Pediatric emergency medicine trisk 3119 3119

associated with an increased risk of lead intoxication in the occupants. Other
unusual sources of lead exposure include the burning of battery casings for heat
or recycling of batteries, water carried by outdated lead pipes, improperly homeglazed ceramics, lead contamination of imported spices or cosmetics, and dust or
dirt contaminated by vehicles which once used leaded gasoline.
Absorption of lead occurs through GI and pulmonary routes; the former is
predominant in pediatric intoxications. Lead is then compartmentalized into three
main areas: bone, soft tissues, and blood. Excretion occurs slowly through urine,
feces, and sweat. Children are probably at double jeopardy compared with adults;
animal studies show that younger animals have increased absorption and also a
heavier distribution into soft tissues (including the brain). Concomitant nutritional
deficiency, especially low dietary iron and calcium, may enhance intestinal lead
absorption. Unfortunately, the same children at greatest risk for lead poisoning by
virtue of age and residence are also likely to be at risk for dietary deficiency,
especially iron.
Lead exerts its toxic effect principally by two mechanisms: (1) interference
with calcium function at the cellular level and (2) enzyme inhibition, particularly
enzymes rich in sulfhydryl groups. In humans, the most obvious effects are on
neurologic function and on the hemesynthesis pathway, which is interrupted at
several points, resulting in abnormally high levels of porphyrins and their
precursors.
Clinical Considerations. Early signs and symptoms of plumbism are notably and
nonspecific. Abdominal complaints, including colicky pain, constipation,
anorexia, and intermittent vomiting, are common; of course, these same
symptoms are often ascribed to relatively normal 2-year-old children by their
parents. The child with early plumbism may also show listlessness and irritability.
When encephalopathy begins, the child develops persistent vomiting and
becomes drowsy, clumsy, or frankly ataxic. As encephalopathy worsens, the level
of consciousness deteriorates further, and seizures commonly occur. Pathologic
examination of brains of children who have died of lead encephalopathy shows
severe cerebral edema with vascular damage; intracranial pressure is often
increased during the encephalopathy. Peripheral neuropathy often occurs in adults

with lead poisoning but is rare in children, although it is seen occasionally in
those with an underlying hemoglobinopathy. Other organs may be damaged by
lead. The kidneys may develop disturbances that range from slight aminoaciduria
to a full Fanconi syndrome with glycosuria and phosphaturia (in addition to
aminoaciduria). High blood lead level (BLL) is also associated with a microcytic