SAT-589 Thyrotoxic Periodic Paralysis: A Rare Presentation of Thyrotoxicosis

Abstract

Background. Periodic paralysis (PP) is a rare muscle disorder caused by ion channel dysfunction and manifesting as episodes of painless muscle weakness. Most cases of PP are autosomal dominant, though thyrotoxic PP may complicate any etiology of hyperthyroidism. We present a case of thyrotoxic PP occurring in a patient with Graves’ thyrotoxicosis. Case. A 34 year-old Caucasian male was brought to the emergency department due to abrupt onset of diffuse muscle weakness and inability to ambulate. One week prior to onset of muscle symptoms, the patient had been diagnosed with Graves’ thyrotoxicosis during evaluation of atrial fibrillation. Examination was notable for tachycardia, irregularly irregular rhythm, small and smooth goiter, 3/5 upper extremity strength, and 2/5 lower extremity strength. Admission laboratories revealed TSH < 0.03 mIU/L (0.45-5.33), free T4 2.4 ng/dL (0.5-1.3), total T3 223 ng/dL (87-178), and potassium level 2.3 mM (3.5-5.1). A regimen of high dose oral propranolol (3 mg/kg/d), methimazole (80 mg/d), supersaturated potassium iodide (SSKI), and prednisone was immediately started, and the critical care team administered 80 mEq of potassium in two divided doses during the first hospital day. By the next day, muscle weakness had resolved, and potassium level was 4.2 mM. The patient required three additional days of treatment to bring atrial fibrillation under rate control. At hospital discharge, SSKI and prednisone were stopped, and the patient was discharged home on extended release propranolol and methimazole. Unfortunately, he was lost to outpatient endocrinology follow up. Conclusion. Thyrotoxic PP occurs most commonly in association with Graves’ disease, has a very strong male predominance, usually manifests initially in the third decade of life, and is reported much more commonly in Asian populations than among other ethnic groups. In some series, thyrotoxic PP has a prevalence of approximately 10% among Asian men with Graves’ thyrotoxicosis. The prevalence of thyrotoxic PP is 0.1-0.2% in non-Asian populations. Hypokalemia of thyrotoxic PP appears to be due to increased skeletal muscle sodium-potassium ATPase activity induced by enhanced beta-adrenergic responsiveness of the ion channel and hyperinsulinemia that occur in the setting of significant thyroid hormone excess. Weakness is typically most severe in proximal muscles and lower extremities. Potassium supplementation and non-selective beta-blockade (e.g. propranolol) can rapidly reverse hypokalemia and muscle weakness, though doses of supplemental potassium exceeding 90 mEq in 24 hr predispose to rebound hyperkalemia. Restoration of euthyroidism is required to entirely eliminate episodes of thyroxic PP.