Aneurysms& Dissections
Dr. Ashraf Abdelfatah Deyab
Assistant Professor of Pathology
Majmaah University- Collage of Medicine
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
.
Normal vessel- cross section
Aneurysms- definition
 Aneurysm: one of the vascular disorders
considered as leading cause of death in all
over the world, esp. developed and western
societies.
 Aneurysm: is localized, permanent, abnormal
dilatation “blood-filled” of a blood vessel or
heart, with extension to all three wall layers
(intima, media, and adventitia).
 Aneurysm-site: small, medium, large BV+HRT.
 Male : female ratio (5:1)\ Age group > 5th decade
Aneurysm classification-1
Different ways and system for classification;
 I. Based on morphological findings:
 A) Cylindrical, saccular, fusiform (macroscopic)
 B) True or False aneurysms (based on microscopic
appearance).
 II. Based on etiological issue- (congenital
or acquired causes).
 III. Based on location: Aneurysms can also be
classified by their location(arterial>venous) (brain,
aorta, kidneys, leg, ect..)
Aneurysms- classified based on morphology-1
 1) classified based on shape (of no clinical
value) :
 Fusiform aneurysm (symmetrical spindle-shaped
dilatation)
 Cylindroid or tubular (lengthy dilatation in the form of a
cylinder)
 Saccular aneurysm (sack-like bulging on one side of the
artery)
 Berry aneurysm (small saccular aneurysm the size of a
berry)
Aneurysms- based on morphological types-2
 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, over tear in the intima and media
confined next to the vessel, surrounded by
fibrous tissue - this enough to seal the leak, or
may rupture out of the surrounding tissue.
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 classification-based on etiology
1) Atherosclerosis& HTN: as result of persistant
mechanical force>> lead to wall weakness&
degeneration , (90%)occur in the abdominal
aorta; Capillary micro-neurysm (HTN, DM&
smoking): Brain& retina.
2) Infections& Mycotic aneurysm: bacterial
sepsis& IE, sites: Brain, abdomen ,neck ,leg &arm.
a) Syphilitic Aortitis (third stage) occur in the
ascending& arch of aorta, which is due to
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 elastin fibers.
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
AAA- introduction
 AAA is localized abnormal ballooning dilatation
of AA exceeding normal diameter- outer aortic
diameter >3 cm (normal 2 cm).
 associated with atherosclerosis majority of
cases occurs infra-renal, a few para-renal and
supra-renal.
 Occur frequently in men and in smokers
 Most commonly in elderly over 60 yrs.
 CLASSIFED based on size& symptoms(> 5.5cm- Surgery )
AAA pathogenesis
 Atherosclerotic plaque in the intima compresses
the underlying media and compromises nutrient
and waste diffusion from the vascular lumen into
the arterial wall.
 The media therefore undergoes degeneration and
necrosis that results in arterial wall weakness and
consequent thinning.
 The degradation of tunica media by means of
proteolytic process& exposure of ECM>>> lead to
elimination of elastin
 Reduced perfusion& nutrition of vasa vasorum in
the AA (compared to thoracic A.)- damage of the
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: dense periaortic
fibrosis containing abundant lymphoplasmacytic
inflammation with many macrophages and often giant
cells (uncertain cause)
 2) Mycotic Aortic Aneurysm: infected by the lodging
of circulating microorganisms in the wall, particularly
in bacteremia from a primary Salmonella
gastroenteritis- destroys the media-thinning.
AAA clinical features
 They tend to cause no symptoms.
 Pressure symptoms and signs: pain, erosion
of vertebra and ureter& legs pain (blood flow).
 Obstruction of vessel branch+ pulsating mass.
 The major complication of AA is rupture, into
the abdominal cavity, and can lead to shock&
death within minutes.
 Embolization+ Fistula formation
 Mortality of rupture repair in the hospital is 60% to 90%.
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 Dissection
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) or acquired connective tissue
causing abnormal vascular ECM(e.g., Marfan
syndrome, Ehlers-Danlos syndrome, vitamin C
deficiency, copper metabolic defects).
3) Large groups of A. dissection remain unknown, a few
with disruption of penetrating vessels of the vasa vasorum can give
rise to an intramural hematoma without an intimal tear.
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.
5) Hematomas “Thrombus”, the dissecting hematoma reenters
the lumen of the aorta through a second distal intimal tear, creating
a new vascular channel “double-barreled aorta” = false channel,
which with time endothelialized (become chronic dissection )
Histologic view of the dissection demonstrating
an aortic intramural hematoma
Aorta dissecting Aneurysm
clinical features
Aortic Dissection- clinical feature The nature of complications depend on site.
(most serious complications: dissections of the
aorta from the aortic valve to the arch).
 Symptoms sudden onset of pain, begin in the
anterior chest, radiating to the back, moving
downward as the dissection progresses;
confused as MI.
 The common cause of death is rupture outward
into the pericardial , pleural, or peritoneal
cavities.
 Aortic insufficiency, and myocardial infarction
summary of common complications
The nature of complications depend on site.
(most serious complications: dissections of the aorta
from the aortic arch).
 1-Cardiac tamponade. 2- Aortic insufficiency.
 3-Myocardial infarction.
 4-Renal, mesenteric, or iliac arteries, causing
critical vascular obstruction
 5-Compression of spinal arteries may cause
transverse myelitis. 6-Thrombo-embolism
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
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