[A Case of Acute Pulmonary Edema after Open Abdominal Aortic Aneurysm Repair]

A 61-year-old man, who had previously undergone percutaneous coronary intervention (PCI) of the left anterior descending artery (LAD), was scheduled for open abdominal aortic aneurysm repair under general anesthesia. Although the left ventricular (LV) ejection fraction was 63%, diastolic dysfunction was identified (E/A 0.61). The patient received inhalation induction with 5% sevoflurane and an infusion of remifentanil (0.2μg · kg⁻¹ · min⁻¹). Rocuronium (0.6 mg · kg⁻¹) was administered and tracheal intubation was performed. Anesthesia was maintained with air-oxygen- sevoflurane, an infusion of remifentanil, and 700 μg fentanyl administered intravenously. An infusion of fentanyl (25 μg · hr⁻¹) in combination with rectus sheath block was administered for postoperative anal- gesia. Intraoperatively, we used arterial pressure-based cardiac output (CO), stroke volume variation (SVV), and transesophageal echocardiography as a guide for circulatory management The intraoperative net fluid in-out balance was 5,296 ml, and the duration of the procedure was 5.5 hr. The patient was extubated in the operating room because no significant findings were observed on the postoperative chest X-ray, and PaO₂/FI0₂ (P/F) ratio was 405. At the termination of anesthesia, systolic blood pressure increased to 200 mmHg. The hypertension lasted until after extubation, following which SpO₂ diminished gradually. And SpO₂ was 78% and PaO₂ was 56.7 Torr under 8 l of oxygen. A chest X-ray at this time showed pulmonary edema. There were no findings of ischemic heart disease on either ECG or echocardiography. Immediate vasodilator treatment for the hypertension and non-invasive posi- tive pressure ventilation for the hypoxia were commenced. The P/F ratio recovered to 240 by the night of the surgery, and a chest X-ray showed that the pul- monary edema had resolved. The patient was moved out of the ICU on the first day after the surgery. This case highlights the fact that even when LV systolic function is preserved, diastolic dysfunction may occur, leading to pulmonary congestion due to increased afterload.