What is the most likely diagnosis and initial management for an adult with venous pH 7.41, anion gap 19 mEq/L, bicarbonate 21 mEq/L, blood glucose 404 mg/dL, and ketones 2.46 mmol/L?

Euglycemic Diabetic Ketoacidosis (Euglycemic DKA)

This patient has euglycemic diabetic ketoacidosis (euglycemic DKA), characterized by ketoacidosis with a relatively normal blood glucose (404 mg/dL is only mildly elevated), elevated ketones (2.46 mmol/L), elevated anion gap (19 mEq/L), low bicarbonate (21 mEq/L), and normal pH (7.41). 1, 2

Diagnosis

This presentation meets criteria for euglycemic DKA rather than classic DKA because:

• Blood glucose is <600 mg/dL (404 mg/dL) with significant ketosis (2.46 mmol/L) 2, 3
• Anion gap is elevated at 19 mEq/L (normal ≤12), indicating unmeasured anions from ketoacids 1, 4
• Bicarbonate is reduced at 21 mEq/L (normal 22-28), though not meeting classic DKA threshold of <15 mEq/L 5, 1
• Venous pH is normal at 7.41, suggesting either very early/mild ketoacidosis or compensated metabolic acidosis 1, 2

The normal pH with elevated anion gap and ketones indicates this is mild euglycemic DKA or a pre-DKA state that requires immediate intervention to prevent progression. 2, 3

Immediate Management Algorithm

Step 1: Fluid Resuscitation

• Begin isotonic saline (0.9% NaCl) at 15-20 mL/kg/hour for the first hour to restore intravascular volume 5, 1, 4
• Continue aggressive fluid replacement targeting 6-9 L deficit over 24 hours 1, 4

Step 2: Dextrose Administration (Critical in Euglycemic DKA)

• Immediately add 5-10% dextrose to IV fluids because glucose is only 404 mg/dL 1, 6, 2
• In euglycemic DKA, dextrose must be started alongside saline from the beginning of insulin treatment to prevent hypoglycemia while clearing ketones 6, 7, 2
• Target glucose 150-200 mg/dL during treatment 6, 3

Step 3: Insulin Therapy

• Start continuous IV regular insulin at 0.1 units/kg/hour (no bolus needed given mild presentation) 5, 1, 2
• Continue insulin infusion despite normal glucose because ketone clearance requires both insulin AND glucose substrate 1, 6, 2
• Do not stop insulin until anion gap normalizes (≤12 mEq/L) and ketones clear, even if glucose normalizes first 6, 8, 3

Step 4: Potassium Management

• Check serum potassium immediately before starting insulin 1, 4
• If K+ 3.3-5.5 mEq/L: add 20-30 mEq/L potassium to IV fluids (2/3 KCl, 1/3 KPO4) 5, 4
• If K+ <3.3 mEq/L: delay insulin and aggressively replace potassium first to prevent fatal arrhythmias 5, 1
• If K+ >5.5 mEq/L: hold potassium supplementation and recheck frequently 1

Step 5: Monitoring

• Draw labs every 2-4 hours: venous pH, bicarbonate, anion gap, glucose, electrolytes (especially K+), BUN, creatinine 5, 1, 6
• Monitor β-hydroxybutyrate directly if available—do not rely on urine ketones (nitroprusside method) as they only measure acetoacetate/acetone, not β-hydroxybutyrate, and can falsely suggest worsening during treatment 5, 1
• Venous pH is sufficient for monitoring; repeat arterial blood gases are unnecessary 5, 1

Resolution Criteria

DKA is resolved when ALL of the following are met:

• Glucose <200 mg/dL 5, 6
• Serum bicarbonate ≥18 mEq/L 5, 6
• Venous pH >7.3 5, 6
• Anion gap ≤12 mEq/L 5, 6, 4

Transition to Subcutaneous Insulin

Once resolution criteria are met:

• Administer basal subcutaneous insulin (NPH, detemir, glargine, or degludec) 2-4 hours BEFORE stopping IV insulin to prevent rebound hyperglycemia and recurrent ketoacidosis 5, 1, 6
• Continue IV insulin for 1-2 hours after starting subcutaneous regimen to ensure adequate plasma insulin levels 5, 6
• Start multiple-dose regimen combining short/rapid-acting and intermediate/long-acting insulin 5, 6

Critical Pitfalls to Avoid

• Never discontinue IV insulin when glucose normalizes—ketone clearance takes longer than glucose correction, and premature insulin cessation causes recurrent ketoacidosis 6, 8, 3
• Never withhold dextrose in euglycemic DKA—insulin cannot clear ketones without adequate glucose substrate; the liver continues producing ketones even with insulin if carbohydrate is absent 1, 6, 2
• Never rely on urine ketones or nitroprusside method for monitoring treatment response—these miss β-hydroxybutyrate (the predominant ketoacid) and paradoxically worsen as β-hydroxybutyrate converts to acetoacetate during treatment 5, 1
• Never delay potassium replacement—insulin drives potassium intracellularly, causing rapid decline despite total body depletion of 3-5 mEq/kg 5, 1

Identify and Treat Precipitating Cause

Common triggers for euglycemic DKA include:

• SGLT-2 inhibitor use (most common in current era) 7, 2, 3
• Starvation or reduced oral intake 2, 3
• Infection 9
• Alcohol use 2
• Pregnancy 2
• Insulin omission or inadequate dosing 9

Obtain cultures (blood, urine, throat) if infection suspected, review medication list for SGLT-2 inhibitors, and assess for other precipitants. 1, 9