Background: Central hypopituitarism is an under-recognized mimic of far more common inpatient diagnoses. Because secondary adrenal insufficiency and central hypothyroidism blunt the classic biochemical alarms of primary endocrine failure, the presentation can be misattributed to psychiatric decompensation, sepsis, or simple deconditioning — delaying a diagnosis that is, once suspected, straightforward to confirm and treat.

Case Presentation: A 68-year-old woman with COPD, bipolar disorder, chronic liver disease, and a recent tracheostomy for laryngeal cancer was admitted for acute hypoxic respiratory failure secondary to COPD exacerbation. Her respiratory status improved with bronchodilators, antibiotics, and steroids, but she developed progressive weakness, hypotension refractory to fluid resuscitation, and an acute change in affect — becoming mute and withdrawn, initially raising concern for depression. Laboratory evaluation revealed an inappropriately normal TSH in the setting of low free T4 and T3, a low random cortisol, and a blunted (rather than absent) response on ACTH stimulation testing — a biochemical signature pointing away from primary organ failure and toward a central process. MRI confirmed a 4 mm nonenhancing pituitary lesion. Glucocorticoid replacement was initiated before thyroid hormone repletion to avoid precipitating adrenal crisis, with prompt clinical recovery.

Conclusion: This case illustrates how central hypopituitarism can masquerade as psychiatric illness or refractory shock, and underscores two teaching points with direct bedside impact: thyroid function tests must be interpreted as a pair rather than in isolation, and hormone replacement sequencing — steroids before thyroid hormone — is a patient-safety issue, not an academic nicety.