Aortic Dissection

Aortic Dissection
Author: Mary C Mancini, MD, PhD; Chief Editor: John Geibel, MD, DSc, MA
Updated: Mar 5, 2013 Practice Essentials

Signs and symptoms
Aortic dissectionthe separation of the layers within the aortic wall that occurs when
blood pushes into the intima-media space through a tear in the intimal layercan be
rapidly fatal, with many patients dying before presentation to the emergency department
or before diagnosis is made in the ED.
No one sign or symptom can positively identify acute aortic dissection. Clinical
manifestations include the following:
Sudden onset of severe chest pain that often has a tearing or ripping quality
(classic symptom)
Chest pain may be mild
Anterior chest pain: Usually associated with anterior arch or aortic root dissection
Neck or jaw pain: With aortic arch involvement and extension into the great
vessels
Tearing or ripping intrascapular pain: May indicate dissection involving the
descending aorta
No pain in about 10% of patients
Syncope
Cerebrovascular accident (CVA) symptoms (eg, hemianesthesia, and hemiparesis,
hemiplegia)[1]
Altered mental status
Numbness and tingling, pain, or weakness in the extremities
Horner syndrome (ie, ptosis, miosis, anhidrosis)
Dyspnea
Hemoptysis
Dysphagia
Flank pain (with renal artery involvement
Abdominal pain (with abdominal aorta involvement)
Fever
Anxiety and premonitions of death
See Clinical Presentation for more detail.
Diagnosis
The diagnosis of acute aortic dissection requires a high index of suspicion and involves
the following:
History and physical examination

Imaging studies
Electrocardiography
Complete blood count, serum chemistry studies, cardiac marker assays
Possible physical examination findings include the following:
Hypertension
Hypotension
Interarm blood pressure differential greater than 20 mm Hg
Signs of aortic regurgitation (eg, bounding pulses, wide pulse pressure, diastolic
murmurs)
Findings suggestive of cardiac tamponade (eg, muffled heart sounds, hypotension,
pulsus paradoxus, jugular venous distention, Kussmaul sign)
Neurologic deficits (eg, syncope, altered mental status)
Peripheral paresthesias
Horner syndrome
New diastolic murmur
Asymmetrical pulses (eg, carotid, brachial, femoral)
Progression or development of bruits
Possible laboratory study findings include the following:
Leukocytosis: Stress state

Decreases in hemoglobin and hematocrit values: Leaking or rupture of the
dissection
Elevation of the blood urea nitrogen and creatinine levels: Renal artery
involvement or prerenal azotemia
Elevation of the myocardial muscle creatine kinase isoenzyme, myoglobin, and
troponin I and T levels: Myocardial ischemia from coronary artery involvement
Lactate dehydrogenase elevation: Hemolysis in the false lumen
Smooth muscle myosin heavy-chain assay: Increased levels in the first 24 hours
are 90% sensitive and 97% specific for aortic dissection
Fibrin degradation product (FDP) elevation: In symptomatic patients, a plasma
FDP of 12.6 g/mL or higher suggests possible aortic dissection with a patent
false lumen; an FDP level of 5.6 g/mL or higher suggests the possibility of
dissection with complete thrombosis of the false lumen[2]
Imaging studies
Chest radiography:
Initial imaging technique if it is readily available at the bedside

Widening of the mediastinum is the classic finding
Hemothorax may be evident if the dissection has ruptured
Computed tomography with contrast:
The definitive test in most patients with suspicion of aortic dissection[3]

Useful only in hemodynamically stable patients
Findings help determine whether hypothermic circulatory arrest is necessary for
surgery
Echocardiography:
Transesophageal echocardiography (TEE) is more accurate than transthoracic

echocardiography (TTE)[4]
TTE is most useful in ascending aortic dissections
TEE is as sensitive and specific as CT scanning and magnetic resonance imaging
TEE is strongly dependent on operator experience
MRI:
The most sensitive method for diagnosing aortic dissection

Specificity is similar to that of CT scanning
Aortography:
Has been the diagnostic criterion standard study for aortic dissection
Is being replaced by newer, safer imaging modalities
See Workup for more detail.
Management
Acute aortic dissection can be treated surgically or medically. In surgical treatment, the
area of the aorta with the intimal tear is usually resected and replaced with a Dacron
graft. Endovascular repair is emerging as the preferred treatment for descending aortic
dissection.
Medical management includes the following:
Decreasing the blood pressure and the shearing forces of myocardial contractility
Antihypertensive therapy, including beta blockers, is the treatment of choice for
all stable chronic aortic dissections
Pain management: Narcotics and opiates are the preferred agents
Emergency surgical correction is the preferred treatment for the following:
Stanford type A (DeBakey type I and II) ascending aortic dissection

Complicated Stanford type B (DeBakey type III) aortic dissections with specific
clinical or radiologic evidence
See Treatment and Medication for more detail.
Image library
Image A represents a Stanford A or a DeBakey type 1 dissection. Image

B represents a Stanford A or DeBakey type II dissection. Image C represents a Stanford
type B or a DeBakey type III dissection. Image D is classified in a manner similar to A
but contains an additional entry tear in the descending thoracic aorta. Note that a primary
arch dissection does not fit neatly into either classification.
Background
Aortic dissection is defined as separation of the layers within the aortic wall. Tears in the
intimal layer result in the propagation of dissection (proximally or distally) secondary to
blood entering the intima-media space. An acute aortic dissection (< 2 wk) is associated
with high morbidity and mortality rates. Mortality is highest in the first 7 days; indeed,
many patients die before presentation to the emergency department (ED) or before
diagnosis is made in the ED. Patients with chronic aortic dissection (>2 wk) have a better
prognosis. The aortic dissection mortality rate is still high despite advancements in
diagnostic and therapeutic modalities.[5, 6]
Although acute aortic dissection classically produces sudden onset of severe chest pain
that often has a tearing or ripping quality, no one sign or symptom can positively identify
acute aortic dissection. The clinical manifestations are diverse, making the diagnosis
difficult and requiring a high index of suspicion.[5, 7, 6] (See Presentation.) An estimated
38% of acute aortic dissections are missed on initial evaluation.[8, 1, 9]
There are no validated clinical decision rules to help identify acute aortic dissection. The
diagnosis is best made when there is high clinical suspicion. A good patient history and
physical examination are essential, along with imaging studies, electrocardiography, and
laboratory studies (see Workup).
graft. (See the Treatment section and the Medication section.)
For patient education information, see the Heart and Blood Vessels Center, Circulatory
Problems Center, and Heart Center, as well as Chest Pain.
History of aortic dissection and its repair

The first well-documented case of aortic dissection occurred in 1760, when King George
II of England died while straining on the commode. In 1761, the celebrated Italian
anatomist Giovanni Battista Morgagni provided the first detailed pathologic description
of aortic dissection.
Aortic dissection was associated with a high mortality rate before the introduction of the
cardiopulmonary bypass in the 1950s, which led to aortic arch repair and construction.
DeBakey performed the first successful operative repair in 1955.
Modern techniques of diagnosing and repairing thoracic aortic dissections transformed
the condition from a death sentence to a treatable disorderas shown by the experience
of Dr. DeBakey himself, who developed aortic dissection at age 97, and at age 98 became
the oldest patient to survive the surgical procedure he pioneered.[10]
Recent advances in the field of stent placement and percutaneous aortic fenestrations
have further reduced mortality rates. However, despite these advances, the mortality rate
associated with aortic dissection remains high, as illustrated by the deaths of Princess
Diana, actor John Ritter, and diplomat Richard Holbrooke.[5, 6]
Anatomy
The aorta is composed of the intima, media, and adventitia. The intima, the innermost
layer, is thin, delicate, lined by endothelium, and easily traumatized.
The media is responsible for imparting strength to the aorta and consists of laminated but
intertwining sheets of elastic tissue. The arrangement of these sheets in a spiral provides
the aorta with its maximum allowable tensile strength. The aortic media contains very
little smooth muscle and collagen between the elastic layers and thus has increased
distensibility, elasticity, and tensile strength. This contrasts with peripheral arteries,
which, in comparison, have more smooth muscle and collagen between the elastic layers.
The outermost layer of the aorta is adventitia. This largely consists of collagen. The vasa
vasorum, which supplies blood to the outer half of the aortic wall, lies within the
adventitia. The nervi vascularis, bundles of nerve fibers found in the aortic adventitia, are
involved in the production of pain, which occurs with acute stretching of the aortic wall
from a dissection.[11] .The aorta does not have a serosal layer.
The aorta plays an integral role in the forward circulation of the blood in diastole. During
left ventricular contraction, the aorta is distended by blood flowing from the left
ventricle, and kinetic energy from the ventricle is transformed into potential energy stored
in the aortic wall. During recoil of the aortic wall, this potential energy is converted to
kinetic energy, propelling the blood within the aorta to the peripheral vasculature.
The volume of blood ejected into the aorta, the compliance of the aorta, and resistance to
blood flow are responsible for the systolic pressures within the aorta. Resistance is
mainly due to the tone of the peripheral vessels, although the inertia exerted by the
column of blood during ventricular systole also plays a small part.
The aorta has thoracic and abdominal regions. The thoracic aorta is divided into the
ascending, arch, and descending segments; the abdominal aorta is divided into suprarenal
and infrarenal segments. The ascending aorta is the anterior tubular portion of the
thoracic aorta from the aortic root proximally to the innominate artery distally. The
ascending aorta is 5 cm long and is made up of the aortic root and an upper tubular
segment.
The aortic root consists of the aortic valve, sinuses of Valsalva, and left and right
coronary arteries. It extends from the aortic valve to the sinotubular junction and supports
the base of the aortic leaflets. The aortic root allows the 3 sinuses of Valsalva to bulge
outward, facilitating the full excursion of the leaflets in systole. The left and right
coronary arteries arise from these sinuses.
The upper tubular segment of the ascending aorta starts at the sinotubular junction and
ends at the beginning of the aortic arch. The ascending aorta lies slightly to the right of
the midline, with its proximal portion in the pericardial cavity. Structures around the aorta
include the pulmonary artery anteriorly; the left atrium, right pulmonary artery, and right
mainstem bronchus posteriorly; and the right atrium and superior vena cava to the right.
The arch of the aorta curves upward between the ascending aorta and descending aorta.
The brachiocephalic arteries originate from the aortic arch. Arteries that arise from the
aortic arch carry blood to the brain via the left common carotid, innominate, and left
subclavian arteries.
The initial part of the aortic arch lies slightly left and in front of the trachea; the arch ends
posteriorly to the left of the trachea and esophagus. Inferior to the arch is the pulmonary
artery bifurcation, the right pulmonary artery, and the left lung. The recurrent laryngeal
nerve passes beneath the distal arch, and the phrenic and vagus nerves lie to the left. The
junction between the aortic arch and the descending aorta is called the aortic isthmus. The
isthmus is a common site for coarctations and trauma.
The descending aorta extends from the area distal to the left subclavian artery to the 12th
intercostal space. Initially, the descending aorta lies in the posterior mediastinum to the
left of the course of the vertebral column. It passes in front of the vertebral column in its
descent and ends behind the esophagus before passing through the diaphragm at the level
of the 12th thoracic vertebra.
The abdominal aorta extends from the descending aorta at the level of the 12th thoracic
vertebra to the level of bifurcation at the fourth lumbar vertebra. The splanchnic arteries
branch from the abdominal aorta. The thoracoabdominal aorta is the combination of the
descending thoracic and abdominal aorta.
With increasing age, the elasticity and distensibility of the aorta decline, thus inducing the
increase in pulse pressure observed in elderly individuals. The progression of this process
is exacerbated by hypertension, coronary artery disease, or hypercholesterolemia.
Histologically, the loss of distensibility is marked by fragmentation of elastin and the
resultant increase in collagen and, thus, a higher collagen-to-elastin ratio. This, along
with impairment in flow in the vasa vasorum, may be responsible for the age-related
changes. These factors cumulatively lead to increased left ventricular systolic pressure
and wall tension with associated increases in end-diastolic pressure and volume.
Pathophysiology
The aortic wall is exposed to high pulsatile pressure and shear stress (the steep slope of
the pressure curve; ie, the water hammer effect), making the aorta particularly prone to
injury and disease from mechanical trauma. The aorta is more prone to rupture than any
other vessel, especially with the development of aneurysmal dilatation, because its wall
tension, as governed by the Laplace law (proportional to the product of pressure and
radius), is intrinsically high.
An aortic dissection is a split or partition in the media of the aorta; this split is frequently
horizontal or diagonal. An intimal tear connects the media with the aortic lumen, and an
exit tear creates a true lumen and a false lumen, resulting in a double-barreled aorta (see
the image below).
Aortic dissection. True lumen and false lumen separated

by an intimal flap.
The true lumen is lined by intima, and the false lumen is within the media. Although the
false lumen is within the media, suggesting that it is "lined" with media is misleading; if
the aortic dissection becomes chronic, the lining becomes a serosal pseudointima.
The true lumen is frequently smaller than the false lumen, but not invariably. Typically,
flow in the false lumen is slower than in the true lumen, and the false lumen often
becomes aneurysmal when subjected to systemic pressure. The dissection usually stops at
an aortic branch vessel or at the level of an atherosclerotic plaque.
Most classic aortic dissections begin at one of the following 3 distinct anatomic locations:
Approximately 2.2 cm above the aortic root

Distal to the left subclavian artery
The aortic arch
The most common site of dissection is the first few centimeters of the ascending aorta,
with 90% occurring within 10 cm of the aortic valve. The second most common site is
just distal to the left subclavian artery. Between 5 and 10% of dissections do not have an
obvious intimal tear. These often are attributed to rupture of the aortic vasa vasorum as
first described by Krukenberg in 1920.
Keeping the descending aorta in mind is important. The descending aorta is the location
of most late clinical events after any dissection of the aorta.[12]
Ascending aortic involvement may result in death from wall rupture, hemopericardium
and tamponade, occlusion of the coronary ostia with myocardial infarction, or severe
aortic insufficiency. The nervi vascularis (ie, bundles of nerve fibers found in the aortic
adventitia) are involved in the production of pain.
Classification
Two major anatomic classification schemes for aortic dissection are the DeBakey and the
Stanford systems (see the images below).
DeBakey and coworkers classify aortic dissection into 3 types, as follows:
Type I: the intimal tear occurs in the ascending aorta, but the descending aorta is
also involved
Type II: only the ascending aorta is involved
Type III: only the descending aorta is involved; type IIIA originates distal to the
left subclavian artery and extends as far as the diaphragm, while type IIIB
involves the descending aorta below the diaphragm
The Stanford classification has 2 types, as follows:
Type A: the ascending aorta is involved (DeBakey types I and II)

Type B: the descending aorta is involved (DeBakey type III)
This system also helps delineate treatment. Type A dissections usually require surgery,
whereas type B dissections are managed medically under most conditions.[13]
Image A represents a Stanford A or a DeBakey type 1 dissection.

Image B represents a Stanford A or DeBakey type II dissection. Image C represents a
Stanford type B or a DeBakey type III dissection. Image D is classified in a manner
similar to A but contains an additional entry tear in the descending thoracic aorta. Note
that a primary arch dissection does not fit neatly into either classification.
Etiology
Congenital and acquired factors, alone or in combination, can lead to aortic dissection.
Aortic dissection is more common in patients with hypertension, connective tissue
disorders, congenital aortic stenosis, or a bicuspid aortic valve,[14] as well as in those with
first-degree relatives with a history of thoracic dissection. These diseases affect the media
of the aorta and predispose it to dissection.
Congenital causes
Aortopathy may be due to the following heritable diseases:
Marfan syndrome
Ehlers-Danlos syndrome
Annuloaortic ectasia
Familial aortic dissections
Adult polycystic kidney disease
Turner syndrome
Noonan syndrome
Osteogenesis imperfecta
Bicuspid aortic valve
Coarctation of the aorta
Connective tissue disorders
Metabolic disorders (eg, homocystinuria, familial hypercholesterolemia)
Acquired conditions
Arterial hypertension is an important predisposing factor for aortic dissection.[6] Of
patients with aortic dissection, 70% have elevated blood pressure. Hypertension or
pulsatile blood flow can propagate the dissection.
Pregnancy can be a risk factor for aortic dissection, particularly in patients with an
underlying anomaly such as Marfan syndrome. An estimated 50% of all cases of aortic
dissection that occur in women younger than 40 years are associated with pregnancy.
Most cases occur in the third trimester or early postpartum period.
Other acquired causes of aortic dissection include the following:
Syphilitic aortitis
Deceleration injury possibly with related chest trauma
Cocaine use
Cystic medial necrosis

The normal aorta contains collagen, elastin, and smooth muscle cells that contribute the
intima, media, and adventitia, which are the layers of the aorta. With aging, degenerative
changes lead to breakdown of the collagen, elastin, and smooth muscle and an increase in
basophilic ground substance. This condition is termed cystic medial necrosis.
Atherosclerosis that causes occlusion of the vasa vasorum also produces this disorder.
Cystic medial necrosis is the hallmark histologic change associated with dissection in
those with Marfan syndrome.
Cystic medial necrosis was first described by Erdheim in 1929. Sources disagree over the
accuracy of this term in elderly patients because the true histopathologic changes are
neither cystic nor necrotic. Researchers have used the term cystic medial degeneration.
Early on, cystic medial necrosis described an accumulation of basophilic ground
substance in the media with the formation of cystlike pools. The media in these focal
areas may show loss of cells (ie, necrosis). This term still is used commonly to describe
the histopathologic changes that occur.
Iatrogenic causes
Iatrogenic aortic dissection can result from cardiologic procedures such as the following:
Aortic and mitral valve replacements

Coronary artery bypass graft surgery
Percutaneous catheter placement (eg, cardiac catheterization, percutaneous
transluminal coronary angioplasty)
Aortic dissection occurs when the layers are split in the process of cannulation or
aortotomy.
Epidemiology
In the United States, aortic dissection is an uncommon disease. The true frequency of
aortic dissection is difficult to estimate, and most estimates are based on autopsy studies.
Evidence of aortic dissection is found in 1-3% of all autopsies (1 in 350 cadavers).[15] The
incidence of aortic dissection is estimated to be 5-30 cases per 1 million people per year.
Aortic dissection occurs once per 10,000 patients admitted to the hospital; approximately
2,000 new cases are reported each year in the United States.[16]
Aortic dissection is more common in blacks than in whites and is less common in Asians
than in whites. Also, it is more common in males than females, with a male-to-female
ratio of 2-3:1.
Approximately 75% of dissections occur in those aged 40-70 years, with a peak in the
range of 50-65 years.[6] Patients with Marfan syndrome present earlier, usually in the third
and fourth decades of life.
Prognosis
Hospital-based mortality rates for aortic dissection are approximately 30%. Patients with
type A aortic dissection who undergo surgical treatment have a 30% mortality rate;
patients who receive medical treatment have a mortality rate of 60%. Comorbidities and
advanced aged can pose a contraindication to surgery in selected patients. Medically
treated patients with type B dissection have a 10% mortality rate; surgically treated
patients with type B dissection have a 30% mortality rate.
An acute aortic dissection (< 2 wk) is associated with high morbidity and mortality rates
(highest mortality in the first 7 d). From 1 to 2% of patients with aortic dissection die per
hour for the first 24-48 hours. Patients with chronic aortic dissection (>2 wk) have a
better prognosis.
History
Patients with acute aortic dissection typically present with the sudden onset of severe
chest pain, although this description is not universal. Some patients present with only
mild pain, often mistaken for a symptom of musculoskeletal conditions in the thorax,
groin, or back. Consider thoracic aortic dissection in the differential diagnosis of all
patients presenting with chest pain.
The location of the pain may indicate where the dissection arises. Anterior chest pain and
chest pain that mimics acute myocardial infarction usually are associated with anterior
arch or aortic root dissection. This is caused by the dissection interrupting flow to the
coronary arteries, resulting in myocardial ischemia. Pain in the neck or jaw indicates that
the dissection involves the aortic arch and extends into the great vessels.
Tearing or ripping pain in the intrascapular area may indicate that the dissection involves
the descending aorta. The pain typically changes as the dissection evolves.
The pain of aortic dissection is typically distinguished from the pain of acute myocardial
infarction by its abrupt onset and maximal severity at onset, although the presentations of
the 2 conditions overlap to some degree and are easily confused. Aortic dissection can be
presumed in patients with symptoms and signs suggestive of myocardial infarction but
without classic electrocardiographic (ECG) findings.
Aortic dissection is painless in about 10% of patients.[1] Painless dissection is more
common in those with neurologic complications from the dissection and those with
Marfan syndrome.
Neurologic deficits are a presenting sign in up to 20% of cases. Syncope is part of the
early course of aortic dissection in approximately 5% of patients and may be the result of
increased vagal tone, hypovolemia, or dysrhythmia. [1] Cerebrovascular accident (CVA)
symptoms include hemianesthesia and hemiparesis or hemiplegia.[1] Altered mental status
is also reported. Patients with peripheral nerve ischemia can present with numbness and
tingling, pain, or weakness in the extremities.
Horner syndrome is caused by interruption in the cervical sympathetic ganglia and
manifests as ptosis, miosis, and anhidrosis. Hoarseness from recurrent laryngeal nerve
compression has also been described.
Cardiovascular manifestations involve symptoms suggestive of congestive heart failure[1]
secondary to acute severe aortic regurgitation. These include dyspnea and orthopnea.
Respiratory symptoms can include dyspnea and hemoptysis if dissection ruptures into the
pleura or if tracheal or bronchial obstruction has occurred. Physical findings of a
hemothorax may be found if the dissection ruptures into the pleura.
Other manifestations include the following[17] :
Dysphagia from compression of the esophagus

Flank pain if the renal artery is involved
Abdominal pain if the dissection involves the abdominal aorta.
Fever
Anxiety and premonitions of death
A retrospective chart review of 83 patients with a thoracic aortic dissection revealed that
only 40% of alert patients were asked the basic questions about their pain. Remember to
cover the P, Q, R, S, and T (position, quality, radiation, severity, and timing) of pain in all
able patients. Timing includes the rate of onset, duration, and frequency of episodes. Also
ask about migration of pain, aggravating or alleviating factors, and associated symptoms.
Physical Examination
Hypertension may result from a catecholamine surge or underlying essential
hypertension.[1, 18] Hypotension is an ominous finding and may be the result of excessive
vagal tone, cardiac tamponade, or hypovolemia from rupture of the dissection.
An interarm blood pressure differential greater than 20 mm Hg should increase the
suspicion of aortic dissection, but it does not rule it in. Significant interarm blood
pressure differentials may be found in 20% of people without aortic dissection.
Signs of aortic regurgitation include bounding pulses, wide pulse pressure, and diastolic
murmurs. Acute, severe aortic regurgitation may result in signs suggestive of congestive
heart failure[1] : dyspnea, orthopnea, bibasilar crackles, or elevated jugular venous
pressure.
Other cardiovascular manifestations include findings suggestive of cardiac tamponade
(eg, muffled heart sounds, hypotension, pulsus paradoxus, jugular venous distention,
Kussmaul sign). Tamponade must be recognized promptly. Superior vena cava syndrome
can result from compression of the superior vena cava from a large, distorted aorta. Wide
pulse pressure and pulse deficit or asymmetry of peripheral pulses are reported.
Patients with right coronary artery ostial dissection may present with acute myocardial
infarction, commonly inferior myocardial infarction. Pericardial friction rub may occur
secondary to pericarditis.
Neurologic deficits are a presenting sign in up to 20% of cases. The most common
neurologic findings are syncope and altered mental status. 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. 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.
Peripheral nerve ischemia can manifest as numbness and tingling in the extremities.
Hoarseness from recurrent laryngeal nerve compression also has been described. Horner
syndrome is caused by interruption in the cervical sympathetic ganglia and presents with
ptosis, miosis, and anhidrosis.
Other diagnostic clues include a new diastolic murmur or asymmetrical pulses. Pay
careful attention to carotid, brachial, and femoral pulses on initial examination and look
for progression of bruits or development of bruits on reexamination. Physical findings of
a hemothorax may be found if the dissection ruptures into the pleura.
Complications
Complications are diverse and numerous; anatomic-related complications are deducible
and include the following:
Hypotension and shock as a result of aortic rupture, with eventual death from
exsanguination
Pericardial tamponade secondary to hemopericardium; this complicates type A
aortic dissection
Acute aortic regurgitation as a complication of proximal aortic dissection
propagating into a sinus of Valsalva with resultant aortic valve insufficiency
Pulmonary edema secondary to acute aortic valve regurgitation
Rare occurrence of right or left coronary ostium involvement leading to
myocardial ischemia
Neurologic findings due to carotid artery obstruction - Ischemic cerebrovascular
accident (CVA), hemiplegia, hemianesthesia (aortic branch involvement can lead
to spinal cord ischemia, ischemic paraparesis, and paraplegia)
Mesenteric and renal ischemia - Can lead to bowel or visceral ischemia, renal
infarction, hematuria, or acute renal failure (ARF)
Compressive symptoms, such as superior vena cava syndrome, Horner syndrome
(when it affects the superior cervical ganglia), dysphagia (when it involves the
esophagus), airway compromise, and hemoptysis (when it compresses the

bronchus)
Other compressive symptoms - Can be associated with vocal cord paralysis and
hoarseness
Claudication - Can develop from extension of the dissection into the iliac arteries
Redissection and progressive aortic diameter enlargement
Aneurysmal dilatation and saccular aneurysm
Diagnostic Considerations
Consider thoracic aortic dissection in the differential diagnosis of all patients presenting
with chest pain. The pain is usually localized to the front or back of the chest, often the
interscapular region, and typically migrates with propagation of the dissection.
The pain of aortic dissection is typically distinguished from the pain of acute myocardial
infarction by its abrupt onset, although the presentations of the 2 conditions overlap to
some degree and are easily confused. Aortic dissection can be presumed in patients with
symptoms and signs suggestive of myocardial infarction but without classic
electrocardiographic findings.
Differential Diagnoses
Aortic Regurgitation Imaging

Aortic Stenosis Imaging
Cardiogenic Shock in Emergency Medicine
Emergent Management of Pleural Effusion
Mechanical Back Pain
Myocardial Infarction
Myocarditis
Pleural Effusion
Pulmonary Embolism
Thoracic Outlet Syndrome Imaging
Approach Considerations
Aortic dissection is usually diagnosed by using imaging techniques before the result of
blood work is interpreted. The choice of imaging techniques depends in part on whether
or not the patient is hemodynamically stable.
Chest radiography is the initial imaging technique and may or may not reveal any
abnormality. Computed tomography (CT) is useful in hemodynamically stable patients;
emergency CT angiography with 3-dimensional reconstruction is rapidly becoming the
diagnostic test of choice. Magnetic resonance imaging (MRI) is as accurate as CT and
may benefit patients who have adverse reactions to the use of intravenous contrast agents.
For hemodynamically unstable patients, echocardiography is ideal.
Aortography is still considered by some as the diagnostic criterion standard test for aortic
dissection. However, it is being replaced by newer imaging modalities. For more
information on imaging in this disorder, see the Medscape Reference article Aortic
Dissection Imaging.
All patients with suspected thoracic aortic dissection should have a 12-lead
electrocardiogram (ECG). However, the ECG often demonstrates a nonspecific
abnormality or normal results.
Blood Studies
A complete blood count (CBC), serum chemistry studies, and cardiac marker assays
should be performed. On the CBC, leukocytosis may be present, which usually represents
a stress state. Decreases in hemoglobin and hematocrit values are ominous findings
suggesting that the dissection is leaking or has ruptured.
Elevation of the blood urea nitrogen (BUN) and creatinine levels may indicate
involvement of the renal arteries or prerenal azotemia resulting from blood loss or
associated dehydration (mainly when the BUN-to-creatinine ratio exceeds 20). Patients
with dissection involving the renal arteries may also exhibit hematuria, oliguria, or even
anuria (< 50 mL/day).
Myocardial muscle creatine kinase isoenzyme, myoglobin, and troponin I and T levels
are elevated if the dissection has involved the coronary arteries and caused myocardial
ischemia. The lactate dehydrogenase level may be elevated because of hemolysis in the
false lumen.
Measurement of the degradation products of plasma fibrin and fibrinogen can facilitate
the diagnosis of acute aortic dissection. In symptomatic patients, aortic dissection with a
patent false lumen should be considered if the plasma fibrin degradation product (FDP)
level is 12.6 g/mL or higher; the possibility of dissection with complete thrombosis of
the false lumen should be considered if the FDP level is 5.6 g/mL or higher.[2]
Some authors suggest that a D-dimer assay should be a part of the initial workup if aortic
dissection is suspected.[19] A negative result makes the presence of the disease less likely.
Smooth Muscle Myosin Heavy-Chain Assay

A smooth muscle myosin heavy-chain assay is performed in the first 24 hours. Increased
levels in the first 24 hours are 90% sensitive and 97% specific for aortic dissection. levels
are highest in the first 3 hours. A cutoff of 2.5 has a sensitivity of 91%, a specificity of
98%, and an accuracy rate of 96%, respectively.
The smooth muscle myosin heavy-chain assay has greater sensitivity and specificity than
transthoracic echocardiography (TTE), CT scanning, and aortography, but it has less
sensitivity and specificity than transesophageal echocardiography (TEE), MRI, and

helical CT scanning.
Chest Radiography
Although chest radiography is not the definitive imaging study for aortic dissection, it
should be performed as the initial imaging technique if it is readily available at the
bedside and does not cause delay in obtaining a CT or MRI.[3] Chest radiography (see the
images below) may or may not reveal any abnormality. Widening of the mediastinum is
the classic finding.
Chest radiograph demonstrating widened mediastinum in a
patient with aortic dissection.
widening.
Aortic dissection. Mediastinal
Aortic dissection. Mediastinal widening.
In 2000, the International Registry of Acute Aortic Dissection published data on 464
patients. Chest radiography showed a widened mediastinum in approximately 62% of
patients.[5]
If the patient is hemodynamically stable and cooperative, an anteroposterior (AP)
radiograph can be obtained at bedside. A widened mediastinum is sometimes difficult to
identify on a portable AP radiograph. Look for a mediastinal width greater than 8 cm on
the AP view.
A tortuous aorta, common in hypertensive patients, may be hard to distinguish from a

widened mediastinum. If in doubt, a good posterior-anterior radiograph is recommended.
The differential diagnosis of a widened mediastinum includes tumor, adenopathy,
lymphoma, and enlarged thyroid.
If an aortic dissection ruptures, blood can extravasate into the ipsilateral pleural space,
causing a hemothorax (see the image below).
Chest radiograph of a patient with aortic dissection presenting

with hemothorax.
With type A dissection, an abnormal aortic contour is observed in a minority of patients.
An 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.
Other radiologic abnormalities seen on chest radiography include the following:
Pleural effusion
Left apical cap
Tracheal deviation to the right
Depression of left main stem bronchus
Esophageal deviation
Loss of the paratracheal stripe
The International Registry for Aortic Dissection revealed that over 12% of the chest
radiographs of patients with aortic dissection were read as normal.[5] 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.
Computed Tomography
CT scanning with contrast is used more frequently in emergency department (ED)
settings. CT scanning is useful only in hemodynamically stable patients, because of its
lack of portability and its potential limitations in patients with contraindications to
intravenous contrast agents.
A 2008 guideline from the American College of Radiology recommends CT angiography
as the definitive test in most patients with suspicion of aortic dissection.[3] CT
angiography provides detailed anatomic definition of the dissection as well as
information on plaque formation. Prospective studies have shown a sensitivity of 83-94%

and a specificity of 87-100%. However, 3-D reconstruction may not be available in
smaller centers.[20]
Spiral CT scanning is associated with a higher rate of detection and better resolution than
incremental CT scanning. Faster scanners have decreased the acquisition time to the
range of a breath hold, resulting in less motion artifact from breathing. High-quality 2-D
and 3-D 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. One
recent study reported that extended hypothermic circulatory arrest times, as a
consequence of disease severity, contribute to a higher mortality rate, as do redo surgery
and the overall extent of disease. Emergency surgery and extracardiac arteriopathy are
associated with increased risk of neurological injury. Age, however, was not associated
with increased risk for neurologic injury or mortality.[21]
Drawbacks include the following:
Transportation of a patient in potentially unstable condition from the ED, even for
the relatively short time needed for this procedure, places the patient at risk
CT angiography requires the injection of iodinated contrast, which may harm a
patient who has impaired renal function or an allergy to contrast media
CT scanning provides no information on aortic regurgitation
See the images below for CT scans showing aortic dissection.
Aortic dissection. CT scan showing a flap (right side of
image).
Aortic dissection. True lumen versus false lumen
in an intimal flap.
Aortic dissection. Left subsegmental
atelectasis and left pleural effusion. Flap at lower right of image.
Aortic dissection. Significant left pleural effusion.
Aortic dissection. CT scan showing a flap (center of image).
Aortic dissection. CT scan showing a flap (center of
image).
Aortic dissection. CT scan showing a flap.
dissection. CT scan showing a flap.
Thrombus and a patent lumen.
Aortic
Aortic dissection.
Aortic dissection. Thrombus.
Aortic dissection. True lumen and false lumen separated by an
intimal flap.
Aortic dissection. Intimal flap and left pleural effusion.
Aortic dissection.
Patient with an
ascending type A aortic dissection showing the intimal flap. Image courtesy of Kaiser-
Permanente.
Patient with an ascending type A aortic
dissection showing the intimal flap. Image courtesy of Kaiser-Permanente.
Patient with an ascending type A aortic dissection showing
the intimal flap. Image courtesy of Kaiser-Permanente.

Patient with an ascending type A aortic dissection showing the intimal flap. Image
courtesy of Kaiser-Permanente.
Patient with a type A
aortic dissection involving the ascending and descending aorta. Image courtesy of Kaiser-
Permanente.
Patient with a type A aortic dissection involving
the ascending and descending aorta. Image courtesy of Kaiser-Permanente.
Patient with a type A aortic dissection involving the ascending

and descending aorta. Image courtesy of Kaiser-Permanente.
Patient with a type A aortic dissection involving the

ascending and descending aorta. Image courtesy of Kaiser-Permanente.
Patient showing a type B aortic dissection with

extravasation of blood into the pleural cavity. Image courtesy of Kaiser-Permanente.



Echocardiography
Echocardiography is an important imaging modality for detecting aortic dissection.[22, 4]
Echocardiography also is useful in diagnosing cardiac tamponade and aortic
regurgitation.
Transesophageal echocardiography (TEE) has greater sensitivity (97-99% versus 80%)
and specificity (97-100% versus 90%) than transthoracic echocardiography (TTE).[4] TTE
is most useful in ascending aortic dissections, especially those closest to the aortic root
and within a few centimeters of the aortic valve. Sensitivity is highest in this location.
TTE is much less accurate for arch and descending aortic dissections.
TEE is as accurate as CT scanning and MRI in terms of sensitivity and specificity, and it
can be used at the bedside, which makes it ideal for hemodynamically unstable patients.
It is a relatively quick study to perform and relatively noninvasive. However, obesity, a
narrow intercostal space, pulmonary emphysema, and mechanical ventilation decrease
the accuracy of TEE. False-positive results with TEE are about 10%.[22, 4]
In one study, color Doppler TEE using biplanar views detected intimal flaps in 18 of 18
patients with type A dissections and in 10 of 39 with type B dissections.[23] Intimal tears
were detected in 15 (83%) patients with type A and in 35 (90%) patients with type B
(both confirmed by surgery or angiography). Intimal entry was detected in 16 of 18
patients using biplanar views and in 34 of 39 patients using single planar views.
Using longitudinal views, only 2 intimal entries were detected in 18 patients. Using
biplanar views, the intimal entries in 2 patients with type B entries were not visualized by
TEE because the dissection was in the aortic arch and was obscured by the trachea and
the left mainstem bronchus. The intimal entries in 2 patients with type B entries were in
the abdominal aorta.[23]
Color Doppler TEE using biplanar views has the advantages of additional acoustic
windows, ease of spatial orientation, more accurate visualization of the entry, and ease of
application.
The main drawback of TEE is its strong dependence on operator experience. Other
drawbacks are that false-positive results can occur from reverberations in the ascending
aorta and that the upper ascending aorta and arch may not be visualized well, leading to
false-negative results. TEE cannot be performed in patients with esophageal varicosities
or stenosis. If the findings are negative and clinical suspicion remains high, a second
diagnostic test is recommended.
Magnetic Resonance Imaging

MRI has approximately 98% sensitivity and specificity for detecting thoracic aortic
dissection. It is the most sensitive method for diagnosing aortic dissection and has similar
specificity to CT scanning.
MRI shows the site of intimal tear, type and extent of dissection, and presence of aortic
insufficiency, as well as the surrounding mediastinal structures. Other benefits are that
MRI requires no contrast medium and no ionizing radiation. It is the preferred modality
for patients with renal failure and those with an allergy to iodine, as well as for imaging
chronic dissections and postsurgical follow-up. Its use in acute dissection is limited
because it is not portable.[24]
A study of 53 consecutive patients with clinically suspected aortic dissection found that
for type A dissection, MRI was 100% sensitive and specific, while TEE was 100%
sensitive and 78% specific. In patients with type B dissection, MRI was 100% sensitive
and specific, while TEE was 90% sensitive and 97% specific.[25]
With regard to epiphenomena, visualization of the site and spatial extent of the intimal
flap with TEE was 78% specific in the ascending aorta, 94% in the aortic arch, and 92%
in the descending aorta. MRI and TEE were equal in the detection of the site of entry of
the aortic dissection. Sensitivity in the detection and localization of intraluminal thrombi
was 75% for TEE and 100% for MRI.[25]
Contrast-enhanced magnetic resonance angiography (CE-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 (however, most patients
with prosthetic heart valves or coronary stents can safely have an MRI)
Electrocardiography
All patients with suspected thoracic aortic dissection should have a 12-lead ECG.
However, the ECG often demonstrates a nonspecific abnormality or normal results
(approximately 31% of patients). One study reported normal findings in 63 (90%) of 70
patients.
In acute thoracic aortic dissection, the ECG changes can mimic those seen in acute
cardiac ischemia. In the presence of chest pain, these signs can make distinguishing
dissection from acute myocardial infarction very difficult (see the image below). Keep
this in mind when administering thrombolytics to patients with chest pain.
Electrocardiogram of a patient presenting to the ED with chest

pain; this patient was diagnosed with aortic dissection.
The incidence of abnormal ECG findings is greater in Stanford type A dissections than in
other types of dissections. ST segment elevation can be seen in Stanford type A
dissections because the dissection interrupts blood flow to the coronary arteries. In one
study, 8% of patients with type A dissections had ST segment elevation, whereas no
patients with type B dissections had ST segment elevation. More commonly, the ECG
abnormality is ST segment depression.
If the dissection involves the coronary ostia, the right coronary artery is most commonly
involved. This can result in ST segment elevation in leads II, III, and aVF, a pattern
similar to that seen in inferior wall infarctions.
Aortography
Aortography has been the diagnostic criterion standard study for aortic dissection, but it
is difficult to perform in patients with hemorrhage, shock, and/or cardiac tamponade.
Aortography is being replaced by newer imaging modalities because of risks associated
with invasiveness and adverse reactions to intravenous contrast agents.
Aortography (see the image below) 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.
Angiogram demonstrating dissection of the aorta in a

patient with aortic dissection presenting with hemothorax.
The procedure is invasive

The patient must be transported to the radiology department, leaving the ED
The use of contrast media may be harmful to patients who have renal
insufficiency or an allergy to iodine
The false lumen and intimal flap may not be visualized if the false channel is
thrombosed, which can lead to misdiagnosis
Simultaneous opacification of the true and false lumens may make discerning the
presence of a dissection difficult
Approach Considerations
graft.
Emergent surgical correction is the preferred treatment for Stanford type A (DeBakey
type I and II) ascending aortic dissection. It is also preferred for complicated Stanford
type B (DeBakey type III) aortic dissections with clinical or radiologic evidence of the
following conditions:
Propagation (increasing aortic diameter)

Increasing size of hematoma
Compromise of major branches of the aorta
Impending rupture
Persistent pain despite adequate pain management
Bleeding into the pleural cavity
Development of saccular aneurysm
Cautions and relative contraindications to surgery include the following:
Cerebrovascular accident
Severe left ventricular dysfunction
Coagulopathy
Pregnancy
Postmyocardial infarction (< 6 mo)
Significant arrhythmias
Advanced age
Severe valvular disease
Medical management remains the treatment of choice for descending aortic dissections
unless they are leaking or ruptured. With the progress in stenting technology, descending
dissections can be approached with this modality in selected cases.[6, 13, 26, 27, 28, 29] Medical
therapy is also administered to surgical patients preoperatively, intraoperatively, and
postoperatively to prevent progression or recurrence of aortic dissection.
Medical management consists of decreasing the blood pressure and the shearing forces of
myocardial contractility in order to decrease the intimal tear and propagation of the
dissection. Medical management with antihypertensive therapy, including beta-blockers,
is the treatment of choice for all stable chronic aortic dissections.[30]
Pain management is an important but difficult aspect of medical therapy. Narcotics and
opiates are the preferred agents.
For more information, see the Medscape Reference article Emergent Management of
Acute Aortic Dissection.
Reducing Blood Pressure and Cardiac Contractility

Initiate medical therapy as soon as the diagnosis is considered. To guide medical therapy,
admit the patient to the intensive care unit or coronary care unit for hemodynamic
studies, as follows:
Arterial blood pressure monitoring with an arterial line

Central venous pressure monitoring with a central catheter
Cardiac performance and filling pressures with Swan-Ganz catheterization
Urine output monitoring with a Foley catheter and bag
Initiate therapy to reduce cardiac contractility. Administer drugs with negative inotropic
effects, such as beta-blockers (the agents of choice); administer calcium channel blockers
if beta-blockers are contraindicated. The following beta-blockers are commonly used,
intravenously or orally:
Labetalol
Propranolol
Esmolol
Initiate therapy to reduce systemic arterial pressure and shear stress if the patient's blood
pressure allows for this type of intervention. The following agents are commonly used:
Intravenous nitroprusside drip

Intravenous labetalol: it has a dual effect of decreasing blood pressure and cardiac
contractility
Calcium channel blockers (eg, diltiazem): they lower blood pressure and cardiac
contractility
The following conditions contraindicate beta-blocker therapy:
Hypersensitivity to drug/class
Severe asthma
Heart block
Uncompensated heart failure
Bradycardia (heart rate < 60 beats/min)
Severe chronic obstructive pulmonary disease
Hypotension
The following conditions contraindicate calcium channel blocker therapy:
Second- or third-degree atrioventricular block
Sick sinus syndrome
Hypotension
Left ventricular dysfunction
Pulmonary congestion
The following conditions contraindicate nitroprusside infusion:
Poor cerebral perfusion
Poor coronary perfusion
Surgical Overview
The major objectives of surgery for aortic dissection are to alleviate the symptoms,
decrease the frequency of complications, and prevent aortic rupture and death. The
affected layers of the aorta are sutured together, and the aorta is reinforced with a Dacron
graft.
Improved cardiopulmonary bypass circuits have decreased the prevalence of injury to
blood elements. Morbidity and mortality rates associated with this highly invasive
surgery have decreased with the introduction of profound hypothermic circulatory arrest
and retrograde cerebral perfusion.[31]
A number of advances have resulted in a decreased frequency of complications associated
with surgery on the aorta. Dacron grafts with impregnated collagen or gelatin have been
developed that are impervious to blood. The development of more impermeable grafts
has greatly enhanced the surgical repair of thoracic aortic dissections. Such grafts include
the following:
Woven Dacron
Collagen-impregnated Hemashield (Meadox Medicals) aortic grafts
Gel-coated Carbo-Seal Ascending Aortic Prosthesis (Sulzer CarboMedics)
The operative mortality rate with ascending aortic dissection is usually less than 10%.
Serious complications are rare.
Dissections involving the arch are more complicated than those involving only the
ascending aorta because the innominate, carotid, and subclavian vessels branch from the
arch. Deep hypothermic arrest is usually required. If the arrest time is less than 45
minutes, the rate of CNS complications is less than 10%. Retrograde cerebral perfusion
may improve the protection of the CNS during the arrest period.
The mortality rate associated with aortic arch dissections is approximately 10-15%.
Significant neurologic complications occur in an additional 10% of patients.
Postoperative complications for extensive disease involving the thoracoabdominal aorta
include myocardial infarction, respiratory failure, renal failure, stroke, and paraparesis or
paraplegia. The use of adjunct procedures has decreased the frequency of procedurerelated spinal cord injury during descending aorta and thoracoabdominal surgeries. These
include the following:
Distal aortic perfusion

Induction of profound hypothermia
Cerebrospinal fluid drainage
Monitoring of somatosensory and motor evoked potentials in the brain and spinal
cord
Endovascular therapy is rapidly emerging as the preferred treatment for descending aortic
dissection, provided vascular access is available. This methodology still remains
controversial for ascending dissection.[32, 33, 34, 35, 36] A 2011 study that included 28
complicated acute aortic dissection patients treated with endovascular repair supports that
this technique has improved mortality versus traditional surgical interventions.[37]
Preoperative details
Numerous factors may increase mortality and morbidity rates for surgical intervention on
the aorta, including a history of myocardial infarction, respiratory failure, renal failure, or
stroke. Preoperative evaluation is, therefore, essential in patients with these histories.
Because aortic dissection is more common in elderly patients (ie, aged 70-80 years), this
group of patients has different comorbidities.
Patients older than 50 years have a high prevalence of atherosclerotic heart disease and
may require a thorough cardiac workup. Symptoms of aortic dissection are always
difficult to differentiate from those of myocardial infarction.
Patients with electrocardiographic (ECG) changes suggestive of myocardial infarction or
ischemia undergo workups with emergency cardiac catheterization and angiography,
followed by percutaneous transluminal coronary angioplasty or coronary artery bypass
grafting concomitant with aortic repair or construction.
Patients with valvular heart disease undergo workups with echocardiography or coronary
angiography. If any valvular abnormalities are found, appropriate surgical correction
(valve replacement or commissurotomy) is performed prior to or simultaneous with aortic
repair.
Surgeries involving the descending or thoracoabdominal aorta require a lateral
thoracotomy. A history of smoking or chronic obstructive pulmonary disease is of
significant concern; perform pulmonary function testing on such patients. Additionally,
arterial blood gas testing may be required. In elective cases, treat reversible restrictive
diseases and excessive sputum production with antibiotics and bronchodilators.
Preoperative renal dysfunction is considered the most important predictor of
postoperative acute renal failure (ARF). Preoperative management to decrease the
frequency of ARF involves adequate hydration; hypotension, a low cardiac output state,
and hypovolemia must be avoided.
Perform appropriate workups for patients presenting with any neurologic signs suggestive
of central nervous system pathology (eg, stroke). This usually consists of Doppler
imaging of the carotid arteries and, if needed, angiography of brachiocephalic and
intracranial arteries. If the study findings are positive, perform a carotid endarterectomy
before the aortic surgery.
Intraoperative details
The objectives of surgical therapy for aortic dissection are to resect the damaged
segment, excise the intimal tear, and obliterate the entry into the false lumen. Suturing the
edges of the dissected aorta both proximally and distally obliterates the entry into the
false lumen. The desirability of obliterating the entrance to the false lumen is
controversial because of multiple portals. Aortic continuity after dissection of a diseased
segment is reestablished by means of a prosthetic sleeve graft between the 2 ends of the
aorta.
Repairing Type A Dissections

Patients with type A dissections are treated with immediate surgical correction. This
involves transfer to the operating room, where median sternotomy is performed.
Profound hypothermia is initiated after the patient is placed on cardiopulmonary bypass.
Cardiopulmonary bypass is performed by femoral-femoral cannulation and through the
superior vena cava for retrograde cerebral perfusion.
Myocardial temperature is kept below 15C (59F) by cardioplegic perfusion via the
coronary sinus. This provides myocardial protection throughout the procedure.
Ventricular distention is avoided by decompressing the left ventricle by venting through
the left superior pulmonary vein or artery. The pump is stopped when the
electroencephalogram is isoelectric and the nasopharyngeal temperature reaches 12C
(53.6F). Retrograde cerebral perfusion is then started via the superior vena cava.
The ascending aorta is inspected for the site and extent of the tear and the involvement of
the transverse arch and for an assessment of intimal disruption that requires repair.
Through a longitudinal approach, the ascending aorta is opened and transected just
proximal to the innominate artery.
In patients with involvement of the transverse aortic arch, either the proximal arch or the
total arch is replaced. If the intima is fragmented or shows evidence of rupture, the whole
arch is replaced. If the transverse arch is free of reentry, the intima and adventitia are
sutured together with fine 4-0 and 5-0 polypropylene suture. A gelatin- or collagenwoven Dacron graft is sutured to the reinforced proximal aortic arch in end-to-end
fashion and reinforced from both inside and outside with 4-0 pledgeted sutures.
At the time of completion of the distal anastomosis, retrograde cerebral perfusion is
stopped and cardiopulmonary bypass is restarted via the femoral artery. This evacuates all
air and debris from the brachiocephalic vessels. The graft is clamped proximal to the
origin of the innominate artery. Flow to the cerebral and systemic circulation is restored
after clamping the graft proximal to the origin of the innominate artery.
Hypothermic circulatory arrest is a valuable tool in aortic dissection repair. Emptying the
major vessels allows ingress of air, which causes complications related to air embolism, a
major hazard associated with this procedure. Ensure that the patient's head is not
elevated; rather, depress it and allow blood to gravitate into the head vessels, thus
displacing the air (upward) to the periphery. This is essential.
The patient is rewarmed with restoration of anterograde flow through a side arm line
inserted in the ascending aorta. The aortic valve is suspended with 4-0 polypropylene
pledgeted sutures if it is normal and no evidence of aortic root dilatation is present. The
intima and adventitia of the aorta superior to the coronaries are sutured together and
reinforced from inside the graft. If the aortic valve or the root is dilatated, a composite
valve graft is placed.
A button or modified Cabrol technique is used to reattach the coronary arteritis. When
aortic regurgitation is present, simple decompression of the false lumen may be all that is
required to allow resuspension of the aortic leaflets and restoration of valvular
competence. More often, however, the 2 layers of the dissected aortic wall are
approximated, and resuspension of the commissures is accomplished with pledgeted
sutures. Prosthetic aortic valve replacement also may be necessary in certain situations.
After the procedure is completed, the patient is brought to sinus rhythm by defibrillation.
The patient is then weaned from cardiopulmonary bypass.
Repairing Type B Dissections

Surgical management of acute type B aortic dissections is undertaken only in the
presence of indications such as the following:
Persistent pain
Aneurysmal dilatation greater than 5 cm
End-organ or limb ischemia
Evidence of retrograde dissection to the ascending aorta
Patients without such indications are treated with intensive medical therapy.[13]
The operation involves transection of the proximal descending aorta distal to the left
subclavian artery. The proximal and distal intima and adventitia of the transected aorta
are reinforced in the same manner as that for the ascending aorta, with a 4-0
polypropylene suture.
A gelatin- or collagen-woven Dacron graft is sewn directly to the reinforced acutely
dissected proximal thoracic aorta, with the posterior row reinforced using interrupted
polypropylene sutures. Blood is rechanneled into the true lumen of the distal aorta by
cutting the descending thoracic graft and suturing it to the reinforced distal aorta.
Adjunct procedures are used to minimize complications. The entire thoracoabdominal

aorta is opened if extensive involvement of the descending and abdominal aorta is present
that requires replacement. The septum between the false and true lumen is excised, and
the visceral vessels and renal arteries are reattached to the graft directly or via a Dacron
graft.
In chronic dissections, the intercostal arteries (T9-T12) are reimplanted by side graft or a
side hole. This is in contrast to acute dissections, in which the intercostals and lumbar
arteries are ligated. Newer surgical techniques have been developed that use fibrin sealant
or gelatin-resorcin-formaldehyde glue.
Glue replaces the use of pledgeted sutures to seal the false lumen of the aortic stumps
after resection of the diseased aortic segment and before the implantation of the Dacron
prosthesis. The glue hardens and reinforces the dissected aortic tissue. Other advantages
include simplification of the operation, facilitation of the resuspension of the aortic valve,
and, possibly, reduction in the frequency of late aortic root aneurysm formation.
Endovascular Repair
Because of high operative mortality rates in patients with renal or visceral artery
compromise from dissection, endovascular techniques are under investigation. Several
endovascular techniques are available.[26, 29, 38] One involves the formation of a site of
reentry to allow blood to pass from the false lumen to the true lumen. This requires
passing a wire past the intact intimal flap, passing a balloon-tipped catheter over the wire,
and tearing a hole in the intimal flap by inflating the balloon.
Another technique involves percutaneous stenting to decrease the ischemic complications
of aortic dissection. This is performed on arteries that have compromised flow from the
dissection. Sutureless intraluminal prostheses placed during cardiopulmonary bypass are
also being used.
Another technique involves percutaneously placed intraluminal stent-grafts using a
transfemoral catheter technique. This procedure results in the closure of the site of entry
into the false lumen and decompresses and promotes thrombosis of the false lumen. It
also alleviates obstruction of the branch vessels complicating a dissection.
Thoracic endovascular aortic repair (TEVAR) is a minimally invasive approach used to
treat patients who cannot tolerate open surgical repair. A study of outcomes following
TEVAR in patients with retrograde type A aortic dissection (RAAD) and an entry tear in
the descending aorta found it to be safe and effective for this group of highly selected
patients. All surgeries were technically successful, with all patients surviving through the
follow-up period. TEVAR resulted in a significant decrease in the diameter and the false
lumen of both the ascending and descending aortas.[39]
For endovascular therapy, the patient is prepared for general anesthesia and open
procedure. The patient is then taken to the vascular suite, and after the induction of
general anesthesia, bilateral groin cutdowns are performed to gain access to the common
femoral artery. Due to the large size of the sheath needed to introduce the stent, a
synthetic graft may be sewn to the artery to gain access. Once groin access is obtained,
the patient is heparinized and the stent is positioned and deployed using radiographic
guidance.[36]
Intramural Hematomas and Penetrating Ulcers

Intramural hematomas and penetrating atherosclerotic ulcers of the aorta are conditions
that result in aortic dissection or rupture. Both are more common in the descending aorta;
medical therapy is first-line treatment. When the ascending aorta or the arch is affected,
the need for surgery is more likely.
Intramural hematomas are hemorrhages into the medial layer of the aortic wall without an
intimal tear. Because these hematomas have a natural history similar to that of aortic
dissection and aneurysm, they are treated similarly. Surgical therapy is initiated for
patients with proximal hematomas; medical therapy is reserved for patients with distal
hematomas. Medical therapy consists of optimizing blood pressure control, decreasing
aortic pulse pressure, controlling risk factors for atherosclerosis, and maintaining close
long-term follow-up care.
Penetrating atherosclerotic ulcers penetrate the internal elastic lamina, causing hematoma
formation within the media of the aortic wall. Almost all are in the descending aorta.
Because the natural history of these ulcers is undefined, a definitive treatment strategy
has not been formulated.
Consider surgery in patients with penetrating atherosclerotic ulcers who are
hemodynamically unstable or who have evidence of pseudoaneurysm formation or
transmural rupture. Other indications for surgery include recurrent pain, distal
embolization, and progressive aneurysmal dilatation from the ulcer. If patients present
without these complications, they are treated with antihypertensive medications and close
monitoring.[40]
Consultations and Long-Term Monitoring

Once a thoracic dissection is suspected, consult a thoracic surgeon. Because many
patients with this disorder have concomitant medical illness, the emergency department
physician should consult the patient's primary care provider to expedite preoperative
preparation. Early consultation is encouraged when ordering further imaging studies if
the patient requires rapid operative intervention. Consult a radiologist prior to obtaining
aortography.
Provide the following long-term care for patients with aortic dissection, whether treated
medically or surgically:
One-month follow-up check for any new symptoms, such as chest or back pain,
and signs suggestive of progression of the aortic dissection
Adequate blood pressure control, with the systolic blood pressure maintained at
90-120 mm Hg
Routine chest radiographs, CT scans with contrast, and MRIs, at 3-, 6-, and 12month intervals, respectively, in an outpatient setting to evaluate any progression
of the condition
Medication Summary
Initial therapeutic goals include the elimination of pain and the reduction of systolic
blood pressure to 100-120 mm Hg or to the lowest level commensurate with adequate
vital organ (ie, cardiac, cerebral, renal) perfusion. Whether systolic hypertension or pain
is present, beta-blockers are used to reduce arterial delta pressure/delta time (dP/dt).
To prevent exacerbations of tachycardia and hypertension, treat patients with intravenous
morphine sulfate. This reduces the force of cardiac contraction and the rate of rise of the
aortic pressure. It then retards the propagation of the dissection and delays rupture.
Antihypertensives, Other
Class Summary
These agents are used to reduce arterial dP/dt. For acute reduction of arterial pressure, the
potent vasodilator sodium nitroprusside is effective. To reduce dP/dt acutely, administer
an IV beta-blocker in incremental doses until a heart rate of 60-80 beats/min is attained.
When beta-blockers are contraindicated, such as in second- or third-degree
atrioventricular block, consider using calcium channel blockers. Sublingual nifedipine
successfully treats refractory hypertension associated with aortic dissection.
View full drug information
Esmolol (Brevibloc)
Esmolol is an ultrashort-acting beta2-blocker. It is particularly useful in patients with
labile arterial pressure, especially if surgery is planned, because it can be discontinued
abruptly if necessary. This agent is normally used in conjunction with nitroprusside. It
may be useful as a means to test beta-blocker safety and tolerance in patients with a
history of obstructive pulmonary disease who are at possible risk of bronchospasm from
beta-blockade. The elimination half-life of esmolol is 9 minutes.
Labetalol (Trandate)
Labetalol blocks alpha-, beta1-, and beta2-adrenergic receptor sites, decreasing blood
pressure.
Propranolol (Inderal LA, InnoPran XL)

Propranolol is a class II antiarrhythmic nonselective beta-adrenergic receptor blocker. It
has membrane-stabilizing activity and decreases the automaticity of contractions.
Propranolol is not suitable for emergency treatment of hypertension. Do not administer
propranolol IV in hypertensive emergencies.
Metoprolol (Lopressor, Toprol XL)

Metoprolol is a selective beta1-adrenergic receptor blocker that decreases the
automaticity of contractions. During IV administration, carefully monitor the blood
pressure, heart rate, and electrocardiogram (ECG). When considering conversion from IV
to oral (PO) dosage forms, use the ratio of 1 mg IV to 2.5 mg PO metoprolol.
Nitroprusside (Nitropress)
Nitroprusside causes peripheral vasodilation by direct action on venous and arteriolar
smooth muscle, thus reducing peripheral resistance. It is commonly given intravenously
because of its rapid onset and short duration of action. It is easily titratable to reach the
desired effect.
Nitroprusside is light sensitive; both bottle and tubing should be wrapped in aluminum
foil. Before initiating nitroprusside, administer a beta-blocker to counteract the
physiologic response of reflex tachycardia that occurs when nitroprusside is used alone.
This physiologic response increases shear forces against the aortic wall, thus increasing
dP/dt. The objective is to keep the heart rate at 60-80 bpm.
Nifedipine (Procardia)
Nifedipine is one of the more common channel blockers used for hypertension.
Analgesics
Class Summary
Pain control is essential to quality patient care. It ensures patient comfort, promotes
pulmonary toilet, and prevents exacerbations of tachycardia and hypertension.
Morphine sulfate (Astramorph, Infumorph, MS Contin, Avinza)

Morphine is the drug of choice for narcotic analgesia because of its reliable and
predictable effects, safety profile, and ease of reversibility with naloxone. Like fentanyl,
morphine sulfate is easily titrated to the desired level of pain control. If administered IV,
morphine may be dosed in a number of ways; it is commonly titrated until the desired
effect is obtained.
NEW TOPIC
Emergent Management of Acute Aortic

Dissection
Author: John M Wiesenfarth, MD, FACEP, FAAEM; Chief Editor: Barry E

Brenner, MD, PhD, FACEP
Updated: Mar 8, 2013 Overview

Aortic dissection is the most common catastrophe of the aorta, 2-3 times more common
than rupture of the abdominal aorta. When left untreated, about 33% of patients die
within the first 24 hours, and 50% die within 48 hours. The 2-week mortality rate
approaches 75% in patients with undiagnosed ascending aortic dissection.
The establishment of the International Registry of Acute Aortic Dissection in 1996, which
gathers information from 24 centers in 11 countries, has helped in the development of an
understanding of the complexity of aortic dissection.
Dissections of the thoracic aorta have been classified anatomically by 2 different

methods. The more commonly used system is the Stanford classification, which is based
on involvement of the ascending aorta and simplifies the DeBakey classification.
Go to Aortic Dissection for complete information on this topic.
Stanford classification
The Stanford classification divides dissections into 2 types, type A and type B. Type A
involves the ascending aorta (DeBakey types I and II); type B does not (DeBakey type
III).
This system helps to delineate treatment. Usually, type A dissections require surgery,
while type B dissections may be managed medically under most conditions.
DeBakey classification
The DeBakey classification divides dissections into 3 types, as follows:
Type I involves the ascending aorta, aortic arch, and descending aorta
Type II is confined to the ascending aorta
Type III is confined to the descending aorta distal to the left subclavian artery
Type III dissections are further divided into IIIa and IIIb. Type IIIa refers to dissections
that originate distal to the left subclavian artery but extend proximally and distally,
mostly above the diaphragm.
Type IIIb refers to dissections that originate distal to the left subclavian artery, extend
only distally, and may extend below the diaphragm.
Thoracic aortic dissections should be distinguished from aneurysms (ie, localized
abnormal dilation of the aorta) and transections, which are caused most commonly by
high-energy trauma.
Prehospital Care
Assure adequate breathing, maintain oxygenation, treat shock, and obtain useful
historical information.
Establishing the diagnosis in the field is usually difficult or impossible, but certain salient
features of aortic dissection may be observed. It is life threatening if not quickly
recognized and treated.
Radio communication with the receiving hospital permits the medical control physician
to direct care and select a capable destination hospital, while permitting the emergency
department (ED) to mobilize appropriate resources.
In the rare event that the diagnosis can be made based on prehospital information, the
physician directing prehospital care should request transport to a facility capable of
operative treatment of an aortic dissection.
Emergency Department Care

The mortality rate of patients with aortic dissection is 1-2% per hour for the first 24-48
hours. Initial therapy should begin when the diagnosis is suspected. This includes 2 largebore 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
(dP/dt) 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.
End organ perfusion should be evaluated. Balancing the risks of dP/dt on the aortic wall
versus the benefits of acceptable end organ perfusion may be a difficult clinical decision.
Retrograde cerebral perfusion may increase the protection of the central nervous system
during the arrest period.
The mortality rate from aortic arch dissections is about 10-15%, with significant
neurologic complications occurring in another 10% of patients. The mortality rate is
influenced by the patient's clinical condition.
The American College of Radiology has established ACR Appropriateness Criteria for
the diagnosis and treatment of suspected aortic dissection.[1]
Type A dissections
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%, and serious complications are rare
with ascending aortic dissections.
The development of more impermeable grafts, such as woven Dacron, collagenimpregnated Hemashield (Meadox Medicals, Oakland, NJ), aortic grafts, and gel-coated
Carbo-Seal Ascending Aortic Prothesis (Sulzer CarboMedics, Austin, Tex), has greatly
enhanced the surgical repair of thoracic aortic dissections.
With the introduction of profound hypothermic circulatory arrest and retrograde cerebral
perfusion, the morbidity and mortality rates associated with this highly invasive surgery
have decreased.
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%.
Aortic stent grafting is a challenging technique. It may prove feasible and has offered
good results in a small series of patients. It may be a reasonable alternative in high-risk
patients in the near future.
Type B dissections
The definitive treatment for type B dissections is less clear.
Uncomplicated distal dissections may be treated medically to control blood pressure.
Distal dissections treated medically have a mortality rate that is the same as or lower than
the mortality rate in patients who are treated 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 in
patients with a distal thoracic aortic dissection.
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.
A series of patients with type B dissections demonstrated that aggressive use of distal
perfusion, CSF drainage, and hypothermia with circulatory arrest improves early
mortality and long-term survival rates.
Endovascular stenting remains an option for treatment of some type B dissections. Some
studies recommend that patients with complicated acute type B dissections undergo
endovascular stenting with the goal of covering the primary intimal tear.[2]
Definitive treatment
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 reconstructionvalve 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%.
In a study by Mimoun et al of patients with Marfan syndrome who had acute aortic
dissection, the patients were found to have a better event-free survival when there were
no dissected portions of the aorta remaining after surgery.[3]
Consultations
Once a thoracic dissection is suspected, consult a thoracic surgeon. Because many
patients with this disorder have concomitant medical illness, consult the patient's primary
care provider to expedite preoperative preparation. Early consultation is encouraged
when ordering further imaging studies if the patient requires rapid operative intervention.
Consult a radiologist prior to obtaining aortography.
Inpatient Care
Patients with symptomatic dissection should undergo immediate repair, especially if it is
leaking or expanding.
Symptomatic patients require admission to a center experienced in cardiopulmonary
bypass and operative care.
Completely asymptomatic patients may have their repair performed electively but may
require admission to expedite their evaluation or for preoperative stabilization of their
condition.
Patients with chest pain should undergo serial echocardiograms (ECGs) and creatine
kinase (CK) determinations if acute myocardial infarction (AMI) is indicated.
Outpatient Care
Follow-up examinations with radiologic studies are recommended at 3-month intervals
for the first year and every 6 months for the next 2 years.
After this, follow up annually.
Transfer
Symptomatic patients require care at a facility equipped to perform cardiopulmonary
bypass with aortic and/or valvular repair.
Contact the receiving physician as soon as possible to transfer patients before their
condition deteriorates.
Early airway management is indicated in the presence of hemoptysis or stridor.
If coronary insufficiency is suspected, nitrates may be used, but therapy with
thrombolytic agents and aspirin should be avoided.
Patients should be monitored and accompanied by personnel capable of resuscitation.
If a prolonged ground transport time is anticipated, consider air transport.

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Updated: Mar 5, 2013 Practice Essentials

See Clinical Presentation for more detail.

History and physical examination

Possible physical examination findings include the following:

Possible laboratory study findings include the following:

Leukocytosis: Stress state

Initial imaging technique if it is readily available at the bedside

Computed tomography with contrast:

The definitive test in most patients with suspicion of aortic dissection[3]

Transesophageal echocardiography (TEE) is more accurate than transthoracic

The most sensitive method for diagnosing aortic dissection

See Workup for more detail.

Emergency surgical correction is the preferred treatment for the following:

Stanford type A (DeBakey type I and II) ascending aortic dissection

See Treatment and Medication for more detail.

Image A represents a Stanford A or a DeBakey type 1 dissection. Image

History of aortic dissection and its repair

Aortic dissection. True lumen and false lumen separated

Approximately 2.2 cm above the aortic root

The Stanford classification has 2 types, as follows:

Type A: the ascending aorta is involved (DeBakey types I and II)

Image A represents a Stanford A or a DeBakey type 1 dissection.

Cystic medial necrosis

Aortic and mitral valve replacements

Dysphagia from compression of the esophagus

esophagus), airway compromise, and hemoptysis (when it compresses the

Aortic Regurgitation Imaging

Smooth Muscle Myosin Heavy-Chain Assay

sensitivity and specificity than transesophageal echocardiography (TEE), MRI, and

Chest radiograph demonstrating widened mediastinum in a

patient with aortic dissection.

Aortic dissection. Mediastinal

Aortic dissection. Mediastinal widening.

A tortuous aorta, common in hypertensive patients, may be hard to distinguish from a

Chest radiograph of a patient with aortic dissection presenting

information on plaque formation. Prospective studies have shown a sensitivity of 83-94%

See the images below for CT scans showing aortic dissection.

Aortic dissection. CT scan showing a flap (right side of

Aortic dissection. True lumen versus false lumen

Aortic dissection. Significant left pleural effusion.

Aortic dissection. CT scan showing a flap (center of image).

Aortic dissection. CT scan showing a flap (center of

Aortic dissection. CT scan showing a flap.

Aortic dissection. CT scan showing a flap.

Aortic dissection. CT scan showing a flap.

Aortic dissection. CT scan showing a flap.

Aortic dissection. CT scan showing a flap.

dissection. CT scan showing a flap.

Thrombus and a patent lumen.

Aortic dissection. Thrombus.

Aortic dissection. True lumen and false lumen separated by an

Aortic dissection. CT scan showing a flap.

Aortic dissection. Intimal flap and left pleural effusion.

Patient with an ascending type A aortic dissection showing

the intimal flap. Image courtesy of Kaiser-Permanente.

Patient with a type A aortic dissection involving the ascending

Patient with a type A aortic dissection involving the

Patient showing a type B aortic dissection with

Patient showing a type B aortic dissection with

Patient showing a type B aortic dissection with

Patient showing a type B aortic dissection with

Magnetic Resonance Imaging