2026 FSA Podium and Poster Abstracts

A 75-year-old man with diabetes, hypertension, and a 40-year history of heavy smoking presented to the ED with lower abdominal and back pain, abdominal distension, and one syncopal episode. On exam his blood pressure was 90/57 mmHg, heart rate 122/min, and SpO2 90%. CTA revealed a ruptured infrarenal abdominal aortic aneurysm measuring 9.1 × 6.7 cm. Initial labs showed hemoglobin 7.6 g/dL, platelets 120, and creatinine 1.26. After urgent multidisciplinary discussion, the patient underwent emergent endovascular aneurysm repair (EVAR) via bilateral femoral cut-down; left leg thrombectomy was required intraoperatively for loss of left femoral pulses. He was intubated, paralyzed, and received heparin, 10 L of crystalloids, and 14 units of PRBCs. Blood pressure management required intermittent nicardipine dripduring crucial times for management of strict blood pressure management and phenylephrine for hypotensive episodes. Three hours after ICU arrival he acutely decompensated with severe hypotension (80/45 mmHg) despite epinephrine, norepinephrine, and phenylephrine infusions. Concern for abdominal compartment syndrome prompted a bedside decompressive laparotomy, during which he received an additional 6 units PRBCs, 6 units FFP, and 2 units platelets. 

This case presents perioperative management challenges of abdominal compartment syndrome following EVAR for ruptured AAA and its potential to precipitate multi-organ failure and increased mortality. Rapid, often misdiagnosed, progression of ACS complicates patient outcomes. The possible risk factors for acute coronary syndrome after endovascular aortic aneurysm repair (EVAR) are explained, including the use of an aortic occlusion balloon, severe coagulopathy, massive transfusion, and the emergency conversion from modular bifurcated grafts to aortouniiliac devices. This case highlights the need for anticipatory anesthetic planning such as aggressive pre-induction resuscitation, readiness with vasopressors, careful choice of induction agents, and continuous hemodynamic and respiratory monitoring, to mitigate the profound physiologic derangements associated with ACS.