An Atypical Presentation of Myxedema Coma Masked by Underlying Renal Failure

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Introduction: Myxedema Coma is a manifestation of severe hypothyroidism typically manifesting as hypothermia, altered mentation, hypotension and bradycardia and has a high mortality rate. We report a case of Myxedema Coma with an atypical presentation, masked by underlying renal failure and metabolic disturbances resulting in a difficult diagnosis and resolution of symptoms with prompt treatment with intravenous T3 and T4.

Case Presentation: Our patient is 60‐year‐old female with a history of toxic multinodular goiter, status post radioactive iodine ablation and End Stage Renal disease requiring hemodialysis. She presented to the Emergency Department with lethargy and left sided weakness, initially suspected of having a stroke. Computed Tomography (CT) head was normal. Initial vitals were a Temperature of 96.1 F°, Blood Pressure 160/110 mmHg, Pulse 76/min and Respiratory Rate 19/min. Labs showed a serum TSH 153 uIU/ml (normal 0.30‐5.00 uIU/ml) and free T4 0.6ng/dL (normal 0.7‐1.7ng/dL). She was started on Intravenous T3 and T4 and admitted to the medical intensive care unit. White Cell Count remained normal and blood cultures remained negative. 24 hours later, her hypothermia resolved. Repeat TSH two weeks later was 42 uIU/mL and free T4 was 1.4ng/dL. She was transitioned to oral levothyroxine 100mcg daily and discharged from the hospital.

Discussion: Myxedema Coma is defined as severe life‐threatening hypothyroidism which can classically manifest as bradycardia, hypotension, altered sensorium, hypothermia, electrolyte abnormalities and facial and limb swelling. There are however, cases reported of atypical presentations of myxedema coma because of an underlying metabolic disturbance such as diabetic ketoacidosis that masks its typical presentation resulting in a difficult diagnosis that can potentially delay treatment. In our case, the patient had underlying renal failure requiring hemodialysis resulting in a baseline metabolic disturbance along with absence of hypotension and bradycardia as typically seen in myxedema coma patients. Given that immediate treatment with intravenous thyroid hormone resulted in resolution of the symptoms without any additional treatment, not only confirmed the diagnosis of myxedema coma but also emphasized the importance of prompt diagnosis of the disorder in the setting of co‐morbidities that can mask its typical presentation.


This abstract was published in Thyroid, Volume 32, Issue Supplement 1.

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