Discussion: Hypokalemic periodic paralysis (HPP) is a rare neuromuscular disorder, with a prevalence estimated at 1/100,000. The male to female ratio is approximately four to one. HPP may be inherited in an autosomal dominant pattern. Genetic mutations have been identified that affect skeletal muscle sarcolemma calcium and sodium channels, resulting in inadequate depolarization. In a minority of cases of HPP, identical pathophysiologic abnormalities are acquired rather than hereditary, most often in the setting of hyperthyroidism. Attacks may be precipitated by stress or vigorous physical exertion, where excessive adrenergic stimuli trigger decompensation by promoting intracellular potassium shift. High carbohydrate intake, with endogenous increases in insulin, and a similar effect on intracellular potassium movement, has also been identified as an etiologic factor. The acute paralysis is always reversible, but a chronic progressive secondary myopathy occurs with aging. Treatment is the cautious replenishment of serum potassium. A rebound effect may occur as intracellular potassium moves back to the extracellular environment. Because of the risk of cardiac arrhythmias, treatment should take place in the setting of continuous cardiac monitoring. Long-term pharmacologic treatment includes carbonic anhydrase inhibitors and potassium sparing diuretics. Vigorous physical exertion and high carbohydrate meals should be avoided.
Conclusions: Hypokalemic periodic paralysis should be included in the differential diagnosis of any patient presenting with acute paralysis and unchanged mental status. Because of the potential for life-threatening cardiac complications, prompt recognition and treatment is imperative. Patient education regarding precipitating factors, in conjunction with pharmacotherapy, may mitigate morbidity and mortality.