Chapter 134
Thoracic and Thoracoabdominal Aortic Aneurysms
Evaluation and Decision Making
Gilbert R. Upchurch Jr.,
Aortic diseases, including aortic aneurysms, are the 12th leading cause of death in the United States.1 Although abdominal aortic aneurysms (AAAs) and ascending aortic aneurysms are more common, descending thoracic aortic aneurysms (TAAs) and thoracoabdominal aortic aneurysms (TAAAs) are not rare, with an estimated incidence of 5.9 cases per 100,000 person-years.2 A study by Clouse and associates suggested that this incidence is increasing and is closer to 10.4 cases per 100,000.3 TAA repair is associated with a high morbidity and mortality. Even though TAAs, including those of the ascending aorta, aortic arch, and descending aorta, course anatomically from the ascending aorta to the diaphragm, the focus of this chapter is on descending TAAs and TAAAs. TAAAs, which can occur from the left subclavian artery to the aortic bifurcation, are defined by anatomic criteria.
Thoracic aortic disease is complex and induced by a myriad of histopathologic processes. Most TAAs and TAAAs are secondary to either medial degeneration or aortic dissection. Medial degeneration is characterized by disruption and loss of elastic fibers and increased deposition of proteoglycans. Many other thoracic aortic diseases, including acute aortic syndromes (aortic dissection, intramural hematoma, and penetrating aortic ulcers) and various forms of vasculitis (giant cell arteritis, Takayasu’s arteritis, and Behçet’s disease), can induce TAAAs. Whereas isolated AAAs were once called atherosclerotic, TAAs associated with frank atherosclerosis are much rarer. Other histopathologic processes associated with thoracic aortic disease include coarctations, various brachiocephalic anomalies (i.e., aberrant right subclavian arteries), and tumors. Disastrous complications of thoracic aortic disease also include pulmonary and enteric fistulae.
This chapter is intended to provide an overview of thoracic aortic disease to help the caregiver of patients with these pathologic conditions in decision making. Guidelines for the diagnosis and management of patients with thoracic aortic disease have recently been published4; contemporary reviews on the management of thoracic and thoracoabdominal aortic aneurysms are also available.5–7
Thoracic Aorta: Anatomy and Epidemiology of Thoracic and Thoracoabdominal Aortic Aneurysms
Whereas the techniques of open and endovascular TAAA repair are discussed in more detail in Chapters 135 and 136, it is important to provide a description of the normal anatomy as well as of the many and varied pathologic changes that are associated with TAAs (Fig. 134-1).
Figure 134-1 A, Multiple CT scan levels documenting a ruptured thoracoabdominal aortic aneurysm (TAAA). The single arrow denotes dissection associated with the rupture. The double arrow points to a right-sided pleural effusion. B, A repeated CT scan 8 months after placement of a thoracic endograft shows resolution of the effusion and exclusion of the TAAA. The arrow denotes a stent-graft.
Definition
TAAAs are localized dilatations in the thoracic and abdominal aorta secondary to weakening and subsequent expansion of the aortic wall. A TAAA by definition is a dilatation at least 1.5 times its normal value.8 When all aneurysms of the thoracic aorta are considered, those of the ascending aorta are the most common (40%). Aneurysms of the descending thoracic aorta account for 35% of TAAs, whereas aortic arch aneurysms (15%) and TAAAs (10%) account for a smaller percentage (Table 134-1).2,9 Defining these anatomic aortic sizes is critical to help identify pathologic aortic growth because TAAA diameter is the strongest predictor of rupture, with a reported mean aortic diameter of ruptured TAAAs of 6.1 cm.10
Normal and Pathologic Aortic Size
The normal thoracic aorta is divided into four parts: the aortic root, the ascending aorta, the aortic arch, and the descending thoracic aorta.4 The normal thoracic aortic wall is composed of three layers, similar to all blood vessels, which include the intima, media, and adventitia. The aorta normally enlarges as it progresses from the aortic root to the terminal aorta.9 In addition, gender, age, and body surface area influence aortic diameter (Table 134-2). Even after adjustment for age and body surface area, mean aortic size is significantly smaller, usually 2 to 3 mm, in women than in men.11–14 Body surface area is reported to be a better predictor of aortic diameter than height or weight.14 Normal and pathologic growth rates are also important. A mean increase in TAAA cross-sectional diameter of 0.4 cm/y has been reported.10 Importantly, the growth rates of TAAAs are not predictable or linear. However, there is consensus that TAAAs, similar to AAAs, have growth rates that accelerate as they enlarge.15 For example, TAAAs larger than 5 cm expand at a growth rate of 0.79 cm/y, whereas TAAAs less than 5 cm experience growth rates of 0.17 cm/y.10 Dapunt and associates documented that patients with ruptured TAAAs experienced growth rates of 0.7 cm/y.10
Table 134-2
Normal Adult Thoracic Aortic Diameters by Gender4
| Thoracic Aorta | Range of Reported Mean (cm) | Assessment |
| Mid-descending, female | 2.45-2.64 | CT |
| Mid-descending, male | 2.39-2.98 | CT |
| Diaphragmatic, female | 2.40-2.44 | CT |
| Diaphragmatic, male | 2.43-2.68 | CT |
CT, Computed tomography.
The terms saccular and fusiform should also be defined for TAAAs because the morphology of an aneurysm will often dictate treatment options as well as indicate specific causes (i.e., mycotic aneurysms are often saccular and at high risk of rupture).16 Most TAAAs are fusiform, a chronic uniform dilatation involving the whole circumference of the aorta. In contrast, saccular aneurysms often represent an eccentric dilatation of the aorta (Fig. 134-2). The size at which eccentric saccular aneurysms are repaired has not been well studied; however, most would concur that a lower threshold is an acceptable indication for repair.
Population Affected
TAAAs are primarily a disease of the elderly. The average age of patients with TAAAs is 65 years, with a male-to-female ratio of 1.7 : 1.2 In contrast, in patients with AAAs whose mean age is 75 years, the male-to-female ratio is 6 : 1.17 TAAAs clearly have a genetic component in that more than 20% of patients will have a first-degree relative affected by aneurysm disease.18–20
Risk Factors for Disease and Rupture
Many risk factors common in patients with AAAs, including hypertension, smoking, and atherosclerosis in other arteries, are also common in patients with TAAAs.2,21–23 Although TAAAs are most often described as degenerative, in up to 20% of patients they are the sequelae of chronic aortic dissection,24 wherein aneurysm dilatation of the outer wall of the false lumen necessitates late aortic repair in up to 40% of patients irrespective of initial medical or surgical treatment of the dissection. Systemic hypertension (in particular, elevated diastolic blood pressure higher than 100 mm Hg) has been associated with aortic growth and rupture.10,25
Multiple genetic syndromes, in addition to the standard connective tissue syndromes such as Marfan’s syndrome, have been associated with TAAs and dissections. Familial aggregation studies have shown that between 11% and 19% of patients referred for TAA or dissection repair have a first-degree relative with a TAA or dissection.21,26,27 Patients with a strong family history of TAA tend to present at a younger age than those without a positive history and yet at an older age than those with connective tissue disease. This disease appears to be inherited in an autosomal dominant fashion with variable expression.28 Mapping studies have shown that there is significant genetic heterogeneity in these patients with familial TAAs and dissection (TAAD). Causative genes have been identified for TAAD2 (due to TGFBR2 mutation), 16p (due to MYH11 mutation), and TAAD4 (due to ACTA2 mutation), suggesting that mutations to the basic aortic wall building blocks of actin and myosin are responsible for these syndromes.29–31 Further studies have suggested that rare copy number variants disrupt genes responsible for smooth muscle cell adhesion and contraction in patients with both sporadic and familial TAA disease.32 The genetics of TAAs and dissections is the subject of many contemporary reviews.33,34
Because most patients with TAAAs are asymptomatic, treatment is aimed at preventing rupture. Natural history studies of TAAAs are rarer than those of isolated infrarenal AAAs, probably related to their much less frequent occurrence. In addition, studies on TAAAs often include patients with both acute and chronic aortic dissection, which serves to complicate natural history data. Initial studies from the 1970s by Pressler and McNamara documented that approximately 40% of patients who did not undergo surgical repair died of TAAA rupture, whereas 32% died of other cardiovascular diseases. Mean survival was less than 3 years. During the extended period of observation, more than 90% of patients sustained aortic rupture, with 68% of ruptures occurring more than 1 month after the diagnosis.35,36 The 5-year survival rate for patients with 6.0-cm TAAAs is 54%, with a risk of rupture of 3.7%/y and a risk of death of 12%/y. Median survival in patients with untreated TAAAs is poor at only 3.3 years.37 In a natural history study of patients who were not candidates for surgery by Crawford et al, the survival rate was just 24% at 2 years, with more than half the deaths related to aneurysm rupture. Chronic obstructive pulmonary disease (COPD) was noted in 80% of the subgroup with rupture.38 Similar studies in patients with small infrarenal AAAs have confirmed COPD as a significant risk factor for rupture.39 Cambria and colleagues followed a series of 57 patients with TAAAs who were not considered operative candidates. In addition to COPD, the authors found an association (P = .06) between rupture and chronic renal failure.40 In a study by Griepp and colleagues, 165 patients with TAAAs were monitored after being assigned nonoperative status. Twenty percent of patients eventually suffered rupture. Important risk factors for rupture included older age, COPD, uncharacteristic continued pain, and aortic diameter. Patients with aortic dissection ruptured at smaller aortic diameters than did those with nondissected degenerative aneurysms.41
Aneurysm diameter is the most important risk factor for rupture. Dapunt and coworkers documented that TAAAs larger than 8 cm have an 80% risk of rupture within 1 year of diagnosis.10 However, the size at which TAAAs rupture is unpredictable. Similar to AAAs, it appears that aneurysm growth rates play a role. The average expansion rate of a TAAA is approximately 0.10 to 0.42 cm/y.37,42–44 Coady and associates suggested that expansion by more than 1 cm/y signals impending rupture.42 Juvonen and colleagues examined 114 patients with TAAAs in detail.45 Multivariate analysis suggested that increasing age, pain (even atypical), COPD, descending thoracic aortic diameter, and abdominal aortic diameter were predictive of rupture (Table 134-3).
Table 134-3
Risk Factors for Thoracoabdominal Aortic Aneurysm Rupture45
| Risk Factor | Relative Rate | P Value |
| Chronic obstructive pulmonary disease | 3.6* | .004 |
| Age | 2.6† | .02 |
| Pain | 2.3 | .04 |
| Descending aortic diameter | 1.9 | .003 |
| Abdominal aortic diameter | 1.50‡ | .05 |
* The relative rate increases by a factor of 1.9 for each centimeter of descending aortic diameter.
† The relative rate increases by a factor of 2.6 for each decade of age.
‡ The relative rate increases by a factor of 1.5 for each centimeter of abdominal aortic diameter.
Incidence and Prevalence
The incidence and prevalence of TAAAs have been increasing during the last several decades.2 Clouse and coauthors documented that the incidence of TAAAs in the United States is 10.4 cases per 100,000.3 Olsson examined the prevalence of TAAAs in a large contemporary population. All subjects with thoracic aortic dissections or aneurysms from 1987 to 2002 were identified in the Swedish National Healthcare Registry. Of 14,229 individuals with thoracic aortic disease, the diagnosis was made in 11,039 (78%) before death. The incidence of thoracic aortic disease rose by 52% in men and 28% in women to reach 16.3 and 9.1 per 100,000 per year, respectively. The authors concluded that the prevalence and incidence of thoracic aortic disease were higher than previously reported and increasing (Fig. 134-3).46 The increasing prevalence of TAAAs has been attributed to a number of factors, including improved imaging techniques, an aging population, and increased patient and physician awareness.47
Figure 134-3 Increasing incidence of thoracoabdominal aortic aneurysms and dissection in the Swedish population (men and women), 1987 to 2002 (cases per million). (From Olsson C, et al: Thoracic aortic aneurysm and dissection: increasing prevalence and improved outcomes reported in a nationwide population-based study of more than 14,000 cases from 1987 to 2002. Circulation 114:2611-2618, 2006.)
Pathogenesis
The development of a TAAA is a multifactorial event that involves a complex interaction of genetic factors, cellular imbalance, and altered hemodynamic factors.48 The increased incidence of TAAAs in patients with Marfan’s syndrome and other connective tissue disorders inherited in a mendelian manner as well as the familial inheritance of nonsyndromic TAADs typically inherited in an autosomal dominant fashion with marked variability in the age at onset and decreased penetrance suggests a varying genetic role along different segments of the aorta.28–31 More recent studies have suggested that genetic variation in extracellular matrix (ECM) actin and myosin may contribute to the development of TAAAs.49,50 Wang and coauthors examined genetic signatures in the peripheral blood of patients with TAAAs (n = 58) and control patients (n = 36). This study documented a number of gene families that were different between the two groups, including those involved in the cell cycle, DNA metabolism, glycolysis, interferon-γ signaling, and transcription. The authors concluded that analysis of peripheral blood to determine expression signatures may help identify patients with TAAAs with high accuracy.51
Formation of TAAAs, similar to that of other aneurysms, is therefore a complicated, dynamic process involving both extracellular and cellular processes (see Chapter 129). Once the process is initiated through a combination of the aforementioned factors, inflammation and pathologic remodeling of the ECM occur. A large body of evidence suggests that ECM degradation by matrix metalloproteinases (MMPs) exceeds matrix production and repair during aneurysm formation. Although the biomechanical properties and composition of the aorta, including the role of elastin and collagen in the arterial matrix, are discussed in Chapter 129, it is important to emphasize that there are significant differences in the composition of the aortic wall as one progresses from the ascending aorta to the iliac bifurcation. Andreotti and colleagues documented that the ascending aorta has a greater concentration of elastin and is therefore more compliant than the descending aorta. This alteration in elastin concentration leads to a progressive decrease in the elastin-collagen ratio as the aorta progresses from the ascending aorta to the abdominal aorta.52 The media also becomes thinner as one progresses from proximal to distal along the aorta.53
A number of studies have documented the overexpression and increased activity of various ECM proteinases, specifically the MMPs, in human TAAAs.54 These proteolytic enzymes, which have been more extensively studied in AAAs, are clearly critical as well during the formation of TAAAs. Sinha and coworkers documented asymmetrical production of MMP9 in the expanding human TAAA wall, which correlated with increased numbers of macrophages.55 In contrast, MMP2 was documented to be increased in the wall of the TAAA that was preserved, in particular, at the point where smooth muscle cells were more abundant and the wall was preserved. Ikonomidis and associates studied the role of MMPs in a murine model of TAAAs.54 These authors documented that MMP9 gene deletion attenuated TAA formation despite increases in MMP2 activity. They concluded that interactions between MMP9 and MMP2 are necessary to facilitate TAAA progression. Studies by Ikonomidis and others have documented altered membrane type 1 MMP and tissue inhibitor of MMP2 (TIMP2, an inhibitor of MMPs) in the murine TAA model.56
Aortic Wall Histology
The histology of TAAAs is most closely associated with medial degeneration, formerly known as cystic medial necrosis (Fig. 134-4). Medial degeneration is characterized by fragmentation and loss of elastic fibers; loss of smooth muscle cells; and collections of interstitial collagenous tissue, basophilic ground substance, and proteoglycans.57,58 Although medial degeneration is considered part of the normal aging process, it is accelerated by certain clinical conditions, such as hypertension and atherosclerosis.59 Given the relatively widespread process along the thoracic aorta, medial degeneration is most closely associated with the development of fusiform aneurysms. Genetic abnormalities, such as Marfan’s syndrome, also accelerate aortic medial degeneration.60 Although TAAAs were originally described as noninflammatory, studies have shown that infiltration of leukocytes contributes to the formation and development of TAAAs. The significant difference in the epidemiology and histology of TAAAs and AAAs suggests distinct causes.
Etiology
Eighty percent of TAAAs are secondary to medial degeneration; approximately 15% to 20% are caused by aortic dissection (Box 134-1) (see Chapter 138). TAAAs secondary to aortic dissection typically occur in younger patients and involve more extensive aortic segments than do degenerative aneurysms.61 The aorta in patients with Marfan’s syndrome is particularly prone to aortic dissection and subsequent TAAA formation.62 Both systemic autoimmune disorders, such as Takayasu’s arteritis, and chronic nonspecific aortitis can destroy the aortic media with progressive aneurysm formation. Aneurysms associated with arteritis are seen in women more commonly than degenerative aneurysms are. Aneurysms of the upper thoracic aorta can also be secondary to congenital aortic coarctations, either in unrepaired coarctations or after repair.63–65
TAAAs may also form secondary to infection. Although saccular aneurysms have been described as mycotic, these aneurysms are most often bacterial and occur because of hematogenous spread of emboli laden with bacteria. Infected TAAAs usually arise as a result of seeding of atherosclerotic plaque in the aorta, the development of a focal inflammatory process in the aortic wall, and ultimately the formation of a false aneurysm. Infected TAAAs present many challenging dilemmas. The goals of therapy are to debulk the infection and to restore arterial continuity. For years this has involved in situ repair with its attendant lifetime risk of reinfection. Recent reports of treatment of infected TAAAs with endovascular prostheses are beginning to accumulate.66,67
Anatomic Classification
Evaluation of a patient with a TAAA as well as the technical performance of either open or endovascular repair is closely aligned with the Crawford classification (Fig. 134-5).68–70 Classification of TAAAs also has important therapeutic implications for the operation to be performed as well as for the risk of specific complications. Type I TAAAs account for approximately 25% of all TAAAs; they involve the entire descending thoracic aorta and extend only to the upper abdominal aorta. Type II TAAAs (approximately 30% of TAAAs) involve the entire descending thoracic aorta and most or all of the abdominal aorta (Fig. 134-6A). Type III TAAAs (less than 25%) involve variable lengths of the descending thoracic aorta and extend into the abdominal aorta (Fig. 134-6B). Type IV TAAAs (<25%) are limited to most or all of the abdominal aorta, including the visceral and renal arteries.
Figure 134-5 Crawford classification of thoracoabdominal aortic aneurysms. Type I, distal to the left subclavian artery to above the renal arteries. Type II, distal to the left subclavian artery to below the renal arteries. Type III, from the sixth intercostal space to the renal arteries. Type IV, from the 13th intercostal space to the iliac bifurcation (entire abdominal aorta). Type V, below the sixth intercostal space to just above the renal arteries.
Clinical Findings
History and Physical Examination
Most patients with TAAAs have no symptoms attributable to their disease at the time of diagnosis.23,36,71 The diagnosis is therefore often made when the patient is being evaluated for unrelated conditions. Although most patients with TAAAs are often asymptomatic, most aneurysms will become symptomatic before they rupture.71 Panneton et al71 documented that 57% of patients with degenerative TAAAs will have symptoms before rupture. The recent American Heart Association guideline for thoracic aortic disease has issued recommendations regarding the history and physical examination for the general approach to the patient with suspected thoracic aortic disease4 (Box 134-2). The authors have suggested on the basis of class I, level C evidence that “the clinician should perform a focused physical examination, including a careful and complete search for arterial perfusion differentials in both upper and lower extremities, evidence of visceral ischemia, focal neurologic deficits, a murmur of aortic regurgitation, bruits, and findings compatible with possible cardiac tamponade.”72–74
The most common initial symptom in patients with TAAAs is vague pain, which can occur in the chest, back, flank, or abdomen. The differential diagnosis in a patient with a symptomatic TAAA therefore includes angina, aortic dissection, and degenerative disease of the spine. The chronic pain associated with TAAAs may easily be dismissed in patients with TAAAs before the diagnosis of a TAAA has been made. Typical of most aneurysms when they are enlarging, pain may increase in severity dramatically. Juvonen and coworkers suggested that the back pain associated with a TAAA can indeed be chronic and have a pattern and implication different from those noted with AAAs, in which the back pain is more often acute and suggests pending rupture.45 Symptoms may also occur in patients with TAAAs from compression of the thoracic aorta by structures in the thoracic cavity. Hoarseness can develop in patients with TAAAs as a result of stretching or compression of the left recurrent laryngeal nerve. Tracheal deviation, persistent cough, or other respiratory symptoms may also be present.35,75 Dysphagia is an uncommon, nonspecific complaint reported by patients with TAAAs that is due to compression of the aneurysm by the esophagus.76 Sudden and catastrophic hemoptysis or hematemesis may occur as a result of erosion of the TAAA into the bronchial and pulmonary space or the esophagus, respectively. Patients with TAAAs may rarely have neurologic deficits, including paraplegia. This is much more common in those with aortic dissection. Embolization to the visceral, renal, and lower extremity arteries has been reported.77 Patients with an abdominal component of their aneurysm may have gastrointestinal hemorrhage, aortoenteric fistulae, or a functional small bowel obstruction secondary to compression of the duodenum. Most patients with symptoms have TAAAs that have attained a diameter greater than 5 cm.
Patients with TAAAs generally have no obvious physical findings in the chest area unless tracheal deviation is present.78 Patients with an abdominal component of their TAAA may have a pulsatile abdominal mass similar to pure AAAs. No controlled or blinded study has been performed that reproducibly stratifies patients with TAAAs into groups predictive of poor outcomes.4 The critical issue is to identify those patients who are acutely ill from their thoracic aortic disease and to triage them accordingly.
Synchronous Aneurysm Risk
Studies examining the natural history of patients with TAAAs indicate that between 20% and 30% will also have an AAA.35,79 In a series of 1500 patients, Crawford et al documented that 13% harbored aneurysms in other segments.80 This appears to be true of patients who undergo TAAA repair as well, of whom as many as a third will have undergone previous aortic repair.81 Most commonly, patients with TAAAs have undergone previous infrarenal AAA repair. Patients with TAAAs are also at risk of discontinuous aneurysms or aneurysms proximal to their TAAA. Synchronous proximal ascending and arch aneurysms are noted in 6% to 13% of patients with TAAAs.71 Even after repair, at least 10% of patients with TAAAs will require subsequent aneurysm repair in noncontiguous aortic segments.82 Patients with Marfan’s syndrome who have suffered a type A dissection appear to be at high risk for this type of manifestation. As discussed in subsequent chapters, there is clearly an increasing trend in treating complex arch aneurysms and TAAAs with sequential open and endovascular therapies.83–85
Diagnostic Evaluation
Imaging
Accurate and precise determination of the anatomy of a patient with a TAAA is mandatory in determining both the need for and the details of operative repair as well as the prescribed follow-up in patients with TAAAs who have not reached a diameter threshold for repair. Recommendations for aortic imaging techniques to determine the presence of progression of thoracic aortic disease have been modified and are summarized in Box 134-3.
Patients with TAAAs frequently have significant coexisting medical conditions, including hypertension, coronary artery disease, COPD, congestive heart failure, cerebrovascular occlusive disease, and peripheral vascular occlusive disease. Cross-sectional imaging, mainly by computed tomography (CT), is the primary method to visualize the thoracic and abdominal aorta for determining aneurysm diameter and extent. Because most TAAAs are small when they are discovered, serial imaging is required; however, level A and B evidence regarding the timing of surveillance is lacking. Serial imaging is typically performed at 6- to 12-month intervals but varies by the initial diameter and extent of the aneurysm.
Chest Radiography
A chest radiograph (Fig. 134-7) or plain films of the abdomen in patients with TAAA may suggest an enlarged thoracic aorta secondary to a calcified aortic wall. Indirect findings suggestive of TAAA on chest radiography include a widened mediastinum, enlargement of the aortic knob, and tracheal deviation. Whereas chest films are part of the routine preoperative workup of every patient going for TAAA repair, they are inadequate to definitely exclude the presence or absence of thoracic aortic disease. A study of data pooled from 10 studies suggested that the predictive sensitivity of a widened mediastinum or an abnormal aortic contour associated with thoracic aortic disease is 64% and 71%, respectively.86 In contrast, a prospective study of more than 200 patients with thoracic aortic disease documented a specificity of 86% for chest radiography.87
Computed Tomography
Spiral CT scanning with three-dimensional reconstructions is now the “gold standard” for evaluating the aorta in patients with TAAAs as it helps diagnose the pathologic process as well as measure the aortic diameter. New-generation multidetector CT scans have been shown to have sensitivities and specificities of well above 95%.88–91 Spiral CT using 360-degree rotation of the x-ray beam source can document the extent of the aortic aneurysm and provide accurate serial measurement of aneurysm diameter. Computer programs can generate sagittal, coronal, and oblique images as well as three-dimensional renderings that can be used to determine whether a patient is a candidate for a stent-graft.92 A general assessment of other organs in the chest, abdomen, and pelvis is also obtained with CT, which allows the detection of other pathologic processes, including cancer, that might affect patient management and surgical planning.93,94 In patients with renal insufficiency, CT without iodinated contrast agents can be useful to determine TAAA size or extent but will not provide accurate data about the atherosclerotic burden of branch vessels or the presence of a dissection. It is my general impression, supported by studies,95 that given the standard use of low-osmolar, smaller boluses of contrast material in performing computed tomographic angiography (CTA), contrast-related acute renal failure after CTA is in fact rare and, when it does occur, mild.
CTA also importantly allows other essential information to be obtained, including assessment of occlusive disease in branch vessels. In addition, CTA documents the patency of important intercostals that might be reimplanted into the aortic graft if extensive open TAAA repair is being considered. CTA further documents the presence of thrombus, inflammatory changes, dissection, and retroperitoneal blood suggestive of a ruptured aneurysm. The relative advantages of CT scanning over magnetic resonance imaging (MRI) include its being less expensive, quicker to perform and thus less claustrophobia inducing, useful in patients with previous implanted ferromagnetic devices, and widely available.
A word of caution is needed regarding CTA and the timing of TAAA repair. Because of the nephrotoxicity of iodinated contrast agents, in the elective surgery and endovascular therapy setting, repair is best delayed for at least 24 hours after CT, especially in patients with chronic renal insufficiency. The administration of N-acetylcysteine and intravenous hydration are current strategies used to limit contrast-induced nephropathy.96,97 If contrast-induced nephropathy does occur, elective repairs should be delayed until renal function returns to baseline.
Magnetic Resonance Imaging and Magnetic Resonance Angiography
MRI and magnetic resonance angiography (MRA) can be considered in the evaluation of patients with TAAAs, especially those with renal insufficiency, because it avoids the use of iodinated contrast material (Fig. 134-8). MRA has also been used to map the spinal cord circulation before TAAA repair.98
