Lisinopril Should Be Stopped Immediately
In this elderly patient with DVT and severe hyperkalemia (K+ 6.0 mEq/L), lisinopril must be discontinued immediately as it is the primary cause of the life-threatening hyperkalemia. 1, 2
Clinical Reasoning
The Hyperkalemia Crisis
- Potassium of 6.0 mEq/L represents moderate-to-severe hyperkalemia requiring immediate intervention, and ACE inhibitors like lisinopril are the most common culprit in patients with declining renal function 2, 3
- The American Geriatrics Society specifically warns that ACE inhibitors in elderly diabetic patients significantly increase hyperkalemia risk, particularly when combined with declining renal function (creatinine 120 μmol/L, up from baseline 115) 1
- The European Society of Cardiology recommends discontinuing RAAS inhibitors immediately when K+ >6.5 mEq/L, and this patient at 6.0 mEq/L is approaching that threshold 2
Why Not the Other Medications?
Furosemide (Loop Diuretic):
- Loop diuretics actually reduce hyperkalemia risk by promoting urinary potassium excretion and should be continued 2
- The FDA label confirms furosemide causes hypokalemia, not hyperkalemia 4
- Stopping furosemide would worsen hyperkalemia 2
Metformin:
- Metformin does not cause hyperkalemia and has no direct effect on potassium homeostasis 2
- While metformin should be held during acute illness with volume depletion to prevent lactic acidosis 5, this patient has DVT without evidence of severe volume depletion
- The concern with metformin is lactic acidosis in renal dysfunction, not hyperkalemia 6
Heparin:
- Heparin can cause hyperkalemia through aldosterone suppression, but this typically occurs with prolonged use (>7 days) and is less pronounced than ACE inhibitor-induced hyperkalemia 2
- Stopping heparin in acute DVT would be dangerous, risking pulmonary embolism and death 7
- The prolonged PT/APTT suggests therapeutic anticoagulation is being achieved, which is essential for DVT treatment 7
Immediate Management Algorithm
Step 1: Discontinue Lisinopril Immediately
- The American College of Cardiology recommends discontinuing ACE inhibitors as the primary intervention in moderate hyperkalemia with declining renal function 2
Step 2: Obtain ECG
- Check for hyperkalemia-related changes (peaked T waves, widened QRS, loss of P waves) 2
Step 3: Recheck Potassium and Creatinine Within 24-48 Hours
- Monitor response to lisinopril discontinuation 2
Step 4: If K+ Remains >5.5 mEq/L After Stopping Lisinopril
- Initiate sodium zirconium cyclosilicate or patiromer 2
- Avoid sodium polystyrene sulfonate (Kayexalate) in elderly patients due to serious gastrointestinal adverse events 2
Step 5: Continue All Other Medications
- Continue heparin for DVT treatment 7
- Continue furosemide to promote potassium excretion 2
- Continue metformin (no contraindication with current creatinine) 2
Long-Term Blood Pressure Management
Once Potassium Normalizes (4.0-5.0 mEq/L):
- Consider reintroducing lisinopril at a lower dose (5 mg daily) with close monitoring if blood pressure control requires it 2
- Alternative: Switch to calcium channel blocker (amlodipine) that does not affect potassium homeostasis 2
- Newer potassium binders (patiromer or sodium zirconium cyclosilicate) can enable continuation of RAAS inhibitors in patients requiring them for cardio-renal protection 1, 2
Critical Pitfalls to Avoid
- Do not stop heparin - this would be life-threatening in acute DVT 7
- Do not stop furosemide - this would worsen hyperkalemia by reducing potassium excretion 2
- Do not use Kayexalate in elderly patients - serious GI complications including colonic necrosis 2
- Monitor renal function closely - the combination of ACE inhibitor, diuretic, and diabetes puts this patient at high risk for further renal deterioration 1, 8