Abstract: FR-PO0603
A Thirst for Clues: Arginine Vasopressin Deficiency Unmasking Central Nervous System (CNS) Tuberculosis in a Patient with Pott Disease
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Clinical - 2
November 07, 2025 | 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
- Adams Chahin, Juan J., Universidad de Puerto Rico Recinto de Ciencias Medicas, San Juan, Puerto Rico
- Burgos Martinez, Lidynell M, Universidad de Puerto Rico Recinto de Ciencias Medicas, San Juan, Puerto Rico
- Vazquez-Fernandez, Paola M., Universidad de Puerto Rico Recinto de Ciencias Medicas, San Juan, Puerto Rico
- Ocasio Feliciano, Edilberto Jose, Universidad de Puerto Rico Recinto de Ciencias Medicas, San Juan, Puerto Rico
- Ocasio Melendez, Ileana E., Universidad de Puerto Rico Recinto de Ciencias Medicas, San Juan, Puerto Rico
- Rivera-Bermudez, Carlos G., Universidad de Puerto Rico Recinto de Ciencias Medicas, San Juan, Puerto Rico
Introduction
Arginine vasopressin deficiency (AVP-D) is a rare disorder that can present life-threatening hypernatremia due to excessive water loss through polyuria. Although tuberculous involvement of the spine—known as Pott’s disease—can lead to spinal cord compression and neurologic deficits, its association with AVP-D is exceedingly uncommon and often underrecognized.
Case Description
A 52-year-old male with type 2 diabetes, hypertension, and chronic neck pain presented with sudden-onset paraplegia. Upon admission, his condition rapidly worsened, requiring intubation and vasopressors. Initial laboratories demonstrated stable renal parameters with no major disturbances. Imaging revealed cervical spine osteolytic lesions and a prevertebral abscess causing spinal cord compression, suggestive of tuberculous spondylitis. Despite a negative PPD, IGRA was positive, thus, antituberculous drugs were started. Several days into hospitalization, the patient developed acute and severe hypernatremia with polyuria of 6.8 liters over a 6-hour period. Laboratories revealed a serum sodium >180 mmol/L, chloride >140 mmol/L, potassium 3.1 mmol/L, creatinine 1.05 mg/dL, and BUN 26.7 mg/dL. Urine studies showed an osmolality of 179 mOsm/kg and urine sodium <20 mmol/L, with total osmolar excretion <800 mOsm/day. Brain MRI demonstrated increased signal intensity within the subarachnoid space of the left frontoparietal region, with associated signal loss on gradient-echo sequences, suggesting subarachnoid exudates such as seen in CNS tuberculosis. The patient was managed with intravenous 5% dextrose at 4 mL/kg/hr, continuous nasogastric administration of tap water at 150 mL/hr, and intravenous desmopressin (2 mg every 8 hours), which led to marked improvement in hypernatremia and polyuria.
Discussion
This case highlights the complexities involved in diagnosing and managing a critically ill patient with spinal tuberculosis who develops abrupt, severe hypernatremia and polyuria. It emphasizes the need to consider endocrine disorders, such as arginine vasopressin deficiency, particularly when CNS involvement is present. Prompt recognition and appropriate management of fluid and electrolyte imbalances are vital to reducing complications and enhancing patient outcomes.