MON-379 - Sympathetic Camouflage: A Reversible Cause of Altered Mental Status Hidden by Drug Withdrawal

Introduction
Altered mental status (AMS) is a common reason for hospitalization and is frequently attributed to intoxication or withdrawal in patients with substance use disorders. Severe hypothyroidism is a reversible but often overlooked cause of AMS, and its recognition depends on classic hypodynamic features. Conditions that induce sympathetic overactivity, such as opioid or alcohol withdrawal, may mask these hallmark signs, delaying diagnosis of impending myxedema crisis.

Case Description
A 38-year-old woman with hypothyroidism, polysubstance abuse, alcohol use disorder, and major depressive disorder was admitted from a rehabilitation facility for altered mental status and slowed responses. Laboratory evaluation revealed profound hypothyroidism with TSH 156 µIU/mL and free T4 < 0.42 ng/dL. Although examination demonstrated features of hypothyroidism, classic manifestations of myxedema crisis including hypothermia, bradycardia, hypotension, and hypoxemia were absent.

Instead, the patient exhibited tachycardia and hypertension attributed to acute opioid, alcohol, and polysubstance withdrawal. This withdrawal-related hyperadrenergic state was felt to mask the expected hypodynamic physiology of severe hypothyroidism. She was treated with intravenous levothyroxine and monitored closely.

Baseline cortisol was low, but cosyntropin stimulation testing demonstrated an appropriate adrenal response. Empiric stress-dose glucocorticoids were initiated due to concern for hypothalamic-pituitary axis suppression in the setting of profound hypothyroidism and were tapered as thyroid function improved. Serial free T4 levels showed biochemical improvement.

Discussion
This case emphasizes severe hypothyroidism as a reversible yet frequently underrecognized cause of AMS, particularly in patients with substance use disorders. Withdrawal-induced sympathetic activation can directly counterbalance the classic hypothermia, bradycardia, and hypotension seen in myxedema crisis, creating a misleading clinical picture. Attribution of AMS solely to withdrawal risks delayed recognition of life-threatening endocrine pathology. Early thyroid function testing should be considered in withdrawal patients with unexplained cognitive slowing or encephalopathy.

Conclusion
Severe hypothyroidism and impending myxedema crisis may be clinically masked by opioid and polysubstance withdrawal. Clinicians should maintain a high index of suspicion for this reversible endocrine cause of AMS, even when classic features are absent. Early identification and appropriate endocrine management are critical to improving outcomes.

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