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10. Follow-Up Strategy. After discharge, follow-up by CT or MRI is indicated depending on technique availability, preferential informa- tion sought, and patient characteristics such as age, renal function, and test tolerance at 3, 6, 12 months and annually thereafter. C. IMH 1. Introduction. Advances in aortic imaging technology, including TEE, CT, and MRI, have led to increasing recognition of aortic IMH among patients with AAS. IMH, generally considered to be a variant of aortic dissection, accounts for approximately 10% to 25% of AAS ( Table 10
). IMH was first described in 1920 as ‘‘dissection without intimal tear’’ 212 and was believed to result from rupture of the vasa vasorum, allowing bleeding between the elastic lamina of the aortic media.
79,212,213 However, recent findings suggest that at least some IMHs may be initiated by small intimal tears that are undetectable by current aortic imaging modalities and are often overlooked on gross inspection of the aorta at the time of surgery or autopsy. 214-217
IMH is not a single entity but can be associated with several conditions, including spontaneous (‘‘typical’’) aortic dissection, penetrating ulcer, aortic trauma, and iatrogenic dissection (cardiac catheterization, cardiac surgery). 2. Imaging Hallmarks and Features. The imaging hallmarks of classic aortic dissection—the presence of a dissection flap and the pres- ence of a double channel aorta—are both absent in IMH ( Figure 38 ) In
addition, there is usually no reentry site. General imaging features of IMH are listed in Table 11 . Typically, IMH appears as thickening of the Figure 42 CTA illustrating an IMH. The arrow points to the crescent-shaped thickened wall due to the IMH. Note the lumen (L) is preserved. Figure 41 This diagram illustrates the different appearances of the hemiazygos sheath (a normal structure), atherosclerotic plaque, and an aneurysm containing a mural thrombus from an IMH. Journal of the American Society of Echocardiography Volume 28 Number 2 Goldstein et al 149 aortic wall > 0.5 cm in a crescentic or concentric pattern ( Figures 39 and 40 ). As mentioned, a mobile dissection flap is absent. The aortic lumen’s shape is preserved, and the luminal wall is curvilinear and usually smooth, as opposed to a rough, irregular border seen with aortic atherosclerosis and penetrating ulcer, although both may coexist. There is no Doppler evidence of communication between the hematoma and the true lumen, but there may be some color Doppler flow within the hematoma. There may also be areas of echolucency within the aortic wall hematoma. IMH is generally a more localized process than classic aortic dissection, which typically propagates along the entire aorta to the iliac arteries. IMH may weaken the aortic wall and either progress outward with aortic expansion and/or rupture or inward with disruption of the intima-media, resulting in typical aortic dissection. Evangelista et al. described seven evolution patterns: regression, progression to classical dissection with longitudinal propagation, progression to localized dissection, development of fusiform aneurysm, development of saccular aneurysm, development of pseudoaneurysm, and persis- tence of IMH. Therefore, serial imaging is necessary to rule out pro- gression in patients who receive only medical treatment, because clinical signs and symptoms cannot predict progression. Although there are no established guidelines for the optimal frequency and lon- gitudinal duration for surveillance imaging of patients with IMH, Evangelista et al., 154 on the basis of the significant dynamic evolution of IMH, recommended imaging at 1, 3, 6, 9, and 12 months from the time of diagnosis. Once stability has been documented, surveillance imaging may be annual. IMHs present a more difficult diagnostic challenge than typical aortic dissections because of the lack of both flow and an oscillating dissection flap. Because IMH thickness may be progressive, establish- ing the diagnosis of IMH may require observation time and repeat im- aging. Evangelista et al. 218 demonstrated that the initial imaging test results were negative in >12% of patients and that a repeat study was required hours to several days later. IMH can be difficult to distin- guish from a thrombosed false lumen of classic aortic dissection, because they can both appear as a crescent-shaped thickening of the aortic wall. However, in aortic dissection, the diameter of the thrombosed false lumen is usually larger than that of most, but not all, IMHs. Conversely, the circumferential extent of an IMH is usually larger than that of an aortic dissection. The appearance of a crescent- shaped thickening of the aortic wall can be mimicked by a normal structure, the hemiazygos sheath, which is a periaortic fat pad. 219 This fat pad is typically present on TEE when the tip of the probe is 30 to 35 cm from the incisors. Aortic atherosclerosis results in thickening of the aortic wall but produces an irregular intraluminal surface that differentiates it from IMH, which has a smooth luminal surface. Moreover, the ‘‘lumpy-bumpy’’ appearance of atherosclerosis tends to vary along each centimeter of the aorta, unlike IMH, which tends to be smooth over a greater length of the aorta. Mural thrombus may appear lining a TAA, most often in the descending aorta, but typi- cally has an irregular luminal surface, narrows the lumen and does not extend longitudinally as much as IMH. Figure 41 illustrates the different features of several of these entities from IMH. Aortitis causes thickening of the aortic wall that is typically concentric and typically has normal segments interspersed between the involved sites. Detection of IMH by CT shows thickening of the aortic wall with higher attenuation than intraluminal blood (from 40 to 70 Hounsfield units) on contrast-enhanced CT ( Figure 42 ). It is vitally important to perform unenhanced CT as the first step in the computed tomographic imaging evaluation of a suspected AAS, because contrast material within the lumen may obscure the IMH. On imaging follow-up of IMH, the appearance of ulcerlike projec- tions (ULPs) is frequently observed, likely representing intimal rup- tures that allow communication between the aortic lumen and the medial wall hematoma. 220 MRI offers the possibility of diagnosing in- tramural bleeding in the hyperacute phase because the hematoma shows an isointense signal on T1-weighted images and a hyperintense signal on T2-weighted images. From the first 24 hours, the change from oxyhemoglobin to methemoglobin determines a hyperintense signal on both T1- and T2-weighted images that together with fat sup- pression is useful for differentiating periaortic fat from IMH. Although greater availability and shorter examination duration favor the use of Table 12
IMH: key points IMH represents hemorrhage into medial layer of aorta Absence of dissection flap between a double-channel aorta Crescentic or concentric thickening of aortic wall Can progress to localized or frank dissection or rupture IMH thickness and maximal aortic diameter predict risk for pro- gression CT appearance is high-attenuation eccentric or concentric wall thickening on noncontrast image Subtle wall thickening can be missed at inexperienced centers Figure 43 Diagram illustrating the characteristic features of a penetrating atherosclerotic ulcer: presence of severe athero- sclerosis and penetration of the ulcer or ‘‘outpouching’’ into the media. Figure 44 Gross pathology specimen from a patient with a ruptured penetrating atherosclerotic ulcer (small arrow) associ- ated with IMH and blood external to the aortic wall (large arrow). 150 Goldstein et al Journal of the American Society of Echocardiography February 2015 CT in the acute setting, MRI may be complementary for the diagnosis of IMH. The greater contrast among tissues can allow MRI to detect even small IMHs that may go unnoticed by CT. In addition, mural thrombi in TAAs are easier to distinguish from IMH by MRI because mural thrombus shows a hypo- or isointense signal in both T1- and T2-weighted sequences. 3. Imaging Algorithm. CT may be considered the first-line diag- nostic imaging modality for IMH, particularly in the acute setting. Detection is based on the high-attenuation signal of acute bleeding by noncontrast enhancement. When findings on CTor TEE are equiv- ocal, MRI may be valuable, as the hyperintense signal in the aortic wall can facilitate a correct diagnosis. 4. Serial Follow-Up of IMH (Choice of Tests). As above, IMH may evolve by reabsorption, aneurysm formation, or conversion to classic dissection. 154
In one series, IMH regressed completely in 34%, led to aneurysm in 20% and pseudoaneurysm in 24%, and progressed to aortic dissection in 12%. Because of their wide field of vision allowing the identification of landmarks, MRI and CT are superior to TEE for defining this dynamic evolution. On surveillance imaging of IMH, the appearance of ULP is frequently observed, and such ulcers may rupture and allow communication between the medial hematoma and the aortic lumen. 221,222 MRI offers the possibility of diagnosing the intramural bleeding evolution and new asymptomatic intramural rebleeding episodes. 5. Predictors of Complications. Most of these predictors may be defined by imaging techniques: 1. Maximum aortic diameter in the acute phase is one of the major predictors of progression in type B IMH and therefore should be reported. Patients with maximum aortic diameters > 40 to 50 mm have a higher risk for dissection, regardless of the location within the descending aorta. 216,223-229 2. Wall thickness has been described as a predictor of progression; however, not all studies have supported this finding. The thickness threshold for pre- dicting progression has been variably reported to be 10, 12, or 15 mm. 228
3. The incidence of periaortic hemorrhage or pleural effusion is higher in IMH than in aortic dissection; in some studies, this incidence reaches to 40%. Some series related pleural effusion to worse prognosis in IMH; however, this remains controversial. Two mechanisms have been described: leakage of blood from the aorta through microperforations or a nonhemorrhagic exudate believed to be inflammatory in origin owing to the proximity of the IMH to the adventitia. 210,230
The likely different prognostic significance of the two pathogenic theories proposed may explain the discordance in the medical literature. Key points related to IMH are listed in Table 12 . D. PAU 1. Introduction. The term penetrating aortic ulcer describes the con- dition in which ulceration of an atherosclerotic lesion penetrates the aortic internal elastic lamina into the aortic media ( Figure 43 ). 231 Although the clinical presentation of PAU is similar to that of classic aortic dissection, PAU is considered to be a disease of the intima (i.e., atherosclerosis), whereas aortic dissection and its variant (IMH) are fundamentally diseases of the media (degenerative changes of the elastic fibers and smooth muscle cells are paramount), and most patients with aortic dissection typically have little atherosclerotic dis- ease. PAUs may occur anywhere along the length of the aorta but appear most often in the mid and distal portions of the descending thoracic aorta, and they are uncommon in the ascending aorta, arch, and abdominal aorta. 232 PAUs are sometimes multifocal, which is to be expected because aortic atherosclerosis is a diffuse process. They may occur in an aorta of normal caliber but are more often pre- sent in aortas of increased diameter. 232-235
Typically, when an ulcer penetrates into the media, a localized IMH develops ( Figure 44 ). In most patients, this IMH is localized, but occa- sionally it can involve the entire descending aorta. 223
Rarely, the medial hematoma ruptures back into the aortic lumen, resulting in a classic-appearing dissection with flow in both lumens. Once formed, PAUs may remain quiescent, but the weakened aortic wall may provide a
for saccular, fusiform, or false aneurysm formation. 231,233,224-227 External rupture into the mediastinum or right or left pleural space may occur but is uncommon. 233,234
Embolization of thrombus or atherosclerotic debris from the ulcer to the distal arterial circulation may also occur. 2. Imaging Features. The diagnosis of PAU requires demonstra- tion of an ‘‘ulcerlike’’ or ‘‘craterlike’’ out-pouching in the aortic wall (the internal elastic lamina is not visible on imaging studies), as seen in Figure 45 . Because protrusion through the internal elastic lamina cannot be identified, PAUs can be detected only when they protrude outside the contour of the aortic lumen. Atheromatous ulcers that do not enter the media may be hard to distinguish from PAUs. Therefore, a diagnosis of PAU must be made with caution, especially if the sus- pected aortic defect has been detected incidentally. Another entity that may be mistaken for a PAU is a ULP that may evolve from an IMH, as described above. These are localized, Figure 45 Transesophageal echocardiogram from a patient with a penetrating atherosclerotic ulcer (arrow). Note the prom- inent aortic atheroma (not labeled). Table 13 PAUs: imaging parameters to report Lesion Location Lesion width, length, depth Aortic diameter at the level of the lesion Presence/absence/extent of IMH Contrast extension beyond/outside aortic wall Mediastinal hematoma Pleural effusion Presence and length of false lumen Journal of the American Society of Echocardiography Volume 28 Number 2 Goldstein et al 151
blood-filled pouches that protrude into the IMH, with a wide communicating orifice of >3 mm. ULPs are felt to be the conse- quence of a focal dissection and a short intimal flap resulting in a small pseudoaneurysm. Differentiation from a PAU may be diffi- cult. Generally, a PAU has jagged edges, is accompanied by multi- ple irregularities in the intimal layer, and may be accompanied by localized hematoma. TEE, CT, and MRI may all detect PAU and its complications. Once identified, attention should be directed to assessing (1) the maximum depth of penetration of the ulcer, measured from the aortic lumen; (2) its maximum width at the entry site; and (3) the axial length of the associated medial hematoma. Observations that should be re- ported are listed in Table 13
. 3. Imaging Modalities. a. CT.–The typical computed tomographic finding of a PAU is a localized contrastlike out-pouching of the aortic wall communicating with the lumen. Its appearance has been likened to a ‘‘collar button.’’ 228
As mentioned above, PAUs are most often found in the mid or distal descending thoracic aorta. 226 Thickening (enhance- ment) of the aortic wall external to sites of intimal calcification suggests localized IMH. These findings are usually in conjunction with severe atherosclerosis. CT has certain advantages over TEE. It can examine areas of the aorta not covered by TEE, allowing more complete identi- fication of the out-pouching produced by PAUs. Moreover, it can also identify calcified atherosclerotic plaques surrounding the ulcer. Computed tomographic angiography is also more likely than TEE to demonstrate extraluminal abnormalities, including pseudoaneurysm or fluid in the mediastinum or pleural space.
which appear as areas of high signal intensity within the aortic wall on T1-weighted images. 79,229
Yucel et al. 236
demonstrated that MRI is superior to conventional CT for differentiating acute IMH from atherosclerotic plaque and chronic intraluminal thrombus. MRI has the additional advantage of providing multiplane images without the use of contrast material.
nosis of PAU but may be of value when the results of CT and MRI are inconclusive. The characteristic finding, similar to what is seen on CT and MRI, is a craterlike out-pouching of the aortic wall, often with jag- ged edges, usually associated with extensive aortic atheroma. Although uncommon, a localized aortic dissection may occur, but the dissection flap, if present, tends to be thick, irregular, nonoscillat- ing, and usually of limited length. 237 The reason for the limited length of the dissection may be that the dissection plane is lost because of scarring or atrophy of the media and secondary to the atherosclerotic process.
to diagnose PAU because of the superiority of current axial imaging modalities and the high definition of TEE. These modalities also Table 14
Recommendations for choice of imaging modality for PAU Modality
Recommendation Advantages Disadvantages CT First-line Superior to TEE for detecting PAU, especially small PAUs Permits assessment of entire aorta and other thoracic structures Detects extraluminal abnormalities better than TEE (e.g., pseudoaneurysm, mediastinal fluid) Follow-up by CT recommended Ionizing radiation exposure and iodinated contrast material MRI Second-line Provides multiple images without contrast Excellent for detecting associated IMH complicating PAU Excellent for differentiating primary IMH from atheroscle- rotic plaque and intraluminal thrombus Less widely available than CT Operator dependent TEE Third-line Differential diagnosis between PAU and ULP Less well studied than CT or MRI Semi-invasive Operator dependent Table 15 Etiologies of TAAs 1. Marfan syndrome 2. BAV-related aortopathy 3. Familial TAA syndrome 4. Ehlers-Danlos syndrome type IV (vascular type) 5. Loeys-Dietz syndrome 6. Turner syndrome 7. Shprintzen-Goldberg (marfanoid-craniosynostosis) syndrome 8. Noninfectious aortitis (e.g., GCA, TA, nonspecific arteritis) 9. Infectious aortitis (mycotic syndrome) 10. Syphilitic aortitis 11. Trauma 12. Idiopathic Figure 46 Diagram illustrating the two morphologic types of aortic aneurysms: saccular and fusiform. 152 Goldstein et al Journal of the American Society of Echocardiography February 2015 provide superior definition of the surrounding wall, making identifi- cation of associated IMH easier. The characteristic aortography finding, a contrast medium–filled out-pouching resembling an ulcer of the gastrointestinal tract, is typically associated with ‘‘cobbleston- ing’’ of the aortic wall in the region of the ulcer consistent with diffuse atherosclerosis, in the absence of a dissection flap or false lumen. 4. Imaging Algorithm. CTA is considered the first-line diagnostic imaging modality. 226,234,238-240 It is widely available, permits assessment of other thoracic structures, and provides
3D reconstructed images that are essential in planning surgery or TEVAR. Moreover, CT is superior to TEE for detecting small ulcers. It is also efficient for the evaluation of the degree of ulcer penetration and bleeding into or outside the aortic wall. MRI is excellent for differentiating PAUs from IMH, atherosclerotic plaque, and intraluminal chronic mural thrombus. 241,242
However, MRI is less widely available than CT and is unable to detect displacement of intimal calcification, which frequently accompanies PAU. Recommendations for choice of imaging modalities for PAUs are summarized in Table 14
. Despite differences in opinion regarding the natural history and management of PAUs, there is agreement that all PAUs, even those found incidentally, warrant close clinical and imaging follow-up, usu- ally by CTA. Findings concerning for progression include an increase in aortic diameter or wall thickening or the appearance of a thin- walled saccular aneurysm. Rupture is indicated by the presence of extra-aortic blood. 5. Serial Follow-Up of PAU (Choice of Tests). The natural history of PAU is unknown. As with IMH, several outcomes have been described. Many patients with PAUs do not need immediate aortic repair but do require close follow-up with serial imaging studies, by CT or MRI, to document disease progression. Although many authors have documented the propensity for aortic ulcers to develop progressive aneurysmal dilatation, the progression is usually slow. Spontaneous complete aortic rupture is uncommon but may occur. Some PAUs are found incidentally, in which case size and progressive enlargement are the only predictors of complications. Both CT and MRI provide superior assessment to TEE in the follow-up of PAU. Yüklə 9,02 Mb. Dostları ilə paylaş:
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