Chapter 53. Descending and Thoracoabdominal Aortic Aneurysms

Treating aneurysms that arise from the aortic segments distal to the left subclavian artery poses challenges that are distinct from those presented by aneurysms of the more proximal ascending and arch segments. The distal aortic segments comprise the descending thoracic aorta, which extends from the left subclavian artery to the diaphragm within the chest, and the abdominal segment that extends from the diaphragm to the iliac bifurcation. The diaphragm divides the thoracic aorta from the abdominal aorta.

An aortic aneurysm that is limited to the chest is classified as a descending thoracic aortic aneurysm (DTAA). An aortic aneurysm that traverses the diaphragm and extends into both the chest and the abdomen to any degree is considered a thoracoabdominal aortic aneurysm (TAAA) (Fig. 53-1). Aneurysms in these locations can be extensive and can involve many or all of the aortic branch vessels. Modern critical care and surgical adjuncts for organ protection have improved the outcomes of surgical repair; however, operative treatment of DTAA and TAAA continues to represent a significant clinical challenge to the cardiovascular surgeon.

The etiology of DTAA and TAAA has changed over time. Whereas tertiary syphilis was the most common cause of thoracic aneurysms in the early 1900s, other causes are more prevalent today. Well-established causes of DTAA and TAAA include medial degeneration, atherosclerosis, aortic dissection, connective tissue disorders, aortitis (eg, Takayasu's arteritis), aortic coarctation, infection, and trauma. As our understanding of genetics increases and as more advanced genetic testing becomes available, classification systems are likely to evolve to include more molecular factors. Perhaps partly because of improved screening for aneurysmal disease and the increasing age of the population, it is certain that the incidence and prevalence of thoracic aortic aneurysm are increasing over time.1

The most common types of aneurysms of the descending and thoracoabdominal aorta today are grouped into the category of atherosclerotic aneurysms. Unfortunately, although this term may be descriptive, it may not accurately describe the mechanism of aneurysmal changes. Although atherosclerosis and aortic aneurysms share common risk factors and frequently coexist, thoracic aortic aneurysms are primarily the result of age-related medial degeneration, which is characterized by changes in elastin and collagen that reduce aortic integrity and strength. Subsequent aortic enlargement and aneurysm formation provide fertile ground for superimposed intimal atherosclerosis and further degeneration of the aortic wall. The usual histologic changes in the aging aorta include elastin fragmentation, fibrosis with increased collagen, and medial degeneration.2 As with most aneurysmogenic processes, medial degeneration usually causes diffuse, fusiform aortic dilatation. In some cases, however, medial degeneration produces saccular aneurysms along the descending thoracic aorta. These saccular aneurysms may be superimposed on or coexist with more generalized, fusiform aneurysmal disease of the thoracoabdominal aorta.

Risk factors for aortic dissection and aortic aneurysm overlap to a great extent, but once an aorta becomes dissected, the dissection itself becomes an independent risk factor for subsequent dilation and aneurysmal changes. Aortic dissections occur in the medial layer separating the intima from the adventitia; blood flows through the true aortic lumen and through one or more false lumen channels that can form at various points along the aorta. This process weakens the outer aortic wall, making it prone to progressive aneurysmal dilatation (Fig. 53-2). Persistence of a pressurized false lumen has been associated with subsequent aneurysm formation, need for intervention, and increased mortality.3,4 Recent endovascular strategies have included stent exclusion of the false lumen in an attempt to thrombose the false channel, thus decreasing the risk of late aneurysm formation, although this technique remains controversial.5 In a randomized series, endovascular stenting in uncomplicated type B aortic dissections failed to show differences in survival and aortic outcomes at 2 years when compared to standard medical management.6 Penetrating aortic ulcers and intramural hematomas are two variants of aortic dissection that can occur in the descending and abdominal aortic segments. Penetrating aortic ulcers are disrupted atherosclerotic plaques that can penetrate the aortic wall, leading to classic dissection or rupture. Intramural hematomas are collections of blood within the aortic wall that occur without an intimal tear; growth of the hematoma can result in classic dissection.

Genetic mutations or defects can give rise to defective components of the aortic extracellular matrix, leading to aortic aneurysm and dissection. Aortic aneurysms that occur in patients with these genetic disorders can be a part of a named syndrome, accompanied by a constellation of extraaortic symptoms, or they may be part of a heterogenous group of familial thoracic aortic aneurysms and dissections that occur in isolation. In a national registry of genetically triggered thoracic aortic aneurysms, Marfan syndrome is the most common genetic cause of thoracic aneurysms (36%).7 Marfan syndrome is a connective tissue disorder that results from a fibrillin-1 gene mutation that causes fragmentation of elastic fibers and the deposition of extensive amounts of mucopolysaccharides in the aortic extracellular matrix. The aorta in Marfan syndrome patients is prone to dissection, which is the most common cause of DTAAs and TAAAs in these patients.8 Ehlers-Danlos syndrome causes 5% of genetically triggered thoracic aneurysms and results from abnormal collagen synthesis. Loeys-Dietz syndrome is a recently identified, particularly aggressive aortic disorder resulting from mutations in the transforming growth factor (TGF)-beta receptor I (TGFBR1) and II (TGFBR2) genes.9,10

Both chronic, nonspecific aortitis and systemic autoimmune disorders, such as Takayasu's arteritis, giant cell arteritis (temporal arteritis), and rheumatoid aortitis, can cause destruction of the aortic media and progressive aneurysm formation. Although Takayasu's arteritis usually causes obstructive lesions related to severe intimal thickening, the associated medial destruction can result in aneurysmal dilatation.

Aneurysms involving the upper descending thoracic aorta can develop in patients with congenital aortic coarctation. These aneurysms occur concomitantly with unrepaired coarctation or after coarctation repair.11 The postrepair aneurysms appear to be most common in patients who have had patch graft aortoplasty operations.12 Histologic examination of the aneurysmal tissue has revealed medial degeneration, smooth muscle cell necrosis, and loss and fragmentation of elastic fibers.13

Infection can produce a saccular “mycotic” aneurysm in a localized area of the aortic wall that has been damaged by the infectious process. For unknown reasons, such mycotic aneurysms tend to occur along the lesser curvature of the transverse aortic arch or the upper abdominal aorta adjacent to the origins of the visceral branches. In such cases, only a portion of the aortic circumference is affected; consequently, localized weakening causes a diverticular or saccular outpouching.

Each of the disease processes described above causes aneurysms through progressive degeneration and dilatation of the aortic wall. In contrast, pseudoaneurysms of the thoracic aorta form as the result of chronic leaks through discrete defects in the aortic wall. These leaks are initially contained by surrounding tissue; the accumulation of organized thrombus and the associated fibrosis forms the wall of the pseudoaneurysm. Pseudoaneurysms can develop after surgical or percutaneous repair of aortic coarctation, dissection, or aneurysm.14 Unrepaired blunt and penetrating injuries are the other common cause of aortic pseudoaneurysms. Chronic traumatic pseudoaneurysms typically develop in the proximal descending thoracic aorta after blunt aortic injuries13; the management of these lesions is covered in detail in a subsequent chapter.

An untreated aneurysm in the thoracic and thoracoabdominal aorta can progress to dissection, rupture, or both if given enough time. A dissected aorta that was originally of normal caliber will tend to dilate and become aneurysmal. The causes and genetics of these aneurysms vary, but there are commonalities in the mechanical and pathophysiologic aspects of their formation and development. Understanding these processes will help surgeons to determine the timing and nature of the operative intervention needed.

An aneurysm is defined as a permanent dilation of an artery to at least 1.5 times its normal diameter at a given location.15 However, the normal aortic diameter is perhaps more difficult to define. At the level of the mid-descending thoracic aorta, the average aortic diameter is 28 mm for men and 26 mm for women; at the level of the celiac axis, it is 23 mm for men and 20 mm for women; and at the infrarenal aorta, it is 19.5 mm for men and 15.5 mm for women.16 The normal aortic diameter also varies with a person's age and body surface area. Aortic enlargement with advancing age has been reported in several studies.17–19 Even when adjusted for age and body surface area, mean aortic size is significantly smaller in women than in men; on average, aortic diameter is 2 to 3 mm greater in men than women. Body surface area is a better predictor of aortic size than is height or weight, particularly in patients less than 50 years of age.17,20

The descending thoracic aorta has a slightly higher rate of expansion over time than the ascending aorta and is noted to average 1 to 4 mm/year.21 The rate is not constant, and it increases as the diameter increases. A dissection in an otherwise small aneurysm can lead to a sudden increase in the rate of growth. The relationship among pressure, vessel diameter, and vessel wall tension is described by Laplace's law. As the luminal diameter increases, there is increasing wall tension, which in turn contributes to the cycle of progressive dilatation. Unfortunately, at some point as the dilation progresses, the wall tension becomes too great for the maximally stretched aortic wall. A tear can occur within the intimal and medial layers, resulting in a dissection that propagates down the length of the aorta, or a tear can penetrate the full thickness of the aortic wall, resulting in contained or free rupture. The aortic size at which this event occurs is determined by several factors, including the presence or absence of a connective tissue disorder, the presence and severity of hypertension, and the patient's body size. In a large series of patients, Elefteriades and colleagues22 have shown that in the thoracic aorta, there is a sharp increase in the incidence of aortic complications at aneurysmal diameters greater than 6 cm, with a 14% combined risk of rupture, dissection, and death. In a population-based study, the 5-year risk of rupture doubled from 16% for aneurysms 4 to 5.9 cm in diameter to 31% in aneurysms 6 cm or more in diameter.23

At the time of diagnosis, patients with DTAAs and TAAAs are commonly asymptomatic. For example, Panneton and Hollier24 reported that degenerative TAAAs are asymptomatic in roughly 43% of patients. In asymptomatic patients, DTAAs and TAAAs are often discovered when imaging studies are performed to evaluate unrelated problems. For example, chest radiographs may show widening of the descending thoracic aortic shadow, which may be outlined by a rim of calcification outlining the dilated aneurysmal aortic wall (Fig. 53-3). Aneurysmal calcium may also be seen in the upper abdomen on standard radiograms.

Although DTAAs and TAAAs remain asymptomatic for long periods of time, most ultimately produce a variety of symptoms before they rupture. Degenerative TAAAs produce symptoms in approximately 57% of patients; 9% of patients present with rupture.24 The most frequent symptom is back pain between the scapulae. When the aneurysm is large in the region of the aortic hiatus, pressure on adjacent structures may cause mid-back and epigastric pain. Other potential signs and symptoms related to compression or erosion of adjacent organs include stridor, wheezing, cough, hemoptysis, dysphagia, and gastrointestinal obstruction or bleeding. Hoarseness results from traction on the vagus nerve as the distal aortic arch expands and causes recurrent laryngeal nerve paralysis. Thoracic or lumbar vertebral body erosion (Fig. 53-4) causes back pain, spinal instability, and neurologic deficits from spinal cord compression; mycotic aneurysms have a peculiar propensity to destroy vertebral bodies. Additionally, neurologic symptoms, including paraplegia, paraparesis, or both, may result from thrombosis of intercostal and lumbar arteries. This is most frequently seen with acute aortic dissection, which may occur primarily or be superimposed on medial degenerative fusiform aneurysmal disease. Thoracic aortic aneurysms, like aneurysms in other locations, may produce distal emboli of clot or atheromatous debris that gradually obliterate and thrombose visceral, renal, or lower-extremity branches.

Imaging technology is critical in diagnosis and determining anatomical details for operative planning. Computed tomography (CT) scanning and magnetic resonance angiography (MRA) enable clinicians to obtain excellent images without the potential morbidity or cost associated with angiography. Computed tomography scanning is widely available and can image the entire thoracic and abdominal aorta, major branch vessels, and virtually all adjacent organs. Computer programs can construct sagittal, coronal, and oblique images, as well as three-dimensional reconstructions, from CT data.25–27 Contrast-enhanced CT scanning (Figs. 53-2, 53-4, and 53-5) also provides information about the aortic lumen, intraluminal thrombus, presence of aortic dissection, intramural hematoma, mediastinal or retroperitoneal hematoma, aortic rupture, and periaortic fibrosis associated with inflammatory aneurysms.28 Computed tomographic angiography with multiplanar reconstruction is especially useful for planning endovascular procedures. Advantages of CT include being less expensive and somewhat quicker to perform than MRA and, at present, the wider availability of CT expertise. Also, CT can be used with patients who have implanted ferromagnetic prostheses or other devices, which can cause injury in patients undergoing MRA.29 The chief advantages of MRA are that it does not expose the patient to ionizing radiation and that it reveals disease within the aortic wall, including intramural hemorrhage. The gadolinium-based contrast agents used in MRA were once considered to be safer for patients with renal insufficiency than CT contrast media. Ironically, recent reports have associated the use of certain gadolinium-based contrast agents with nephrogenic systemic fibrosis (NSF)—a scleroderma-like fibrotic process that can affect not only the skin but also internal organs—in patients with renal insufficiency.30 The current recommendation is to avoid using such agents in patients with advanced renal failure (ie, with a glomerular filtration rate <30 mL/min) or in patients who are dialysis dependent.31

Ongoing improvements in noninvasive imaging modalities have substantially reduced the role of catheter aortography in assessing thoracic aortic aneurysms. However, catheter aortography remains useful in situations in which noninvasive methods are not feasible; for example, when artifact or heavy calcification obscures the area of interest.32 Anterior, posterior, oblique, and lateral views provide detailed information about branch vessels. The risks posed by aortography include renal toxicity from the large volumes of contrast material required to adequately fill large aneurysms. There is also a risk of embolization from laminated thrombus secondary to manipulation of intraluminal catheters. Furthermore, angiography underestimates the size of an aneurysm in areas of laminated thrombus. Nonetheless, angiography can be helpful in patients with suspected renal or visceral ischemia, aortoiliac occlusive disease, horseshoe kidney, or peripheral aneurysms.

Once an aneurysm involving the descending thoracic or thoracoabdominal aorta has been discovered, precise determination of the extent and severity of disease is the critical next step toward clarifying the specific diagnosis, determining the appropriate treatment, and, when repair is indicated, planning the appropriate intervention.

Indications for Operation

In asymptomatic patients, the decision to consider surgical repair is based primarily on the diameter of the aneurysm. To prevent fatal rupture, elective operation is recommended when diameter exceeds 5 to 6 cm or when the rate of dilatation exceeds 1 cm per year. In patients with connective tissue disorders, such as Marfan syndrome and related disorders, the threshold for operation is lower for both absolute size and rate of growth.8 Nonoperative management—which consists of strict blood pressure control, cessation of smoking, and at least yearly surveillance with imaging studies—is appropriate for asymptomatic patients who have small aneurysms. Symptomatic patients, however, are at increased risk of rupture and warrant expeditious evaluation and urgent aneurysm repair, even when the mentioned threshold diameters have not been reached. The onset of new pain in a patient with a known aneurysm is particularly concerning and often heralds significant expansion, leakage, or impending rupture. Malperfusion caused by chronic dissection is also an indication for TAAA repair. Degenerative DTAAs and TAAAs with superimposed acute dissection are especially prone to rupture and are therefore treated with emergent operation.

Endovascular Considerations

Descending thoracic aortic aneurysm is an approved and widely accepted indication for endovascular stent repair,33–35 and several stent-grafts have been approved by the US Food and Drug Administration (FDA) for this purpose. Endovascular repairs are covered in detail in a subsequent chapter, but all patients in our practice are evaluated for possible endovascular intervention, and an individualized surgical option best suited for the patient is selected. Two important factors to consider when deciding between open and endovascular aneurysm repair are the patient's physiologic reserve and vascular anatomy.36 Open repairs have well-documented outcomes and excellent long-term durability, and they allow repair of aneurysms with complex anatomy. However, the patients must have considerable physiologic reserve to undergo and recover from these procedures.

Repairing DTAAs with stent grafts is an attractive alternative to standard open procedures, especially in patients who have compromised cardiac, pulmonary, or renal status, who have undergone previous complex thoracic aortic procedures, or who are very elderly. Recent data show that, in general, endovascular repair of the descending thoracic aorta is associated with less early mortality and morbidity than is open repair.33–35 Appropriate anatomy, however, is critical for successful endovascular repair. Landing zones that have inadequate length, excessive angulation, extensive intraluminal thrombus, or severe vessel calcification will not allow secure endograft fixation, precluding endovascular repair. Furthermore, the long-term durability of these repairs remains unclear, particularly in patients with complex aortic disease, such as chronic aortic dissection, or with connective tissue disorders.

Combining open and endovascular procedures capitalizes on the principal benefits of both by creating durable repairs in patients with complex anatomy while minimizing physiologic stress and postoperative complications. Accordingly, combined approaches—commonly called “hybrid” procedures—appear well-suited for patients with limited physiologic reserve (precluding standard open repair) and complex aneurysmal anatomy (precluding standard endovascular repair).37 For example, in patients with DTAAs that have an insufficient proximal landing zone, an open procedure to reroute the brachiocephalic circulation can convert the aortic arch into a satisfactory landing zone for a stent-graft.38 Similarly, if arch aneurysms and DTAAs exist concurrently, a hybrid “frozen elephant trunk” repair can be performed that combines open arch replacement with stent-grafting of the DTAA.39 Thoracoabdominal aortic aneurysms have also been repaired with hybrid approaches: open visceral bypass grafting, performed to secure organ perfusion, is followed by stent-graft coverage of the entire aneurysm, including branch-vessel ostia.40–42 Although hybrid procedures are feasible and may be associated with reduced postoperative morbidity and mortality, the durability of these repairs is unclear. In contrast with endovascular repair of DTAA, purely endovascular approaches to TAAA repair require the use of fenestrated or branched endografts to maintain branch-vessel perfusion, and these repairs remain experimental to date.43–45

Endovascular stent devices are being used for evolving and expanding indications, including blunt aortic injuries, descending thoracic aortic ruptures, mycotic aneurysms, DeBakey type III aortic dissections, and hybrid descending aortic stenting during concurrent open repair of DeBakey type I aortic dissection. Although these indications remain controversial, the procedures are often performed in clinical scenarios with limited options. In endovascular stenting of a dissected descending thoracic aorta, some data suggest that a persistent patent false lumen is a predictor of poorer long-term outcome. Whether stent intervention will prevent the dissected thoracoabdominal aorta from following its typical natural history remains controversial, and late outcomes are not known.46

What is certain is that as endovascular aortic stent-graft use increases, these devices are increasingly encountered in subsequent open operations. Stent-graft failure may result from progression of the aneurysmal process to an adjacent portion of the aorta that is not amenable to further endovascular treatment, progressive dilation of the treated segment owing to persistent endoleak, infection of the endovascular device, or device migration. In general, the endovascular devices do not incorporate into the aneurysm thrombus and aortic intima in the way that conventional Dacron grafts incorporate into the periadventitial tissue. Explantation of the endovascular device and open graft replacement of the thoracic aorta can be accomplished with relatively good success.47,48 In the absence of infection, salvaging the device or portions of the device is also possible.49 We have applied the aortic cross-clamp to a proximal aortic segment with an endovascular stent-graft in place and repaired a distal segment in an open fashion. Suturing an existing stent-graft to a standard Dacron graft in a hemostatic fashion is also feasible, particularly if the surrounding aortic tissue can be incorporated into the suture line.

In each patient, the indications for operation discussed above are weighed against the risks posed by surgical intervention.50,51 The Crawford classification of TAAA (Fig. 53-6) permits standardized reporting of the extent of aortic involvement, thereby allowing appropriate risk stratification, choice of specific treatment modalities according to the extent of the aneurysm, and a type-specific determination of the risks for neurologic deficits and other morbidities and mortality associated with TAAA repair. Extent I TAAA repairs involve replacing most or all of the descending thoracic aorta and the upper abdominal aorta. Extent II repairs involve most or all of the descending thoracic aorta and extend into the infrarenal abdominal aorta. Extent III repairs involve the distal half or less of the descending thoracic aorta and varying portions of the abdominal aorta. Extent IV repairs involve most or all of the abdominal aorta.

An adequate preoperative assessment of physiologic reserve is critical in evaluating operative risk. Unless they require emergency operation, patients undergo a thorough preoperative evaluation, with emphasis on cardiac, pulmonary, and renal function.

Cardiac Status

Impaired myocardial contractility and reduced coronary reserve are common among elderly patients who undergo aortic reconstruction. Patients need substantial cardiac reserve to tolerate clamping of the thoracic aorta. Given the prevalence of preoperative cardiac disease and the physiologic strain of aortic clamping, it is not surprising that cardiac complications are a major cause of postoperative mortality. Reports indicate that cardiac disease has been responsible for 49% of early deaths and 34% of late deaths after TAAA repair, attesting to the importance of careful preoperative cardiac evaluation.24,52

Several imaging techniques are useful in preoperative screening for cardiac disease. Transthoracic echocardiography is noninvasive and can satisfactorily evaluate both valvular and biventricular function. Dipyridamole-thallium myocardial scanning identifies regions of myocardium that are reversibly ischemic, and it is more practical than exercise testing in this generally elderly population, whose exercise capacity is often limited by concurrent lower-extremity peripheral vascular disease. In patients with evidence of reversible ischemia on noninvasive studies, and those with a significant history of angina or an ejection fraction of 30% or less, cardiac catheterization and coronary arteriography are performed. Patients who have asymptomatic aneurysms and severe coronary artery occlusive disease (ie, significant left main, proximal left anterior descending, or triple-vessel coronary artery stenosis) undergo myocardial revascularization before aneurysm repair. In appropriate patients, percutaneous transluminal angioplasty is carried out before surgery. If clamping proximal to the left subclavian artery is anticipated in patients in whom the left internal thoracic artery has been used as a coronary artery bypass graft, a left-common-carotid-to-subclavian bypass is necessary to prevent cardiac ischemia when the aortic clamp is applied.53

Renal Status

Preoperative renal insufficiency has been a major risk factor for early mortality throughout the history of TAAA repair.50,54 It was among the predictive variables selected in Svensson et al.'s54 multivariable analysis of Crawford's complete experience with TAAA surgery in 1509 patients treated between 1960 and 1991. However, patients with preoperative renal failure who are being treated with an established hemodialysis program appear to have a level of risk similar to that of patients with normal renal function. Patients with severely impaired renal function who are not receiving long-term hemodialysis frequently require temporary hemodialysis early after operation and are clearly at increased risk for postoperative complications.

Although patients are not rejected as surgical candidates on the basis of renal function, careful assessment of renal function aids in estimating perioperative risk and adjusting treatment strategies accordingly. Renal function is assessed preoperatively by measuring serum electrolytes, blood urea nitrogen, and creatinine. Kidney size and perfusion can be evaluated by using the imaging studies obtained to assess the aorta. Patients who have poor renal function secondary to severe proximal renal artery occlusive disease are revascularized at operation by renal arterial endarterectomy, stenting, or bypass grafting, with the expectation that renal function will stabilize or improve.52

Because of the nephrotoxic effects of vascular contrast agents, surgery is delayed (if possible) for 24 hours or longer after CT scanning or aortography has been performed. This is especially important in patients with preexisting renal impairment. Strategies to reduce the risk of contrast-induced nephropathy include periprocedural administration of acetylcysteine and intravenous hydration. If renal insufficiency occurs or worsens after contrast administration, the surgical procedure is postponed until renal function returns to baseline or is satisfactorily stabilized.

Pulmonary Status

Pulmonary complications are the most common form of postoperative morbidity in patients who undergo DTAA and TAAA repairs. Most patients undergo pulmonary function screening with arterial blood gases and spirometry.55,56 Patients with an FEV₁ greater than 1.0 and a PCO₂ less than 45 are satisfactory surgical candidates. In suitable patients, borderline pulmonary function frequently is improved by smoking cessation, progressive treatment of bronchitis, weight loss, and a general exercise program that the patient follows for a period of 1 to 3 months before operation. However, surgery is not withheld from patients with symptomatic aortic aneurysms and poor pulmonary function. In such patients, preservation of the left recurrent laryngeal nerve, phrenic nerve, and diaphragmatic function is particularly important.

Anesthetic Strategies

Coordination among the surgeon, anesthesiologist, and perfusionist is critical during a DTAA or TAAA repair procedure. Management of hemodynamics during aortic clamping and unclamping, blood volume management, anticoagulation and hemostasis, and proper lung management occur in real time, with anticipation and preparation by the anesthesia team. Swan-Ganz catheters are routinely used for hemodynamic monitoring. The arterial catheter is placed in the right radial artery whenever the left subclavian artery flow may be interrupted during aortic clamping. A large-bore central venous line is necessary for volume return. We re-infuse filtered, unwashed whole blood from the cell-saver through a rapid infusion system during periods of substantial blood loss. With careful scavenging of shed blood and meticulous surgical hemostasis, operations without the use of blood and blood products are frequently possible. However, when coagulopathy does occur after the cross-clamp is released, rapid replacement of blood components with fresh-frozen plasma, platelets, and cryoprecipitate is necessary. Left lung isolation, usually by a double-lumen endobronchial tube, is necessary for exposure, although this may not be critical in extent IV TAAA repairs. The lung is handled minimally during anticoagulation to prevent lung hematoma and contusion. Deflating the left lung reduces retraction trauma to the lung, improves exposure, and alleviates the risk of cardiac compression. When motor evoked potentials are used for spinal cord monitoring, muscle paralytics must be avoided. Sodium bicarbonate solution is routinely infused to prevent acidosis during aortic cross-clamping, and mannitol can be given before cross-clamping to enhance renal perfusion. Proximal blood pressure, afterload, and cardiac performance are closely monitored by Swan-Ganz catheter and transesophageal echocardiography probe when necessary and are aggressively maintained.

Surgical Adjuncts for Organ Protection

Organ ischemia is a major source of the morbidity related to DTAA and TAAA repair. We currently employ a multimodal approach (Table 53-1) in an attempt to maximize organ protection during these operations (Fig. 53-7).57 The rationale for and details of several important strategies are discussed in the following sections.

Heparin

Potential benefits of heparinization include preserving the microcirculation and preventing embolization. Additionally, by inhibiting the clotting cascade, the use of heparin may help to reduce the incidence of disseminated intravascular coagulation.

Heparin (1 mg/kg) is administered intravenously before aortic clamping or the start of left heart bypass (LHB). After this small heparin dose is administered, the activated clotting time generally ranges from 220 to 270 seconds.

Hypothermia

Hypothermia decreases the metabolic demand of tissues and is protective during ischemic states. The protective effects of hypothermia on the spinal cord are well accepted.58,59 Mechanisms of spinal protection may involve membrane stabilization and reduced release of excitatory neurotransmitters.60,61 We routinely use mild passive systemic hypothermia during DTAA and TAAA repairs. The patient's temperature is allowed to drift down to a nasopharyngeal temperature of 32 to 33°C. After the aortic repair, rewarming can be accomplished by irrigating the thoracic and abdominal cavities with warm saline.

Profound systemic hypothermia on full cardiopulmonary bypass is an operative strategy for organ protection. Kouchoukos and colleagues62–64 have published several reports showing that hypothermic cardiopulmonary bypass with circulatory arrest can safely and substantially protect against paralysis and renal, cardiac, and visceral organ system failure during operations on the thoracic and thoracoabdominal aorta. Despite these protective effects, many clinicians avoid using this approach, principally because of the associated risks of coagulopathy, pulmonary dysfunction, and massive fluid shift. We use hypothermic circulatory arrest selectively when the aneurysm anatomy precludes safe proximal clamping.

Left Heart Bypass

Disruption of blood flow to the spinal cord and abdominal viscera contributes significantly to the development of ischemic complications. Conversely, maintaining flow through spinal and visceral arteries during all or part of the anatomic repair should reduce the duration of organ ischemia and prevent associated morbidity.65 Borst et al.66 found that using LHB for distal perfusion during DTAA and TAAA repair effectively unloads the proximal circulation during aortic occlusion and maintains adequate perfusion of distal vital organs, thereby reducing early mortality and renal failure. Further, combined distal perfusion and aggressive reattachment of distal intercostal arteries decreased the risk of spinal cord damage.

Typically used during the proximal aortic anastomosis, LHB is achieved by establishing a temporary bypass from the left atrium to either the femoral artery (most commonly the left) or the distal descending thoracic aorta with a closed-circuit in-line centrifugal pump (Fig. 53-7B). The left atrial cannula is placed via an opening in the inferior pulmonary vein (see Fig. 53-7B). When we first began using LHB, cannulation of the distal descending thoracic aorta (usually at the level of the diaphragm) was used solely as an alternative to femoral artery cannulation in patients with femoral or iliac artery occlusive disease. However, because this technique causes few complications and eliminates the need for femoral artery exposure and repair, distal aortic cannulation has become our preferred approach. Careful examination of CT or MR images assists selection of an appropriate site for direct aortic cannulation. Areas with intraluminal thrombus (see Fig. 53-4) are avoided because cannulation could lead to distal embolization. Bypass flows are adjusted to maintain normal proximal arterial and venous filling pressures. Flows between 1500 and 2500 mL/min are generally used. Left heart bypass facilitates rapid adjustment of proximal arterial pressure and cardiac preload, thereby reducing the need for pharmacologic intervention. Because LHB effectively unloads the left ventricle, it is useful in patients with suboptimal cardiac reserve.

Spinal Cord Protection

Paraplegia remains an index complication specific to distal aortic surgery. Historically, paraplegia rates have been as high as 30% for extensive aortic replacements. With modern operative techniques and spinal adjuncts, paraplegia rates in aortic centers are currently 2 to 5%.67–69 Because multiple adjuncts are used in combination, it is difficult to attribute the improvements in outcome to one technique.

Spinal Cord Monitoring

Somatosensory evoked potential (SSEP) and motor evoked potential (MEP) monitoring have been used for intraoperative assessment of spinal cord function. Motor evoked potential monitoring involves electrical excitation of the motor cortex or motor neurons and measuring the amplitude of the resulting motor response in the peripheral muscles of the arms and legs. Monitoring MEPs allows real-time assessment of spinal cord motor function and was approved for this use during surgical TAAA repair by the FDA in 2003. Because the motor function of the anterior horn of the spinal cord is more susceptible than the posterior horn to ischemia and infarction, MEP changes are a sensitive indicator of spinal cord ischemia and are predictive of adverse neurologic events.70–72 In contrast, SSEP monitoring is less sensitive because the sensory pathways on the dorsal horn are more resistant to injury and are sometimes spared when ischemic injury occurs. Irreversible loss of either MEPs or SSEPs is highly predictive of immediate neurologic deficit on recovery.73 Monitoring MEPs precludes the use of neuromuscular paralytic agents.

Significant attenuation or loss of MEPs can occur within 2 minutes of acute spinal cord ischemia, and infarction can occur within 10 minutes at normothermia.74 Several studies have examined the use of MEP monitoring to guide spinal perfusion–enhancing measures (eg, reattaching more segmental arteries, increasing distal and proximal perfusion pressures, and enhancing cerebrospinal fluid [CSF] drainage) to improve the outcomes of TAAA and DTAA repair. For example, Jacobs et al.75 published excellent results in a series of 184 patients who underwent TAAA repair with a protocol that included LHB, CSF drainage, and MEP monitoring. The authors found that MEP was a sensitive technique for assessing spinal cord ischemia and identifying the segmental arteries that critically contribute to spinal cord perfusion. With this protocol, the incidence of neurologic deficit after TAAA repair was 2.7%. Other series of TAAA and DTAA repairs have found similarly low rates of postoperative paraplegia and paraparesis when MEP is used in this fashion.72,76 Our current practice is to monitor MEP in all extent II TAAA repairs and selectively in any other high-risk aortic repairs in which prolonged cross-clamping is anticipated, such as reoperative repairs and those involving difficult anatomy.

Cerebrospinal Fluid Drainage

The drainage of CSF in the context of aortic surgery for spinal cord protection was tested in animal models in the early 1960s.77 The rationale for CSF drainage was that it would enhance spinal perfusion by decreasing the pressure on the cord during aortic cross-clamping. Today, the practice is well accepted in TAAA repair, although the exact mechanisms of this adjunct's benefits remain controversial.78–82 In our study of 145 patients who underwent extent I or II TAAA repair, patients were randomly assigned to receive CSF drainage or no CSF drainage. Postoperatively, paraplegia or paraparesis developed in nine patients (13%) in the control group but in only two patients (2.6%) in the CSF drainage group (p = .03).83 Additionally, a meta-analysis of eight studies (three randomized controlled trials and five cohort studies) of CSF drainage in TAAA repair found that CSF drainage substantially reduced the incidence of postoperative neurologic impairment (p < .0001).84 Although the safety of CSF drainage has been shown clinically,85 known risks include intra-cranial bleeding, perispinal hematoma, meningitis, and spinal headaches.

We routinely use CSF drainage in patients undergoing Crawford extent I or II TAAA repairs because of the higher risks of paraplegia in these extensive TAAA repairs. We selectively use CSF drainage during less extensive repairs, such as DTAA or extent III or IV TAAA repairs, depending on the individual risk factors involved; for example, we would use CSF drainage in a redo aortic operation in which the spinal collateral is compromised and a long cross-clamp time is anticipated because of the complex configuration of the aneurysm. The intrathecal catheter is placed through the second or third lumbar space preoperatively after induction of anesthesia and is maintained 2 to 3 days postoperatively in the intensive care unit. The catheter allows both monitoring of the CSF pressure and therapeutic drainage of the fluid. The CSF is allowed to drain passively from the catheter and can be aspirated with a closed collection system as needed to keep the CSF pressure between 8 and 10 mm Hg during the operation and between 10 and 12 mm Hg during the early postoperative period. Once the patients are awake and neurologic exams confirm that they are able to move their legs, the CSF pressures are allowed to rise to a higher range of 15 to 18 mm Hg. To prevent intracranial hemorrhage, we avoid draining more than 25 mL per hour.

Regional Spinal Hypothermia

Regional spinal cord hypothermia can be accomplished by direct infusion of cold perfusate into the epidural or intrathecal space and intravascular cold perfusion of isolated thoracic aortic segments (with the expectation that the intercostal vessels will deliver the cold perfusate to the spinal cord). Epidural cooling for regional spinal cord hypothermia is effective in preventing paraplegia after aortic cross-clamping in canine and leporine models.86–89 Additionally, a series of 337 TAAA repairs reported by Cambria and colleagues90 showed that, in patients who underwent extent I, II, or III TAAA repairs, the incidence of spinal cord ischemic injury was reduced from 19.8 to 10.6% after the introduction of epidural cooling at their institution in 1993. A similar technique, cold perfusion into isolated aortic segments, has been tested in animal models to show that cord temperature and, consequently, the extent of ischemic spinal cord injury can be effectively reduced by this method.91

Left Heart Bypass for Spinal Protection

Left heart bypass appears to provide the greatest benefit to patients who undergo the more extensive repairs. Our own retrospective review of 1250 consecutive extent I or extent II TAAA repairs found that using LHB (in 666 cases) reduced the incidence of spinal cord deficits only in patients who underwent extent II repairs.92 In patients who underwent extent I repairs, the incidence of paraplegia was similar in the LHB and no-LHB groups, even though the LHB group had significantly longer aortic clamp times. This finding suggests that, by providing spinal cord protection, LHB gives the surgeon more time to create secure anastomoses. A propensity-score analysis of 387 of our patients who underwent DTAA repair with (n = 46) or without (n = 341) LHB during the construction of the proximal anastomosis found no effect of LHB on postoperative paraplegia and paraparesis rates.93 Data from series in which LHB and CSF drainage were used together suggest that combining these adjuncts may further reduce rates of spinal cord injury.94,95 Because patients who undergo extensive TAAA repairs (extents I and II) are at greatest risk of postoperative paraplegia or paraparesis, we routinely use LHB to provide distal aortic perfusion during the proximal portion of the aortic repair.

Segmental Artery Reattachment and Sequential Graft Clamping

Because of the often tenuous nature of the blood supply to the spinal cord, we take an aggressive approach to reattaching patent segmental arteries. Intimal atherosclerosis, particularly in medial degenerative fusiform aneurysms, obliterates many intercostal and lumbar arteries and complicates matters anatomically. Patent segmental arteries from T7 to L2 are selectively reattached as patches to one or more openings made in the graft (Fig. 53-7G). Large arteries with little or no back-bleeding are considered particularly important. When none of these arteries is patent, endarterectomy of the aortic wall and removal of calcified intimal disease can be considered as a means of identifying arteries suitable for reattachment. After intercostal arteries are reattached, the proximal clamp is often moved down the graft to restore intercostal perfusion. Sequential clamping restores perfusion to the proximal branch vessels and will decrease the ischemic time to the spinal cord. However, this benefit must be weighed against the additional time needed to control the potential bleeding from the proximal aortic anastomosis, the intercostal patch, and the collateral intercostal and lumbar branches that often results when the clamp is moved below the intercostal patch.

Postoperative Management

Postoperative management remains critical to spinal cord protection. Adequate blood pressure, preload, and cardiac inotropic state are carefully maintained to keep spinal perfusion sufficient. In the absence of postoperative bleeding, blood pressure should be kept near its preoperative baseline level. Delayed paraplegia can arise hours to days after aortic surgery.67 In the immediate postoperative period, strategies to reverse paraplegia and paraparesis include inducing systemic hypertension; placing a CSF drain, if one is not already present; decreasing CSF pressure; administering cardiac inotropes, mannitol, or steroids; correcting anemia; and preventing fever. Recovery from paraplegia is possible, but if cord function does not return promptly after these measures are taken, such a recovery is not likely.

Postoperative renal failure after DTAA and TAAA remains an important complication and is predictive of mortality.96 Distal aortic perfusion with LHB provides renal perfusion during proximal anastomosis. Once the renal vessels are exposed during distal repair, the renal arteries can be directly perfused with cold (4°C) crystalloid (Fig. 53-7G). Our current technique is to infuse 400 to 600 mL of cold lactated Ringer's (LR) solution every 6 to 10 minutes. We have previously reported on a group of patients who underwent Crawford extent II TAAA repair with LHB and who were randomly assigned to receive either renal artery perfusion of cold LR solution for renal cooling or to isothermic blood perfusion from the LHB circuit.97 Multivariate analysis confirmed that cold crystalloid perfusion was independently protective against acute renal dysfunction. Other groups continue to selectively perfuse the renal arteries with blood from the LHB circuit.

Visceral Protection

Similarly, distal aortic perfusion by LHB provides flow to the mesenteric branches during the initial portion of a TAAA repair. Once the visceral origins are exposed, selective visceral perfusion can be delivered through separate balloon perfusion catheters that are placed within the origins of the celiac and superior mesenteric arteries; these catheters are attached to the LHB circuit via a Y-line from the arterial perfusion line (Fig. 53-7B). This system provides oxygenated blood to the abdominal viscera while the intercostal and visceral branches are being reattached to the graft (Figs. 53-7G,H). Reducing hepatic ischemia in this fashion may decrease the risk of postoperative coagulopathy, and reducing bowel ischemia may decrease the risk of bacterial translocation.

Operative Techniques

Incisions and Aortic Exposure

Aneurysms limited to the descending thoracic aorta are approached through a full posterolateral thoracotomy (Fig. 53-8A). In most cases, the left pleural space is entered through the sixth intercostal space; however, if the aneurysm predominantly involves the upper portion of the descending thoracic aorta, the fifth intercostal space provides better access to the distal aortic arch. Exposure of the distal descending thoracic aorta is enhanced by dividing the costal margin without dividing the diaphragm.

The full thoracoabdominal incision extends from the left posterior chest (between the scapula and the spine), crosses the costal margin, and traverses obliquely to the umbilicus. The length and level vary according to the anatomy of the aneurysm. The incision is gently curved as it crosses the costal margin to reduce the risk of tissue necrosis at the apex of the lower portion of the musculoskeletal tissue flap (Fig. 53-9A). Stabilized on a bean bag, the patient is placed in a modified right lateral decubitus position with the shoulders placed at 60 to 80 degrees and the hips rotated to 30 to 40 degrees from horizontal. In extent I and II repairs, which require access to the left subclavian artery and distal arch in the upper chest, our standard approach is through the sixth intercostal space. The upper or lower ribs may be divided posteriorly to achieve additional proximal or distal exposure, respectively, as needed. For extent III aneurysm repairs, entering through the seventh or eighth intercostal space will allow adequate access. Extent IV aneurysms are approached via a straight oblique incision through the ninth or tenth interspace (Fig. 53-9B). Ending the incision distally at the level of the umbilicus will allow access to the aortic bifurcation. The incision can be extended toward the pubis if iliac aneurysms also require repair.

For thoracoabdominal access, the diaphragm is divided partially or completely in a circular fashion to protect the phrenic nerve and preserve as much diaphragm as possible. The crus of the diaphragm is divided at the hiatus, and a 3- to 4-cm rim of diaphragmatic tissue is left posterolaterally on the chest wall to facilitate closure when the operation is complete. Below the diaphragm, the retroperitoneum is entered lateral to the left colon, and medial visceral rotation is performed to expose the aorta. A dissection plane is developed anterior to the psoas muscle, and the left kidney, left colon, spleen, and left ureter are retracted anteriorly and to the right. The abdominal aortic segment is approached transperitoneally; opening the peritoneum permits direct inspection of the abdominal viscera and its blood supply after aortic reconstruction is completed. An entirely retroperitoneal approach can be used in patients with a “hostile abdomen,” ie, patients with multiple prior abdominal operations or a history of extensive adhesions, peritonitis, or both.

The left renal artery is identified but generally does not require mobilization. The aorta is approached laterally to avoid injury to the mesenteric vessels and the abdominal organs. Commonly, a large lumbar branch of the left renal vein courses posteriorly around the aorta. This branch may be ligated and divided as needed. An anomalous retroaortic left renal vein is occasionally encountered and should be preserved. If the retroaortic renal vein or its tributaries require division for exposure, direct reanastomosis or interposition grafting to the inferior vena cava can be performed if the left kidney appears congested and shows distended collaterals.

Proximal Anastomosis

For DTAA and extent I and II TAAA repairs, options for establishing proximal control include applying a proximal aortic clamp distal to the left subclavian artery; applying an aortic clamp between the left subclavian and the left carotid artery and applying a separate bulldog clamp to the left subclavian artery; applying an aortic clamp to an existing graft during an elephant trunk operation; or open anastomosis under hypothermic circulatory arrest with full cardiopulmonary bypass when an aortic clamp cannot be safely applied. The decision is based on the anatomy of the aneurysm. We use aortic clamping distal to the left subclavian artery whenever possible, although others have advocated using circulatory arrest routinely.98

In aneurysms suitable for aortic clamping, the distal aortic arch is gently mobilized by dividing the remnant of the ductus arteriosus. The vagus and recurrent laryngeal nerves are identified (see Fig. 53-7C). The vagus nerve may be divided below the recurrent nerve to provide additional mobility, thereby protecting the recurrent nerve from injury. Preserving the recurrent laryngeal nerve is particularly important in patients with chronic obstructive pulmonary disease and reduced pulmonary function. If the aneurysm encroaches on the left subclavian artery, clamping proximal to the left subclavian artery should be anticipated; the left subclavian artery is then circumferentially mobilized to enable placement of a bulldog clamp.

After heparin is administered, the proximal clamp is applied to the proximal descending thoracic aorta or the distal transverse aortic arch between the left common carotid and left subclavian arteries (see Figs. 53-7B and 53-8A). When LHB is used, it is initiated at a flow rate of 500 mL/min just before the proximal aorta is clamped. After the proximal clamp is applied, LHB flow is increased to 2 L/min and a second distal aortic clamp is placed between T4 and T7 (Fig. 53-8C). After the aorta is opened, patent upper intercostal arteries are oversewn (Fig. 53-7D). In cases of chronic dissection, the partition between the true and false lumens is completely removed. The aorta is transected 2 to 3 cm beyond the proximal clamp and is separated from the esophagus to allow the surgeon to place full-thickness sutures in the aortic wall without injuring the esophagus. A 22- or 24-mm, gelatin-impregnated woven Dacron graft is used in most patients. The proximal anastomosis is performed with continuous polypropylene suture (Fig. 53-7E). Most anastomoses are made with 3-0 polypropylene suture; however, in patients with particularly fragile aortic tissues, such as patients with acute aortic dissection or Marfan syndrome, 4-0 polypropylene sutures are commonly used. Felt strips are generally not used; instead, intermittent polypropylene mattress sutures with felt pledgets are used to reinforce selected portions of the anastomoses. The use of surgical adhesives is avoided in these operations.

Open Anastomosis under Hypothermic Circulatory Arrest

In repairs of large aneurysms at the distal arch or aneurysms with contained rupture, or in redo operations in which safe dissection and clamping are not possible, an alternative strategy is total cardiopulmonary bypass with hypothermic circulatory arrest. Arterial inflow is established by placing a cannula in the distal aorta or the femoral artery. Venous drainage is usually established by inserting a long percutaneous cannula into the femoral vein and advancing it into the right atrium with transesophageal echocardiographic guidance. The left atrium or left ventricle can be vented via a right-angled sump cannula placed in the left pulmonary vein to prevent cardiac distension. Total cardiopulmonary bypass is initiated, and the patient is cooled to electrocerebral silence. Circulatory arrest is initiated, and the aneurysm is opened. Direct antegrade cerebral perfusion into the left carotid artery can be accomplished via a separate balloon catheter arising from the arterial limb of the circuit. An open proximal anastomosis is performed. After this anastomosis is completed, a Y-limb from the arterial line is connected to a side-branch of the graft. The graft is deaired and clamped, pump flow to the upper body is resumed, and the remainder of the aortic repair is performed.

Elephant Trunk Repairs

A staged operative procedure is preferred in patients who present with extensive aneurysmal disease involving the ascending aorta, aortic arch, and descending thoracic or thoracoabdominal aorta (Fig. 53-10A). When the DTAA or TAAA is not causing symptoms and is not substantially larger than the ascending aorta, the proximal aortic repair is performed first. This allows treatment of valvular and coronary artery occlusive disease during the first operation.

Our current preference for reconstruction of the innominate, left carotid, and left subclavian artery is separate end-to-end anastomoses with a branched trifurcated graft (Fig. 53-10B). The bypass to the left subclavian artery during the first stage is not critical, and the left subclavian artery origin can remain intact on the native aorta. The aorta itself can be replaced with a skirted elephant trunk graft, which facilitates the distal aortic anastomosis to aneurysmal tissue. The proximal aortic anastomosis is placed to the supravalvar ascending aorta, and the distal skirt anastomosis can be placed fairly anteriorly on the aortic arch at the level of the innominate artery, facilitating hemostasis. The proximal end of the trifurcated graft is then anastomosed to an opening in the mid-ascending aspect of the aortic graft. The distal aortic anastomosis later becomes unimportant when the distal elephant trunk anastomosis to the descending aorta is completed at the second stage (Fig. 53-10C-E). The presence of the graft elephant trunk within the descending aorta allows secure clamping of even very large aneurysms distal to the left subclavian artery. If this artery was not bypassed during the arch vessel reconstruction, a side branch from the descending aorta can be anastomosed to the subclavian artery from the left chest during the second stage.99

Reversed Elephant Trunk Repairs

Conversely, in patients with similarly extensive aneurysmal disease who present with a DTAA or TAAA that has ruptured, causes symptoms (eg, back pain), or is considerably larger than the ascending aorta, the DTAA or TAAA is treated during the initial operation, and the ascending aorta and transverse aortic arch are repaired in a second procedure. During this “reversed” elephant-trunk repair (Fig. 53-11), a portion of the proximal end of the aortic graft is inverted down into the lumen during the first operation and is later used to facilitate second-stage repair of the ascending and transverse aortic arch.100

Intercostal Patch Anastomosis and Completion of the DTAA Repair

After the proximal anastomosis is completed, LHB is discontinued and the distal aortic clamp is removed. The remainder of the aneurysm is opened longitudinally to its distal extent (Fig. 53-7F). The blood in the open aorta is scavenged via cell saver and returned as whole blood by a rapid infuser system. If the aneurysm was clamped proximal to the left subclavian artery, the aortic clamp is moved down onto the graft and the left subclavian artery clamp is removed; this restores blood flow to the left vertebral artery and to spinal collaterals. For repairs that extend to the diaphragm or beyond, patent lower intercostal arteries are selected and reattached to an opening cut in the side of the graft (Fig. 53-7G). If the aortic tissue is particularly friable, a separate, 8-mm graft can be attached in an end-to-end fashion to the selected intercostal vessels. In DTAA repairs, the distal anastomosis is then performed (Fig. 53-8B) to the open distal aorta. For aneurysms arising from chronic dissections, the membrane between the true and false lumen is fenestrated distally to ensure that both lumens are perfused.

Visceral Branch Vessel Anastomoses

In patients with TAAAs, after the descending thoracic aortic repair is completed, the remainder of the aneurysm is opened longitudinally (Fig. 53-7F). This incision runs posterior to the origin of the left renal artery and continues to the distal extent of the aneurysm. When present, the remaining dissecting membrane is excised. The origins of the visceral and renal branches are identified. Cold crystalloid is intermittently delivered to the renal arteries via balloon catheters (Fig. 53-7G). In patients receiving LHB, balloon cannulas are also placed in the celiac and superior mesenteric arteries so that selective visceral perfusion can be delivered from the pump circuit. Subsequently, the celiac, superior mesenteric, and renal arteries are reattached. In extent I repairs, the reattachment of the visceral arteries is often incorporated into a beveled distal anastomosis (Fig. 53-11C), but in extent II and III repairs, the visceral artery origins are reattached to one or more oval openings in the graft (Fig. 53-7H). In 30 to 40% of patients, the origin of the left renal artery is displaced laterally and is best attached to a separate opening in the graft (Fig. 53-7I). Patients with genetic disorders such as Marfan or Loeys-Dietz syndrome are prone to aneurysms involving their visceral reattachment patch; a multibranched graft enables separate bypasses to each of the vessels, thereby minimizing the amount of remaining aortic tissue and reducing the risk of recurrent aneurysms. Multibranched grafts are also useful in patients with large aneurysms that have caused wide displacement of the celiac, superior mesenteric, and renal arterial ostia (Fig. 53-12). Visceral artery stenosis is encountered in at least 25% of patients and necessitates endarterectomy (if anatomically suitable), stenting, or interposition bypass grafting.54,101

Distal Aortic and Iliac Anastomoses

When the TAAA extends below the renal arteries, a distal anastomosis is performed near the aortic bifurcation (Fig. 53-7J). In patients with iliac artery aneurysms, a bifurcation graft is sewn onto the end of the straight graft; the graft's limbs are then anastomosed to the common iliac, external iliac, or common femoral artery, depending on the extent of disease. The right limb of the bifurcation graft is tunneled retroperitoneally into the pelvis near the right iliac artery. Exposure of the left iliac artery is more straightforward from the left retroperitoneal incision. Care is taken to preserve circulation to at least one of the internal iliac arteries.

Closure

After all clamps are removed, heparin is reversed with protamine sulfate. Hemostasis is achieved by surgically reinforcing the anastomoses and administering blood products as necessary. The renal, visceral, and peripheral circulations are assessed. To ensure that renal function is adequate, blue dye is administered intravenously, and transit time to urine output is measured. The bowel, spleen, and liver are all assessed for adequacy of perfusion. The spleen is examined for capsular injury; if a splenic hematoma is present, the spleen is removed to avoid postoperative bleeding and hypotension. The aneurysm wall is then loosely wrapped around the aortic graft. Two posteriorly located thoracic drainage tubes and a closed-suction retroperitoneal drain are placed before closure. The diaphragm is closed with continuous polypropylene suture; postoperative disruption of the diaphragmatic repair is exceedingly rare.

Since 1986, we have performed open surgical repair of 3159 DTAAs and TAAAs. Combined hospital and 30-day operative mortality was 5.6% (n = 178). Complications that are commonly associated with an increased risk of death include paraplegia, renal failure, respiratory failure, cardiac events, and bleeding. The incidence of paraplegia and paraparesis in our series was 4.4% (n = 107), and the incidence of renal failure necessitating hemodialysis was 5.7% (n = 181). Our most recent data (from 2006 to 2009), which reflect the results of our current organ-protection strategies, are shown in Table 53-2.

The rate of return to the operating room for bleeding has been 2.5% in our experience. Postoperative blood pressure management is critical and must be balanced between hypertension (which can cause bleeding) and hypotension (which can lead to paraplegia/paraparesis). Because aortic anastomoses are often extremely fragile during the early postoperative period, even brief episodes of hypertension may disrupt suture lines and cause severe bleeding or pseudoaneurysm formation. In most cases, we use nitroprusside, intravenous β-antagonists, and intravenous calcium-channel blockers to keep the mean arterial blood pressure between 80 and 90 mm Hg. In patients with severely friable aortic tissue, such as those with Marfan syndrome, we use a target range of 70 to 80 mm Hg.

Vocal cord paralysis can contribute to respiratory complications; it should be suspected in patients with postoperative hoarseness and confirmed by direct examination. This complication can be treated effectively by direct cord medialization (ie, type 1 thyroplasty) or, in higher-risk patients, by polytetrafluoroethylene injection.102

Patients who have undergone DTAA or TAAA repair remain at risk for developing new aneurysms in other aortic segments or in reattachment patches. Progressive weakening of aortic tissue at suture lines can lead to pseudoaneurysm formation. To detect new aortic disease before life-threatening complications occur, we recommend that all patients undergo annual CT or MR imaging of the chest and abdomen. This strategy of lifelong surveillance is especially important in patients with genetic disorders.8,9 Subsequent aortic repairs can be performed with surprisingly low mortality and morbidity risk, particularly when done electively.103

The authors thank Scott A. Weldon and Carol P. Larson for their outstanding medical illustrations and Stephen N. Palmer and Susan Y. Green for invaluable editorial support.