704 - The Sodium Swing: Unmasking the Triphasic Pituitary Dance Post-TBI

Friday, February 20, 2026

5:00 PM - 6:30 PM AST

Presenting Author(s)

JA

Jonathan Arias, DO

Resident Physician
Temple University Hospital
Allentown, Pennsylvania, United States

Co-Author(s)

AA

Ayan N. Ahmed, MD

Resident Physician
Temple University Hospital
Sewickley, Pennsylvania, United States
AS

Andrej Sodoma, DO

Resident Physician
Northwell South Shore University Hospital
Islip, New York, United States
AP

Angelina Prince, BA

Medical Student
New York Institute of Technology College of Osteopathic Medicine
Glen Head, New York, United States

Submitter(s)

JA

Jonathan Arias, DO

Temple University Hospital
Allentown, Pennsylvania, United States

Case Diagnosis: A 21-year-old male sustained a traumatic brain injury (TBI) after being ejected during a motor vehicle accident. He developed a rare triphasic neuroendocrine response due to pituitary stalk injury, marked by sequential phases of arginine vasopressin deficiency (AVP-D), syndrome of inappropriate antidiuretic hormone secretion (SIADH), and a return to AVP-D.

Case Description: The patient presented to the emergency department with a subdural hematoma and scalp contusions, initially alert with stable vitals. Within 24 hours, he developed polyuria and hypernatremia (Na 150 mmol/L), consistent with AVP-D, and responded to IV fluids and desmopressin. Three days later, his sodium dropped to 119 mmol/L with concentrated urine and elevated urine sodium, meeting criteria for SIADH. Management included hypertonic saline, fluid restriction, and salt tablets. Subsequently, a return to AVP-D was observed with hypernatremia and low urine osmolality, necessitating re-initiation of desmopressin therapy. He stabilized and was discharged with normal sodium levels and outpatient follow-up.

Discussions: The triphasic pituitary response is an uncommon sequela of stalk injury typically seen in pediatric craniopharyngioma resections and rarely post-TBI. It results from initial neuronal shock and vasopressin depletion (AVP-D), followed by unregulated release of stored AVP (SIADH), and eventually permanent or transient neuronal loss leading back to AVP-D. Differentiating these phases is essential, as treatment strategies vary significantly—ranging from desmopressin and fluid replacement to fluid restriction and hypertonic saline. This case underscores the importance of vigilant electrolyte monitoring in post-TBI patients, even when they are clinically stable.

Conclusions: Triphasic pituitary response post-TBI, while rare, demands early recognition and phase-specific interventions to prevent life-threatening sodium derangements. This case illustrates successful diagnosis and management through meticulous clinical monitoring and interdisciplinary care.