How to manage diabetic ketoacidosis (DKA)?

Management of Diabetic Ketoacidosis (DKA)

The management of diabetic ketoacidosis requires immediate administration of intravenous fluids, insulin therapy, electrolyte replacement, and identification and treatment of precipitating factors to reduce morbidity and mortality. 1, 2

Initial Assessment

• Perform laboratory evaluation including plasma glucose, blood urea nitrogen/creatinine, serum ketones, electrolytes with calculated anion gap, osmolality, urinalysis, urine ketones, arterial blood gases, complete blood count, and electrocardiogram 3, 1
• Obtain bacterial cultures (urine, blood, throat) if infection is suspected and administer appropriate antibiotics 2
• Identify potential precipitating factors: infection, cerebrovascular accident, alcohol abuse, pancreatitis, myocardial infarction, trauma, drugs, or insulin discontinuation/inadequacy 1

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
• Subsequent fluid choice depends on hydration status, serum electrolyte levels, and urine output 1
• 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, 2
• Total fluid replacement should aim to correct estimated deficits within 24 hours 1

Insulin Therapy

• Start with continuous intravenous regular insulin infusion at 0.1 units/kg/hour (preferred method for moderate to severe DKA) 1, 2
• If plasma glucose does not fall by 50 mg/dL from initial value 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 3, 1
• When plasma glucose reaches 250 mg/dL, decrease insulin infusion to 0.05-0.1 units/kg/hour and add dextrose to IV fluids 3, 2
• 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

Electrolyte Management

• Monitor potassium levels closely as insulin therapy and correction of acidosis can cause hypokalemia 1, 4
• 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 <5.5 mEq/L 3, 1
• In patients with relatively low plasma potassium levels, temporarily delay insulin administration and first administer potassium chloride intravenously to bring plasma potassium close to 4 mmol/L 5
• Maintain serum potassium between 4-5 mmol/L throughout treatment 1, 2

Monitoring During Treatment

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

Bicarbonate Administration

• Bicarbonate administration is generally not recommended for DKA patients with pH >7.0 1, 6
• Consider bicarbonate in adult patients with moderately severe acidemia (pH <7.20 and plasma bicarbonate <12 mmol/L) who are at risk for worsening acidemia, particularly if hemodynamically unstable 5
• Bicarbonate should not be administered to children with DKA, except if acidemia is very severe and hemodynamic instability is refractory to saline administration 5

Transition to Subcutaneous Insulin

• Once DKA resolves (glucose <200 mg/dL, serum bicarbonate ≥18 mEq/L, venous pH >7.3, and anion gap ≤12 mEq/L), transition to subcutaneous insulin 1, 2
• When the patient can eat, start a multiple-dose schedule using a combination of short/rapid-acting and intermediate/long-acting insulin 1, 7
• Administer basal insulin 2-4 hours before stopping the IV insulin infusion to prevent recurrence of ketoacidosis 2

Common Pitfalls to Avoid

• Premature termination of insulin therapy before complete resolution of ketosis can lead to recurrence of DKA 1, 2
• Interruption of insulin infusion when glucose levels fall without adding dextrose is a common cause of persistent or worsening ketoacidosis 1, 2
• Inadequate monitoring and replacement of electrolytes, particularly potassium 1, 4
• Relying on nitroprusside method to measure ketones is misleading as it only measures acetoacetic acid and acetone, not β-hydroxybutyrate 3, 2
• Overzealous treatment with insulin without glucose supplementation can lead to hypoglycemia 1, 4
• Excessive saline resuscitation and rapid decrease in effective plasma osmolality early in treatment may increase risk of cerebral edema, especially in children 5, 6