This document provides a guide on abdominal aortic aneurysms (AAAs) for medical students. It defines AAAs as abnormal dilatations of the aorta between the diaphragm and iliac arteries. AAAs are usually asymptomatic but can rupture, causing severe abdominal pain and shock. Risk factors include smoking, male sex, age, and family history. Ultrasound is used to detect AAAs by measuring diameter. Larger AAAs have higher rupture risks and may require elective open or endovascular repair surgery to prevent rupture. Complications after endovascular repair include endoleaks, where blood bypasses the graft. Ruptured AAAs require emergency open repair surgery.

1. Abdominal Aortic Aneurysms. A rough
guide for medical students
By Nick Harper
Student Number 0606273
Word Count 2066
October 2009

2. www.vascularsociety.org.uk
Abdominal Aortic Aneurysms. A rough
guide for medical students
What are Aortic Aneurysms?
An Aortic Aneurysm is abnormal focal dilatation of the aorta.
For Abdominal aortic aneurysms (AAA), this must
occur somewhere between the aortic hiatus in the
diaphragm (level of the T12 vertebra) and the
bifurcation into the common iliac arteries (Level of
L4).
The diameter of the normal aorta varies slightly
between individuals and in men, is between 16 to
22mm. A ≥50% increase in this diameter is classically
used as the cut off to define a significant aneurysm
(Johnston, K.W. et al. 1991). This means ≥30mm for
the average man.
AAAs typically grow at a rate of around 2.6 – 3.2mm
per year (Baxter, B.T. et al. 2008). The larger they
grow, the greater their risk of rupture.
Ruptured AAAs account for 1.5% of deaths in men between the age of 65 and 85 and 8000 deaths in
total per year in the UK (Sakalihasan, N. et al. 2005)
Prevalence of AAAs
Men between 3 to 8%
Women between 0.5 to 1.5%
Risk factors
Smoking One of the main risk factors for developing AAA.
Smokers are 4 times more likely to develop an AAA compared to lifelong non
smokers. Daily smoke exposure appears to be more important than the number of
years spent smoking (Vardulaki, K.A. et al. 2000)
For the ≥50 age group (Wilmink, A.B. &
Quick, C.R., 1998).

3. Sex Being male increases the risk of AAA by roughly 6 times (Vardulaki, K.A. et al. 2000).
As the number of women who smoke increases however, we may see a change in
this male:Female distribution
Age
Family Up to 20% of patients with AAA report a family history (Sakalihasan, N. et al. 2005).
Other risk factors include Hypertension, Hyperlipidaemia and Previous vascular
disease
Several studies have reported that Diabetes Mellitus has a protective effect against the expansion of
AAAs. This is possibly due to the increased wall thickness and decreased wall stress observed in
diabetics (Diehm, N. et al. 2007)
Types of Aneurysm
True aneurysms can develop into 2
main morphologies:
1. Fusiform – A dilatation parallel to
the long axis of the aorta
2. Saccular – An outpouching of the
aortic wall. Usually thought of being at
a higher risk of rupture than fusiform
(Pappu, S. et al. 2008)
False or pseudoaneurysms occur
when blood leaks out from a small tear in
the aorta and forms a haematoma. This
encapsulates the tear but still
communicates with the vessel beneath.
A common finding in all types of AAA is thrombus formation within the lumen. This can narrow the
vessel to the point of reducing blood flow and will further increase the haemodynamic strain within
the aneurysm.
This graph shows how
the prevalence of
both small (29 to
49mm) and large
(≥49mm) AAAs
increases with age
(From Wilmink, A.B. &
Quick, C.R., 1998)
Fig 1.

4. Anatomical considerations
The media of the Aortic wall contains
elastin for distensibility and collagen
for tensile strength. This extracellular
matrix is crucial for pulse propagation
and if weakened can lead to dilatation
of the aorta.
The number of medial elastin lamellae
within the aorta decreases as it
progresses from thoracic to abdominal.
This is thought to underlie the fact that
AAAs are 3 times more frequent than
thoracic aortic aneurysms (TAAs)
(Allaire, E. et al. 2009)and that most
AAAs occur below the renal arteries
(Infrarenal AAA).
What causes AAAs?
A complex interaction between: genetic predisposition, atherosclerosis, haemodynamic strain,
thrombus formation and enzymatic degradation.
Other causes of AAA include vasculitis, syphilis, cystic medial necrosis and trauma.
Genetic
The recognition of a familial component to AAAs sparked the search for a genetic contribution. So
far, the following mutations have all been linked to AAA development (Allaire, E. et al. 2009):
• Marfans
• Loyes-Dietz & TGFβ signalling mutations
• Vascular type IV Ehlers – Danlos
• ACTA2
• MYHII
Proteases
Proteases are found in abundance in aortic aneurysms and may possibly underlie AAA progression
by digesting the structural proteins within the aortic wall. The main players in this process identified
so far include:
Matrix Metalloproteinases (MMPs) Proteases that can break down both Elastin and Collagen
Tissue inhibitors of MMPs (TIMPs) Overexpression has been shown to prevent AAA formation
in animal models
Fig 2. From
http://www.anatomyatlases.org/Microscopic
Anatomy/Section08/Plate08152.shtml

5. Proposed model for Protease mediated aneurysm formation:
Fig 3. (1)Thrombus within the lumen traps Neutrophils. These Neutrophils release proteases which
diffuse into the media causing breakdown of Collagen and Elastin. (2) These proteases also kill
vascular smooth muscle cells (VSMCs). (3) As VSMCs normally release protease inhibitors (TIMPs),
Protease action is left unchecked. (4) Finally, angiogenesis within the adventitia, a recognised
feature of AAAs causes influx of yet more protease producing leukocytes (Allaire, E. et al. 2009).
Net Result:
Decreased elastin, collagen and smooth muscle within the aortic wall leading to dilatation and
possible rupture
How to detect AAAs
Presentation
Most unruptured AAAs are asymptomatic and as such are picked up by chance during other
investigations (chest X-ray, ultrasound etc). Others may present with:
• Pain in the abdomen, chest or lower back
• Peripheral vascular disease if thrombus formation within the aneurysm, or mural emboli
decrease blood flow to the periphery.
• Ureteric obstruction if the Aneurysm is causing compression
Adventitia
Media
Thrombus
Elastin
Collagen VSMC
P
P
P
TIMP
Neutrophils
1
2
3
4

6. Examination
Pulsatile mass found by bimanual palpation above the umbilicus. The larger the aneurysm is, the
higher the probability of detection. The larger the patient’s abdomen is, the lower the probability of
detection.
A bruit may be heard over the aneurysm due to turbulent blood flow
Imaging
Ultrasound
• The method of choice for initial
assessment and follow up
• Quick, easy, cheap and with no
radiation.
• Can measure the size of the aorta
to the nearest 3mm (Pleumeekers,
H.J. et al. 1998)
• Duplex scans allow visualisation of
blood flow
Fig 4. Transverse section through an infrarenal AAA showing the lumen, surrounding thrombus and
aortic wall (from http://www.nzma.org.nz/journal/116-1169/335/)
Aortic Wall
Lumen Thrombus

7. CT scan
• Must be performed if considering a surgical
procedure
• More accurate measure of aneurismal size
with very high sensitivity and specificity
• CT angiography allows prior surgical planning
based on the patient’s own anatomy
• Limitations include cost, time and radiation
exposure
Elective repair
The decision whether to repair an aneurysm is a balance between the risk that it will rupture and the
risk of the procedure.
Currently, the only reliable way of determining the risk of rupture is by measuring the diameter of
the aneurysm.
Size of AAA Risk of rupture per year
4cm or less Low risk
4 - 5cm 1 in 100 per year
5 - 6cm 1 in 12 per year
6 - 7cm 1 in 6 per year
Over 7cm 1 in 4 per year or higher
Fig 6. 3D reconstruction angiogram showing an
AAA (From www.cardiologyrounds.com)
Fig 5. Non enhanced CT of an AAA
showing a hyperattenuating crescent
sign. An indicator of impending rupture.
(From Gonsalves, C.F. 1999)

8. There are currently 2 main methods for elective repair: Open repair and endovascular aortic
aneurysm repair (EVAR)
Open repair
(1) Performed under general anaesthesia
(2) The abdominal cavity is entered via a
midline incision
(3) The AAA is identified
(4) Proximal control – Clamp the Aorta
(preferably below the renal arteries)
(5) Distil Control – Clamp the common iliac
arteries
(6) The aneurysm is opened and any
thrombus is removed
(7) A graft is anastamosed to either end of
the affected section
(8) Clamps are removed and blood flow is returned
Mortality rates following elective open repair:
• 4.6% 30 days post-op
• 6.3% after 4 Years (AAA related mortality only)
EVAR
The AAA is repaired by deploying a stent graft system within the aneurysm. This requires careful CT
angiography to determine the anatomy of the aneurysm prior to treatment.
www.vascularsociety.org.uk
Fig 7.
Fig 8.

9. EVAR was first carried out in 1991 and approved by the FDA for AAAs in 1999 (Eliason, J.L. &
Upchurch, G.R Jr., 2008)
The graft typically comprises of 2 components, both inserted on catheters under fluoroscopic
guidance. The procedure can be performed under local anaesthetic with sedation, epidural, or spinal
block.
Main body stents the aorta and ipsilateral common iliac artery
Contralateral Limb stents the contralateral common iliac artery
The main body is inserted into the aorta via the common femoral artery. Once deployed, the
contralateral limb is then inserted via the other femoral artery, cannulated into the main body and
deployed. This system provides an entirely new lumen for the distal aorta and proximal common
iliac arteries and prevents blood flow into the aneurysm.
Mortality rates following elective EVAR
• 1 to 2% 30 days post-op
• 3.5% after 4 Years (AAA related mortality only)
Fig 9. EVAR endograft before and after
deployment (From
http://midlandvascularcentres.com/evar.htm)
Catheter
EVAR stent graft
Main body
Contralateral
limb
Deployment
Fig 10. (A) Positioning the stent before deployment. (B) Deployment. (C) Final aortogram
showing the completed procedure. (From Eliason, J.L. & Upchurch, G.R Jr., 2008)

10. EVAR or Open repair?
The following table is a summary of a meta-analysis of 21,178 patients who underwent AAA repair
(Lovegrove, R.E. et al. 2008). This includes the EVAR1 and DREAM trials.
Comparing EVAR to open repair
Advantages No difference Disadvantages
• Can be performed without
general anaesthesia
• Long term all cause
mortality
• Higher rates of
complication (see section
on endoleak)
• Shorter postoperative stay
by on average 5 days
• Graft stenosis or
infection
• Secondary intervention
more likely to be required.
This is successful in 84% of
cases
• Lower 30 day mortality
(odds ratio 0.46)
• More expensive ≈ £12,000
for EVAR compared to ≈
£10,000 for open repair
• Lower long term aneurysm
related mortality (hazard
ratio 0.39)
• In younger patients open
repair may be a longer term
solution
Endoleak
One of the main complications of EVAR is that of “endoleak” This occurs when blood manages to
bypass the graft and re-enter the aneurysm. Classification is dependent on the route of re-entry (see
fig 12.), with treatment typically involving source embolization or conversion to open repair.
Fig 11. (A) Aortogram and (B) Transverse CT angiogram of
endoleaks following EVAR repair. (From Stavropoulos, S.W. &
Charagundla, S.R., 2007)
A B

11. Fig 13. Possible sites for AAA rupture: (1) into the
abdominal cavity, (2) retroperitoneal, (3) rupture of
a retroperitoneal sac, (4) into the duodenum, (5)
into the inferior vena cava (From Sakalihasan, N. et
al. 2005).
Ruptures
EMERGENCY! 100% mortality if untreated!
Sudden & severe abdominal pain which may
radiate to the back and groin.
Shock – depends on the size of rupture and
duration of haemorrhage. Small tears can
quickly develop into larger ones!
Acute management
• Call a vascular surgeon or anaesthetist
• Get wide bore IV access X2
• If the shock is severe give O Rh –ve blood
but keep systolic BP ≤100mmHg
• ECG & blood amylase
• Crossmatch blood
• Take the patient to theatre for open
repair
Fig 12. Classification of
endoleak from type I to IV.
(From Eliason, J.L. &
Upchurch, G.R Jr., 2008)

12. In some cases a small rupture may temporarily seal itself. If the patient is stable a CT scan may be
useful to confirm diagnosis and plan treatment. As the main ΔΔ includes acute pancreatitis, also
check serum amylase/lipase levels.
Prevention
Controlling risk factors
Stopping smoking is currently the best method for preventing AAA development.
Long term statin use has been shown to reduce mortality after AAA repair (Kertai, M.D. et al. 2004).
It is unclear whether this effect is due to a reduction in cholesterol or due to the fact that statins can
also reduce MMP expression.
Screening
A ruptured AAA has an average mortality of around 80% whilst the mortality of elective repair is only
3 to 8%. Ultrasound imaging is easy and cheap to carry out so why not screen everyone?
A meta analysis of 4 large randomised control trials: MASS, Western Australia, Vilborg County and
Chichester studies was carried out by Fleming, C. et al. (2005). Results showed that Ultrasound
screening roughly halves AAA related mortality in men over the age of 65.
Screening in women showed no advantage.
On the basis of these results, a national AAA screening programme is being introduced
into the UK from spring 2009. This screening will only be available for men aged 65 years and older.
Further information on this screening programme and patient leaflets can be found at
http://aaa.screening.nhs.uk/.

13. References
Allaire, E., Schneider, F., Saucy, F., Dai, J., Cochennec, F., Michineau, S., Zidi, M., Becquemin, J-P.,
Kirsch, M. & Gervais, M. (2009) New insight in aetiopathogenesis of aortic diseases. European
Journal of Vascular & Endovascular Surgery. 37(5), 531-537
Baxter, B.T., Terrin, M.C. & Dalman, R.L. (2008) Medical management of small abdominal aortic
aneurysms. Circulation. 117(14), 1883-1889
Diehm, N., Dick, F., Schaffner, T., Schmidli, J., Kalka, C., Di Santo, S., Voelzmann, J. & Baumgartner, I.
(2007) Novel insight into the pathobiology of abdominal aortic aneurysm and potential future
treatment concepts. Progress in Cardiovascular Diseases. 50(3), 209-217
Dobrin, P.B., Baker, W.H. & Gley, W.C. (1984) Elastolytic and collagenolytic studies of arteries.
Implications for the mechanical properties of aneurysms. Archives of Surgery. 119(4), 405-409
Eliason, J.L. & Upchurch, G.R Jr. (2008) Endovascular abdominal aortic aneurysm repair. Circulation.
117(13), 1738-1744
Fleming, C., Whitlock, E.P., Beil, T.L. & Lederle, F.A. (2005) Screening for abdominal aortic aneurysm:
a best-evidence systematic review for the U.S. Preventive Services Task Force. Annals of Internal
Medicine. 142(3), 203-211
Gonsalves, C.F. (1999) The hyperattenuating crescent sign. Radiology. 211(1), 37-38
Johnston, K.W., Rutherford, R.B., Tilson, M.D., Shah, D.M., Hollier, L. & Stanley, J.C. (1991) Suggested
standards for reporting on arterial aneurysms. Subcommittee on Reporting Standards for Arterial
Aneurysms, Ad Hoc Committee on Reporting Standards, Society for Vascular Surgery and North
American Chapter, International Society for Cardiovascular Surgery. Journal of Vascular Surgery.
13(3), 452-458
Kertai, M.D., Boersma, E., Westerhout, C.M., van Domburg, R., Klein, J., Bax, J.J., van Urk, H. &
Poldermans, D (2004) Association between long-term statin use and mortality after successful
abdominal aortic aneurysm surgery. american journal of medicine. 116(2), 96-103
Lovegrove, R.E., Javid, M., Magee, T.R. & Galland, RB (2008) A meta-analysis of 21178 patients
undergoing open or endovascular repair of abdominal aortic aneurysm. british journal of surgery.
95(6), 677-684
Pappu, S., Dardik, A., Tagare, H., Gusberg, R.J. (2008) Beyond fusiform and saccular: a novel
quantitative tortuosity index may help classify aneurysm shape and predict aneurysm rupture
potential. Annals of Vascular Surgery. 22(1), 88-97
Pleumeekers, H.J., Hoes, A.W., Mulder, P.G., van der Does, E., Hofman, A., Lameris, J.S. & Grobbee,
D.E. (1998) Differences in observer variability of ultrasound measurements of the proximal and distal
abdominal aorta. Journal of Medical Screening. 5(2), 104-108

14. Sakalihasan, N., Limet, R. & Defawe, O D. (2005) Abdominal aortic aneurysm. Lancet. 365(9470),
1577-1589
Stavropoulos, S.W. & Charagundla, S.R. (2007) Imaging techniques for detection and management of
endoleaks after endovascular aortic aneurysm repair. Radiology. 243(3), 641-655
Vardulaki, K.A., Walker, N.M., Day, N.E., Duffy, S.W., Ashton, H.A. & Scott, R.A. (2000) Quantifying
the risks of hypertension, age, sex and smoking in patients with abdominal aortic aneurysm. British
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Wilmink, A.B. & Quick, C.R. (1998) Epidemiology and potential for prevention of abdominal aortic
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www.cardiologyrounds.com
www.midlandvascularcentres.com/evar.htm
www.nzma.org.nz/journal/116-1169/335
www.vascularsociety.org.uk