What is the treatment for hyperkalemia?

Evaluation and Treatment of Hyperkalemia

Immediate Assessment and Risk Stratification

Obtain an ECG immediately and check for cardiac manifestations—this determines whether you have minutes or hours to act. 1, 2

The severity classification guides your treatment urgency:

• Mild: 5.0-5.5 mEq/L 1
• Moderate: 5.5-6.0 mEq/L 1, 2
• Severe: >6.0 mEq/L 1, 2

Any ECG changes (peaked T waves, flattened P waves, prolonged PR interval, widened QRS complex) mandate immediate hospital admission and emergency treatment regardless of the potassium level. 1, 2

First, rule out pseudohyperkalemia from hemolysis, poor phlebotomy technique, or delayed sample processing—repeat the measurement if suspected. 3, 1, 2

Emergency Treatment Algorithm for Severe Hyperkalemia

Step 1: Cardiac Membrane Stabilization (Acts Within Minutes)

Administer calcium chloride 10% at 5-10 mL (500-1000 mg) IV over 2-5 minutes as first-line therapy. 2 This provides more rapid increase in ionized calcium than calcium gluconate and is more effective in critically ill patients. 2

• Alternative: Calcium gluconate 10% at 15-30 mL IV over 2-5 minutes 2
• Use central venous access when possible—extravasation of calcium chloride through peripheral IV causes severe tissue injury 2
• Monitor heart rate during administration and stop if symptomatic bradycardia occurs 2
• Critical caveat: Calcium does NOT lower potassium levels; it only protects against arrhythmias for 30-60 minutes 2

Step 2: Shift Potassium Into Cells (Acts Within 15-30 Minutes)

Administer multiple agents simultaneously for additive effect:

Insulin with glucose: 10 units regular insulin IV with 25g glucose (50 mL of D50W) over 15-30 minutes 2

• Onset: 15-30 minutes, duration: 4-6 hours 2
• Monitor for hypoglycemia

Nebulized albuterol: 10-20 mg over 15 minutes 2

• Reduces potassium by approximately 0.5-1.0 mEq/L 2
• Can be used concurrently with insulin/glucose

Sodium bicarbonate: 50 mEq IV over 5 minutes 2

• Most effective when concurrent metabolic acidosis is present 2

Warning: These are temporary measures lasting only 1-4 hours, and rebound hyperkalemia can occur after 2 hours. 2 You must initiate potassium elimination strategies immediately.

Step 3: Eliminate Potassium From the Body (Longer-Term Effect)

Loop diuretics: Furosemide 40-80 mg IV 1, 2

• Only effective with adequate renal function 2

Potassium binders:

• Newer agents (patiromer, sodium zirconium cyclosilicate): Preferred over traditional resins due to superior safety profile 2, 4
• Sodium polystyrene sulfonate (Kayexalate): 15-50 g orally or rectally 2
  • FDA limitation: Should NOT be used for emergency treatment due to delayed onset of action 5
  • Associated with risk of intestinal necrosis 5
  • Avoid concomitant sorbitol—increases intestinal necrosis risk 5

Hemodialysis: Most effective method for severe hyperkalemia, especially with renal failure 2

Management of Moderate Hyperkalemia (5.5-6.0 mEq/L)

If ECG is normal and patient is asymptomatic, you can manage outpatient with close monitoring rather than immediate hospitalization. 1

Immediate Actions:

1. Obtain ECG to confirm no cardiac effects 1
2. Review and adjust medications:
   • Discontinue or reduce RAAS inhibitors (ACE inhibitors, ARBs, MRAs), NSAIDs, potassium-sparing diuretics, beta-blockers 3, 1, 2
   • Stop potassium supplements, salt substitutes, trimethoprim-sulfamethoxazole 3
3. Restrict dietary potassium to <3 g/day 1
   • Avoid bananas, oranges, melons, potatoes, tomatoes, salt substitutes, herbal supplements 1
4. Consider loop diuretics (furosemide 40-80 mg) if adequate kidney function 1

Monitoring Protocol:

• Recheck potassium within 24-48 hours 1
• Additional measurement within 1 week 1
• If on RAAS inhibitors, check potassium within 1 week after any dose adjustment 1

Escalation Criteria:

Immediate hospital referral if:

• Potassium rises above 6.0 mEq/L 1
• ECG changes develop 1
• Symptoms develop (muscle weakness, paresthesias) 1
• Rapid deterioration of kidney function 1

Chronic/Recurrent Hyperkalemia Management

The critical principle: Do NOT permanently discontinue RAAS inhibitors in patients with heart failure or proteinuric kidney disease—these drugs reduce mortality and morbidity. 3, 1, 2

Preferred Strategy:

For patients on RAAS inhibitors with potassium >5.0 mEq/L: Initiate potassium-lowering agents (newer binders preferred) and maintain RAAS inhibitor therapy. 2 Only reduce or discontinue RAAS inhibitors if potassium exceeds 6.5 mEq/L. 2

Additional Measures:

• Ensure effective diuretic therapy 6
• Correct metabolic acidosis if present 6
• Dietary modification nuance: Focus on reducing nonplant sources of potassium rather than blanket restriction—evidence for strict dietary restriction is lacking 6
• Consider SGLT2 inhibitors to assist potassium management 6

High-Risk Populations Requiring Closer Monitoring

Hyperkalemia occurs in up to 73% of patients with advanced CKD and 40% of patients with chronic heart failure. 3

Patients requiring intensive monitoring:

• Advanced CKD (prevalence up to 73%) 3
• Heart failure (prevalence up to 40%) 3
• Diabetes mellitus 3, 1
• Concurrent use of multiple RAAS inhibitors 3
• Elderly patients 3

Critical Pitfalls to Avoid

Do not delay treatment of severe hyperkalemia while waiting for repeat laboratory confirmation if clinical suspicion is high and ECG changes are present. 1

Do not prematurely discontinue beneficial RAAS inhibitors—dose reduction plus potassium binders is preferred to maintain cardioprotective and renoprotective benefits. 1, 2

Do not ignore the need for repeat potassium measurement to confirm hyperkalemia and monitor treatment response. 1

Do not use sodium polystyrene sulfonate for emergency treatment—it has delayed onset and is reserved for subacute management. 5, 7