SAT-349 - Severe Primary Hypothyroidism Masked by Septic Shock: Recognizing Discordant Recovery Patterns in Critical Illness

Introduction
Severe hypothyroidism and myxedema coma remain challenging to recognize in critically ill patients because early manifestations overlap with sepsis-related organ dysfunction. Delayed recognition is associated with significant morbidity and mortality. This case highlights a diagnostic pitfall in which severe hypothyroidism becomes clinically apparent only after resolution of the inciting infection, emphasizing the importance of identifying discordant clinical trajectories—particularly cardiovascular, neurologic, and renal deterioration despite sepsis control.

Case Presentation
A 71-year-old nursing home resident with known hypothyroidism, atrial fibrillation, chronic kidney disease, diabetes mellitus, and chronic Foley catheter use presented with altered mental status and hypotension. On arrival, vital signs revealed a mean arterial pressure of 64 mmHg, heart rate 60 bpm, respiratory rate 14/min, and temperature 35 °C. She was admitted to the medical intensive care unit with septic shock secondary to catheter-associated urinary tract infection and community-acquired pneumonia, complicated by severe Clostridioides difficile infection requiring vasopressor support. During the shock phase, she developed stress hyperglycemia managed with a critical-care insulin infusion for 24 hours. Septic shock resolved after three days with discontinuation of vasopressors, and she was transferred to the medical ward on hospital day five.
Despite infection control and negative cultures, the patient exhibited a discordant clinical course on the ward, including persistent waxing and waning mental status (GCS 14/15), worsening renal function, progressive peripheral edema, hypothermia, bradycardia, and atrioventricular conduction abnormalities, without evidence of recurrent sepsis. Thyroid evaluation demonstrated a thyroid-stimulating hormone level of 319 mIU/L (confirmed at 290 mIU/L) with free thyroxine < 0.42 ng/dL, consistent with severe decompensated hypothyroidism.

Endocrine Management and Outcomes
Empiric stress-dose glucocorticoids were administered prior to thyroid hormone replacement, followed by intravenous levothyroxine 200 mcg once, then 60 mcg daily, dose-reduced for advanced age, cardiovascular disease, and renal impairment. The patient demonstrated gradual improvement in hemodynamics, mental status, renal function, and peripheral edema.

Conclusion
This case emphasizes that severe hypothyroidism should be actively suspected in critically ill patients whose sepsis resolves but neurologic, cardiovascular, or renal dysfunction persists or worsens. Key clinical clues include hypothermia, bradycardia, altered mental status, edema, and unexplained renal deterioration. Early thyroid testing and prompt endocrine intervention are essential to prevent progression to myxedema coma and improve outcomes.

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