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| Journal of the New Zealand Medical Association,
24-February-2012, Vol 125 No 1350
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Abdominal aortic aneurysm disease in New Zealand:
epidemiology and burden between 2002 and 2006
Nisha Nair, Caroline Shaw, Diana Sarfati, James
Stanley
Abdominal aortic aneurysms (AAAs) are present in about 5 to
10% of men aged 65 to 79 years.1 Generally,
they expand without causing symptoms until they rupture, or, the individual dies
of an unrelated cause. AAA rupture is a surgical emergency, and less than half
of rupture patients reach the hospital alive. Emergency repair itself carries a
high operative mortality of 30 to 65%,2–4
attributable to haemodynamic compromise, advanced age, and medical
comorbidities. Overall, AAA rupture carries a mortality rate as high as 80 to
90%.3,5–8 In contrast, elective repair is
associated with a considerably lower operative mortality, between 3 and
10%.9–14
Population-based AAA screening programmes use abdominal
ultrasound scans to detect AAAs before they rupture. Four major randomised
controlled trials evaluating AAA population screening have been performed to
date.9 15-17 Meta-analysis of these shows that
AAA screening reduces AAA-related mortality by about 40% in males aged 65 to 79
years.18 However, issues of concern include the
risk of overtreatment, the benefit-harm balance of elective repair, and health
system capacity. (see companion article in this NZMJ issue for further
discussion on AAA screening).
The United Kingdom began gradually implementing population
screening for AAA in 2009, screening males aged 65
years.19 In the United States, Medicare has
covered AAA screening in male ever-smokers aged 65 to 75 and females with a
family history of AAA since 2007.20 There is
currently no policy for AAA screening in New Zealand, although “awareness
of the research evidence for screening is
high.”21
The evidence base for AAA screening draws heavily from
international studies. The relatively small body of local research has been
focused mainly on in-hospital mortality from rupture, selection criteria for
emergency repair, clinical presentation of rupture, risk factors, and
endovascular repair analysis. There is a lack of recent national-level
information on overall epidemiology of AAA events and deaths, both in and out of
hospital. This information is essential to inform any policy around AAA
screening in New Zealand.
Accordingly, the objective of this study is to describe the
burden of AAA disease in New Zealand by AAA events, AAA-related deaths, and
vascular surgical workload. It also aims to describe AAA events and deaths by
age, sex, ethnicity, and operative status. This is the first of two papers; the
second evaluates the evidence for population screening for AAA in New Zealand
against screening criteria.
MethodologyStudy population—Records with
ICD-10 codes for AAA [ I71.3 ‘abdominal aortic aneurysm, ruptured’
and I71.4 ‘abdominal aortic aneurysm, without mention of
rupture’]22 were extracted from two
national databases, the Mortality Collection and the National Minimum Dataset
(NMDS).23
Collectively, these datasets contained all deaths
between 2002 and 2006 for which the underlying cause of death was AAA,
and all publicly funded hospital discharges from 2002 to 2006 with any
diagnosis of AAA. From these datasets, three populations were defined: AAA
Events, AAA Deaths, and AAA Alive Discharges (Figure 1).
In order to identify these three populations, firstly,
hospital discharges that involved a AAA operation were identified from the NMDS
dataset (using ICD-10 operation codes for emergency and elective repair). These
were then separated into AAA Operative Deaths (within 30 days of procedure) and
AAA Alive Discharges using the event end type codes. All AAA Operative Deaths
were then matched against the Mortality Collection, and duplicates
identified.
The non-duplicates were assumed to be AAA Non-Operative
Deaths, as AAA rupture without surgery carries a 100%
mortality.[1]
Variables—The analysis was
limited to the AAA Events and AAA Deaths populations. These were then analysed
by age (<55 yrs; 55-64 yrs; 65-74 yrs; 75-84 yrs; 85+ yrs); sex; ethnicity
(prioritised ethnicity fields were provided by the Ministry of Health
Information Directorate as per Ministry of Health ethnicity data protocols and
categorized as European, Māori, Pacific Island, Asian, and
Other),24,25 and operative status (elective
repair, emergency repair after rupture, or no surgery after rupture).
Figure 1. Populations identified from datasets
used
 Statistical methods—The tables
show frequency counts and proportions for AAA Events and AAA Deaths. Operative
mortality (AAA operative deaths/AAA operative events x100), case fatality rates
(AAA deaths/AAA events X 100), and age and sex standardised mortality and event
ratios have been calculated. The reference population for standardised ratios
was the 2006 Census Usually Resident Population
(CURP),26 apart from the prioritised ethnicity
analysis (which utilised 2001 census data as prioritized ethnicity data by age
and sex for the 2006 census were not available at the time of
analysis).27 Statistical analysis was performed
using SAS version 9.1 software. Confidence intervals for case fatality rates
were calculated using OpenEpi version 2.3
software.28 Confidence intervals for indirectly
standardised event and mortality ratios were calculated using the formulae from
Rothman, Green & Lash.29
Prevalence and incidence of AAAs could not be
calculated because it was not possible to identify individuals with AAAs too
small for elective repair, those who do not qualify for/refuse elective repair,
and those with intact but undiagnosed AAAs.
Ethical approval—Ethical
approval was obtained from the Multi-Region Ethics
Committee.30 The Ngāi Tahu Research
Consultation Committee was also consulted before project
initiation.31
ResultsTable 1 is an overview of AAA events and deaths, by
operative status. There were 1182 AAA-related deaths between 2002 and 2006,
equating to about 236 deaths per year. Almost 80% of these deaths were in
patients after rupture who did not undergo surgery, and 13% and 7.5% in those
not surviving emergency repair and elective repair, respectively.
There were 1774 AAA repairs between 2002 and 2006; about 25%
of these were emergency repairs and 75% elective repairs. This equates to about
87 emergency repairs and 267 elective repairs each year. The 30-day operative
mortality rate was 35.2% for emergency repair, and 6.7% for elective repair.
Table 1. AAA events, AAA deaths, and operative
mortality between 2002 and 2006
* Due to rounding, percentages may not add up to
exactly 100%.
†This table shows a discrepancy of 13 individuals
between ‘deaths’ and ‘events’. This is due to 13 people
who underwent repair but died beyond the 30-day mark. From the AAA events
perspective, they were counted as repairs. However, these 13 did not fulfil
definition of an ‘operative death’ (i.e. within 30 days of
operation) and so by default had to be included in the non-operative
group.
Table 2 shows AAA events, deaths, case fatality, and
operative mortality rates by age group. About 89% of all AAA events and almost
94% of all AAA deaths occurred in individuals aged > 65 years.
The overall emergency repair operative mortality rate was
35.2%, and the elective repair mortality rate was 6.7%. Predictably, operative
mortality rates increased with increasing age. Operative mortality in
individuals aged > 85 years was about 58% for emergency repair, and almost
12% for elective repair.
Table 2. AAA events, deaths, case fatality and
operative mortality by age group between 2002 and 2006
Table 3 shows AAA events by operative status in each age
group. There is a pattern of reduced surgical intervention (both elective and
emergency repair) with increasing age. Elective repairs predominated in younger
age groups, and non-operative events predominated in older age groups. In
individuals aged ≥85 years, non-operative events constituted almost 81% of
all AAA events. Reduced surgical intervention at older ages is expected given
that advanced age is a predictor of poor
outcome.32,33
Table 3. AAA events by age group and operative
status between 2002 and 2006
* Small event numbers in this age group, should be
interpreted with caution
§ Due to rounding, percentages
may not add up to exactly 100%.
Table 4 shows AAA events and deaths by sex and ethnicity,
along with age and sex standardised event and mortality ratios.
Table 4. AAA events and AAA deaths by sex and
ethnicity between 2002 and 2006, with age and sex standardised event and
mortality ratios
* reference population for indirect standardisation in
sex analysis was 2006 CURP males.
†reference population for indirect
standardisation in ethnicity analysis was 2001 CURP for each ethnicity
# 46 events were missing ethnicity
data.
About 72% of AAA events, and 64% of AAA deaths occurred in
males. After indirect standardisation, the observed AAA event rate in females
was about 23% that of males. The death rate in females was about 30% of that in
males. The disparity between sexes in AAA death rates is narrower than in AAA
event rates. One explanation for this is the higher case fatality in females
(56%) compared to males (39%).
In other analyses not shown here, higher case fatality in
females was evident in each age group, and females also presented at older ages
for rupture and elective repair.
Almost 91% of AAA events between 2002 and 2006 occurred in
New Zealand Europeans, 6% in Māori, and about 1% in each of Pacific, Asian
and ‘Other’. After age and sex standardisation, Māori had a AAA
event rate about 1.5 times higher than New Zealand Europeans. However, the
standardised mortality rate of Māori was about double that of New Zealand
Europeans. In other analyses not shown here, Māori also presented at
younger ages for rupture and elective repair.
The results suggest that Pacific people have somewhat lower
event rates but higher mortality, although neither are statistically
significant. Both event and mortality ratios suggest a lower disease burden
among Asian people, but considerably higher burden among those in
‘Other’ ethnic groups.
DiscussionBetween 2002 and 2006, there were on average 236 diagnosed
AAA-related deaths per year. Almost 94% of these occurred in individuals aged
> 65 years. Almost 80% of AAA deaths occurred in a non-operative
setting, 13% associated with emergency repair, and 7.5% associated with elective
repair. There was an average of 267 elective repairs and 87 emergency repairs
per year, with associated operative mortality rates of 6.7% and 35.2%
respectively. Although over 70% of AAA events occurred in males, females had
higher case fatality across every age group. Similarly, although over 90% of AAA
events and deaths occurred in New Zealand Europeans, Māori had a
standardised mortality rate twice as high as New Zealand Europeans.
The total number of AAA repairs here is similar to the 1868
repairs reported by Rossaak et al between 1993 and 1997. Any change in the
relative proportions of elective and emergency repair between 1993-97 and
2002-2006 cannot be commented on, as Rossaak et al used three categories of AAA
repair (emergency, urgent, and elective) as compared to the two categories used
here.34 The emergency repair operative
mortality rate of 35.2% is similar to that reported by Grant et al (37.8%) and
slightly lower than the 40% reported in a 2007 NZVASC
audit.35 36 It compares favourably with
international estimates, which range from 30 to
65%.2-4 The relatively low emergency repair
mortality rate in New Zealand may reflect surgical expertise, good postoperative
care, a stricter selection policy for emergency repair, or some combination
thereof. The elective repair mortality rate of 6.7% is slightly higher than the
4% reported in the 2007 NZVASC audit,36 and is
in line with international estimates of 3 to
10%.9-14 Based on this study, the risk of dying
was five times higher with emergency repair than with elective repair.
This analysis identified three populations that appear to be
particularly vulnerable. Firstly, individuals > 65 years account for
the vast majority of AAA deaths, and case fatality is particularly high in
individuals > 85 years. This is not surprising given AAA prevalence is
estimated to increase by 6% per decade after 65
years.3 Advanced age is also associated with
lower rates of surgical intervention and significantly higher operative
mortality rates from both elective and emergency
repair.37-40 However, less
incidental/opportunistic detection of AAAs in this age group may also play a
role, along with a higher likelihood of declining repair even when offered.
Secondly, although females have lower AAA prevalence and
mortality than males, they have higher case fatality across every age group.
This is consistent with both national and international
evidence.35 41 42 Possible reasons include
higher risks of rupture, lower rates of emergency repair being offered, and
higher operative mortality from emergency repair. Internationally, concerns have
been raised about possible gender bias in diagnosis of or selection for surgical
treatment in AAA.43
Thirdly, Māori have higher AAA event and mortality
rates as compared with New Zealand Europeans, and also present with the
condition at a younger age. This is consistent with Rossaak et al’s
findings when analysing AAA admissions in New Zealand between 1993 and 1997.
Additionally, more emergency procedures and a higher proportion of admissions
for rupture was also reported.34 The
disproportionate burden of AAA disease in Māori is likely to be
multifactorial. Higher prevalence of smoking in Māori is a risk factor for
both AAA development and AAA rupture.44 Higher
prevalence of high blood pressure,45
smoking,44 diabetes, and
obesity46 may also increase mortality from
emergency and elective repair. Māori also have poorer access to primary
care, which may mean less opportunity for AAA detection. Additionally, there is
increasing evidence (particularly from studies in cardiovascular disease
management) that secondary and tertiary services may serve Māori less well
than non- Māori.47-49
Strengths and limitations—The major
strength of this study is that it combines mortality and hospital datasets to
provide a more comprehensive picture of AAA burden. Previous studies have
largely utilised hospital data, and this is a highly selected group given less
than half of rupture patients reach the hospital alive. The wider view afforded
by this study is essential in planning a population-based intervention.
Coding inaccuracies within the datasets used is a potential
limitation of this study. This was minimized by using AAA operation codes to
identify individuals with AAA-related diagnoses, rather than more subjective AAA
diagnosis codes. Individuals admitted with AAA who did not undergo repair would
not have had operation codes. However, these individuals would have been
represented in the mortality dataset due to the fatal nature of this condition.
The analysis of AAA events and deaths by age, sex, and
ethnicity provide valuable information on the demographics of individuals with
AAA. However, in certain populations (< 55 years and some ethnicities),
numbers were small and results should be interpreted with caution. This analysis
also was not able to differentiate between endovascular and open repair. Trends
in endovascular repair have significant implications for decisions relating to
population-based screening. Finally, undercounting of Māori should always
be considered. Studies have shown that there is no net undercount of Māori
on mortality records from this period, but hospitalisation data may be less
reliable.50
The study population was not able to include individuals
with AAAs too small for elective repair, individuals who do not qualify
for/refuse elective repair, and individuals with undiagnosed but intact AAAs.
Thus, this study cannot reliably comment on AAA prevalence or incidence. It is
also likely that the figure of 236 AAA-related deaths per year may be an
underestimate. While deaths from elective or emergency repair are reliable, the
same cannot be said for non-operative AAA deaths. Firstly, there are significant
inaccuracies in death certification, particularly in the elderly. In particular,
in an elderly individual with an undiagnosed AAA, there is a tendency for sudden
death to be attributed to a more common condition like coronary artery
disease.51 52 Secondly, low autopsy rates
(particularly in the elderly) compound the risk of misclassifying the cause of
death.51 53 54 The only way of overcoming this
knowledge gap is a population prevalence study.
Implications for policy—This study
describes AAA events, deaths, and vascular surgical workload over a five-year
period. Alongside other local studies, it provides a baseline for assessing the
appropriateness and feasibility of a AAA screening programme in New Zealand.
However, a population-based prevalence study would provide a more complete
picture of AAA burden. Additionally, the drivers of high event and mortality
rates in Māori, and high case fatality in females warrant further
investigation. An understanding of existing inequalities in AAA disease is vital
if a potential AAA screening programme is to avoid exacerbating them. Knowledge
of vulnerable populations and existing service gaps is imperative in formulating
AAA screening policy, identifying target areas for implementation, and guiding
quality assurance measures.
Competing interests: Caroline Shaw is
a member of the National Screening Advisory Committee which provides independent
advice to the Director General of Health on screening issues.
Author information: Nisha Nair, Public
Health Registrar, University of Otago Wellington School of Medicine & Health
Sciences, Wellington; Caroline Shaw, HRC Clinical Training Research
Fellow/Public Health Physician, Department of Public Health, University of Otago
Wellington School of Medicine & Health Sciences, Wellington; Diana Sarfati,
Senior Lecturer/Public Health Physician, Cancer Control and Screening Research
Group, University of Otago Wellington School of Medicine & Health Sciences,
Wellington; James Stanley, Biostatistician/Research Fellow, University of Otago
Wellington School of Medicine & Health Sciences, Wellington
Correspondence: Nisha Nair, Public Health
Registrar, c/o Cancer Control and Screening Research Group, University of Otago,
Wellington, PO Box 7343, Wellington South. Phone (04)9186042, fax (04)3895319,
email nisha.nair1004@gmail.com
References:
[1]
In a very small number of patients with AAA rupture, the surrounding tissue
seals off the bleeding and the patient remains haemodynamically stable. This is
termed chronic AAA rupture and patients can survive for a prolonged length of
time. However, risk of free rupture is very high and prompt surgical repair is
clinically indicated. For the purposes of this paper we have assumed a 100%
mortality as this small group is unlikely to alter the findings.
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