Abstract
Traumatic brain injuries (TBIs) cause damage to the brain. Various brain structures can be vulnerable during acceleration-deceleration accidents, such as, in some cases, the pituitary organ. We present the case of a 21-year-old male with no past medical history who came to the ED of a tertiary care center after a motor vehicle accident (MVA). The patient was an unrestrained passenger ejected through the windshield of a car; he developed fluctuating sodium levels. This case demonstrates a rare occurrence of the triphasic pituitary response secondary to stalk injury, consisting of arginine vasopressin deficiency (AVP-D), syndrome of inappropriate antidiuretic hormone secretion (SIADH), and again AVP-D in a patient post traumatic brain injury (TBI). Clinical symptoms vary at each stage of the response, with management tailored accordingly. The patient in this case was admitted and diagnosed with AVP-D, initially being asymptomatic, followed shortly by hypernatremia and polyuria. In the first and last stages of AVP-D, the patient was treated with fluids and desmopressin. During the SIADH stage, the patient experienced net fluid negative and hyponatremia that was treated with fluid restriction, 3% normal saline, and conversion to salt tablets. Maintaining normal sodium levels in TBI patients is essential for preventing damage from rapid changes in osmolarity. In this case, we highlight the importance of close monitoring in the titration of sodium levels and present a successful treatment of the triphasic pituitary response secondary to stalk injury in a TBI patient.