A 75 year-old male presented to the hospital with abdominal pain, nausea, vomiting, and dizziness for two weeks. He also endorsed a gradual onset of generalized weakness, and decreased oral intake over the past six months. His past medical history was remarkable for diet-controlled hypertension, and type II diabetes mellitus for which he was taking insulin.
Physical exam revealed signs of mild hypovolemia. He was also hypotensive at 90/54 mmHg. Laboratory studies showed serum sodium of 112 mmol/L, blood urea nitrogen of 17 mg/dL, and creatinine of 0.743 mg/dL. Normal saline infusion for hypovolemic hyponatremia was started. Serum osmolality was 242 mOsm/kg, urine osmolality was 364 mOsm/kg, and urine sodium was 65 mmol/L. Over the next three days, the sodium level gradually increased and plateaued at 123-126 mmol/L. The patient appeared euvolemic clinically. Repeat studies showed serum osmolality of 258 mOsm/kg, urine osmolality of 285 mOsm/kg, and urine sodium of 73 mmol/L. A diagnosis of Syndrome of Inappropriate Anti-Diuretic Hormone (SIADH) was presumed. However, patient remained hyponatremic despite fluid restriction.
Workups for adrenal and thyroid causes of hyponatremia were initiated. Morning cortisol was depressed at 3.1 mcg/dL, and adrenocorticotropic hormone was elevated at 700 pg/mL. Plasma renin activity and aldosterone were 1.71 mg/mL/H and <1 ng/dL. Thyroid-stimulating hormone and free thyroxine were unremarkable. The patient was started on stress dose of Hydrocortisone, and both blood pressure and sodium level normalized. Magnetic resonance imaging did not show adrenal enlargement or nodules. A positive anti-21-hydroxylase antibody confirmed the diagnosis of Addison’s disease. The patient was discharged home with Hydrocortisone and Fludrocortisone.
Hyponatremia was observed in 42.6% of hospitalized patient. It is a highly challenging diagnosis due to myriad of causes. In our patient, the initial correction of hypovolemia improved serum sodium but did not completely correct his sodium to normal range until another etiology, Addison’s disease, was discovered and appropriately treated. Addison’s disease is characterized by chronic primary adrenal insufficiency which resulted in cortisol and mineralocorticoid deficiency. The diagnosis of Addison disease is often delayed due to its insidious onset and vague symptoms. SIADH appeared to be a plausible cause based on the urine studies when he was euvolemic. However, as a diagnosis of exclusion, other causes need to be ruled out. Further workups when the patient failed to improve finally disclosed the true culprit.
Hyponatremia is an extremely common electrolyte abnormality among hospitalized patients and carries a high morbidity and mortality. Clinicians must maintain a high index of suspicion, and be ready to entertain mixed etiologies of hyponatremia in order to effectively address patients’ hyponatremia.
To cite this abstract:Yang, A . “IS IT SIMPLY TOO MUCH ANTIDIURETIC HORMONE?”: A CASE OF HYPONATREMIA WITH MIXED ETIOLOGY. Abstract published at Hospital Medicine 2017, May 1-4, 2017; Las Vegas, Nev. Abstract 798. Journal of Hospital Medicine. 2017; 12 (suppl 2). https://www.shmabstracts.com/abstract/is-it-simply-too-much-antidiuretic-hormone-a-case-of-hyponatremia-with-mixed-etiology/. Accessed September 19, 2019.