratories to quantify low levels of blood lead resulting in false negatives [26]. However, any detectable lead ≥3.5 mcg/dL (0.17 micromol/L) warrants careful evaluation and an attempt at determining the source of lead exposure.

This approach to detectable BLLs recognizes that there is no safe lead level. Thus, even children with detectable BLLs <3.5 mcg/dL (0.17 micromol/L) may be at risk for neurocognitive deficits [27-30]. The reference level set by the CDC is not necessarily a level in which specific action is taken but one that documents the level at which the large majority (ie, 97.5 percent) of US children who have been tested for lead exposure fall.

Furthermore, all children should be monitored regularly for developmental and behavioral problems, and parents/caregivers should receive anticipatory guidance that promotes optimal development for their children regardless of their BLL. (See "Developmental-behavioral surveillance and screening in primary care", section on 'Approach to surveillance'.)

Chelation is not recommended for BLL <45 mcg/dL (2.17 micromol/L). (See 'Lead level 15 to 44 mcg/dL' below.)

Lead level 15 to 44 mcg/dL — Children with BLLs 15 to 44 mcg/dL (0.72 to 2.13 micromol/L) should have a confirmatory venous BLL within one to four weeks (table 2). Retesting should be performed even if the original specimen was a venous sample to make sure that the BLL is not increasing rapidly. If the level remains the same or is decreasing, then monitoring of the level should occur every three months until it is <3.5 mcg/dL (0.17 micromol/L).

Once the elevated BLL is confirmed, management consists of the general approach described above and for levels <3.5 mcg/dL (table 2). (See 'Approach' above and 'Detectable BLL 3.5 to 14 mcg/dL' above.)

In addition, a plain abdominal radiograph is warranted in patients with pica behaviors (eg, eating paint chips or excessive mouthing) or in patients in whom the BLL is significantly increased from baseline testing. We suggest that children with leaded foreign bodies or flecks (image 1) that are located in the small bowel receive gastrointestinal decontamination with whole bowel irrigation. (See 'Gastrointestinal decontamination' below and "Gastrointestinal decontamination of the poisoned patient", section on 'Whole bowel irrigation'.)

We recommend that children with BLLs <45 mcg/dL (2.17 micromol/L) not receive chelation therapy. Although chelation with oral agents (eg, succimer or meso-2,3-dimercaptosuccinic acid [DMSA] or penicillamine) has been shown to transiently reduce BLL, limited evidence, including one randomized controlled trial, has not found improved neurodevelopmental outcomes in children with BLLs <45 mcg/dL who receive chelation [1,20,31-35]. Furthermore, even if chelation is provided, the primary treatment remains removal of the child from further lead exposure.

As an example, in a blinded, placebo-controlled trial of 780 children (aged 12 to 33 months) with BLLs of 20 to 44 mcg/dL (0.96 to 2.13 micromol/L) that compared up to three courses of succimer and lead abatement to lead abatement alone, mean BLL in the treatment group was 4.5 mcg/dL (95% CI, 3.7-5.3 mcg/dL) lower than in the control group during the first six months of the trial [1]. However, at the end of the trial, there was no significant difference in BLLs indicating that removal from the source was as effective as chelation therapy. Furthermore, neurodevelopmental function was followed over a period of 36 months [1] and again at age seven years [36]. At seven years of age, no statistically significant differences were observed between treatment and control groups in the areas of cognition, behavior, learning, memory, attention, or neuromotor performance [36]. Thus, although chelation therapy in general, and succimer in particular, is effective in lowering BLLs in children with BLLs less than 45 mcg/dL (2.17 micromol/L), it is not associated with improvement in neurodevelopmental outcomes and thus, is not indicated. Additionally, use of chelation therapy has resulted in mild to severe adverse drug reactions, putting the child’s health at higher risk for harm.

Lead level 45 to 69 mcg/dL — Asymptomatic children with venous BLLs 45 to 69 mcg/dL (2.17 to 3.33 micromol/L) should have a confirmatory venous lead level within 48 hours. These patients should also receive the same general management as for children with lower levels as described above and listed in the table (table 2). (See 'Approach' above.)

In addition to the general management described for children with levels of 15 to 45 mcg/dL (0.72 to 2.17 micromol/L) (table 2), these patients also warrant additional testing (table 5) as follows:

Abdominal radiograph to identify lead paint chips or leaded foreign bodies in the gastrointestinal tract (image 1)

Free erythrocyte protoporphyrin (if not already obtained)

Serum electrolytes (including sodium to assess for syndrome of inappropriate secretion of antidiuretic hormone [SIADH])

Blood urea nitrogen

Serum creatinine

Serum calcium

Serum magnesium

Serum aspartate aminotransferase and alanine aminotransferase

Serum iron, total iron binding capacity (TIBC), and transferrin saturation

Urinalysis

We suggest that children with leaded foreign bodies or flecks (image 1) that are located in the small bowel receive gastrointestinal decontamination with whole bowel irrigation. (See 'Gastrointestinal decontamination' below and "Gastrointestinal decontamination of the poisoned patient", section on 'Whole bowel irrigation'.)

We recommend that asymptomatic children with BLL ≥45 mcg/dL (2.17 micromol/L) receive chelation therapy. Treatment should begin as soon as possible after the BLL is confirmed, and only when the child is in a lead-safe environment. We suggest that chelation be performed orally with succimer (table 6) rather than by continuous infusion of calcium disodium edetate (CaNa2EDTA) or oral penicillamine. If succimer is contraindicated, not tolerated, or causes significant adverse reactions, then CaNa2EDTA is suggested [37]. Chelation should be performed in consultation with a toxicologist or clinician who has experience with the chelating agents. (See 'Pharmacologic agents for chelation' below.)

In most instances, patients should be hospitalized to begin chelation therapy and to ensure a lead-safe environment. Hospitalization serves several purposes: it permits the monitoring of children for potential adverse effects during chelation therapy, removes the child from the lead-containing environment until the origin of lead exposure can be identified, and ensures compliance with therapy [38].

After initial chelation, ongoing care and decisions about further treatment are best made in consultation with a physician with expertise in childhood lead poisoning (eg, pediatric toxicologist).

Ongoing care includes:

BLLs should be measured weekly at the end of oral chelation until the lead level plateaus to ensure no sudden increase from re-exposure. The interval for testing may be increased once the level plateaus and no ongoing exposure occurs.

Retreatment with chelation therapy should occur if the BLL rebounds to >80 percent of the original lead level and is ≥45 mcg/dL (2.17 micromol/L).

An acute rise in levels may signify a new exposure to lead, and repeat evaluation, including a plain abdominal radiograph, and renewed surveillance of the child's environment will be necessary. This is especially true if the "rebound" levels rise above pre-chelation levels.

Treatment of symptomatic children with BLL 45 mcg/dL is provided below. (See 'Symptomatic lead poisoning' below.)

Although chelation of children with BLLs 45 mcg/dL (2.17 micromol/L) has not been associated with improved clinical outcomes in randomized trials [39], it does reduce the BLL which would be expected to reduce toxicity, and, when combined with lead abatement, can prevent progression to symptomatic lead poisoning, including encephalopathy.

The efficacy of intravenous CaNa2EDTA and oral succimer therapy in the treatment of asymptomatic lead toxicity were compared in a controlled trial of 19 hospitalized children [40]. Succimer was more effective in reducing mean BLL after five days of therapy (61 versus 45 percent) and was well tolerated. BLL 14 days after discharge depended upon outpatient therapy: The mean BLL was 73 percent of pretreatment levels with no additional therapy, 66 percent of pretreatment levels with low-dose succimer (350 mg/m2 per day), and 50 percent of pretreatment levels with high-dose DMSA (750 mg/m2 per day). Furthermore, oral therapy with succimer avoids the need for intravenous access, and monitoring for adverse effects is not as intensive. (See 'Succimer' below and 'Calcium disodium edetate' below.)

Oral of administration of D-penicillamine can also effectively lower BLLs. However, given the potential for significant adverse events (including leukopenia, thrombocytopenia, hematuria, abnormal liver function, urticaria, angioedema, Stevens Johnson Syndrome, and nephritic syndrome), use of this agent is not generally recommended, and consultation with a clinician with expertise in managing pediatric lead poisoning with D-penicillamine chelation is advised before starting this treatment. (See 'D-penicillamine' below.)

Lead level ≥70 mcg/dL — Asymptomatic children with BLLs ≥70 mcg/dL (3.38 micromol/L) warrant a repeat BLL within 24 hours, urgent evaluation with baseline studies (table 5), hospitalization, and chelation therapy [41,42]. (See 'Initial evaluation' below and 'Chelation' below.)

These patients should also receive the same general management as for asymptomatic children with lower lead levels as described above and in the table (table 2). (See 'Approach' above.)

We suggest that children with leaded foreign bodies or flecks (image 1) that are located in the small bowel receive gastrointestinal decontamination with whole bowel irrigation. (See 'Gastrointestinal decontamination' below and "Gastrointestinal decontamination of the poisoned patient", section on 'Whole bowel irrigation'.)

We suggest that asymptomatic children with BLLs ≥70 mcg/dL (3.38 micromol/L) receive succimer and CaNa2EDTA rather than combination therapy with dimercaprol for three to five days, and CaNa2EDTA for five days or single-agent chelation with succimer (table 7). We typically start the 19-day course of succimer and, after 48 hours, give a 5-day intravenous course of CaNa2EDTA.

Chelation should occur as part of an overall treatment plan that ensures careful monitoring of lead levels, parental education, and assurance of a lead-safe environment in the child's home at discharge. (See 'Approach' above.)

Chelation is associated with a markedly reduced risk of mortality in children with lead encephalopathy. Based upon observational studies, children with BLLs ≥70 mcg/dL (3.38 micromol/L) are at increased risk for developing symptomatic lead poisoning, including encephalopathy [41,42]. Although chelation with succimer alone has been associated with successful lowering of BLLs with low mortality in children in resource-limited settings [43], combination therapy with succimer and CaNa2EDTA is preferred because parenteral portion of the regimen ensures adherence to the chelation regimen with timely lowering of the BLL. This approach also avoids multiple shots and adverse effects associated with dimercaprol. Furthermore, succimer is more easily obtained for chelation than dimercaprol.

SYMPTOMATIC LEAD POISONING — Symptoms attributable to lead poisoning can include intermittent vomiting, anorexia, and abdominal pain (lead colic); intermittent irritability or lethargy; and/or lead encephalopathy (eg, persistent vomiting, persistent lethargy or coma, headache, or afebrile convulsions) (table 8). (See "Childhood lead poisoning: Clinical manifestations and diagnosis", section on 'Clinical manifestations'.)

Initial evaluation — Symptomatic lead intoxication is a medical emergency warranting an emergency repeat blood lead level (BLL) for confirmation, emergency evaluation, hospitalization, and chelation [37,42]. Children with lead encephalopathy should be admitted to a pediatric intensive care unit.

In addition to a complete blood count, ferritin, and C-reactive protein, these children should undergo the baseline studies to identify contraindications to chelation therapy, complications of lead toxicity, and baseline values of minerals that may be affected by chelation therapy (table 5):

Abdominal radiograph to identify lead paint chips or leaded foreign bodies in the gastrointestinal tract (image 1).

Free erythrocyte protoporphyrin (if not already obtained).

Serum electrolytes (including sodium to assess for syndrome of inappropriate secretion of antidiuretic hormone [SIADH]).

Blood urea nitrogen.

Serum creatinine.

Serum calcium.

Serum magnesium.

Serum aspartate aminotransferase and alanine aminotransferase.

Serum iron, total iron binding capacity (TIBC), and transferrin saturation.

Urinalysis.

Neuroimaging (eg, computed tomography of the brain) in patients with encephalopathy.

Screening for glucose-6-phosphate dehydrogenase (G6PD) deficiency should be performed in patients who will be treated with dimercaprol if they are of an ethnicity with high prevalence for the disease (eg, African American, Mediterranean descent). However, chelation should not be delayed while awaiting results. (See "Diagnosis and management of glucose-6-phosphate dehydrogenase (G6PD) deficiency", section on 'Epidemiology'.)

G6PD deficiency is discussed in detail separately. (See "Diagnosis and management of glucose-6-phosphate dehydrogenase (G6PD) deficiency".)

Performing a lumbar puncture should be avoided in encephalopathic children unless absolutely necessary to rule out meningitis because lead intoxication can cause increased intracranial pressure. Extreme caution should be exercised if lumbar puncture is attempted, and only a small amount of spinal fluid (less than 1 mL) should be removed [44]. (See "Lumbar puncture in children".)

Initial stabilization

Encephalopathy — Children with lead encephalopathy warrant general measures as described separately for children with elevated intracranial pressure. Patients with lead encephalopathy may present with altered mental status or refractory seizures secondary to increased intracranial pressure (ICP) and frequently need stabilization, including acute management of airway and breathing with endotracheal intubation and mechanical ventilation. If necessary, rapid sequence intubation should be performed using agents that provide protection against further elevations of ICP. (See "Elevated intracranial pressure (ICP) in children: Management", section on 'Initial stabilization' and "Elevated intracranial pressure (ICP) in children: Management", section on 'Ongoing Management'.)

In addition, these patients warrant emergency chelation as described below.

Seizures — Children with symptomatic lead poisoning are at risk for seizures and status epilepticus, especially patients who are encephalopathic. Benzodiazepine administration (eg, lorazepam) is the first-line therapy (table 9). Seizures may be difficult to control.

If additional medications are needed, levetiracetam or phenobarbital is preferred to phenytoin as the second agent because it has greater efficacy for toxin-induced seizures (table 9). Patients with refractory status epilepticus warrant escalation of therapy to continuous infusions of pentobarbital, midazolam, or propofol, depending upon their hemodynamic stability. (See "Management of convulsive status epilepticus in children", section on 'Emergency antiseizure treatment' and "Management of convulsive status epilepticus in children", section on 'Refractory status epilepticus'.)

Once seizures have stopped, the patient should receive maintenance anticonvulsant doses of phenobarbital.

Fluid administration — Maintaining adequate urine output is essential to permit chelation and excretion of blood and tissue lead. This goal is achieved by the administration of intravenous fluids containing dextrose and maintenance amounts of sodium (eg, 5 percent dextrose with normal saline [154 mEq/L sodium chloride]) at a rate to maintain a minimum daily urine output between 300 and 350 mL/m2. After urine flow has been established, fluids should be administered cautiously and restricted to maintenance requirements with correction for losses from vomiting and dehydration using normal saline. (See "Maintenance intravenous fluid therapy in children".)

Close monitoring of fluid intake and output, repeated measures of electrolytes, and patient weight are essential to permit early detection of syndrome of inappropriate secretion of antidiuretic hormone (SIADH). (See "Hyponatremia in children: Etiology and clinical manifestations", section on 'Syndrome of inappropriate ADH secretion'.)

Gastrointestinal decontamination — We suggest that children with lead flecks (image 1) or leaded foreign bodies demonstrated on abdominal radiographs receive gastrointestinal decontamination with whole bowel irrigation (WBI). However, decontamination is only of value in children with lead flecks in the small bowel since lead is not absorbed from the large bowel. The clinical efficacy of WBI has not been clearly established, however, and therefore should not delay the initiation of chelation therapy in symptomatic children. (See "Gastrointestinal decontamination of the poisoned patient", section on 'Whole bowel irrigation'.)

Chelation — Chelation therapy in these children, particularly those with encephalopathy, can be life-saving [41,45]. Chelation therapy should be performed in consultation with physician with expertise in managing childhood lead poisoning. In the United States, these clinicians can be found through regional health department lead programs, Pediatric Environmental Health Specialty Units, or by contacting the regional poison control center (1-800-222-1222). In other parts of the world, the clinician should contact an international poison control center; contact information for poison centers around the world is provided separately. (See 'Additional resources' below.)

We recommend that children with lead encephalopathy receive combined chelation therapy with dimercaprol (also called British anti-Lewisite [BAL]) and calcium disodium edetate (CaNa2EDTA) (table 7). A clinician with expertise in managing pediatric lead poisoning should guide the selection of alternative methods of chelation in settings where CaNa2EDTA and/or dimercaprol is not available or advisable (eg, patients with peanut allergy or liver insufficiency who cannot receive dimercaprol or patients with renal disease or hepatitis who cannot receive CaNa2EDTA).

Treatment should be administered to symptomatic young children (eg, encephalopathic and younger than five years of age) who have supportive evidence of lead toxicity (eg, history of pica, history of elevated lead levels, known lead exposure, elevated erythrocyte protoporphyrin, basophilic stippling, plain abdominal radiograph showing lead flecks or metallic radiopaque foreign body) even if the diagnosis of lead poisoning has not been confirmed. (See "Childhood lead poisoning: Clinical manifestations and diagnosis", section on 'Symptomatic patients'.)

We suggest that symptomatic children whose BLL is ≥45 mcg/dL but who do not have encephalopathy receive dimercaprol for three to five days and CaNa2EDTA for five days rather than combination therapy with succimer and CaNa2EDTA or chelation with a single agent [41]. This treatment is designed to avoid mobilization of lead into the brain which can cause lead encephalopathy. The duration of dimercaprol treatment is determined by the degree of symptoms and the BLL.

Suggested baseline tests and laboratory monitoring during chelation therapy is provided in the table (table 7) and discussed separately. (See 'Initial evaluation' above and 'Pharmacologic agents for chelation' below.)

Once the initial course of chelation is completed, ongoing monitoring of BLLs and decisions regarding additional regimens of chelation should be performed by a physician with expertise in managing childhood lead poisoning. (See 'Follow-up' below.)

Chelating agents remove lead from the blood and soft tissues, including the brain. Thus, chelation can reverse acute encephalopathy and alleviate vomiting, abdominal pain, anemia, and renal insufficiency caused by lead intoxication [46]. The use of dimercaprol or CaNa2EDTA as single agents in the treatment of children with acute severe lead encephalopathy was found to reduce mortality from 66 percent to 28 to 45 percent [47]. When used together, mortality in this population was further reduced to 1 to 2 percent [45]. In contrast to the effects on mortality and acute symptoms, chelation therapy does not affect the chronic neurocognitive effects of lead toxicity [47]. Reexposure or chronic exposure to lead increases morbidity and mortality. (See "Childhood lead poisoning: Clinical manifestations and diagnosis", section on 'Neurologic'.)

Although dimercaprol and CaNa2EDTA are the recommended treatment for severe lead poisoning, oral chelation with succimer has been performed successfully in resource-limited settings. As an example, a single course of oral chelation with succimer in 1156 Nigerian children, including 36 percent of patients with venous BLLs ≥80 mcg/dL, was associated with an absolute mean decrease in BLL of 29.4 ug/dL for the initial course delivered, and a mean decrease in BLL of 22.3 ug/dL per course across all courses administered [43]. Minimal adverse effects, primarily moderate serum alanine aminotransferase (ALT) elevations occurred in <2.5 percent of 3180 treatment courses. Inpatient administration, higher pretreatment lead levels, and 28-day treatment courses were associated with better responses. Mortality for all children (including those without severe lead poisoning) was 2 percent during the period of the study. Thus, treatment with succimer for severe lead poisoning may be an option if dimercaprol and CaNa2EDTA are not available or cannot be safely administered. Dosing and methods of oral administration that increase patient acceptance are described separately. (See 'Succimer' below.)

Chelation should occur as part of an overall treatment plan that ensures careful monitoring of lead levels, parental education, and assurance of a lead safe environment in the child's home at discharge (table 7). (See 'Approach' above.)

Ensure lead-safe housing — Ensuring that the source of lead exposure is identified and removed from the child's environment is critical to treatment of these patients. The physician should contact the appropriate public health jurisdiction to report the presence of life-threatening lead poisoning and need to ensure that the child has lead-safe housing to go to once they are ready for discharge. (See 'Approach' above and "Childhood lead poisoning: Exposure and prevention", section on 'Additional resources'.)

Disposition — Once inpatient chelation has finished, the child must be discharged to a lead-free environment.

Other criteria for discharge include:

Improvement in clinical status

BLL <25 mcg/dL (1.21 micromol/L)

Parental possession of discharge medication (eg, succimer) and demonstrated knowledge on administration to child

Follow up appointments scheduled

The family must receive education regarding ways to maintain a lead-free environment and to reduce the absorption of gastrointestinal lead (table 3).

As zinc levels may decrease with chelation therapy, assessment for zinc deficiency should occur with supplementation as needed after chelation has ended. The diagnosis and treatment of zinc deficiency in children is discussed separately. (See "Zinc deficiency and supplementation in children", section on 'Diagnosis' and "Zinc deficiency and supplementation in children", section on 'Treatment'.)

In patients with iron deficiency, iron supplementation should be given after chelation is finished. The diagnosis and treatment of iron deficiency is discussed separately. (See "Iron deficiency in infants and children <12 years: Treatment", section on 'Diagnosis' and "Iron deficiency in infants and children <12 years: Treatment", section on 'Oral iron therapy'.)

Follow-up — Retreatment with chelation therapy is warranted if the BLL rebounds to greater than 80 percent of the original lead level and is ≥45 mcg/dL (2.17 micromol/L). BLLs should be measured periodically until the lead level is less than 3.5 mcg/dL (0.17 micromol/L).

PHARMACOLOGIC AGENTS FOR CHELATION

Succimer — Succimer (meso-2,3-dimercaptosuccinic acid) is a water-soluble analog of dimercaprol (British anti-Lewisite, BAL) that can be administered orally [48,49]. Like dimercaprol and CaNa2EDTA, succimer increases the urinary excretion of lead.

Indications – Succimer is appropriate for chelation of asymptomatic children with lead levels 45 to 69 mcg/dL (2.17 to 3.33 micromol/L) and may also be used in combination with CaNa2EDTA for chelation of children with symptomatic lead poisoning, although dimercaprol is preferred to succimer for combination chelation therapy for children with lead encephalopathy. (See 'Lead level 45 to 69 mcg/dL' above and 'Chelation' above.)

Succimer can be administered orally and has little toxicity. Unlike CaNa2EDTA, it is relatively specific for lead and causes less urinary loss of essential minerals [40,50]. Unlike dimercaprol, it may be administered concurrently with iron [40,51].

Contraindications – Chelation should not occur on an outpatient basis until a lead-safe environment is assured. Succimer should be used with caution in patients with renal impairment. Although succimer is dialyzable, the lead chelates are not.

Succimer is also contraindicated in children with allergic reactions to it or who develop hepatitis or signs of renal injury while taking it.

Dose and administration – Succimer is given at a dose of 10 mg/kg or 350 mg/m2 (rounded to the nearest 100 mg) three times per day for five days followed by the same dose two times per day for 14 days (table 6). At approximately five years of age, mg/kg dose and the mg/m2 doses are equivalent; for younger children, calculations based upon body surface area provide higher doses, which are recommended [52].

Succimer is supplied in 100 mg gelatin capsules that contain medicated beads. Succimer, preferably, can be administered by sprinkling the beads onto food (eg, apple sauce, chocolate syrup, or jelly).

Alternatively, dissolving succimer into juice at the time of the dose may be effective and can help mask the sulfur odor which is the largest disadvantage to its use [38]. The beads may be difficult to dissolve. Juice containing the dissolved medication may be better tolerated if it is given through a straw from a cup with a lid. During administration in juice, the beads may settle to the bottom and additional juice may need to be added to the cup to ensure ingestion of the entire dose. It is expected that the blood lead level (BLL) should decrease quickly (eg, <25 mcg/dL by day three). If this has not occurred, medication is not getting into the child and an alternative administration vehicle should be considered.

The child must also be encouraged to drink at least two to three glasses of milk per day (total volume 24 ounces per day) for calcium supplementation, and to include other dairy products such as yogurt and cheese. Additionally, children should be encouraged to use a multivitamin that includes trace metals. Additional oral calcium supplementation sometimes is required if calcium levels cannot be maintained (20 to 65 mg/kg per day of elemental calcium in four divided doses).

Monitoring – BLLs may rebound after discontinuation of succimer therapy because of re-equilibration of lead from other body compartments. The rebound usually plateaus between two to three weeks after completion of therapy and may be as high as 78 percent of pretreatment levels [38,50,53,54]. Thus, a venous BLL should be examined 10 to 14 days after completion of succimer therapy. It should be noted that re-exposure should be always considered when increases of BLLs above the pre-chelation levels are seen. This should precipitate a repeat environmental and clinical evaluation, including a plain radiograph of the abdomen to assess for acute ingestions of lead sources.

Adverse effects – Adverse effects of succimer include rash, neutropenia, elevation of serum liver transaminases, and gastrointestinal upset [38,55]. It has also been associated with hemolysis in a patient with glucose-6-phosphate dehydrogenase (G6PD) deficiency [56].

Calcium disodium edetate — In 1950, calcium disodium edetate (CaNa2EDTA), was found to be clinically useful in the treatment of lead poisoning. Like dimercaprol, CaNa2EDTA increases the urinary excretion of lead through the formation of a nonionizing, soluble chelate.

Indications – CaNa2EDTA is used as a single chelator for asymptomatic patients with blood lead 45 to 69 mcg/dL (2.17 to 3.33 micromol/L), especially those who cannot tolerate or have contraindications to succimer treatment and is also be used in combination with dimercaprol for patients with lead encephalopathy. (See 'Lead level 45 to 69 mcg/dL' above and 'Chelation' above.)

Because the use of CaNa2EDTA may cause increased lead concentration in the central nervous system (CNS) and consequently increased intracranial pressure [57,58], CaNa2EDTA should be administered after dimercaprol in children with lead encephalopathy. Dimercaprol lowers lead levels acutely without causing the elevated CNS levels of lead that are induced by CaNa2EDTA. CaNa2EDTA can be administered four hours after the first dose of dimercaprol and once urine output is established [48].

The use of CaNa2EDTA is crucial because mistaken use of Na2EDTA for chelation has resulted in severe hypocalcemia and death [31,59].

Contraindications – CaNa2EDTA should not be administered before dimercaprol in patients with lead encephalopathy. It should also not be given to patients with anuria, active renal disease, or hepatitis.

Dosing and administration – CaNa2EDTA can be administered intravenously (IV) as a continuous (preferred) or bolus infusion in children with encephalopathy but without cerebral edema. Product labeling suggests that it should be given intramuscularly (IM) in children with cerebral edema to avoid a potentially lethal increase in intracranial pressure [60,61]. This can be avoided with slow IV infusion. Patients with encephalopathy should be managed in consultation with a toxicologist or clinician who has experience with the chelating agents [31]. Rapid infusions should be avoided. Caution is needed when using the intravenous route as there is a risk for overhydration and SIADH. However, continuous intravenous infusion is the preferred route.

When administered IV, the total daily dose should be diluted in 250 to 500 mL of NS or D5W at a concentration less than 5 mg/mL (0.5 percent). Thrombophlebitis has occurred following infusions of concentrations >30 mg/mL (3 percent). It is not compatible with D10W and has not been tested with Lactated Ringer.

When administered IV, the dose is 1000 to 1500 mg/m2 per day (or 35 to 50 mg/kg per day) for five days. It can be administered in two to four divided doses or by continuous infusion (which is the preferred method, given EDTA's ultra-short elimination half-life) [48]. If administered in divided doses, each dose should be administered at the slowest rate of infusion that is clinically feasible to avoid mobilization of lead to the brain which can produce acute encephalopathy [31]. If the child is not encephalopathic, not vomiting, and BLL has decreased below 70 mcg/dL, CaNa2EDTA may be changed to succimer.

When administered IM, the dose is 250 mg/m2 per dose every four hours for five days. A local anesthetic (eg, procaine) should be used to mitigate the pain of injection if the IM route is to be used. CaNa2EDTA must be administered in a separate syringe and at a separate site from dimercaprol.

The dose should be adjusted for patients with renal insufficiency.

Monitoring – The hepatic and renal function of the patient must be observed carefully during chelation therapy. Daily monitoring of transaminases (serum aspartate and alanine aminotransferases), serum electrolytes, blood urea nitrogen, and serum creatinine is warranted in severe cases, and on days two, five, and before each treatment course in less severe cases. Frequent urine analysis also should be performed looking for renal epithelial cells, hematuria, or proteinuria that may indicate possible toxicity from CaNa2EDTA. CaNa2EDTA should be temporarily discontinued if the patient becomes anuric; however, dimercaprol should be continued [45].

Neurologic assessment must be monitored carefully because chelation therapy can increase the risk for an elevated intracranial pressure.

BLLs should be measured after each three- to five-day course of therapy to assess the need for future chelation therapy, and two days later.

The parenteral chelating agents, dimercaprol and CaNa2EDTA, are the mainstay of therapy for children with severe lead toxicity (table 7). Na2EDTA (edetate disodium, Endrate) is another chelating agent that has been used to treat hypercalcemia. Na2EDTA should never be used for treating lead or other heavy metal poisoning in children because it causes hypocalcemia, which can lead to tetany and death [59,62].

CaNa2EDTA mobilization tests, once used as indicators of potential response to chelation therapy in children with moderate lead intoxication, are NOT recommended. They are thought to be unnecessary because most patients with BLL greater than 40 mcg/dL (1.93 micromol/L) have an adequate response. In addition, they are expensive and difficult to administer [31,61,63,64].

Adverse effects – In addition to the possible elevation of the concentration of lead in the central nervous system, the major side effects of CaNa2EDTA include local reactions at the injection site, fever, hypocalcemia, renal dysfunction (manifest by increasing BUN, proteinuria, hematuria, and/or epithelial cells), and the excretion of other essential minerals [48,59].

Dimercaprol — Dimercaprol (2,3-dimercapto-1-propanol), also known as British Anti-Lewisite or BAL, was developed in 1946 by the British to counteract German arsenical war gases. It was the first chelating agent found to be useful in the treatment of childhood lead poisoning. Dimercaprol increases the fecal and urinary excretion of heavy metals through the formation of stable, nontoxic, soluble chelates. Dimercaprol lacks stability in water and must be dissolved in peanut oil for deep intramuscular injection.

IndicationsDimercaprol is indicated for the treatment of symptomatic lead poisoning, especially lead encephalopathy.

ContraindicationsDimercaprol is contraindicated in patients with hepatic insufficiency or peanut allergy and must be used cautiously in children with renal impairment or hypertension (table 10 and table 11).

Patients with G6PD deficiency should be monitored for hemolysis during treatment with dimercaprol [65].

Dose and administration – Recommended administration of dimercaprol in children is as follows:

Dimercaprol is administered as a deep intramuscular injection at a dose of 75 mg/m2 (or 3 to 5 mg/kg) every four hours (table 7). Pretreatment with diphenhydramine (eg, 1 mg/kg IV or orally every six hours as needed, maximum single dose 50 mg) is recommended to prevent the adverse effects of dimercaprol that are related to histamine release [31,66].

The duration of therapy varies depending upon the type and presence of symptoms. Encephalopathic patients are treated for five days; other patients with symptomatic lead toxicity are treated for three to five days depending upon their degree of symptomatology and the BLL [31,48].

A daily urine flow of 300 to 350 mL/m2 or 0.5 mL/kg per hour should be maintained. Intravenous fluids may be necessary to maintain urine output because nausea and vomiting are two of the major side effects of dimercaprol.

Iron therapy should be discontinued during dimercaprol therapy because the combination of iron and dimercaprol increases nephrotoxicity. Transfusion therapy should be considered as an alternative to iron in children with lead poisoning and concurrent iron deficiency anemia that requires treatment [60].

Monitoring – BLLs should be measured after each three- to five-day course of therapy to assess the need for future chelation therapy, and two days later. In addition to the lab tests necessary to monitor during administration of CaNa2EDTA as described below, a complete blood count with differential and smear should be obtained daily to assess for hemolysis. (See 'Calcium disodium edetate' above.)

Adverse effects – Common adverse effects include tightness sensation in the chest, limbs, jaw and abdomen, injection site pain, nausea, vomiting, headache, paresthesias, tremor, lacrimation, and nasal discharge. Serious reactions include hypertension (frequent), tachycardia (frequent), infection site abscess, and fever (occurs in 30 percent of children).

D-penicillamine — D-penicillamine is another oral chelating agent. It was developed originally to reduce serum copper concentration in patients with Wilson disease [67]. American Academy of Pediatrics (AAP) guidelines for the treatment of lead toxicity describe penicillamine as a third-line agent, indicated only when unacceptable reactions have occurred to succimer or CaNa2EDTA, and continued therapy is required. Given the potential for significant adverse events (including leukopenia, thrombocytopenia, hematuria, abnormal liver function, urticaria, angioedema, Stevens-Johnson syndrome, and nephritic syndrome), use of this agent is not generally recommended and consultation with a clinician with expertise in managing pediatric lead poisoning with D-penicillamine chelation is advised before starting this treatment [31,37,68,69].

PERINATAL LEAD EXPOSURE — Since publication of guidance for perinatal lead exposure discussed below, the Centers for Disease Control and Prevention (CDC) has lowered the reference level for elevated blood lead in United States children to 3.5 mcg/dL (0.17 micromol/L). Consultation with experts in perinatal lead exposure is advised for mothers with blood lead levels (BLLs) between 3.5 and 5 mcg/dL.

Prenatal exposure — In the United States, blood lead screening is recommended for pregnant women with risk factors for lead exposure. Providers for pregnant women with elevated BLLs should ensure that the maternal lead level is known by the provider managing the newborn infant. Levels of both the mother and infant should be documented in their medical records. Indications for blood lead screening during pregnancy and postpartum are discussed separately (figure 1). (See "Lead exposure, toxicity, and poisoning in adults", section on 'Pregnancy and breastfeeding'.)

Lead inspection of the home and abatement, as needed, is a key intervention for pregnant women with elevated BLLs. (See "Childhood lead poisoning: Exposure and prevention", section on 'Prevention'.)

According to the CDC, infants of mothers with BLLs ≥3.5 mcg/dL (0.17 micromol/L) should have cord blood samples sent for blood lead testing at the time of delivery or venous BLLs measured soon after birth [70]. Additional testing is indicated for neonates with an initial venous or cord BLL ≥3.5 mcg/dL (0.17 micromol/L). The frequency of repeated testing and the need for other interventions vary according to the degree of blood lead elevation (table 12 and figure 1). These guidelines apply to infants up to age six months. Screening intervals differ for older infants and children. (See "Childhood lead poisoning: Clinical manifestations and diagnosis", section on 'Diagnosis'.)

Breastfeeding — Based upon estimates of infant BLL elevation occurring from breast milk ingestion (table 13) and the proven benefits of breastfeeding in young infants, breastfeeding should be encouraged for all mothers with a venous BLL <40 mcg/dL (1.93 micromol/L) [70]. In the United States, infants whose mothers have a BLL ≥40 mcg/dL (1.93 micromol/L) should not breastfeed initially. The mother should be instructed to pump her breast milk and discard it. Breastfeeding should be instituted if the maternal BLL falls below 40 mcg/dL (1.93 micromol/L). Whether the risks of breastfeeding for mothers with a BLL ≥40 mcg/dL (1.93 micromol/L) who live in a resource-limited regions outweigh the benefits is uncertain. Measurement of levels of lead in breast milk is not recommended.

Infant monitoring of BLLs during breastfeeding should proceed according to recommendations for follow-up screening of neonates and infants under six months of age (table 12 and table 14). Continuation of breastfeeding is based upon whether there is evidence that breast milk is contributing to elevated infant lead levels on the follow-up maternal and infant screening (table 15) [70]:

Infant BLL <5 mcg/dL (0.24 micromol/L) or has declined by at least 5 mcg/dL from the neonatal baseline – Continue breastfeeding.

Infant BLL failing to decline by at least 5 mcg/dL (0.24 micromol/L) from the neonatal baseline, and maternal BLL ≤20 mcg/dL (0.96 micromol/L) – Environmental and other sources of lead exposure should be evaluated. Mother can continue breastfeeding.

Infant BLL failing to decline by at least 5 mcg/dL (0.24 micromol/L) from the neonatal baseline, and maternal BLL >20 mcg/dL (0.96 micromol/L) – Consider interruption of breastfeeding until maternal levels decline.

Additional monitoring of maternal BLL during breastfeeding depends upon the most recently obtained maternal BLL (immediately postpartum if possible) (table 16). (See "Lead exposure, toxicity, and poisoning in adults", section on 'Pregnancy and breastfeeding'.)

ADDITIONAL RESOURCES

Lead poisoning management resources — To identify a physician and other clinicians with expertise in managing childhood lead poisoning, contact the regional health department, regional poison control center, or, in the United States a Pediatric Environmental Health Specialty Unit.

In the United States, additional sources for information for the general public and professionals include the Centers for Disease Control and Prevention (CDC; 1-800-CDC-INFO [1-800-232-4636]), Pediatric Environmental Health Specialty Units, and the National Lead Information Center (1-800-424-LEAD [5323]).

Regional poison control centers — Regional poison control centers in the United States are available at all times for consultation on patients with known or suspected poisoning, and who may be critically ill, require admission, or have clinical pictures that are unclear (1-800-222-1222). In addition, some hospitals have medical toxicologists available for bedside consultation. Whenever available, these are invaluable resources to help in the diagnosis and management of ingestions or overdoses. Contact information for poison centers around the world is provided separately. (See "Society guideline links: Regional poison control centers".)

Society guideline links — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Lead and other heavy metal poisoning".)

SUMMARY AND RECOMMENDATIONS

Approach – Because there is no known safe threshold for lead exposure, certain actions should be taken in all children with blood lead levels (BLLs) greater than or equal to the United States reference value (3.5 mcg/dL [0.17 micromol/L] in 2021); the timing, urgency, and setting of the interventions vary, depending upon the severity of lead toxicity (table 2). The mainstay of treatment at all BLLs is removal of lead from the child's environment. (See 'General management' above.)

BLL <45 mcg/dL (2.17 micromol/L) – We recommend that children with BLLs <45 mcg/dL (2.17 micromol/L) do not receive chelation therapy (Grade 1B) (see 'Lead level 15 to 44 mcg/dL' above). The major interventions for patients with BLLs <45 mcg/dL (2.17 micromol/L) are (see 'Approach' above):

Confirm elevated BLLs by repeat venous blood lead testing.

Perform a history and physical examination focused on the history of lead exposure and signs and symptoms of lead toxicity (table 8).

Perform laboratory screening for iron deficiency anemia consisting of a complete blood count, serum ferritin, and C-reactive protein.

Perform a plain abdominal radiograph in patients with pica behaviors (eg, eating paint chips or excessive mouthing). We suggest that children with leaded foreign bodies or flecks (image 1) that are located in the small bowel receive gastrointestinal decontamination with whole bowel irrigation (WBI) (Grade 2C). (See 'Gastrointestinal decontamination' above.)

Provide nutritional interventions and lead education to the family (table 3).

Ensure screening of other children at risk, including those in foster care with frequent caregiver changes, who may be placed in homes not evaluated for lead risks.

Notify the appropriate public health authority.

Facilitate identification and abatement of the lead source by a licensed contractor.

Carry out follow-up screening with a schedule determined by the original BLL.

BLL ≥45 mcg/dL (2.17 micromol/L) – In addition to the interventions described for lower BLLs, all patients with BLL ≥45 mcg/dL (2.17 micromol/L) need chelation as described below. Chelation therapy for lead poisoning should be performed in consultation with a physician with expertise in managing childhood lead poisoning. In the United States, contact the regional public health department, the regional Pediatric Environmental Health Specialty Unit, or a regional poison control center (1-800-222-1222). In other parts of the world, contact the regional public health department or poison control center (see 'Additional resources' above):

Confirmatory testing prior to chelation – Asymptomatic children with BLLs 45 to 69 mcg/dL (2.17 to 3.33 micromol/L) should have a confirmatory venous lead level within 48 hours. Patients with BLLs ≥70 mcg/dL (3.38 micromol/L) and patients with signs or symptoms of lead toxicity (table 8) require confirmatory levels within 24 hours. Additional laboratory testing prior to chelation is also indicated (table 5). (See 'Lead level 45 to 69 mcg/dL' above and 'Initial evaluation' above.)

Asymptomatic patients (BLLs of 45 to 69 mcg/dL [2.17 to 3.33 micromol/L]) – We recommend that asymptomatic children with BLLs of 45 to 69 mcg/dL (2.17 to 3.33 micromol/L) receive chelation therapy (Grade 1C). We suggest that chelation be performed orally with succimer (table 6) rather than by intravenous administration of calcium disodium edetate (CaNa2EDTA) or oral penicillamine (Grade 2C). Treatment should begin as soon as possible after the BLL is confirmed, and only when the child is in a lead-safe environment. In most instances, asymptomatic patients with BLLs of 45 to 69 mcg/dL should be hospitalized. (See 'Lead level 45 to 69 mcg/dL' above and 'Pharmacologic agents for chelation' above.)

Asymptomatic patients with BLLs ≥70 mcg/dL (3.38 micromol/L) and symptomatic patients without encephalopathy – Asymptomatic children with BLLs ≥70 mcg/dL (3.38 micromol/L) and children with symptomatic lead poisoning warrant emergency evaluation and consultation with a physician with expertise in managing childhood lead poisoning. We suggest that asymptomatic children with BLLs ≥70 mcg/dL (3.38 micromol/L) and symptomatic children whose BLL is ≥45 mcg/dL but who do not have encephalopathy receive succimer and CaNa2EDTA rather than combination therapy with dimercaprol and CaNa2EDTA or single-agent chelation with succimer (Grade 2B). (See 'Lead level ≥70 mcg/dL' above and 'Chelation' above and 'Symptomatic lead poisoning' above.)

Lead encephalopathy – Initial treatment priorities in children with lead encephalopathy include emergency chelation, management of increased intracranial pressure, seizures (table 9), and establishing and maintaining urine output while avoiding excess fluid administration. These patients also warrant emergency neuroimaging. Lumbar puncture should be avoided. (See 'Initial stabilization' above.)

We recommend that children with lead encephalopathy receive combined chelation therapy with dimercaprol (also called British Anti-Lewisite [BAL]) and calcium disodium edetate (CaNa2EDTA) (table 7) (Grade 1A). (See 'Chelation' above.)

Perinatal lead exposure – In the United States, blood lead screening is recommended for pregnant women with risk factors for lead exposure. Providers for pregnant women with elevated BLLs should ensure that the maternal lead level is known by the provider managing the newborn infant. Levels of both the mother and infant should be documented in their medical records. A summary of interventions for the mother and infant is provided in the figure (figure 1). Breastfeeding is encouraged for mothers with venous BLLs <40 mcg/dL (1.93 micromol/L). (See 'Perinatal lead exposure' above.)

ACKNOWLEDGMENT

The editorial staff at UpToDate acknowledge both Richard L Hurwitz, MD and Dean A Lee, MD, PhD, who contributed to earlier versions of this topic review.

The UpToDate editorial staff acknowledges extensive contributions of Donald H Mahoney, Jr, MD to earlier versions of this topic review.

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Topic 6494 Version 56.0

References

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