Case Presentation: A 39-year-old Hispanic male presented to his primary care physician with progressive fatigue, leg weakness, and occasional falls. His past medical history was unremarkable. A clinical diagnosis of disk herniation was made and treated conservatively.  Two weeks later, he presented to our emergency department (ED) with upper and lower extremity weakness, unable to stand or walk. He denied prior history of recent trauma or illness. His vital signs in the ED were normal except for a heart rate of 130 beats per minute. Physical exam revealed a moderately enlarged goiter, fine tremor, preserved sensation, and decreased motor strength in all four extremities. Deep tendon reflexes were diminished. Initial laboratory studies were concerning for a serum potassium of 1.4 mg/dL. Electrocardiogram showed sinus tachycardia. Treatment was initiated with intravenous potassium with subsequent resolution of the patient’s paralysis. Further workup included a thyroid panel that showed suppressed thyroid stimulating hormone of <0.02 mIU/L, elevated free thyroxine of 3.76 ng/dl, and elevated thyroid stimulating immunoglobulin of 507%. Thyroid peroxidase antibodies were normal. Subsequent thyroid ultrasound (Figure 1) showed multiple bilateral thyroid nodules with the largest solid nodule measuring 2.1 cm. I-123 radioactive iodine uptake scan established a diagnosis of Grave’s disease. Methimazole and as-needed propranolol were initiated with complete recovery and permanent resolution of patient’s muscle paralysis.  

Discussion: Thyrotoxic periodic paralysis (TPP) is a largely unrecognized and potentially lethal complication of hyperthyroidism, with a reported incidence of approximately 0.2% in the United States. Massive intracellular shift of potassium can lead to sudden muscle paralysis, potentially progressing to life-threatening cardiopulmonary complications. Although potassium replacement can offer a short term solution, recurrent thyrotoxic induced hypokalemia will inevitably result in persistent episodic paralysis, making accurate diagnosis and subsequent intervention crucial.

This case demonstrates that recognizing and treating the underlying hyperthyroidism is key. Diagnosis is often missed or delayed given the subtleness of thyrotoxicosis on presentation, the similarities of TPP with other more common causes of weakness/paralysis, and general physician unawareness. Although TPP has been described mainly in Asian males, it is being increasingly recognized in non-Asian populations, including Caucasians and Hispanics, and usually affects young adults 20-40 years of age with up to a 70:1 male-to-female predominance. The proposed mechanism is increased production or activity of the Na/K-ATPase pump in genetically predisposed individuals with underlying hyperthyroidism, hyperadrenergic state, and an exaggerated insulin response. Clinicians should be educated about this rare clinical entity for prompt detection and definitive management. On a larger scale, we realize that pinpointing an exact diagnosis in patients with electrolyte abnormalities is essential; it is not enough to simply treat a laboratory result. 

Conclusions: TPP is a rare but serious complication of hyperthyroidism and requires prompt diagnosis and treatment. Diagnosis is based on clinical presentation and laboratory data showing a thyrotoxic state. Successful treatment entails correction of hypokalemia and treatment of the underlying hyperthyroid state.