Abstract: PUB103
Na+ So Fast: A Cautionary Chlorthalidone Tale
Session Information
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Burgos Guntin, Eusebio Felipe, NYC Health + Hospitals / Elmhurst, Icahn School of Medicine at Mount Sinai, Queens, New York, United States
- Mace de Lepinay, Beatrice, NYC Health + Hospitals / Elmhurst, Icahn School of Medicine at Mount Sinai, Queens, New York, United States
- Stern, Aaron S., NYC Health + Hospitals / Elmhurst, Icahn School of Medicine at Mount Sinai, Queens, New York, United States
Introduction
Thiazide-induced hyponatremia (TIH) is a common cause of hyponatremia that is especially prevalent in elderly women.This case describes a prolonged course of hyponatremia shaped by the use of a long-acting thiazide-like diuretic, chlorthalidone.
Case Description
An 84-year-old woman with hypertension (on chlorthalidone 25 mg daily), controlled hypothyroidism and gout (on allopurinol) presented to the emergency department with acute confusion, nausea, and vomiting.
On arrival, she was unable to provide a history. Her mucous membranes were dry. Initial laboratory evaluation revealed serum sodium 109 mmol/L, glucose 192 mg/dL, and serum osmolality 236 mOsm/kg. Uric acid was low at 2.1 mg/dL (on allopurinol), TSH 5.6 U/ml with normal free T4 and AM cortisol 17 μg/dl (within normal range). Urine sodium was 142 mmol/L and urine osmolality 633 mOsm/kg. Head CT showed no acute intracranial pathology. On ultrasound, her Inferior Vena Cava was <2cm in diameter and collapsed >50% with inspiration.
She was admitted to the ICU. Serum sodium remained unchanged after 200cc of 3% saline, then increased from 109 to 116–117 mmol/L within 24 hours, prompting discontinuation of 3% saline and initiation of desmopressin and dextrose 5% in water. Despite discontinuation of chlorthalidone on admission, sodium remained persistently low over the next four days (118–124 mmol/L), with repeat urine studies demonstrating persistently elevated urine sodium (up to 163 mmol/L) and urine osmolality (up to 619 mOsm/kg).
Management included fluid restriction to 1 L/day and initiation of oral urea (15 g twice daily), after which serum sodium gradually improved to 126 mmol/L by day five and 132 mmol/L by day six.
Discussion
In this case, hyponatremia was likely multifactorial. Nausea and vomiting likely contributed through non-osmotic antidiuretic hormone (ADH) release and reduced oral intake. However, chlorthalidone use and its prolonged half-life (1–3 days) played a central role in delayed normalization. The elevated urine sodium reflected ongoing renal sodium wasting from the thiazide use, while high urine osmolality reflected appropriate ADH release in the setting of hypovolemia.
In TIH, hyponatremia is usually induced within 2 weeks of starting the medication, but it can occur at any time. The pathophysiological mechanisms underlying TIH are unclear, but three main factors are implicated: stimulation of ADH secretion, reduced free-water clearance, and increased water intake.