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Case Presentation:A 59-year-old female with a history of hypertension was brought to a local hospital after being found unresponsive at home. Computed tomography angiography (CTA) of the chest showed type A aortic dissection (TAAD) with maximal aortic dimension of 9.0 cm. She was transferred to our center for escalation of care. She had poor neurological status but stable hemodynamic status, without malperfusion or acute cerebrovascular accident. Lab studies showed severely elevated thyroid-stimulating hormone of 80.4 mIU/ML and free thyroxine 4 (T4) less than 0.2 ng/dL, indicating severe hypothyroidism consistent with myxedema coma. Due to her low functional baseline status, surgical repair was deferred. Anti-impulse therapy was initiated with short acting beta blocker and calcium channel blocker infusion to maintain control of heart rate (HR) and blood pressure (BP). Her clinical course was complicated by pulseless electrical arrest and acute renal failure. After 100 mcg of intravenous levothyroxine, she was extubated and regained renal function. After 40 days, she was discharged to an acute rehabilitation center. 6 weeks later, she showed marked improvement in her frailty index, and medications were optimized. She underwent elective aortic repair, coronary bypass surgery, and was discharged to home.Discussion:Due to the patient’s initial neurological status, repair of her TAAD with aneurysmal degeneration was deferred. She was later diagnosed with myxedema coma and her TAAD was deemed chronicrather than acute. Surgical repair of both acute and chronic TAAD remains the gold standard; however, medical therapy with strict control of HR and BP parameters may stabilize the patient for future surgical repair.1,2In this case, by treating the patient’s underlying hypothyroidism and managing risk factors, her surgical risk was reduced, and she underwent successful aortic repair, reporting drastically improved functional status and quality of life. |
