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(mainly hypokalemia), such as thyrotoxicosis, aldosteronism, 17 hydroxylase de ciency (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 insuf ciency or disorders due to 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 paralysis Thyrotoxicosis with Periodic Paralysis This is another and 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 extraction In Japan, Okinaka and associates found that 89 percent of males with thyrotoxicosis had periodic paralysis but this was the case in only 04 percent of females; in China, the corresponding gures were 130 and 017 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 inexcitable Potassium chloride restores power in paralytic attacks, and treatment of the hyperthyroidism prevents their recurrence (see page 1236) Hypokalemic Weakness in Primary Aldosteronism Hypokalemic weakness due to hypersecretion of the major adrenal mineralocorticoid aldosterone was rst described by Conn and associates in 1955 In primary aldosteronism, the cause of the hypersecretion is in the adrenal gland itself usually an adrenal cortical adenoma, less often adrenal cortical hyperplasia The disorder is not common (occurring in about 1 percent of unselected hypertensive patients), but its recognition is essential, since it can be treated effectively Persistent aldosteronism is frequently associated with hypernatremia, polyuria, and alkalosis, which predispose the patient to attacks of tetany as well as to hypokalemic weakness Conn and associates (1964), in an analysis of 145 patients with primary aldosteronism, found that persistent muscular weakness was a major complaint in 73 percent; intermittent attacks of paralysis occurred in 21 percent; and tetany in 21 percent These manifestations were much more frequent in women than in men, in contrast to the preponderance of men among patients with hypokalemic periodic paralysis of familial type Rarely, as already noted, primary aldosteronism is produced by the chronic ingestion of licorice; this is due to its content of glycyrrhizic acid, a potent mineralocorticoid (Conn et al, 1968) The muscle bers of patients with primary aldosteronism show necrosis and vacuolation Ultrastructurally, the necrotic areas are characterized by a dissolution of myo laments with degenerative vacuoles; nonnecrotic bers contain membrane-bound vacuoles and show dilatation of the sarcoplasmic reticulum and abnormalities of the transverse tubular system, suggesting that a vulnerability of the latter structures may be responsible for the muscle ber necrosis (Atsumi et al).

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This dramatic syndrome is observed during general anesthesia in susceptible individuals It is characterized by rapidly rising body temperature, extreme muscular rigidity, and a high mortality rate Since the original report by Denborough and Lovell in 1960, as larger experience was gained with this entity, it proved to be a metabolic polymyopathy inherited as a dominant trait, rendering the individual vulnerable to any potent volatile anesthetic agent, particularly halothane, and to the muscle relaxant succinylcholine The fundamental cause in a large proportion of cases is an aberration in a component of the calcium channel Malignant hyperthermia has been estimated to occur approximately once in the course of every 50,000 administrations of general anesthesia The full clinical picture is striking but anesthesiologists have become adept at detecting its earliest stages As halothane or a similar inhalational anesthesia is induced or succinylcholine is given for muscular relaxation, the jaw muscles unexpectedly become tense rather than relaxed, and soon the rigidity extends to all of the muscles Thereafter, the body temperature rises to 42 F or 43 F (55 C or 61 C) with tachypnea and tachycardia Arterial CO2 may exceed 100 mmHg, and blood pH may fall to 700 or below There may be gross myoglobinuria, and serum CK often reaches extraordinarily high levels Circulatory collapse and death may ensue in approximately 10 percent of cases, or the patient may survive with gradual recovery In some cases there is the same sequence of events (increased temperature and acidosis) without muscular spasm With the patient s early death, the muscle may appear normal by light microscopy In case of survival for several days, samples of muscle reveal scattered segmental necrosis and phagocytosis of sarcoplasm without in ammation Regenerative activity is in progress Multicores, which are characteristic of a particular congenital polymyopathy, may be found in the muscle of patients who have had such episodes Pathophysiology The pathogenesis of this reaction has been the subject of a number of investigations During the rigor phase, oxygen consumption in muscle increases threefold and serum lactate, 15- to 20-fold Muscle from most affected individuals is abnormally sensitive to caffeine, which induces contracture in vitro It has been postulated that halothane acts in a manner similar to caffeine that is, to release calcium from the sarcoplasmic reticulum and prevent its reaccumulation, thus interfering with relaxation of the muscle There is a breed of pigs, inbred for muscular development, in which muscle spasm (true contracture) and hyperthermia follow the administration of anesthetic agents These swine have an inherited defect in the ryanodine receptor, a protein component of the calcium channel of the sarcoplasm that is sensitive to both caffeine and ryanodine However, one of several similar defects in ryanodine is found in somewhat fewer than 20 percent of human beings It is presumed that other yet unidenti ed allelic mutations of this receptor protein or another that controls the structure of the calcium channel account for the remainder of cases The essential physiologic change is one of increased intracellular calcium The cause of the high fever is not known; it is probably due to the muscle spasm, but an effect of the anesthetic on heatregulating centers cannot be excluded Clues as to which patients are at risk for this condition come from several sources Other members of the family may have collapsed or died during anesthesia Some of the susceptible individuals exhibit certain myopathic and musculoskeletal abnormalities.

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