Should a patient with Acute Kidney Injury (AKI) on Continuous Renal Replacement Therapy (CRRT) and in euglycemic Diabetic Ketoacidosis (DKA) be started on a DKA protocol?

Management of Euglycemic DKA in Patients on CRRT

Yes, patients with AKI on CRRT who develop euglycemic DKA should be started on a DKA protocol, but with critical modifications to prevent life-threatening hypoglycemia and electrolyte disturbances unique to this dual pathology.

Core Principle: Treat the Metabolic Emergency

The fundamental goal remains resolving the ketoacidosis and metabolic derangement, regardless of glucose level. Euglycemic DKA (glucose <250 mg/dL) requires the same insulin therapy to clear ketones and close the anion gap, but demands heightened vigilance for hypoglycemia 1.

Critical Modifications Required for CRRT Patients

Insulin Administration Strategy

• Initiate continuous insulin infusion as per standard DKA protocol to resolve ketoacidosis, but at potentially lower rates given the euglycemic state 1, 2
• Expect shorter duration on insulin infusion compared to hyperglycemic DKA (mean 13.5 vs 19.4 hours), but with 3-fold higher hypoglycemia risk (18.2% vs 4.8%) 1
• Add dextrose-containing fluids early (D5 or D10) once glucose approaches 200-250 mg/dL to prevent hypoglycemia while continuing insulin to clear ketones 1, 2

Fluid Management Considerations

• Severely restrict fluid resuscitation volumes in patients on CRRT, as these patients cannot handle standard DKA fluid protocols (typically 1-2 liters initial bolus followed by 250-500 mL/hr) 3, 4
• CRRT already provides precise fluid balance control; coordinate fluid administration with CRRT prescription to avoid volume overload 3, 5
• The standard DKA fluid resuscitation approach must be abandoned in favor of CRRT-guided fluid management 6, 3

Electrolyte Replacement Protocol

• Potassium management becomes exponentially more complex: euglycemic DKA patients present with lower initial potassium (4.3 vs 5.3 mmol/L) 1, while CRRT can rapidly shift potassium levels
• Monitor potassium hourly initially, as both insulin therapy and CRRT dialysate composition affect serum levels 4, 1
• Adjust CRRT dialysate potassium concentration based on frequent measurements rather than relying on standard DKA potassium replacement protocols 3, 5
• Hypokalemia risk remains substantial (27.3% in euglycemic DKA) 1

Bicarbonate and Acid-Base Management

• Use bicarbonate-based CRRT replacement fluids rather than lactate-based solutions, as metabolic acidosis from DKA compounds with potential lactic acidosis in critically ill patients 6, 3, 5
• CRRT will assist in correcting metabolic acidosis, but insulin remains essential to stop ketone production and resolve the underlying DKA 2
• Monitor pH and bicarbonate every 2-4 hours initially to assess response 1, 2

Monitoring Requirements

• Glucose monitoring every 1 hour while on insulin infusion due to extreme hypoglycemia risk 1, 2
• Electrolytes (including potassium, phosphate, magnesium) every 2-4 hours initially, then every 4-6 hours once stable 4, 1
• Venous pH and bicarbonate every 2-4 hours until anion gap closes and bicarbonate >18 mmol/L 1, 2
• Beta-hydroxybutyrate or urine ketones to confirm ketone clearance 2

Common Pitfalls to Avoid

• Do not delay insulin therapy because glucose is "normal" - the ketoacidosis still requires insulin to resolve 1, 2
• Do not use standard DKA fluid protocols - this will cause volume overload in CRRT patients 3, 4
• Do not rely on standard potassium replacement algorithms - CRRT dialysate composition must be adjusted dynamically 5, 4
• Do not wait for hyperglycemia to develop before adding dextrose - proactive dextrose administration prevents hypoglycemia while allowing continued insulin therapy 1, 2

Etiology Recognition

• In euglycemic DKA, identify the precipitating cause: insulin use prior to arrival (57%), poor oral intake with baseline insulin (29%), or SGLT2 inhibitor use (14%) 1
• If SGLT2 inhibitors are involved, discontinue immediately and do not restart 7, 2

Resolution Criteria

• DKA resolution defined as: glucose <200 mg/dL, bicarbonate ≥18 mmol/L, venous pH >7.3, and anion gap ≤12 1, 2
• Transition to subcutaneous insulin only after metabolic parameters normalize and patient tolerates oral intake 2
• Continue CRRT based on renal indications independent of DKA resolution 6, 3

Special Consideration for Citrate Anticoagulation

• If using regional citrate anticoagulation for CRRT (recommended approach), be aware this can affect acid-base status interpretation 6, 5
• Citrate metabolism generates bicarbonate, potentially masking ongoing ketoacidosis 6
• Monitor ionized calcium and total calcium/ionized calcium ratio to detect citrate accumulation 6