Abstract
BEFORE the availability of insulin, diabetic ketoacidosis was a uniformly fatal catastrophe. In the 50 years since insulin treatment has been employed, a progressive decline in mortality has been achieved to current levels of 3 to 10 per cent.1 Despite the marked improvement in success rate, considerable controversy still exists over the optimal mode of treatment. Recommendations differ about "large" versus "small" doses of insulin, the use of isotonic saline rather than hypotonic solutions, and the need for bicarbonate administration. Two basic principles are applicable to any therapeutic approach: successful treatment depends in large measure on individualization of therapy rather . . .