Aneurysms

1. ANEURYSMS

2. Learning Objectives
• Definition
• Classification
• Pathology
• Complication

3. Definition
• Localized abnormal dilation of blood vessel or heart due to
blood vessel wall stress.
• Weak spot on a blood vessel wall that causes an outward
bulging, likened to a bubble or balloon
• Congenital or acquired.
• Nidus for thrombosis and embolization.
• Increase in size Risk of rupture Uncontrolled bleeding
• Arises in the heart following a myocardial infarction.

4. Definition

5. Classification
A. Depending upon composition of the wall

6. Classification
A. Depending upon composition of the wall
Trauma to vessel wall

7. Classification

8. Classification
1. Saccular having large spherical outpouching.
2. Fusiform having slow spindle-shaped dilatation.
3. Cylindrical with a continuous parallel dilatation.
4. Serpentine or varicose which has tortuous dilatation of
the vessel.
5. Racemose or circoid having mass of
intercommunicating small arteries and veins.
B. Depending upon shape :

9. Classification

10. Classification
Lateral left carotid arteriogram shows an
irregular channel of the giant serpentine
aneurysm
Cirsoid aneurysm in the right occipital and
post-auricular regions in a 19 year old
male patient

11. Classification
C. Depending upon location
A. Arterial and venous, with arterial being more common.
B. Capillaries, specifically capillary aneurysms.
C. The heart, including coronary artery aneurysms,
ventricular aneurysms, aneurysm of sinus of Valsalva,
and aneurysms following cardiac surgery.
D. The aorta, namely aortic aneurysms including thoracic
aortic aneurysms and abdominal aortic aneurysms.
E. The brain, including cerebral aneurysms, berry
aneurysms, and Charcot–Bouchard aneurysms.
F. The legs, including the popliteal arteries.[citation
needed]
G. The kidney, including renal artery aneurysm and
intraparechymal aneurysms.

12. Classification
D. Depending upon pathogenetic mechanisms :
1. Atherosclerotic (arteriosclerotic) aneurysms are the
most common type.
2. Syphilitic (luetic) aneurysms found in the tertiary stage
of the syphilis.
3. Dissecting aneurysms (Dissecting haematoma) in
which the blood enters the separated or dissected wall
of the vessel.
4. Mycotic aneurysms resulting from weakening of the
arterial wall by microbial infection.
5. Berry aneurysms which are small dilatations especially
affecting the circle of Willis in the base of the brain.

13. Pathology
Etiology
• Atherosclerosis especially in aortic aneurysms
• Hypertension especially in ascending aortic aneurysms
• Trauma
• Vasculitis
• Congenital defects
– Fibromuscular dysplasia
– Berry aneurysms typically in the circle of willis
• Infections -
– Syphilic aneurysms
– Mycotic aneurysms
– From embolization of a septic embolus - complication of infective endocarditis
– As an extension of an adjacent suppurative process
– By circulating organisms directly infecting the arterial wall.

14. Pathology
• Occur when structure or function of the connective tissue
within the vascular wall is compromised.
• Poor intrinsic quality of the vascular wall connective
tissue.
• Imbalance in vascular wall collagen degradation and
synthesis caused by inflammation and associated
proteases.
• Weakening of vascular wall due to
– loss of smooth muscle cells
– synthesis of non-collagenous /non-elastic extracellular matrix.

15. Pathology
 Poor intrinsic quality of the vascular wall connective tissue
– defective synthesis of fibrillin leads to aberrant TGF-β activity and
weakening of elastic tissue in the aorta, this may result in progressive
dilation in Marfan syndrome.
– mutations in TGF-β receptors lead to defective synthesis of elastin
and collagens I and II in Loeys-Dietz syndrome.
– Weak vessel walls due to defective type III collagen synthesis are
also a hallmark of the vascular forms of Ehlers-Danlos syndrome.
– altered collagen cross-linking associated with Vitamin C deficiency
(scurvy)

16. Pathology
Imbalance in vascular wall collagen degradation & synthesis
• Increased matrix metalloprotease (MMP) expression,
especially by macrophages in atherosclerotic plaque or in
vasculitis degrade virtually all components of the extracellular
matrix in the arterial wall (collagens, elastin, proteoglycans,
laminin, fibronectin).
• Decreased expression of tissue inhibitors of metalloproteases
(TIMPs)
• May be associated with MMP & TIMP polymorphisms.

17. Pathology
Weakening of vascular wall
• Ischemia of the inner media occurs when there is
atherosclerotic thickening of the intima.
• Systemic hypertension causes significant narrowing of
arterioles of the vasa vasorum.
• Medial ischemia may lead to “degenerative changes” of
the aorta.
• Smooth muscle cell loss/change in synthetic phenotype
leads to scarring (and loss of elastic fibers), inadequate
extracellular matrix synthesis, and production of
increasing amounts of amorphous ground substance
(glycosaminoglycan).

18. Pathology

19. ATHEROSCLEROTIC ANEURYSMS
• Most common form of aortic aneurysms.
• More commonly seen in males over the age of 50 years.
• Most common sites abdominal aorta, thoracic aorta,
iliac arteries and other large systemic arteries.
• Pathogenesis :

20. ATHEROSCLEROTIC ANEURYSMS

21. External view, gross photograph
of a large aortic aneurysm that ruptured
Opened view, with location of rupture tract
indicated by a probe. The wall of the aneurysm is
exceedingly thin, with lumen filled by large uantity
of layered but largely unorganized thrombus

22. ATHEROSCLEROTIC ANEURYSMS
COMPLICATIONS :
1. Rupture
• Most serious and fatal complication.
• Depends upon the size and duration of the aneurysm and the blood pressure.
• Rupture of abdominal aneurysm may occur either into the peritoneum or into the
retroperitoneum resulting in sudden and massive bleeding.
• Occasionally, there may be slow progressive leak from the aneurysm.
• A ruptured aneurysm is more likely to get infected.
2. Compression
• The atherosclerotic aneurysm may press upon some adjacent structures such as compression
of ureter and erosion on the vertebral bodies.
3. Arterial occlusion
• Atherosclerotic aneurysms of the abdominal aorta may occlude the inferior mesenteric
artery, or there may be development of occlusive thrombosis.
• Collateral circulation develops slowly and is nearly always sufficient so as not to produce
effects of ischaemia.
• Thromboembolism is rather common in abdominal aneurysms.

24. Obliterative endarteritis:
• Luminal narrowing and
obliteration, scarring of the vessel
wall, and a dense surrounding rim
of lymphocytes and plasma cells
that may extend into the media
• The aorta loses its elastic recoil
with destruction of the media
and becomes dilated, producing
an aneurysm.
• Valvular insufficiency and massive
volume overload lead to
hypertrophy of the left ventricle.
• The greatly enlarged hearts are
sometimes called "cor bovinum"
(cow's heart).

28. COMPLICATIONS
1. Rupture
• Causes massive and fatal haemorrhage into the pleural cavity, pericardial
sac, trachea and oesophagus.
2. Compression
• The aneurysm may press on the adjacent tissues and cause symptoms :
 on trachea causing dyspnoea,
 on oesophagus causing dysphagia,
 on recurrent laryngeal nerve leading to hoarseness
 and erosion of vertebrae, sternum and ribs due to persistent pressure.
3. Cardiac dysfunction
• When the aortic root and valve are involved, syphilitic aneurysm produces
aortic incompetence and cardiac failure.
• Narrowing of the coronary ostia may further aggravate cardiac disease.

35. Dissecting aneurysm of the aorta
(Aortic dissection)
• Refers to a dissecting haematoma in which the blood
enters the separated (dissected) wall of the vessel and
spreads for varying distance longitudinally.
• The most common site is the aorta and is an acute
catastrophic aortic disease.
• The condition occurs most commonly in men in the age
range of 50 to 70 years.
• In women, dissecting aneurysms may occur during
pregnancy.

36. Dissecting aneurysm of the aorta
(Aortic dissection)
The aortic wall has split (dissected) at the level of the media producing an outer false
lumen running parallel to the central true lumen which is narrowed.

37. Dissecting aneurysm of the aorta
(Aortic dissection)
PATHOGENESIS
1. Hypertension in about 90% cases of dissecting
aneurysm.
2. Marfan’s syndrome
3. Development of cystic medial necrosis of Erdheim,
especially in old age.
4. Iatrogenic trauma during cardiac catheterisation or
coronary bypass surgery
5. Pregnancy, for some unknown reasons

38. Dissecting aneurysm of the aorta
(Aortic dissection)
CLASSIFICATION

39. Dissecting aneurysm of the aorta
(Aortic dissection)
HISTOLOGY
i. Focal separation of the
fibromuscular and elastic tissue
of the media.
ii. Numerous cystic spaces in the
media containing basophilic
ground substance.
iii. Fragmentation of the elastic
tissue.
iv. Increased fibrosis of the media.

40. Dissecting aneurysm of the aorta
(Aortic dissection)
COMPLICATIONS
1. Rupture
• Haemorrhage from rupture results in mortality in 90% of cases.
• Haemorrhage occurs into the pericardium; less frequently it may rupture into
thoracic cavity, abdominal cavity or retroperitoneum.
2. Cardiac disease
• Involvement of the aortic valve results in aortic incompetence.
• Obstruction of coronaries results in ischaemia causing fatal myocardial infarction.
• Rarely, dissecting aneurysm may extend into the cardiac chamber.
3. Ischaemia
• Obstruction of the branches of aorta by dissection results in ischaemia of the
tissue supplied.
• There may be renal infarction, cerebral ischaemia and infarction of the spinal cord.

41. To summarize…
• An aneurysm is a permanent abnormal dilatation of a blood vessel due to
congenital or acquired weakening or destruction of the vessel wall.
• ŒBased on pathogenetic mechanisms, aneurysms are atherosclerotic,
syphilitic (luetic), dissecting, mycotic and berry aneurysms; the last ones
are seen in the circle of Willis in the base of the brain.
• ŒAtherosclerotic aneurysms are the most common,affecting abdominal
aorta more often and may rupture or cause compression on adjacent
tissues.
• Syphilitic aneurysm occurs due to syphilitic aortitis and affects ascending
and arch of aorta.
• Dissecting haematoma is often preceded by hypertension and affects the
arch and ascending aorta most often.