What is the management of diabetic ketoacidosis (DKA)?

Management of Diabetic Ketoacidosis

Begin immediate treatment with isotonic saline at 15-20 mL/kg/hour for the first hour, followed by continuous intravenous regular insulin at 0.1 units/kg/hour, and never stop insulin infusion when glucose falls—instead add dextrose to prevent hypoglycemia while continuing insulin until complete resolution of ketoacidosis. 1, 2, 3

Initial Diagnostic Assessment

Obtain the following laboratory studies immediately upon presentation 4, 2:

• Arterial blood gases (venous pH acceptable for monitoring)
• Complete blood count with differential
• Plasma glucose, electrolytes with calculated anion gap
• Blood urea nitrogen, creatinine, osmolality
• Serum ketones (β-hydroxybutyrate preferred over nitroprusside method)
• Urinalysis with ketones
• Electrocardiogram
• Chest X-ray and bacterial cultures (blood, urine, throat) if infection suspected

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, 3

Critical pitfall: The nitroprusside method only measures acetoacetic acid and acetone, not β-hydroxybutyrate (the predominant ketone body in DKA). During treatment, β-hydroxybutyrate converts to acetoacetic acid, which may falsely suggest worsening ketosis—therefore, do not use nitroprusside measurements to guide therapy. 4, 1

Fluid Resuscitation Protocol

First hour: Administer isotonic saline (0.9% NaCl) at 15-20 mL/kg/hour (approximately 1-1.5 L in average adults) to restore circulatory volume and tissue perfusion 1, 2, 3

Subsequent fluid management: Continue fluid replacement based on hydration status, serum electrolyte levels, and urine output, aiming to correct estimated deficits within 24 hours 2, 3

When glucose reaches 250 mg/dL: Switch to 5% dextrose with 0.45-0.75% NaCl to prevent hypoglycemia while continuing insulin therapy to clear ketosis 4, 1, 2

Insulin Therapy

Standard regimen for moderate-to-severe DKA: Start continuous intravenous regular insulin infusion at 0.1 units/kg/hour without an initial bolus 1, 2, 3

Target glucose decline: 50-75 mg/dL per hour 4, 2

If glucose does not fall by 50 mg/dL in the first hour: Check hydration status; if adequate, double the insulin infusion rate every hour until steady glucose decline is achieved 4, 2

Critical management principle: 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, 2, 3

When glucose falls below 250 mg/dL: Do NOT stop insulin—add dextrose-containing fluids and decrease insulin infusion rate to 0.05-0.1 units/kg/hour (3-6 units/hour) 4, 1

Alternative for mild uncomplicated DKA: Subcutaneous rapid-acting insulin analogs combined with aggressive fluid management may be equally effective and safer than IV insulin, with potential cost savings 2, 3

Potassium Management Algorithm

If K+ <3.3 mEq/L: HOLD insulin therapy and aggressively replace potassium until levels reach ≥3.3 mEq/L to prevent life-threatening cardiac arrhythmias and respiratory muscle weakness 2, 3

If K+ 3.3-5.5 mEq/L: Add 20-30 mEq potassium per liter of IV fluid (use 2/3 KCl and 1/3 KPO₄) once adequate urine output is confirmed 4, 1, 2

If K+ >5.5 mEq/L: Withhold potassium initially but monitor closely, as levels will drop rapidly with insulin therapy and acidosis correction 4, 2

Target range throughout treatment: Maintain serum potassium between 4-5 mEq/L 1, 2, 3

Rationale: Despite potential hyperkalemia at presentation, total body potassium depletion is universal in DKA. Insulin therapy, acidosis correction, and volume expansion all decrease serum potassium concentration. Hypokalemia occurs in approximately 50% of patients during treatment and is a leading cause of mortality in DKA. 4, 2, 3

Bicarbonate Therapy

Do NOT administer bicarbonate for pH >6.9-7.0 1, 2, 3

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. 1, 2

Exception: Consider bicarbonate only if pH <6.9, or when pH <7.2 and/or bicarbonate <10 mEq/L pre- and post-intubation to prevent hemodynamic collapse from apnea during intubation 5

Monitoring During Treatment

Blood glucose: Check every 1-2 hours 1

Comprehensive metabolic panel: Draw blood every 2-4 hours for serum electrolytes, glucose, blood urea nitrogen, creatinine, osmolality, and venous pH 4, 1, 2

Venous vs arterial pH: Venous pH is typically 0.03 units lower than arterial pH and is adequate for monitoring; repeat arterial blood gases are generally unnecessary 4, 2

Follow venous pH and anion gap to monitor resolution of acidosis rather than relying on ketone measurements 4, 1

Resolution Criteria

DKA is resolved when ALL of the following parameters are met 1, 2, 3:

• Glucose <200 mg/dL
• Serum bicarbonate ≥18 mEq/L
• Venous pH >7.3
• Anion gap ≤12 mEq/L

Important: Ketonemia typically takes longer to clear than hyperglycemia—do not use ketone clearance as the primary indicator of resolution 4, 1

Transition to Subcutaneous Insulin

Timing is critical: Administer basal insulin (intermediate or long-acting) 2-4 hours BEFORE stopping IV insulin infusion to prevent recurrence of ketoacidosis and rebound hyperglycemia 1, 2, 3

For newly diagnosed patients: Initiate 0.5-1.0 units/kg/day as a multidose regimen of short- and intermediate-/long-acting insulin, with subsequent modification based on glucose testing 4

If patient remains NPO: Continue IV insulin and fluid replacement, supplementing with subcutaneous regular insulin as needed 2

British guideline alternative: Adding subcutaneous insulin glargine along with continuous IV insulin has shown faster DKA resolution and shorter hospital stays compared to IV insulin alone 5

Identification and Treatment of Precipitating Factors

Identify and treat underlying causes 2, 3:

• Infection (most common precipitant)
• Myocardial infarction
• Cerebrovascular accident
• Pancreatitis
• Insulin omission or inadequacy
• SGLT2 inhibitor use (can cause euglycemic DKA)
• Trauma, alcohol abuse, drugs

SGLT2 inhibitor management: Discontinue 3-4 days before any planned surgery to prevent euglycemic DKA 2, 3

Special Consideration: Euglycemic DKA

Diagnostic criteria: pH <7.3, bicarbonate <15 mEq/L, presence of ketonemia/ketonuria, but blood glucose may be normal or only mildly elevated 1

Key management difference: Add dextrose-containing fluids EARLIER in treatment to maintain adequate glucose levels while continuing insulin therapy to clear ketosis 1

Never interrupt insulin infusion when glucose levels fall in euglycemic DKA—this is the most common cause of persistent or worsening ketoacidosis 1, 2

Common Pitfalls to Avoid

• Premature termination of insulin therapy before complete resolution of ketosis (all four resolution criteria must be met) 1, 2
• Interrupting insulin infusion when glucose falls without adding dextrose 1, 2
• Starting insulin therapy when K+ <3.3 mEq/L 2, 3
• Inadequate potassium monitoring and replacement 1, 2
• Relying on nitroprusside ketone measurements to guide therapy 4, 1
• Stopping IV insulin without 2-4 hour overlap with subcutaneous basal insulin 1, 2, 3
• Overly rapid correction of osmolality (increases cerebral edema risk, particularly in children) 2
• Using bicarbonate for pH >6.9-7.0 1, 2, 3