What is the management approach for Diabetic Ketoacidosis (DKA) in an Intensive Care Unit (ICU) setting?

Management of Diabetic Ketoacidosis in the ICU

Initial Assessment and Diagnosis

For critically ill and mentally obtunded patients with DKA in the ICU, continuous intravenous regular insulin at 0.1 units/kg/hour is the standard of care. 1, 2

Diagnostic Criteria

• Confirm DKA diagnosis with all three criteria: blood glucose >250 mg/dL, arterial pH <7.3, serum bicarbonate <15 mEq/L, and presence of ketonemia or ketonuria 2
• Obtain comprehensive laboratory workup immediately: plasma glucose, arterial blood gases, complete metabolic panel with calculated anion gap, serum ketones (β-hydroxybutyrate preferred), osmolality, urinalysis with ketones, complete blood count with differential, and electrocardiogram 2
• Identify precipitating factors: infection (obtain blood, urine, throat cultures if suspected), myocardial infarction, stroke, pancreatitis, trauma, insulin omission, or SGLT2 inhibitor use 2

Fluid Resuscitation Protocol

Begin with isotonic saline (0.9% NaCl) at 15-20 mL/kg/hour (approximately 1-1.5 L in the average adult) during the first hour to restore intravascular volume and tissue perfusion. 2

• After initial resuscitation, adjust fluid choice based on hydration status, serum electrolytes, and urine output 2
• When serum glucose reaches 250 mg/dL, switch to 5% dextrose with 0.45-0.75% saline while continuing insulin infusion to prevent hypoglycemia and ensure complete ketoacidosis resolution 2
• Target total fluid replacement to correct estimated deficits within 24 hours 2

Critical Pitfall to Avoid

• Never interrupt insulin infusion when glucose falls below 250 mg/dL—this is a common cause of persistent or worsening ketoacidosis; instead, add dextrose-containing fluids 2

Insulin Therapy

Start continuous IV regular insulin infusion at 0.1 units/kg/hour after confirming adequate potassium levels (K+ ≥3.3 mEq/L). 2

• If plasma glucose does not fall by 50 mg/dL in the first hour, verify adequate hydration; if acceptable, double the insulin infusion rate hourly until achieving steady glucose decline of 50-75 mg/dL per hour 2
• Continue insulin infusion until complete resolution of ketoacidosis (pH >7.3, serum bicarbonate ≥18 mEq/L, anion gap ≤12 mEq/L) regardless of glucose levels 2
• Target glucose between 150-200 mg/dL during treatment, but do not stop insulin until metabolic parameters normalize 2

Electrolyte Management

Potassium Replacement (Critical)

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

• Total body potassium depletion averages 3-5 mEq/kg body weight in DKA, and insulin therapy will unmask this by driving potassium intracellularly 2
• Once K+ is 3.3-5.5 mEq/L and adequate urine output confirmed, add 20-30 mEq potassium per liter of IV fluid (use 2/3 KCl and 1/3 KPO₄) 2
• If K+ >5.5 mEq/L initially, withhold potassium but monitor closely as levels will drop rapidly with insulin therapy 2
• Target serum potassium of 4-5 mEq/L throughout treatment 2
• Check potassium levels every 2-4 hours during active treatment 2

Bicarbonate Administration

Bicarbonate is NOT recommended for DKA patients with pH >6.9-7.0, as multiple studies show no difference in resolution of acidosis or time to discharge, and it may worsen ketosis, cause hypokalemia, and increase cerebral edema risk. 2

Monitoring Protocol

Draw blood every 2-4 hours to determine serum electrolytes, glucose, BUN, creatinine, osmolality, and venous pH. 2

• Follow venous pH (typically 0.03 units lower than arterial pH) and anion gap to monitor resolution of acidosis 2
• Direct measurement of β-hydroxybutyrate in blood is the preferred method for monitoring DKA, as the nitroprusside method only measures acetoacetic acid and acetone 2
• Monitor for signs of cerebral edema (altered mental status, headache, neurological deterioration), particularly in younger patients 2

Resolution Criteria

DKA is resolved when ALL of the following are achieved: glucose <200 mg/dL, serum bicarbonate ≥18 mEq/L, venous pH >7.3, and anion gap ≤12 mEq/L. 2

Transition to Subcutaneous Insulin

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

• Once DKA is resolved and the patient can eat, start a multiple-dose schedule using a combination of short/rapid-acting and intermediate/long-acting insulin 2
• If the patient remains NPO after DKA resolution, continue IV insulin and fluid replacement, supplementing with subcutaneous regular insulin as needed 2
• Recent evidence shows adding low-dose basal insulin analog during IV insulin infusion may prevent rebound hyperglycemia without increasing hypoglycemia risk 2

Treatment of Underlying Precipitating Factors

Identify and treat correctable underlying causes concurrently: administer appropriate antibiotics if infection is suspected, manage myocardial infarction or stroke, and discontinue SGLT2 inhibitors immediately (do not restart until 3-4 days after metabolic stability). 2

Special Considerations for Mild-Moderate Uncomplicated DKA

• For hemodynamically stable, alert patients with mild-moderate uncomplicated DKA, subcutaneous rapid-acting insulin analogs combined with aggressive fluid management are equally effective, safer, and more cost-effective than IV insulin 1, 2
• This approach requires adequate fluid replacement, frequent point-of-care glucose monitoring, treatment of concurrent infections, and appropriate follow-up 1
• However, continuous IV insulin remains the standard of care for critically ill and mentally obtunded ICU patients 1, 2

Common Pitfalls in ICU Management

• Premature termination of insulin therapy before complete resolution of ketosis leads to DKA recurrence 2
• Failure to add dextrose when glucose falls below 250 mg/dL while continuing insulin therapy 2
• Inadequate potassium monitoring and replacement is a leading cause of mortality in DKA 2
• Overly rapid correction of osmolality increases risk of cerebral edema 2
• Stopping IV insulin without prior administration of basal subcutaneous insulin causes rebound hyperglycemia and ketoacidosis 1, 2