Lead in a case of encephalopathy.

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 Chelation therapy was started but, unfortunately, he did not make a neurological recovery, and care was withdrawn.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.

High prenatal and postnatal lead exposure associated lead encephalopathy in an infant.

An 11-month-old child presented with persistent seizures requiring ventilator support. The child had global developmental delay, was staying in the premises of battery manufacturing unit, had microcytic and hypochromic anemia with basophilic stripling on peripheral smear, lead line on radiograph of the long bones and BLL of 244 µg/dl. The CT scan of the brain revealed cerebral atrophy. The mother also had high BLL and lead line in the radiograph of the long bones. The child was managed with chelation therapy. Given the continuing lead exposure among occupational and general populations in India, this case study highlights the need for prompt environmental preventive actions as well as nutritional and preventive counseling for occupational populations.

Encephalopathy from lead poisoning masquerading as a flu-like syndrome in an autistic child.

Acute encephalopathy from childhood lead poisoning is fortunately rare. However, in pediatric patients with developmental disabilities and pica, there is a risk of lead exposure at a dose commensurate with encephalopathy, coupled with a risk of delayed diagnosis because of difficulty in distinguishing between baseline and altered behavior. We report here a 4-year old autistic boy who presented to the pediatrician's office with gastrointestinal symptoms and behavioral changes and was at first thought to have a viral syndrome. He returned 2 days later with a worsening illness; increasing pallor, vomiting, abdominal colic, and changes in consciousness were recognized in the emergency department as lead-induced anemia and encephalopathy, associated with a positive abdominal film for paint chips and a blood lead level equal to 216 microg/dL (10.43 micromol/L) (reference, <10 microg/dL or 0.483 micromol/L). As this case illustrates, prompt recognition is dependent on the skills and suspicions of an astute clinician, especially in the busy emergency department.

Sickle cell disease and plumbism in children.

Childhood lead poisoning is common, affects multiple organs and is preventable. Co-existence of plumbism and sickle cell disease (SCD) is uncommon, with major overlap in signs and symptoms. We describe a patient with SCD and plumbism. Dysfunctional eating patterns may cause ingestion and increased absorption of lead in these patients. Routine screening for pica and other dysfunctional eating habits with appropriate behavioral interventions is emphasized. Annual screening for lead in patients with SCD of all ages (1-21years) and supplementation of micronutrients like zinc and iron in deficient cases may help prevent plumbism in these patients.

Pseudotumor cerebral maligno en niños por intoxicación plumbica / Lead poisoning presenting as malignant pseudotumor cerebri in children

Introducción: El pseudotumor cerebral (PTC), o hipertensión endocraneana benigna, se caracteriza por sintomatología compatible con aumento de la presión endocraneana en ausencia de lesión espacio-ocupante o dilatación ventricular por obstrucción en la circulación del LCR. Se presenta con cefalea, náuseas-vómitos, y variadas alteraciones visuales con edema de papila. Las causas subyacentes son múltiples: alteraciones endocrinas y metabólicas, obesidad, medicamentos, trombosis senos venosos, megadosis de vitamina A, sinusopatías, etc. como así también intoxicación plúmbica. Objetivo: Detectar etiología tóxica en pacientes con PTC en los cuales no se evidenció factor causal mediante interrogatorio dirigido a pesquisa de fuentes contaminantes de plomo. Material y Métodos: Análisis prospectivo de pacientes ambulatorios o internados con diagnóstico de PTC. Estudios de Rx de cráneo, oftalmológicos y neuroimágenes. Aplicación de protocolo de investigación de contacto con plomo. Determinaciones en sangre y orina del bioperfil plúmbico: ALA-D, ALA-U, plombemia, PPE, coproporfirinas III. Comparación con grupo control de los niños intoxicados. Aplicación del test de Fisher. Resultados: Fueron evaluados 66 niños entre 4 meses y 13 años, 49 varones. Las manifestaciones clínicas fueron: cefalea (85 por ciento), náuseas-vómitos (94 por ciento), alteraciones visuales: diplopia, disminución agudeza visual, estrabismo (91 por ciento), edema de papila (89 por ciento). Hipertensión radiológica (55 por ciento). Neuroimágenes: negativas para tumor (100 por ciento), compatible con edema cerebral (27 por ciento). Los factores etiológicos fueron identificados en 55 casos (83 por ciento) obesidad, endocrinopatía, corticoterapia, megadosis de vitamina A, sinusopatías, etc. En el 17 por ciento restante (11 casos) se sospechó etiología tóxica, comprobándose intoxicación plúmbica en 8 niños (12 por ciento). Conclusiones: Sugerimos aplicar interrogatorio dirigido hacia pesquisa de fuentes contaminantes de plomo en casos de PTC sin causa establecida, y confirmación con análisis de nivel de plomo en sangre y bioperfil plúmbico. El diagnóstico y tratamiento oportunos evitarán el pronóstico desfavorable de la afección, por eso consideramos como "maligno" a este tipo de pseudotumor. (AU)