Abstract: TH-PO331
Polyuria without Thirst: Adipsic Arginine Vasopressin Deficiency as a Sequela of Pituitary Surgery
Session Information
- Sodium, Potassium, and Volume Disorders: Clinical
October 24, 2024 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Siddiqui, Nabeel, Southeast Health, Dothan, Alabama, United States
- Meek, Kevin, Southeast Health, Dothan, Alabama, United States
- Kaur, Rupinder, Southeast Health, Dothan, Alabama, United States
- Qureshi, Muhammad, Southeast Health, Dothan, Alabama, United States
- Shah, Bhoomi, Southeast Health, Dothan, Alabama, United States
- Ibie, Nowoghomwenma Charles, Southeast Health, Dothan, Alabama, United States
Introduction
Arginine vasopressin deficiency (AVP-D) stems from impairment or absence of vasopressinergic neurons in the hypothalamus and posterior pituitary, resulting in an inability to concentrate urine. Patients typically present with polyuria and polydipsia. Acute AVP-D mostly occurs following surgery for pituitary tumors. Here, we present a case of AVP-D following surgical resection of a suprasellar mass and an unusual absence of thirst response indicative of adipsia.
Case Description
26-year-old female with complaints of headache, nausea, vomiting, loss of appetite, and unintentional weight loss. She had low TSH, ACTH, cortisol, and IGF-1. MRI head showed a large sellar and suprasellar mass abutting her optic chiasm. She underwent a total macroscopic transcranial resection with findings of extensive sellar and suprasellar lesions displacing the optic nerve and compressing the pituitary. Post-surgery, she had polyuria, a sodium level of 183 with decreased density, serum osmolality of 396, and urine osmolality of 182. The maximum urine output recorded was 5.6 liters in 24 hours. She was treated with desmopressin. Despite sodium levels in the 170s, she denied experiencing thirst.
Discussion
Postoperative AVP-D involves disruption of the hypothalamic-pituitary axis during surgery. Classically, patients with AVP-D experience polyuria and compensatory polydipsia. Increased plasma sodium levels typically trigger the thirst response. Adipsic AVP-D is a rare subset that results when injury to the hypothalamus impairs thirst osmoreceptors and ADH-synthesizing neurons, leading to the absence of thirst in response to hypernatremia. AVP-D following pituitary tumor surgery is a challenging complication requiring comprehensive evaluation and management. Early recognition, appropriate fluid and electrolyte replacement, and tailored ADH replacement therapy are crucial for optimal patient outcomes. This case underscores the importance of prompt recognition and tailored management of AVP-D post-surgery, particularly in patients with complications such as adipsia. Further research is needed to refine diagnostic approaches, optimize treatment strategies, and improve long-term outcomes for patients with postoperative AVP-D.