What is the management protocol for diabetic ketoacidosis (DKA) in the Intensive Care Unit (ICU)?

Management of Diabetic Ketoacidosis in the ICU

In critically ill and mentally obtunded patients with DKA, continuous intravenous regular insulin at 0.1 units/kg/hour (without initial bolus) combined with aggressive isotonic saline resuscitation at 15-20 mL/kg/hour is the standard of care, with treatment continuing until metabolic acidosis resolves (bicarbonate ≥18 mEq/L, venous pH >7.3, anion gap ≤12 mEq/L)—not just until glucose normalizes. 1, 2, 3

Initial Assessment and Diagnostic Workup

Upon ICU admission, immediately obtain:

• Arterial blood gas (pH must be <7.3 for DKA diagnosis; severe DKA has pH <7.00) 2
• Complete metabolic panel with calculated anion gap [Na⁺ - (Cl⁻ + HCO₃⁻)] which should be >10-12 mEq/L 2, 3
• Direct blood β-hydroxybutyrate measurement (preferred over urine ketones, which miss the predominant ketone body) 2, 4
• Serum bicarbonate (<18 mEq/L for DKA; <10 mEq/L indicates severe DKA) 2
• Blood glucose (>250 mg/dL in classic DKA, but can be normal in euglycemic DKA) 2, 4
• Corrected sodium using formula: measured Na + [(glucose - 100)/100 × 1.6] 2
• Potassium level before starting insulin (total body potassium is depleted despite potentially normal initial levels) 2, 3
• Cultures (blood, urine, throat) if infection suspected as precipitating cause 2, 3

Critical pitfall: Never rely on urine ketones or nitroprusside-based tests for diagnosis or monitoring—they only detect acetoacetate and acetone, completely missing β-hydroxybutyrate, and paradoxically worsen during treatment as β-hydroxybutyrate converts to acetoacetate. 2, 4

Fluid Resuscitation Protocol

First Hour

• Begin with isotonic saline (0.9% NaCl) at 15-20 mL/kg/hour to restore circulatory volume and tissue perfusion 1, 2, 3
• In severely dehydrated patients, this may need repeating, but initial reexpansion should not exceed 50 mL/kg over first 4 hours in pediatric patients 1
• Monitor for fluid overload in patients with renal or cardiac compromise 3

Subsequent Fluid Management

• Total fluid replacement should correct estimated deficits within 24 hours 1, 2
• Subsequent fluid choice depends on hydration state, serum electrolytes, and urine output 2, 3
• The induced change in serum osmolality should not exceed 3 mOsm/kg H₂O per hour to prevent cerebral edema 1

Recent evidence suggests balanced crystalloid solutions may achieve faster DKA resolution than normal saline alone, though isotonic saline remains the guideline standard. 5

Insulin Therapy

Initiation

• Do NOT start insulin if serum potassium <3.3 mEq/L—aggressively replace potassium first to prevent fatal cardiac arrhythmias 2, 3
• Start continuous IV regular insulin at 0.1 units/kg/hour WITHOUT an initial bolus (bolus not recommended in pediatric patients) 1, 2, 3
• Target glucose decline of 50-75 mg/dL per hour 1, 2, 3

Dose Adjustment

• If glucose does not fall by 50 mg/dL in the first hour, check hydration status; if acceptable, double the insulin infusion hourly until steady decline achieved 1, 2, 3

Preventing Hypoglycemia While Clearing Ketones

• When glucose falls to 200-250 mg/dL, add dextrose 5-10% to IV fluids while continuing insulin infusion 2, 4, 3
• This is the most critical step: never stop insulin based on glucose levels alone—ketoacidosis resolution requires continued insulin until metabolic acidosis clears 4, 3
• Ketonemia typically takes longer to clear than hyperglycemia 1, 2

In euglycemic DKA (glucose <250 mg/dL at presentation), immediately add dextrose to IV fluids from the start while maintaining insulin infusion—stopping insulin when glucose normalizes is the most critical error. 4

Potassium Replacement

Critical Monitoring

• Check potassium before starting insulin—total body potassium is always depleted in DKA despite potentially normal or elevated initial levels due to acidosis-induced extracellular shift 2, 4, 3
• Insulin therapy and acidosis correction will drive potassium intracellularly, causing life-threatening hypokalemia 3

Replacement Protocol

• If K⁺ <3.3 mEq/L: Hold insulin, aggressively replace potassium first 2, 3
• If K⁺ 3.3-5.5 mEq/L: Add 20-30 mEq/L potassium to IV fluids (2/3 KCl and 1/3 KPO₄) 1, 2, 3
• If K⁺ >5.5 mEq/L: Do not add potassium initially, but monitor closely as levels will fall rapidly with treatment 3
• Goal: maintain serum potassium 4-5 mEq/L throughout treatment 2

Monitoring Protocol

Frequency

• Check blood glucose every 1-2 hours 3
• Draw blood every 2-4 hours for electrolytes, glucose, BUN, creatinine, osmolality, and venous pH 2, 3
• Monitor β-hydroxybutyrate every 2-4 hours (not urine ketones) 2

What to Follow

• After initial arterial blood gas, venous pH suffices for monitoring acidosis resolution (venous pH typically 0.03 units lower than arterial) 2
• Follow venous pH and anion gap to track metabolic acidosis correction 2, 3
• Monitor mental status closely, especially in pediatric patients, to rapidly identify cerebral edema 1, 6

Resolution Criteria and Transition

DKA is Resolved When ALL of the Following Are Met:

• Glucose <200 mg/dL 2, 3
• Serum bicarbonate ≥18 mEq/L 2, 3
• Venous pH >7.3 2, 3
• Anion gap ≤12 mEq/L 2, 3

Transition to Subcutaneous Insulin

• Administer basal subcutaneous insulin (long-acting analog or NPH) 2-4 hours BEFORE stopping IV insulin to prevent rebound hyperglycemia and recurrent ketoacidosis 1, 2, 3
• British guidelines suggest adding subcutaneous glargine along with continuous IV insulin during treatment, which has shown faster DKA resolution and shorter hospital stays 5

Controversial and Special Considerations

Bicarbonate Therapy

• Bicarbonate use is NOT recommended in most patients—multiple studies show no difference in acidosis resolution or time to discharge 1
• Consider bicarbonate ONLY if pH <6.9, or when pH <7.2 pre-intubation to prevent hemodynamic collapse from apnea 2, 5
• Bicarbonate can worsen ketosis, cause hypokalemia, and increase cerebral edema risk 5

Cerebral Edema Prevention

• Most common cause of death in pediatric DKA 6
• Risk factors include: severity of acidosis, greater hypocapnia (after adjusting for acidosis), higher BUN at presentation, bicarbonate treatment, and overly aggressive fluid resuscitation 1, 6, 5
• Avoid rapid overcorrection of hyperglycemia—osmolality changes should not exceed 3 mOsm/kg H₂O per hour 1
• Monitor mental status continuously; any deterioration warrants immediate evaluation for cerebral edema 1, 6

Phosphate Replacement

• Include 1/3 of potassium replacement as KPO₄ (with 2/3 as KCl) 1, 2
• Monitor for hypophosphatemia, hypomagnesemia during treatment 5

Airway Management in Critically Ill Patients

• BiPAP is NOT recommended due to aspiration risk 5
• For impending respiratory failure, proceed with intubation and mechanical ventilation 5
• Consider bicarbonate if pH <7.2 pre-intubation to prevent metabolic acidosis worsening and hemodynamic collapse during apneic period 5

Early Nutrition

• Early initiation of oral nutrition has been shown to reduce ICU and overall hospital length of stay 5

Identifying and Treating Precipitating Causes

The most common triggers include:

• Infections (obtain cultures early) 3, 7
• New diagnosis of diabetes 7
• Insulin nonadherence or omission 7
• SGLT2 inhibitor use (can cause euglycemic DKA; discontinue 3-4 days before surgery) 3, 7
• Myocardial infarction, stroke, sepsis 1

Failing to identify and treat the underlying precipitating cause will lead to DKA recurrence. 2

ICU vs. General Ward Placement

Severe DKA (pH <7.00, bicarbonate <10 mEq/L) requires ICU admission for intensive monitoring, including potential central venous and intra-arterial pressure monitoring. 2

Mild to moderate DKA may sometimes be treated in emergency departments or step-down units with subcutaneous rapid-acting insulin analogs combined with aggressive fluid management, which can be safer and more cost-effective than IV insulin—but this requires adequate staffing for frequent bedside testing and close monitoring. 1, 8