THE TREATMENT OF ACUTE LEAD ENCEPHALOPATHY IN CHILDREN

Abstract

The findings of the present report are based upon study of 36 children with acute lead encephalopathy who were treated parenterally with one or more courses of edathamil calcium disodium. The group included 22 mild cases and 14 severe cases of whom 5 died. Comparison of this group with a similar, but not simultaneously studied, group of patients treated with BAL indicates that while edathamil calcium disodium may have reduced the incidence of residual neurologic damage to a certain extent, it has not significantly reduced mortality from this disease. Review of these patients further suggested that edathamil calcium disodium was no more effective than BAL for quickly terminating coma, convulsions and increased intracranial pressure in an episode of acute lead encephalopāthy. During the period of these manifestations most of the deaths occurred. The only present hope for a further reduction in mortality from lead encephalopathy would appear to lie in earlier diagnosis, prompt removal of the child from exposure to lead and careful supportive management during the first 48 to 72 hours of administration of edathamil calcium disodium. The data presented indicate that this duration of drug administration is required in severe cases before the high toxic concentrations of lead initially present in tissues can be sufficiently reduced to remove the danger to life. In view of the unpredictable and fulminant manner in which acute lead encephalopathy may develop in children, both mild and severe cases should be managed during the first few days of observation on the assumption that all are potentially severe cases. Clinical and laboratory observations which may facilitate earlier diagnosis are discussed. In the present study no significant variations in total 24-hour output of lead in urine were found when the parenteral routes and time intervals of injection were varied while total dosage of edathamil calcium disodium was kept constant. Intermittent intramuscular injection was the most convenient. No significant local reactions thereto were observed. Parenteral administration of edathamil calcium disodium produced no measurable increase in the fecal excretion of lead in four patients. The rationale for the use of repeated courses of edathamil calcium disodium during the convalescent phase following initial clinical recovery, in an effort to prevent continuing lead toxicity to cerebral tissue, is discussed. It has been reported elsewhere that the quantity of lead excreted in the urine during administration of edathamil calcium disodium can be predicted from the antecedent output of coproporphyrin in the urine. Serial, quantitative determinations of coproporphyrin in urine were used as the principal biochemical indication for repeated courses of chelation therapy. In patients recovering from an initial episode of acute lead encephalopathy, a high incidence of severe permanent damage to the central nervous system may be anticipated unless re-exposure to lead is strictly prevented. Close clinical, laboratory and social service control are necessary to assure this. Prevention of re-exposure to lead in combination with repeated courses of edathamil calcium disodium offers new hope of reducing the incidence of the more subtle but equally incapacitating forms of late damage to mentality. Final conclusions with respect to such late damage to mentality of survivors of acute lead encephalopathy incurred during late infancy must await the re-evaluation of these patients during the early school years.