Treatment Options for the Management of Acute Hyperkalemia

Prescribed medications are a primary cause of hyperkalemia in 35-75% of hospitalized patients.¹ High-risk patients are those with underlying renal impairment, hypoaldosteronism, and taking combination of drugs that can increase potassium level. Several classes of medications can induce hyperkalemia by different mechanisms.² Recognition and close monitoring of those medications is necessary to reduce morbidity and mortality related to hyperkalemia.

Drug-induced hyperkalemia may range from asymptomatic to life threatening.³ Symptoms are mainly related to cardiac and muscular functions. The most serious manifestations include muscle weakness or paralysis, respiratory failure, cardiac conduction abnormalities, and cardiac arrhythmias.

There are 3 major mechanisms of drug-induced hyperkalemia:

• Impaired renal excretion of potassium
• Extracellular potassium shift
• Excessive potassium intake.

Drug classes that are known to cause hyperkalemia are listed below (table 1).

Table 1. Drugs known to cause hyperkalemia and their mechanism of action^1,2

Impaired renal excretion

Extracellular potassium shift

Excessive potassium intake

ACE inhibitors, ARBs

Direct renin inhibitors

NSAIDs

Aldosterone agonists

Potassium-sparing diuretics

Trimethoprim, pentamidine

Cyclosporine, tacrolimus

Heparin, LMWH

β blockers

Digoxin intoxication

Intravenous cationic amino acids (lysine, arginine)

Mannitol

Suxamethonium

Verapamil

Salt substitutes

Penicillin G

Stored blood products

Drug-induced hyperkalemia can be prevented by slow dose titration and close monitoring of serum potassium within the first week of therapy and after each dose adjustment. NSAIDs, especially chronic use, should be avoided in the elderly, dehydrated patients, patients with renal insufficiency, and those taking other drugs known to increase potassium. Alternative therapies with non-NSAID analgesics or topical agents should be recommended.

Management of acute hyperkalemia should be guided by the serum potassium level and severity of symptoms.^4,5

Treatment

Mechanism

Onset/ Duration

Comments

Furosemide

40-80 mg IV

Increases renal excretion of potassium

15 min./

4 hours

Monitor volume status

Sodium polystyrene sulfonate (SPS)

50 mg PO or rectal

Removes potassium from the gut in exchange of sodium

1-2 hours/ 4-6 hours

May lead to sodium retention

Regular insulin

5-10 units IV with 50 ml of 50% dextrose

Shifts potassium from the vascular space into the cells

30 min./

4-6 hours

Lower dose recommended in renal insufficiency

Monitor for hypoglycemia

Albuterol 0.5 mg IV

or 10-20 mg via nebulizer over 10 minutes

Shifts potassium intracellularly

30 min./

2-4 hours

Monitor for tachycardia

Potentially ineffective in patients receiving beta-blockers

Sodium bicarbonate

50-100 mEq IV bolus over 5 minutes

Shifts potassium intracellularly

5-10 min./

2 hours

Used in patients with metabolic acidosis

Calcium gluconate

15-30 mL of 10% solution

Membrane potential stabilizer

1-3 min./

30 min.

Goal: normalization of ECG changes

No effect on potassium level

Hemodialysis

Removes potassium from the body

Immediate

Used in refractory hyperkalemia and

renal failure

References:

• Perazella MA. Drug-induced hyperkalemia: old culprits and new offenders. Am J Med. 2000; 109(4):307—14.
• Ben Salem CB, Badreddine A, Fathallah N,et al. Drud-induced hyperkalemia. Drug Saf. 2014; 37:677-692.
• Noize P, Bagheri H, Durrieu G, et al. Life-threatening drug-associated hyperkalemia: a retrospective study from laboratory signals. Pharmacoepidemiol Drug Saf. 2011; 20(7):747—53.
• Rossignol P, Legrand M, Kosiborod M, et al. Emergency management of severe hyperkalemia guidelines for best practice and opportunities for the future. Pharmacol Res. 2016; 113(ptA):585-591.
• Weisberg LS. Management of severe hyperkalemia. Crit Care Med. 2008; 36(12):3246-3251.