SUN-315 - Sepsis, Steroids and Suppressed Thyroid Function: A Diagnostic Consideration

Euthyroid sick syndrome (ESS) is characterized by alterations in the levels of thyroid hormones due to non-thyroidal illness without intrinsic thyroid or hypothalamic- pituitary dysfunction. It is most commonly seen in hospitalized, critically ill patients. The typical biochemical pattern is low total and free triiodothyronine (T3) with low or normal thyroxine (T4) and thyroid-stimulating hormone (TSH). It can result from various etiologies such as sepsis, stress, burns or medications such as dopamine or corticosteroids. We present a case of critically ill patient with abnormal thyroid labs likely due to ESS in setting of glucocorticoid use.

A 66-year-old female with a history of COPD and HTN was brought to ED for fever, dyspnea, fatigue, decreased responsiveness. On arrival, she was hypotensive, tachycardic, tachypneic, and hypoxic with increased work of breathing, requiring non-rebreather support and eventually intubation. She received brief vasopressor support, which stabilized her blood pressure. She was also started on antibiotics and corticosteroids for treatment of sepsis likely due to pneumonia. Her blood culture later turned positive for streptococcus pneumoniae. Initial thyroid function tests were normal. During the course of her hospitalization, she developed bradycardia and repeat thyroid testing showed low TSH, free and total T4, and free and total T3. Considering her clinical condition, she received a dose of IV levothyroxine; however, her heart rate showed minimal improvement. Subsequent thyroid labs demonstrated normalization of TSH and free T4 within a few days, although reverse T3 was elevated. Her thyroglobulin antibodies were negative. Repeat testing one week later confirmed persistent normalization of thyroid labs. These findings were thought likely due to euthyroid sick syndrome in setting of sepsis, and likely aggravated by corticosteroid therapy, rather than primary thyroid dysfunction. No ongoing thyroid directed treatment was indicated.

While ESS is common in the setting of severe illness, our case highlights a unique presentation where both bradycardia and corticosteroids were confounding variables in determining a diagnosis. Elevation in reverse T3 will be seen, however, the rapid normalization of TSH and FT4 levels are often sufficient in diagnosing. In the critically ill patient, one should consider ESS as a cause of abnormal thyroid testing, being mindful of how corticosteroids can impact thyroid levels.

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