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Stem
A 4-year-old boy is brought by his parents with progressive irritability, intermittent vomiting, and over the last 24 hours drowsiness, ataxia, and a witnessed generalized seizure. The family lives in a 1960s-built rented house with peeling paint that the child is known to pick at and eat (pica). On examination he is drowsy (GCS 12), afebrile, with a blood pressure of 110/70, no meningeal signs, and no focal motor deficit. A capillary blood lead done at the clinic was 86 micrograms/dL. A full blood count shows microcytic hypochromic anaemia; the blood film shows basophilic stippling. A venous blood lead is pending.
Questions
a) What is the most likely diagnosis, and which two pathophysiological mechanisms explain his anaemia and the blood-film finding? (2 marks)
b) List five sources of lead exposure relevant to this case and to children generally. (2 marks)
c) Outline your immediate resuscitative and definitive management, including the specific chelation regimen (drug, route, dose, sequence) and its rationale. (4 marks)
d) Name two complications of chelation therapy and one absolute contraindication to dimercaprol (BAL). (1 mark)
e) What public-health and follow-up measures are essential, and why is the developmental prognosis guarded despite successful treatment? (1 mark)
Model answers
a) Acute lead poisoning (plumbism) with lead encephalopathy. Mechanisms: (i) lead inhibits delta-aminolaevulinic acid dehydratase and ferrochelatase → sideroblastic microcytic anaemia with raised zinc protoporphyrin (ZPP); (ii) basophilic stippling = aggregated degenerated ribosomes in the lead-damaged red cell.
b) Sources: lead-based paint/dust (peeling paint, pica — this child), contaminated water (lead pipes/solder), industrial (battery recycling, smelting, ammunition, foundry, demolition — take-home exposure), traditional cosmetics (surma/kohl, sindoor), Ayurvedic/herbal medicines (Bhasmas), ceramic glazes, moonshine, leaded-petrol-contaminated soil, retained bullets.
c) Resuscitation — ABCDE; secure airway (GCS impaired), oxygen, IV access; treat seizures with IV lorazepam; control raised ICP (head-up, normocapnia, hypertonic saline; avoid over-hydration); ICU admission. Confirm with venous blood lead. Decontamination — whole-bowel irrigation with polyethylene glycol if radiopaque material on abdominal X-ray; remove from source. Definitive chelation — dimercaprol (BAL) IM FIRST at 75 mg/m2 deep IM every 4 hours for 5 days, THEN calcium disodium EDTA IV (CaNa2 EDTA) at 1000–1500 mg/m2/day continuous infusion for 5 days, starting 4 hours after the first BAL dose; add oral succimer (DMSA) when tolerated. Rationale: BAL crosses the blood-brain barrier and chelates brain lead first; EDTA given alone mobilises lead from bone and transiently raises brain lead, worsening encephalopathy. ALWAYS the calcium disodium salt — disodium EDTA causes fatal hypocalcaemia. Source removal is essential.
d) Complications of chelation: EDTA nephrotoxicity; succimer transaminitis, rash, neutropenia; depletion of zinc/copper/iron; rebound blood lead requiring repeat courses. Absolute contraindication to BAL: severe G6PD deficiency (haemolysis) — also contraindicated in peanut allergy (formulated in peanut oil).
e) Public health — report to public health authorities; environmental investigation and lead-paint abatement by certified contractors before the child returns home; screen siblings and pregnant household members; nutritional supplementation (iron, calcium, zinc). Prognosis — guarded because neurodevelopmental harm (IQ loss) is irreversible even when chelation lowers blood lead (TLC Trial); the child needs developmental surveillance and early-intervention support.