Key Points

• Presentation in diabetic ketoacidosis always requires hospitalization for fluid resuscitation and insulinization.

• Fluid resuscitation is a critical part of treating DKA. Intravenous solutions replace extravascular and intravascular fluids and electrolyte losses.

• Protracted symptoms suggest hypokalemia and total-body potassium depletion.

• If diagnosis of DKA is made immediately by history, physical examination, or fingertip glucose determination, and confirmed with tests demonstrating metabolic acidosis, specific treatment should not be delayed by pending laboratory results.

• Sodium bicarbonate is safely delivered isotonically as 100 mEq or 100 mL added to 1 L of 0.45% normal saline.

• In a previously known diabetic patient, an episode of ketoacidosis results from the patient's inability to recognize deterioration in glucose control and react promptly with insulin.

• When transitioning to subcutaneous insulin from continuous infusion, basal SC insulin dose should precede cessation of insulin infusion by 4 to 6 hours to prevent recurrent ketosis.

In only a few emergencies in medicine has an understanding of the pathophysiology reduced mortality from 100% to less than 1% in less than 50 years. One example is the discovery and rapid clinical deployment of insulin in 1921 as the major intervention shutting down the diabetic keto-genic state and preventing profound acidosis with cerebral dehydration and edema. With the introduction of low-dose insulin infusion protocols in the early 1970s, the residual mortality of 6% to 8% associated with potassium and water shifts common with overaggressive insulin treatment was reduced to 1%. Cerebral edema and hypokalemic deaths from ketoacidosis in adults are now rare.

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