Title: A Case of Thyrotoxic Hypokalemic Periodic Paralysis

Authors: Ma. Beatrice Camille Gaviola, MD; Megan Lileas, MD; Hilmer Negrete MD; Milad Saleh Abusag, MD; Erdal Sarac MD

Email: mgaviola@mercy.com

Introduction: Hyperthyroidism can have widespread effects on various organs and organ systems, especially when uncontrolled. One very rare complication of this common condition is thyrotoxic hypokalemic periodic paralysis (TPP), characterized by recurrent episodes of severe hypokalemia accompanied by weakness typically affecting the lower extremities. Reported cases in the literature predominantly involve Asian males between 20-39 years old. We present the case of a white male with recurrent hypokalemia and paralysis, ultimately diagnosed to have TPP.

Case Report(s): A 30-year-old white male presented to the ED with a 1-day history of lower extremity weakness, shortness of breath, and palpitations. His past medical history included Graves’ disease which has been inadequately treated since diagnosis, hypertension, celiac disease, and recurrent hypokalemia leading to multiple hospital admissions. He was tachycardic with mildly elevated blood pressure. On neurological exam, he had 3/5 strength on bilateral hip and knees, 4/5 strength on ankles and feet, and no motor deficits on bilateral upper extremities. EKG revealed sinus tachycardia with a 1st degree AV block. His potassium (K) was 2.2 mmol/L, TSH <0.01 mU/L, Free T4 2.5 ng/dL. Continuous K replacement was initiated and he was started on Methimazole and Propranolol. His symptoms and serum K levels eventually improved, and he was discharged in stable condition.

Discussion: TPP is a rare but potentially life-threatening condition, with severe cases progressing to involve all extremities and respiratory musculature. Its exact mechanism is not well understood, but various pathogenesis have been theorized. Increased thyroid activity in thyrotoxicosis triggers increased catecholamine activation. This heightened state of energy increases the activity of the Na-K ATPase pump, which causes the K intracellular shift and the hyperpolarization of cells. After establishing the diagnosis, quick but careful K replacement should be initiated with close monitoring of serum K due to the risk of rebound hyperkalemia. Beta blockade is also recommended since it does improve the neuromuscular symptoms by reducing the intracellular shift of K. Treatment of the underlying thyrotoxicosis should also be initiated. In patients who present with acute paralysis and hypokalemia, underlying hyperthyroidism should be ruled out despite the absence of other symptoms of thyrotoxicosis. The diagnosis can have a significant impact on these patients since it is relatively straightforward to manage once identified.