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Abstract: SA-PO714

Arginine Vasopressin Deficiency in the Hypoxic Brain

Session Information

Category: Fluid, Electrolytes, and Acid-Base Disorders

  • 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical


  • Ritchie, Leanna V., Mayo Foundation for Medical Education and Research, Jacksonville, Florida, United States
  • Basit, Abdul, Mayo Foundation for Medical Education and Research, Jacksonville, Florida, United States
  • Baker, Lyle Wesley, Mayo Foundation for Medical Education and Research, Jacksonville, Florida, United States

Hypernatremia is an electrolyte disorder most commonly related to limited access to water or suppression of the thirst compensatory mechanism. Uncommonly hypernatremia may be associated with interruption in the anti-diuretic hormone (ADH) cascade either from a central (pituitary) or nephrogenic etiology. ADH is released in response to elevated serum sodium from the posterior pituitary gland to bind with V2 receptors in the distal tubules and collecting ducts in the kidney to facilitate water reabsorption. If this phenomenon is interrupted, termed arginine vasopressin deficiency (AVD), a patient may present with hypernatremia and polyuria. The most common etiologies of AVD are secondary to infiltrative disease, primary or secondary tumors and traumatic brain injury.

Case Description

Here presented is a case of a 58 year old female with a past medical history remarkable for hypertension, diabetes, seizure disorder and obesity who presented to the hospital after cardiac arrest. The patient had asystole and achieved return of spontaneous circulation after 1 hour of advanced cardiac life support. Following cardiac arrest she developed hypernatremia with polyuria. CT head indicated global hypoxemic brain injury. The patient had absent brainstem reflexes. The patient developed acute kidney injury secondary to renal ischemia and was started on continuous veno-venous hemofiltration (CVVH). Despite renal replacement therapy the patient developed hypernatremia with polyuria. Initially free water flushes were initiated, however the patient developed refractory hypernatremia. Renal replacement therapy was discontinued. Urine osmolality was 259 mOsm/kg, consistent with AVD. The patient's urine volume reduced in response to desmopressin administration with correction of hypernatremia. She was diagnosed with central AVD secondary to anoxic brain injury. Unfortunately neurological evaluation identified brain death and the patient was terminally extubated.


This case has a unique etiology secondary to hypoxic injury versus a trauma, infiltrative disease or brain mass. The pathophysiology of AVD post hypoxic brain injury is poorly understood. It is hypothesized that damage to the hypothalamus or posterior pituitary gland may hinder ADH secretion. This is an uncommon presentation of cerebral injury post cardiac arrest and may be a negative prognostic indicator for recovery.