2. Case history
• Md.Rokibul hasan 38 years old hypertensive,smoker presented in ED
of NHFRI with severe centrtal chest pain with sweating for 1 day
• On examination:
• Pulse: 110b/min with radioradial delay;
• BP-190/110mm of Hg
• CVS & Lung NAD
• ECG : Sinus Tachycardia
• Clinical diagnosis:ACS
Anything else?????
5. What is dissection of aorta?
• Tear in the aortic intima that directly exposes an
underlying diseased medial layer to the driving
force (or pulse pressure) of intraluminal blood
• cleaves the media longitudinally
• thereby dissecting the aortic wall
• This aortic tear propagates anterogradely or less
common retrograde
6. Lumen
• The blood-filled space between the
dissected layers becomes the false lumen.
• Distention of the false lumen with blood
may cause the intimal flap to bow into the
true lumen and thereby narrow its caliber
and distort its shape
7. How Big Is The Problem?
• Incidence and prevalence uncertain.
• 5-30 cases per 1 million population per year.
• Available information: 2000 cases/year in U.S.
• Early mortality is as high as 5%per hour if untreated
• Male:Female= 3:1
• Descending dissections: 60-70 years old
• Ascending dissections: 50-59 years old
• (<40 years: Marfan, pregnancy, AV disease/Coarctation of Ao)
8. Classifications
• Acute: when diagnosis is made within 2 weeks of initial onset of
symptoms
• Chronic: >2 weeks of symptoms
• One third of patients fall into the chronic category
9. Classifications
DEBAKEY
• Type I
• Ascending aorta extending beyond arch
• Type II
• Ascending aorta only
• Type III a
• Descending aorta distal to left subclavian
(above diaphragm)
• Type III b
• Descending aorta distal to LSA extending
below diaphragm
• STANFORD
• A – Ascending aorta
• B – Not involving Ascending Aorta
10.
11. Location
-Most classic aortic dissections
begin at 3 distinct anatomic
locations:
• the aortic root
• 2 cm above the aortic root
• just distal to the left
subclavian artery.
12. Risk factor
• 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).
• Family history: Recently recognized is a genetic, nonsyndromic
familial form of thoracic aortic dissection
• Trauma (deceleration/torsional injury) .
13. • Congenital and inflammatory disorders:
• Present as Marfan syndrome in almost 5% of total patients and half of
those patients under age 40 years
• Other associated congenital disorders include
• Ehlers-Danlos syndrome, Loeys-Dietz syndrome, bicuspid aortic valve,
aortic coarctation, Turner syndrome, Takayasu and giant-cell aortitis,
relapsing polychondritis (Behcet disease,spondyloarthropathies)
14. Pregnancy
• Associated with 50% of dissections in women under age 40
• most frequently occurring in the third trimester.
• This might be attributable to
• elevations in cardiac output during
pregnancy that cause increased wall stress
15. • 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
16. Natural history
• Mortality Rates (if untreated)
– 5% per hour
– 25% die within 24 hr
– 50% die within a week
– 90% within a year
17. Death usually caused
by
-Cardiac tamponade with
type A dissection
– Acute aortic
regurgitation
– Major branch vessel
obstruction
– Aortic Rupture ( into
pericardium, L pleural
cavity, or mediastinum)
19. Aortic Dissection – Pulse Loss
• 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
20. Other menifestation
• Myocardial ischemia or infarction
• by an expanding false lumen that compresses the proximal coronary
or by extension of the dissection flap into the coronary artery ostium
• Cardiac tamponade is diagnosed in 8% to 10% of patients seen with
acute type A dissections
• Cardiogenic shock
• In approximately 6% of cases
21. • Syncope
• Syncope is a well-recognized clinical feature of dissection, occurring in up
to 13% of cases.
• Neurological symptom
• 17% of patients were seen initially with neurologic symptoms, 53% of
which represented ischemic stroke.
22. • Acute paraplegia in 1% to 3% of patients
• Up to 50% of neurologic symptoms may be transient.
• Aortic Regurgitation:
• AR in 18-50% cases
• Diastolic murmur reported in 25% pts.
• 3 possible mechanisms for acute AR in dissection
23. B. Dilatation of
aortic root
C.Pressure from D. Intimal flap prolapse
dissecting hematoma
may depress one
leaflet
24. Clues to Proximal Dissection
• Substernal chest pain
• Neck, jaw, throat or face pain
• Aortic Insufficiency
• Decreased pulse or BP in Rt arm
• Pulse abnormalities are seen in 50% of proximal dissections
• ECG changes
• Marfans Syndrome
• Hypotension
• Syncope – 12%
• CVA – 5-10%
25. Clues to Distal Dissection
• Interscapular pain
• HTN less commonly associated about 35%
• Left Pleural effusion
• Pulse defecits are less frequent about 15%
• Usually involve femoral or left subclavian
• Spinal Cord Ischemia (10%)
– Transverse Myelitis
– Paraplegia
– Quadriplegia
27. Investigation
• GOALS
Confirm the diagnosis
Classify the dissection and determine extent
Detect pericardial involvement
Detect and grade AI
• CHOICES
CXR
TTE/TEE
CT
MRI
Aortography
28. ECG
• ECG: 1/3 exhibit LVH
• ECG is important to rule out any ischemic changes or MI which would
lead to an alternate diagnosis
• ECG may display infarction
• ECG – usually shows nonspecific ST-T wave changes.
29. CHEST X-RAY
1. widened mediastinum, (seen: 44-80%)
2. Calcium sign -Displaced intimal calcification (>10mm) from outer
aortic wall– useful in older patients
3.pleural effusion (involvement of descending aorta)
4.Normal
30. Mediastinal widening is the most
common plain radiographic finding
in aortic dissection; it is noted in
80% of patients
Inward displacement of aortic wall calcification
by more than 10 mm
31. TTE
• Indicated as an initial test if patient is very unwell and other
modalities of imaging not readily available
• Can be performed bedside
• Can detect intimal flap and AR
• Limitation: No information beyond aortic root
and early part of proximal aorta
32.
33. TEE
• Procedure of first choice for dissection, if readily available
• High sensitivity (98%) and specificity(97%)
• Limitations : Unable to visualize distal part of asc. Aorta (beginning of
aortic arch) and desc. Aorta below stomach
36. CT SCAN WITH CONTRAST
• Sensitivity 98-100% Specificity 98-100%
• Typical CT findings in acute dissection include :
-Detection of intimal flap which separates two lumen
Limitations:
• Use of contrast
• Inability to identify site of tear
• No evaluation of aortic regurgitation
• Limited information on branch vessels
Useful for follow-up of dissections
37.
38.
39. MRI
• Gold Standard for Diagnosis
■ Sensitivity and Specificity of 98-100%
■ Disadvantages:
– Limited Availability
– Relatively CI in unstable patients.
– CI:
• Pacemakers
• Certain types of vascular clips
• Older metallic heart valves
40.
41. AORTOGRAPHY
• Considered Gold standard in olden days
Sensitivity (88%) Specificity (94%)
Identify intimal flap, true and false lumen
Aortic insufficiency, branch vessel involvement
• Limitations
• Invasive
• Use of contrast
• Time delay in preparation
43. MANAGEMENT
• Therapy is targeted at halting the progression of the dissection
• Goal:
– Reduction of SBP (100-120)
– Dimunition of dp/dt (reflects force of LV ejection) through use of a
beta blocker.
– HR around 60
- Control of pain
44. • The ideal antihypertensive regimen must decrease blood pressure
without increasing cardiac output through peripheral vasodilatation
• Intravenous b-blockers (commonly esmolol,labetalol, propranolol, or metoprolol)
are considered the first-line medical stabilization regimen because they affect all
three parameters
• In patients who are unable to tolerate B- blockade,nondihydropyridine calcium
channel antagonists (verapamil, diltiazem) offer an acceptable alternative.
45. • If b-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
• Other agents, such as Nicardipine, nitroglycerin, and fenoldopam are
also acceptable
46. Other Considerations
• Hypotension must ensure if its true or false
• Fluids first then use norepinephrine or phenylephrine
• Dopamine & epinephrin should be avoided since it can raise dP/dT unless
used at low doses for renal perfusion
• Cardiac Tamponade: Pericardiocentesis may be harmful
• Pericardiocentesis in AD only if marked hypotension, and aspirate only
enough pericardial fluid to raise BP
47. INDICATIONS FOR SURGERY
• Stanford type A (DeBakey type I and II) ascending aortic dissection
• Complicated Stanford type B (DeBakey type III)aortic dissections with
clinical or radiological evidence of the following conditions:
• Propagation (increasing aortic diameter)
• Increasing size of hematoma
• Compromise of major branches of the aorta
• Impending rupture
48. Sugery
• Objectives of surgery are to remove the most severely damaged
segments of the aorta and to obliterate the false lumen by suturing
the most proximal segment
• Surgery with AR: Bentall procedure
• Percutanous EVAR for typeB AD: potentially effective
• Long Term Outcome: who survive their hospital stay is:
– 65-80% at 5 years
– 50% at 10 years
49.
50. Follow-up
• CT/MRI at 1,3,6 & 12 month,then yearly
• Long term aggressive control of BP,heart rate,lipid profile & smoking
cessation indicated
51. Surgery
• In 2019,Total 11 surgery done for Aortic dissection of which 3 are
acute & 8 are chronic in NHFRI
53. TAKE HOME MESSAGE
• High clinical suspicion. Should consider as a
differential diagnosis with all chest pain.
• Examine Pulse in all ACS pt
• Thrombolytic ,Anticoagulants and anti platelet therapy may be
catastrophic.
• Refer to appropriate center
• Early diagnosis + prompt action = SURVIVAL