Annals of Indian Academy of Neurology
ORIGINAL ARTICLE
Year
: 2013  |  Volume : 16  |  Issue : 2  |  Page : 211--217

Clinical and biochemical spectrum of hypokalemic paralysis in North: East India


Ashok K Kayal, Munindra Goswami, Marami Das, Rahul Jain 
 Department of Neurology, Gauhati Medical College, Guwahati, Assam, India

Correspondence Address:
Ashok K Kayal
Department of Neurology, Gauhati Medical College Hospital, Guwahati, Assam
India

Background: Acute hypokalemic paralysis, characterized by acute flaccid paralysis is primarily a calcium channelopathy, but secondary causes like renal tubular acidosis (RTA), thyrotoxic periodic paralysis (TPP), primary hyperaldosteronism, Gitelman«SQ»s syndrome are also frequent. Objective: To study the etiology, varied presentations, and outcome after therapy of patients with hypokalemic paralysis. Materials And Methods: All patients who presented with acute flaccid paralysis with hypokalemia from October 2009 to September 2011 were included in the study. A detailed physical examination and laboratory tests including serum electrolytes, serum creatine phosphokinase (CPK), urine analysis, arterial blood gas analysis, thyroid hormones estimation, and electrocardiogram were carried out. Patients were further investigated for any secondary causes and treated with potassium supplementation. Result: The study included 56 patients aged 15-92 years (mean 36.76 ± 13.72), including 15 female patients. Twenty-four patients had hypokalemic paralysis due to secondary cause, which included 4 with distal RTA, 4 with Gitelman syndrome, 3 with TPP, 2 each with hypothyroidism, gastroenteritis, and Liddle«SQ»s syndrome, 1 primary hyperaldosteronism, 3 with alcoholism, and 1 with dengue fever. Two female patients were antinuclear antibody-positive. Eleven patient had atypical presentation (neck muscle weakness in 4, bladder involvement in 3, 1 each with finger drop and foot drop, tetany in 1, and calf hypertrophy in 1), and 2 patient had respiratory paralysis. Five patients had positive family history of similar illness. All patients improved dramatically with potassium supplementation. Conclusion: A high percentage (42.9%) of secondary cause for hypokalemic paralysis warrants that the underlying cause must be adequately addressed to prevent the persistence or recurrence of paralysis.


How to cite this article:
Kayal AK, Goswami M, Das M, Jain R. Clinical and biochemical spectrum of hypokalemic paralysis in North: East India.Ann Indian Acad Neurol 2013;16:211-217


How to cite this URL:
Kayal AK, Goswami M, Das M, Jain R. Clinical and biochemical spectrum of hypokalemic paralysis in North: East India. Ann Indian Acad Neurol [serial online] 2013 [cited 2019 Aug 25 ];16:211-217
Available from: http://www.annalsofian.org/article.asp?issn=0972-2327;year=2013;volume=16;issue=2;spage=211;epage=217;aulast=Kayal;type=0