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Abstract: TH-PO357

Thyrotoxic Periodic Paralysis Complicated by Severe Rebound Hyperkalemia

Session Information

Category: Fluid, Electrolytes, and Acid-Base Disorders

  • 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical

Authors

  • Ravender, Raja, The University of New Mexico, Albuquerque, New Mexico, United States
  • Shareef, Zan, The University of New Mexico, Albuquerque, New Mexico, United States
  • Garcia, Pablo, The University of New Mexico, Albuquerque, New Mexico, United States
  • Teixeira, J. Pedro, The University of New Mexico, Albuquerque, New Mexico, United States

Group or Team Name

  • UNM Nephrology.
Introduction

Thyrotoxic periodic paralysis (TPP) is a rare, acquired subtype of periodic paralysis in which muscle weakness develops from profound hypokalemia in the setting of hyperthyroidism. We present a case of TPP complicated by severe rebound hyperkalemia.

Case Description

A 31-year-old Hispanic man without medical history presented with severe generalized weakness. His physical exam was notable for proptosis and tremor. Initial labs included hypokalemia (serum potassium 1.6 mEq/L), undetectable thyroid-stimulating hormone (TSH), free T4 2.3 ng/dL, and urine potassium 5 mEq/L. He was admitted to intensive care with a diagnosis of TPP and treated with methimazole, propranolol, and aggressive potassium replacement (100 mEq IV + 220 mEq PO in 24 hours). His weakness improved, but he subsequently developed severe hyperkalemia with peak serum potassium of 7.4 mEq/L (Figure 1). His hyperkalemia resolved with medical therapy. He was diagnosed with Graves’ disease based on a positive TSH receptor antibody, and he was discharged home on methimazole and propranolol.

Discussion

TPP is a potentially fatal complication of hyperthyroidism characterized by episodes of sudden paralysis and hypokalemia, classically triggered by carbohydrate intake or exercise and often predating overt clinical hyperthyroidism. Though common in East Asian men, other non-white minorities, including Hispanics, appear to be at increased risk. Rather than potassium depletion, the primary cause of acute hypokalemia in TPP is transcellular shift caused by a hyperadrenergic state. As such, aggressive potassium repletion — particularly as the underlying hyperthyroidism abates with treatment — carries a risk of rebound hyperkalemia which can be lethal. Thus, initial treatment for TPP must focus on the underlying hyperthyroidism with antithyroid therapy and non-selective beta-blockade, with recommended potassium replacement limited to ≤90 mEq PO in 24 hours.