Management and Surgical Treatment of Ruptured
Intracranial Aneurysms
PETER D.
MOYES, M.D., F.R.C.S.[C], Vancouver,
B.C.ABSTRACT
The
advantages,
methods and results ofsurgical
intracranial obliteration of aneur¬ysms in conjunction with the use of intra¬
cranial or neck
ligation
of arteries werestudied in 177
patients
made up of thefollowing
groups:(a)
internal carotidaneurysms.48, (b)
anterior cerebral.an¬terior
communicating.37, (c)
middle cere¬bral.20, (b) basilar.two, (e) posterior
cerebral.one. The overall
mortality
ratewas 23%.
Following
conservative treat¬ment, 69patientswithsubarachnoid hemor¬
rhage
without demonstrated aneurysms had amortality
rate of 30%. In this seven-year
study
the value of team work involv¬ing a second neurosurgeon, well-trained
nursing personnel
and expert anesthetistswas
amply
demonstrated.rPHE treatment of
ruptured
intracranial aneur-¦*¦ ysms constitutes one of the most
challenging
areas in
neurology
and neurosurgerytoday.
Advo- catedtherapy
hasranged
fromstrictly
medicaltreatment ofall
patients.irrespective
of the ageof thepatient,
site of aneurysm, orseverity
and fre¬quencyof
rupture.to surgical
treatmentwithdeep hypothermia
and total arrest of circulation.Current Concepts est Aneurysm Surgery
Despite McKissock,
Paine and Walsh's1 con- clusion that there is noproof
that the results ofsurgical
treatment are any better than those ofconservative treatment in
comparable
groups ofpatients,
most neurosurgeons,rightly
orwrongly,
believe that the results of
surgical
treatment arebetter and that the additional
security
andfreedom fromphysical
restrictionsresulting
from successfulsurgical
treatment are further factorsworthy
of consideration.Some facts with
regard
to subarachnoid hemor¬rhage
have become clear:1. There is a
high early mortality.
We are notlikely
in the immediate future to reduce the num¬ber of deaths that occur in the first 24 hours after
hemorrhage except
in thosepatients
in whom localized hematoma ispresent.
SOMMAIRE
L'auteur a etudie sur 117
patients
les avantages, methodes et resultats de Te- liminationchirurgicale
d'anevrismes intra-craniens,
associee a laligature
d'art&res intracraniennes ou cervicales. Les maladesont ete repartis dans les groupes suivants:
(a)
anevrismesdela carotideinterne48cas,(b)
cerebrale anterieure et communicante anterieure37cas,(c)
c£r£bralemoyenne20 cas,(d)
basilaire deux cas,(e)
c£r£brale posterieure un cas. La mortaliteglobale
aet6 de 23%.
Apres
traitement conservateur, chez 69 maladesatteintsd'hemorragie
sous-arachnoidienne sans evidence
d'anevrismes,
la mortalite a atteint 30%. Cette
&ude, qui
a couvert uneperiode
de sept ans, apermis de d£montrer
amplement
la valeur du travaild'equipe
comportant lapresence
d'un second
neuro-chirurgien,
depersonnel
infirmier competent et d'anesthesistes bien entrain£s.
From theDepartmentofSurgery (Neurosurgery), University
of British Columbia, Vancouver, B.C.
Presented in part at the 34th Annual Meetingof the Royal College of Physicians and Surgeons of Canada, Toronto, January 23, 1965.
2. The more severe the
hemorrhage
and theworse the basic health of the
patient,
the worse are the results ofanykindoftreatment.3.
Except
when a localized hematomaispresent,
the purpose ofsurgical
intervention is toprevent
furtherhemorrhage,
not to treat the currentepisode.
4. Patients who survive a subarachnoid hemor¬
rhage
and in whom no aneurysm can be demon¬strated, despite adequate
visualization of both carotid and both vertebral arteries and theirbranches,
appear to have agood prognosis.2"4
5.
Vasospasm
is one of themajor factors,
if notthe
major factor, responsible
formortality
andmorbidity,
andanadequate
method ofdealing
with this response wouldundoubtedly greatly
enhanceour
ability
to deal withruptured
aneurysms.Certain
techniques
arebeing developed
andapplied
to the treatment of intracranial aneurysms such aselectrocoagulation,5 pilojection,6
intra¬luminal
manipulations7
anddeep hypothermia.8*9
One or more of these
techniques
may provesuperior
tothosepresently
ingeneral
use butvalid conclusions cannotyet
be drawn aboutthem. How¬ever, differences of
opinion
existconcerning
thetechniques
nowgenerally available,
and this com¬munication will outline my
attempts
to use, to the bestpossible advantage,
oneor more ofthefollow¬ing
methods: intracranial obliteration of theaneurysm, reinforcement of the aneurysm
by muscle,
muslin orplastic material,
andligation
ofa
proximal artery.either intracranially
or in the neck.Management of Intracranial Hemorrhage
at theVancouver General Hospital
When a
patient
with asuspected
subarachnoidhemorrhage
is seenby
one of the members of theNeurosurgical
Service of the Vancouver GeneralHospital,
he or she is assessedclinically
and thediagnosis
is confirmedby
lumbarpuncture using
a
small-gauge
needle andobtaining only
a smallamount of
cerebrospinal
fluid. When doubtexists,
xanthochromia or the presence of crenated red blood cells in thespinal
fluid willusually provide positive
confirmation.If the
patient
has focalsigns compatible
with an intracerebralhematoma,
carotidarteriography
iscarried out as soon as
possible
and is followedby craniotomy
if indicated. Otherwise thepatient
is well sedated ifrestless,
and the blood pressure is reducedby
a moderate amount if elevated. He is maintained oncomplete
bed rest and may be catheterized. Thenursing
careduring
thisperiod
is very
important.
Carotidarteriography
is carriedout within 24 to 48 hours and should include
oblique
views andcross-compression
when an anteriorcommunicating
aneurysm issuspected.
Ifno aneurysm is discovered at this
examination,
vertebralarteriography
is carried out in 48hours;
open brachial
retrograde arteriography,
as de¬scribed
by Kuhn,10
isusually
done.When the aneurysm is
located,
another neuro-surgeon on the service is called upon to
help
de- cide whether or notoperation
should be carried out, whattype
ofoperation
should be done and when it should be done. He also assists at theoperation.
I agree with Pool11 that
operation
should be carried out within sevendays
ofhemorrhage
if the condition of thepatient
warrantsit,
because thedanger
of recurrenthemorrhage beyond
this timeis considerable. In the
interim,
thepatient
ismain¬tained on
complete
bed rest and is well sedated.Various factors must be considered when decid-
ing
on thetiming
ofsurgical
intervention in a pa¬tient with
rupture
of an intracranial aneurysm.Despite
the fact that thedanger
of recurrenthemorrhage
isgreat beyond
sevendays,
it is still difficult to decide whether or not tooperate
in the first sevendays
because vascular spasm isgreater
during
thisperiod
than it is several weeks later.provided
recurrenthemorrhage
has not occurred.The
operation
is done toprevent
recurrent hemor¬rhage but,
infact,
often increases thedegree
of spasm and this spasm is theprincipal
factor inpostoperative mortality
andmorbidity.
Thetiming
of
operation
is therefore decided afterweighing
thesetwofactors:
If,
onclinical andradiographical grounds,
considerable spasm seems to bepresent,
one would be inclined to wait
longer
than sevendays;
if it isslight,
one wouldproceed
within theseven-day period.
It must be remembered
that, except
when asignificant
intracranial hematoma ispresent, attempts
toprevent
recurrenthemorrhage
maycause further
damage by
virtue of retraction ofalready
swollenbrain,
andmanipulation
ofalready spastic
arteries.Thereason
why
thepresence ofhematoma alters the situation withrespect
totiming
is because such hematoma constitutes aspace-occupying
mass,which may increase insize
owing
to osmoticattrac¬tion of fluid. Since this mass can be removed
surgically,
its removal isusually highly
beneficial and this benefit islikely
to begreater
thanthe dis-advantage
ofpossibly increasing
spasm.Fig. 1..Patient in position with the scalp flap marked and the collar incision for carotid exposure already made.
The patient is lying on her back with her head turned 45°
to the left.
Operation
iscarried
out underhypothermia, using
atemperature
of about 84° F. attainedby
means of a
cooling
blanket.Hyperventilation
and the intravenous administration of urea or mannitolare also used to shrink the brain and allow maximum exposure with minimum retraction. The carotid arteries are
exposed
in the neck for intra¬cranial
operations
on carotid and anterior com¬municating
aneurysms, but not forprocedures
onmiddle cerebral aneurysms in which a
Mayfield clip
can beapplied
to the middle cerebralartery
itself fortemporary
occlusion. As soon as the aneurysm has beenobliterated, re-warming
iscommenced and
hyperventilation
is discontinued.Papaverine
isapplied locally
to the vessels inproximity
to the aneurysm. Some ofthe features ofa
procedure
carried out for the control of an aneurysm of theright
internal carotidartery
areillustrated in
Figs.
1-3.Case Material
The case material
presented
in this communica¬tion was that seen over a
period
of seven yearsFig. 2..Viewobtained withtherightfrontalloberetracted to expose (from.left to right) the right optic nerve, the internalcarotidarterywith the aneurysm projecting postero- laterally from it, and the third nerve in close lateral proximity to the aneurysm.
Fig. 3..Thesame view asthatillustrated in theprevious photograph, showing an Olivecrona clip occluding the neck of theaneurysm.
and consists of 108 cases in which aneurysms were
proved
and 69 in which subarachnoid hemor¬rhages
occurred but in which no aneurysms werefound: a totalof 177cases. With
respect
to evalua¬tion,
thepatients
have been divided into fourcategories: good.no significant
residual neuro¬logic deficit; fair.significant neurologic
deficitbut able to lead
essentially
normal lives.thatis,
they
have resumedprevious employment
ormanagement
of ahousehold;
andpoor.unable
to resume their
previous occupation.
In a fourthcategory
arepatients
who died as a result of the aneurysm no matter howlong
afteroperation
death occurred
(Table I).
There were many more women than men in this series andalthough
this is common to otherstudies,
we have anusually high percentage
ofwomen.Our
mortality
rateof23%
in agroupofsurgically
treated
patients
withruptured berry
aneurysmsmayseem
high. However,
in other studies whereonly
ideal
patients
were chosen for surgery and wherea lower
surgical mortality
rateobtains, proportion- ately greater
numbers ofpatients
died preopera¬tively
than died in this group,thereby raising
the overallmortality.
Hencethe end resultis much thesame.
TABLE I..Proved Berry Aneurysms Total108>Male28,Female80 Notsurgicallytreated. 25
Good. 2
Fair. 1
Poor. 1
Died. 21 Intracranialoperations. 78
Good. 49
Fair. 6
Poor. 5
Died. 18
Mortalityrate.23%
Carotidligationinneck. 5
Good. 2
Fair. 1
Poor. 1
Died. 1
Multiple Aneurysms
Eleven
patients
hadmultiple
aneurysms; thelargest
number of aneurysms in asingle patient
was five. At
postmortem examination,
twopatients
were found in whom
rupture
of more than one aneurysm had occurred. In twopatients,
two aneurysms were attackedintracranially
atseparate operations.
One isdoing
well and the otherisblindas a result ofvitreous
hemorrhages
which occurredat the time of theintracranial
bleeding.
In anotherpatient
two aneurysms were attacked at the sameoperation
but furtherhemorrhage
occurred fromone of the aneurysms which had been
wrapped
but not
occluded,
and thepatient
died.In this entire
series, only
thosepatients
who re-fused
operation,
or were considered unsuitable foroperation,
were not treatedsurgically. By
andlarge, they
constituted apoor-risk
group and the results in thesepatients (Tables I, II,
III andIV)
are not
representative
of the results obtainedinthenon-surgical
treatment ofruptured
aneurysms.Internal CarotidAneurysms
These involved either the
posterior
communicat-ing artery
or the bifurcation of the carotidartery,
and were the commonesttype
in this series(Figs.
4 and
5). They
sometimespresented
in associdtion with a third-nervepalsy
andoccasionally
withcontralateral hemiparesis,
butveryoftenthere were nolocalizing signs.
Patients inthis group are some¬times considered for
ligation
of the carotidartery
in the neck without
intracranial
obliteration. This method is more effective when the aneurysm is sofar
proximal
on the intracranialposition
of theartery
thatdifficulty
maybeexperienced
ingetting
around the neck of the aneurysm.
In one
patient
an internal carotid aneurysm wasobliterated
intracranially
but it was evident that this area had not been the source of the hemor¬rhage. Subsequent
vertebralarteriography
demon¬strated an aneurysm of the
posterior
inferior cere-bellar
artery.
Thispatient
refused a second opera¬tion at the time but after
moving
away from Van¬couver had a further
subarachnoid hemorrhage
and the aneurysm was
successfully obliterated.
InFig. 4..Arteriogram showingan internalcarotidaneurysm of thetype sometimes referred toas aposteriorcommunicat-
Ing aneurysm.
another
patient
awrapping procedure
was carriedout and a further mild
hemorrhage
followed sixweeks later. The carotid
artery
was then occluded in the neck and shehas since donewell. In a thirdpatient
with a third cranialnervepalsy
an internal carotid aneurysm wasligated
but atoperation
the aneurysm didnotappeartohave beencompressing
the nerve.
TABLE II..InternalCarotidAneurysms Total48,Male9,Female89
Notsurgicallytreated. 9
Good. 1
Fair. 1
Poor. 1
Died. 6
Intracranialoperations. 34
Good. 23
Fair. 1
Poor. 1
Died. 9
Mortalityrate.27%
Carotidligationinneck. 5
Good. 2
Fair. 1
Poor. 1
Died. 1
During operation,
severalpatients
with internal carotid aneurysms died because the aneurysm hadbeen
sheared off from theparent trunk, leaving
ahole in the arterial
wall,
andligation
of theartery
had been necessary to controlhemorrhage.
Whenimproved patching techniques
such as that de¬scribed
by Carton,
Heifetz and Kessler12 are em¬ployed, ligation
of theparent artery
willprobably
notoften benecessary in the future.
Thetreatmentofsomecarotidaneurysmssituated in a somewhat
postero-medial position
should be either carotidligation
in the neck alone or carotidligation
followedby
intracranialligation
or rein-forcement.
Fig. 5..Arteriogramonthesamepatientafterobliterating
the neck of the aneurysm withan Olivecrona clip. Thiswas an uncomplicated operation, yetmarkedspasmofthecarotid arteryjust proximal to the aneurysm can be seen.
Vasospasm
will continue to cause death in somepatients
in this group until it can besatisfactorily
overcome. It is
usually present
in theartery
adjacent
to the aneurysm but it can also befairly generalized throughout
the intracranial arteries and is often increasedby operative manipulation during ligation
of the aneurysm. Its exact cause isnot
known,
butit isprobably
aprotective
mechan¬ism induced
by
blood in thecerebrospinal
fluid orby
the aneurysmitself,
and is accentuatedby operative
maneuvers; inbrief,
it is a result of acombination offactors known and unknown. What¬
ever the cause,
postoperative
deaths are attributedmore often to vascular spasm than to any other factor.
Anterior Cerebral.Anterior Communicating Aneurysms
In four
patients
in this group(Table III) wrapping procedures
werecarriedout tostrengthen
and
protect
the walls of aneurysms which seemedtoo
large
to obliterate. Muscle was used in the earlier cases butrecently
I have usedmethacrylate
as described
by
Dutton.13 Three of the four aredoing
well. One diedfollowing
recurrent hemor¬rhage
afewdays
later afteroperation.
Ihavesome-TABLEIII..AnteriorCerebral.Anterior Communica-
ingAneurysms Total37,Male12,Female 25
Notsurgicallytreated.All 8 died Intracranialoperations
Good.. 18
Fair. 2
Poor. 2
Died.. 7
Mortalityrate.24%
Fig. 6..Marked vasospasm associated with an anterior communicating aneurysm before operative intervention.
times
placed
aclip
across the aneurysm at a site other than the neck of the aneurysm if itappeared
that
clamping
of the neck(i.e.
near theparent
artery)
wouldjeopardize
thepatency
of the anterior cerebral arteries. One of the fourpatients
mentioned above did well after
operation
but suffered a furtherhemorrhage
at home as'a result ofrupture
of the aneurysmproximal
to theclip.
In similar situations I now
usually
reinforce the whole aneurysm withmethacrylate.
However,
thegreatest
difficultiesexperienced
inthis group of 37
patients (Table III)
were relatedto vasospasm, and
operation
isusually
deferred whenthe clinical and/orarteriographic findings
aresuggestive
of vasospasm(Figs.
6 and7).
The blood pressure is held at a levelapproximately
20%
below thepatient's
normalsystolic
pressure until the clinical status hasimproved,
unless re¬current
hemorrhages
indicate that there is lessdanger
inoperating.
It is in thisparticular
group that the team
approach
affordedby
the second neurosurgeon andspecialized nursing
facilities has been most
helpful
and successful.Middle Cerebral Aneurysms
More often than in othervessels middle cerebral aneurysms are associated with localized
neurologic deficit,
characterizedby varying degrees
of hemi-paresis,
andoccasionally,
when the dominant hemi¬sphere
isinvolved,
thepatient
is alsodysphasic.
Two
patients
in this group of 20(Table
IVandFig. 8)
had not had recent subarachnoid hemor¬rhage
but one had suffered a serioushemorrhage
someyears
previously
andhisaneurysmwasjudged
to have increased in size inthe interim.
In addition to the
patients
included in the fore¬going tables, during
this seven-yearperiod
I en¬countered two
patients
with basilar aneurysms, both of whom died withouthaving
hadoperative intervention,
and onepatient
who hadan aneurysm of theposterior
cerebralartery.
In this lastpatient,
Fig. 7..Anexample ofdiminishedvasospasm in thesame
patient asFig. 6 followingobliteration of the aneurysm. Fig. 8..Atypical aneurysm atthe trifurcation of the left middle cerebral artery.
TABLE IV.-MIDDLE CEREBRAL ANEURYSMS
Total 20, Male 5, Female 15 Not surgically treated.
Good..6 Died.5
Intracranial operations..14 Good.8
Fair.2 Poor.2 Died.2 Mortality rate-14%
the posterior cerebral artery was ligated just proxi- mal to the aneurysm with very little subsequent neurologic deficit.
Sui.1.cINom HEMORRHAGE WITHOUT DEMONSTRATED ANEURYSMS
In this group of patients with subarachnoid hemorrhage but without demonstrated aneurysm, the mortality rate was 30%. At postmortem ex- animation only rarely were very small discrete aneurysms found and in most cases the source of the bleeding was not revealed.
TABLE V.-SUBARACHNOID HEMORRHAGE WITHOUT DEMON- STRATED ANEURYSMS
Total 69, Male 24, Female 45 Conservativetreatment..66
Good.39 Fair.4 Poor.4 Died.19 Mortality rate-30%
Surgicallyexplored.
Good..3 -Died.1
There are two theories as to the mechanism of subarachnoid hemorrhage without demonstrable source. One is that the aneurysm bleeds and then becomes thrombosed, in which case the patient theoretically should survive. The second theory, which postmortem examination tends to support, is that a small aneurysm actually destroys itself during the* bleeding and the hole seals itself off.
Microarteriography to demonstrate vessels in- visible to standard carotid arteriography is in the process of development, but whether such lesions are amenable to surgical attack with our present surgical techniques is not yet clear.
In the last three patients in Table V, in whom exploration was carried out because aneurysms were thought to have been demonstrated arterio- graphically, no aneurysm was found at operation.
DIscussIoN
The results of any form of treatment depend upon - many factors. The overall mortality rate of 23% for the group subjected to intracranial surgery seems high, but this is due in part to the policy that every patient was operated upon whose chances of survival were considered to be greater with surgical intervention than without.
In my experience, the influence of age, presence and degree of vascular hypertension, severity of hemorrhage and degree of vascular spasm is the same as that described by Botterell et al.14 except that the chronological age of the patient seems less important than is sometimes stated. For example, one patient, aged 70, had successful obliteration of an anterior communicating aneurysm: he was exceptionally healthy and had no evidence of atherosclerosis in either cerebral or other vessels.
In other words, the health of the vessels is more important than the chronological age of the patient.
The patients least suitable for surgical treatment are often those least suitable for an aggressive hypotensive regimen, but the judicious induction of moderate hypotension is a valuable adjunct in the management of these patients.
There is no single ideal intracranial approach to any particular type of aneurysm. A consideration of the various approaches has been omitted from this discussion because each neurosurgeon will use the approach that is most suitable for him.
Specific ways in which present results of treat- ment can be improved have been mentioned, but the most important lesson I have learned concerns the value of the team approach in which a second surgeon helps in the management of the patient, well-trained nurses are on hand in the ward and in the operating room, and good anesthesia has been assured. The results that can be achieved with techniques now generally available can be quite en- couraging and rewarding.
SUMMARY
The results of treatment of 177 patients including 108 patients with proved intracranial aneurysms are reported. The overall mortality rate among 78 pa- tients who had intracranial operations was 23%.
A concerted team approach is advocated in the management of each patient in order to achieve maxi- mum benefit from the methods of treatment at preseilt generally available.
I wish to thank Drs. F. A. Turnbull, P. 0. Lehmann, J. W. Cluff and G. B. Thompson for their help in the treatment of the patients referred to in this report.
REFERENCES
1. McKlssocK, W., PAINE, K. W. E. AND WALSH, L. S.:
J. Neurosurg., 17: 762, 1960.
2. PARKINSON, D.: Ibid., 12: 565, 1955.
3. DUNSMORE, R. H. AND POLCYN, J. L.: Ibid., 13: 165, 1956.
4. BJ6RKESTEN, G. AS'. AND TROUPP, H.: Ibid., 14: 434, 1957.
5. MIJLLAN, S.: Induced thrombosis in an aneurysm, paper presented at the Harvey Gushing Society Meeting, Los Angeles, April 20-22, 1964.
6. GALLAGHER, J. P.: J. Ncurosurg., 21: 129, 1964.
7. LUESSENHOP, A. J. AND VELASQUEZ, A. C.: Ibid., 21: 85, 1964.
8. USHLEIN, A. et al.: Ibid., 19: 237, 1962.
9. MACCARTY, C. S., MICHENFELDER, J. D. AND UIHLEIN, A.:
Ibid., 21: 372, 1964.
10. KUHN, R. A.: Ibid., 17: 955, 1960.
11. PooL, J. L.: Ibid., 19: 378, 1962.
12. CARTON, C. A., HEIPETE, M. D. AND KESSLER, L. A.: Ibid., 19: 887, 1962.
13. DUTTON, J.: Brit. Med. .T., 2: 597, 1959.
14. BOTTERELL, E. H. et al.: .T. Neurosurg., 15: 4, 1958.