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February 2, 1979, Vol 241, No. 5 >
ARTICLE | February 2, 1979

Diabetic Ketoacidosis

Richard Bienia, MD; Ignacio Ripoll, MD
JAMA. 1979;241(5):510-511. doi:10.1001/jama.1979.03290310050019.
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IN RECENT years there has been a great deal of controversy over optimal insulin therapy for diabetic ketoacidosis. The disputes have centered on the issues of traditional high-dose vs low-dose insulin regimens and intravenous (IV) vs intramuscular (IM) administration.1-4 The results with any of the accepted regimens are acceptable, implying that the physician should use the protocol with which he is both familiar and comfortable.

Pathophysiology  The hallmark of diabetic ketoacidosis is a relative insulin deficit. This results in hyperglycemia with glycosuria once the renal threshold for glucose is exceeded. The resulting osmotic diuresis leads to dehydration, which is intensified if the patient vomits.In the absence of adequate insulin, the body is unable to use glucose as an energy source and must turn to long-chain fatty acids that are mobilized from adipose stores. The end products of this metabolism are β-hydroxybutyric acid and acetoacetic acid, generally in a

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