Aneurysms& Dissections
Dr. Ashraf Abdelfatah Deyab
Assistant Professor of Pathology
Majmaah University- Collage of Medicine
Aneurysm & Dissection
objectives
Aneurysms: define, classify& causes.
 Etiology, pathogenesis, morphology and clinical
course of Aortic
aneurysm.
 Discuss etiology, pathogenesis, morphology and
clinical course of syphilitic
aneurysm.
 Etiology, pathogenesis, morphology and clinical course
of aortic
dissection.
 Suggested Ref: Robbins Basic Pathology 8th edition 357 – 362
Aneurysms- definition
 Vascular disorder chr. By localized abnormal
permanent “blood-filled” dilations of blood
vessels and the Heart.

Result due to weakening of the vessel wall, with
extension to all three wall layers (intima, media, and
adventitia)..

Site: small, medium, large BV+HRT

Have the tendency to rupture. “inevitable”.

Male : female ratio (5:1).

Age group > 5th decade

Why it’s important?? leading cause of death in all over
the world, esp. developed and western•3societies.
Aneurysm classification
 Aneurysms are classified by:

Location ( e.g AAA, brain, kidney).

Etiology (congenital: MS, EDS or Acquired: e.g.
mycotic, syphilitic, atherosclerotic aneurysm).

Shape\morphology:
- Shape :(e.g. fusiform, saccular, Cylindrical)
- Integrity of vascular wall: (True or False aneurysms)
Aneurysms- based on morphology
 A true aneurysm
 is dilatation without tear, due to weakness that involves all 3
layers of the vascular wall (intima, media & adventitia), e.g.
Atherosclerotic, syphilitic , and congenital A.
, ventricular aneurysms
 A false aneurysm, or pseudo-aneurysm,
characterized by peri-vascular hematoma\
thrombus, after intimal& medial tear, surrounded by
fibrous tissue - this enough to seal the leak.
II. False Aneurysms classification
•An. varix
 The following are the types of false aneurysms:
(1) Pulsating Haematoma (Simple False
Aneurysm)
(2) Arterio-venous Fistula- Caused by traumatic
injury to an artery, and adjacent vein. The injury
results in either Aneurysmal varix, Varicose
aneurysm
•Simple false A.
•Varicose A
Aneurysm- etiology
1) Atherosclerosis& HTN: due to DM or smoking,
persistent mechanical force>> lead to wall
weakness&media degeneration , (AAA, Capillary
micro-aneurysm), organ involved; Aorta Brain&
retina.
2) Infections& Mycotic aneurysm: bacterial sepsis&
IE, sites: Brain, abdomen ,neck ,leg &arm.
*
a) Syphilitic Aortitis (third stage)- ascending& arch
of aorta, obliterative endarteritis of the vasa
vasorum.
b) Mycosis in immune-deficient patients.
Aneurysm classification-based on etiology
3) Congenital weakness of the media: Causes
congenital cerebral aneurysms. Berry A. occurs in
the circle of Willis; rupture of one arteries and lead
to subarachnoid - hemorrhages
4) Trauma: Causes false aneurysms.
5) Immunologically mediated aneurysms (e.g.,
in polyarteritis nodosa).
6) Copper Deficiency. Rare cases of aneurysms=
lead to a decreased activity of the lysyl
oxidase enzyme, affecting intergrity of elastin fibers.
Aneurysm & Dissection
objectives
Aneurysms: define, classify& causes.
 Etiology, pathogenesis, morphology and clinical
course of Aortic
aneurysm.
 Discuss etiology, pathogenesis, morphology and
clinical course of syphilitic
aneurysm.
 Etiology, pathogenesis, morphology and clinical course
of aortic
dissection.
 Suggested Ref: Robbins Basic Pathology 8th edition 357 – 362
Aortic Aneurysm introduction
 It is a localized abnormal ballooning dilatation
exceeding normal diameter The symptoms & severity measures based on size (close
follow-up& intervention)

We going to address two important clinical
condition based on Etiological factors:
1) Abdominal aortic aneurysm- AAA
Atherosclerosis (infra- with a few para- and supra-renal)
or other congenital factor.\ commonest.
2) Syphilitic aneurysm: T.pallidum Infection.
Abdominal aortic aneurysms (AAA)

Mainly occur as one of complications of atherosclerosis

Usually located below the renal artery orifices
proximal to bifurcation
 Frequently in men > 50 yrs & heavy smokers.
 The risk to rupture is directly related to the size,
Most expand at a rate of 0.2 to 0.3 cm/yr, but 20%
expand more rapidly.
 Endoluminal approaches using stent grafts
as replacement of surgical bypass.
•11
AAA pathogenesis
 1) Atherosclerotic plaque in the intima: Compression
of the media lead to compromises nutrient and waste diffusion.
 2) Then media become degenerated& necrotic
>>>> that results in arterial wall weakness and
consequent thinning.
 3) The degradation of tunica media by means of
proteolytic process& exposure of ECM>>> lead to
elimination of elastin
 4) Reduced perfusion& nutrition of vasa vasorum in
the AA >>>- damage of the tunica media.
 5) Familial factors & structural defects in connective tissue
AAA morphology
 Usually below renal& above bifurcation.
 Saccular or fusiform, up to 15 cm diameter up
to 25 cm in length.
 Intimal surface showed severe complicated atherosclerosis
with thinning of the underlying.
 laminated, poorly organized mural thrombus
 Renal, superior or inferior mesenteric arteries:
AA producing direct pressure or by narrowing or
occluding vessel ostia with mural thrombi
 Rupture as main complications
AAA morphology-VARIANTS
 AAA-two variants:
 1) Inflammatory Aortic Aneurysm: (uncertain cause)
dense periaortic fibrosis containing abundant
lymphoplasmacytic inflammation with many
macrophages and often giant cells
 2) Mycotic Aortic Aneurysm: infected by the lodging
of circulating microorganisms in the wall, particularly in
bacteremia from a primary Salmonella gastroenteritisdestroys the media-thinning.
 Diagnosis: Abdominal ultrasound is the gold
standard test.
Syphilitic aneurysm: Etiology& Pathogenesis
 Syphilis is chronic venereal dis. caused by
T.pallidum infection- (microaerophilic Spirochetes\ easy to
be visualized by silver stain, IF)- lead to multi-system disorders.
 Chr. by outer covering membrane called an outer sheath, which
may mask bacterial antigens from the host immune response
. Typically affect those age below 50 years old.
 Sexual contact is usual mode of spread + vertical spread.
 Affect the HRT& aorta in late stages (tertiary syphilis)
 Commonest site affected is the vasa vasorum of the
ascending and transverse portions of aortic arch.
•15
Syphilitic aneurysm: Etiology& Pathogenesis
______________________________________

Pathogenesis of syphilitic Aneurysm:
 1) Aortitis is caused by endarteritis of the vasa
vasorum (endarteritis obliterans) of the proximal aorta.
 2) This result in occlusion of the vasa vasorum.
 3) Results in Ischemia& scarring of the media of the
proximal aortic wall, causing a loss of elasticity>>>>>
 Morphological changes: chr. plasma cell infiltrate in
vessel wall with  focal necrosis and scarring of
media  diffuse Dilatation of the aorta and aortic
valve ring.. Also roughened intimal surface imparts a
“tree bark” appearance.
•16
AAA- Clinical course& consequences
1. Either asymptomatic or symptomatic based on size
2. Presentation as an abdominal mass with
pressure – pain + erosion+ fistula formation.
3. Rupture- abdominal or pericardial hemorrhage- shock
4. Impingement on adjacent structures
5. Occlusion of proximate vessel
6. Embolism from mural thrombosis
Mortality is high 60% to 90%
•17
Aneurysm & Dissection
objectives
Aneurysms: define, classify& causes.
 Etiology, pathogenesis, morphology and clinical
course of Aortic
aneurysm.
 Discuss etiology, pathogenesis, morphology and
clinical course of syphilitic
aneurysm.
 Etiology, pathogenesis, morphology and clinical course
of aortic
dissection.
 Suggested Ref: Robbins Basic Pathology 8th edition 357 – 362
Aortic dissection-introduction
Aortic dissection is medical emergency, previously
called dissecting “aortic” aneurysm, associated with (HTN,
AA, Marfan’s syndrome)
Dissecting aneurysm occurs when blood splays apart
the laminar planes of the media to form a blood-filled
channel, under high forceful pressure with obvious
perforation of the intima, (intra-mural hematoma).
 The word dissecting mean hematoma dissecting between
the intima and the media or the media and the adventitia
or through the layers of the media.
Dissecting aneurysm : may or may not associate with
dilatation.(not similar to athersclerotic& syphilitic aneurysms)
Aortic dissection- Risk group
(1)Adult aged 40 to 60, with antecedent HTN (>
90% of cases of dissection.
(2) Younger patients with systemic or localized
abnormalities of connective tissue affecting the aorta
(e.g., Marfan syndrome).
3) Iatrogenic causes, after cardiac cathetrization.
4) Rare –of unknown etiology– after pregnancy.
Key note: Dissection is unusual in the presence of
atherosclerosis or syphilis, because of the medial
scarring, fibrosis - inhibits propagation of the dissection.
Aortic dissection- causes
 Hypertension- major risk factor.
 Connective tissue diseases
 Chest trauma.
 Vasculitis (rare).
Aortic dissection- pathogenesis
1) Pressure-related mechanical injury: Aortas of hypertensive
pt. have medial hypertrophy of the vasa vasorum with
degenerative changes with loss of smooth muscle of
Aortic media. ( (due to diminished flow through the Vasa
Vasorum).
2) Inherited (congenital) connective tissue abnormlity
causes e.g Marfan syndrome (defect in elastic tissuefibrillin), Ehlers-Danlos syndrome (collagen defect).
3) Acquired connective tissue abnormality of vascular ECM
due to (e.g, vitamin C deficiency, copper metabolic
defects).+\- Ageing.
4) Large groups of A. dissection remain unknown.
Aortic dissection- morphology
1) Site: common portion (The ascending aorta), usually
within 10 cm of the aortic valve.
2) cystic medial degeneration: most frequent
preexisting histologically is. and is characterised by
mucoid degeneration and elastic fibres fragmentation
3) Intimal tear with typically transverse or oblique and
1 to 5 cm in length, with sharp, jagged edges, not
going retrograde towards the heart.
4) No significant inflammation or atheroma.
5) Hematomas “Thrombus”,\ Double-barreled aorta, formed
by second Intimal tear filled with hematoma, creating a new
vascular channel “” = false channel, which with time
endothelialized (become chronic dissection )
Cystic
•Histologic
Medial view of the
•Normal
dissection:
media
degeneration
An aortic intramural hematoma
•24
Aortic dissection- clinical findings:
 Acute onset of severe sudden onset retrosternal pain
radiating to the back. Pain described as tearing. (severity
depend on the site- the most serious is Aortic arch dissec.)
 Aortic insufficiency, and myocardial infarction.
 AV regurgitation: aortic valve ring dilatation; Echo-findings.
 Compression symptoms & signs: subclavian artery> loss of
upper extremity pulse& spinal arteries> cause transverse
myeliti, renal and mesenteric arteries pressure .
 Rupture: usually into the pericardial sac (tamponade most
common cause of death), pleural or peritoneal cavities.
 Diagnosis:
 Increased aortic diameter on chest X ray, CT-angiography,
U\S.
•25
Clinical classification of Aorta dissections
Dr. Michael DeBakey (vascular surgeon)
DeBakey type I =
Type A (proximal)
Ascending & Descending aorta,
with extensive aorta dissection
DeBakey type II =
Type A (proximal)
involves Ascending aorta, in
isolation.
DeBakey type III =
Type B (distal (
dissections arise beyond the
take off of the great vessels
(distal to subclavian)
-.
DeBkey’s Classification of dissections
Type I
Type II
Type III
Aortic Dissection- management
 the mortality is at least 50% at 48 hours,
and 90% within 1 week.
 I. Reducing blood pressure: immediate
aim to control the propagating hematoma
by reducing
 II. Surgical repair (plication of aorta wall) is
feasible if the process affects the proximal
aorta.
NB: However thrombosis with organization and
fibrosis may be regarded as a cure.
•The end
Aneurysm pathogenesis
Aneurysms- Pathogenesis-1
 Arteries are dynamically remodeling
tissues.
 weakening of vessel walls due to inherited
defects in connective tissues, is important
in the common, sporadic forms.
 The intrinsic quality of the vascular wall
connective tissue is poor, e.g. in Marfan
syndrome, due to defective synthesis of
scaffolding protein fibrillin which lead–
weakening of elastic fibers.
Cystic medial degeneration- cross-section of aortic media
from a patient with Marfan syndrome showing marked
elastic fragmentation (A), comparison to normal media (A)
Aneurysm – Pathogenesis-2
 The balance of collagen degradation and
synthesis is altered by local inflammatory
infiltrates and the destructive proteolytic
enzymes they produce, such as in
atherosclerosis.
 The vascular wall is weakened through loss
of smooth muscle cells or the inappropriate
synthesis of non-collagenous or non-elastic
ECM, e.g. thickening of the intima+ medial
ischemia of aorta in (atherosclerotic&HTN)
Aneurysm morphology
Aneurysms –Morphology-1
 The intimal surface of the aneurysm
shows severe atherosclerosis with
destruction of the media.
 The aneurysm –contains poorly organized
mural thrombus.
 The aneurysm can affect the renal and
superior or inferior mesenteric arteries,
either by producing direct pressure or by
narrowing or occluding vessel ostia with
mural thrombi.
Aneurysms –Morphology-2
 Tow general variants:
 Chronic Inflammation: dense periaortic
fibrosis, abundant lymphoplasmacytic
inflammation with many macrophages and
often giant cells.
 Infection – bacterial infection with
suppuration - destroys the media, lead to
rapid dilation and rupture.
Aneurysm clinical features
Aneurysms-Clinical features-1
 Pressure symptoms& signs:
Impingement
on an adjacent structure, e.g., compression of a
ureter or erosion of vertebrae..
 Rupture into the peritoneal cavity or
retroperitoneal tissues with massive,
potentially fatal hemorrhage
 Obstruction of a branch vessel resulting in
ischemic injury of downstream tissues,
iliac (leg), renal (kidney), mesenteric (GIT),
or vertebral (spinal cord) arteries
Aneurysms-Clinical features-2
 Thrombo-embolism from Atheroma or
mural thrombus.
 Presentation as an abdominal mass (often
palpably pulsating) that simulates a tumor
Complications of Aneurysms:
(1) Pressure atrophy on the surroundings.
(2) Spontaneous rupture - hemorrhagic shock will
dominate the clinical picture: Acute risk to
cerebral function (intra-craniazl&, subarachanoid)+
Acute pericardial tamponade
(3) Thrombosis with ischaemic effects.
4) Emboli to distal vessels.
5) Dissection, serious complications predominantly occur
in the region from the aortic valve through the arch with
no underlying atherosclerosis
Aneurysm & Dissection
objectives
Aneurysms: definition & classification.
 Pathogenesis, morphology and clinical
course of abdominal aortic aneurysm.
 Pathogenesis, morphology and clinical
course of aortic dissection.
Robbins Basic Pathology, 8th ed. p. 357 – 362
.
Aneurysm & Dissection
objectives
Aneurysms: definition & classification.
 Pathogenesis, morphology and clinical
course of abdominal aortic aneurysm.
 Pathogenesis, morphology and clinical
course of aortic dissection.
Robbins Basic Pathology, 8th ed. p. 357 – 362
.
Abdominal aortic Aneurysm
AAA