Page 14 of 31
PH9.3 | PH9.3 | Heavy Metal Poisoning and Chelation — SDL Guide — SDL Guide (Part 3)
Self-Assessment
Test your understanding of heavy metal toxicology and chelation pharmacology.
- Match each metal to its preferred chelating agent(s): (a) lead with encephalopathy, (b) acute iron poisoning, (c) Wilson's disease, (d) acute arsenic poisoning, (e) inorganic mercury poisoning.
- Why is dimercaprol (BAL) contraindicated in iron poisoning? Explain the mechanism of the adverse effect.
- A patient with Wilson's disease who has been on D-penicillamine for 3 years decides to stop taking it because she feels well. What is the risk, and what will you advise?
- What is basophilic stippling and in which conditions is it seen? How does lead cause this finding?
- Describe the 'vin rosé' sign in deferoxamine therapy — what causes it, and what is its clinical significance?
SELF-CHECK
A child with severe lead encephalopathy (blood lead 85 mcg/dL) needs chelation. Which is the correct management sequence?
A. Start calcium EDTA immediately by IV infusion; add BAL 4 hours later
B. Give D-penicillamine orally for 3 weeks, then reassess
C. Give dimercaprol (BAL) IM first; add calcium EDTA 4 hours later (after BAL has penetrated the CNS)
D. Deferoxamine IV infusion plus BAL IM combination
Reveal Answer
Answer: C. Give dimercaprol (BAL) IM first; add calcium EDTA 4 hours later (after BAL has penetrated the CNS)
In lead encephalopathy (BLL >70 mcg/dL with CNS symptoms), the sequence is BAL IM FIRST, then EDTA 4 hours later. The rationale: EDTA mobilises lead from bone into blood, which can worsen encephalopathy if lead then crosses into the brain. BAL, given first, provides CNS-penetrant chelation (it crosses the blood-brain barrier as a lipid-soluble complex) and protects the brain during the EDTA mobilisation phase. D-penicillamine alone is insufficient for acute lead encephalopathy. Deferoxamine is for iron, not lead.