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Lead poisoning often causes minimal symptoms at first but can cause acute encephalopathy or irreversible organ damage, commonly resulting in cognitive deficits in children. Diagnosis is by whole blood lead level. Treatment involves stopping lead exposure and sometimes using chelation therapy with succimer or edetate Ca disodium, with or without dimercaprol.
There is no blood lead level that does not have deleterious effects. The Centers for Disease Control and Prevention (CDC) recommend that children with blood lead levels > 5 μg/dL must have remediation, retesting, and serial monitoring as well as assessment for vitamin deficiency and general nutritional status.
Leaded paint was commonly used until 1960, used to some degree until the early 1970s, and mostly eliminated in 1978. Thus, for a significant number of older housing units, leaded paint still poses some hazard. Lead poisoning is usually caused by direct ingestion of leaded paint chips (from cracked, peeling paint). During home remodeling, patients may be exposed to significant amounts of aerosolized lead in the form of particles scraped or sanded off during surface preparation for repainting.
Some ceramic glazes contain lead; ceramic ware (eg, pitchers, cups, plates) that is made with these glazes (common outside the US) can leach lead, particularly when in contact with acidic substances (eg, fruits, cola drinks, tomatoes, wine, cider). Lead-contaminated moonshine whiskey and folk remedies are possible sources, as are occasional lead foreign objects in the stomach or tissues (eg, bullets, curtain or fishing weights). Bullets lodged in soft tissues near synovial fluid or CSF may increase blood lead levels, but that process takes years.
Occupational exposure can occur during battery manufacture and recycling, bronzing, brass making, glass making, pipe cutting, soldering and welding, smelting, or working with pottery or pigments. Certain ethnic cosmetic products and imported herbal products and medicinal herbs contain lead and have caused cluster outbreaks of lead poisoning in immigrant communities. Fumes of leaded gasoline (in countries other than the US) recreationally inhaled for CNS effects may cause lead poisoning.
Lead poisoning is most often a chronic disorder and may not cause acute symptoms. With or without acute symptoms, poisoning eventually has irreversible effects (eg, cognitive deficits, peripheral neuropathy, progressive renal dysfunction).
Symptoms of lead poisoning are roughly proportional to lead levels, but there are no safe levels of lead. Risk of cognitive deficits increases when the whole blood lead level (PbB) is ≥ 10 μg/dL (≥ 0.48 mmol/L) for an extended period, although the cutoff may be even lower. Other symptoms (eg, abdominal cramping, constipation, tremors, mood changes) may occur if PbB is > 50 μg/dL (> 2.4 mmol/L). Encephalopathy is likely if PbB is > 100 μg/dL (> 4.8 mmol/L).
Acute lead poisoning may cause irritability, decreased attentiveness, and acute encephalopathy. Cerebral edema develops over 1 to 5 days, causing persistent and forceful vomiting, ataxic gait, seizures, altered consciousness, and, finally, intractable seizures and coma. Encephalopathy may be preceded by several weeks of irritability and decreased play activity.
Chronic lead poisoning in children may cause intellectual disability, seizure disorders, aggressive behavior disorders, developmental regression, chronic abdominal pain, and anemia.
Lead poisoning is suspected in patients with characteristic symptoms. However, because symptoms are often nonspecific, diagnosis of lead poisoning is often delayed. Evaluation includes CBC and measurement of serum electrolytes, BUN, serum creatinine, plasma glucose, and PbBs. An abdominal x-ray should be taken to look for lead particles, which are radiopaque. X-rays of long bones are taken in children. Horizontal, metaphyseal lead bands representing lack of RBC remodeling and increased Ca deposition in the zones of provisional calcification in children’s long bones are somewhat specific for poisoning with lead or other heavy metals but are insensitive. Normocytic or microcytic anemia suggests lead toxicity, particularly when the reticulocyte count is elevated or RBC basophilic stippling occurs; however, sensitivity and specificity are limited. Diagnosis is definitive if PbB is ≥ 5 μg/dL.
Because measuring PbB is not always possible and can be expensive, other preliminary or screening tests for lead poisoning can be used. Capillary blood testing for lead is accurate, inexpensive, and quick. All positive tests should be confirmed with PbB. The erythrocyte protoporphyrin (also called zinc protoporphyrin or free erythrocyte protoporphyrin) test is often inaccurate and now is seldom used.
Children with PbB > 5 μg/dL should be assessed clinically and, if necessary, with testing for nutritional and vitamin deficiencies (eg, iron, Ca, vitamin C deficiencies).
Provocative urine metal testing for lead and other metals in which chelation agents (eg, dimercaptosuccinic acid, dimercaptopropane sulfonic acid, calcium disodium edetate) are given to the patient and then urinary levels of excreted metals are measured has not been scientifically validated, has no shown benefit, and may be harmful in the assessment and treatment of patients in whom there is concern for metal poisoning.
For all patients, the source of lead is eliminated. If lead chips are visible on abdominal x-ray, whole-bowel irrigation with a polyethylene glycol electrolyte solution at 1 to 2 L/h for adults or 25 to 40 mL/kg/h for children is done until repeat x-ray shows no lead. Administration via NGT may be necessary to deliver these large volumes and care must be taken to protect the airway; intubation may be necessary. If the cause is bullets, surgical removal should be considered. Children with PbB > 70 μg/dL (> 3.40 μmol/L) and all patients with neurologic symptoms should be hospitalized. Patients with acute encephalopathy are admitted to an ICU.
Chelating drugs (eg, succimer [meso-2,3-dimercaptosuccinic acid], CaNa 2 EDTA, dimercaprol [British antilewisite, or BAL]) can be given to bind lead into forms that can be excreted. Chelation should be supervised by an experienced toxicologist. Chelation is indicated for adults with symptoms of poisoning plus PbB > 70 μg/dL and for children with encephalopathy or PbB > 45 μg/dL (> 2.15 μmol/L). Liver and kidney disorders are relative contraindications for chelating drugs. Chelating drugs should not be given to any patient with ongoing exposure to lead because chelation can increase GI absorption of lead. Chelation removes only relatively small amounts of metal. If total body burden of lead is very large, multiple chelations over many years may be required.
Patients with encephalopathy are treated with dimercaprol 75 mg/m 2 (or 4 mg/kg) IM q 4 h and CaNa 2 EDTA 1000 to 1500 mg/m 2 IV (infusion) once/day. The first dose of dimercaprol should precede the first dose of CaNa 2 EDTA by at least 4 h to prevent redistribution of lead into the brain. Dimercaprol may be stopped after the first few doses depending on lead levels and symptom severity. Dimercaprol-CaNa 2 EDTA combination therapy is given for 5 days, followed by a 3-day washout period; then the need for continued chelation is reassessed.
Patients without encephalopathy are usually treated with succimer 10 mg/kg po q 8 h for 5 days, followed by 10 mg/kg po q 12 h for 14 days. If these patients have symptoms, they can alternatively be treated for 5 days with dimercaprol 50 mg/m 2 via deep IM injection q 4 h plus CaNa 2 EDTA 1000 mg/m 2 IV once/day.
Dimercaprol, which can cause vomiting, is given with parenteral or oral fluids. Dimercaprol can also cause pain at the injection site, numerous systemic symptoms, and, in patients with G6PD deficiency, moderate to severe acute intravascular hemolysis. This drug should not be given concurrently with iron supplements. Dimercaprol is formulated with peanut derivatives and thus is contraindicated in patients with known or suspected peanut allergy.
CaNa 2 EDTA can cause thrombophlebitis, which can be prevented by giving the drug IM, not IV, and by using an IV concentration of < 0.5%. Before beginning treatment with CaNa 2 EDTA, adequate urine flow must be confirmed. Serious reactions to CaNa 2 EDTA include renal insufficiency, proteinuria, microscopic hematuria, fever, and diarrhea. Renal toxicity, which is dose-related, is usually reversible. Adverse effects of CaNa 2 EDTA are probably due to zinc depletion.
Succimer may cause rash, GI symptoms (eg, anorexia, nausea, vomiting, diarrhea, metallic taste), and transient elevations of liver enzymes.
Patients at risk should be screened by measuring PbB. Measures that reduce risk of household poisoning include regular hand washing, regular washing of children’s toys and pacifiers, and regular cleaning of household surfaces; drinking water, household paint (except in houses built after 1978), and ceramic ware made outside the US should be tested for lead. Adults exposed to lead dust at work should use appropriate personal protective equipment, change their clothing and shoes before going home, and shower before going to bed.
Houses painted before 1978 (particularly when remodeled or repainted), certain ceramic ware (eg, pitchers, cups, plates) that has a leaded glaze, and certain occupational exposures increase the risk of lead poisoning.
Test patients by measuring capillary levels or PbB.
Remove the source of lead (eg, by whole-bowel irrigation for lead in the GI tract).
Arrange chelation therapy for adults with PbB > 70 μg/dL and for children with encephalopathy or PbB > 45 μg/dL.
Use succimer or CaNa 2 EDTA, with or without dimercaprol, for chelation therapy.
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