Abstract Background Severe traumatic brain injury (TBI) can precipitate hypothalamic-pituitary failure with central adrenal insufficiency (AI), central hypothyroidism (CeH), and central diabetes insipidus (DI). In the unstable neurotrauma patient, timely endocrine replacement may be lifesaving. We report endocrine-guided stabilization in a young TBI patient with biochemical pan-hypopituitarism. Case Presentation A 27-year-old male bike vs vehicle arrived with GCS 3T noted to have craniofacial fractures, bilateral pneumothoraces and severe TBI due to bifrontal/cerebellar hemorrhagic contusions, subarachnoid and subdural hemorrhage. He underwent emergent right decompressive craniectomy. The patient required multiple vasopressors (norepinephrine, vasopressin, phenylephrine) and hyperosmolar therapy. Over hospital days 2 to 4 he developed hypernatremia and polyuria: sodium (Na) rose to 175 mEq/L with serum osmolality 333 mOsm/kg, urine osmolality 83 mOsm/kg, urine Na 20 mEq/L, which was diagnostic of central DI. Concurrent endocrine testing showed thyroid stimulating hormone (TSH) 23 μIU/mL with low free T4 0.63 ng/dL and serum cortisol 12 μg/dL. Hormone replacement using hydrocortisone, desmopressin (plus adjunct vasopressin), free-water replacement guided to neurosurgical Na goal 145-155, and levothyroxine. Following hormone replacement, urine output decreased (from 300 mL/h to 20-60 mL/h), sodium trended down to 140s to 150s, acid-base status improved, and vasopressors were weaned off by day 6. Neurologically, he progressed from no purposeful movement to GCS 11T; he underwent tracheostomy/PEG and transitioned to long term rehabilitation planning. Discussion This case demonstrates that acute hypothalamic-pituitary failure can be a primary and reversible driver of hemodynamic instability in TBI. The patient’s presentation with rapid onset polyuria, rising serum sodium, low urine osmolality, vasopressor-refractory hypotension, and low free T4 with inadequate cortisol response was consistent with combined anterior and posterior pituitary dysfunction. The presence of skull base and frontal calvarial fractures placed the pituitary stalk at high shear risk, and diffuse cerebral edema likely compounded ischemic pituitary injury.The sequenced hormone replacement strategy was central to stabilization. Central diabetes insipidus was confirmed biochemically and responded to DDAVP/vasopressin titration and targeted free-water replacement. Cortisol deficiency can present subtly during catecholamine-dependent shock, stress-dose hydrocortisone was initiated before thyroid replacement, preventing the risk of precipitating adrenal crisis. Subsequently, levothyroxine was added for central hypothyroidism, improving perfusion stability and facilitating ventilatory weaning. The patient transitioned from triple vasopressor dependence to hemodynamic stability, with meaningful neurologic recovery. This report provides ICU-level, time-sequenced evidence that early recognition and staged endocrine replacement can reverse shock physiology previously attributed to “severe TBI” alone. This abstract is funded by: none
Gray et al. (Fri,) studied this question.