What is the initial treatment for Diabetic Ketoacidosis (DKA)?

Initial Treatment of Diabetic Ketoacidosis (DKA)

Begin immediate fluid resuscitation with isotonic saline (0.9% NaCl) at 15-20 mL/kg/hour during the first hour, followed by continuous intravenous regular insulin at 0.1 units/kg/hour without an initial bolus, while closely monitoring and replacing potassium to prevent life-threatening hypokalemia. 1, 2, 3

Immediate Fluid Resuscitation

• Start with isotonic saline (0.9% NaCl) at 15-20 mL/kg/hour (approximately 1-1.5 liters in the average adult) during the first hour to restore intravascular volume and renal perfusion 1, 2, 3
• After the initial hour, switch to 0.45% NaCl at 4-14 mL/kg/hour if corrected serum sodium is normal or elevated; continue 0.9% NaCl if corrected sodium is low 1
• Correct serum sodium for hyperglycemia by adding 1.6 mEq to the measured sodium value for each 100 mg/dL glucose above 100 mg/dL 1
• When serum glucose reaches 250 mg/dL, add 5% dextrose to IV fluids (dextrose with 0.45-0.75% NaCl) to prevent hypoglycemia while continuing insulin to clear ketosis 2, 3

Insulin Therapy Protocol

• Start continuous IV regular insulin at 0.1 units/kg/hour without an initial bolus after confirming adequate potassium levels (>3.3 mEq/L) 1, 2, 3
• If plasma glucose does not fall by 50 mg/dL in the first hour, double the insulin infusion rate hourly until achieving a steady decline of 50-75 mg/dL per hour 3, 4
• Never interrupt insulin infusion when glucose falls—instead add dextrose to IV fluids to maintain glucose 150-200 mg/dL while continuing insulin until ketoacidosis resolves 2, 3
• Continue insulin until complete resolution: pH >7.3, serum bicarbonate ≥18 mEq/L, anion gap ≤12 mEq/L, and glucose <200 mg/dL 1, 3, 4

Critical Potassium Management

• Delay insulin therapy if initial potassium is <3.3 mEq/L to avoid cardiac arrhythmias, cardiac arrest, and respiratory muscle weakness 1, 4
• Once potassium falls below 5.5 mEq/L and urine output is adequate, add 20-30 mEq/L potassium to each liter of IV fluid (2/3 KCl and 1/3 KPO₄) 1, 2
• Maintain serum potassium between 4-5 mEq/L throughout treatment, as insulin therapy and acidosis correction cause rapid intracellular potassium shifts 2, 3

Essential Laboratory Monitoring

• Initial labs: plasma glucose, arterial blood gases, complete metabolic panel with calculated anion gap, serum ketones (β-hydroxybutyrate preferred), urinalysis, complete blood count, and electrocardiogram 1, 3, 4
• Check blood glucose every 1-2 hours during active treatment 2, 3
• Draw blood every 2-4 hours for electrolytes, glucose, BUN, creatinine, osmolality, and venous pH to monitor acidosis resolution 2, 3
• Follow venous pH and anion gap (venous pH is typically 0.03 units lower than arterial pH) rather than repeated arterial blood gases 3, 4

Bicarbonate Administration (Rarely Indicated)

• Do NOT give bicarbonate if pH >7.0, as studies show no clinical benefit and potential harm including worsening ketosis, hypokalemia, and cerebral edema risk 1, 3, 4
• If pH <6.9, consider 100 mmol sodium bicarbonate in 400 mL sterile water at 200 mL/hour 1, 4
• If pH 6.9-7.0, consider 50 mmol sodium bicarbonate in 200 mL sterile water at 200 mL/hour 1, 4

Transition to Subcutaneous Insulin

• When DKA resolves (glucose <200 mg/dL, bicarbonate ≥18 mEq/L, pH >7.3, anion gap ≤12 mEq/L), administer basal insulin (intermediate or long-acting) 2-4 hours BEFORE stopping IV insulin to prevent recurrence of ketoacidosis and rebound hyperglycemia 1, 2, 3, 4
• For newly diagnosed patients, initiate approximately 0.5-1.0 units/kg/day as a multidose regimen of short- and intermediate/long-acting insulin 1, 4

Identifying and Treating Precipitating Causes

• Obtain bacterial cultures (urine, blood, throat) if infection is suspected and administer appropriate antibiotics 3, 4
• Discontinue SGLT2 inhibitors 3-4 days before surgery, as they can cause euglycemic DKA 4
• Search for myocardial infarction, stroke, medication non-compliance, or other acute stressors 4

Critical Pitfalls to Avoid

• Premature termination of insulin before complete ketoacidosis resolution (pH >7.3, bicarbonate ≥18 mEq/L, anion gap ≤12 mEq/L) is the most common cause of DKA recurrence 2, 3
• Stopping insulin when glucose normalizes without adding dextrose perpetuates ketosis—glucose and ketone clearance occur at different rates 2, 3
• Inadequate potassium monitoring and replacement can cause life-threatening arrhythmias, as total body potassium is always depleted despite potentially normal or elevated initial levels 1, 4
• Relying on nitroprusside method for ketone measurement is misleading, as it only detects acetoacetic acid and acetone, not β-hydroxybutyrate (the predominant ketone body)—direct β-hydroxybutyrate measurement is preferred 2, 3, 4
• Rapid correction of hyperglycemia and osmolality (>3 mOsm/kg/hour) increases cerebral edema risk, particularly in children—aim for gradual correction 1, 4, 5

Special Consideration for Euglycemic DKA

• In euglycemic DKA (glucose <250 mg/dL with ketoacidosis), add dextrose-containing fluids earlier while maintaining full-dose insulin to clear ketosis 2
• Never reduce or stop insulin based on glucose levels alone—resolution requires normalization of pH, bicarbonate, and anion gap 2