Management of Diabetic Ketoacidosis in Adults
Begin aggressive isotonic saline resuscitation at 15–20 mL/kg/hour in the first hour, followed by continuous IV regular insulin at 0.1 units/kg/hour once potassium is ≥3.3 mEq/L, and continue insulin until complete resolution of ketoacidosis regardless of glucose levels. 1, 2
Initial Diagnostic Workup
Obtain the following laboratory studies immediately upon presentation:
- Plasma glucose, arterial or venous pH, serum electrolytes with calculated anion gap 1, 2
- β-hydroxybutyrate (β-OHB) in blood—this is the preferred ketone test, not nitroprusside-based urine or serum tests which miss the predominant ketone body 1, 2, 3
- BUN, creatinine, calculated effective serum osmolality (2 × [Na] + glucose/18) 1, 2
- Complete blood count, urinalysis with ketones, electrocardiogram 1, 2
- Bacterial cultures (blood, urine, throat) if infection is suspected 1, 2
Diagnostic criteria for DKA: glucose >250 mg/dL, arterial pH <7.3, serum bicarbonate <15 mEq/L, positive serum/urine ketones, and anion gap >12 mEq/L 1, 2, 3
Fluid Resuscitation Protocol
First Hour
Administer isotonic saline (0.9% NaCl) at 15–20 mL/kg/hour (approximately 1–1.5 L in an average adult) to restore intravascular volume and renal perfusion 4, 1, 2
The typical total body water deficit in DKA is 6–9 L 1, 2
After First Hour
Calculate corrected serum sodium: add 1.6 mEq/L for each 100 mg/dL glucose above 100 mg/dL 1, 2
- If corrected sodium is normal or elevated: switch to 0.45% NaCl at 4–14 mL/kg/hour 4, 1, 2
- If corrected sodium is low: continue 0.9% NaCl at 4–14 mL/kg/hour 4, 1, 2
When Glucose Reaches 250 mg/dL
Change IV fluids to 5% dextrose with 0.45–0.75% NaCl while continuing insulin infusion to prevent hypoglycemia and ensure complete ketoacidosis resolution 4, 1, 2
Critical pitfall: Stopping insulin when glucose normalizes leads to recurrent ketoacidosis because ketonemia takes longer to clear than hyperglycemia 1, 2
Aim to correct the fluid deficit over 24 hours while limiting osmolality change to ≤3 mOsm/kg H₂O per hour to reduce cerebral edema risk 4, 1
Potassium Management
Total body potassium depletion is universal in DKA (approximately 3–5 mEq/kg) even when serum levels appear normal or elevated 1, 2
Potassium replacement algorithm:
- If K⁺ <3.3 mEq/L: Hold insulin and aggressively replace potassium at 20–40 mEq/hour until K⁺ ≥3.3 mEq/L to prevent life-threatening arrhythmias, cardiac arrest, and respiratory muscle weakness 1, 2
- If K⁺ 3.3–5.5 mEq/L: Add 20–30 mEq potassium per liter of IV fluid (approximately 2/3 KCl and 1/3 KPO₄) once adequate urine output is confirmed 4, 1, 2
- If K⁺ >5.5 mEq/L: Withhold potassium initially but monitor every 2–4 hours as levels will drop rapidly with insulin therapy 1, 2
Target serum potassium throughout treatment: 4–5 mEq/L 1, 2
Insulin Therapy
Confirm serum potassium ≥3.3 mEq/L before starting insulin 1, 2
Administer IV bolus of regular insulin 0.15 units/kg, then start continuous infusion of 0.1 units/kg/hour 4, 1, 2
Target a glucose decline of 50–75 mg/dL per hour 4, 1, 2
If glucose does not fall by 50 mg/dL in the first hour and hydration is adequate, double the insulin infusion rate each hour until a steady decline is achieved 4, 1, 2
Continue insulin infusion until complete DKA resolution regardless of glucose level 1, 2:
- pH >7.3
- Serum bicarbonate ≥18 mEq/L
- Anion gap ≤12 mEq/L
- Glucose <200 mg/dL
Alternative for Mild-to-Moderate Uncomplicated DKA
For hemodynamically stable, alert patients with mild-to-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, 2, 5
Continuous IV insulin remains the standard of care for critically ill and mentally obtunded patients 1, 2
Monitoring During Treatment
Draw blood every 2–4 hours for 1, 2:
- Serum electrolytes, glucose, BUN, creatinine
- Venous pH (typically 0.03 units lower than arterial pH—repeat arterial gases are generally unnecessary) 1, 2
- Calculated osmolality and anion gap
Monitor β-hydroxybutyrate levels to track ketosis resolution—this is superior to nitroprusside-based tests 1, 2, 3
Common pitfall: Nitroprusside-based ketone tests only measure acetoacetate and acetone, missing β-OHB (the predominant ketone body), and may paradoxically appear worse during treatment as β-OHB converts to acetoacetate 1, 2, 3
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
Consider bicarbonate only if pH <6.9: administer 100 mEq sodium bicarbonate in 400 mL sterile water at 200 mL/hour 2
Identification and Treatment of Precipitating Causes
Common precipitants that must be sought and treated concurrently 1, 2:
- Infection (most common): obtain cultures and start appropriate antibiotics
- Myocardial infarction, cerebrovascular accident
- Insulin omission or inadequacy
- Pancreatitis, trauma
- SGLT2 inhibitor use: discontinue immediately and do not restart until 3–4 days after metabolic stability 1, 2
- Glucocorticoid therapy
- Pregnancy
Transition to Subcutaneous Insulin
Administer basal insulin (intermediate or long-acting such as glargine, detemir, or NPH) 2–4 hours BEFORE stopping the IV insulin infusion to prevent recurrence of ketoacidosis and rebound hyperglycemia 1, 2
Critical pitfall: Stopping IV insulin without prior administration of basal subcutaneous insulin causes rebound hyperglycemia and ketoacidosis 1, 2
Recent evidence shows that adding low-dose basal insulin analog during IV insulin infusion may prevent rebound hyperglycemia without increasing hypoglycemia risk 1, 2
Once the patient can eat, start a multiple-dose schedule using short/rapid-acting plus intermediate/long-acting insulin 1, 2
For newly diagnosed patients, start with approximately 0.5–1.0 units/kg/day total daily insulin dose 1, 2
Special Considerations
Cerebral Edema
Cerebral edema occurs more commonly in children and adolescents than adults but remains one of the most serious complications 1, 2
Prevention strategies:
- Avoid overly rapid correction of osmolality (limit to ≤3 mOsm/kg H₂O per hour) 4, 1
- Monitor mental status continuously for signs of altered consciousness, headache, or neurological deterioration 1, 2
- Avoid excessive fluid administration in patients with cardiac or renal compromise 1, 2
Euglycemic DKA
SGLT2 inhibitors are the leading contemporary cause of euglycemic DKA (glucose <200–250 mg/dL with ketoacidosis) 2
These agents lower the renal glucose threshold, masking hyperglycemia that normally alerts clinicians to DKA 2
Management: Same fluid, insulin, and electrolyte protocols apply; discontinue SGLT2 inhibitors immediately 2
Discharge Planning
Prior to discharge, ensure 1, 2:
- Identified outpatient diabetes care provider
- Patient education on recognition, prevention, and management of DKA
- Education on glucose monitoring, insulin administration, and recognition/treatment of hyperglycemia and hypoglycemia
- Appropriate insulin regimen prescribed with attention to medication access and affordability
- All prescriptions filled and reviewed with patient and family
- Follow-up appointment scheduled