Initial Treatment of Diabetic Ketoacidosis (DKA)
Begin immediate fluid resuscitation with isotonic saline (0.9% NaCl) at 15-20 mL/kg/hour for the first hour, followed by continuous IV regular insulin infusion at 0.1 units/kg/hour once serum potassium is ≥3.3 mEq/L. 1, 2
Immediate Initial Assessment
Obtain stat laboratory evaluation including: 1, 2
- Plasma glucose, arterial or venous blood gases
- Complete metabolic panel with calculated anion gap
- Serum ketones (β-hydroxybutyrate preferred if available)
- Electrolytes, osmolality
- Complete blood count with differential
- Electrocardiogram
- Urinalysis with urine ketones
Critical diagnostic criteria for DKA: blood glucose >250 mg/dL, arterial pH <7.3, serum bicarbonate <15 mEq/L, and presence of ketonemia or ketonuria. 2
Identify precipitating factors immediately: infection (obtain bacterial cultures of urine, blood, throat if suspected), myocardial infarction, stroke, pancreatitis, trauma, insulin omission, or SGLT2 inhibitor use. 1, 2
Fluid Resuscitation Protocol
Start with isotonic saline (0.9% NaCl) at 15-20 mL/kg body weight/hour (approximately 1-1.5 L in average adult) during the first hour. 1, 2 This aggressive initial fluid replacement is critical to restore tissue perfusion and improve insulin sensitivity. 2
After the first hour, adjust fluid rate based on hydration status, serum sodium, and urine output, with total fluid replacement approximating 1.5 times the 24-hour maintenance requirements. 1, 3
When serum glucose reaches 250 mg/dL, switch to 5% dextrose with 0.45-0.75% NaCl to prevent hypoglycemia while continuing insulin therapy until DKA resolves. 2 This is a critical step—do not stop insulin when glucose normalizes, as this is a common cause of persistent or worsening ketoacidosis. 2
Potassium Management (Critical Safety Step)
DO NOT start insulin if serum potassium is <3.3 mEq/L—this is an absolute contraindication. 1, 2 Insulin will further lower serum potassium and can cause life-threatening cardiac arrhythmias, respiratory muscle weakness, and death. 1, 3
- Delay insulin therapy completely
- Aggressively replace potassium until levels reach ≥3.3 mEq/L
- Continue isotonic saline and obtain ECG to assess cardiac effects
- Add 20-40 mEq/L potassium to IV fluids once renal function confirmed
- Add 20-30 mEq potassium per liter of IV fluid (use 2/3 KCl and 1/3 KPO₄)
- Proceed with insulin therapy
- Target serum potassium of 4-5 mEq/L throughout treatment
If K+ >5.5 mEq/L: 2
- Withhold potassium initially
- Monitor closely as levels will drop rapidly with insulin therapy
- Begin replacement once levels fall below 5.5 mEq/L
Despite normal or elevated initial potassium, total body potassium depletion is universal in DKA, and inadequate monitoring/replacement is a leading cause of mortality. 2
Insulin Therapy
Start continuous IV regular insulin infusion at 0.1 units/kg/hour (without initial bolus for critically ill/intubated patients; with 0.1 units/kg IV bolus for others) once K+ ≥3.3 mEq/L. 1, 2, 3 Continuous IV insulin is the standard of care for moderate to severe DKA and all critically ill or mentally obtunded patients. 2, 3
Target glucose decline of 50-75 mg/dL per hour. 1, 2 If plasma glucose does not fall by 50 mg/dL in the first hour, check hydration status; if acceptable, double the insulin infusion rate every hour until steady glucose decline is achieved. 2
Continue insulin infusion until complete resolution of ketoacidosis (pH >7.3, serum bicarbonate ≥18 mEq/L, anion gap ≤12 mEq/L) regardless of glucose levels. 1, 2 Premature termination of insulin before complete resolution of ketosis is a common pitfall leading to DKA recurrence. 2
Alternative for Mild-Moderate Uncomplicated DKA
For uncomplicated mild-to-moderate DKA in non-critically ill patients, subcutaneous rapid-acting insulin analogs at 0.15 U/kg every 2-3 hours combined with aggressive fluid management may be equally effective, safer, and more cost-effective than IV insulin. 2, 4 However, continuous IV insulin remains standard for severe DKA, critically ill patients, or those who are mentally obtunded. 2, 3
Monitoring Protocol
Draw blood every 2-4 hours for: 1, 2, 3
- Serum electrolytes, glucose
- Blood urea nitrogen, creatinine
- Osmolality, venous pH
- β-hydroxybutyrate (preferred marker if available)
Check blood glucose every 2-4 hours. 1 Follow venous pH (typically 0.03 units lower than arterial pH) and anion gap to monitor resolution of acidosis. 2
Bicarbonate Administration
Bicarbonate is NOT recommended for DKA patients with pH >6.9-7.0. 2 Studies show no difference in resolution of acidosis or time to discharge with bicarbonate use, and it may worsen ketosis, cause hypokalemia, and increase cerebral edema risk. 2
Resolution Criteria
DKA is resolved when ALL of the following are met: 1, 2, 3
- Glucose <200 mg/dL
- Serum bicarbonate ≥18 mEq/L
- Venous pH >7.3
- Anion gap ≤12 mEq/L
Target glucose between 150-200 mg/dL until these resolution parameters are met. 2
Transition to Subcutaneous Insulin
Once DKA is resolved and the patient can eat, administer basal insulin (glargine, detemir, or NPH) 2-4 hours BEFORE stopping the IV insulin infusion. 1, 2, 3 This overlap period is essential to prevent recurrence of ketoacidosis and rebound hyperglycemia—stopping IV insulin without prior basal insulin administration is the most common error leading to DKA recurrence. 1
For patients who remain NPO (intubated), continue IV insulin and supplement with subcutaneous regular insulin every 4 hours as needed. 3
When the patient can eat, start a multiple-dose insulin schedule using a combination of short/rapid-acting and intermediate/long-acting insulin. 1, 2
Common Pitfalls to Avoid
- Starting insulin when K+ <3.3 mEq/L (can cause fatal arrhythmias) 1, 2
- Stopping insulin when glucose normalizes instead of continuing until ketoacidosis resolves 2
- Failing to add dextrose when glucose falls below 250 mg/dL while continuing insulin 2
- Inadequate potassium monitoring and replacement 2
- Stopping IV insulin without prior basal insulin administration 1, 2
- Overly rapid correction of osmolality (increases cerebral edema risk, especially in children) 2