How to treat hyperkalemia caused by vancomycin (Vancomycin) intravenous (IV) infusion?

Treatment of Vancomycin-Induced Hyperkalemia

Critical First Step: Verify the Diagnosis

Vancomycin does NOT cause hyperkalemia—it actually causes hypokalemia (low potassium). 1 The case report evidence demonstrates that vancomycin induces renal potassium wasting, leading to critically low potassium levels, not elevated levels. 1

• If hyperkalemia is present in a patient receiving vancomycin IV, look for alternative causes immediately rather than attributing it to the vancomycin itself. 2
• Exclude pseudo-hyperkalemia from hemolysis or improper blood sampling by repeating the measurement with appropriate technique or arterial sampling. 2, 3

Identify the True Cause of Hyperkalemia

Review all concurrent medications that commonly cause hyperkalemia in hospitalized patients receiving vancomycin:

• RAAS inhibitors (ACE inhibitors, ARBs, mineralocorticoid receptor antagonists) are the most common culprits. 2
• Potassium-sparing diuretics (spironolactone, amiloride, triamterene). 2
• NSAIDs impair renal potassium excretion. 2, 4
• Trimethoprim-sulfamethoxazole (often used concurrently with vancomycin for MRSA coverage). 2
• Heparin (frequently administered in hospitalized patients). 2
• Beta-blockers decrease potassium excretion. 2

Acute Hyperkalemia Management Algorithm

Step 1: Assess Severity and ECG Changes

• Severe hyperkalemia is defined as potassium ≥6.5 mEq/L. 3
• ECG changes (peaked T waves, flattened P waves, prolonged PR interval, widened QRS) indicate urgent treatment regardless of the exact potassium level. 3
• Absent or atypical ECG changes do NOT exclude the necessity for immediate intervention. 5

Step 2: Cardiac Membrane Stabilization (if K+ >6.5 mEq/L OR ECG changes present)

Administer IV calcium immediately:

• Calcium chloride 10%: 5-10 mL (500-1000 mg) IV over 2-5 minutes (preferred for rapid effect). 3
• Alternative: Calcium gluconate 10%: 15-30 mL IV over 2-5 minutes. 3
• Onset within 1-3 minutes, but effects last only 30-60 minutes. 3
• Calcium does NOT lower potassium—it only stabilizes cardiac membranes temporarily. 3
• Monitor ECG continuously; if no improvement in 5-10 minutes, repeat the dose. 3

Step 3: Shift Potassium into Cells

Administer all three agents together for maximum effect:

• Insulin with glucose: 10 units regular insulin IV with 25g glucose (50 mL of D50W) over 15-30 minutes. 3, 5

  • Onset: 15-30 minutes; duration: 4-6 hours. 3
  • Never give insulin without glucose—hypoglycemia can be life-threatening. 4

• Nebulized albuterol: 10-20 mg over 15 minutes. 3

  • Onset: 15-30 minutes; duration: 4-6 hours. 3

• Sodium bicarbonate: 50 mEq IV over 5 minutes ONLY if metabolic acidosis is present (pH <7.35, bicarbonate <22 mEq/L). 3, 4

  • Do NOT use sodium bicarbonate without metabolic acidosis—it is ineffective and wastes time. 4

Step 4: Eliminate Potassium from the Body

Choose based on renal function and clinical context:

• Loop diuretics (furosemide 40-80 mg IV) if adequate renal function exists. 3, 4

  • Only effective in patients with eGFR sufficient for diuresis. 3

• Newer potassium binders (preferred over sodium polystyrene sulfonate):

  • Sodium zirconium cyclosilicate (SZC/Lokelma): 10g three times daily for 48 hours, then 5-15g once daily. 4
    • Onset: ~1 hour. 4
  • Patiromer (Veltassa): 8.4g once daily, titrated up to 25.2g daily. 4
    • Onset: ~7 hours. 4

• Hemodialysis is the most effective method for severe hyperkalemia, especially in renal failure. 3, 4

Medication Management During Acute Episode

Temporarily discontinue or reduce the following medications:

• RAAS inhibitors if K+ >6.5 mEq/L. 2, 4
• NSAIDs, potassium-sparing diuretics, trimethoprim, heparin, beta-blockers. 4
• Potassium supplements and salt substitutes. 2, 4

Continue vancomycin—it is NOT the cause of hyperkalemia. 1

After Acute Resolution: Preventing Recurrence

Do NOT permanently discontinue RAAS inhibitors in patients with cardiovascular disease or proteinuric kidney disease:

• Initiate a potassium binder (patiromer or SZC) and restart RAAS inhibitors at a lower dose once potassium <5.5 mEq/L. 4
• RAAS inhibitors provide mortality benefit and slow CKD progression. 2, 4

Monitor potassium levels:

• Check within 1 week of restarting or escalating RAAS inhibitors. 4
• Reassess at 1-2 weeks, 3 months, then every 6 months. 4

Critical Pitfalls to Avoid

• Never delay treatment while waiting for repeat lab confirmation if ECG changes are present. 4
• Never attribute hyperkalemia to vancomycin—look for other causes. 1
• Never use sodium bicarbonate without metabolic acidosis. 4
• Never give insulin without glucose. 4
• Remember that calcium, insulin, and beta-agonists are temporizing measures only—they do NOT remove potassium from the body. 3, 4
• Avoid sodium polystyrene sulfonate (Kayexalate) due to risk of bowel necrosis and lack of efficacy data. 2, 4