Reversible electrophysiological abnormalities in acute secondary hyperkalemic paralysis

Abstract

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.

Keywords: Conduction block; hyperkalemia; nerve conduction studies; secondary hyperkalemic paralysis.

Figure 1

Motor nerve conduction studies in right median and ulnar nerves stimulated at wrist (A, D), elbow (B, E) and arm (C, F). At admission, distal latencies are prolonged with reduction of CMAP amplitude and duration on proximal stimulation (1a) which improved after dialysis (1b)

Figure 2

The F-wave studies in right median nerve at admission (a) and on day 3 after clinical improvement (b) revealing increased latencies of M and F response in the first study which improved after correction of hyperkalemia. Timescale 10ms/d.

Figure 3

The electrocardiogram at admission revealing broad QRS complexes with tall peaked T waves