What is the management protocol for diabetic ketoacidosis (DKA)?

Management Protocol for Diabetic Ketoacidosis (DKA)

The management of diabetic ketoacidosis requires immediate fluid resuscitation with isotonic saline at 15-20 mL/kg/hour initially, followed by continuous intravenous insulin at 0.1 units/kg/hour, careful electrolyte monitoring and replacement, and identification of precipitating factors. 1, 2

Diagnosis and Initial Assessment

• DKA is diagnosed by the presence of blood glucose >250 mg/dL, arterial pH <7.3, serum bicarbonate <15 mEq/L, and moderate ketonuria or ketonemia 1, 2
• Severity classification:
  • Mild: pH 7.25-7.30, bicarbonate 15-18 mEq/L, alert mental status 2
  • Moderate: pH 7.00-7.24, bicarbonate 10-15 mEq/L, drowsy mental status 2
  • Severe: pH <7.00, bicarbonate <10 mEq/L, stupor/coma 2
• Initial laboratory evaluation should include:
  • Arterial blood gases, complete blood count with differential
  • Blood glucose, blood urea nitrogen, creatinine
  • Electrolytes with calculated anion gap, serum ketones
  • Urinalysis, electrocardiogram 1, 2
• Obtain bacterial cultures of urine, blood, and throat if infection is suspected 3, 2

Treatment Protocol

1. Fluid Therapy

• Begin with isotonic saline (0.9% NaCl) at 15-20 mL/kg/hour during the first hour to restore intravascular volume and renal perfusion 3, 1, 2
• Subsequent fluid choice depends on hydration state, serum electrolytes, and urine output:
  • If corrected serum sodium is normal or elevated: use 0.45% NaCl at 4-14 mL/kg/hour 3
  • If corrected serum sodium is low: continue with 0.9% NaCl 3, 1
• Target fluid replacement to correct estimated deficits within 24 hours 1
• Add dextrose 5% to IV fluids when blood glucose falls below 250 mg/dL while continuing insulin infusion to clear ketones 1, 2

2. Insulin Therapy

• Start continuous intravenous regular insulin at 0.1 units/kg/hour without an initial bolus 1, 2, 4
• Continue insulin therapy until resolution of ketoacidosis (pH >7.3, bicarbonate ≥15 mEq/L, and normalized anion gap), regardless of glucose levels 1, 2
• Never discontinue insulin when glucose levels fall; instead, add dextrose to prevent hypoglycemia while continuing insulin to clear ketosis 1, 5
• Transition to subcutaneous insulin:
  • Administer basal insulin 2-4 hours before stopping IV insulin to prevent rebound hyperglycemia 1, 2
  • Consider overlapping IV insulin with subcutaneous insulin during transition 1

3. Electrolyte Management

• Monitor potassium closely as total body potassium is depleted despite potentially normal or elevated initial serum levels due to acidosis 1, 2
• Once renal function is assured and serum potassium is known, add potassium to IV fluids:
  • If serum K+ <3.3 mEq/L: hold insulin and give 40 mEq/L K+ until >3.3 mEq/L 1
  • If serum K+ 3.3-5.3 mEq/L: add 20-30 mEq/L K+ (2/3 KCl and 1/3 KPO₄) to IV fluids 1, 2
  • If serum K+ >5.3 mEq/L: do not add K+, but check frequently 1
• Typical electrolyte deficits in DKA include:
  • Potassium: 3-5 mEq/kg
  • Phosphate: 5-7 mEq/kg
  • Magnesium: 1-2 mEq/kg
  • Calcium: 1-2 mEq/kg 1
• Bicarbonate therapy is generally not recommended except in cases where pH <6.9 2, 6

Monitoring During Treatment

• Check blood glucose hourly 1, 2
• Check electrolytes, blood urea nitrogen, creatinine, and osmolality every 2-4 hours until stable 1, 2
• Monitor venous pH and anion gap to assess resolution of acidosis 1, 2
• Assess for signs of volume overload, particularly in patients with renal or cardiac compromise 1

Resolution Criteria

• Blood glucose <200 mg/dL 1, 2
• Serum bicarbonate ≥15 mEq/L 1, 2
• Venous pH >7.3 1, 2
• Anion gap normalized 1, 2

Common Pitfalls to Avoid

• Inadequate potassium replacement leading to arrhythmias 1, 2
• Overly rapid correction of hyperglycemia and hyperosmolality 1, 7
• Insufficient monitoring of electrolytes and acid-base status 1
• Premature discontinuation of insulin therapy before ketoacidosis resolves 1, 5
• Not overlapping IV insulin with subcutaneous insulin during transition 1
• Failing to identify and treat the underlying precipitating cause of DKA 2, 8
• Relying solely on urine ketones for diagnosis or monitoring response to treatment, as the nitroprusside method doesn't measure β-hydroxybutyrate, the predominant ketone body in DKA 5
• Cerebral edema, particularly in children and adolescents, associated with rapid correction of hyperglycemia 9, 7