What are the immediate management steps for Diabetic Ketoacidosis (DKA)?

Immediate Management of Diabetic Ketoacidosis (DKA)

The immediate management of DKA requires aggressive fluid resuscitation with isotonic saline 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, and careful electrolyte monitoring with potassium replacement once levels fall below 5.3 mEq/L. 1, 2

Initial Assessment and Diagnosis

• 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 1
• Diagnostic criteria for DKA: plasma glucose >250 mg/dL, arterial pH <7.30, serum bicarbonate <18 mEq/L, and positive serum and urine ketones 1
• Obtain bacterial cultures (urine, blood, throat) if infection is suspected and administer appropriate antibiotics 1, 2
• Direct measurement of β-hydroxybutyrate in blood is preferred over nitroprusside method, which only measures acetoacetic acid and acetone 3, 2

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 1, 3
• Continue fluid replacement to correct estimated deficits within the first 24 hours 2
• For mild DKA, use 1.5 times the 24-hour maintenance requirements (5 mL/kg/h) for smooth rehydration; do not exceed twice the maintenance requirement 2
• When serum glucose reaches 250 mg/dL, add dextrose to IV fluids to prevent hypoglycemia while continuing insulin to clear ketosis 1, 3

Insulin Therapy

• Start continuous intravenous regular insulin infusion at 0.1 units/kg/hour without an initial bolus 1, 3, 2
• If plasma glucose does not fall by 50 mg/dL in the first hour, double the insulin infusion rate hourly until a steady glucose decline between 50-75 mg/hour is achieved 1, 2
• When serum glucose reaches 250 mg/dL, decrease insulin infusion to 0.05-0.1 units/kg/hour and add dextrose to IV fluids 1
• Never interrupt insulin infusion when glucose levels fall; instead, add dextrose to prevent hypoglycemia while continuing insulin to clear ketosis 3, 2

Electrolyte Management

• Monitor potassium levels closely as insulin therapy and correction of acidosis can cause hypokalemia 1, 3, 2
• Include 20-30 mEq/L potassium in IV fluids once renal function is assured and serum potassium is <5.3 mEq/L 1, 3
• Maintain serum potassium between 4-5 mmol/L throughout treatment 1, 3
• Bicarbonate administration is generally not recommended for DKA patients with pH >6.9 1, 2
• For adult patients with pH <6.9, administer 100 mmol sodium bicarbonate in 400 mL sterile water at 200 mL/h 2

Monitoring During Treatment

• Check blood glucose every 1-2 hours 1, 3
• 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, 3, 2

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, 3, 2
• When DKA resolves, transition to subcutaneous insulin 1, 2
• Administer basal insulin 2-4 hours before stopping the IV insulin infusion to prevent recurrence of ketoacidosis 4, 1, 3
• Administration of a low dose of basal insulin analog in addition to intravenous insulin infusion may prevent rebound hyperglycemia 4, 3

Common Pitfalls to Avoid

• Premature termination of insulin therapy before complete resolution of ketosis can lead to recurrence of DKA 1, 3
• Inadequate monitoring of potassium levels during insulin therapy can cause dangerous hypokalemia 1, 2
• Interruption of insulin infusion when glucose levels fall without adding dextrose is a common cause of persistent or worsening ketoacidosis 1, 3
• Relying on nitroprusside method to measure ketones is misleading as it only measures acetoacetic acid and acetone, not β-hydroxybutyrate 1, 3
• Cerebral edema is a rare but frequently fatal complication of DKA, occurring more commonly in children and adolescents 2, 5
• Risk factors for cerebral edema include severity of acidosis, greater hypocapnia, higher blood urea nitrogen concentration at presentation, and treatment with bicarbonate 5, 6

Identification and Treatment of Precipitating Causes

• Common precipitating causes include infections, new diagnosis of diabetes, and nonadherence to insulin therapy 7
• SGLT2 inhibitors should be discontinued 3-4 days before surgery to prevent DKA 4, 2
• Patients prescribed SGLT2 inhibitors should be monitored for euglycemic DKA, which can occur with normal or only mildly elevated blood glucose levels 3