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167
occurred in approximately 20% of patients and caused 13% of
all death and disability aer SAH2,18).
Although angiographic vasospasm may occur in up to 70% of
patients, symptomatic vasospasms only occur in about 30% of
patients10). Delayed ischemic neurologic decits (DIND) may
occur in about 50% of patients with angiographic vasospasm,
which may lead to stroke or death despite maximal therapy26).
Although much has been elucidated regarding pathophysiol-
ogy of the vasospasm, its exact pathophysiologic mechanism
remains an incompletely solved problem. e presence of blood
or its breakdown products within the subarachnoid space and
cisterns is clearly associated with vasospasm9). So, thick SAH
completely lling cistern has been shown to be an independent
predictor of DIND2). Considerable clinical and experimental
evidences have been reported that the volume and duration of
INTRODUCTION
e management of patients with acutely ruptured intracra-
nial aneurysms should achieve two major goals : 1) prevention
of subsequent bleeding and 2) prevention and treatment of de-
layed ischemia or infarction due to vasospasm29). Early surgical
clipping or endovascular coiling can prevent the subsequent
aneurysm bleeding and can allow active management of vaso-
spasm. In spite of marked development in the treatment of an-
eurysmal subarachnoid hemorrhage (SAH), the cerebral vaso-
spasm still remains a signicant cause of cerebral ischemia and
neurologic decits in patient with SAH. e prevalence of va-
sospasms have been reported 20–35% in aneurysmal SAH pa-
tients, although in those with a higher blood load, this may be
as high as 40%2,18). Some authors reported that cerebral infarcts
The Effectiveness of Lumbar Cerebrospinal Fluid
Drainage to Reduce the Cerebral Vasospasm after
Surgical Clipping for Aneurysmal Subarachnoid
Hemorrhage
Soojeong Park, M.D., Narae Yang, M.D., Euikyo Seo, M.D., Ph.D.
Department of Neurosurgery, School of Medicine, Ewha Womans University, Seoul, Korea
Objective : Removal of blood from subarachnoid space with a lumbar drainage (LD) may decrease development of cerebral vasospasm. We evalu-
ated the effectiveness of a LD for a clinical vasospasm and outcomes after clipping of aneurysmal subarachnoid hemorrhage (SAH).
Methods : Between July 2008 and July 2013, 234 patients were included in this study. The LD group consisted of 126 patients, 108 patients in
the non LD group. We investigated outcomes as follow : 1) clinical vasospasm, 2) angioplasty, 3) cerebral infarction, 4) Glasgow outcome scale
(GOS) score at discharge, 5) GOS score at 6-month follow-up, and 6) mortality.
Results : Clinical vasospasm occurred in 19% of the LD group and 42% of the non LD group (p<0.001). Angioplasty was performed in 17% of the
LD group and 38% of the non LD group (p=0.001). Cerebral infarctions were detected in 29% and 54% of each group respectively (p<0.001). The
proportion of GOS score 5 at 6 month follow-up in the LD group was 69%, and it was 58% in the non LD group (p=0.001). Mortality rate showed
5% and 10% in each group respectively. But, there was no difference in shunt between the two groups.
Conclusion : LD after aneurysmal SAH shows marked reduction of clinical vasospasm and need for angioplasty. With this technique we have
shown favorable GOS score at 6 month follow-up.
Key Words : Aneurysm · Subarachnoid hemorrhage · Lumbar drainage · Cerebral vasospasm · Surgical clipping.
Clinical Article
• Received : July 13, 2014 • Revised : July 21, 2014 • Accepted : December 15, 2014
• Address for reprints : Euikyo Seo, M.D., Ph.D.
Department of Neurosurgery, School of Medicine, Ewha Womans University, 1071 Anyangcheon-ro, Yangcheon-gu, Seoul 158-710, Korea
Tel : +82-2-2650-5952, Fax : +82-2-2650-0948, E-mail : drekseo@ewha.ac.kr
• This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0)
which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
J Korean Neurosurg Soc 57 (3)
: 167-173, 2015
http://dx.doi.org/10.3340/jkns.2015.57.3.167
Copyright © 2015 The Korean Neurosurgical Society
Print ISSN 2005-3711 On-line ISSN 1598-7876
www.jkns.or.kr
168
J Korean Neurosurg Soc 57 | March 2015
tients with Fisher grade 1 were excluded. e patients who had
received second operation like decompressive craniectomy or
removal of intracerebral hematoma, were also excluded. We ex-
perienced 4 cases of non functioning drainage due to broken
catheter, thick blood clot, insertion into epidural space. All non
functioning drainage patients were excluded in this study.
Finally, we disqualied the patients who presented for surgi-
cal clipping 4 or more days aer initial SAH. 234 patients were
le as the patient population for this study.
Clinical management
At admission, we conducted brain computed tomography
(CT) and neurologic examination and recorded Hunt and Hess
grade, modied Fisher grade according to density of SAH on
initial CT scan. We create a new modied Fisher grade 3+4 cate-
gory for patients with both dense subarachnoid blood clot and
intraventricular hemorrhages of 5 mL shown in Fig. 1.
All patients were treated with appropriate medication and
procedure including intubation, mannitol, anticonvulsant, se-
dation and central vein catheterization for stabilization of sys-
temic and neurologic condition.
All patients were managed according to our SAH manage-
ment protocol. Our protocol included surgical clipping or coil-
ing of ruptured aneurysms as soon as possible, at least within
24 hours after initial ictus, nimodipine administration, daily
transcranial Doppler (TCD) examination, monitoring and cor-
rection of electrolyte and blood gas, control of intracranial pres-
sure (ICP), pain management, and so on. e patients under-
went CT or diusion magnetic resonance imaging (MRI) and
digital subtraction angiography (DSA) if vasospasm was sus-
pected based on clinical symptoms and signs and TCD exam.
We conrmed the vasospasm with DSA, and then the inter-
ventional radiologist usually treated vasospasm with either re-
peated intra-arterial vasodilator infusion or balloon angioplasty.
From the start, treatment was provided in the form of intra-
venous nimodipine at a dose of 0.5 mg/h with gradual dose in-
crements over the next 6 hours up to 2 mg/h in the absence of
adverse hemodynamic eects, and was continued via the oral
route at a dose of 60 mg every 4 hours.
subarachnoid blood clots are directly related to the develop-
ment and severity of the cerebral vasospasm9,38). Moreover, the
removal of blood clots and irrigation of the cisterns performed
during surgery have been reported to reduce the risk of cerebral
vasospasm15,20). Because hemolysis of blood is the primary in-
citing agent for vasospasms, it follows that strategies to facilitate
the clearance of blood from the subarachnoid spaces shall de-
crease cerebral vasospasm. is strategy has been studied by a
number of investigators7,13,15,19,22,27,32). A number of Japanese
groups have advocated cisternal irrigation therapy with inow
and outow catheters placed in the cranial subarachnoid spac-
es22-24,31,36).
Lumbar drainage (LD) is thought to be a simple and eective
method to facilitate brain relaxation during aneurysmal SAH
surgery, remove blood cell mass from the subarachnoid spaces,
and decrease the incidence of vasospasm. Draining cerebrospi-
nal uid (CSF) from the lumbar subarachnoid space would be
expected to promote circulation of clear, newly formed CSF
from the cerebral ventricles through the subarachnoid spaces.
Moreover, LD would also promote removal of the red cell mass
from the intrathecal space, which represents the largest of all
subarachnoid cisterns.
We have been using LD aer SAH, and now report how this
aects the incidence of vasospasm and improvement in clinical
outcome in comparison to a group of patients whose SAH was
managed with LD or no CSF drainage.
MATERIALS AND METHODS
Patient demographics and data
Between July 2008 and July 2013, 427 patients with aneurys-
mal SAH were hospitalized and treated in my hospital. 193 pa-
tients were excluded from this study for various reasons. We ex-
cluded patients whose neurological conditions at admission
were too poor to manage the aneurysm properly and to allow
clinical recognition of signs and symptoms those, who died
within 7 days aer rupture of aneurysm. e patients who were
treated with endovascular coiling were also excluded. Because
of minimal eect of LD for prevention of vasospasm, the pa-
Fig. 1. Non-contrast axial CT scan showing the modified Fisher grade 3+4. A : CT scan shows dense subarachnoid hemorrhage in basal cistern and
small amount of intraventricular hemorrhage in both lateral ventricle. B : Non-contrast CT scan demonstrates thick subarachnoid hemorrhage in basal
cistern and small amount of intraventricular hemorrhage in 3rd ventricle and lateral ventricle.
A B
169
LP Drainage to Reduce Vasospasm after SAH | S Park, et al.
ages, and ranges. Tests of associations between the outcome cri-
teria and the LD were performed using chi-square test or Fish-
er’s exact test. We used Student t-test for continuous variables to
compare two groups. Statistical signicance was considered at
probability values of less than 0.05. Subgroup specic analysis
according to modified Fisher grade was also performed also.
All statistical analyses were performed with commercially avail-
able soware (version 22.0, SPSS Institute, Chicago, IL, USA).
RESULTS
ere were no signicant dierences in patient age, Hunt and
Hess grade, aneurysm location and modied Fisher grade be-
tween the two groups (Table 1). Table 2 shows the favorable ef-
fects of LD on our numerous outcome criteria. e incidence of
clinical vasospasm showed 19% in the LD group and 42% in
the non LD group. Angioplasty for vasospasm treatment was
performed in 17% of the LD group patients and 38% of the non
LD group patients. On routine CT or MRI at discharge, the in-
cidence of cerebral infarction was 29% in the LD group and
54% in the non LD group. e proportion of GOS score 5 at 6
month follow-up in the LD group was 69%, whereas 40% in the
non LD group. LD group had 2 times fewer patients than that
of the non LD group in poor GOS score of 1 and 2. Modied
Fisher grade 3+4 category had the highest risk of clinical vaso-
spasm (71%) in the non LD group and second high risk in the
LD group (Table 3). Irrespective of LD, 33% of modied Fisher
grade 3 patients and 50% of modied Fisher grade 3+4 patients
suered from clinical vasospasm (Table 3).
Mean CSF drainage was 174 mL/24 hours and the mean du-
ration of drainage was 13.5 days (9–16.2 days).
Complications associated with lumbar drains are presented in
Table 4. Culture-positive meningitis developed in three patients
Definition of vasospasm
We defined clinical vasospasm using the tirilizad trials18) as
following : 1) newly developed neurological decits such as con-
fusion, disorientation, increased sleeping tendency, focal motor
or speech decits, and pupil reex change; 2) no other cause of
neurological decits such as hyponatremia, hypoxia, infection,
pulmonary edema, and drug toxicity; 3) negative findings on
brain CT scan of secondary hemorrhage, cerebral edema, hy-
drocephalus; 4) evidence of vasospasm on serial TCD ultraso-
nography examinations. If the clinical symptoms and signs of
vasospasm were suspected, we performed DSA immediately to
conrm the vasospasm.
Transcranial Doppler (TCD)
TCD exploration was carried out with 2 MHz ultrasound
probe through the craniotomy site window in the case of a rou-
tine pterional approach and the temporal window in the case of
supraorbital approach. TCD study was carried out in the rst 24
hours and daily for 14 days following SAH. The studies were
made by 3 physician assistants with extensive experience in ultra-
sonic Doppler examination. In both hemispheres, we recorded
the mean velocity (MV) of the proximal middle cerebral artery
(MCA). Also TCD exploration was made of the homolateral ex-
tracranial internal carotid artery (ex ICA) at submandibular level,
with calculation of the Lindegaard index (LI) : MV MCA/MV ex
ICA. e patients who presented over 150 m/s of MV or increas-
es of more than 50 cm/s a day or an MV MCA/MV ex ICA ratio
greater than 3 were classied as clinical vasospasm. DSA was car-
ried out for accurate confirmation of arterial spasm and treat-
ment of vasospasms.
Cerebrospinal fluid drainage methods
We performed the LD if there were no evidences of the ob-
structive hydrocephalus and mass eect causing midline shi
with CT scan. We randomly selected the patient on whom LD
was performed at operation. LD was typically performed dur-
ing clipping surgery. If the postoperative CT scan demonstrated
no contraindication, the LD was opened. LD was continued
throughout the vasospasm risk period (about 14 days after
SAH). We used closed drainage system with infusion pump to
drain the CSF slowly and continuously and the drain rate was
5–10 mL/h (Fig. 2). We examined CSF analysis every 3 days for
detecting CSF infection.
Outcome measure
e outcomes measure were 1) prevalence of clinical vaso-
spasm, 2) incidence of angioplasty, 3) rate of cerebral infarction
on MRI at discharge, 4) persisting neurological decit at dis-
charge by Glasgow outcome scale (GOS) score, 5) GOS score at
6-month follow-up, and 6) mortality rate.
Statistical analysis
Categorical variables are summarized as frequencies, percent-
Fig. 2. Photograph shows closed lumbar drainage kit composed infusion
pump and closed drainage bag. We performed lumbar CSF drainage
slowly and continuously with drainage rate 5 to 10 mL/hour. CSF : cere-
brospinal fluid.
170
J Korean Neurosurg Soc 57 | March 2015
signicantly decreased over past years.
According to many studies for treatment
aer aneurysmal SAH, clinically signif-
icant vasospasm aected 5–13.5% of pa-
tients with permanent neurologic decit
and account for 33% of deaths and dis-
abilities7,18). e current standard treat-
ment for vasospasm aer ruptured an-
eurysm surgery consists of triple-H (3H)
therapy, calcium-channel blocker, and
the endovascular angioplasty with pa-
paverine or nimodipine injection. A
number of studies have shown that 3H
therapy and calcium channel blocker
such as nimodipine reduced the patients
with severe cerebral vasospasm18,28). En-
dovascular angioplasty and injection of
intra-arterial chemical vasodilators en-
abled to treatment of vasospasm and
thus improve their overall outcome3,6,8).
But these current therapies can’t prevent
the occurrence of vasospasm in all pa-
tients, so cerebral vasospasm still con-
tributes to poor outcome in approxi-
mately 10–40% of patients with dense
SAH.
All patients were operated on and
treated by one surgeon in the cerebro-
vascular center of our hospital with a
consistent aneurysmal SAH manage-
ment protocol. Although much has been
elucidated regarding pathophysiology of
vasospasm, the exact mechanisms are
not completely understood. The blood
in subarachnoid space or its breakdown
products within the subarachnoid space
is clearly associated with vasospasm2,15).
Biochemical factors, such as oxygen free radicals, oxyhemoglo-
bin, iron, intracellular adhesion molecule-1, endothelins, nitrous
oxide, reduced form of nicotinamide-adenine dinucleotide phos-
phate oxidase, vascular endothelial growth factor, arachidonic
acid, and protein kinase C from blood clots within subarachnoid
space and cistern are known to be related to cerebral vaso-
spasm4,16,17,21). Because hemolysis of blood is the primary inciting
agent for vasospasm, there have been numerous clinical investi-
gation that early clearance of subarachnoid blood clot or even
massive subarachnoid irrigation would reduce the risk of vaso-
spasm7,15,19,22,27,32). Many Japanese groups have applied massive ir-
rigation therapy with catheters located in the subarachnoid spac-
es13,23,24,31,36), and this therapy is usually accompanied with daily
head shaking and brinolytic therapy. But these therapies have
not been accepted widespreadly, because the results were equivo-
cal and there were risks of potential complication of cerebral
of the LD group. Aer removal of drainage and treatment with
proper antibiotics, these infections were resolved without per-
manent neurologic decits. Five patients demonstrated micro-
organism growth on catheter tip culture without symptoms of
meningitis, which was thought to be contaminated from skin.
Two patients complained low intracranial pressure associated
headache developed on several weeks aer removal of the lum-
bar drain. eir headaches subsided aer treatment with blood
patch.
DISCUSSION
Despite advances in management of vasospasm, cerebral va-
sospasm is the still a signicant cause of morbidity and mortali-
ty in treatment of aneurysmal SAH. e incidence and impact
of vasospasm on clinical outcome aer aneurysmal SAH has
Table 1. Baseline characteristics of the lumbar drain and non-lumbar drain groups in 234 patients
with aneurysmal subarachnoid hemorrhage underwent surgical clipping
Characteristics Group p value
LD Non LD
No. of patients 126 108
Mean age (range) 56.7 (23–76) 54.8 (26–75) 0.148
Sex, male : female 1 : 1.6 1 : 1.4
Hunt & Hess grade (%) 0.426
I 13 (10) 10 (9)
II 48 (39) 29 (26)
III 42 (33) 45 (42)
IV 18 (14) 18 (17)
V 5 (4) 6 (6)
Modied Fisher grade (%) 0.625
2 45 (36) 33 (30)
3 40 (32) 42 (39)
3+4 29 (23) 21 (20)
4 12 (9) 12 (11)
Ruptured aneurysm location (%) 0.626
Anterior circulation
ACoA 63 (50) 44 (40)
PCoA 14 (11) 15 (14)
OA 1 (1) 1 (1)
AChA 3 (2) 3 (3)
MCA 38 (30) 31 (29)
ACA 4 (3) 8 (7)
Posterior circulation (%)
BA bif 1 (1) 2 (2)
PICA 2 (2) 4 (4)
Multiple aneurysm, % 12 17
Intraoperative rupture (%) 5 (4) 5 (3)
Daily drainage (range) 174 mL (145–214 mL)
Duration of drainage (range) 13.5 days (9–16.2 days)
LD : lumbar drainage, ACoA : anterior communicating artery, PCoA : posterior communicating artery, OA : oph-
thalmic artery, AChA : anterior choroidal artery, MCA : middle cerebral artery, ACA : anterior cerebral artery distal
to ACoA, BA bif : basilar artery bifurcation, PICA : posterior inferior cerebellar artery
171
LP Drainage to Reduce Vasospasm after SAH | S Park, et al.
also be combined in a single ratio : vintracranial MCA/vextracra-
nial ICA which is frequently called the LI25). LI>3 in patients with
elevated MV in MCA oers high specicity (94–100%) in detect-
ing vasospasm in MCA1,34). We used TCD parameters such as
LI>3, increase of more than 50 cm/s a day, >150 cm/s of MCA
velocity as vasospasm diagnostic criteria in this study. In my se-
ries, 3 patients among 30 clinical vasospasm patients showed no
vasospasm on DSA in the LD group. LI were over 3 in two pa-
tients and one patient revealed that MV was 195 m/sec and in-
hemorrhage and infection33,36).
It is impossible to clear completely
blood clots in subarachnoid spaces and
cisterns by surgery. e rationale of our
use of lumbar CSF drainage in aneurys-
mal SAH is that it evacuates the large
reservoir of bloody CSF from the spinal
cistern, that it promotes CSF circulation
from the ventricles through the subara-
chnoid spaces, and that it also removes
the biochemical substance to mediate
vasospasm from subarachnoid space.
Several reports have indicated that direct
ventricular CSF drainage could reduce
the incidence of vasospasm aer aneu-
rysmal SAH15,19). However, CSF drainage
directly from the ventricles through ex-
traventricular drainage (EVD) may dis-
turb CSF circulation, and contribute to
stasis of hemorrhage within the sub-
arachnoid cisterns, so that ventricular
drainage in those patients may actually
add to the risk that cerebral vasospasm
will develop. We excluded the patients
with EVD in this study.
We routinely checked TCD parameter (MCA velocity, daily
velocity trend, and LI) to detect vasospasm early from post SAH
day 1 to day 14. MCA velocity above 200 cm/s may indicate
moderate to severe vasospasm37). Other criterion for the possibil-
ity of development of severe vasospasm is increases of more than
50 cm/s per day5). It should be cautioned that velocity or increas-
es in TCD velocity cannot distinguish vasospasm from cerebral
hyperemia. So another criterion for detection of vasospasm was
introduced. e extracranial and intracranial measurements can
Table 2. Outcomes of the lumbar drainage and non-lumbar drainage groups in 234 patients with aneurysmal subarachnoid hemorrhage underwent
surgical clipping
Outcomes Group p-value
LD Non LD
No. of patients 126 108
Clinical vasospasm (%) 24 (19) 45 (42) <0.001
Angioplasty (%) 21 (17) 41 (38) 0.001
Infraction on MRI at discharge (%) 37 (29) 58 (54) <0.001
No. of patients with GOS of 4–5 at discharge (%) 87 (69) 63 (58) 0.084
GOS score at 6 months follow up (%) 0.001
1 6 (5) 11 (10)
2 4 (3) 6 (6)
3 13 (10) 15 (13)
4 16 (13) 33 (31)
5 87 (69) 43 (40)
Shunt (%) 26 (21) 28 (26) 0.428
Death (%) 6 (5) 11 (10) 0.273
LD : lumbar drainage, GOS : Glasgow outcome scale
Table 3. Clinical vasospasm according to modified Fisher grade
Outcomes Group p-value
LD Non LD
Modied Fisher grade 2 (%)
No. of patients 45 33
Clinical spasm 2 (4) 2 (7) 0.264
Angioplasty 1 (2) 1 (3) 0.475
Infarction at discharge 4 (9) 7 (21) 0.153
Modied Fisher grade 3 (%)
No. of patients 40 42
Clinical spasm 7 (18) 20 (48) 0.009
Angioplasty 7 (18) 17 (40) 0.019
Infarction at discharge 10 (25) 23 (55) 0.007
Modied Fisher grade 3+4 (%)
No. of patients 29 21
Clinical spasm 10 (34) 15 (71) 0.042
Angioplasty 8 (28) 15 (71) 0.031
Infarction at discharge 15 (52) 19 (90) 0.013
Modied Fisher grade 4 (%)
No. of patients 12 12
Clinical spasm 5 (42) 8 (67) 0.412
Angioplasty 5 (42) 8 (67) 0.408
Infarction at discharge 8 (67) 9 (75) 0.678
LD : lumbar drainage
172
J Korean Neurosurg Soc 57 | March 2015
was well controlled with proper antibiotics. ere was no per-
manent morbidity associated with infection. We did not experi-
ence the complication of LD like spinal nerve root injury or
tension pneumocephalus. To avoid complication and for the
safe use of postoperative LD in patients with aneurysmal SAH,
experienced team in my institute consisted of vascular neuro-
surgeon and neurosurgery nurse practitioner trained in the
neurological critical care is fully occupied with strict attention
to detail, close surveillance to the patient.
ere are some limitations to our study. Selection bias is al-
ways a potential problem, although case assignment did have a
randomizing eect. We did not distinguish the opening the lam-
inar terminalis during clipping of surgery, which change the
CSF pathway from 3rd ventricle to subarachnoid cistern direct-
ly and thus may aect the development of vasospasm.
CONCLUSION
In this study, clinical vasospasm and endovascular procedure
to manage the vasospasm were marked reduced with LD aer
aneurysmal SAH surgery. Also, this method favorably influ-
enced the GOS score at 6 month follow-up. Clearance of blood
clots and its various derivatives from subarachnoid space and
improvement of CSF circulation with LD were believed to be
possible mechanisms to decrease incidence of cerebral vaso-
spasm. ere was no permanent morbidity and mortality relat-
ed with LD. is report was only surgical series, we would ex-
pect investigation of vasospasm comparing surgical clipping
series with endovascular coiling series. A randomized, prospec-
tive study will be able to overcome the limitations of our study.
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Complication No. of patients Results
CSF infection 3No complications with proper antibiotics
Microorganism growth on routine drainage tip culture 5No complications without antibiotics
Low pressure headache continued aer removal of drainage 2Improved with lumbar blood patch
Pseudomeningocele on lumbar MRI several week aer discharge 2Symptoms improved without treatment
CSF : cerebrospinal fluid
173
LP Drainage to Reduce Vasospasm after SAH | S Park, et al.
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