Abstract
IN recent years the widespread use of edathamil (EDTA)‡ for treatment of acute lead encephalopathy has led to a marked reduction in the incidence of severe neurologic abnormalities after therapy.1 , 2 There has been no concomitant reduction of mortality, however, and the death rate remains at 15 to 25 per cent.2 3 4 5 Marked elevation of intracranial pressure has frequently been observed during the first forty-eight hours after the onset of edathamil therapy, and most fatal cases have occurred during that period.2 The problems and frequently disappointing results associated with the usual methods of managing increased intracranial pressure recently led to the trial . . .