Three major changes have occurred in the treatment of diabetic ketoacidosis during the past decade: (1) a trend toward continuous intravenous (IV) infusion of insulin, (2) a trend toward the use of lower doses of insulin, and (3) the reintroduction of phosphate replacement. These changes are based on sound theoretical considerations, but their effects on mortality and morbidity are still being evaluated. Despite any changes, intelligent treatment of diabetic ketoacidosis still requires an understanding of the underlying pathophysiology.
PATHOGENESIS OF DIABETIC KETOACIDOSIS
There are two major abnormalities in diabetic ketoacidosis—metabolic acidosis and hyperglycemia. Each of these is caused by insulin deficiency.
An understanding of fatty acid and ketone metabolism is required to understand the pathogenesis of acidosis.1,2 Fatty acids are stored as triglycerides within fat cells. Fatty acids released by fat cells are taken up and metabolized by the liver, and ketone bodies (acetoacetic acid, β-hydroxybutyric acid,