Drug-induced hypokalaemia: Part 1

Abstract

SummaryDrug-induced hypokalaemia is common in therapeutic dose and overdose. It arises via several mechanisms that can be simply divided based on urine potassium excretion rate. When the urinary potassium excretion is low, drugs can induce hypokalaemia by acute transcellular potassium shift (&bgr;2-adrenergic agonists, insulin, thyroxine, calcium-channel blockers, thiopental sodium, chloroquine), gastrointestinal tract potassium loss (laxatives, drug-induced diarrhoea and vomiting, cation-exchange resin), or former renal potassium wasting (diuretics ‘off’ action). The drugs that induce hypokalaemia because of high urine potassium excretion rate can cause excessive mineralocorticoid effects (hydrocortisone, licorice), or renal tubular defects with either metabolic alkalosis (diuretics, antibiotics with nonreabsorbale anions, aminoglycoside, cisplatin) or metabolic acidosis (carbonic anhydrase inhibitor, antiretrovirals, antifungal drugs, aristolochic acid, chemotherapy). The management of drug-induced hypokalaemia incorporates assessment of the onset and degree of hypokalaemia, cessation of the culprit drug, consideration of potassium replacement, assessment of the risk of potassium therapy, and management of associated illness. Early recognition of drug-induced hypokalaemia with prompt management is still the key to avoid potential life-threatening complications.