What is the treatment for Diabetic Ketoacidosis (DKA)?

Treatment of Diabetic Ketoacidosis (DKA)

The cornerstone of DKA treatment consists of aggressive fluid resuscitation with isotonic saline, continuous intravenous insulin infusion until resolution of ketoacidosis, and careful electrolyte management, particularly potassium replacement. 1, 2

Initial Assessment

• Diagnostic criteria for DKA include blood glucose >250 mg/dL, arterial pH <7.3, serum bicarbonate <15 mEq/L, and presence of ketonemia or ketonuria 1
• Laboratory evaluation should include plasma glucose, blood urea nitrogen/creatinine, serum ketones, electrolytes (with calculated anion gap), osmolality, urinalysis, urine ketones, arterial blood gases, complete blood count with differential, and electrocardiogram 1, 3
• Identify potential precipitating factors: infection, cerebrovascular accident, alcohol abuse, pancreatitis, myocardial infarction, trauma, drugs, or insulin discontinuation/inadequacy 1

Treatment Protocol

Fluid Therapy

• Begin with isotonic saline (0.9% NaCl) at 15-20 mL/kg/hour (approximately 1-1.5 L in the average adult) during the first hour 1, 2
• When serum glucose reaches 250 mg/dL, change fluid to 5% dextrose with 0.45-0.75% NaCl to prevent hypoglycemia while continuing insulin therapy 1
• Total fluid replacement should aim to correct estimated deficits within 24 hours 1
• Balanced crystalloid solutions like Sterofundin may lead to faster DKA resolution compared to normal saline (13.8 vs 18.1 hours) 4

Insulin Therapy

• Start with continuous intravenous regular insulin infusion at 0.1 units/kg/hour (preferred method for moderate to severe DKA) 1, 3
• If plasma glucose does not fall by 50 mg/dL in the first hour, check hydration status; if acceptable, double the insulin infusion rate every hour until a steady glucose decline of 50-75 mg/h is achieved 1
• Continue insulin infusion until resolution of ketoacidosis (pH >7.3, serum bicarbonate ≥18 mEq/L, and anion gap ≤12 mEq/L) regardless of glucose levels 1, 2
• When glucose falls below 250 mg/dL, add dextrose (5-10%) to IV fluids while continuing insulin to clear ketones 1
• For mild to moderate DKA, subcutaneous insulin may be an effective alternative with fewer hypoglycemic events compared to IV insulin 5

Electrolyte Management

• Include 20-30 mEq/L potassium (2/3 KCl and 1/3 KPO₄) in the infusion once renal function is assured and serum potassium is known 1, 3
• Monitor potassium levels closely, as insulin administration can cause hypokalemia; maintain serum K⁺ between 4-5 mmol/L 1
• Bicarbonate administration is generally not recommended for DKA patients with pH >7.0 1
• Consider bicarbonate only if pH <6.9 or when pH <7.2 with bicarbonate <10 mEq/L, particularly before intubation to prevent hemodynamic collapse 6

Monitoring During Treatment

• Draw blood every 2-4 hours to determine serum electrolytes, glucose, blood urea nitrogen, creatinine, osmolality, and venous pH 1, 3
• Follow venous pH (typically 0.03 units lower than arterial pH) and anion gap to monitor resolution of acidosis 1
• Direct measurement of β-hydroxybutyrate in blood is the preferred method for monitoring DKA 1

Resolution Parameters and Transition to Subcutaneous Insulin

• DKA resolution requires: glucose <200 mg/dL, serum bicarbonate ≥18 mEq/L, venous pH >7.3, and anion gap ≤12 mEq/L 1, 2
• When DKA resolves and the patient can eat, start a multiple-dose insulin schedule using a combination of short/rapid-acting and intermediate/long-acting insulin 1, 2
• Administer basal insulin 2-4 hours before stopping the IV insulin infusion 3

Common Pitfalls to Avoid

• Premature termination of insulin therapy before complete resolution of ketosis can lead to recurrence of DKA 1
• Interruption of insulin infusion when glucose levels fall is a common cause of persistent or worsening ketoacidosis 1
• Failure to add dextrose when glucose falls below 250 mg/dL while continuing insulin therapy 1
• Inadequate monitoring and replacement of electrolytes, particularly potassium 1, 7
• Overzealous treatment with insulin without glucose supplementation can lead to hypoglycemia 1
• Rapid overcorrection of hyperglycemia can lead to cerebral edema, particularly in children and adolescents 6