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Amiodarone induced myxedema coma presenting with cardiogenic shock and junctional rhythm
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We describe the case of an elderly female, with no prior history of thyroid dysfunction, who presented with facial swelling and worsening fatigue. She was found to have myxedema coma, with thyroid-stimulating hormone (TSH) 98.90 uIU/mL and free thyroxine (fT4) 0.8 ng/dL, following two months of amiodarone therapy for paroxysmal atrial fibrillation. The patient developed cardiogenic shock and received liothyronine, levothyroxine, stress dose steroids, inotropic and vasopressor therapy while in the intensive care unit (ICU). She was weaned off vasopressors and switched to oral levothyroxine with a gradual steroid taper. Two months following hospital discharge, the patient remained asymptomatic while on oral levothyroxine. Literature lacks cases of amiodarone-induced myxedema coma and to our knowledge, myxedema coma secondary to amiodarone use has never been reported in patient on treatment for as short as two months. This case demonstrates the significance of early diagnosis and prompt treatment for rapid progression of signs and symptoms of amiodarone-induced myxedema coma to optimize outcomes. Although transient changes are seen while on amiodarone therapy, continuous monitoring is essential to examine for apparent thyroid dysfunction. Thyroid function testing prior to initiation of amiodarone and in cases of cardiac dysrhythmias or cardiogenic shock can help to avoid potentially fatal complication of hypothyroidism.
Title: Amiodarone induced myxedema coma presenting with cardiogenic shock and junctional rhythm
Description:
We describe the case of an elderly female, with no prior history of thyroid dysfunction, who presented with facial swelling and worsening fatigue.
She was found to have myxedema coma, with thyroid-stimulating hormone (TSH) 98.
90 uIU/mL and free thyroxine (fT4) 0.
8 ng/dL, following two months of amiodarone therapy for paroxysmal atrial fibrillation.
The patient developed cardiogenic shock and received liothyronine, levothyroxine, stress dose steroids, inotropic and vasopressor therapy while in the intensive care unit (ICU).
She was weaned off vasopressors and switched to oral levothyroxine with a gradual steroid taper.
Two months following hospital discharge, the patient remained asymptomatic while on oral levothyroxine.
Literature lacks cases of amiodarone-induced myxedema coma and to our knowledge, myxedema coma secondary to amiodarone use has never been reported in patient on treatment for as short as two months.
This case demonstrates the significance of early diagnosis and prompt treatment for rapid progression of signs and symptoms of amiodarone-induced myxedema coma to optimize outcomes.
Although transient changes are seen while on amiodarone therapy, continuous monitoring is essential to examine for apparent thyroid dysfunction.
Thyroid function testing prior to initiation of amiodarone and in cases of cardiac dysrhythmias or cardiogenic shock can help to avoid potentially fatal complication of hypothyroidism.
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