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Thoracic aortic surgery is required for a spectrum of disease, including degenerative aneurysm, acute and chronic dissection, pseudoaneurysm, coarctation, and traumatic aortic tear. Thoracoabdominal aortic aneurysm (TAA) repair is often regarded as the most challenging surgical case in terms of overall anesthetic and perioperative management. Since the first TAA repair in 1955,[313] tremendous advances have been made in the field. These advances have led to significant reductions in operative mortality and perioperative complications. However, even in centers where numerous procedures are performed, morbidity and mortality rates are high, especially for patients with dissecting or ruptured aneurysms. To successfully care for these patients, the anesthesiologist must be knowledgeable in the areas of one-lung ventilation; extracorporeal circulatory support, including circulatory arrest; renal and spinal cord protection; induced hypothermia; invasive hemodynamic monitoring, including TEE; massive transfusion; and management of coagulopathy. Intraoperative management requires a team effort, with intimate cooperation among surgeons, anesthesiologists, perfusionists, nurses, and electrophysiologic monitoring staff. Endovascular repair of lesions that affect the descending thoracic and thoracoabdominal aorta is evolving, but much more slowly than with infrarenal aortic aneurysm. However, accumulating experience with stent graft repair of thoracic aortic aneurysm, dissection, and traumatic tear indicates that it will likely be an effective alternative to open repair for select patients.
Aneurysms of the thoracoabdominal aorta occur primarily because of atherosclerotic degenerative disease (80%) and chronic aortic dissection (17%). [314] The remainder are caused by trauma, connective tissue diseases involving the aortic wall from conditions such as Marfan's syndrome, cystic medial degeneration, Takayasu's arteritis, or syphilitic aortitis.[315] The true incidence of TAA is unknown, but population studies suggest a prevalence much less than infrarenal abdominal aortic aneurysm. Degenerative and dissecting TAAs differ in their associated risk factors, extent of aortic involvement, and natural history.[316] [317] Complete characterization of each TAA is required to formulate a comprehensive treatment plan. Development of degenerative and dissecting TAA is ultimately related to weakening of the aortic wall. Although the natural history of TAA without surgery is uncertain, enlargement tends to be progressive and nonoperative management is generally associated with a poor prognosis. With progressive enlargement, the nutritional blood flow to the aorta is compromised. The increasing diameter is associated with increased wall tension, even when arterial pressure is constant (i.e., law of LaPlace). The high incidence of associated systemic hypertension enhances aneurysm enlargement.
Degenerative and dissecting TAAs are symptomatic at the time of presentation in 57% and 85% of patients, respectively.[316] [317] The most common presenting complaint
In addition to cause, aneurysms of the thoracoabdominal aorta may be classified according to their anatomic location. In 1986, Crawford and colleagues, [314] recognizing the correlation between aneurysm extent and clinical outcome, proposed a classification based on extent of aortic involvement ( Fig. 52-14 ). The Crawford classification defines aneurysms as extent types I, II, III, and IV. Type I aneurysms involve all or most of the descending thoracic aorta and the upper abdominal aorta. Type II aneurysms involve all or most of the descending thoracic aorta and all or most of the abdominal aorta. Type III aneurysms involve the lower portion of the descending thoracic aorta and most of the abdominal aorta. Type IV aneurysms involve all or most of the abdominal aorta, including the visceral segment. Types II and III are most difficult to repair because they involve the thoracic and abdominal segments of the aorta. The Crawford classification is appropriately applied to aneurysms of all causes (degenerative and dissecting). Patients with Crawford type II aneurysms are at greatest risk for paraplegia and renal failure from ischemia to the spinal cord and kidneys during cross-clamp. Even with extracorporeal circulatory support, there is an obligatory period when blood flow to these organs is interrupted because the origin of the blood flow is between the cross-clamps. For this reason, protective measures to prevent ischemic injury are important in reducing morbidity.
Figure 52-14
The Crawford classification of thoracoabdominal aortic
aneurysms is defined by anatomic location and the extent of involvement. Type I
aneurysms involve all or most of the descending thoracic aorta and the upper abdominal
aorta; type II aneurysms involve all or most of the descending thoracic aorta and
all or most of the abdominal aorta; type III aneurysms involve the lower portion
of the descending thoracic aorta and most of the abdominal aorta; and type IV aneurysms
involve all or most of the abdominal aorta, including the visceral segment. (Adapted
from Crawford ES: Thoracoabdominal and suprarenal abdominal aortic aneurysm. In
Ernst CB, Stanley JC [eds]: Current Therapy in Vascular Surgery. Philadelphia,
Decker, 1987, pp 96–98.)
Aortic dissection, with or without aneurysm formation, has likewise been classified based on extent of aortic involvement. The most widely used classification, proposed by DeBakey and colleagues, defines aortic dissection as types I, II, and III ( Fig. 52-15 ).[321] Type I aneurysms begin in the ascending aorta and extend throughout the entire aorta. These lesions are usually repaired by use of a two-stage approach, with the first procedure on the ascending aorta and aortic arch and the second procedure on the descending thoracic aorta. Type II aneurysms are confined to the ascending aorta. Types I and II often involve the aortic valve, causing aortic regurgitation, and sometimes involve the ostia of the coronary arteries. Type III aneurysms begin just distal to the left subclavian artery and extend to the diaphragm (type IIIA) or to the aortoiliac bifurcation (type IIIB). Another commonly used classification of aortic dissection is the Stanford classification.[322] This more simplified classification divides aortic dissection into those that involve the ascending aorta (Stanford type A) and those that do not involve the ascending aorta (Stanford type B). Aortic dissection is also classified by duration, with those less than 2 weeks classified as acute and those greater than 2 weeks classified as chronic. This classification has very significant mortality implications, with much higher mortality in the acute phase.
Acute aortic dissection involving the ascending aorta (DeBakey type I and II, Stanford type A) is a surgical emergency and requires immediate cardiac surgical repair[323] (see Chapter 50 ). Acute dissections involving the descending aorta (DeBakey type III, Stanford type B) are most often treated conservatively (i.e, blood pressure and pain control) because surgical repair has no proven benefit over medical or interventional treatment in stable patients.[324] Early surgical intervention may be required for a variety of reasons, including aneurysmal formation, impending rupture, leg, renal, or visceral ischemia and
Figure 52-15
The DeBakey classification of dissecting aneurysms of
the aorta. Type I has an intimal tear in the ascending aorta with dissection extending
down the entire aorta. Type II has an intimal tear in the ascending aorta with dissection
limited to the ascending aorta. Type III has an intimal tear in the proximal descending
thoracic aorta with dissection limited to the thoracic aorta (type IIIA) or extending
distally to the abdominal aorta or aortoilic bifurcation (type IIIB). (Adapted
from DeBakey ME, Beall AC Jr, Cooley DA, et al: Dissecting aneurysms of the aorta.
Surg Clin North Am 46:1045–1055, 1966.)
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