Aortic Dissection: Causes, Symptoms, and Classification

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MAGDI AWAD SASI DISSECTINGAORTICA.
Dissection, Aortic
Aortic dissectionis the most commoncatastrophe of the aorta, 2-3 times more
common thanrupture of the abdominal aorta. When left untreated, about 33%
of patients die withinthe first 24 hours, and50% die within48 hours. The 2-
week mortality rate approaches 75% inpatients withundiagnosedascending
aortic dissection.
The DeBakey classificationdividesdissections into3 types.
 Type I involves the ascending aorta, aortic arch, and descending aorta.
 Type II is confinedto the ascending aorta.
 Type III is confinedto the descending aortadistal tothe left subclavian
artery.
o Type III dissectionsare further dividedintoIIIaand IIIb.
o Type IIIa refers todissections that originatedistal tothe left
subclavianartery but extendbothproximally and distally, mostly
above the diaphragm.
Type IIIb refers todissections that originatedistal tothe left subclavianartery,
extendonly distally andmay extendbelowthe diaphragm.
CLASSIFICATION
DEBAKEY
Type I
Ascending aorta extending beyond
arch
Type II
Ascending aorta only
Type III a
Descending aorta distal to left
subclavian (above diaphragm)
Type III b
Descending aorta distal to LSA
extending below diaphragm
STANFORD
 A – Ascending aorta
 B – Not involving
Ascending Aorta

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Thoracic aortic dissections shouldbe distinguishedfromaneurysms (ie, localized
abnormal dilationof the aorta) and transections, whichare causedmost
commonly by high-energy trauma.
Race
Aortic dissectionis more commonin blacks than inwhites and less common in
Asians thanin whites.
Sex
The male-to-female ratiois 3:1.
Age
75% of dissections occur inthose aged40-70 years, withapeak in 50-65 years

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Pathophysiology:
The essential feature of aortic
dissectionis atear in the intimal
layer, followedby formationand
propagationof a subintimal
hematoma. The dissecting
hematoma commonly occupies
about half and occasionally the
entire circumference of the
aorta. This produces a false
lumenor double-barreledaorta,
which can reduce bloodflow to
the major arteries arising fromthe aorta. If the dissectioninvolves the
pericardial space, cardiac tamponade may result.
Cystic medial necrosis
The normal aorta contains collagen, elastin, andsmoothmuscle cells that
contribute the intima, media, and adventitia, whichare the layers of the aorta.
Withaging, degenerativechanges leadtobreakdownof the collagen, elastin,
and smooth muscle and an increase in basophilic groundsubstance. This
conditionis termedcystic medial necrosis. Atherosclerosis that causes occlusion

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of the vasa vasorum alsoproduces this disorder. Cystic medial necrosis is the
hallmark histologic change associatedwithdissectioninthose with Marfan
syndrome.
Researchershave usedthe termcystic medial degeneration inelder patients.
Early on, cystic medial necrosis describedanaccumulationof basophilic ground
substance inthe media withthe formationof cystlike pools. The mediain these
focal areas may show loss of cells (ie, necrosis). This termstill is usedcommonly
to describe the histopathologic changes that occur.
Dissectionsites
The most common site of dissectionis the first fewcentimetersof the ascending
aorta, with90% occurring within10 centimetersof the aortic valve. The second
most common site is just distal tothe left subclavianartery. Between5% and
10% of dissectionsdonot have an obvious intimal tear. These oftenare
attributedtorupture of the aortic vasa vasorum as first describedby
Krukenberg in1920.

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Mortality/Morbidity
 From 1-2% of patients withaortic dissectiondie per hour for the first 24-
48 hours.
 Aortopathy may be present inheritable diseases suchas Marfan
syndrome, Ehlers-Danlos syndrome, annuloaortic ectasia, familial aortic
dissections, adult polycystic kidney disease, Turner syndrome, Noonan
syndrome, osteogenesisimperfecta, bicuspidaortic valve, coarctationof
the aorta, and connective tissuedisorders. It is alsoseeninheritable
metabolic disorders suchas homocystinuriaandfamilial
hypercholesterolemia.
 Incidence is increasedinpregnancy and syphilis. Thoracic aortic dissection
also is associatedwithcrack cocaine use and iatrogenic causes, suchas
cardiac catheterization.
SYMPTOMS:
No one signor symptom can positively identify acute aortic dissection(AAD). An
estimated 38% of acute aortic dissections are missedoninitial evaluation
There are no validatedclinical decisionrulesto helpidentify acute aortic
dissection(ADD). The diagnosis is best made whenthere is highclinical
suspiciongiventhe overall evaluationof the patient, including the history,
physical examination, and supporting testsincluding ECG, laboratory studies,
and radiology.
". . . Spontaneous tear of the arterial coats is associatedwithatrocious pain, with
symptoms, indeed, inthe case of the aortaof angina pectoris andmany
instances have beenmistakenfor it"WilliamOsler, 1910.
 Chest pain is the most common presenting symptominpatients withan
aortic dissection. Consider thoracic aortic dissectioninthe differential
diagnosis of all patients presenting with sudden chest pain.
o The pain usually is describedas ripping or tearing.
o The suddenonset of chest painhas beenshown to have a
sensitivity of 84%.
o This descriptionis not universal, andsome patients present with
only mildpain, oftenmistakenfor musculoskeletal conditions,
locatedin the thorax, groin, or back.

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o The pain of aortic dissectiontypically is abrupt onset.
o Aortic dissectionshouldbe consideredstrongly inall patients
reporting acute, sudden, andsevere chest painthat is maximal at
onset.
o The nervi vascularis, bundles of nerve fibers foundinthe aortic
adventitia, are involvedinthe productionof pain.
 The descriptionof the pain may indicate where the dissectionarises.
o Anterior chest painandchest pain that mimics AMI usually are
associatedwithanterior archor aortic root dissection. This is
causedby the dissectioninterrupting flowtothe coronary arteries,
resulting inmyocardial ischemia.
o Pain that is describedinthe neck or jaw indicates that the
dissectioninvolves the aortic archand extends intothe great
vessels of the arch.
o Tearing or ripping pain that is felt inthe intrascapular areamay
indicate that the dissectioninvolves the descending aorta. The pain
typically changes as the dissectionevolves.
 Aortic dissectionis painlessinabout 10% of patients. Painless dissectionis
more common in those withneurologic complications fromthe dissection
and those withMarfan syndrome.
 Presenting signs andsymptoms inacute thoracic aortic dissectioninclude:
o Anterior chest pain - Ascending aortic dissection
o Neck or jaw pain - Aortic archdissection
o Interscapular tearing or ripping pain - Descending aortic dissection
o Chest pain
o Myocardial infarction
o Neurologic symptoms
Syncope
Stroke symptoms
Alteredmental status
Limb paresthesias, pain, or weakness
Hemiparesis or hemiplegia
Horner syndrome
o Dyspnea
o Dysphagia

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o Orthopnea
o Anxiety andpremonitions of death
o Flank pain if renal artery is involved
o Dyspneaand hemoptysis if dissectionruptures intothe pleura
 SUMMARY=AAA is characterizedby:
1. Acute chest painwithacute inferior MI
2. Acute LVF/PULMONARY ODEMAdue toacute AR
3. Acute CVA
AND wide mediastinum (aortic shadow widened)
 ABDOMINAL AORTA ANEURYSM
Nonspecific abdominal symptoms (constipation,pain)
Pulsating abdominal mass/backage
Lower limbs intermittent cludication
Physical
 Bloodpressure may increase or decrease.
o Hypertensionmay result froma catecholamine surge or underlying
essential hypertension.
o Hypotensionis an ominous finding and may be the result of
excessivevagal tone, cardiac tamponade, or hypovolemiafrom
rupture of the dissection.
o A bloodpressure differential of greater than20 mmHg was an
independent predictorof aortic dissection. A pressuredifferential
of greater than20 mm Hg shouldincrease the suspicionof aortic
dissection, but it does not rule it in. Significant interarmblood
pressure differentials may be found in 20% of people without aortic
dissection.
 Neurologic deficits are a presenting sign in up to 20% of cases.
o The most common neurologic findings are syncope and altered
mental status.
o Syncope is part of the early course of aortic dissection in about 5%
of patients and may be the result of increased vagal tone,
hypovolemia, or dysrhythmia.
o Other causes of syncope or altered mental status include strokes
from compromised blood flow to the brain or spinal cord and
ischemia from interruption of blood flow to the spinal arteries.
o Peripheral nerve ischemia can manifest with numbness and tingling
in the extremities.

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o Hoarseness from recurrent laryngeal nerve compression also has
been described from AAA (ASCENDING AORTA).
o Horner syndrome is caused by interruption in the cervical
sympathetic ganglia and presents with ptosis, miosis, and
anhidrosis.
o Superior vena cava syndrome, caused by compression of the
superior vena cava from a large distorted aorta, may occur.
 Dyspnea may be causedby congestive heart failure or tracheal or
bronchial compression.
 Dysphagia from compressionof the esophagus may be present.
 Findings suggestive of cardiac tamponade, such as muffledheart sounds,
hypotension, pulsus paradoxus, jugular venous distension, andKussmaul
sign, must be recognizedquickly.
 Other diagnostic clues include anewdiastolic murmur, asymmetrical
pulses, andasymmetrical bloodpressure measurements. Pay careful
attentiontocarotid, brachial, and femoral pulses on initial examination
and look for progressionof bruits or development of bruits on
reexamination.
 Physical findings of a hemothorax may be found if the dissectionruptures
intothe pleura.
Causes
Aortic dissection is more common in patients with hypertension, connective
tissue disorders, congenital aortic stenosis or bicuspid aortic valve, and in those
with first-degree relatives with history of thoracic dissections. These diseases
affect the media of the aorta and predispose it to dissection.
 Aortopathy may be due to the following heritable diseases:
A . Hereditary Connective Tissue Diseases
 Marfan Syndrome
 Ehler Danlos Syndrome
B. Chromosomal Aberrations
 Turners Syndrome
 Noonans Syndrome
C.
Aortic Diseases

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 Aortic Dilatation
 Aortic Aneurysm
 Anuloaortic ectasia
 Aortic Arteritis
 Bicuspid Aortic Valve
 Hypertension or pulsatile blood flow can propagate the dissection.
 An estimated 50% of all cases of aortic dissection that occur in women
younger than 40 years are associated with pregnancy.
 Syphilis may cause aortic dissection.
 Crack cocaine use may precipitate aortic dissection.
 Iatrogenic causes of aortic dissection include cardiac catheterization.
 Differential Diagnoses
Aortic Regurgitation Pericarditis and Cardiac Tamponade
Back Pain, Mechanical Pleural Effusion
Gastroenteritis Pulmonary Embolism
HypertensiveEmergencies Shock, Cardiogenic
Myocardial Infarction Shock, Hypovolemic
Thoracic Outlet Syndrome
Pancreatitis
Laboratory Studies
 Blood studies
o Usually, the diagnosis is made before the blood work is returned;however,
leukocytosis may be present.
o BUN and creatinine are elevated if the dissection involves the renal
arteries.
o Troponin and creatine kinase (CK) can be elevated if the dissection has
caused myocardial ischemia.
o Decreases in the hemoglobin and hematocrit are ominous findings
suggesting the dissection either is leaking or has ruptured.
o Some studies suggest that D-dimer should be a part of the initial workup if
aortic dissection is suspected.Anegative result makes the presence of the
disease less likely.
o Hematuria, oliguria, and even anuria (<50 mL/d) may occur if the dissection
involves the renal arteries.
o Routine bloods – non diagnostic
o D-dimer < 500ng/ml unlikely to be dissection

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ECG
All patients with suspected thoracic aortic dissection should have an ECG. 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 . Keep this in mind when administering thrombolytics to patients with chest pain.
ST elevation can be seen in Stanford type A dissections because the dissection
interrupts blood flow to the coronary arteries.
 The incidence of abnormal ECG findings is greater in Stanford type A
dissections than in other types of dissections.
 In one study, 8% of patients with type A dissections had ST elevation, while
no patients with type B dissections had ST elevation.
 More commonly, the ECG abnormality is ST depression.
 If the dissection involves the coronary ostia, it is the right coronary artery
that is most commonly involved, leading to inferior ST-segment elevation
pattern.
DIAGNOSTIC EVALUATION
 Chest radiograph
 Tran thoracic echocardiogram
 Tran esophageal echocardiogram*
 Computed tomography*
 Magnetic resonance imaging*
 Aortography
*Choice based on rapid availability and quality of performance

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Chest radiography
Findings are abnormal in 80% of patients and are abnormal in ascending aorta D.
A widened mediastinum is sometimes difficult to identify on a portable anteroposterior
(AP) radiograph. If the patient is hemodynamically stable and cooperative, an AP
radiograph can be obtained at bedside. Look for a mediastinal width greater than 8 cm on
AP chest radiograph. A tortuous aorta, common in hypertensive patients, may be hard to
distinguish from a widened mediastinum(44-80%). If in doubt, a good posterior-anterior
radiograph is recommended. The differential diagnosis of a widened mediastinum
includes tumor, adenopathy, lymphoma, and enlarged thyroid.
Abnormal (ie, blunted) aortic knob was observed in 66% of patients in one study.
Ring sign (displacement of the aorta >5 mm past the calcified aortic intima) is considered
a specific radiographic sign.
Calcium sign -Displaced intimal calcification (>10mm) from outer aortic wall– useful in
older patients.
Other radiologic abnormalities seen on chest radiography include the following:
 Left apical cap
 Tracheal deviation
 Depression of left main stem bronchus
 Esophageal deviation
 Loss of the paratracheal stripe
Over 12% of the chest radiographs of patients with aortic dissection were read as
normal.
Several studies concluded that the overall diagnosis of aortic dissection is not
determined by any one sign, rather a combination of all findings leads to suspicion of
dissection.

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TTE
 Indicated as an initial test if patient is veryunwell and other imaging not available.
 Can be performed bedside ,Can detect intimal flap and AR
 Limitation: No information beyond aortic root and early part of proximal aorta.
TRANSESOPHAGEAL ECHO
 Procedure of first choice for
dissection, if readily
available
 Portability of equipment
facilities in emergency to ER
or ICU
 High sensitivity (98%) and
specificity(97%)
 Limitations :Unable to
visualize distal part of
ascending Aorta(beginning
of aortic arch) and
descending Aortabelow
stomach .

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Angiography
Still considered by some as the diagnostic standard test for aortic dissection, it is
being replaced by newer imaging modalities.
Angiography leads to accurate diagnosis of aortic dissection in over 95% of
patients and aids the surgeon in planning the repair operation because blood
vessels of the arch can be assessed easily. Benefits include visualization of the
true and false lumens, intimal flap, aortic regurgitation, and coronary arteries.
Drawbacks include the following:
 The procedure is invasive.
 The patient must be transported to the radiology department .
 The use of contrast media may be harmful to patients who have renal
insufficiency or an allergy to iodine.
isdiagnoses can occur if the false channel is thrombosed. In this instance, the
false lumen and intimal flap may not be visualized. Possible simultaneous
opacification of the true and false lumens may make discerning the presence
of a dissection difficult.
Computedtomography (CT) scanning:
The accepteddiagnostic criterionstandard, angiography, is being challengedby
state-of-the-art CTangiography.
Withthe advent of helical CT withmultiplanar and 3D reconstructionandCT
angiography, CT scanning is quickly replacing angiography as the diagnostic test
of choice in many institutions
Spiral CT scanning is associated with a higher rate of detection and better
resolution than incremental CT scanning. High-quality 2D and 3D reconstructions
are possible with spiral CT scanning, which greatly adds to the usefulness of this
imaging modality. More importantly, imaging information, including the type of
lesion, location of the pathologic lesion, extent of the disease, and evaluation of
the true and false lumen can be assessed quickly and help the surgeon plan the
operation. This information helps determine if hypothermic circulatory arrest is
necessary for surgery; this procedure increases the complexity, length,
morbidity, and mortality associated with surgery.

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Faster scanners have decreased the acquisition time to the range of a breath
hold, resulting in less motion artifact from breathing.
 Transportation of a patient in potentially unstable condition from the ED,
places the patient at risk.
 Requires the injection of iodinated contrast.
 The use of contrast material may harm a patient who has impaired renal
function or an allergy to contrast media.
 No information on aortic regurgitation
MRI
 MRI has over 90% sensitivity andgreater than95% specificity. It is the
most sensitive methodfor diagnosing aortic dissectionandhas similar
specificity toCTscanning. MRI shows the site of intimal tear, type and
extent of dissection, andpresenceof aortic insufficiency, as well as the
surrounding mediastinal structures. Other benefits are that MRI requires

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no contrast mediumand no ionizing radiation. It is the preferredmodality
for patients withrenal failure andthose withan allergy toiodine.
Contrast-enhanced magnetic resonance angiography (CE-MRA) is a principle
technique for evaluating the thoracic aorta. MRI is the preferred tool for imaging
chronic dissections and postsurgical follow-up.
Contrast 3D MRA is an accurate noninvasive imaging modality. It has the
advantage of being able to evaluate the aortic valve more effectively than CT
angiography.
 MRI is not readily available at most institutions, requiring transportation of
patients in unstable condition away from the ED.
 MRI requires much more time to acquire images than CT scanning.
 Patients with permanent pacemakers cannot undergo MRI. Most patients
with prosthetic heart valves or coronary stents can safely have an MRI.
MRA
• Good alternative toTEE or CT, if readily available
• Highsensitivity (98%)
and specificity (98%)
• Provides three
dimensional
reconstruction
• Can detect site of
intimal tear and
involvement of branch
vessels
• Non-invasive;neither
x-rays nor contrast
needed
• Limitation:
claustrophobic, more
costly, not readily
available

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Immediate management:
 Initial therapy should begin when the diagnosis is suspected. This includes
2 large-bore intravenous lines (IVs), oxygen, respiratory monitoring, and
monitoring of cardiac rhythm, blood pressure, and urine output..
 Clinically, the patient must be assessed frequently for hemodynamic
compromise, mental status changes, neurologic or peripheral vascular
changes, and development or progression of carotid, brachial, and femoral
bruits.
 Aggressive management of heart rate and blood pressure should be
initiated.
 Beta-blockers should be given initially to reduce the rate of change of
blood pressure and the shear forces on the aortic wall.
 The target heart rate should be 60-80 beats per minute.
 The target systolic blood pressure should be 100-120 mm Hg.
 Treat hypotension/ hypertension –aim for MAP 60-70
 Betablockers
eg esmalol, propranolol, labetalol
 Vasodilators Nanitroprusside
 Calcium channel blockers
eg verapamil, diltiazem
Indications for Definitive Surgical
and Medical Therapy in AD

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 Urgent surgical intervention is required in type A dissections.
 The area of the aorta with the intimal tear usually is resected and
replaced with a Dacron graft.
 The operative mortality rate is usually less than 10%.
 Dissections involving the arch are more complicated that those
involving only the ascending aorta because the innominate, carotid,
and subclavian vessels branch from the arch. Deep hypothermic
arrest usually is required. If the arrest time is less than 45 minutes,
the incidence of central nervous system complications is less than
10%.
 The definitive treatment for type B dissections is less clear(distal D.).
 Control blood pressure.
 Mortality rate - the same medically treated or surgically.
 Surgery is reserved for distal dissections that are leaking, ruptured,
or compromising blood flow to a vital organ.
 Acute distal dissections in patients with Marfan syndrome usually
are treated surgically.
 Inability to control hypertension with medication is also an indication
for surgery.
 Patients with a distal dissection are usually hypertensive,
emphysematous, or older.
 Long-term medical therapy involves a beta-adrenergic blocker
combined with other antihypertensive medications. Avoid
antihypertensives (eg, hydralazine, minoxidil) that produce a
hyperdynamic response that would increase dP/dt (ie, alter the
duration of P or T waves).
 Survivors of surgical therapy also should receive beta-adrenergic
blockers.
 Definitive treatment involves segmental resection of the dissection with
interposition of a synthetic graft.
 When thoracic dissections are associated with aortic valvular
disease, replace the defective valve.
 With combined reconstruction–valve replacement, the operative
mortality rate is approximately 5% with a late mortality rate of less
than 10%.
 Operative repair of the transverse aortic arch is technically difficult,
with an operative mortality rate of 10% despite induction of
hypothermic cardiocirculatory arrest.
 Repair of the descending aorta is associated with a higher incidence
of paraplegia than repair of other types of dissections because of
interruption of segmental blood supply to the spinal cord.
 The operative mortality rate is approximately 5%

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Sodium Nitroprusside
Causes peripheral vasodilationby direct actionon venous and arteriolar
smoothmuscle, thus reducing peripheral resistance.
Commonly usedIV because of rapid onset and short durationof action.
Easily titratable toreachdesiredeffect.
Light sensitive; bottle andtubing shouldbe wrappedin aluminum foil.
Prior to initiating nitroprusside, administer beta-blocker tocounteract
physiologic response of reflex tachycardiathat occurs whennitroprusside
usedalone. This physiologic response increases shear forcesagainst aortic
wall, thus increasing dP/dt. Objectiveis tokeepheart rate at 60-80 bpm
 Sodium Nitroprusside for acute reduction starting 10 – 20 mcg/min and titrated
upward
 Adding IV BB prior until desired effect such as HR 60 – 80s (propranolol 1 mg Q 3-5
minutes max 10 mg)
 Then Q 4-6 hrs at a dose of 2 – 6 mg
 0.5-3 mcg/kg/min IV; rates >4 mcg/kg/min may lead to cyanide toxicity
Labetolol
 Effectively lowersdP/dTas well as reducing arterial pressure
 Blocks alpha-, beta1-, and beta2-adrenergic receptor sites, decreasing
BP.

 Initial dose is 20mg followedby 40 to 80 mg Q 10 – 15 minutes (max
300mg IV)
 Once BP controlledmaintenance by continuous infusion
 Infusionat 2mg/min titrating upto5 –10 mg/min
Esmolol
 Ultrashort acting BB for those withlabile blood pressure or those that are
surgical candidates. (Long acting medications may affect intraoperative
bp management)
 Load with 500 mcg/kg bolus
 Infusionstarts @ 50mcg/kg/mintitrate to200 mcg/kg/minfor control
 Can be usedin patients withuncertainrisk for bronchospasm

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