Slow release potassium chloride treatment.

-brain levels of HCP varied between 0-442 and 1-204 nmol[g (0-18 and 0 49 ig/g).4 So myelinopathy in case 2 was probably attributable to HCP, despite the absence of clinical signs of toxicity. The trace level in case 1 suggests that myelinopathy was unrelated to HCP, for other causes of infantile spongioform myelinopathy are known, though none has been identified in small premature infants. Nevertheless, case 1 may have lived long enough (24 days) for HCP to have been cleared from the brain. In rats HICP myelinopathy takes months to resolve, whereas the half-life of a dose of HCP is 19 hours. Until now, the only direct evidence that HCP may cause myelinopathy in premature babies has been the correlation between spongy change and the extent of exposure to HCP.5 The amount of the compound recovered from our second case indicates that myelinopathy may result from the normal clinical use of a 3% solution of HCP on very immature infants.