Management of Diabetic Ketoacidosis (DKA)
Begin immediate treatment with isotonic saline (0.9% NaCl) at 15-20 mL/kg/hour for the first hour, followed by continuous intravenous regular insulin at 0.1 units/kg/hour once potassium is ≥3.3 mEq/L, while aggressively replacing potassium to maintain levels between 4-5 mEq/L throughout treatment. 1
Initial Diagnostic Workup
Obtain the following laboratory studies immediately 1:
- Plasma glucose, serum ketones, arterial blood gases
- Complete metabolic panel with calculated anion gap
- Serum osmolality, urinalysis with urine ketones
- Complete blood count with differential
- Electrocardiogram
- Blood, urine, and throat cultures if infection suspected 1
Diagnostic criteria for DKA: blood glucose >250 mg/dL, arterial pH <7.3, serum bicarbonate <15 mEq/L, and presence of ketonemia or ketonuria 1
Identify precipitating factors: infection (most common), myocardial infarction, stroke, pancreatitis, trauma, insulin omission, SGLT2 inhibitor use, or alcohol abuse 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 tissue perfusion 1, 2
After initial resuscitation, adjust fluid rate based on hydration status, electrolyte levels, and urine output, aiming to correct estimated deficits within 24 hours 1
Critical transition point: When serum glucose reaches 250 mg/dL, switch to 5% dextrose with 0.45-0.75% NaCl to prevent hypoglycemia while continuing insulin therapy until ketoacidosis fully resolves 1, 2
Insulin Therapy
For Moderate-to-Severe or Critically Ill Patients
Administer continuous intravenous regular insulin at 0.1 units/kg/hour without an initial bolus 1, 2
If plasma glucose does not fall by 50 mg/dL in the first hour, verify adequate hydration, then double the insulin infusion rate hourly until achieving a steady decline of 50-75 mg/dL per hour 1
Do NOT stop insulin when glucose normalizes—continue insulin infusion until complete resolution of ketoacidosis (pH >7.3, bicarbonate ≥18 mEq/L, anion gap ≤12 mEq/L) regardless of glucose levels 1, 2
For Mild-to-Moderate Uncomplicated DKA
For hemodynamically stable, alert patients with mild-moderate DKA, subcutaneous rapid-acting insulin analogs at 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
This approach requires adequate fluid replacement, frequent point-of-care glucose monitoring, and treatment of concurrent infections 1
Electrolyte Management
Potassium Replacement (Critical)
Total body potassium depletion averages 3-5 mEq/kg body weight in DKA, and insulin therapy will unmask this depletion by driving potassium intracellularly 1
If initial potassium <3.3 mEq/L: DELAY insulin therapy and aggressively replace potassium until levels reach ≥3.3 mEq/L to prevent life-threatening arrhythmias, cardiac arrest, and respiratory muscle weakness 1, 2
If potassium 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 is confirmed 1, 2
If potassium >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: 4-5 mEq/L throughout treatment 1, 2
Bicarbonate Administration
Bicarbonate is NOT recommended for DKA patients with pH >6.9-7.0—multiple studies show no difference in resolution of acidosis or time to discharge, and bicarbonate may worsen ketosis, cause hypokalemia, and increase cerebral edema risk 1, 2, 3
Consider bicarbonate only if pH <6.9 or when pH <7.2 pre-intubation to prevent hemodynamic collapse 3
Phosphate and Magnesium
Monitor phosphate and magnesium levels to prevent refeeding syndrome, particularly in malnourished patients 2, 4
Monitoring During Treatment
Draw blood every 2-4 hours for 1, 2:
- Serum electrolytes, glucose, BUN, creatinine, osmolality
- Venous pH (typically 0.03 units lower than arterial pH)
- Anion gap calculation
Monitor blood glucose every 1-2 hours 2
Continuous cardiac monitoring is necessary due to electrolyte shifts and arrhythmia risk 2
Direct measurement of β-hydroxybutyrate in blood is the preferred method for monitoring DKA, as the nitroprusside method only measures acetoacetic acid and acetone 1
Resolution Criteria
DKA is resolved when ALL of the following are met 1, 2:
- Glucose <200 mg/dL
- Serum bicarbonate ≥18 mEq/L
- Venous pH >7.3
- Anion gap ≤12 mEq/L
Target glucose between 150-200 mg/dL until these resolution parameters are achieved 1
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, 3
This overlap period is essential—stopping IV insulin without prior subcutaneous basal insulin administration causes rebound hyperglycemia and ketoacidosis 1
Once the patient can eat, start a multiple-dose schedule using a combination of short/rapid-acting and intermediate/long-acting insulin 1
If the patient remains NPO after DKA resolution, continue IV insulin and fluid replacement, supplementing with subcutaneous regular insulin as needed 1
Treatment of Precipitating Causes
Administer appropriate antibiotics if infection is suspected based on cultures 1, 2
Evaluate for myocardial infarction (can both precipitate and be masked by DKA), stroke (assess for focal neurological deficits), or pancreatitis 1, 2
Discontinue SGLT2 inhibitors immediately and do not restart until 3-4 days after metabolic stability is achieved, as these medications can precipitate euglycemic DKA 1, 2
Critical Pitfalls to Avoid
Premature termination of insulin therapy before complete resolution of ketosis leads to recurrent DKA 1
Interruption of insulin infusion when glucose falls is a common cause of persistent or worsening ketoacidosis—add dextrose instead 1
Failure to add dextrose when glucose falls below 250 mg/dL while continuing insulin therapy leads to hypoglycemia 1
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 and adolescents 1, 3
Stopping IV insulin without prior subcutaneous basal insulin causes rebound hyperglycemia 1
Special Populations
Pregnancy
Requires tailored management with lower glucose targets and heightened monitoring for fetal complications 5
Chronic Kidney Disease
Adjust fluid rates cautiously; if anuric or oliguric, potassium repletion must be more cautious with nephrology consultation 1, 5
Congestive Heart Failure
Monitor fluid status closely to avoid volume overload during aggressive fluid resuscitation 6
Euglycemic DKA (SGLT2 Inhibitor-Associated)
Recognize that glucose may be <250 mg/dL; diagnosis relies on ketosis and acidosis 1, 5
Discharge Planning
Identify outpatient diabetes care provider before discharge 1
- Recognition and prevention of DKA
- Glucose monitoring and home glucose goals
- Insulin administration technique
- Sick-day management
- When to call healthcare professional
Ensure appropriate insulin regimen is prescribed with attention to medication access and affordability 1
Schedule follow-up within 1-2 weeks 2