Abdominal aortic aneurysm surveillance: application
of the UK Small Aneurysm Trial to a New Zealand tertiary hospital
Timothy Buckenham, Justin Roake, David Lewis, Malcolm
Gordon, Isabel Wright
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Abstract
Aims We present 5-year results of an
abdominal aortic aneurysm surveillance programme at Christchurch Hospital, based
on the UK Small Aneurysm Trial.
Method Patients with infrarenal abdominal
aortic aneurysms between 30 and 55 mm were placed in an ultrasound-based
surveillance programme with an intention to treat when their aneurysms reached
the Vascular Service determined threshold, when the AAA became symptomatic, or
when rapid AAA growth was demonstrated. Patients were divided into three groups:
Group 1, those currently under or those who had completed surveillance (n=198);
Group 2, those excluded from surveillance and therefore treatment due to
unsuitability for open surgical or endoluminal exclusion who had not completed
surveillance (n=18); and Group 3, those who declined surgery on completion of
surveillance (n=5). We looked at the number of aneurysm-related deaths in these
groups and examined any issues that arose during or upon completion of
surveillance.
Results There were five aneurysm-related
deaths in Group 1. There was one aneurysm-related death in Group 2, and one in
Group 3.
Conclusion The data highlights problems
related to setting threshold diameters for abdominal aortic aneurysms in women,
and to the interval between completion of surveillance and undergoing
endoluminal or open surgical repair.
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Abdominal aortic aneurysm surveillance has become an
established policy in many vascular units following the publication of the UK
Small Aneurysm Trial, which demonstrated no significant difference in mortality
at 9 years, if patients with aneurysms less than 55 mm were observed with
regular ultrasound surveillance and intervention was restricted to aneurysms
reaching the size threshold or becoming symptomatic. The outcome of this trial
was that 25% of the observation surveillance cohort did not require repair of
their aortic aneurysms over 9 years. The Aneurysm Detection and Management
(ADAM) group in the United States performed a similar randomised controlled
trial that drew similar conclusions. We started an abdominal aortic aneurysm
surveillance programme based on the findings of the UK Small Aneurysm Trial.
We present the 5-year results of this programme. We have
attempted to benchmark our data to that of the UK Small Aneurysm Trial, and we
also discuss some of the issues that arose when trying to implement a
surveillance programme in New Zealand.
Methods
The abdominal aortic aneurysm (AAA) surveillance
programme at Christchurch Hospital was commenced in November 2000. For the
purpose of this audit, we studied the period from November 2000 to September
2005 inclusive. During this time, the protocol at our institution was as
follows:
Definition
The infrarenal aorta was considered aneurysmal when the
dilated segment was 1.5 times greater in diameter than the adjacent normal
segment or when the infrarenal aorta exceeded 3 cm in maximum AP
diameter.4
Inclusion
Population screening for AAA did not take place in our
region during the audit period. Patients with a known AAA of ≤55 mm
(discovered incidentally on imaging for other indications or on physical
examination either by GP or hospital staff) were clinically reviewed by the
Vascular Service prior to inclusion into the surveillance programme. Only
patients that were deemed fit enough to undergo elective AAA repair were
included in surveillance. Upon entry to the programme, patients were set an
individual threshold for review, namely the AAA diameter at which that patient
would undergo vascular surgical review with a view to repair.
Ultrasound imaging
Technique and equipment—All
patients were scanned on a GE Logiq 700 ultrasound scanner, using the 546L
linear probe (imaging frequency set at 2.5, 3.0 or 4.0 MHz as deemed
appropriate) using the ‘virtual convex’ setting to provide a convex
field of view, or 384c curvilinear probe (imaging frequency set at 2.5, 3.0 or
4.0 MHz as deemed appropriate).
The entire aorto-iliac segment was imaged (abdominal
aorta, common iliac arteries [CIA], external iliac arteries [EIA], and proximal
internal iliac arteries if visualised) from the level of the coeliac axis to the
inguinal ligament. Key images of aneurysmal disease were recorded: in transverse
section; the maximum antero-posterior (AP) external diameter was measured from
the B-mode image of the AAA; and the same measurement taken from the CIA and EIA
bilaterally. (This measurement has been shown to be the most repeatable and
accurate;5 we do not take transverse/
“side-to-side” measurements).
The distance of the AAA from the superior mesenteric
artery (SMA) origin was measured from a longitudinal B-mode image, and the
external AP diameter of the aorta at the level of one of the renal artery
origins was measured from a transverse B-mode image if possible. If the
suprarenal aorta was suspected to be aneurysmal, its external AP diameter in the
transverse plane was measured, at the level of the coeliac axis origin if
possible.
Ultrasound scan recall
frequency—The recall frequency was determined by the most
recently measured maximum AP diameter in the transverse plane. Table 1
demonstrates recall frequency in relation to the AAA diameter. Prior to June
2004, all patients followed the male recall schedule. Thereafter females
followed a different recall schedule (see Table 1). A few selected patients had
a different recall frequency as requested by the referring vascular surgeon, for
example, one female patient with a 33 mm AAA was recalled annually rather than
every two years due to anxiety about her AAA following the death of her husband
from AAA rupture.
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FEMALE AAA Size
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Scan Frequency
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30–34 mm
35–39 mm
40–50
mm
≥50 mm
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2 years
1 year
6 months
Vascular
Review
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MALE AAA Size
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Scan Frequency
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30–34 mm
35–39 mm
40–44
mm
45–55 mm
≥55 mm
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4 years
2 year
1 year
6
months
Vascular Review
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Completion of surveillance
Patients
completed surveillance upon their AAA reaching a threshold diameter, or if they
became symptomatic or experienced rapid (>10 mm per year or >7 mm in 6
months’) 3,6 growth. Prior to June 2004,
the threshold for most patients was 55 mm. After that time for most patients
(for reasons discussed below) the threshold for review was subsequently altered
to 50 mm and 55 mm respectively for most females and males. For a patient
considered at high risk from AAA repair, the referring vascular surgeon could
request a customised threshold (e.g. >55 mm).
Exclusion from surveillance
Patients could be excluded from surveillance prior to
reaching ‘completion’ as defined above for several reasons.
Death—The vascular unit learned
of the death of a surveillance patient either via notification from the GP or
from hospital records. In every instance the cause of death was recorded, as was
whether a post-mortem was performed, for audit purposes.
Ill-health—Precluding them from
consideration for elective repair. Patients were reviewed in vascular or other
outpatient clinics for other indications and deemed to be unfit for elective
repair, or the patient’s GP had contacted the programme co-ordinator to
inform the vascular unit of a patient’s new, significant co-morbidities.
Upon communication of this to the programme co-ordinator and the patient, the
patient was excluded from surveillance. Since mid 2005, as part of the
surveillance programme, the health of each patient was assessed annually by the
vascular unit by writing to the general practitioner. If the general
practitioner felt that the patient’s health had deteriorated and was now a
contraindication to repair, they were referred for vascular surgical opinion and
thus could be removed from the programme.
Suprarenal component—The patient
was found to have a suprarenal (component to their) aneurysm. Patients with such
dilatation were not able to be part of the surveillance programme, as the UK
Small Aneurysm Trial only included infrarenal abdominal aortic aneurysms. This
group was managed by clinical review by the combined vascular and cardiothoracic
surgical departments and decisions made as to appropriateness of surgery or
continued monitoring.
Patient lost to system—It was
possible, as had happened with our other surveillance programmes, that the
occasional patient may have moved home and, usually due to their GP not knowing
their whereabouts, become lost to recall.
Patient relocates—As had
happened with our other surveillance programmes, a patient may relocate to
outside our catchment area. When informed of this, we would contact the
patient’s new GP requesting that surveillance be continued and supplied
relevant imaging from our institution.
Results
Overview
The entire cohort comprised 221 patients (162 males, 59
females) of age 73 (38–85) years [median (range)] at inclusion. The
baseline (initial scan) AAA diameter was 45 (28–78) mm [median (range)]
and the length of follow-up was 20.2 (0.0–59.5) months [median (range)].
The expansion rate was 0.5 (0.0–15.5) mm per year
[median (range)]. For analysis purposes, we divided the patients into three
groups:
- Group
1: Those who were currently on surveillance and those who had completed
surveillance;
- Group
2: Those excluded from surveillance prior to ‘completion’;
and
- Group
3: “Self-excluders”, i.e. those who declined treatment on
completion of the surveillance programme.
Group 1 results
Group 1 comprised 198 patients aged 72 (38-85) years [median
(range)]. There were 148 males and 50 females in this group. Baseline AAA
diameter at entry to surveillance is shown in Figure 1; it was 45 (28-78) mm
[median (range)]. Length of follow-up was 19.7 (0.0-59.5) months [median
(range)]. The expansion rate for AAA in this group was 0.5 (0.0–15.5) mm
per year [median (range)], assuming any apparently negative growth represented
inter-observer error and was therefore considered as no change in diameter.
Outcomes—In this group there were 28
patients who underwent elective surgical (n=24) or endoluminal (n=4) exclusion
of their abdominal aortic aneurysm—3 additional patients who underwent
urgent repair, 10 patients awaiting treatment, 128 on active surveillance, and
11 patients who (on clinical review), having reached their threshold, were too
ill to proceed to treatment (Figure 2).
Of the urgent repairs, all three patients had reached their
threshold but had become symptomatic. None of these aneurysms were ruptured. All
three patients survived their urgent repair. The 30-day mortality for elective
and for urgent repair was 0%. There were no emergency repairs in this group.
All-cause mortality—23 deaths
occurred in this group of 198 patients (11.6% all-cause
mortality over the audit period); 16 patients died during surveillance, 2 died
having completed surveillance and awaiting repair, and 5 who had been excluded
due to ill health (untreated) died.
In total, 9 of these 23 deaths were AAA-related and they are
discussed below. The other causes of death were myocardial infarction (MI) (5),
cerebrovascular accident (CVA) (2), cancer (2), heart failure (1), biliary
sepsis (1), pneumonia (1), unknown (1), and ruptured thoracic aortic dissection
(1), with all but the latter not confirmed by post-mortem.
Group 2 results
Group 2 comprised 18 patients aged 77 (44–82) years
[median (range)]. There were 9 males and 9 females in this group. Baseline AAA
diameter at entry to surveillance is shown in Figure 3; it was 42 (36–56)
mm [median (range)]. Length of follow-up was 23.3 (0.7–51.3) months
[median (range)]. The expansion rate for AAA in this group was 0.8
(0.0–5.1) mm per year [median (range)], assuming any apparently negative
growth represented inter-observer error and was therefore considered as no
change in diameter.
Outcomes—This is the group that had
been deemed unsuitable for surgical or endoluminal exclusion of their abdominal
aortic aneurysm prior to their reaching threshold. This was either due to
ill-health (12 patients) or due to discovery of a suprarenal component to the
patient’s abdominal aortic aneurysm (n=6). No patients were lost to the
programme, nor did any relocate to outside the catchment area.
All-cause mortality—Within the group
of 12 patients excluded due to ill health, there were 3 deaths, one from
myocardial infarction and two from cancer. These all occurred in the community
without post-mortem.
In the suprarenal group (n=6), there were two deaths (n=2)
despite these patients being monitored by the combined cardiothoracic and
vascular surgical team: one death was AAA-related and is discussed below, and
the other from a ruptured thoracic aortic aneurysm. (The latter patient died 2
weeks post-AAA repair awaiting repair of his thoracic aortic aneurysm; no
post-mortem was performed). Hence for Group 2, the all-cause mortality was 27.8%
over the audit period.
Group 3 results
Group 3 comprised 5 patients aged 75 (70–79) years
[median (range)]; all were male. Baseline AAA diameter at entry to surveillance
was 52 (49–57) mm [median (range)]. Length of follow-up was 25.0
(0.0–41.7) months [median (range)]. The expansion rate for AAA in this
group was 2.3 (1.3–2.4) mm per year [median (range)], assuming any
apparently negative growth represented inter-observer error and was therefore
considered as no change in diameter.
Outcomes—These patients chose to
decline surgical or endoluminal repair on reaching their threshold diameter and
completing surveillance, after discussion with a vascular surgeon.
All-cause mortality—Two of these
patients subsequently died. Both deaths occurred in the community without
post-mortem; one death was AAA-related whilst the other cause of death was
unknown. Hence for Group 3, all-cause mortality was 40.0% over the audit
period.
Hence for the entire cohort, all-cause mortality was 13.6%
over the audit period.
AAA-related mortality for all groups
Group 1—In those patients fit for
treatment, there were five aneurysm-related deaths. Three deaths were from
ruptures of abdominal aortic aneurysms during surveillance, i.e. between
scheduled surveillance scans. The threshold for review for all three AAAs was 55
mm.
Of these, the first patient, a female, had a 50-mm abdominal
aortic aneurysm; she presented to the Emergency Department with a suspected
rupture, no operation was performed and this patient died, with the rupture
confirmed on post-mortem. The second patient, also female, died in the community
with a 51-mm ruptured aneurysm confirmed on post-mortem. The third patient, a
male, ruptured at 51 mm and presented to the Emergency Department, where the
rupture was confirmed by imaging and after clinical assessment; no operation was
performed and this patient subsequently died.
The other two deaths were of patients awaiting repair. Both
patients had reached their modified threshold of 60 mm. Patient 1 was a male
with a 61-mm sac, and he died within 3 days of ending surveillance. Patient 2, a
female, died 6 months after completing surveillance. Both patients died in the
community prior to repair; neither had post-mortem, with the cause of death
being attributed to ruptured AAA. These five deaths represent 2.5 % of Group
1.
Group 2—One patient excluded from
surveillance due to their aneurysm having a suprarenal component died from a
ruptured AAA; no post-mortem was performed, but the AAA appeared ruptured on CT.
None of the 12 patients excluded due to ill-health died of ruptured AAA. Hence
for Group 2, the AAA-related mortality was 5.6% over the audit period.
Group 3—One death was attributed to
rupture of the patient’s abdominal aortic aneurysm, although no
post-mortem was performed. Hence for Group 3, the AAA-related mortality was
20.0% over the audit period.
Discussion
We commenced our surveillance program in Christchurch
Hospital, New Zealand, in November 2000. Christchurch Hospital is the biggest
tertiary, teaching, and research hospital on the South Island, with 650 beds
serving approximately 36,000 inpatients and 13,000 day patients each year.
Our approach to surveillance was based primarily on the
findings of the UK Small Aneurysm Trial,1,6
although in this paper we shall also compare some of our results and experiences
with the US ADAM trial3 and other smaller
published studies.
Briefly, the UK Small Aneurysm
Trial1 was a randomised controlled trial
designed to compare the outcomes and costs of electively repairing AAA of
40–55 mm versus ultrasonographic surveillance of these lesions. It found
no advantage in early repair: there was no significant difference in mortality
between the two groups at 9 years, if patients with aneurysms less than 55 mm
were observed with regular ultrasound surveillance and intervention was
restricted to aneurysms reaching the size threshold or becoming symptomatic.
The US ADAM trial3 compared
outcomes and costs of electively repairing AAA of 40–55 mm versus
ultrasonographic or computed tomographic surveillance with a slightly different
(almost exclusively male) cohort, but essentially drew the same conclusions:
that trends in survival did not favour immediate repair and that there was no
significant reduction in mortality between the two groups.
There are potential problems when adapting level one data
achieved in one country to the local circumstances in another country due to
several factors such as resources and service delivery; patient numbers and
geography; influences of ethnicity, demography, etc upon the natural history of
a particular condition; and other factors.
This audit was carried out to assess our 5-year experience
of a surveillance programme, and to examine the data to identify problems that
have arisen and ways to improve the surveillance programme. Our surveillance
cohort (27% female) closely resembles that of the UK trial. Their trial
population comprised both males and females (roughly 80% male to 20% female).
Subjects (with known AAA) were aged between 60 and 76 years;
they were referred from general practitioners, non-vascular specialists, and
hospital or community-based screening programmes to vascular surgeons for
assessment for suitability for inclusion to the programme. The US ADAM
cohort2 was predominantly (~99%) male and aged
50–79 years with incidentally-discovered as well as known or
screen-discovered AAA.
The main purpose of a surveillance programme is to reduce
deaths due to ruptured AAA. In relation to this we found two main issues, namely
that of setting a suitable threshold for review in females, and the time between
decision to repair and the operation itself. A further secondary issue was that
of patients reaching their threshold for review and being (appropriately) denied
elective repair due to existing comorbidities, or deciding that they no longer
wanted treatment, that may have had unnecessary surveillance. Equally, it is not
known whether those excluded prior to reaching threshold due to ill health were
removed from the surveillance programme in a timely manner.
Considering the latter first, Group 2 partly comprised those
excluded prior to reaching threshold of the clinical opinion that death was more
likely from their comorbidities than from their aneurysm. These 12 patients
(5.4% of cohort) were excluded due to ill-health before reaching their
threshold. This is not comparable with the UK Small Aneurysm Trial since we have
no record of those patients that were excluded prior to being placed on the
surveillance programme. Moreover, this figure reflects only those who have
become ill during the surveillance programme.
In the UK Small Aneurysm Trial, exclusion due to ill-health
was performed at the time of enrolment in the trial, rather than progressively
throughout the trial;7 they reported 16% of
their patients were excluded due to being unfit at the time of randomisation.
Eleven patients in Group 1 (5.0% of cohort) reached their
threshold for review but were denied surgery on the grounds of ill-health, hence
a total of 10.4% of our patients were excluded due to ill-health. They also
found that 4.8% of the early-surgery group became unfit for repair whilst on the
waiting list. This figure is, however, comparable with our percentage of
patients excluded during surveillance.
In the US randomised trial, patients underwent cardiac
thallium scanning before randomisation to reduce the difference in coronary
artery disease management between the two groups and to reduce the number of
patients to be found unfit for surgery after
randomisation.2
Regarding Group 3, it is unclear as to why these patients
declined treatment when at the threshold; they represent 2.3% of the cohort.
Unsurprisingly, 40% (2/5) of this group have died; neither had post-mortem, with
the cause of death being ruptured AAA (1) and unknown (1). The Chichester study
found that 5 (3.3%) of the 153 AAA patients they reviewed declined surgery upon
reaching threshold; 3 died “having refused screening recalls or
surgery”.8
Hence 16 patients underwent surveillance (7.2% of the
cohort) and reached their threshold without receiving treatment. Whilst the
patient clearly has a right to refuse treatment if correctly informed, from a
fiscal perspective it would be preferable to exclude patients no longer suitable
for/desirable of elective treatment before they reached threshold. As we were
not able to clearly identify why these patients refused treatment, after
accepting the possibility initially, we were not able to develop a strategy for
predicting such refusal at an earlier stage in their surveillance. An additional
cost is the potential psychological one to those patients reaching threshold and
then being denied repair.
Indeed, following the end of this audit, we have introduced
an annual letter to each surveillance patient’s GP asking if they are
aware of any comorbidities that would preclude the patient from elective
treatment and hence surveillance. We shall audit these results in the future to
ascertain whether this is an efficient use of resources.
The above problems aside, of most concern are the patients
who would have been fit for elective repair but who died before it was
performed. These fall into two categories—those who died during
surveillance and those during the wait for repair. Both groups contributed to
the AAA-related mortality of our cohort. In the latter group, there were two
ruptures that occurred after completion of surveillance but prior to open
surgical or endoluminal exclusion, representing 4.9% of the subset of Group 1
comprising patients awaiting or having had repair (n=41).
One of these patients suffered a ruptured abdominal aortic
aneurysm 2 days after completing surveillance whilst awaiting repair, and one
patient ruptured 6 months after completion of surveillance. Given that the
annual risk of rupture of a 55-mm abdominal aortic aneurysm is approximately
6–10%9 and that the median time for
surgical or endoluminal exclusion of these aneurysms at our institution is 6
months, one would anticipate 3–5% of patients having completed
surveillance but waiting for surgery to rupture, with a mortality approaching
90% (as has been our experience).
There is little published data on the time to repair in
other papers. The Huntingdon (UK) aneurysm screening programme, whereby men in
the district over 50 years deemed fit for elective repair are routinely screened
for AAA, found 4 (0.5%) of its 768 screen-detected AAA over a 9-year period
ruptured whilst being worked up.10 They do not
state their average waiting time for repair nor the time-lag for all four cases,
but cite a patient dying whilst waiting 2 months for repair and one who was
apparently lost to their system with a 72 mm AAA who died 3 years after being
scheduled for repair.
In the Chichester (UK)
study8 (a randomised trial of ultrasonographic
screening for men over 65 years with a threshold for review of 60 mm), 3 (1.8%)
of 170 reviewed AAAs ‘ruptured before outpatient appointment’ having
reached this threshold. Whilst the UKSMAT1 was
a multicentre study and hence the time to treat will vary with centre, this will
have contributed to the final mortality results, and knowledge of their median
waiting time would assist in applying the recommendations. The message from this
paper is that once the patient has reached threshold they should be repaired
expeditiously, as they are at the point of where the balance of risk favours
surgery.
At a public hospital institution such as ours, if 6 months
is the necessary time needed to effect surgical repair then it is important to
identify the factors contributing to this and we intend to publish further on
this topic. We are unsure as to whether our waiting list is excessive or average
and are considering restructuring the surveillance schedule or reducing review
thresholds to incorporate a 6-month wait for repair.
Finally in our first and largest group, those intended for
treatment or who have completed treatment, there were three fatal ruptures (1.4%
of cohort, followed for on average 1.7 years, giving annual rate of death due to
rupture of 0.8%) in between routine scheduled surveillance scans.
Comparison of our data with the randomised trials from the
UK and United States has been made. The ADAM
trial,3 reported an annual risk of rupture of
0.6% in the surveillance cohort, although it was ~99% male and a substantial
number of AAA-related deaths in our group were female. The UK Small Aneurysm
Trial reported 3.8% of deaths in its surveillance group to be attributable to
AAA rupture (including AAA >55 mm, but excluding those deemed unfit for
surgery and those who refused surgery) over a median follow-up of 4.6
years—yielding an annual death rate of
0.8%.6
In this Christchurch study, these five ruptures (2.5% of
cohort) over a median follow-up of 1.7 years yield an annual death rate of 1.4%
which (given the relatively small size of our sample) appears similar to that in
the UK trial.
The three ruptures during surveillance highlighted the
issues surrounding surveillance of women. Whilst one was an 82-year-old male
with a 51-mm AAA, two of these patients were female (aged 78 and 76 years, with
50- and 51-mm AAA respectively). We initially applied the 55-mm threshold, but
following the two female ruptures mentioned above we reviewed the 55-mm
threshold in women and reduced it to 50 mm. This practice is clearly not
evidence-based, and the problem of setting an appropriate intervention threshold
is one of the main issues surrounding the management of AAA in women.
The prevalence of AAA in women is approximately one-quarter
to one-sixth of that in men.11,12 There is some
evidence in comparison to men that female aortas have a proclivity to rupture at
a slightly lesser diameter and this may be due to having a smaller aorta
initially.13 A study in Norway found more rapid
expansion in AAA in women than men (2.43 vs 1.65 mm per
year).14 The UK Small Aneurysm
Trial1 found the risk of rupture in women to be
four times that of men. A Finnish study of ruptured AAA found that the diameter
was less than 55 mm in 24% of females with
rupture.15
There is also evidence that once the AAA has ruptured, women
are less likely to be considered for emergency repair than
men16 and that they have a lower survival rate
post-emergent repair.17
The UK Small Aneurysm Trial was not powered to make
recommendations about females with abdominal aortic
aneurysms.1 Unlike the US ADAM
trial,2 it did include a significant proportion
of women but concludes that, whilst the 5.5 cm threshold for repair may be too
high for females, the diameter at which surgery should be recommended for women
cannot be ascertained from their study. No asymptomatic females have ruptured
since our local change in threshold. In retrospect, had the threshold been 50 mm
in women, the death from rupture may have been prevented.
Conclusion
We present the experience of an abdominal aortic aneurysm
surveillance programme based on the UK Small Aneurysm Trial, as well as some
problems that were identified. The study was attempted to confirm the
feasibility of applying the UK Small Aneurysm Trial data to the local population
in New Zealand.
The main problems encountered were setting a threshold for
intervention in women; the interval between completion of surveillance and
undergoing endoluminal or open surgical repair; and the number of exclusions
from surveillance group, mainly due to ill health.
We conclude that the annual risk of death due to rupture in
our New Zealand surveillance group is similar to the UK Small Aneurysm Trial (at
approximately 1% per annum), but the ruptures and urgent repairs that occurred
after completion of surveillance are concerning.
Competing interests: None.
Author information: Timothy Buckenham,
Clinical Professor of Radiology and Vascular Radiologist, Department of
Radiology, Christchurch Hospital, Christchurch; Justin Roake, Professor of
Surgery, Department of Surgery, Christchurch Hospital, Christchurch; David
Lewis, Vascular Surgeon, Department of Surgery, Christchurch Hospital,
Christchurch; Malcolm Gordon, Vascular Surgeon, Department of Surgery,
Christchurch Hospital, Christchurch; Isabel Wright, Sonographer, United Kingdom
(former employee of Department of Radiology, Christchurch Hospital,
Christchurch)
Correspondence: Professor Timothy
Buckenham, Department of Radiology, Christchurch Hospital, Private Bag 4710,
Christchurch. Fax: (03) 364 0620; email: TimB2@cdhb.govt.nz
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