Introduction

Pulmonary embolism is a major complication of Deep Vein Thrombosis (DVT). In severe cases, it causes an increase in pulmonary arterial pressure and right ventricular post-charge that results in right-sided heart failure. The enlargement of the right-sided cavities facilitates the opening of right-to-left shunts, thereby allowing the passage of thrombi into the systemic circulation, i.e., paradoxical embolism.

Case Presentation

A 54-year-old man was admitted to our emergency department with a 3-day history of severe dyspnea, chest and left arm pain, and transient paresthesia. The patient had no history of cardiac or pulmonary events but was treated for a comminuted fracture of the distal leg by osteosynthesis 6 weeks ago. Until 4 days before the onset of symptoms, the patient had been prescribed preventive anticoagulant therapy (Enoxaparin 40 mg). The patient was never tested for activated protein C resistance or other hemostatic abnormalities and did not have a history of DVT. All other blood parameters were normal.

A chest X-ray showed bilateral lower lung infiltrations (Figure 1). A thoracic Computed Tomography (CT) scan with contrast, performed to exclude a pulmonary embolism, showed thrombi in both pulmonary arteries with large, floating thrombi in the aortic arch and the descending part of the aorta and total occlusion of the left subclavian artery (Figure 2).

Transthoracic echocardiography showed that the right heart was dilated, with a left ventricle ejection fraction of 70% and an estimated pulmonary artery systolic pressure of 48 mm Hg plus central venous pressure. Neither a diagnosed valve dysfunction nor a Patent Foramen Ovale (PFO) was observed on transthoracic echocardiography. The clinical condition of the patient worsened very rapidly and an emergent pulmonary and aortic embolectomy was planned. Transesophageal Echocardiography (TEE) performed in the operating room after the administration of general anesthesia revealed a small PFO. A Cardio-Pulmonary Bypass (CPB) was initiated through a median sternotomy; the arterial cannula was introduced into the brachiocephalic artery 2 cm from its origin after ensuring that it was free of any thrombi, and a two-stage atrio-caval cannula was placed through the right atrium. The patient was cooled to a temperature of 32^°C. After cross-clamping, antegrade cardioplegia was given through the sino-tubulary junction. During the cooling process, a bilateral pulmonary embolectomy was performed through an incision in the transverse pulmonary trunk.

When a temperature of 32^°C was reached, circulatory arrest was initiated after a second clamp was placed proximally to cross clamp the brachiocephalic artery. The flow in the arterial cannula was reduced to 10 mL/kg/min to maintain selective antegrade cerebral perfusion through the right carotid artery. A transverse aortotomy revealed a fresh thrombus that was obstructing the aortic arch and the subclavian artery. A 7-French embolectomy-catheter was deployed through the aortotomy to reach the origin of the subclavian and left common carotid arteries (Figure 3), and the PFO was closed through a right atriotomy during circulatory arrest.

Twelve minutes after initiating circulatory arrest, the aorta was closed and the circulatory arrest discontinued. The patient was rewarmed and easily weaned from the CPB after 25 minutes of cross-clamping time. The procedure was performed under pericardial carbon dioxide flooding. The patient recovered well except for residual grade I dyspnea. A post-operative lower leg ultrasound examination revealed a DVT that was treated by warfarin. Post-procedure cardiac echography did not show any residual thrombi in the cardiac chambers and a chest CT scan showed that the aorta and the pulmonary arteries were thrombus-free. Complementary investigations of hemostatic or coagulation dysfunction (antithrombin deficiency, C-protein and S-protein, factor VIII, and resistance to C-reactive protein) did not reveal any abnormalities, and treatment with a vitamin K antagonist (Acenocoumarin) was initiated. One year after the procedure, the patient remained free of thrombotic disease and neurological deficits.

Discussion

We report a rare case of a pulmonary embolism with an intra-aortic thrombus occluding the left subclavian artery in a young patient. A PFO discovered peri-operatively was found to be responsible for the paradoxical aortic thrombus that occurred after DVT developed, despite enoxaparin prophylaxis. Patients undergoing orthopedic or trauma surgery are at high risk for Venous Thromboembolism (VTE) [1]. Therefore, anticoagulation therapy is recommended for the prevention of VTE after orthopedic surgery, but this regimen does not completely prevent DVT or VTE [2]. A PFO is present in about 25% of the general population [3] and increases the mortality rate related to pulmonary embolism from 13% to 44% and the incidence of stroke from 2% to 13% [4]. In this case, an acute increase in right-sided cardiac pressure due to the pulmonary embolism led to a right-to-left shunt responsible for the paradoxical embolism [5]. Because our patient was in a critical condition, we decided to perform emergent surgery. In the operating room, after general anesthesia had been administered, TEE, which is a very reliable method to detect septal defects [6], revealed the presence of a PFO. After ensuring that the brachiocephalic trunk was free of any thrombotic material, a CPB was initiated by cannulating it distally. This approach was used to maintain antegrade flow in the arch and to avoid dislodging the thrombus located in the left subclavian artery. The entire procedure was performed under carbon dioxide flooding to minimize the risk of air embolism [7].

Under conditions of tepid hypothermic circulatory arrest with selective antegrade perfusion of the right carotid, the aortic and subclavian embolectomies were completed and the PFO was closed to prevent future emboli or stroke [8]. These operative conditions were decided upon prior to the procedure to limit the duration of circulatory arrest, post-operative bleeding, and CPB time [9]. In cases of total aortic arch obstruction, cannulation of the apex of the heart is considered a safe option [10], but, if possible, cardiac manipulations should be limited to avoid embolization or thrombus fragmentation. Similarly, atrio-caval cannulation and closing of the PFO during circulatory arrest avoid the need for slinging the caval veins when closing the PFO during a CPB. The mortality of massive pulmonary embolisms reaches 52.4% at 90 days [11]. The main complication of thrombolysis is intracranial hemorrhage which accounts for 3% [12]. Surgical embolectomy is indicated for pulmonary embolism with arterial hypotension and cardiogenic shock [13]. Several studies show a higher mortality and recurrence rate in the medically treated group [14,15], but also a low mortality rate for pulmonary embolectomies [16].

Conclusion

Cases of thrombi in the ascending aorta are rare, and surgical management appears to be the most frequently used option, with low mortality rates [17].

Declarations

Acknowledgments

None.

Funding

GK, AB, and BR were supported by “Fondation Mont-Godinne” (Belgium).

The funding agency had no role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript. This does not alter our adherence to all the Journal of Cardiothoracic Journal policies on sharing data and materials.

Availability of Data and Materials

The data supporting the conclusions of this article are included within the article.

Authors’ Contributions

GK wrote the report, PS performed the surgery, and AB and BR revised the manuscript. All authors read and approved the final manuscript.

Competing Interests

The authors declare that they have no competing interests.

Consent for Publication

Written informed consent was obtained from the patient for publication of this case report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.

Ethics Approval and Consent to Participate

Not required.

Figure 1: Pre-operative chest X-ray showing bi basal infiltration.

Figure 2: Thoracic CT scan showing a concomitant embolism of the aortic and pulmonary arteries. Panel A, axial view; panel B, sagittal view;  and panel C, coronal view.

Figure 3: Thrombi specimens after removal from the pulmonary arteries (panel A) and aortic-subclavian arteries (panel B).

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