Case presentation

A two-year-old girl was referred to the paediatric outpatient clinic in September 2025 following recent consumption of non-nutritive substances, or pica, including peeling paint from the walls. She had a known background of iron deficiency anaemia secondary to excessive cow’s milk intake, with no other identified underlying cause of anaemia, including inherited causes, such as thalassaemia. She was on regular Macrogol 350 (with potassium chloride, sodium bicarbonate, and sodium chloride; two sachets daily) to ensure opening of her bowels once daily. She was eating, but her appetite was slightly reduced.

The girl was born preterm at 33.5 weeks via a caesarean section for maternal pre-eclampsia. She required 23 days of neonatal care. Her developmental age was appropriate. Her siblings were fit and well, and there was no family history of similar complaints.

On examination, she appeared well, and full systemic examination was completely normal, other than a general appearance of pallor. However, given this pica background and known iron deficiency anaemia, the clinical suspicion for further nutritional deficiencies and potential heavy metal exposure was raised. She had bloods taken, including full blood count (FBC), liver function tests (LFTs), iron profile, lead levels, and vitamin D (see Table 1).

Blood test | Normal range | Result from the September clinic visit
White blood cells | 6.0-17.0 109/L | 7.3
Haemoglobin | 101.0-138.0 g/L | 52
Haematocrit | 0.300-0.400 L/L | 0.230
MCV (mean corpuscular volume) | 73.00-88.00 fL | 49.90
MCH (mean corpuscular haemoglobin) | 24.0-30.0 pg | 11.3
MCHC (mean corpuscular haemoglobin concentration) | 310-350 g/L | 226
Neutrophils | 1.00-8.50 109/L | 2.41
Alanine transaminase (ALT) | 1-35 IU/L | 19
Alkaline phosphatase (ALP) | 90-540 U/L | 214
Total bilirubin | 0-21 µmol/L | 4
Albumin | 28-40 g/L | 30
Iron | 5.0-25.0 µmol/L | 1.4
Transferrin | 2.20-3.37 g/L | 4.06
Transferrin saturation | 15.0-45.0 % | 1.4
Lead | <0.1 µmol/L | 0.89
Total 25-hydroxy vitamin D | >50 nmol/L | 18.8

Given the low haemoglobin levels, she was asked to attend hospital. After discussion with haematology, they advised discharging with oral iron replacement to complete a three-month course.

The lead level was also raised at 0.89 µmol/L. Public health authorities were informed, and there was a plan put in place for her lead levels to be monitored regularly following these raised results. There was also discussion surrounding the environmental source for the lead ingestion, believed secondary to paint in the house, which the patient’s mother had been trying to reduce.

On outpatient follow-up in early January, the patient was clinically well. The mother reported that the patient’s appetite had been improving. Her systemic examination was once more normal, though there was still mild pallor. Bloods were repeated, including repeat lead levels, and she was sent home from clinic.

Then, at the end of January, her blood lead levels returned as 3.34 µmol/L (normal <0.1 µmol/L), indicating a significantly elevated result. The paediatric consultant discussed this result with the National Poisons Information Service (NPIS) regarding this result, and a plan was made for the child to be admitted to the Children’s Unit at the hospital for treatment. The treatment in question was chelation therapy with calcium disodium EDTA (ethylenediaminetetraacetic acid) at a dose of 75 mg/kg intravenously, with daily monitoring of bloods, including renal function, liver function, and lead levels. They also requested additional tests, including zinc levels (to be replaced if required), coeliac screen, and repeat vitamin D levels. The patient was to have their urine output monitored, with administration of intravenous fluids if necessary, and their clinical state monitored for any signs of encephalopathy. There was also a request for a plain radiograph of the long bones to assess growth plates and bone density. The patient’s parents were contacted, and she was brought to hospital.

As an inpatient, the patient remained clinically well on examination with good appetite. Their bowels habits remained normal. A more in-depth history surrounding the pica background was obtained, uncovering that the paint was peeling from the walls in a rented house, and it was unclear how long it had been since the paint was replaced.

As an inpatient, her admission bloods were as follows (see Table 2).

Blood test | Normal range | Result on admission
White blood cells | 6.0-17.0 109/L | 11.6
Haemoglobin | 101.0-138.0 g/L | 89
Haematocrit | 0.300-0.400 L/L | 0.340
MCV (mean corpuscular volume) | 73.00-88.00 fL | 56.10
MCH (mean corpuscular haemoglobin) | 24.0-30.0 pg | 14.7
MCHC (mean corpuscular haemoglobin concentration) | 310-350 g/L | 262
Neutrophils | 1.00-8.50 109/L | 5.32
Sodium | 133-146 mmol/L | 139
Potassium | 3.5-5.0 mmol/L | 4.4
Urea | 2.5-6.5 mmol/L | 2.5
Creatinine | 15-31 µmol/L | 23
Alanine transaminase (ALT) | 1-35 IU/L | 16
Alkaline phosphatase (ALP) | 90-540 U/L | 245
Total bilirubin | 0-21 µmol/L | 3
Albumin | 28-40 g/L | 36
Adjusted calcium | 2.20-2.70 mmol/L | 2.47
Phosphate | 1.10-2.00 mmol/L | 1.50
Magnesium | 0.70-1.00 mmol/L | 0.83
Parathyroid hormone | 1.2-6.3 pmol/L | 1.8
Iron | 5.0-25.0 µmol/L | 2.0
Transferrin | 2.20-3.37 g/L | 3.96
Transferrin saturation | 15.0-45.0% | 2.0
Lead | <0.1 µmol/L | 1.64
Zinc | 10.0-18.0 µmol/L | 7.7
Total 25-hydroxy vitamin D | >50 nmol/L | 96.7
TTG (tissue transglutaminase) IgA antibody (serum) | 0.0-14.9 kU/L | <0.5

She had a plain radiograph of her left knee including the distal femur and proximal tibia to assess for growth plate changes, which showed mildly increased metaphyseal sclerosis - a feature of lead poisoning (see Figure 1).

Figure 1: Plain radiograph of the left knee: anterior-posterior view on the left and lateral views on the right.There is mild increased metaphyseal sclerosis, but no further metaphyseal sclerotic bands. Bone density appears normal.'L' = left; 'Xp' = X-ray photograph

Her renal function remained stable as an inpatient. She received a total of five days of chelation therapy. Due to a turnover of seven days for lead levels to return, she was discharged without any confirmed lead levels, with a plan to repeat the levels after her discharge with regular follow-up.

Three months after this hospital stay, she attended a follow-up clinic, where she had repeat blood tests (see Table 3) and was clinically assessed. She had been doing well, and there had been no further exposure to paint following the installation of wallpaper in the home. Her dietary intake had improved, and she was no longer exhibiting pica behaviours. She was opening her bowels regularly, and her parents had no current concerns regarding constipation. Clinically, she appeared well, and her systemic examination was unremarkable.

Blood test | Normal range | Result from the April clinic visit
Haemoglobin | 101.0-138.0 g/L | 96
MCV (mean corpuscular volume) | 73.00-88.00 fL | 55.30
Lead | <0.1 µmol/L | 1.60
Iron | 5.0-25.0 µmol/L | 2.2
Transferrin | 2.20-3.37 g/L | 4.23
Transferrin saturation | 15.0-45.0% | 2.1

Her most recent lead levels taken on the last day of her January admission had measured 1.47 µmol/L, and although still elevated, displayed significant improvement compared to prior to admission. The lead levels taken in this clinic level were chased and returned as 1.60 µmol/L, showing a mild increase compared to previous (see Table 4 for the trend of lead levels). Given the rise, she is due for further follow-up with repeat bloods this July.

Timeline | Stage in treatment | Lead levels in µmol/L
September 2025 clinic | Initial screening in the clinic | 0.89
November 2025 clinic | Follow-up clinic lead levels prompting further monitoring | 0.85
January 2026 clinic | Follow-up clinic lead levels prompting admission | 3.34
Day 1 of January 2026 admission | Whilst on chelation therapy | 1.64
Day 2 of January 2026 admission | 1.56
Day 3 of January 2026 admission | 1.47
April 2026 clinic | First follow-up post-chelation therapy | 1.60