What is the appropriate treatment for a diabetic patient presenting with euglycaemic diabetic ketoacidosis and a base excess of -13 mmol/L?

Treatment of Euglycemic Diabetic Ketoacidosis with Base Excess of -13 mmol/L

In a diabetic patient presenting with euglycemic DKA (normal glucose) and a base excess of -13 mmol/L, you must initiate continuous IV regular insulin at 0.1 units/kg/hour while simultaneously starting dextrose-containing IV fluids (5% dextrose with 0.45–0.75% NaCl) from the outset to prevent hypoglycemia while clearing ketones. 1, 2

Understanding the Clinical Scenario

A base excess of -13 mmol/L indicates moderate-to-severe metabolic acidosis (typically corresponding to a bicarbonate of approximately 10–12 mEq/L and pH around 7.0–7.1), which meets criteria for moderate DKA despite the euglycemia. 1, 3 This presentation is increasingly common with SGLT2 inhibitor use, pregnancy, starvation states, or recent insulin administration. 4, 5, 6

The absence of hyperglycemia does not reduce the urgency or severity of the metabolic emergency—euglycemic DKA carries the same morbidity and mortality risk as classic DKA. 5, 7

Immediate Management Algorithm

Step 1: Fluid Resuscitation (First Hour)

• Begin isotonic saline (0.9% NaCl) at 15–20 mL/kg/hour (approximately 1–1.5 L in the first hour) to restore intravascular volume and renal perfusion. 1, 2, 3
• This initial bolus is identical to classic DKA management regardless of glucose level. 1

Step 2: Critical Potassium Assessment (Before Any Insulin)

Check serum potassium immediately and apply this algorithm: 1, 2, 3

• If K⁺ < 3.3 mEq/L: Hold all insulin, aggressively replace potassium at 20–40 mEq/hour until K⁺ ≥ 3.3 mEq/L, obtain ECG, and continue isotonic saline. 1, 2 This is a Class A contraindication to insulin initiation. 1
• If K⁺ 3.3–5.5 mEq/L: Insulin may be started safely; add 20–30 mEq/L potassium to IV fluids (2/3 KCl + 1/3 KPO₄) once adequate urine output confirmed. 1, 2, 3
• If K⁺ > 5.5 mEq/L: Start insulin immediately without potassium supplementation initially, but monitor K⁺ every 2–4 hours as levels will drop rapidly. 1, 2

Step 3: Simultaneous Insulin and Dextrose Initiation

This is the critical difference from classic DKA management:

• Start continuous IV regular insulin at 0.1 units/kg/hour (no initial bolus needed in euglycemic DKA). 1, 2
• Simultaneously begin 5% dextrose with 0.45–0.75% NaCl at 150–250 mL/hour to provide approximately 150–200 grams of carbohydrate per 24 hours. 1, 2, 8
• Do not wait for glucose to fall—in euglycemic DKA, dextrose must be given from the start because insulin alone cannot clear ketones without adequate glucose substrate. 1, 2, 7

The rationale: Insulin requires both adequate insulin levels AND glucose availability to suppress ketogenesis and clear ketones. 1, 2 Without carbohydrate provision, the liver continues producing ketones despite insulin administration. 1

Step 4: Monitoring Protocol

Draw blood every 2–4 hours for: 1, 2, 3

• Serum electrolytes (especially potassium—target 4.0–5.0 mEq/L throughout treatment) 1, 2
• Venous pH and bicarbonate 1, 3
• Anion gap 1, 3
• Blood glucose 1, 2
• β-hydroxybutyrate (preferred over urine ketones) 1, 3

Check capillary glucose every 1–2 hours to prevent hypoglycemia, which is a higher risk in euglycemic DKA. 1, 2

Step 5: Insulin and Dextrose Titration

• If glucose falls below 150 mg/dL: Increase dextrose concentration to 10% while maintaining the same insulin infusion rate. 2, 8
• If glucose rises above 250 mg/dL: Continue current dextrose concentration and insulin rate; do not reduce dextrose. 1, 2
• Never reduce or stop insulin infusion until ketoacidosis fully resolves, regardless of glucose level. 1, 2, 3

The insulin infusion rate should remain at 0.1 units/kg/hour (or be increased if acidosis is not improving) until resolution criteria are met. 1, 2

Resolution Criteria (All Must Be Met)

DKA is resolved only when all of the following are achieved simultaneously: 1, 2, 3

• Venous pH > 7.3 1, 3
• Serum bicarbonate ≥ 18 mEq/L 1, 3
• Anion gap ≤ 12 mEq/L 1, 3
• β-hydroxybutyrate < 1.0 mmol/L 1
• Glucose < 200 mg/dL (though this is already met in euglycemic DKA) 1, 3

Ketonemia clears more slowly than hyperglycemia—this is why insulin must continue even after glucose normalizes. 1, 3

Transition to Subcutaneous Insulin

Once all resolution criteria are met and the patient can tolerate oral intake: 1, 2, 3

• Administer basal insulin (glargine or detemir) 2–4 hours BEFORE stopping the IV insulin infusion. 1, 2, 3
• Continue IV insulin for 1–2 hours after the basal dose to ensure adequate absorption and prevent rebound ketoacidosis. 1, 2
• Premature discontinuation of IV insulin is the most common cause of recurrent DKA. 1, 2

Critical Pitfalls to Avoid in Euglycemic DKA

1. Delaying diagnosis because glucose is normal—euglycemic DKA is easily missed, leading to delayed treatment and worse outcomes. 5, 6, 7

2. Starting insulin without dextrose—this perpetuates ketogenesis because the liver needs both insulin AND glucose to stop producing ketones. 1, 2, 8

3. Stopping insulin when glucose normalizes—ketone clearance lags behind glucose normalization by hours; premature insulin cessation causes recurrent ketoacidosis. 1, 2, 3

4. Using urine ketones or nitroprusside tests for monitoring—these miss β-hydroxybutyrate (the predominant ketone) and can falsely suggest worsening ketosis during treatment. 1, 3

5. Inadequate potassium monitoring and replacement—total body potassium depletion is universal (≈3–5 mEq/kg) despite potentially normal initial levels; insulin drives K⁺ intracellularly, causing rapid decline. 1, 2, 3

6. Initiating insulin when K⁺ < 3.3 mEq/L—this can precipitate fatal cardiac arrhythmias and is an absolute contraindication. 1, 2

Identifying and Treating the Precipitating Cause

Simultaneously investigate and treat the underlying trigger: 1, 2, 3

• SGLT2 inhibitors: Discontinue immediately and do not restart until 3–4 days after metabolic stability. 4, 1, 9
• Infection: Obtain cultures (blood, urine, throat) and start appropriate antibiotics. 1, 2, 3
• Pregnancy: Recognize that pregnant individuals frequently present with euglycemic DKA and mixed acid-base disturbances. 4
• Starvation/reduced oral intake: Common in acute illness with nausea/vomiting. 4, 5, 6
• Alcohol use, chronic liver disease, pancreatitis, myocardial infarction, stroke: All recognized precipitants. 1, 2, 3, 5

Special Consideration: Bicarbonate Therapy

Bicarbonate is NOT recommended for pH > 6.9–7.0 (which includes your patient with BE -13, likely pH ≈7.0–7.1), as multiple studies show no benefit in resolution time and potential harms including worsened ketosis, hypokalemia, and increased cerebral edema risk. 1, 2, 3