8431 Triphasic response of pituitary stalk post anoxic injury in a mechanically ventilated patient
Authors: Feliz Pamela Henriquez , Neizer Hannah , Alshdifat Esra’a , Abdulkarim Faridat , Mazhude Tawana , Zahra Tasneem 
Published: October 2024

Disclosure: P. Henriquez Feliz: None. H. Neizer: None. E. Alshdifat: None. F. Abdulkarim: None. T. Mazhude: None. T. Zahra: None.

Introduction: A phenomenon may manifest wherein the pituitary undergoes a triphasic response following an inciting event. Phases include diabetes insipidus (DI) followed by Syndrome of inappropriate Antidiuretic Hormone (ADH), and finally a recurrence of DI. Research has established that this is a common complication to neurosurgical interventions but there are limited reports following anoxic brain injury. This case demonstrates a potential pituitary stalk injury after an anoxic brain injury. Case: Unknown 30 year old male found by EMS with pulseless electrical activity cardiac arrest likely from polysubstance use. Returned of spontaneous circulation after 30 minutes in the emergency department. Total downtime unknown. Managed by Intensive Care Unit. Scans were negative. Initial blood work showed eunatremia with a specific gravity (sg) 1.068 and serum osmolarity (Sosm) 311. Eventually, developed hypernatremia, 163 mmol/L, and a urine osmolarity (Uosm) of 428 mosm, raising concern for central DI (CDI). Responded to hypotonic fluids not requiring desmopressin at that time. On day 10, developed severe hyponatremia 113 mmol/L with a Uosm of 774, suggesting ADH mediated response or excessive free water intake. Sodium normalized after managed with fluid restriction. On day 16, patient developed hypernatremia, 178 mmol/L, and Uosm of 869 mosm. Suggestive of CDI recurrence. Treated with desmopressin and hydrocortisone. Discussion: Changes in water-electrolyte balances may occur after anoxic brain injury. The mechanism is believed to arise from axonal shock due to disruptions in vascular supply leading to unregulated release of ADH from degenerating posterior pituitary, causing oliguria and hyponatremia, and subsequent permanent DI from loss of neurons. These stages may last 5-7 days on initial phase, and the second phase can extend anywhere from 2-14 days. In this case, phases one and two lasted four and three days, respectively. It is important to acknowledge that timelines may vary based on management initiation and recognition of transition between stages. CDI treatment involves hypotonic fluids with desmopressin. Our patient was initially managed with free water due to low suspicion for CDI. During shift towards suspected second phase, Uosm increased, urine output and sodium dropped significantly. However, it is uncertain whether this was due to axonal injury causing SIADH or a consequence of hypotonic fluids causing increased response of ADH. As predicted during triphasic response, patient became oliguric with a net negative fluid balance of &gt;10L and Uosm of 869. Therefore, desmopressin was started with good response. Further follow up was unattainable as neurological status deteriorated preceding to brain death. Most cases reported showed hypoattenuation lesion of posterior pituitary on MRI; MRI would have been required to determine if there was injury to the pituitary in this case.

Presentation: 6/2/2024