Management of Diabetic Ketoacidosis (DKA)
Begin immediate fluid resuscitation with isotonic saline at 15-20 mL/kg/hour for the first hour, followed by continuous IV regular insulin at 0.1 units/kg/hour (after confirming potassium ≥3.3 mEq/L), aggressive potassium replacement, and identification of the precipitating cause—this remains the standard of care for moderate-to-severe DKA. 1, 2
Initial Assessment and Diagnostic Workup
Obtain the following laboratory tests immediately:
- Plasma glucose, serum ketones (preferably β-hydroxybutyrate), electrolytes with calculated anion gap, arterial or venous blood gas, BUN/creatinine, osmolality 1, 2
- Urinalysis with urine ketones, complete blood count with differential, electrocardiogram 1, 2
- Bacterial cultures (blood, urine, throat) if infection is suspected—infection is one of the most common precipitating causes 1, 3
- Chest X-ray only if clinically indicated (not routine) 1
Diagnostic criteria for DKA: glucose >250 mg/dL, arterial pH <7.3, serum bicarbonate <15 mEq/L, and presence of ketonemia or ketonuria 2
Identify precipitating factors immediately: infection (most common), insulin omission/inadequacy, myocardial infarction, stroke, pancreatitis, SGLT2 inhibitor use, new diabetes diagnosis 1, 2, 4
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 tissue perfusion 1, 3, 2
Subsequent fluid management:
- Continue isotonic or hypotonic saline based on hydration status, electrolyte levels, and urine output 2
- When glucose reaches 200-250 mg/dL: Switch to 5% dextrose with 0.45-0.75% saline while continuing insulin infusion—this prevents hypoglycemia and ensures complete ketoacidosis resolution 1, 2
- Total fluid replacement should approximate 1.5 times 24-hour maintenance requirements 1
Critical pitfall: Inadequate fluid resuscitation worsens DKA and delays resolution 3
Insulin Therapy
Standard IV Insulin Protocol (Moderate-to-Severe DKA)
DO NOT start insulin if potassium <3.3 mEq/L—this can cause life-threatening cardiac arrhythmias and respiratory muscle weakness 1, 2
Once potassium ≥3.3 mEq/L:
- Give IV bolus of 0.1 units/kg regular insulin 1, 2
- Start continuous infusion at 0.1 units/kg/hour regular insulin 1, 2
- Target glucose decline: 50-75 mg/dL per hour 1, 2
If glucose does not fall by 50 mg/dL in first hour:
- Verify adequate hydration status 1, 2
- If hydration acceptable, double insulin infusion rate hourly until steady decline achieved 1, 2
Continue insulin infusion until DKA resolution (pH >7.3, bicarbonate ≥18 mEq/L, anion gap ≤12 mEq/L, glucose <200 mg/dL)—do NOT stop insulin when glucose normalizes 1, 3, 2
Critical pitfall: Interrupting insulin infusion when glucose falls below 250 mg/dL is a common cause of persistent or worsening ketoacidosis—instead add dextrose to IV fluids 3, 2
Alternative Approach for Mild-to-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, 3, 2
Requirements for subcutaneous approach:
- Patient must be hemodynamically stable and alert 1, 2
- Adequate fluid replacement must be ensured 3, 2
- Frequent point-of-care glucose monitoring required 2
- Concurrent infections must be treated 2
Continuous IV insulin remains mandatory for: critically ill patients, mentally obtunded patients, and severe DKA 1, 2
Electrolyte Management
Potassium Replacement (CRITICAL)
Total body potassium depletion averages 3-5 mEq/kg in DKA—insulin therapy will unmask this by driving potassium intracellularly 2
Potassium replacement protocol:
- If K+ <3.3 mEq/L: HOLD insulin, aggressively replace potassium until ≥3.3 mEq/L to prevent fatal arrhythmias 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 confirmed 1, 2
- If K+ >5.5 mEq/L: Withhold potassium initially but monitor closely—levels will drop rapidly with insulin 2
- Target serum potassium: 4-5 mEq/L throughout treatment 1, 2
Monitor potassium every 2-4 hours during active treatment—inadequate monitoring is a leading cause of mortality in DKA 2
Critical pitfall: Confirm adequate renal function (urine output) before aggressive potassium repletion; if anuric/oliguric, consult nephrology 2
Bicarbonate Administration
Bicarbonate is NOT recommended 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, 3, 2
Consider bicarbonate only if pH <6.9 or in specific circumstances like pre/post-intubation when pH <7.2 to prevent hemodynamic collapse 5
Monitoring During Treatment
Check every 2-4 hours:
- Blood glucose (can check more frequently) 1, 3, 2
- Serum electrolytes, BUN, creatinine, osmolality 1, 2
- Venous pH (typically 0.03 units lower than arterial pH) 3, 2
- Anion gap to monitor acidosis resolution 3, 2
Preferred ketone monitoring: Direct measurement of β-hydroxybutyrate in blood (nitroprusside method only measures acetoacetic acid and acetone) 3, 2
Avoid routine arterial blood gases, ECGs, and chest X-rays—perform only when clinically indicated to reduce costs without compromising outcomes 6
DKA Resolution Criteria
ALL of the following must be met:
Note: Ketonemia typically takes longer to clear than hyperglycemia 3
Transition to Subcutaneous Insulin
CRITICAL STEP: Administer basal insulin (glargine or detemir) 2-4 hours BEFORE stopping IV insulin infusion—this prevents recurrence of ketoacidosis and rebound hyperglycemia 1, 3, 2
Transition protocol:
- Once DKA resolution criteria met and patient can tolerate oral intake, give basal insulin subcutaneously 1, 2
- Continue IV insulin for 1-2 hours after subcutaneous insulin administered to allow absorption 1, 2
- Start multiple-dose regimen with combination of short/rapid-acting and intermediate/long-acting insulin 1, 2
Alternative approach: Adding low-dose basal insulin analog during IV insulin infusion may prevent rebound hyperglycemia without increasing hypoglycemia risk 2
If patient remains NPO after DKA resolution: Continue IV insulin and fluid replacement, supplement with subcutaneous regular insulin as needed 2
Most common error: Stopping IV insulin without prior basal insulin administration leads to DKA recurrence 1, 2
Special Considerations and Complications
Cerebral Edema
More common in children and adolescents than adults—one of the most dire complications of DKA 2
Risk factors: Overly rapid correction of osmolality, excessive fluid administration 2
Monitor closely for: Altered mental status, headache, neurological deterioration 2
SGLT2 Inhibitors
Discontinue immediately if patient on SGLT2 inhibitors—these can precipitate euglycemic DKA 2, 4
Do not restart until: 3-4 days after metabolic stability achieved and infection resolved 2
Concurrent Medical Emergencies
Myocardial infarction can both precipitate and be masked by DKA—maintain high index of suspicion 2
Stroke can precipitate DKA—assess for focal neurological deficits 2
Treat underlying precipitating cause simultaneously with metabolic correction 2
Discharge Planning
Before discharge, ensure:
- Identification of outpatient diabetes care providers 2
- Patient/family education on glucose monitoring, insulin administration, recognition of hyperglycemia/hypoglycemia 2
- Appropriate insulin regimen prescribed with attention to medication access and affordability 2
- Follow-up appointment scheduled 2
- Education on DKA prevention, sick day management, and when to seek medical care 3, 4
Most patients can be discharged in 3 days—few require ICU admission with this protocol 6