Lead in a case of encephalopathy

Abstract

A 2-year-old boy with a history of pica was admitted with vomiting and treated overnight for viral tonsillitis. A week later, he presented with a prolonged afebrile seizure and required intubation and ventilation. Antibiotics and acyclovir were started. Despite extensive investigations including MRI head, no cause was identified. Four days later, he deteriorated with signs of raised intracranial pressure. On day 5, blood lead concentration in the sample collected at admission was reported as grossly elevated, consistent with a diagnosis of severe lead poisoning from ingesting lead-containing paint at the family home. Chelation therapy was started but, unfortunately, he did not make a neurological recovery, and care was withdrawn. A serious case review identified a lack of awareness of lead poisoning and its relation to pica as a root cause. We report this case to share our experience and the importance of considering lead poisoning in children with pica.

Case epidemiology from the first three years of a pilot laboratory-based surveillance system for elevated blood-lead concentrations among children in England, 2014–17: implications for public health action

“…The effect can be significant. For example, clinician education and electronic prompts to paediatricians and GPs to consider BLC testing in children with pica instituted by Leeds SAS laboratory (based in Yorkshire and Humber) following the death of a child from lead exposure (the same case as in our results) 26 resulted in a 90% increase in BLC test requests in the subsequent 12 months. 27 This may also partly explain the higher case incidence in Yorkshire and Humber.…”

Disparity in Risk Factor Severity for Early Childhood Blood Lead among Predominantly African-American Black Children: The 1999 to 2010 US NHANES

“…Continuous BLLs were rounded to the first decimal place to maintain significant figures. EBLLs ≥5 µg/dL were assigned by using the current CDC guideline of rounding BLLs to one decimal place so that measurements ≥4.5 µg/dL are identified [21]. Children who are younger than 12 months of age are not included in blood sample draws by the NHANES.…”

“…Infants and preschool-aged children are at higher risk of Pb exposure in part due to their increased body surface area, increased heart and respiratory rates, the ingestion and inhalation of contaminated dust or soil from greater hand-to-mouth activity, pica, crawling, and their low stature to the ground [19]. Exposure to Pb during early childhood that results in blood Pb concentrations between 30 and 100 µg/dL leads to the development of clinical lead poisoning, which is characterized by a severe hemolytic anemia, nephropathy, and encephalopathy proceeding to coma and death beginning at BLLs of approximately 100 to 150 µg/dL [20][21][22][23].…”

Central nervous system infections versus lead toxicity in the differential diagnosis of encephalopathy

“…[ 1 ] The signs and symptoms of lead encephalopathy include headache, delirium, hallucinations, lethargy, agitation, tremor, memory loss, and single or recurrent seizures. [ 1 2 3 ] A tonic–clonic seizure is the most typical seizure type in these patients. [ 3 ] Delirium induced by lead may increase over a period of several days.…”

“…[ 1 2 3 ] A tonic–clonic seizure is the most typical seizure type in these patients. [ 3 ] Delirium induced by lead may increase over a period of several days. [ 1 ] Coma is an uncommon presentation of lead encephalopathy, and progressive cerebral edema and increased intracranial pressure may result in death.…”