SAT-381 More Than Just Hypothermia: A Case Of Myxedema Coma With Normal Thyroid-Stimulating Hormone

Abstract Disclosure: N. Alkhawam: None. K. Mitrollari: None. D. Kaul: None. P. Halon: None. T. Yasmeen: None. Background: Myxedema coma is a rare complication of severe hypothyroidism that could lead to mortality if left untreated. It is characterized by altered mental status, hypothermia, bradycardia, hypotension, and hypoventilation. Laboratory findings include an elevated thyroid-stimulating hormone (TSH) with a low serum free T3 and T4 level. Clinical case: An 81-year-old female with past medical history of type 2 diabetes presented for progressive lethargy. On presentation, HR was 32 bpm, blood pressure was 69/31 mmHg, and temperature was 79.3°F. Patient was administered atropine with no response. EKG noted a third-degree heart block. Transvenous pacing and vasopressors were initiated emergently. Patient was rewarmed with warming blankets. She was admitted to the intensive care unit (ICU) for suspected myxedema coma versus septic shock. Stress dose steroids were initiated with IV hydrocortisone 100 mg, followed by 50 mg every 6 hours. Labs were remarkable for TSH 2.1 mcUnits/mL (normal 0.35-5 mcUnits/mL), free T4 0.7 ng/dL (normal 0.8-1.5 ng/dL), free T3 0.48 pg/mL (normal 2.2-4 pg/mL). Computed tomography (CT) imaging without contrast showed no abnormalities in the pituitary or adrenal glands. Blood and urine cultures were negative. Stress dose steroids were maintained; however, levothyroxine was initially withheld due to return to normothermia with warming blankets, decreased pressure support requirements, and resolution of bradycardia. On day 3 of admission, the patient required norepinephrine intermittently overnight, with otherwise stable temperature on warming blankets. In light of persistent clinical features of severe hypothyroidism, IV levothyroxine 75 mcg daily was initiated. On day 8 of admission, the patient was switched to oral levothyroxine with tapering of her hydrocortisone dose. The patient was then discharged on oral levothyroxine 75 mcg daily, with outpatient endocrinology follow-up arranged. Conclusion: This case highlights the importance of maintaining a high suspicion for myxedema coma based on clinical presentation, even when laboratory values are not profoundly abnormal, as thyroid function tests can be confounded by non-thyroidal illness in critically ill patients. Early recognition and treatment are essential to preventing mortality and improving outcomes in patients with myxedema coma. Presentation: Saturday, July 12, 2025

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Journal of the Endocrine Society
Published
2025-10-01
DOI
https://doi.org/10.1210/jendso/bvaf149.2297
Primary Topic
Cancer, Hypoxia, and Metabolism
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article
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article

SAT-381 More Than Just Hypothermia: A Case Of Myxedema Coma With Normal Thyroid-Stimulating Hormone

Diksha Kaul, Kristjana Mitrollari, Tahira Yasmeen, Noor Alkhawam et al.
Journal of the Endocrine Society
Cancer, Hypoxia, and Metabolism
article

SAT-381 More Than Just Hypothermia: A Case Of Myxedema Coma With Normal Thyroid-Stimulating Hormone

Diksha Kaul, Kristjana Mitrollari, Tahira Yasmeen, Noor Alkhawam, Piotr Halon
article en

Abstract

Abstract Disclosure: N. Alkhawam: None. K. Mitrollari: None. D. Kaul: None. P. Halon: None. T. Yasmeen: None. Background: Myxedema coma is a rare complication of severe hypothyroidism that could lead to mortality if left untreated. It is characterized by altered mental status, hypothermia, bradycardia, hypotension, and hypoventilation. Laboratory findings include an elevated thyroid-stimulating hormone (TSH) with a low serum free T3 and T4 level. Clinical case: An 81-year-old female with past medical history of type 2 diabetes presented for progressive lethargy. On presentation, HR was 32 bpm, blood pressure was 69/31 mmHg, and temperature was 79.3°F. Patient was administered atropine with no response. EKG noted a third-degree heart block. Transvenous pacing and vasopressors were initiated emergently. Patient was rewarmed with warming blankets. She was admitted to the intensive care unit (ICU) for suspected myxedema coma versus septic shock. Stress dose steroids were initiated with IV hydrocortisone 100 mg, followed by 50 mg every 6 hours. Labs were remarkable for TSH 2.1 mcUnits/mL (normal 0.35-5 mcUnits/mL), free T4 0.7 ng/dL (normal 0.8-1.5 ng/dL), free T3 0.48 pg/mL (normal 2.2-4 pg/mL). Computed tomography (CT) imaging without contrast showed no abnormalities in the pituitary or adrenal glands. Blood and urine cultures were negative. Stress dose steroids were maintained; however, levothyroxine was initially withheld due to return to normothermia with warming blankets, decreased pressure support requirements, and resolution of bradycardia. On day 3 of admission, the patient required norepinephrine intermittently overnight, with otherwise stable temperature on warming blankets. In light of persistent clinical features of severe hypothyroidism, IV levothyroxine 75 mcg daily was initiated. On day 8 of admission, the patient was switched to oral levothyroxine with tapering of her hydrocortisone dose. The patient was then discharged on oral levothyroxine 75 mcg daily, with outpatient endocrinology follow-up arranged. Conclusion: This case highlights the importance of maintaining a high suspicion for myxedema coma based on clinical presentation, even when laboratory values are not profoundly abnormal, as thyroid function tests can be confounded by non-thyroidal illness in critically ill patients. Early recognition and treatment are essential to preventing mortality and improving outcomes in patients with myxedema coma. Presentation: Saturday, July 12, 2025

Journal of the Endocrine SocietyVol. 9(Supplement_1)
Advocate Christ Medical Center (US)
Openalex Percentile: Top 63%
Cancer, Hypoxia, and Metabolism
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