Hypokalemic Paralysis: A Report of Two Different Cases

Abstract

Hypokalemic paralysis is characterized by symmetric muscle weakness due to low serum potassium levels, which is completely disappeared when the potassium levels become normalized. It can be classified into primary (familial) or secondary depending on the etiology. Primary hypokalemic paralysis, which is called hypokalemic periodic paralysis (HPP), is mostly caused by a gene mutation that codes calcium or sodium channel in skeletal muscle. It is quite rare, with an estimated prevalence of 1 in 100,000. Secondary hypokalemic paralysis can be caused by potassium ion loss through the gastrointestinal or renal system. It can also be developed by an intracellular shift of potassium ion by pharmacologic causes such as insulin and beta-adrenergic agonists [1-3]. Although hypokalemic paralysis can be suspected with clinical features, electromyography (EMG) can be used to help to establish the diagnosis. During the attack of paralysis, compound muscle action potential (CMAP) amplitude declines and increased small polyphasic motor unit action potentials (MUAPs) with decreased interference pattern can be observed on the needle EMG. However, the routine electrodiagnostic examination can be normal between the attacks. Therefore, many provocative tests have been proposed. Among them, the long exercise test