Abstract: PUB179
A Rare Case of Aspirin-Induced Symptomatic Hyponatremia
Session Information
Category: Fluid‚ Electrolyte‚ and Acid-Base Disorders
- 1002 Fluid‚ Electrolyte‚ and Acid-Base Disorders: Clinical
Authors
- Chung, Madeline S., The Ohio State University Wexner Medical Center, Columbus, Ohio, United States
- Yau, Amy, The Ohio State University Wexner Medical Center, Columbus, Ohio, United States
Introduction
Prostaglandins in the kidney act to attenuate the actions of antidiuretic hormone (ADH). Non-steroidal anti-inflammatory drugs (NSAIDs) inhibit the synthesis of prostaglandins resulting in an increased response to ADH in the kidney leading to free water retention and hyponatremia, especially under conditions which also promote hyponatremia.
Case Description
We present a 61-year-old man with past medical history significant for hypertension and basal and squamous cell skin carcinomas who presented complaining of excessive urination and generalized weakness for 3 days and altered mentation. Blood pressure was 153/76 mmHg and other vitals unremarkable. He was lethargic with delayed response to questions and euvolemic on exam. Medications included losartan 50mg daily with no diuretics.
Admission labs were significant for a serum sodium of 111 mEq/dL, urine sodium of 135 mmol/L, urine osmolality of 542 mOsm/L, TSH 1.633 μIU/mL and cortisol 53.52 μg/mL. Two weeks prior, his serum sodium level was 138 mEq/dL. CT head and chest X-ray were negative for any acute pathologies. He was started on 3% saline with improvement in symptoms but 24 hours later developed a brisk water diuresis. Labs were significant for a serum sodium of 122 mEq/dL, urine sodium of 12 mmol/L, and urine osmolality of 98 mOsm/L.
Further history revealed a high water intake based on advice from his physician and new intake of aspirin 325mg three times a day due to shoulder pain. His hyponatremia was managed with DDAVP, free water, and saline. It remained normal prior to discharge without any additional intervention. Pan-CT and MRI brain were obtained and negative.
Discussion
SIADH attributable to NSAIDs is a rare occurrence, especially since prostaglandins present in the kidneys inhibit the actions of ADH while prostaglandins present in the central nervous system stimulate the secretion of ADH. But NSAID use can lead to an effect similar to SIADH in the setting of other situations which also promote ADH secretion such as pain and/or nausea. In our case, there were multiple factors that likely contributed to hyponatremia including pain, increased free water intake, and new NSAID use. The half-life of aspirin increases with higher plasma concentrations and is anywhere from 3-10 hours. Clinicians should be careful about encouraging excessive water intake especially in the setting of other risk factors for hyponatremia to include NSAID use.