Treatment of Diabetic Ketoacidosis
Begin immediate fluid resuscitation with isotonic saline (0.9% NaCl) at 15-20 mL/kg/hr in the first hour, followed by continuous intravenous regular insulin at 0.1 units/kg/hr after confirming potassium >3.3 mEq/L, while aggressively monitoring and replacing electrolytes to prevent life-threatening complications. 1
Initial Assessment and Diagnostic Confirmation
Before initiating treatment, confirm DKA diagnosis with the triad of:
- Blood glucose >250 mg/dL (though euglycemic DKA can occur, particularly with SGLT2 inhibitor use) 1, 2
- Arterial pH <7.3 and bicarbonate <15 mEq/L 1
- Moderate ketonemia or ketonuria 1
Critical pitfall: Measure β-hydroxybutyrate in blood directly rather than relying on urine ketones, as the nitroprusside method only detects acetoacetic acid and acetone, missing the predominant acid in DKA 1. This is a common error that can lead to underestimation of ketoacidosis severity.
Immediately assess for precipitating factors including infection (most common), medication non-adherence, new-onset diabetes, trauma, or surgery 1, 3.
Fluid Resuscitation Protocol
Hour 1: Administer 15-20 mL/kg/hr (approximately 1-1.5 L) of isotonic saline to restore circulatory volume and tissue perfusion 1, 4. This aggressive initial resuscitation is critical for reversing shock and improving insulin sensitivity.
After Hour 1: Continue at 4-14 mL/kg/hr based on hemodynamic status and hydration assessment 1. The typical total water deficit in DKA is substantial, requiring careful ongoing monitoring.
When glucose reaches 200-250 mg/dL: Add dextrose (D5W or D10W) to IV fluids while continuing insulin infusion 1, 4. This prevents hypoglycemia while allowing continued ketone clearance—a crucial concept many clinicians miss.
Insulin Therapy Algorithm
Do NOT give insulin until potassium is confirmed >3.3 mEq/L to avoid life-threatening cardiac arrhythmias 4, 5.
Start continuous IV regular insulin at 0.1 units/kg/hr after fluid resuscitation has begun 1, 4. Some protocols suggest an initial bolus of 0.1-0.15 U/kg, though this is not universally recommended 6.
If glucose fails to decrease by 50-75 mg/dL in the first hour: Double the insulin infusion rate 1. This indicates insulin resistance requiring more aggressive dosing.
Target glucose reduction: 50-75 mg/dL per hour 4. Faster correction risks cerebral edema, particularly in children.
Continue insulin infusion until DKA resolves: pH >7.3, bicarbonate ≥18 mEq/L, and anion gap normalized 1. Do not stop insulin when glucose normalizes—ketoacidosis may persist despite euglycemia 4.
Electrolyte Replacement Strategy
Potassium Management (Critical)
Monitor potassium every 2-4 hours as insulin therapy drives potassium intracellularly, causing potentially fatal hypokalemia 1, 4.
Begin potassium replacement when serum levels fall below 5.2-5.5 mEq/L (provided adequate urine output exists) 1, 4. Typical replacement is 20-30 mEq per liter of IV fluid 1.
Major pitfall: Severe hypokalemia increases risk of poor outcomes approximately 4-fold 3. Inadequate potassium supplementation is a leading cause of preventable DKA mortality 3.
Phosphate
Monitor levels and consider replacement if <1.0 mg/dL, especially with cardiac dysfunction, anemia, or respiratory depression 1.
Bicarbonate
Generally NOT recommended unless pH <6.9 1. Bicarbonate therapy can paradoxically worsen intracellular acidosis and increase cerebral edema risk.
Monitoring Protocol
Blood glucose: Every 1-2 hours until stable, then every 4 hours 1, 4
Electrolytes, BUN, creatinine, venous pH: Every 2-4 hours 1, 4
Osmolality changes: Should not exceed 3-8 mOsm/kg/hr to prevent cerebral edema 4, 6. This is particularly critical in children and young adults who are at highest risk 1, 4.
Watch for cerebral edema signs: Headache, altered mental status, seizures, bradycardia—treat immediately if suspected 1, 4.
Transition to Subcutaneous Insulin
Once DKA resolves (glucose <200 mg/dL, bicarbonate ≥18 mEq/L, pH >7.3):
- Administer subcutaneous basal insulin 2-4 hours BEFORE discontinuing IV insulin 1, 4
- Continue IV insulin for 1-2 hours after starting subcutaneous insulin to ensure adequate plasma levels and prevent rebound ketoacidosis 1
Critical error to avoid: Never stop IV insulin abruptly without overlapping subcutaneous coverage—this causes rapid recurrence of DKA 4.
Special Considerations and Complications
Hypoglycemia during treatment: The most common preventable complication 3. Prevent by adding dextrose when glucose <200-250 mg/dL while maintaining insulin infusion 1, 5.
Infection as precipitant: Most common trigger (29-40% of cases) 3. Antibiotics were administered in 39% of DKA cases, emphasizing the importance of identifying and treating underlying infections 3.
SGLT2 inhibitor use: Increases risk of euglycemic DKA 7. Educate patients to stop SGLT2 inhibitors and seek urgent care if experiencing nausea, vomiting, abdominal pain, or weakness—even with normal glucose readings 7.
Cardiac complications: In patients with heart failure or pleural effusions, avoid excessive fluid administration which worsens pulmonary edema 4. Consider thoracentesis if effusions significantly compromise respiration 4.
Treatment of Precipitating Factors
Identify and aggressively treat underlying causes 1, 4:
- Infection (most common—obtain cultures, start empiric antibiotics if indicated) 3
- Medication non-adherence (40% of cases) 3
- Myocardial infarction or stroke 6
- New-onset diabetes 1
In-hospital mortality from DKA is approximately 12%, with most deaths related to correctable causes including inadequate potassium supplementation and insulin-induced hypoglycemia 3. This mortality is unacceptable given that these are preventable complications.