An aortic dissection is a tear in the inner layer of the aorta that allows blood to flow between the layers of the aortic wall, creating a false passageway. It is a medical emergency that requires prompt diagnosis and treatment. Type A dissections, which involve the ascending aorta, require emergency surgery while type B dissections, involving only the descending aorta, are generally treated medically with blood pressure control. Surgical treatment of type A dissections aims to remove the damaged aortic segment and restore blood flow through the aorta using a graft.

1. AORTIC DISSECTION

2. 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. • Prompt diagnosis and appropriate treatment are
critical to maximize the possibility of survival.
• Significant dissections are often fatal and rarely
survive to clinical attention;
• 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

7. • In 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,
• in 10% of patients it occurs in the aortic arch.
• Only rarely is an intimal tear identified in the
abdominal aorta.

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

9. • 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

11. • 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

12. • 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.

13. • 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 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.

14. • 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%.
• 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

15. Risk factors

16. • 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

17. • 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

18. Other associated congenital disorders
• Ehlers-Danlos syndrome,
Loeys-Dietz syndrome,
• bicuspid aortic valve,
• aortic coarctation,
• Turner syndrome,
Takayasu and giant-cell aortitis, relapsing
polychondritis (Behcet disease,
spondyloarthropathies),

19. • confirmed genetic mutations known to
predispose to dissections
• (TGFBRI, TGFBRP, FBNI, ACTAP, or MYHI I ) .

20. • 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.

21. 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

22. • The common clinical signs and symptoms of
aortic dissection

23. 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

24. • 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.

25. 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.

26. • 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.

27. 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

28. 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
caused by widening of the aortic annulus
resulting in incomplete valve closure
• actual disruption of the aortic valve leaflets
from the dissection flap

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

31. 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.
• MI IS DANGEROUS FOR A PATIENT OF AORTIC
DISSECTION

32. • 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

33. • 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

34. • 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

36. 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

37. 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.

38. • 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)

39. 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

40. 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

41. • 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

42. • 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

45. • (CT), (MRI), and (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

50. 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

51. • A recent metaanalysis found that all three
imaging techniques provided equally reliable
results.

52. • 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.

53. 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 .

54. Differentiate between the
management of Stanford type A and
type B dissections
• An acute type A dissection is a surgical emergency
• medical management is critical to halt progression
of dissection while diagnostic work-up takes place

55. • Pain management
• gradual down-titration of blood pressure
• are critical to prevent extension of dissection

56. • blood products and intravascular access should be
available in event of aortic rupture.
• Patients with uncomplicated type B dissection are
preferably managed medically with B- 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

57. •
Ongoing advances with less invasive interventions
(endovascular stent grafts and endovascular
fenestration procedures) suggest an expanded role
for interventional management in treatment of
acute type B dissection, especially in experienced
centers.

58. 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,
to determine need for surgical or
endovascular intervention.

59. • 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

60. • 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,
• velocity of ventricular contraction .

61. • 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 dissection

62. • Intravenous B-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

63. • 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.

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

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

66. 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 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.

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

68. Recent alternatives to surgical repair o
• 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 anatomic features of the lesion,
clinical presentation and course, patient
comorbidities, and anatomic constraints
related to endograft technology

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

71. • For type B dissection, an increasing number of
reports show better results with endovascular
repair versus open surgical repair.

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

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

75. 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.

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