What is the treatment for diabetic ketoacidosis (DKA) in a patient with hyperglycemia and metabolic acidosis?

Treatment of Diabetic Ketoacidosis

Initial Fluid Resuscitation

Begin immediately with isotonic saline (0.9% NaCl) at 15-20 mL/kg/hour (approximately 1-1.5 liters in the first hour) to restore intravascular volume and renal perfusion. 1, 2, 3 This aggressive initial fluid replacement is critical for restoring tissue perfusion and improving insulin sensitivity. 2

• After the first hour, adjust fluid choice based on hydration status, serum electrolyte levels, and urine output. 1, 3
• Total fluid replacement should approximate 1.5 times the 24-hour maintenance requirements. 1, 3
• When serum glucose reaches 250 mg/dL, switch to 5% dextrose with 0.45-0.75% saline while continuing insulin infusion to prevent hypoglycemia and ensure complete ketoacidosis resolution. 2, 3

Potassium Management: The Critical First Step Before Insulin

Do not start insulin if serum potassium is <3.3 mEq/L—this is an absolute contraindication that can cause life-threatening cardiac arrhythmias and death. 1, 2 Despite patients often presenting with normal or elevated potassium, total body potassium depletion is universal in DKA (averaging 3-5 mEq/kg body weight), and insulin therapy will unmask this by driving potassium intracellularly. 2

Potassium Replacement Protocol:

• If K+ <3.3 mEq/L: Delay insulin therapy and aggressively replace potassium (20-40 mEq/L in IV fluids) until levels reach ≥3.3 mEq/L. 1, 2
• If K+ 3.3-5.5 mEq/L: Add 20-30 mEq potassium per liter of IV fluid (use 2/3 KCl and 1/3 KPO₄) once adequate urine output is confirmed. 1, 2, 3
• If K+ >5.5 mEq/L: Withhold potassium initially but monitor closely, as levels will drop rapidly with insulin therapy. 2
• Target serum potassium of 4-5 mEq/L throughout treatment. 2, 3
• Check potassium levels every 2-4 hours during active treatment. 2

Insulin Therapy

Once potassium is ≥3.3 mEq/L, start continuous IV regular insulin infusion at 0.1 units/kg/hour (with or without an initial 0.1 units/kg IV bolus) for moderate to severe DKA. 1, 2, 3 This remains the standard of care for critically ill and mentally obtunded patients. 2

Insulin Adjustment Protocol:

• Target glucose decline of 50-75 mg/dL per hour. 1, 2
• If plasma glucose does not fall by 50 mg/dL in the first hour, verify adequate hydration, then double the insulin infusion rate hourly until achieving steady glucose decline. 1, 3
• When serum glucose reaches 250 mg/dL, decrease insulin infusion to 0.05-0.1 units/kg/hour and add dextrose to IV fluids. 1, 3 This is a critical step—do not stop insulin when glucose normalizes, as ketoacidosis resolution requires continued insulin therapy regardless of glucose levels. 2, 3

Alternative Approach for Mild-Moderate Uncomplicated DKA:

For hemodynamically stable, alert patients with mild-moderate DKA, subcutaneous rapid-acting insulin analogs combined with aggressive fluid management are equally effective, safer, and more cost-effective than IV insulin. 1, 2 This approach requires adequate fluid replacement, frequent point-of-care glucose monitoring, and treatment of concurrent infections. 2

Resolution Criteria and Transition to Subcutaneous Insulin

DKA is resolved when ALL of the following criteria are met: glucose <200 mg/dL, serum bicarbonate ≥18 mEq/L, venous pH >7.3, and anion gap ≤12 mEq/L. 1, 2, 3

Critical Transition Protocol:

Administer basal insulin (glargine or detemir) 2-4 hours BEFORE stopping the IV insulin infusion to prevent recurrence of ketoacidosis and rebound hyperglycemia. 1, 2, 3 This overlap period is essential—stopping IV insulin without prior basal insulin administration is the most common error leading to DKA recurrence. 1, 2

• Continue IV insulin for 1-2 hours after administering subcutaneous insulin. 1
• Once the patient can eat, start a multiple-dose schedule using a combination of short/rapid-acting and intermediate/long-acting insulin. 1, 2
• Recent evidence shows adding low-dose basal insulin analog during IV insulin infusion may prevent rebound hyperglycemia without increasing hypoglycemia risk. 2

Bicarbonate Administration: Generally Not Recommended

Bicarbonate is NOT recommended for DKA patients with pH >6.9-7.0. 2, 3 Multiple studies show no difference in resolution of acidosis or time to discharge with bicarbonate use, and it may worsen ketosis, cause hypokalemia, and increase cerebral edema risk. 2, 3 Consider bicarbonate only if pH falls below 6.9, or when pH is <7.2 pre- and post-intubation to prevent hemodynamic collapse. 4

Monitoring Protocol

Check blood glucose every 1-2 hours during active treatment. 3

Draw blood every 2-4 hours for serum electrolytes, glucose, BUN, creatinine, osmolality, and venous pH. 1, 2, 3 Follow venous pH (typically 0.03 units lower than arterial pH) and anion gap to monitor resolution of acidosis. 2, 3

Direct measurement of β-hydroxybutyrate in blood is the preferred method for ketone monitoring, as the nitroprusside method only measures acetoacetic acid and acetone, not the predominant ketone body. 1, 3

Initial Diagnostic Workup

Obtain plasma glucose, BUN/creatinine, serum ketones, electrolytes with calculated anion gap, osmolality, urinalysis, urine ketones, arterial blood gases, complete blood count with differential, and electrocardiogram. 1, 2, 3

Obtain bacterial cultures (urine, blood, throat) if infection is suspected and administer appropriate antibiotics, as infection is the most common precipitating cause (30-50% of cases). 5, 2, 6 Consider chest X-ray if clinically indicated. 1

Common Pitfalls to Avoid

• Starting insulin before correcting severe hypokalemia (K+ <3.3 mEq/L) can cause life-threatening arrhythmias. 1, 2
• Stopping IV insulin without prior basal insulin administration causes rebound hyperglycemia and DKA recurrence. 1, 2
• Interrupting insulin infusion when glucose falls without adding dextrose perpetuates ketoacidosis. 2, 3
• Premature termination of insulin therapy before complete resolution of ketosis (all four resolution criteria must be met). 2, 3
• Inadequate potassium monitoring and replacement is a leading cause of mortality in DKA. 2
• Overly rapid correction of osmolality increases cerebral edema risk, particularly in children. 2, 3

Special Considerations

Discontinue SGLT2 inhibitors immediately and do not restart until 3-4 days after metabolic stability is achieved, as these medications increase the risk of euglycemic DKA. 2, 7

Identify and treat underlying precipitating causes such as infection, myocardial infarction, stroke, pancreatitis, trauma, or insulin omission. 5, 2, 6