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Coiling and clipping in aneurysmal subarachnoid hemorrhage [Elektronische Ressource] / vorgelegt von Zhiyu Nie

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87 pages
Aus der Sektion Neuroradiologie der Albert-Ludwigs-Universität Freiburg i.Br. Coiling and Clipping in Aneurysmal Subarachnoid Hemorrhage INAUGURAL - DISSERTATION Zur Erlangung des Medizinischen Doktorgrades der Medizinischen Fakultät der Albert-Ludwigs-Universität Freiburg i.Br. Vorgelegt 2004 von Zhiyu Nie geboren in Liaoning, China Dekan: Prof. Dr. med. J. Zentner 1. Gutachter: Prof. Dr. med. Martin Schumacher 2. Gutachter: PD. Dr. med. S. Rosahl Jahr der Promotion: 2004 ii本论文献给一贯支持我事业的妻子曲玉波女士和儿子聂嘉彤 To my wife,Yubo Qu and My son, Jiatong Nie iiiContents 1. Introduction …………………………………………………………………… 1 1.1 General introduction of aneurysmal SAH …………………………………. 1 1.2 Introduction of coiling and clipping modalities ……….…………………... 3 1.3 The current situation: coiling and clipping therapies ……………………… 5 1.4 The aim of this study ….…………….……………………………………….. 92. Material and Methods ...……………………………….…………………….…. 11 112.1 Patients population .…………………………..…….……………………….. 2.2 Protocol for aneurysm treatment ……………………….…………..….…….. 12 2.3 Review of Angiography .…………………………………………….………. 12 2.4 Procedures …………….………………………………………………….….. 14 2.5 Statistical analyses …….....…………………………………………….….…. 153. Result ……….…………………….……………………………………………... 16 3.1 Patients selection …………………………………………………………….. 16 3.
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Aus der Sektion Neuroradiologie
der Albert-Ludwigs-Universität Freiburg i.Br.
Coiling and Clipping
in Aneurysmal Subarachnoid Hemorrhage
INAUGURAL - DISSERTATION
Zur Erlangung des Medizinischen Doktorgrades der Medizinischen Fakultät der Albert-Ludwigs-Universität Freiburg i.Br.
Vorgelegt 2004
von
Zhiyu Nie
geboren in Liaoning, China
Dekan:Prof. Dr. med. J. Zentner
1. Gutachter:Prof. Dr. med. Martin Schumacher
2. Gutachter:PD. Dr. med. S. Rosahl
Jahr der Promotion: 2004
ii
To my wifeYubo Qu
and My son, Jiatong Nie
iii
15
2.4 Procedures ....
2.5 Statistical analyses ........
16
16
Result .....
3.
3.1 Patients selection ..
16
18
3.2 Characteristics of the patients at hospital admission .
3.3 Age distribution ....
18
3.4 Aneurysm locations ..
19
3.5 Comparability of the patients with SAH between two groups .
19
3.6 Procedure-related complications .
19
3.6.1 Procedure-related complications in the endovascular treatments .
26
3.6.2 Procedure-related complications in the neurosurgical treatments ...
3.8 Learning curve of the coiling skill 
31
3.7 Causes of death and in-hospital mortality 
30
3.9 Technical outcome of the first procedure ..
32
37
3.10 Occlusion rates of aneurysms in primary procedures .
34
3.12 Crossover between treatment groups ..
38
3.11 Clinical outcome.
3.13 Recoiling and reclipping ....
40
3.14 Non procedure-related rebleeding ..
42
40
Discussion ..
4.
Introduction
1.
1 1
3
Contents
iv
5
9
11
1.2 Introduction of coiling and clipping modalities ....
1.1 General introduction of aneurysmal SAH .

2.
12
11
1.4 The aim of this study ....
1.3 The current situation: coiling and clipping therapies 
14
2.3 Review of Angiography ...
2.1 Patients population ...... 2.2 Protocol for aneurysm treatment ......
12
Material and Methods ......
v
49
45
4.2 Aneurysm occlusion rates......
4.1 Treatment feasibility and failure....
43
7.
77
Zusammenfassung 
Reference
Summary ...
6.
63
5.
65
64
4.7 Rebleeding ....
62
60
4.6 Clinical outcome ...
4.5 Crossover therapy, recoiling and reclipping ..
57
4.4 Mortality and morbidity.
56
4.3.3 Coil dislocation and coil stretching ...
55
4.3.2 Parent artery occlusion and thromboembolic events ....
52
4.3.1 Aneurysm rupture ..
49
4.3 Procedure-related complications ..
11.
Curriculum Vitae
...81
Abbreviations.
9.
10.
Acknowledgments..
Appendices.....
8.
79
80
Coiling and Clipping
in Aneurysmal Subarachnoid Hemorrhage 1. Introduction
1.1 General introduction of aneurysmal SAH
Subarachnoid hemorrhage (SAH), from rupture of an intracranialaneurysm, is a
common and serious disorder with a high mortality and morbidity. The prevalence of
aneurysmal SAH is about 0.5% to 6% in adults, according to angiography and
autopsy studies (Schievink, 1997 b). A Meta-Analysis indicated that the incidence is
between 7.8 and 21.4 per 100 000 person years in most western populations and the
actual incidence of SAH has remained stable over the last three decades. Despite
considerable advances in the management of patients with SAH, with a decreasing
case-fatality rate of 0.5% per year (Hop et al., 1997), the outcome for patients with
SAH remains poor. Patients with SAH face a mortality rate of between 35% and 50%,
and an associated morbidity from 18% to 25% (Adams et al., 1981; Ljunggren et al.,
1984; Rosenorn et al., 1987). In other words, only about 30% of SAH patients will
have a good outcome, meaning return to premorbid functionality (Johnston et al.,
2002; Bryan et al., 1997).
According to epidemiological studies, 8% to 15% of patients with SAH diedbefore
receiving medical attention (Phillips et al., 1980; Bonita et al., 1985; Ingall et al.,
1989; Inagawa et al., 1995;) and the overall case-fatalityrate was 35% within 8 hours
after onset of SAH (Kiyohara et al., 1989), 20% to 37%within 48 hours ( Bonita et al.,
1983; Bonita et al., 1985), 39% to 43% in the first week (Bonita et al., 1983; Bonita et
al., 1985; Kiyohara et al., 1989) and 46% to 61% at 1 month (Bonita et al., 1983;
Sacco et al., 1984; Kiyohara et al., 1989; Bamford et al., 1990; Sarti et al., 1991;
Broderick et al., 1993). The total mortality rate is still reported as between 32 and
67%, most of the patients died asthe initial bleeding or its immediatea result of
complications (Hop et al., 1997). About 20% -50% of the survivors will be left with
1
long term dependence due to brain damage (Hijdra et al., 1987; Hop, et al., 1997).
Mortality due to rerupture is as high as 74%, and only 19% of patients with a rebleed
had a good outcome (Juvela S., 1989).
SAH is due to rupture of an intracranial aneurysm in 75% of cases, which usually
arises from the circle of Willis or branch artery (Wardlaw et al., 2000). The risk of
rupture is approximately 1% to 2% per year for asymptomatic, as-yet-unruptured
aneurysms (Wiebers et al., 1987; Juvela et al., 1993; Yasui et al., 1997). The published
results of ISUIA (International Study of Unruptured Intracranial Aneurysms) in 1998
indicated that for the patients without prior history of SAH, a rupture rate of 0.05%
per year in patients with aneurysms <10 mm in diameter and of approximately 1% per
year for those with aneurysms10 mm in diameter. The rupture rate was 6% in the
first year among patients with giant (25 mm) UIAs (Unruptured intracranial
aneurysms, International Study of Unruptured Intracranial Aneurysms Investigators,
1998). For patients with prior history of SAH, even with unruptured aneurysm < 10
mm in diameter, the rupture rates were 11 times higher (about 0.5% per year) than for
patients without prior SAH with the same size aneurysms. A more recent published
data of this study revealed that five year cumulative rupture rates for patients who did
not have a history of subarachnoid hemorrhage with aneurysms located in internal
carotid artery, anterior communicating or anterior cerebral artery, or middle cerebral
artery were 0%, 2.6%, 14.5%, and 40% for aneurysms less than 7 mm, 7-12 mm,
13-24 mm, and 25 mm or greater, respectively, compared with rates of 2.5%, 14.5%,
18.4%, and 50%, respectively, for the same size categories involving posterior
circulation and posterior communicating artery aneurysms (Wiebers et al., 2003). The
cumulative hemorrhage rate is 20% at 10 years after diagnosis and 35% at 15 years.
The probability of rupture is significantly higher for multiple aneurysms (Yasui et al.,
1997).
Aneurysms are typically lesions of adults, although they may occur at any age but
are most common in those aged 40 to 60; the mean age for rupture is 50 years (Rinkel
et al., 1998). Aneurysms are more common in women with 1.6  4.5 times higher than
in men (Linn et al., 1996).
2
Most aneurysms occur on the circle of Willis or at the middle cerebral artery
bifurcation. Approximately 90% of intracranial aneurysms are located on the anterior
circulation whereas only 10% occur in the vertebrobasilar system. About 1/3 of all
aneurysms are found at the anterior communicating artery, 1/3 are located at the
posterior communicating artery-internal carotid artery junction, and 1/5 occur at the
middle cerebral artery bi- or trifurcation (Schreiber et al., 1977; Rosenorn et al., 1987;
Osborn AG., 1994).
Multiple aneurysms account for approximately 20% of all intracranial aneurysms,
predominately in females. A recent report showed the overall frequency of multiple
aneurysms was 20.2% in women, which was significantly higher than 12.4% in men
(Kaminogo et al., 2003). However the previous reported frequency of multiple
aneurysms varies widely ranging from a low of 14% to nearly 45% of all cases
examined (Rinne et al., 1994). Vasculopathies such as fibromuscular dysplasia and
polycystic kidney disease are associated with an increased incidence of multiple
aneurysms (Schievink., 1997 a; Neumann et al., 1999).
For ruptured aneurysms, the riskof subsequent rupture is high, with approximately
20% risk of rerupture in the first 2 weeks after subarachnoid hemorrhage (Mayberg et
al., 1994). In the prospective Cooperative Aneurysm Study (Kassell et al., 1983),
rebleeding was 4% on the first day after SAH and then constant at a rate of 1% to 2%
per day over the subsequent 4 weeks. The other prospective follow-up study has
demonstrated that the risk of rebleeding with conservative therapy is between 20%
and 30% for the first month after hemorrhage and approximately 3% per year
thereafter (Winn et al., 1977).
1.2 Introduction of both coiling and clipping modalities
In 1937, Walter Dandy reported the first successful surgicalclipping of the neck of
an aneurysm (Johnston et al., 2002). Since then, with the development of surgical
approaches and instruments, including the introduction of the operation microscope,
metal aneurysm clip (consisting of platinum, titanium,tungsten, and steel alloys),
3
advances in anaesthetic and intensive care management, improved diagnostic facilities, neurosurgical techniqueshave steadily evolved. Repair of aneurysmsin nearly all
intracranial locations is possible by clipping the neck of the aneurysm, thus excluding
it from the cerebral circulation. The risk of surgery for ruptured intracranial
aneurysms was reduced. Neurosurgical clipping for treatment of intracranial
aneurysm had been the standard approach of the therapy of cerebral aneurysm
(Schievink. 1997 b). Nonetheless, even with these advances, relatively few patients
return to a normal lifestyle after SAH, and many have persistent disabling
neurological or cognitive defects (Powell et al., 2002).
In 1991, a new kind of treatment for aneurysm emerged. Guido Guglielmi was the first to describe the techniqueof Guglielmi detachable coils(GDCs) which occlude aneurysms from an endovascular approach with electrolyticdetachable platinum coils
(Guglielmi et al., 1991, a and b). GDCs are introduced directly into the aneurysm througha microcatheter and detached from a stainless steel micro guide wireby an electrical current. The aneurysm is packedwith one or more GDCs. The goal of the
treatment is to prevent the flow of blood into the aneurysm sack by filling the aneurysm with coils. As clinical experience with this technique has increased andcoil
design has improved, coil embolization has been used withincreasing frequency even
in patients who could be treated byconventional surgical clipping (Johnston et al.,
2000; Johnston et al., 2001). Furthermore, some centersare treating patients with
surgical clipping only if they cannotbe treated primarily by endovascular coil
embolization therapy (Raftopoulos et al., 2000). Up to 1995, more than 16,000
patients with ruptured and unruptured aneurysms have been treated worldwide with
the GDC method (Graves et al., 1995). In August 2002, it was estimated that 100,000
patients with intracranial aneurysms had been treated with GDCs at sites throughout
the world, with approximately 1500 patients being treated per month (Hopkins et al.,
2001). Theoretically, there are several advantages of GDC over surgery. However,
there are some drawbacks of endovascular coiling therapy including the potential for
bleeding from nonobliterated aneurysms after the procedure, aneurysm perforation
during the manipulation of the microcatheter or delivering the coils into the aneurysm,
4
its effect on the incidence of vasospasm,and the inherent complications of the
technique (Dovey et al., 2001).
1.3 The current situation: coiling and clipping therapies
Since 1995, endovascular coiling embolization has become widely used in patients
with ruptured and unruptured intracranial aneurysms (Brilstra et al., 1999; Johnston et
al., 2002), which offered the prospect of reducing the risk of further rupture without
the need for craniotomy. However, the occlusion rate of aneurysms and outcomes
after the endovascular coiling treatment varied widely. A small series study (Raymond
et al., 1997 b) of ruptured aneurysms in 75 patients treated by coiling embolization
showed that immediate angiographic results were: the complete obliteration in 40%;
remnant neck in 37%. And the clinical outcomes as measured by Glasgow coma scale
(GCS) at 6 months were as follows: GOS score of 1 in 50 patients (66.7%); GOS
score of 2 in 4 patients (5.3%); GOS score of 3 in 4 patients (5.3%); and GOS score of
5 in 17 patients (22.7%, Raymond., 1997 b). In another study report, complete
aneurysm occlusion was observed in 70.8% of small aneurysms with a small neck,
35% of large aneurysms, and 50% of giant aneurysms. A small neck remnant was
observed in 21.4% of small (4-10 mm) aneurysms with a small neck, 57.1% of large
(11-25 mm) aneurysms, and 50% of giant (>25 mm) aneurysms (Viñuela et al., 1997).
84.9% of patients had good outcome or unchanged clinical status, 8.9% had poor
outcome or deterioration, and 6.2% died (Viñuela et al., 1997). Raymond et al.
reported the immediate angiographic results of endovascular coiling of ruptured and
unruptured basilar tip aneurysms: complete obliteration in 42%, residual neck and dog
ear in 52% and incomplete occlusion in 6% (Raymond et al., 1997 a). For the 23
patients with acute ruptured basilar tip aneurysms, 83% (19 patients) had a good early
clinical outcome (GOS 1 or 2), 17% (4 cases) had poor outcomes (GOS 3, 4 and 5)
(Raymond et al., 1997 a).In a meta-analysis concerning 48 eligible studies with a
total number of 1383 patients, only 54% of aneurysms were completely occluded after
initial coil embolization, with 88% more than 90% occlusion (Brilstra et al., 1999).
5
Intracranial aneurysm treatment, by either neurosurgical clipping or endovascular
coiling, may precipitate a complication that could lead to newsymptoms, disability, or
death. The reported rates of procedure related complications referred to both
modalities were also varied widely, some even controversial. The complications
occurring in endovascular coiling treatment reported atrates of 2.1% to 8.0% for
aneurysmal perforation, 1.6% to 6.5%for thromboemboli, 3.2% to 5.0% for parent
vessel occlusion, and 1.1% to 1.3% for coil migration (Dovey et al., 2001; Viñuela et
al., 1997). With endovascular coiling of intracranial aneurysms, procedure related
morbidity and mortality were also variable. The morbidity and mortality were 9.1%
and 7.8% (Kuether et al., 1998), 4.0%and 2.0% (Cognard et al., 1998). 8.1%
morbidity and 6.4% mortality rates in anterior circulation aneurysms and 9.6%
morbidity and 6.1% mortality rates in posterior circulation aneurysms, respectively
(Viñuela et al., 1997). In contrast to these results, the previous surgical seriesoverall
morbidity23% and 21% (Säveland et al., 1992)and mortality is relatively higher, of
and 14% and 27% (Seiler et al., 1998). Also outcomes after cerebral aneurysm clip
occlusion were closely related to hospital treatment volume, very low volume
hospitals demonstrated higher mortality rates than very high volume hospitals for both
elective patients (9.4% compared with 4.5%) and emergency (14.7% compared with
8.8%) (Cowan et al., 2003). A large, international prospective study of unruptured
aneurysm treatment (Wiebers et al., 2003) indicated that 30 days post procedure
related morbidities (mRS 3 5) and mortalities were 2.2% and 2.0% in endovascular
and 3.0% and 1.8% in neurosurgical groups, and were 1.0% and 3.4% in endovascular
and 1.4% and 2.7% in neurosurgical groups at 1 years for unruptured aneurysms in
patients without SAH from a separate aneurysm. A Meta-Analysis about mortality and
morbidity of surgery for unruptured intracranial aneurysms, which included 61 studies
in 2460 patients with 2568 aneurysms (27% > 25 mm, 30% located in the posterior
circulation), the report concluded that mortalitywas 2.6% and permanent morbidity
was 10.9% (Raaymakers et al., 1998).
The incidence of angiographic vasospasm ranged between 19% and 97%,
dependent on the day after SAH on which angiography was performed (Schumacher
6