5160 Acute Onset Myxedema Coma After Pituitary Surgery

5160 垂体手术后急性发作性黏液性水肿昏迷

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Abstract

Disclosure: D. Krinsky: None. E. Krug: None. J.A. Mullally: None. Introduction: Myxedema coma is a rare endocrine emergency. The classic presentation is progressive worsening of hypothyroidism, over the course of months, usually in the setting of improper intake of levothyroxine. Here, we present a unique case in which a 91-year-old male presented with myxedema coma 3 weeks after resection of a non-functioning pituitary macroadenoma. Case Presentation: A 91-year-old male with history of hypertension and atrial fibrillation initially presented with progressive bitemporal hemianopsia due to an enlarging 2.4 cm pituitary macroadenoma with compression of the optic chiasm. Pre-operative pituitary labs, including thyroid function tests, were normal and he underwent transsphenoidal resection. Free T4 and cortisol levels were normal post-op day 3 and the patient did not require hormone replacement on discharge. 3 weeks later, the patient presented with hypotension and altered mental status. On admission, he was oriented to self only, able to follow simple commands, with dry oral mucosa, and bilateral non-pitting lower extremity edema. Laboratory studies indicated a normal TSH of 0.386 mlU/L (reference range 0.35-4.7). The following day, the patient became unresponsive, bradycardic, and had hypothermia to 30° C. His free T4 was found to be low at 0.4ng/dL (reference range 0.7-1.9) The diagnosis of myxedema coma was made, and intravenous levothyroxine was initiated after administration of intravenous hydrocortisone to prevent adrenal crisis. After initiation of treatment, the patient’s mental status improved, and he was discharged on long term thyroid hormone and glucocorticoid replacement. Discussion: Myxedema coma is a clinical diagnosis and requires urgent treatment as it has a mortality rate as high as 30-50%. This case was unusual because myxedema coma most often occurs in the setting of primary hypothyroidism with inadequate intake of thyroid hormone supplementation over the course of months. In contrast, our patient presented only 3 weeks after pituitary surgery, with a new diagnosis of central hypothyroidism and myxedema coma. Our case demonstrates central hypothyroidism and myxedema coma can develop quite rapidly after pituitary surgery. Clinical guidelines recommend checking a FT4 between 4-6 weeks after pituitary surgery. Our patient presented with severe biochemical hypothyroidism and myxedema coma only 3 weeks post-operatively despite having a normal FT4 3 days post-op. Based on our case, there may be a benefit to checking FT4 at an earlier post-op time point. Additionally, initially only a TSH was checked for our patient and was normal. When considering a diagnosis of myxedema coma in a patient with recent pituitary surgery, a FT4 must be checked as the TSH will not be reliable in central hypothyroidism. Clinicians should be aware of the potential for new central hypothyroidism and even myxedema coma within weeks of pituitary surgery. Presentation: 6/2/2024

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