SAT-458 A Case of Cardiac Arrest Due to Hashimoto’s Thyroiditis Associated Cardiac Tamponade

Introduction: Myxedema coma is currently an uncommon medical emergency. We present a case of undiagnosed Hashimoto’s thyroiditis with myxedema coma and cardiac tamponade leading to cardiac arrest. Case Presentation: A 35 year-old man with no significant past medical history was brought to the emergency department after being found unresponsive. The patient was hypoglycemic (17 mg/dL), hypothermic (34°C), tachypneic (26/min), hypotensive (84/50 mmHg), and hypoxemic (90% on ambient air). Physical exam showed mild anasarca, jugular vein distention, clear lung sounds, and muffled heart sounds. Laboratory findings showed TSH 168.16 uIU/mL (0.45–5.33 uIU/mL), fT4 <0.25 ng/dL (0.58–1.64 ng/dL), fT3 1.33 pg/mL (2.5–3.9 pg/mL), cortisol 5.7 mcg/dL (3–16 mcg/dL). Chest x-ray demonstrated markedly enlarged, globular heart. ECG revealed sinus rhythm and low voltage of QRS complexes. Echocardiogram was significant for a very large pericardial effusion. Resuscitation was started with intravenous thyroxine and hydrocortisone, during which the patient was found to be in a cardiac arrest with pulseless electrical activity. CPR per ACLS protocol was initiated with return of spontaneous circulation. Clear fluid (2000 ml) was evacuated from the pericardial space. He was diagnosed with Hashimoto thyroiditis (thyroid peroxidase antibody level 355 IU/mL, normal <9 IU/mL). He recovered without neurological deficits and was discharged home with thyroid replacement therapy (levothyroxine 100 mcg). Discussion: Myxedema coma occurs as a complication of undiagnosed/untreated thyroid disease. It may be precipitated by an event such as infection, drug overdose, or myocardial infarction. The mainstay of treatment is T4 replacement along with supportive therapy, and glucocorticoids to counter possible underlying adrenal insufficiency. Massive pericardial effusion due to hypothyroidism, especially resulting in cardiac tamponade, is extremely rare. The incidence of pericardial effusion in patients with hypothyroidism has significantly decreased from 30–80% to 3–6%, due to early recognition of this common disorder. Our case highlights the importance of prompt recognition of hypothyroidism as a cause of cardiac tamponade, thus allowing rapid life-saving treatment. In patient populations with limited access to health care, it should be remembered that very late and potentially fatal complications of otherwise easily treatable conditions can occur. Awareness of this may help limit morbidity and mortality. References: Kabadi UM, Kumar SP. Pericardial effusion in primary hyperparathyroidism. Am Heart J. 1990; 120:1393.