At blood lead concentrations of 70 mcg/dL symptoms may be minimal, but acute encephalopathy may occur abruptly and unpredictably, for which reason the child should be hospitalized for chelation therapy (see below). Some children with a blood lead level of 50 mcg/dL may have symptoms of severe encephalopathy, whereas others may be asymptomatic. In the latter case, an attempt should be made to discover and remove the source of lead intoxication and the child should be reexamined at frequent intervals. The seriousness of lead encephalopathy is indicated by the fact that most of the children who become stuporous or comatose remain mentally retarded despite treatment. The physician’s aim, therefore, is to institute treatment before the severe symptoms of encephalopathy have become manifest.
Pathology In children who die of acute lead encephalopathy, the brain is massively swollen, with herniation of the temporal lobes and cerebellum, multiple microscopic ischemic foci in the cerebrum and cerebellum, and endothelial damage and deposition of proteinaceous material and mononuclear inflammatory cells around many of the small blood vessels. There are also hyperplastic changes in arteries and arterioles and in some places, perivascular infiltrates of lymphocytes and mononuclear cells. In the territories of some of these vessels there are foci of ischemic necrosis with surrounding glial reaction appropriate for the age of the lesion. Similar changes are present in the kidneys.
Treatment The plan of therapy includes the establishment of urinary flow, following which intravenous fluid therapy is restricted to basal water and electrolyte requirements. In cases of acute encephalopathy, combined chelation therapy with 2,3-dimercaprol (British anti-Lewisite [BAL]; 12 to 24 mg/kg) and CaNa2 EDTA (0.5 to 1.5 g/m2 body surface area) for 5 to 7 days. This is followed by a course of oral penicillamine (40 mg/kg, not exceeding 1 g/d). In acute cases the goal is to reduce the serum lead levels below 40 mcg/dL. Once the absorption of lead has ceased, chelating agents remove lead only from soft tissues and not from bone, where most of the lead is stored. Any intercurrent illness may result in a further mobilization of lead from bones and soft tissues and an exacerbation of symptoms of lead intoxication.
Repeated doses of mannitol may be used for relief of cerebral edema. Microcytic hypochromic anemia is treated with iron once the chelating agents have been discontinued. Seizures are best controlled with intravenous diazepam or midazolam.
Prevention The prevention of reintoxication (or initial intoxication) demands that the child be removed from the source of lead. Although this is axiomatic, it is often difficult to accomplish, despite the best efforts of local health departments and hospital and city social workers. Nevertheless, an attempt to eliminate the environmental factor must be made in each case. Such attempts, among other things, have resulted in a marked decrease in the incidence of acute lead encephalopathy in the past two decades. Although florid examples of this encephalopathy are now uncommon, undue exposure to lead (blood levels greater than 30 mcg/dL) remains inordinately prevalent and a continuing source of concern to public health authorities.