A51-08 Atypical Presentation of Myxedema Coma in Metastatic Squamous Cell Lung Carcinoma

Abstract Introduction Myxedema coma is a rare, life-threatening endocrine emergency characterized by severe hypothyroidism and multi-organ dysfunction, with mortality rates ranging from 25-70% despite advances in critical care. Classic findings include hypothermia, bradycardia, and altered mental status, though presentations may be atypical or masked by malignancy, prior radiation, or concurrent illness. Diagnosis can be challenging, particularly when thyroid function tests are discordant, making prompt recognition and treatment critical to improving survival. Case Report A 59-year-old woman with stage IV squamous cell lung carcinoma (mediastinal and adrenal metastases), hypothyroidism, chemotherapy-induced neuropathy, and prior radiation presented with odynophagia, hypotension, and hypothermia. She was admitted to the ICU for persistent hypothermia, bradycardia, encephalopathy, and autonomic instability. Extensive infectious, neurologic, and endocrine evaluations - including MRI brain/spine, CT head, lumbar puncture, and paraneoplastic panels - were unrevealing. Empiric levothyroxine and steroids for possible adrenal insufficiency were ineffective. Despite supportive care, her encephalopathy worsened. Repeat thyroid testing revealed low T3 with normal T4 and fluctuating TSH, raising suspicion for atypical myxedema coma. Intravenous liothyronine was initiated, resulting in rapid normalization of temperature, mental status, and hemodynamics. She was subsequently weaned from high-flow oxygen, diuresed for edema, and transferred out of the ICU for ongoing thyroid titration and rehabilitation. Discussion This case highlights the diagnostic challenge of myxedema coma in the setting of atypical thyroid function and complex comorbidities. The combination of persistent hypothermia, bradycardia, and encephalopathy without infectious, neurologic, or adrenal causes prompted consideration of myxedema coma despite near-normal thyroid indices. Non-thyroidal illness and pituitary suppression can blunt TSH elevation, while impaired peripheral conversion can lower T3, obscuring the typical biochemical pattern. Increasing evidence supports that myxedema coma may occur even without classic lab findings, particularly under physiological stress. Current American Thyroid Association guidelines emphasize initiating thyroid hormone therapy based on clinical suspicion alone. Intravenous levothyroxine is the mainstay, with liothyronine added in critically ill patients, and glucocorticoids given to prevent adrenal crisis. In this case, early combination therapy led to rapid recovery, underscoring the importance of empiric, guideline-driven management. This report adds to limited literature on atypical myxedema coma and reinforces the need for clinical judgment over strict laboratory interpretation. Maintaining a high index of suspicion and initiating timely hormone replacement can be lifesaving in critically ill patients with unexplained hypothermia and encephalopathy. This abstract is funded by: None