Spectrum of hypokalemic paralysis from a tertiary care center in India

Hypokalemic paralysis is an important and reversible cause of acute flaccid paralysis. The treating physician faces unique diagnostic and therapeutic challenges. We did a prospective study and included all patients with acute flaccid weakness and documented serum potassium of <3.5 mEq/L during the period between January 2009 and August 2015. We studied the incidence, etiology, clinical profile, and acid-base disturbances in patients presenting with hypokalemic paralysis and analyzed the significance of periodic and non-periodic forms of hypokalemic paralysis on patient's outcome. Two hundred and six patients were studied with a mean follow-up of 3.6 ± 1.2 years. Mean age was 37.61 ± 2.2 years (range 18-50 years). Males were predominant (M:F ratio 2.1:1). The nonperiodic form of hypokalemic paralysis was the most common (61%). Eighty-one (39%) patients had metabolic acidosis, 78 (38%) had normal acid-base status, and 47 (23%) patients had metabolic alkalosis. The most common secondary cause was distal renal tubular acidosis (RTA) (<i>n</i> = 75, 36%), followed by Gitelman syndrome (<i>n</i> = 39, 18%), thyrotoxic paralysis (<i>n</i> = 8, 4%), hyperaldosteronism (<i>n</i> = 7, 3%), and proximal RTA (<i>n</i> = 6, 4%). Patients with non-periodic paralysis had more urinary loss (40.1 vs. 12.2 mmol, <i>P</i> = 0.04), more requirement of potassium replacement (120 vs. 48 mmol, <i>P</i> = 0.05), and longer recovery time of weakness (48.1 vs. 16.5 h, <i>P</i> = 0.05) than patients with periodic paralysis. Non-periodic form of hypokalemic paralysis was the most common variant in our study. Patients with periodic paralysis had significant incidence of rebound hyperkalemia.