Diabetic Ketoacidosis (DKA) Treatment Guidelines
The management of diabetic ketoacidosis requires immediate fluid replacement, insulin therapy, electrolyte monitoring and replacement, and identification of precipitating causes, with careful attention to preventing complications such as cerebral edema. 1
Initial Assessment and Diagnosis
- DKA is characterized by hyperglycemia (blood glucose >250 mg/dL), metabolic acidosis (pH <7.3, serum bicarbonate <18 mEq/L), and elevated ketones 1
- Initial laboratory evaluation should include plasma glucose, blood urea nitrogen, creatinine, serum ketones, electrolytes with calculated anion gap, osmolality, urinalysis, arterial blood gases, complete blood count with differential, and electrocardiogram 1
- Direct measurement of β-hydroxybutyrate in blood is preferred over nitroprusside method (which only measures acetoacetic acid and acetone) for monitoring DKA 1
Fluid Therapy
- Begin with balanced electrolyte solutions at 15-20 mL/kg/h during the first hour to restore circulatory volume and tissue perfusion 1
- Continue fluid replacement to correct estimated deficits within the first 24 hours, with careful monitoring to prevent rapid changes in serum osmolality 1
- For mild DKA, 1.5 times the 24-hour maintenance requirements (5 mL/kg/h) will accomplish smooth rehydration; do not exceed twice the maintenance requirement 2
Insulin Therapy
- After confirming adequate potassium levels, administer an intravenous bolus of regular insulin at 0.15 U/kg body weight, followed by continuous infusion at 0.1 U/kg/h 1
- If plasma glucose does not fall by 50 mg/dL from initial value in the first hour, double the insulin infusion every hour until a steady glucose decline between 50-75 mg/h is achieved 1
- For mild DKA, subcutaneous regular insulin may be given every 4 hours (5-unit increments for every 50 mg/dL increase in blood glucose above 150 mg/dL, up to 20 units for blood glucose of 300 mg/dL) 2
Electrolyte Management
Potassium
- Monitor potassium levels closely as total body potassium deficits are common despite potentially normal or elevated initial serum levels due to acidosis 1
- Begin potassium replacement after serum levels fall below 5.5 mEq/L, assuming adequate urine output 2
- Add 20-30 mEq potassium (2/3 KCl and 1/3 KPO4) in each liter of infusion fluid to maintain serum potassium concentration within 4-5 mEq/L 2
- If significant hypokalemia is present initially, delay insulin treatment until potassium concentration is restored to >3.3 mEq/L to avoid arrhythmias, cardiac arrest, and respiratory muscle weakness 2
Bicarbonate
- Bicarbonate therapy is generally not recommended for DKA patients with pH >7.0 1
- For adult patients with pH <6.9, administer 100 mmol sodium bicarbonate in 400 mL sterile water at 200 mL/h 2
- For patients with pH 6.9-7.0, administer 50 mmol sodium bicarbonate in 200 mL sterile water at 200 mL/h 2
Phosphate
- Studies have failed to show beneficial effects of routine phosphate replacement on clinical outcomes in DKA 2
- Consider phosphate replacement only in patients with cardiac dysfunction, anemia, respiratory depression, or serum phosphate <1.0 mg/dL 1
Monitoring and Resolution Parameters
- Draw blood every 2-4 hours to determine serum electrolytes, glucose, blood urea nitrogen, creatinine, osmolality, and venous pH 1
- Venous pH (typically 0.03 units lower than arterial pH) and anion gap can be followed to monitor resolution of acidosis 2
- DKA resolution requires: glucose <200 mg/dL, serum bicarbonate ≥18 mEq/L, venous pH >7.3, and anion gap ≤12 mEq/L 1
Transition from IV to Subcutaneous Insulin
- When DKA is resolved and the patient can eat, transition to a multiple-dose regimen using a combination of short/rapid-acting and intermediate/long-acting insulin 2
- Administer basal insulin 2-4 hours before stopping the intravenous insulin to prevent recurrence of ketoacidosis and rebound hyperglycemia 1
- For newly diagnosed patients, initiate a multidose regimen of short- and intermediate/long-acting insulin at approximately 0.5-1.0 units/kg/day 2
Prevention of Complications
Cerebral Edema
- Cerebral edema is a rare but frequently fatal complication of DKA, occurring in 0.7-1.0% of children with DKA 2
- Risk factors include severity of acidosis, greater hypocapnia, higher blood urea nitrogen at presentation, and treatment with bicarbonate 3
- To prevent cerebral edema, follow recommendations for gradual correction of glucose and osmolality, and judicious use of isotonic or hypotonic saline 2
Identification and Treatment of Precipitating Causes
- Obtain bacterial cultures of urine, blood, and other sites as needed and administer appropriate antibiotics if infection is suspected 1
- SGLT2 inhibitors should be discontinued 3-4 days before surgery to prevent DKA 1
- Common precipitating factors include infection, inadequate insulin therapy, new-onset diabetes, and medication non-adherence 4
Discharge Planning and Prevention
- Provide education on recognition, prevention, and management of DKA for all individuals affected by or at high risk for these events 1
- Schedule follow-up appointments with appropriate providers to ensure continuity of care and prevent recurrence 1
- Develop a structured discharge plan tailored to the individual to reduce length of hospital stay and readmission rates 1