Journal of Cardiothoracic and Vascular Anesthesia ] (]]]]) ]]]–]]]

Contents lists available at ScienceDirect

Journal of Cardiothoracic and Vascular Anesthesia

journal homepage: www.jcvaonline.com

Review Article

Intramural Hematoma
Andrew Maslow, MD*, , Michael K. Atalay, MD, PhD, FSCCT†,
1

Neel Sodha, MD‡

*
Departments of Anesthesiology, Rhode Island Hospital, Providence, Rhode Island
†
Department of Radiology, Rhode Island Hospital, Providence, Rhode Island
‡
Department of Surgery, Rhode Island Hospital, Providence, Rhode Island

Key Words: intramural hematoma; aortic syndromes; computed tomography; transesophageal echocardiography

ACUTE AORTIC SYNDROMES (AAS) are vascular emer-
gencies that are associated with significant short- and long-term
morbidity and mortality.1,2 AAS includes intramural hematoma
(IMH), penetrating aortic ulcer (PAU; the “A” may also be
“atherosclerotic”), aortic dissection (AD), aortic rupture/transec-
tion, and an expanding/symptomatic aortic aneurysm (thoracic
and/or abdominal) (Table 1).2,3 Because AAS are defined by
their acuity, an aortic aneurysm is generally not included in the
group of AAS, unless it is symptomatic or has shown rapid
expansion (Z0.5 cm/y). The incidence of AAS is estimated to
be 2.6 to 3.5 cases per 100,000 person-years, the majority of
which are AD (65%-75%), followed by IMH (4%-32%), and
PAU (o10%).1,4–13 Multiple lesions may coexist.7,13
This review focuses on IMH, which can be a particularly
challenging diagnosis with potentially dire complications.
Familiarity with anatomy, pathology, diagnosis, management,
prognosis, and outcomes of IMH—which differ from other
AAS—is the objective of this review.
Normal Aortic Anatomy
Aortic injuries are described by the layer(s) and segment(s)
involved, aortic diameter and wall thickness, and associated
complications. Knowledge of the normal aortic anatomy is
important to understanding the pathology of IMH. The aortic
wall consists of 3 layers: intima, media, and adventitia2,7 (Fig 1).
1
Address reprint requests to A. Maslow, MD, Department of Anesthesia,
Rhode Island Hospital, 63 Prince Street, Providence, Rhode Island.
E-mail address: amaslow@rcn.org (A. Maslow).
The intima (tunica intima) is the innermost layer and is in direct
contact with luminal blood. It consists of a single-cell layer of
endothelial cells supported by delicate connective tissue and an
internal elastic lamina. The medial layer (tunica media) is the
thickest layer, consisting of smooth muscle, collagen, and elastic
tissue. This layer is responsible for vascular tone. The outermost
layer, the adventitia, consists of connective tissue that provides
passive structural support. Blood supply to the wall itself comes
from vasa-vasorum, which are small arteries that enter through
the adventitia, arborize, and terminate near the junction of
middle and outer thirds of the media.2,26 By way of the vasa-
vasorum, the coronary and brachiocephalic arteries perfuse the
ascending aorta, the intercostal arteries perfuse the descending
thoracic aorta, and the lumbar and mesenteric arteries supply the
abdominal aorta.7,27
By convention, the aorta is divided into segments2
(Figs 1 and 2). The ascending thoracic aorta extends from
the aortic annulus to the brachiocephalic (or innominate)
artery. The proximal portion, referred to as the aortic root,
spans the annulus to sinotubular junction and includes the
aortic valve and coronary artery ostia. The aortic arch gives
rise to the head and neck vessels starting at the brachiocephalic
artery and ending at the left subclavian artery. The descending
aorta extends from the left subclavian artery to the iliac
bifurcation and is subdivided into the descending thoracic
aorta and the abdominal aorta, which give rise respectively to
the intercostal and brachial arteries, and the mesenteric, renal
and lumbar arteries.
The normal aortic wall thickness is o 3 mm.2 The aortic
diameter varies between segments and by age, sex, and patient

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Table 1
Acute Aortic Syndromes.

Lesion Layer affected Demographics Presentation Location Appearance Complication

IMH Medial layer 65-70 y AAS Descending 4 Ascending 4 Arch Crescentic thick Rupture
HTN Circumferential thick Dissection
Males Varying length Aneurysm
Iatrogenic No intimal flap
Trauma No false lumen
AD Intimal tear 58-63 y AAS Ascending 4 Descending Intimal flap Peripheral ischemia
Intimal flap HTN Dual lumen: True/False Embolization
Medial false CTD Low-flow false lumen Aneurysm
lumen Coarctation False 4 True lumen Rupture
Bicuspid
AoV
Pregnancy
Trauma
 Iatrogenic
AA Intima 50-60 y Asymptomatic Ascending 4 Descending 4 4 4 Dilation Rupture
Media Males Compression of proximal Arch No intimal flap Embolization
Adventitia structures No dual lumen Fistula
Fistula related No false lumen
PAU Intimal layer 70 y AAS Descending 4 4 4 Arch 4 4 Irregular surface IMH
Males Ascending Crater-like protrusion Aneurysm
HTN No intimal flap Embolization
Tobacco No dual lumen Dissection
CAD No false lumen Rupture
COPD
ULP Intimal layer 65 y Asymptomatic Distal Arch Single Aneurysm
Males Proximal descending 4 4 4 Contrast-Filled Regression
Ascending and Distal Descending outpouchings across
intima into medial layer
No connections with
aortic branches
IBP Medial layer 60-62 y Asymptomatic Descending 4 4 4 Arch 4 4 Multiple pools medial Disappear
Males Ascending layer
No communication
Near branch vessels

NOTE. Adapted from various references.1–25

Abbreviations: AA, aortic aneurysm; AAS, acute aortic syndrome; AD, aortic dissection; AoV, aortic valve; CAD, coronary artery disease; COPD, chronic
obstructive pulmonary disease; CTD, connective tissue disorder; HTN, hypertension; IBP, intramural blood pool; IMH, intramural hematoma; PAU, penetrating
atherosclerotic (aortic) ulcer; ULP, ulcer-like projection.

size. Aortic diameters are larger in older men with higher body
surface areas2,28 (Table 2). Except in very large individuals, a
normal the aortic diameter is rarely 4 4 cm. An ascending
aorta 4 4 cm is abnormal, and 4 5 cm is aneurysmal, whereas
a descending aorta 4 4 cm is considered aneurysmal.2,26
Normalized mean values and upper limits of normal for adults
are 1.8 7 0.2 cm/m2 and 2.1 cm/m2 in the ascending aorta,
and 1.4 7 0.2 cm/m2 and 1.8 cm/m2 in the descending
aorta2,28 (Fig 1).
Intramural Hematoma
Aortic IMH was first described by Kruckenberg in 1920 as
“dissection without intimal tear” that results from hemorrhage
within the aortic wall31 (Fig 3). It has long been suggested that
an IMH results from the spontaneous rupture of vasa-vasorum
in the medial layer due to a combination of wall stress, fragile
vessels, chronic hypertension, and inflammation.5,14–16 The
lack of a clear communication between the lumen and the
aortic wall at imaging or surgery is the hallmark of sponta-
neous IMH. Hemorrhage within the wall causes smooth,
crescentic or circumferential mural thickening ( 4 5 mm) at
cross-sectional imaging (Figs 4 and 5). The longitudinal extent
of the IMH can be very short (
1 cm) or can extend the full
length of the aorta. In the case of type A IMH, aortic wall
thickening creates a separation between the aortic lumen and
the right atrial appendage where such a separation normally
does not exist (Figs 4–6). This anatomic occurrence helps to
distinguish IMH from other AAS.
Rarely with IMH does mural thickening sufficiently narrow
the vascular lumen to impair blood flow or compromise branch
vessel flow.
More recently, perhaps due to improved imaging technology
and resolution, small intimal tears have been detected in as
many as 70% to 80% of IMH cases, and may represent a site
of initial insult.32–36 In a report of IMH, intimal tears were

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Fig 1. CT of normal aortic anatomy. Thoracic aortic segmental anatomy. Coronal-oblique image (A) from a contrast-enhanced ECG-gated CT of the AA and
proximal DA. The thoracic aorta comprises the ascending segment (AA), the arch, and the descending segment (DA). The aortic root (annulus to sinotubular
junction) encompasses the aortic valve (parentheses) and the coronary artery ostia (black arrows). (B) A schematic cross-section of the aorta and a sample section
of the aortic wall denoted by the blue circle and arrow. The different layers of the vascular wall including the adventitial layer, across which the vasa-vasorum
traverses, the medial layer, which consists of smooth muscle cells, and the intimal or inner layer, which is a thin 1-cell layer that is in direct contact with the
vascular lumen. AA, ascending aorta; Adv, adventitia or external layer of the vascular wall; CT, computed tomography; DA, descending aorta; ECG,
electrocardiography; Int, intimal layer of the vascular wall; LA, left atrium; LPA, left pulmonary artery; LV/RV, left/right ventricle; RAA, right atrial appendage.

found in 36% of type A IMH and 60% of type B IMH cases.34
As a consequence, some consider an IMH to be a subset of AD
with little or no flow in the false lumen.36 These intimal
defects have been referred to as ulcer-like projections (ULP) or
focal intimal disruptions (FID) and can be found at initial
presentation or during follow-up, either during imaging or
surgery34–39 (Figs 7–10). Since the terms ULP and FID may
be used interchangeably, for the remainder of this review, only
the term ULP will be used.34–36 Intimal tears r 3 mm are
typically associated with a more favorable outcome.35 ULPs
have a larger neck ( 4 3mm) and protrude from the lumen into
the thrombosed media, potentially leading to adventitial
bulging and even resulting in a pseudo-aneurysm formation
or rupture7,15,35 (Figs 7 and 8).
ULPs resemble the defect of PAU, but PAU is the result of
ulceration through an atheromatous plaque with or without
focal outward bulging of the adventitia with surrounding
inflammatory changes.17 A PAU may progress to IMH, AD,
or aneurysm.
Another type of intimal defect seen in some cases of IMH is
termed intramural blood pool (IBP)37–39 (Figs 7C, 8, and 10).
IBPs, which probably represent pseudoaneurysms of intercos-
tal or lumbar arteries, do not communicate with the lumen, or
do so almost imperceptibly32,38 (Fig 10).

Fig 2. Normal thoracic aortic anatomy as seen in vivo. Left anterior oblique (A) and left posterior oblique (B) volume rendered images of the normal thoracic aorta
obtained using contrast-enhanced ECG-gated CTA. Coronary artery ostia (white dashed arrows) and left-sided intercostal arteries (white solid arrows) are shown.
AA segment, arch, and DA segment are evident. The right ventricle and pulmonary arteries have been removed. AA, ascending aorta; CTA, computed tomography
angiography; DA, descending aorta; ECG, electrocardiography; LAA, left atrial appendage; LV, left ventricle.

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Table 2 Because the pathophysiologic mechanism of the classically

Presentation of Intramural Hematoma. described IMH involves a weakened outer medial layer near the
Sign/Symptom Type A IMH Type B IMH
adventitia, there is a high risk for developing aneurysms or
rupture.7,11,20,23
Age (y) 465 465
Aortic pain (%) 490 490
Chest pain (%) 82.5 77.3 Stanford Classification
Back pain (%) 41 78.7
Abdominal pain (%) 13.1 36.8 Intramural hematomas are first classified by their aortic
Radiating pain (%) 45.9 35.3
location to predict outcome and guide urgent therapeutic
Acute Onset pain (%) 86.7 82.6
Hypertension (%) 32.2 58.6 decisions.40 As originally defined, type A injury “indicates
Hypotension (%) 11.9 2.3 involvement of the ascending aorta” and type B lesions “are
Aortic regurgitation (%) 25-35 o10 limited to the descending aorta”41 (Fig 11). Controversy has
Pulse deficit (%) 15 o10 existed for lesions starting in the aortic arch, but this has been
Renal complications (%) o10 o10
subsequently clarified—namely, “type A or not type A”—and
Pericardial effusion (%) r70 o5
Tamponade (%) r50 o5 1 group has recently proposed that when acute aortic pathol-
Coronary ischemia (%) r30 r20 ogy starts in the arch it be referred to as “type B with arch
Hemodynamic instability (%) r20 o5 involvement.”41 Although the incidence may vary, 450%
(58%-63%) of IMH cases are classified as type B.7,8,34,43 By
NOTE. Adapted from various references.1–3,5,8,11,18,19,21,22,25,29,30,47
Abbreviation: IMH, intramural hematoma. contrast, the majority of classic AD cases are type A (72.8% v
27.2%).8
The value of this classification is demonstrated by
Complications of IMH include extension or expansion of the reports describing a 1% to 2% mortality per hour for untreated
IMH, conversion to a classic AD, aneurysm or pseudoaneurysm type A AD for the first 24 to 48 hours and r50% by the
formation, branch vessel compromise, and rupture.18–20 end of the first week.9,19,20 Although the incidences of

Fig 3. Acute aortic syndrome schematics. Cross-sectional schematics of the appearances of 3 aortic layers in various acute aortic syndromes. (A) Normal aorta.
Throughout the figures, the short arrow points to the adventitial layer and the long, dashed arrow points to the intimal layer. The long solid arrow points to the
medial layer. The figures represent the 3 main types of AAS: IMH (B and C); PAU (aortic) (D); 2 representations of an AD (E and F). In B and C, the double arrow
points to a crescentic IMH with starry circles to represent ruptured vasa-vasorum. (C) shows a circumferential IMH. (D) demonstrates the erosion or ulceration
through the middle of the Ath and into the medial layer creating a IMH. E and F demonstrate AD characterized by a TL and FL lumen, and an IT in (E). (F) shows
the FL to be larger than the true lumen with the intimal wall concave toward the TL, which is typical during ventricular diastole. AAS, acute aortic syndromes; AD,
aortic dissection42,45; Ath, atheroma; FL, false lumen; IMH, intramural hematoma; IT, intimal tear; PAU, penetrating atherosclerotic ulcer; TL, true lumen.

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Fig 4. Intramural hematoma relation of ascending aorta to right atrial appendage. Type A IMH with rupture. Transaxial (A and B) and coronal (C) postcontrast CT
images demonstrate crescentic soft-density material (yellow arrows) around the opacified ascending aortic lumen representing the IMH, separating (black arrows) it
from the RAA (white arrow), consistent with type A IMH. Moreover, hemorrhage within the pericardium (short white arrows) and along the PA—a so-called PA
sheath hematoma (dashed white arrow)—provides evidence of rupture. AA, ascending aorta; CT, computed tomography; DA, descending aorta; IMH, intramural
hematoma; PA, pulmonary artery; RAA, right atrial appendage.

type A and B may differ between IMH and classic AD,
morbidity and mortality parallel one another.36,44 Guidelines
have suggested that type A IMH be managed similarly with
surgery as type A AD.36,44 As with most type B AD, type B
IMH are usually managed medically or with an endovascular
stent.21,36
Presentation
AAS cases have similar clinical presentations, and suspicion
alone should prompt emergent imaging8,21,22 (Table 2).
Cases are described as hyperacute (o 24 hours), acute
(2-7 days), subacute (8-30 days), or chronic (4 30 days).37,43

Fig 5. Intramural hematoma of the ascending aorta. (A and B) Mid-esophageal long axis views of a type A IMH that demonstrate the increased separation between
the RAA and the AscAo lumen (black arrows). (C) shows an example of an AscAo aneurysm in which the RAA and the aorta abut one another (blue circle). A and
B demonstrate the absence of a false lumen flow. (D and E) demonstrate a classic type A AD with a mobile, prolapsing intimal flap (white arrows). (F) shows the
dissection involving the aortic arch and demonstrates the true and false lumens. Also, note in D and E that the blue circle demonstrates a normal distance between
the RAA and the aortic lumen (albeit false lumen). AD, aortic dissection; AscAo, ascending aorta; IMH, intramural hematoma; RAA, right atrial appendage.

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Fig 6. Normal relation of ascending aorta to right atrial appendage Transaxial (A) and coronal (B) ECG-gated computed tomographic images through the AA show
that the normal aortic wall is very thin ( o3 mm) and that there is typically no separation between the RAA (white arrow) and the aorta (black arrowheads). AA,
ascending aorta; ECG, electrocardiography; LA, left atrium; LV/RV, left/right ventricle; RAA, right atrial appendage.

Patients with IMH are typically older than those with
AD (69 v 62 years), more likely to be men, and, as
with PAU, have a greater incidence of hypertension and
atherosclerosis.5,11,16,21,29,46
Although trauma is occasionally implicated (Fig 12), the
vast majority (90%) of IMH cases are spontaneous (ie,
nontraumatic). Approximately 5% of spontaneous IMH cases
are associated with erosion of a PAU into the media with
subsequent hemorrhage.5,7 IMH can occur during catheter-
based aortic procedures. These are sometimes referred to as
thrombosed dissections (Figs 13 and 14). Various AAS lesions
may coexist, and IMH may be present in both AD and PAU.
Patients with IMH may present with signs and symptoms
related to vascular complications.18,19
Although the majority of IMH cases are symptomatic, a few
are asymptomatic and incidentally diagnosed at imaging
conducted for an unrelated reason. More than 90% of patients
present with aortic pain, characterized as an abrupt or sudden
excruciating anterior or posterior chest pain that may radiate to
the neck, back, or chest.5,8,21 It may be further qualified as
either ripping, tearing, or stabbing, and in severe cases the pain
may extend to the low back and limbs. Data from the

Fig 7. Aortic dissection. True and false lumen, PAU, and ULP. AD and PAU at postcontrast CT in 3 different patients. Transaxial CT image demonstrates Type A
AD with a compressed TL (*) (A). Note the intimomedial flap (blue arrows). Transaxial CT image near the diaphragm demonstrates a type B PAU (white arrow)
that appears as a mushroom-like luminal outpouching with overlying edges (B). Note the concomitant indistinct high-density IMH also present (dashed arrows).
Coronal CT image demonstrates a ULP (white arrow) along the undersurface of the proximal DA (C). AA, ascending aorta; AD, aortic dissection; CT, computed
tomography; DA, descending aorta; FL, false lumen; IMH, intramural hematoma; LA, left atrium; PAU, penetrating atherosclerotic ulcer; RPA, right pulmonary
artery; TL, true lumen ULP, ulcer-like projection.

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aortic dissection. In the acute setting, pulse pressure may be

Fig 8. Ulcer-like projection (white arrow) in type A IMH (*). Axial post-
contrast CT image demonstrates a type A IMH with a ULP (solid arrow),
which confers greater likelihood for adverse events. This patient also has a PA-
sheath hematoma (dashed arrows) consistent with aortic rupture. AA,
ascending aorta; CT, computed tomography; PA, pulmonary artery; ULP,
ulcer-like projection.
International Registry of Acute Aortic Dissection (IRAD), a
multicenter database with 4 3,500 cases of AAS, indicate that
aortic pain is the common presenting symptom in both acute
type A and B IMH and may persist despite therapies.24 Other
potential diagnostic considerations include acute coronary
syndrome, pericarditis, pulmonary embolism, musculoskeletal
issues, spinal pain, or cholecystitis.1
On physical examination, tachycardia may be present due to
pain, or in response to acute aortic regurgitation or tamponade.
Patients are typically hypertensive at presentation. Hypoten-
sion related to AAS is an ominous sign and may suggest a
complication such as myocardial infarction, tamponade, aortic
insufficiency, or rupture.5,8,30 Blood pressure (BP) should be
assessed in both upper extremities to assess for asymmetry,
which is possible with IMH but more likely due to classic
narrowed. A widened pulse pressure should heighten suspicion
for aortic regurgitation,47 and likewise for a diastolic murmur
at auscultation. Jugular venous distension, pulsus paradoxus,
and decreased heart sounds may indicate a significant peri-
cardial effusion.
Branch vessel occlusion, differential BPs, pulse deficits, and
aortic valve dysfunction are less common with IMH than with
AD and less common with type B IMH than with type A.8,25
Pulse deficits were recorded in 31% and 19% of type A and B
AD cases, respectively, compared with 15% and o 10% for
IMH cases.8,25 Syncope has been reported in r 15% of cases
of IMH,1 and renal complications occur in 9% of IMH cases
compared with 14% of AD cases.25
Type A IMH may result in aortic valve insufficiency in up
to one-third of patients and should be suspected if diastolic
murmurs are detected or if the pulse pressure is widened.30 In
patients with IMH, as with AD, aortic insufficiency can result
from leaflet tethering in the case of root dilation, or from
prolapse due to disruption of the leaflet support.5,43,48,49
A pericardial effusion results from aortic rupture into the
pericardial space.5 A higher rate of pericardial effusion has
been reported with type A IMH than with type A AD (66.7% v
50.6%), with a corresponding higher rate of tamponade (50% v
31%), but an identical rate of cardiogenic shock (20%).11,23
The occurrence of a pericardial effusion suggests rupture into
the pericardial space, which is, perhaps, explained by the
initial IMH injury occurring in the outer medial layer near the
adventitia.11,23 Not surprisingly, type A IMH has a greater
incidence of aortic regurgitation (25%-30%), pericardial effu-
sion (r 70%), and shock ( r 20%), than type B IMH ( o 5%
for all).30
Electrocardiographic (ECG) abnormalities have approxi-
mately the same incidence for IMH cases as for AD.8 ECG
abnormalities (ST segment changes) are seen in about 30% of
type A IMH and 20% of type B IMH.30 Abnormalities may

Fig 9. Penetrating atherosclerotic (aortic) ulcer. CT (A) and TEE (B) of a PAU (white arrows) seen in the Desc Ao resulting in an IMH. The luminal surface
appears irregular (ie, not smooth like a normal intimal surface or that associated with an IMH). Instead the luminal interface is irregular due to Ath. Ath, atheroma;
CT, computed tomography; DA, descending aorta; Desc Ao, descending aorta; IMH, intramural hematoma; LV, left ventricular; PAU, penetrating atherosclerotic
ulcer; RV, right ventricular; TEE, transesophageal echocardiography.

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Fig 10. Intramural hematoma with intramural blood pool. Resolving type B IMH with IBP. Axial postcontrast CT image demonstrates type B IMH (solid arrows)
with an IBP (dashed arrow) at the level of the celiac axis (*) (A). The IBP does not appear to be connected by any channel to the TL. Both findings nearly
completely resolve on follow-up imaging 8 months later (B). CT, computed tomography; IBP, intramural blood pool; IMH, intramural hematoma; TL, true lumen.

reflect coronary ischemia or pericardial effusion. Sinus tachy-
cardia is the most common finding.
There are no specific biomarkers for the diagnosis of IMH
or the differentiation between the causes of AAS. However,
D-dimer may be useful when assessing a thrombotic state
associated with aortic injury.21 The sensitivity ranges from
52% to 100% and the specificity from 33% to 89%.41 D-dimer
is elevated between 6 and 12 hours after the onset of
symptoms of an IMH case.1 Serial C-reactive protein levels
may be helpful in predicting which patients may progress to a

Fig 11. Classification of intramural hematoma. The Stanford classification identifies a type A defect as including the AA, while a type B defect does not include the
AA. The latter may include the aortic arch. Representative images of type B (A and B; CT study) and a type A (C and D; MRI study) IMH are seen in both a
sagittal (left) and a short axis (right) images. The AA, the aortic arch, and the DA are seen. The IMH is shown by the white solid arrows and the right atrial
appendage identified by the white arrow. A small ulcer-like projection is seen in A (yellow arrow). AA, ascending aorta; CT, computed tomography; DA,
descending aorta; IMH, intramural hematoma; MRI, magnetic resonance imaging; PA, pulmonary artery.

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Fig 12. Traumatic intramural hematoma. Axial postcontrast CT images through the upper abdomen before (A) and 3 hours after (B) cardiopulmonary resuscitation
demonstrate a traumatic type B IMH (white solid arrows in an abdominal aortic aneurysm [white dashed arrow]). CT, computed tomography; IMH, intramural
hematoma.

classic aortic dissection or rupture, but have limited value
during the initial evaluation.50
Imaging
The diagnosis of IMH can be challenging—even in the
presence of strongly suggestive clinical findings—and
accurate, timely imaging plays a crucial role in preventing
adverse outcomes.7,13,18,19,51–53 A report from the IRAD
database shows that as many as 60% of IMH cases were first
diagnosed at the tertiary IRAD institution instead of the
referring center.8 Explanations for a delayed diagnosis include
unavailable imaging technology and/or lack of expert inter-
pretation.7,52,53 Timely detection requires familiarity with the
lesion and heightened diagnostic diligence.
The ideal modality for imaging clinical aortic pathology is
readily available, fast, noninvasive, easy to perform and
interpret, and provides a high-resolution comprehensive trans-
mural assessment of the entire aorta and its branch vessels.
Pertinent IMH metrics for prognosis and management include
measurements of maximum short axis wall thickness, and
maximum aortic diameter (MAD) measured between the outer
walls of the aorta to reflect mural involvement.2,54,55 Beyond
yielding a diagnosis, imaging is crucial for identifying the

Fig 13. Intramural hematoma due to catheter injury. Injury to the descending thoracic aortic intima (black box) during cerebral angiography resulted in an IMH as
demonstrated during angiographic inspection of the aorta (A), and on subsequent axial (B) and coronal (C) postcontrast CT images (white arrows) extending from
the root (*) and the aortic valve to DA and the bifurcation of the iliac arteries (yellow arrowhead). Abbreviations: AscAo, ascending aorta; AoV, aortic valve; CT,
computed tomography; DA, descending aorta; IMH, intramural hematoma; LV/RV, left/right ventricles.

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Fig 14. Intramural hematoma during TAVR. These images were obtained after TAVR showing the SAX (A) and LAX (B) of the aortic valve during
transesophageal echocardiographic imaging. (A and B) Thickening (white arrows) can be seen around the newly placed AoV (TAVR) with hypoechoic spaces
consistent with fresh blood. These figures represent traumatic IMH of the AscAo. (C and D) SAX views that demonstrate color Doppler flow within the hematoma.
Acute aortic syndromes occur in o1% of TAVRs. Risk factors include older age, annular and aortic calcifications, and multiple inflations and dilations. AscAo,
ascending aorta; AoV, aortic valve; IMH, intramural hematoma; LA, left atrium; LAX, long axis; RV, right ventricle; RVOT, right ventricular outflow tract; PA,
pulmonary artery; RA, right atrium; SAX, short axis; TAVR, transcatheter aortic valve replacement.

presence of intimal tears, associated defects, and vascular
complications. Other complications such as myocardial infarc-
tion related to coronary artery involvement, aortic valve
insufficiency, pericardial effusion/tamponade, and hemody-
namic instability typically require additional imaging modal-
ities combined with clinical and laboratory findings for
detection.
Although there are a several imaging modalities available
for imaging the aorta, computed tomography (CT), magnetic
resonance imaging (MRI), and echocardiography are the
primary tools used evaluate, diagnose, and differentiate
AAS. CT and MRI are true 3-dimensional modalities that
are capable of imaging the entire aorta, and have greater
sensitivity and specificity for IMH detection than transesopha-
geal echocardiography (TEE).21,56 Although CT and MRI
have both sensitivities and specificities of 90% to 100%, the
values for TEE are 86% to 100% and 75% to 100%,
respectively.21,56 After the initial detection and management
of AAS, serial follow-up imaging is accomplished with CT or
MRI to document resolution, stability, or progression.6,22
Chest radiography and nuclear medicine have little role in
the initial diagnosis and management of IMH. Although chest
radiography is easy and quick to perform, and may reveal
findings that prompt urgent cross-sectional imaging, it is
seldom useful in providing an actionable diagnosis of AAS.
Nuclear medicine may be able to distinguish AAS from
inflammatory and infectious aortitis in the nonurgent setting,
but it is time-intensive, not readily available (especially off
hours), and provides little useful anatomic data. Moreover, the
clinical and laboratory findings of aortitis combined with aortic
mural enhancement typically seen at MRI and CT usually
suffice for rendering an appropriate diagnosis. Chest radio-
graphy and nuclear medicine are not discussed further here.
The appearance of an aortic IMH at cross-sectional imaging
is a circular or crescentic thickening of the medial layer with a
smooth luminal interface (Figs 4 and 5; Videos 1 and 2).
Blood in the medial layer typically appears organized and
homogeneous but, in a minority of cases, may have a
heterogeneous appearance. At ultrasound imaging, IMH
is usually echogenic, but may be hypoechoic or even
echolucent, in which case it might be reported as a
contained aortic dissection.15 In contrast to AD, there is no
color flow or pulsatile grayscale movement seen within the
vascular wall.
Distinguishing an IMH from other pathologies is important
to determine prognosis and management. A classic AD has an
intimomedial flap separating true and false lumens that are in
communication via Z1 intimomedial defect with blood flow
present the majority of the time in the false lumen (Figs 5, 7,
and 15; Videos 1 and 2). The false lumen in classic AD may
be sufficiently pressurized to compress the true lumen during
the cardiac cycle (Figs 5, 7, and 15; Videos 1 and 2). For this
reason and the greater chance that branch vessels may arise
from the false lumen, there is a greater risk for end-organ
ischemia with classic AD. IMH, by contrast, has no dissection
flap or false lumen (Fig 15). The aortic lumen in IMH is
typically smooth compared with the irregular luminal surface
and focal outpouching or adventitial bulge seen with a PAU
(Figs 7B and 9). Although an IMH may occur throughout the
aorta, a PAU is rarely found in the ascending aorta, infre-
quently seen in the arch, whereas 4 90% are seen in the
descending aorta.1,2,4

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Fig 15. Intramural hematoma versus aortic dissection. TEE views of the descending aorta showing type B ADs and IMHs. The figure shows ADs from 2 different
patients to demonstrate the relative sizes of the TLs and FLs during the cardiac cycle demonstrating the collapse (A and C) and expansion (B and D) of the TL
during the diastole (A and C) and systole (B and D), respectively, using both 2-dimensional and color Doppler imaging. (E) The TLs and FLs during ventricular
systole and highlights, using color Doppler imaging, the intimal tear and communication within the yellow circle. (F, G, and H) An IMH that does not compress the
vascular lumen. A hypoechoic area (white arrow) that could represent an intramural blood pool (F and H). A dilated aorta (MAD 45 cm) (G). Note that, during
TEE examination of the descending aorta, the anterior aortic wall is not well visualized and may lead to underestimation of the MAD as well as miss pathology.
AD, aortic dissection; FL, false lumen; IMH, intramural hematoma; MAD, maximum aortic diameter; TEE, transesophageal echocardiography; TL, true lumen.

Although an absence of a clear communication between the
lumen and the aortic wall is the chief feature of IMH,
previously described intimal defects such as ULPs and IBP
(discussed earlier) may be present32,37–39 (Figs 7C, 8, and 10).
Iatrogenic and traumatic aortic injuries resulting in an IMH are
likely to have an intimal defect (Figs 12–14).
Computed Tomography
CT is the preferred modality for urgent evaluation of
suspected AAS.57 It is accurate, widely available, fast,
relatively operator-independent, and noninvasive, requiring
only the rapid injection of intravenous iodinated contrast.
The actual scan time is typically measured in seconds. The
relative risks are very low and relate primarily to the risks of
radiation, contrast allergy, and contrast-related renal injury.
The sensitivity and negative predictive value approach 100%
with multidetector CT.18,19,58,59 Because CT is a true 3-dimen-
sional imaging modality, image reconstruction in any con-
ceivable orientation is permissible for clarification of findings
and confirmation of diagnosis. However, unlike echocardio-
graphy, CT does not provide functional assessment of the heart
and valves.
Noncontrast chest CT and postcontrast CT angiography
(CTA) both demonstrate abnormal findings associated with
IMH, and are considered complementary methods in the
evaluation of AAS. It has been shown that accuracy for the
detection of IMH by CT increases when a combined approach
Please cite this article as: Maslow A, et al. (2018), http://dx.doi.org/10.1053/j.jvca.2018.01.025
is employed.60 CTA generically refers to a postcontrast CT
imaging protocol that employs a relatively high-contrast
injection rate, scan-acquisition timed to the vascular region
in question—in this case the aorta—and thin-slice reconstruc-
tion of data, all to better display detailed vascular anatomy.7
Noncontrast CT demonstrates a conspicuous, high-density
crescent that has greater attenuation that the adjacent lumen.
On postcontrast imaging, the high attenuation within the vessel
lumen renders this crescent less visually conspicuous, although
unchanged in measured density15,60 (Figs 16 and 17). If thin,
the IMH may be quite subtle on postcontrast imaging and a
confident diagnosis may hinge on noncontrast findings.
Central displacement of intimal calcification is a characteristic
of both AD and IMH and can help distinguish IMH from
mural atheroma/thrombus (Figs 7B and 18).
Although both non- and postcontrast CT can show findings
of aortic rupture such as mediastinal and pulmonary artery
sheath hematomas, pericardial hemorrhage, and pleural effu-
sions, CTA demonstrates these findings to better advantage
(Figs 4 and 19). Contrast is also critical for the demonstration
of an intimomedial flap in aortic dissection (Figs 7 and 20), for
distinguishing IMH from PAU (Figs 7 and 9), and for
visualizing ULPs, and IBPs when present (Figs 7, 8, 10, and
17). ULPs may confer an increased risk for adverse events
(AEs), especially with larger lesions61–63; however, limited
data suggest that this is probably not true for IBPs.38 ECG-
gating during CTA acquisition may eliminate pulsation artifact
—especially around the aortic root—but is not typically
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Fig 16. Crescentic intramural hematoma. Pre- and postcontrast CT of type A IMH. Transaxial pre- (A) and post- (B) contrast CT images demonstrate crescentic
soft-density material (white arrows) around the ascending aortic lumen (AA), further highlighted with a yellow line, consistent with type A IMH (with aneurysm
formation). Also note the subtle involvement of the DA at this level (highlighted with yellow line). IMH has relatively high density on precontrast imaging,
confirming the diagnosis, particularly in subtle cases. AA, ascending aorta; CT, computed tomography; DA, descending aorta; IMH, intramural hematoma; PA,
pulmonary artery.

necessary, adds slight technical complexity, and is not always
available. ECG-gating also can be used for problem- solving if
prior imaging is inconclusive.
Magnetic Resonance Imaging
MRI has superior soft tissue contrast, no harmful radiation,
and is highly accurate for the diagnosis of AAS. Regarding
IMH, MRI has virtually 100% sensitivity and negative
predictive value.15,58,59 It is less widely available than CT,
more technically challenging to perform and interpret,
and requires a longer procedural time. Monitoring of critically
ill patients in the MR environment can be challenging.
Finally, gadolinium-based MRI contrast carries a small but
finite risk for nephrogenic systemic fibrosis in patients with
moderate to severe renal impairment and is contraindicated.
For these reasons, MRI is generally relegated to problem
solving and follow-up imaging when urgency is not
paramount.
MRI, like CT, can be regarded as a true 3-D imaging
modality offering a variety of different perspectives for view-
ing, measuring, and characterizing the entire aorta. It also
benefits from a host of different pulse sequences that can act to
highlight tissue abnormalities and enhance their conspicuity.

Fig 17. Crescentic intramural hematoma. Resolving type A IMH with ULP. Axial noncontrast (A) and postcontrast (B) CT images demonstrate type A IMH (solid
arrows and highlighted by yellow line) with a ULP seen in the AA (dashed arrow). Whereas the IMH regresses on follow-up axial postcontrast (C) CT imaging
after 2 months, the ULP persists. AA, ascending aorta; CT, computed tomography; DA, descending aorta; IMH, intramural hematoma; ULP, ulcer-like projection.

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Fig 18. Intramural hematoma, an ulcer-like projection, and central displacement of calcification.
Type B IMH with ULP at CT treated with endovascular stenting. Noncontrast (A), and postcontrast axial (B) and sagittal-oblique (C) CT images demonstrate a type
B IMH (yellow arrows) with a mid-DA ULP (white arrow). Due to persistent pain, angiography was performed and an endovascular stent was placed to exclude
the ULP as a potential entry site (D and E). Note the central displacement of the intimal calcification (dashed white arrow) on axial CT images (A and B)
confirming intramural pathology. AA, ascending aorta; CT, computed tomography; DA, descending aorta; IMH, intramural hematoma; ULP, ulcer-like projection.

A detailed discussion of MRI methodology is outside the
scope of this review, but, in general, imaging of the aorta is
conducted using so-called bright-blood and dark-blood pulse
sequences. MR angiography (MRA) with gadolinium-based
contrast is usually included in the examination when renal
function permits (Fig 21). MRA is specifically performed to
analyze vascular anatomy in greater detail and relies on a
relatively fast contrast injection, with data acquisition timed
for optimal visualization of the vascular region in question.
MRA provides detailed delineation of vascular anatomy and
improved detection of dissection flaps and of subtle lesions
such as ULPs and IBPs. In some settings, cine bright-blood

Fig 19. Descending aortic rupture. Ruptured type B IMH with ULP at CT treated with endovascular stenting. Axial (A) and sagittal-oblique (B) postcontrast CT
images demonstrate a type B IMH (yellow arrows) with a mid-DA ULP (white arrows). Mediastinal (black asterisk) and pleural (white asterisks) hemorrhage
confirm aortic rupture. Angiographic examination (C) shows the site of rupture (white solid arrow). Endovascular stent (dashed arrow) placement was undertaken
and the ULP excluded (D and E). Follow-up postcontrast axial CT (E) demonstrates resolution of IMH, mediastinal hematoma, and pleural effusions. AA,
ascending artery; CT, computed tomography; DA, descending aorta; IMH, intramural hematoma; PA, pulmonary artery; ULP, ulcer-like projection.

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Fig 20. Type A IMH conversion to AD. Sagittal oblique postcontrast CT images taken 28 days apart demonstrate type A IMH (white arrows) throughout the
thoracic Ao (A) converting to AD with a complex intimomedial flap (black arrows) (B). AA, ascending aorta; AD, aortic dissection; Ao, aorta; CT, computed
tomography; DA, descending aorta; IMH, intramural hematoma.

imaging may be of benefit, particularly for dynamic visualiza- Conventional Angiography

tion of a dissection membrane. In principle, this type of
imaging would also allow functional evaluation of the heart
and valves.
Because of the various well-known effects on T1- and T2-
weighted MRI of various states of hemoglobin (ie, oxyhemo-
globin, deoxyhemoglobin, intra- and extracellular methemo-
globin, and hemosiderin), the use of specific pulse sequences
permits the detection and characterization of blood products
within a hematoma.8 These blood products loosely correspond
to the chronological age of the injury, namely hyperacute
(oxyhemoglobin), acute (deoxyhemoglobin), early subacute
(intracellular methemoglobin), late subacute (extracellular
methemoglobin), and chronic (hemosiderin) (Figs 22 and 23).
Coronary angiography is a 2-D luminography technique that
requires intra-arterial catheterization, iodinated contrast, and
radiation. The risks for contrast include nephrotoxicity and
allergy. The diagnostic utility of coronary angiography for
AAS is suspect, with a false-negative rate of 10% to 20% for
AD and frequently missing IMH altogether.1,13 In fact, intimal
injury may occur during coronary angiography (Fig 13). With
the advent of reliable and accurate cross-sectional imaging
methods for the evaluation of acute aortic pathology, coronary
angiography has largely been relegated to a role of treatment.
In particular, coronary angiography is chiefly used for endo-
vascular stenting of type B aortic pathology when medical

Fig 21. Magnetic resonance imaging/angiography. Type A IMH converting to dissection. Dark (A) and bright (B) blood transaxial noncontrast MRI demonstrate a
crescent of abnormal signal intensity in the AA and DA (white arrows) consistent with type A IMH. A single transaxial postcontrast CT image taken 4 hours later
shows interval conversion to AD with acute aneurysm formation of the ascending aortic segment (C). Although hemorrhage in the wall remains evident, an
intimomedial dissection flap has appeared (dashed arrow). Yellow arrows point to pleural effusions. AA, ascending aorta; AD, aortic dissection; DA, descending
aorta; IMH, intramural hematoma; MRI, magnetic resonance imaging.

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Fig 22. Type B IMH at MRI. Dark-blood transaxial and sagittal oblique T1-weighted (A and B), and T2-weighted (C and D), MRI demonstrates type B IMH
(white arrows). The intramural blood products are bright on both T1- and T2-weighted images corresponding to extracellular methemoglobin which has late
subacute chronicity. AA, ascending aorta; DA, descending aorta; IMH, intramural hematoma; MRI, magnetic resonance imaging.

management fails and a luminal defect (eg, PAU, ULP) is
identified (Figs 18 and 19).
Echocardiography
Echocardiography is commonly employed for cardiovascular
assessment for patients with suspected AAS, and is obtained in
450% of IMH cases to compliment CT or MRI.13,25,40,64 It is a
readily available, non- (TTE) or semi-invasive (TEE) modality
that can be performed at the bedside (and/or intraoperatively),
and allows assessment of heart function as well as the aorta.
Transthoracic echocardiography (TTE) is frequently combined
with CT imaging for a comprehensive, expeditious cardiovas-
cular evaluation, including ventricular and valvular functions,
and pericardial assessment.64 For the unstable patient, TTE may
be the first test obtained. However, compared with CT and MRI,
TTE is highly operator-dependent, has limited depth of view, is
relatively constrained with regard to viewing angles and imaging
planes, and does not have the same detailed soft tissue
characterization. Patient habitus may impose further restrictions
on imaging. For these reasons, its versatility is somewhat offset
by its lower accuracy (sensitivity o40%) for detecting and
diagnosing aortic pathology due to limited views of the entire
aorta.64
TEE overcomes the limitations of TTE by positioning the
probe closer to the aorta with fewer viewing impediments,
with the notable exception of a 2- to 3-cm segment of the arch
where the distal trachea and left mainstem bronchus are
interposed between the esophagus and aorta. High-resolution
imaging of the thoracic aorta, the aortic arch, and the
descending aorta is permits differentiation between IMH,
AD, PAU, and atheroma (Figs 9, 15, and 24; Videos 1 and 2).
However, it is a semi-invasive study, not readily available and,
requires considerable expertise. These factors restrict its
routine utility in the emergent nonoperative setting. It is
unclear if advances in TEE technology such as 3-D imaging
are advantageous for the detection and diagnosis of IMH.13 In
some cases, abdominal ultrasound may be used to evaluate the
abdominal aorta and branches.
Management/Outcome
Outcomes for IMH vary between institutions, regions, and
countries.1,6,8,11,17,20,22,29,44,64–67 An IMH may progress,

Fig 23. Type A IMH at MRI. Dark-blood transaxial and sagittal oblique T1-weighted (A and B), and T2-weighted (C and D), MR images demonstrating type A
IMH (white arrows). The blood products have intermediate intensity with T1-weighting and hyperintensity with T2-weighting corresponding to oxyhemoglobin,
which has hyperacute chronicity. AA, ascending aorta; DA, descending aorta; IMH, intramural hematoma; MRI, magnetic resonance imaging.

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Fig 24. Intramural hematoma of the ascending aorta. These figures highlight the characteristics of an IMH of the AA. A type A IMH is seen using transesophageal
echocardiography from mid-esophageal long axis windows. (A and B) Heterogeneous, isoechoic aortic wall thickening (*) obtained during ventricular systole
(white solid arrows showing aortic valve leaflets) ventricular diastole (aortic valve leaflets closed), respectively. The increased distance between the RAA and the
AA lumen (black arrows) is noted. That absence of change in the IMH helps to differentiate it from a classic AD, which show changes in the true and false lumen
sizes. (C and D) Hypo- and hyperechoic type A IMH (white arrows). The former would be considered high risk for progression to an AD, while the latter, with a
thickness of 7 mm is considered lower risk for complications. AA, ascending aorta; AD, aortic dissection; AoV, aortic valve; IMH, intramural hematoma; LA, left
atrium; RAA, right atrial appendage.

regress, or even resolve over the first 30 days to 1 year, or as
long as 5 years after presentation.1,6,8,11,17,20,22,29,34,44,64–67
The large majority of aortic-related deaths occur during the
acute phase of the disease (ie, within the first 8 days).34,35
Imaging evidence of progression, or weakening of the
vascular wall includes extension and expansion of the hema-
toma, aneurysmal changes, development of intimal defects
including ULP, conversion to a classic AD, or aortic
rupture.1,7,8,23,30,44,62,65,68 Clinical complications include pulse
deficits, cardiovascular dysfunction, or both. Progression and
adverse outcomes are more likely with type A than type B
IMH (88% v 3%-14%).1,17,34,44,62,64,68
Aggressive medical management of IMH involving pain
control and reduction of aortic wall stress has been associated
with increased stabilization or even resolution, thereby redu-
cing or preventing complications.1,6,15,17,22,44,64,69 The deci-
sion to perform surgery depends on a host of factors including
the extent of pathology, Stanford classification, the presence of
complications, and the predicted likelihood of regression or
progression. Therapeutic decisions heavily rely on imaging.
For all patients diagnosed with IMH, medical management
is instituted emergently and includes aggressive heart rate and
BP control to reduce aortic wall tension, as well as pain
abatement. Pain control reduces the sympathetic response and
associated tachycardia and hypertension. “Antipulse” therapy
using β-blockers, calcium channel blockers, and antihyperten-
sive medications reduces vascular wall stress by reducing
ventricular contractility, heart rate, and BP.30 Emergent
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administration of pain control and antipulse therapy limits
disease progression and promotes resolution.30,36 Hemody-
namic goals include heart rate o70 beats/min and systolic BP
o110-120 mmHg.1,11,29 Aortic regurgitation with compensa-
tory tachycardia or hemodynamic instability requires careful β-
blocker titration.
Type A IMH
Emergency surgery for type A IMH is the current recom-
mendation from the American Heart Association Guidelines
for the Diagnosis and Management of Patients with Thoracic
Aortic Disease69 and Society of Thoracic Surgeons Guidelines
for Aorta Management.70,71 This is particularly true if there is
cardiovascular instability, the presence of ULPs, or evidence
of an impending or suspected rupture, the latter including
hemopericardium, mediastinal hematoma, or a
hemothorax.6,22,23,30 Additional indications for surgery include
persistent or refractory pain, evidence of end-organ dysfunc-
tion/ischemia, continued aortic dilation, or progression to a
classic dissection. The optimal timing of surgery is debated.
The risk for progression and acute complications is greatest at
8 days.34,35,72 For a hemodynamically stable patient, emergent
surgery (ie, o 6 hours from presentation) is not necessary, and
a delay of up to 3 days is considered safe.72 Although
management varies, 480% of type A IMH patients undergo
early surgery and o20% are managed medically in North
American/European centers.8,65
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In-hospital and long-term mortality for type A IMH is as
high as 30% and 40%, respectively.1,6,8,11,20,22,43,65–67 Pro-
gression of a type A IMH to a classic AD occurs in 15% to
87%.17,62,64,73 Support for early surgery comes from reported
low postoperative in-hospital mortality of 4.3%,23 the risk for
progression to a classic AD,74 and lower early (8% v 55%) and
long-term (24% v 40%) mortalities for surgical management
compared with medical management.8,30,65
Selection of medical management, in lieu of urgent/emer-
gent surgery for type A IMH is controversial but evol-
ving.11,29,75–77 For stable cases, medical management is
more frequently selected in Asian (Japan/Korea) cohorts
(78%) than in North American/European groups (49%).
Follow-up data from Asian populations report a 40% resolu-
tion of type A IMH in medically managed cases.75,76 Overall,
Asian studies report a lower 30-day (or hospital) mortality
(9.4% v 20.6%) than North American/European groups, and an
83% survival at 3 years for IMH cases.78,79 These data suggest
that medical therapy is a viable and safe option for selected
type A IMH patients, and may even be preferred.
Although outcome differences between populations support
the benefits of aggressive medical therapy, they also might
represent different diagnostic capabilities, different severities
of disease, and different population demographics. IRAD data
reported inaccuracies with diagnostic imaging resulting in
delayed diagnoses.8 Diagnostic differences are further high-
lighted by different incidences of IMH.5–12 Although IMH
represents 4% to 11% of AAS cases in North American/
European populations, the occurrence is as high 32% in Asian
populations.5–12 All considered, emergent accurate imaging,
earlier detection, and aggressive medical therapy reduces
progression and complications.8,9,29,44,57,80,81
Although some Asian investigators have concluded that
aggressive medical therapy is a feasible option, progression,
complications, or surgery still occur in Z40% of medically
managed cases.77 Of 66 patients with type A IMH, 21
presented with complications (aortic insufficiency, tamponade,
stroke), and 16 of these 21 underwent urgent or emergent
surgery. Fifty of the 66 (76%) were managed medically.77 The
30-day mortalities for emergent surgical (n ¼ 16) and medical
(n ¼ 50) management were 6% and 4%, respectively.8,65,77
During follow-up, 30 of the 50 (60%) medically managed
cases showed regression or disappearance of the IMH. How-
ever, 20 of 50 (40%) had an increase in IMH size, develop-
ment of a ULP, or progression to a classic AD. Sixteen of
these 20, or 32% of the 50 initially medically managed
patients, underwent late surgery with no operative mortality.77
Overall, in this study, 32 of 66 (48%) patients with type A
IMH underwent surgery.77 The overall actuarial survival for
type A IMH was excellent at 1, 5, and 10 years; 96%, 94%,
and 89%, respectively.77
In another report of 101 patients with type A IMH, 16
underwent emergent surgery.29 The in-hospital survival of the
16 patients who had surgery and the 85 who were managed
medically were 87% and 93%, respectively.29 Of 79 medically
managed hospital survivors, 28 (36%) had surgery, complica-
tions, or both within 6 months of the diagnosis. Overall, 28%
Please cite this article as: Maslow A, et al. (2018), http://dx.doi.org/10.1053/j.jvca.2018.01.025
17
of type A IMH cases had surgery (16 emergent and 12
delayed). Survival for type A IMH was 4 80% at 1, 2, and
3 years.11,29
Two conclusions can be drawn from these data.11,29,77 The
first is that there still remains significant progression with a
significant number of patients undergoing late surgery despite
aggressive medical therapy, supporting the need for careful
clinical and imaging surveillance. Second, despite the risks for
progression, initial medical management is a feasible option in
some cases with excellent long-term outcomes. The decision to
medically or surgically manage cases balances risk for
progression, with a low surgical mortality with delayed
surgery, and possible regression of the IMH in a high
percentage of cases.11,29,30,77 Surveillance imaging is recom-
mended at 3 and 7 days, 1, 3, 6, and 12 months.7 Follow-up
thereafter depends on previous imaging and determined risks
for progression and complications.
Type B IMH
Medical management for type B IMH is preferred unless
complications are present or anticipated.7,36,58 Approximately
90% of type B IMH patients are managed medically and
o10% surgically.8,65
In a review of 30 manuscripts, including 925 patients with
type B IMH, the 30-day and 3-year mortality, regardless of
management, was 3.9% and as high as 14.3%, respec-
tively.17,64 After 1 year, 4 50% of medically managed cases
were either stable (10%), regressed (30%), or resolved
(60%).17,64 Of those patients who progressed, approximately
33% developed either a classic AD or aneurysm, and 25%
developed a localized AD or ULP.8,17,25 Less than 5% were
complicated by rupture.17
The 30-day and long-term (3-5 years) mortalities for
medical, open surgical, and thoracic endovascular aortic
aneurysm repair (TEVAR) treatments ranged from 3% to
19% (median 8%), 11% to 33% (median 17%), and 0% to 6%
(median 2%), respectively.17,21,64 Mortality for open surgery is
consistently greater than for TEVAR.1,17,44,64 Although the
use of TEVAR to treat type B IMH is relatively recent, its
preference over open surgical replacement is increasing.8,65
Open surgical repair or TEVAR is considered for compli-
cated cases or cases considered high risk (see predictors in the
next section). Continued aortic dilation or progression to an
aortic dissection warrants invasive therapy. Other concerning
findings include periaortic hematoma and pleural effusions17,64
(Fig 25). Based on relatively lower perioperative mortality
rates with TEVAR, some groups advocate intervention even in
the absence of complication.82
The chief concerns for using TEVAR in the management of
type B IMH are the absence of a localized hematoma and/or
intimal defect to target stent deployment, as well as concerns
over inducing retrograde aortic dissection or rupture. Optimal
anatomy to accept the stent includes aortic segments proximal
and distal to the IMH of o40 mm inner diameter and 4 20
mm in length based on CT imaging. Fluoroscopy, TEE, and/or
intravascular ultrasound are used to guide the procedure.
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Fig 25. Type A IMH with inclusion of the arch and descending aorta managed with endovascular stent. Pre- and post-stenting computed tomographic views of an
IMH. Although a type A IMH with extension to the DA was initially found (white dashed arrow) (A), it appeared to progress a week later (B) with concerns of a
DA rupture suggested by the pleural effusion (white solid arrow). Thoracic endovascular aortic repair (TEVAR) was performed by placing a vascular stent in the
DA and into the distal aortic arch (yellow arrows) (C and D). AA, ascending aorta; DA, descending aorta; IMH, intramural hematoma; PA, pulmonary artery.

Fig 26. Computed tomography: Resolution of type B IMH. Axial postcontrast CT images demonstrate a type B IMH (white arrows) that gradually resolves with
medical management. Images were obtained at the time of diagnosis (A), at 10 days (B), at 2 months (C), at 4 months (D), and at 4 years (E). Note the gradual
decrease in IMH thickness at this level. At 10 days, a pleural effusion was noted (*). AA, ascending aorta; CT, computed tomography; DA, descending aorta; IMH,
intramural hematoma.

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Table 3
Adverse Outcomes and Predictors*.
Adverse outcomes Hospital/30-d mortality
Long-term mortality
Progression, AA, AD, rupture
Surgery
Predictors of adverse outcome Persistent pain
Hemodynamic instability
Pleural effusion
Pericardial effusion
Para-aortic hematoma
Echolucency
Rapid aortic growth
Intimal tear (ULP/FID)
PAU-related IMH
MAD
Wall thickness
NOTE. Adapted from various references.1,2,6–9,11,12,15,22,23,29,30,34,35,40,41,44,62–69,72–77
AA, aortic aneurysm; AD, aortic dissection; FID, focal intimal disruption; IMH, intramural hematoma; MAD, maximum aortic diameter; PAU, penetrating
atherosclerotic (aortic) ulcer; ULP, ulcer-like projection.
n
Echolucency suggests an unstable medial layer with blood flow. Intimal tears include ULP, which also may be referred to as focal intimal disruptions.
At the conclusion of the TEVAR procedure, angiography is
performed to assess for a type I endo-leak, which indicates
insufficient seal at the proximal or distal ends of the stent.
Uncomplicated type A and B IMH cases can be managed
medically (antipulse therapy) with low morbidity and mortality
(Fig 26). Surveillance imaging using either CT or MRI are
preferred as they allow a more complete aortic assessment and
are more easily compared with prior examinations. Surveil-
lance imaging in the first year should be conducted at 3 and
7 days, and 1, 3, 6, and 12 months.7 Subsequent follow-up is
tailored to the individual patient or based on institutional
protocol. Imaging results that suggest progression warrant
more aggressive management whether it be medical or
surgical.7 With improved CT resolution and an increased
detection of intimal tears, consideration of TEVAR for
uncomplicated type B IMH has increased as it has for type
B AD.36
Predictors of Outcome
A number of clinical and radiologic findings predict
progression of aortic pathology and complications
(Table 3).6,22,64,72 Clinical predictors of AEs include persistent
or refractory pain, hemodynamic instability, and evidence of
peripheral ischemia.6,22,64,72 Radiologic measurements used to
predict progression of IMH include the MAD and maximum
aortic wall thickness (Figs 24D and 27). A MAD of the
ascending aorta 455 mm (range 448 to 4 60 mm) and a
maximum aortic diameter of the descending aorta 4 40 mm
(range 440 to 4 60mm) are predictors of progression.1,7,68 A
wall thickness 4 10 mm (range 410 to 4 15mm) also is
considered high risk for progression and complications for
both type A and type B IMH.1,7,9,12,17,68,77 The luminal
compression ratio (minimum:maximum transverse luminal
Please cite this article as: Maslow A, et al. (2018), http://dx.doi.org/10.1053/j.jvca.2018.01.025
19
IMH Type A Intramural Hematoma Type B
10-30% 4-20%
r40% 4-14%
r90% up to 50%
r50% o 10%
45 mm/y 4 5 mm/y
Uncommon 4 10 mm depth
445 to 460 mm 4 40 to 4 60 mm
410 to 15 mm 4 10 to 15 mm
diameters at the site of the maximal hematoma thickness)
describes the extensiveness of the injury, and is further
predictive of adverse outcomes. Specifically, a luminal com-
pression ratio o 0.75 is predictive of AEs.29,62,83
For type A IMH, predictors of progression of 50 medically
treated cases included a maximum aortic diameter 450 mm
(sensitivity [Sens], 75%; specificity [spec], 90%; positive
predictive value [PPV], 83%; negative predictive value
[NPV], 84%), a maximum IMH thickness 4 10 mm (sens,
75%, spec, 63%, PPV, 58%, NPV, 79%).77 In other data, a
maximum aortic diameter 4 50 mm was a stronger predictor
of progression and adverse outcome than an IMH wall
thickness 4 10 mm.75,77,84 By contrast, Song et al found that
the hematoma thickness (4 11 mm) was the only independent
predictor for adverse outcomes with a sensitivity of 89% and a
specificity of 69%12 Data suggest that surgery for lower-risk
(ie no complications noted) type A IMH cases (maximum
aortic diameter o 50 mm and/or an IMH thickness of o 10
mm) can be postponed for 24 to 72 hours or indefinitely
depending on patient stability and follow-up imaging.1,12
For type B IMH, anatomic predictors of progression include
an early or acute-phase maximum aortic diameter 4 45 mm
and/or a wall thickness of 4 10 to 15 mm64 In the chronic
phase, an aorta diameter 4 50 mm or increase of 40.5 cm/
year is indication for surgery.64 Type B IMH patients (N ¼
107) with intimal tears (ULP) that were found in the acute
phase were more likely to have MAD 4 60 mm that was
associated with an aortic-related mortality of 36%.35 Intimal
tears found after discharge did not increase the incidence of
aortic-related deaths.35 Finally, progression of a type B IMH to
a type A IMH is consistent with an unstable aorta.75,77,84
The presence of periaortic hematoma, pericardial effusion,
and pleural effusions suggest that an injury to the adventitial
wall may be present.6 A PAU that causes persistent pain or
20 A. Maslow et al. / Journal of Cardiothoracic and Vascular Anesthesia ] (]]]]) ]]]–]]]
Fig 27. Computed tomography of a type A IMH. Three images showing a type A IMH extending throughout the AA, arch, and DA. (A) Cross-sections of the AAs
and DAs. (B) The aortic arch. The IMH is shown by the white arrows. (C) The measurement of the DA. The MAD and maximum wall thickness are 47 mm and 18
mm, respectively. AA, ascending aorta; DA, descending aorta; IMH, intramural hematoma; MAD, maximum aortic diameter.
one that has a depth 4 10 mm are risk factors for developing a
complication.64 Interestingly, PAU-related IMH may carry a
higher risk for adverse outcome as it already demonstrates
progression and weakening of the aortic wall.64
An echolucent or heterogeneous appearance during ultra-
sound or CT imaging might be suggestive of an unstable IMH,
and predict progression to a classic aortic dissection versus
absence of echolucency or a more homogenous appearance
(78% v 34%, respectively).68 During follow-up, 33% to 39%
of all IMH cases show progressive aortic enlargement and
aneurysmal development.8,25 Development of an aneurysm
(saccular of fusiform) is indicative of progressive weakening
of all 3 layers of the aortic wall.68 A fusiform aneurysm is
more common. Saccular aneurysms are more likely to occur in
the aortic arch over the first 2 to 3 years.68 Saccular aneurysms
may start out as a ULP, and, eventually, develop into a
pseudoaneurysm.68
Conclusions
Aortic IMH is an AAS characterized by hemorrhage within
the medial layer of the aortic wall without evidence of flow or
clear luminal communication at imaging or surgery. It may
arise spontaneously or after trauma. A timely diagnosis is
paramount, and relies on high clinical suspicion, and prompt
imaging with CT serving as the preferred first-line option for
stable patients. Echocardiography is a frequently used adjunct
to assess cardiovascular functions, and may be the first
modality used in unstable patients. MRI is typically reserved
for problem solving in the acute setting and for serial follow-
up imaging, along with CT, in the chronic or postsurgical
setting to assess for resolution, stability, or progression.
The management of IMH depends on its location, appear-
ance, dimensions, and associated pathology. When these
features are taken together, the risk for progression or
regression can be assessed. Although all hemodynamically
stable cases warrant emergent medical management, the
factors affecting the decision to emergently perform surgery
are evolving. In general, Stanford type A AAS lesions warrant
urgent surgical repair. However, recent data suggests that some
Please cite this article as: Maslow A, et al. (2018), http://dx.doi.org/10.1053/j.jvca.2018.01.025
patients will respond well to aggressive medical management
alone. By contrast, the majority of type B lesions are managed
medically, with endovascular stenting performed in those
experiencing complications or at heightened risk. Imaging
biometrics, such as IMH thickness and outer wall diameter
help predict progression or regression and may serve as
arbiters of which patients to treat medically and which to
send for surgery. Effusions (pleural or pericardial) and/or
periaortic hematoma suggest that small tears in the adventitia
may exist. Additional imaging findings (eg, ULP, PAU,
hypoechoic areas) may offer additional management guidance.
Outcomes for appropriately managed patients are favorable.
The urgency of assessment and management cannot be
understated and is the key toward improving outcome.
Appendix A. Supplementary material
Supplementary data associated with this article can be found
in the online version at http://dx.doi.org/10.1053/j.jvca.2018.
01.025.
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