For an acute attack, 0.25 mEq KCl/kg should be given orally or, if this is not tolerated, some other K salt may be tried. This dose may be insufficient and if there is no improvement in 1 or 2 h, KCl may have to be given intravenously: 0.05 to 0.1 mEq/kg initially in a bolus at a safe rate, followed by 20 to 40 mEq KCl in 5 percent mannitol, avoiding glucose or NaCl as the carrier solution. For the late-progressive polymyopathy that follows many severe attacks of periodic paralysis, Dalakas and Engel report successful restoration of strength by the long-term administration of dichlorphenamide. Regular exercise (not too strenuous) to keep the patient fit is desirable.
In addition to the hereditary kalemic paralyses described earlier, transitory episodes of weakness are associated with a number of acquired derangements of potassium metabolism (mainly hypokalemia); these include thyrotoxicosis, aldosteronism, 17α-hydroxylase deficiency (Yazaki et al), barium poisoning (Lewi and Bar-Khayim), glycyrrhizic acid ingestion (a substance in licorice that has mineralocorticoid activity), and abuse of thyroid hormone (Layzer). Other forms of secondary hypokalemic weakness have been observed in patients suffering from chronic renal and adrenal insufficiency or disorders caused by a loss of potassium, as occurs with excessive use of diuretics or laxatives (the most common cause in practice). (Renal failure with hyperkalemia can also induce considerable weakness.)
This is a special form of secondary hypokalemic periodic paralysis and occurs mainly in young adult males (despite the higher incidence of thyrotoxicosis in women), with a strong predilection for those of Japanese and Chinese origin (Pothiwala). In Japan, Okinaka and associates found that 8.9 percent of men with thyrotoxicosis had periodic paralysis, but this was the case in only 0.4 percent of women; in China, the corresponding figures were 13.0 and 0.17 percent (McFadzean and Yeung). The paralytic disorder is unrelated to the severity of the hyperthyroidism. In patients with the familial forms of periodic paralysis, the induction of hyperthyroidism is said not to increase the frequency or intensity of attacks. Therefore, it seems likely that thyrotoxicosis has unmasked another type of hereditary periodic paralysis, although a familial occurrence in the thyrotoxic cases is exceptional. Clinically, the attacks of paralysis are much the same as those of familial hypokalemic type except for a greater liability to cardiac irregularity. As in the familial form, the paralyzed muscles are electrically inexcitable. Potassium chloride restores power in paralytic attacks, and treatment of the hyperthyroidism prevents their recurrence.