Management of Diabetic Ketoacidosis
For critically ill and mentally obtunded patients with DKA, continuous intravenous insulin is the standard of care, combined with aggressive isotonic saline resuscitation at 15-20 mL/kg/hour initially, potassium replacement when levels fall below 5.5 mEq/L, and identification/treatment of the precipitating cause. 1, 2, 3
Initial Assessment and Diagnostic Criteria
Obtain STAT laboratory studies including arterial blood gases, complete blood count with differential, urinalysis, plasma glucose, BUN, electrolytes, chemistry profile, creatinine, and ECG 2. DKA is diagnosed when blood glucose >250 mg/dL, venous pH <7.3, bicarbonate <15 mEq/L, and moderate ketonemia or ketonuria are present 2.
Correct serum sodium for hyperglycemia by adding 1.6 mEq to the sodium value for each 100 mg/dL glucose above 100 mg/dL 2. This corrected sodium is critical for accurate assessment of volume status and osmolality.
Identify and treat the precipitating cause immediately, such as sepsis, myocardial infarction, stroke, or medication non-adherence 1, 2, 3. Obtain chest X-ray and cultures as clinically indicated 2.
Fluid Resuscitation
Begin with isotonic saline (0.9% NaCl) at 15-20 mL/kg/hour for the first hour to restore circulatory volume and tissue perfusion 2, 3, 4. This aggressive initial resuscitation is essential for reversing the profound volume depletion that characterizes DKA.
After initial resuscitation, adjust fluid rate based on hemodynamic status, electrolyte levels, and urine output 2. Continue fluid replacement to maintain adequate perfusion while monitoring for signs of fluid overload, which can precipitate cerebral edema, particularly in pediatric patients 2.
When glucose falls below 200-250 mg/dL, add dextrose (5-10%) to IV fluids while continuing insulin therapy to maintain glucose between 150-200 mg/dL until acidosis resolves 2, 4. This prevents hypoglycemia while allowing continued clearance of ketones.
Insulin Therapy
For Adults with Moderate to Severe DKA:
Administer IV bolus of regular insulin at 0.15 units/kg body weight, followed by continuous infusion at 0.1 unit/kg/hour (typically 5-7 units/hour) 2, 4. The bolus should only be given after confirming serum potassium is ≥3.3 mEq/L to prevent life-threatening hypokalemia 4.
If plasma glucose does not fall by 50 mg/dL in the first hour, check hydration status; if acceptable, double insulin infusion rate hourly until glucose decline of 50-75 mg/dL per hour is achieved 2.
When glucose falls below 200 mg/dL, decrease insulin infusion to 0.05-0.1 unit/kg/hour (3-6 units/hour) and add dextrose to IV fluids to maintain glucose between 150-200 mg/dL until acidosis resolves 2.
For Pediatric Patients:
Do NOT give an initial insulin bolus; start continuous infusion at 0.1 unit/kg/hour 2, 4. The bolus is omitted in children to reduce the risk of cerebral edema.
For Mild or Moderate Uncomplicated DKA:
Subcutaneous rapid-acting insulin analogs combined with aggressive fluid management may be used in the emergency department or step-down units 1, 2. This approach is safer and more cost-effective than IV insulin for uncomplicated cases, but requires adequate fluid replacement, frequent bedside glucose monitoring, and appropriate follow-up 1.
Electrolyte Management
Potassium:
Despite total body potassium depletion, mild to moderate hyperkalemia is common initially 2. Insulin administration drives potassium intracellularly, causing potentially dangerous hypokalemia.
Begin potassium replacement when serum levels fall below 5.5 mEq/L, assuming adequate urine output 2. Add 20-30 mEq potassium (2/3 KCl and 1/3 KPO₄) per liter of infusion fluid to maintain serum potassium 4-5 mEq/L 2, 4.
If initial potassium is <3.3 mEq/L, start potassium replacement BEFORE insulin therapy to prevent cardiac arrhythmias 2. Delay insulin administration temporarily and give potassium chloride intravenously to bring plasma potassium close to 4 mmol/L 5.
Bicarbonate:
Bicarbonate administration is generally NOT recommended as studies show it makes no difference in resolution of acidosis or time to discharge 1, 2, 3. The acidosis resolves with insulin therapy and volume resuscitation alone.
Monitoring During Treatment
Check blood glucose every 1-2 hours until stable 2. Monitor serum electrolytes, glucose, BUN, creatinine, osmolality, and venous pH every 2-4 hours 2, 3, 4.
Follow venous pH (typically 0.03 units lower than arterial pH) and anion gap to monitor acidosis resolution 2. Direct measurement of β-hydroxybutyrate in blood is the preferred method for monitoring DKA 2, 4.
Do NOT use the nitroprusside method (urine ketones) to monitor treatment response as it only measures acetoacetic acid and acetone, not β-hydroxybutyrate, which is the predominant ketone body 2, 4.
Resolution Criteria
DKA is resolved when glucose <200 mg/dL, serum bicarbonate ≥18 mEq/L, venous pH >7.3, and anion gap ≤12 mEq/L 2, 4. Ketonemia typically takes longer to clear than hyperglycemia, so insulin therapy must continue until ketoacidosis resolves even if blood glucose normalizes 2, 4.
Transition to Subcutaneous Insulin
Once DKA resolves and the patient can eat, start a multiple-dose insulin regimen with combination of short/rapid-acting and intermediate/long-acting insulin 2.
Administer basal insulin 2-4 hours BEFORE stopping IV insulin to prevent recurrence of ketoacidosis and rebound hyperglycemia 1, 2, 3, 4. This overlap period is critical—premature discontinuation of IV insulin before subcutaneous insulin takes effect is a common pitfall that leads to recurrent DKA.
Continue IV insulin infusion for 1-2 hours after starting subcutaneous insulin 2. Recent studies show that administering a low dose of basal insulin analog in addition to IV insulin infusion may prevent rebound hyperglycemia without increased risk of hypoglycemia 1, 3, 4.
If the patient remains NPO, continue IV insulin and fluids; supplement with subcutaneous regular insulin as needed every 4 hours (5-unit increments for every 50 mg/dL increase in blood glucose above 150 mg/dL) 2.
Critical Complications to Monitor
Cerebral edema is the most common cause of mortality and morbidity, especially in children 5. Monitor for headache, altered mental status, and seizures 2. Risk is minimized by avoiding insulin bolus in pediatrics, excessive saline resuscitation, and rapid decrease in effective plasma osmolality early in treatment 5.
Hypokalemia can cause cardiac arrhythmias and is associated with increased inpatient mortality when severe (<2.5 mEq/L) 3. Monitor potassium levels closely and replace aggressively 2, 3.
Recurrent DKA occurs when transition to subcutaneous insulin is inadequate 2. Ensure proper overlap of IV and subcutaneous insulin as described above.
Discharge Planning
Begin discharge planning at admission 3. Schedule follow-up appointments prior to discharge, as this increases the likelihood that patients will attend 1, 3.
Provide structured education on sick-day management, ketone monitoring, recognition and treatment of hyperglycemia and hypoglycemia, insulin administration, and when to call a healthcare provider 1, 3.
Ensure medication reconciliation with cross-checking of home and hospital medications 4. Prescriptions for new or changed medications should be filled and reviewed with the patient before discharge 1.
Transmit discharge summaries to the primary care provider as soon as possible with information on medication changes, pending tests, and follow-up needs 1, 4.