Thoracoabdominal Aortic Aneurysms
Sharon McCartney
Stephen Gregory
J. Mauricio Del Rio
Mani A. Daneshmand
Madhav Swaminathan
A 68-year-old man presents for surgical repair of a thoracoabdominal aortic aneurysm (TAAA). He has a significant past medical history that includes a type A aortic dissection 12 years ago, for which he underwent a Bentall repair, poorly controlled hypertension, chronic obstructive pulmonary disease (COPD), tobacco use (45 pack-years), and stage III chronic kidney disease (CKD). His type A dissection event was complicated by end-organ ischemia, including ischemic colitis and renal failure. He has been undergoing routine surveillance of his aorta, and computed tomography (CT) reveals his aortic aneurysm has recently enlarged to 5.5 cm starting at the innominate artery and extending into the abdominal aorta, proximal to the renal arteries. Chest radiograph demonstrates thoracic aortic aneurysmal dilation, without compression of surrounding structures. Transthoracic echocardiogram demonstrates normal left and right ventricular function, trivial aortic insufficiency (AI), and trivial mitral insufficiency. Laboratory studies indicate a hemoglobin of 14.5 g per dL, hematocrit 44%, blood urea nitrogen (BUN) 22 mg per dL, and creatinine 1.8 mg per dL.
A. Pathophysiology and Differential Diagnosis
What is a thoracic aortic aneurysm (TAA) and how does it typically present?
How are TAAs classified?
What is the pathogenesis of aortic aneurysms and what genetic conditions predispose to their formation?
What are the risk factors for TAA rupture?
What is the natural history and medical management of thoracic aneurysms?
What is a thoracic aortic dissection, and how does it typically present?
How are thoracic aortic dissections classified?
B. Preoperative Evaluation and Preparation
What are the indications and timing of surgical intervention for TAAs?
Which patients are candidates for endovascular aortic repair, and what are the advantages to this approach?
What are the preoperative considerations for the anesthesiologist before TAA repair?
What is the preoperative management of a patient presenting with acute aortic dissection (AAD)?
What is the spinal cord blood supply?
C. Intraoperative Management
What are the surgical approaches to thoracic aneurysm repair?
How is the open repair performed?
How are the endovascular repair of TAAAs performed?
What are the specific considerations for anesthetic management of the patient presenting for open TAAA repair?
What are the specific considerations for anesthetic management of the patient presenting for endovascular TAAA repair?
What hemodynamic monitors should be used for the patient undergoing thoracic aneurysm repair?
What strategies are used for spinal cord protection during a TAAA repair?
What strategies are used for mesenteric and renal preservation?
What is the pathophysiology of aortic clamping and unclamping?
Why does coagulopathy ensue and how is it prevented/treated?
D. Postoperative Anesthetic Management
What are the postoperative complications after open TAAA repair?
What are the postoperative complications after endovascular TAAA?
A. Pathophysiology and Differential Diagnosis
A.1. What is a thoracic aortic aneurysm (TAA) and how does it typically present?
Thoracic and TAAAs are abnormal dilations of the thoracic and/or abdominal aorta to greater than 150% of its expected diameter. They can occur at any point along the aorta, including the root, arch, and descending portions with occasional extension into branching vessels. The dimensions that define normal aortic size are determined by patient age, gender, and body surface area.
One of the greatest challenges in the care of patients with thoracic aortic disease is identifying them prior to the onset of a catastrophic aortic event. Despite their propensity for life-threatening complications, TAAs are often clinically silent and are often diagnosed during imaging for an unrelated disorder. When symptoms do occur, they are often nonspecific, and diagnosis requires a high index of clinical suspicion. Symptoms of TAAs frequently result from compression of adjacent structures. Patients may exhibit hoarseness from recurrent laryngeal nerve compression, stridor from bronchial or tracheal compression, dyspnea from lung compression, dysphagia from esophageal compression, and facial edema from superior vena cava (SVC) compression. Pain in the neck, jaw, back, shoulders, or abdomen may also be present. Additionally, new-onset heart failure symptoms may occur as aortic enlargement results in progressive AI (Fig. 9.1).
Once identified, dedicated imaging with either CT (Fig. 9.2) or magnetic resonance imaging (MRI) should be undertaken to delineate the extent of the aneurysm, its maximum dimension, branch vessel involvement, and the presence or absence of a coexisting intramural hematoma (Fig. 9.3) or penetrating aortic ulcer. Transthoracic echocardiography (TTE) is also performed to assess for valvular disease, evaluate cardiac function, and more carefully assess the anatomy of the aortic root (Fig. 9.4).
Booher AM, Eagle KA. Diagnosis and management issues in thoracic aortic aneurysm. Am Heart J. 2011;162:38.e1-46.e1.
Hiratzka LF, Bakris GL, Beckman JA, et al. 2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM guidelines for the diagnosis and management of patients with thoracic aortic disease. A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, American Association for Thoracic Surgery, American College of Radiology, American Stroke Association, Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, Society of Interventional Radiology, Society of Thoracic Surgeons, and Society for Vascular Medicine. J Am Coll Cardiol. 2010;55(14):e27-e129.
A.2. How are TAAs classified?
Ascending TAAs do not follow a specific classification system but are described by the extent of the aorta that is involved, including the aortic valve (AV), aortic root, and aortic arch.
 FIGURE 9.1 Midesophageal aortic valve long-axis view on TEE demonstrating moderate central aortic insufficiency secondary to ascending aortic dilatation in a young woman with Turner syndrome. |
TAAAs are described using the modified Crawford classification, which subdivides TAAAs into five types according to the extent of the surgical repair required (Fig. 9.5).
Type I begins distal to the left carotid artery and extends down below the diaphragm to above the renal arteries.
Type II begins distal to the left carotid above the sixth intercostal space. They extend through the diaphragm and end below the renal arteries.
Type III begins below the sixth intercostal space but above the diaphragm. They extend below the renal arteries.
Type IV begins below the diaphragm but above the renal arteries, with extension to below the renal arteries.
Type V begins above the diaphragm and end above the renal arteries.
Crawford ES, Crawford JL, Safi HJ, et al. Thoracoabdominal aortic aneurysms: preoperative and intraoperative factors determining immediate and long-term results of operations in 605 patients. J Vasc Surg. 1986;3:389-404.
Frederick JR, Woo YJ. Thoracoabdominal aortic aneurysm. Ann Cardiothorac Surg. 2012;1(3):277-285.
Hoel AW. Aneurysmal disease: thoracic aorta. Surg Clin North Am. 2013;93:893-910.
A.3. What is the pathogenesis of aortic aneurysms and what genetic conditions predispose to their formation?
TAAs primarily arise from focal degeneration of the elastic and muscular tissue of the aortic wall. The resulting tissue weakness predisposes the wall to dilate under the stress of high pressures within the aorta. The dilation of the aorta is associated with decreased vessel wall compliance, increased wall stress, and a propensity for subsequent rupture of the aneurysm.
 FIGURE 9.2 Three-dimensional (3D) CT reconstruction demonstrating a thoracoabdominal aneurysm that begins in the descending thoracic aorta and extends to the infrarenal aorta, above the bifurcation into the iliac arteries. Also seen in a chronic type B aortic dissection. |
 FIGURE 9.3 Descending aorta in short axis (left) and long axis (right) on TEE demonstrating an intramural hematoma (arrow) in a patient with a thoracoabdominal aneurysm. |
 FIGURE 9.4 A. Midesophageal aortic valve long-axis view on TEE demonstrating aortic valve annulus, sinus, and sinotubular junction dimensions at mid-systole. B. Ascending aorta in short axis demonstrating aneurysmal enlargement with a diameter of 5.3 cm in a young woman with Turner syndrome. |
 FIGURE 9.5 The modified Crawford classification of thoracoabdominal aortic aneurysms. (Used with permission from Frederick JR, Woo YJ. Thoracoabdominal aortic aneurysm. Ann Cardiothorac Surg. 2012;1[3]:277-285.) |
Although the majority of TAAs follow a degenerative pattern, there are a number of congenital disease processes that are associated with aneurysm formation.
Marfan syndrome (MFS) is an autosomal dominant disorder caused by a mutation in the fibrillin-1 gene. Patients with MFS have characteristic overgrowth of the long bones of the arms and legs, increased finger length (arachnodactyly), and joint laxity. They can also demonstrate ocular abnormalities, most commonly lens dislocation. In addition to the musculoskeletal and ocular manifestations of MFS, patients are also at increased risk of aortic root dilation, ascending and descending aortic aneurysms, and aortic dissection. Valvular disease can also be present, with mitral regurgitation and associated pulmonary hypertension being the most common cause of MFS-related infant mortality. On a molecular level, mutations in the fibrillin-1 gene result in disordered formation of the microfibril matrix, leading to disruption of the elasticity of the aorta. More recent evidence suggests that excessive transforming growth factor β (TGF-β) signaling also plays a role in the clinical phenotype of MFS.
Vascular Ehlers-Danlos syndrome (vEDS) is the result of mutation in the COL3A1 gene coding for type III procollagen. Mutations in type III procollagen can result in a number of complications, including spontaneous intestinal or uterine rupture, fragile skin, and vascular dissection. Children may also present with inguinal hernias, pneumothoraces, or recurrent joint dislocations. Although diagnosis is often made clinically, many patients are only diagnosed after a major arterial or gastrointestinal event.
Loeys-Dietz syndrome (LDS) is a heterogeneous disease stemming from mutations in either the TGFBR1 or TGFBR2 gene, resulting in a relative increase in TGF-β signaling. LDS presents with characteristic craniofacial, skeletal, and cardiovascular anomalies with a broad range of phenotype. Because patients with milder disease exhibit limited skeletal features and no typical ophthalmologic manifestations of the disease, the diagnosis is often made within a family after a significant aortic event. These patients are also at risk of complicated cerebral aneurysms, and imaging of all major arterial structures is recommended after diagnosis.
Turner syndrome is a genetic disorder characterized by the lack of an X-chromosome in a female patient (45, X). Women with Turner syndrome are often short in stature, have dysfunctional ovaries, and are at increased risk of cardiovascular disease. Bicuspid AV disease is present in between 10% and 25% of women with Turner syndrome, and approximately 8% have coarctation of the aorta. The risk of AAD is also increased in women with Turner syndrome and tends to occur at a younger age and smaller aortic diameter than the general population.
Less common genetic etiologies of thoracic and thoracoabdominal aortic disease include mutations in the MYH11, ACTA2, MYLK, SLC2A10, or SMAD3 gene. Despite progress in discerning the genetic mechanisms of familial TAAs, up to 80% are without a clear molecular etiology.
There are a number of rheumatologic diseases that may affect the thoracic aorta. Takayasu arteritis, giant cell arteritis, Behçet disease, and ankylosing spondylitis have all been demonstrated to contribute to the development of aneurysmal dilation of the aorta with varying degrees of frequency.
Patients may also develop aneurysms with an infectious etiology, although this is rare. There are several mechanisms by which this can occur, including direct spread from adjacent structures, septic embolic events from bacterial endocarditis, and hematogenous seeding of the aorta from bacteremia. Although most infections are caused by bacteria, immunosuppressed patients are also susceptible to fungal and mycobacterial infection. Interestingly, HIV infection also appears to be associated with an increased risk of TAA formation.
Finally, patients with a bicuspid AV have a markedly increased risk of TAA formation. Aortic dilation in bicuspid AV disease most commonly involves enlargement of the ascending aorta in addition to dilation of the aortic root (Fig. 9.6). Risk factors for aneurysm development include older age, male sex, systolic hypertension, valve stenosis or regurgitation, and the specific morphology of the valve itself. Although a specific unifying gene remains elusive, bicuspid aortic disease demonstrates familial inheritance.
Boodhwani M, Andelfinger G, Leipsic J, et al. Canadian Cardiovascular Society position statement on the management of thoracic aortic disease. Can J Cardiol. 2014;30:577-589.
Hoel AW. Aneurysmal disease: thoracic aorta. Surg Clin North Am. 2013;93:893-910.
Jondeau G, Boileau C. Genetics of thoracic aortic aneurysms. Curr Atheroscler Rep. 2012;14:219-226.
Jones JA, Ikonomidis JS. The pathogenesis of aortopathy in Marfan syndrome and related diseases. Curr Cardiol Rep. 2010;12:99-107.
Pomianowski P, Elefteriades JA. The genetics and genomics of thoracic aortic disease. Ann Cardiothorac Surg. 2013;2(3):271-279.
Ramanath VS, Oh JK, Sundt TM III, et al. Acute aortic syndromes and thoracic aortic aneurysm. Mayo Clin Proc. 2009;84(5):465-481.
Verma S, Siu SC. Aortic dilatation in patients with bicuspid aortic valve. N Engl J Med. 2014;370:1920-1929.
A.4. What are the risk factors for TAA rupture?
The size of a TAA is the most important predictor of rupture (Table 9.1). For every 1 cm increase in aneurysm diameter, the risk of rupture roughly doubles. The “hinge point” at which the risk of rupture increases dramatically is approximately 6 cm in diameter for ascending aneurysms and 7 cm for descending aneurysms, although 31% and 43%, respectively, of patients will have experienced rupture or dissection by the time they reach this point. Patients with COPD, advanced age, and symptomatic aneurysms appear to have an increased risk of rupture. Although women tend to develop TAAs later in life, they appear to also have an increased risk of aneurysm rupture relative to their male counterparts.
Chau KH, Elefteriades JA. Natural history of thoracic aortic aneurysms: size matters, plus moving beyond size. Prog Cardiovasc Dis. 2013;56:74-80.
Davies RR, Goldstein LJ, Coady MA, et al. Yearly rupture or dissection rates for thoracic aortic aneurysms: simple prediction based on size. Ann Thorac Surg. 2002;73:17-27.
Elefteriades JA. Natural history of thoracic aortic aneurysms: indications for surgery, and surgical versus nonsurgical risks. Ann Thorac Surg. 2002;74:S1877-S1880.
Frederick JR, Woo YJ. Thoracoabdominal aortic aneurysm. Ann Cardiothorac Surg. 2012;1(3):277-285.
A.5. What is the natural history and medical management of thoracic aneurysms?
The location and etiology of thoracic and thoracoabdominal aneurysms determines their rate of growth and subsequent propensity for rupture. Ascending TAAs typically grow at a rate of 0.1 cm per year, whereas descending aneurysms grow slightly faster at 0.3 cm per year. The rate of growth is greater in patients with larger aneurysms, dissected aortas, and certain familial causes of TAA. The aortic size is a strong predictor of the risk of complications, with a marked increase in risk profile as the aneurysm increases to greater than 6 cm.
 FIGURE 9.6 A. Midesophageal aortic valve short-axis view on TEE showing a bicuspid valve, with fusion of the left and right coronary cusps. B. Midesophageal aortic valve long-axis view on TEE demonstrating the characteristic doming of a stenotic bicuspid aortic valve and blunting of the sinotubular junction due to aortic root dilatation. |
TABLE 9.1 Annual Rate of Rupture for Thoracic Aortic Aneurysms | ||||||||
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Medical therapy to slow aneurysm growth or to reduce the risk of dissection or rupture has only been modestly successful thus far. Initial therapy consists of lifestyle modifications including smoking cessation and minimization of heavy lifting to avoid significant spikes in systolic blood pressure, which may precipitate rupture or aortic dissection.
Despite a relative paucity of clinical evidence, β-blocker therapy is often prescribed with the goal of reducing the rate of aortic dilatation by decreasing left ventricular contractility and subsequently decreasing shear stress. Although this has been demonstrated to be beneficial in patients with MFS, evidence for its use in the broader population of patients with TAAs is still lacking. Statins have also recently been shown to be beneficial in the medical management of TAAs, with patients receiving statin therapy showing a slower rate of aneurysmal growth, a smaller percentage requiring surgery, and a decrease in the overall number of adverse events.
Angiotensin receptor blockade has shown promise in the murine model of MFS, with a small human study showing a decrease in the rate of aneurysmal growth. This data formed the basis for the ongoing MARFANSARTAN trial (Study of the Efficacy of Losartan on Aortic Dilatation in Patients with Marfan Syndrome). Current recommendations suggest aggressive blood pressure reduction with β-blockers and angiotensin-converting enzyme (ACE)-inhibitors or angiotensin receptor blockers to the lowest level that patients can tolerate without adverse effects.
Brooke BS, Habashi JP, Judge DP, et al. Angiotensin II blockade and aortic-root dilation in Marfan’s syndrome. N Engl J Med. 2008;358:2787-2795.
Chau KH, Elefteriades JA. Natural history of thoracic aortic aneurysms: size matters, plus moving beyond size. Prog Cardiovasc Dis. 2013;56:74-80.
Danyi P, Elefteriades JA, Jovin IS. Medical therapy of thoracic aortic aneurysms. Trends Cardiovasc Med. 2012;22(7):180-184.
Devereux RB, Roman MJ. Aortic disease in Marfan’s syndrome. N Engl J Med. 1999;340:1358-1359.
Stein LH, Berger J, Tranquilli M, et al. Effect of statin drugs on thoracic aortic aneurysms. Am J Cardiol. 2013;112(8):1240-1245.
A.6. What is a thoracic aortic dissection, and how does it typically present?
An AAD typically develops when a tear in the intimal layer of the aorta permits blood to enter into the medial layer, creating a false lumen that may rapidly expand both proximally and distally (Fig. 9.7). This can cause ischemia of the brain and viscera because the vasculature supplying these organs is occluded. Proximal dissection may cause AI, cardiac ischemia from coronary artery occlusion, or accumulation of blood in the pericardium resulting in tamponade (Fig. 9.8). Finally, the false lumen can rupture, resulting in rapid exsanguination.
Hypertension is the most common comorbid disease in patients experiencing aortic dissection, although hyperlipidemia, tobacco use, and cocaine use are other risk factors. Pregnancy can also increase the risk of AAD, with most women typically presenting during their third trimester or in the early postpartum period. There are several genetic conditions that increase the risk of AAD, including MFS, Ehlers-Danlos syndrome, familial aortic dissection, LDS, and annuloaortic ectasia. AAD can also occur iatrogenically during cardiac surgery, cardiac catheterization, and insertion of an intra-aortic balloon pump.
 FIGURE 9.7 Midesophageal aortic valve short-axis view on TEE demonstrating an acute aortic dissection (arrow) that extends proximally to the aortic valve in a young patient with Marfan syndrome. |
 FIGURE 9.8 Transgastric midpapillary view on TEE demonstrating accumulation of blood in the posterior pericardial space (arrow) after acute aortic dissection. |
Patients typically present with the acute onset of severe chest and back pain, although this is not a universal finding. Less commonly, patients can present with abdominal pain, syncope, or symptoms of limb or visceral malperfusion. In roughly 6% of cases, the aortic dissection is painless and presents as new-onset heart failure, stroke, or syncope. These patients tend to be diabetic, have a history of aortic aneurysm, or a history of prior cardiac surgery. Hypertension is common on initial presentation, and the diastolic murmur of AI is present in 44% of patients with a type A dissection. Hypotension is an ominous sign and portends a poor clinical prognosis.
It is important to differentiate AAD from acute coronary syndrome (ACS) because they may have similar presentations. Symptomatically, patients with AAD typically present with acute, severe chest pain, whereas patients with ACS typically have pain that is more gradual in onset. This differentiation is important because the treatment of ACS (antiplatelet agents, anticoagulation, and occasionally thrombolytics) is potentially catastrophic in patients with aortic dissection. AAD should be in the differential diagnosis for any patient presenting with syncope; new-onset chest, abdominal, or back pain; acute heart failure; or clinical evidence of malperfusion. Diagnosis is most commonly made via spiral CT scan (Fig. 9.9) or transesophageal echocardiogram (TEE), although aortography and MRI may also be used.
Ramanath VS, Oh JK, Sundt TM III, et al. Acute aortic syndromes and thoracic aortic aneurysm. Mayo Clin Proc. 2009;84(5):465-481.
Tsai TT, Trimarchi S, Nienaber CA. Acute aortic dissection: perspectives from the International Registry of Acute Aortic Dissection (IRAD). Eur J Vasc Endovasc Surg. 2009;37:149-159.
 FIGURE 9.9 CT scan demonstrating an acute aortic dissection that extends from the aortic root to the iliac arteries. |
A.7. How are thoracic aortic dissections classified?
There are several systems used to classify aortic dissections that focus on anatomic or clinical factors noted on presentation (Fig. 9.10).
DeBakey Classification
The DeBakey classification system categorizes aortic dissections based on their site of origin and degree of distal extension.
Type I dissection originates in the ascending aorta and propagates to at least the level of the aortic arch and often beyond, sometimes extending as distal as the iliac arteries.
Type II dissection begins in, and is limited to, the ascending aorta. Although these occur on occasion in patients with MFS, they are the rarest form of aortic dissection. Type I and type II dissections are almost always treated surgically.
 FIGURE 9.10 The Stanford and DeBakey classifications of aortic dissections. (Used with permission from Nienaber CA, Eagle KA. Aortic dissection: new frontiers in diagnosis and management: part I: from etiology to diagnostic strategies. Circulation. 2003;108:628-635.) |
Type IIIa dissection begins beyond the origin of the left subclavian artery and is limited to the descending thoracic aorta.
Type IIIb dissection begins beyond the left subclavian origin and extend more distally beyond the diaphragm. Type III dissections are often managed medically.
Stanford Classification
The Stanford classification system is similar to the DeBakey system in that it describes aortic dissections based on their anatomic site of origin.
Stanford type A aortic dissections originate in the ascending aorta and include DeBakey type I and type II dissections.
Stanford type B aortic dissections originate in the descending aorta and include DeBakey type IIIa and IIIb dissections. These may occasionally also propagate proximally into the ascending aorta or aortic arch.
A notable limitation to both the Stanford and DeBakey classification systems is their inability to classify dissections originating in the aortic arch.
Penn Classification
More recently, patients with acute Stanford type A aortic dissection have been subcategorized according to ischemic symptoms noted on presentation in what has been termed the Penn classification. This has been successfully validated as a predictor of perioperative mortality.
Penn Class Aa patients have no ischemic symptoms on presentation. This is the most common clinical finding in type A aortic dissection, encompassing approximately 60% of all patients. It is also associated with the best clinical outcome with a 30-day mortality of 3% and a 5-year cumulative survival approaching 85% in one cohort.
Penn Class Ab patients present with branch vessel malocclusion producing clinically significant organ ischemia. This includes patients presenting with stroke, paraplegia, renal dysfunction, mesenteric malperfusion, and occlusion of vascular supply to the extremities.
Penn Class Ac patients present with circulatory collapse with or without cardiac involvement. Class Ab and Ac patients have similar perioperative and long-term survival profiles.
Penn Class Abc patients present with symptoms of both local and generalized ischemia. These patients have the worst prognosis with a 30-day perioperative mortality of 40%. Most deaths are secondary to multisystem organ failure, hemorrhage, cardiac failure, or central nervous system (CNS) dysfunction.
Augoustides JG, Geirsson A, Szeto WY, et al. Observational study of mortality risk stratification by ischemic presentation in patients with acute type A aortic dissection: the Penn classification. Nat Clin Pract Cardiovasc Med. 2009;6:140-146.
Daily PO, Trueblood HW, Stinson EB, et al. Management of acute aortic dissections. Ann Thorac Surg. 1970;10:237-247.
DeBakey ME, Cooley DA, Crawford ES, et al. Aneurysms of the thoracic aorta; analysis of 179 patients by resection. J Thorac Surg. 1958;36:393-420.
Hiratzka LF, Bakris GL, Beckman JA, et al. 2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM guidelines for the diagnosis and management of patients with thoracic aortic disease. A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, American Association for Thoracic Surgery, American College of Radiology, American Stroke Association, Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, Society of Interventional Radiology, Society of Thoracic Surgeons, and Society for Vascular Medicine. J Am Coll Cardiol. 2010;55(14):e27-e129.
Kimura N, Ohnuma T, Itoh S, et al. Utility of the Penn classification in predicting outcomes of surgery for acute type A aortic dissection. Am J Cardiol. 2014;113(4):724-730.
Nienaber CA, Eagle KA. Aortic dissection: new frontiers in diagnosis and management: part I: from etiology to diagnostic strategies. Circulation. 2003;108:628-635.
B. Preoperative Evaluation and Preparation
B.1. What are the indications and timing of surgical intervention for TAAs?
Patients diagnosed with aneurysms of the thoracic aorta require frequent surveillance to assess for aneurysmal expansion. The goal is to facilitate surgical intervention prior to the onset of aortic dissection or aneurysm rupture. Important considerations include the
appropriate interval for surveillance imaging and the diameter at which surgical intervention should be recommended.
appropriate interval for surveillance imaging and the diameter at which surgical intervention should be recommended.
TABLE 9.2 Guidelines for Elective Intervention in Patients with Ascending or Descending Thoracic Aortic Aneurysms | ||||||||||||
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Patients diagnosed with thoracic and TAAAs should undergo initial CT or MRI to define the size and extent of the aneurysm. Follow-up surveillance imaging is typically performed 6 months after diagnosis, with continued follow-up imaging at an interval determined by the rate of growth. These aneurysms tend to grow slowly, with arch and ascending aneurysms growing 0.1 cm per year and descending aneurysms growing 0.3 cm per year.
Determining when to intervene depends on the underlying pathology, size, rate of expansion, and presence or absence of symptoms (Table 9.2). In patients without known connective tissue disease, surgical repair is recommended at 5.5 cm in ascending aortic aneurysms and 6.5 cm in descending aneurysms. In patients with concomitant AV disease who are scheduled to undergo AV replacement, an aneurysm should be repaired if it is greater than 4.5 cm in diameter. Patients with symptomatic aneurysms of any size should be considered for surgical intervention. Very large and very small patients may be better managed by indexing aortic diameter to body size to determine the appropriate timing of repair.
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