Intravascular Ultrasound-Guided Pulmonary Artery Embolectomy for Saddle Pulmonary Embolism
Saturday, September 19, 2020
9:00 AM – 11:00 AM
Overview: Background The coexistence of chronic kidney disease (CKD) and acute massive or submassive pulmonary embolism (PE) portends a greater morbidity and mortality. A percutaneous catheter-directed embolectomy approach for the treatment of PE is preferred among patients at significant risk of bleeding with thrombolytics. However, the risk of intravenous (IV) contrast-induced nephropathy (CIN) during the catheter-directed procedure is significant, which can further increase morbidity and mortality.
Case Presentation A 61-year-old morbidly obese African American woman (BMI of 46.9 kg/m2) with multiple comorbidities, including a provoked PE 3 years prior and CKD (GFR 33 mL/min/1.73/m2), presented to the emergency department (ED) with 3 weeks of dyspnea on exertion which worsened in past 3-5 days preceding her ED visit. Up until 3 weeks prior, she was on a direct oral anticoagulant, which was stopped given the provoked nature of her initial PE and subsequent hematuria. On examination, her blood pressure was elevated and her oxygen saturation was 96% on 3 liters of oxygen, which worsened to 88% on 5 liters. She was in mild respiratory distress with bilateral 2+ lower extremity pitting edema. Laboratory tests were remarkable for troponin = 0.06 ng/mL (ref. < 0.04), B-type natriuretic peptide = 932 pg/mL (ref. ≤ 78), arterial oxygen partial pressure = 56 (ref. 80 – 110) and hemoglobin = 10.1 g/dL (ref. 11.3 – 15.0). Computed tomography pulmonary angiography (CTPA) performed with IV contrast showed a saddle embolus with evidence of right heart strain with an RV/LV ratio of 2.05. A transthoracic echocardiogram showed a dilated, mildly hypokinetic right ventricle with normal left ventricular systolic function. Her right heart catheterization showed mean pulmonary artery pressure (mPA) of 53 mm Hg (was 44 mm Hg three years prior). Given her intermediate risk of bleeding (RIETE score = 4; creatinine > 1.2 mg/dL, hemoglobin < 12 g/dL, clinical PE), a percutaneous pulmonary embolectomy was favored over catheter-directed lysis. Given her CKD stage IV, to avoid a higher dose of IV contrast (from the CTPA and pulmonary embolectomy procedure) which carries a greater risk of CIN with increased morbidity and mortality, we decided to utilize intravascular ultrasound (IVUS) along with fluoroscopy to confirm the clot and roadmap to guide the aspiration site (see Figure). She underwent a successful catheter-directed pulmonary embolectomy with utilization of IVUS and fluoroscopy, and without IV contrast. Post procedure, there was a modest decrease in her right-sided pressures (mPA from 53 mmHg to 49 mmHg and mean right atrial pressure from 22 mmHg to 17 mmHg), reduction in dyspnea and a significant improvement in her arterial oxygen saturation (> 96% on 2 liters of oxygen).
Conclusions In patients with concomitant massive or submassive PE and CKD, who are at a moderate-to-high risk of bleeding with thrombolysis, a percutaneous catheter-directed approach to therapy is feasible. To the best of our knowledge, this is the first reported case of an “IVUS-only” approach in this scenario. Limiting contrast volume in these patients could reduce morbidity and mortality associated with CIN.