Abstract: FR-PO0873
Profound Hypervolemic Hyponatremia from Hypothalamic-Pituitary-Adrenal Axis Suppression After an Intra-Articular Glucocorticoid Injection
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Case Reports - 1
October 23, 2026 | Location: Exhibit Hall A, 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
- Dabech, Abdulaziz, The University of Texas Medical Branch at Galveston, Galveston, Texas, United States
- Pierluissi Rivera, Valeria Andrea, The University of Texas Medical Branch at Galveston, Galveston, Texas, United States
- Gamilla-Crudo, Ann Kathleen N., The University of Texas Medical Branch at Galveston, Galveston, Texas, United States
Introduction
Hyponatremia evaluation relies on volume status and urine studies, which can be confusing. In hypervolemic hyponatremia from CHF, nephrotic syndrome and cirrhosis, urine osmolality is high, but urine sodium is low, indicating decreased effective arterial blood volume. We present our patient with secondary adrenal insufficiency (SAI) who has lab and urine findings typically seen in SIADH, i.e., high urine sodium and osmolality but has hypervolemia. While chronic systemic corticosteroids cause iatrogenic SAI, profound hypothalamic-pituitary-adrenal (HPA) axis suppression from a single intra-articular glucocorticoid injection is under-recognized.
Case Description
A 54-year-old male with heavy alcohol use presented with dyspnea and lower extremity edema. Initial serum sodium of 122 mmol/L rapidly declined to 116 mmol/L. His serum osmolality was 254 mOsm/kg, urine osmolality 300 mOsm/kg, and urine sodium of 96 mEq/L. Work-up showed normal thyroid, cardiac, kidney and liver functions. Initially treated as beer potomania or SIADH, his sodium failed to improve despite fluid restriction and loop diuretics. Endocrine workup revealed an AM cortisol of 10.9 µg/dL, low baseline ACTH of 6.9 pg/mL, and a blunted peak cortisol of 13.8 µg/dL following cosyntropin stimulation. Renin and aldosterone were normal. He received a 40 mg methylprednisolone intraarticular hip injection two weeks prior. He had no recent illnesses or hospitalizations. The patient was started on oral hydrocortisone replacement resulting in rapid clinical improvement with a discharge sodium of 134 mmol/L. Outpatient follow-up demonstrated sustained normonatremia.
Discussion
This case illustrates the phenomenon of iatrogenic secondary AI caused by localized depot steroid injections which can unmask or exacerbate severe hyponatremia through the non-osmotic release of antidiuretic hormone. Notably, the patient had normal kidney, cardiac, and liver function by imaging and laboratory studies ruling out classic hypervolemic etiologies. This highlights the importance of suspecting glucocorticoid deficiency in treatment-refractory hyponatremia and the necessity of obtaining a comprehensive pharmacological history including joint injections.