Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3711_Библиотеки_им_академика_М_И_Перельмана

Diagnosis and management of these entities remains challenging due to their rarity relative to other cardiovascular complications, the non-specic nature of symptoms in the acute phase, and their lack of associated symptoms in the chronic phase even when adverse remodeling is occurring. In the acute phase, rapid diagnosis is essential as the risk of death or major complication is particularly high early in the clinical course. Establishing and characterizing the diagnosis may maximize the opportunity for successful therapeutic intervention [1, 2]. Typically, acute aortic syndromes that do not involve the ascending aorta (Type B) have been managed medically unless complications are present [3]. The role of endovascular aortic intervention including fenestration and stent grafting (TEVAR) in the management of patients with Type B acute aortic syndromes is rapidly evolving. Clinically, vigilance is necessary as patients may evolve early in their course and experience complications requiring intervention after initial triage to medical management. As patients transi-

Acute aortic syndromes involving the descending aorta include AoD, IMH, penetrating aortic ulcer (PAU), acute aneurysm expansion, and trauma [3, 4]. These entities may present alone or in combination and represent a spectrum and evolution of aortic disruption. Aortic dissection typi­cally results from an intimal tear that allows pressurized blood into the often weakened medial layer leading to prop­agation of the plane front either antegrade or retrograde directions [4]. The resulting ap of tissue divides the aorta by creating a second or “false” lumen along the native or true lumen. The intimal ap may lead to complications such as malperfusion through branch vessel occlusion. The patency and degree of fenestration of the false lumen may impact patency and pressurization. The false lumen may communicate with the true lumen via one or more re-entry tears distal to the entry site, which may allow for false lumen decompression. Alternatively, there may be no or limited re­entry tears, causing the false lumen to functionally act as a “wind sock” characterized by elevated false lumen pres­sures. This pressurized space may lead to further propaga­tion, outward remodeling and aneurysm formation, compromise of the true lumen, occlusion of branch vessels, or ultimately progression resulting in rupture. Observational studies have described this status of ow within the false lumen as prognostically important in patients with Type B dissection [5]. Although medial disruption is generally a unifying feature in dissection, cases of isolated intimal tears without false lumen formation do occur [6].

the highest incidence in the third trimester and early postpar­tum period [18]. This risk is greatest in those with a bicuspid aortic valve, Marfan, Ehlers–Danlos, or Turner syndrome [18–20]. In pregnant women with Turner syndrome, the risk of acute aortic syndrome is greater than 2%, and that for death is increased approximately 100-fold [18, 19].

Medial degeneration often characterized as cystic medial necrosis is generally invoked as the pathobiology underlying the development of acute aortic syndromes [3, 4]. This nd­ing is not etiology specic and is associated with typical risk factors such as age and hypertension as well as several other disorders. In general, any process that damages the tunica media leading to degeneration will increase the risk of aneu­rysm or dissection. Several biological processes have been discussed as contributing to the etiology including inam­mation, oxidative stress, and disrupted P53-MDM2 signal-

Acute aortic disruption may also occur in the setting of procedures (iatrogenic) or in the setting of trauma. These events may be more common in the ascending rather than the descending aorta as they have been associated with cardiac procedures [24]. Aortic transection can occur in the setting of rapid deceleration such as occurs in chest trauma and motor vehicle accidents. Cocaine ingestion may result in

and the need for surgical management, although the latter is likely a reection of the presence of complications [28]. It is important to recognize that complications may develop after presentation in patients who appear uncomplicated at the time of diagnosis and that complications may be dynamic. Identifying early, evolving, and dynamic complications in patients with Type B dissection is critical for risk stratica­tion and timely intervention [3].