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Abdominal Aortic Aneurysm
1. Faculty of Medicine
Dr Mohd Firdaus Che Ani
General Surgeon & Lecturer
Department of General Surgery
Universiti Teknologi MARA (UiTM)
firdaus.7431@uitm.edu.my
Abdominal Aortic Aneurysm
2. • Abdominal aortic aneurysm is the most common aortic
aneurysm; infra renal segement is more prone for aneurysm
formation.
• Incidence is 2%. It is more common in males.
• Transverse diameter of aorta in an aneurysm should be 3
cm or more.
• Common in elderly; chance of getting aneurysm in
genetically related first-degree relatives is 10 times more.
• Common in smokers -- 8:1with nonsmokers.
Introduction:
3. • From aortic hiatus of the
diaphragm, anterior to the lower
border of vertebra T7/T8.
• It descends to the level of
vertebra L4 it is slightly to the left
of midline.
• The terminal branches of the
abdominal aorta are the two
common iliac arteries.
• Normal Diameter ranges from 16-
22 mm.
Anatomy: Abdominal Aorta
4. • The wall of the mature aorta is composed of three
layers:
• Tunia intima, with its single layer of endothelial cells;
• Tunica media, made up of smooth muscle cells within a
structural protein matrix; ELASTIN is the main load bearing
part.
• Tunica adventitia, a tough layer of collagen fiber and
fibroblasts.
AnatomyofAorta
5.
6. Definition: Aneurysm
• Pathological dilatation of localised segments
of the arterial system more than 1.5 of its
normal diameter.
• True aneurysms - contained three layers of
the arterial wall in the aneurysm sac
• False aneurysms - a single layer of fibrous
tissue as the wall of the sac as seen in
aneurysm following trauma
8. Based on shape of the
aneurysm
• Fusiform—uniform dilatation
ofentire circumference of
arterial wall
• Saccular—dilatation of part
of circumference of the
arterial wall
Classification: Morphology (shape) of a
True Aneurysm
9. • Atherosclerosis (as degenerative process) is the most
common facilitating cause (95%).
• Familial aortic aneurysm(25% of AAA)
• more prevalent in females.
• related to decrease in type III collagen, α1 antitrypsin
and lysyl oxidase.
• i.e in Marfan’s, Ehler Danlos syndromes
• Others: Salmonella infection, Syphilis, trauma, collagen
diseases, arteritis
Etiology
10. Pathophysiology
• Based on a study conducted by the US National Heart,
Lung, and Blood Institute:
• Proteolytic degradation of aortic-wall connective
tissue
• Inflammation and immune responses
• Biomechanical wall stress
• Molecular genetics
11. Development Expansion Rupture
Tobacco use AdvancedAge Female gender
Hypercholesterolemia Severe Cardiac
Disease
↓ FEV1
Hypertension Previous Stroke Larger initialAA
diameter
Male Gender Tobacco Use Cardiac or renal
transplantation
Family History Cardiac Or Renal
Transplantation
Higher mean blood
pressure
Current tobacco use
(length of time smoking
≫ amount)
Risk Factors
12. Clinical Features
• Patients with AAAs are typically asymptomatic
• Typical symptoms;
• back pain,
• abdominal pain,
• Pulsatile abdominal mass
• Associated with underlying
• Hypertension,
• diabetes,
• cardiac problems
• Lower limb ischaemia and embolic episodes can occur.
14. • *UK Small Aneurysm Trial: implication for surgical
treatments of abdominal aortic aneurysms, J Vasc Surg
1999
Diameter of AAA vs Risk of Rupture
15. • Predicting the behavior of an aneurysm over time is
difficult. Risk factors for rupture include
• chronic obstructive pulmonary disease
• tobacco use (smoking)
• female gender
• cardiac or renal transplantation.
• larger initial AAAdiameter
• **The most widely adopted surrogate for rupture risk is
maximal cross-sectional aneurysm diameter
Risk Factors of a ruptured AAA
16. Prognosis of a ruptured AAA
• Only 1/3 of all ruptured AAA reaches hospital alive (~33%)
• Out of the 1/3 reached hospital:
• Another 1/3 is stable enough and will undergo surgery (~11%)
• Out of the 1/3 who undergone surgery
• Only 1/3 will survive (~4%)
Therefore, it is crucial to be able to identify early those who
reached hospital so that treatment delivery can be given
immediately
17. Plain Film of Abdomen (PFA):
• In about 90% of the cases, X-rays of the
abdomen show calcium deposits in the
aneurysm wall. But plain x-rays of the
abdomen cannot determine the size
and the extent of the aneurysm.
Investigations :
18. Ultrasound Abdomen usually gives a clear
picture of the size of an aneurysm. Ultrasound has
about 98% accuracy in measuring the size of the
aneurysm and is safe and non-invasive.
Advantages: Non-invasive , no risk of radiation,
and contrast media, it is an excellent choice for
screening.
Drawbacks: Ultrasound is not an ideal method
for detecting rupture as it is unable to image all
portions of the aortic wall. Cannot determine
whether AAA is leaking
Imaging: Ultrasound
Ultrasonogram of an aortic
aneurysm showing the large
clot-filled sac with a small central
lumen
19. Provides excellent imaging of AAA compared to
ultrasound. CT, particularly with the adjunctive use of
iodinated contrast agents to perform CT angiography
(CTA) which provides:
• anatomic information
• detects vessel calcification thrombus
• concurrent arterial occlusive disease
• permits multiplanar and three-dimensional reconstruction and
analysis for operative planning.
• Also it can be determined if there is leaking of the aneurysm which
may lead to imminent rupture
Drawbacks include substantial radiation exposure, particularly in
the setting of serial examinations and the use of iodinated
contrast media in a population with a high incidence of contrast
induced nephropathy (CIN).
Imaging: Computed tomography
Infrarenal abdominal aortic
aneurysm demonstrating aortic wall
calcification and intraluminal
thrombus
20. Recommendations for Screening
Ultrasound is the screening modality of choice.
Candidates for Screening:
• AAA size of:
• less than 4cm – yearly
• 4.0 to 5.0cm – 6 monthly
• More than 5cm – recommended for surgical
intervention
22. When to offer surgical intervention
• The size criterion for elective repair:
• 5.5 cm for men and 5 cm for women
• or a 12-month growth rate of equal to or greater than 10 mm
in both sexes.
• saccular aneurysms, dissection of mural thrombus, or fracture
of saccular calcification.
• Symptomatic AAA regardless of size
• *patient’s condition should be optimized prior to intervention
• Emergency Repair:
• Leaking AAA
• Ruptured AAA
23. Post-operative complications
Common complications after open repair are
• cardiac (ischaemia and infarction)
• respiratory (atelectasis and lower lobe consolidation)
• colonic ischemia due to lack of collateral supply
• Renal failure
• Neurological-sexual dysfunction and spinal cord ischaemia.
• Aortoduodenal fistula –uncommon
• Prosthetic graft infection
• Distal Thrombo-embolism
• DVT
24.
25. Pre-op optimizations of comorbidities, such as:
Coronary artery disease (CAD)
Renal insufficiency
Peripheral arterial occlusive disease
Diabetes
Obstructive lung disease
Vitamin K antagonists should be stopped 5 to 7 days prior to surgery and
bridging anticoagulation provided, if indicated, using LMWH or
unfractionated heparin in pts on blood thinning therapy.
Pre operative evaluation and management
26. Called as endo-aneurysmorrhaphy with intraluminal graft placement
• Under general anaesthesia, via full-length midline or supraumbilical
transverse incision is made.
Open Surgical Procedure
27. EndoVascular Aortic Aneurysm Repair
(EVAAR)
• About 50 per cent of infrarenal aneurysms are suitable for EVAR.
• Common causes of unsuitability include a short, flared or angulated
neck and difficult iliac artery access because of narrowing or tortuosity
• The endovascular prosthesis (‘stent graft’) is usually made up of three
separate parts – a main body and two limbs which are enclosed in
separate delivery catheters .
• Some types have only two pieces – a main body with ipsilateral limb
attached and a separate contralateral limb.
• The prosthesis is made from Dacron or PTFE with integral metallic
stents for support.
30. Endoleak
Most common indication for re-intervention after EVAR.
• Type I endoleak is defined as failure to achieve a satisfactory seal at either
the proximal (type Ia) or distal (type Ib)seal zone, representing a failure to
exclude the aneurysm sac.
• Type I endoleak should be addressed at the time of detection.
Placement of additional graft components to extend the seal zone
Placement of balloon-expandable stents within the seal zone
• One FDA-approved device uses helical EndoAnchors delivered with a
deflectable sheath to address both type I endoleak and migration
31. Type II Endo-leaks
• Most common form and represent continued filling of the aneurysm sac by
lumbar branches or the inferior mesenteric artery.
• Treatment may include embolization of feeding branches by selective
catheterization (transarterial technique) or direct sac puncture (translumbar
technique) or laparoscopic or open surgical ligation of these vessels.
Type III Endo-leaks
• Represent failure of an individual component or of the seal between
components of a modular graft system.
• All type III endoleaks should be treated, typically by relining the offending
area with new graft components
32. Type IV Endoleaks
• Seepage through porous graft material and are typically self-limited,
resolving when procedural anticoagulation is reversed.
• An entity known as ENDOTENSION is sometimes considered a fifth type of
endoleak. This represents persistent growth of the aneurysm sac in the
absence of a detectable leak. It is proposed that this phenomenon is due to
either the passage of serous ultrafiltrate across an excessively porous fabric
or the existence of an undetected endoleak of one of the prior types.
33. Post Op Care
• smoking cessation to reduce the risk of AAA growth and rupture.
Open repair:
• contrast-enhanced CT imaging of the entire aorta at 5-year after open
repair
EVAAR:
• baseline imaging (CT Aortogram) in the first month after EVAR with
contrast enhanced CT and color duplex ultrasound imaging. In the
absence of an endoleak or sac enlargement, imaging should be
repeated in 12 months using contrast-enhanced CT or color duplex
ultrasound imaging
• Yearly CT Aortogram for-life
