Abstract

Periodic Paralysis (PP) is a rare inherited neuromuscular disorder caused by a sodium-potassium ion channel defect leading to hypo- or hyperkalemia. Thyrotoxic periodic paralysis (TPP) is a sporadic form of hypokalemic PP associated with a hyperthyroid state, most commonly Graves’ disease. It clinically presents as painless proximal muscle weakness often precipitated by exercise, stress, or a high carbohydrate diet. Here we present a case of hypokalemic TPP. A 63-year-old female from Thailand with a history of meningioma treated with gross total resection (without radiation) three years ago presented to the Emergency Department (ED) with two weeks of neck pain, subjective weight loss, and tremors after receiving the influenza vaccine. Due to elevated thyroid function tests, she was discharged on steroids for presumed subacute thyroiditis with plan for Endocrinology follow up. One week later, she returned to the ED for a potassium of 2.5 mmol/L (3.5-5.1 mmol/L) on outpatient labs. On physical exam, vitals were notable for a heart rate of 99 and palpable goiter. Her neurologic exam demonstrated mildly decreased strength with hip flexion (4/5), shoulder abduction (4-/5), and elbow flexion and extension (4/5). Labs were notable for a potassium of 2.4 mmol/L with undetectable TSH, elevated T4 4.80 mcg/dl (0.60-1.12 mcg/dl), and T3 315 ng/dL (80-210 ng/dL). The TSI was 4.7 IU/L (< 1.3 IU/L) and TSH receptor antibody 4.46 IU/L (< 1.75 IU/L). EKG demonstrated U-waves. The patient was admitted to telemetry and repleted with intravenous and oral potassium. Repeat potassium was 3.8 mmol/L without rebound hyperkalemia. She was also started on propranolol 20 mg twice daily and methimazole 20 mg three times daily for treatment of Graves’ disease. Periodic paralysis (PP) is an autosomal dominant hereditary form of channelopathy that is classified as either hypo- or hyperkalemic. Acquired cases of PP present at an older age and mostly in the context of hyperthyroidism—in these cases the diagnosis is termed thyrotoxic periodic paralysis (TPP). The condition is more common in Asian men, unlike most cases of hyperthyroidism which have a female predominance. Diagnostic lab findings include hypokalemia with hyperthyroidism. Treatment in the acute setting is directed at correcting hypokalemia with cardiac monitoring during the first 24 hours as rebound hyperkalemia occurs in 40-60% of cases. Recommended potassium repletion is 30 mEq every 2 hours, with a maximum dose of 90 mEq in 24 hours. Oral supplementation is preferred. Propranolol and potassium supplementation can be used to prevent attacks until euthyroid state is achieved.

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