Aortic dissection is a severe condition affecting the aorta, with high mortality if untreated, and is classified based on the location of the tear. Diagnosis relies on imaging techniques, primarily CT with contrast, and management may require surgical intervention for type A dissections or medical management for type B cases. Key risk factors include hypertension, male sex, and connective tissue diseases, while symptoms often include severe chest or back pain and hypertension.

1. Aortic Dissection and Acute
Aortic Syndrome
Brant Clatterbuck

2. • Nothing to disclose

3. The problem
• Most common catastrophic event affecting the
aorta
– Incidence ranging from 2.9 – 3.5 per 100,000
person years
• Without treatment, majority of patients die
within 3 months

4. Anatomy
• Aorta is largest artery in the body
– Aortic Root: includes AV, starts at
annulus ends at sinotubual junction.
– Ascending Aorta: sinotubual
junction to takeoff of the Inominate
Artery (brachiocephalic artery).
– Aortic Arch: ends at the Subclavian
Artery. Curves anterior to posterior
– Descending Aorta: from subclavian
to diaphragm
– Abdominal aorta: from diaphragm
until division into iliacs

5. Anatomy – Layers
• Endothelium
• Intima
– Smooth surface for laminar
flow
• Media
– Muscles and elastic fibers
• Allows for stretch and
contraction
• Adventitia
– Surrounding connective
tissue
– Vasa vasorum originate here

6. Pathophysiology
• Aortic Dissection (AD) occurs when a defect in the
intimal layer of the aorta permits blood to create a false
channel within the aortic wall
– Typically occurs between media and adventitia
• Typically transverse and longitudinal
– Originates
• ascending aorta in 65%
• descending aorta in 25%
• arch and abdominal aorta in 10%
• Aorta is divided into true and false lumens, separated by
a dissection flap
• Blood courses antegrade or retrograde through the
newly created space

7. Pathophysiology
• Penetrating atherosclerotic ulcer and intramural hematoma
are also considered to be variants of aortic dissection.
– These lesions may eventually extend into the media and evolve
into a true dissection

8. Pathophysiology
• Fenestrations (connections
between the true and false
lumens) occur within the
intimal flap downstream
– usually at branch vessel
ostia
• These serve as sites where
blood flows back from the
false lumen into the true
lumen
– This flow allows the false
lumen to persist, rather than
thrombose

9. Malperfusion Syndromes
• Systemic effects of AD
largely depend on
involved branches
• Aortic branch
compromise is
present in 31% of
cases

10. Aortic Branch Vessel Compromise
• Dynamic obstruction: the
compressed true lumen cannot
provide enough volume due to low
flow or intimal flap prolapse into the
branch vessel
– Most common, 80%
– Severity based on circumference of AD,
cardiac output, BP, HR, and peripheral
resistance at the branch vessel
• Static Obstruction: dissection
extends into the branch vessel,
narrowing the lumen
– False lumen is highly thrombogenic, so
thrombosis beyond the compromised
area can occur

11. Anatomical Classification
• 2 schemes of classification based on intimal tear location
– Origin of the entry tear is known to be key predictor of early outcomes
• Debakey also considered extent of dissection in its classification
• Debakey
– Type I: Dissection originates in the ascending aorta, extends through the aortic
arch, and continues into the descending aorta and/or abdominal aorta for a
varying distance
– Type II: Dissection originates in and is confined to the ascending aorta
– Type IIIa: Dissection originates in the descending aorta and is limited to same.
– Type IIIb: Dissection involves descending and variable extents of the abdominal
aorta.
• Stanford
– Type A: originates in the ascending aorta
– Type B: originates in the descending aorta distal to the origin of the left
subclavian

12. Anatomical Classification

13. Temporal Classification
• Acute
– Traditionally a dissection is considered acute for the first
2 weeks after onset of symptoms
• Based on autopsy studies, 74% on patient deaths occur within
the first 2 weeks
• Subacute
– 2 weeks to 3 months
• Dissection flap remains pliable
• Chronic
– > 90 days, remodeling is taking place (for better or worse)

14. Risk Factors - Traditional
• HTN
– Especially if uncontrolled
• Male sex
– 4:1 predilection over females
• Age 60-80
– Avg age range for Type A is 50-60
– Avg age range for Type B is 60-70
• Family History
• Connective Tissue disease
– Marfan syndrome accounts for 50% of AD in patients < 40 years old
• Pregnancy
– Uncommon overall (5.5 per million pregnant women)
– 4x increased risk when compared to similar non-pregnant women
• Associated with pre-eclampsia

15. Risk Factors – Less Common
• Cardiovascular conditions
– Bicuspid aortic valve with or without aortic root
dilatation
– Congenital aortic diseases (coarctation, aortic arch
hypoplasia, etc…)
• Turner’s syndrome
• Coccaine/Crack use
• Thoracic Aortic aneurysm
• Trauma/Iatrogenic

17. Signs and Symptoms
• Pain
– Located in back, chest, or abdomen
– 93% of AD patients have pain
• 90% say “the worst ever”
– 85% report abrupt onset
• Hypertension
– Present in 70% of Type B, but only 25-35% of Type A
• Peripheral vascular complications
– Pulse deficits (most commonly femoral pulses)
• Hypotension
– More common with Type A, usually indicates AV disruption or tamponade
• Syncope/neurologic
– Present in 5-10%, may indicate tamponade or brachiocephalic vessel
involvement
– 2-10% of Type B AD cause spinal cord ischemia

18. Diagnosis
• Imaging required for
diagnosis
• Plain X-Ray
– Positive findings are
nonspecific
– Include widening of
mediastinum or
cardiac/aortic silhouette,
displacement of aortic
calcifications, or effusions

19. Diagnosis - CT
• CT with contrast is the mainstay of
imaging diagnosis
– Fast
– 90% sensitive, up to 100% specific
– Excellent anatomic data
• ability to localize the entry tear and
fenestrations
• assessment of branch vessel patency
• Detect extravasation of contrast
material consistent with rupture
– Effect of iodinated contrast on renal
function is main drawback

20. Diagnosis - Echocardiography
• Transthoracic Echo
– Widely variable
sensitivity/specificity
– Blind spot behind trachea and left
mainstem bronchus
• Transesophageal Echo
– Sensitivity as high as 98%
– May give useful surgical anatomical
information
– Often done in peri-operative period

22. Management – If suspected
• Obtain EKG, look for signs of ACS
– Extension of type A dissection to coronary ostia can cause coronary
ischemia
• Right coronary most commonly affected
• Labs:
– D-dimer. If <500 ng/dL is less likely to be aortic dissection
– CBC, basic electrolytes, LDH, coagulation parameters
– Cardiac markers
– Type and crossmatch
• This could become very important very soon
• Chest radiograph
– Widened mediastinum and/or unexplained pleural effusion are consistent
with dissection, particularly if unilateral.
• Proceed with vascular imaging as patient stability allows

23. Management – Once Diagnosed
• Two large bore IV’s. Continuous monitoring. Consider early arterial line
• Control heart rate and blood pressure.
– Maintain heart rate <60 BPM and systolic blood pressure between 100 and 120
mmHg.
• Esmolol - Loading dose plus drip
• Labetalol – 20 mg bolus followed q10 min boluses, or start drip
• Verapamil, diltiazem, or nicardipine if beta blockers not tolerated
• Once heart rate is consistently <60 BPM, give vasodilator therapy.
– For SBP > 120, start nitroprousside drip or nicardipine drip
– DO NOT use vasodilators without first controlling the heart rate
• Give IV opioids for analgesia (eg, fentanyl).
• Place Foley catheter for assessment of urine output and kidney
perfusion.
• Surgical Consultation

24. Surgical Consultation
• Obtain immediate surgical consultation (CT surgery, vascular surgery) as
soon as the diagnosis is strongly suspected
– Especially if ascending aorta is involved
• Type A aortic dissection is a cardiac surgical emergency
– Transesophageal echocardiography should be routinely performed in the
operating room to assess AV function, tamponade, etc
• Type B aortic dissection WITH evidence of malperfusion is treated with
urgent aortic stent-grafting or surgery
• Type B aortic dissection without evidence of malperfusion is admitted to
the ICU for medical management of hemodynamics and serial aortic
imaging
• If appropriate surgical services are not available, transfer without delay

25. Surgical Repair – Type A
• Surgical treatment
involves:
– Excision of the intimal
tear
– Obliteration of entry
into the false lumen
proximally
– Reconstitution of the
aorta with
interposition of a
synthetic vascular
graft
– Repair or replacement
of the aortic valve

26. Surgical Repair – Type A
• Endovascular repair has not been utilized
widely, still being studied

27. Management – Type B
• Type B dissection is generally managed medically
initially, with surgical intervention reserved for those
who develop complications related to the dissection
(eg, dissection extension, malperfusion)
– Early intervention to prevent malperfusion becoming more
common
– For uncomplicated Type B, endovascular intervention vs best
medical mgmt had equivocal 2-year survival (INSTEAD trial)
• Endovascular treatment had much more favorable aortic
remodeling (91% vs 14%) when compared to medical, but clinically
little difference was seen at 5 years (INSTEAD-XL trial)

28. Surgical Repair – Type B
• Indications for repair
– Evidence of end-organ malperfusion (see 'End-organ malperfusion' below)
– Refractory pain in spite of adequate medical treatment (subacute or
chronic)
– A rapidly expanding false lumen seen in first months after diagnosis
– Impending or frank rupture (acute or chronic)
– Aneurysmal dilation in a chronic type B dissection
• Open repair generally met with high mortality
– Reserved for those with anatomically unfavorable aorta or threatened or
actual rupture of proximal intima with no identifiable proximal landing zone
– Mortality ranges 6 – 70%
– Spinal cord ischemia in 32% of successful cases

29. Surgical Repair – Type B
• Endovascular repair was initially
used for complicated type B
dissections with malperfusion or
(impending) rupture
– promotion of aortic remodeling has
promise for all patients with type B
dissections
• Goals of TEVAR
– Cover proximal entry tear
– Obliterate false lumen 
thrombosis
– Restore flow to visceral vessels

30. Surgical Repair – Type B
• Fenestrated grafts allow for selected
angioplasty/stenting of involved branch vessels
– Promotes false lumen obliteration and reverses
malperfusion
– Technically challenging, not available everywhere