aortic dissection topic is good for medical students

1. AORTIC DISSECTION
DR RAKESH ROSHAN

2. Review of
Aortic
Anatomy

3. Layers of Aorta…

4. What is dissection of aorta?
 Tear in the aortic intima that directly
exposes an underlying diseased medial
layer to the driving force (or pulse
pressure) of intraluminal blood.
 This blood penetrates the diseased medial
layer and cleaves the media longitudinally ,
thereby dissecting the aortic wall.
 Driven by persistent intraluminal pressure,
the dissection process extends a variable
length along the aortic wall, typically
antegrade but sometimes retrograde from
the site of the intimal tear.

5.  The blood-filled space between the
dissected layers of the aortic wall
becomes the false lumen.
 Shear forces may lead to further tears in
the intimal flap (the inner portion of the
dissected aortic wall) and produce exit
sites or additional entry sites for blood
flow into the false lumen.
 Distention of the false lumen with blood
may cause the intimal flap to bow into
the true lumen and thereby narrow its
caliber and distort its shape.

6. EPIDEMIOLOGY :
 Uncommon but potentially catastrophic illness.
 Occurs with an incidence of at least 2000 cases
per year.
 Early mortality is as high as 1 % per hour if
untreated.
 The peak incidence – fifth and sixth decades of
life,
 Male to female--- 3:1

7. Clinical Presentation :
 Sudden onset of sharp , tearing , intractable
chest pain, may radiate to the back, esp,
interscapular region.
 Asymmetrical peripheral pulse
 Diastolic murmur or bruit
 Pulmonary edema
 Previously hypertensive , now in shock

8. LOCATION :
 Ascending aorta 65%
 Descending aorta, 20%
just distal to the origin of the left subclavian
artery at the site of the ligamentum
arteriosum.
 Aortic arch 10% and
 Abdominal aorta 5%

9. Commonly used classifications:
 Stanford types A and B and ,
 DeBakey types I, II, and III
Anatomical categories "proximal" and "distal”

10.  Stanford : Type A
:All dissections involving
the ascending aorta,
regardless of the site of
origin.
 Type B: All dissections
not involving the
ascending aorta

11. DeBakey’s :
DeBakey’sType I Originates in the
ascending aorta, propagates at least to
the aortic arch and often beyond it
distally
Type II Originates in and is confined to
the ascending aorta
Type III Originates in the descending
aorta and extends distally down the
aorta or, rarely, retrograde into the
aortic arch and ascending aorta

12. Proximal Includes:DeBakey
types I and II or Stanford
type A
Distal Includes :DeBakey
type III or Stanford type B

13. ETIOLOGY:
 Hypertension 72 – 80% ( most common)
 cystic Medial degeneration , as evidenced by
deterioration of medial collagen and elastin, is most
common predisposing factor.
 Atherosclerosis
 Connective tissue disorder (Marfan, Ehlers-Danlos)
 Takayasu (giant cell) arteritis
 Pregnancy (normal women during 3rdtrimester)
 Congenital bicuspicaortic valve
 Aortic coarctation
 Skeletal abnormalities (scoliosis, pectus)
 Mycotic aneurysm
 Aortic laceration

14. Rare causes
 Trauma
 Iatrogenic :
1. Intraarterial catheterization and
2. the insertion of intraaortic balloon pumps
3. Cardiac surgery Aortic valve replacement

15. Predisposing conditions:
 Bicuspid aortic valve. 7 -14 %,
 Coarctation of the aorta.
 Noonan and Turner syndromes.
 Cocaine abuse
 Pregnancy: third trimester & postpartum period

16. ACR Appropriateness Criteria for Aortic Dissection

17. Laboratory data
1. Decreases in the hemoglobin and hematocrit are
ominous findings suggesting the dissection either is
leaking or has ruptured.
2. BUN and creatinine are elevated if the dissection involves
the renal arteries.
3. Hematuria, oliguria, and even anuria(<50 mL/d) may
occur if the dissection involves the renal arteries.
4. CKMB and TroponinT may be elevated in acute thoracic
aorta dissection

18. In acute thoracic dissection, ECG can mimic the
changes seen in acute cardiac ischemia. In the
presence of chest pain, these signs can make
distinguishing dissection from AMI very difficult.
STT depression and T wave
inversion

19. IMAGING FINDINGS
o Chest X – Ray
 Mediastinal widening
 Left paraspinal stripe
 “ Calcium sign “is a
finding that suggests
aortic dissection. It is
the separation of the
intimal calcification
from the outer aortic
soft tissue border by
10 mm.

20. Other radiographic findings include the following:
Double aortic knob sign (present in 40% of patients)
Diffuse enlargement of the aorta with poor definition or irregularity
of the aortic contour
Inward displacement of aortic wall calcification by more than 10 mm
Tracheal displacement to the right
Pleural effusion (more common on the left side; suggests leakage)
Pericardial effusion
Cardiac enlargement
Displacement of a nasogastric tube

23. CT and CTA
 CT, especially with arterial contrast enhancement
(CTA) is the investigation of choice, able not only to
diagnose and classify the dissection, but also evaluate
for distal complications.
 Post contrast CT (CTA preferably) gives excellent
detail. Findings include:
 intimal flap
 double lumen
 dilatation of aorta

24.  Identification of true lumen is important : Helpful featurees
 True lumen :
 Surrounded by calcifications (if present)
 Smaller than false lumen
 Usually origin of celiac trunk, SMA and right renal artery
 False Lumen :
 Flow or occluded by thrombus (chronic).
 Delayed enhancement
 Wedges around true lumen (beak-sign)
 Collageneous media-remnants (cobwebs)
 Larger than true lumen
 Circular configuration (persistent systolic pressure)
 Outer curve of the arch
 Usually origin of left renal artery
 Surrounds true lumen in Type A dissection
Chronic dissection flaps are often thicker and straighter than those seen in acute
dissections

27. Intimomedial
flap in
ascending
aorta
Contrast
extravasation into
anterior
mediastinum
intimomedial
flap in aortic
Mediastinal arch
hematoma
False lumen: hypodense
compared to true lumen
True lumen: hyperdense
compared to false lumen

29. Type A dissection with
clear intimaflap seen
within the aortic arch.
RIGHT: Type B
dissection. Entry point
distal to left subclavian
artery

30. Type B dissection. Green
arrow indicates entry.
False lumen is indicated
by yellow arrows and is
seen spiraling around the
true lumen

31. Cobweb seen within the false
lumen

32. Dissection into abdominal arteries
The celiac trunc, SMA and right renal
artery flow usually originates from
the true lumen.
Left renal artery flow mostly
originates from the false lumen.
Impaired perfusion of end-organs can
be due to 2 mechanisms:
1) static = continuing dissection in the
feeding artery (usually treated by
stenting)
2) dynamic = dissection flap hanging
in front of ostium like a curtain
(usually treated with fenestration.
Left: Continued dissection into the celic
trunk showing bigger false lumen,
significantly contributing to organ
perfusion.Right: : SMA and renal artery
involvement, illustrating possible cause of
organ malperfusion

33. Rupture into pericardium and
thoracic cavity :
Even the slightest amount of fluid in
pericardium, mediastinum or
pleural cavity is suggestive of
rupture of the dissection.
The cases on the left show evident
rupture, with presence of extensive
hematoma.
Note extreme hematothorax and
hematomediastinum, causing shift
of the mediastinum and
compression on the pulmonary
veins and even aorta.
No pericardial effusion visible.
Left: pericardial fluid / hematoma indicates
rupture of the dissected aorta.Right:
Massive hematoma caused by rupture of
the dissected aorta into the mediastinum
and pleural cavity, no pericaldial hematoma

34. Aneurysm with thrombus
versus thrombosed dissection :
It can be difficult to differentiate an
aneurysm with thrombus from a
dissection with a thrombosed false
lumen.
If there are intima calcifications this
will be very helpfull.
A false lumen displaces the intimal
calcifications.
LEFT: Dissection with a thrombosed false lumen.
RIGHT: Aneurysm with thrombus on the inner side of the intimal calcifications

35. INTRAMURAL HEMATOMA :
Intramural Hematoma is a result of
ruptured vasa vasorum
Brief facts:
•Spontaneous hemorrhage caused
by rupture of vasa vasorum in media
13% of dissections, usually no pulse
deficit.
•Difficult to distinguish from
thrombosedAD
•Can proceed to classic dissection
(16-47%)
•Long time to diagnosis: usually
overlooked due to lack of non-enhanced
scan
•Mortality at 1 year after adismission
~ 25%

36. Classic example of IMH. Hyperdense
hematoma on NECT. Intima calcifications
surround the true lumen.
Same case. CECT of Intramural
hematoma

37. Non-contrast CT shows a cuff of high attenuation around the aortic
lumen in the acute phase that is low attenuation on post-contrast CT.
Intimal calcification may be displaced inwards.
Unlike aortic dissection, no intimal flap is present.
Contrast‐filld
CT
No contrast in aorta
intramural
hematoma

38. Penetrating Atherosclerotic Ulcer
PAU is defined as an ulceration of an
atheromatous plaque that has eroded the inner
elastic layer of the aortic wall.
It has reached the media and produced a
hematoma within the media.
Brief facts:
Patients with severe systemic atherosclerosis
Rarely rupture, yet worse prognosis due to
extensive atherosclerosis which causes organ
failure (e.g. acute myocardial infarction)
Cause of most saccular aneurysms
Located in arch and descending aorta
Often multiple (therefore surgical treatment
difficult, mostly treated medically)

39. Imaging features
Extensive atherosclerosis with severe intimal calcifications and atherosclerotic
plaques
Focally displaced and separated intima calcifications
Crater and/or contrast extravasation
-Focal IMH, longitudinal spread limited by mediafibrosis
Possibly enhancing aortic wall
Typical illustration of PAU, focal outpouchings of
contrast, separating extensive intimal calcifications

40. Complications
Complications of all types of aortic dissection include:
dissection and occlusion of branch vessels
abdominal organ ischaemia
limb ischaemia
ischaemic stroke
paraplegia: involvement of artery of Adamkiewicz
distal thromboembolism
aneurysmal dilatation: this is an indication for endovascular or
surgical intervention
aortic rupture
A type A dissection may also result in:
coronary artery occlusion
aortic incompetence
rupture into pericardial sac with resulting cardiac tamponade

41. MRI
1. Intimal flap
2. Slow flow and clot in false lumen
Lumen Partition of a three-dimensional
contrast-enhanced MRA shows intimal flap
(arrows ) in the distal aortic arch and descending
aorta.

42. Transesophgeal echocardiogram
1. Freely movable flap within the lumen of the vessel
2. Differential Doppler detection of true v.s. false lumen
Freely movable flap within the aorta

43. Angiography
1. Intimalflap
2. True and false lumen (may be failure if the false
channel is thrombosed)
3. Aortic regurgitation
4. Coronary artery.
Oblique arteriogram of the thoracic
aorta demonstrates the double-barrel
aorta sign of aortic dissection.
Both the true and false lumina are
opacified

44. .
MANAGMENT
Type A aortic dissection
Treatment for type A aortic dissection may include
:
Surgery. Surgeons remove as much of the dissected aorta as possible,
block the entry of blood into the aortic wall and reconstruct the aorta
with a synthetic tube called a graft. If the aortic valve leaks as a result of
the damaged aorta, it may be replaced at the same time. The new valve
is placed within the graft used to reconstruct the aorta.
Medications. Some medications, such as beta blockers and
nitroprusside (Nitropress), reduce heart rate and lower blood pressure,
which can prevent the aortic dissection from worsening. They may be
given to people with type A aortic dissection to stabilize blood pressure
before surgery.

45. Type B aortic dissection
Treatment of type B aortic dissection may include:
Surgery. The procedure is similar to that used to correct a
type A aortic dissection. Sometimes stents — small wire
mesh tubes that act as a sort of scaffolding — may be placed
in the aorta to repair complicated type B aortic dissections.
Medications. The same medications that are used to treat
type A aortic dissection may be used without surgery to treat
type B aortic dissections.
After treatment, you may need to take blood pressure
lowering medication for life. In addition, you may need
follow-up CTs or MRIs periodically to monitor your condition.