What question did this study set out to answer?

This case aims to clarify the diagnostic dilemma between myxedema coma and SREAT in a patient with profound hypothyroidism.

May 20, 2026

A51-02 Hypothyroidism Presenting as Coma: A Diagnostic Challenge of Differentiating Myxedema Coma From SREAT

Key Points

This case aims to clarify the diagnostic dilemma between myxedema coma and SREAT in a patient with profound hypothyroidism.
Case presentation of a 59-year-old man with severe hypothyroidism and altered mental status.
Laboratory tests included TSH, T4, and TPO antibodies, followed by EEG and MRI assessments.
Treatment involved levothyroxine, hydrocortisone, methylprednisolone, and IVIG based on evolving symptoms.
Initial diagnosis of myxedema coma with TSH of 542 mIU/mL and undetectable T4 levels.
Intravenous treatment did not improve neurological status, leading to reconsideration of SREAT.
High-dose IV medications were initiated based on persistent encephalopathy and elevated antibodies.

Abstract

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

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Cite This Study

Karam et al. (Fri,) studied this question.

synapsesocial.com/papers/6a0d4fbff03e14405aa9b2cc https://doi.org/https://doi.org/10.1093/ajrccm/aamag162.4899

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