What is the management protocol for hyperkalemia?

Hyperkalemia Management Protocol

Initial Assessment and Classification

Immediately verify the result is not pseudohyperkalemia from hemolysis, repeated fist clenching, or poor phlebotomy technique before initiating treatment. 1

• Classify severity: mild (5.0-5.9 mEq/L), moderate (6.0-6.4 mEq/L), or severe (≥6.5 mEq/L) 1
• Obtain an ECG immediately—look for peaked T waves, flattened P waves, prolonged PR interval, and widened QRS complexes, though these findings are highly variable and less sensitive than laboratory values 1
• ECG changes indicating cardiac toxicity mandate urgent treatment regardless of the absolute potassium level 1

Acute Hyperkalemia Management (Severe or with ECG Changes)

Step 1: Cardiac Membrane Stabilization (Acts in 1-3 minutes)

Administer calcium gluconate 10% solution: 15-30 mL IV over 2-5 minutes to stabilize cardiac membranes and prevent arrhythmias. 2, 1

• Effects begin within 1-3 minutes but are temporary (30-60 minutes) and do not reduce serum potassium 1
• If no effect within 5-10 minutes, repeat the dose 2
• Alternative: calcium chloride 10%: 5-10 mL IV over 2-5 minutes (more potent but requires central access) 1

Step 2: Intracellular Potassium Shift (Acts in 15-30 minutes)

Administer insulin 10 units regular insulin IV with 50 mL of 50% dextrose (25 grams glucose) to shift potassium intracellularly. 3, 4

• Effects begin within 15-30 minutes and last 4-6 hours 2, 1
• Monitor glucose closely to prevent hypoglycemia—patients with low baseline glucose, no diabetes, female sex, and altered renal function are at higher risk 1
• Verify potassium is not below 3.3 mEq/L before administering insulin 1
• Can be repeated every 4-6 hours as needed, monitoring potassium every 2-4 hours 1

Add albuterol 10-20 mg nebulized as adjunctive therapy to enhance intracellular shift. 3, 4

• Effects last 2-4 hours 1
• Beta-agonists work synergistically with insulin 2

Consider sodium bicarbonate ONLY if concurrent metabolic acidosis is present (pH <7.35, bicarbonate <22 mEq/L). 2, 1

• Promotes potassium excretion through increased distal sodium delivery and counters acidosis-induced potassium release 2, 1
• Effects take 30-60 minutes to manifest 1
• Do not use in patients without metabolic acidosis—it is only indicated when acidosis is present 1

Step 3: Potassium Removal from the Body

For patients with adequate kidney function, administer furosemide 40-80 mg IV to increase renal potassium excretion. 1, 4

• Loop diuretics promote urinary potassium excretion by stimulating flow to renal collecting ducts 2, 1
• Effectiveness depends on residual kidney function 2

Hemodialysis is the most reliable and effective method for potassium removal in severe cases, especially with renal failure, oliguria, or cases unresponsive to medical management. 2, 1, 5

• Should be instituted as adjunctive therapy after other approaches 2
• Most efficient means of removing excess potassium from the body 1

Chronic Hyperkalemia Management

Medication Review and Adjustment

Review and adjust medications that contribute to hyperkalemia: ACE inhibitors, ARBs, mineralocorticoid antagonists, NSAIDs, and beta-blockers. 1

• For patients on RAAS inhibitors with potassium >5.0 mEq/L, initiate a potassium-lowering agent and maintain RAAS inhibitor therapy unless an alternative treatable cause is identified 1
• When potassium >6.5 mEq/L, discontinue or reduce RAAS inhibitors temporarily, initiate a potassium-lowering agent, and monitor closely 1

First-Line Chronic Management

Use loop or thiazide diuretics as first-line agents to promote urinary potassium excretion. 2, 6, 1

• Stimulate flow and delivery of potassium to renal collecting ducts 2
• Effectiveness relies on residual kidney function 2
• May increase risk of gout, volume depletion, and worsening kidney function 2

Potassium Binders

Newer FDA-approved potassium binders—patiromer (Veltassa) and sodium zirconium cyclosilicate (Lokelma)—are preferred for long-term management over older agents. 2, 6, 1

• These agents facilitate elimination of bound potassium in feces 2
• Allow continuation of beneficial RAAS inhibitor therapy 2

Sodium polystyrene sulfonate (Kayexalate) should not be used as emergency treatment due to delayed onset of action and is not efficacious for acute management. 7, 3

• Avoid chronic use, especially with sorbitol, due to risk of intestinal necrosis 8

Alternative Agents

Fludrocortisone increases potassium excretion but carries significant risks of fluid retention, hypertension, and vascular injury—use with caution 2, 1

Monitoring Protocol

Check potassium within 7-10 days after starting or increasing RAAS inhibitor doses. 1

• More frequent monitoring required in high-risk patients: those with CKD, diabetes, heart failure, or history of hyperkalemia 1
• Individualize monitoring frequency based on comorbidities and medications 1

Critical Pitfalls to Avoid

• Do not rely solely on ECG findings—they are highly variable and less sensitive than laboratory tests 1
• Remember that calcium, insulin, and beta-agonists only temporize—they do not remove potassium from the body 1
• Always administer glucose with insulin to prevent hypoglycemia 1
• Sodium bicarbonate is contraindicated without concurrent metabolic acidosis 1
• Avoid chronic sodium polystyrene sulfonate use due to gastrointestinal complications 8

Team-Based Approach

Optimal chronic hyperkalemia management requires a multidisciplinary team including cardiologists, nephrologists, primary care physicians, nurses, pharmacists, social workers, and dietitians. 2, 6, 1

• Educational initiatives on newer potassium binders are needed, especially in regions where specialist services may not be readily available 2
• Dietary counseling for low-potassium diet is essential 9