Clinical and biochemical features of hypokalemic paralysis: a study from rural Eastern India.

Background: Hypokalemic paralysis is characterized by episodic attacks of flaccid muscle weakness of variable duration and severity associated with hypokalemia. Overall, there is a scarcity of data regarding hypokalemic paralysis from Indian subcontinent particularly from rural areas. Methods: A total of 50 consecutive patients of hypokalemic paralysis who were admitted in our hospital were recruited in this study. Results: Fifty patients of hypokalemic paralysis were admitted to our department over a period of 4 years. Forty-two (84%) patients presented with classic acute onset quadriparesis, while eight patients had atypical presentation. Five patients had paraparesis, two had hemiparesis and one patient presented with isolated neck muscle weakness without any limb weakness. Thirty-two patients had primary hypokalemic periodic paralysis (HoPP) and 18 had secondary hypokalemic paralysis. There was no significant difference in severity of weakness (p = 0.53), number of episodes of weakness (p = 0.66) and serum CPK levels (p = 0.36) between primary and secondary hypokalemic paralysis. Secondary cases required significantly prolonged time for recovery as well as higher potassium supplements as compared to the primary HoPP. The severity of weakness of proximal muscles measured in MRC grading showed a significant correlation with serum potassium levels (p = 0.010), but did not show any correlation with CPK Levels (p = 0.86). Conclusion: Hypokalemic paralysis is an important cause of acute flaccid paralysis in the Emergency Room that often improves dramatically with potassium supplements. While secondary cases often require treatment of underlying etiology, primary hypokalemic paralysis often requires chronic treatment with acetazolamide and/or potassium-sparing diuretics. Key Message: Hypokalemic paralysis is an important differential diagnosis of acute flaccid paralysis that rapidly recovers with treatment. Most of the cases are primary, usually a calcium channel disorder (Type I) or very rarely a sodium channel disorder (Type II). However, secondary causes should be evaluated for and reasonably excluded before labeling the disorder as primary hypokalemic paralysis. [ABSTRACT FROM AUTHOR]