Recommended Citation
Halon P, Krasny R, Alkhawam N. Myxedema Coma in the Setting of a Normal TSH. Presented at Scientific Day; May 20, 2026; Milwaukee, WI.
Abstract
Background/Significance:
Myxedema coma (MC) is an endocrine emergency precipitated by physiological stress and characterized by hypothermia, bradycardia, hypoglycemia, and altered mental status. Diagnosis is primarily clinical but is typically associated with low Free T4/T3 and elevated TSH, although cases with normal or minimally abnormal thyroid tests have been reported. There is a paucity of literature on the benefit of thyroid hormone replacement therapies and steroids in critically ill patients with features of MC with nondiagnostic labs.
Description:
An 81-year-old female with a history type two diabetes and chronic kidney disease presented with altered mental status and weakness. She was bradycardic (HR 30’s), hypotensive (69/31) and hypothermic (79.3 F). EKG revealed a third-degree AV block. On exam she was lethargic, with bilateral pitting edema and pulmonary crackles. Warming and vasopressors had minimal hemodynamic response prompting emergent transvenous pacing. Imaging demonstrated pulmonary edema with bilateral lower lobe consolidations, and broad-spectrum antibiotics were initiated. While in the intensive care unit (ICU), worsening lethargy, hypercapnia, and persistent anuria prompted intubation and CRRT. Stress-dose steroids were initiated given persistently high vasopressor requirements. Echocardiography showed preserved ventricular function and her blood cultures were negative. Despite some clinical improvement, she remained lethargic and vasopressor dependent. Thyroid studies showed a mildly low-free T4 (0.7), free T3 (0.8), and a normal TSH (2.1). Due to persistent concern for MC, IV levothyroxine was initiated on day 5. By day 7, vasopressors were discontinued, and steroids were tapered. She was discharged on day 14 on oral levothyroxine.
Discussion:
Undifferentiated shock remains difficult given limited early diagnostic clarity. The patient’s AV block was likely secondary to profound hypothermia. Concern for septic shock remained high despite negative cultures, which occur in up to half of cases. Several case reports document MC with normal biomarkers, associated with subclinical hypothyroidism, central hypothyroidism, or non-thyroidal illness. Evidence suggests that there is a poor correlation between thyroid biomarkers and disease severity. Therefore, patients with strong clinical suspicion for MC may benefit from empiric thyroid hormone therapy.
Presentation Notes
Presented at Scientific Day; May 20, 2026; Milwaukee, WI.
Full Text of Presentation
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Document Type
Poster
Open Access
Available to all.
Myxedema Coma in the Setting of a Normal TSH
Background/Significance:
Myxedema coma (MC) is an endocrine emergency precipitated by physiological stress and characterized by hypothermia, bradycardia, hypoglycemia, and altered mental status. Diagnosis is primarily clinical but is typically associated with low Free T4/T3 and elevated TSH, although cases with normal or minimally abnormal thyroid tests have been reported. There is a paucity of literature on the benefit of thyroid hormone replacement therapies and steroids in critically ill patients with features of MC with nondiagnostic labs.
Description:
An 81-year-old female with a history type two diabetes and chronic kidney disease presented with altered mental status and weakness. She was bradycardic (HR 30’s), hypotensive (69/31) and hypothermic (79.3 F). EKG revealed a third-degree AV block. On exam she was lethargic, with bilateral pitting edema and pulmonary crackles. Warming and vasopressors had minimal hemodynamic response prompting emergent transvenous pacing. Imaging demonstrated pulmonary edema with bilateral lower lobe consolidations, and broad-spectrum antibiotics were initiated. While in the intensive care unit (ICU), worsening lethargy, hypercapnia, and persistent anuria prompted intubation and CRRT. Stress-dose steroids were initiated given persistently high vasopressor requirements. Echocardiography showed preserved ventricular function and her blood cultures were negative. Despite some clinical improvement, she remained lethargic and vasopressor dependent. Thyroid studies showed a mildly low-free T4 (0.7), free T3 (0.8), and a normal TSH (2.1). Due to persistent concern for MC, IV levothyroxine was initiated on day 5. By day 7, vasopressors were discontinued, and steroids were tapered. She was discharged on day 14 on oral levothyroxine.
Discussion:
Undifferentiated shock remains difficult given limited early diagnostic clarity. The patient’s AV block was likely secondary to profound hypothermia. Concern for septic shock remained high despite negative cultures, which occur in up to half of cases. Several case reports document MC with normal biomarkers, associated with subclinical hypothyroidism, central hypothyroidism, or non-thyroidal illness. Evidence suggests that there is a poor correlation between thyroid biomarkers and disease severity. Therefore, patients with strong clinical suspicion for MC may benefit from empiric thyroid hormone therapy.
Affiliations
Advocate Christ Medical Center