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Thyrotoxic Periodic Paralysis: The Peril of Potassium Replacement

Hypokalemic periodic paralysis (HPP) is a clinical condition of sudden-onset, recurrent transient episodes of weakness caused by severe hypokalemia. Thyrotoxic periodic paralysis (TPP) is a specific subgroup of the HPP spectrum, where hypokalemia occurs in the setting of thyrotoxicosis, and the repl...

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Detalles Bibliográficos
Autores principales: Yoon, Sean Ho, Raza, Hassan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Cureus 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9872846/
https://www.ncbi.nlm.nih.gov/pubmed/36699760
http://dx.doi.org/10.7759/cureus.32926
Descripción
Sumario:Hypokalemic periodic paralysis (HPP) is a clinical condition of sudden-onset, recurrent transient episodes of weakness caused by severe hypokalemia. Thyrotoxic periodic paralysis (TPP) is a specific subgroup of the HPP spectrum, where hypokalemia occurs in the setting of thyrotoxicosis, and the repletion of potassium must be performed with caution. A male in his second decade of life with hyperthyroidism non-adherent to methimazole presented with acute-onset bilateral lower extremity weakness. On physical examination, the patient had diffuse thyromegaly and tremors on outstretched hands. Bilateral lower extremity weakness and decreased reflexes were also noted, with preserved muscle tone and normal passive range of motion. Labs demonstrated hyperactive thyroid function and severe hypokalemia at 1.7 mEq/L, with U waves present on the electrocardiogram. In the intensive care unit, the patient received methimazole and propranolol for thyrotoxicosis and a total dose of 60 mEq/L of potassium replacement therapy. Despite the expected correction by 0.6 mEq/L, his follow-up potassium level dramatically increased to 5.7 mEq/L, resulting in the actual correction of 4.0 mEq/L. Within a few hours, the patient regained his baseline strength with a significant improvement in tremors. Patients with TPP present with acute-onset extremity weakness and severe hypokalemia, which reverses quickly with potassium repletion. Clinicians should not only treat thyrotoxicosis but also avoid overly aggressive repletion of potassium as this may lead to rebound hyperkalemia when the initial transcellular potassium shift is reversed.