What is the protocol for managing Diabetic Ketoacidosis (DKA)?

Management Protocol for Diabetic Ketoacidosis (DKA)

Begin immediate fluid resuscitation with isotonic saline at 15-20 mL/kg/hour during the first hour, followed by continuous IV regular insulin at 0.1 units/kg/hour without a bolus, while aggressively monitoring and replacing potassium to prevent life-threatening arrhythmias. 1, 2

Initial Diagnosis and Assessment

Diagnostic Criteria

DKA requires all three components to be present: 3, 1, 2

• Blood glucose >250 mg/dL (though euglycemic DKA can occur with normal glucose, especially with SGLT2 inhibitors) 1, 4
• Arterial or venous pH <7.3 3, 1, 2
• Serum bicarbonate <15 mEq/L 3, 1, 2
• Moderate ketonuria or ketonemia (preferably measured as β-hydroxybutyrate, not nitroprusside method) 1, 2
• Anion gap >10-12 mEq/L calculated as [Na+] - ([Cl-] + [HCO3-]) 3, 2

Severity Classification

Categorize severity to guide monitoring intensity: 3, 2

• Mild DKA: pH 7.25-7.30, bicarbonate 15-18 mEq/L, alert mental status
• Moderate DKA: pH 7.00-7.24, bicarbonate 10-15 mEq/L, drowsy mental status
• Severe DKA: pH <7.00, bicarbonate <10 mEq/L, stupor/coma (requires ICU with central venous and intra-arterial monitoring)

Initial Laboratory Workup

Obtain immediately: 1, 2

• Arterial or venous blood gas (venous pH is 0.03 units lower than arterial and adequate for monitoring after initial diagnosis)
• Complete metabolic panel with calculated anion gap
• Serum β-hydroxybutyrate (not nitroprusside-based ketone tests)
• Complete blood count with differential
• Urinalysis
• Blood urea nitrogen, creatinine, osmolality
• Electrocardiogram
• Bacterial cultures (blood, urine, throat) if infection suspected

Critical pitfall: Correct serum sodium for hyperglycemia by adding 1.6 mEq/L for every 100 mg/dL glucose above 100 mg/dL before assessing true sodium status. 3, 2

Fluid Resuscitation

First Hour

Administer isotonic saline (0.9% NaCl) at 15-20 mL/kg/hour (approximately 1-1.5 liters in average adult) to restore intravascular volume and renal perfusion. 3, 1, 2 This aggressive initial resuscitation is critical even in patients with cardiac compromise, though closer monitoring is required. 1

Subsequent Fluid Management

After the first hour, fluid choice depends on corrected serum sodium: 3, 1

• If corrected sodium is normal or elevated: Use 0.45% NaCl at 4-14 mL/kg/hour
• If corrected sodium is low: Continue 0.9% NaCl at 4-14 mL/kg/hour
• Target: Correct estimated fluid deficits (typically 6-9 liters total body water deficit) within 24 hours 3, 1

Monitor for fluid overload, particularly in patients with renal or cardiac disease, by assessing blood pressure, urine output, and clinical examination. 1, 2

Insulin Therapy

Initiation

Do not start insulin until potassium is ≥3.3 mEq/L to avoid fatal cardiac arrhythmias. 2 If potassium <3.3 mEq/L, delay insulin and aggressively replace potassium first. 2

Start continuous IV regular insulin at 0.1 units/kg/hour without an initial bolus. 1, 2, 5 The bolus-free approach is now standard per American Diabetes Association guidelines. 1

Insulin Titration

• If 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/dL per hour 2
• Never stop insulin based on glucose levels alone—continue until ketoacidosis resolves 1, 4

Dextrose Addition

When serum glucose reaches 250 mg/dL (or if glucose is already <250 mg/dL at presentation in euglycemic DKA), add dextrose 5-10% to IV fluids while continuing insulin infusion. 1, 4 This prevents hypoglycemia while allowing continued ketone clearance, which is the actual therapeutic target. 4

Critical pitfall: In euglycemic DKA (increasingly common with SGLT2 inhibitors), immediately add dextrose to fluids while maintaining insulin infusion—discontinuing insulin when glucose normalizes is the most dangerous error. 4, 6

Electrolyte Management

Potassium Replacement

Total body potassium is severely depleted (3-5 mEq/kg deficit) despite potentially normal or elevated initial serum levels due to acidosis-induced extracellular shift. 3, 1, 2

Replacement protocol based on serum potassium: 1, 2

• <3.3 mEq/L: Hold insulin, aggressively replace potassium first
• 3.3-5.5 mEq/L: Add 20-30 mEq/L potassium to IV fluids (2/3 KCl and 1/3 KPO4)
• >5.5 mEq/L: Do not add potassium, recheck in 2 hours

Continue potassium supplementation until patient is stable and can tolerate oral intake. 3, 1 Target serum potassium 4-5 mEq/L throughout treatment. 2

Phosphate, Magnesium, and Calcium

Typical deficits include phosphate (5-7 mEq/kg), magnesium (1-2 mEq/kg), and calcium (1-2 mEq/kg). 3, 1 Replace as part of potassium supplementation (1/3 as KPO4) and monitor levels every 2-4 hours. 1, 2

Bicarbonate Therapy

Bicarbonate is NOT recommended for routine DKA management and may worsen outcomes by causing hypokalemia, paradoxical CNS acidosis, and cerebral edema. 1, 7

Consider bicarbonate only if: 1, 7

• pH <6.9, or
• pH <7.2 with hemodynamic instability or impending intubation to prevent metabolic collapse during apnea

Monitoring During Treatment

Frequency

• Blood glucose: Every 1 hour 1, 2
• Electrolytes, BUN, creatinine, osmolality: Every 2-4 hours until stable 1, 2
• Venous pH and anion gap: Every 2-4 hours to monitor acidosis resolution (arterial blood gases not needed after initial diagnosis) 1, 2
• β-hydroxybutyrate: Every 2-4 hours (superior to urine ketones, which paradoxically worsen as patient improves) 2, 4

Monitoring for Complications

Watch for: 1, 2

• Cerebral edema: Especially with overly rapid correction of hyperglycemia and hyperosmolality (more common in children but can occur in adults)
• Hypokalemia: Leading to cardiac arrhythmias
• Hypoglycemia: From inadequate dextrose supplementation
• Fluid overload: Particularly in renal or cardiac disease

Resolution Criteria

DKA is resolved when ALL of the following are met: 1, 2, 4

• Blood glucose <200 mg/dL
• Serum bicarbonate ≥15-18 mEq/L
• Venous pH >7.3
• Anion gap ≤12 mEq/L (normalized)

Do not stop insulin until all criteria are met—ketoacidosis takes longer to clear than hyperglycemia. 1, 4

Transition to Subcutaneous Insulin

Administer basal subcutaneous insulin (long-acting) 2-4 hours before stopping IV insulin to prevent rebound hyperglycemia and recurrent ketoacidosis. 1, 4 This overlap period is essential for smooth transition. 1

Identification and Treatment of Precipitating Causes

The most common triggers are: 6, 8

• Infections (most common)
• New diagnosis of diabetes
• Insulin nonadherence or omission
• SGLT2 inhibitor use (causes euglycemic DKA)
• Acute coronary syndrome or stroke
• Pancreatitis
• Medications (corticosteroids, antipsychotics)

Failure to identify and treat the underlying cause leads to recurrence. 1, 6

Special Considerations

Euglycemic DKA

Increasingly common with SGLT2 inhibitors—maintain high suspicion when pH <7.3 and ketones present despite glucose <250 mg/dL. 4, 6 Immediately add dextrose to fluids while continuing insulin. 4

Severe DKA Requiring ICU

Patients with pH <7.0, altered mental status, or hemodynamic instability require ICU admission with central venous and intra-arterial monitoring. 2, 7

Airway Management

For impending respiratory failure, avoid BiPAP due to aspiration risk. 7 Proceed with intubation and mechanical ventilation, considering bicarbonate administration pre-intubation if pH <7.2 to prevent hemodynamic collapse during apnea. 7

Common Pitfalls to Avoid

• Starting insulin before checking potassium or when K+ <3.3 mEq/L (causes fatal arrhythmias) 2
• Stopping insulin when glucose normalizes before ketoacidosis resolves (most critical error in euglycemic DKA) 1, 4
• Using nitroprusside-based ketone tests instead of β-hydroxybutyrate (falsely suggests worsening) 2, 4
• Inadequate potassium replacement despite normal initial levels (total body depletion exists) 1, 2
• Overly rapid correction of hyperglycemia and hyperosmolality (causes cerebral edema) 1, 2
• Not overlapping IV and subcutaneous insulin during transition (causes rebound DKA) 1, 4
• Routine bicarbonate use (worsens outcomes) 1, 7
• Failing to identify precipitating cause (leads to recurrence) 1, 6