Treatment for Euglycemic Diabetic Ketoacidosis
For euglycemic DKA, begin aggressive fluid resuscitation with isotonic saline at 15-20 mL/kg/hour AND immediately add dextrose-containing fluids (5% dextrose) alongside continuous intravenous insulin to prevent hypoglycemia while correcting ketoacidosis—this is the critical difference from standard DKA management. 1
Initial Assessment and Recognition
Euglycemic DKA is characterized by metabolic acidosis (pH <7.3), ketosis, and blood glucose levels below 250 mg/dL (often <200 mg/dL). 1, 2 The normal glucose levels can delay diagnosis, making high clinical suspicion essential. 3
Key diagnostic workup includes: 1
- Arterial blood gas for metabolic acidosis
- Serum ketones (β-hydroxybutyrate preferred over nitroprusside method)
- Electrolytes with calculated anion gap
- Blood glucose monitoring every 2-4 hours
Common precipitating factors to identify: 1, 2
- SGLT2 inhibitor use (most common in modern practice)
- Ketogenic/low-carbohydrate diets
- Pregnancy, fasting, or reduced food intake
- Pancreatitis, infection, or other acute illness
- Gastroparesis or persistent vomiting
Fluid Resuscitation Protocol
Start with isotonic saline (0.9% NaCl) at 15-20 mL/kg/hour for the first hour to restore circulatory volume and tissue perfusion. 1 This aggressive initial fluid therapy is critical for both DKA resolution and treatment of any underlying condition like pancreatitis. 1
Unlike standard DKA, immediately incorporate dextrose-containing fluids (5% dextrose with 0.45-0.75% saline) from the outset or very early in treatment to provide carbohydrate substrate while insulin is administered. 1, 4, 2 This prevents hypoglycemia and provides the glucose needed for insulin to effectively suppress ketogenesis.
Insulin Therapy
Continuous intravenous insulin remains the standard of care for euglycemic DKA, particularly in critically ill or mentally obtunded patients. 1
Critical timing consideration: In some cases of severe euglycemia (glucose <100 mg/dL), delay insulin infusion until blood glucose rises above 150-200 mg/dL with dextrose administration. 4 However, for most euglycemic DKA cases with glucose 150-250 mg/dL, start insulin immediately at 0.1 units/kg/hour alongside dextrose-containing fluids. 1
Monitor blood glucose every 2-4 hours and adjust insulin accordingly, maintaining glucose between 150-200 mg/dL during treatment. 1
Continue insulin infusion until complete resolution of ketoacidosis (pH >7.3, bicarbonate ≥18 mEq/L, anion gap ≤12 mEq/L), regardless of glucose levels. 5, 1 The absence of hyperglycemia does not indicate resolution—monitor β-hydroxybutyrate or anion gap closure.
Electrolyte Management
Potassium replacement is critical: 1
- Check potassium before starting insulin
- If K+ <3.3 mEq/L, delay insulin and aggressively replace potassium first 5
- Once K+ ≥3.3 mEq/L and urine output confirmed, add 20-30 mEq/L potassium to IV fluids (2/3 KCl and 1/3 KPO₄) 1
- Target serum potassium 4-5 mEq/L throughout treatment 5
Monitor electrolytes, venous pH, and anion gap every 2-4 hours. 1
Bicarbonate is NOT recommended for pH >6.9-7.0, as it provides no benefit and may worsen ketosis, cause hypokalemia, and increase cerebral edema risk. 5, 1
Resolution Criteria and Transition
Euglycemic DKA is resolved when ALL of the following are met: 1
- pH >7.3
- Serum bicarbonate ≥18 mEq/L
- Anion gap ≤12 mEq/L
- Clinical symptom improvement
When transitioning to subcutaneous insulin: 1
- Administer basal insulin (glargine or detemir) 2-4 hours BEFORE stopping IV insulin infusion
- This overlap prevents recurrence of ketoacidosis and rebound hyperglycemia
- Continue monitoring for several hours after transition
Critical Pitfalls to Avoid
Inadequate carbohydrate administration alongside insulin perpetuates ketosis in euglycemic DKA—this is the most common error. 1 Unlike standard DKA where you wait until glucose falls to 250 mg/dL to add dextrose, euglycemic DKA requires dextrose from the beginning.
Premature discontinuation of insulin before complete resolution of ketosis leads to DKA recurrence. 1 Normal glucose does not equal resolved ketoacidosis—follow the anion gap and pH.
Failure to recognize SGLT2 inhibitors as the precipitating cause: These medications must be discontinued immediately and not restarted until 3-4 days after metabolic stability is achieved. 5, 6 The prolonged half-life of SGLT2 inhibitors may extend the duration of euglycemic DKA. 6
Inadequate fluid resuscitation worsens both DKA and any underlying condition like pancreatitis. 1
Special Considerations
For SGLT2 inhibitor-associated euglycemic DKA: The pathophysiology involves chronic low-level ketones from the medication, with any additional ketone formation precipitating ketoacidosis while the glycosuric effect prevents hyperglycemia. 6 Treatment duration may be prolonged due to the drug's half-life. 6
Dietary causes (ketogenic diets): Severe carbohydrate restriction creates a relative carbohydrate deficit state, requiring emphasis on adequate dextrose administration during treatment. 4, 2