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Acute lead encephalopathy in early infancy--clinical presentation and outcome
A al Khayat1, N S Menon, M R Alidina
1Department of Pediatrics, Al Wasl Maternity & Pediatric Hospital, Dubai, United Arab Emirates.
Insights
Acute lead encephalopathy in infants can occur at lower lead levels than previously thought, even below 70 micrograms/dl. This study highlights risks associated with traditional medicines containing lead.
Area of Science:
- Pediatric Neurology
- Environmental Health
- Toxicology
Background:
- Traditional medicines are sometimes contaminated with toxic heavy metals like lead.
- Infants are particularly vulnerable to lead poisoning due to their developing brains.
Purpose of the Study:
- To investigate acute lead encephalopathy in infants exposed to lead via traditional medicines.
- To determine the lead level threshold for encephalopathy in this vulnerable population.
Main Methods:
- Studied 19 infants with suspected lead encephalopathy.
- Assessed clinical symptoms, brain imaging (CT scans), cerebrospinal fluid analysis, and blood lead levels.
- Correlated lead levels with neurological outcomes post-chelation therapy.
Main Results:
- Median lead level was 3.6 mumol/l (74.5 micrograms/dl).
- Seven infants had levels below 56.9 micrograms/dl, yet showed encephalopathy symptoms.
- Thirteen infants developed brain damage, with lead levels at 2 months post-chelation correlating with neurological deficits.
Conclusions:
- Acute lead encephalopathy in infants may occur at lead levels lower than the commonly accepted threshold of 70 micrograms/dl.
- Lead exposure from traditional medicines poses a significant risk to infant neurodevelopment.
- Early detection and intervention are crucial for managing lead poisoning in infants.
Abstract:
We studied 19 infants with a mean age of 3.8 months who presented with features consistent with acute lead encephalopathy following the use of traditional medicines. All presented with convulsions; CT scans of the brain on admission showed brain oedema in four, atrophy in four and normal findings in 11. Cerebrospinal fluid analysis in nine patients showed pleocytosis in six and a high protein content in eight. The median lead level in these 19 infants which encephalopathy was 3.6 mumol/l (74.5 micrograms/dl). Seven had a mean lead level of only 2.7 mumol/l (56.9 micrograms/dl) which is much below 70 micrograms/dl, the level usually proposed as the threshold for encephalopathy. Thirteen infants developed brain damage during follow-up; statistical analysis correlated the lead level at 2 months post chelation with an abnormal neurological outcome. Our findings indicate that in very young infants acute lead encephalopathy may occur at lead level lower than previously reported.