AORTIC DISSECTION DIAGNOSIS AND MANAGEMENT

1. AORTIC DISSECTION
2015
SAMIR EL ANSARY

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3. Aortic dissection
An aortic dissection is a tearing of the layers
within the aortic wall, classically associated
with sudden-onset chest or back pain, a pulse
deficit, and mediastinal widening on a chest
radiograph.
Depending on size and degree of aortic
involvement, it may result in marked
hemodynamic instability and, often, a rapid
death.

4. Aortic dissection.
Prompt diagnosis and appropriate treatment
are critical to maximize the possibility of
survival.
Significant dissections are often fatal and
rarely survive to clinical attention; the majority
of dissections seen in the critical care
environment are either
Subacute, contained, or sparing the
major aortic vessels.

5. Anatomy of injury in aortic
dissection
The tear usually originates in the intima.
It then propagates into the media creating a
false channel for blood to flow and hematoma
to form.
The dissection process may alternatively
originate with hemorrhage
in the media that secondarily causes
disruption of the intima.

6. In approximately 70% of patients, the intimal
tear, which is the beginning of the dissection,
occurs in the ascending aorta.
In 20% of patients it occurs in the descending
thoracic aorta, and in 10% of patients it occurs
in the aortic arch.
Only rarely is an intimal tear identified in the
abdominal aorta.

7. DeBakey classifications of aortic
dissection
The two classification systems most
commonly used both have anatomic
as well as management
implications.

8. The DeBakey classification describes three
types of dissection :
Type I: extends from aortic root to beyond the
ascending aorta
Type 11: involves only the ascending aorta
Type Ill: Begins distal to the takeoff of the left
subclavian artery and has two subtypes
Type III A: limited to the thoracic aorta
Type 111 B: extends below the diaphragm

9. The Stanford classification has
two types of dissection
Type A: involves the ascending
aorta
Type B: involves the descending
aorta, distal to the left subclavian
artery

10. Approximately 75% of patients with ruptured
aortic aneurysm will reach an emergency
department alive.
Whereas for aortic dissection 40% die
immediately.
Furthermore, only 50% to 70% will be alive 5
years after surgery depending on age and
underlying cause.

11. For untreated acute dissection of the
ascending aorta the mortality rate is 1 % to 2%
per hour after onset.
For type A dissections treated medically it is
approximately 20% within the first 24 hours and
50% by 1 month after presentation.
Even with surgical intervention
the mortality rate for type A dissection may be
as high as 10% after 24 hours and nearly 20%
1 month after repair.

12. Although type B dissection is less dangerous
than type A, it is still associated with an
extremely high mortality.
The 30-day mortality rate for an uncomplicated
type B dissection approaches 10%.
However, patients with type B dissection who
have complications such as limb ischemia,
renal failure, or visceral ischemia have a 2-day
mortality upwards of 20% and may prompt the
need for surgical intervention.

13. AORTIC DISSECTION
Risk factors
.

14. Hypertension: Present in 70% to 90% of
patients with acute dissection.
Advanced age: Mean of 63 years in the
International Registry of Acute Aortic
Dissection (IRAD).
Male sex: Represented by 65% of patients in
the IRAD.
Family history: Recently recognized is a
genetic, nonsyndromic familial form of thoracic
aortic dissection.

15. Trauma (deceleration/torsional
injury) .
Congenital and inflammatory
disorders:
Present as Marfan syndrome in
almost 5% of total patients in the
IRAD and half of those patients under
age 40 years.

16. Other associated congenital disorders
include
Ehlers-Danlos syndrome, Loeys-Dietz
syndrome, bicuspid aortic valve, aortic
coarctation, Turner syndrome, Takayasu
and giant-cell aortitis, relapsing
polychondritis (Behcet disease,
spondyloarthropathies), or confirmed
genetic mutations known to predispose
.to dissections (TGFBRI, TGFBRP, FBNI,
ACTAP, or MYHI I ) .

17. Pregnancy
Associated with 50% of dissections in
women under age 40 and most
frequently occurring in the third
trimester.
This might be attributable to
elevations in cardiac output during
pregnancy that cause increased
wall stress.

18. Circadian and seasonal
variations
Producing a higher frequency of dissection
in the morning hours and in the winter
months.
Iatrogenic
Occurring as a consequence of invasive
procedures or surgery, especially when the
aorta has been entered or its main
branches have been cannulated, such as
for cardiopulmonary bypass.

19. The common clinical
signs and symptoms of
aortic dissection.

20. Pain
The most common presenting symptom is
chest pain, occurring in up to 90% of
patients with acute dissection.
Classically, for type A dissections, sudden
onset of severe anterior chest pain with
extension to the back occurs that is
described as ripping or tearing in nature.

21. The pain is usually of maximal intensity
from its inception and is frequently
unremitting.
It may migrate along the path of the
dissection.
The pain of aortic dissection may mimic
that of myocardial ischemia.
Patients with type B dissections are more
likely to be seen with back pain ( 64%)
alone.

22. Syncope
Syncope is a well-recognized clinical
feature of dissection, occurring in up to
13% of cases.
Impairments of cerebral blood flow can
be due to
Acute hypovolemia, low cardiac output,
or dissection-involvement of the cerebral
vessels.

23. Syncope
Patients with a presenting syncope were
significantly more likely to die than were
those without syncope (34% vs. 23%),
likely because of
the frequent correlation with associated
cardiac tamponade, stroke,
decreased consciousness, and
spinal cord ischemia.

24. The common clinical
findings associated with
aortic dissection.

25. Neurologic symptoms
17% of patients were seen initially with neurologic
symptoms, 53% of which represented
ischemic stroke.
Neurologic complications may result from
hypotension, malperfusion, distal thromboembolism,
or nerve compression.
Acute paraplegia as a result of spinal cord
malperfusion has been described as a primary
manifestation in 1% to 3% of patients.
Up to 50% of neurologic symptoms may be
transient.

26. Cardiovascular manifestations
The heart is the most frequently involved end-organ
in acute proximal aortic dissections.
Acute aortic regurgitation
may be present in 41 % to 76% of patients with
proximal dissection and may be caused by widening
of the aortic annulus resulting in incomplete valve
closure or actual disruption of the aortic valve
leaflets from the dissection flap.

27. Clinical manifestations of dissection-
related aortic regurgitation span from
mere diastolic murmurs without clinical
significance to overt congestive heart
failure and cardiogenic shock.

28. Myocardial ischemia or infarction
May result from compromised coronary artery flow
by an expanding false lumen that compresses the
proximal coronary or by extension of the dissection
flap into the coronary artery ostium.
This occurs in 7% to 19% of patients with proximal
aortic dissections.
Clinically, these present as electrocardiographic
changes consistent with primary myocardial
ischemia and/or infarction.

29. Cardiac tamponade is diagnosed in 8% to
10% of patients seen with acute type A
dissections.
It is associated with a high mortality and
should prompt consideration for emergent
drainage and aortic repair.
Hypertension occurs in greater than 50% of
patients with dissection, more commonly with
distal disease.
Ongoing renal ischemia can produce severe
hypertension.

30. Hypotension/shock may present in up to 20% of
patients with dissection.
This may be a result of cardiac tamponade from aortic
rupture into the pericardium, dissection, or
compression of the coronary arteries, acute aortic
regurgitation, acute blood loss, true lumen
compression by distended false lumen, or an intra-
abdominal catastrophe.
Cardiogenic shock
In approximately 6% of cases.
This can be due to acute aortic
regurgitation or ongoing myocardial
ischemia.

31. Peripheral vascular complications
Can manifest as pulse and/or blood pressure
differentials or deficits and occur in
approximately one third to one half of patients
with proximal dissection.
Etiology is partial compression, obstruction,
thrombosis, or embolism of
the aortic branch vessels, resulting in
cerebral, renal, visceral, or limb ischemia.
Peripheral pulse deficits should alert the clinician to
possible ongoing renal or visceral ischemia unable to
be detected from physical examination or laboratory
values alone.

32. Pulmonary complications
May manifest as pleural effusions, which
occur most frequently on the left.
Causes include rupture of the dissection
into the pleural space or weeping of fluid
from the aorta as an inflammatory
response to the dissection.

33. Laboratory abnormalities
associated with aortic dissection
Laboratory data are usually unrevealing, but
anemia from blood loss into the false lumen
can occur.
A moderate leukocytosis (10,000-14,000
white cells per mL) is sometimes seen.
Lactic acid dehydrogenase and bilirubin
levels may be elevated because of hemolysis
within the false lumen.

34. Laboratory abnormalities
associated with aortic dissection
Disseminated intravascular coagulation has
been reported.
Currently, randomized controlled data do not
support the use of D-dimers or experimental
serum markers (plasma smooth muscle
myosin heavy chain protein, high-sensitivity
C-reactive protein).

35. Imaging modalities
used to diagnose aortic
dissection
On the basis of clinical risk factors and
conditions, presentation, and associated
examination findings, patients are
stratified into
Low- intermediate- or high-
risk categories.

36. Further work-up is dictated by this pretest
probability index.
Some patients with acute dissection initially
have no high-risk features, creating a
diagnostic dilemma.
According to most recent guidelines, if a
clear alternative diagnosis is not established
after the initial evaluation, then obtaining a
diagnostic aortic imaging study should be
considered.

37. Although lacking specificity, a chest
radiograph should be obtained as part
of the initial diagnostic evaluation.
A radiograph abnormality is seen in up
to 90% of patients with aortic
dissection; most frequent is widening
of the aorta and mediastinum.

38. Other findings may include a localized hump on
the aortic arch, displacement of calcification in
the aortic knob, and pleural effusions.
However, approximately 40% of radiographs in
acute dissection lack a widened mediastinum,
and as many as 16% are normal.
Thus a negative radiograph must not delay
definitive aortic imaging in patients deemed at
high risk for aortic dissection by initial
screening.

39. Computed tomography (CT) scanning,
magnetic resonance imaging (MRI), and
Transesophageal
echocardiography (TEE)
Are all highly accurate imaging modalities that
may be used to make the diagnosis; all can
provide acceptable diagnostic accuracy.
Transthoracic echocardiography has
limited diagnostic accuracy.

40. Aortography
Which was once the test of choice, is no
longer used routinely because it is invasive and
time-consuming and involves exposure to
intravenous contrast dye.
The most recent comparative study with
nonhelical CT, MRI, and TEE showed 100%
sensitivity for all modalities, with better
specificity of CT (100%) as compared with TEE
or MRI.

41. A recent metaanalysis found that all three
imaging techniques provided equally
reliable results.
Although each imaging modality offers
advantages and disadvantages, the
choice among CT, MRI, and TEE is
probably best based on which is most
readily available.

42. It should be noted, however, that the diagnosis
of acute aortic dissection can be difficult and
occasionally cannot be absolutely excluded by
a single imaging study.
If a high clinical suspicion exists despite initially
negative imaging, then consideration should be
given to a second imaging modality.
Regardless, prompt surgical consultation
should be initiated in any patient with a
suspected dissection.

43. Regardless, prompt surgical
consultation should be
initiated in any patient with a
suspected dissection.

44. Diagnosis could be confused
with Aortic dissection
Acute myocardial infarction
Pulmonary embolism
Acute cholycystitis
Pleuritis
Pericarditis
Atherosclerotic emboli
Cerebrovascular accidents . .
Acute aortic regurgitation
Thoracic nondissecting aneurysm . .
Mediastinal cysts or tumors
Cholecystitis .
Musculoskeletal pain
Atherosclerotic emboli

45. Differentiate between the
management of Stanford type A
and type B dissections
An acute type A dissection is a surgical
emergency
However, medical management is critical to
halt the progression of the dissection while the
diagnostic work-up takes place and while
preparations are made to bring the patient to
the operating room for definitive treatment.

46. While the diagnosis work-up proceeds and a
cardiothoracic surgeon is consulted, the
patient's condition should be carefully
monitored and stabilized in an intensive care
unit.
Pain management and gradual down-titration of
blood pressure are critical to prevent extension
of the dissection.

47. Sufficient blood products and intravascular
access should be available in the event of
aortic rupture.
Patients with uncomplicated type B dissection
are preferably managed medically with p-
blockers and other antihypertensive agents.
Surgical intervention has no demonstrable
superiority except in cases of failed medical
management manifesting as malperfusion,
aortic expansion with potential for imminent
rupture, or intractable pain.

48. Ongoing advances with less
invasive interventions
(endovascular stent grafts and
endovascular fenestration
procedures) suggest an expanded
role for interventional management
in the treatment of acute type B
dissection, especially in experienced
centers.

49. The strategies for medical
management of dissection and
commonly used medications
The goals of medical therapy are to treat
pain, to aggressively control blood
pressure, and to determine need for
surgical or endovascular intervention.

50. Patients who are seen with hypotension
should receive the following:
Prompt but judicious volume resuscitation and
hemodynamic support with intravenous
vasopressors to maintain a goal mean
arterial pressure of 70 mm Hg .
Rapid search for underlying etiology
(tamponade, myocardial dysfunction, acute
hemorrhage)
Emergent surgical consultation for operative
management

51. In those who are seen initially with
hypertension, the blood pressure should
generally be lowered to a systolic of 100 to
120 mm Hg, to a mean of 60 to 65 mm Hg,
or to the lowest level that is compatible with
perfusion of the vital organs.
The aortic wall stress is affected by the
heart rate, blood pressure, and velocity of
ventricular contraction (dP/dt).

52. The ideal antihypertensive regimen must
decrease blood pressure
without increasing
cardiac output
through peripheral vasodilatation.
This is because an increased cardiac output
can increase flow rates producing higher
aortic wall stress and thus propagating the
dissection.

53. Intravenous p-blockers (commonly esmolol,
labetalol, propranolol, or metoprolol) are
considered the first-line medical stabilization
regimen because they affect all three parameters
without increases
in cardiac output and aortic wall stress.
In patients who are unable to tolerate B- blockade,
nondihydropyridine calcium channel antagonists
(verapamil, diltiazem) offer an acceptable
alternative.

54. Often, single-drug therapy alone is
inadequate to optimize blood pressure
management.
Adequate pain control is essential not only
for patient comfort but also to decrease
sympathetic mediated increases in heart rate
and blood pressure.
This may be accomplished with intravenous
opioid analgesics.

55. .
If p-blockade and adequate pain control
are ineffective to control blood pressure,
the addition of a rapidly acting, easily
titratable intravenous vasodilator, such
as
nitroprusside
should be considered.

56. Other agents, such as
Nicardipine, nitroglycerin, and
fenoldopam
are also acceptable.
Vasodilator therapy without prior p-blockade
may cause reflex tachycardia and increased
force of ventricular contraction leading to
greater wall stress and potentially causing
false lumen propagation; therefore adequate
p-blockade must be established first, before
the vasodilator is initiated.

57. The surgical approach for repair of Stanford
type A dissection.
The purpose of surgery is to resect the aortic
segment containing the proximal intimal tear, to
obliterate the false channel, and to restore aortic
continuity with a graft or by reapproximating the
transected ends of the aorta.
For patients with aortic insufficiency, it may be
possible to resuspend the aortic valve, but in
some cases replacement of the aortic valve is
necessary.
.

58. In some cases of proximal dissection,
reimplantation of the coronary arteries is
required.
If a DeBakey type II dissection is present,
the entire dissected aorta should be
replaced.
Surgery to repair an aortic dissection
generally requires cardiopulmonary bypass
and, often, deep hypothermic circulatory
arrest.

59. Recent alternatives to surgical repair of
aortic dissection
An endovascular technique of stent-grafting
and/or balloon fenestration may be used for
initial surgical treatment of some dissections.
Indications for open or endograft treatment are
based on the anatomic features of the lesion,
clinical presentation and course, patient
comorbidities, and anatomic constraints
related to endograft technology.

60. Dissections pose a complex situation because
the branches of the aorta may be perfused
from either the true or false lumen.
Often, both the true and false lumens are
patent and some of the visceral, renal, or lower
extremity vessels are fed by one channel and
the remainder by the other.
Consideration must be given to how blood flow
reaches vital organs before considering
treatment of a dissection with an endovascular
stent-graft.

61. For type B dissection, an increasing
number of reports show better results
with endovascular repair versus open
surgical repair.
The role of endovascular stent-graft
versus optimal medical therapy was
recently examined in the literature, but
no difference was noted in survival or
number of adverse events.

62. However, longer-term (5 year)
data are needed to fully assess
the potential impact of stent-
grafting for acute dissection,
including
Effects on survival, clinical
outcomes, and long-term
aortic remodeling.

63. The use of fenestrated endografts
A new era in the treatment of aortic
dissections.
Unsuitable anatomy is a significant barrier
to the use of endovascular stent-grafts for
most forms of aortic disease, where the
ostia of major vessels would otherwise be
partially or completed covered with the
deployment of a stent-graft.
.

64. The use of fenestrated endografts
Using preoperative
Three-dimensional CT aortic
reconstruction
customized stents can be constructed,
featuring holes (fenestrations) or side-
branches matched to patient-specific
anatomy to ensure perfusion to major
aortic branch vessels.

65. The use of fenestrated endografts
Current trials are underway in
Europe and the United States for
their use for
complex aneurysmal disease, and
expectations are high for similar
application to aortic dissection.

66. SAMIR EL ANSARY
ICU PROFESSOR
AIN SHAMS
CAIRO
elansarysamir@yahoo.com
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