Introduction Thyrotoxic periodic paralysis is a medical emergency. It is a very rare presentation of uncontrolled hyperthyroidism. It is more common among Asian and Latin American males and is often precipitated by rest after exercise, stress, or a carbohydrate meal. Immediate replacement of potassium, preventing overcorrection, is lifesaving. It can be prevented by adequate and timely management of hyperthyroidism.
Case Report We report a case of a 22-year-old Hispanic male who presented to our emergency department with quadriplegia upon awakening from sleep. Symptoms started the night before with bilateral lower extremity weakness that developed after eating a heavy meal of pizza and beer. The patient had a history of palpitations and excessive sweating for 2 years but was never worked up. He had no significant past medical or family history. Physical examination revealed quadriplegia and pure motor weakness. Workup for neurologic causes of the above deficit was nonrevealing. Laboratory studies revealed a potassium of 1.7 mEq, thyroid-stimulating hormone of < 0.05 mIU/mL, triiodothyronine of 719 ng/dL, and free thyroxine of 5.66 ng/dL. He was diagnosed with thyrotoxic periodic paralysis and was appropriately treated with potassium, inderal, and propylthiouracil. The patient's neurologic symptoms resolved dramatically with therapy. He was observed in the intensive care unit for 2 days and then discharged. Thyroid-stimulating immunoglobulin level (> 200) was followed up.
Discussion Hypokalemic periodic paralysis is a medical emergency characterized by episodes of muscle weakness resulting from hypokalemia. The commoner variant is the inherited or familial form (autosomal dominant), but rarely encountered is the acquired variety secondary to uncontrolled hyperthyroidism. Acute attacks are due to transcellular shift of potassium. Hypokalemia is often accompanied by hypophosphatemia and hypomagnesemia. It has been proposed that thyrotoxic patients with periodic paralysis have higher Na-K-ATPase activity than those without paralytic episodes, and thyroxine increases this pump activity even further (thereby tending to drive potassium into cells resulting in very low serum potassium values). A possibility of a mutated calcium channel has also been proposed. In addition, these patients become vulnerable to hypokalemic action of insulin and epinephrine, and often this leads to paralytic episodes.
Conclusion The above-illustrated case proves the fact that certain metabolic derangements can have presentations that mimic neurologic emergencies. All patients with paralysis do not have stroke or spinal cord pathology.
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