bubble_chart Overview

Pediatric lead poisoning is mostly caused by ingestion through the digestive tract, and the oral dose that causes acute lead poisoning is approximately 5mg/kg.

bubble_chart Etiology

Infant poisoning often results from licking lead-containing powders on their mothers' faces, sucking lead-containing ointments applied to their mothers' nipples, or ingesting the breast milk of mothers with lead poisoning. When children's baby teeth erupt, they often enjoy biting objects, which can lead to poisoning from chewing on lead-containing paint layers on bed frames, toys, etc. Children with pica may develop lead poisoning from swallowing large amounts of peeling paint from floors or walls. Consuming acidic foods cooked or stored in lead-containing utensils (such as tinware or low-quality ceramic glazes or enamels, which contain lead) or ingesting water and food contaminated with lead can also cause lead poisoning. Leaving leftover canned food in tin cans and storing them in the refrigerator is another cause of lead poisoning.

Accidental ingestion of excessive amounts of lead-containing medications, such as epilepsy pills, minium, black tin pill, litharge, etc., can cause acute poisoning. Lead toxins can also be absorbed through the respiratory tract, such as lead-containing talcum powder (which can be inhaled by infants) or fumes containing lead compounds produced by burning battery casings, both of which can lead to inhalation poisoning in infants and young children. Children living in environments surrounded by lead dust may regularly inhale certain amounts of lead. If the work clothes of lead industry workers are brought home for long periods and contaminate the dust, their children may frequently inhale lead-contaminated dust, leading to symptomatic lead poisoning.

bubble_chart Pathogenesis

After lead enters the human body, it is absorbed into the bloodstream and circulates primarily in forms such as dibasic lead phosphate, lead glycerophosphate, protein complexes, and lead ions. Initially distributed throughout the body, approximately 95% is subsequently stored in bone tissue as tribasic lead phosphate, with small amounts remaining in the liver, kidneys, spleen, lungs, heart, brain, muscles, bone marrow, and blood. About 95% of the lead in the blood is distributed within red blood cells. When lead concentrations in the blood and soft tissues become too high, toxic effects can occur. Lead stored in bones does not cause poisoning symptoms; however, when the body's acid-base balance is disrupted due to infections, trauma, fatigue, consumption of alcoholic beverages, or intake of acidic medications, the insoluble tribasic lead phosphate in bones converts to soluble dibasic lead phosphate and moves into the bloodstream. A significant increase in blood lead levels can then lead to symptoms of lead poisoning.

Lead toxicity primarily inhibits enzymes containing sulfhydryl groups within cells, disrupting the body's generation and transformation and physiological functions. This can cause small stirred pulse spasms, injury to capillary endothelial cells, impair energy metabolism, lead to porphyrin metabolism disorders, hinder the synthesis of methemoglobin, alter the normal properties of red blood cells and their membranes, and inhibit the resynthesis of phosphocreatine in muscles, among other effects. These changes result in a series of pathological alterations, with the most notable impacts observed in the nervous system, kidneys, hematopoietic system, and blood vessels.

bubble_chart Clinical Manifestations

Children with acute poisoning may experience a metallic taste in the mouth, drooling, nausea, vomiting (the vomitus often appears as white, milk-like clumps due to the formation of white lead chloride in the stomach), abdominal pain, sweating, dysphoria, and refusal to eat. When acute lead encephalopathy occurs, sudden and persistent vomiting (which may be projectile) appears, accompanied by increased respiratory and pulse rates, ataxia, strabismus, convulsions, unconsciousness, etc. At this stage, elevated blood pressure and optic disc edema may also be present. In infants, the anterior fontanelle may be full or even bulging, with widened cranial sutures and an enlarged head circumference. Severe lead poisoning often presents with paroxysmal colicky abdominal pain and may lead to hepatomegaly, jaundice, oliguria or anuria, and circulatory failure. A few cases may exhibit gastrointestinal bleeding and paralytic ileus. Most children show no fever or only mild fever. Patients with prolonged illness may also develop anemia, with a grayish complexion (lead pallor), accompanied by palpitations, shortness of breath, and lack of strength. Teeth and nails may appear black due to lead deposition, though the black "lead line" on the gums is rarely seen in young children. Numbness in the limbs and distal limb manifestations such as wrist drop or foot drop are uncommon in infants; older children often complain of numbness in the fingers and toes. Occasionally, limb paralysis may occur, and if intercostal muscle paralysis develops, respiratory distress or even respiratory failure may ensue. Chronic lead poisoning is more common in children over 2–3 years old, with symptoms typically appearing 3–6 months after lead exposure.

The main manifestations include severe central nervous system disorders such as epileptic seizures, hyperactivity, aggressive behavior, delayed or lost language development, etc., but without signs of acute intracranial hypertension. Such chronic encephalopathy may be a sequela of acute encephalopathy or related to chronic excessive lead intake. Epileptic seizures and behavioral changes in the sequelae of lead encephalopathy may gradually lessen by adolescence, but intellectual disabilities persist; severe cases may result in blindness and hemiplegia. Recent studies have found that retinal stippling often appears before abnormal urinary lead excretion, serving not only as an early sign of lead poisoning but also showing a high positive rate in lead absorption cases, though false positives and negatives have also been reported.

X-ray findings: Dense white bands appear in the metaphyses of long bones, broader and more pronounced than those seen during the convalescent stage of rickets. Large deposits of bismuth or phosphorus in the bone ends may produce similar shadows, though this is rare. X-ray changes in the long bones of children under 2 years old with lead poisoning are often inconspicuous, and even severe cases may show no abnormalities. Abdominal X-rays may reveal radiopaque substances.

bubble_chart Auxiliary Examination

1. Lead Measurement: Blood lead levels of 1.44–2.4 μmol/L (30–50 μg/dL) are generally considered diagnostically significant. However, since lead leaves the bloodstream relatively quickly, this test is most valuable for diagnosing acute poisoning. In children, blood lead levels exceeding 2.88 μmol/L (60 μg/dL) may cause noticeable neurological damage and signs; persistent levels above 1.92 μmol/L (40 μg/dL) can lead to varying degrees of neurological impairment. Recent studies on children aged 4–12 showed that blood lead levels above 1.18 μmol/L (24.5 μg/dL) may result in abnormal mental development. Currently, the U.S. Centers for Disease Control and Prevention defines lead poisoning as a whole-blood lead concentration ≥1.2 μmol/L (≥25 μg/dL), as even asymptomatic lead exposure at this level can adversely affect red blood cells, peripheral nerves, kidneys, immune system, bones, and central nervous system function. Urinary lead measurement can serve as a diagnostic reference, with a normal upper limit of 0.39 μmol/L (0.08 mg/L), though variations may occur due to influencing factors. For detecting lead in talcum powder, a small amount of vinegar can be added, followed by a drop of 1% potassium iodide solution; a golden yellow color indicates the presence of lead.
2. Peripheral Blood Tests: Children with grade II or higher lead poisoning may exhibit reduced red blood cells and hemoglobin, increased basophilic stippling, and elevated reticulocytes and polychromatic erythrocytes, though these findings lack specificity. Fluorescent erythrocyte testing is a valuable method for early lead poisoning diagnosis, with the following criteria: <1% is normal, 2–10% indicates grade I increase, and >10% is considered excessive. However, this is not a specific diagnostic method for lead poisoning.
3. Provocation Test for Lead: For children with lead exposure history but no obvious symptoms and normal urinary lead levels, a provocation test can be performed. Typically, calcium disodium edetate (Na₂CaEDTA) is administered as a single intramuscular injection of 500 mg/m², followed by an 8-hour urine collection for lead measurement. If the urinary lead excretion exceeds 4.83 μmol (1 μg) per mg of injected calcium disodium edetate, it suggests a blood lead concentration above 2.64 μmol/L (55 μg/dL).
4. Porphyrin Measurement: Quantitative urinary coproporphyrin testing is reliable, with a normal upper limit of <0.15 mg/L. The qualitative coproporphyrin test by Benson and Chisolm is simpler and can detect children with blood lead levels exceeding 4.83 μmol/L (100 μg/dL). Erythrocyte protoporphyrin levels are significantly elevated (normal values: <0.72 μmol/L erythrocytes (40 μg/dL erythrocytes) or <0.144 μmol/g hemoglobin (3 μg/g hemoglobin)). Tests for erythrocyte δ-aminolevulinic acid dehydratase (δ-ALAD) and urinary δ-aminolevulinic acid (δ-ALA): Reduced δ-ALAD activity is currently regarded as a sensitive indicator of lead exposure. A study by Shanghai First Medical College on 49 healthy individuals with no lead exposure established a normal lower limit of 126.4 units for blood δ-ALAD activity. Due to its extreme sensitivity to lead, δ-ALAD is more suitable for assessing environmental lead pollution than for diagnosing lead poisoning. In China, the upper limit for urinary δ-ALA is set at 6 mg/L, with increased excretion strongly correlating with lead poisoning severity. Its diagnostic value for lead poisoning is roughly comparable to that of urinary coproporphyrin.
5. Cerebrospinal fluid examination: The pressure can be as high as 58.8～78.4 kPa, with high protein content, but the white blood cell count generally does not increase, occasionally reaching around 0.03×10⁹/L (30/mm3), mostly lymphocytes, and normal glucose levels.
6. Other examinations: Lead-poisoned children may occasionally have bright red blood or occult blood in their stool, caused by significant lead irritation to the intestines. Additionally, blood sugar levels often increase.

bubble_chart Diagnosis

Acute moderate to severe lead poisoning can usually be diagnosed based on clinical manifestations and laboratory tests. However, for chronic, low-level lead poisoning in children, simple and feasible examination methods are still being explored. Since such children often exhibit varying degrees of intellectual impairment, this issue has now attracted widespread attention.

In the initial stage [first stage] of lead poisoning, when gastrointestinal symptoms appear, it should be differentiated from acute gastroenteritis and viral hepatitis; when abdominal colicky pain occurs, it must be distinguished from acute abdomen; when signs of encephalopathy appear, it should be differentiated from encephalitis, subcutaneous node encephalitis, brain tumors, and hand-foot convulsion syndrome; when symptoms and signs of peripheral neuritis are present, it must be distinguished from poliomyelitis and diphtheritic nerve paralysis.

bubble_chart Treatment Measures

1. Prevent further lead poisoning

In patients with mild lead poisoning, cutting off the source of lead can already halt severe symptoms. For children poisoned by ingesting large amounts of lead-containing medication, the first step must be to induce vomiting (using syrup of ipecac), followed by gastric lavage with 1% sodium sulfate or magnesium sulfate. Then, 15–20g of sodium sulfate or magnesium sulfate should be introduced into the stomach to form insoluble lead sulfide, after which gastric lavage is performed again to remove the precipitated lead sulfide. Subsequently, administering a relatively large amount of milk or raw egg whites can convert the remaining lead into less soluble salts and protect the gastric mucosa. Finally, saline cathartics should be administered 1–2 times to induce defecation.

2. Promote the excretion of lead The currently common method for lead removal therapy involves adding calcium disodium edetate (Na2CaEDTA) at 15–25mg/kg to a 5% glucose solution to form a 0.3%–0.5% solution, which is then administered via intravenous drip or slow intravenous injection. This allows the formation of non-toxic lead edetate salts, which are excreted in the urine.

The total daily dose generally does not exceed 50 mg/kg, administered via intravenous drip over 6 to 12 hours or divided into two slow intravenous injections, continued for 2 to 3 days, with an interval of 5 to 10 days constituting one treatment course. Typically, 3 to 5 courses may be applied consecutively, followed by subsequent lead removal therapy at intervals of 3 to 6 months based on the condition. Intravenous administration may cause kidney damage, so urine routine and renal function must be frequently monitored during treatment. If abnormal renal function or anuria occurs, the medication should be discontinued immediately. For pediatric patients undergoing this therapy, it is advisable to start with a small dose, i.e., dissolving 0.2 g in 200 ml of 5% glucose solution and administering it slowly via intravenous drip over at least 1 hour. If no adverse reactions occur within 4 hours, the aforementioned dose may be administered. Chronic poisoning may be treated with intramuscular injection. This drug is poorly absorbed in the gastrointestinal tract and can form lead disodium edetate with lead, which is absorbed into the body, increasing lead toxicity; thus, oral administration is not recommended. The domestically produced detoxification agent sodium dimercaptosuccinate (DMSA) is no less effective than edetate for treating lead poisoning. The dosage and usage are detailed in the section on antimony poisoning. For severe cases or when blood lead levels exceed 4.83 μmol/L (100 μg/dL), combination therapy may be used. The drug dosage and administration are as follows: first, administer dimercaprol (BAL) at 4 mg/kg per dose, intramuscularly every 4 hours; simultaneously or shortly thereafter, administer calcium disodium edetate at 12.5 mg/kg per dose (maximum daily dose of 75 mg/kg) via intravenous or intramuscular injection (the two drugs should be injected intramuscularly at different sites). For patients who can take oral medication, administer penicillamine as soon as possible at 20–25 mg/kg daily, divided into four oral doses, with a maximum daily dose of 1 g. A penicillin allergy test should be performed before administration. The combination therapy lasts 3 to 5 days until blood lead levels normalize, followed by a 2-day break before the next course. In repeated courses, the daily dose should be appropriately reduced (calcium disodium edetate at 50 mg/kg daily, dimercaprol at 15 mg/kg daily). Throughout the use of these drugs, attention must be paid to their side effects. If anuria occurs, discontinue calcium disodium edetate immediately. During dimercaprol administration, iron supplements should not be used concurrently. Patients with anuria lasting over 4 hours should undergo hemodialysis simultaneously. For blood lead levels between 3.84–4.83 μmol/L (80–100 μg/dL), administer calcium disodium edetate and dimercaprol for 2 days, followed by oral penicillamine for 5 days. If no lead is present in the intestines, calcium disodium edetate alone may be used for 5 days or dimercaprol plus calcium disodium edetate for 3 days. For blood lead levels between 2.88–3.84 μmol/L (60–80 μg/dL), short-term calcium disodium edetate or longer-term penicillamine therapy may be used. Patients with blood lead levels <2.88 μmol/L (60 μg/dL) generally do not require lead removal therapy unless other lead poisoning symptoms are present. Additionally, calcium trisodium pentetate (CaNa3DTPA) is also effective for lead removal and may be used as appropriate. The dosage is 15–30 mg/kg per administration, dissolved in saline to form a 0.2%–0.5% solution, administered via intravenous drip, with a regimen of 3 days on and 3 days off constituting one course. In cases of acute poisoning, sodium citrate may also be used to form lead citrate with lead. Although soluble in blood, it does not readily dissociate, thus posing no toxic effects and can be excreted in urine without causing poisoning. The daily dose is 3–8 g (adult dose), divided into multiple oral administrations, or a 2.5% solution may be used for intravenous injection if necessary.

3. Treatment of acute abdominal pain

If the abdominal pain is severe, atropine, 654-2, vitamin K, etc. can be used to relieve intestinal spasms, and 10 ml of 10% calcium gluconate can be slowly injected intravenously. In addition to alleviating abdominal colicky pain, this also promotes the deposition of lead in the bones and reduces blood lead levels. If necessary, compound formula camphor tincture can be administered, and older children may receive a small subcutaneous injection of morphine.

4. Treatment of acute cerebral symptoms

Generally, drugs such as diazepam, paraldehyde, and phenobarbital sodium are used to control convulsions. To reduce intracranial pressure, intravenous infusion of 50% glucose or 20% mannitol can be administered to alleviate cerebral edema. Fluid intake should meet the basic requirements, typically 40–60 ml/kg per day (equivalent to 800–1200 ml/m²), while also correcting electrolyte imbalances. If symptoms such as vomiting, convulsions, or fever are present, the minimum estimated fluid loss should also be supplemented.

bubble_chart Prognosis

Early cessation of lead absorption leads to a good prognosis. However, once brain symptoms appear, even with treatment, sequelae such as epilepsy and intellectual developmental disorders often occur.