Aortic dissection 2015

AORTIC DISSECTION2015

SAMIR EL ANSARY

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Aortic dissection

An aortic dissection is a tearing of the layers

within the aortic wall, classically associated

with sudden-onset chest or back pain, a pulse

deficit, and mediastinal widening on a chest

radiograph.

Depending on size and degree of aortic

involvement, it may result in marked

hemodynamic instability and, often, a rapid

death.

Aortic dissection.

Prompt diagnosis and appropriate treatment

are critical to maximize the possibility of

survival.

Significant dissections are often fatal and

rarely survive to clinical attention; the majority

of dissections seen in the critical care

environment are either

Subacute, contained, or sparing the

major aortic vessels.

Anatomy of injury in aortic

dissection

The tear usually originates in the intima.

It then propagates into the media creating a

false channel for blood to flow and hematoma

to form.

The dissection process may alternatively

originate with hemorrhage

in the media that secondarily causes

disruption of the intima.

In approximately 70% of patients, the intimal

tear, which is the beginning of the dissection,

occurs in the ascending aorta.

In 20% of patients it occurs in the descending

thoracic aorta, and in 10% of patients it occurs

in the aortic arch.

Only rarely is an intimal tear identified in the

abdominal aorta.

DeBakey classifications of aortic

dissection

The two classification systems most

commonly used both have anatomic

as well as management

implications.

The DeBakey classification describes three

types of dissection :

Type I: extends from aortic root to beyond the

ascending aorta

Type 11: involves only the ascending aorta

Type Ill: Begins distal to the takeoff of the left

subclavian artery and has two subtypes

Type III A: limited to the thoracic aorta

Type 111 B: extends below the diaphragm

The Stanford classification has

two types of dissection

Type A: involves the ascending

aorta

Type B: involves the descending

aorta, distal to the left subclavian

artery

Approximately 75% of patients with ruptured

aortic aneurysm will reach an emergency

department alive.

Whereas for aortic dissection 40% die

immediately.

Furthermore, only 50% to 70% will be alive 5

years after surgery depending on age and

underlying cause.

For untreated acute dissection of the

ascending aorta the mortality rate is 1 % to 2%

per hour after onset.

For type A dissections treated medically it is

approximately 20% within the first 24 hours and

50% by 1 month after presentation.

Even with surgical intervention

the mortality rate for type A dissection may be

as high as 10% after 24 hours and nearly 20%

1 month after repair.

Although type B dissection is less dangerous

than type A, it is still associated with an

extremely high mortality.

The 30-day mortality rate for an uncomplicated

type B dissection approaches 10%.

However, patients with type B dissection who

have complications such as limb ischemia,

renal failure, or visceral ischemia have a 2-day

mortality upwards of 20% and may prompt the

need for surgical intervention.

AORTIC DISSECTION

Risk factors

.

Hypertension: Present in 70% to 90% of

patients with acute dissection.

Advanced age: Mean of 63 years in the

International Registry of Acute Aortic

Dissection (IRAD).

Male sex: Represented by 65% of patients in

the IRAD.

Family history: Recently recognized is a

genetic, nonsyndromic familial form of thoracic

aortic dissection.

Trauma (deceleration/torsional

injury) .

Congenital and inflammatory

disorders:

Present as Marfan syndrome in

almost 5% of total patients in the

IRAD and half of those patients under

age 40 years.

Other associated congenital disorders

include

Ehlers-Danlos syndrome, Loeys-Dietz

syndrome, bicuspid aortic valve, aortic

coarctation, Turner syndrome, Takayasu

and giant-cell aortitis, relapsing

polychondritis (Behcet disease,

spondyloarthropathies), or confirmed

genetic mutations known to predispose

.to dissections (TGFBRI, TGFBRP, FBNI,

ACTAP, or MYHI I ) .

Pregnancy

Associated with 50% of dissections in

women under age 40 and most

frequently occurring in the third

trimester.

This might be attributable to

elevations in cardiac output during

pregnancy that cause increased

wall stress.

Circadian and seasonal

variationsProducing a higher frequency of dissection

in the morning hours and in the winter

months.

IatrogenicOccurring as a consequence of invasive

procedures or surgery, especially when the

aorta has been entered or its main

branches have been cannulated, such as

for cardiopulmonary bypass.

The common clinical

signs and symptoms of

aortic dissection.

Pain

The most common presenting symptom is

chest pain, occurring in up to 90% of

patients with acute dissection.

Classically, for type A dissections, sudden

onset of severe anterior chest pain with

extension to the back occurs that is

described as ripping or tearing in nature.

The pain is usually of maximal intensity

from its inception and is frequently

unremitting.

It may migrate along the path of the

dissection.

The pain of aortic dissection may mimic

that of myocardial ischemia.

Patients with type B dissections are more

likely to be seen with back pain ( 64%)

alone.

Syncope

Syncope is a well-recognized clinical

feature of dissection, occurring in up to

13% of cases.

Impairments of cerebral blood flow can

be due to

Acute hypovolemia, low cardiac output,

or dissection-involvement of the cerebral

vessels.

Syncope

Patients with a presenting syncope were

significantly more likely to die than were

those without syncope (34% vs. 23%),

likely because of

the frequent correlation with associated

cardiac tamponade, stroke,

decreased consciousness, and

spinal cord ischemia.

The common clinical

findings associated with

aortic dissection.

Neurologic symptoms

17% of patients were seen initially with neurologic

symptoms, 53% of which represented

ischemic stroke. Neurologic complications may result from

hypotension, malperfusion, distal thromboembolism,

or nerve compression.

Acute paraplegia as a result of spinal cord

malperfusion has been described as a primary

manifestation in 1% to 3% of patients.

Up to 50% of neurologic symptoms may be

transient.

Cardiovascular manifestations

The heart is the most frequently involved end-organ

in acute proximal aortic dissections.

Acute aortic regurgitation

may be present in 41 % to 76% of patients with

proximal dissection and may be caused by widening

of the aortic annulus resulting in incomplete valve

closure or actual disruption of the aortic valve

leaflets from the dissection flap.

Clinical manifestations of dissection-

related aortic regurgitation span from

mere diastolic murmurs without clinical

significance to overt congestive heart

failure and cardiogenic shock.

Myocardial ischemia or infarction

May result from compromised coronary artery flow

by an expanding false lumen that compresses the

proximal coronary or by extension of the dissection

flap into the coronary artery ostium.

This occurs in 7% to 19% of patients with proximal

aortic dissections.

Clinically, these present as electrocardiographic

changes consistent with primary myocardial

ischemia and/or infarction.

Cardiac tamponade is diagnosed in 8% to

10% of patients seen with acute type A

dissections.

It is associated with a high mortality and

should prompt consideration for emergent

drainage and aortic repair.

Hypertension occurs in greater than 50% of

patients with dissection, more commonly with

distal disease.

Ongoing renal ischemia can produce severe

hypertension.

Hypotension/shock may present in up to 20% of

patients with dissection.

This may be a result of cardiac tamponade from aortic

rupture into the pericardium, dissection, or

compression of the coronary arteries, acute aortic

regurgitation, acute blood loss, true lumen

compression by distended false lumen, or an intra-

abdominal catastrophe.

Cardiogenic shock

In approximately 6% of cases.

This can be due to acute aortic

regurgitation or ongoing myocardial

ischemia.

Peripheral vascular complications

Can manifest as pulse and/or blood pressure

differentials or deficits and occur in

approximately one third to one half of patients

with proximal dissection.

Etiology is partial compression, obstruction,

thrombosis, or embolism of

the aortic branch vessels, resulting in

cerebral, renal, visceral, or limb ischemia. Peripheral pulse deficits should alert the clinician to

possible ongoing renal or visceral ischemia unable to

be detected from physical examination or laboratory

values alone.

Pulmonary complications

May manifest as pleural effusions, which

occur most frequently on the left.

Causes include rupture of the dissection

into the pleural space or weeping of fluid

from the aorta as an inflammatory

response to the dissection.

Laboratory abnormalities

associated with aortic dissection

Laboratory data are usually unrevealing, but

anemia from blood loss into the false lumen

can occur.

A moderate leukocytosis (10,000-14,000

white cells per mL) is sometimes seen.

Lactic acid dehydrogenase and bilirubin

levels may be elevated because of hemolysis

within the false lumen.

Laboratory abnormalities

associated with aortic dissection

Disseminated intravascular coagulation has

been reported.

Currently, randomized controlled data do not

support the use of D-dimers or experimental

serum markers (plasma smooth muscle

myosin heavy chain protein, high-sensitivity

C-reactive protein).

Imaging modalities

used to diagnose aortic

dissection

On the basis of clinical risk factors and

conditions, presentation, and associated

examination findings, patients are

stratified into

Low- intermediate- or high-

risk categories.

Further work-up is dictated by this pretest

probability index.

Some patients with acute dissection initially

have no high-risk features, creating a

diagnostic dilemma.

According to most recent guidelines, if a

clear alternative diagnosis is not established

after the initial evaluation, then obtaining a

diagnostic aortic imaging study should be

considered.

Although lacking specificity, a chest

radiograph should be obtained as part

of the initial diagnostic evaluation.

A radiograph abnormality is seen in up

to 90% of patients with aortic

dissection; most frequent is widening

of the aorta and mediastinum.

Other findings may include a localized hump on

the aortic arch, displacement of calcification in

the aortic knob, and pleural effusions.

However, approximately 40% of radiographs in

acute dissection lack a widened mediastinum,

and as many as 16% are normal.

Thus a negative radiograph must not delay

definitive aortic imaging in patients deemed at

high risk for aortic dissection by initial

screening.

Computed tomography (CT) scanning,

magnetic resonance imaging (MRI), and

Transesophageal

echocardiography (TEE) Are all highly accurate imaging modalities that

may be used to make the diagnosis; all can

provide acceptable diagnostic accuracy.

Transthoracic echocardiography has

limited diagnostic accuracy.

Aortography

Which was once the test of choice, is no

longer used routinely because it is invasive and

time-consuming and involves exposure to

intravenous contrast dye.

The most recent comparative study with

nonhelical CT, MRI, and TEE showed 100%

sensitivity for all modalities, with better

specificity of CT (100%) as compared with TEE

or MRI.

A recent metaanalysis found that all three

imaging techniques provided equally

reliable results.

Although each imaging modality offers

advantages and disadvantages, the

choice among CT, MRI, and TEE is

probably best based on which is most

readily available.

It should be noted, however, that the diagnosis

of acute aortic dissection can be difficult and

occasionally cannot be absolutely excluded by

a single imaging study.

If a high clinical suspicion exists despite initially

negative imaging, then consideration should be

given to a second imaging modality.

Regardless, prompt surgical consultation

should be initiated in any patient with a

suspected dissection.

Regardless, prompt surgical

consultation should be

initiated in any patient with a

suspected dissection.

Diagnosis could be confused

with Aortic dissectionAcute myocardial infarction

Pulmonary embolism

Acute cholycystitis

Pleuritis

Pericarditis

Atherosclerotic emboli

Cerebrovascular accidents . .

Acute aortic regurgitation

Thoracic nondissecting aneurysm . .

Mediastinal cysts or tumors

Cholecystitis .

Musculoskeletal pain

Atherosclerotic emboli

Differentiate between the

management of Stanford type A

and type B dissections

An acute type A dissection is a surgical

emergency

However, medical management is critical to

halt the progression of the dissection while the

diagnostic work-up takes place and while

preparations are made to bring the patient to

the operating room for definitive treatment.

While the diagnosis work-up proceeds and a

cardiothoracic surgeon is consulted, the

patient's condition should be carefully

monitored and stabilized in an intensive care

unit.

Pain management and gradual down-titration of

blood pressure are critical to prevent extension

of the dissection.

Sufficient blood products and intravascular

access should be available in the event of

aortic rupture.

Patients with uncomplicated type B dissection

are preferably managed medically with p-

blockers and other antihypertensive agents.

Surgical intervention has no demonstrable

superiority except in cases of failed medical

management manifesting as malperfusion,

aortic expansion with potential for imminent

rupture, or intractable pain.

Ongoing advances with less

invasive interventions

(endovascular stent grafts and

endovascular fenestration

procedures) suggest an expanded

role for interventional management

in the treatment of acute type B

dissection, especially in experienced

centers.

The strategies for medical

management of dissection and

commonly used medications

The goals of medical therapy are to treat

pain, to aggressively control blood

pressure, and to determine need for

surgical or endovascular intervention.

Patients who are seen with hypotension

should receive the following:

Prompt but judicious volume resuscitation and

hemodynamic support with intravenous

vasopressors to maintain a goal mean

arterial pressure of 70 mm Hg .

Rapid search for underlying etiology

(tamponade, myocardial dysfunction, acute

hemorrhage)

Emergent surgical consultation for operative

management

In those who are seen initially with

hypertension, the blood pressure should

generally be lowered to a systolic of 100 to

120 mm Hg, to a mean of 60 to 65 mm Hg,

or to the lowest level that is compatible with

perfusion of the vital organs.

The aortic wall stress is affected by the

heart rate, blood pressure, and velocity of

ventricular contraction (dP/dt).

The ideal antihypertensive regimen must

decrease blood pressure

without increasing

cardiac output

through peripheral vasodilatation.

This is because an increased cardiac output

can increase flow rates producing higher

aortic wall stress and thus propagating the

dissection.

Intravenous p-blockers (commonly esmolol,

labetalol, propranolol, or metoprolol) are

considered the first-line medical stabilization

regimen because they affect all three parameters

without increases

in cardiac output and aortic wall stress.

In patients who are unable to tolerate B- blockade,

nondihydropyridine calcium channel antagonists

(verapamil, diltiazem) offer an acceptable

alternative.

Often, single-drug therapy alone is

inadequate to optimize blood pressure

management.

Adequate pain control is essential not only

for patient comfort but also to decrease

sympathetic mediated increases in heart rate

and blood pressure.

This may be accomplished with intravenous

opioid analgesics.

.

If p-blockade and adequate pain control

are ineffective to control blood pressure,

the addition of a rapidly acting, easily

titratable intravenous vasodilator, such

as

nitroprussideshould be considered.

Other agents, such as

Nicardipine, nitroglycerin, and

fenoldopamare also acceptable.

Vasodilator therapy without prior p-blockade

may cause reflex tachycardia and increased

force of ventricular contraction leading to

greater wall stress and potentially causing

false lumen propagation; therefore adequate

p-blockade must be established first, before

the vasodilator is initiated.

The surgical approach for repair of Stanford

type A dissection.

The purpose of surgery is to resect the aortic

segment containing the proximal intimal tear, to

obliterate the false channel, and to restore aortic

continuity with a graft or by reapproximating the

transected ends of the aorta.

For patients with aortic insufficiency, it may be

possible to resuspend the aortic valve, but in

some cases replacement of the aortic valve is

necessary.

.

In some cases of proximal dissection,

reimplantation of the coronary arteries is

required.

If a DeBakey type II dissection is present,

the entire dissected aorta should be

replaced.

Surgery to repair an aortic dissection

generally requires cardiopulmonary bypass

and, often, deep hypothermic circulatory

arrest.

Recent alternatives to surgical repair of

aortic dissection

An endovascular technique of stent-grafting

and/or balloon fenestration may be used for

initial surgical treatment of some dissections.

Indications for open or endograft treatment are

based on the anatomic features of the lesion,

clinical presentation and course, patient

comorbidities, and anatomic constraints

related to endograft technology.

Dissections pose a complex situation because

the branches of the aorta may be perfused

from either the true or false lumen.

Often, both the true and false lumens are

patent and some of the visceral, renal, or lower

extremity vessels are fed by one channel and

the remainder by the other.

Consideration must be given to how blood flow

reaches vital organs before considering

treatment of a dissection with an endovascular

stent-graft.

For type B dissection, an increasing

number of reports show better results

with endovascular repair versus open

surgical repair.

The role of endovascular stent-graft

versus optimal medical therapy was

recently examined in the literature, but

no difference was noted in survival or

number of adverse events.

However, longer-term (5 year)

data are needed to fully assess

the potential impact of stent-

grafting for acute dissection,

including

Effects on survival, clinical

outcomes, and long-term

aortic remodeling.

The use of fenestrated endografts

A new era in the treatment of aortic

dissections.

Unsuitable anatomy is a significant barrier

to the use of endovascular stent-grafts for

most forms of aortic disease, where the

ostia of major vessels would otherwise be

partially or completed covered with the

deployment of a stent-graft.

.

The use of fenestrated endografts

Using preoperative

Three-dimensional CT aortic

reconstructioncustomized stents can be constructed,

featuring holes (fenestrations) or side-

branches matched to patient-specific

anatomy to ensure perfusion to major

aortic branch vessels.

The use of fenestrated endografts

Current trials are underway in

Europe and the United States for

their use for

complex aneurysmal disease, and

expectations are high for similar

application to aortic dissection.

SAMIR EL ANSARYICU PROFESSOR

AIN SHAMSCAIRO

[email protected]

GOOD LUCK

Global Critical Carehttps://www.facebook.com/groups/1451610115129555/#!/groups/145

1610115129555/ Wellcome in our new group ..... Dr.SAMIR EL ANSARY