Aneurysm Pathology Brief summary

1. Blood Vessels
ANEURSYM

2. • PA 27.2: Describe the etiology, dynamics, pathology
types and complications of aneurysms including
aortic aneurysms
• SPECIFIC LEARNING OBJECTIVES:
• Define aneurysm, classify it based on anatomical and
macroscopic features with help of an illustration
• Discuss pathogenesis of aneurysms with special
reference to Abdominal Aortic Aneursyms,its
morphological variants and clinical complications
• Explain the Aortic Dissections types and its outcome

3. Aneurysms are
congenital or
acquired dilations
of blood vessels or
the heart
It can be
• Congenital
• acquired.

4. pseudo-aneurysm
A false aneurysm results when a wall
defect leads to the formation of an
extravascular hematoma that
communicates with the intravascular
space (“pulsating hematoma”)
a leak at the suture site of a
vascular graft with a natural
artery may also be a cause

5. True Aneurysm
True aneurysm involves an intact
attenuated arterial wall or thinned
ventricular wall of the heart
Predisposing Factors
Aortic Aneurysms:
Atherosclerosis (AS)(abdominal)
Hypertension (HT) (ascending aorta)
Tertiary syphilis (now rare) (ascending
aorta)
Ventricular – Post Transmural MI
Other conditions include
trauma, vasculitis,
congenital defects (Berry)
infections (mycotic)

6. Types of Aneurysms
Saccular aneurysms:
Eccentric spherical
outpouchings; 5 to 20 cm in
diameter & often contain
thrombus.
Fusiform aneurysms:
diffuse, circumferential
dilation of a long segment;
vary in diameter (up to 20
cm) & length, involve the
aortic arch, abdominal aorta,
or the iliac arteries.

7. Pathogenesis
 Inadequate or abnormal connective
tissue synthesis.
 Excessive connective tissue degradation.
 loss of smooth muscle/inappropriate
synthesis of ECM.

8. Inadequate or abnormal connective
tissue synthesis.
• Marfan syndrome: defective
fibrillin synthesis leads to elastic
tissue weakening
• Loeys-Dietz syndrome: mutations
in TGF-β receptors in fibroblasts
lead to abnormalities in elastin &
collagen I/III formation.
• Ehlers- Danlos syndrome: Weak
vessel walls due to defective type III
collagen synthesis
• vitamin C deficiency altered
collagen cross-linking
PATHOGENESIS

9. Excessive connective tissue degradation.
• By inflammatory infiltrates & increased ^ MMP
production, by macrophages in atherosclerotic plaque or in
vasculitis.
• Decreased tissue inhibitor of metalloproteinase (TIMP)
expression can contribute to the ECM degradation.
• Genetic predisposition to aneurysm formation -
polymorphisms of MMP &/or TIMP genes are noted.
Adventitial inflammatory
infiltrate and thickening of
the vasa-vasorum (HE
staining)

10. Weakened vascular wall due to loss of smooth
muscle/inappropriate synthesis of ECM.
Ischemia due to atherosclerosis (the inner
media blood supply is compromised) or
hypertension (outermedia vaso-
vasorum) leads to smooth muscle cell
loss (ischemia) & “degenerative
changes,” (fibrosis, loss of elastic
fibres, inadequate ECM synthesis,
and production of excessive amorphous
ground substance - glycosaminoglycan)
• Histologically these nonspecific
changes are collectively called cystic
medial degeneration (also seen in
Marfan disease and scurvy)

11. ABDOMINAL AORTIC
ANEURYSM
• Atherosclerosis (1st) is a major
cause.
• More frequently in men and
smokers, and rare before 50 years
of age
• Usually positioned below the renal
arteries and above the bifurcation of
the aorta, can be saccular or
fusiform,
– Inflammatory (2) AAAs
• Mycotic AAAs (3) occur when
circulating microorganisms (as in
bacteremia from a Salmonella
gastroenteritis) seed the aneurysm wall
or the associated thrombus;
up to 15 cm in diameter, and up
to 25 cm in length
frequently contains a bland, laminated,
mural thrombus

12. The Clinical Consequences Of AAA
• Rupture into the peritoneal cavity or retroperitoneal
tissues with massive, potentially fatal haemorrhage
• Obstruction of a branch vessel resulting in ischemic
injury of downstream tissues: iliac (leg), renal,
mesenteric (GIT) or vertebral arteries
• Embolism from atheroma or mural thrombus
• Compression of an adjacent structure, e.g., of a
ureter or erosion of vertebrae
• Simulates an abdominal tumor (often pulsating)

13. Thoracic Aortic
Aneurysms
• Most commonly with hypertension,
Marfan, Loeys -Dietz syndromes
• Signs & symptoms referable to
encroachment
– on mediastinal structures,
– On lungs & airways with
respiratory difficulties
– On oesophagus with difficulty in
swallowing
– On recurrent laryngeal nerve with
persistent cough
– On ribs and vertebrae with erosion
& bone pain
• Aortic valve dilation (syphilitic) with
valvular insufficiency or narrowing of
the coronary ostia leads to MI

14. Arterial
dissection
• Occurs when blood enters
the arterial wall itself, as a
hematoma dissecting
between its layers.
Dissections are often but
not always aneurysmal.
• Dissections can rupture,
often with catastrophic
consequences.

15. Aortic Dissection
Occurs principally in two groups:
• men aged 40 to 60, with antecedent hypertension
(more than 90% of cases of dissection);
• younger patients with connective tissue abnormalities
of affecting the aorta (Marfan’s)
Iatrogenic: complicating arterial cannulations during
catheterization or cardiopulmonary bypass
Rarely, for unknown reasons, during or after pregnancy.

16. Aortic Dissection
• starts with an intimal tear.
• In majority of cases the tear
is in the ascending aorta,
usually within 10 cm of
the aortic valve, transverse
or oblique, 1 to 5 cm in
length.
• The dissecting hematoma
spreads usually between
the middle & outer thirds of
laminar planes

17. Aortic Dissection
Proximal lesions (type A
dissections) (More common
and dangerous), involving
the ascending aorta with or
without descending aorta
(types I and II of the
DeBakey)
Distal lesions beginning
distal to the subclavian
artery (type B dissections or
DeBakey type III)

18. Symptoms & Outcome of Aortic
Dissection
• Sudden onset of excruciating pain, mimicking MI
• The most common cause of death is rupture of the
dissection outward into the pericardial (cardiac
tamponade), pleural, or peritoneal cavities.
• Rapid diagnosis and institution of intensive
antihypertensive therapy, coupled with surgical
procedures involving plication of the aortic wall, permit
65% to 75% survival