aneurysm is a fairly common incidental finding at postmortem examination,
with a prevalence ranging from 1 to 6 percent among adults in large
autopsy series. Many of these aneurysms, however, are very small, and the
prevalence of incidental intracranial aneurysms among adults undergoing
cerebral angiography is between 0.5 and 1 percent.
aneurysms remain asymptomatic until they rupture and cause a subarachnoid
Some of them grow to a
large size and compress the
neighborhood nerves and present with
Saccular (Berry) aneurysms:
Approximately 85% of
all spontaneous hemorrhages into the subarachnoid space arise from rupture
of saccular aneurysms at the base of the brain. Such aneurysms are not
congenital, but develop during the course of life. Cerebral aneurysms
almost never occur in neonates and they are also rare in children. In
those exceptional cases, there is usually a specific underlying cause for
the aneurysm, such as trauma, infection or connective-tissue disorder.
The majority of
intracranial aneurysms (80 to 85 percent) are located in the anterior
circulation, most commonly at the junction of the internal carotid artery
and the posterior communicating artery, the anterior communicating-artery
complex, or the trifurcation of the middle cerebral artery.
Aneurysms of the
posterior circulation are most frequently located at the bifurcation
of the basilar artery or the junction of a vertebral artery and the
ipsilateral posterior inferior cerebellar artery.
intracranial aneurysms, usually two or three in number, are found in
20 to 30 percent of patients. In rare cases, as many as 13
intracranial aneurysms have been detected in a patient.
cerebral system 36%
3. Middle cerebral
basilar system 5%
It is largely unknown
why only some adults develop aneurysms at arterial bifurcations and most
do not. The once popular notion of a congenital defect in the muscle layer
of the wall (tunica media) being a weak spot has not been accepted now.
Any defect in the muscle layer is located not at the neck of the aneurysm,
but somewhere in the wall of the aneurysmal sac.
A role of acquired
changes in the arterial wall is likely because hypertension, smoking and
alcohol abuse are risk factors for SAH in general. It may well be the
influence of these factors that leads to local thickening of the intimal
layer ( ‘intimal pads') in the arterial wall, distal and proximal to a
branching site, changes that some investigators regard as the earliest
stage in the formation of aneurysms. The formation of these pads, in which
the intimal layer is inelastic, may cause increased strain in the more
elastic portions of the vessel wall. Also, structural abnormalities in
structural proteins of the extracellular matrix have been identified in
the arterial wall at a distance from the aneurysm itself.
Aneurysms arising from
the intracranial arteries are much more common than those arising from
extracranial arteries of similar size. One possible reason for this
discrepancy is that as compared with their extracranial counterparts,
intracranial arteries have an attenuated tunica media and lack an external
elastic lamina. On microscopical examination, the typical saccular, or
berry, aneurysm has a very thin tunica media or none, and the internal
elastic lamina is either absent or severely fragmented. Thus, the wall of
the aneurysm is generally composed of only intima and adventitia, with
variable amounts of fibrohyaline tissue interposed between these two
intracranial aneurysms, especially those that rupture, have an irregular
appearance, with one or more daughter sacs and variable wall thickness.
The point of rupture is generally in the dome of the aneurysm.
intracranial aneurysms are much more common than has generally been
appreciated. According to several epidemiologic studies, 7 to 20 percent
of patients with aneurismal subarachnoid hemorrhage have a first or second
degree relative with a confirmed intracranial aneurysm. The familial
aggregation of intracranial aneurysms was first described in 1954 by
Chambers et al. Considerable evidence supports the role of genetic factors
in the pathogenesis of intracranial aneurysms.
Recent studies have
also indicated that the familial aggregation of intracranial aneurysms is
not a matter of chance. Among first-degree relatives of patients with
aneurismal subarachnoid hemorrhage, the risk of a ruptured intracranial
aneurysm is approximately four times higher than the risk in the general
In most families with
intracranial aneurysms, only two or three members are known to be
affected, and the inheritance pattern is unclear. The two main lines of
evidence are the association of intracranial aneurysms with heritable
connective-tissue disorders and their familial occurrence. Of the numerous
heritable connective-tissue disorders that have been associated with
intracranial aneurysms, the most important are autosomal dominant
polycystic kidney disease, Ehlers–Danlos syndrome type IV,
neurofibromatosis type 1, and Marfan's syndrome. It is not known to what
extent these specific heritable disorders are present in the population of
patients with intracranial aneurysms.
As compared with
sporadic intracranial aneurysms, familial aneurysms rupture at an earlier
age, may be smaller when they rupture, and are more often followed by the
formation of a new aneurysm.
Affected siblings are
often in the same decade of life at the time of the rupture.
Of the various
environmental factors that may confer a predisposition to aneurismal
subarachnoid hemorrhage, cigarette smoking is the only factor that
has consistently been identified in all the populations studied, and it is
also the most easily preventable. The estimated risk of an aneurismal
subarachnoid hemorrhage is approximately 3 to 10 times higher among
smokers than among nonsmokers. In addition, the risk increases with the
number of cigarettes smoked, and patients who continue to smoke after an
initial subarachnoid hemorrhage may be at especially high risk for the
development of a new aneurysm.
It is unclear how
cigarette smoking affects the development of aneurysms, but several
hypotheses have been proposed. Cigarette smoking has been shown to
decrease the effectiveness of 1-antitrypsin,
the main inhibitor of proteolytic enzymes (proteases) such as elastase,
and the imbalance between proteases and antiproteases in smokers may
result in the degradation of a variety of connective tissues, including
the arterial wall. In support of this hypothesis is the observation that
patients with a genetically determined 1-antitrypsin
deficiency may also be at increased risk for the development of
is the most frequently studied risk factor for the development and rupture
of intracranial aneurysms. Several studies have shown that hypertension is
associated with an increased risk of aneurismal subarachnoid hemorrhage,
as well as unruptured intracranial aneurysms. Although the data are
inconsistent, taken together they suggest that hypertension poses a risk
of aneurismal subarachnoid hemorrhage, but probably not as high a risk as
that associated with cigarette smoking.
The incidence of
aneurysmal subarachnoid hemorrhage, unlike other types of stroke, is
higher among women than among men. Before the fifth decade of life,
however, aneurismal subarachnoid hemorrhage occurs more frequently in men,
suggesting the role of hormonal factors.
The use of low-dose
oral contraceptives by premenopausal women does not increase and
may even decrease the risk of subarachnoid hemorrhage.
The risk of
aneurismal subarachnoid hemorrhage is lower among postmenopausal women
receiving hormone replacement therapy than among postmenopausal women not
receiving such therapy, but not as low as the risk among premenopausal
women. These data suggest that premenopausal women have a low risk of
aneurismal subarachnoid hemorrhage, postmenopausal women have a relatively
high risk, and postmenopausal women receiving hormone-replacement therapy
have an intermediate risk.
level of alcohol consumption is an independent risk factor for aneurismal
subarachnoid hemorrhage. Recent, heavy use of alcohol (binge drinking) in
particular appears to increase the risk of subarachnoid hemorrhage.
The data on
hypercholesterolemia as a risk factor for aneurismal subarachnoid
hemorrhage are inconsistent.
Other causes of
Infected tissue debris
entering the blood stream may lodge in the wall of cerebral arteries and
lead to aneurysmal dilatation. The traditional term`mycotic aneurysms'
refers only to fungi and should perhaps be discarded; after all, bacterial
endocarditis is more common as an underlying condition than aspergillosis.
Aneurysms associated with infective endocarditis are most often located on
distal branches of the middle cerebral artery, but 10% of these aneurysms
develop at more proximal sites, and rupture of a septic aneurysm causes an
intracerebral hematoma in most patients, but some have a basal pattern of
hemorrhage on CT that is very similar to that of a ruptured saccular
Septic aneurysms in patients with
aspergillosis are usually located on the proximal part of the basilar
or carotid artery. Rupture of such an aneurysm causes a massive SAH in the
basal cisterns, indistinguishable from that of a saccular aneurysm.
Aspergillosis is difficult to diagnose, but should particularly be
suspected in patients undergoing long-term treatment with antibiotics or
children may develop cerebral aneurysms secondary to generalized
arteriopathy. In HIV-infected adults, aneurismal SAH can also be
intracranial tumors: Aneurysms associated with tumor are
usually incidental. It is suggested that neoplasm increases local blood
flow which predispose to aneurysms. Some (meningoma) may have dysgenetic
factors. Hormone factors are suggested because of high frequency of
pituitary adenoma with aneurysms.
Cerebral metastases may in
exceptional cases infiltrate the wall of an intracranial artery, and thus
cause an aneurysm to develop, even >1 year after operation on the primary
include radiation therapy, acrylate applied externally for microvascular
decompression and operation for a superficial temporal artery-middle
cerebral artery bypass, with the aneurysm at the site of the anastomosis.
Asymptomatic Intracranial Aneurysms:
The discrepancy between
the prevalence of incidental intracranial aneurysms at autopsy and the
incidence of aneurismal subarachnoid hemorrhage indicates that most
aneurysms never rupture. With the widespread use of computed tomographic
scanning and magnetic resonance imaging, many unruptured asymptomatic
intracranial aneurysms can now be detected.
The natural history of
such aneurysms is incompletely understood, but all the large studies have
reported annual rupture rates of 0.5 to 2 percent.
The rate of rupture
increases with the size of the aneurysm but appears to be unrelated to the
age or sex of the patient or to the presence or absence of hypertension.
Data suggest that only intracranial aneurysms that are 10 mm or larger in
diameter carry a significant risk of subsequent rupture, but there is
still considerable controversy about the size below which the risk of
rupture is negligible.
The natural history of
asymptomatic intracranial aneurysms is not well defined, and the benefits
of screening have never been quantified. Screening for asymptomatic
intracranial aneurysms appears to be warranted, because aneurismal
subarachnoid hemorrhage has a dismal prognosis, whereas the treatment of
most asymptomatic intracranial aneurysms is associated with a fairly low
rate of morbidity (less than 5 percent) and mortality (less than 2
Screening has been
suggested for patients at high risk for the development of an aneurysm.
The two groups of
patients most commonly screened are those with a family history of
intracranial aneurysms, and
those with autosomal
dominant polycystic kidney disease.
In the absence of any
clinical feature or biologic marker that can identify persons in whom
intracranial aneurysms are most likely to develop, screening is generally
recommended for asymptomatic members of families with two or more affected
members. Although the extent of screening depends on the apparent
inheritance pattern in a particular family, usually only first-degree
relatives are screened. Using such a screening program, Detection rate is
about 9 percent with affected family members.
Some investigators have
suggested screening of persons even with only a single affected family
member. However, the absolute lifetime risk of subarachnoid hemorrhage for
persons with one affected first-degree relative is small (1 percent at the
age of 50 and 2 percent at the age of 70), even though they have a risk of
aneurismal rupture that is four times higher than that in the general
population. Screening is therefore not recommended for such persons.
Approximately 5 to 10
percent of asymptomatic adults with autosomal dominant polycystic kidney
disease who undergo screening are found to have saccular intracranial
aneurysms. Clustering of intracranial aneurysms has been reported in
several families with autosomal dominant polycystic kidney disease, and
screening reveals asymptomatic aneurysms in 20 or 25 percent of the
members of such families. Therefore, although screening for asymptomatic
intracranial aneurysms in patients with autosomal dominant polycystic
kidney disease remains controversial, most investigators agree that
screening is indicated for those patients who also have family histories
of intracranial aneurysms.
Dott successfully wrapped a
ruptured berry aneurysm in 1931. Dandy was the first to use a metal clip
in 1944. Since then great strides have been made. The aim of the surgical
intervention is to prevent a rebleed unless it is for hydrocephalus or
1) Duration since last bleed:
About 40% patients with ruptured aneurysms die following the first
hemorrhage.40% of survivors will rebleed in the I year.25% will rebleed in
2 weeks, with the incidence markedly decreasing over the next 6wks. Beyond
this, the rebleed rate is about 3% and death is about 2% per year The
proponents of early operation (within 3 days) believe that
overall mortality can be improved by correction of vasospasm by means of
induced vascular hypertension and cerebral perfusion in the presence of a
secured aneurysms. They also claim, irritating blood products from the
basal cisterns, which are presumed to be the cause for vasospasm can be
removed during surgery. Others feel operative manipulation offset the
Certainly it should not be delayed beyond the period of vasospasm.
2) Clinical grades & dynamic trend:
If the trend is toward a poorer grade, many believe the surgery should be
delayed. If the trend is towards a better grade, surgery may be
Generally patients above 60 years do not tolerate major cerebrovascular
procedures as well as the younger do. However each patient should be
considered with her or his prebleed life style and other factors.
4) Associated medical problems:
The systemic problems, such
as diabetes must be corrected before surgery to a reasonable level.
5) Blood pressure:
Rise in blood pressure, assumed due to elevated catecholamines, is usual
in SAH. A relentless increase may herald vasospasm and should alert the
surgeon to possible operative complications Reasonable stabilization is
advised before surgery. A stable blood pressure even on the higher side is
preferable to unstable B.P.
6) Study of the angiography:
Discussion with the radiologist helps, as also presence of the surgeon
during angiography. The site, size, walls, configuration, the number
aneurysms must be studied which will help the surgeon in deciding
the optimal approach.
Length of supraclinoid carotid gives a clue on required frontal
lobe retraction at surgery. State of cross circulations, asymmetry of
circle of Willis, anomalous anterior cerebral artery, carotid basilar anastamosis,
aplasia of one carotid or vertebral must be studied.
In the absence of ophthalmic artery, meningo orbital artery
(superior orbital branch of middle meningial artery) may be the primary
blood supply to retina and warn the surgeon while drilling the lesser
wing at surgery.
7) Local physiological & anatomical assessment:
Local pathological changes
clot, vasospasm, edema & hydrocephalus can be studied with CT and or MRI
along with angio. When hydrocephalus (10%) or hematoma (10%)requires
surgical intervention to save life, it is prudent that the aneurysms
should be secured at the same sitting.
8) Associated conditions:
a) Reports suggest that 1-2%
of aneurysms are associated with AVM and 5% of AVM are associated with
aneurysm. Ideally both must be treated in one sitting which is not
possible always. Generally, aneurysms is the assumed culprit and treated
b) Carotid stenosis (associated with aneurysms) may be treated first
if the aneurysm has not bleed. In the presence of bleed, aneurysms
gets the priority. Of course, ideal will be if both can be treated
c) In Moyamoya disease, the aneurysms represent a false one
and may disappear without surgery.
d) Aneurysms associated with tumor are usually incidental. It is suggested
that neoplasm increases local blood flow which predispose to aneurysms.
Some (meningoma) may have dysgenetic factors. Hormone factors are
suggested because of high frequency of pituitary adenoma with aneurysms.
Treatment is directed to symptomatic tumor.
e) Aortic stenosis and polycystic kidney are the only 2
congenital anomalies with correlation with aneurysms. They may have
congenital origin, but they also cause high BP which may be a factor.
f) Connective tissue diseases such as fibromuscular dysplasia, Ehler
Danlos syndrome, Marfan's, Lupus erythematosis, have sporadic association
Ehler Danlos lack collagen and the adventitia and elastic
g) Familial aneurysms and need to screen the family members are still
h) Aneurysms detected during pregnancy are treated as any other.
i) Mycotic aneurysms carries higher (80%) mortality because of their
have been reported. Septic aneurysms can be obliterated by surgical or
endovascular treatment, but they usually resolve after adequate antibiotic
j) Aneurysms in cancer patients are due to oncotic emboli, destroying the
wall of the artery. Cancer gets the priority in treatment.
k) Traumatic ones are fragile and normally at distal anterior cerebral and
intracavernous int. carotid and need surgical intervention.
9) Special Tests:
Special tests such as PET, Isotope Scan, Doppler provide information on
CBF and during temporary occlusion.
10) In case of multiple aneurysms:
Ideally all the aneurysms on
one side are attended to simultaneously.
If it is not possible, the
aneurysms which have bled, shall get the priority.
following will help to decide the aneurysms which one has bled ,
a) History and clinical exam.
Isotope scan-Rapid flow suggest perfusion; Static flow suggest infarct.
d) CT &
MRI-reveals midline shift, hemotoma and SAH.
Cerebral angiography-from displacement of vessels due to clot, from
contour of the aneurysms with nipple like protrusion, from seepage
Largest, in the absence of
above, is assumed to be the one which has bled.
The subarachnoid space:
The regular compartmentalization of the subarachnoid space allows the
surgeon to follow an orderly pattern of dissection. The key landmark
is the junction of the several cisterns which lies above the
bifurcation of ICA just lateral to the optic chiasm.
carotid cistern (containing the carotid and the origin of its
branches) extends anteriorly to the ant.clinoid.
sylvian cistern (containing the MCA) extends back into the sylvian
olfactory cistern (containing the olfactory tract) is above on the
base of the frontal lobe.
lamina terminalis cistern (containing the ACA, the A.COM.A and their
branches) is in the midline.
the chiasmatic cistern (containing the optic nerves, chiasm and
the pituitary stalk) is in the midline.
6. the interpeduncular cistern ( containing the P.COM arteries and
their branches, the oculomotor nerves, and many components of the
basilar artery circulation) lies beneath the carotid, and chiasmatic
cisterns. The anterior wall reaches from the medial surface of one
temporal lobe to the other.
the crural cistern
(containing the anterior choroidal artery) lies medial to the sylvian
Care must be taken with thickened bands of archnoid which cross
the origins of the middle cerebral and anterior cerebral arteries.
The optic nerve is the landmark in this region. It should be
identified early at exposure.
medially from supraclinoid ICA underneath the ant.clinoid process
(from the subdural portion in 90% and at the carotid-dural ring in 2%
and extradural portion in 8%).It runs along the inferior surface of
the optic nerve, enters the optic canal, penetrates the orbit and
curves medially above or below the nerve.
They are multiple arteries from ICA underneath the optic nerve. They
supply the pituitary stalk, ant.pituitary and part of optic nerve and
chiasm and anastomose with counterparts from the opposite ICA
and inferior hypophysial arteries from cavernous ICA.
It originates from the
inferior wall of the supraclinoid IAC just distal to the anterior clinoid
process and exits from the carotid cistern , runs medially (hidden from
the surgeon in a subfrontal approach) to enter the interpedunclar cistern
to join the posterior cerebral artery. In 10% of the patients it is absent
or hypoplastic. Its branches supply the optic chiasm and tract, mammilary
bodies, hypothalamus and inferior thalamus.
Anterior Choroidal Artery:
It arises few mms distal to P.com.artery and runs laterally, following the
optic tract posteriorly. It is duplicated in about 30% of patients. It
gives off 'uncal artery' which supplies the uncus, part of amygdala, and
anterior hippocampus. The main trunk supplies the choroid plexus and
anastomoses distally. In its course through the carotid cistern it
supplies, through perforating branches, to inferior chiasm, parts of optic
tract & globus pallidus, the genu of the internal capsule, part
of cerebral peduncle, red nucleus, the subthalamus and thalamic nuclei and
further distally, to lateral geniculate body, the internal capsule and the
optic radiations. Obviously loss of this vessel is devastating.
Middle Cerebral Artery:
The ICA bifurcates at a variable distance from the anterior clinoid. The
middle cerebral, from the origin to bifurcation is termed the
'M1'segment which gives off the superior lateral and the inferior medial
perforating branches (lenticulo-striate) at its proximal part. The
lenticulo-striate branches supply the anterior commisure, the putamen, the
lateral globus pallidus, the superior internal capsule and the head and
body of the caudate nucleus. The surgeon must look for these during
archnoid dissection. The 'M2'segment is distal to the bifurcation. In
about 20% of the patients there is a trifurcation instead of
bifurcation. The orbitofrontal, pre-frontal, angular and posterior
temporal arteries arise proximally from 'M2' and supply the cortex.
Anterior Cerebral Artery:
Anomalies are common, especially in patients with aneurysms. The 'A1'
segment extends from the carotid bifurcation to the anterior
communicating artery and the rest is termed the 'A2' segment.
Typically one A1 is
dominant. The proximal perforators postero inferiorly and distal
perforators close to the anterior communicating artery, and perforators
from the anterior communicating artery (typically from the inferior side
of the neck of the aneurysm) supply the infundibulum, optic chiasm, fornix,
internal capsule, striatum and hypothalamus. In 25% of the patients the
communicator has various anomalies.
The recurrent artery of Heubner usually arise close to A.Com.Art. from
A1 or A2 segment and runs parallel to the anterior cerebral artery
laterally along the inferior frontal lobe and at risk during resection of
the rectus gyrus. It supplies parts of caudate nucleus, the putamen, the globus
pallidus,and internal capsule.
It is the 1st branch of the subclavian and enters the transverse foramen
of C6. At C3 it turns laterally and enters the foramen at C2 and exits
through the foramen of C2 behind atlantoaxial joint and lies along the
posterior arch of C1. It penetrates the dura at foramen magnum, goes
laterally and then ventrally to join the contralateral artery to form the
In 15%, one artery is
dominant. In addition to the posterior inferior cerebellar artery and
anterior spinal artery, it gives off perforators to the to medulla and
occasional posterior spinal artery and few meningeal branches.
Posterior Inferior Cerebellar Artery:
It is quite variable. In about 10%, it is absent. In about 50% it arises
from the proximal vertebral artery. It loops along the lateral medulla and
turns superiorly to complete the caudal loop. It then passes superiorly as
a cranial loop and then crosses the cerebellar tonsil. The artery supplies
the choroid plexus of the 4th ventricle, cerebellar tonsil, vermis and
The vertebral arteries join along the anterior surface of the medulla,
close to the pontomedullary junction. The artery is deviated to the side
of the smaller vertebral artery. It extends along the ventral surface
of the pons and terminates in the interpeduncular cistern into posterior
cerebral arteries. In about 50%, the tip is at the level of the posterior
clinoid. In 15%, the labyrinthine or the internal auditory artery arises
from the basilar artery. The perforating arteries from the trunk project
posteriorly. The anterior cerebellar artery and superior cerebellar artery
are the major branches.
Anterior Inferior cerebellar Artery:
In most, it arises from the proximal basilar. Typically the right and left
arteries arise at the same level. It runs inferiorly and laterally to the
IAM. The labyrinthine artery arises from AICA in about 85% of the
patients. It also supplies the pons, middle cerebellar peduncle, flocculus,
tegmentum and cerebellar hemisphere.
Superior Cerebellar Artery:
In 85% of the patients, the left and right ones arise from the basilar as
a single trunk. At its origin, it is separated from the posterior cerebral
artery by the 3rd nerve. It supplies the superior the superior aspect of
the cerebellar hemispheres, the superior cerebellar peduncle, the dentate
nucleus and a portion of the middle cerebellar peduncle.
1) A binocular dissecting microscope with its superb
magnification, clearer stereoscopic images, and improved illumination is a
must, needless to say. It makes it possible for a smaller exposure with
less brain retraction. Micro instruments along with bipolar forceps,
lyla retractors and fine tipped suckers are essential for fine
2) Clips: Generally, shorter clips have more closing pressure,
the pressure is more near the shank.
(a) Yasargill's clips
are cross action clips and popular. Their small shank do not obscure
(b) Sugita's clips are some what similar and comes in various angles.
(c) Heifetz clips have broader wings with an internal spring action and
are preferred for thin, friable walls by some.
(d) less commonly malleable clips are used.
(e) Temporary clips differ from permanent clips with their closing
pressure not exceeding 25-40 gm.
(f) Fenestrated and the right angled ones are ideal for larger aneurysms
with a broad neck, especially at the internal carotid and basilar tree.
3) Other agents:
Protective coatings include muscle, fascia, gelatin, cotton and
synthetic agents such as methylmethacrylate, EDH adhesive (bioband) come
handy when surgeon is faced with unclippable aneurysm. Cotton is the only
one with proven effect.
click for intraoperative videos
With the exception of
distal arterial aneurysms which are rare, all the anterior circulation
aneurysms can be clipped through a pterional flap of various sizes. In
fact basilar tip aneurysms especially the ones which project above
the level of posterior clinoid can be successfully clipped trough this
zygomotomy helps in minimizing the brain retraction. Pterion is the
point where zygomatic process of the frontal bone, orbital ridge and
temporal bone meet. Pterional flap is really a modified Dandy's fronto
the lesser wing of the sphenoid should be shaved down to ant. clinoid
until the meningo orbital branch of the middle meningeal artery is
encountered. On occasions, removing the anterior clinoid helps. It is
a must, for medially projecting internal carotid artery aneurysms
(ophthalmic) to visualize both sides of the neck.
L.P. drainage, as
preferred by some, may be started at this stage (to restrict the brain
retraction) after the dural-pericranial hitch stitches. Others prefer
to open the sylvian fissure and other basal interns and let out the
CSF. L.P. drainage hinders arachnoid dissection and may injure the
Opening the sylvian
fissure is harmless, the bridging veins from the frontal lobe to
sylvian vein may be cauterized and cut so that the major vein is
Extension of the neck
at this stage further minimizes the brain retraction.
Presence of a temporal
hemtoma may warrant an approach through superior temp gyrus in middle
cerebral artery aneurysm. Some prefer this approach as a routine to
avoid brain retraction although
getting a proximal control (in case of
accidental rupture of the aneurysm) is difficult.
Similarly a small
group of surgeons approach ant. com. art. aneurysm. through an inter
approach may be, fine arachnoid dissection of
the neck, without exposing too
much of the distal artery is necessary.
Intermittent use of temp.
clips, not to exceed 10 - 15 mts each time, help in dissection.
The B.P. should kept
above normal BP during temp.occlusion to maintain adequate collateral
circulation. On occasions, it may be wise to puncture the aneurysm
(preferably with temp clips in place) to facilitate dissection.
(a) Basilar tip aneurysm
can be approached through a
zygomatico orbitotomy or a sub-temporal approach with or without
temp. lobe resection. Side of the approach depends on the projection
of the dome which is to be avoided.
It is prudent to avoid
dominant, side every thing else being equal.
b) Sub temp.approach is
well suited for post. Cerebral artery aneurysms.
(c) Vertebro basilar
aneurysms below the level of int. auditory meatus are normally
approached through a suboccipital approach. Lately, extended lateral
approach has been recommended basically to gain better exposure with
lesser retraction. The patient in park bench position, a lateral suboccipital
craniectomy is performed.
The arch of the atlas is
removed. The inter transverse process space of C1&2 exposed and
posterior root of C2 is cut to expose the vertebral artery which is
protected and the dura is opened medial to the dural entrance of the
vertebral artery. L.P. drainage at this stage helps to minimize brain
retraction. The occipital condyle is shaved to such an extent that the
dural flap falls flat over the shaven condyle, rather than getting
Aneurysms above the level of IAM are better approached through trans
tentorial approach. petrosectomy helps in minimizing brain retraction.
Lately, a new approach,
the trans petrosal approach where-in a window is made through the apex
of the petrous extra durally, has been described. This avoids brain
retraction and injuries to the cranial nerves which is almost
inevitable in posterior and postero lat. approach.
approach, the basics, such as adequate exposure and fine arachnoid
dissection of the neck before applying the clip, must be adhered to.
The temp.clips may be kept longer (20 - 30mts) in posterior
They may be saccular or
Fenestrated clip for Rt.A.com.An
Rt. P.com. art
Rt.AICA.An-transpetrous app. with 5th and 6th nerve
(a) Saccular aneurysms must
be considered for clipping these days, whatever the size is, as they are
not ideal for interventional radiology as it stands today. Broad neck,
calcification at the neck, presence of intraluminal thrombus are more
common in giant aneurysms and make clipping a difficult proposition.
Angled, fenestrated, strong and extra strong clips are required. It is
unusual that a single will suffice.
Three basic systems of clip
application are often used.
(1) Piggyback or booster clip
is a second clip placed so as to increase and reinforce the closing
pressure of the primary clip.
(2) Tandem clipping involves application of 2 or more clips across the
neck usually with short blades across the distal neck. With progressive
distal application of these clips, a neck can be fashioned and occluded.
(3) Picket fence or parallel clipping is a system wherein clips
are applied parallel to one another usually perpendicular to the plane
of neck, lined up like a picket fence. It is wise to expose the
proximal artery such as carotid or vertebral before dissection.
Temporary proximal occlusion or aspiration of the sac or the use of an
encircling silk ligature to narrow the neck may make clip occlusion
possible. Rarely hypothermia (down to 16 degree c) and cardiopulmonary by
pass in selected cases may be useful.
(b) Fusiform aneurysms
have no neck and not amenable for clipping. Excision and anastomosis with
graft is ideal. But proximal (Hunterian ligation) or trapping are more
commonly used with or without bypass.
radiology has largely
replaced the need of these measures. When such measures are contemplated
without bypass, the following pre op tests help to assess the viability of
1) Mata's test - Common carotid is compressed at bed side for 10 mts. and
the pt is examined clinically for a deficit (unreliable
2) Temp. occlusion (at surgery) for 30 mts and the pt is observed with or
without EEG. This reveals only pts who are immediately intolerant and is
of no help in the rest.
3) During angiography a cross
circulation may be assessed with contra-lateral compression. 70% of those
with giant aneurysms will show filling of opposite AC & MC and are good
candidates. 25% of them fill only AC and ligation may be considered with
4) Carotid artery pressure determinations are reliable. Both carotids are
exposed and the clamp applied. The pressure of the carotid stump distal to
the clamp is measured. If the reduction of the pressure is not more than
50% when compared to the unclamped one the procedure is safe.
5) Ideal is Xenon study with temp clamping. If the CBF is more than 40ml/mt/100gm
the procedure is safe. Less than 20 ml it is not safe. In between it is
probably safe if the reduction is less than 25%. Crutch field clamp is
Post operative care:
Absolute bed rest with head kept flat and close surveillance
of electrolytes is warranted. Some prefer to institute, 'triple H' (Hypervolemic,
hypertensive, hemodilution) treatment for 2-3 days. Anti-convulsants are
routinely given as the incidence of post op fits is next only to that of
It is wise to repeat angiogram in cases where there is doubt of complete
occlusion. If facilities available an intra operative angiogram may be
arranged. If done, brain swelling must be anticipated.
Whatever discussed above is for some one at the bottom of the learning
curve. As they go up in the curve, they form their own principles and
technique, after all, medicine is an ever changing field!!.