Hashimoto Heartbreak: The Silent Squeeze of Autoimmune Hypothyroidism

Abstract Background: Cardiac tamponade is a life-threatening condition characterized by the accumulation of fluid in the pericardial space, leading to compromised cardiac function. Common etiologies include but are not limited to malignancy, infections, or trauma; however, autoimmune diseases – like Hashimoto's thyroiditis – are rare culprits. Case Presentation: A 58-year-old female presented to the emergency department with a 1-week history of worsening shortness of breath. She reported a 75-pound weight gain over the past year due to fluid overload, along with dyspnea on exertion. She had a known history of Hashimoto's thyroiditis but was not on any thyroid replacement therapy, relying solely on supplements prescribed by a homeopathic physician. Physical exam revealed 3+ pitting edema extending to the lower abdomen, bilateral lung crackles, and an S4 heart sound. Laboratory tests revealed a TSH of 115 mIU/L, T3 of 0.49 ng/mL, and pro-BNP of 2118 pg/mL. Echocardiography revealed a large pericardial effusion with right atrial collapse, indicating cardiac tamponade. The patient was started on IV furosemide 40 mg BID, PO metoprolol 25 mg, and IV levothyroxine 100 mcg. Due to the effusion size and her clinical status – hypotensive, tachypneic, and in atrial flutter – pericardiocentesis was deferred, and Cardiothoracic surgery performed a subxiphoid pericardial window, yielding 400 mL of serous fluid. Management and Outcomes: The intervention provided significant symptomatic relief, with stabilizing her hemodynamics and improving respiratory status. Her recovery in the ICU was uneventful. Follow-up imaging confirmed resolution of the effusion. She was discharged on colchicine, furosemide, metoprolol, dapagliflozin, and levothyroxine, with outpatient follow-up for echocardiogram and ischemic evaluation. Discussion: This case underscores the rare occurrence of cardiac tamponade secondary to untreated Hashimoto's thyroiditis. Thyroid hormone deficiency affects cardiovascular function, contributing to fluid retention and heart failure. In our patient, delayed management of her autoimmune thyroid condition likely resulted in significant pericardial effusion and tamponade. The successful resolution of the effusion following a pericardial window emphasizes timely intervention. This case adds to the limited literature linking autoimmune thyroiditis with cardiac tamponade, highlighting the importance of adequate thyroid hormone replacement to avoid life-threatening complications. Conclusion: Cardiac tamponade, although rare, can result from untreated Hashimoto's thyroiditis. Clinicians should consider autoimmune thyroid disease in the differential diagnosis of pericardial effusions. Early recognition and appropriate management, including surgical intervention, can lead to favorable outcomes. Further studies are necessary to explore the pathophysiological mechanisms linking Hashimoto's thyroiditis to pericardial effusions.