Aortic Dissection

Categories: ACCS Acute, CAP7, HAP8, HST Acute, Vascular emergencies

Authors: Gary L A Cumberbatch
Publication Date: Nov 15, 2009
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Jump to: Top | Introduction | Clinical Assessment | Investigation
Strategies | Management | Prognosis & Followup strategies | Safety pearls and
Pitfalls | References | Comments

Introduction
(a) Context

The challenge for the Emergency Physician is in making the diagnosis of acute aortic
dissection and in doing so as expediently as possible as the mortality rate is 1-2% per
hour. It is often a difficult diagnosis to make due to the multitude of different clinical
presentations of the disease. The aim of this review is to provide a firm knowledge base
about aortic dissection and to increase its consideration in the differential diagnosis of
any patient with appropriate signs and symptoms of the disease.

The image illustrates an aortic dissection from the ascending aorta into the descending aorta.

(b) Definition

Aortic dissection occurs following a tear in the aortic intima with subsequent separation
of the tissue within the weakened media by the propagation of blood.

At the point of dissection the aorta is NOT aneurysmal and the term dissecting
aneurysm is incorrect and may be misleading.

A ruptured or leaking abdominal aneurysm is a different disease, requires immediate

surgery with only occasional need for any imaging, can be performed in most hospitals
by a vascular surgeon and does not require the use of cardiopulmonary bypass.

(c) Classification

Stanford classification
There are 4 different classifications of aortic dissection and the commonest one used is
the Stanford classification dividing them into Type A and Type B. A type A dissection
involves the ascending aorta and/or the arch whilst type B dissections involve only the
descending aorta and occur distal to the origin of the left subclavian artery.

DeBakeys Classification

The other commonly used classification is DeBakeys classification which divides aortic
dissections into 3 types: I, II and III (Figure 1). Type I dissections involve the entire aorta
whilst type II only involves the ascending aorta and, or the arch of the aorta. Type III
involves only the descending aorta.
 Figure 1: Classification of aortic dissection: Stanford Classification (Type A and B) and DeBakeys
Classification (I, II and III)

Reul and Cooley further subdivided De Bakeys classification into subtypes IIIa and IIIb.
In IIIa the dissection involves the aorta just distal to the left subclavian artery but
extends proximal or distal to this but is largely above the diaphragm. In IIIb the
dissection occurs only distal to the left subclavian artery and may extend below the
diaphragm.

Svenssons classification

A more recent classification has been made by Svensson, because intramural

haematoma and aortic ulcers may be the only signs of evolving aortic dissection and
are not accounted for in the other classification systems.

Class Classic dissection with flap between true and false aneurysm and
1 clot in false lumen

Class
2 Intramural hematoma

Class
3 Limited intimal tear with eccentric bulge at tear site

Class Penetrating atherosclerotic ulcer with surrounding hematoma,

4 usually subadventitial

Class Iatrogenic or traumatic dissection illustrated by coronary catheter

5 causing dissection

(d) Pathophysiology

Aortic dissection occurs following a tear in the intimal layer of the aorta with subsequent
anterograde or retrograde flow of blood within the outer third of the tunica media. It is
thought that this occurs because of medial degeneration and certain conditions
predispose to this (see Table 1).

Table 1: Predisposing factors for aortic dissection

 Hypertension

Marfans Syndrome

Ehlers-Danlos Syndrome

Annuloaortic ectasia and familial aortic

dissection

Bicuspid aortic valve

Coarctation of the aorta

Pregnancy

Turners Syndrome

Cocaine abuse

Giant cell arteritis

Iatrogenic

Notably essential hypertension is by far the commonest risk factor being present in
approximately 70% of cases. It causes weakening of the tunica media layer of the aorta.

Marfans Syndrome is associated with an inherited connective tissue disorder resulting in

a weakened aortic media and progressive aortic dilatation. Marfans Syndrome is likely
to be present in 50% of cases of dissection presenting under the age of 40.

Bicuspid aortic valve is associated with aortic root dilatation and with a congenitally
weakened aortic wall.

Intimal tear

The channel created by the dissection process is called the false lumen and occasionally
the blood may re-enter the true lumen through a more distal tear in the intima.

The majority of intimal tears occur in the ascending aorta (see Figure 1) due to greater
pressure on the aortic wall as it is closer to the left ventricular outflow.
Dissection

Once the dissection process occurs blood tracks through the media to varying degrees
and may dissect down from the aortic root to the bifurcation of the common iliac
arteries in a matter of seconds and typically causes maximum pain at this time.

aortic dissection from the ascending aorta extending to the bifurcation of the common iliacs.

The incidence of the location of primary aortic tears

Location of primary Inciden

aortic tear ce

Ascending aorta 70%

Descending thoracic aorta 15-20%

Arch of the aorta 10%

Abdominal aorta <5%

(e) Pathophysiological consequences of AAD

1) Rupture into various body cavities (see Table 2):

 AAD can result in rupture of the dissection into various body cavities (see Table 2).

haemopericardium (syncope and /or

sudden death)
right haemothorax (invariably sudden
Ascending
death
aorta

mediastinal haematoma
interatrial septal haematoma (cardiac
conduction defects)
compression of pulmonary trunk/ artery
Arch of aorta

left haemothorax (sudden death)

rarely into oesophagus (profuse
Descending
haematemesis)
aorta

retroperitoneal haemorrhage (back pain

with shock)
rarely intraperitoneal haemorrhage (shock
Abdominal
and acute abdomen
aorta

(2) Occlusion of any of the branch vessels of the aorta with consequent distal organ
ischaemia (see Table 3):

Pulse deficits are a classic feature of AAD and represent occlusion of branch vessels of
the aorta. There are two ways this can happen:

1. Smaller branches may be simply compressed at the point of origin without the
dissection progressing within the tunica media.
2. The dissection progresses within the media of the branch vessel and the false
lumen becomes so large it compresses the true lumen of the vessel.

Occasionally an obstructed branch vessel can have its blood flow restored either
because of a re-entry tear into the true lumen or because an intimal flap only
intermittently obstructs the origin of the vessel as the flap extends or moves with aortic
blood flow.

Table 4: Branch vessel occlusion and consequences

ST elevation myocardial
Coronary vessel(s) infarction

Common carotid(s) any type of stroke

an acutely ischaemic upper

Subclavian(s) limb

Coeliac/mesenteric
vessel(s) ischaemic bowel

Renal vessel(s) frank haematuria

 sudden onset painless
Spinal artery(ies) paraplegia

(3) Acute or progressive aortic regurgitation:

This occurs when the dissection process extends into or around the aortic valvular
support. When this happens the aortic root can dilate so much that the aortic leaflets
cannot fully appose during diastole thereby allowing regurgitation of blood through the
cusps. The resultant murmur may be of any grade of intensity and may be inaudible if
there is associated haemopericardium. Patients who survive the dissection process may
have a delayed presentation with cardiac failure.

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Clinical Assessment
A substantial amount of what we now know about the disease is due a large series of
patients in a review by Hirst (1) and also to the ongoing data submitted to the
International Registry of acute Aortic Dissection (IRAD) (2).

(a) The history

The history is the most essential part of the assessment of a patient as it will be the
patients symptoms that will alert you to the possibility of aortic dissection. The most
common symptom is pain and in 85% of patients in the IRAD series this pain was abrupt
in onset. The pain is often so sudden that the patient can describe exactly what they
were doing at the moment of onset and the pain is almost always at its maximum at
this point. This history helps distinguish between the pain of aortic dissection from the
more gradual onset of chest pain that occurs with acute coronary syndromes. In
addition the pain of aortic dissection is commonly sharp in nature whilst it is described
as an ache or tightness in acute coronary syndrome. The classic tearing interscapular
pain was found to occur in only 50% of patients in the IRAD series regardless of whether
they had a type A or type B dissection.

The pain in aortic dissection occurs in the anterior chest 70-80% of the time in patients
with a type A dissection and back pain occurs only in 50% of all patients (2) . Abdominal
pain was found to be the third commonest site of initial pain and other sites described
were the throat, neck and extremities.

Patients may also describe the classic migration of pain from the chest, back or
abdomen to one or more limbs or to the neck and this is thought to be due to peripheral
extension of the dissection from the primary intimal tear. The physician must beware
that the pain, however severe initially, may completely resolve by the time the patient
presents to hospital and often this is because the dissection process has for the moment
stopped or there is relief of the pressure within the aortic wall by the spontaneous re-
entry of blood back into the true lumen.

It is on these features alone that the physician should suspect aortic dissection even if
subsequent clinical examination and other bedside tests do not support the diagnosis.
 This suspicion should be raised further if the patient has any of the predisposing factors
such as hypertension, Marfans Syndrome, etc.

In 5-15% of patients however, no pain occurs at all and this is typically the case in those
patients presenting with syncope, stroke, congestive cardiac failure or the elderly.

(b) Physical examination

The physical examination of these patients needs to be thorough but also must be done
quickly. The chest should be specifically examined for a pleural effusion which may
represent a haemothorax.

When examining the cardiovascular system one must search for the following:

1. Signs relating to haemopericardium: pulsus paradoxus, faint or absent heart

sounds, distended neck veins, shock
2. Signs relating to aortic root dilatation: wide pulse pressure, diastolic murmur over
the aortic area
3. Compression of the true aortic lumen: systolic murmur over any part of the aorta
4. Pulse deficits: a difference of 20mmHg or more in blood pressure between arms,
a weaker central or peripheral pulse compared to the contralateral side or palpable
thrills or audible bruits over pulses
5. If the patient is hypotensive one must quickly determine whether this is
secondary to hypovolaemia, pump failure or neurogenic as the treatments for each of
these is very different.

Hypovolaemia may be caused by a massive haemothorax, loss of blood into an

extensive aortic wall false lumen, bowel ischaemia with or without haematemesis or
retroperitoneal haemorrhage.

Cardiac failure can be secondary to haemopericardium with tamponade; left ventricular

dysfunction due to myocardial infarction as a result of a coronary artery dissection
(3,4,5) ; or complete heart block following haemorrhage into the interatrial septum (6,7)
.

Neurogenic shock can simply be caused by spinal cord ischaemia or infarction and
should be considered when the patient has an obvious para- or tetraplegia with
bradycardia and hypotension and warm peripheries.

Abdominal examination is essential to exclude other potential causes of the patients

symptoms such as pancreatitis, perforated hollow viscus and ruptured abdominal aortic
aneurysm.

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Investigation Strategies
(a) ECG
The 12 lead electrocardiogram is not as helpful as one may think in distinguishing aortic
dissection from acute coronary syndrome as it is only completely normal in 30% of
patients with dissection. In the IRAD series 3% of all aortic dissection patients had ST
elevation myocardial infarction pattern; 15% acute ischaemic changes and 41% had
non-specific ST segment and T wave changes.

If the history suggests aortic dissection, a diagnosis of acute coronary syndrome should
not be made even if the ECG has obvious STEMI or NSTEMI patterns as antiplatelet
treatment, heparin or thrombolysis may worsen the prognosis of the patient. It is always
better to withhold these treatments when aortic dissection is considered and
immediately arrange for urgent aortic imaging to clarify the diagnosis.

The image displays a 12 lead ECG

(b) Chest Radiography

The portable erect chest x-ray is very helpful as it may demonstrate mediastinal
widening or provide another diagnosis for the patients symptoms e.g. spontaneous
pneumothorax.

An abnormal chest x-ray is present most of the time and the following radiological signs
must be sought in patients with AAD:

A widened mediastinum and other radiological signs

Mediastinal widening (see Figure 2) however is only present in 60% of patients with
dissection and other radiological signs are important to elicit (see Figure 3). These are
an abnormal aortic contour which occurs in 50% of patients; a soft tissue shadow
peripheral to a calcified aortic annulus which occurs in 15% of patients and represents
blood within the false lumen extending around the aortic annulus; a globular heart may
suggest haemopericardium and a pleural effusion may represent a haemothorax(8).

Pleural effusion

A pleural effusion, representing a haemothorax (invariably massive) occurs in 20% of

patients. This typically occurs when the dissection process involves the descending
thoracic aorta, and when rupture occurs here it is almost always into the left pleural
space.
 Figure 2: Mediastinal widening on the CXR

Figure 3: Other radiological features suggestive of thoracic aortic dissection

 A soft tissue shadow peripheral to a calcified aortic annulus occurs in 15% of patients.

A globualr heart suggesting a large haemopericardium

Pleural effusion

It is however possible to have a normal chest radiograph and this occurred in 12% of
patients in the IRAD series.

(c) Transthoracic Echocardiography

Although transthoracic echocardiography (TTE) can be performed at the bedside in the
resuscitation room it must not delay more definitive investigations such as CT or
transoesophageal echocardiography.

TTE may help make the diagnosis of aortic dissection by identifying a free intimal flap
within the aortic lumen but its sensitivity is approximately 80% for type A dissections
but only 50% for type B (9). Such imaging rarely identifies the extent of the dissection
and a more definitive investigation is always required. It does however accurately
detect a pericardial effusion, aortic regurgitation and the degree of aortic valvular
disruption all of which provide valuable information for the surgeon. It is therefore
ideally performed whilst awaiting interhospital transfer or whilst awaiting theatre in
centres with Cardiothoracic surgery on site.

(d) Transoesophageal Echocardiography

Transoesophageal echocardiography (TOE) is an ideal test because it can be performed

in the resuscitation room, has a sensitivity of 90-98%; can easily delineate the extent of
the dissection and can visualise the aortic root and valve (9). In the UK, this test is
limited by its availability out-of-hours. It can also cause surges in blood pressure whilst
instrumenting the awake patient particularly if the operator is inexperienced in its use.

(e) CT scan of mediastinum

Aortic dissection is diagnosed on CT by identifying two distinct lumens with a visible

intimal flap (see Figure 4). It can also delineate branch vessel involvement, visualise the
entire aorta and has a sensitivity ranging between 83 and 100% (9). CT will also reveal
pericardial fluid (see Figure 5) which is not a direct confirmatory test for aortic
dissection but will suggest this diagnosis in the right clinical context.

A distinct advantage of CT over other modalities of aortic imaging is that currently most
hospitals in the UK are able to transfer these images to a regional cardiothoracic centre
if required. This gives the surgeons adequate information on whether to transfer the
patient and allows them to plan the type of surgery required prior to patient arrival.

The sensitivity of CT detection for AAD is not yet 100%: it may miss a dissection if there
is complete thrombosis of one lumen or if there is similar opacification of both the true
and false lumens; also, intramural haematoma may be missed as the findings are often
subtle and only evident on pre-contrast images.

Intimal flaps
 Figure 4: Aortic dissection The arrows demonstrate the intimal flaps in both the ascending aorta
(anterior) and the descending aorta (posterior). TL is the true lumen as this has contrast within it whilst
the darker false lumen (FL) does not.

Lumens

The image illustrates two distinct lumens at the level of the arch of the aorta.

Dissection flap
 The arrow on the image demonstrates a dissection flap within the left common carotid artery as it
comes off the arch of the aorta.

Peridcardial fluid

CT will also reveal pericardial fluid which is not a direct confirmatory test for aortic
dissection but will suggest this diagnosis in the right clinical context. The white arrow
highlights the pericardial fluid.
 Figure 5: Aortic dissection with rupture into the pericardial sac The white arrow demonstrates the
pericardial effusion

(f) MRI and aortography

Although these imaging modalities can be used to detect aortic dissection they are
rarely used (9). MRI requires that these critically ill patients be placed on different
monitoring which is magnet-proof and doesnt allow for quick access to the patient
should they deteriorate once the scan has commenced. MRI at the moment also takes
considerable time to acquire the necessary images.

Aortography is invasive and is not performed at most hospitals. It is now rarely used as
non-invasive imaging can provide the required information.

It is essential that there is an agreed imaging modality for patients with suspected
aortic dissection in individual hospitals and that the regional Cardiothoracic surgeons
are happy to act on whatever imaging is to be used (10).

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Management
(a) General principles

Patients with suspected dissection are often in pain and opiate analgesia is important
both for comfort and to reduce the sympathetic response to pain which itself can cause
progression of the dissection process.

Definitive treatment depends upon the type of dissection:

Type A dissections require open surgery to prevent rupture into the pericardial
sac.
Type B dissections are managed medically but may require endovascular stenting
if the patient has persistent pain, a rapidly expanding aortic diameter, or malperfusion
of branch vessel organs.

It is important that patients with a type B dissection are still managed in a High
Dependency Unit and referred to a vascular interventional team if complications arise
(11-14).

(b) Control of blood pressure

It is vital that patients with suspected or proven dissection should have their blood
pressure actively reduced if higher than a systolic of 120 mmHg otherwise the
dissection process may progress. In order to facilitate this an arterial line must be
placed; intravenous labetalol (a mixed - and -blocker) is the ideal agent to be used in
this setting (15). Labetalol is both an alpha and beta- blocker and should be given as an
initial bolus and then as an infusion with invasive arterial monitoring used to guide the
actual dose.
Vasodilators and -blockers must not be used on their own. If a vasodilator is used it will
cause a reflex increase in contractility of the left ventricle which will potentially worsen
the dissection. A -blocker may cause unopposed alpha receptor stimulation with
increased peripheral vasoconstriction. These agents can, however, be used to good
effect if administered together.

The characteristics of the drugs used to manage hypertension in AAD (either singly or in
conjunction) are presented in Box 1.

0.25mg/kg (usually 20mg) as

a bolus over 2 minutes.
Further boluses of 20-80mg
are usually required every
and - 10 minutes once BP
blocker:Labetal controlled a continuous Cardiogenic shock, AV block,
ol infusion at 2mg/min bradycardia, COPD

200mcg/kg/min loading dose

over 1 min
Maintenance infusion
50mcg/kg/min for 4 mins.
Repeat loading dose and
- increase maintenance by
blockers:Esmol 50mcg/kg/min for 4 mins if Cardiogenic shock, AV block,
ol BP remains elevated. bradycardia, COPD

Bolus up to 5mg at rate 1-

2mg/min
Repeated after 5 mins to a Cardiogenic shock, AV block,
Metoprolol total dose of 10-15mg bradycardia, COPD

Vasodilators

Glyceryl Hypotension, hypovolaemia

Trinitrate Titrate 2 to 10mg/hour HOCM, aortic stenosis

Severe vitamin B12 deficiency,

hypotension, hypovolaemia
Beware cyanide toxicity as a side
Sodium Titrate an infusion at a rate effect hyperventilation
Nitroprusside of 0.5 to 1.5 mcg/kg/min arrhythmias, severe metabolic

(c) Management of haemopericardium in patients with AAD

In patients with haemopericardium it is imperative that pericardiocentesis is not

performed as a number of case series have demonstrated that rapid decompression of
the pericardium can restart fresh bleeding with rapidly fatal consequences (16,17,18) .

It is thought that the pressure gradient between the false lumen and the pericardial sac
is suddenly increased when pericardiocentesis is performed thereby causing sudden
and catastrophic bleeding into the pericardial sac.
 As a result of this case series and several case reports also highlighting this problem,
the Recommendations of the Task Force on Aortic Dissection also discourage
pericardiocentesis in this context(19).

(d) Definitive treatment

Type A

Patients with a type A dissection require urgent transfer for cardiothoracic surgery:
many patients die whilst waiting especially when an inter-hospital transfer is necessary.

Urgent surgery is required for type A dissections because they have the potential to
rupture into the pericardium with rapidly fatal consequences. Once a patient with a Type
A dissection survives to operation the subsequent in-patient mortality after surgery is
26%(2)

Type B

Patients with a type B dissection for whom open surgery is not indicated must be
assessed for the presence of complications of the dissection process. These are:

1. persistent intractable pain

2. a rapidly expanding aortic diameter
3. development of a periaortic or mediastinal haematoma
4. malperfusion of a branch vessel organs
5. malperfusion due to aortic lumen compression

A meta-analysis of endovascular stent-graft placements for type B AAD showed that the
procedure was successful in 95% of the patients selected for such treatment (13).

Depending upon the aetiology of the branch vessel occlusion either a stent placed in
the origin of the vessel or percutaneous balloon fenestration can be used to alleviate
pain or other complications.
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Prognosis & Followup strategies

1. Aortic tears occur most commonly in the ascending aorta; subsequent
haemopericardium is the leading cause of death from AAD.
2. The aorta may dissect along its entire length in only a few seconds and the
patient may be subsequently aymptomatic at the time of presentation to hospital.
3. An abrupt or sudden onset of thoracic pain occurs in 85% of patients with aortic
dissection.
4. The presence of an aortic diastolic murmur in the dyspnoeic patient must always
alert the physician to the possibility of aortic dissection.
5. Pulse deficits, including a significant difference in BP in both arms, only occurs in
20% of patients.
6. The 12 lead ECG is only completely normal in 30% of patients with more than
40% having ST segment or T wave changes.
7. Patients with proven or suspected aortic dissection who have a pericardial
effusion must not have pericardiocentesis performed even if cardiac tamponade is
present as this procedure may cause sudden death n this context (Grade C).
8. Hypertension in suspected or proven aortic dissection must be aggressively
treated with intravenous labetalol using invasive arterial monitoring to reduce the
progression of the dissection process (Grade D)The use of only a vasodilator or a -
blocker can accentuate the dissection.
9. Patients with a Type B dissection with complications should be considered for
endovascular intervention (Grade B).
10. Patients with Type A dissections for whom surgery is considered appropriate must
be transferred urgently.
11. There should be an agreement in place between individual hospitals and the
regional Cardiothoracic centre on which imaging modality is most appropriate to avoid
unnecessary delays.
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Safety pearls and Pitfalls

1. Pain is not adequately treated for fear that intravenous opiates may accentuate
hypotension
2. The unwary may change their initial diagnosis of aortic dissection because of a
lack of supporting physical signs, a normal mediastinum on CXR or ischaemic changes
on the ECG and as a consequence miss the diagnosis altogether.
3. Insufficient time given to obtaining the history, which is pivotal in making the
diagnosis.
4. Belief that a normal transthoracic echocardiogram excludes the diagnosis.
5. Lowering the threshold for making the diagnosis of aortic dissection because
there is no significant difference in the blood pressures between the arms.
6. Allowing the blood pressure to remain high whilst awaiting tests/transfer or
treating them with the wrong drugs eg just a vasodilator or only a -blocker.
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