Case Presentation: Hypokalemia, especially serum potassium concentrations of < 2.5 mmol/L, is a well-recognized etiology of generalized muscle weakness. While hypokalemia, weakness, and thyroid disorders are common clinical entities, thyrotoxic periodic paralysis (TPP) is a rare condition driven by both increased gene transcription and increased intrinsic activity of the Na-K-ATPase pump. Here, we present a case of TPP in a young, previously healthy male.A 23-year-old male without pertinent past medical history presented with one month of progressive, diffuse weakness. The patient presented to an outside hospital one week prior to admission to our institution with profound weakness, found to have a potassium level of 2.3 mmol/L. After receiving potassium repletion, his symptoms resolved and he was discharged. His symptoms started to return within 3 days of discharge from ED and progressively worsened.On the day of admission to our institution, the patient had to be carried off of a plane because of profound, acute weakness. In addition to extremity weakness, he endorsed mild dysphagia, dysarthria, and myalgias. The patient’s physical exam was remarkable for tachycardia and 1/5 strength in bilateral upper and lower extremities with intact reflexes, cranial nerve exam, and sensation to light touch. Notable laboratory results included a potassium level of 2.0 mmol/L, TSH of < 0.01 uIU/mL, T4 of 4.3 ng/dL, and T3 of 15.6 pg/mL and an elevated TSH immunoglobulin of 13.30 units IU/L. A thyroid ultrasound demonstrated a diffusely heterogeneous thyroid gland without nodules. An electrocardiogram revealed accelerated junctional rhythm with a prolonged QTc interval.Given the clinical presentation and objective data, the patient was diagnosed with TPP in the setting of Grave’s disease. The patient was treated with potassium repletion, methimazole, and propranolol. Within 24 hours of presentation, the patient was able to ambulate without assistance and the patient’s strength had improved to 5/5 in all extremities.Unfortunately, the patient presented 3 days after discharge with a similar presentation in the setting of a recent high carbohydrate meal. He initially required the intensive care unit but was quickly transferred to the general medicine floor and then discharged after aggressive potassium repletion and continuation of his methimazole and beta blocker.
Discussion: TPP is an uncommon but dangerous presentation seen in patients with thyrotoxicosis. Rapid recognition and treatment of the underlying thyroid disorder and aggressive electrolyte repletion is critical for not only symptom management but also prevention of serious cardiopulmonary complications. Additionally, cautioning patients against high carbohydrate meals and strenuous exercise, which further activate the Na-K-ATPase channel, may help prevent recurrence of paralysis.
Conclusions: In patients presenting with periodic paralysis or diffuse muscle weakness, clinicians should maintain a high degree of suspicion for underlying thyroid dysfunction in order to not miss this rare clinical entity.