2025 FSA Podium and Poster Abstracts

Introduction: Postoperative diabetes insipidus (DI) is a significant yet uncommon complication of aortic arch repair. It is associated with transient cerebral ischemia or hypothalamic-pituitary axis dysfunction due to surgical interventions, including cardiopulmonary bypass or hypothermic circulatory arrest. DI causes excessive urine output and polydipsia, resulting from impaired secretion of or renal response to antidiuretic hormone (ADH). Anesthesiologists play a critical role in identifying and managing this complication; delayed diagnosis can lead to severe hypernatremia and associated morbidity. Early detection requires vigilant perioperative monitoring of fluid balance, electrolytes, and osmolality, particularly in high-risk patients undergoing complex cardiovascular surgeries.

Case Report: We present the case of a 76-year-old female with a significant family history of aortic dissection who was admitted to the emergency department with shortness of breath. Initial workup revealed an elevated D-dimer, normal troponin levels, and a Type A thoracic mural hematoma spanning zones 0–5 on CTA PE protocol. The patient was started on esmolol for blood pressure control and transferred to the intensive care unit for management.

The patient underwent replacement of the ascending aorta, bioprosthetic aortic valve replacement, creation of a right axillary artery chimney graft, hypothermic circulatory arrest with antegrade cerebral perfusion, left atrial appendage ligation, and intraoperative transesophageal echocardiography. Postoperatively, she required vasopressin, norepinephrine, and epinephrine for hypotension. She developed hypernatremia (serum sodium 150 mmol/L), atrial fibrillation, and a pulmonary effusion necessitating bedside chest tube placement. High-flow nasal cannula oxygen therapy was initiated.

During recovery, her pressure support was gradually reduced, atrial fibrillation resolved, and oxygen requirements decreased. Unfortunately, her serum sodium trended upward, reaching 173 mmol/L, followed by symptoms of polyuria. Pertinent lab findings included a serum osmolality of 372 mOsm/kg, urine osmolality of 199 mOsm/kg, and urine sodium of 8 mmol/L, consistent with a diagnosis of DI. This diagnosis was delayed due to the masking effects of vasopressin therapy used for hemodynamic support. Consultation with nephrology confirmed the diagnosis and desmopressin therapy was initiated, leading to subsequent improvement in sodium levels and clinical symptoms.

Discussion: There is an important interplay between surgical complexity, perioperative management, and postoperative monitoring; therefore, intensivists must remain highly vigilant for complications such as DI, particularly in patients undergoing hypothermic circulatory arrest or cardiopulmonary bypass, where transient cerebral ischemia can impair ADH secretion. In this case, vasopressin, a critical agent for hemodynamic support, masked the hallmark signs of DI, including polyuria and severe hypernatremia. This underscores the need for routine monitoring of serum sodium, urine output, and osmolality in the postoperative period, even when vasopressin is administered.

Conclusion: This case highlights the importance of a multidisciplinary approach to perioperative care, as anesthesiologists are responsible for recognizing and managing complications such as DI. A high index of suspicion and early recognition are critical and require careful review of laboratory findings, especially in patients receiving vasopressin. Early intervention with desmopressin is essential to prevent severe hypernatremia and its sequelae. By implementing routine monitoring protocols, perioperative teams can ensure better outcomes for patients undergoing complex cardiovascular surgeries.