Initial 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, obtain critical laboratory studies, and start continuous IV insulin at 0.1 units/kg/hour ONLY after confirming serum potassium is ≥3.3 mEq/L. 1, 2, 3
Immediate Diagnostic Workup
Upon presentation, obtain the following laboratory studies to confirm DKA and guide management 1, 2:
- Plasma glucose (expect >250 mg/dL)
- Arterial blood gas (expect pH <7.30)
- Serum bicarbonate (expect <18 mEq/L)
- Serum and urine ketones (positive)
- Complete metabolic panel with calculated anion gap (expect >10-12 mEq/L)
- Serum osmolality
- Complete blood count with differential
- Electrocardiogram (assess for cardiac effects of electrolyte abnormalities)
- Bacterial cultures (blood, urine, throat) if infection suspected 1, 2
The diagnostic triad requires all three: hyperglycemia >250 mg/dL, arterial pH <7.30, and positive ketones. 1, 2
Fluid Resuscitation (First Priority)
Start isotonic saline (0.9% NaCl) at 15-20 mL/kg/hour (approximately 1-1.5 L in average adults) during the first hour. 1, 2, 3 This aggressive initial fluid replacement is critical to restore tissue perfusion and improve insulin sensitivity. 2
After the first hour, adjust fluid choice based on 1, 2:
- Hydration status assessment
- Serum electrolyte levels (particularly sodium)
- Urine output confirmation
Total fluid replacement should approximate 1.5 times the 24-hour maintenance requirements. 1, 3
Critical Potassium Assessment Before Insulin
This is the most critical safety step: Check serum potassium BEFORE starting insulin. 2, 3
Potassium-Based Insulin Decision Algorithm:
If K+ <3.3 mEq/L: DO NOT start insulin. Delay insulin therapy and aggressively replace potassium with 20-40 mEq/L in IV fluids until K+ reaches ≥3.3 mEq/L to prevent life-threatening cardiac arrhythmias and death. 2, 3
If K+ 3.3-5.5 mEq/L: Safe to start insulin. Add 20-30 mEq/L potassium to IV fluids (use 2/3 KCl and 1/3 KPO₄) once adequate urine output is confirmed. 1, 2, 3
If K+ >5.5 mEq/L: Start insulin but withhold potassium initially. Monitor closely as levels will drop rapidly with insulin therapy. 2
Despite possible hyperkalemia on presentation, total body potassium depletion is universal in DKA, and insulin therapy will further lower serum potassium by driving it intracellularly. 2, 4 Target maintenance of serum potassium between 4-5 mEq/L throughout treatment. 1, 2
Insulin Therapy
For moderate to severe DKA, start continuous IV regular insulin infusion at 0.1 units/kg/hour without an initial bolus. 1, 2 This is the standard of care for critically ill and mentally obtunded patients. 2
Insulin Titration Protocol:
- Target glucose decline: 50-75 mg/dL per hour 1, 2, 3
- If glucose does not fall by 50 mg/dL in the first hour: Check hydration status; if acceptable, double the insulin infusion rate hourly until steady glucose decline is achieved 1, 2
- When glucose reaches 250 mg/dL: Decrease insulin to 0.05-0.1 units/kg/hour AND add dextrose (5% dextrose with 0.45-0.75% NaCl) to IV fluids 1, 2
Critical pitfall to avoid: Never stop insulin when glucose falls below 250 mg/dL. Continue insulin infusion with dextrose supplementation until complete resolution of ketoacidosis, not just glucose normalization. 1, 2 Interruption of insulin when glucose levels fall is a common cause of persistent or worsening ketoacidosis. 1, 2
Alternative for Mild-to-Moderate Uncomplicated DKA:
Subcutaneous rapid-acting insulin analogs combined with aggressive fluid management may be equally effective, safer, and more cost-effective than IV insulin for uncomplicated mild DKA. 2, 3 However, continuous IV insulin remains standard for critically ill patients. 2
Monitoring During Treatment
Glucose Monitoring:
Laboratory Monitoring:
Draw blood every 2-4 hours to assess 1, 2, 3:
- Serum electrolytes (especially potassium)
- Glucose
- Blood urea nitrogen and creatinine
- Serum osmolality
- Venous pH (typically 0.03 units lower than arterial pH)
- Anion gap
Direct measurement of β-hydroxybutyrate in blood is the preferred method for monitoring ketone clearance, as the nitroprusside method only measures acetoacetic acid and acetone, not β-hydroxybutyrate. 1, 2
Bicarbonate Administration
Bicarbonate is NOT recommended for DKA patients with pH >6.9-7.0. 1, 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 criteria 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 achieved. 2
Transition to Subcutaneous Insulin
Administer basal insulin (intermediate or long-acting such as glargine or detemir) 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. 2, 3
Critical pitfall: Stopping IV insulin without prior basal insulin administration is the most common error leading to DKA recurrence. 3
When the patient can eat, start a multiple-dose insulin schedule using a combination of short/rapid-acting and intermediate/long-acting insulin. 2, 3
Identify and Treat Precipitating Factors
The most common precipitating causes include 1, 2, 4, 5:
- Infection (most common—obtain cultures and start appropriate antibiotics)
- Medication noncompliance or insulin omission
- New diagnosis of diabetes
- Myocardial infarction
- Cerebrovascular accident
- Acute pancreatitis
- SGLT2 inhibitor use (can cause euglycemic DKA—discontinue 3-4 days before any planned surgery) 2
Concurrent treatment of the underlying precipitating event is crucial for successful DKA management. 2, 5
Common Pitfalls Summary
- Inadequate potassium monitoring and replacement is a leading cause of mortality in DKA 2
- Starting insulin with K+ <3.3 mEq/L can cause life-threatening arrhythmias 2, 3
- Premature termination of insulin therapy before complete resolution of ketosis leads to DKA recurrence 1, 2
- Stopping IV insulin without prior basal insulin causes rebound hyperglycemia and ketoacidosis 2, 3
- Overly rapid correction of osmolality increases cerebral edema risk, particularly in children 2