Chapter 16. Echocardiography for Aortic Surgery

Diseases involving the aorta can present a challenge to both surgeons and anesthesiologists. Aortic dissection and rupture are life threatening, require rapid and accurate diagnosis, and need definitive medical and/or surgical management due to their high risk of morbidity and mortality.1,2 A key ingredient in the efficient management of these patients is imaging of the thoracic aorta. Transesophageal echocardiography (TEE) has become an essential noninvasive diagnostic modality for acute thoracic aortic pathologies, and is a standard part of the echocardiographer's armamentarium in the operating room.3–6 It is important for the echocardiographer to quickly and accurately verify the diagnosis, distinguish true pathology from the many common confounding artifacts, and clearly communicate precise echocardiographic findings of the aorta and related cardiac anatomy to the surgeon in order to guide intervention. The following text reviews aortic anatomy and pathology and associated echocardiographic features that assist with imaging during aortic surgery.

In order to truly appreciate the invaluable role that TEE plays in the assessment for diseases of the aorta, a detailed understanding of the aorta and surrounding anatomic structures is crucial. The thoracic aorta can be divided into three anatomic segments: ascending thoracic aorta, aortic arch, and descending thoracic aorta (Figure 16–1). The ascending thoracic aorta originates at the level of the aortic valve annulus. As previously described in Chapter 9, the aortic valve comprises three crescent-shaped leaflets that coapt to form three commissures. Immediately distal to the aortic valve apparatus is a short and dilated aortic segment—the sinus of Valsalva—which is subdivided into the noncoronary, left coronary, and right coronary sinuses. As the nomenclature suggests, the left and right coronary arteries each originate from their respectively named sinus. Distal to the sinus of Valsalva, the aorta slightly narrows, forming the sinotubular junction (STJ). From this point, the ascending aorta crosses beneath the main pulmonary artery, then courses in an anterior, cranial, and rightward direction over the origin of the right pulmonary artery.

The ascending aorta terminates and continues as the aortic arch at the origin of the brachiocephalic (innominate) artery. The aortic arch then proceeds to curve in a posterior and leftward direction with cranial convexity. Three arteries arise from the aortic arch: the brachiocephalic, left common carotid, and left subclavian arteries. It is often difficult to visualize the distal ascending thoracic aorta and proximal aortic arch with TEE because the trachea is positioned between the esophagus and aorta, effectively preventing ultrasound transmission. Immediately beyond the origin of the left subclavian artery, at the point of attachment of ligamentum arteriosum (remnant of the fetal ductus arteriosus), is a second narrowing called the aortic isthmus. Unlike the heart and proximal part of the aorta, the aortic isthmus and descending thoracic aorta are relatively fixed. Consequently, deceleration injury secondary to trauma is most often confined to this level. Distal to the aortic isthmus, the descending aorta follows a caudal, slightly anterior, and rightward trajectory towards the aortic diaphragmatic hiatus. Along its intrathoracic course, the descending thoracic aorta and the esophagus are in close proximity. While the esophagus courses almost straight downward, anterior to the midline of the vertebral bodies, the aorta travels in a smooth, curved direction from the anterolateral side of the 4th thoracic vertebral body to the anterior side of the 11th vertebral body.

During its thoracic descent, multiple intercostal arteries branch off the aorta and may occasionally be imaged with TEE using color-flow Doppler (CFD). Spinal branches of these intercostal arteries supply blood to the spinal cord through radicular arteries. The radicular artery anatomy in this area is quite variable, with 4 to 10 radicular branches typically contributing to the thoracic spinal cord. The anterior spinal cord blood supply is tenuous in the thoracic region, thus it is at great risk for cord ischemia. Frequently, one radicular artery—the arteria radicularis magna, or the artery of Adamkiewicz—is very developed and is responsible for the majority of anterior spinal cord blood supply, and it is typically found between T9 and T12.

Below the diaphragm, the abdominal aorta lies posterior to the stomach. Because the stomach is a large cavity that is highly deformable, the position of the abdominal aorta in relation to the intragastric TEE probe is somewhat variable. The celiac artery and mesenteric arteries originate from the anterior side of the abdominal aorta. The renal arteries arise from the left and right sides of the aorta, slightly below the mesenteric vessels.

The wall of the aorta is composed of three tunicae: the intima, media, and adventia. The inner layer, the intima, consists of simple squamous epithelium and underlying connective tissue. The tunica media consists of circularly arranged smooth muscle and elastic tissue. The outer adventitial layer is mainly a loose layer of connective tissue, lymphatics, and vasa vasorum (ie, “vessels of the vessels”). TEE provides the ability to assess the aortic wall for many pathologies including thickening of the tunica intima due to arteriosclerosis and/or atherosclerosis, intimal tears/dissections, and aneurysmal dilatation.

As described in Chapter 5, insertion of the TEE probe must be performed gently and should never be forced through areas of resistance. This is especially important in patients with suspicion of major aortic pathology. First, intubation of the esophagus with the TEE probe can be very stimulating and may result in hypertensive episodes, increasing the risk of further tearing or rupture of a dissection or aneurysm. Second, resistance encountered during advancement of the probe may represent esophageal compression by a large aneurysm, and if so, consideration should be given to abandon the examination. Finally, in aortic dissection, because the adventitia is the sole layer of the wall of the false lumen, aortic rupture may occur if the TEE probe is not manipulated cautiously.

As with any TEE examination, a systematic approach is required to thoroughly evaluate the thoracic aorta. As per the SCA/ASE guidelines, there are six short-axis and two long-axis imaging planes that enable imaging of most of the thoracic aorta.7 Although many sequences are possible, the authors recommend the following order: Begin with the midesophageal (ME) aortic valve (AV) short-axis (SAX), “Mercedes-Benz” view, which is obtained at the midesophageal level with the scan angle rotated forward to 30° to 60° (see Figure 5–19B). From here, the angle can be rotated by another 90° to about 120° to 150° to identify the ME AV long-axis (LAX) view (see Figure 5–20B). The long-axis view is particularly important because it allows evaluation of the aortic valve and proximal ascending aorta. Measurements can be made of the left ventricular outflow tract (LVOT), aortic valve annulus, sinuses of Valsalva, STJ, and ascending aorta if aortic valve repair and/or root reconstruction are planned (Figure 16–2). In order to visualize the ascending aorta in short axis, rotate back to a scan angle of 0° and slowly withdraw from the level of the aortic valve (ie, ME ascending aorta SAX view; see Figure 5–30B). By rotating forward to a 120° scan angle, a ME ascending aorta LAX view is obtained (see Figure 5–32B). It is crucial in these two views to carefully examine the aorta for dissections. Artifacts are frequently encountered within the ascending aorta, and it is important to distinguish artifacts from true pathology as discussed in Chapter 3.

Following examination of the ascending aorta, the TEE probe should be advanced to the level of the ME four-chamber view and rotated towards the patient's left. This should result in the descending aorta SAX view in which the aorta appears as a circular image at the top of the screen (Figure 16–3). As the descending aorta is about 3 to 4 cm in diameter at this level, reducing the scan depth to 6 to 8 cm and selecting a high transducer frequency improves both the spatial and temporal resolutions of the image. Almost the entire descending thoracic aorta may be visualized in short axis by advancing and withdrawing the TEE probe. By rotating the scan angle forward to 90°, the descending aorta can be seen longitudinally (see Figure 16–3). Alternating between short- and long-axis views may help demonstrate aortic pathology more comprehensively. While withdrawing the TEE probe and maintaining the descending aorta in the short-axis view (at 0°), the aorta will change in appearance from circular to longitudinal at the level of the aortic arch (upper esophageal [UE] aortic arch LAX; see Figure 5–34). Frequently, the origins of the left subclavian and carotid arteries can be seen. Adding CFD with the Nyquist limit set at 50 cm/s may aid in visualizing these vessels. Finally, by rotating forward to 90°, the UE aortic arch SAX will be obtained (see Figure 5–31B). Most aortic pathologies can be identified by adding pulsed-wave Doppler (PWD) and continuous-wave Doppler (CWD), as well as gray-scale and color M-mode to the two-dimensional (2D) examination above.

An aortic aneurysm is a localized or diffuse dilation of the aorta to twice its diameter involving all three layers of the vessel wall. The estimated annual incidence is six cases per 100,000 persons.8 TEE is useful for the diagnosis and classification of thoracic and upper abdominal aortic aneurysms. Thoracoadominal aneurysms (TAAs) are categorized into four types based on the Crawford classification system (Figure 16–4).9 Type I involves the entire descending thoracic aorta to the abdominal aorta above the renal arteries. Type II originates in the proximal descending thoracic aorta and terminates distal to the renal arteries. Type III affects the distal half of the thoracic aorta and the abdominal aorta to the bifurcation. Type IV is limited to the distal portion of the descending thoracic aorta and the abdominal aorta to the bifurcation.

Aneurysms are generally thought to be a disease of aging and a consequence of degeneration and atherosclerosis. Aging results in a pathological process that involves the development of eccentric fibrous intimal thickening, lipid deposition, and calcification, leading to weakening of the aortic wall and dilation.10 According to Laplace law (Tension = Pressure × Radius), as the diameter of the lumen increases, the wall tension increases resulting in progressive dilation. Other causes of TAAs include connective tissue diseases (ie, Marfan's, type IV Ehlers-Danlos and Loeys-Dietz syndromes), infections (ie, bacteria, mycotic, or syphilitic), trauma, and increased wall tension secondary to hypertension or a high-velocity jet originating from aortic stenosis.

The decision to surgically repair a TAA is based upon the size and etiology of the aneurysm. According to recommendations by the Society of Thoracic Surgeons, a thoracic fusiform aneurysm should be surgically repaired if it is greater than 5.5 cm in diameter or twice the diameter of the normal contiguous aorta.11 Indications for saccular aneurysm have not been determined, but it is considered reasonable to intervene if the width is greater than 2 cm. Patients with connective tissue diseases, such as Marfan's syndrome, may be considered for early operative repair because of their increased risk of dissection or rupture. A strong family history of aortic aneuryms may also prompt early intervention. Finally, symptomatic patients should be considered for operative treatment regardless of the size of the aneurysm. Symptoms include persistent pain, malperfusion, and compression of nearby structures leading to dysphagia, cough, hoarseness, or Horner's syndrome. Descending TAAs can also be treated by endovascular stent grafting. There are no established guidelines regarding which patients should be managed with endovascular aortic repair (EVAR). In general, patients at high risk for complications from either conventional open repair or medical management may benefit from this relatively less invasive approach. Another emerging alternative for complex aortic pathology is the “hybrid” approach in which an open surgical technique is combined with an EVAR. This approach is thought to maximize the benefit of complete repair of complex lesions while minimizing the risk of a total open technique.

TEE may be used to detect the patency of aortic side branches and to evaluate for the presence of organ malperfusion. In the thoracic region, the identification of the left subclavian artery and its patency may be particularly important in EVAR and hybrid approaches. Intraoperative TEE is also an excellent monitoring tool, especially if aortic cross-clamping is performed, and may be helpful during cannulation if total or partial extracorporeal circulatory support is required. Monitoring of cardiac function is an added benefit of TEE during aortic aneurysm surgery. While the aorta remains the focus of intraoperative imaging, the effects of aortic manipulation on cardiac function can also be evaluated. This enables clinicians to make informed decisions on pharmacological support, should it be required.

An aortic dissection is a separation in the aortic wall that allows blood flow within the tunica media. Currently, there are two proposed etiologies for aortic dissections.12 In the first hypothesis, the intima is ruptured along the edge of an atheromatous plaque or at a penetrating ulcer. The high pressure in the aorta forces blood through the intimal tear into the tunica media, creating a false lumen. The intimal layer that separates the false lumen from the true lumen (normal conduit of blood in the aorta) is termed the intimal flap. While intimal injury per se does not lead to dissection, it is a common precipitating factor, especially when the aortic medial layer is diseased. In the second hypothesis, the dissection is attributed to spontaneous rupture of the vasa vasorum or degeneration of the collagen and elastin that make up the tunica media. This medial layer can be affected by poor structural integrity as seen in old age or with primary connective tissue diseases such as Marfan's syndrome. Apart from medial integrity, the time required for extension of an intimal tear and development of a dissection depends on the rate of rise of systolic pressure, pulsatile pressure, diastolic recoil, and mean arterial pressure.

Aortic dissection is the most common cause of death among all conditions involving the aorta. The incidence of thoracic aortic dissection in North America is about 5 to 10 cases per million people per year.13 The mortality associated with acute aortic dissection is extremely high, with 21% of patients dying before hospital admission.14 The mortality rate from acute aortic dissection has been shown to be 1% to 3% per hour for the first 24 to 48 hours, and as high as 80% by 2 weeks.15 Due to this high mortality, early diagnosis is considered crucial for appropriate management to be initiated.

Magnetic resonance imaging (MRI) is currently the gold standard test for the detection and assessment of aortic dissections with a sensitivity and specificity of 98% and 98%, respectively.16 However, there are many contraindications to MRI examination including implanted medical devices (ie, pacemaker, orthopedic hardware, etc) and hemodynamic instability. Consequently, TEE is increasingly becoming an important and convenient modality for diagnosis of acute aortic dissection. TEE, similar to MRI, is highly sensitive and specific for the diagnosis of aortic dissection, with a sensitivity of 97% and specificity of 100%.17 TEE is an attractive first-choice diagnostic procedure because of its accuracy, speed, relatively low cost, portability, and noninvasiveness.18 However, a major limitation of TEE in the diagnosis of aortic dissection is the inability to reliably visualize the distal ascending aorta and proximal aortic arch. The frequent presence of artifacts such as mirror images in aortic imaging makes TEE prone to important false-positive diagnoses of dissection (Figure 16–5).

There are two main classification systems utilized for thoracic aortic dissections (see Figure 16–4).19 The DeBakey classification system recognizes three types of aortic dissections.19,20 In type I, the entire aorta is dissected; in type II, only the ascending aorta is involved; and in type III, the ascending aorta and arch are spared, while the descending aorta is dissected. Type III is further subclassified into type IIIA, involving the descending thoracic aorta alone, and type IIIB, extending into the abdominal aorta. The Stanford system classifies dissections into two types.20 In Type A the ascending aorta is affected, while in Type B the ascending aorta is spared. A classification system from Europe has also been proposed to replace the DeBakey and Stanford classification systems.21,22 This classification groups dissection into five types based on etiology (Table 16–1).

These classification systems have important prognostic and therapeutic consequences.11,23 Type A aortic dissection is a formal indication for surgical intervention because the reported mortality rate with medical therapy far exceeds that reported for surgical treatment.24–26 Unlike Type A aortic dissections, the correct management for Type B aortic dissections remains controversial.27–29 Medical management is advocated for most Type B dissections as most studies show no clear survival advantage with surgical management. Some indications for surgery in Type B dissection include organ malperfusion, persistent pain, hemodynamic instability, or any signs of impending or ongoing rupture, notably the accumulation of pleural, pericardial, periaortic, or mediastinal fluid; propagation of the dissection; increasing size of hematoma; and development of a saccular aneurysm. In addition, echocardiographic evidence of a wide-open false lumen with communication to the true lumen increases the risk of progression of the dissection, and therefore is considered an indication for surgery.

Though an intimal tear is the classic finding for aortic dissection, it is not always present. The presence of an intimal flap is therefore considered a classical sign of dissection, but not a mandatory one. The TEE examination of a patient with aortic dissection involves several components including characterization of the dissection, assessment of flow in aortic branches, and determination of cardiac complications. The dissection flap is a thin, mobile echogenic membrane found within the aortic lumen; however, to avoid a false-positive diagnosis, the intimal flap must be identified in multiple image planes.18,30,31 Although identification of the site of the intimal tear can be challenging, CFD imaging is useful in the assessment of entry and exit sites. It can sometimes be very difficult to distinguish the true lumen from the false lumen. In contrast to the false lumen, the true lumen tends to be smaller, round in appearance, shows enlargement during systole, and often has normal PWD and CFD profiles. In addition, M-mode imaging can help determine the direction of movement of the flap in systole, and thereby identify the location of the true lumen (Figure 16–6). The false lumen is usually larger and crescent shaped, and often demonstrates spontaneous echo contrast suggesting sluggish blood flow.

Closure of the tear to prevent further spread of the dissection is an essential part of the surgical repair.32 Ascending aortic dissection usually requires a formal sternotomy, while descending aortic dissections can be managed by open (thoracotomy), EVAR, or hybrid techniques. The two most common sites of intimal tear are 1 to 3 cm above the sinuses of Valsalva (70%) and the ligamentum arteriosum (30%).33–35

Other variants of aortic dissection include intramural hematoma (IMH) and aortic ulcers. Intramural hematoma (ie, European Heart Society class II dissection) is a common finding with a prevalence of up to 30%.36,37 The false lumen is believed to be due to rupture of vasa vasorum in the tunica media resulting in hematoma formation.12 There are two distinctive types of IMH.38 Type I IMH has a smooth intraluminal surface, a diameter less than 3.5 cm, and a wall thickness greater than 0.5 cm, while type II IMH has a rough intraluminal surface, a diameter greater than 3.5 cm, and a wall thickness greater than 0.6 cm. Both types have a longitudinal extension of at least 11 cm.

Atherosclerotic aortic plaques can also ulcerate (ie, European Heart Society class IV dissection) leading to the formation of aneuryms, aortic rupture, or dissections.39 The ulcers predominantly affect the descending thoracic aorta and are not usually associated with longitudinal extension. On TEE, these lesions are characterized by a discrete ulcer penetrating the aortic wall with or without intramural hematoma.

While identification and characterization of the dissection remains extremely important, there are several other crucial aspects of the echocardiographic examination for a patient with aortic dissection. Functional aortic insufficiency (AI) occurs frequently in patients with acute Type A aortic dissection, with approximately 44% being severe AI.5 The mechanisms of the AI include incomplete leaflet closure due to leaflet tethering in a dilated aorta, aortic leaflet prolapse due to disruption of leaflet attachments, and dissection flap prolapse through the aortic valve orifice. The management of AI associated with aortic dissection is controversial. If the aortic valve leaflets are otherwise normal, preservation of the native valve can be achieved in up to 86% of Type A dissections.40

The aorta has several side branches, including the coronary arteries, cerebral vessels, celiac and mesenteric vessels, renal arteries, and spinal cord vessels, which can be compromised as a consequence of dissection. The incidence of coronary artery involvement in aortic dissection can be as high as 10% to 20%.41 The left main and right coronary arteries can often be reliably visualized in the ME AV SAX view.17 Direct evidence of coronary involvement is the presence of a dissection flap extending into the ostium of the coronary vessel. Indirect evidence includes electrocardiographic (ECG) changes, cardiovascular instability, and echocardiographic findings of regional wall motion abnormalities. Although branch arteries of the aortic arch can be reliably visualized with TEE,42,43 the use of additional modalities including epiaortic scanning and surface Doppler directly over the carotid arteries to assess dissection extent into the arch vessels is highly recommended.44 The remaining side branches including the renal, intestinal, and spinal cord vessels are more difficult to examine with TEE.

Other important echocardiographic findings include the presence of pericardial and left pleural effusions. Although pericardial effusions can result from the rupture of the dissection through the wall of the aortic root, the most common cause is from the transudation of fluid across the false lumen.4,45 The development of left pleural effusion is similar except for the fact that the rupture occurs in the descending thoracic aorta.46,47 A pericardial effusion appears as an echolucent space between the parietal and visceral pericardium on TEE. Echocardiographic signs suggesting tamponade include early diastolic collapse of the right ventricle, late diastolic/early systolic collapse of the right or left atrium, decreased size of the cardiac chambers, and abnormal ventricular septal wall motion with inspiration. A left pleural effusion is best seen in the descending aorta SAX view as an echolucent space that resembles a “claw” (Figure 16–7).

Intraoperatively, TEE is a valuable tool to monitor volume status and global and regional left ventricular function. It can also assist with cannulation and discern whether the malperfused side branches originate from the false or the true lumen—information that is essential in the surgical decision to reimplant these vessels. Finally, TEE can be used to evaluate the success of the surgical repair (ie, absence of blood flow in the false lumen) and assess for the presence of residual AI and resolution of wall motion abnormalities or pericardial and pleural effusions.

Stroke continues to be a significant cause of morbidity and mortality after cardiac surgery. Strokes occur in approximately 1% to 6% of patients following cardiac surgery and account for nearly 20% of deaths.48–50 The association between aortic atheromatous disease and stroke has been clearly defined.51–53 Techniques for detecting the presence of aortic atheromas include manual palpation, x-ray, magnetic resonance and tomographic scans, and cardiac catheterization. However, TEE and epiaortic ultrasound are generally considered to be superior imaging modalities.54,55

Several classification systems for grading the severity of aortic atheromas have been proposed. A commonly used system is that of Katz and colleagues who divided the severity of atherosclerosis into five grades (Table 16–2).52 It should be noted, however, that these measurement and categorization schemes are limited because they measure only maximal thickness and do not account for total plaque area (ie, “atheroma burden”) within any given segment of aorta. Furthermore, the thickness measurement is just a one-dimensional estimate of a three-dimensional atherosclerotic lesion. Another limitation of grading systems is that gray-scale density, calcification, surface texture, and ulceration are highly subjective atheroma characteristics and prone to interobserver variability. Irrespective of the specific classification system used, patients with advanced aortic atherosclerosis are at high risk for adverse outcomes—patients with grade 5 lesions have a 1-year mortality rate of 25%.52,56

Although TEE has been useful in diagnosing aortic atheromatous disease, it is not without limitations. The usual site for aortic cannulation and cross-clamping during cardiopulmonary bypass is the distal ascending aorta and proximal arch, which are difficult areas to visualize with TEE.57,58 It is also believed that aortic manipulation may result in plaque embolism and subsequent neurological injury.59 It is therefore possible to miss the presence of severe aortic disease with TEE alone. Konstadt et al found that severe atherosclerosis in the ascending aorta was not detected in 19% of cases.57 Epiaortic ultrasound has been shown to overcome this limitation and has emerged as the gold standard for detecting the extent and distribution of ascending aortic atherosclerosis.44,60 It is important to note that although it is possible to accurately detect atheromatous disease with a combination of TEE and epiaortic scanning, any subsequent alteration in surgical management has not been conclusively shown to reduce the incidence of neurological sequelae.61,62 There are numerous surgical techniques that focus on reducing the manipulation of the ascending aorta in an effort to decrease embolic events. These include using alternate atheroma-free sites for cannulation, cross-clamping, and placement of proximal anastomoses; deep hypothermic circulatory arrest for improved neurologic protection; off-pump approaches; and avoidance of cross-clamping altogether.60,63–66

Traumatic aortic disease is associated with an exceptionally high mortality.67,68 The reported mortality rate of patients who present to the hospital with a traumatic aortic injury is about 30%. Severe deceleration is the most common etiology, with the injury most commonly occurring at the aortic isthmus (approximately 54% to 67% of the time).67 Other sites of injury, in order of decreasing frequency, are the descending thoracic aorta, the aortic arch, and the abdominal aorta. Computed tomography (CT) scan and aortography remain the diagnostic imaging modalities of choice.69 However, these modalities can be time consuming, require transport of a potentially unstable patient, and necessitate administration of nephrotoxic contrast agents. In contrast, TEE, with a reported 91% sensitivity and 100% specificity, is noninvasive, can be performed at the bedside, and avoids the use of contrast agents, but may also be limited by availability of suitably trained personnel.6

Three types of lesions may be encountered: a subadventitial traumatic aortic rupture, a traumatic aortic intimal tear, or a mediastinal hematoma.6 The subadventitial traumatic aortic rupture may be partial, subtotal, or complete, and is characterized by the presence of blood flow on both sides of the disruption. A flap consisting of intima and media can also be found. There may be a disrupted aortic wall and a deformed aortic contour, although the aortic diameter is usually preserved. It can sometimes be very difficult to differentiate subadventitial traumatic aortic rupture from aortic dissection. Echocardiographic findings supporting subadventitial traumatic aortic rupture include asymmetrical contour at the level of aortic isthmus, thick and highly mobile medial flap, absence of tear, presence of mediastinal hematoma, similar blood flow velocities on both sides of the flap, and mosaic color Doppler flow surrounding the disruption. In contrast, TEE findings supporting aortic dissection include symmetrical enlargement of the aortic contour, thin and less mobile intimal flap, entry and exit tears, no mediastinal hematoma, thrombus formation in the false lumen, different blood flow velocities in both the true and false lumens, and finally, absence of mosaic color Doppler flow mapping on both sides of the intimal flap.

Traumatic aortic intimal tears appear echocardiographically as thin, mobile intraluminal appendages of aortic wall that are located in the region of the aortic isthmus. Since these lesions are small and superficial, the contour and diameter are unaffected, and color-flow mapping does not demonstrate turbulence. Mediastinal hematomas have three characteristic TEE findings: increasing space between the probe and the wall of the aorta, double contour aortic wall, and a distinct echogenic space between the bright aortic wall and the visceral pleura. This space is typically seen in the far field adjacent to the posterolateral aortic wall.

Associated lesions with traumatic aortic injury have been reported by Goarin and colleagues.70 These consist of pulmonary contusion, left pleural effusion, rib fractures, diaphragmatic rupture, mediastinal hematoma, hemopericardium, myocardial contusion, valvular lesions, and hypovolemia. Some of these lesions become apparent much later after the initial injury; hence, a follow-up TEE examination is mandatory.

In the early 1990s, the use of endovascular stents to treat aortic pathologies was introduced. Since then, stents have become an increasingly utilized alternative to conventional aortic surgery.71,72 There was initial skepticism for their use in the thoracic aorta due to concerns about their durability in this region with higher hemodynamic stress. However, as experience grew with their use in the thoracic aorta, endovascular stenting became a widely adopted practice and has been routinely used since the early 2000s for the treatment of complex aortic diseases.

On March 23, 2005, the U.S. Food and Drug Administration (FDA) approved the Gore TAG thoracic endoprosthesis. Since then, two other thoracic stent graft systems have received approval: the Medtronic Talent (Medtronic Vascular, Santa Rosa, CA, USA) and the Zenith TX-2 (Cook Medical Inc, Bloomington, IN, USA). Currently, the only FDA-approved indication for the use of these devices is for the treatment of thoracic aortic aneurysmal disease. However, endovascular stents are now being successfully used for other aortic pathology such as acute and chronic dissection, transection, and aorto-bronchial fistulae. The early results have been very promising, and long-term data on durability are awaited.73 In aneurysmal disease, the goal of the stent is to exclude the aneurysmal sac so that further dilation and disease progression can be prevented. In aortic dissection, the goal of the sent is to exclude the intimal tear, thus preventing its evolution. During an EVAR procedure, TEE is extremely valuable and can be used to verify pathology such as the site of the intimal tear, to identify the true and false lumen, to guide stent placement, to detect endoleaks, and to assess cardiac performance.74 It can also be used to take measurements of the aorta and the aortic lesion, document side branch patency, and detect static or dynamic obstruction. An added benefit of TEE is the noninvasive visualization and direction of guidewires and catheters on short- and long-axis views of the aorta, thus reducing the need for nephrotoxic contrast agents. A guidewire appears as a linear echo-dense intraluminal structure. TEE is also an excellent hemodynamic monitor, especially during inflation of the balloon to unfold the stent. Similar to cross-clamping of the aorta, inflation of the balloon can cause significant aortic occlusion and subsequent strain on the heart, and result in regional or global myocardial ischemia. Newer endoaortic balloons, however, incorporate a nonocclusive design that permits partial flow, thereby reducing the extent of myocardial strain. However, TEE use is limited by the poor visualization of the distal ascending aorta and proximal arch, and by the need for general anesthesia. There is also the potential interference of the TEE probe with fluoroscopy during procedures in the aortic arch.

Although an off-label indication, the use of EVAR for dissection deserves special consideration. First, sizing of the endograft is based solely on the diameter of the aorta at the proximal landing zone, since the distal zone will include both the true and false lumens. This is in contrast to aneurysms where both proximal and distal aortic diameters must be considered. Second, it is critical for the guidewire of the endograft delivery system to be within the true lumen. This can be easily facilitated with TEE, which is superior to angiography in this regard. Finally, TEE can be useful in identifying distal fenestrations between the true and false lumens, which may determine the number of endografts to be used.

Another emerging indication for EVAR is traumatic aortic transections. These patients are typically young, have multiple injuries, and are critically ill. They are also hyperdynamic, which makes endograft deployment challenging. TEE imaging can also be difficult in a setting where there may be multiple surgical specialties involved, and facial or spinal injuries may limit the opportunities for esophageal imaging. A distinct feature from an echocardiographic perspective is that the left subclavian artery is almost always covered, and loss of flow on CFD imaging should be expected.

An endoleak is a common complication following endovascular repair of the aorta. It is characterized by persistent blood flow within the aneurysmal sac or adjacent vascular segment being treated by the stent, and may occur in 20% of patients.75 Endoleaks are characterized into four types based on location (Table 16–3)76 and can also be classified on the basis of time of occurrence: primary endoleaks are detected within the first 30 days postoperatively while secondary endoleaks occur after 30 days. Endoleaks can also be detected by TEE, which has been demonstrated to be more sensitive than angiography (Figure 16–8).77,78 A limitation of angiography is that it relies on a fixed volume of contrast to circulate within the endoleak. Therefore, smaller leaks may be overlooked because the volume of contrast within the leak may not be detectable by fluoroscopy, or the imaging angle may not be aligned to detect the endoleak. Most endoleaks can be detected using CFD in the region of the aneurysmal sac. However, endoleaks that are in the far field may be obscured by echo-dense endograft material. Additionally, the color scale for CFD may need to be reduced in order to visualize low-flow leaks. Another echocardiographic sign of an endoleak is the development of spontaneous echo contrast (SEC, or “smoke”) within the aneurysmal sac following the deployment of the stent.79 The sudden development of SEC in a previously quiescent aneurysmal sac should alert the echocardiographer to the potential presence of an endoleak. Contrast that swirls or moves around the sac may indicate an endoleak, while static contrast indicates no movement or flow within the sac, suggesting the absence of any endoleak. Detecting endoleaks intraoperatively also provides the opportunity for immediate corrective interventions.

Coarctation of the aorta is a congenital narrowing of the aorta at the level of the aortic isthmus. Described more completely in Chapter 18, a coarctation can be preductal, ductal, or postductal, and can vary in length. It is commonly associated with other cardiac abnormalities including bicuspid aortic valve and patent ductus arteriosus. The classical presentation is arterial hypertension in the right arm with normal to low blood pressure in the lower extremities. TEE findings include narrowing of the aorta distal to the subclavian artery and turbulent blood flow on CFD. The anatomical position of this lesion makes transthoracic echocardiography the imaging modality of choice. The coarctation is best visualized with the transducer at the suprasternal notch.

Transesophageal echocardiography is invaluable for perioperative imaging of the aorta. The anatomical juxtaposition of the aorta and esophagus makes TEE an ideal imaging tool, especially for thoracic aortic pathology. From complex lesions in the ascending aorta to endovascular stenting, TEE can provide valuable information to the intraoperative echocardiographer, including lesion identification, measurement of aortic dimensions, quantification of associated abnormalities like aortic incompetence, and detection of complications such as endoleaks.