presentation on Aortic dissection include classification, cause, symptoms, diagnosis and its management.

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Aortic
Dissection
Dr Khushal

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The tragedies of life are largely arterial.
— SirWilliamOsler

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Introduction
 An aortic dissection is a serious condition in
which the inner layer of the aorta, the large
blood vessel branching off the heart, tears.
 Blood surges through the tear, causing the inner
and middle layers of the aorta to separate
(dissect).
 In classic aortic dissection an intimal flap exists
between the two lumens (true and false lumens)

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Acute aortic syndrome
 ClassicAortic dissection
 Aortic intramural
hematoma(IMH) - 10-20%
 Penetrating atherosclerotic aortic
ulcer(PAU) ~5%

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Features
 Incidence of aortic dissection at 2 to 6 cases per 100,000 person-years
 In autopsy series the prevalence of aortic dissection ranges from
0.2% to 0.8%.
 Male > Female (2:1)
 Age: most often 50-60 yrs.
 Very high early mortality: ~ 1% per hour reported in the first 24 hours
before surgery for type A dissection

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Hypothesis
1. Primary tear in the aortic intima with blood from the aortic lumen
penetrating into the diseased media and leading to dissection and
creation of fast and true lumen.
2. Rupture of vasa vasorum leading to haemorrhage in aortic wall ->
intimal disruption -> intimal tear and aortic dissection.
 Malperfusion syndrome: Distention of the false lumen with blood
causes the intimal flap to compress the true lumen and narrow its
calibre

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Classification
ATHEROSCLEROTIC
CARDIOVA
associated with Noonan syndrome, unicuspid aortic valve, supraval-
vular aortic stenosis, aberrant right subclavian artery (Kommerell
diverticulum), right-sided aortic arch, polycystic kidney disease, and
Alport syndrome (in males).1,17
Type A Type B
I II III
FIGURE 63.11 Classi cation schemes of acute aortic dissection. DeBakey clas-
si cation: Type I dissection originates in the ascending aorta and extends at least
to the aortic arch and often to the descending aorta (and beyond). Type II dissection
originates in the ascending aorta and is con ned to this segment. Type III dissection
TABLE 63.3 Classi cation Schemes of Acute
Aortic Dissection
TYPE DESCRIPTION
DeBakey Classi cation
I Dissection originates in the ascending aorta and extends at
least to the aortic arch and often to the descending aorta
(and beyond).
II Dissection originates in the ascending aorta and is con ned
to this segment.
III Dissection originates in the descending aorta, usually just
distal to the left subclavian artery, and extends distally.
Stanford Classi cation
A Dissection involves the ascending aorta (with or without
into subsets of importance for endovascular management.37
Cause and Pathogenesis
Several conditions predispose the aorta to dissection (Table 63.5),
most from disruption of the integrity of the aortic wall or marked
increases in aortic wall circumferential stress (see earlier discussion
on TAAs). Approximately 75% of all patients with aortic dissection
have hypertension. Hypertension may affect the elastic propertiesof
the arterial wall and increase stiffness, predisposing to aneurysm or
dissection. However, hypertension alone is not usually associated
with significant aortic dilation, and the vast majority of hypertensive
patients never have aortic dissection. In the IRAD registry of 4428
patients, conditionsassociated with dissection included: hypertension
(77%), atherosclerosis (27%), previouscardiac surgery (16%), known
aortic aneurysm (16%), MFS(4%), and iatrogenic condition (3%).38
Genetically triggered aortic syndromes, congenital heart diseases,
inflammatory vascular diseases, and cocaine and methamphetamine
use are also risk factorsfor aortic dissection. CMD commonly underlies
aortic dissection but does not indicate the cause (see Fig. 63.2).
Excessive signalingin the TGF-β pathway and abnormalitiesin function
of the SMCcontractile element may underlie certain aortic aneurysm
syndromes6,12,17
(see Table 63.1, Fig. 63.6, and eFig. 63.2). Patients
with MFS have a high risk for aortic root aneurysm and especially

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According to duration
 DISSECT system of classification divides patients into subsets of
importance for endovascular management
 Approx 65% of intimal tears occur in the ascending aorta, 30% in the
descending aorta, <10% in the aortic arch and ~ 1% in the abdominal
aorta.

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Causes
 Hypertension (~75%)
 Heritable or genetic thoracic aortic disease and syndromes
 Congenital diseases/syndromes
 Atherosclerosis
 Trauma, blunt or iatrogenic
 Cocaine/methamphetamine use
 Inflammatory/infectious diseases
 Pregnancy (with underlying aortopathy)
 Weightlifting (with underlying aortopathy)

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Clinical manifestation
Symptoms
 May mimic various conditions, high index suspicion
 Abrupt onset of severe chest or back pain is the most classic feature
 Severe sudden onset and maximum at the time of inception
 Quality: sharp, severe, stabbing, tearing, ripping, sense of doom
 Migratory (17%)- tend to follow the path of dissection through aorta
 Radiation from chest to back or vice versa
 “Painless” aortic dissection (6% ) more common in those with diabetes,
previous aortic aneurysm, and prior cardiac surgery

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Physical finding
organ system complication
 Hypertension
 Common inType B
 Type A normotensive or hypotensive
 Pulse deficit, AR and neurological
manifestation more common in Asc AD
 Mal perfusion
 Dynamic- over pressurized false lumen
pushing septum to true lumen
 Static - stenosis or occlusion of a branch
artery caused by the dissection flap,
hematoma embolism, or thrombosis.

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Aortic regurgitation
 Key diagnostic feature of type A dissection. (41-73%)
 Murmur ofAR varies in intensity, depending on BP
and the degree of heart failure
 Mechanism:-
 Incomplete coaptation of leaflet due to dilatation
 Leaflet prolapse cause by dissection flap
 extensive or circumferential dehiscing intimal flap
prolapsing into LVOT in diastole
 pre-existingAR resulting from an underlying aortic
root aneurysm or BAV disease

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Neurological manifestation
 17-40%, more common in type A.
 Persistent or transient ischemic stroke, spinal cord ischemia, ischemic
neuropathy, and hypoxic encephalopathy.
 Syncope (type A 19%, 3% type B)
 Acute Hypotension, obstruction of a cerebral vessel, or activation of
cerebral baroreceptors
 Coma and cerebral mal perfusion are associated with poor outcomes

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 Acute MI
 False lumen obstructing coronary ostium, dissection flap
involving CA.
 Most frequently involves RCA.
 Renal artery involvement (5-10%) - renal ischemia, infarction,
renal insufficiency, refractory hypertension
 Mesenteric Ischemia <5%
 Acute haemothorax
 Acute cardiac tamponade as a result of rupture with
hemopericardium, related to worst outcome.

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Lab finding
Initial evaluation
 Chest X ray- nonspecific finding, normal sometime
 ECG – nonspecific
 Ischemia or infraction related changes
 Low voltage QRS complex
 Evaluating the complications-CBP, Lactate,Troponin, LDH,
metabolic profile

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Diagnostic technique
 CECT,TTE,TEE, MRI.
 Each modality has advantages
and disadvantages with respect to
diagnostic ability, speed,
convenience and risk
 one must consider the diagnostic
information needed

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Contrast enhance CT
 Aortic dissection is diagnosed by the presence of two
distinct lumens with a visible intimal flap
 CECT is highly accurate in diagnosing aortic dissection,
with a sensitivity and specificity of 98% to 100%.
 Limitations:
Coronary Artery and Aortic valve evaluation
Streak Artifact in implanted device
Motion artifact of cardiac movement
Contrast nephropathy

18. z Spiral (helical) CECT allows three-dimensional reconstruction
for evaluation of the dissection and branch vessels and is critical for
planning endovascular repair.

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Magnetic resonance imaging
 Sensitivity and specificity of 98%
 It does not require IV iodinated contrast material or
ionizing radiation
 MRI permits multiplanar imaging with three-dimensional
reconstruction
 may detect pericardial effusion, aortic rupture, entry
points, and exit points with a high level of accuracy
 Limitations:Contraindicated in implantable devices and
implants,Time consuming and limited availability in
emergency

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Ultrasound
 Presence of an undulating intimal flap with independent
motion within the aortic lumen.
 Color flow Doppler demonstrates differential flow in the
two lumens
 TTE has sensitivity of 70% to 80% and specificity of 93% to
96% for the identification of type A aortic dissection
 Less sensitive for type B (33-55%)
 Bedside Availability

21. z Trans Esophageal Echocardiography
 TEE is highly accurate in the evaluation and diagnosis
 Sensitivity ~ 98%; specificity ~ 95%
 Accuracy is operator dependent
 visualize the intimal tear in 75% to 100% of cases,
differentiate the true and false lumens, and identify
fenestrations in the intimal flap.
 TEE is 100% sensitive in detecting AR complicating
dissection and may define its mechanism
 Access LV function , PE, Prox coronaries.

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Evaluation and management

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Management
 Initial medical management includes stabilizing the patient,
controlling pain, and lowering BP with beta blockers to reduce
the rate of rise in the force (dP/dt) of left ventricular
contraction.
 Aortic dissection has high mortality rate
 require urgent multidisciplinary evaluation and management.
 Emergency surgery leads to improved survival in patients with
acute type A dissection
 Initial medical therapy is recommended for acute type B
dissections

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Blood pressure reduction
 Reduction of systolic BP to ~ 100 to 120 mmHg or the lowest level
necessary for adequate perfusion and a heart rate of 60 to 80
beats/min is recommended.
 B Blocker should be administered-– Esmolol / labatolol
 Sodium nitroprusside leads to rapid reduction of BP
 Multiple agent IV NTG, IV ACE inhibitor, IV Nicardipin
 Refractory Hypertension – rule out renal malperfusion

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Management of cardiac tamponade
 8-31% in type A
 present with hypotension, syncope, or altered mental status
 Pericardiocentesis can result in recurrent bleeding and acute
hemodynamic collapse
 Hypotension or shock from hemopericardium secondary to
ascending dissection requires emergency aortic surgery
 Pericardiocentesis with aspiration of only enough pericardial
fluid to stabilize the patient before surgery may be lifesaving

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Thoracic endovascular Aortic repairTEVAR
In type B
 Entails lower morbidity and mortality thanOSR
 TEVAR covers the area of the primary intimal tear
and redirects flown to the true lumen, promoting
thrombosis of the false lumen and allowing aortic
remodelling
 corrects mal perfusion syndromes and branch vessel
ischemia

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Long term therapy and follow up
 It includes medical therapy, BP control, screening the patient and first-degree
relatives, serial imaging of the aorta, lifestyle modifications, and education.
 Treatment of hypertension – b blocker, CCB’s, ACE inhibitors.
 To look for underlying genetic aortic syndrome (MFS, BAV)
 Regular imaging of aorta and its branches for complications.
 A patent false lumen and a dilated descending aorta (>45 mm) are risk factors
for aneurysm and reintervention.
 Rapid aortic growth (>5 mm/yr) or aortic diameter greater than 60 mm are
risk factors for rupture

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