Electrolyte and muscle disorder with acute muscle weakness and hypokalemia.
An uncommon and potentially life-threatening complication of hyperthyroidism characterized by episodic and abrupt muscle weakness with hypokalemia.
Highest incidence among Asian people but is seen among other ethnic groups.
Will likely recur if hyperthyroidism is not adequately treated.
Can lead to death from respiratory failure and ventricular arrhythmias.
Ultrasound of the thyroid gland shows a diffusely enlarged goiter in keeping with thyroiditis.
Thyroid peroxidase antibodies are elevated.
It most commonly affects eastern Asian and Hispanic men in the second or third decade of life.
It is becoming increasingly present in the western world as a result of population mobility.
Postulated that excess thyroid hormone enhances the activity of the sodium-potassium adenosine triphosphatase pump driving potassium into cells, resulting in hypokalemia without a total body deficit of potassium.
Compensatory mechanisms expected to shift potassium out of skeletal muscles are impaired in these patients creating a cycle of hypokalemia and suppression of sodium-potassium adenosine triphosphatase activity resulting in muscle inexcitability and worsening paralysis.
The degree of hypokalemia present correlates with the severity of muscle weakness.
Excess thyroid hormone may precipitate paralysis by increasing susceptibility to the hypokalemic actions of adrenaline or insulin.
Insulin also activates the sodium-potassium adenosine triphosphatase pump and may act synergistically with thyroid hormone to shift potassium intracellularly.
Attacks often occur postprandially.
Clinical manifestations include episodic muscular weakness commonly occurring at night or early in the morning, and exacerbations may be precipitated by exercise, high carbohydrate or salt load and alcohol binges.
Weakness that is experienced is highly variable from heavy legs to flaccid paralysis and areflexia.
Weakness has a predilection for lower limbs.
The pattern of weakness can fluctuate from attack to attack.
Bulbar, ocular, respiratory muscle involvement is rare but potentially serious complications.
Sensation and cognition are preserved as is sphincter function.
Management requires treatment of thyrotoxicosis, and intravenous potassium replacement.
The only way to achieve complete remission of thyrotoxic periodic paralysis is by normalizing thyroid hormone levels.
Beta blockers can counteract the peripheral effects of thyrotoxicosis, and is beneficial as an antiarrhythmic drug, and improves muscle strength.
Hypokalemia precipitates arrhythmias lengthen the action potential refractory period, it causes EKG changes reflecting abnormal ventricular repolarization.