What is the treatment for severe hyperkalemia?

Treatment of Severe Hyperkalemia

For severe hyperkalemia (≥6.5 mEq/L or any ECG changes), immediately administer IV calcium to stabilize cardiac membranes, followed simultaneously by insulin with glucose and nebulized albuterol to shift potassium intracellularly, then initiate definitive potassium removal via diuretics or hemodialysis. 1

Step 1: Immediate Cardiac Membrane Stabilization (Within 1-3 Minutes)

Administer calcium first—this is your cardiac protection and takes priority over everything else. 2, 1

• Calcium chloride (10%): 5-10 mL (500-1000 mg) IV over 2-5 minutes 2, 1

  • Preferred in critically ill patients as it provides more rapid increase in ionized calcium 1
  • Must use central line when possible—peripheral extravasation causes severe tissue necrosis 1

• Calcium gluconate (10%): 15-30 mL IV over 2-5 minutes 2, 1

  • Alternative option, safer for peripheral IV access 1
  • Requires larger volume to achieve equivalent effect 1

• Critical caveat: Calcium does NOT lower potassium—it only protects against arrhythmias for 30-60 minutes 1, 3

• Monitor heart rate continuously and stop if symptomatic bradycardia develops 1

• May repeat dose in 5-10 minutes if no ECG improvement 1

Step 2: Shift Potassium Into Cells (Onset 15-30 Minutes, Duration 4-6 Hours)

Give all three agents together for maximum effect—they work synergistically. 1, 3

Insulin with Glucose (Most Effective)

• 10 units regular insulin IV mixed with 25g glucose (50 mL of D50W) over 15-30 minutes 2, 1
• Onset: 15-30 minutes, duration: 4-6 hours 1
• Critical pitfall: Never give insulin without glucose—hypoglycemia can be life-threatening 3
• Monitor glucose closely in patients with low baseline glucose, no diabetes, female sex, or renal dysfunction 1
• Can repeat every 4-6 hours if hyperkalemia persists, with careful glucose and potassium monitoring 1

Nebulized Beta-2 Agonist

• Albuterol 10-20 mg nebulized over 15 minutes 2, 1
• Reduces potassium by approximately 0.5-1.0 mEq/L 1
• Onset: 15-30 minutes, duration: 2-4 hours 1, 3
• Augments insulin effect but provides only temporary benefit 1

Sodium Bicarbonate (ONLY if Metabolic Acidosis Present)

• 50 mEq IV over 5 minutes 2, 1
• Only use if pH <7.35 and bicarbonate <22 mEq/L 1, 3
• Onset: 30-60 minutes 3
• Common pitfall: Do not use without documented acidosis—it is ineffective and wastes time 1, 3

Step 3: Remove Potassium From Body (Definitive Treatment)

Remember: Steps 1 and 2 are temporizing only—you MUST remove potassium to prevent rebound. 1, 3

Loop Diuretics (If Adequate Renal Function)

• Furosemide 40-80 mg IV 2, 1
• Increases renal potassium excretion by stimulating flow to collecting ducts 3
• Only effective with adequate kidney function 1
• Titrate to maintain euvolemia, not primarily for potassium management 3

Hemodialysis (Most Effective Method)

• Most reliable and effective for severe hyperkalemia 2, 1, 3
• Indications: Severe cases unresponsive to medical management, oliguria, or end-stage renal disease 1, 3
• Critical consideration: Potassium can rebound 4-6 hours post-dialysis as intracellular stores redistribute 3
• Monitor potassium every 2-4 hours initially after dialysis if initial level >6.5 mEq/L 3

Potassium Binders (Subacute Treatment)

• Sodium polystyrene sulfonate (Kayexalate): 15-50 g orally or rectally with sorbitol 2
• FDA warning: Should NOT be used as emergency treatment due to delayed onset of action 4
• Serious safety concern: Associated with intestinal necrosis, colonic necrosis, and gastrointestinal injury—avoid in favor of newer agents 1, 3, 4

Newer Potassium Binders (Preferred for Chronic Management)

• Sodium zirconium cyclosilicate (SZC): 10g three times daily for 48 hours, then 5-15g once daily 1, 3

  • Onset: 1 hour (fastest) 1, 3
  • Highly selective potassium binding 3

• Patiromer: 8.4g once daily, titrate up to 25.2g daily 1, 3

  • Onset: ~7 hours 1, 3
  • Must separate from other medications by 3 hours 3
  • Monitor magnesium levels—causes hypomagnesemia 3

Step 4: Medication Management During Acute Episode

Temporarily discontinue or reduce these medications at K+ ≥6.5 mEq/L: 1, 3

• RAAS inhibitors (ACE inhibitors, ARBs, mineralocorticoid antagonists) 1, 3
• NSAIDs 1, 3
• Potassium-sparing diuretics (spironolactone, amiloride, triamterene) 3
• Trimethoprim 3
• Heparin 1, 3
• Beta-blockers 1, 3
• Potassium supplements and salt substitutes 1, 3

Step 5: Preventing Recurrence

Do NOT permanently discontinue RAAS inhibitors in patients with cardiovascular disease or proteinuric CKD—they provide mortality benefit. 1, 3

• Restart RAAS inhibitors at lower dose once potassium <5.0-5.5 mEq/L 1, 3
• Initiate potassium binder (patiromer or SZC) to enable continuation of life-saving medications 1, 3
• Monitor potassium 7-10 days after restarting or escalating RAAS inhibitors 1, 3
• Target potassium 4.0-5.0 mEq/L to minimize mortality risk 3

Critical Pitfalls to Avoid

• Never delay treatment waiting for repeat labs if ECG changes are present 3
• Never rely solely on ECG findings—they are highly variable and less sensitive than laboratory tests 3
• Never use sodium bicarbonate without documented metabolic acidosis 1, 3
• Never give insulin without glucose 3
• Remember calcium, insulin, and beta-agonists do NOT remove potassium—they only temporize 1, 3
• Exclude pseudohyperkalemia from hemolysis or improper sampling before aggressive treatment 1, 3
• Watch for rebound hyperkalemia 2-4 hours after temporary measures 1, 3

Monitoring Protocol

• Check potassium every 2-4 hours after initial treatment until stable 1
• Obtain ECG if initial presentation included cardiac changes to document resolution 3
• Monitor glucose closely during and after insulin administration 1
• Monitor magnesium if using patiromer 3
• More frequent monitoring needed in patients with ongoing potassium release (tumor lysis syndrome, rhabdomyolysis) 3