VASCULAR SURGERY I
Surgery for aortic aneurysms
Seamus C Harrison
Robert D Sayers
Abstract
Abdominal aortic aneurysm (AAA) is a dilatation of the infra-renal abdom-
inal aorta to greater than 3 cm. Population screening is offered to men in
their 65th year in the UK. Patients with small AAAs (<5.5 cm) are entered
into surveillance programs and should have cardiovascular risk factors
managed aggressively. AAA 5.5 cm diameter should be considered for
repair to prevent rupture. Endovascular aneurysm repair (EVAR) has
lower perioperative mortality than open repair and is first line treatment
in many centres with an elective mortality rate <1% in the UK. Ruptured
AAA can be treated with open or endovascular approaches but the mor-
tality rate for intervention remains in excess of 35%. Developments in
endovascular technology allow treatment of juxta-renal, aorto-iliac and
thoracoabdominal aneurysms, but should be thoroughly investigated in
well designed clinical trials before introduction to routine clinical practice.
Keywords Aorta; aneurysm; AAA; surgery; vascular
Introduction
An aneurysm is a focal, permanent dilatation of an artery or
chamber to more than 50% of its normal diameter. The natural
history of aneurysms is asymptomatic growth followed by
rupture, which is catastrophic in many cases. In the infra-renal
abdominal aorta, an absolute diameter of 3 cm is the threshold
at which a diagnosis of abdominal aortic aneurysm (AAA) is
made. The prevalence of AAA in men between the ages of 65 and
79 years is approximately 5%, and it is estimated to cause
approximately 4000 deaths per year in the United Kingdom (UK).
In the UK there is a national AAA screening programme and
approximately 8000 operations are carried out each year for
AAA. This article will review the options and evidence for repair
of AAA.
Epidemiology and risk factors for AAA
Large-scale cross-sectional studies of AAA screening with ultra-
sound scans have demonstrated that the prevalence of an infra-
renal aortic diameter greater than 3 cm is approximately 5% in
men over the age of 65 years,1 though this may be decreasing.2
There have been no comparably large studies in the female
population but the prevalence is though to be about fivefold
lower as compared to males and for this reason females are not
currently offered screening.3 Despite this, approximately 40% of
deaths attributed to AAA occur in females, suggesting a more
Seamus C Harrison PhD FRCS is a Lecturer in Vascular Surgery
at the University of Leicester, Leicester, UK. Conflicts of interest:
none declared.
Robert D Sayers MD FRCS is Professor of Vascular Surgery
at the University of Leicester, Leicester, UK. Conflicts of interest:
none declared.
SURGERY 33:7
malignant course in this group and a need to direct more re-
sources at tackling this problem. Other non-modifiable risk fac-
tors for AAA include increasing age (AAA is very rare before the
age of 55 years) and positive family history for the disease.
Having a first-degree relative affected by AAA increases the risk
approximately fourfold, implicating both genes and shared
environmental exposures in AAA development. The major
modifiable risk factor for AAA is cigarette smoking. Prospective
observational studies have demonstrated that current cigarette
smoking can increase the risk of AAA development by as much
as eightfold compared to those that have never smoked. Indeed,
it is likely that public health measures aimed at smoking cessa-
tion may, in part, explain the reduction in AAA prevalence seen
in the past 10e15 years. Other risk factors for development of
AAA include hypercholesterolaemia, hypertension and other
atherosclerotic diseases. Interestingly, diabetes appears to pro-
tect against both the development and progression of AAA. The
mechanism for this unexpected observation is unclear at present
but could provide clues to developing novel pharmacological
treatments for AAA.
Clinical presentation
Most AAAs are asymptomatic until rupture. Occasionally, large
AAAs may compress surrounding structure such as the ureters,
inferior vena or duodenum, leading to development of symp-
toms, but this is unusual. It is more common for AAA to be
discovered incidentally, as part of the diagnostic work-up for
unrelated conditions or to be found as part of the national
screening programme. Patients with AAA may also present with
ischaemic symptoms in the lower limbs secondary to acute
thrombosis or embolization to the peripheral circulation, but
again this is not common.
AAA rupture classically presents as a triad of abdominal pain
radiating to the back, shock and a palpable pulsatile abdominal
mass. It is important to recognize that not all cases of AAA will
have all of these features. It is unfortunately not uncommon for
patients with ruptured AAA to be misdiagnosed as ureteric colic,
musculoskeletal back pain or other diagnoses commonly pre-
senting to the emergency department. Therefore there should be
a high clinical suspicion of ruptured AAA in at-risk patients
presenting to the emergency department with unexplained
abdominal, back or loin pain.
Screening for AAA
The aim of surgery for AAA is to prevent rupture, which has a
mortality exceeding 80%, but a major challenge has been the fact
that AAA often remains occult until rupture occurs. This fact has led
to the development of screening asymptomatic at-risk individuals
with an ultrasound scan, which is safe, inexpensive and has both a
high specificity and sensitivity. The evidence for AAA screening
comes from randomized controlled trials in the UK, Australia and
Denmark. The largest study is the UK based Multicentre Aneurysm
Screening Study (MASS) that randomized 68,700 males aged 65e79
to receive an invitation to US screening or not.1 The risk of aneu-
rysm related death was reduced by 42% in the group invited for
ultrasound screening after 4 years of follow-up. Currently in the UK,
a national aneurysm-screening programme has been implemented,
in which men are invited for an USS in their 65th year.
330 2015 Elsevier Ltd. All rights reserved.
 VASCULAR SURGERY I
Intervention to prevent rupture of AAA
The risk of aneurysm rupture should be weighed against the risk
of the intervention to repair it. Aneurysm size is the major
determinant of rupture risk (Table 1). Post-mortem studies have
demonstrated that the majority of deaths secondary to AAA
rupture occurred in AAA greater than 6 cm. There was, therefore
a degree of equipoise in the best strategy for management of
patients with smaller AAA and the UK Small Aneurysm Trial
(UKSAT) provided pivotal evidence in this regard.4 This study
randomized 1090 individuals with AAA measuring 4e5.5 cm to
receive either surgical repair or ultrasound surveillance pro-
gramme and surgery was offered to AAA exceeding 5.5 cm. After
5 years of follow-up there was no discernible survival benefit
with early surgical intervention and surveillance of AAA sized 4
e5.5 cm was found to be a safe strategy with low rupture rate.
Therefore in the UK, the current recommendation for small
asymptomatic AAA (<5.5 cm) is ultrasound-based surveillance.
The vast majority of AAAs identified by screening are small.
There are currently no medical therapies that have been proven
to alter the history of small AAA. Observational studies have
reported an association between statin use and slower AAA
growth, but this has been inconsistent and there are no high
quality randomized trials.5 Trials of anti-platelets, beta-blockade
and doxycycline have not shown any strong effect whereas trials
of ACE inhibitors are currently ongoing. Despite this, patients
with small AAA can be considered at high risk of other cardio-
vascular disorders and their risk factors should be examined and
treated.
Open surgery for AAA
Open surgery to repair AAA is nearly always performed under
general anaesthesia. Routine use of epidural anaesthesia reduces
the respiratory and gastrointestinal complications associated
with other forms of postoperative analgesia. The approach to the
aorta is usually transperitoneal via a longitudinal or transverse
laparotomy, but some surgeons favour a retroperitoneal
approach via a left flank incision. The intraperitoneal contents
are mobilized to the right side of the abdomen and the infra-renal
aorta exposed by incision of the posterior peritoneum. The du-
odenum is mobilized off the aortic neck and the left renal vein
marks the upper extent of the dissection in most cases. A clamp
site in the proximal infra-renal aortic neck is exposed and pre-
pared. Approximately 2/3 of infra-renal AAA can be repaired
with a tube graft but the presence of iliac aneurysmal and/or
Annual rupture rate of AAA by AAA diameter11
AAA Size (cm) Annual rupture rate (%)
<3 0
3e3.9 0.4
4e4.9 1.1
5e5.9 3.3
6e6.9 9.4
7e7.9 24
Table 1
SURGERY 33:7
occlusive disease necessitates the use bifurcated grafts extending
to the iliac or femoral arteries. Prior to proximal and distal
clamping of the vessels it is usual to administer intravenous
heparin to prevent thrombotic complications. A longitudinal
aortotomy is made and back bleeding vessels (e.g. lumbar, me-
dian sacral and inferior mesenteric arteries) are carefully over-
sewn after removal of the thrombus. A suitably sized synthetic
graft is selected and sutured into the aneurysm with poly-
propylene sutures using an inlay technique (Figure 1). Following
haemostasis the aneurysm sac and posterior peritoneum are
closed over the graft to reduce the chances of graft infection and/
or aorto-enteric fistula. Laparoscopic repair of AAA is described
and practiced in a few centres in the UK, and uses the same
principles as conventional open repair.
Randomised controlled trials have reported an early mortality
rate of 4e6% for open AAA repair and recent nationwide audits
have reported a mortality rate of 3.8% in the UK.6 Factors
determining outcomes from open surgery include age, aneurysm
size and renal function, in addition to the experience of the
treating surgeon and/or centre.
Endovascular aneurysm repair (EVAR)
EVAR is a minimally invasive technique used to repair AAA and
has been widely adopted into vascular practice. The procedure
involves placement of a stent-graft in the infra-renal aorta usually
via the femoral arteries. A variety of stent-grafts are available on
the market, all of which are a modular design of two or more
separate pieces (Figure 2). The stent-grafts are anchored in the
aorta by the radial force of the stent and/or barbs that penetrate
the wall of the aorta. A major benefit of the endovascular
approach is that there is no need for a laparotomy and aortic
cross clamping, diminishing the potential risk of the procedure
and improving recovery time. EVAR is described in more detail in
the following article by White & Wyatt.
EVAR or open surgery
EVAR has been comprehensively evaluated by a number of
randomized surgical trials. The UK EVAR 1 trial randomized
1082 patients to either open repair or EVAR. The 30-day mor-
tality for EVAR was 1.7% compared to 4.7% in open repair, but
at 6 years there were late deaths in the EVAR group from AAA
rupture.7 These results have been mirrored in other trials from
the Netherlands and US.8,9 Given the early mortality advantage,
EVAR has therefore become widely adopted for AAA repair with
an overall mortality in the UK of 0.8%.6 Many models have been
developed to predict mortality and other graft related outcomes
but few have the diagnostic precision to warrant widespread
uptake, though this continues to be an active area of clinical
research. The Achilles heal of EVAR has been long-term dura-
bility and lifelong screening with US and/or CT scans is required.
Ruptured AAA
Ruptured AAA is a surgical emergency and almost universally
fatal if not treated expediently. While the classic presentation of
ruptured AAA is sudden onset back pain and circulatory collapse,
this is by no means universal and patients may initially present
with back and/or loin pain and relatively normal haemodynamic
331 2015 Elsevier Ltd. All rights reserved.
 VASCULAR SURGERY I

Open repair of an infra-renal AAA with a synthetic graft

Inferior
vena cava

Left renal vein

Left renal artery
Proximal aortic neck
Polypropylene (clamp zone)
suture line Opened aortic sac

Ligated segmental
vessels
(e.g. IMA, lumbars)

Synthetic
vascular graft
Polypropylene
suture line

Common iliac arteries

(distal clamp zone)

Figure 1

observations. Free intraperitoneal AAA rupture is rapidly fatal

and most patients in whom this occurs do not survive. Some
Endovascular aneurysm repair
ruptures may, however, be temporarily arrested by retroperito-
neal structures, providing a window of opportunity for repair.
The widespread uptake of EVAR in elective practice led to
many centres developing protocols for using EVAR in the emer-
gency situation, with excellent results reported in highly selected
Fixation barbs
case series. Proponents for EVAR in the rupture scenario argued
that it could be performed rapidly with minimal trauma to an
Main body already traumatized patient. Opponents argued that the
requirement for CT scans and extra equipment added unnec-
essary delay to management of patients with an immediately life-
threatening condition. The IMPROVE randomized controlled trial
Contralateral gate aimed to address the question of open surgery versus EVAR for
treatment of ruptured AAA; 613 patients with a clinical diagnosis
Ipsilateral limb of ruptured AAA were randomized to receive either open or
Contralateral endovascular repair. Mortality rates were similar in both groups
limb extension
(35% in EVAR vs. 37% in open repair) as was the overall costs of
the procedures and hospital stay.10 In subgroup analyses, it was
shown that patients who received EVAR under local anaesthesia
had a mortality of just 15%, though it is not clear if this was a
self selecting group of patients with suitable anatomy and
physiology for this approach. The ramifications of this study are
Figure 2

SURGERY 33:7 332 2015 Elsevier Ltd. All rights reserved.

 VASCULAR SURGERY I
probably that most major vascular centres should be able to offer
both treatments for patients with ruptured AAA with decision
being dependent upon the AAA morphology and patient
physiology.
Summary
AAA is a common life-threatening condition. Its aetiology is
multi-factorial and there are no pharmacological therapies that
have been proven to prevent its development or progression.
Intervention to prevent rupture should be offered to patients with
AAA >5.5 cm and acceptable surgical risk and EVAR has a lower
perioperative mortality but increased necessity for long-term
surveillance and re-intervention. Developments in endovascular
technology continue to overcome morphological barriers to
EVAR but their introduction to routine clinical practice should be
subject to rigorous clinical evaluation. A rysms. N Engl J Med 2005; 352: 2398e405.
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333 2015 Elsevier Ltd. All rights reserved.