Aortic intramural - PowerPoint Presentation

Slide1

Aortic intramural haematoma: pathogenesis, clinicalfeatures and imaging evaluation

Department

of

Cardiology,

Radiology,

Heart of, Birmingham

,

UK, England

Postgrad Med J 2012Slide2

INTRODUCTIONIntramural haematoma

(IMH) is a

localised

haemorrhage

within

the aortic wall

.

It accounts

for

10–20

% of cases of acute aortic syndrome (AAS)

(aortic

dissection (AD) and penetrating

atherosclerotic ulcer).

It similar

clinical

manifestations and

prognosis to

AD.

carries

a similarly

high mortality

rate.Slide3

INTRODUCTIONImaging plays

a central

role in diagnosing IMH, differentiating

it from

AD and assessing for complications

.

Imaging provides

lesion location and

extent, which

is vital for clinical decision making

.

Key tool:

Multidetector

CT (MDCT)

and MRI.Slide4

This article reviews the IMH from

pathogenesis

clinical features

complications

the

role of advanced

imaging techniques

in its evaluation including

differentiation from other pathological

conditions of

the thoracic

aorta.Slide5

PATHOGENESIS OF IMHIn most cases IMH is thought

to begin

with spontaneous rupture of the

vasa

vasorum

.

it can

also occur

secondary to aortic trauma or a

penetrating aortic ulcer.Slide6

IMH propagates along the media layer, weakening the wall, and may progress either to outward aneurysm formation/rupture or to inward fracture of the intima, the latter resulting in a communicating AD.Slide7

Dissection has been reported as a complication of IMH in 12–47% of cases.

a recent

study of

300

patients regression

in 34

% over

a mean

follow-up period

of 3

years.Slide8

Some authors have recently questioned the classical mechanism of IMH formation.They have postulated that small intimal tears may be the initiating pathology in some cases.

It

is generally

agreed that

the same Stanford classification system as

is used

to classify AD be used for

IMH.Slide9

CLINICAL FEATURESIMH median age at presentation of 68

years.

male

predominance (61

%).

It

exhibits nearly

identical clinical signs, symptoms and

risk factor

profile to classic AD,

and systemic hypertension

recognised

as the most common

predisposing factor.

Physical examination is frequently normal.Slide10

auxiliary examinationMore

often than not the radiograph will have a normal appearance

.

It may occasionally mediastinum may be Widened.

It will not be reliably detected with catheter-directed angiography.Slide11

ultrasound Transthoracic echocardiography (TTE) is a valuable means

to assess

complicating features of type A

IMH.

Transoesophageal

echocardiography (TOE

)

gives improved spatial

resolution,

with a reported sensitivity and

specificity of

98% and 95

%.Slide12

MDCT Definite distinction between IMH and normal findings with TOE often requires a second imaging modality

such as MDCT or

MRI to confirm or refute the

diagnosis.

In recent years MDCT has become established as the

leading technique

for diagnosis and classification of

IMH.Slide13

MRI MRI is rarely used to investigate the initial presentation of suspected AAS due to prolonged examination times (

20–30

min for a typical aortic protocol) and incompatible

life support

and monitoring equipment which is usually

required for

critically ill

patients.

MRI can also be used to

estimate the

age of a

haematoma

based on differing

signa

characteristics .Slide14

MDCT techniqueScan coverage should be from above the aortic arch

to below

the aortic

bifurcation.

The application of ECG

gating reduces

cardiac motion-related

artefact

.

however, it carries a

significant additional

radiation

burden.

an initial unenhanced

study must

be performed as this is crucial for diagnosing IMH

and for

the detection of any

mediastinal

haemorrhage

or

haemorrhagic

pericardial effusion.Slide15

MDCT technique this does not require ECG gating and

a slice thickness of 2–3 mm is

adequate.

Injection

rate of 3–4 ml/s

is usually

adequate and a slice thickness of 1–2 mm is used

to provide

isotropic spatial

resolution.Slide16

Findings

The hallmark non-contrast MDCT finding of IMH is high attenuation (60–80 HU) eccentric crescent-shaped thickening of the aortic wall

.

Thickening is nearly always

>

7

mm

IMH

does not

enhance

.Slide17

In contrast to dissection, the aortic thickening does not spiral around the opacified aortic lumen which is rarely compromised.

A

combined unenhanced

and contrast-enhanced MDCT protocol has

been shown

to have a sensitivity approaching 100% for the

detection of IMH.Slide18

MRI techniqueBreath-hold ECG-gated

fast spin echo images acquired with T1 and

T2 weighting

are used to assess aortic

calibre

, aortic wall

thickness and

aortic wall signal change

.

These are acquired as

contiguous transverse

sections from the apices to the

infrarenal

abdominal aorta

and also as sections

parallelling

the long axis of the

aortic arch

.Slide19

Dynamic steady state free precession (SSFP) sequences are used to assess aortic valve function and the calibre

of the

aortic root

. These are acquired in both transverse and coronal

planes through

the LVOT.

If

AR is present, its severity can be

quantified via

flow sensitive phase contrast sequences.

Finally

,

a gadolinium-enhanced

aortic angiography study is performed.Slide20

Findings

IMH

appears as a focal area of mural thickening with

signal characteristics

that depend upon its acuity and relate to

the slow

conversion

of

oxyhaemoglobin

to

methaemoglobin

and their

differing paramagnetic

properties.Slide21

Acute IMH (0–7 days) demonstrates intermediate signal intensity on T1-weighted spin-echo

images caused by a predominance of

oxyhaemoglobin

making

it sometimes difficult to distinguish from the

normal aortic

wall.

Oxyhaemoglobin

exhibits

high

T2 signal in the acute

phase, making

it appear

conspicuous.

With increasing

methaemoglobin

content

, both T1 and T2 signals increase

within IMH.

In the absence of expected signal intensity

evolution,

rebleeding

should be

considered.Slide22

DIFFERENTIAL DIAGNOSESother causes of aortic wall thickening atherosclerosis, mural thrombus,

thrombosed

dissection and

aortitis

.

Atherosclerotic wall thickening and mural

thrombus has

an

typically irregular

contour

of inner margin.

IMH which

is usually smooth.

However ,it is a

distinction

challenging IMH

develops within an area

of atherosclerosis. In

such situations early

interval repeat

scanning may be the only means of discrimination.Slide23

AD comprises a laceration of the intima and inner layer with resultant intimomedial

flap and

formation of

a double-channel

aorta

with

communication

between true

and false

lumens.

Evidence of an intimal tear is the key

discriminating feature

from

IMH.

Another important

distinguishing feature

is the spiral course of AD in contrast to the

constant crescent-shaped

appearance of

IMH.Slide24

Aortitis is most often caused by vasculitides such as

Takayasu

arteritis and giant cell

arteritis.

Active

aortitis

manifests on

imaging as diffuse or segmental thickening of

the vessel wall.

often with accompanying inflammatory changes

in the

periaortic

fat.

Key discriminating

features :

Aortitis

are circumferential

mural thickening, mural

enhancement and

a patchy distribution with normal intervening

segments.Slide25

COMPLICATIONS AND ADVERSE PROGNOSTIC INDICATORSType A IMH carries a substantially higher risk of major complications than

a type

B

lesion

.

Early complications

include fluid

extravasation into

the pericardial space with

tamponade

,

mediastinal

extravasation, acute AR and development of

AD.Slide26

clinical outcome of IMH

It

may

be spontaneous regression

over

time

.

It

may be complicated by

saccular

or

fusiform aneurysmal dilatation, rupture or

late progression

to AD

.

main adverse clinical

feature

is patient

age

>70 years carrying the

highest risk

of

progression.

imaging

characteristics be correlated

with increased mortality

rates.Slide27

Imaging findings associatied with increased mortality in intramural

haematoma

Stanford

type A lesion

Mural thickening >10 mm

Aortic diameter >5 cm

Coexistent penetrating ulcer

Evidence of

rebleeding

on serial imaging

Extension of thrombus on serial imagingSlide28

Development of an ulcer

is strongly

associated with AD, with one study showing 70%

of ulcers

within areas of

IMH progressing

to AD, especially

in type

A

lesions.

Recent data have shown that an

intimal defect

of >5 mm in a type B lesion

predicts progression with sensitivity

, specificity and

postive

and negative

predictive values

of 84%, 95%, 94% and 86%,

respectively.Slide29

Given the propensity for complications, close follow-up imaging during the 30 days after initial presentation is recommended for

all patients being treated

medically.

If there is

longitudinal progression

of aortic involvement, progressive

luminal dilation

, penetrating ulcer, enlarging IMH or overt

dissection

surgical or endovascular treatment should be

strongly considered.Slide30

MANAGEMENT Slide31

IMAGING FOLLOW-UPThe decision to use MDCTor MRI is guided by the

patient’s age

and renal

function.

with

MRI preferred in young patients

and those with renal impairment

Imaging

at 1, 3, 6, 9 and 12 months from diagnosis has

been suggested

by EvangelistaSlide32

CONCLUSIONSIMH is a localised

haemorrhage

within the aortic wall

.

It

has overlapping

clinical manifestations with AD and carries a

similarly high

mortality rate

.

Imaging is central to the diagnosis

of IMH

and its differentiation from AD and other causes of

aortic wall

thickening

.

Imaging can also provide crucial

information concerning

lesion location and extent which is essential

for treatment

planning.Slide33

MDCT is the modality of choice for diagnosis and classification of IMH.

imaging findings are considered

adverse prognostic indicators:

mural thickness >10 mm

and aortic

diameter >5 cm

.

Different type need different management.Slide34

Thanks for attention!