Hypotonic hyponatremia is caused by a serum sodium level of <135 mEq/L in the setting of excess solute loss accompanied by free water retention because of antidiuretic hormone release, subsequent to decreased effective arterial blood volume. Acute hyponatremia can have various neurological manifestations, including drowsiness, lethargy, coma, seizures, respiratory depression, and even death. In this article, we present a case of a 41-year-old man who presented with hyponatremia as a result of sodium containing biliary fluid loss and resultant renal free water retention in response to increased antidiuretic hormone secretion. He underwent placement of a cholecystostomy tube for acalculous cholecystitis and was found to be persistently hyponatremic despite repletion with sodium-containing fluids. Once the cholecystostomy tube was removed, the patient’s sodium levels improved, and his symptoms resolved. Our case highlights choleuresis as an unusual but significant cause of hyponatremia in patients who have external biliary drainage.

Heyde syndrome is a multisystem disorder characterized by the classical triad of aortic stenosis, gastrointestinal (GI) angiodysplasias, and acquired von Willebrand syndrome. GI angiodysplasias, common in older patients, are tortuous, thin-walled blood vessels seen in the mucosa or submucosa of the GI tract and are highly prone to rupture resulting in GI bleeds. In this case report, we describe an elderly female with a past medical history of end-stage renal disease and chronic anemia who presented to the emergency department (ED) with complaints of dark-tarry stools and associated abdominal cramping. Patient reported a history of dark-tarry stools and multiple blood transfusions in the past, secondary to severe anemia. An inpatient echocardiogram was performed, revealing severe aortic stenosis. Additionally, gastroenterology was consulted for esophagogastroduodenoscopy and colonoscopy, which were negative for active bleeding. About a year ago, the patient underwent capsule endoscopy at an outlying facility, which was positive for angiodysplasia. Therefore, due to high clinical suspicion, presence of aortic stenosis, and GI angiodysplasia, a platelet function assay was ordered. It was found to be abnormal, pointing to the presence of acquired von Willebrand syndrome. Hence, a diagnosis of Heyde syndrome was established. The patient gradually improved and was discharged with a follow-up appointment with the cardiologist for a possible transcatheter aortic valve replacement procedure. The patient underwent the procedure without complications, after which she did not report episodes of GI bleeding. In this case report, we discuss the presentation, pathophysiology, diagnostic approach, and management of patients with Heyde syndrome.