Introduction: Hyponatremia is a common electrolyte disturbance in critically ill patients and is associated with increased morbidity after cardiac surgery. Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is an underrecognized cause in this setting. We report the interdisciplinary management of severe hyponatremia with associated postoperative delirium following complex cardiac surgery. Methods: An 82-year-old woman with hypertension, hyperlipidemia, OSA, and an ascending aortic aneurysm underwent elective aortic valve replacement, ascending aortic repair, and left atrial appendage clip placement. Intraoperative management included propofol, isoflurane, and rocuronium, with norepinephrine and epinephrine for hemodynamic support. She required re-exploration for mediastinal bleeding and remained on vasopressors and sedatives postoperatively. Results: Serum sodium decreased from 135 mmol/L on POD2 to 123 mmol/L on POD7, reaching a nadir of 121 mmol/L on POD8. The patient developed intermittent confusion, initially attributed to ICU delirium. Nephrology diagnosed SIADH based on laboratory findings and clinical context. The differential for euvolemic hypotonic hyponatremia included SIADH, hypothyroidism, adrenal insufficiency, and reset osmostat; normal cortisol and acute onset supported SIADH. Contributing factors included CPB-related fluid shifts, perioperative stress, and chronic serotonergic and opioid use (citalopram, trazodone, oxycodone). Management consisted of fluid restriction, oral sodium supplementation, and dexmedetomidine for sedation to minimize delirium while preserving spontaneous ventilation. Sodium normalized to 138 mmol/L over five days. The patient recovered without neurologic sequelae and was discharged on POD13 with home health and outpatient sodium monitoring. Conclusions: Postoperative SIADH is an uncommon but critical cause of hyponatremia after cardiac surgery. Perioperative factors such as cardiopulmonary bypass, vasopressor use, anesthetic agents, and serotonergic medications likely contributed to non-osmotic ADH secretion. Early recognition, targeted therapy, and collaboration between anesthesiology and critical care teams are essential to prevent neurologic complications and improve outcomes.
Bruns et al. (Sun,) studied this question.