What is the immediate treatment for a patient presenting with diabetic ketoacidosis (DKA)?

Immediate Treatment of Diabetic Ketoacidosis

Begin aggressive fluid resuscitation with isotonic saline (0.9% NaCl) at 15-20 mL/kg/hour in the first hour, followed by continuous intravenous insulin infusion at 0.1 units/kg/hour once adequate urine output is confirmed and potassium is ≥3.3 mEq/L. 1, 2

Initial Fluid Resuscitation

• Administer 1-1.5 liters of isotonic saline (0.9% NaCl) at 15-20 mL/kg/hour during the first hour to restore intravascular volume and tissue perfusion. 1, 2
• Subsequent fluid choice depends on hydration status, serum electrolyte levels, and urine output. 2
• When serum glucose falls to 200-250 mg/dL, switch to 5% dextrose with 0.45-0.75% saline while continuing insulin infusion to prevent hypoglycemia and ensure complete resolution of ketoacidosis. 2

This aggressive initial fluid replacement is critical as it restores tissue perfusion and improves insulin sensitivity before insulin therapy begins. 2

Insulin Therapy Protocol

Critical Pre-Insulin Check: Potassium Level

• Do NOT start insulin if potassium is <3.3 mEq/L—aggressively replace potassium first to prevent life-threatening cardiac arrhythmias and respiratory muscle weakness. 2
• Despite presenting potassium levels, total body potassium depletion averages 3-5 mEq/kg body weight in all DKA patients, and insulin will further drive potassium intracellularly. 2

Insulin Administration

• For moderate-to-severe DKA or critically ill/mentally obtunded patients: continuous intravenous regular insulin at 0.1 units/kg/hour is the standard of care. 1, 3, 2
• Target a glucose decline of 50-75 mg/dL per hour. 2
• If glucose does not fall by 50 mg/dL in the first hour, double the insulin infusion rate hourly until steady decline is achieved (after confirming adequate hydration). 2
• 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, 3, 2

Alternative for Mild-Moderate Uncomplicated DKA

• For hemodynamically stable, alert patients with mild-moderate DKA: subcutaneous rapid-acting insulin analogs (0.15 units/kg every 2-3 hours) combined with aggressive fluid management are equally effective, safer, and more cost-effective than IV insulin. 2
• This approach requires adequate fluid replacement, frequent point-of-care glucose monitoring, and treatment of concurrent infections. 2

Electrolyte Management

Potassium Replacement (Critical)

• 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. 2
• If K+ >5.5 mEq/L: withhold potassium initially 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

Common Pitfall: Inadequate potassium monitoring and replacement is a leading cause of mortality in DKA. 2

Bicarbonate Administration

• Bicarbonate is NOT recommended for pH >6.9-7.0, as multiple studies show no benefit in resolution time or outcomes. 1, 2
• Bicarbonate may worsen ketosis, cause hypokalemia, and increase cerebral edema risk. 2

Monitoring During Treatment

• Draw blood every 2-4 hours to measure serum electrolytes, glucose, BUN, creatinine, osmolality, and venous pH. 1, 2
• Direct measurement of β-hydroxybutyrate in blood is the preferred method for monitoring DKA resolution (not urine ketones, which only measure acetoacetic acid and acetone). 3, 2
• Follow venous pH (typically 0.03 units lower than arterial pH) and anion gap to monitor resolution of acidosis. 2

Resolution Criteria

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

• 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 met. 1

Transition to Subcutaneous Insulin

• Administer basal insulin (glargine or detemir) 2-4 hours BEFORE stopping IV insulin infusion to prevent recurrence of ketoacidosis and rebound hyperglycemia. 1, 3, 2
• This overlap period is essential—stopping IV insulin without prior basal insulin administration is a common cause of rebound hyperglycemia and ketoacidosis. 3, 2, 4
• Once the patient can eat, start a multiple-dose schedule using combination of short/rapid-acting and intermediate/long-acting insulin. 1, 2

Identify and Treat Precipitating Causes

Concurrent treatment of underlying triggers is crucial: 2

• Obtain bacterial cultures (urine, blood, throat) if infection is suspected and administer appropriate antibiotics. 2
• Consider myocardial infarction, stroke, pancreatitis, trauma, or insulin omission as precipitating factors. 2
• Discontinue SGLT2 inhibitors immediately if the patient is taking them—these can precipitate euglycemic DKA. 2

Critical Pitfalls to Avoid

• Premature termination of insulin therapy before complete resolution of ketosis leads to recurrent DKA. 2, 4
• Failure to add dextrose when glucose falls below 250 mg/dL while continuing insulin causes hypoglycemia and interrupts ketoacidosis resolution. 2
• Starting insulin when potassium <3.3 mEq/L can cause fatal cardiac arrhythmias. 2
• Stopping IV insulin without prior basal subcutaneous insulin causes rebound hyperglycemia. 3, 2
• Overly rapid correction of osmolality increases cerebral edema risk, particularly in children and adolescents. 2

Special Populations

Children and Adolescents

• Initial treatment should address hyperglycemia and metabolic derangements regardless of ultimate diabetes type, as presentation often overlaps between type 1 and type 2 diabetes. 5
• Cerebral edema occurs more commonly in children and adolescents—monitor closely for altered mental status, headache, or neurological deterioration. 2

Pregnancy and Chronic Kidney Disease

• Management principles remain the same, but closer monitoring is required. 6
• If anuric or oliguric, potassium repletion must be more cautious with nephrology consultation. 2