This document discusses acute aortic syndrome (AAS), which includes acute aortic dissection, intramural hematoma, and penetrating atherosclerotic ulcer. AAS is caused by disruption of the aortic wall layers from tears or ulcers, allowing blood to track within the layers. The most common type is aortic dissection, where blood passes through a tear separating the vessel layers. Presenting symptoms typically include sudden severe chest or back pain. Diagnosis involves imaging like CECT, MRI, or TEE to identify abnormalities. Prognosis depends on factors like involvement of the ascending aorta and complications. Classification systems differentiate type A dissections involving the ascending aorta from type B.

1. Acute aortic
syndromes
Dipak Patade

4. Normal range for size of aorta

6. Acute aortic syndrome (AAS)
• Acute aortic syndrome (AAS) is a modern term to describe interrelated
emergency aortic conditions with similar clinical characteristics and
challenges.
• These conditions include :
 Acute aortic dissection(80-90 %)
 Intramural haematoma (IMH): bleeding in the aortic wall occurs without
evidence of an intimal tear or dissection flap( 10% to 20%)IMH, where
 penetrating atherosclerotic ulcer. PAU: (5% )
Other closely related :
 trauma to the aorta with intimal laceration
 Ruptured aneurysm

7. Acute aortic syndrome (AAS)
• AAS : disruption of the media layer of the aorta resulting in separation of the
layers of the aorta (dissection),
• IMH:with bleeding in the the wall of the aorta
• disruption transmurally through the wall in the case of ruptured PAU or trauma.
In the majority of patients (90%), an intimal disruption is present
• a tear or an ulcer allows blood to penetrate from the aortic lumen into the media
or within rupture of the ‘vasa vasorum’ within the media;
• intimal disruption results in tracking of the blood in a dissection plane within
the media potentially rupturing through the adventitia or back through the
intima into the aortic lumen.
• the inflammatory response to blood in the media may lead to aortic dilatation
and rupture.
• The most common aortic syndrome is aortic dissection.

10. Pathophysiology
• a tear in the aortic intima
• commonly preceded by medial wall degeneration or cystic media necrosis.
• Blood passes through the tear separating the intima from media or
adventitia creating a false lumen.
• Propagation of dissection can proceed in an anterograde or retrograde
fashion from the initial tear involving side branches and causing
complications such as tamponade, aortic valve, insufficiency, or proximal or
distal malperfusion syndromes.

11. Pathophysiology
• In the presence of atherosclerosis, the inflammatory response to
thrombus in the further necrosis and apoptosis of SMC
• degeneration of elastic tissue, which potentiates the risk of medial
rupture
• increased risk of AAS in patients with inflammatory disorders such
as periarteritis nodosa, Takayashu’s syndrome, or Behcet’s
syndrome.
• Prevalent in genetic aortic syndromes

12. Contributing conditions for aortic dissection

13. Genetic risk factors

14. Clinical symptoms

15. Clinical symptoms
• Variable.
• Needs high index of suspicion.
• Abrupt onset of severe chest or back pain is the most classic feature.
• sudden onset, with maximum intensity occurring at its inception. The pain
may be accompanied by a “sense of doom.”
• quality :“sharp,” “severe,” or “stabbing,” “tearing” or “ripping”
• “stabbed in the chest with a knife” or “hit in the back with a baseball bat,”
• burning, pressure, or pleuritic pain.
Painless aortic dissection: occurs in 6% of patients and is more common in
those with diabetes, previous aortic aneurysm, and prior cardiac surgery.

17. Laboratory Findings
(1) CXR:
• abnormal aortic contour or widening of the aortic silhouette, which appears
in approximately 80% of cases
• (83% of type A; 72% of type B).
• Pleural effusions :20% of dissections.
• normal chest x-ray findings on presentation were found in 29% of type A and
36% of type B dissections.
(2) ECG:
• Acute MI
• Low voltage complex in hemopericrdium

19. labs
(3) Elevated D-dimer levels:
• seen within the first 24 hours of onset, a D-dimer level lower than 500 ng/mL had a negative
likelihood ratio of 0.07 and a negative predictive value of 95%.
• sensitivity of 97% and a specificity of 47%.
(4) dedicated aortic imaging:
 CECT :the modality of choice most often used
• Fast and reliable
• allows rapid acquisition of thinly collimated images of the entire aorta during arterial transit of
contrast bolus
• CECT is highly accurate in diagnosing aortic
• a sensitivity and specificity of 98% to 100%.
• Risk: Contarst induced neohropathy

20. MRI:
• infrequently used as the initial test for evaluation of acute dissection, but
• given its imaging detail and lack of ionizing radiation, it is particularly attractive for
the long-term follow-up of aortic dissection.
• visualization of blood flow, differentiation of slow flow and clot, evaluation of intimal
flap mobility, and detection of AR ,to assess branch vessel morphology when combined
with contrast-enhanced MRA.
• pericardial effusion, aortic rupture, entry points, and exit points with a high level of
accuracy; MRA may detect and quantify AR.
• ECHO:
• TTE has sensitivity of 70% to 80% and specificity of 93% to 96% for the identification
of type A aortic dissection, but it is much less sensitive (31% to 55%) than other
modalities for the diagnosis of type B aortic dissection.

21. • TEE :
• highly accurate in the evaluation and diagnosis
• sensitivity 98%; specificity, 95% but its accuracy is operator dependent
• may not completely visualize the distal ascending aorta and proximal aortic
arch, but it interrogates the remaining thoracic aortic segments well.
• TEE may visualize the intimal tear in 75% to 100% of cases, differentiate
the true and false lumens, and identify fenestrations in the intimal flap

22. Complications of dissection
• a. Type A dissections
i. Aortic regurgitation
ii. Coronary artery involvement
iii. Pericardial effusion/hemopericardium
• b. Aortic rupture or leakage
• c. Branch vessel involvement
• d. Malperfusion
• e. Aneurysmal enlargement

23. AORTIC DISSECTION

25. Classification
• In 80% to 90% of acute aortic syndromes, classic aortic dissection is present
• Regarding time from the onset of initial symptoms to the time of
presentation
• 1- Acute dissection: within 2 weeks of onset of pain
• 2- Subacute: between 2 and 6 weeks from the onset of pain
• 3- Chronic: more than 6 weeks from the onset of pain

26. Anatomical classification
• according to -either the origin of the intimal tear or whether the dissection
involves the ascending aorta (regardless of the site of origin)
• Accurate classification is important as it drives decisions regarding surgical vs.
non-surgical management
• The two most commonly used classification schemes are the
1. DeBakey system and the
2. Stanford systems
For the purpose of Classification :
the ascending aorta refers to the aorta proximal to the brachiocephalic artery,
and the descending aorta refers to the aorta distal to the left subclavian artery.

27. Types of dissections

28. The DeBakey classification system
• categorizes dissections based on the origin of the intimal tear and the extent
of the dissection
• Type I: Dissection originates in the AA and propagates distally to include at
least the aortic arch and typically the DA (surgery usually recommended)
• Type II: Dissection originates in and is confined to the AA (surgery usually
recommended)
• Type III: Dissection originates in the descending aorta and propagates most
often distally (non-surgical treatment usually recommended).
Type IIIa: Limited to the descending thoracic aorta.
Type IIIb: Extending below the diaphragm.

29. The Stanford classification
• The Stanford classification system divides dissections into two categories,
those that involve the ascending aorta and those that do not.
• Type A: All dissections involving the ascending aorta regardless of the site of
origin (surgery usually recommended).
• Type B: All dissections that do not involve the ascending aorta (non-surgical
treatment usually recommended).
• Note that involvement of the aortic arch without involvement of the
ascending aorta in the Stanford classification is labelled as Type B.

30. Prognostic considerations :
• The risk of death is increased in patients who present with or develop
complications of pericardial tamponade, involvement of coronary arteries
causing AMI, or malperfusion of the brain.
• Other predictors of increased in-hospital death : age ≥70 years old,
hypotension or cardiac tamponade, RF, and pulse deficits.
• Iatrogenic aortic dissection carries a mortality higher than non-iatrogenic
(35 vs. 24%)
• In the absence of immediate surgery, medical management of proximal
dissection is associated with a mortality of 20% by 24 h after presentation
30% by 48 h, 40% by Day 7, and 50% by 1 month
• Even with surgical repair, mortality rates are 10% by 24 h, 13% by 7 days,
and 20% by 30 days tamponade, RF, and pulse deficits.

31. Prognostic considerations :
• Patients with uncomplicated Type B dissection have a 30-day mortality of
10%
• However, patients who develop ischaemic complications such as RF, visceral
ischaemia, or contained rupture often require urgent aortic repair which
carries a mortality of 20% by Day 2 and 25% by Day 3.
• Similar to Type A dissection, advanced age, rupture, shock, and
malperfusion are important independent predictors of early mortality.
• The chronic use of crack cocaine appears to predispose patients to AAD.

33. Inntramural hematoma
• Intramural hematoma is defined as a bleeding of the vasa vasorum in the
medial layer of the aorta with no blood flow within the media .
• aortic wall apoplexy.
• Systemic hypertension is the leading cause.
• Other causes – Aortic trauma, penetrating aortic ulcer.
• Intramural hematoma most frequently involves the ascending or proximal
descending aorta—up to 70% of cases.
• Intramural hematoma is classified in the same way as aortic dissection: type
A when the ascending aorta is involved and type B when involvement is
limited to the descending aorta.

34. • True lumen is surrounded by calcification
most of the times and its usually smaller
than false lumen
• False lumen spirals around true lumen
• In M mode, the flap moves to the false
lumen in systole.
• Spontaneous echo contrast and thrombus
can be seen in the false lumen.
• With color Doppler is delayed systolic
flow seen by secondary or re-entry tear to
the false lumen.
• The false lumen (especially in chronic
dissections) tends to be larger in
comparison to the true lumen

35. Dissection vs IMH
IMH does not spiral around the lumen as seen in AD

36. TEE
Type A dissection visualized in
the longitudinal and short-axis
view; white arrows indicate
dissection lamella (A) and an
intimal tear in close proximity of
the aortic leaflets (B).
Colour flow mapping in a patient
with chronic Type B dissection
shows vigorous flow into the false
lumen, demonstrating the
communication between the true
and false lumen (C).
Partial thrombosis in the
aneurysmatic false lumen in
chronic Type B dissection (D).
FL, false lumen; TL, true lumen.

37. Inntramural hematoma
• Aortic IMH is considered a precursor of dissection
• IMH may, progress, dissect, regress, or resorb;
• two-thirds of cases are located in the descending aorta and are typically
associated with hypertension.
• Similar to dissection, chest pain is more common with ascending (proximal)
• IMH, whereas back pain is more common with descending (distal) IMH.
• Nonetheless, the diagnosis of IMH cannot be made on clinically grounds
alone-CT

38. Intramural hematoma
• Acute IMH : for 5–20% of all AAS,
• regression : 10%,
• progression to classic aortic dissection : 28–47%,
• and a risk of rupture : 20–45%.
• Although there is ongoing debate on the natural history of IMH Caucasian
patients benefit from surgical repair in proximal IMH.
• an association between increasing hospital mortality and the proximity of
IMH to the aortic valve, irrespective of medical or surgical treatment.
(In the IRAD registry of 1010 patients)

39. Penetrating aortic ulcer

40. Penetrating aortic ulcer
• account for 7.5% of all cases of acute aortic syndrome.
• Deep ulceration of atherosclerotic aortic plaques can lead to IMH
• present as acute pain syndrome with aortic dissection or perforation.
• disease process that often complicates IMH and appears as an ulcer-like
projection into the haematoma.
• PAUs almost exclusively seen in patients with Type B IMH.
• PAUs originate from atherosclerotic aortic segments and are localized in the
descending thoracic aorta in over 90%.
• the classic appearance is mushroom-like outpouching of the aortic lumen
with overhanging edges.
• Symptomatic ulcers with signs of deep erosion are more prone to develop
dissection or rupture.
• Transthoracic endovascular repair with stent grafting (TEVR) is an
attractive therapeutic modality.

41. Penetrating aortic ulcer
• Typically, penetrating atherosclerotic ulcers are seen in older male patients
with :
history of hypertension (up to 92%),
smoking (up to 77%) and
coronary artery disease (up to 46%) as well as
chronic obstructive pulmonary disease (24-68%)

42. Diagnostic evaluation by imaging modalities

43. Treatment concepts
• Acute aortic syndromes (dissection or IMH) involving the ascending aorta
are surgical emergencies;
• acute aortic pathology confined to the descending aorta is subject to medical
treatment unless complicated by organ or limb malperfusion, progressive
dissection, extraaortic blood collection (impending rupture), intractable pain,
or uncontrolled hypertension.
• Initial management of AAS :
• Aortic dissection :limiting propagation of dissected wall components by
control of blood pressure and reduction in dP/dt (pressure development).
• Reduction in pulse pressure to just maintain sufficient end-organ perfusion
is a priority with the use of intravenous b-blockade as first-line therapy.

44. Treatment concepts
• Initial therapy:
• intravenous b-blockade. Labetalol, Esmolol with both a- and b-blockade, is useful for
lowering both blood pressure and dP/dt, with a target systolic pressure of 100–120 mmHg
and a heart rate of 60–80 b.p.m.
• Often multiple agents are required, with patients ideally managed in an intensive care
setting.
• Opiate analgesia should be prescribed to attenuate the sympathetic release of
catecholamines to pain with resultant tachycardia and hypertension.
• endovascular intervention :is dictated by the site of the lesion and evidence of
complicationsn(persisting pain, organ malperfusion), as well as evidence of disease
progression on serial imaging.
• Pericardiocentesis: generally avoided in acute type A dissection and urgent surgery is
recommended(can result in recurrent bleeding and acute hemodynamic collapse,
especially if a larger volume of fluid is removed and increased BP leads to further brisk
bleeding into the pericardial space.

45. Treatment concepts
• Acute Type A dissection: has a mortality of 1–2% per hour during the first
24–48 h of presentation.
• if left untreated up to 50% of the patients will be dead in 1 week.
• Death is caused by proximal or distal extension of the dissection leading to
valvular dysfunction, pericardial tamponade, arch vessel occlusion, or
rupture.
• Medical management alone is associated with a mortality of 20% by 24 h
and 30% by 48 h;
• In experienced centers, 30-day surgical mortality for acute type A dissection
is 10% to 35%.
• Factors increasing mortality included shock, heart failure, cardiac
tamponade, MI, renal failure, age, and malperfusion

46. Treatment concepts
• Patients with acute type B aortic dissection have a lower acute mortality
rate than those with acute type A dissection.overall in-hospital mortality
rates of approximately 10%.
• complicated type B dissection carries a much higher mortality rate,
especially when accompanied by shock or malperfusion.
• In the IRAD era, 57% of patients with acute type B dissection were treated
medically, 32% received endovascular therapy, and 7% were treated with
OSR with in-hospital mortality rates of 10%, 14%, and 21%, respectively.
• TEVAR covers the area of the primary intimal tear and redirects flow to the
true lumen, promoting thrombosis of the false lumen and allowing aortic
remodeling.often corrects malperfusion syndromes and branch vessel
ischemia
• The STABLE trial :30-day mortality rate of 4.7%.
• The DISSECTION trial treated complicated type B dissection with TEVAR,
reporting a 30-day mortality of 8% and 12-month mortality of 15%.

49. For type A dissection

50. For type A dissection

51. For type B dissection
(TEVR)