Abstract Introduction Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is an uncommon postoperative complication and is exceptionally rare after ambulatory facial cosmetic procedures. When unrecognized, it can progress to profound hyponatremia and neurologic injury. We report a case of severe post-rhytidectomy SIADH requiring intensive care unit (ICU) admission and treatment with 3% hypertonic saline (HTS). Case Presentation A 76-year-old female with irritable bowel syndrome, prior diverticulitis status-post laparoscopic rectosigmoid resection, and major depressive disorder on chronic escitalopram underwent an uncomplicated elective rhytidectomy. Four hours postoperatively, she developed lethargy, persistent nausea, nonbloody nonbilious emesis, and severe headache, prompting emergency department (ED) evaluation. Despite multimodal antiemetics (ondansetron, metoclopramide, prochlorperazine, droperidol), multiple doses of ketorolac, and a 1-liter normal saline (NS) bolus, symptoms persisted. Initial serum sodium was 133 mmol/L, declining to 126 and then 119 mmol/L with ongoing emesis. Urine studies showed inappropriately concentrated, sodium-rich urine (urine osmolality 597 mOsm/kg; urine sodium 224 mmol/L). She was transferred to the ICU for severe symptomatic acute hyponatremia and started on continuous HTS with close electrolyte monitoring, nephrology consultation, aggressive antiemetics, cessation of nonsteroidal anti-inflammatory drugs (NSAIDs), withholding escitalopram, and serial serum/urine studies. After 24 hours in the ICU receiving HTS, serum sodium increased to 122 mmol/L; repeat urine studies remained consistent with antidiuresis (urine osmolality 546 mOsm/kg; urine sodium 172 mmol/L; urine potassium 37 mmol/L). After a total of 48 hours in the ICU, serum sodium increased to 127 mmol/L and symptoms resolved. HTS was discontinued, and the patient was transferred to the medical ward. Discussion To our knowledge, only two isolated cases of severe postoperative SIADH after elective rhytidectomy are documented, underscoring this presentation’s rarity. As in those reports, this patient had refractory emesis, progressive hyponatremia, and clinical deterioration after isotonic saline; early paired serum and urine studies demonstrated markedly negative electrolyte-free water clearance, providing a physiologic explanation for the paradoxical sodium decline after NS administration. The most plausible mechanism was non-osmotic antidiuretic hormone release triggered by anesthesia and refractory nausea, likely potentiated by NSAID exposure with a possible contribution from chronic selective serotonin reuptake inhibitor use; all of which are recognized precipitants of SIADH. This case highlights a practical, implementable approach: recognize persistent postoperative emesis with hyponatremia; obtain early serum and urine studies; avoid isotonic saline when urine remains concentrated and sodium-rich; and, when indicated, initiate goal-directed HTS with nephrology involvement, strict fluid restriction, and removal of SIADH-inducing medications to prevent neurologic complications. This abstract is funded by: None
Gallub et al. (Fri,) studied this question.