3. B.Adhiwidjaja
History of AAA
The first description of abdominal aortic aneurysm (AAA)
by the 16th century: Vesalius.
In 1923,Matas first successful aorta ligation in patient with
AAA.
In 1948, Rea wrapped reactive cellophane to induce a
fibrotic reaction.
In 1949, Nissen used the technique to treat the AAA in
Albert Einstein.
In 1951, Dubost, Schaffer, Creech popularized
endoaneurysmorrhaphy with intraluminal graft placement.
4. B.Adhiwidjaja
INTRODUCTION
In the US , ruptured AAA are the 15th leading cause
of death overall and the 10th leading cause of death in
men older than age 55.
In 1991 , 30-40% patients with ruptured AAA die
after reaching a hospital but without operation. When
combined with an operative mortality rate 40-50%,
this results in an overall mortality of 80-90% for
AAA rupture.
5. B.Adhiwidjaja
Since 1990 elective AAA repair is one of the
most frequent vascular surgery procedures,
with a relatively constant volume of 40,000
operations annually.
Despite the frequency of elective repair,
however, death from AAA rupture has remain
relatively constant because many AAA are
undetected or untreated.
7. B.Adhiwidjaja
Aortic wall structure
The aortic wall contains vascular smooth muscle,
matrix proteins elastin, collagen, which are arranged
in organized, concentric layers to withstand arterial
pressure.
Gradual but marked reduction in the number of
medial elastin layers from proximal thoracic aorta to
the infrarenal aorta, accompanied by medial thinning
and intimal thickening in the more distal aorta.
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AAA represent a chronic degenerative disease
with life-threatening implications.
Localized form of arterial wall injury
superimposed on degenerative changes related
to age, hemodynamic, systemic risk factors, and
a genetically predisposition, but the exact nature
or sequence of these events is unknown.
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Several processes contribute to the pathologic changes
observed in AAA and the most important are chronic
inflamation, destructive remodeling of the extracellular
matrix, and depletion of vascular smooth muscle cells
(SMC).
Progression of these changes results in segmental aortic
dilatation and alterations in vessel geometry
Redistribution of hemodynamic wall stresses and
diminished tensile strength, thereby increasing the
potential for rupture.
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AAA
90% of aneurysm involve the infra-renal abdominal
aorta.
10% involve the descending and thoracic aorta.
Peripheral aneurysms 3,5%.
ANEURYSM are defined as a focal dilatation at least
50% larger than the expected normal arterial
diameter.
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CLINICAL FEATURES
Majority asymptomatic, often incidental finding on US exam.
Back pain (posterior erosion into vertebral bodies), pulsatile
mass in the abdomen.
Distal embolism
Acute thrombosis
Rupture: classical presentation :Sudden onset back
pain/abdominal pain associated with hypotension, tachycardia
and hypovolemic shock
Obstruction of neighboring structure (ureter, vena cava)
Rare presentation: aorto- caval fistula or primary aorto-
duodenal fistula
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MANAGEMENT
ASYMPTOMATIC AAA
Assess the operative risk of morbidity and
mortality versus the risk of Rupture and premature
death associated with non-operative management
FACTOR to consider: SIZE OF ANEURYSM
5 year risk of rupture if<4cm=10%
5 year risk of rupture if>7cm=95%
Mortality rate for elective AAA repair is 5%
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Medical Status of Patient
Co-existent cardiac or respiratory disease
Aneurysm repair not indicate in the presence
of advance malignancy
Age alone, not factor, but should be considered
versus risk of rupture
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Medical Management
No therapeutic approaches are proven to reduce the
rate of aneurysm expansion.
Cronenwett : COPD is associated with a greater rate
expansion and rupture.
Smoking cessation.
Poorly controlled hypertension is associated with
AAA.
Propranolol.
Non-steroid anti-inflamatory drugs.
Metalloproteinase inhibitor.
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MANAGEMENT OF RUPTURED
AAA
Immediate transfer to operating theatre
Consider withholding surgery in the following circumstances:
Unconscious patient with fixed dilated pupils
Prolonged hypotension and anuria> 8 hours
Severe cardiac/respiratory disease
Known suprarenal or thoracoabdominal aneurysm
History of widespread malignancy or severe degenerative
neurological disorder
Survival rates who undergo emergency repair 40-60%
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EVAR
Endovascular repair of selected AAA is
feasible
Long term results are awaited before its role in
the overall management of AAA can become
clear
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ADVANTAGES of EVAR
Avoidance of aortic cross-clamp
Less patient discomfort
Shorter hospital stay
The mayor disadvantage is the EXPENCE of
the stent graft device.
NEW ALTERNATIVE TO OPEN
SURGICAL procedure.
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COMPLICATIONS of EVAR
ENDOLEAKS (immediate, early, late)
Continued aneurysm expansion
Stent –graft migration, displacement and
dislocation
Mortality rates after EVAR are between 0%
and 5%.
Re-interventions between 10% and 20%.
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EVAR
The perplexing problems of endoleaks and
graft failure continue to be challenges which
technological innovations must address.
Until solutions for endoleaks and stent failure
are found, EVAR remains an imperfect long-
term treatment and requires regular life-long
graft surveillance.
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EVAR
Based on the available evidence, EVAR is an
appropriate treatment for selected patients,
especially those at high risk for open surgical
repair’.
