What is the best course of action for a 24-year-old female with type 1 diabetes, presenting with diabetic ketoacidosis (DKA), impaired renal function, metabolic acidosis, and hyperketonemia, who has been non-adherent to her prescribed Lantus (insulin glargine) regimen?

Management of Severe Diabetic Ketoacidosis with Renal Impairment and Insulin Non-Adherence

This patient requires immediate hospitalization for aggressive intravenous fluid resuscitation, continuous IV insulin infusion, careful potassium monitoring and replacement, and treatment of any precipitating factors—with special attention to her impaired renal function which will affect fluid and electrolyte management. 1

Immediate Initial Management

Fluid Resuscitation

• Begin with isotonic saline (0.9% NaCl) at 15-20 mL/kg/hour (approximately 1-1.5 L in the first hour) to restore circulatory volume and tissue perfusion. 2, 1
• However, given her elevated creatinine (1.42) and reduced GFR (53), monitor closely for fluid overload and consider reducing the rate after initial resuscitation. 3
• Total fluid replacement should aim to correct estimated deficits within 24 hours, but proceed more cautiously in patients with renal compromise. 1, 3
• When serum glucose reaches 250 mg/dL, change fluid to 5% dextrose with 0.45-0.75% NaCl to prevent hypoglycemia while continuing insulin therapy. 2, 1

Insulin Therapy

• Start continuous intravenous regular insulin infusion at 0.1 units/kg/hour without an initial bolus. 1, 3
• Target a steady glucose decline of 50-75 mg/dL per hour. 2, 1
• 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 steady decline is achieved. 1
• Continue insulin infusion until resolution of ketoacidosis (pH >7.3, serum bicarbonate ≥18 mEq/L, and anion gap ≤12 mEq/L) regardless of glucose levels. 2, 1
• Do not stop insulin when glucose normalizes—ketoacidosis takes longer to resolve than hyperglycemia, and premature cessation causes recurrence. 2, 1, 3

Critical Electrolyte Management

Potassium is the most critical electrolyte concern in DKA management:

• Despite total body potassium depletion averaging 3-5 mEq/kg, initial serum levels may be normal or elevated. 1, 3
• Insulin therapy will drive potassium intracellularly, causing rapid and potentially life-threatening decline. 1, 3
• Check potassium levels every 2-4 hours during active treatment. 2, 1

Potassium replacement algorithm: 2, 1, 3

• If K+ <3.3 mEq/L: Delay insulin therapy and aggressively replace potassium first to prevent fatal cardiac arrhythmias. Do not start insulin until K+ ≥3.3 mEq/L.
• 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 is confirmed.
• If K+ >5.5 mEq/L: Withhold potassium initially but monitor closely, as levels will drop rapidly with insulin therapy.
• Target serum potassium of 4-5 mEq/L throughout treatment. 2, 1

Special Considerations for Renal Impairment

• With GFR 53, this patient has moderate renal impairment (CKD Stage 3a). 3
• Confirm adequate urine output before aggressive potassium repletion; if anuric or oliguric, potassium repletion must be more cautious with nephrology consultation. 1
• Monitor for fluid overload more carefully than in patients with normal renal function. 3
• Bicarbonate administration is generally NOT recommended for pH >6.9-7.0, as it provides no benefit and may worsen ketosis, cause hypokalemia, and increase cerebral edema risk. 2, 1

Monitoring During Treatment

• Draw blood every 2-4 hours to measure serum electrolytes, glucose, BUN, creatinine, osmolality, and venous pH. 2, 1, 3
• After initial diagnosis, venous pH (typically 0.03 units lower than arterial pH) and anion gap adequately monitor acidosis resolution without repeated arterial sticks. 2, 1, 3
• Direct measurement of β-hydroxybutyrate in blood is the preferred method for monitoring DKA, as the nitroprusside method only measures acetoacetic acid and acetone. 2, 1, 3
• Monitor for signs of cerebral edema, especially with overly aggressive fluid resuscitation. 3

Resolution Criteria

DKA is resolved when ALL of the following are met: 2, 1, 3

• Glucose <200 mg/dL
• Serum bicarbonate ≥18 mEq/L
• Venous pH >7.3
• Anion gap ≤12 mEq/L

Note that ketonemia typically takes longer to clear than hyperglycemia. 2, 3

Transition to Subcutaneous Insulin

• Once DKA is resolved, administer basal insulin (intermediate or long-acting) 2-4 hours BEFORE stopping IV insulin infusion to prevent recurrence of ketoacidosis and rebound hyperglycemia. 2, 1, 3
• This overlap period is essential—stopping IV insulin without prior administration of basal subcutaneous insulin causes rebound hyperglycemia and ketoacidosis. 1
• Start a multiple-dose schedule using a combination of short/rapid-acting and intermediate/long-acting insulin when the patient is able to eat. 2, 1
• Long-acting insulin therapy alone (like Lantus monotherapy) is NOT sufficient for type 1 diabetes because of the absence of pancreatic function after beta-cell destruction. 4
• Starting total daily requirement can be estimated at 0.3-0.4 units/kg/day, with half given as prandial coverage in divided doses and half as once-daily long-acting analog. 4

Addressing the Precipitating Factor

The most common precipitating causes for DKA include infections, new diagnosis of diabetes, and nonadherence to insulin therapy. 5

• In this case, the patient took only 10 units of Lantus instead of her prescribed 22 units, representing insulin non-adherence. 5
• Identify any concurrent infections or other precipitating factors (myocardial infarction, stroke, pancreatitis) and treat appropriately. 2, 1, 3
• Obtain bacterial cultures (urine, blood, throat) if infection is suspected and administer appropriate antibiotics. 1, 3

Common Pitfalls to Avoid

• Premature termination of insulin therapy before complete resolution of ketosis leads to recurrence of DKA. 2, 1
• Interruption of insulin infusion when glucose levels fall is a common cause of persistent or worsening ketoacidosis. 2, 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, which is a leading cause of mortality in DKA. 1, 3
• Overzealous fluid resuscitation in patients with renal or cardiac compromise can lead to fluid overload. 3
• Relying on urine ketones for monitoring response to treatment—they don't measure β-hydroxybutyrate and can falsely suggest worsening ketosis during treatment. 3

Discharge Planning and Prevention

• Education is critical to learn skills like responding to hypoglycemia, anticipating exercise, monitoring for DKA, and carbohydrate counting. 4
• Early endocrinology consultation is a high priority for all patients. 4
• Ensure appropriate insulin regimen is prescribed with attention to medication access and affordability. 1
• Educate on recognition, prevention, and management of DKA to prevent recurrence. 1, 3
• Future episodes of DKA can be reduced through patient education programs focusing on adherence to insulin and self-care guidelines during illness. 5