Exploring Etiologies of Hypokalemic Paralysis: A Case Series

Hypokalemic paralysis is a rare but potentially life-threatening neuromuscular emergency characterized by the sudden onset of flaccid weakness due to reduced serum potassium. While inherited channelopathies represent primary causes, secondary etiologies-particularly endocrine, renal, and metabolic disorders-are more frequently encountered and require timely recognition to avoid complications.

We report four patients presenting with acute flaccid paralysis associated with documented hypokalemia (serum potassium <3.5 mmol/L). The first case involved a pregnant woman with primary hyperaldosteronism due to an adrenal adenoma, managed initially with spironolactone and subsequently cured by adrenalectomy. The second case was a normotensive female diagnosed with distal renal tubular acidosis (dRTA) in the setting of Sjögren's syndrome, treated with potassium citrate and sodium bicarbonate. The third case was a young male with thyrotoxic periodic paralysis (TPP) secondary to Graves' disease, who improved with antithyroid drugs and beta-blockers. The fourth case described a young male with primary hypokalemic periodic paralysis (HPP), presenting with exertion-induced weakness, successfully treated with intravenous potassium supplementation.

This case series underscores the diverse etiologies of hypokalemic paralysis, spanning endocrine, renal, autoimmune, and genetic causes. A systematic diagnostic approach, guided by clinical and biochemical evaluation, is essential for timely treatment. Identifying the underlying cause not only ensures effective acute management but also prevents recurrence and reduces the risk of serious complications, including cardiac arrhythmias.