How is hyperkalemia treated?

Hyperkalemia Treatment

Hyperkalemia treatment requires a stepwise approach starting with calcium gluconate for cardiac membrane stabilization in severe cases (>6.5 mmol/L or with ECG changes), followed by insulin with glucose for intracellular potassium redistribution, and ultimately potassium removal through diuretics, potassium binders, or hemodialysis. 1

Severity Assessment and Initial Management

Severity Classification:

• Mild: >5.0 to <5.5 mmol/L
• Moderate: 5.5 to 6.0 mmol/L
• Severe: >6.0 mmol/L 1

Emergency Treatment for Severe Hyperkalemia:

1. Cardiac Membrane Stabilization:

   • Calcium gluconate 10% solution, 15-30 mL IV over 2-5 minutes
   • Onset: 1-3 minutes, Duration: 30-60 minutes
   • Protects against cardiac toxicity but does not lower potassium levels 1
   • Note: Sodium polystyrene sulfonate should NOT be used for emergency treatment due to its delayed onset of action 2

2. Intracellular Potassium Shift:

   • Insulin with glucose: 10 units regular insulin IV with 50 mL of 25% dextrose
   • Inhaled beta-agonists: 10-20 mg salbutamol (albuterol) nebulized over 15 minutes
   • Salbutamol has been shown to significantly reduce serum potassium compared to placebo, with peak effect at 90-120 minutes 3

3. Potassium Removal:

   • Loop diuretics: 40-80 mg IV (for patients with adequate kidney function)
   • Hemodialysis (for severe cases or when other measures fail) 1

Non-Emergency Management

1. Medication Review:

   • Evaluate and adjust medications that contribute to hyperkalemia:
     • ACE inhibitors/ARBs
     • Potassium-sparing diuretics
     • NSAIDs
     • Beta-blockers
     • Calcineurin inhibitors
     • Trimethoprim 1, 4

2. Potassium Binders:

   • For chronic management: patiromer or sodium zirconium cyclosilicate
   • Sodium polystyrene sulfonate for subacute treatment 1, 5

3. Dietary Modifications:

   • Focus on reducing non-plant sources of potassium rather than strict overall potassium restriction 4

Management in Special Populations

Heart Failure Patients:

• Balance between optimizing RAAS inhibitors and managing hyperkalemia is crucial

• In patients with K+ levels between 4.5 and 5 mEq/L not on maximum tolerated RAAS inhibitor therapy:

  • Titrate/start RAAS inhibitors and monitor K+ levels closely
  • If K+ rises above 5.0 mEq/L, initiate K+ lowering measures 6, 7

• In patients with K+ levels >5 mEq/L on maximum tolerated RAAS inhibitor therapy:

  • Initiate K+ lowering agents
  • Monitor K+ levels according to clinical status 6

• In patients with K+ levels >5 mEq/L not on maximum tolerated RAAS inhibitor therapy:

  • Start K+ lowering agents
  • When K+ levels are <5 mEq/L, titrate RAAS inhibitor therapy 6

Monitoring

• Serum potassium: Within 1 week of treatment initiation, more frequently in high-risk patients
• Serum creatinine and eGFR: Regularly, especially in CKD patients
• ECG monitoring: To assess response to calcium gluconate and detect cardiac complications 1

Common Pitfalls and Caveats

1. Rebound Hyperkalemia: Treatments that shift potassium intracellularly (insulin/glucose, beta-agonists) have temporary effects. Monitor for rebound increases in potassium levels 5

2. Hypoglycemia Risk: When using insulin/glucose therapy, monitor blood glucose levels to prevent hypoglycemia 1

3. Overtreatment Risk: Excessive treatment can lead to hypokalemia, which may be more dangerous than hyperkalemia 6

4. RAAS Inhibitor Management: Avoid unnecessary discontinuation of RAAS inhibitors in heart failure and proteinuric kidney disease patients, as these medications improve outcomes 4, 7

5. Calcium Administration: In cardiac arrest due to hyperkalemia, calcium chloride may be preferred over calcium gluconate due to more rapid ionization 1