Management 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 intravenous regular insulin infusion at 0.1 units/kg/hour without an initial bolus, while aggressively monitoring and replacing potassium to prevent life-threatening hypokalemia. 1, 2
Initial Assessment and Laboratory Evaluation
Obtain the following labs immediately upon presentation 1, 2:
- Plasma glucose, blood urea nitrogen, creatinine
- Serum ketones (β-hydroxybutyrate preferred over nitroprusside method) 2
- Electrolytes with calculated anion gap
- Serum osmolality
- Arterial blood gases
- Complete blood count with differential
- Urinalysis with urine ketones
- Electrocardiogram (continuous cardiac monitoring in severe DKA) 2
Diagnostic criteria confirming DKA: plasma glucose >250 mg/dL, arterial pH <7.30, serum bicarbonate <18 mEq/L, and positive serum/urine ketones 1
Fluid Resuscitation Protocol
First hour: Administer isotonic saline (0.9% NaCl) at 15-20 mL/kg/hour to restore intravascular volume and renal perfusion 1, 2. Recent evidence suggests balanced electrolyte solutions may achieve faster DKA resolution, though isotonic saline remains the standard 3.
Subsequent fluid management: Continue fluid replacement to correct estimated deficits within 24 hours, targeting 1.5-2 times the 24-hour maintenance requirements 1. Change serum osmolality should not exceed 3 mOsm/kg/hour to prevent cerebral edema 2.
Insulin Therapy
Start continuous IV regular insulin at 0.1 units/kg/hour without an initial bolus 1. The American Diabetes Association recommends this approach as standard of care for critically ill patients 4.
If plasma 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/hour 1, 2.
Once glucose reaches 200 mg/dL, add dextrose to IV fluids while continuing insulin infusion to clear ketones and resolve acidosis 2. Target blood glucose of 100-180 mg/dL during treatment 2.
Critical caveat: Some evidence suggests adding low-dose subcutaneous basal insulin analog (e.g., glargine) alongside IV insulin may prevent rebound hyperglycemia and shorten hospital stays, though this is not yet standard practice in all guidelines 4, 3.
Electrolyte Management: Potassium is Critical
Potassium monitoring is absolutely essential as total body potassium is depleted despite potentially normal or elevated initial levels due to acidosis 1, 2.
Before starting insulin:
- If serum potassium <3.3 mEq/L: DELAY insulin therapy until potassium is restored above 3.3 mEq/L to prevent life-threatening arrhythmias, cardiac arrest, and respiratory muscle weakness 2
Once insulin is started:
- When potassium falls below 5.5 mEq/L (with adequate urine output): Add 20-40 mEq/L potassium to IV fluids 2
- Maintain serum potassium between 4-5 mEq/L 2
- Use combination of 2/3 KCl and 1/3 KPO4 2
Phosphate replacement: Generally not recommended routinely as studies show no benefit on clinical outcomes 2. Consider only if cardiac dysfunction, anemia, respiratory depression, or serum phosphate <1.0 mg/dL 2.
Bicarbonate therapy: NOT recommended for pH >7.0 as it provides no benefit and may worsen outcomes 2. Consider only if pH <6.9 (administer 100 mmol sodium bicarbonate in 400 mL sterile water at 200 mL/h) or pH 6.9-7.0 (50 mmol in 200 mL at 200 mL/h) 2. Bicarbonate risks include worsening ketosis, hypokalemia, and cerebral edema 3.
Monitoring During Treatment
Blood glucose: Check every 1-2 hours 1
Comprehensive metabolic panel: Draw blood every 2-4 hours for electrolytes, glucose, BUN, creatinine, osmolality, and venous pH 1, 2
Follow venous pH and anion gap to monitor resolution of acidosis (venous pH typically 0.03 units lower than arterial pH) 2
Identifying and Treating Precipitating Causes
Obtain cultures (blood, urine, other sites as indicated) and start appropriate antibiotics if infection suspected 2. Common precipitants include 5:
- Infections (most common)
- New diagnosis of diabetes
- Insulin nonadherence
- SGLT2 inhibitors (can cause euglycemic DKA—discontinue 3-4 days before surgery) 1, 2
Search for myocardial infarction, stroke, or other acute stressors 4.
Resolution Criteria and Transition to Subcutaneous Insulin
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 protocol: Administer basal insulin (intermediate or long-acting) 2-4 hours BEFORE stopping IV insulin to prevent recurrence of ketoacidosis and rebound hyperglycemia 4, 1, 2. This timing is critical and non-negotiable.
For newly diagnosed patients, initiate multidose regimen at approximately 0.5-1.0 units/kg/day using combination of short/rapid-acting and intermediate/long-acting insulin 2.
Critical Complications to Monitor
Cerebral edema: Rare (0.7-1.0% in children) but frequently fatal 2. Risk factors include 6:
- Severe acidosis at presentation
- Greater hypocapnia (after adjusting for acidosis)
- Higher BUN at presentation
- Bicarbonate treatment
- Rapid overcorrection of hyperglycemia
Prevention: Avoid rapid osmolality changes (≤3 mOsm/kg/hour), use judicious fluid replacement, and avoid bicarbonate unless absolutely necessary 2, 3.
Hypokalemia: Most dangerous complication during treatment—can cause fatal arrhythmias 1, 2, 7.
Special Considerations for Mild DKA
For uncomplicated mild DKA, subcutaneous rapid-acting insulin analogs may be used in emergency department or step-down units with aggressive fluid management, which may be safer and more cost-effective than IV insulin 4. However, this requires adequate fluid replacement, frequent glucose monitoring, and appropriate follow-up 4.
Airway Management in Critically Ill Patients
For impending respiratory failure: Intubation and mechanical ventilation are recommended 3. Do NOT use BiPAP due to aspiration risk 3. Consider IV bicarbonate pre- and post-intubation if pH <7.2 or bicarbonate <10 mEq/L to prevent hemodynamic collapse from apnea during intubation 3.