Management of Diabetic Ketoacidosis in Adults
For critically ill adult patients with DKA, initiate aggressive fluid resuscitation with isotonic saline at 15-20 mL/kg/hour, start continuous IV regular insulin at 0.1 units/kg/hour (after confirming potassium >3.3 mEq/L), add dextrose to fluids when glucose falls below 250 mg/dL while continuing insulin until acidosis fully resolves, and administer basal subcutaneous insulin 2-4 hours before stopping the IV infusion. 1, 2, 3
Initial Assessment and Diagnosis
Confirm DKA diagnosis immediately by obtaining venous blood gases, complete metabolic panel, and direct measurement of β-hydroxybutyrate—not urine ketones, which miss the predominant ketoacid. 2, 3 DKA requires all three criteria: blood glucose >250 mg/dL, venous pH <7.3, and serum bicarbonate <15 mEq/L with moderate ketonuria or ketonemia. 2, 3
Calculate the anion gap using [Na⁺] - ([Cl⁻] + [HCO₃⁻]); it should be >10-12 mEq/L in DKA. 2, 3 Correct serum sodium for hyperglycemia by adding 1.6 mEq/L for every 100 mg/dL glucose above 100 mg/dL. 2, 3
Classify severity to guide monitoring intensity: mild (pH 7.25-7.30, bicarbonate 15-18 mEq/L), moderate (pH 7.00-7.24, bicarbonate 10-15 mEq/L), or severe (pH <7.00, bicarbonate <10 mEq/L). 2 Severe DKA requires intensive monitoring including potential central venous and intra-arterial pressure monitoring. 2
Obtain bacterial cultures of urine, blood, and throat if infection is suspected, as sepsis is a common precipitating factor. 2
Fluid Resuscitation Protocol
Begin with isotonic saline (0.9% NaCl) at 15-20 mL/kg/hour during the first hour to restore circulatory volume and tissue perfusion. 1, 2, 3 The typical total body water deficit in DKA is 6-9 liters. 2
After the first hour, switch to 0.45% NaCl at 4-14 mL/kg/hour if corrected serum sodium is normal or elevated. 3 Target total fluid replacement to correct estimated deficits within 24 hours, approximately 1.5 times the 24-hour maintenance requirements. 2
Monitor closely for fluid overload in patients with renal or cardiac compromise, adjusting infusion rates accordingly. 2 This is a critical pitfall in elderly patients and those with heart failure. 4
Potassium Management: The Critical First Step
Check serum potassium before starting insulin therapy. 3 This is non-negotiable because DKA causes total body potassium depletion of 3-5 mEq/kg despite normal or elevated initial serum levels due to acidosis-driven extracellular shift. 2
If initial potassium is <3.3 mEq/L, delay insulin therapy and aggressively replace potassium first to prevent fatal cardiac arrhythmias. 2, 3 Hypokalemia occurs in roughly 50% of patients during DKA treatment, and severe hypokalemia (<2.5 mEq/L) is linked to higher in-hospital mortality. 2
Once potassium is 3.3-5.5 mEq/L and adequate urine output is confirmed, add 20-30 mEq/L potassium to IV fluids using 2/3 KCl and 1/3 KPO₄. 2, 3 The phosphate component prevents severe hypophosphatemia. 2
Insulin Therapy Protocol
Start continuous IV regular insulin infusion at 0.1 units/kg/hour without an initial bolus once potassium is safe. 2, 3 For critically ill and mentally obtunded patients, continuous intravenous insulin is the standard of care. 1
If glucose does not fall by 50 mg/dL in the first hour, double the insulin infusion rate hourly until achieving a steady decline of 50-75 mg/dL per hour. 2
When blood glucose falls to 200-250 mg/dL, immediately add dextrose 5-10% to IV fluids while continuing insulin infusion. 1, 2, 3 This is the most critical management principle: insulin must continue until ketoacidosis resolves, not until glucose normalizes. 2, 5 Adults require 150-200 grams of carbohydrate daily to reduce starvation ketosis, and without carbohydrate substrate, the liver continues producing ketones even with insulin administration. 2
Never stop insulin based on glucose levels alone—this is the most common and dangerous error in DKA management. 3, 5 Ketoacidosis takes longer to resolve than hyperglycemia, and premature insulin cessation causes recurrence. 2
Monitoring During Treatment
Monitor blood glucose, electrolytes, BUN, creatinine, venous pH, and β-hydroxybutyrate every 2-4 hours. 2, 3 After initial diagnosis, venous pH and anion gap adequately monitor acidosis resolution without requiring repeated arterial blood gases. 2
Do not rely on urine ketones or nitroprusside-based tests for monitoring treatment response. 2, 5 These only measure acetoacetate and acetone, completely missing β-hydroxybutyrate—the predominant ketoacid. During treatment, β-hydroxybutyrate converts to acetoacetate, paradoxically making nitroprusside tests appear worse even as the patient improves. 2
Resolution Criteria
DKA is resolved when ALL of the following are met: 2, 3
- Blood glucose <200 mg/dL
- Serum bicarbonate ≥18 mEq/L
- Venous pH >7.3
- Anion gap ≤12 mEq/L
Continue monitoring β-hydroxybutyrate until it normalizes, as ketonemia typically takes longer to clear than hyperglycemia. 2
Transition to Subcutaneous Insulin
Administer basal subcutaneous insulin (NPH, detemir, glargine, or degludec) 2-4 hours before stopping IV insulin infusion to prevent rebound hyperglycemia and recurrent ketoacidosis. 1, 2, 3 This overlap period is essential for successful transition. 1
Calculate total daily dose by averaging the IV insulin rate over the preceding 12 hours (e.g., an average of 1.5 units/hour translates to approximately 36 units per 24 hours) or estimate 0.5-0.8 units/kg/day. 2, 3
Ensure the patient is stable before transition: glucose values stable for ≥4-6 hours, normal anion gap, resolved acidosis, hemodynamic stability, and a defined nutrition plan. 2
Special Considerations
Bicarbonate therapy is not recommended for routine DKA management and should be reserved only for pH <6.9. 1, 2 Multiple studies show bicarbonate provides no benefit in acidosis resolution time or hospital length of stay. 1
For euglycemic DKA (glucose <250 mg/dL at presentation, often seen with SGLT2 inhibitor use), immediately add dextrose to IV fluids while starting insulin infusion. 5 The fundamental principle remains: insulin therapy must continue until ketoacidosis resolves, not until glucose normalizes. 5
Monitor closely for cerebral edema during treatment, especially with overly aggressive fluid resuscitation. 2 This is particularly important in younger patients and those with severe hyperglycemia at presentation.
For uncomplicated mild-to-moderate DKA, subcutaneous rapid-acting insulin analogs combined with aggressive fluid management may be used in emergency departments or step-down units as a safer and more cost-effective alternative to IV insulin. 1 However, this requires adequate fluid replacement, frequent bedside glucose monitoring, infection treatment if warranted, and appropriate follow-up. 1
Discharge Planning
Identify the outpatient diabetes care provider before discharge and schedule follow-up appointments prior to discharge to improve compliance. 2
Provide education on: 2
- Recognition, prevention, and management of DKA
- Sick-day management (continuing insulin during illness, monitoring ketones, maintaining hydration)
- Hypoglycemia and hyperglycemia recognition and treatment
- Proper insulin administration technique
Verify that all new or adjusted medication prescriptions are filled and reviewed with the patient and family prior to discharge. 2 Ensure adequate outpatient insulin supply. 3
Transmit discharge summaries to the primary care clinician as soon as possible after discharge, including information on medication changes, pending tests, and follow-up needs. 1