Open AccessReversible electrophysiological abnormalities in acute secondary hyperkalemic paralysis
Author(s) -
Karkal Ravishankar Naik,
Aralikatte Onkarappa Saroja,
Mallikarjun S Khanpet
Publication year - 2012
Publication title -
annals of indian academy of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.427
H-Index - 31
eISSN - 1998-3549
pISSN - 0972-2327
DOI - 10.4103/0972-2327.104354
Subject(s) - hyperkalemia , medicine , paralysis , guillain barre syndrome , anesthesia , acute flaccid paralysis , neuromuscular disease , periodic paralysis , pediatrics , disease , surgery , immunology , virus , poliovirus
Hyperkalemia manifests clinically with acute neuromuscular paralysis, which can simulate Guillain Barré syndrome (GBS) and other causes of acute flaccid paralysis. Primary hyperkalemic paralysis occurs from genetic defects in the sodium channel, and secondary hyperkalemic paralysis (SHP) from diverse causes including renal dysfunction, potassium retaining drugs, Addison's disease, etc. Clinical characteristics of SHP have been addressed in a number of publications. However, electrophysiological evaluations of these patients during neuromuscular paralysis are infrequently reported and have demonstrated features of demyelination. The clinical features and electrophysiological abnormalities in secondary hyperkalemia mimic GBS, and pose diagnostic challenges. We report the findings of nerve conduction studies in a middle-aged man who was admitted with rapidly reversible acute quadriplegia resulting from secondary hyperkalemic paralysis.