Management of DKA with AKI and CKD
In adults with diabetic ketoacidosis complicated by acute kidney injury and chronic kidney disease, initiate aggressive fluid resuscitation with isotonic saline at 15-20 ml/kg/hour (1-1.5 liters in the first hour), followed by insulin therapy and intensive potassium monitoring, while adjusting fluid rates and insulin dosing based on renal function and avoiding rapid osmolality shifts. 1
Initial Laboratory Evaluation
Essential Diagnostic Tests
- Arterial blood gas to document metabolic acidosis with pH <7.3 1
- Serum β-hydroxybutyrate specifically (not nitroprusside-based tests, which miss this predominant ketone and should not be used for monitoring) 1
- Serum glucose (typically >250 mg/dL, though euglycemic DKA exists with glucose <250 mg/dL, particularly with SGLT2 inhibitor use) 1, 2
- Serum bicarbonate to confirm levels <15-18 mEq/L 1
- Electrolytes with calculated anion gap (>10 mEq/L in mild DKA, >12 mEq/L in moderate-severe) 1, 3
- BUN/creatinine to assess renal function and hydration status, critical given the AKI/CKD context 1
- Corrected serum sodium by adding 1.6 mEq/L for each 100 mg/dL glucose above 100 mg/dL 1
Additional Monitoring Tests
- Serum phosphate, magnesium, and calcium (typical deficits: phosphate 3-5 mmol/kg, magnesium 4-6 mEq/kg, calcium 1-2 mEq/kg) 1
- Complete blood count with differential to identify infection as precipitating cause 2
- Urinalysis (though avoid relying on urine ketones alone for diagnosis) 1, 2
- A1C for baseline glycemic control assessment 2
- ECG to evaluate for cardiac complications and hyperkalemia 2
- Blood and urine cultures if infection suspected 2
Critical Diagnostic Pitfalls
- Never rely on urine ketone testing alone as it is insufficient and misleading 1
- Exclude other causes of high anion gap metabolic acidosis including lactic acidosis, salicylate toxicity, methanol/ethylene glycol ingestion, uremia, and alcoholic ketoacidosis 1, 3
- Recognize euglycemic DKA particularly in patients on SGLT2 inhibitors 2
Fluid Resuscitation Protocol
Initial Fluid Management
- Isotonic saline (0.9% NaCl) at 15-20 ml/kg/hour during the first hour (1-1.5 liters in average adult) in absence of cardiac compromise 1
- Consider balanced electrolyte solutions as recent evidence shows faster DKA resolution (mean difference -5.36 hours) compared to 0.9% saline, with lower post-resuscitation chloride and sodium levels 4
- After initial hour, adjust to either 0.9% or 0.45% NaCl based on corrected serum sodium and hydration status 5
Renal-Specific Considerations
- Target correction of estimated deficits within 24 hours with serum osmolality change not exceeding 3 mOsm/kg H₂O per hour to prevent cerebral edema 1
- Monitor fluid overload carefully given impaired renal clearance in AKI/CKD 6
- Typical total body deficits: water 6-9 liters, sodium 7-10 mEq/kg, potassium 3-5 mEq/kg, chloride 5-13 mEq/kg 1
Insulin Therapy
Insulin Administration
- Begin insulin therapy after initial fluid resuscitation (not before, to avoid worsening hypovolemia) 7, 8
- Continue insulin infusion until acidosis resolves (bicarbonate ≥18 mEq/L, venous pH >7.3), not just until glucose normalizes 3
- Add dextrose to IV fluids when glucose reaches 200 mg/dL to prevent hypoglycemia while continuing insulin to clear ketoacidosis 3
Critical Insulin Management Error
- Never stop insulin when glucose normalizes before acidosis resolves as this causes rebound hyperglycemia and ketoacidosis 3
Electrolyte Replacement
Potassium Management (Critical in Renal Dysfunction)
- Initiate potassium replacement once renal function is assured (urine output established) 1, 5
- Add 20-30 mEq/L potassium to IV fluids (2/3 KCl and 1/3 KPO₄) until patient is stable and can tolerate oral supplementation 1
- Monitor potassium every 2-4 hours as insulin drives potassium intracellularly, risking life-threatening hypokalemia despite total body depletion 1, 7
- Exercise extreme caution in AKI/CKD as impaired renal excretion increases hyperkalemia risk 9
Bicarbonate Therapy
- **Only consider bicarbonate therapy when pH <6.9** (not necessary if pH >7.0) 3
- In CKD patients with chronic acidosis (serum bicarbonate <22 mmol/L), oral bicarbonate supplementation can be given to maintain normal range once acute DKA resolves 6
Phosphate Considerations
- Typical phosphate deficit is 3-5 mmol/kg 1
- Replacement included in potassium supplementation (1/3 as KPO₄) 1
Monitoring Protocol
Frequency of Assessments
- Check arterial blood gases and serum electrolytes every 2-4 hours during active treatment 3
- Monitor venous pH and anion gap every 2-4 hours to track resolution 3
- Continuous assessment of vital signs, fluid input/output, and mental status 1
- Hemodynamic monitoring to track blood pressure improvement 1
Resolution Criteria
- DKA resolution requires: serum bicarbonate ≥18 mEq/L, glucose <200 mg/dL, and venous pH >7.3 3
- Anion gap closure indicates resolution of ketoacidosis 3
Treatment Complications to Monitor
- Hypoglycemia from excessive insulin 3
- Hypokalemia from insulin-driven intracellular shift 3, 7
- Hyperchloremic acidosis from excessive saline administration (less common with balanced solutions) 3, 4
- Fluid overload particularly in AKI/CKD patients with impaired clearance 6
- Cerebral edema from overly rapid osmolality correction 1
Nephrology Consultation Indications
Refer to nephrology for: 6
- GFR <30 ml/min/1.73 m² (baseline CKD)
- Abrupt sustained fall in GFR (AKI component)
- Progression of CKD (drop in eGFR from baseline by 25% or sustained decline >5 ml/min/1.73 m²/year)
- Need for renal replacement therapy consideration 6
Special Considerations in AKI/CKD Context
Contrast Avoidance
- Avoid gadolinium-containing contrast if GFR <15 ml/min/1.73 m² unless no alternative 6
- If GFR <30 ml/min/1.73 m² and gadolinium required, use macrocyclic chelate preparation 6
- For iodinated contrast with GFR <60 ml/min/1.73 m²: avoid high-osmolar agents, use lowest dose, withdraw nephrotoxic agents, ensure adequate hydration, measure GFR 48-96 hours post-procedure 6
Medication Adjustments
- Withdraw potentially nephrotoxic agents during acute illness 6
- Consider ACE-I/ARB discontinuation during acute DKA with AKI, with careful re-initiation planning 6