Immediate Management of Diabetic Ketoacidosis
Begin aggressive fluid resuscitation with isotonic saline (0.9% NaCl) at 15-20 mL/kg/hour for the first hour, followed by continuous IV regular insulin at 0.1 units/kg/hour once potassium is ≥3.3 mEq/L, while closely monitoring and replacing potassium to maintain levels between 4-5 mEq/L. 1, 2
Initial Assessment and Diagnosis
- Confirm DKA diagnosis using the triad: blood glucose >250 mg/dL, arterial pH <7.3, serum bicarbonate <15 mEq/L, and presence of moderate ketonuria or ketonemia 3, 1, 4
- Obtain immediate laboratory evaluation including plasma glucose, electrolytes with calculated anion gap, venous blood gases, serum ketones (preferably direct β-hydroxybutyrate measurement), BUN/creatinine, complete blood count, urinalysis, and electrocardiogram 1, 2
- Correct serum sodium for hyperglycemia by adding 1.6 mEq/L for every 100 mg/dL glucose above 100 mg/dL 3, 4
- Obtain bacterial cultures (blood, urine, throat) if infection is suspected and identify other precipitating factors such as myocardial infarction, stroke, pancreatitis, insulin omission, or SGLT2 inhibitor use 1, 2
Fluid Resuscitation Protocol
- Start with isotonic saline (0.9% NaCl) at 15-20 mL/kg/hour (approximately 1-1.5 L in average adults) during the first hour to restore intravascular volume and renal perfusion 3, 1, 2
- After initial resuscitation, switch to 0.45% NaCl at 4-14 mL/kg/hour if corrected serum sodium is normal or elevated; continue 0.9% NaCl if corrected sodium is low 3, 1
- When serum glucose reaches 200-250 mg/dL, change to 5% dextrose with 0.45-0.75% NaCl while continuing insulin infusion to prevent hypoglycemia and allow complete ketoacidosis resolution 1, 2, 4
- Total fluid replacement should correct estimated deficits (typically 6-9 L water deficit) within 24 hours 3, 1
Insulin Therapy
Critical: Do not start insulin if serum potassium is <3.3 mEq/L—aggressively replace potassium first to prevent life-threatening cardiac arrhythmias. 1, 2
- Once K+ ≥3.3 mEq/L, begin continuous IV regular insulin infusion at 0.1 units/kg/hour (an initial bolus of 0.1 units/kg may be given but is not mandatory) 1, 2
- Target glucose decline of 50-75 mg/dL per hour 1, 2
- If glucose does not fall by 50 mg/dL in the first hour, verify adequate hydration status; if acceptable, double the insulin infusion rate hourly until steady glucose decline is achieved 1, 2
- Continue insulin infusion until complete DKA resolution (pH >7.3, bicarbonate ≥18 mEq/L, anion gap ≤12 mEq/L, glucose <200 mg/dL) regardless of glucose normalization 1, 2, 4
Potassium Management
Potassium replacement is critical—total body potassium depletion averages 3-5 mEq/kg despite normal or elevated initial serum levels, and insulin therapy will unmask this depletion. 1
- If K+ <3.3 mEq/L: Hold insulin, aggressively replace potassium with 20-40 mEq/L in IV fluids until K+ ≥3.3 mEq/L 1, 2
- If K+ 3.3-5.5 mEq/L: Add 20-30 mEq/L potassium to IV fluids (use 2/3 KCl and 1/3 KPO₄) once adequate urine output is confirmed 3, 1, 2
- If K+ >5.5 mEq/L: Withhold potassium initially but monitor closely every 2-4 hours, as levels will drop rapidly with insulin therapy 1
- Target serum potassium of 4-5 mEq/L throughout treatment 1, 2
Bicarbonate Administration
Do NOT administer bicarbonate for pH >6.9-7.0—multiple studies show no benefit in resolution time or outcomes, and it may worsen ketosis, cause hypokalemia, and increase cerebral edema risk. 1, 5
- Bicarbonate is only considered for pH <6.9 or patients in cardiogenic shock 1, 6
- The FDA label indicates bicarbonate for "severe diabetic acidosis," but current guidelines restrict use to extreme acidosis 5
Monitoring During Treatment
- Draw blood every 2-4 hours to measure electrolytes, glucose, BUN, creatinine, osmolality, and venous pH 1, 2, 4
- Venous pH (typically 0.03 units lower than arterial) and anion gap adequately monitor acidosis resolution without repeated arterial blood gases 1, 4
- Direct measurement of β-hydroxybutyrate in blood is preferred over nitroprusside methods, which only measure acetoacetate and acetone and can falsely suggest worsening ketosis during treatment 1, 4
- Monitor for cerebral edema, particularly in children and adolescents—watch for altered mental status, headache, or neurological deterioration 1, 7, 8
Resolution Criteria
DKA is resolved when ALL of the following are met 1, 2, 4:
- Glucose <200 mg/dL
- Serum bicarbonate ≥18 mEq/L
- Venous pH >7.3
- Anion gap ≤12 mEq/L
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, 2
- Once DKA is resolved and patient can eat, start multiple-dose insulin schedule combining short/rapid-acting and intermediate/long-acting insulin 1, 2
- Continue IV insulin for 1-2 hours after administering subcutaneous insulin to allow for absorption 2
- If patient remains NPO after DKA resolution, continue IV insulin and fluid replacement with subcutaneous regular insulin supplementation as needed 1
Alternative Approach 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 1, 2
- This approach requires adequate fluid replacement, frequent point-of-care glucose monitoring, and treatment of concurrent infections 1
- Continuous IV insulin remains the standard of care for critically ill, mentally obtunded, or severe DKA patients 1, 2
Critical Pitfalls to Avoid
- Never stop IV insulin when glucose normalizes—ketoacidosis takes longer to resolve than hyperglycemia, and premature cessation causes recurrence 1, 4
- Never discontinue IV insulin without prior basal insulin administration—this is the most common error leading to DKA recurrence 1, 2
- Never fail to add dextrose when glucose falls below 250 mg/dL—continue insulin to clear ketones while preventing hypoglycemia 1, 4
- Never start insulin with K+ <3.3 mEq/L—correct potassium first to prevent fatal arrhythmias 1, 2
- Inadequate potassium monitoring and replacement is a leading cause of mortality in DKA 1
- Overly rapid correction of osmolality increases cerebral edema risk, particularly in children 1, 7