Management of Diabetic Ketoacidosis in Type 1 Diabetes
For a patient with T1DM presenting with DKA, you must immediately initiate continuous intravenous regular insulin at 0.1 units/kg/hour alongside aggressive isotonic saline resuscitation at 15-20 mL/kg/hour, while simultaneously correcting electrolyte abnormalities—particularly potassium—and identifying the precipitating cause. 1
Initial Assessment and Diagnostic Workup
Upon presentation, confirm DKA diagnosis with the following criteria: blood glucose >250 mg/dL, arterial pH <7.3, serum bicarbonate <15 mEq/L, and presence of ketonemia or ketonuria 1. Obtain comprehensive laboratory evaluation including plasma glucose, electrolytes with calculated anion gap, serum ketones (preferably β-hydroxybutyrate), blood urea nitrogen/creatinine, osmolality, arterial blood gases, complete blood count, urinalysis with urine ketones, and electrocardiogram 1, 2. If infection is suspected based on fever, leukocytosis, or clinical signs, obtain bacterial cultures from urine, blood, and throat, and initiate appropriate antibiotics immediately 1, 2.
Critical pitfall: Direct measurement of β-hydroxybutyrate in blood is the preferred method for monitoring ketosis, as the nitroprusside method only detects acetoacetic acid and acetone, potentially underestimating the severity of ketoacidosis 1.
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 renal perfusion 1, 2. Subsequent fluid choice depends on hydration status, serum electrolyte levels, and urine output 1. When serum glucose reaches 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 1, 2. Total fluid replacement should correct estimated deficits within 24 hours 1.
Insulin Therapy
Start continuous intravenous regular insulin infusion at 0.1 units/kg/hour (this is the standard of care for moderate-to-severe DKA or critically ill/mentally obtunded patients) 1, 2. Target a glucose decline of 50-75 mg/dL per hour 1, 2. If plasma glucose does not fall by 50 mg/dL from the initial value in the first hour, verify adequate hydration status; if acceptable, double the insulin infusion rate every hour until achieving steady glucose decline 1, 2.
Continue insulin infusion until complete resolution of ketoacidosis (pH >7.3, serum bicarbonate ≥18 mEq/L, and anion gap ≤12 mEq/L) regardless of glucose levels 1, 2. This is crucial—stopping insulin prematurely when glucose normalizes is a common error that leads to persistent or worsening ketoacidosis 1.
Alternative Approach for Mild-Moderate Uncomplicated DKA
For hemodynamically stable, alert patients with mild-to-moderate DKA (glucose <400 mg/dL, pH 7.0-7.3, bicarbonate 10-18 mEq/L), subcutaneous rapid-acting insulin analogs combined with aggressive fluid management are equally effective, safer, and more cost-effective than IV insulin 1, 2. However, continuous IV insulin remains the standard for critically ill or mentally obtunded patients 1, 2.
Electrolyte Management: The Potassium Imperative
This is the most critical and dangerous aspect of DKA management. Total body potassium depletion in DKA averages 3-5 mEq/kg body weight, yet many patients present with normal or even elevated serum potassium due to transcellular shifts from acidosis 1, 2. Insulin therapy will unmask this depletion by driving potassium intracellularly, creating life-threatening hypokalemia 1, 2.
Potassium Replacement Algorithm:
If K+ <3.3 mEq/L: DO NOT start insulin therapy—this is an absolute contraindication 1, 2. Delay insulin and aggressively replace potassium with 20-40 mEq/L in IV fluids until K+ ≥3.3 mEq/L to prevent cardiac arrhythmias and death 1, 2.
If K+ 3.3-5.5 mEq/L: Add 20-30 mEq/L potassium to IV fluids (use 2/3 KCl or potassium-acetate and 1/3 KPO₄) once adequate urine output is confirmed 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, 2.
Target serum potassium of 4-5 mEq/L throughout treatment 1, 2. Inadequate potassium monitoring and replacement is a leading cause of mortality in DKA 1.
Bicarbonate: Generally Contraindicated
Do not administer bicarbonate for pH >6.9-7.0 1, 2. Multiple studies demonstrate no benefit in resolution time or outcomes, and bicarbonate may worsen ketosis, cause hypokalemia, and increase cerebral edema risk 1, 2, 3. Bicarbonate administration is only considered for pH <6.9 3.
Monitoring Requirements
Check blood glucose every 2-4 hours and measure serum electrolytes, glucose, blood urea nitrogen, creatinine, osmolality, and venous pH every 2-4 hours during active treatment 1, 2. Venous pH is typically 0.03 units lower than arterial pH and is adequate for monitoring 1. Follow the anion gap to monitor resolution of acidosis 1.
Resolution Criteria
DKA is resolved when ALL of the following are met: glucose <200 mg/dL, serum bicarbonate ≥18 mEq/L, venous pH >7.3, and anion gap ≤12 mEq/L 1, 2.
Transition to Subcutaneous Insulin
This is where most errors occur. Once DKA is resolved and the patient can tolerate oral intake, administer basal insulin (glargine or detemir) subcutaneously 2-4 hours BEFORE stopping the IV insulin infusion 1, 2. This overlap period is essential to prevent recurrence of ketoacidosis and rebound hyperglycemia 1, 2. Stopping IV insulin without prior basal insulin administration is the most common error leading to DKA recurrence 2.
Start a multiple-dose schedule using a combination of short/rapid-acting insulin (0.05-0.1 units/kg/meal) and intermediate/long-acting insulin (0.2-0.3 units/kg/day) 4, 1. Continue IV insulin for 1-2 hours after subcutaneous insulin is administered 2.
Identifying and Treating Precipitating Causes
The most common precipitating causes include infections (30-50% of cases, particularly urinary tract infections and pneumonia), new diagnosis of diabetes, and nonadherence to insulin therapy 5, 6. Other causes include myocardial infarction, stroke, pancreatitis, trauma, and SGLT2 inhibitor use 1, 2. Treat the underlying cause concurrently with DKA management 1, 2.
SGLT2 inhibitor consideration: If the patient was on SGLT2 inhibitors, discontinue immediately and do not restart until 3-4 days after metabolic stability is achieved 1.
Special Considerations for T1DM
Patients with T1DM have absolute beta cell failure and require lifelong insulin therapy 4. Following DKA resolution, these patients need comprehensive diabetes education including hypoglycemia management, stress dosing, ketone monitoring, sick day management, and DKA prevention 4. Consider eligibility for supportive technologies including insulin pump therapy and continuous glucose monitoring 4.
Disposition
ICU admission is indicated for cardiovascular instability, inability to protect the airway, obtundation, severe metabolic derangements, or if adequate monitoring capacity is unavailable 7. Most patients with moderate-to-severe DKA require ICU-level care initially 1.