A CASE OF THYROTOXICOSIS INDUCED PERIODIC PARALYSIS R. Poudel MD, N. Sahami Department of Internal Medicine, Leonard J. Chabert Medical Center, Houma, LA
INTRODUCTION: Thyrotoxicosis brings to mind many different symptomatic complications. As thyroid hormones essentially effects every cell in the body, it’s important to consider some of the potentially fatal complications.
CASE: A 28 year old man with hyperthyroidism and atrial fibrillation presented with acute onset paralysis and palpitations one hour prior to arrival. He had been evaluated due to malaise, palpitations, cough, and congestion and treated with dexamethasone 80mg IM and IVF. He later awoke from sleep and was unable to move his extremities secondary to diffuse weakness. He reported noncompliance with his home medications that included levothyroxine, methimazole and atenolol. His examwas positive for a diffuse, non-nodular goiter, tachycardia with an irregularly irregular rhythm and 2/5 strength in all extremities. Relevant lab studies showed K<2.0, Mg 1.4, TSH 0.015, T4 >5.00. EKG revealed atrial fibrillation, incomplete right bundle branch block and a QTc of 706 ms. Initial management included prophylthiouracil hydrocortisone , Lugol’s solution, cholestyramine, and magnesium supplementation which resolved the EKG changes, electrolyte disturbances and his symptoms by day two. He was discharged with counselling on triggering factors for periodic paralysis secondary to hyperthyroidism. DISCUSSION: Thyrotoxicosis and thyroid storm are dangerous complications of hyperthyroid states which can be life threatening. With the overall prevalence of hyperthyroidism in the U.S. at around 1.3%, it’s important to recognize and educate patients on the complications of ineffective treatment leading to acquired hypokalemic periodic paralysis. Specific signs of this acquired condition include sudden generalized weakness with preserved consciousness. The mechanism is currently not well understood but it’s proposed that thyroid hormone stimulates beta-adrenergic receptors which increase NA/K ATPase activity on skeletal muscles. This shifts potassium into cells causing hypokalemia resulting in hyperpolarization of the muscle membrane and decreased “excitability” of the muscle fibers leading to paralysis. Moreover, a hyperthyroid state also potentiates the hypokalemic action of epinephrine and insulin which also activates Na/K ATPase pump contributing further to hypokalemia. Keys to decreasing morbidity and mortality lies in the early detection of hyperthyroid induced hypokalemia with mindful correction of potassium as these patients are susceptible to rapid potassium shifts which may precipitate severe hyperkalemia.
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