2024 FSA Podium and Poster Abstracts

P018: LIFE-THREATENING MASSIVE INTRAOPERATIVE PULMONARY EMBOLISM
Mariah Gosling, MD; Gisele Wakim, MD; Miguel Abalo, MD; University of Miami/Jackson Health System

Introduction: The incidence of intraoperative acute pulmonary embolism (APE) ranges from 0.3-1.6% to as high as 30% in orthopedic surgeries [1] and is the third most common cause of death among patients with cardiovascular disease [2]. Surgical patients are at particular risk of venous thromboembolism due to immobility, acute inflammation from tissue trauma, as well patient comorbidities such as obesity, malignancy and smoking history. The typical symptoms of anxiety, dyspnea and tachycardia are masked by general anesthesia, making detection difficult. The anesthesiologist must rely on their clinical skills to recognize APE as hypotension, tachycardia, decreased ETCO2 and hypoxemia. Prompt diagnosis is crucial as APE is associated with significant morbidity and mortality during the perioperative period [5].

Case presentation: 62-year-old-male with unknown medical history was brought in by air rescue after being found down for an unknown duration. Upon arrival, the patient was a GCS 5 and was intubated for airway protection. CT imaging revealed possible RLL/RUL pulmonary embolism and was started on a heparin gtt. The next morning, the patient self extubated and was found to have left sided hemiplegia. Head CT demonstrated a right parietal acute intra-axial hematoma with diffuse subarachnoid hemorrhage and a 8 mm leftward midline shift with subfalcine herniation. The patient was reintubated, protamine was administered and neurosurgery was consulted. Patient was brought to the OR for emergency craniectomy, the patient was hemodynamically stable on a nicardipine, fentanyl and propofol drip. After starting sevoflurane for maintenance, administering keppra and mannitol, an arterial line was placed. During the surgery, the patient quickly desatted to the low 80s and became hypotensive 35/23 with a sudden drop in ETCO2. HR remained in the 80s. No rise in the peak airway pressures were noted. At this point, a pulmonary embolism was suspected. The surgeon was informed. Nicardipine was discontinued. Epinephrine and bicarbonate were given with a response in blood pressure. Manual ventilation subsequently also improved hemodynamics. An ABG revealed a respiratory acidosis (7.18/59/100/22/-6) with an ETCO2 and PaCO2 gradient of 23. The patient proceeded to desaturate and became tachycardic to the 120s, an epinephrine and vasopressin drip was started. At the end of the case, significant right heart strain on an informal transthoracic echocardiogram was suggestive of an APE. Considering the patient’s intracranial hemorrhage, anticoagulation with heparin or thrombolysis therapy was contraindicated.

Discussion: This case illustrates the importance of early identification of perioperative APE and supportive measures to prevent sequela such as cardiac arrest. The preferred definitive diagnostic modality is CT pulmonary angiography, however transthoracic echocardiogram is utilized intraoperatively. Electrocardiographic findings include right heart strain, right bundle branch block and an S1Q3T3 pattern. Duplex ultrasound of the lower extremities is utilized to identify the source of the clot. When a large APE occurs, focus is on maintaining hemodynamic stability before considering treatment options. Treatment options include systemic thrombolysis, catheter-based thrombus fragmentation (thrombolysis or thromboaspiration) and surgical embolectomy.