Immediate Management: Check Serum Potassium and ECG
The most appropriate next step is to obtain STAT serum potassium, creatinine, and ECG, as this patient on lisinopril with CKD presenting with drowsiness, fatigue, and nausea is at high risk for life-threatening hyperkalemia. If hyperkalemia is confirmed with ECG changes, calcium gluconate (option D) should be administered immediately to stabilize the cardiac membrane 1, 2.
Clinical Reasoning
This patient's presentation is highly concerning for hyperkalemia-induced cardiac toxicity:
- ACE inhibitor (lisinopril) in CKD dramatically increases hyperkalemia risk, with rates of severe hyperkalemia (K+ >6.0 mmol/L) approaching 4% in clinical trials and likely higher in real-world practice 1
- Drowsiness with fatigue and nausea are classic but non-specific symptoms of hyperkalemia that can rapidly progress to cardiac arrhythmias, respiratory paralysis, and death 2
- CKD stage 3b-4 (implied by erythropoietin and vitamin D use) significantly impairs potassium excretion 1
Diagnostic Workup Priority
Obtain immediately (within 30 minutes):
- Serum potassium, creatinine, BUN 1
- 12-lead ECG to assess for hyperkalemic changes (peaked T waves, widened QRS, loss of P waves) 2
- Blood glucose to rule out hypoglycemia (patient on insulin) 2
- Venous blood gas if available (to assess for metabolic acidosis, which worsens hyperkalemia) 3
Treatment Algorithm Based on Results
If Hyperkalemia Confirmed (K+ >5.5 mmol/L):
With ECG changes (peaked T waves, QRS widening):
- Calcium gluconate 10% 10-20 mL IV over 2-3 minutes immediately to stabilize cardiac membrane (Answer D is correct in this scenario) 2
- Insulin 10 units IV with D50W 25g to shift potassium intracellularly 2
- Consider sodium bicarbonate if metabolic acidosis present 1
- Hold lisinopril temporarily 1
Without ECG changes but K+ 5.5-6.5 mmol/L:
- Insulin/dextrose protocol 2
- Sodium polystyrene sulfonate or patiromer for GI potassium removal 1
- Reduce or hold lisinopril dose 1
- Dietary potassium restriction 1
If Hyperkalemia Absent:
Consider alternative diagnoses:
- Hypoglycemia (check fingerstick glucose immediately) - treat with D5W or oral glucose 2
- Uremia from CKD progression - may require dialysis evaluation 3
- Volume overload - consider diuretics (Answer C) if evidence of fluid retention 1
- Metabolic acidosis - consider NaHCO3 (Answer A) if pH <7.2 and bicarbonate <15 mEq/L 1
Critical Monitoring After ACE Inhibitor Initiation
The KDIGO guidelines emphasize that serum creatinine and potassium must be monitored within 2-4 weeks after starting or increasing ACE inhibitor dose 1, 4. This patient's presentation suggests this monitoring may have been inadequate.
Continue ACE inhibitor unless:
- Creatinine rises >30% within 4 weeks (suggests acute kidney injury, volume depletion, or renal artery stenosis) 1, 4
- Uncontrolled hyperkalemia despite medical management 1
- Symptomatic hypotension 1
Common Pitfall to Avoid
Do not empirically treat with diuretics, bicarbonate, or D5W without first confirming the diagnosis. While these may be appropriate treatments for specific conditions (volume overload, metabolic acidosis, hypoglycemia), administering them blindly could worsen the patient's condition:
- D5W without insulin in hyperkalemia will worsen potassium levels 2
- Diuretics may worsen volume depletion if patient is euvolemic 1
- NaHCO3 is only indicated for metabolic acidosis and can worsen volume overload 1
The drowsiness is the red flag here - this suggests either severe hyperkalemia, hypoglycemia, or uremia, all of which require immediate laboratory confirmation before treatment 2, 3.