Thoracic aortic aneurysms . This section will analyze aneurysms corresponding to the thoracic aorta, that is, the ascending aorta, the aortic arch, and the descending thoracic aorta.
Summary
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- 1 Etiology
- 2 Pathological anatomy
- 3 Clinical picture
- 4 Signs and Symptoms
- 5 Diagnosis
- 6 Differential diagnosis
- 7 Forecast
- 8 Treatment
- 9 Source
Etiology
Thoracic aortic aneurysms are the result of degenerative disease of the middle layer, a dissection (see above), autoimmune diseases (aortitis), infectious or fungal processes, trauma (pseudoaneurysms), and / or atherosclerosis. . In the thoracic aorta, unlike in the abdominal aorta, atherosclerosis is a process added to aneurysmal disease. The most frequent cause involved in the formation of thoracic aortic aneurysms is degenerative media disease. Inflammatory processes such as Takayasu disease or giant cell arteritis have been less frequently involved . The term fungal aneurysm is used to describe arterial dilation secondary to destruction of the vascular wall by fungi.or bacteria . Until before the antibiotic era, it was not uncommon to find aneurysms of lutic origin, characteristically saccular and located in the ascending aorta. Other microorganisms have been isolated from the wall of fungal aneurysms: Sta-philococcus , Streptococcus , Salmonella and Escherichia coli. False thoracic aneurysms or pseudoaneurysms are the result of trauma or secondary to previous surgical repairs. The typical traumatic injury due to deceleration involves shearing of the aortic wall frequently in the minor curvature of the origin of the descending thoracic aorta corresponding to the ductus arteriosus. The contained rupture of the aorta generates a hematoma in communication with the aortic lumen (pseudoaneurysm).
Pathological anatomy
The destruction of the elastic fibers and the destructuring of the muscular layer leads to the weakening of the arterial wall, which is the immediate cause of aneurysmal formation. Fusiform aneurysms generally correspond to degeneration of the mean, which includes the following pathological varieties: mucoid degeneration, myxomatous degeneration, and cystic necrosis of the mean. Fungal aneurysms, generally saccular, present a leukocyte infiltrate and areas of necrosis in the media. When atherosclerosis is involved in the formation of the aneurysm, the presence of cells is notedfoamy, varying degrees of necrosis, calcification, and intraplate hemorrhage with destruction of elastic and collagen fibers. Pure atherosclerotic thoracic aneurysms are frequently saccular. Pseudoaneurysms are limited by collagen fibers and little inflammatory infiltration with more or less extensive calcification depending on the chronicity of the process. The presence of the so-called mural thrombus that covers the interior of the aneurysmal sac is common. It is formed as a consequence of the turbulence generated by the changes in the caliber of the aneurysmal vessel, in an attempt to harmonize hemodynamics.
Clinical picture
Usually, thoracic aneurysms, as in other locations, are usually asymptomatic. Fungal aneurysms can be associated with febrile episodes and nonspecific chest pain. Pain is not exclusive to this type of aneurysm. When it occurs it constitutes an alert symptom, due to growth or breakage. Sometimes it has anginal characteristics, radiating to the back or the epigastrium.
Signs and symptoms
Thoracic aneurysms generate symptoms and signs depending on their size and location. A root dilating aneurysm of the ascending aorta would cause aortic regurgitation with or without secondary heart failure . More rarely, it can cause superior vena cava syndrome. An arch or descending aortic aneurysm can cause dysphonia due to compression of the recurrent nerve, dyspnea or stridor due to compression of the upper respiratory tract, hemoptysis due to erosion of the trachea or of a bronchus. A descending thoracic aortic aneurysm can compress the esophagusand cause dysphagia and / or hematemesis due to erosion. Patients with Marfan syndrome or other inherited connective tissue disorders, such as Ehlers-Danlos syndrome type IV, more frequently develop aneurysms of the ascending thoracic aorta or of various segments of the aorta. The semiology of these syndromes should warn of the possibility of association with thoracic aneurysms. The thrombotic content of the aneurysmal sac is the cause of embolisms towards the supraortic trunks, the extremities or towards the visceral arteries , giving rise to ischemic symptoms.. Dissection is a possible evolution of a thoracic aneurysm. Similarly, rupture constitutes a final phase of this nosological entity. If the rupture occurs towards the pericardial sac, an acute hemopericardium tamponade occurs. If it ruptures into the right ventricle or atrium or into the pulmonary artery, a large left-right shunt is created with severe heart failure and death. If it ruptures into the mediastinum, into the pleural cavity (massive hemothorax), or into the retroperitoneal space, a hypovolemic shock with generally fatal consequences results.
Diagnosis
Diagnostic suspicion through history or physical examination is exceptional. Auscultation of chest murmurs and palpation of a pulsating mass in the suprasternal socket in a young patient with Marfan syndrome is a rare form of presentation of this entity. Most thoracic aortic aneurysms are evident on plain chest radiography. It presents as a mediastinal widening or mass, with or without compression of neighboring structures, attributable to an aneurysm of the ascending or descending aorta or the aortic arch. The left lateral view offers additional information. However, this diagnostic method is not ideal for correct localization or to differentiate between aneurysm and tortuosity of the aorta. Computed tomography (CT) is the most useful diagnostic method to determine the diameter of the aorta and the extent of the aneurysm. It provides information on the characteristics of the arterial wall, degree of calcification, thickness and distribution of the mural thrombus and the state of the periaortic tissue. The contrast tomographic study also reports possible dissections or leaks due to cracking or rupture. Current helical CT models allow three-dimensional reconstruction of the aneurysm anatomy and its relationship with large-caliber aortic branches. Precisely, one of the limitations of this diagnostic method is the low resolution to visualize small branches of the aorta. Another drawback is the risk of causing kidney failure with the use of iodinated contrast. It is also unable to report cardiac function or the degree of aortic valve insufficiency. Magnetic resonance imaging (MRI) provides information similar to that provided by CT. MRI can report blood flow status without the need to inject iodinated contrast; however, the time required for each examination and the cost are greater than for CT. In addition, until now, its availability is reduced. Recent technical improvements have allowed the study of cardiac and valvular functionalism. Transesophageal echocardiography (TEE) provides excellent images of the structure and function of the heart, aorta, and large thoracic vessels, using the esophagus as an ultrasonic window. The association with pulsed or color Doppler offers the possibility of studying blood flow, the presence of mural thrombus, dissection, rupture, or periaortic hematoma. It has the advantage of being a bloodless and very cheap method. If the possibility of surgical treatment is anticipated, the preoperative study should consider the analysis of cardiac, renal and pulmonary function. Likewise, a hemodynamic vascular study of the lower extremities should be performed to rule out the concomitance of peripheral vascular disease.
Differential diagnosis
If the patient presents with chest pain, other causes such as ischemic heart disease, aortic dissection, spontaneous esophagus rupture (Boerhaave syndrome), gastroduodenal ulcus, esophageal hiatus hernia, pericarditis, osteoarticular thoracic processes, or pleural processes should be ruled out. inflammatory. If it is based on a suspicious chest radiographic image, a differential diagnosis can be made with mediastinal tumors or tortuosity of the large thoracic vessels. If hemoptysis or hematemesis is the first clinical manifestation, other bronchopulmonary or esophageal-gastroduodenal processes must be ruled out. In any case, given the danger that would entail starting clinical research with biopsies or mediastinoscopies, it is preferable to start the vascular diagnostic study with CT.
Forecast
As previously mentioned, the spontaneous evolution of thoracic aneurysms is towards dissection or rupture. 80% break after 5 years from diagnosis. Breakage usually leads to death from hypovolemic shock or severe heart failure. For this reason, patients with acceptable surgical and anesthetic risk should be operated to avoid this fatal outcome. Patients with connective diseases such as Marfan syndrome require several reparative interventions throughout their shortened life due to the multi-segmental nature of their aortic disease.
Treatment
The treatment of thoracic aortic aneurysms is surgical. Surgical repair is indicated in patients with acceptable surgical and anesthetic risk, with symptomatic or asymptomatic thoracic aneurysm that has a diameter that exceeds twice the adjacent normal aorta. The technique used varies according to the location, extension and shape of the aneurysm. Currently, aneurysms that compromise the ascending aorta are treated by replacing the aneurysmal segment with a tubular prosthesis. If, in addition, it affects the valve, it must be replaced with a valved composite prosthesis and the coronary arteries are reimplanted (a technique introduced in 1968 by Bentall and DeBono, modified by Cabrol in 1981).). When the aortic arch is affected, if the aneurysm is saccular, it can be repaired with resection of the aneurysm and closure of the aorta with a polyester patch. If it is fusiform, the aortic segment is replaced by a tubular graft with reimplantation of the supraortic trunks. If only the descending thoracic aorta is affected, if the aneurysm is saccular, it is resected and the aorta is closed with a patch, and if it is fusiform, it is replaced by a tubular prosthesis. In the case of a diffuse aneurysmal disease (mega-aorta) involving the ascending aorta, the arch, the descending aorta, or the thoraco-abdominal aorta, repair is performed sequentially starting with the ascending aorta and aortic arch (elephant trunk technique ) so that in a second operation the rest of the aorta is repaired. The morbidity and mortality associated with this type of surgical repairs makes it advisable to perform them by surgical groups with extensive experience. Recently, as in the case of abdominal aortic aneurysms, the repair of aneurysms of the descending thoracic aorta is being evaluated using endoluminal techniques. This revolutionary technique, introduced by Parodi in1991 allows the aneurysm to be excluded through the implantation of a stent that, folded inside a carrying catheter, is advanced from the femoral artery or from the iliac artery to the place to be repaired, where it is deployed. This procedure avoids thoracotomy, the need for extracorporeal circulation, reduces morbidity and mortality. However, it is still too early to advise this treatment widely since its long-term results are unknown.
