SAT-340 - Hyperthyroid Periodic Paralysis: A Rare but Reversible Endocrine Emergency

Introduction

Hyperthyroid periodic paralysis (HPP) is a rare but potentially life-threatening complication of hyperthyroidism. It results from an intracellular shift of potassium into skeletal muscle due to increased activity of Na⁺/K⁺-ATPase pumps, leading to profound hypokalemia and acute muscle weakness or paralysis. HPP may occur regardless of the degree of biochemical hyperthyroidism and can be the initial presenting manifestation of Graves disease. It predominantly affects males of Asian descent between 20 and 40 years of age and is frequently underrecognized, particularly in the absence of classic thyrotoxic symptoms.

Clinical Case

A 31-year-old Asian male with a history of Graves disease diagnosed eight years earlier, who was noncompliant with methimazole therapy, presented with acute-onset, symmetric, rapidly progressive weakness of all four extremities, predominantly involving proximal muscles. Symptoms began early in the morning, rendering him unable to stand or walk. He denied tremors, palpitations, heat intolerance, weight loss, or other symptoms of thyrotoxicosis. On examination, he was hypertensive and tachycardic, with a diffusely enlarged thyroid gland and no evidence of ophthalmopathy. Neurologic examination revealed hypotonia and decreased deep tendon reflexes with intact sensation. Laboratory evaluation demonstrated severe hypokalemia (K⁺ 1.8 mmol/L; normal: 3.5–5.3) and biochemical evidence of uncontrolled hyperthyroidism: TSH < 0.01 mIU/L (normal: 0.27–4.2), free T4 4.02 ng/dL (normal: 0.8–1.7), and free T3 7.8 pg/mL (normal: 2.2–4.0). Symptoms improved rapidly following potassium repletion, with muscle strength returning to baseline within 24 hours. High-dose methimazole was initiated in addition to propranolol to reduce the frequency and severity of recurrent paralytic episodes until a euthyroid state was achieved.

Conclusion

This case highlights the importance of recognizing HPP as a rare, serious, yet reversible cause of acute flaccid paralysis, particularly in Asian males with hyperthyroidism. HPP may present without classic thyrotoxic symptoms and does not correlate with the degree of biochemical hyperthyroidism, contributing to frequent misdiagnosis. It should be distinguished from other causes of acute paralysis; features favoring HPP include sudden, symmetric proximal weakness, preserved sensation, and absence of ocular or bulbar involvement, which make Guillain–Barré syndrome, anterior horn cell disease, and myasthenia gravis less likely. Timely recognition, prompt correction of hypokalemia, and definitive management of the hyperthyroid state are essential for rapid recovery and prevention of recurrence and serious complications, including cardiac arrhythmias. Increased clinical awareness is crucial to avoid diagnostic delays and improve patient outcomes.

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