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) ( = 75, 36%), followed by Gitelman syndrome ( = 39, 18%), thyrotoxic paralysis ( = 8, 4%), hyperaldosteronism ( = 7, 3%), and proximal RTA ( = 6, 4%). Patients with non-periodic paralysis had more urinary loss (40.1 vs. 12.2 mmol, = 0.04), more requirement of potassium replacement (120 vs. 48 mmol, = 0.05), and longer recovery time of weakness (48.1 vs. 16.5 h, = 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.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6146732PMC
http://dx.doi.org/10.4103/ijn.IJN_225_17DOI Listing

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