A case of acute lead poisoning in a 2‐year‐old child

Abstract

Lead poisoning still remains a matter of concern, especially in children, in spite of widespread preventive practices [1]. Children are particularly vulnerable through mouthing behaviour [2–4] and high absorption from the gastrointestinal tract as compared with adults. This may adversely affect the developing nervous system, with neurocognitive effects and IQ decline in chronic intoxication [5]. We describe a sporadic case of severe lead poisoning rapidly treated by therapeutic means including surgery, thereby avoiding possible death through encephalopathy. In January 2004 while his parents were looking on, a 2-year-old boy with pica behaviour swallowed toy money made from pure metallic lead. No specific abdominal pain or vomiting was noted by the attending physician. What is more, the child’s behaviour did not change, and he showed no loss of appetite. On the second day (D2), possible elimination of the object in stools was found to be negative, so the child was admitted to a hospital paediatric ward, which ordered blood lead (Pb) measurement, a blood and urine check-up and an X-ray abdominal examination. Blood Pb concentrations were assessed by electrothermal atomic absorption spectrometry with Zeeman background correction. Analytical efficiencies have been monitored by participation in an interlaboratory survey, the Quebec Toxicology Centre Interlaboratory Comparison Programme [6]. The results of 1.51 ± 0.02 µmol l−1 (mean ± SD, in triplicate) already indicated Pb overload in this child, largely exceeding the threshold defined by the 1998 Centers for Disease Control and Prevention [1] (CDC) ( 2.17 µmol l−1, chelation therapy is strongly recommended [1]. On D4, calcium disodium edetate (CaNa2 EDTA) diluted in 5% isotonic glucose solution was infused slowly by intravenous administration (500 mg m−2 day−1) over 5 h for 5 days. No symptoms such as headache, fatigue and nausea were noted. Samples of urine were collected on D3 to D7. High urinary lead excretion from D3 to D5 (1560 µg 24 h−1, 810 µg 24 h−1 and 510 µg 24 h−1, respectively) indicated accelerated elimination of this toxic metal (reference value in urine: <100 µg 24 h−1) [7] and thereby confirmed body lead burden in the child. After the results for D6-D7 in urine (190 µg 24 h−1 and 150 µg 24 h−1, respectively), body pools tended to equilibrate. A decrease of blood lead was observed from D4 to D8 (2.04 ± 0.39 µmol l−1, 1.86 ± 0.02 µmol l−1, 1.54 ± 0.04 µmol l−1, 1.50 ± 0.04 µmol l−1, 1.52 ± 0.04 µmol l−1) vs. D2 (2.95 ± 0.04 µmol l−1). Over the months of February, March, April and May 2004, we noted a relative stability in blood Pb concentrations (1.45 ± 0.01 µmol l−1, 1.25 ± 0.01 µmol l−1, 1.20 ± 0.01 µmol l−1, 1.20 ± 0.01 µmol l−1, respectively), but the concentrations remained high for a child [1]. Figure 1 (A) Child’s anteroposterior abdominal radiography. Toy money is located in the gastric area (black arrow) with minimal colon dilatation. (B) Picture of toy money. Specifications of the toy money: 4 g pure metallic lead, diameter 2 cm Furthermore, in May, an increase of zinc protoporphyrin (ZPP) and a microcytic anaemia (5 µg g−1 Hb; reference value: <1 µg g−1 Hb) was noted. In this acute lead poisoning, clinically speaking, no symptom or loss of appetite was observed, nor was there any intellectual impairment or decline in cognitive function. Lastly, a decrease of blood Pb concentrations appeared over the course of June, July, August and September 2004 (0.85 ± 0.02 µmol l−1, 0.82 ± 0.04 µmol l−1, 0.82 ± 0.04 µmol l−1, 0.75 ± 0.02 µmol l−1, respectively), and was likewise correlated with the ZPP determination in August (1.9 µg g−1 Hb). These concentrations constantly remained above the CDC [1]. It was only during the tenth month (October 2004) that the child’s blood Pb and ZPP concentrations (0.48 ± 0.01 µmol l−1 and 1 µg g−1 Hb, respectively) came within the previously mentioned reference values. It is a well-known fact that the average fractional gastrointestinal absorption of lead is much greater in children than in adults [5] and subsequently, without rapid medical intervention, the extremely high concentrations in this child could have provoked possibly devastating effects on his nervous system [8].