A risk-adjusted analysis of mortality and severe morbidity in patients with ruptured
abdominal aortic aneurysm from February 1994 till February 2010 in the OLVG,
Amsterdam
Master program medical science, scientific rotation
University of Groningen, the Netherlands
O.N.H. Kahmann
Onze Lieve Vrouwe Gasthuis, Amsterdam
Department of vascular surgery
03/03/2010 - 21/07/2010
Supervised by:
Dr. A.C. Vahl, vascular surgeon OLVG, clinical epidemiologist
Dr. J.J.A.M. van den Dungen, vascular surgeon UMCG
ABSTRACT
Background. A ruptured abdominal aortic aneurysm (RAAA) is a life-threatening
disorder. It is associated with a risk of death approaching 80-90%, including
operative therapy. Despite improved perioperative care, the operative mortality rate
(40-50%) has not changed during recent decades. Given the preoperative variability
in presentation of patients, it is difficult to compare postoperative outcomes. The
purpose of the present study was to make a retrospective risk-adjusted analysis of
the outcomes of RAAA during a 16-year period in the Onze Lieve Vrouwe Gasthuis
in Amsterdam.
Methods. Over a 16-year period (February 1994 to February 2010) 206 patients
underwent conventional open surgery or endovascular repair for RAAA. Through a
retrospective review of the patient’s hospital charts, data were collected to determine
the actual mortality and severe morbidity. These findings were compared with the
preoperative risk assessment according to the V-POSSUM (Vascular – Physiological
and Operative Severity Score for enUmeration of Mortality and morbidity) method
and the GAS (Glasgow Aneurysm Score).
Results. The 30-day mortality rate was 45/206 (22%) in the whole cohort, 41/179 (23%,
95% Confidence Interval (CI) 17-30) after open repair and 4/27 (15%, 95% CI 6-32)
after emergency EndoVascular Aneurysm Repair (eEVAR). The patient population
did not significantly change over time according to age, gender, GAS and VPOSSUM. Neither did the 30-day mortality rate. 54 patients (26%) required intensive
care treatment for more than 5 days and 72 (35%) had one or more major
complications. The mean GAS in patients who did not survive RAAA repair was 102
(± SD 11), compared to 89 (± SD 15) among patients who survived (P<0.001). The GAS
appeared to be a reasonable predictor of postoperative outcome for both open and
endovascular RAAA repair, with an AUC (Area Under the Curve) of 0.73 (± SD 0.04;
95% CI 0.65-0.80; P<0.001) . The mean V-POSSUM among patients who died was 73
(± SD 21), compared with 54 (± SD 28) among survivors (P<0.001). The V-POSSUM
predicted mortality was less accurate: AUC 0.69 (± SD 0.05; 95% CI 0.60-0.77;
P<0.001). The only preoperative variables independently predicting 30-day mortality,
were age (P=0.006) and lowest preoperative systolic blood pressure (P=0.032).
Conclusion. In this study the 30-day mortality rate after RAAA repair was low
(22%). It did not change significantly over the past 16 years. A noticeable trend was
that the introduction of a less invasive operation technique (eEVAR) resulted in a
lower amount of severe postoperative complications. The GAS appeared to be a
reasonable predictor for outcome after both open and endovascular RAAA repair.
The V-POSSUM scoring method had limited predictive value and overestimated
preoperative risk. The preoperative measures for risk assessment we used, did not
identify the high risk patients at an individual level. Therefore it appears that V2
POSSUM and GAS do not aid in determining whether or not an attempted operation
is appropriate. Nevertheless these methods can be used in surgical audit or for interhospital comparisons.
3
INDEX
Abstract
2
I. Introducion
Epidemiology
Etiology
Symptoms
Risk of rupture
Treatment
Predictors for outcome
Measures predicting outcome
Aim
5
5
6
6
7
7
8
9
II. Patients and methods
Study population
Study method
Data collection and definitions
Outcome measures
Statistical analyses
10
10
10
11
11
III. Results
12
IV. Discussion
17
V. Conclusion
21
VI. Samenvatting
22
VII. References
24
4
I. INTRODUCTION
Epidemiology
All reported incidences of RAAA vary due to variability in data retrieval methods,
sample selection, sex, age, and autopsy rate. The incidence of RAAA is
approximately 6.0/100,000 per year and has not changed over recent decades.(1-3)
The incidence rate of RAAA between men and women is about 3:1.(1;2;4) Gender
related differences in AAA development seems to be caused by an estrogen mediated
reduction in proteases derived from macrophages. These proteases are causing
extracellular matrix breakdown, leading to aneurysm formation.(5;6) Using the same
diameter (≥ 3 cm) in defining AAA, most prevalence studies underestimate AAA
incidence in women, not taking into account gender associated differences in normal
aortic diameter.(7)
Despite advances in surgical health care and in perioperative intensive care, RAAA
remains a life-threatening condition with an estimated overall mortality of 80-90%.
More than 50% of patients die before reaching hospital or without operation.(1;2) A
graduate reduction of mortality after RAAA repair is seen in a meta-analysis over a
50-year period.(8) Mortality rate in patients reaching the hospital alive, remains as
high as 48%; multi organ failure being the predominant cause.(9)
A meta-analysis of articles published between 1991 and 2006 showed a constant inhospital mortality rate of 48.5%.(10) According to the authors this lack of
improvement is caused by the increased age of patients undergoing RAAA repair.
In the Netherlands Visser et al. found an in-hospital mortality rate of 41% that did
not change in a 10-year period (1991-2000).(11) They found age and hospital type to
be the most significant predictors of mortality. Highest mortality rates were found in
University hospitals and lowest in the smaller hospitals (0-399 beds).
In industrialized countries RAAAs cause 1 to 2% of all deaths.(12;13) Age being one
of the main risk factors in developing AAAs, the number of RAAAs will increase
because of the proportional rise in the ageing population.
Etiology
The normal aortic diameter is approximately 2.0 cm, with a range of 1.4 to 3.0 cm. An
AAA is most commonly described as an abdominal aortic measuring 3.0 cm or more
in diameter.(14) The underlying cause of developing an AAA is often uncertain.
There is considerable evidence for genetic predisposition.(5;15) The role of
atherosclerotic disease in causing AAA is questionable.(5;6) Histologicaly, there is a
destruction of elastin and collagen in the tunica media and the tunica adventitia of
the arterial wall. The medial wall is characterized by smooth muscle cell loss and
5
there is infiltration of lymphocytes and macrophages. Inflammation and proteases
play an important role in this process.(5;6;16)
Symptoms
AAAs expand at a variable rate and are usually asymptomatic. When the strength of
the aortic wall is insufficient to sustain the intraluminal pressure, the aneurysm
ruptures. One of the symptoms is pain in abdomen and back, possibly radiating to
the groin and legs. Other symptoms are nausea, vomiting, pallor, sweating,
tachycardia and hypotension.(1) Immediate surgical treatment is the only way to
save the life of a patient with RAAA. Only when the rupture is contained, symptoms
can be less acute or even missing. Operative treatment can then be performed with a
delay of some days or even weeks.(17)
Risk of rupture
13% of all AAAs will eventually rupture.(1) Several studies evaluated the factors that
may contribute to AAA rupture. The maximum diameter of an AAA is an important
predictor of rupture, with risk increasing markedly at diameters more than 5.5 cm
(Figure I).(18)
Figure I
Risk of rupture through time according to initial diameter
While male sex is a risk factor for developing an AAA, female gender is considered
to be a risk factor associated with rupture.(5) This can simply be explained by the
difference in normal aortic diameter, which is smaller in women than in men.
Therefore an increased aortic diameter reflects a greater degree of dilatation in
women than in men. Nevertheless, for both genders the current threshold for elective
repair is similar. A lower threshold for women with AAA should be considered.(7)
6
Besides aneurysm diameter and gender, aneurysm growth rate and biomechanical
factors are other important factors associated with a higher risk of rupture.(5;18;19)
Other factors increasing the risk of rupture are continued smoking, uncontrolled
hypertension and increased wall stress.(20)
Treatment
When the risk for aneurysm rupture is clearly higher than the expected operative
mortality, elective surgery is indicated. Open surgery used to be the standard
procedure for ruptured or intact AAA repair. The first successful elective AAA repair
occurred in 1952.(21) In 1991 Parodi and Volodos published their first results after
introduction of a new technique for elective AAA surgery: endovascular aneurysm
repair (EVAR).(22;23) This treatment was used as a less invasive alternative
technique and appeared to be suitable for both elective and emergency repair.
Through the femoral arteries, under fluoroscopic guidance, an endograft is placed to
act as a false lumen excluding the aneurysm lumen.
The first report of emergency endovascular repair of a RAAA (eEVAR) was
published in 1994.(24) Not all patients with a RAAA are suitable for eEVAR. Based
on the dimensions of the endovascular graft, the infrarenal aortic neck and both iliac
arteries must have a sufficient length and diameter. To evaluate the possibility of
endovascular repair a CT angiography must be performed.
In the OLVG the first eEVAR took place in October 1999. Since 2004 the OLVG is one
of the three hospitals in Amsterdam participating in the Amsterdam Acute
Endovascular Treatment to Improve Outcome of Ruptured Aortoiliac Aneurysm trial
(AJAX trial). This trial is aiming to study the combined outcome of conventional
emergency surgery versus endovascular treatment for RAAA. All patients with a
suspected RAAA are transported to the trial centre on duty. CT-angiography is
performed to prove anatomical suitability. If patients are unfit for eEVAR because of
unfavourable anatomy or if they are in an unstable condition before or during CTscanning, immediate open surgery is performed. All other patients are randomized.
Outcomes of all patients are recorded and compared.(25) First results are expected
late 2010.
Predictors for outcome
Most vascular surgeons practice a selective policy of operative intervention for
patients with RAAA. Determining whether or not an attempted operation is
appropriate, is largely a subjective decision. The evidence on which to base operative
selection remains uncertain.(26) In previous studies several factors have been
mentioned as possible predictors for outcome after RAAA repair. Higher age was
associated with a higher mortality rate.(3;11;27;28) Co-morbidity (COPD,
cerebrovascular disease, renal insufficiency, coronary heart disease), along with
advanced age, affected mortality after RAAA.(28) In contrast, other studies
7
suggested there is no association between preoperative co-morbidity and
outcome.(29;30) Gender did not seem to affect postoperative mortality.(11;28)
Measures predicting outcome
Many previous studies reported the outcomes after RAAA repair. These mortality
rates have varied depending on the patient’s clinical condition at presentation. Crude
numbers of mortality and morbidity alone are insufficient to reflect the quality of
care. Appropriate risk adjusted analysis of patients with RAAA would support
comparative audit between different institutions and surgeons, allowing better
evaluation of RAAA repair.(31;32) In addition to surgical audit, risk stratification can
be useful in preoperative decision-making. Several scoring systems were developed
to estimate preoperative risk. The POSSUM scoring system and the Glasgow
Aneurysm Scale are two such statistical models.
POSSUM scoring system. The Physiological and Operative Severity Score for the
enUmeration of Mortality and morbidity (POSSUM) is a method that is developed
for standardizing patient data and for comparative audit in series of surgical
patients.(33) It was described and prospectively validated by Copeland et al. in
1991.(34) The original POSSUM scoring system was designed for a broad range of
general surgery patients. A special method was developed for patients undergoing
vascular surgery, the V-POSSUM, using the same variables in an other equation.(35)
The V-POSSUM data set consists of 12 preoperative variables (age, cardiac signs,
respiratory signs, systolic blood pressure, pulse rate, Glasgow coma scale, serum
urea, serum sodium, serum potassium, hemoglobin level, white blood cell count,
electrocardiogram) and 6 intra-operative variables (grade of operation, number of
procedures, total blood loss, peritoneal soiling, presence of malignancy, timing of
operation). The combined physiologic scores and operative scores are used to
generate risk equations by logistic regression analyses that convert the data into a
predicted percentage mortality.
GAS scoring system. The Glasgow Aneurysm Score is a preoperative scoring
system, established in 1994, for predicting outcome after open repair of intact or
ruptured AAA. The preoperative score is calculated using the following formula:
Risk score = age in years + 17 points for shock + 7 points for myocardial disease + 10
points for cerebrovascular disease + 14 points for renal insufficiency.(28) ‘Shock’ is
based on the clinical information of hypotension, tachycardia, pallor and sweating.
Myocardial disease refers to previous myocardial infarction and/or ongoing angina
pectoris. Cerebrovascular disease refers to all grades of stroke, including transient
ischemic attacks. Renal insufficiency includes a history of acute and chronic renal
failure, and/or a serum urea level > 20 µmol/l and or serum creatinine level > 150
µmol/l at presentation. A preoperative score < 70 is associated with a low risk of
8
mortality after RAAA repair. A high risk of mortality is seen in patients with a GAS >
85. A GAS > 95 correlated with a mortality rate of 80 % in a group of 92 patients.(36)
Aim
The main purpose of this study was to make an analysis of mortality and severe
morbidity in patients with RAAA in the OLVG from February 1994 till February
2010, adjusted for the variability in preoperative risk using the V-POSSUM and the
GAS scoring systems. Main interests were changes of patient population and
postoperative outcome over the years, investigating the effect of the introduction of
eEVAR and the AJAX trial.
The second aim was to evaluate independent preoperative variables which influence
the outcome after RAAA repair.
9
II. PATIENTS AND METHODS
Study population
All consecutive patients who underwent RAAA repair in the Onze Lieve Vrouwe
Gasthuis in Amsterdam between February 1994 and February 2010 were included in
this survey. Patients were included if they underwent either open surgery or
endovascular repair. RAAA was defined as blood outside the aortic wall and was
determined by preoperative ultrasound or computed tomography (CT) or intraoperative findings. Intra-operative deaths were also included for analysis. The
patients who died on their way to the hospital and the patients who did not survive
the transport to the operation room were excluded.
Study method
Through a retrospective review of the patients’ hospital charts, data were collected to
determine the actual mortality and severe morbidity. These findings were compared
with the predicted mortality yielded by two different outcome predicting scoring
systems: The V-POSSUM method and the Glasgow Aneurysm Scale.
Data collection and definitions
Retrospectively collected data included: patient characteristics (i.e. gender, age,
known cardiac and respiratory co-morbidity, history of cerebrovascular disease and
renal insufficiency), patients hemodynamic condition upon arrival at the emergency
room (i.e. highest and lowest systolic blood pressure and pulse rate), other clinical
signs of shock at presentation (i.e. pallor, sweating), preoperative V-POSSUM
variables (i.e. Glasgow coma scale, serum urea, serum sodium, serum potassium,
hemoglobin level, white blood cell count, electrocardiogram), use of CT-scan for
diagnosis, morphology of the AAAA (suprarenal, juxtarenal or infrarenal), time to
treatment, which mode of repair was performed (open surgery or eEVAR) and 6
intra-operative V-POSSUM variables (grade of operation, number of procedures,
total blood loss, peritoneal soiling, presence of malignancy, timing of operation).
Postoperative data include: days in hospital, days on intensive care unit, minor
morbidity (pneumonia, urinary tract infection, conservatively treated wound
infection, temporary kidney insufficiency) severe morbidity (myocardial infarction,
stroke, graft thrombosis, permanent kidney insufficiency, major amputation, bowel
ischemia, spinal cord ischemia, prothesis infection, inevitable re-operation and the
reason for re-operation) and 30-day mortality (intra-operative mortality and death ≤
30 days after operation).
If there were missing data regarding medical history, the risk factor was assumed not
to be present.
10
Outcome measures
The V-POSSUM score and the Glasgow Aneurysm Score were retrospectively
calculated. Preoperative scores were related to postoperative outcome.
Statistical Analyses
Results were tabulated and analysed using SPSS Statistics for Windows version 17.0
(SPSS Inc, Chicago, Il). Patient demographics and continuous variables were
summarised using measures of central tendency (i.e. mean) and dispersion (i.e.
standard deviation). Categorical data were summarised using number and
percentage.
To assess the distribution of continuous variables in different subgroups we used the
Student’s t-test. Chi-square and Fisher’s exact test were used for univariate analysis
in categorical data.
The discriminative ability of the preoperative risk assessments (GAS and POSSUM
score) was evaluated by using receiver operating characteristics (ROC) curves. If the
area under the ROC curve (AUC) is 0.5 there is no discriminative ability. The better
the discriminative ability, the closer the AUC gets to 1.0. AUC values >0.8 represent
good discriminative ability, whereas values of 0.7–0.8 represent reasonable
discrimination.
Preoperative variables with P<0.05 at univariate analysis were included for a
multivariate analysis. We used the logistic regression with backward stepwise
selection to evaluate the factors affecting the 30-day mortality. A P<0.05 was
considered statistically significant.
11
III. RESULTS
Patient population. Between February 1994 and February 2010, a total of 206 patients
underwent RAAA repair. This study cohort with a mean age of 74 (± SD 8) consisted
of 174 males (84.5%). 179 patients underwent open repair and 27 underwent
emergency endovascular repair. The patient demographics and characteristics are
listed in Table I.
Mean V-POSSUM score is lower (P<0.001) in the eEVAR group as favourable
operative factors (i.e. blood loss, peritoneal contamination) are taken into account.
All patients with an altered Glasgow Coma Scale (i.e. <15) were in the open surgery
group, because further preoperative CT imaging and thus eEVAR were impossible.
Taking into account the endovascular group was small (13% of the whole cohort),
there were no other statistically significant differences between both groups.
Table I
Patient demographics and characteristics
Whole cohort
(n = 206)
Male
Open surgery
(n = 179)
eEVAR
(n = 27)
174
(85)
151
(84)
23
(85)
Mean age
74
(8)
74
(8)
75
(8)
CVA/TIA
34
(17)
28
(16)
6
(21)
Renal insufficiency
42
(20)
36
(20)
6
(21)
Cardiac co-morbidity
73
(35)
63
(35)
10
(36)
Respiratory co-morbidity
44
(22)
38
(22)
6
(21)
Mean systolic blood pressure
98
(45)
96
(45)
110
(45)
Abnormal ECG
65
(32)
56
(31)
9
(32)
Mean heart rate
87
(22)
87
(22)
87
(21)
Altered GCS (i.e. <15)
13
(7)
13
(8)
0
(0)
Shock
133
(65)
120
(67)
14
(50)
Cardiac arrest
30
(15)
27
(15)
3
(11)
Mean hemoglobin
7,1
(2)
7,1
(2)
7,2
(1)
Mean white cell count
12,9
(6)
13
(5)
12,4
(6)
Mean serum sodium
139
(4)
139
(4)
138
(3)
4
(1)
4
(1)
3,9
(1)
Mean serum urea
8,5
(4)
8,5
(4)
8,8
(4)
Mean serum creatinine
118
(43)
118
(42)
117
(49)
Mean GAS
92
(15)
92
(15)
91
(17)
Mean V-POSSUM mortality rate
58
(28)
62
(26)
32
(24)
Length of stay (days)
19
(12)
20
(13)
14
(10)
Observed 30-day mortality
45
(22)
41
(23)
4
(15)
Mean serum potassium
All variables are in no (%) or mean (+-SD) where appropriate.
12
Mortality. The 30-day mortality rate was 45/206 (22%) in the whole cohort, 41/179
(23%; 95% Confidence Interval (CI) 17-30) after open repair and 4/27 (15%: 95% CI 632) after eEVAR (P=0.34). Intra-operative death occurred in 19 patients (42% of 45
patients not surviving RAAA repair). The mean survival period of the 26 patients
who died in the 30-day postoperative period was 7 days.
Complications. 54 patients (26%) required intensive care treatment for more than 5
days and 72 (35%) had one or more major complications (myocardial infarction,
stroke, graft thrombosis, permanent kidney insufficiency, major amputation, bowel
ischemia, prosthesis infection, inevitable re-operation). Details of postoperative major
and minor complications are listed in Table II. Especially infections and severe renal
failure were seen more often after open surgery. There were more major
complications after open surgery, although not statistically significant (P=0.055).
Table II
Postoperative complications
Whole cohort
(n = 206)
N (%)
Open surgery
(n = 179)
N (%)
eEVAR
(n = 27)
N (%)
Infections
Pneumonia
32
(16)
27
(15)
4
(15)
Urinary tract infection
17
(8)
17
(10)
0
(0)
Wound infection
14
(7)
14
(8)
0
(0)
Sepsis
13
(6)
12
(7)
1
(4)
Intra-abdominal abces
11
(5)
11
(6)
0
(0)
CVC infection
5
(2)
5
(3)
0
(0)
Prothesis infection
4
(2)
4
(2)
0
(0)
Renal failure not requiring dialyis
32
(16)
25
(14)
7
(26)
Renal failure requiring temporary dialyis
21
(10)
21
(12)
0
(0)
Renal failure requiring permanent dialyis
5
(2)
5
(3)
0
(0)
Bleeding
23
(11)
22
(12)
1
(4)
Intestinal ischemia
20
(10)
18
(10)
2
(7)
Second look
15
(7)
14
(8)
1
(4)
Lower limb ischemia
13
(6)
12
(7)
1
(4)
Abces
12
(6)
12
(7)
0
(0)
8
(4)
7
(4)
1
(4)
54
(26)
48
(27)
6
(22)
Re-operation
Wound dehiscence
>5 Days intensive care treatment
CVA
1
(1)
1
(1)
0
(0)
Myocardial infarction
12
(6)
10
(6)
2
(7)
≥1 Major complication
72
(35)
67
(38)
5
(18)
13
GAS. The mean GAS in the group of patients who did not survive RAAA repair was
102 (± SD 11), compared to 89 (± SD 15) among patients who survived (P<0.001). In
Figure III mean postoperative mortality rate is shown for different quartiles of the
GAS. All patients with a GAS <85 survived. 8 of 18 patients (44%) with the highest
GAS (>115) died.
Figure III
Mean 30-day mortality rates (%) among quartiles of the Glasgow Aneurysm Score and the V-POSSUM calculated mortality
risk
V-POSSUM. The mean V-POSSUM among patients who died was 73 (+/- SD 21),
compared with 54 (+/- SD 28) among survivors (P<0.001). The mean 30-day
postoperative mortality rate is shown for different quartiles of the V-POSSUM score
in Figure III. Only one person (2.6%) died in the lowest risk group (0-25%). 48 of 72 of
the patients in the highest risk group (predicted mortality of 75-100%) survived
(66.7%). The observed-to-expected (O:E) ratios were calculated for each quartile
(Table III). The overall O:E ratio was 0.38. This reflects the high number of predicted
deaths (120) compared to the number of actual deaths (45). In each group there was a
difference between observed and predicted mortality which was most obvious in the
low risk group (O:E ratio 0.17). The V-POSSUM over-predicted risk in all quartiles.
Table III
V-POSSUM predicted mortality compared with actual 30-day mortality
Score
Number of
patients
Actual deaths
(%)
Mean
predicted
mortality risk
0-25%
39
1
(3)
15.9
25-50%
36
4
(11)
37.6
50-75%
59
16
(27)
75-100%
72
24
Total
206
45
Predicted
deaths
O:E ratio
(6)
6
0.17
(7)
14
0.29
62.3
(7)
37
0.43
(33)
88.0
(7)
63
0.38
(22)
58.2
(28)
120
0.38
14
(SD)
Receiver operating characteristics curve. The ROC curve was plotted to analyze the
relationship between the preoperative risk measures and the 30-day mortality
(Figure IV). The AUC of the GAS was 0.73 (SD 0.04; 95% CI 0.65-0.80; P<0.001). This
represented a reasonable discrimination of the preoperative risk assessment by the
GAS. The AUC of the V-POSSUM predicted mortality was 0.69 (SD 0.05; 95% CI 0.600.77; P<0.001) representing a less favourable discriminative ability of the predicted
mortality by the V-POSSUM scoring method.
Figure IV
The ROC curve of the Glasgow Aneurysm Score (AUC 0.73; SD 0.04; 95% CI 0.65-0.80; P<0.001) and of the V-POSSUM
predicted mortality (AUC 0.69; SD 0.05; 95% CI 0.60-0.77; P<0.001)
Predicting risk. Predictors of 30-day mortality are listed in Table IV. The only
preoperative variables that were independent predictors for 30-day mortality were
age (P=0.006) and lowest preoperative systolic blood pressure (P=0.032).
Table IV
Preoperative variables associated with 30-day mortality
Variables
Univariate analysis
Multivariate analysis
Age
P = 0.002
P = 0.006
Cardiac comorbidity
P = 0.001
Cerebrovascular comorbidity
P < 0.0001
Renal comorbidity
P < 0.0001
Lowest systolic blood pressure
P = 0.021
Shock
P < 0.0001
Cardiac arrest
P < 0.0001
Hemoglobin concentration
P = 0.003
Creatinine concentration
P = 0.002
Ureum concentration
P = 0.043
15
P = 0.032
16 years of RAAA repair. The number of procedures performed each year increased
significantly over the past 16 years (Figure V). In 2010 three patients underwent
RAAA repair in the period until February. This was when data collection was
aborted.
Figure V
Number of procedures over the years, split by way of repair
To evaluate preoperative variables and postoperative outcome in time, patients were
subdivided into two groups. The first group were treated before the start of the AJAX
trial (1994-2003), the second group during the AJAX trial (2004-2010). The patient
population, divided into two time groups, did not significantly change over time,
according to age, gender, GAS and V-POSSUM. Neither did the 30-day mortality
(Table V).
Table V
Characteristics of the patient population, split in three time groups.
1994-2003 (n=85)
n/year
9
(3)
Age
74
Male
70
GAS
V-POSSUM
Mortality
2004-2010 (n=121)
20
(3)
(8)
74
(8)
(83)
104
(86)
90
(15)
93
(16)
59
(29)
58
(27)
17
(20)
28
(23)
All variables are in no (%) or mean (+-SD) where appropriate.
16
IV. DISCUSSION
Mortality. The 30-day mortality rate in this study compared favourably to those
mentioned in a recently published prospective multicentre trial in the Netherlands;
57/143 (40%) after open repair and 15/58 (26%) after eEVAR.(37) Veith et al.
examined the collected data from 49 centres over the world and found an overall 30day mortality rate of 21% after eEVAR and 36% after open RAAA repair.(38)
Collected data included details of 1037 patients treated by eEVAR and 763 patients
who underwent open repair.
The mean in-hospital mortality rates reported in previous studies and meta-analyses
were 40-50%.(8;10) In our study 5 patients who survived the first 30 postoperative
days, died in days or weeks after the first month, in hospital. Therefore the inhospital mortality rate in the OLVG was 50/206 (24%), which was still low compared
to mortality rates in previous reports.
Ouriel et al. correlated inter-hospital differences in mortality rates after RAAA repair
with surgical experience, delay in treatment and differences in patient
population.(39) Although reports on mortality rates in high and low volume centres
remain contradicting, hospital volume might influence outcome after RAAA
repair.(10;11;40;41) The OLVG is a referral hospital for elective and acute AAA repair
with well developed emergency care, diagnostic facilities, preoperative care and
postoperative intensive care. As can be seen in table V, patient population did not
significantly change over time. This was in contrast with previous studies, which
suggested the lack of improvement of RAAA repair is caused by the increased age of
patients undergoing RAAA repair.(9;10) Mortality rates remained the same, which
suggested a constant pre-, per-, and postoperative quality of care.
As patients who were not operated were not included in this study, it was unclear
which role preoperative selection plays in these postoperative outcomes in the
OLVG. Mean age and mean preoperative scoring measures were comparable or even
higher than scores mentioned in previous studies, suggesting the proportion of
operated high-risk patients was comparable or even higher in the OLVG.(13;30;31;4244) For example, Harris et al. found an overall mortality of 46% and a V-POSSUM
predicted mortality rate of 50%, compared to an overall mortality of 22% and a VPOSSUM of 58% in our study cohort.(30) However, further research into the group of
non-operated patients is necessary to provide clarity on this subject.
Open surgery vs. eEVAR. Veith et al., who examined the collected experience of
eEVAR from 49 centres to clarify the controversial role of this treatment for RAAA,
concluded that eEVAR was better than open repair, provided the patient had a
favourable anatomy and that adequate logistics and skills were available and optimal
techniques and strategies were employed.(38) In the present study, as can be seen in
table 1, eEVAR was not significantly correlated with a lower mortality rate than open
17
RAAA repair (P=0.34). The small amount of patients who underwent eEVAR (n=27)
may have contributed to a lack of significance in outcome differences. These
differences might be explained by preoperative selection bias. Beacause of the fact
eEVAR patients should be hemodynamically stable undergoing a preoperative CTscan, all critically ill and high risk patients were in the open repair group. High
quality evidence to demonstrate superiority of eEVAR over open RAAA repair is
lacking.(9) A randomized controlled trial, like the ongoing AJAX trial, will provide
more insight into this topic, comparing both ways of RAAA repair.
Complications. Despite being an important factor in surgical outcome, postoperative
complications after RAAA repair were not often described in previously published
reports. Compared with results of Leo et al., who published their complications after
open RAAA repair in a group of 114 patients, complication rate in the present survey
appeared to be high in all categories.(32) Their high mortality rate (45%) with a mean
survival of 0.02 days after the operation, may contribute to a low complication rate;
all patients who died in the first postoperative days were less susceptible to
complications like pneumonia and sepsis.
Although not statistically significant, there appeared to be a trend in complication
rate, comparing open and endovascular repair, suggesting favourable outcome after
endovascular repair (P=0.055). However, the small amount of endovascular patients
and the above mentioned preoperative selection bias should be taken into account.
The AJAX trial may provide clarity on this subject.
Hospital volume. The number of procedures performed each year increased
significantly over the past 15 years, with a mean of 9 procedures a year until 2003
and a mean amount of 20 procedures a year since 2004 (Figure V). This was when the
smaller centres in the Amsterdam area started to refer their patients to one of the
main centres on duty for the AJAX trial, explaining the increase of RAAA repair in
the OLVG in this period.
GAS. Several previous studies validated the GAS for RAAA repair. Results were
inconsistent. Leo et al. found the GAS as a highly predictive risk-scoring method of
postoperative death in open RAAA repair, in a retrospective study (AUC 0.91).(32)
All patients with a GAS >100 died in this study. As mentioned before Samy et al.,
who designed the GAS, reported in a prospective evaluation of their scoring system
80% of patients with a GAS >95 did not survive open RAAA repair.(36) In Finland
Korhonen et al. described a mortality rate of approximately 80% of patients with a
GAS >98, with an AUC of 0.75.(43) More recently, Gatt et al. described a mortality
rate of 74% of patients with a GAS >95.(13;43) Tambyraja et al. found the GAS as a
poor predictor for postoperative death with their prospective data. 12 of 28 patients
(43%) with a GAS >105 survived (AUC 0.61).(44) In the present study we found even
higher survival rates in the high-risk group (GAS >105): 22 of 38 patients (58%)
survived. The lower overall mortality rate may have contributed to the poor positive
18
predicting values, but lack of specificity in the preoperative test may be another
cause. Nevertheless, the sensitivity was quite good: no patients in the lowest risk
group (GAS <85) died. Overall the GAS appeared to have a reasonable discriminative
ability with an AUC of 0.73 in the whole cohort. The AUC in the open repair group
alone was also 0.73 (SD 0.07, P=0.02). Although the GAS was developed in a time
open surgery was the standard procedure for RAAA repair, we found even better
discriminative values when using outcomes of endovascular repair alone (AUC 0.88,
SD 0.04, P<0.001). These results are in contradiction with the recently published
findings of Visser et al. from a prospective multicentre study in the Netherlands,
concluding that the discriminative ability of the GAS is limited.(37) The authors
suggested this may be caused by the introduction of eEVAR and they updated the
GAS by adding the type of procedure performed. Further investigation of (updated)
preoperative scoring systems is needed to evaluate their validity in different
procedures.
V-POSSUM The V-POSSUM score was originally designed for standardizing patient
data and for comparative audit in series of surgical patients.(33) It has never been
recommended for outcome prediction.(44) In this retrospective study it appeared to
be difficult to collect all 18 V-POSSUM variables, especially in the hemodynamically
unstable patients who went to the operating room immediately and died during
operation. In these high-risk patients, preoperative variables and risk factors were
often missing. The V-POSSUM method scores missing data as normal. Therefore,
using an incomplete database will lead to reduced V-POSSUM scores, especially in
the critically ill patients. Nevertheless in the present study the V-POSSUM score
overestimated preoperative risk in all quartiles (Table III). Furthermore,
discriminative ability seamed to be limited with regards to an AUC of 0.69, which
did not change analysing the different ways of repair separately. Tang et al.
demonstrated the V-POSSUM method was not a valid tool for comparing outcome
after elective and emergency open AAA repair, in their prospective study.(33)
According to the authors predicted outcomes were easily influenced by missing data.
Harris et al. found V-POSSUM scores that accurately predicted early mortality after
RAAA repair.(30) These data were collected retrospectively and overall mortality
(46%) was much higher.
Predicting risk. As found in previous studies, we could not discover a direct
association between preoperative co-morbidity and outcome.(29;30) Age and lowest
preoperative systolic blood pressure appeared to be the only preoperative variables
that were independent predictors for 30-day mortality. Nevertheless, the two oldest
patients who were operated, both 90 years old, survived. Therefore we can conclude
that age alone is no exclusion criteria for RAAA repair, neither is one of the other
independent risk factors. Other factors, not taken into consideration in the present
study, like terminal illness (e.g. cancer), may be more important in decision-making.
19
16 years of RAAA repair. Despite promising results of observational studies, there is
lack of level one evidence demonstrating the advantages of eEVAR over open RAAA
repair.(9) That is why, since 2004, the OLVG is one of the three hospitals in
Amsterdam participating in the AJAX trial, evaluating the outcome of conventional
open emergency surgery versus endovascular treatment for RAAA. Until February
2010, 40 patients were included in this trial at the OLVG. This number of patients
was too small for conclusions to be drawn. In addition, as the trial was still going on
and the patients were blinded, these patients were not analysed separately in this
report. Nevertheless, we can conclude that despite considerable improvements in
emergency care, diagnostic facilities and perioperative care and the introduction of a
less invasive operation technique, 30-day mortality rate did not change significantly
over the past 16 years of RAAA repair in the OLVG.
We could not find a reasonable explanation for the lack of significant progress over
the past 16 years. The mortality rate was already very low, due to excellent
postoperative care. Further improvements may not be realistic.
20
V. CONCLUSION
In this study the 30-day mortality rate after RAAA repair was low (22%). It did not
change significantly over the past 16 years. A noticeable trend was that the
introduction of a less invasive operation technique (eEVAR) resulted in a lower
amount of severe postoperative complications. The patient population did not
significantly change over time, according to age, gender, GAS and V-POSSUM.
The GAS appeared to be a reasonable predictor for outcome after both open and
endovascular repair. The V-POSSUM scoring method had limited predictive value
and overestimated preoperative risk.
The preoperative measures for risk assessment we used, did not identify the high
risk patients at an individual level. Therefore it appears that V-POSSUM and GAS do
not aid in determining whether or not an attempted operation is appropriate.
Nevertheless these methods can be used in surgical audit or for inter-hospital
comparisons.
The only preoperative variables that were independent predictors for 30-day
mortality appeared to be age and lowest preoperative systolic blood pressure. Age
alone is no exclusion criteria for RAAA repair, neither is one of the other
independent risk factors. Other factors, not taken into consideration in the present
study, may be more important in decision-making.
21
VI. SAMENVATTING
Achtergrond. Een ruptuur van een aneurysma aortae abdominalis (RAAA) is een
levensbedreigende aandoening. Het is geassocieerd met een risico op overlijden van
80 tot 90%. Ondanks verbeterde perioperatieve zorg, is de operatieve sterfte niet
veranderd in de afgelopen decennia (40-50%). Gezien de onderlinge preoperatieve
verschillen binnen de patiëntenpopulatie, is het moeilijk om postoperatieve
resultaten met elkaar te vergelijken. Het doel van deze studie was om een
retrospectieve, risico gewogen analyse van de uitkomsten na RAAA operaties te
maken, over een periode van 16 jaar in het Onze Lieve Vrouwe Gasthuis in
Amsterdam.
Methoden. Over een periode van 16 jaar (van februari 1994 tot februari 2010)
ondergingen 206 patiënten een open buik operatie of een endovasculaire
behandeling in verband met een RAAA. Door middel van een retrospectief
statusonderzoek van de betreffende patiënten werden gegevens verzameld om de
werkelijke sterfte en de ernstige morbiditeit vast te stellen. Deze bevindingen werden
vergeleken met de preoperatieve risicobeoordeling volgens de V-POSSUM methode
(Vascular – Physiological and Operative Severity Score for enUmeration of Mortality
and morbidity) en de GAS (Glasgow Aneurysma Score).
Resultaten. De 30-dagen mortaliteit bedroeg 45/206 (22%) in het gehele cohort,
41/179 (23%, 95% betrouwbaarheidinterval (BI) 17-30) na open chirurgische
behandeling en 4 / 27 (15%, 95% BI 6-32) na eEVAR (emergency EndoVascular
Aneurysm Repair). De patiëntenpopulatie liet geen significante verandering zien in
de loop der tijd, gemeten naar leeftijd, geslacht, GAS en V-POSSUM. De 30-dagen
mortaliteit bleef in de loop der jaren ook constant. De gemiddelde GAS bij patiënten
die operatieve behandeling van RAAA niet overleefden was 102 (± SD 11),
vergeleken met 89 (± SD 15) bij patiënten die wel overleefden (P<0.001). De GAS
bleek een redelijke voorspeller van postoperatieve uitkomst voor zowel open als
endovasculaire RAAA behandeling, met een AUC (Area Under the Curve) van 0.73
(± SD 0.04; 95% betrouwbaarheidsinterval 0.65-0.80; P<0.001). De V-POSSUM bleek
minder nauwkeurig: AUC 0.69 (± SD 0.05; 95% BI 0.60-0.77; P<0.001). De enige
onafhankelijke preoperatieve voorspellers van de 30-dagen mortaliteit, waren leeftijd
(P=0.006) en de laagste preoperatieve systolische bloeddruk (P=0.032).
Conclusie. In deze studie bleek de 30-dagen mortaliteit na behandeling van RAAA
laag (22%). Ondanks de invoering van een minder invasieve operatietechniek
(eEVAR), is de mortaliteit niet significant veranderd in afgelopen 16 jaar. Er leek wel
een trend zichtbaar ten gunste van de endovasculaire procedure wat betreft de
postoperatieve morbiditeit. De GAS bleek een redelijke voorspeller van de mortaliteit
na zowel open als endovasculaire RAAA behandeling. De V-POSSUM
scoringsmethode had beperkte voorspellende waarde en overschatte het
22
preoperatieve risico. De preoperatieve risico-evaluaties die werden gebruikt bleken
ongeschikt om hoog risico patiënten op individueel niveau aan te wijzen. Daaruit
blijkt dat de V-POSSUM en de GAS geen rol kunnen spelen in het oordeel om wel of
niet te opereren. Niettemin kunnen deze methodes worden gebruikt bij chirurgische
audit of voor het vergelijken van resultaten van verschillende ziekenhuizen.
23
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28