Aortic Dissection

Kriswanto , MD
Yudi Her Oktaviono , MD. PHD
Departement of cardiology
Dr. Soetomo General Hospital - Airlangga University
Surabaya - indonesia

Historical Note
Recognized since 16 th century.
Lannaec (French physician) introduced term Dissection aneurysm in 1819.

 King George 2 of Great Britain died (october 25,1760) while training on the
commode and was the first well documented case of an aortic dissection.

Historical Note
First successful outcome of modern treatment of aortic dissection was attributed to
Dr. DeBakey in his report, 1955 and later he devised a classification that is widely
used today as Debakey classification.

Anatomy of aorta

Overview of vessel histology

ARTERY

VEIN
Tunica intima
endothelium
basement membrane
internal elastic lamina

Tunica media
circular smooth muscle
external elastic lamina

Tunica adventitia

CAPILLARY

endothelium

basement membrane

Large or elastic arteries

Aortasection H&E 4x objective

A = tunica intima (interna) B = tunica media C = tunica adventitia (externa)

Large or elastic arteries

Aortasection H&E high magnification

With H&E, elastin fibers and smooth muscle cells are hard to discern. Under
high power, focus up and down with the fine focus knob, and look for fibers
that are birefringent (they look like they glow). These are elastin fibers.

arrowheads = elastic fibers

arrows = nuclei of smooth muscle

Large or elastic arteries

Aortasection Verhoeffs stain for elastin fibers 4x objective

Verhoeffs stain is used to visualize elastin fibers because it stains

them purple-black. How many layers of elastin fibers can you count
in the tunica media?
Large vessels are so thick that they must have their own blood
supply. This is the vasa vasorum.

A = tunica intima (interna) B = tunica media C = tunica adventitia (externa) arrowheads = vasa
vasorum

1.25

Classification

Percentage
Type

60%

10-15%

DeBakey I

DeBakey II

25-30%
DeBakey III

Stanford A

Stanford B

Proximal

Distal

Classification of aortic dissection

Incidence
Ranges from 2-10 per 100,000 person-years
Evidence of dissection is found in 1-3% of all autopsies
International Registry of Acute Aortic Dissection (IRAD)
65% men
mean age 63yrs
Women tend to present older (67 vs. 60yrs)

Highest incidence in patients 50 to 70 years old.

Male-to-female ratio 2:1
Half of dissections in females before age 40 occur during
pregnancy

Mortality
When left untreated
33% of patients die within the first 24 hours
50% die within 48 hours
~75% die within 2-weeks

Aortic dissection mimickers

Myocardial ischemia due to an acute coronary syndrome with or without ST segment
elevation
Pericarditis
Pulmonary embolus
Aortic regurgitation without dissection
Aortic aneurysm without dissection
Musculoskeletal pain
Mediastinal tumors
Pleuritis
Cholecystitis
Atherosclerotic or cholesterol embolism
Peptic ulcer disease or perforating ulcer
Acute pancreatitis

Predisposing factors
Older patients

HTN (72% of IRAD patients)

Younger patients

Pre-existing aneurysm (13%)

Inflammatory disease (giant cell, takayasu, RA, syphilitic aortitis)
Collagen disorders (Marfans [50% of pts <40], Ehlers-Danlos, Pseudoxanthoma
elasticum
Coarctation (Turners syndrome)
Family history (up to 19% of pts, # of mutations identified)
Bicuspid aortic valve
Trauma/Iatrogenic
Crack cocaine, (37% in largely AA, inner-city population study)
mean duration from last cocaine use ~12 hours. Mechanism may be abrupt, transient
hypertension due to catecholamine release.

Clinical Features
Abrupt onset of severe, sharp or "tearing" posterior chest or back
pain (70-90%)
Pulse deficit
weak/absent carotid, brachial, or femoral pulse resulting from
intimal flap or compression by hematoma
HTN at initial presentation is more common in those with a type B
dissection (70 vs 36%)

Clinical presentation

Clinical presentation

If dissection involves ascending aorta

Acute aortic insufficiency --> diastolic decrescendo murmur, hypotension,
or heart failure (1/2 to 2/3 of pts)
Acute MI due to coronary occlusion (1-2%). RCA most commonly involved (L
main sudden death) and, in infrequent cases, leads to complete heart
block.
Tamponade
Hemothorax (if extends through adventitia)
Stroke (if involves carotids)
Horner syndrome (compression of superior cervical sympathetic ganglion)
or vocal cord paralysis (compression of the left recurrent laryngeal nerve)

DIAGNOSTIC
EKG Findings
normal (31%)
nonspecific ST--T wave changes (30-42%)
(commonly, LVH and strain patterns associated with HTN)

ischemic changes (15%)

acute MI (5%)
>98% do not show ST elevation
***Based on 464 IRAD patients

Labs
D-dimer ?

14-center international study of 220 patients (87 with AD, 133 controls)
D-dimer levels 3213 1465 and 3574 1430 for type A and B
respectively
Sensitivity 96.6%, Specificity 46.6%
Possibility that D-dimer could be used to help rule-out aortic dissection

Suzuki et. al. Diagnosis of Acute Aortic Dissection by D-Dimer. Circulation 2009; 119,
2702-2707

Chest X Ray

Imaging
Summary of specialized imaging techniques
Angiography

CT

MRI

TEE

Sensitivity

Poor

Average

Excellent

Excellent

Specificity

Good

Good

Excellent

Good

Site of tear

Good

Poor

Excellent

Good

Excellent

Useless

Excellent

Excellent

Pericardial
effusion

Useless

Poor

Excellent

Good

Coronaries

Excellent

Useless**

Good

Average

Aortic
Regurgitation

Modified from Cigarroa JE et al.

ECHOCARDIOGRAPHY

0.50

TEE

0.21

CT Scan

Angiography
First definitive test for aortic dissection
Traditionally considered the gold standard
Involves injection of contrast media into the aorta

Identifies the site of the dissection

Major branches of the aorta
Communication site between true & false lumen
Can detect thrombus in the false lumen

Disadvantages

Not very practical in critically ill patients

Nephrotoxic contrast
Risks of an invasive procedure

Medical management
Basic management
Type A dissection surgery
Type B dissection medical management, TEVAR

Surgery -- prevents medial extension reaching the pericardium

and producing fatal tamponade or worsening other complications

Medical therapy
Reduce systolic BP to 100 to 120 mmHg or the lowest level that is tolerated
IV Beta blockers

Propanolol (1-10 mg load, 3mg/hr)

Labetalol (20 mg bolus, 0.5 to 2 mg/min)

If SBP remains >100mmHg, nitroprusside should be added

Do not use without beta blockade
Avoid hydralazine

Bentall procedure

What is the optimal treatment

TEVAR

1.20

Long Term Outcome

Type A
Survival at 5 yrs 68%
Survival at 10 yrs 52 %

Type B
5 yrs 60 - 80%
10 yrs 40 80%
Spontaneous healing of dissection is uncommon

Long-Term Management
Medical therapy

Oral Beta-blockers (reduces aortic wall stress)

Keep BP < 135/80 mmHg (combination therapy)
Avoidance of strenuous physical activity

Serial imaging

Thoracic MR scan prior to discharge

f/u scans at 3, 6, and 12 months
Subsequent screening studies done every 1-2 yrs if no evidence of progression

Overview
Incidence of aortic dissection is at least 2000 new cases per year
Peak incidence is in the sixth to seventh decade
Men are affected twice as commonly as women
Mortality in the first 48 hours is 1% per hour
Early diagnosis is essential

Pathophysiology
The chief predisposing factor is degeneration of collagen and elastin in
the aortic intima media
Blood passes through the tear into the aortic media, separating the
media from the intima and creating a false lumen
Dissection can occur both distal and proximal to the tear

Classification
Debakey system
Type I
Originates in the ascending aorta, propagates to the aortic arch and beyond it distally

Type II
Confined to the ascending aorta

Type III
Confined to the descending aorta, and extends distally, or rarely retrograde into the aortic
arch

Classification
The Stanford system
Type A
All dissections involving the ascending aorta

Type B
All other dissections regardless of the site of the primary intimal tear

Ascending aortic dissections are twice as common as descending

Predisposing factors
Age, 60-80 yrs old
Long standing history of hypertension
80% of cases have co-existing HTN

Takayasus arteritis
Giant cell arteritis
Syphilis
Collagen disorders
Marfan syndrome (6-9% of aortic dissections)
Ehlers-Danlos syndrome

Other Risk Factors

Congenital Cardiac Anomalies

Bicuspid aortic valve (7-14% of cases)

Coarctation of the aorta

Cocaine

Abrupt HTN, due to catecholamine release

Trauma

Pregnancy (50% of dissections in women <40 yrs)

Iatrogenic (cardiac cath, IABP, cardiac surgery, s/p valve replacement)

Clinical Symptoms
Severe, sharp, tearing posterior chest pain or back pain (occurs in 74-90% of pts)
Pain may be associated with syncope, CVA, MI, or CHF
Painless dissection relatively uncommon

Chest pain is more common with Type A dissections

Back or abdominal pain is more common with Type B dissections

Physical Exam
Pulse deficit
Weak or absent carotid, brachial, or femoral pulses
these patients have a higher rate of mortality

Acute Aortic Insufficiency

Diastolic decrescendo murmur
Best heard along the right sternal border

Clinical signs
Acute MI

RCA most commonly involved

Cardiac tamponade
Pleural effusions
Hypertension or hypotension
Hemothorax
Variation in BP between the arms (>30mmHg)

Neurologic deficits

Stroke or decreased consciousness

Clinical Signs
Involvement of the descending aorta
Splanchnic ischemia
Renal insufficiency
Lower extremity ischemia
Spinal cord ischemia

Diagnosis
Generally suspected from the history and PE
In a recent study in 2000, 96% of acute dissection patients could be identified based
upon a combination of three clinical features
Immediate onset of chest pain
Mediastinal widening on CXR
A variation in pulse and/or blood pressure (>20 mmHg difference between R & L arm

Incidence >83% when any combination of all three variables occurred

Differential Diagnosis

Acute Coronary Syndrome

Pericarditis
Pulmonary embolus
Pleuritis
Cholecystitis
Perforating ulcer

Diagnostic Tests
EKG
Absence of EKG changes usually helps distinguish dissection from angina
Usually non-specific ST-T wave changes seen

CXR
Cardiac Enzymes

Chest X-Ray
May show widening of the aorta with ascending aorta
dissections
Present in 63 % of patients with Type A dissections

Diagnostic Imaging
Not performed until the patient is medically stable
Has been a dramatic shift from invasive to non-invasive diagnostic
strategy

Spiral CT scan
TEE
MRI
Angiography

Imaging
Can identify aortic dissection and other features such as:

Involvement of the ascending aorta

Extent of dissection
Thrombus in the false lumen
Branch vessel or coronary artery involvement
Aortic insufficiency
Pericardial effusion with or without tamponade
Sites of entry and re-entry

Spiral CT

Sensitivity 83%
Specificity 90 - 100%

Two distinct lumens with a visible intimal flap can be identified

Advantages

Noninvasive
Readily available at most hospitals on an emergency basis
Can differentiate dissection from other causes of aortic widening (tumor, periaortic hematoma, fat)

Disadvantages

Sensitivity lower than TEE and MRI

Intimal flap is seen < 75% of cases
Nephrotoxic contrast is required
Cannot reliably detect AI, or delineate branch vessels

TTE
First used to diagnose aortic dissections in the 70s
Sensitivity 59-85%, specificity 63-96%
Image quality limited by obesity, lung disease, and chest wall
deformities

TEE
Sensitivity 98%

Specificity 95%

Advantages

Close proximity of the esophagus to the thoracic aorta

Portable procedure
Yields diagnosis in < 5 minutes
Useful in patients too unstable for MRI
True and false lumens can be identified
Thrombosis, pericardial effusion, AI, and proximal coronary arteries can be readily visualized

TEE
Lower specificity attributed to reverberations atherosclerotic vessels or
calcified aortic disease producing echo images that resemble an aortic
flap
Disadvantages
Contraindicated in patients with esophageal varices, tumors, or strictures
Potential complications: bradycardia, hypotension, bronchospasm

MRI

Most accurate noninvasive for evaluating the thoracic aorta

Sensitivity 98%
Specificity 98%

Advantages

Safe
Can visualize the whole extent of the aorta in multiple planes
Ability to assess branch vessels, AI, and pericardial effusion
No contrast or radiation

Disadvantages

Not readily available on an emergency basis

Time consuming
Limited applicability in pts with pacemakers or metallic clips

Conclusions
Conventional TTE is of limited diagnostic value in assessment of the
thoracic aorta
Both TEE and MRI have excellent sensitivity, however MRI is more
specific
MRI is the study of choice for stable patients
TEE is the study of choice for unstable patients

Treatment
Acute dissections involving the ascending aorta are considered surgical
emergencies
Dissections confined to the descending aorta are treated medically
Unless patient demonstrates continued hemorrhage into the pleural or
retroperitoneal space

Surgical Options
Excision of the intimal tear
Obliteration of entry into the false lumen proximally
Reconstitution of the aorta with interposition of a synthetic
vascular graft

Type A Dissections
Operative mortality varies from 7-35%
27% post-op mortality
Patients who died had a higher rate of in-hospital complications such
as strokes, renal failure, limb ischemia, & mesenteric ischemia

Poor prognostic factors

Hypotension or shock
Renal failure
Age> 70 yrs
Pulse deficit
Prior MI
Underlying pulmonary disease
Preoperative neurologic impairment
Renal and/or visceral ischemia
Abnormal EKG, particularly ST elevation

Aortic Dissection
Matt White
February 8, 2010
Morning Report

Aortic Dissection

Background
Epidemiology
Clinical characteristics
Diagnostic Modalities
Treatment

Aortic Dissection

Background
Epidemiology
Clinical characteristics
Diagnostic Modalities
Treatment

History
First known case was King George II on October, 25, 1760
First successful repair by Dr. Michael DeBakey in 1955.
". . . spontaneous tear of the arterial coats is associated with
atrocious pain, with symptoms, indeed, in the case of the aorta of
angina pectoris and many instances have been mistaken for it"
William Osler, 1910.

Mechanism
Primary event is a tear in the aortic intima.
Degeneration of aortic media, or cystic medial necrosis, is felt to be a
prerequisite nontraumatic aortic dissection
Blood passes into the aortic media through the tear, separating the intima
from the media and creating a false lumen.

Uncertain whether the initiating event is a primary rupture of the

intima with secondary dissection of the media, or hemorrhage
within the media and subsequent rupture of the overlying intima

Mechanism (contd)
Propagation of the dissection can occur both distal and
proximal to the initial tear,
Complications of dissection:
ischemia (coronary, cerebral, spinal, or visceral)
aortic regurgitation
Pericardial effusion/cardiac tamponade

Nomenclature
DeBakey classification system
Type I - Originates in 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 descending aorta, rarely extends proximally but will
extend distally.
Daily (Stanford) classification system
Divided into 2 groups; A and B depending on whether the ascending aorta is
involved.
A = Type I and II DeBakey
B = Type III DeBakey

Aortic Dissection

Background
Epidemiology
Clinical characteristics
Diagnostic Modalities
Treatment

Aortic Dissection

Background
Epidemiology
Clinical characteristics
Diagnostic Modalities
Treatment

Aortic Dissection

Background
Epidemiology
Clinical characteristics
Diagnostic Modalities
Treatment

Pre-OR management
Virtually all non-shocked patients require medical
management prior to surgery
Aim of medical management:
reduce the absolute pressure on the damaged aortic media
Reduce the rate of rise of that pressure (dP/dT).

Medical management
Blood pressure control
Blood pressure control
Blood pressure control
Pain control

Main goals of medical management

Systolic BP < 100 mmHg.

Pain free.
Adequate renal perfusion (urine output > 30 ml/hr).
No evidence of cerebral hypoperfusion.
Minimized shear stress (-blocked to < 55/min).

Antihypertensive choice
Labetalol for beta blockade
Nitroprusside if HR controlled but SBP still >100mmHg

Antihypertensive choice
Start with -blockers
use of a vasodilator in isolation will actually increase
aortic shear stress by widening the pulse pressure and
the dP/dT of left ventricular ejection.

Which arm to measure?

Blood pressure should be measured in the arm with

the highest reading.

References
Davies, Crispin; Bashir, Yaver; Shively. Cardiovascular
Emergencies. London, GBR: BMJ Publishing Group, 2001. p151172
Manning, Warren. Clinical manifestations and diagnosis of aortic
dissection. UptoDate
Suzuki et. al. Diagnosis of Acute Aortic Dissection by D-Dimer.
Circulation 2009; 119, 2702-2707