Management of Diabetic Ketoacidosis
Begin immediate treatment with isotonic saline (0.9% NaCl) at 15-20 mL/kg/hour for the first hour, followed by continuous IV regular insulin at 0.1 units/kg/hour without an initial bolus, while aggressively monitoring and replacing potassium to maintain levels between 4-5 mEq/L. 1
Initial Diagnostic Workup
Confirm DKA with the following criteria 1:
- Blood glucose >250 mg/dL
- Arterial pH <7.3
- Serum bicarbonate <15 mEq/L
- Presence of ketonemia or ketonuria
- Anion gap >12 mEq/L
Obtain comprehensive laboratory evaluation including plasma glucose, blood urea nitrogen/creatinine, serum ketones, electrolytes with calculated anion gap, serum osmolality, urinalysis, urine ketones, arterial blood gases, complete blood count with differential, and electrocardiogram 1. If infection is suspected, obtain bacterial cultures from urine, blood, and throat, and administer appropriate antibiotics 1.
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.
Fluid Resuscitation Protocol
Start 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 1, 2. This aggressive initial fluid replacement restores tissue perfusion and improves insulin sensitivity 1.
After the first hour, adjust fluid choice based on hydration status, serum electrolyte levels, and urine output 1. When serum glucose reaches 250 mg/dL, switch to 5% dextrose with 0.45-0.75% NaCl to prevent hypoglycemia while continuing insulin therapy to ensure complete ketoacidosis resolution 1, 2.
Total fluid replacement should correct estimated deficits within 24 hours, ensuring serum osmolality changes do not exceed 3 mOsm/kg/hour 2.
Insulin Therapy
For moderate-to-severe DKA or critically ill/mentally obtunded patients, use continuous intravenous regular insulin at 0.1 units/kg/hour without an initial bolus 1, 2. The initial bolus is not recommended as it increases hypoglycemia risk 3.
If plasma glucose does not fall by 50 mg/dL from initial value in the first hour, check hydration status; if acceptable, double the insulin infusion rate every hour until a steady glucose decline of 50-75 mg/h is achieved 1.
Critical: 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. Interruption of insulin infusion when glucose levels fall is a common cause of persistent or worsening ketoacidosis 1.
Target glucose between 150-200 mg/dL until DKA resolution parameters are met 1. Monitor blood glucose every 1-2 hours 2.
Alternative Approach for Mild-Moderate Uncomplicated DKA
For hemodynamically stable, alert patients with mild-moderate uncomplicated 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 Priority)
Despite potentially normal or elevated initial levels due to acidosis, total body potassium depletion is universal in DKA, averaging 3-5 mEq/kg body weight 1, 2. 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 is 3.3-5.5 mEq/L, add 20-30 mEq/L potassium (2/3 KCl and 1/3 KPO₄) to IV fluids once adequate urine output is confirmed 1, 2. If anuric or oliguric, potassium repletion must be more cautious with nephrology consultation 1.
If potassium >5.5 mEq/L, withhold potassium initially but monitor closely, as levels will drop rapidly with insulin therapy 1.
Maintain serum potassium between 4-5 mEq/L throughout treatment 1, 2. Check potassium levels every 2-4 hours during active treatment 1. Inadequate potassium monitoring and replacement is a leading cause of mortality in DKA 1.
Bicarbonate Administration
Bicarbonate is NOT recommended for DKA patients with pH >6.9-7.0 1, 2. Multiple studies show no difference in resolution of acidosis or time to discharge with bicarbonate use, and it may worsen ketosis, cause hypokalemia, and increase cerebral edema risk 1, 2.
Monitoring During Treatment
Draw blood every 2-4 hours to determine serum electrolytes, glucose, blood urea nitrogen, creatinine, osmolality, and venous pH 1, 2. Follow venous pH (typically 0.03 units lower than arterial pH) and anion gap to monitor resolution of acidosis 1.
Continuous cardiac monitoring is necessary due to electrolyte shifts and arrhythmia risk 2.
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
Transition to Subcutaneous Insulin
Once DKA is resolved, administer basal insulin (intermediate or long-acting such as glargine or detemir) 2-4 hours BEFORE stopping IV insulin infusion to prevent recurrence of ketoacidosis and rebound hyperglycemia 1, 2. This overlap period is essential 1.
Stopping IV insulin without prior administration of basal subcutaneous insulin causes rebound hyperglycemia and ketoacidosis 1. Recent evidence shows adding low-dose basal insulin analog during IV insulin infusion may prevent rebound hyperglycemia without increasing hypoglycemia risk 1.
When the patient is able to eat, start a multiple-dose schedule using a combination of short/rapid-acting and intermediate/long-acting insulin 1, 2.
Identifying and Treating Precipitating Factors
Identify potential precipitating factors: infection, cerebrovascular accident, alcohol abuse, pancreatitis, myocardial infarction, trauma, drugs, or insulin discontinuation/inadequacy 1, 2. Treatment of the underlying cause must occur simultaneously with correction of the metabolic derangement 1.
SGLT2 inhibitors must be discontinued immediately and not restarted until 3-4 days after metabolic stability is achieved, as these medications can precipitate euglycemic DKA 1, 2.
Common Pitfalls to Avoid
- Premature termination of insulin therapy before complete resolution of ketosis can lead to recurrence of DKA 1
- Interruption of insulin infusion when glucose levels fall is a common cause of persistent or worsening ketoacidosis 1
- Failure to add dextrose when glucose falls below 250 mg/dL while continuing insulin therapy 1
- Inadequate monitoring and replacement of electrolytes, particularly potassium 1
- Overzealous treatment with insulin without glucose supplementation can lead to hypoglycemia 1
- Overly rapid correction of osmolality increases the risk of cerebral edema, particularly in children 1
Discharge Planning
Before discharge, ensure identification of outpatient diabetes care providers, educate patients and families on glucose monitoring, insulin administration, recognition and treatment of hyperglycemia/hypoglycemia, and DKA recognition and prevention 1, 2. Ensure appropriate insulin regimen is prescribed with attention to medication access and affordability 1. Schedule follow-up appointments within 1-2 weeks prior to discharge 1, 2.