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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3734_Библиотеки_им_академика_М_И_Перельмана
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Z. Hartley-Blossom et al.
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Fig. 7 Axial (a) and coronal (b) postcontrast CT images of a 75-year old man with chest pain
demonstrating a ruptured type A IMH (white arrows) with an ulcer-like projection in the posterior
ascending aorta (arrowhead). Soft tissue density material surrounding the main and right pulmonary
arteries (MPA, RPA) represents mediastinal blood tracking into the shared adventitia between the
aorta and pulmonary arteries—a ‘shared-sheath’ hematoma (dotted arrows). Note that the irregular
mural atheroma in the mid descending aorta (yellow arrow) is slightly lower density than the IMH
and lacks its smooth crescentic morphology. AA Ascending aorta
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an imaging appearance referred to as the “Chinese ring-sword sign” [45] (Figs.9
and 10). IBPs are most commonly identied in the descending aorta, and do not
confer any specic increased risk for progression or complication, however those
hematomas are less likely to completely resolve [44, 46].
IMH typically results in smooth thickening of the aortic wall. PAU in contrast
has an irregular lumen—due to atheroma—with a focal luminal outpouching, mural
thickening, and bulging of the overlying adventitia (Figs.11 and 12). The appearance
is characteristically mushroom-like, especially at angiography. The location of the
lesion can help differentiate between IMH and PAU if imaging characteristics are
not clear (as can often be the case). PAU is overwhelmingly (>90%) found in the
mid-descending aorta, while IMH lesions can be found anywhere throughout the
aorta [8, 47]. Finally, at least a small IMH is commonly seen with PAU.In these
cases, it can often be best to describe and localize the ndings rather than trying to
specically categorize the lesion.
MRI ndings of IMH and PAU are morphologically similar to CT, with a crescentic region of abnormal signal within the aortic wall with IMH, and a focal atheroma-associated luminal outpouching and accompanying outer wall bulging with
PAU.As discussed previously, cine imaging can offer dynamic visualization of intimal aps in the setting of dissection. With its excellent soft-tissue contrast, MRI can
detect small regions of intramural blood conrming the diagnosis of IMH/PAU in
questionable cases and dynamic postcontrast T1-weighted imaging will reveal the
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Fig. 8 Type B IMH in a 57-year old woman with a few days of chest and back pain. Transaxial CT
images (a–d) obtained on the same day as the MRI study in gure 9 and 3 years later (e–h). There
is a relatively smooth low-density crescent of intramural hemorrhage (arrows) with a few intramural blood pools (IBPs) (arrowheads). Except for minimal mural thickening and a single IBP, there
has been near complete resolution of the lesion on follow-up imaging. AA Ascending aorta; DA
Descending aorta; MPA Main pulmonary artery
absence of enhancement in such cases (Figs.9, 10, and 16). Wall-thickening due to
vasculitis—an occasional IMH mimicker—will on the other hand show mural
enhancement. Moreover, the varying magnetic states of hemoglobin allow MRI to
better date a lesion’s chronicity. Hyperacute hemorrhage (oxyhemoglobin), acute
(deoxyhemoglobin), early subacute (intracellular methemoglobin), late subacute
(extracellular methemoglobin), and chronic (hemosiderin), all have different signal
characteristics on T1- and T2- weighted MRI which aids in ascertaining lesion acuity (Figs.9 and 10).
Diagnostic Pitfalls
As noted in the preceding section IMH and PAU share imaging features and may in
fact co-exist. Other conditions may mimic these lesions, and imaging ndings must
therefore be clearly interpreted in the appropriate clinical context. For example,
large vessel vasculitides such as Takayasu aortitis and giant cell arteritis can result
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Fig. 9 Same patient as in Fig.8. Candy cane (a & b) and transaxial (e-h) magnetic resonance
images using T1-weighted fast spin echo (FSE) with fat saturation (FS) (a) without FS (e),
T2-weighted FSE without (b & f) and with FS (g), and a single frame from a cine acquisition using
steady-state free precession (SSFP) (h). In addition shaded surface display (SSD) (c) and maximum
intensity projection (MIP) images (d) from an MR angiogram are shown. Arrows identify IMH in
the descending thoracic aorta. Bright signal on both T1- and T2-weighted images indicated blood
products chiey in the extracellular methemoglobin phase consistent with a subacute to chronic
lesion. Small outpouchings seen on the MRA images (arrowheads) represent intramural blood
pools (IBP) that are pseudoaneurysms of small branching vessels, in this case intercostal arteries,
within the aortic wall. When multiple IBPs are present the appearance resembles a so-called
Chinese ring-sword. AA Ascending aorta; DA Descending aorta; M PA Main pulmonary artery
in smooth thickening of the aorta that strongly resembles IMH (Figs.13 and 14).
Here, the clinical scenario and laboratory biomarkers may be critical in rendering a
prompt and accurate diagnosis. Heaped-up atheroma with extensive irregularity and
ssuring can mimic PAU (Fig.15). However, non-calcied atheroma has uniformly
low density and does not lead to outward bulging of the adventitia. Moreover, the
periaortic fat should be easily demarcated from the aortic wall, in contrast to the
indistinct appearance typically seen in PAU. On postcontrast CT imaging felt
pledgets commonly used in aortic surgery have a density at CT that is often
indistinguishable from intravascular contrast and may also mimic a PAU (Fig.16).
Correlation with prior surgical history is usually adequate to assuage any concerns,
but if there is lingering question noncontrast CT imaging or MRA will readily
resolve the issue. Uncommonly, uid in the superior aortic pericardial recess may
resemble an IMH.Although familiarity with this and other recesses usually sufces
to avoid any confusion, in rare cases, additional imaging may be necessary. Finally,
motion related artifacts are commonly seen near the aortic root. Here again, while
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Fig. 10 IMH of the abdominal aorta in a 45-year old woman with acute abdominal pain by MRI
(a-d, h) and CT (e-g). Axial (a) and coronal (b) T1-weighted noncontrast MRI demonstrate
crescentic high T1-signal in aortic wall (arrows) consistent with IMH.Subtraction postcontrast
coronal T1-weighted imaging (c) shows no enhancement of the wall as well as small outpouchings
(dotted arrows) representing intramural blood pools (IBP) which are pseudoaneurysms of lumbar
arteries within the aortic wall. These IBPs are also evident on coronal oblique MRA maximum
intensity projection (MIP) (d) and shaded-surface display (SSD) (h) reconstructions that also show
aortic narrowing but that—as luminograms—do not show the IMH itself. Also noted on the MRA
images is an incidental 1.8 cm splenic artery aneurysm (arrowheads). Note also that a right
common iliac artery ulcer-like projection (ULP) is evident on the SSD (red arrowhead). CT images
obtained a few days earlier also show the IMH (arrow) and IBPs (dotted arrows)
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Fig. 11 Penetrating atherosclerotic ulcer. Ten months after a CT scan demonstrated a normal caliber, atherosclerotic descending thoracic aorta (a), this patient presented with acute back pain and
evidence at repeat CT (b) of a new focal aortic ulceration at the site of atheroma consistent with a
PAU (white arrow). There is circumferential high-density thickening of the wall (yellow arrows)
likely due to a component of short-segment IMH, and the aortic wall is indistinct. Images (c) and
(d) demonstrate the lesion at angiography (white arrow) before and after stenting. Notice on (c) the
characteristic mushroom-like outpouching. DA Descending aorta
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a b
Fig. 12 Penetrating atherosclerotic ulcer in a patient with acute chest and back pain. Image (b) is
a zoomed in view of the descending thoracic aorta shown in image (a). A small PAU is seen in the
posterior aspect of the atherosclerotic aorta (white arrow). There is circumferential high-density
thickening of the indistinct aortic wall (yellow arrows) likely due to a component of short-segment
IMH.A small reactive pericardial effusion is seen adjacent to the aorta (dotted white arrows)
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Fig. 13 Aortitis conned to the aortic arch in a 53-year old man with chest pain. Transaxial (a-d)
and coronal (e) images demonstrate asymmetric thickening of the lateral aspect of the aortic arch
(arrows) without increased density on noncontrast imaging (c) conrming that this lesion was not
an acute IMH.Laboratory studies conrmed the diagnosis of vasculitis and follow-up imaging
4months later (f-h) conrmed improvement after appropriate medical management
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Fig. 14 Aortitis of the ascending aorta seen on abdomen CT (a) and unchanged 4months later (b).
Images demonstrate near circumferential thickening of the ascending aorta. This appearance may
be indistinguishable from type A IMH at imaging and careful history and clinical examination
must be undertaken to help differentiate the two entities. A small pericardial effusion present on
the rst study has essentially resolved by the second
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Fig. 15 Axial CT images in a patient with no pertinent symptoms demonstrate irregular atheroma
mimicking a PAU (white arrows). Images (a) & (c) are from the same study and image (b) from a
study 5months later. Notice the similarity of appearance of the ssured and excavated atheroma in
images (a) and (c). Also, note the similarity of appearance to the lesion in Fig.11. The plaque at
this level has uniform low-density. Image (b) demonstrates calcication on both sides of the plaque
in the anterior aorta (arrow). This should not be confused with the medially displaced plaque of
IMH or dissection
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Fig. 16 Axial CT images of a patient who had a prior aortotomy. High density felt pledgets that
are easy to recognize and dismiss on noncontrast CT (a) (arrow) can mimic a PAU on postcontrast
imaging owing to a similar density to luminal contrast (b). Note however that there are no ancillary
ndings such as mural thickening or adjacent fat stranding to suggest an acute aortic injury
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familiarity with the appearance of these artifacts is usually sufcient to rule in or
rule out pathology, persistent concerns should be managed with additional imaging,
including ECG-gated CT, ECG-gated MRI, or echocardiography.
Predictors ofOutcome
The natural history of IMH and PAU is variable. IMH may resolve, stabilize,
enlarge, or progress to aneurysm, dissection, or frank rupture. Hemopericardium
may result in cardiac tamponade; hemorrhage across the shared adventitia of the
ascending aorta and main pulmonary artery gives rise to a so-called ‘shared-sheath’
or ‘pulmonary sheath’ hematoma that can compromise pulmonary blood ow
(Figs.5 and 7); coronary artery involvement may result in myocardial ischemia and
infarction [48]. Various vignettes and outcomes are provided in Figs.8, 11, 13, 17,
18, 19, 20, and 21.
In addition to the presence and size of ULPs described earlier, other imaging
biometrics of IMH are known to correlate with risk of complications. Maximum
aortic diameter (MAD) and maximum aortic wall/IMH thickness have been shown
to correlate with outcomes. A MAD of ≥45–55mm for the ascending aorta and of
>40–41mm for the descending aorta are associated with lesion progression [15,
49–52]. Maximum aortic wall/IMH thickness>10–16mm is also considered high
risk for progression/complications [15, 44, 51, 53] (Fig.16). Finally, a ratio of the
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Fig. 17 Near concurrent MRI (a-d) and CT (e-h) images of a 65-year old man with chest and back
pain demonstrate acute type A IMH (white arrows). Transaxial (a, b) and candy-cane (c, d) magnetic resonance images using single frame from a cine acquisition using steady-state free precession (SSFP) (a), T1-weighted fast spin echo (FSE) with fat saturation (FS) (b), T2-weighted FSE
with FS (c), and T1-weighted gradient echo (GRE) with contrast (d). As expected, there is no
enhancement of the lesion after contrast. The maximum thickness of the IMH is 18mm (g) which
is believed to be a high-risk feature (>10–16mm). The patient was initially treated medically. He
returned with chest pain one month later and CT revealed (h) that the lesion had converted to a
dissection with a complex dissection ap in the aortic arch (yellow arrows). He was subsequently
operated on. AA Ascending aorta; DA Descending aorta
minimum and maximum luminal diameters at the site of maximum IMH thickness—referred to as the luminal compression ratio—of <0.75 is associated with
worse outcomes [54].
Management/Outcomes ofIMH andPAU
Detailed medical and surgical management strategies for IMH and PAU are discussed elsewhere. In general, the management of these lesions is chiey determined by the location of the lesion (Type A or Type B), any associated active or
impending complications, prognostic factors described above, and patient status
including their frailty or robustness for surgery. Historically, surgery is indicated
for Type A lesions and medical therapy or endovascular stenting for Type B
lesions. The necessity for urgent or emergent surgery for Type A IMH has been
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Fig. 18 95-year old woman with chest pain and known ascending aortic (AA) aneurysm. Axial
CT images with contrast (a-d) show a subtle type B IMH involving the proximal descending aorta
(DA) (arrows). A small intramural blood pool associated with an intercostal arrow is evident (solid
yellow arrow) (a). Images from 9months prior (e-h) conrm that the AA aneurysm is stable, but
that the IMH is new. Also note the normal appearance of the intercostal artery in question (dotted
yellow arrow) and the interval increase in mural atheroma (dotted arrows) which has a slightly
lower density than the hemorrhage
challenged by the observation that stabilization and regression are possible in an
appropriately selected subgroup of patients whose imaging biometrics are favorable and whose blood pressure and pain control are adequate. In this population,
a conservative approach has been found to be safe and feasible—though surgery
may at some point be necessary—and outcomes appear to be very good and comparable to surgery [52, 55]. In the acute setting, medical management is virtually
always initiated emergently—including aggressive blood pressure (systolic
<110–120mmHg), heart rate (<70 beats/min), and pain control—while the decision on whether and when to proceed to surgery is considered [1, 37, 51]. For
those IMH and PAU patients who are managed medically, close clinical and imaging surveillance over the rst few days—and temporally more spread-out thereafter—may therefore represent a reasonable initial management strategy. A potential
follow-up strategy includes imaging multiple times in the rst week, then weekly
for 2–4weeks, monthly for the next 3–6months, and at 6–12months thereafter,
unless complications are suspected [53]. Overall, patients with type A IMH are
considerably more likely to progress (88%) than patients with type B IMH
(3–15%) [1, 23, 56].
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Fig. 19 Axial (a-d) and sagittal (e) postcontrast CT images demonstrate a ruptured type B IMH in
an 80-year old woman with acute chest and back pain. High density material consistent with acute
hemorrhage (arrows) is seen around the descending aorta (DA), throughout the posterior
mediastinum, and in the pleural spaces bilaterally, right more than left. Intramural blood pools
(IBPs) are present (dotted arrows). Angiographic views pre- (f) and post- (g) endovascular stent
placement show successful coverage of IBPs and resolution of contrast extravasation. Single axial
postcontrast CT image 18 months later (h) reveals resolution of IMH and hemorrhage. AA
Ascending aorta
Conclusions
Aortic IMH and PAU are two lesions in the spectrum of acute aortic syndromes and
their timely diagnosis is crucial for optimizing patient outcomes. CT is the primary
initial imaging modality because of its accuracy, speed, and widespread and rapid
availability. MRI demonstrates comparable accuracy and is generally used for
problem solving and imaging follow-up. Pitfalls in accurate imaging diagnosis are
important to consider but can usually be resolved with careful scrutiny and repeat or
additional imaging when appropriate.
Management decisions for IMH and PAU are guided by clinical and imaging
ndings, the latter including Stanford classication, maximum aortic diameter,
maximal hematoma thickness, the presence, size, and location of an intimomedial
injury (ULP/FID), and the presence and size of extra-aortic complications such as
pleural and pericardial effusions and mediastinal hematomas. The majority of type
A lesions are treated surgically, although there has been a growing body of literature
showing that medical management may be equally efcacious in appropriately
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