Failed transcatheter pulmonary artery embolization in a patient suffering from massive hemoptysis after thoracic endovascular aortic repair

Abstract

An emergency thoracic endovascular aortic repair (TEVAR) with zone 2 landing without revascularization of the left subclavian artery was performed due to the impending rupture of a distal arch aneurysm in an old patient presenting hemoptysis. Two months later, the patient had recurrent massive hemoptyses and continued after additional zone 0 TEVAR. The lung parenchyma was considered to be the bleeding source and transcatheter pulmonary artery embolization was performed, and the episodes of massive hemoptysis appeared to have ceased. However, the patient died of sudden recurrent massive hemoptysis 40 days later. Inflammation and/or infection of the lung parenchyma adjunct to the aortic aneurysm could be cause of fatal hemoptysis, and aggressive therapy such as lung resection should be considered in such patients.

The Cause of Massive Hemoptysis After Thoracic Endovascular Aortic Repair May Not Always Be an Aortobronchial Fistula: Report of a Case

“…We agree with Anastasiadou et al 8 in that TEVAR should be the first therapy for all patients for hemodynamic stabilization, and could be the definite therapy in cases where an infectious factor is absent. However, our previous case 3 and the present case suggest that when additional TEVAR does not sufficiently treat post TEVAR hemoptysis, it is possible that ABF is not the main pathology; further endovascular repair would have no effect because the bleeding source is not the aorta but the adjacent lung parenchyma. In such cases, one should consider open aortic repair with resection of the diseased aorta and/or lung resection adjacent to the diseased aorta.…”

“…Where does bleeding come from in patients who underwent TEVAR? From our previous study 3 and the present experiences, we think there may be mixed pathologies cases that are commonly construed as ABF. Canaud et al 4 described postulated causes of ABF after TEVAR such as, stent graft coverage of the bronchial arteries leading to ischemic necrosis of the bronchial wall, chronic endoleaks leading to erosion into the adjacent lung, and penetration of the stent graft through the aortic wall into the lung.…”

“…1 Once a patient is diagnosed with ABF, additional or primary TEVAR has become the popular choice for therapy in recent years, 1,2 especially if there is no sign of infection, but hemoptysis continues in some patients despite successful TEVAR procedures without endoleak. We previously reported a different case of a patient who underwent embolization of the pulmonary artery for recurrent massive hemoptyses after additional TEVAR 3 ; from that experience, we have come to think that the cause of massive hemoptysis after TEVAR may not always be an ABF but diffuse inflammatory changes presumably induced by TEVAR. Here we present another patient who suffered from recurrent massive hemoptyses after multiple TEVARs, where hemoptysis was ultimately controlled by pneumonectomy.…”

Treatment of massive hemoptysis after thoracic aortic aneurysm repair

“…A previous study reported that the incidence of ABF after TEVAR was 0.6% (Czerny et al 2015a, b) and that endoleak is one of its major causes (Czerny et al 2015a, b;Karube et al 2019a, b;Sueyoshi et al 2018a, b). In addition to ABF, pulmonary artery pseudoaneurysm rupture associated with a mycotic TAA and chronic inflammatory reactions of the lung parenchyma secondary to the dispersion of atheroma and/or cholesterol embolization of the pulmonary vessel caused during a previous TAA rupture have been reported as etiologies of hemoptysis after the TAA repair Ishikawa et al 2019aIshikawa et al , b, 2020aMotohashi et al 2020a, b).…”

Treatment of Massive Hemoptysis After Thoracic Aortic Aneurysm Repair

“…2015;Karube et al 2019;Sueyoshi et al 2018). On the other hand, hemoptysis in patients with TAA repair is known to occur other than ABF and pulmonary artery aneurysm rupture associated with a mycotic TAA(Ishikawa et al 2019), and the chronic in ammatory reaction of lung parenchyma secondary to dispersion of atheroma and/or cholesterol embolization of pulmonary vessels caused during a previous impending TAA rupture(Ishikawa et al 2020;Motohashi et al 2020) are reportedly its etiology.…”