Management of Diabetic Ketoacidosis in Adults
Initial Resuscitation and Fluid Management
Begin aggressive isotonic saline (0.9% NaCl) at 15–20 mL/kg/hour during the first hour to restore intravascular volume and tissue perfusion; this typically delivers 1–1.5 L in an average adult and is critical for improving insulin sensitivity. 1, 2
After the first hour, calculate corrected serum sodium by adding 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. 1, 2
- If corrected sodium is low: continue 0.9% NaCl at 4–14 mL/kg/hour. 1, 2
When plasma glucose falls to 250 mg/dL, change IV fluids to 5% dextrose with 0.45–0.75% NaCl while maintaining the insulin infusion to prevent hypoglycemia and ensure complete ketoacidosis resolution. 1, 2
The total fluid deficit in DKA averages 6–9 L and should be replaced over 24 hours while limiting the change in serum osmolality to ≤3 mOsm/kg/hour to reduce cerebral edema risk. 1, 2
Potassium Management (Class A Evidence)
Verify serum potassium ≥3.3 mEq/L before initiating insulin therapy—this is an absolute contraindication supported by Class A evidence. 1, 2
Total body potassium depletion is universal in DKA (approximately 3–5 mEq/kg) even when initial serum potassium appears normal or elevated due to acidosis and insulin deficiency. 1, 2
Potassium Replacement Algorithm:
K⁺ <3.3 mEq/L: Hold insulin and aggressively replace potassium at 20–40 mEq/hour until K⁺ ≥3.3 mEq/L to prevent fatal cardiac arrhythmias, respiratory muscle weakness, and cardiac arrest. 1, 2
K⁺ 3.3–5.5 mEq/L: Start insulin and add 20–30 mEq/L potassium to each liter of IV fluid (approximately 2/3 potassium chloride or acetate and 1/3 potassium phosphate) once adequate urine output is confirmed. 1, 2
K⁺ >5.5 mEq/L: Start insulin immediately without potassium supplementation; monitor every 2–4 hours as levels will decline rapidly with insulin therapy, then add potassium once K⁺ falls below 5.5 mEq/L. 1, 2
Target serum potassium of 4.0–5.0 mEq/L throughout treatment—not merely >3.5 mEq/L. 1, 2
Insulin Therapy
Administer continuous IV regular insulin at 0.1 units/kg/hour (an initial bolus of 0.1–0.15 units/kg is optional but not required) once serum potassium is ≥3.3 mEq/L. 1, 2, 3
Target a glucose decline of 50–75 mg/dL per hour. 1, 2
If glucose does not fall by ≥50 mg/dL in the first hour despite adequate hydration, double the insulin infusion rate each subsequent hour until a steady decline is achieved. 1, 2
Continue insulin infusion until DKA resolution is achieved (pH >7.3, bicarbonate ≥18 mEq/L, anion gap ≤12 mEq/L, glucose <200 mg/dL), regardless of glucose levels. 1, 4
When glucose reaches 250 mg/dL, add dextrose to IV fluids while maintaining the insulin infusion—never stop insulin when glucose normalizes, as ketone clearance lags behind glucose correction. 1, 2
Alternative for Mild-Moderate Uncomplicated DKA:
For hemodynamically stable, alert patients with mild-moderate DKA, subcutaneous rapid-acting insulin analogs (0.1–0.2 units/kg every 1–2 hours) combined with aggressive fluid management are equally effective, safer, and more cost-effective than IV insulin. 1, 2
This approach requires adequate fluid replacement, frequent point-of-care glucose monitoring, treatment of concurrent infections, and appropriate follow-up. 1
Laboratory Monitoring
Obtain at presentation: plasma glucose, venous or arterial pH, serum electrolytes with calculated anion gap, β-hydroxybutyrate (preferred ketone test), BUN, creatinine, effective serum osmolality, urinalysis with ketones, CBC with differential, and ECG. 1, 4
Draw blood every 2–4 hours for serum electrolytes (especially potassium), glucose, BUN, creatinine, osmolality, and venous pH until metabolically stable. 1, 2
Use venous pH for ongoing monitoring—it is typically 0.03 units lower than arterial pH and eliminates the need for repeated arterial blood gases. 1, 4
Measure β-hydroxybutyrate in blood as the preferred method for monitoring ketosis resolution—nitroprusside-based tests (urine ketones) only detect acetoacetate and acetone, missing the predominant ketone body (β-hydroxybutyrate), and may delay appropriate therapy. 1, 4
Bicarbonate Administration
Do NOT administer bicarbonate for DKA patients with pH >6.9–7.0—multiple studies show no benefit in resolution of acidosis or time to discharge, and bicarbonate may worsen ketosis, cause hypokalemia, and increase cerebral edema risk. 1, 2
Consider bicarbonate (100 mmol sodium bicarbonate diluted in 400 mL sterile water, infused at 200 mL/hour) only if pH <6.9 after initial fluid resuscitation. 2
Identification and Treatment of Precipitating Causes
Obtain bacterial cultures (urine, blood, throat) if infection is suspected and administer appropriate antibiotics—infection is the most common precipitant of DKA. 1, 2
Actively search for other precipitants: myocardial infarction, cerebrovascular accident, pancreatitis, insulin omission or inadequacy, SGLT2-inhibitor use, glucocorticoid therapy, trauma, and pregnancy. 1, 2
Discontinue SGLT2 inhibitors immediately and do not restart until 3–4 days after metabolic stability is achieved to prevent euglycemic DKA recurrence. 1, 4
Transition to Subcutaneous Insulin
Administer basal insulin (glargine, detemir, or NPH) 2–4 hours BEFORE stopping the IV insulin infusion to prevent rebound hyperglycemia and recurrence of ketoacidosis—this is the most common cause of recurrent DKA. 1, 2
Continue the IV insulin infusion for an additional 1–2 hours after the subcutaneous basal dose to ensure adequate absorption. 1, 2
Calculate the basal dose as approximately 50% of the total 24-hour IV insulin amount given as a single daily injection; divide the remaining 50% equally among three meals as rapid-acting prandial insulin. 2
Once the patient can tolerate oral intake, start a multiple-dose schedule using a combination of short/rapid-acting and intermediate/long-acting insulin. 1, 2
Critical Pitfalls to Avoid
Never start insulin when potassium is <3.3 mEq/L—this can precipitate fatal cardiac arrhythmias. 1, 2
Never stop insulin when glucose falls to 250 mg/dL without adding dextrose—this leads to recurrent ketoacidosis. 1, 2
Never discontinue IV insulin without a 2–4 hour overlap of basal subcutaneous insulin—this is the most common cause of DKA recurrence. 1, 2
Never rely on urine ketones or nitroprusside-based tests for monitoring—they miss β-hydroxybutyrate and may delay appropriate therapy. 1, 4
Inadequate potassium monitoring and replacement is a leading cause of mortality in DKA—monitor every 2–4 hours and maintain K⁺ 4.0–5.0 mEq/L. 1, 2
Overly rapid correction of serum osmolality (>3 mOsm/kg/hour) increases the risk of cerebral edema, particularly in children but also relevant in adults. 1, 2
Discharge Planning
Prior to discharge, ensure the patient has identified an outpatient diabetes care provider to facilitate continuity of care. 1, 2
Provide education on recognition, prevention, and management of DKA, including glucose monitoring, insulin administration, sick-day management, and when to seek medical care. 1, 2
Verify that all new or adjusted medication prescriptions are filled and reviewed with the patient and family prior to discharge. 2
Schedule a follow-up outpatient appointment before discharge to improve post-hospital compliance. 2