Approach to the Treatment of Diabetic Ketoacidosis

• Published in: American journal of kidney diseases Vol. 68; no. 6; pp. 967 - 972
• Main Authors: Kamel, Kamel S., MD, FRCPC, Schreiber, Martin, MD, FRCPC, Carlotti, Ana P.C.P., MD, Halperin, Mitchell L., MD, FRCPC
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01-12-2016
• Subjects: acidemia; Adolescent; cerebral edema; Diabetic ketoacidosis (DKA); Diabetic Ketoacidosis - drug therapy; Humans; hypokalemia; Male; metabolic acidosis; Nephrology; Potassium Chloride - therapeutic use; Sodium Bicarbonate - therapeutic use; type 1 diabetes mellitus (T1DM); Diabetic ketoacidosis (DKA); hypokalemia; metabolic acidosis; cerebral edema; acidemia; type 1 diabetes mellitus (T1DM)
• ISSN: 0272-6386; 1523-6838
• DOI: 10.1053/j.ajkd.2016.05.034

Diabetic ketoacidosis (DKA), a common cause of severe metabolic acidosis, remains a life-threatening condition due to complications of both the disease and its treatment. This Acid-Base and Electrolyte Teaching Case discusses DKA management, emphasizing complications of treatment. Because cerebral edema is the most common cause of mortality and morbidity, especially in children with DKA, we emphasize its pathophysiology and implications for therapy. The risk for cerebral edema may be minimized by avoiding a bolus of insulin, excessive saline resuscitation, and a decrease in effective plasma osmolality early in treatment. A goal of fluid therapy is to lower muscle venous P co2 to ensure effective removal of hydrogen ions by bicarbonate buffer in muscle and diminish the binding of hydrogen ions to intracellular proteins in vital organs (such as the brain). In patients with DKA and a relatively low plasma potassium level, insulin administration may cause hypokalemia and cardiac arrhythmias. It is suggested in these cases to temporarily delay insulin administration and first administer potassium chloride intravenously to bring the plasma potassium level close to 4 mmol/L. Sodium bicarbonate administration in adult patients should be individualized. We suggest it be considered in a subset of patients with moderately severe acidemia (pH < 7.20 and plasma bicarbonate level < 12 mmol/L) who are at risk for worsening acidemia, particularly if hemodynamically unstable. Sodium bicarbonate should not be administered to children with DKA, except if acidemia is very severe and hemodynamic instability is refractory to saline administration.