Immediate Treatment of Diabetic Ketoacidosis (DKA)
Begin aggressive fluid resuscitation with isotonic saline at 15-20 mL/kg/hour in the first hour, followed by continuous intravenous insulin infusion at 0.1 units/kg/hour once serum potassium is ≥3.3 mEq/L, while simultaneously monitoring and replacing electrolytes—particularly potassium—to restore circulatory volume, resolve ketoacidosis, and prevent life-threatening complications. 1, 2, 3
Initial Assessment and Stabilization
Critical Laboratory Evaluation
Before initiating treatment, obtain the following to confirm DKA diagnosis and guide therapy 2, 3:
- Diagnostic criteria: Blood glucose >250 mg/dL, arterial pH <7.3, serum bicarbonate <15 mEq/L, and presence of ketonemia or ketonuria 3
- Plasma glucose, electrolytes with calculated anion gap, serum ketones (β-hydroxybutyrate preferred), arterial blood gases, complete blood count, and electrocardiogram 2, 3
- Blood urea nitrogen/creatinine, osmolality, urinalysis, and urine ketones 2, 3
- Bacterial cultures (blood, urine, throat) if infection suspected 2, 3
Identify Precipitating Factors
Concurrent treatment of underlying causes is essential 4, 3:
- Infection (most common), myocardial infarction, stroke, pancreatitis, trauma 3
- Insulin omission or inadequacy, SGLT2 inhibitor use (discontinue 3-4 days before any surgery) 3
Fluid Resuscitation Protocol
First Hour
Administer isotonic saline (0.9% NaCl) at 15-20 mL/kg/hour (approximately 1-1.5 L in average adult) to restore intravascular volume and renal perfusion. 1, 2, 3
Subsequent Fluid Management
- Continue isotonic or hypotonic saline based on hydration status, electrolyte levels, and urine output 3
- When 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 ketoacidosis resolution 3
- Total fluid replacement should correct estimated deficits within 24 hours 3
Insulin Therapy
Critical Pre-Insulin Check: Potassium Level
DO NOT start insulin if serum potassium <3.3 mEq/L—this is an absolute contraindication that can cause life-threatening cardiac arrhythmias and death. 2, 3
- Delay insulin therapy immediately
- Aggressively replace potassium until levels reach ≥3.3 mEq/L
- Obtain electrocardiogram to assess cardiac effects
- Confirm adequate urine output before potassium replacement
Insulin Initiation (Once K+ ≥3.3 mEq/L)
Start continuous intravenous regular insulin infusion at 0.1 units/kg/hour (preferred method for moderate to severe DKA). 1, 2, 3
- An initial IV bolus of 0.1 units/kg may be given, followed by continuous infusion 2
- Target glucose decline of 50-75 mg/dL per hour 2, 3
- If glucose does not fall by 50 mg/dL in first hour, check hydration status; if adequate, double insulin infusion rate hourly until steady decline achieved 3
Alternative for 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 for uncomplicated mild-moderate DKA. 4, 3
- Requires adequate fluid replacement, frequent point-of-care glucose monitoring, and treatment of concurrent infections 3
- Continuous IV insulin remains standard for critically ill and mentally obtunded patients 4, 3
Electrolyte Management
Potassium Replacement (Critical Priority)
Despite possible normal or elevated initial levels, total body potassium depletion is universal in DKA, and insulin therapy will further lower serum potassium. 3
Potassium replacement protocol 2, 3:
- If K+ <3.3 mEq/L: Delay insulin, aggressively replace potassium until ≥3.3 mEq/L
- 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 confirmed
- If K+ >5.5 mEq/L: Withhold potassium initially but monitor closely, as levels will drop rapidly with insulin therapy
- Target serum potassium of 4-5 mEq/L throughout treatment 3
Bicarbonate Administration
Bicarbonate is NOT recommended for DKA patients with pH >6.9-7.0. 4, 3
- Multiple studies show no difference in resolution of acidosis or time to discharge 4, 3
- May worsen ketosis, cause hypokalemia, and increase cerebral edema risk 3
Monitoring During Treatment
Frequency and Parameters
Draw blood every 2-4 hours to measure 2, 3:
- Serum electrolytes, glucose, blood urea nitrogen, creatinine, osmolality, and venous pH
- Follow venous pH (typically 0.03 units lower than arterial pH) and anion gap to monitor acidosis resolution 3
- Direct measurement of β-hydroxybutyrate in blood is preferred over nitroprusside method 3
Glucose Targets During Treatment
- Target glucose between 150-200 mg/dL until DKA resolution parameters are met 1, 3
- Continue insulin infusion until resolution of ketoacidosis regardless of glucose levels 4, 3
Resolution Criteria
DKA is resolved when ALL of the following are met 1, 3:
- Glucose <200 mg/dL
- Serum bicarbonate ≥18 mEq/L
- Venous pH >7.3
- Anion gap ≤12 mEq/L
Transition to Subcutaneous Insulin
Critical Timing to Prevent Recurrence
Administer basal insulin (glargine, detemir, or NPH) 2-4 hours BEFORE stopping IV insulin infusion to prevent recurrence of ketoacidosis and rebound hyperglycemia. 4, 2, 3
- This overlap period is essential—premature termination of IV insulin is the most common error leading to DKA recurrence 2
- Recent evidence shows adding low-dose basal insulin analog during IV insulin infusion may prevent rebound hyperglycemia without increasing hypoglycemia risk 4, 3
Post-Resolution Insulin Regimen
- Start multiple-dose schedule using combination of short/rapid-acting and intermediate/long-acting insulin
- Continue monitoring electrolytes, particularly potassium, as insulin drives potassium intracellularly 2
If patient remains NPO after DKA resolution 3:
- Continue IV insulin and fluid replacement
- Supplement with subcutaneous regular insulin as needed
Common Pitfalls to Avoid
Critical errors that lead to complications or treatment failure 3:
- Starting insulin before correcting severe hypokalemia (K+ <3.3 mEq/L)—can cause fatal arrhythmias 2, 3
- Stopping IV insulin without prior basal insulin administration—leads to DKA recurrence 2
- Interrupting insulin infusion when glucose falls below 250 mg/dL—causes persistent or worsening ketoacidosis 3
- Failing to add dextrose when glucose falls below 250 mg/dL while continuing insulin therapy 3
- Inadequate potassium monitoring and replacement—leading cause of mortality in DKA 3
- Overly rapid correction of osmolality—increases risk of cerebral edema, particularly in children 3
Special Considerations
Thromboprophylaxis
- DKA creates a hypercoagulable state increasing thrombosis risk 1
- Enoxaparin can be started upon admission after initial fluid resuscitation as part of standard hospital thromboprophylaxis protocols 1
- Monitor renal function regularly, as insulin therapy and fluid resuscitation can improve kidney perfusion and change enoxaparin clearance 1