Management of Diabetic Ketoacidosis
Begin with aggressive fluid resuscitation using isotonic saline at 15-20 mL/kg/h for the first hour, followed by continuous IV regular insulin at 0.1 units/kg/hour (after excluding hypokalemia), and add potassium replacement once levels fall below 5.5 mEq/L with adequate urine output. 1, 2
Initial Assessment and Diagnosis
Obtain the following laboratory studies immediately upon presentation 1, 2:
- Plasma glucose, blood urea nitrogen, creatinine, serum ketones
- Electrolytes with calculated anion gap and osmolality
- Arterial blood gases (venous pH is adequate for ongoing monitoring)
- Complete blood count with differential
- Urinalysis and electrocardiogram
- Bacterial cultures if infection is suspected 1
Direct measurement of β-hydroxybutyrate in blood is the preferred monitoring method, as the nitroprusside method only measures acetoacetic acid and acetone, potentially misleading clinicians during treatment when β-hydroxybutyrate converts to acetoacetic acid 3, 1, 2.
Correct serum sodium for hyperglycemia by adding 1.6 mEq to the sodium value for each 100 mg/dL glucose above 100 mg/dL 3, 4.
Fluid Resuscitation
Start with balanced electrolyte solutions or 0.9% saline at 15-20 mL/kg/h during the first hour to restore circulatory volume and tissue perfusion 1, 2. This initial bolus should precede insulin administration by 1-2 hours 5.
Continue fluid replacement to correct estimated deficits within 24 hours, ensuring the induced change in serum osmolality does not exceed 3 mOsm/kg/h 1, 4. For pediatric patients, use 1.5 times the 24-hour maintenance requirements (5 mL/kg/h); do not exceed twice the maintenance requirement 3, 1.
Monitor fluid input/output, hemodynamic parameters, and clinical examination continuously to assess progress 1, 4.
Insulin Therapy
Administer IV regular insulin at 0.1 units/kg/hour as a continuous infusion after confirming potassium is >3.3 mEq/L 1, 2. The American Diabetes Association now recommends starting continuous IV insulin without an initial bolus as standard of care for critically ill patients 1.
If plasma glucose does not fall by 50 mg/dL in the first hour, check hydration status; if acceptable, double the insulin infusion every hour until achieving a steady glucose decline of 50-75 mg/h 3, 1, 2.
When plasma glucose reaches 250 mg/dL, decrease insulin infusion to 0.05-0.1 units/kg/h and add dextrose (5-10%) to IV fluids 3. Continue insulin infusion until acidosis resolves, not just until glucose normalizes 3, 1.
Alternative Approach for Mild DKA
For uncomplicated mild DKA in emergency departments or step-down units, subcutaneous rapid-acting insulin analogs may be used with aggressive fluid management, which may be safer and more cost-effective than IV insulin 1. Give an initial "priming" dose of regular insulin 0.4-0.6 U/kg (half IV bolus, half subcutaneous/intramuscular), then 0.1 U/kg/h subcutaneously or intramuscularly 3.
Electrolyte Management
Potassium Replacement
Begin potassium replacement immediately once serum levels fall below 5.5 mEq/L, assuming adequate urine output 3, 1, 2. Add 20-40 mEq/L potassium to each liter of infusion fluid (2/3 KCl and 1/3 KPO4) to maintain serum concentration at 4-5 mEq/L 3, 1.
Critical pitfall: If significant hypokalemia (<3.3 mEq/L) is present initially, delay insulin treatment until potassium is restored to avoid life-threatening arrhythmias, cardiac arrest, and respiratory muscle weakness 1. Insulin drives potassium intracellularly, potentially precipitating fatal hypokalemia 4.
Bicarbonate Therapy
Do not administer bicarbonate in DKA patients with pH >7.0, as studies have failed to show beneficial effects on clinical outcomes 1. For adult patients with pH <6.9, give 100 mmol sodium bicarbonate in 400 mL sterile water at 200 mL/h; for pH 6.9-7.0, give 50 mmol in 200 mL at 200 mL/h 1.
Phosphate Replacement
Routine phosphate replacement has not shown beneficial effects on clinical outcomes 1. Consider phosphate replacement (20-30 mEq/L potassium phosphate) only in patients with cardiac dysfunction, anemia, respiratory depression, or serum phosphate <1.0 mg/dL 1, 4.
Monitoring During Treatment
Draw blood every 2-4 hours for serum electrolytes, glucose, blood urea nitrogen, creatinine, osmolality, and venous pH 3, 1, 4. Venous pH (typically 0.03 units lower than arterial pH) and anion gap adequately monitor resolution of acidosis; repeat arterial blood gases are generally unnecessary 3, 1, 4.
Maintain continuous cardiac monitoring in severe DKA to detect arrhythmias early 1.
Target blood glucose of 100-180 mg/dL during treatment 1.
Resolution Criteria
DKA is resolved when all of the following are met 1:
- Glucose <200 mg/dL
- Serum bicarbonate ≥18 mEq/L
- Venous pH >7.3
- Anion gap ≤12 mEq/L
Transition to Subcutaneous Insulin
Administer basal insulin (intermediate or long-acting) 2-4 hours BEFORE stopping IV insulin to prevent recurrence of ketoacidosis and rebound hyperglycemia 1, 2, 4. This overlap is critical and commonly missed.
When DKA is resolved and the patient can eat, transition to a multiple-dose regimen using short/rapid-acting and intermediate/long-acting insulin 1. For newly diagnosed patients, initiate 0.5-1.0 units/kg/day as a multidose regimen 3, 1.
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 1.
Identification and Treatment of Precipitating Causes
Search for and treat underlying triggers 3, 1, 2:
- Infection (obtain bacterial cultures of urine, blood, and other sites; administer appropriate antibodies)
- Myocardial infarction or stroke
- Medication non-compliance or insulin omission
- SGLT2 inhibitors (discontinue 3-4 days before surgery to prevent euglycemic DKA) 1
Critical Complications to Monitor
Cerebral Edema
Cerebral edema is rare (0.7-1.0% in children) but frequently fatal 1. Higher BUN at presentation is a risk factor 1. Monitor for lethargy, behavioral changes, seizures, incontinence, pupillary changes, bradycardia, and respiratory arrest 4, 5.
Prevent cerebral edema by avoiding overly rapid correction of fluid deficits, hyperglycemia, and osmolality, particularly in pediatric patients 2, 4. If cerebral edema develops, treat with mannitol or hypertensive saline infusion and provide ventilatory support as needed 5, 6.
Other Complications
Monitor for hypoglycemia, hypokalemia, and hyperchloremic metabolic acidosis from overzealous insulin treatment, inadequate potassium replacement, or excessive saline administration 4.
Special Populations
Children and Adolescents
In youth with ketoacidosis, initiate subcutaneous or IV insulin immediately to rapidly correct hyperglycemia and metabolic derangement 3, 2. Once acidosis resolves, initiate metformin while continuing subcutaneous insulin 3.
Fluid infusion should precede insulin administration by 1-2 hours 5. Use 0.45% saline after initial bolus, calculated to supply maintenance and replace 5-10% dehydration 5.
Type 2 Diabetes
Some type 2 diabetic patients may be discharged on oral agents and dietary therapy after DKA resolution 3.
Discharge Planning
Develop a structured discharge plan tailored to the individual patient to reduce length of hospital stay and readmission rates 3, 1, 2.
Schedule an outpatient follow-up visit within 1 month of discharge for all patients; if glycemic medications are changed or glucose control is not optimal, schedule within 1-2 weeks 3.
Provide education on recognition, prevention, and management of DKA, including how to adjust insulin during illness, monitor glucose and ketone levels, and the importance of medication compliance 1, 2, 7.