An aneurysm is an abnormal dilation of a blood vessel or heart. True aneurysms involve an intact but thinned wall, while false aneurysms involve a defect in the wall. Aneurysms are usually caused by atherosclerosis or hypertension and can rupture catastrophically. Arterial dissection occurs when blood enters the arterial wall, dissecting between layers. The main types are abdominal aortic aneurysms and thoracic aortic aneurysms. Unruptured aneurysms are generally managed surgically while ruptured aneurysms have high mortality.

1. Aneurysms & dissection
Rana el saeed
Lecturer of pathology
Faculty of medicine, Benha University

2. • An aneurysm is a localized abnormal dilation of
a blood vessel or the heart ; it can be congenital
or acquired.
• true aneurysm :involves an intact attenuated
arterial wall or thinned ventricular wall of the
heart (e. g Atherosclerotic, syphilitic aneurysms)
• false aneurysm (also called pseudo-aneurysm) is
a defect in the vascular wall leading to an
extravascular hematoma that freely
communicates with the intravascular space
(“pulsating hematoma”). E.g a ventricular
rupture after myocardial infarction that is
contained by a pericardial adhesion

3. • arterial dissection arises when blood enters the
arterial wall itself, as a hematoma dissecting
between its layers.
• Dissections are often but not always aneurysmal
• Consequences: true, false aneurysms and
dissections can rupture, often with catastrophic
consequences.

4. Aneurysms are generally classified
by shape and size
• Saccular aneurysms :
spherical outpouchings
Involves only a portion of the vessle wall
 vary from 5 to 20 cm in diameter and often contain
thrombus.
• Fusiform aneurysms
 involve diffuse, circumferential dilation of a long vascular
segment
vary in diameter (up to 20 cm) and in length
can involve extensive portions of the aortic arch,
abdominal aorta, or even the iliac arteries.
• These types are not specific for any disease or clinical
manifestations.

6. pathogensis
• Aneurysms can occur when the structure or
function of the connective tissue within the
vascular wall is compromised.
• weakening of vessel walls is important in both
inherited and sporadic forms of aneurysms as
well.

7. examples of inherited defects in connective
tissues:
• The intrinsic quality of the vascular wall
connective tissue is poor:
In Marfan syndrome: defective synthesis of
protein fibrillin result in progressive dilation
Loeys-Dietz syndrome: “aggressive” course
aneurysms. defective synthesis of elastin and
collagens I and III.
Ehlers-Danlos syndrome: defective type III
collagen synthesis
scurvy : altered collagen cross-linking
associated with vitamin C deficiency . an
example of a nutritional basis for aneurysm
formation

8. • The balance of collagen degradation and
synthesis is altered by inflammation and
associated proteases.
• In particular, increased matrix metalloprotease
(MMP) expression, especially by macrophages in
atherosclerotic plaque or in vasculitis.
• these enzymes have the capacity to 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) can also contribute to
the extracellular matrix degradation

9. • The vascular wall is weakened through loss of smooth
muscle cells or the synthesis of noncollagenous or
nonelastic extracellular matrix.
 Ischemia of the inner media occurs when there is
atherosclerotic thickening of the intima. Decrease
nutreient diffusion
 Systemic hypertension can also cause significant narrowing
of arterioles of the vasa vasorum medial ischemia.
 Medial ischemia “degenerative changes” of the
aorta, whereby smooth muscle cell loss scarring,
inadequate extracellular matrix synthesis, and production
of increasing amounts of amorphous ground substance
 Histologically, these changes are collectively recognized as
cystic medial degeneration , which can be seen in a variety
of settings, including Marfan syndrome and scurvy.

10. A, Cross-section of aortic media from a patient with Marfan syndrome, showing elastin
fragmentation and areas devoid of elastin that resemble cystic spaces but are actually filled
with proteoglycans (asterisks).
B, Normal media for comparison, showing the regular layered pattern of elastic tissue.
In both A and B, elastin is stained black

11. To sum up
• The main 2 causes of aneurysms:
Atherosclerosis (in Abdominal Aortic
Aneurysm (AAA))
Hypertention (in ascending aortic
aneurysms)
• Other causes include trauma, vasculitis,
congenital defects (e.g., fibromuscular
dysplasia and berry aneurysms), and
infections (mycotic aneurysms).

12. • Mycotic aneurysms can originate
(1) from embolization of a septic embolus,
usually as a complication of infective
endocarditis
(2) as an extension of an adjacent
suppurative process
(3) by circulating organisms directly infecting
the arterial wall.

13. Abdominal Aortic Aneurysm (AAA)
• occur more frequently in men and in smokers
• rarely develop before age 50
• Atherosclerosis is a major cause
• other factors contribute.

14. Morphology.
• Grossly:
Usually below the renal arteries and above the
bifurcation of the aorta
can be saccular or fusiform,
up to 15 cm in diameter, and up to 25 cm in
length.
Occasionally 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.

15. A, External view, gross photograph of a large aortic aneurysm that ruptured (rupture site is
indicated by the arrow).
B, Opened view, with the location of the rupture tract indicated by a probe. The wall of the
aneurysm is exceedingly thin, and the lumen is filled by a large quantity of layered but largely
unorganized thrombus.

16. • Histologically:
 the intimal surface of the aneurysm
shows severe complicated atherosclerosis
with destruction and thinning of the
underlying aortic media
frequently contains a bland, laminated,
poorly organized mural thrombus that may
fill some or all of the dilated segment.

17. Two AAA variants merit special mention:
• Inflammatory AAAs : characterized by dense
periaortic fibrosis with abundant
lymphoplasmacytic inflammation with many
macrophages and often giant cells. Their cause is
uncertain.
• Mycotic AAAs : lesions that have become
infected by a circulating microorganisms in the
wall. In such cases suppuration further destroys
the media, potentiating rapid dilation and
rupture.

18. clinical consequences of AAA
• 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, for
example, iliac (leg)
• Embolism from atheroma or mural thrombus
• compression on an adjacent structure, e.g.,
compression of a ureter or erosion of vertebrae
• Presentation as an abdominal mass (often
palpably pulsating) that simulates a tumor

19. prognosis
• The risk of rupture is directly related to the size of the
aneurysm
• aneurysms of 5 cm and larger are managed aggressively,
usually by surgical bypass involving prosthetic grafts
• Currently, aneurysm treatment is evolving toward
endoluminal approaches using stent grafts in selected
patients
• Timely surgery is critical; operative mortality for
unruptured aneurysms is approximately 5%, whereas
emergency surgery after rupture carries a mortality rate of
more than 50%.
• because atherosclerosis is a systemic disease, a person
with AAA is also very likely to have atherosclerosis in
other vascular beds and is at a significantly increased risk
of IHD and stroke.

20. THORACIC AORTIC ANEURYSMS
• most commonly associated with hypertension
• other causes: Marfan and Loeys-Dietz syndromes
• signs and symptoms referable to
(1) encroachment on mediastinal structures
(2) respiratory difficulties due to encroachment on the lungs and airways
(3) difficulty in swallowing due to compression of the esophagus
(4) persistent cough due to irritation of or pressure on the recurrent
laryngeal nerves
(5) pain caused by erosion of bone (i.e., ribs and vertebral bodies
(6) cardiac disease : aortic valve dilation with valvular insufficiency or
narrowing of the coronary ostia causing myocardial ischemia
(7) rupture.
Most patients with syphilitic aneurysms die of heart failure induced by
aortic valvular incompetence.

21. AORTIC DISSECTION
• Def: occurs when blood splays apart the laminar planes of
the media to form a blood-filled channel within the aortic
wall
• aortic dissection may or may not be associated with aortic
dilation.
• Main causes: (1) men aged 40 to 60, with hypertension (2)
younger patients with systemic or localized abnormalities
of connective tissue affecting the aorta (e.g., Marfan
syndrome).
• Other causes: iatrogenic (e.g., during diagnostic
catheterization), during or after pregnancy (unknown
reason),rare with syphilis due fibrosis of media

22. Pathogenesis.
• Hypertension is the major risk factor in aortic dissection.
• Aortas of hypertensive patients have medial hypertrophy of
the vasa vasorum degenerative changes in the aortic
media and variable loss of medial smooth muscle cells.
• A smaller number of dissections are related to inherited or
acquired connective tissue disorders causing abnormal
vascular ECM (e.g., Marfan syndrome, Ehlers-Danlos
syndrome, vitamin C deficiency, copper metabolic defects).
• Regardless the etiology of medial weakness, the trigger for the
intimal tear and initial intramural aortic hemorrhage is not
known in most cases.
• intimal tear blood flow under systemic pressure
dissects through the media progression of the medial
hematoma.

23. Morphology.
• In most cases, no specific underlying causal
pathology is identified in the aortic wall.
• The most frequent preexisting histologically
detectable lesion is cystic medial degeneration
• initiates with an intimal tear which is found in
the ascending aorta, usually within 10 cm of the
aortic valve sometimes into the iliac and femoral
arteries
• Such tears are typically transverse or oblique
and 1 to 5 cm in length, with sharp, jagged
edges.

24. • The dissection can extend along the aorta
retrograde toward the heart as well as distally.
• The dissecting hematoma spreads along the
laminar planes of the aorta, usually between the
middle and outer thirds.
• It often ruptures out through the adventitia
causing massive hemorrhage or cardiac
tamponade
• In some (lucky) instances, the dissecting
hematoma reenters the lumen of the aorta
through a second distal intimal tear forming a
“double-barreled aorta” with a false channel
that may be endothelialized and become chronic
dissections

25. AORTIC DISSECTION
Histologic view of the
dissection
demonstrating an
aortic intramural
hematoma (asterisk).
Aortic elastic layers
are black and blood is
red in this section,
stained with the
Movat stain

26. Clinical Features
• depend strongly on the region(s) affected
• the most serious complications occur with lesions
from the aortic valve to the arch.
• aortic dissections are classified into two types
• More common (and dangerous) proximal lesions
(called type A dissections), involving either both the
ascending and descending aorta or just the
ascending aorta (types I and II of the DeBakey
classification)
• Distal lesions not involving the ascending part and
usually beginning distal to the subclavian artery
(called type B dissections or DeBakey type III)

27. Type A (proximal) involves the ascending aorta, either as part of a more extensive dissection
(DeBakey I) or in isolation (DeBakey II). Type B (distal or DeBakey III) dissections arise beyond
the takeoff of the great vessels. The serious complications predominantly occur in type A
dissections

28. • The main symptoms is sudden onset of
excruciating pain, beginning in the anterior
chest, radiating to the back between the
scapulae, and moving downward as the
dissection progresses; the pain can be confused
with that of myocardial infarction
• The most common cause of death is rupture of
the dissection outward into the pericardial,
pleural, or peritoneal cavities.
• Retrograde dissection into the aortic root can
cause disruption of the aortic valvular
apparatus.

29. • common clinical manifestations include
cardiac tamponade, aortic insufficiency,
and myocardial infarction or extension of
the dissection into the great arteries of the
neck or into the coronary, renal,
mesenteric, or iliac arteries, causing
critical vascular obstruction and associated
ischemic consequences; compression of
spinal arteries may cause transverse
myelitis.

30. prognosis
• In the past aortic dissection was typically
fatal
• the prognosis has markedly improved
• Rapid diagnosis and institution of intensive
antihypertensive therapy, coupled with
surgical procedures involving plication of the
aortic wall, permit 65% to 75% of stricken
individuals to be saved.