Management Protocol for Diabetic Ketoacidosis (DKA)
Begin immediate treatment with isotonic saline (0.9% NaCl) at 15-20 ml/kg/hour for the first hour, followed by continuous IV regular insulin at 0.1 units/kg/hour without a bolus, while closely monitoring potassium and adding replacement once levels fall below 5.5 mEq/L. 1
Diagnostic Criteria
DKA is confirmed when ALL of the following are present: 2, 1, 3
- Blood glucose >250 mg/dL 2, 1
- Arterial pH <7.3 (or venous pH <7.3) 2, 1
- Serum bicarbonate <15 mEq/L 2, 1
- Moderate ketonuria or ketonemia (preferably measured as β-hydroxybutyrate) 1, 3
- Anion gap >10-12 mEq/L (calculated as [Na+] - [Cl- + HCO3-]) 2, 3
Severity Classification
- Mild DKA: pH 7.25-7.30, bicarbonate 15-18 mEq/L, alert mental status 2, 3
- Moderate DKA: pH 7.00-7.24, bicarbonate 10-15 mEq/L, drowsy mental status 2, 3
- Severe DKA: pH <7.00, bicarbonate <10 mEq/L, stupor/coma 2, 3
Initial Laboratory Evaluation
Obtain immediately upon presentation: 2, 1
- Arterial or venous blood gas 2, 1
- Complete metabolic panel (electrolytes, BUN, creatinine, glucose) 2, 1
- Serum β-hydroxybutyrate (preferred over urine ketones) 1, 3
- Calculated anion gap and corrected sodium 2, 1
- Complete blood count with differential 2, 1
- Urinalysis 2, 1
- Electrocardiogram 2, 1
- Blood, urine, and throat cultures if infection suspected 2, 3
- Chest X-ray if clinically indicated 2
Critical pitfall: Do not rely on urine ketones or nitroprusside methods—these only detect acetoacetate and acetone, completely missing β-hydroxybutyrate, the predominant ketoacid in DKA. 1, 3 During treatment, β-hydroxybutyrate converts to acetoacetate, making nitroprusside tests falsely appear worse even as the patient improves. 3
Fluid Resuscitation
Initial Phase (First Hour)
Administer isotonic saline (0.9% NaCl) at 15-20 ml/kg/hour (approximately 1-1.5 liters in average adults) to restore intravascular volume and renal perfusion. 2, 1 This aggressive initial resuscitation is critical regardless of cardiac status, unless overt heart failure is present. 2
Subsequent Fluid Management
After the first hour, fluid choice depends on corrected serum sodium: 2, 1
- If corrected sodium is normal or elevated: Use 0.45% NaCl at 4-14 ml/kg/hour 2
- If corrected sodium is low: Continue 0.9% NaCl at 4-14 ml/kg/hour 2
Correct sodium for hyperglycemia: Add 1.6 mEq/L to measured sodium for every 100 mg/dL glucose above 100 mg/dL. 2, 3
Target total fluid replacement to correct estimated deficits within 24 hours. 2, 1 The induced change in serum osmolality should not exceed 3 mOsm/kg/hour. 2
Critical pitfall: In patients with renal or cardiac compromise, monitor serum osmolality and frequently assess cardiac, renal, and mental status to avoid iatrogenic fluid overload. 2
Insulin Therapy
Initiation
Start continuous IV regular insulin at 0.1 units/kg/hour WITHOUT an initial bolus once potassium is ≥3.3 mEq/L. 1, 3 Do not start insulin if potassium is <3.3 mEq/L—aggressively replace potassium first to prevent fatal cardiac arrhythmias. 3
Dose Adjustment
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. 3
Adding Dextrose
When blood glucose reaches 250 mg/dL, add dextrose 5% to IV fluids while continuing insulin infusion. 1, 4 This is critical—insulin must continue until ketoacidosis resolves, NOT until glucose normalizes. 1, 4
Most critical pitfall: Never discontinue insulin when glucose normalizes. Ketoacidosis will persist or worsen if insulin is stopped prematurely. 4 The therapeutic target is ketone clearance, not glucose normalization. 4
Potassium Management
Assessment Before Insulin
Check potassium before starting insulin—total body potassium is severely depleted in DKA despite potentially normal or elevated initial serum levels due to acidosis-induced extracellular shift. 1, 3
Replacement Protocol
Once renal function is assured (urine output present): 2, 1
- If K+ <3.3 mEq/L: Hold insulin, aggressively replace potassium first 3
- If K+ 3.3-5.5 mEq/L: Add 20-30 mEq/L potassium to IV fluids (2/3 KCl and 1/3 KPO4) 2, 1
- If K+ >5.5 mEq/L: Do not add potassium initially, but monitor closely as levels will fall rapidly with insulin therapy 1, 3
Target serum potassium 4-5 mEq/L throughout treatment. 3
Typical total body potassium deficit in DKA is 3-5 mEq/kg body weight. 2
Monitoring During Treatment
Frequency
- Blood glucose: Every 1 hour 1, 3
- Electrolytes, BUN, creatinine, osmolality, venous pH: Every 2-4 hours until stable 2, 1, 3
- Anion gap: Every 2-4 hours to assess acidosis resolution 1, 3
- β-hydroxybutyrate: Every 2-4 hours (if available) 3
Important note: After initial diagnosis, venous pH adequately monitors acidosis resolution—repeated arterial blood gases are unnecessary. 3 Venous pH is typically 0.03 units lower than arterial pH. 3
Resolution Criteria
DKA is resolved when ALL of the following are met: 1, 3
- Blood glucose <200 mg/dL 1, 3
- Serum bicarbonate ≥15-18 mEq/L 1, 3
- Venous pH >7.3 1, 3
- Anion gap ≤12 mEq/L 1, 3
Ketonemia typically takes longer to clear than hyperglycemia, requiring continued monitoring even after glucose normalizes. 3
Transition to Subcutaneous Insulin
Administer basal subcutaneous insulin 2-4 hours BEFORE stopping IV insulin to prevent rebound hyperglycemia and recurrent ketoacidosis. 1, 4, 3 This overlap period is essential—stopping IV insulin without prior subcutaneous dosing is a common cause of DKA recurrence. 3
Special Considerations
Bicarbonate Therapy
Bicarbonate is NOT recommended for routine DKA management. 3 Consider only if pH <6.9, as bicarbonate can worsen ketosis, cause hypokalemia, and increase cerebral edema risk. 5 If used pre- or post-intubation when pH <7.2 or bicarbonate <10 mEq/L, it may prevent hemodynamic collapse from apnea during intubation. 5
Euglycemic DKA
In patients presenting with DKA criteria but glucose <250 mg/dL (common with SGLT2 inhibitor use): 4
- Immediately add dextrose 5-10% to IV fluids at presentation 4
- Continue insulin infusion until ketoacidosis resolves, not until glucose normalizes 4
- This prevents hypoglycemia while allowing continued ketone clearance 4
Cerebral Edema Risk
More common in children but can occur in adults. Risk factors include: 6, 5
- Severe acidosis at presentation 6
- Greater hypocapnia (after adjusting for acidosis) 6
- Higher BUN at presentation 6
- Bicarbonate treatment 6
- Overly rapid correction of hyperglycemia and hyperosmolality 1, 5
Monitor closely for altered mental status, headache, or neurological deterioration during treatment. 5
Precipitating Factors
Identify and treat underlying causes: 7, 8
- Infections (most common) 7
- New diagnosis of diabetes 7
- Insulin nonadherence 7
- SGLT2 inhibitor use 7
- Myocardial infarction, stroke, pancreatitis 8
Failure to identify and treat the precipitating cause leads to DKA recurrence. 3
Typical Electrolyte Deficits in DKA
Total body deficits per kg body weight: 2