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A3359 - Thyrotoxic Periodic Paralysis and Cardiomyopathy in a Patient with Graves' Disease
Author Block: A. A. Abbasi1, S. S. Gupta2, P. Chandar2, S. Shankar2, Y. Kupfer2; 1Internal Medicine, Maimonides Medical Center, Brooklyn, NY, United States, 2CRITICAL CARE MEDICINE, Maimonides Medical Center, Brooklyn, NY, United States.
INTRODUCTION
Thyrotoxic Periodic Paralysis (TPP) and cardiomyopathy are two established complications of thyrotoxicosis. Emergent management is essential as TPP and cardiac events secondary to thyrotoxic cardiomyopathy can be fatal. We report a unique case of a patient with Graves’ disease presenting with symptoms secondary to both these complications.
CASE REPORT
A 34-year old Hispanic male, diagnosed with Graves’ disease, non-compliant with his medications, presented to the Emergency room with complaints of generalized weakness, palpitations, chest pain and multiple episodes of nausea and vomiting for one day. On presentation, the patient was tachycardiac, had a systolic flow murmur and decreased motor strength in all extremities. Blood work showed a potassium of 1.8 millimoles per liter, cardiac troponin of 0.04 nanograms per milliliter and a thyroid panel consistent with hyperthyroidism. Electrocardiogram showed atrial flutter. In the ER Propranolol, Propylthiouracil and Hydrocortisone were administered to prevent thyroid storm. Potassium was repleted, and the patient developed rebound hyperkalemia. He was given calcium gluconate, insulin, Sodium Polystyrene and admitted to the medical intensive care unit for further management. Echocardiogram revealed severely decreased left ventricular systolic function and an ejection fraction of 26-30%. He was diagnosed with cardiomyopathy secondary to thyrotoxicosis. He was stabilized with Methimazole, Propranolol, Lisinopril and discharged on day nine with these medications and an outpatient follow up appointment.
DISCUSSION
Thyrotoxicosis can be life threatening. This case shows a unique instance where a Hispanic patient presented with two complications of this phenomena. The pathogenesis of TPP involves increased responsiveness of the beta-adrenergic receptors, which leads to increased activity of the Na+/K+ ATPase pump and a transcellular shift of potassium into cells. The condition can resolve acutely with the administration of potassium. It is important to monitor the rate of potassium replacement as rebound hyperkalemia can occur, as this case demonstrates. Propranolol is an integral part of treatment as it is a beta-adrenergic receptor blocker and blocks the peripheral conversion of thyroxine (T4) to triiodothyronine (T3) in high doses.
Thyrotoxic cardiomyopathy is one of the many cardiac complications that can be precipitated by Graves’ disease. One probable cause is the chronic tachycardia that patients with hyperthyroidism develop. Treatment entails managing the hyperthyroidism by starting the patient on beta blockers and anti-thyroid drugs or radioactive iodine uptake. Diuretics can be started to manage patients with heart failure. It is important to identify and treat the condition immediately to prevent grave complications.