Abstract Introduction Myxedema coma is a rare, life-threatening manifestation of severe hypothyroidism, commonly precipitated by infection, drugs, or trauma. It presents with altered mental status, hypothermia, and respiratory depression. Steroid-responsive encephalopathy associated with autoimmune thyroiditis (SREAT), also known as Hashimoto’s encephalopathy, is another uncommon cause of encephalopathy linked to elevated antithyroid antibodies, typically in a euthyroid or mildly hypothyroid state. Differentiating these entities can be challenging when clinical and biochemical features overlap. Case Presentation A 59-year-old man with hypothyroidism, chronic obstructive pulmonary disease (COPD), traumatic brain injury, and seizure disorder presented after being found unresponsive on railroad tracks. On arrival, his Glasgow Coma Scale score was 5 with decerebrate posturing, prompting emergent intubation. Laboratory evaluation revealed a thyroid-stimulating hormone (TSH) of 542 mIU/mL, undetectable thyroxine (T4), and markedly elevated thyroid peroxidase (TPO) antibodies (952 IU/mL). Electroencephalography (EEG) showed diffuse slowing without epileptiform activity, and magnetic resonance imaging (MRI) was initially unremarkable. Myxedema coma was diagnosed, and he was started on intravenous (IV) levothyroxine and stress-dose hydrocortisone. Despite normalization of thyroid indices, his mental status remained unchanged. Repeat MRI demonstrated findings suggestive of postictal or autoimmune etiology, and lumbar puncture revealed mildly elevated protein without pleocytosis. Given persistent encephalopathy and elevated antibodies, high-dose IV methylprednisolone and intravenous immunoglobulin (IVIG) were initiated for suspected SREAT. On hospital day 9, code status was changed to do-not-resuscitate comfort care (DNRCC); he was extubated and transitioned to hospice care, remaining awake but non-verbal. Conclusion This case illustrates the diagnostic overlap between myxedema coma and SREAT. Profound hypothyroidism favored the former, yet lack of neurological recovery and evolving imaging findings suggested concomitant autoimmune encephalopathy, underscoring the need for clinical vigilance and multidisciplinary evaluation. This abstract is funded by: None
Karam et al. (Fri,) studied this question.