How to manage a patient with euglycemic (normal blood sugar levels) Diabetic Ketoacidosis (DKA)?

Management of Euglycemic Diabetic Ketoacidosis

The critical difference in managing euglycemic DKA compared to classic DKA is that you must start dextrose-containing fluids EARLY while continuing insulin infusion—never stop insulin just because glucose is normal, as this perpetuates ketosis. 1, 2

Diagnostic Confirmation

Euglycemic DKA presents with the metabolic derangements of classic DKA but with blood glucose <250 mg/dL (often <200 mg/dL):

• Arterial pH <7.3 2
• Serum bicarbonate <15 mEq/L 2
• Positive ketonemia/ketonuria 2
• Anion gap >10 mEq/L 3

Measure β-hydroxybutyrate directly in blood rather than relying on nitroprusside urine tests, as the nitroprusside method only detects acetoacetate and acetone, missing β-hydroxybutyrate which is the predominant ketone body in DKA. 2 This is a common pitfall that can delay diagnosis.

Initial Fluid Resuscitation

Begin with isotonic saline (0.9% NaCl) at 15-20 mL/kg/hour during the first hour (approximately 1-1.5 liters in average adults). 1, 2 This aggressive fluid management restores circulatory volume and improves tissue perfusion. 1

The Critical Difference: Insulin + Dextrose Strategy

Start continuous IV regular insulin at 0.1 units/kg/hour WITHOUT an initial bolus. 2 The American Diabetes Association guidelines specifically recommend omitting the bolus in euglycemic presentations to avoid precipitous hypoglycemia.

Here is the key algorithmic approach that distinguishes euglycemic DKA management:

When Glucose Falls Below 250 mg/dL (or is already low):

• Immediately add 5% dextrose with 0.45-0.75% NaCl to IV fluids 2
• Continue insulin infusion at full rate (0.1 units/kg/hour) 2
• Never reduce or stop insulin when glucose normalizes—this is the most common error leading to prolonged ketosis 1, 2

The dextrose provides substrate to suppress ketogenesis while insulin clears existing ketones. 2 Without adequate carbohydrate administration alongside insulin, ketosis perpetuates despite normal glucose. 1, 2

Electrolyte Management

Potassium replacement is critical and must begin early:

• Once urine output is established and serum potassium is <5.3 mEq/L, add 20-30 mEq/L potassium (2/3 KCl and 1/3 KPO₄) to IV fluids 2
• Target serum potassium 4-5 mmol/L throughout treatment 2
• Insulin drives potassium intracellularly, and correction of acidosis further lowers serum potassium 2

Bicarbonate administration is NOT recommended unless pH <6.9, as it provides no benefit in resolution of acidosis or time to discharge. 1, 2

Monitoring Protocol

Check blood glucose every 1-2 hours (more frequently than classic DKA due to risk of hypoglycemia). 2

Draw venous blood every 2-4 hours for:

• Electrolytes (sodium, potassium, chloride) 2
• Venous pH and calculated anion gap 2
• Blood urea nitrogen and creatinine 2

Follow venous pH and anion gap rather than serum glucose to determine resolution. 2 This prevents the error of stopping treatment prematurely when glucose normalizes but ketoacidosis persists.

Resolution Criteria

DKA is resolved when ALL of the following are met:

• Venous pH >7.3 2
• Serum bicarbonate ≥18 mEq/L 2
• Anion gap ≤12 mEq/L 2

Note that glucose level is NOT part of resolution criteria. 2

Transition to Subcutaneous Insulin

Administer basal insulin (glargine or detemir) 2-4 hours BEFORE stopping IV insulin infusion. 2 This prevents rebound ketoacidosis, which is the most common error during transition. 4

Consider administering a low dose of basal insulin analog in addition to IV insulin during the final hours of treatment to prevent rebound hyperglycemia without increasing hypoglycemia risk. 1, 2

Common Pitfalls Specific to Euglycemic DKA

Stopping insulin when glucose normalizes—this is the cardinal error. 1, 2 The glucose may be normal but ketoacidosis persists, requiring continued insulin with dextrose supplementation.

Inadequate dextrose administration—failing to provide sufficient carbohydrate substrate perpetuates ketogenesis despite insulin therapy. 1, 2

Relying on urine ketones for monitoring—urine ketones lag behind serum ketones and the nitroprusside method misses β-hydroxybutyrate. 2

Premature discontinuation of IV insulin—stopping IV insulin without prior basal insulin administration leads to DKA recurrence. 4, 2

Special Consideration: SGLT-2 Inhibitor-Associated Cases

If euglycemic DKA is precipitated by SGLT-2 inhibitors, expect a more prolonged course due to the long half-life of these medications (up to 12-13 hours for empagliflozin, canagliflozin). 5 The glycosuric effect continues even after stopping the medication, requiring extended dextrose supplementation with insulin. 5