Initial Management of Diabetic Ketoacidosis in the Inpatient Setting
Begin immediate treatment with isotonic saline (0.9% NaCl) at 15-20 mL/kg/hour for the first hour, followed by continuous intravenous regular insulin at 0.1 units/kg/hour once adequate hydration and potassium levels are confirmed. 1, 2
Diagnostic Confirmation
Before initiating treatment, confirm DKA with the following criteria 1:
- Blood glucose >250 mg/dL (though euglycemic DKA can occur, particularly with SGLT-2 inhibitor use) 3, 4
- Arterial pH <7.3 1
- Serum bicarbonate <15-18 mEq/L 1, 2
- Presence of ketonemia or ketonuria 1
- Anion gap >10-12 mEq/L 1, 4
Obtain the following labs immediately 1, 2:
- Plasma glucose, electrolytes with calculated anion gap, serum ketones (β-hydroxybutyrate preferred over nitroprusside method)
- Blood urea nitrogen, creatinine, osmolality
- Arterial or venous blood gas
- Complete blood count with differential
- Urinalysis with urine ketones
- Electrocardiogram
- If infection suspected: blood cultures, urine cultures, throat cultures, and chest X-ray 1
Step-by-Step Treatment Algorithm
1. Fluid Resuscitation (FIRST PRIORITY)
- Administer isotonic saline (0.9% NaCl) at 15-20 mL/kg/hour (approximately 1-1.5 L in average adult)
- This restores intravascular volume and improves renal perfusion before insulin administration
After Hour 1: 1
- Continue IV fluids based on hydration status, electrolyte levels, and urine output
- Aim to correct estimated fluid deficits within 24 hours
- When glucose reaches 250 mg/dL: Switch to 5% dextrose with 0.45-0.75% NaCl to prevent hypoglycemia while continuing insulin 1, 2
2. Insulin Therapy (Start AFTER initial fluid resuscitation)
- Start continuous IV regular insulin at 0.1 units/kg/hour without an initial bolus
- Do NOT start insulin until adequate hydration is achieved
- If glucose does not fall by 50 mg/dL in the first hour, check hydration status
- If hydration is adequate, double the insulin infusion rate hourly until steady glucose decline of 50-75 mg/hour is achieved
- When glucose reaches 250 mg/dL, decrease insulin to 0.05-0.1 units/kg/hour but never stop insulin 2
Critical Point: Continue insulin infusion until complete resolution of ketoacidosis (pH >7.3, bicarbonate ≥18 mEq/L, anion gap ≤12 mEq/L) regardless of glucose levels 1, 3, 2. This is the most common pitfall—stopping insulin when glucose normalizes before ketosis resolves.
3. Potassium Replacement (ESSENTIAL)
Before starting insulin, check potassium level: 1, 2
- If K+ <3.3 mEq/L: Hold insulin and give potassium replacement first
- If K+ 3.3-5.3 mEq/L: Add 20-30 mEq/L potassium to IV fluids (2/3 KCl and 1/3 KPO₄)
- If K+ >5.3 mEq/L: Hold potassium replacement but recheck frequently
Target: Maintain serum potassium between 4-5 mmol/L throughout treatment 1, 2. Insulin drives potassium intracellularly, causing potentially life-threatening hypokalemia.
4. Monitoring Protocol
- Blood glucose
- Serum electrolytes (especially potassium)
- Venous pH (typically 0.03 units lower than arterial pH)
- Anion gap
- Blood urea nitrogen, creatinine, osmolality
Preferred ketone monitoring: Direct measurement of β-hydroxybutyrate rather than nitroprusside method, which only detects acetoacetic acid and acetone 1, 3
5. Bicarbonate Administration
Generally NOT recommended for pH >6.9-7.0 1, 2. Bicarbonate can worsen hypokalemia, increase risk of cerebral edema, and paradoxically worsen ketosis 5, 6.
Exception: Consider if pH <6.9 or in peri-intubation period to prevent hemodynamic collapse 5
Resolution Criteria and Transition
DKA is resolved when ALL of the following are met: 1, 2
- Glucose <200 mg/dL
- Serum bicarbonate ≥18 mEq/L
- Venous pH >7.3
- Anion gap ≤12 mEq/L
Transition to subcutaneous insulin: 3, 2
- Administer basal insulin (long-acting) 2-4 hours before stopping IV insulin infusion
- This overlap prevents rebound ketoacidosis
- Patient must be able to eat before transitioning
Critical Pitfalls to Avoid
Stopping IV insulin when glucose normalizes before ketoacidosis resolves—this causes recurrent or worsening DKA 1, 3, 2
Failing to add dextrose when glucose falls below 250 mg/dL while continuing insulin therapy 1, 3
Inadequate potassium monitoring and replacement—insulin therapy causes rapid intracellular potassium shift leading to life-threatening hypokalemia 1, 2
Premature termination of insulin therapy before complete resolution of all metabolic parameters 1, 3, 2
Using nitroprusside method alone to measure ketones, which misses β-hydroxybutyrate, the predominant ketone body 1, 3
Overly rapid correction in younger patients increases cerebral edema risk 5, 7